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A Study On The Effect Of Sri Bahusala Gudam As Naimithika Rasayana In The Management Of Industrial Hazards w.s.r. to Tamaka Swasa, K.V.Narasimha Raju, Department of Kayachikitsa, PG unit Dr.BRKR Govt. …

A Study On The Effect Of Sri Bahusala Gudam As Naimithika Rasayana In The Management Of Industrial Hazards w.s.r. to Tamaka Swasa, K.V.Narasimha Raju, Department of Kayachikitsa, PG unit Dr.BRKR Govt. Ayurvedic College, HYDERABAD

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  • 1. POST GRADUATE TRAINING AND RESEARCH UNIT DEPARTMENT OF KAYACHIKITSA Dr. B.R.K.R GOVT. AYURVEDIC COLLEGE & HOSPITAL ERRAGADDA, HYDERABAD.AFFILIATED TO Dr. N.T.R. UNIVERSITY OF HEALTH SCIENCES, VIJAYAWADA. CERTIFICATE This is to certify that the present study entitled ‘A Study On TheEffect Of Sri Bahusala Gudam As Naimithika Rasayana In TheManagement Of Industrial Hazards w.s.r. to Tamaka Swasa’, has beenconducted by Dr. K.V.Narasimha Raju, under our direct supervisionand guidance for the award of Doctor of Medicine in Ayurveda in theSpeciality of Kayachikitsa. The work is completed after a series of scientific discussions andhence, I fully recommend this thesis for acceptance. GUIDE Dr. M.L.NAIDU M.D. (AY) Reader, Post Graduate Unit,Date: Kayachikitsa Department, Dr. B.R.K.R. Govt. Ay. College,Place: Erragadda, Hyderabad. 1
  • 2. ACKNOWLEDGEMENTS I owe an enormous debt to my parents who have been a constantpsychololgical support and backup throughout the research work. I would like to extend special thanks to Dr.M.S.Rao, Principal, Dr. B.R.K.R.Govt. Ay. College, Hyd., for his careful supervision and liberality towardsP.G.Scholars and permitting to attend National and International Seminars, thusenabling us to update our knowledge regarding the system and subject. I express my profound gratitude to our professor Dr. Prakash Chandra,Professor & H.O.D., P.G.Unit, K.C.Dept., for his valuable cooperation andsuggestions. I had the privilege of working under Dr.V.V.S.Rama Sastry, Retd. Professor,P.G. Unit, K.C. Dept., and it gives me great pleasure for experiencing hisunprecedented and uncompromising principles that guided me in shaping the mode ofstudy at the very primary stage of hypothesis. I pay my humble and deep sense of respect to Dr.M.L.Naidu, my Guide &Reader, P.G. Unit, K.C. Dept, who have been a source of constant inspiration andencouragement to me for the successful completion of this work. I’m grateful for the critical reviews provided by Dr.V.Vijaya Babu, Asst.Professor, P.G. Unit, K.C. Dept., and making everything worthwhile, thus impartingthe qualities of approachability and readability to my work. He also provided adviceat the page-proof stage. I am grateful to Dr.Ramalingeshwar Rao, lecturer and technical assistant, forhis forbearance and for checking factual accuracy as well as balance in the text. 2
  • 3. I’m fortunate enough to have friends like D.Dinesh Chakravarthy,Dr.L.Srinivas and Miss.Sana, for their inestimable and invaluable help. I am indebtedto them for my life time as they were instrumental in initiating me into thechallenging task and they continued to keep my morale high all through this periodwith their support and guidance. I convey my special thanks to the staff of General library and Research libraryof the college and Hospital, for their valuable cooperation. It gives me great pleasure in expressing my deep sense of gratitude toMr.C.S.R.Prabhu, Deputy Director of National Informatics Centre (NIC),Mr.K.V.Rao, Social Scientist, PCB, Hyd, for their encouragement and expertise inshaping, collation and illustration regarding my work thus giving an inspirational startto this challenging and exciting task. It’s my pleasure to convey thanks to Mr.Bhatra, G.M and Mr.Rambabu, ChiefOfficer in ‘Surya Vansh’ cotton mills at Bhongir, and the ANM staff of the Healthdept. in Panchayat Office of IDA, Bollarum, without whom the work wouldn’t havebegun. I wish to express my thanks to the workers in Cotton and Chemical Industrieswho have been the skeletal frame work to my thesis. At last, to the many persons who have already helped, I send my sincerethanks. Dr. K.V. NARASIMHA RAJU 3
  • 4. INDEXS.No TITLE Pg. No I INTRODUCTION 1 II HISTORICAL REVIEW 3III LITERARY REVIEW 1 Rachana Shareera 9 2 Kriya Shareera 23 DISEASE REVIEW 1 Definitions & Derivations 40 2 Prevalence of Asthma 42 3 Nidana 44 4 Purva Roopa of Swasa 67 5 Roopa of Tamaka Swasa 69 6 Tamaka Swasa Bhedas 74 7 Samprapti 77 8 Vyavacchedaka Nidana 88 9 Investigations 92 10 Upasaya-Anupasaya 93 11 Sadhya-Asadhya 94 12 Upadrava 95 13 Arista Lakshanas 96 14 Tamaka Swasa Chikitsa 97 15 Pathya-Apathya 103 DRUG REVIEW & CRITERIA 105 4
  • 5. IV CLINICAL STUDY 1 Aims & Objectives 126 2 Material & Materials 127 3 Observations & Results 137 4 Discussion 161 5 Conclusion 165 6 Summary 166V REFERENCES 168VI BIBILIOGRAPHY 173VII APPENDIX 1 Case Sheet 177 2 Master Chart 183 5
  • 6. LIST OF TABLESS.No TITLE Pg.No 1 Solubility Coefficients 31 2 Partial Pressures 31 3 Vata Prakopakara Ahara 45 4 Vata Prakopakara Vihara 45 5 Kapha Prakopakara Ahara 46 6 Other Nidana 46 7 Genes currently implicated in Asthma 48 8 Allergens 49 9 Major Causes of Occupational Asthma 52 10 Causes of OA- Grains, Flours, Plants and gums 60 11 Causes of OA- Animals, Insects and fungi 61 12 Causes of OA- Chemicals/Materials-I 62 13 Causes of OA- Chemicals/Materials-II 63 14 Causes of OA- Isocyanates and metals 64 15 Causes of OA- Drugs and enzymes 65 16 Causes of OA-Woods 66 17 Purva Roopa of Swasa 67 18 Roopa of Tamaka Swasa 69 19 Extrinsic and Intrinsic Asthma 76 20 Types of Samprapti 82 21 Upper and Lower Airway disorders 89 22 D.D of Bronchial Asthma and COPD 90 23 D.D of Bronchial Asthma and Tropical Asthma 90 24 D.D of Bronchial Asthma and Cardiac Asthma 91 25 Pathya Aahara 103 26 Data of Individual variable of all the subjects in Gr.A 130 27 Data of all variables of individual subject in Gr.A 131 28 Data of Individual variable of all the subjects in Gr.B 132 6
  • 7. 29 Data of all variables of individual subject in Gr.B 13330 IgE Values of Gr.A 13431 IgE Values of Gr.B 13432 Distribution of Patients acc.to Age 13733 Distribution of Patients acc. to Sex 13834 Distribution of Patients acc. to Socio Economic status 13935 Distribution of Patients acc. to Diet 14036 Distribution of Patients acc. to Prakriti 14137 Distribution of Patients acc. to Heredity 14238 Distribution of Patients acc. to Chronicity 14339 P values of individual variables in both Groups 14440 P values of individual subjects of Gr.A 14741 P values of individual subjects of Gr.B 14942 Means and Percentage diff. of individual selected variable in all 151 subjects of Gr.A43 Means and Percentage diff. of all the selected variables in individual 153 subject of Gr.A44 Means and Percentage diff. of individual selected variable in all 155 subjects of Gr.B45 Means and Percentage diff. of all the selected variables in individual 157 subject of Gr.B 7
  • 8. LIST OF GRAPHSS.No TITLE Pg.No 1 Distribution of Patients acc. to Age 137 2 Distribution of Patients acc. to Sex 138 3 Distribution of Patients acc. to Socio Economic status 139 4 Distribution of Patients acc. to Diet 140 5 Distribution of Patients acc. to Prakriti 141 6 Distribution of Patients acc. to Heredity 142 7 Distribution of Patients acc. to Chronicity 143 8 Means of individual selected variable in all subjects of Gr.A 152 9 Percentage diff. of individual selected variable in all subjects of Gr.A 152 10 Means of all selected variables in individual subject of Gr.A 154 11 Percentage diff. of all selected variables in individual subject of Gr.A 154 12 Means of individual selected variable in all subjects of Gr.B 156 13 Percentage diff. of individual selected variable in all subjects of Gr.B 156 14 Means of all selected variables in individual subject of Gr.B 158 15 Percentage diff. of all selected variables in individual subject of Gr.B 158 16 Internal Comparison between individual parameters of two Groups 159 8
  • 9. INTRODUCTION Ayurveda, the science of life is the supreme theory with unerring factors basedon Tridosha and Panchabhautic principles. This system, with its eight divisions encompassed every angle of a person’shealth, ailments and treatments which were highly comprehensive. Ayurveda, thoughancient, still contemporary and potential enough in dealing the diseases of presentday. This system of medicine has got its own modes of handling a pathologicalcondition where by the consequences are absolutely desirable. Over the centuries, the etiology of a particular disease has been enrolling widenumber of factors rendering incurable status to that disease. Tamaka swasa is thedisease of such status which is though manageable at the early onset, still not curableat the chronic stage (after 1 year duration), as the term ‘Yapya’ suggests to itsprognosis. Swasa, a disease of antiquity, also was considered for treatment ever since itoriginated. In Vedic period the efforts started to keep the respiration unimpairedthrough Prayers and Mantras. Later, in Samhitas the treatment methods wereelucidated. The significance of this disease is magnified by the high incidence andfrequency of recurrence. Bronchial Asthma is a global health problem that claimsabout a million unnecessary deaths each decade. The prevalence appears to haveincreased continuously since the 1970s and it now affects 4-7% of people world wide.As a number of substances and conditions that precipitate asthmatic attacks have beenidentified, it is reasonable to conclude that no single mechanism or mediator isresponsible for an asthmatic attack. Tamaka swasa, the disease from the past, has incarnated as an IndustrialHazard in recent decades with the name Occupational Asthma (OA). This is due to 9
  • 10. the Industrialization in the developing countries where an additional causative factorin the form of Industrial Pollutant has been implicated. Such recent advances in a disease were expected long back, as explained in theAyurvedic literature, the concept of Janapadodhwamsa, an Epidemic of disease.Hence in the present study Tamaka Swasa is being dealt as an Occupational Asthma,which results from industrial pollutants. Despite increased scientific knowledge and improved therapeutic options, thedisease continue to cause significant morbidity and mortality. In an attempt to ascertain the therapeutic and Rasayana effects in the asthmaticattacks related to Industrial work places, a safe and scientifically approved drug ‘SriBahusala Gudam’ is considered for research with appreciable results. 10
  • 11. HISTORICAL REVIEW Swasa vyadhi reveals its evolution through ages, with origin in Vedic age,existence in medieval age and persistence in modern age. Over the centuries differentcausative factors have been attributed, which proved potential in stimulating thisdisease. The history of Swasa vyadhi is now reviewed referring back to its antiquity.VEDAS:‘SWASA’ as a disease or as a symptom received no contribution from Vedas orKausika Sutra, and the term was completely obscure.In Antharvana Veda1, a disease nearer to the condition of Swasa Roga, called as‘BALASA’ was referred many times2.The commentary by “SAYANACHARYA’ explains Balasa as a Sleshma Rogaassociated with Kasa & Swasa and causing depreciation of Bala.Balasa is described as Balamasyatiti balasah i.e., that which takes away Bala3.Asthi, Parva, Sandhi, Hridaya and Anga of the body are the sthanas of Balasa4.Balasa is mentioned as upadrava of Jwara5.Different prayers were mentioned in Atharvana Veda which aims at alleviating Balasafrom the body.Different remedies were given for this condition like ‘Anjanam’6, ‘Cheepudru’7,‘Balasa nasani8, ‘Jangida’9. 11
  • 12. PURANAS:Garuda Purana allotted an entire chapter for the description of Swasa.The disease has been mentioned in Vishnupurana10, Bhagavata purana11, ShankaraBhasya on Bhagawatgeeta12 and Garga samhita.Swasa is described as blowing of bellows, in Kadambari Purana13.Swasa is described as a symptom in serious diseases in Harsha Charitra, Kausika14and in Brihat Samhita15.It is mentioned as one of the symptoms in Sannipata Jwara, in Kausika.It is mentioned as a complication of Rajayakshma in Harsha Charitra, Kautilya’sArthasastra16 and Kamandakiya Neetisatra.SAMHITAS & SANGRAHAS:The disease has been described by most of the authors of samhitas like – Charaka,Susruta, Hareeta, Kashyapa etc, and also by Sangraha grandhas.(The word Balasa is used to denote ‘Kapha’ in Ayurveda. It is used by Vaghbhata todenote Sandhigata Netra Vyadhi, and a complication of Jwara).MODERN:Asthma is not a recent condition, but a disease of antiquity.‘Asthma’ is a Greek word derived from the verb ‘aazein’, meaning to exhale withopen mouth, to pant, to gasp, or a sharp breathe.The word first appeared in Homer’s Iliad. 12
  • 13. HIPPOCRATES (460-367 B.C), Father of Medicine, was the first to use the term inreference to the medical condition – in his text ‘Corpus Hippocraticum’.AURELIUS CORNELIUS CELSUS (? 1st Century B.C/A.D) says:-When the difficulty of breathing is moderate and not suffocating it is calledDyspnoea, when it is more vehement so that the breathing is more sonorous andwheezing, it constitutes Asthma, when breathing can only take place in an uprightposition it is termed as Orthopnea.ARETAEUS of Cappadocia (81-138 A.D) described well about Bronchial orSpasmodic Asthma.GALEN (130-200 A.D) wrote much about Asthma, noting that it is caused by partialor complete bronchial obstruction.In 1190 A.D MOSES MAIMONIDES a Medieval ‘Rabbi’ Philosopher physicianwrote a treatise on asthma for his royal patient, prince Al-Afdal, describing itsprevention, diagnosis and treatment.The term Asthma has been in use in English since 14th century. However in 1390, wefind the word ASTHMATICUS.In 1552 the famous physician JEROME CARDON (1501-1576) of Pavia was calledespecially from Italy to Edinburgh to treat John Hamilton who was the Arch Bishopof St.Andrews and was suffering from Asthma for 10 yrs. He had been cured – orrelieved-by diet, regular exercise and sleep, and by prohibiting the use of feathers inhis bed.JEAN BAPTISTE VAN HELMONT, a Belgium Physician during the 16th Century,wrote that asthma originated in the pipes of the lungs.In 1618 the 1st edition of the London Pharmacopoeia mentioned the saying of BENMESUE that – “Let persons troubled with asthma take two drachms of dried andpowdered fox lung in their drink”. 13
  • 14. GALEN said that many cure Asthma with owl’s blood given in wine.In 17th Century, BERNARDINO RAMAZZINI, Father of Occupational Medicine,noted a connection between Asthma and organic dust. The modern history of the disease begins with THOMAS WILLS (1614-1715), who was the first to suggest tentatively that the disease mainly constitutes thespasm of bronchial muscles.SIR JOHN FLOYER in a ‘Treatise on Asthma’ published in 1698, appears to havebeen the first to mention the contraction of the muscle fibers of the bronchi.In 1707 FRIEDRICH HOFFMANN (1660-1742) was one of the first to describeConvulsive Asthma with dropsy.In 1769 MILLAR published a treatise on Asthma and whooping cough.In 1806 JEAN NICOLAS DESMARETS was the first to describe dyspnoea of effort.In 1810 SAMUEL HAHNEMANN described the use of Ipecacuanha for Asthma.In 1844 ALFRED WILHELM VOLKAMANN demonstrated that stimulation of thevagus nerve produces constriction of bronchi.In 1851 F.A.ZENKER described colourless needles like crystals of phosphate foundin the sputum of patients with bronchial Asthma and allied conditions.In 1853 CHARCOT & LEYDEN (1869) noted the same crystals and hence known as‘Charcot – Leyden Crystals’.In 1860 HENRY HYDE SALTER (1823-1871) called attention to emanations fromrabbits, cats, dogs etc., as cause of Asthma. 14
  • 15. Found in Egypt in 1870s, the ‘GEORG EBERS PAPYRUS’ contains a writtenevidence of Asthma.In 1873 CHARLES HARRISON BLACKLEY (1820-1900) demonstrated that pollencan cause Asthma, Catarrh and skin reactions in sensitive subjects.In 1883 CURSCHMANN described the presence of respiratory epithelial cells in thesputum of Asthma patients.In 1876 EDVARD HEINRICH HENOCH (1820-1910) described dyspeptic Asthma.In 1902 CHARLES HOBER RICHET introduced the term “Anaphylaxi”.In 1902 FORTIER gave the first satisfactory description of ‘Anaphylaxis’.In 1907 BELA SCHICK introduced the term ‘Allergy”.In 1910 JOHN AUER & PAUL A.LEWIS showed that in true anaphylaxis in guineapig’s death is due to asphyxia caused by tetanic contraction of the bronchial musclespreventing any air from entering the lungs.In 1910 SAMUEL JAMES MELTZER suggested that the mechanism or productionof an attack of asthma was similar and thus included among allergic disorders.In 1917 JOHN SCOTT HALDANE introduced modern Oxygen therapy.In 1925 WILLIAM STORMVAN LEEUWEN, a Dutch Physician (1882-1933)demonstrated the benefit of high altitudes in cases of Asthma.In 1929 PHILIP DRINKER invented Iron Lung.In 1931 BARTOSCH, FIELEBERG AND BEGEL showed that when lungs werechallenged there was a release of histamine. 15
  • 16. In 1940 KELLAWAY and TRETHWIE showed the release of a substance now calledas Slow Reacting Substance in anaphylaxis (SRS-A).The United States bureau of labour in 1956, listed over 100 occupations related toasthma, while in France in 1960, the first occupational asthma to be recognized wasthat associated with handling Penicillin17.In 1962 NAYLOR has drawn attention to the presence of compact clusters ofcolumnar epithelial cells or creola bodies in the sputum of Asthmatics.In 1968 GELL & COOMBS described the possible roles of immunologicalmechanism in Asthma. The prevalence and severity of Asthma have increased in recent years. Amongthe factors implicated in this ‘epidemic’ are indoor and outdoor airborne pollutants.Urbanization with its high levels of Industrial pollutants, vehicle emissions andwesternized life style parallels the increase in Asthma in most industrializedcountries18. 16
  • 17. RACHANA SHAREERA The Swasa Kriya is performed by the cumulative effect of different organsincluded under Swasana samsthana. Pranavaha Srotas is the one which involves allthese organs and considers Pranavata and Udanavata for their functioning. In relation to the respiratory system the Pranavata, located in Murdha19 holdsthe higher centres in the brain like Tractus solitarius, Nucleus ambiguus and Nucleusretroambiguus and receives the stimulation through the Glossopharyngeal and Vagusnerves from Phraynx, Larynx, Lungs and Diaphragm which are responsible for theregulation. Udanavata located in Urahsthana20 acts as accessory to the Pranavata inperforming the act of respiration. PRANAVAHA SROTAS 21MULA STHANA: Hridaya and Maha Srotas The structural description of pranavahasrotas involves the anatomical partsfrom Nasa, extending up to anilayanani. This explanation also needs to be understoodon modern lines to make the concept more comprehensive. The respiratory system predominantly consists of the lungs, and the passagesthrough which air passes to reach them. The passages are the nasal cavities, thepharynx, the larynx, the trachea, the bronchi & their intrapulmonary continuations.1) NASA: It is the first part of Prana vaha srotas whose cavity is divided into two, whichopen externally and are mentioned under the 9 bahirmukha srotases22.Paryayas: - Ghrana, Gandhavaha, Ghona, Nasa, Nasika etc23.Asthis present in Nasa are Tarunasthis24.Asthis of Nasa are termed as Nasa Tarunasthis by Dalhana25.Charaka mentions that the 3 bones present in Nasa are Ghonasthis26. 17
  • 18. Susrutha mentioned the presence of 8 asthis27 and one sandhi in Nasa28, and 2 asthisnear Kaninika29.Ghrana mula is the term used by charaka in the context of pratisyaya, in RajaYakshma30.Ghrana randhra is the term mentioned in Bhava prakasha in the context of Dinacharya31.Nasa puta bahirbhaga is the term used by Dalhana, commenting on susruta’s referencefor the pramana of nasa puta.Nasa nadi is the term used by susruta in the context of ‘Tala yantra’, used for salyanirharana32. Nasa Srotas is the term used by Ashtanga Hridayakara for the same33.Nasa vamsha is the term mentioned by susruta for nasal bridge, which wascommented by chakrapani as ‘Nasa asthi danda’34.There are 2 peshis35 and 6 siras in Nasa36.According to Arunadatta Ghranendriya is located in Nasa.Two Gandha vaha nadis are present in Nasa for Gandha gnana37.In Ghrana marga, on both sides there are marmas called phanas (2) which are ofardhangula pramana. They perform Gandha vahana and injury to these marma causesGandha agnanam38.NOSE:a) External Nose: It has a skeletal frame work that is partly bony and partlycartilaginous. Bones are the nasal bones, which form the bridge of the nose, and thefrontal process of the maxillae. The cartilages are the superior and inferior nasalcartilages, the septal cartilage, and some small cartilages.b) Nasal Cavity: It extends from the external nares to the posterior nasal apertures. Itis subdivided into right & left halves by nasal septum. Each half has a roof, a floorand medial & lateral walls. Each half is 5 cm in ht, 5-7 cm in length and 1.5 cm inwidth near the floor. The roof is about 7cm long and 2mm wide.c) Nasal Septum: It is the median osteocartilaginous partition between the two halvesof the nasal cavity. On each side it is covered by mucous membrane and forms themedial wall of both nasal cavities. 18
  • 19. Nasal septum has 3 parts: 1. The bony part: - Formed by the vomer, and the perpendicular plate of the ethmoid. 2. The cartilaginous part: Formed by the septal cartilage & the septal processes of inferior nasal cartilages. 3. The cuticular part: Formed by the fibro-fatty tissue covered by skin.Nasal septum has 4 Borders: Superior, Inferior, Anterior & Posterior. 2 Surfaces: Right and LeftArterial Supply: 1. Ethmoid artery 2. Superior labial branch of the facial artery. 3. Sphenopalatine artery.VenousDrainage: Venous plexus is formed in the lower part of the septum (little’s area). The plexus drains into facial vein and pterygoid venous plexus.Nerve Supply: General sensory by Trigeminal nerve. Special sensory by Olfactory nerve.Lymphatic Drainage: 1. Submandibular nodes anteriorly. 2. Retropharyngeal & deep cervical nodes posteriorly.d) Lateral wall of Nose: It is irregular owing to the presence of 3 shelf like bonyprojections called Conchae, which increases the surface area of the nose for effectiveconditioning of the inspired air.It is subdivided into 3 parts: 1. Vestibule 2. Atrium of middle meatus 3. Conchae.The skeleton of the lateral wall is partly bony and partly cartilaginous and partly madeup of soft tissue. 19
  • 20. e) Nasal Conchae: These are curved bony projections directed downwards andmedially. They are 3 in number: 1. Inferior, 2. Middle, 3. Superiorf) Meatuses of the Nose: These are the passages beneath the overhanging conchae.Each meatus communicates freely with the nasal cavity proper.Arterial Supply:1. Antero superior quadrant is supplied by anterior ethmoidal artery, posterior ethmoidal artery and facial arteries.2. Antero inferior quadrant is supplied by facial & greater palatine arteries.3. Postero superior quadrant is supplied by Sphenopalatine arteries.4. Posteroinferior quadrant is supplied by greater palatine artery.Venous Drainage: Venous drainage is mainly into facial vein, pharyngeal plexus ofveins and pterygoid plexus of veins.Nerve Supply:General Sensory: By anterior ethmoidal nerve, anterior superior alveolar nerve,posterior superior lateral nasal branches, and from pterygopalatine ganglion.Special Sensory: By Olfactory nerve.Lymphatic Drainage: To submandibular nodes, retropharyngeal and upper deepcervical nodes.2) KANTHA: This is the part where Nasa marga and Mukha marga join and get separated atits lower end.It is mentioned as one of the Dasa pranayatanas39.In the context of Garbha, it is told that the Garbhastha sishu cannot cry because ofsome factors of which kantha being filled with kapha is one40.Kantha is one of the seven parts of Mukha in the context of Mukha Rogas.PHARYNX: 20
  • 21. It is a wide muscular tube, situated behind the nose, the mouth and the larynx.The upper part transmits only air, the lower part only food, but the middle part iscommon passage for both air and food.Parts of Pharynx:The cavity of the Pharynx is divided into 3 parts: 1. The Nasopharynx (nasal part) – This is the upper part of the Pharynx situated behind the nose and above the lower border of soft palate. It is respiratory in function. 2. The Oropharynx (oral part) – This is the middle part of the pharynx situated in the oral cavity. It communicates with nasopharynx through the pharyngeal isthmus. It communicates with oral cavity through oropharyngeal isthmus. It opens into laryngopharynx at the level of upper border of epiglottis. Behind it is supported by the body of the axis of the vertebra and the upper part of the body of the C3 vertebra. Its lateral wall presents the palatine tonsil which lies in the tonsillar fossa. 3. The Laryngopharynx (laryngeal part) – This is situated behind the larynx. It extends from upper border of the epiglottis to the lower border of the cricoid cartilage.Structure of the Pharynx: -The wall of the pharynx is composed of 5 layers from within outwards: Mucosa Submucosa Pharyngobasilar fascia Muscular Coat Buccopharyngeal fasciaArterial Supply: 1. Ascending Pharyngeal branch of external carotid artery. 2. Ascending palatine and tonsilar branches of the facial artery. 3. Dorsal lingual branches of the lingual artery. 4. Greater palatine, pharyngeal and pterygoid branches of maxillary artery. 21
  • 22. Venous Drainage:The venous plexus on the posterolateral aspect of the pharynx receives blood frompharynx, soft palate and prevertebral region. It drains into internal jugular veins andfacial veins.Nervous Supply:Pharynx is supplied by the pharyngeal plexus of nerves which lies chiefly on themiddle constrictor.The plexus is formed by pharyngeal branches of the vagus, the glosso pharyngealnerve, and the superior cervical sympathetic ganglion.Motor fibers are derived from the cranial accessory nerve through the branches of thevagus.Sensory fibers travel through glossopharyngeal & Vagus nerves.Parasympathetic secretomotor fibers are derived from the greater petrosal nervethrough the lesser palatine branches of the pterygopalatine ganglion.Lymphatic Drainage:Lymph drains into retro pharyngeal and deep cervical lymph nodes.3) SWARA YANTRA: Though this term is being used in the recent literatures, many words like swarabheda, swara sada, swara kshaya, swaropaghata, gadgada, muka etc., used by samhita& sangrahakaras implies the presence of the knowledge regarding swara yantra longbefore.LARYNX: It is the organ for voice production and air passage. It lies in the anteriormidline of the neck extending from the root of the tongue to the trachea. It is 44mmlength in males and 36mm in females.Larynx is made up of a skeletal framework of cartilages, which are connected byjoints, ligaments and membranes, and are moved by a number of muscles. The cavityof the larynx is lined by mucous membrane. Larynx contains 9 cartilages of which 3 are unpaired and 3 paired.Unpaired Cartilages: 1. Thyroid 2. Cricoid 22
  • 23. 3. EpiglotticPaired Cartilages: - 1. Arytenoids 2. Corniculate 3. CuneiformArterial supply:Upto Vocal folds: By superior laryngeal artery, a branch of superior thyroid artery.Below Vocal folds: By inferior laryngeal artery, a branch of inferior thyroid artery.Venous Drainage:Upto Vocal folds: - The superior laryngeal vein drains into superior thyroid vein.Below Vocal folds: - Inferior laryngeal vein drains into the inferior thyroid vein.Nerve Supply:Motor: - By recurrent laryngeal & External laryngeal nerve.Sensory: Above the level of Vocal folds by Internal laryngeal nerve and below thelevel of vocal folds by recurrent laryngeal nerve.Lymphatic Drainage:Above Vocal folds: Drain through superior thyroid vessels to the anterior superiorgroup of deep cervical nodes.Below Vocal folds: Drain into the postero inferior group of deep cervical nodes andprelaryngeal nodes.4) KANTHA NADI:This is trachea, a tubular structure between larynx and bronchi.Kantha srota41 and Gala marga42 are the terms used by Ashtanga Hridayakara forkantha nadi.The term Gala sandhi is used by Charaka in the context of Vidalika and by Susruthain the context of valaya.Antargala is the term used by susruta for Kantha43, and Charaka used the term Galavaahya for Greeva44. 23
  • 24. Gala nalaka is the term used by Dalhana for Swara yantra & trachea and GalaNalakasthis is used for hyoid, thyroid and Cricoid cartilages45.Kantha nadi consists of 40 asthis and 20 sandhis46. These asthis are Taruna type andare mentioned as Mandalasthis47.On either side of Kantha nadi there are 4 dhamanis – 2 Neelas & 2 Manyas. Injury tothese causes Mukata, swara vaikrutam and Arasagraha48.The Kantha nadi (trachea) divides into two (bronchi), which lead into lungs afterfurther division. These are described as Apastambha marmas and injury to thesecauses vata purna koshtata, and marana with kasa and swasa49.These divided Kanthanadis are attached to, and enter into puppusas on dakshina andvama parshvas and divide further into numerous bronchioles.The terms Tundikeri (tonsils), Gala sundi (uvula), Adhijihvika (epiglottis), Upajihvika(palatine tonsils) indicates the awareness and knowledge of the Acharyas towards thisconcept.TRACHEA: It is a wide tube lying more or less in the midline, in the lower part of the neckand in the posterior mediastinum. Its upper end is continuous with the lower end ofthe larynx and its lower end ends by dividing into right and left principal bronchi.Trachea is 4-6 inches in length. Its external diameter is 2 cm in males and 1.5 cm infemales.The upper end of the trachea lies at the lower border of the cricoid cartilage, oppositeC6 vertebra.Trachea has a fibroelastic wall supported by a cartilaginous skeleton formed by C-shaped rings. The rings are about 16-20 in number and make the tube convexanterolaterally. Posteriorly there is a gap which is closed by a fibroelastic membraneand contains transversely arranged smooth muscle. 24
  • 25. Arterial Supply: Inferior thyroid arteries.Venous Drainage: Into the left branchiocephalic vein.Nerve supply: Parasympathetic is by vagus through the recurrent Laryngeal nerve. Sympathetic fibers are from the middle cervical ganglion.Lymphatic Drainage: To the pretracheal and paratracheal nodes.5) PUPPUSAS: Puppusas are mentioned in Atharvaveda as ‘Plasih’ which denotes their shape,i.e., ‘Parvatakara’50, resembling the conical shape of the lung.Charaka did not used the term puppusa, but mentioned ‘Dvau sleshma Bhavau’ in thecontext of pratyangas, which may be understood as puppusas51.Susruta and Vagbhata have used the term in singular number and mentioned it underkoshtangas52. This type of expression may be according to panineeya sutram, whichdescribes the way of expressing similar things in singular number by the quote‘Jatyaika Vachanam”53.Susruta54 and Sarangadhara55 mention puppusa to the left of hridaya, where asVagbhata56 mentions it to the right. These may be interpreted as the presence ofpuppusas on both the sides.Susruta mentions the embryological development of puppusas as from the Phena ofshonita57, which clearly resembles the anatomical and morphological structure of thelung.In the context of swaraghna, susruta mentioned the term ‘anilayana’58 (alveolus),which was commented by Dalhana as ‘Vayu Bhaga’. 25
  • 26. LUNGS: These are a pair of respiratory organs situated in the thoracic cavity. Each lunginvaginates the corresponding pleural cavity. The right and left lungs are separated bythe mediastinum.Lungs are spongy in texture and right lung weighs about 625 gms. It is about 50 gmheavier than the left lung.Features of the Lungs:Each lung is conical in shape.It has: 1. An apex at the upper end 2. A base resting on the diaphragm 3. 3 borders – Anterior, Posterior & Inferior 4. 2 surfaces – Costal and MedialFissures and lobes of the lungs:Right lung is divided into 3 lobes – superior, middle and inferior by two fissures,oblique and horizontal.Left lung is divided into 2 lobes by the oblique fissure.The tongue shaped projection of the left lung below the cardiac notch is calledlingula, which corresponds to the middle lobe of the right lung.Root of the Lung:It is a short, broad pedicle which connects the medial surface of the lung to themediastinum. It is formed by structures which either enter or come out of the lung atthe hilum. The roots of the lungs lie opposite the bodies of T5, T6, T7 vertebrae.Contents of Root of the Lung: 1. Principal bronchus on the left side, eparterial and hyparterial bronchi on right side. 2. One pulmonary artery 3. Two pulmonary veins, superior and inferior 4. Bronchial arteries, one on the right side and two on the left side. 26
  • 27. 5. Bronchial veins 6. Anterior and posterior pulmonary plexuses of nerves 7. Lymphatics of the lung. 8. Bronchopulmonary lymph nodes. 9. Areolar tissue.Arterial supply of the lung:Bronchial arteries supply nutrition to the bronchial tree and to the pulmonary tissue.On the right side there is one bronchial artery and on the left side there are 2 bronchialarteries.Deoxygenated blood is brought to the lungs by the pulmonary arteries and oxygenatedblood is returned to the heart by the pulmonary veins.There are precapillary anastomoses between bronchial and pulmonary arteries.Venous drainage:Blood is drained through bronchial veins. Usually there are 2 bronchial veins on eachside. The right bronchial veins drain into the azygous vein.The left bronchial veins drain either into the left superior intercostal vein or into thehemiazygous vein.The greater part of the venous blood is drained by the pulmonary veins.Lymphatic Drainage:There are 2 sets of lymphatics, both of which drain into the bronchopulmonary nodes.Superficial vessels drain the peripheral lung tissue lying beneath the pulmonarypleura.Deep lymphatics drain the bronchial tree, the pulmonary vessels and the connectivetissue septa.Nerve supply of the lungs:Parasympathetic nerves are derived from the vagus.Sympathetic nerves are derived from spinal segments T2 to T5.Both parasympathetic and parasympathetic nerves first form anterior and posteriorpulmonary plexuses situated in front and behind the lung roots. From the plexuses,nerves are distributed to the lungs along the blood vessels and bronchi. 27
  • 28. BRONCHIAL TREE: Trachea divides at the level of the lower border of 4th thoracic vertebra into 2principle bronchi, one for each lung. The right principle bronchus is shorter (1 inch),wider and more in line with the trachea than the left principle bronchus. The leftprinciple bronchus is longer (2 inches), narrower and more oblique than the rightbronchus.Each principle bronchus enters the lung through the hilum, and divides into secondaryor lobar bronchi one for each lobe of the lungs i.e., 3 on the right side and 2 on the leftside.Each lobar bronchus divides into tertiary / segmental bronchi, one for each bronchopulmonary segment i.e., 10 on the right side and 8 on the left side.The segmental bronchi divide repeatedly to form very small branches called terminalbronchioles which divide into still smaller branches called respiratory bronchioles.Each respiratory bronchiole aerates a small part of the lung knows as a pulmonaryunit.The respiratory bronchiole ends in microscopic passages which are termed asAleveolar ducts → Atria → Air saccules → Pulmonary alveoli in that order.BRONCHOPULMONARY SEGMENTS: These are well defined sectors of the lung each one of which is aerated by atertiary or segmental bronchus. Each segment is pyramidal in shape with its apexdirected towards the root of the lung. There are 10 segments on the right side and 8 on the left. Each segment issurrounded by connective tissue which is continuous on the surface with pulmonarypleura. Thus the bronchopulmonary segments are independent respiratory units. Theconnective tissue septa between adjoining segments form inter segmental planeswhich are crossed by the pulmonary veins and occasionally by the pulmonary arteries. 28
  • 29. SEGMENTS:Right Lung: Upper Lobe 1. Apical 2. Anterior 3. Posterior Middle Lobe 4. Medial 5. Lateral Lower Lobe 6. Apical 7. Anterior basal 8. Lateral basal 9. Posterior basal 10. Medial basalLeft Lung: Upper Lobe 1.Apico – posterior 2. Anterior 3. Interior 4. Superior Lower Lobe 5. Apical 6. Anterior basal 7. Lateral basal 8. Posterior basal 29
  • 30. HISTOLOGY OF THE RESPIRATORY TRACTNOSE: The vestibule of the nasal cavity is lined by skin continuous with that on theexterior of the nose. Hair and sebaceous glands are present.The respiratory mucosa lies behind the vestibule and is lined by pseudostratifiedciliated columnar epithelium. Apart from these epithelial cells, Goblet cells, non-ciliated columnar cells and basal cells are present.The olfactory mucosa is a small area on the superior nasal concha and on theadjoining part of the nasal septum. This is yellow in colour in contrast to the pinkcolour of the respiratory mucosa. This area consists of olfactory cells which aremodified neurons, sustentacular cells and basal cells.PHARYNX: In nasopharynx the epithelial lining is ciliated columnar or pesudostratifiedciliated columnar.Over the soft palate, oropharynx and laryngopharynx the epithelium is stratifiedsquamous epithelium, as these parts come in contact with food during swallowing.LARYNX: The mucous membrane lining the larynx is predominantly pesudostratifiedciliated columnar. However over some parts like epiglottis, aryepiglottic fold & Vocalfolds that come in contact with food, the epithelium is stratified squamous.TRACHEA & PRINCIPLE BRONCHUS: The lumen of trachea is lined by mucus membrane which consists ofpseudostratified ciliated columnar epithelium. The subepithelial connective tissueconsists of serous and mucous glands & lymphoid tissue aggregations.The right and left principle bronchi have a similar structure as that of trachea. 30
  • 31. LUNGS: As the bronchi become smaller the epithelium first becomes simple ciliatedcolumnar, then non-ciliated columnar, and finally cuboidal.The alveolus has a very thin wall and is lined by flattened squamous cells. 31
  • 32. KRIYA SHAREERA The Nirgama and pravesa of prana vayu by nasika and gala marga is calledswasa. The roga in which avarodha is caused to this process is also called Swasa59. Ayurvedic texts were the first to explain the physiology of the respiration in amost convincing manner. The pulmonary ventilation, diffusion and transport ofpulmonary gases, and the regulation of the respiratory process were completelyencompassed in the Ayurvedic literature. In relation to this, the explanation as given by Sarangadhara60 elucidates thatthe pranavayu, the seat of which is nabhi (Hridaya nabhi), after passing throughHritkamalantaram (lungs) comes out of Kantha to drink Vishnupadamritham(Oxygen) there after taking in the Ambarapiyusha i.e., Vishnupadamritham, rushesinto the body to nourish the whole body in the form of oxygen. JeevamchaJatharanalam is the sustenance of life of the cell by maintaining metabolism within. The shareera of swasa kriya involves the roles of vata and kapha with specificinvolvement of Prana &Udana vata and Avalambaka & Kledaka kapha which regulatethe swasana samsthana and thus establishes the process of normal respiration.VATA: The role of vata: 1) All the sareera karmas are due to Vata and Vata itself is called Prana61. Vata is Ayu, Bala, and Dhata of Sareera and is praised as Prabhu62. 2) The important prakrita karmas of vata according to Charaka are Utsaha, Ucchwasa, Nisswasa, cheshta, Sama Dhatu gati and Moksha of Malas63. 3) Though the Pitta, kapha, Malas and Dhatus are also responsible for roga or arogata, they are all Pangus and are lead by Vata just like megha is lead by Vayu64. 4) Vata is Vibhu, Asukari, and Balavan and can cause Kopana of all others65. 5) ‘Sameerano agneh’ on this Gananath Sen comments as ‘Vata is the regulator of agni karmas of pitta’66. 6) ‘Dosha Samshoshana’, according to Chakrapani is ‘sareerakleda samshoshana’ and according to Gananath Sen it is ‘Shoshana of pitta Sleshmadi doshas67’. 32
  • 33. Prana Vata: The following are the factors supporting the role of Prana vata: 1) The word Prana is derived from the dhatu ‘An’ with ‘Pra’ as upasarga68. Its nirukti is said as – “pranayateeti Pranah”, i.e., which causes Ucchwasa and Nisswasa. ‘An’ is a paryaya to swasa. “Prakarshena anayati pranan iti pranah” is another nirukti, which means it is important in maintaining the pranas. 2) Sthanas of Prana Vata are the sthanas of Prana vaha Srotas itself.. According to Chakrapani Prana vata moves through Prana Vaha srotases69.While the total chemical regulation of the respiration is explained by Sarangadhara,the neuronal regulation of respiration can be better understood through the propertiesof Pranavata.It explains that Pranavata, situated in moordha (Mastishka) region circulates throughKanta (Trachea) and Uras (lungs & Heart). It controls buddhi (Intellect), Hridaya(Mind), Indriya (Sense organs) and is responsible for Nishteevana (Salivation),Kshavathu (sneezing), Udgara (Erructation), Nishwasa (Respiratory movements) &Anna pravesha (Deglutition) 70.This explanation clearly shows that the Pranavata performs its functions at higher andlower levels through Brain Centers, Glossopharyngial & Vagus nerves i.e., thefunctions of higher level, Buddhi Dharana, Hridaya dharana, Indriya dharana andChitta dharana are performed through definite centers in the brain.The lower functions like, Nishteevana, Kshavathu, Udgara etc are well controlled byGlossopharyngial & Vagus supply to Oesophagus, Pharynx, larynx, salivary glands,stomach etc.,Udana Vata: The following factors establish the role of Udana vata in swasa: 1) The meaning of the prefix ‘ut’ is urdhwam i.e., the vata which moves upwards is called udana vata71. This implies the expiration part of swasa. 2) Sthanas of Udana vata are nabhi, uras and kantha72. According to Sarangadhara puppusa is the adhara for Udana vata73. 33
  • 34. The Udana vata, located in Uras, circulates through nasa, nabhi and gala with thespecific functions of Vakravritti, prayatna, Urja, Bali, Smriti & varna74 etc., byinvolving the organs closely related to the respiratory system. Thus Udana vataappears to act as accessory to the Pranavata in regulating respiratory system.(Vyana vayu which is sarva deha chara75 and is responsible for RasaraktadiSamvahana has relation with respiration, as the functions of carrying oxygenatedblood to the cells and venous blood to the lungs come under the purview ofvyanavayu.)KAPHA:. The factors establishing its role: 1) ‘Slish alingane’76 is the dhatu from which Sleshma sabda is derived, and ‘kena jalena phalateeti va kaphah’77 is the nirukti for kapha. 2) The Amasaya which is the udbhava sthana for swasa78 is also the utpatti sthana for sleshma79. 3) The uras which is the seat for swasa80 is also the vishesha sthana for sleshma81.Avalambaka Selshma: The involvement of avalambaka sleshma in swasa is appreciated by the following factors: 1) Uras, the seat for avalambaka sleshma is also the seat for swasa82. 2) Puppusas which are involved in swasa are supported and protected by avalambaka sleshma. This kapha, situated in uras83 and trika regions performs avalambana to sleshmasthanas related to urah pradesha. Its function clearly supports respiratory mechanism.In relation to the respiratory mechanism, the avalambaka kapha functions as pleuralfluid – enabling free and frictionless movements of the lungs, Mucin of bronchi -providing free entry of air into lungs, lung parenchyma - supporting blood vesselsand alveoli etc., 34
  • 35. Kledaka Kapha: The role of Kledaka kapha can be established based on the following factors: 1) The sthana of kledaka kapha is amasaya, which is also the udbhava sthana for swasa84. 2) Kledaka kapha aids in the sukha jarana of ahara by its oudaka guna, and its vriddhi causes Agni vaishamya as seen in swasa85. 3) Kledaka kapha protects the other seats of sleshma by udaka karmas through its prabhava, and its vikruti causes vikruti of other kaphas86.SWASA SANKHYA: Sathapatha brahmana, Varahopanishat, Hamsopanishat, Amrutopanishat, andDhyanabindupanishat have mentioned the Swasa Sankhya as 21,600 per one Ahoratri,which comes to 15 per minute, almost close to normal respiratory rate87. RESPIRATION IN FOETAL LIFEDuring fetal life, the placenta helps in the gas exchanges. As the lungs are fluid filled,there is no air fluid interface. The most obvious effect of birth on the baby is loss of the placental connectionwith the mother and therefore, loss of this means of metabolic support. One of themost important immediate adjustments required of the infant is to begin breathing.With the onset of respiration, pulmonary vascular resistance is greatly decreased withassociated increase in pulmonary blood flow. These changes occur within a minute ortwo. With the fall of pulmonary resistance and along with the increase of resistance inthe abdominal aorta, direction of blood flow through ductus arteriosus is changed.The promptness with which the fetus begins to breathe indicates that breathing isinitiated by sudden exposure to the exterior world, probably resulting from: a. Slightly asphyxiated state incident to the birth process. b. Sensory impulses that originate in the suddenly cooled skin. 35
  • 36. PHYSIOLOGY OF RESPIRATIONThe physiology of respiration in adult human includes:1. Pulmonary ventilation2. Diffusion of Oxygen and Carbon dioxide3. Transport of O2 and Co2 in Blood and Tissue fluids4. Regulation of respiration 1. PULMONARY VENTILATIONMuscles that cause lung expansion and contraction: The lungs can be expanded andcontracted in 2 ways:1) By downward and upward movement of the diaphragm to lengthen or shorten thechest cavity. Normal quiet breathing is accomplished almost entirely by this method.During inspiration, contraction of the diaphragm pulls the lower surfaces of the lungsdownward. During expiration, the diaphragm simply relaxes and the elastic recoil ofthe lungs, chest wall and abdominal structures compresses the lungs and expels theair.2) By elevation and depression of the ribs to increase and decrease the antero-posterior diameter of the chest cavity. This method of expanding the lungs includes raising the rib cage. Thisexpands the lungs because, in the natural resting position, the ribs slant downwardthus allowing the sternum to fall backward toward the vertebral column. But when therib cage is elevated, the ribs project almost directly forward, so that the sternum alsomoves forward, away from the spine, making the anteroposterior thickness of thechest about 20% greater during maximum inspiration than during expiration. 36
  • 37. Therefore all the muscles that elevate the chest cage are classified as muscles ofinspiration and those that depress the chest cage are classified as muscles ofexpiration.Muscles that raise the rib cage (during inspiration) are: External intercostals Sternocleidomastoid Anterior serrate ScaleniMuscles that depress the rib cage (during expiration) are: Abdominal recti Internal intercostals.The ribs during expiration are angled downward, and the external intercostals areelongated forward and downward. As they contract, they pull the upper ribs forwardin relation to the lower ribs, and this cause leverage on the ribs to raise them upward,thereby causing inspiration.The internal intercostals function exactly in the opposite manner, functioning asexpiratory muscles because they angle between the ribs in the opposite direction andcause opposite leverage.PULMONARY VOLUMES: These four pulmonary lung volumes that, when added together, equal themaximum volume to which the lungs can be expanded.i) Tidal Volume: This is the volume of air inspired or expired with each normalbreathe. (VT = 500 ml)ii) Inspiratory Reserve Volume: This is the extra volume of air that can be inspiredover and above the normal tidal volume when the person inspires with full force.(IRV = 3000 ml)iii) Expiratory Reserve Volume: This is the maximum extra volume of air that canbe expired by forceful expiration after the end of a normal tidal expiration.(ERV = 1100 ml) 37
  • 38. iv) Residual Volume: This is the volume of air remaining in the lungs after the mostforceful expiration. (RV = 1200 ml)PULMONARY CAPACITIES:These are the combination of pulmonary volumesi) Inspiratory Capacity: (VT + IRV)This is the amount of air a person breathe in beginning at the normal expiratory leveland distending the lungs to the maximum amount. (IC = 3500 ml.)ii) Functional Residual Capacity: (RV + ERV)This is the amount of air that remains in the lungs at the end of normal expiration.(FRC = 2300 ml.)iii) Vital Capacity: (IRV + VT + ERV)This is the maximum amount of air a person can expel from the lungs to theirmaximum extent and then expiring to the maximum extent. (VC = 4600 ml.)iv) Total Lung Capacity: (VC + RV)This is the maximum volume to which the lungs can be expanded with the greatestpossible effort. (TLC = 5800 ml.) All pulmonary volumes and capacities are about 20-25% less in women thanin men.The ultimate importance of pulmonary ventilation is to continually renew theair in the gas exchange areas of the lungs, where air is in proximity to the pulmonaryblood. These areas include the alveoli, alveolar sacs, alveolar ducts and respiratorybronchioles. The rate at which new air reaches these areas is called alveolarventilation. 2. DIFFUSION OF OXYGEN AND CARBON DIOXIDE After the alveoli are ventilated with fresh air, the next step in the respiratoryprocess is diffusion of oxygen from the alveoli into the pulmonary blood anddiffusion of carbondioxide in the opposite direction, out of the blood.Respiratory unit: - (Respiratory lobule) this is composed of a respiratory bronchiole,alveolar ducts, atria and alveoli. 38
  • 39. There are about 300 million alveoli in the two lungs, and each alveoli has anaverage diameter of about 0.2mm. Between the alveoli, an extensive network ofinterconnecting blood capillaries is present. Because of this the flow of blood in thealveolar wall has been described as a ‘sheet’ of flowing blood. Thus the alveolar gases are in very close proximity to the blood of thepulmonary capillaries. Further, gas exchange between the alveolar air and pulmonaryblood occurs through the membranes of all the terminal portions of the lungs. Allthese membranes are collectively known as Respiratory membrane or pulmonarymembrane. The overall thickness of the respiratory membrane is about 0.6 micrometer.The total surface area of the respiratory membrane is about 70sq.mts. The totalquantity of the blood in the capillaries of the lungs at any given instant is 60 – 140 ml.The average diameter of the pulmonary capillaries is only 5 µm, which means thatRBCs must squeeze through them. The RBC membrane usually touches the capillarywall, so that oxygen and carbondioxide need not pass through significant amounts ofplasma as they diffuse between the alveolus and the red cells.Factors that affect the rate of Gas diffusion through Respiratory membrane:1. The thickness of the membrane2. The surface area of the membrane3. The diffusion coefficient of the gas in the substance of membrane4. ‘Partial pressure’ difference of the gas between the two sides of membrane.Diffusion capacity for oxygen: 21 ml/min/mmHg.Diffusion capacity for carbondioxide: 400 – 450 ml/min/mmHg because the diffusioncapacity of CO2 is slightly more than 20 times that of O2. In respiratory physiology one deals with mixtures of gases, mainly of oxygen,nitrogen and carbondioxide. The rate of diffusion of each of these gases is directlyproportional to the pressure caused by that gas alone, which is called the ‘Partialpressure’ of that gas. 39
  • 40. The partial pressure is directly proportional to the concentration of the gas molecules,and inversely proportional to the solubility coefficient or diffusion coefficient.Partial Pressure = concentration of dissolved gas/ Solubility or Diffusion coefficient.Solubility Coefficients / Diffusion Coefficients: Table No.1 Oxygen 0.024 Carbondioxide 0.57 Carbonmonoxide 0.018 Nitrogen 0.012 Helium 0.008Partial Pressures:Table No.2 Respiratory Atmospheric Humidified air Alveolar air Expired air Gases air (mm Hg) (mm Hg) (mm Hg) (mm Hg) N2 597.0 (78.62%) 563.4 (79.09%) 569.0 (74.9%) 566.0 (74.5%) O2 159.0 (20.84%) 149.3 (19.67%) 104.0 (13.6%) 120.0 (15.7%) CO2 0.3 (0.04%) 0.3 (0.04%) 40.0 (5.3%) 27.0 (3.6%) H2O 3.7 (0.50%) 47.0 (6.20%) 47.0 (6.2%) 47.0 (6.2%) Total 760.0 (100%) 760.0 (100%) 760.0 (100%) 760.0 (100%)One can observe that CO2 is more than 20 times as soluble as O2. Therefore, thepartial pressure of CO2 is less than one twentieth that exerted by oxygen. 3. TRANSPORT OF O2 AND CO2 IN BLOOD AND TISSUE FLUIDSGases can move from one point to another by diffusion and the cause of thismovement is always a partial pressure difference from first point to the next. Thus,oxygen diffuses from the alveoli into the pulmonary capillary blood because the PO2in the alveoli is greater than the PO2 in the pulmonary capillary blood. In the othertissues of the body, a higher PO2 in the capillary blood than in the tissues causesoxygen to diffuse into the surrounding cells. 40
  • 41. Once oxygen has diffused from the alveoli into the pulmonary blood, it is transportedto the peripheral tissue capillaries almost entirely in combination with haemoglobin.Normally, about 97% of oxygen transported from the lungs to tissues is carried inchemical combination with heamoglobin in the RBC. The remaining 3% istransported in the dissolved state in the water of the plasma and blood cells.The presence of haemoglobin in the RBCs allows the blood to transport 30 –100 timesas much oxygen as could be transported in the form of dissolved oxygen in the waterof the blood.Under normal conditions, about 5 ml of oxygen are transported from the lungs to thetissues by each 100 ml of blood flow.About 98% of the blood that enters the left atrium from the lungs has just passedthrough the alveolar capillaries and has become oxygenated upto a PO2 of about 104mmHg.When the arterial blood reaches the peripheral tissues, its PO2 in the capillaries is still95 mmHg. The PO2 in the interstitial fluid that surrounds the tissue cells averagesonly 40 mmHg. Therefore the PO2 of the blood leaving the tissue capillaries andentering the systemic veins is also about 40 mmHg. The intracellular PO2 in theperipheral tissue cells averages 23 mmHg.In the body’s tissue cells, oxygen reacts with various food stuffs and is metabolized toform carbondioxide. This intracellular PCO2 rises to a high value, which causes CO2to diffuse into the tissue capillaries. After blood flow to the lungs, the CO2 diffusesout of the blood into the alveoli, because the PCO2 in the pulmonary capillary blood isgreater than that in the alveoli.Intracellular PCO2 is 46 mmHg.Interstitial PCO2 is 45 mmHg.Pulmonary capillary PCO2 is 45 mmHg.PCO2 in alveolar air is 40 mmHg.CO2 can diffuse about 20 times as rapidly as O2. 41
  • 42. Under normal resting conditions, an average of 4 ml of CO2 is transported from the tissues to the lungs in each 100 ml of blood. CO2,like oxygen also combines with chemical substances in the blood that increases CO2 transport 15 – 20 fold. 4. REGULATION OF RESPIRATION• NEURONAL REGULATION OF RESPIRATION: The nervous system normally adjusts the rate of alveolar ventilation almost exactly to the demands of the body so that the oxygen pressure (Po2) and carbondioxide pressure (Pco2) in the arterial blood is hardly altered. The respiratory centre is composed of several groups of neurons located bilaterally in the medulla oblongata and pons of the brain stem. It is divided into 3 major collections of the neurons. a) Dorsal Respiratory Group: It is located in the dorsal portion of the medulla and extends most of the length. It mainly causes inspiration. Most of its neurons are located with in nucleus of the ‘tractus solitarius’ which is the sensory termination of both vagal and glossopharyngeal nerves. Sensory signals are transmitted from peripheral chemoreceptors, baroreceptors and receptors in the lungs. The nervous signal that is transmitted to the inspiratory muscles, mainly the diaphragm begins weakly and increases steadily in a ramp manner for about 2 seconds. Then it ceases abruptly for approximately the next 3 seconds which turns off the excitation of the diaphragm and allows elastic recoil of the lungs and the chest wall to cause expiration. This repeats in a cyclic manner. 42
  • 43. b) Ventral Respiratory Group: This is located in the ventrolateral part of the medulla about 5mm to the dorsal respiratory group. This is found in ‘nucleus ambiguus’ rostrally and the ‘nucleus retroambiguus’ caudally. This group mainly causes expiration and also inspiration to some extent. The neurons of this group remain almost totally inactive during normal quiet respiration. But when the respiratory drive for pulmonary ventilation becomes greater than normal, this group contributes extra respiratory drive. c) Pneumotaxic centre: It is located dorsally in the nucleus parabrachialis of the upper pons and transmits signals to the inspiratory area. This centre mainly controls rate and depth of breathing, thus controlling the duration of the filling phase of the lung cycle. The function of the centre is primarily to limit inspiration. This has a secondary effect of increasing the rate of breathing because limitation of inspiration also shortens expiration and the entire period of each respiration.• CHEMICAL CONTROL OF RESPIRATION: The ultimate goal of respiration is to maintain proper concentrations of oxygen, carbondioxide and hydrogen ions in the tissues. Apart from the three respiratory centres, an additional neuronal area, a ‘chemosensitive area’ located bilaterally, lying only 0.2 mm beneath the ventral surface of the medulla is found to be sensitive to the changes in blood Pco2 or Hydrogen ion concentration. Hydrogen ions do not easily cross the blood-brain barrier, but can excite the chemosensitive area directly. CO2 passes through the blood-brain barrier almost as if the barrier did not exist, but it has little effect in stimulating the neurons in the chemosensitive area. Still CO2 has a potent indirect effect. It does this by reacting with the water of the tissues, to form Carbonic acid, which dissociates into hydrogen 43
  • 44. and bicarbonate ions. The hydrogen ions then have a potent direct stimulatory effecton respiration. Oxygen, in contrast, does not have a significant direct effect on the respiratorycentre of the brain. Instead, it acts almost entirely on the peripheral chemoreceptorslocated in the carotid and aortic bodies, and these in turn transmit appropriate nervoussignals to the respiratory centre for the control of respiration. 44
  • 45. FUNCTIONS OF RESPIRATORY PASSAGES The air is distributed to the lungs by way of respiratory passages viz., nose,trachea, bronchi & bronchioles.Nose: As air passes through the nose, three distinct normal respiratory functions,called ‘air conditioning functions’ are performed by the nasal cavities: 1. The air is warmed by the extensive surfaces of the conchae and sputum, a total area of about 160 sq.cms. 2. The air is almost completely humidified even before it passes beyond the nose. 3. The air is partially filtered. The hairs at the entrance of the nostrils are important for filtering out largeparticles. Much more important, though, is the removal of particles by ‘turbulentprecipitation’. That is, the air passing through the nasal passages hits manyobstructing vanes, the conchae (turbinates), the septum and the pharyngeal wall.During this the particles striking the surfaces of obstructions are entrapped in themucous coating and transported by the cilia to the pharynx to be swallowed.Trachea, Bronchi & Bronchioles: To keep trachea from collapsing, multiple cartilage rings extend about 5/6th ofthe way around trachea. In the walls of the bronchi, less extensive curved cartilageplates also maintain a reasonable amount of rigidity yet allow sufficient motions forthe lungs to expand and contract. These plates become progressively less extensive inthe later generations of bronchi and are gone in the bronchioles, which usually havediameters less than 1.5mm. The bronchioles are not prevented from collapsing by therigidity of their walls. Instead, they are kept expanded mainly by the sametranspulmonary pressures that expand alveoli. In all the areas of trachea and bronchi, not occupied by cartilage plates, thewalls are composed mainly of smooth muscle. Also, the walls of the bronchioles arealmost entirely smooth muscles, with the exception of the most terminal bronchiole, 45
  • 46. called respiratory bronchiole, which is mainly pulmonary epithelium and underlyingfibrous tissue plus a few smooth muscle fibers.MUCUS LINING OF RESPIRATORY PASSAGES: All the respiratory passages are kept moist by a layer of mucus that coats theentire surface. The mucus is secreted partly by individual mucous goblet cells in theepithelial lining of the passages and partly by small submucosal glands. The mucusalso traps small particles out of the inspired air and keeps most of them from everreaching the alveoli.REMOVAL OF MUCUS: The entire surface of respiratory passages is lined with ciliated epithelium,with about 200 cilia on each epithelial cell. These cilia beat continuously at a rate of10-20 times / sec. and the direction of their ‘power stroke’ is always towards pharynx.That is, the cilia in the lungs beat upward, whereas those in the nose beat downward.The mucus flows slowly at a velocity of few mm / min. towards the pharynx. Thus themucus and its entrapped particles are either swallowed or coughed to the exterior. 46
  • 47. PHYSIOLOGICAL CONCEPT OF RASAYANA Rasayana is a disease modifying and prophylactic function, which aims atfortifying the ultimate resistances of an individual viz., the innate immunity andacquired immunity. Rasayana is an evidence based concept which has its origin in Vedas. TheVedic texts, in particular Atharvaveda88 and Sathapadha brahmana89 consistently usedthe term ‘RASA’ in the sense of water. The Vedic age regarded ‘water’ as Rasayanaattributing different functions to it. While Atharvaveda emphasizes the efficacy of Rasayana as – ConferringLustre, putting away old age, resisting diseases and bringing immortality, Samhita andSangrahakaras establishes its therapeutics in diseases like Asthma. The inherent property of a Rasayana exhibits its effect by controlling andmaintaining the immune system of an individual. The term ‘Immunity’ refers to the resistance exhibited by the host towardsinjury caused by the microorganisms and their products. Protection against infectiousdiseases is only one of the consequences of the immune response, which in its entiretyis concerned with the reaction of the body against any foreign antigens.Innate Immunity:Innate or Native Immunity is the resistance to infections which an individual possessby virtue of his genetic and constitutional make up. This includes: Phagocytosis Destruction by acid secretions and digestive enzymes. Resistance of skin Presence of Lysozyme, Basic polypeptides, Complement complex, and Natural killer lymphocytes. 47
  • 48. Acquired Immunity:In addition to these, the human body has the ability to develop extremely powerfulspecific immunity against individual invading agents such as lethal bacteria, viruses,toxins and even foreign tissues from other animals. This is called ‘Acquired’ or‘Adaptive’ Immunity which an individual acquires during life as distinct from theinborn innate immunity.Two basic but closely allied types of acquired immunity occur in the body which isinitiated by antigens:1. Humoral or B-Cell Immunity: In this the body develops circulating antibodieswhich are globulin molecules in the blood plasma that are capable of attacking theinvading agents.2. Cell-mediated or T-Cell Immunity: In this the immunity is achieved through theformation of large numbers of activated T-lymphocytes that are specially crafted inthe lymph nodes to destroy foreign agent.An important undesirable side effect of immunity is the development of allergy orimmunity hypersensitivity, which is due to non ordinary response of the immunesystem thus maintaining an excess Ig E antibody levels in the blood.It is at this level the effect of Rasayana is felt which not only maintains a powerfulimmune mechanism but also neutralizes the side effects of adverse immune reactions. 48
  • 49. DEFINITIONS & DERIVATIONS The word ‘TAMAKA’ is derived from ‘TAMAS’ sabda, which meansAndhakara (Darkness). The word ‘SWASA’ is derived from ‘SWAS-JEEVANE’Dhatu which means living or life90.‘Swasanthyanekarogaharatwat Swasanah Swasapranane’. It means that ‘Swasana’ isthe one which combats many diseases, and is the elixir of life91.‘Swasanthyanena pranina iti swasanah swasapranane’. This means as the cause forthe existence and sustenance of life is Swasana92. Hemachandra mentions Ucchwasa as Antharmukha swasa, and Niswasa asBahirmukhaswasa. According to the commentators of ‘Charaka Samhita’of Jamnagar, theNirgama, (Expiration) and pravesa (Inspiration) of prana vayu through Nasa and Galamarga is called Swasa. The disease in which it is obstructed is called Swasa93. According to Susruta it is a ‘Vikruta Swasa’ Vayu leaving its prakruti,associated with prana vata & kapha, moves in upward direction, which is then calledSwasa94. Word ‘ASTHMA’ is derived from a Greek word ‘aazein’ meaning sharpbreath gasping or panting. Though the word first appeared in Homer’s Iliad,Hippocrates was the first to use the term in reference to the medical condition. Asthma is defined as a chronic inflammatory disease of airways that ischaracterized by increased responsiveness of the tracheobronchial tree to amultiplicity of stimuli. 49
  • 50. Asthma or spasmodic bronchial asthma is a paroxysmal affection. It manifestsitself in attacks of severe respiratory dyspnoea due to bronchospasm excited byperipheral irritation, chemical agencies or cerebral influences. Asthma is defined as a disorder characterized by chronic airway inflammationand increased airway responsiveness resulting in symptoms of wheeze, cough, chesttightness and dyspnoea. Bronchial asthma is a disease characterized by variable air flow obstruction,airway inflammation and bronchial hyperresponsiveness. The clinical syndrome of asthma is defined as “widespread narrowing of theintrapulmonary airways which varies either spontaneously or in response to treatment. According to a compilation work: ‘Should the definition of asthma be clinicalor pathological?’ – Ideally it should contain both aspects i.e., a conditioncharacterized by episodes of breathlessness with wheeze and cough which respondswell to treatment, and other, the bronchospasm due to bronchial hypersensitivity andproduction of thick viscid sputum95. 50
  • 51. PREVALENCE OF ASTHMA The disease can start at any age, but in about one half of cases it starts before10 yrs of age, and another third occur before age 40. It is twice as common amongst boys as girls, whereas in adults the male-female ratio usually equalizes by age 30.Globally, asthma is responsible for around 1, 80,000 deaths annually.It is believed that there are about 300 million people suffering from asthma throughout the world.According to Dr.MARTYN PARTRIDGE, professor / Chairman, NationalRespiratory Training Centre (NRTC), U.K., asthma affects at least 3.5% to over 20%of population in any country.It is estimated that 4% - 5% of population in U.S. is affected.More than 6% of children in United States have been diagnosed with asthma, a 75%increase in recent decades. The rate soars to 40% among some populations of urbanchildren.9% of U.S. children below 18 yrs have asthma in 2001 compared with just 3.6% in1980.Each year, approximately 4, 70,000 hospital admissions and 5000 deaths in U.S areattributed to asthma.7% of adults and upto 15% of children in U.K. have asthma.On the remote South Atlantic Island TRISTAN DA CUNHA, 50% of the populationis asthmatic due to heredity transmission of a mutation in the gene CC16.There is a wide variability in the geographical prevalence of asthma, with the highestrates observed in New Zealand, Australia, and the U.K and the lowest in countriessuch as China & Malaysia. 51
  • 52. According to W.H.O. census 8% of Swiss population suffers from asthma today,compared with just 2% some 25-30 yr ago.W.H.O. estimates 15-20 million asthmatics in India.In India the prevalence is 6%. However it has been reported to vary from 2-17% indifferent study population.In India 5-12% of children and 3.5% adults are sufferers.It is almost certain that the figure is much higher because people with asthma are notdiagnosed properly. Both the prevalence and severity of respiratory allergic diseases such asbronchial asthma have increased in recent years. Among the factors implicated in thisEpidemic are indoor and outdoor airborne pollutants. Urbanization with its high levelsof vehicle emissions, Industrial pollutants and westerned lifestyle parallels theincrease in Asthma in most industrialized countries. 52
  • 53. NIDANANidana is the vyadhi karana96.The ultimate significance of the knowledge of nidana is ‘Nidana parivarjana97, whichpoints at preventing the aetiology in the approach of treatment of a disease.One vyadhi may have one nidana or many and many vyadhis may have one nidana ormany98. Tamaka swasa is such a vyadhi that it has many nidana factors.The contribution to the aetiological factors is also provided by those factors whichvitiate the prana, udaka & Annavaha srotases which are involved in the diseasemanifestation of Tamaka Swasa:a) Pranavaha Sroto dusti Nidana99 – Kshaya, Vegadharane, Ruksha ahara sevana,performing vyayama when hungry.b) Udaka vaha sroto dusti Nidana100: Ushnata, Ama, bhrya, atimadyapana, atisushkaannasevana, trishra etc.c) Ama vaha sroto dusti Nidana101: Atimatra bhojana, Akala bhojana, Ahitabhojana,and agnivaigunya etc.Swasa vyadhi is caused due to vitiated Vata & Kapha. These doshas are vitiatedbecause of specific nidanic factors as told by different authors: 53
  • 54. VATA PRAKOPAKARA AHARA Table No.3 S.No AHARA M.N102 C.S103 S.S104 A.S105 A.H106 1 VIDAHI + + + - - 2 RUKSHA + + + - - 3 SITA PANA + + + + + 4 SITA ASANA + - + - - 5 APATARPANA + + + - - 6 VISHAMASANA - + + - - 7 SAMASANA - - + - - 8 VIRUDDHASANA - + - - - VATA PRAKOPAKARA VIHARA Table No 4S.No VIHARA M.N107 C.S108 S.S109 A.S110 A.H111 1 SITASTHANA + + + - - 2 RAJAS + + + + + 3 DHUMA + + + + + 4 ATAPA + - + - - 5 ANILA + + + + + 6 VYAYAMA + + + - - 7 BHARA + - + - - 8 ADHWA + + + - - 9 VEGAGHATA + - + - - 10 STRI SEVANA/ - + + - - GRAMYA DHARMA 54
  • 55. KAPHA PRAKOPAKARA AHARA Table No. 5 S.No AHARA M.N112 C.S113 S.S114 A.S A.H 1 GURU + + + - - 2 VISHTAMBHI + + + - - 3 ABHISHYANDI + + + - - 4 AMADOSHA - + + - - 5 ADHYASANA - - + - - 6 NISHPAVA - + - - - 7 MASHA - + - - - 8 PINYAKA - + - - - 9 TILA TAILA - + - - - 10 PISHTA - + - - - 11 SHALUKA - + - - - 12 JALAJA PISITA - + - - - 13 ANUPA PISITA - + - - - 14 DADHI - + - - - 15 AMAKSHIRA - + - - - 16 SLESHMAKARA - + - - - OTHER NIDANA Table No. 6S.No NIDANA M.N C.S115 S.S116 A.S117 A.H118 1 ABHIGATA/MARMAGHATA - + + + + 2 KSHAYA/DOURBALYA - + + - - 3 ANAHA - + - - - 4 ATI ROUKSHYA - + - - - 5 ATI SHODANA - + - - - 6 KANTA & URAH PRATIGHATA - + - - - 7 SROTO VIBANDHA - + - - - The Ayurvedic literature encompassed all the factors which are causative to 55
  • 56. Tamaka Swasa. From an etiological stand point of modern literature, asthma isa heterogenous disease and multifactorial in origin.The aetiological factors can be considered as 2 types:1. INDUCING FACTORS:After birth, several factors interact to result in the clinical manifestation of Asthma.Inducing factors actually ‘Switch on’ the initial development of Asthma.a) GENETIC: The concept of hereditary factor has profound roots in Ayurvedic literaturewhere Acharya Susruta mentions Adibala pravritta vyadhis119, and Charaka mentionsBeeja dosha120 relating to the genetic predisposition of such conditions. Genetic contribution to asthma involves polygenic inheritance with severalgenes contributing to the asthmatic tendency in any one individual, and geneticheterogeneity where different combinations of genes lead to asthma in differentindividuals. Genetically determined predisposition to develop localized anaphylacticreaction to inhaled or ingested allergens is called Atopy, and is the single largest riskfactor for the development of Asthma. This is called Atopic or Allergic Asthma. This type of Asthma has its onset in early life. This is often associated with apersonal and / or family history of allergic diseases such as rhinitis, urticaria andeczema with positive wheal-and-flare skin reactions to intradermal injection ofextracts of airborne antigens, with increased levels of Ig E in serum and / or with apositive response to provocation tests involving the inhalation of specific antigen.Symptoms may develop immediately (Immediate Asthmatic response) or 4-6 hrs afterallergen expose (late Asthmatic response). 56
  • 57. GENES CURRENTLY IMPLICATED IN ASTHMA Table No 7PATHOLOGICAL CANDITATE CANDIDATE NORMAL FUNCTION PROCESS REGION GENE(S) OF GENE PRODUCT(S) ATOPIC RESPONSESIgE generation 6p21 HLA complex Antigen presentation 12q14 Interferon-γ Inhibition of TH2 cells and IgE switching 14q11 TCR α / δ T-cell activation complex 16p12-p11 IL-4 receptor Regulates IgE productionMast cell response 11q13 FcεRI-β High-affinity IgE receptor 12q24 Mast cell Mast cell growth growth factorEosinophil 5q31 IL-3,4,5,9,13 Cytokines up-regulatingrecruitment and GM-CSF IgE responseInflammatory 6p21.3 TNF-α Inflammatory cytokineMediator release 12q Nitric oxide Inflammatory mediator synthase 1 BRONCHIAL HYPER-RESPONSIVENESS & BRONCHOCONSTRICTION 5q31 Corticosteroid Mediates inflammation receptor 5q35 Leucotriene C4 Inflammatory mediator synthase 5q32-q34 β2-adrenoceptor Bronchodilation UNKNOWN Wheeze 1 Two asthma loci identified ? in Tristan da cunha population, p < 0.0001: ? Wheeze 2 ( > 10 loci also identified for atopy) b) INFECTION: Childhood virus infection by Respiratory Syncitial Virus (RSV). Bacterial infections by pertusis and mycoplasma. c) SMOKING: Maternal smoking during pregnancy. If parents smoke during first 2 years of their child’s life. 57
  • 58. d) ALLERGENS: Table No 8 AERO-ALLERGENS / INHALANTS INGESTANTS: House dust Milk Mite allergens (found in pillows, mattresses, Eggs upholstered furniture, carpets and drapes) Nuts Tree pollens Chocolates Feathers Fish Cats Shell-fish Cockroaches Strawberries etc., Animal dander Moulds Smoke Paints etc.,2. PROVOKING or TRIGGERING FACTORS:These factors provoke or incite an acute episode of asthma in predisposed individual.a) INFECTION:In Young children – By Respiratory Syncytial Virus & Para influenza virus.In Older children & Adults – By Rhinovirus & Influenza virus. In support of this aetiological factor, different vyadhis behaving asnidanardhakara to tamaka swasa were told by Acharya Charaka121. Tamaka swasamay result either as a chikitsa vikruti or as asadhya lakshana of these vyadhis. 1. Atisara 7. Udavarta 2. Jwara 8. Visuchika 3. Chardi 9. Alasaka 4. Pratisyaya 10. Pandu 5. Kshatakshaya 11. Visha. etc. 6. Raktapittab) ALLERGENS: (Ingestants and Inhalants) 58
  • 59. c) DRUGS: - (Pharmacological Stimuli) Aspirin – The prevalence of aspirin sensitivity is 10%. Typical aspirin sensitivity respiratory syndrome primarily affects adults,although the condition may occur in childhood. The problem usually begins with perennial vasomotor rhinitis that is followedby a hyperplastic rhinosinusitis with nasal polyps. Progressive asthma then appears.On exposure to even very small quantities of aspirin, affected individuals typicallydevelop ocular and nasal congestion and acute, often severe episodes of airwaysobstruction. β – Blockers: Beta2 – adrenoceptor antagonists can induce broncho constriction even when administered in the form of eye drops for the treatment of Glaucoma. Hence β – Blockers are avoided in patients with Asthma and COPD. Cholinergic drugs used for myasthenia gravis. Prostaglandins used to induce abortion. NSAIDSd) FOOD: Egg, Cow’s milk, wheat, peanuts, soy Cold edibles, Ice, Cool drinks Colouring agents like Tartrazine. Sulfating agents – Potassium Meta bisulphate, Sodium and Potassium bisulfite, Sodium sulfite, Sodium dioxide.e) EXERCISE: The attack follows exertion and do not occur during it. It begins within 3minutes after the end of exercise peaks within 10-15 min and then resolves by 60 min.The critical variables that determine the severity of the post exertional airwayobstruction are the levels of ventilation achieved, the temperature and the humidity ofthe inspired air. The higher the ventilation and lower the heat content of the air, thegreater the response. The phenomenon is thought to be the consequence of theairways attempt to warm and humidify an increased volume of expired air duringexercise and the mechanism may be related to a thermally produced hyperemia &capillary leakage in the airway wall. 59
  • 60. Running produces a more severe attack of asthma than walking because of its greaterventilatory cost.Inhalation of cold air markedly enhances asthma.Ice-hockey, cross-country skiing and ice skating are more provocative than swimmingin an indoor heated pool.f) ENVIRONMENT: This condition tends to develop in heavily industrial or densely populatedurban areas and is frequently associated with thermal inversions or other situationscreating stagnant air masses. INDOOR: House dust mites in carpet. Soft furnishing & bedding. Pet-derived allergens (dogs & cats). Fungal spores. Cockroach antigens. Passive exposure to cigarette smoking. OUTDOOR: Nitrogen dioxide (Motor vehicle emissions, fuel-burning industries). Nitrogendioxide reacts with sunlight & oxygen in a photochemical reaction to produce ozone. Sulphur dioxide (by burning fossil fuels and emissions from diesel – powered vehicles) Air-borne particulates (from vehicles) Levels of grass & flower pollens. (From Congress grass, soyabean seed etc.,)g) PSYCHOLOGICAL FACTORS: Severe anxiety and acute emotions can alter bronchial reactivity. These factorsbring changes in airway caliber which seems to be mediated through modification ofvagal afferent activity.Endorphins also play a role to cause this effect. 60
  • 61. h) OCCUPATION: Acute and chronic airway obstructions have been reported to follow exposure to alarge number of compounds used in many types of Industries.H.M.W. compounds induce asthma through immunological mechanism.L.M.W compounds serve haptens or can release bronchoconstrictor substance. Table No.9 Major causes of occupational asthma Occupation at risk Low molecular weight chemicals Isocyanates (eg, toluene diisocyanate, Polyurethane workers, diphenylmethane diisocyanate, roofers, insulators, painters hexamethylene diisocyanate, naphthalene diisocyanate) Anhydrides (eg, trimellitic anhydride, Manufacturers of paint, phthalic anhydride) plastics, epoxy resins Metals (eg, chromic acid, potassium Platers, welders, metal and dichromate, nickel sulfate, vanadium, chemical workers platinum salts) Drugs (eg, beta lactam agents, piperazine Pharmaceutical workers, farm derivatives, psyllium, sulfathiazole, workers organophosphates) Miscellaneous (eg, formaldehyde, Laboratory workers, textile dimethylethanolamine, ethylene oxide, workers, paint sprayers pyrethrin, polyvinyl chloride vapor) High molecular weight organic materials Animal proteins (eg, domestic animals, Farmers, veterinarians, birds, mice, fish glue) poultry processors, laboratory workers, bookbinders, postal workers Plant proteins (eg, wheat, grain dust, Farmers, bakers, textile coffee beans, tobacco dust, cotton, tea) workers, food processors Wood dust (eg, Western red cedar, Carpenters, woodworkers mahogany, oak, redwood) Dyes (eg, anthraquinone, carmine, Fabric and fur dyers, 61
  • 62. paraphenyl diamine, henna extract) beauticians Fluxes (eg colophony, soft core solder) Solderers, electrical workers Enzymes (eg, pancreatic extracts, papain, Pharmaceutical workers, food trypsin, Bacillus subtilis, bromelain, processors, plastic workers, pectinase) detergent manufacturersi) GASTRO-OESOPHAGEAL REFLUX: Reflux of gastric contents in the lower third of oesophagus can provoke asthma.j) ENDOCRINAL: Women may experience catamenial asthma at predictable times during menstrual cycle, which is thought to be due to endocrinal imbalance.k) CARDIAC ASTHMA: Wheezing precipitated by uncompensated congestive heart failure. With such a diversified and comprehensive aetiology, the study on all thefactors would be highly industrious and hence, the present research work considersonly occupational asthma, an industrial hazard which results from the aetiologicalfactors related only to the work place. 62
  • 63. THE CONCEPT OF INDUSTRIAL HAZARDS Industrialization, a social and economic revolution in the culture of a nation isbound to carry with it some associated hazards manifested as occupational hazardsand community health problems.• OCCUPATIONAL HAZARDS (OCCUPATIONAL DISEASES)An industrial worker may be exposed to 5 types of hazards depending upon his/heroccupation:A) PHYSICAL HAZARDS:1) HEAT & COLD:Due to Heat: Common Physical hazard Direct effects are burns, heat exhaustion, heat stroke & heat cramps. Indirect effects are decreased efficiency, increased fatigue and enhanced accident rates.Due to Cold: Chilblains Erythrocyanosis Immersion foot & frostbite General hypothermia2) LIGHT: Acute effects of poor illumination are: Eye strain Headache Eye pain Lacrimation Congestion around cornea 63
  • 64. Eye fatigue Chronic effects include ‘Miner’s Nystagmus’. Exposure to excessive brightness or glare is associated with annoyance & visual fatigue. Intense direct glare may result in blurring of vision.3) NOISE: Temporary or permanent hearing loss Nervousness, fatigue, interference with communication by speech.4) VIBRATION: Vibration, especially in the frequency range 10- 500 Hz usually affects hands & arms.5) U.V. RADIATION: This occurs in arc welding. Effects eyes, causing conjunctivitis & keratitis (welder’s flash)6) IONIZING RADIATION: This is found in medicine industries. CO 60 & P-32 are common. The radiation hazards comprise genetic changes, malformation, cancer, leukaemia, depilation, ulceration, sterility and may be death.B) CHEMICAL HAZARDS: Chemical agents act in 3 ways.1) LOCAL ACTION: Some causes dermatitis, eczema, ulcers & cancers. Systemic effects are caused by aromatic nitro & amino compounds like TNT & ANILINE. Occupational dermatitis. 64
  • 65. 2) INHALATION:Dusts: The soluble dusts slowly dissolve, enter the systemic circulation and are eventually eliminated by body metabolism. The insoluble dusts remain, more or less permanently in the lungs, causing Pneumoconiosis. The most common dust diseases in our country are silicosis & Anthracosis.Gases: Simple & Anaesthetic gases are common causes.Metals & their compounds: The ill effects depend on duration of exposure & dosageof concentration of exposure.3) INGESTION: Ingestion of chemical substances such as Pb, Hg, As, Zn, Cr, Cd &P etc.C) BIOLOGICAL HAZARDS: The exposure to infective and parasitic agents may cause brucellosis,leptospirosis, Anthrase, hydatidosis, psittacosis, tetanus, encephalitis, fungalinfections & schistosomiasis etc. Mechanical Hazards: About 10% of accidents in industry are said to be due to mechanical causes. Psycho Social Hazards: Frustration Drug abuse Lack of Job satisfaction Alcoholism Insecurity Tardiness Poor Human relationships Sickness Emotional tension Astentecism Hostility Fatigue Aggressiveness Headache etc., Anxiety Depression 65
  • 66. COMMUNITY HEALTH PROBLEMS:1) Environmental Sanitation problems: a) Housing (Slum & unsanitary dwellings) b) Water pollution c) Air pollution d) Sewage disposal2) Communicable diseases3) Food Sanitation4) Mental Health5) Accident6) Social problems7) Increased Morbidity & Mortality Thus industrialization pollutes different elements of nature like air, water, land& climate producing disorders in the form of ‘Epidemics”. 66
  • 67. THE CONCEPT OF JANAPADODHWAMSA An epidemic (Epi – upon, Demics – people) is the unusual occurrence in acommunity or region, of disease, specific health related behaviour or other health –related events clearly in excess of expected occurrence. This concept is well explained long back by Acharya Charaka in VimanaSthana as “Janapododhwamsa’122. According to this the population of a community oran area with varied individual prakriti, Ahara, Deha, Bala, Abhyasa, Satwa and Vayascan be adversely affected by the turmoil of 4 important environmental aetiologicalfactors viz., Vayu (Air), Udaka (Water), Desa (Land) & Kala123 (Climate), where inthe potency of the effects caused by these factors increases from vayu towards kala inthat order124. It is an established fact that Epidemics result by sensing & savoring suchenvironmental calamities125. The commonest and the basic environmental factor vulnerable to pollution isvayu, the air factor. The unseasonable and extreme occurrences of the atmosphere air,being polluted with unpleasant gases, vapours, dust, sand particles, and smoke withirritating odour126 is highly attributable as a basic industrial pollutant in causing mostcommon of the Industrial Hazards called Occupational Asthma. 67
  • 68. OCCUPATIONAL ASTHMA (OA) This is a disease characterized by variable airflow obstruction and or nonspecific bronchial hyperresponsiveness due to causes and conditions attributable to aparticular occupational environment and not due to stimuli encountered out side thework place.PREVALENCE: Approximately 5% to 9% of asthmatic subjects identify workplace exposure asthe cause of their asthma. This implies that in approximately one to two of every 20asthmatic subjects, investigation of causal relationship between workplace exposureand asthma is indicated. The number of cases of occupational asthma varies from country to countryand from industry to industry. In Japan, 15% of asthma in males is believed to be occupational. In United States, 2% of all cases of asthma are thought to be occupationalorigin. About 16% of animal handlers develop asthma due to animal hair or dust. Between 10% and 45% of workers who process subtilisms, the ‘proteolyticenzymes’ like ‘Bacillus subtilis’ in the detergent industry develop asthma. About 5% of workers exposed to such chemicals as isocyanates and certainwood dusts develop asthma. 16.9% of total subjects are suffering in silk industries, with 36.2% of themwho are working in the processing of natural silk. The prevalence of Occupational Asthma has increased over the past twodecades. This due partly to a better recognition of the condition and partly to anincrease in the number of new chemicals capable of causing occupational asthma inthe work place. At present, more than 250 agents have been implicated in causingoccupational asthma in the work place. 68
  • 69. Table No 10 Causes of Occupational Asthma- Grains, flours, plants and gums Occupation AgentBakers, millers Wheat / Rye flourChemists, coffee bean baggers and handlers, Castor beansgardeners, millers, oil industry workers,farmers, sea men.Cigarette factory workers Tobacco dustDrug manufacturers, mold makers in sweet Gum acaciafactories, printersFarmers, grain handlers Grain dust, Fertilisers & PesticidesGum manufacturers, sweet makers Gum tragacanthStrawberry growers Strawberry pollenTea sifters and packers Tea dust / fluffTobacco farmers Tobacco leafWoolen industry workers WoolFood process workers Green coffee beanLaxative manufacturers PsylliumFlorist Baby’s breath(gypsophila)Plant keeper Weeping fig 69
  • 70. Table No 11 Causes of Occupational Asthma - Animals, insects and fungi Occupation AgentBird fanciers Avian proteinsCosmetic manufacturers CarmineEntomologists Moths, butterfliesFeather pluckers FeathersField contact workers CricketsFish bait breeders Bee mothsFlour mill workers, bakers, farm workers, grain Grain storage mites,handlers alternaria, aspergillusLaboratory workers Locusts, cockroaches, grain weevils, rats, mice, guinea pigs, rabbitsMushroom cultivators Mushroom sporesOyster farmers HoyaPea sorters Mexican bean weevilsPigeon breeders PigeonsPoultry workers ChickensPrawn processors PrawnsSilkworm sericulturers SilkwormsZoological museum curators Beetles 70
  • 71. Table No 12 Causes of Occupational Asthma – Chemicals/Materials - I Occupation AgentAircraft fitters TriethyltetramineAluminum cable solderers AminoethylethanolamineAluminum pot room workers FluorineAutobody workers Acrylates (resins, glues, sealants, adhesives),cyanoacrylates,methymethacrylateFoundry workers Furfurly alcoholBrewery workers Chloramine-TChemical plant workers, pulp Chlorinemill workersDye weighers Levafix brilliant yellow, drimarene brilliant yellow and blue, cibachrome brilliant scarletElectronics workers, soldering. ColophonyEpoxy resin manufacturers Tetrachlorophthalic anhydride,Maleic, Hexdrahydeophthalic, Himic.Foundry mold makers Furan-based resin binder systemsFur dyers Para-phenylenediamineHairdressers Persulphate salts, henna, Freon, tannic acid. 71
  • 72. Table No 13 Causes of Occupational Asthma – Chemicals/Materials - II Occupation AgentMeat wrappers Polyvinyl chloride vapourPaint manufacturers, plastic molders, Phthalic anhydridetool setters .Paint chemical workers TrimeliticPaint sprayers DimethylethanolamineFabric dye workers Reactive dyesPhotographic workers, shellac EthylenediaminemanufacturersRefrigeration industry workers CFCsSolderers Polyether alcohol, polypropylene glycolManufacture AzodicarbonamideHospital staff HexachloropheneLaboratory workers, dialysis nurses, Formalin/formaldehydephenolic resin moldersHealth care workers, bronchoscopy Glutaraldehyde, latexnurses 72
  • 73. Table No 14 Causes of Occupational Asthma - Isocyanates and metals Occupation AgentBoat builders, foam manufacturers, office Toluene diisocyanateworkers, plastics factory workers, refrigeratormanufacturers, TDI manufacturers/users,printers, laminators, tinners, toy makersBoiler cleaners, gas turbine cleaners VanadiumCar sprayers Hexamethylene diisocyanateCement workers Potassium dichromateChrome platers, chrome polishers Sodium bichromate, chromic acid, potassium chromateNickel platers Nickel sulphatePlatinum chemists Chloroplatinic acidPlatinum refiners Platinum saltsPolyurethane foam manufacturers, printers, Diphenylmethanelaminators diisocyanateRubber workers Naphthalene diisocyanateTungsten carbide grinders CobaltWelders Stainless steel fumes 73
  • 74. Table No 15 Causes of Occupational Asthma - Drugs and enzymes Occupation AgentAmpicillin manufacturers Phenylglycine acid chlorideDetergent manufacturers Bacillus subtilisEnzyme manufacturers Fungal alpha-amylaseFood technologists PapainPharmacists, laboratory workers Gentian powder, flaviastasePharmaceutical workers Methyldopa, salbutamol, dichloramine, piperazine dihydrochloride, spiramycin, penicillins, sulphathiazole, sulphonechloramides, chloramine-T, phosdrin, pancreatic extracts,Cephalosporins, Isoniazid, Cimetidine, IpecacuanhaBread manufacture, pharmaceutical worker, α – amylase, pancreatic extractparents of cystic fibrosis children, PaediatricnurseBlood group laboratories BromelainPoultry workers Amprolium hydrochlorideProcess workers, plastic polymer production Trypsin, bromelinworkers 74
  • 75. Table No 16 Causes of Occupational Asthma – Woods Occupation AgentCarpenters, timber millers, woodworkers Western red cedar (Thuja plicata), cedar of Lebanon (Cedrus libani), iroko, California redwood (Sequoia sempervirens), Ramin (Gonystylus bancanus), African zebrawood (Microberlinia), Tanganyika aningre, African maple (Sefroxylon triplochiton), Eastern white cedar, Ebony (Diospyrus crassiflora), Obeche, Ash (Fraxinus americana), PalisanderSawmill workers, pattern makers Mansonia, oak, mahogany, abiruanaShuttle makers South African boxwoodWood finishers Cocabolla (Dalbergia retusa),Wood machinists Kejaat (Pterocarpus anglensis) 75
  • 76. PURVA ROOPA OF SWASA These are the symptoms which occur prior to the manifestation of the diseaseproper. Though no specific purva roopas are mentioned, few general purva roopas, astold by different authors are listed below: Table No. 17S.No PURVA ROOPA M.N127 C.S128 S.S129 A.S130 A.H131 K.S132 1 HRITPEEDA + + + + + - 2 SOOLA + - - - - - 3 ADHMANA + - - - - - 4 ANAHA + + + + + - 5 VAKTRAVAIRASYA + - + - - - 6 SANKHA NISTODA + - - + + - 7 PRANASYAVILOMATA - + - + + - 8 BHAKTADWESHA - - + - - - 9 ARATI - - + - - - 10 PARSWASOOLA - + + + + - 11 USHNA NISWASA - - - - - +Hritpeeda : This may be because of tightness in the chest due to heavy mucus lodgedin the lungs causing severe discomfort during respiration.Soola: This is due to severe and fast respiratory movements performed with difficultydue to disease. The muscles of the chest, flanks and abdomen are restless andcontinuously get exhausted thereby inducing painful condition as soola and parswasoola.Adhmana & Anaha: These are the symptoms of lower intestinal tract resulted fromthe agnimandya which occurs due to incompatible food intake and other etiologicalfactors. This leads to improper and delayed digestion and metabolism.Arati, Bhaktadwesha and Vaktravairasya: These are the symptoms of upper GITresulting due to the effect of ama produced as a consequence of agnimandya. 76
  • 77. Modern literature strongly supports these by explaining premonitory symptoms whichcan be understood as ‘Asthmatic aura’.They are: Sneezing: This occurs as result of stimulation by any irritating agents. Flatulence: This is due to improper digestion and metabolism leading to sluggish Peristalsis of intestines and delayed evacuation of bowels. Drowsiness: This is due to improper circulation to the brain due to inadequate nourishment to the body tissues. Restlessness: This is mainly because of the respiratory distress caused due to shortness of breath. Irritability: This may be an allergic response either externally or internally, occurring along with asthmatic attack. Dry irritant cough may precede or accompany attacks of wheezy breathlessness. 77
  • 78. ROOPA OF TAMAKA SWASA The pratyatmaniyata lakshana i.e., swasa is same for all the panchavidha swasa. The lakshanas of Tamaka swasa according to various authors are: Table No. 18S.No ROOPA M.N133 C.S134 S.S135 A.S136 A.H137 1 PINASA + + - + + 2 GHURGHURUKA + + + + + 3 TIVRAVEGA SWASA + + - + + 4 PRANA PRAPEEDAKA + + - - - 5 PRATAMYATI + + + + + 6 TRIT + + + + + 7 SANNIRUDDHYATE + + - - - 8 PRAMOHAM KASAMANASCHA + + - + + 9 SLESHMANYAMUCCHYAMANETU + + - - - BHRISAM BHAVATI DUKHITAH 10 VIMOKSHANTE MUHURTAM + + + + + LABHATE SUKHAM 11 KANTHA & ASYA UDDHWAMSA + + - - - 12 KRICCHRACCHAKNOTI + + - - - BHASITAM 13 ANIDRA + + - - - 14 PARSWE TASYAVAGRUHNATI + + - + + 15 ASINOLABHATE SOUKHYAM + + - + + 16 USHNAMCHAIVABHINANDATE + + - + + 17 UCCHRITAKSHA + + - + + 18 LALATENA SWIDYATA + + - + + 19 BHRISAMARTIMAN + + - + + 20 VISUSHKASYA + + - + + 21 MUHUHSWASA / + + - + + MUHUSCHAIVAVADHAMYATE 22 SWEDA - - + - - 23 VAMADHU - - + - - 24 ABALA - - + - - 25 AMADWESHA - - + - - 26 PARIGRUHYA SIRO GREEVAM - - - + + 27 KASA - - - + + 28 ARUCHI - - - + + 29 URAH PEEDA - - - + + 30 VEPATHU - - - + + 31 KASAHA SA KAPHA - - + - - 32 GHOSAHA MAHATAVISHTA - - + - - 33 SWAPATHASCHA VIVARDHATE - - + + + 78
  • 79. The present explanation is according to Charaka138 and Madhavanidana139,which appears as: Vata prakopa and Kapha prakopa occur due to their individual nidanas. This isseen as Pratilomagati of vayu and excessive Kaphasrava in Pranavaha Srotas. Thisresults in pinasa, the premonitory symptom rhinitis, which is an excessive nasalsecretion due to mucosal irritation of nose. Vata cannot perform its prakruta karma of soshana of this excess kapha, butonly tries to expel the dushta Kapha present in pranavah Srotas i.e., Sleshmodeeranadue to which Ghurghuruka, the loud stridor like sounds produced due to theobstruction of the respiratory passages. As the quantity and picchilatwa of kapha have increased than normal, itsexpulsion needs more effort. Kasa is the reflex phenomenon to remove theobstruction or irritants existing in the respiratory tract. Due to severity and recurrent swasa, i.e. difficult in breathing, and Kricchrabhashanam, i.e, difficulty in speaking due to Kantodhwamsa occurs. Bhrisam arti,Parswa peeda and Pramoham are the consequences of the distressed coughed andbreath. Sleshmanyamuchyamanetu dukham and Vimokshante sukham are the extremediscomfort and relief respectively observed by the patient before and after theexpectoration of Kapha. Due to adhika dushta kapha, body becomes deficit of pranavayu where byAteeva teevra Vega Swasa is produced which is the manifestation of the effort put bythe body to compensate the oxygen deficit and to remove the excess CO2 in the body. Pratamyati and Sannirudhyate are the subjective experiences of the patientdue to hypoxia and hypercapnia. Aaseeno labhate soukhyam is the sitting posture which is comfortable to thepatient due to lower level situation of diapharagm. This is in contrast to the lying 79
  • 80. posture of the patient where the position of diaphragm is higher comparativelyresulting in extreme discomfort and sleeplessness i.e, Sayaanasswasa peeditah. Thriving for the air, patient breath through open mouth which consequentlyleads to dryness of mouth followed by thirst i.e., Visushkasya and trishna produceddue to Udaka vaha sroto dushti. Aruchi, Annadwesha and Vamathu are the manifestations of Kaphadhikyataand Anna vaha sroto dushti, which supports the concept of swasa being AmasayaSamudhbhava. Increased blood circulation and pressure leads to Lalata Sweda. The movement of the patient’s trunk in typical sitting posture will be similarto that of an elephant rider, which is told as Avadhamyate. Muhur Swasa is the recurrent attack of swasa which is the nature of thedisease. Seeta guna is common for Kapha and Vata dosha and Ushna guna is itscounter property. Hence Ushna ahara and viharas will be the Upasaya to the patientwho naturally desires them. This is Ushnabhinandati. The classical symptomatology as explained by the clinical features of modernliterature only conveys that Asthma is not a uniform static disease but a broaddynamic syndrome. The typical symptoms of asthma consist of a triad of dyspnoea, cough andwheezing, the last often being regarded as the sinequanon. In its most typical form, allthree symptoms coexist. At the onset of an attack, patient experience a sense of constriction in thechest, often with a non productive cough. Respiration becomes audibly harsh,wheezing in both phases of respiration becomes prominent, expiration becomes 80
  • 81. prolonged, and patients frequently have tachypnoea, tachycardia, and mild systolichypertension.The lungs rapidly become overinflated, and the anteroposterior diameter of the thoraxincreases (pigeon chest). If the attack is severe or prolonged, there may be a loss of adventitial breathsounds, and wheezing becomes very high pitched. Furthermore, the accessorymuscles become visibly active, and a paradoxical pulse often develops. The end of an episode is frequently marked by a cough that produces thick,stringy mucus, which often takes the form of casts of the distal airways (curshmann’sspirals) and shows eosinophils and Charcot-leyden crystals. In extreme situationscentral cyanosis occurs and airflow becomes so restrictive that wheezing / ronchi maylessen markedly or even disappears. Cough may become extremely ineffective andthere may be a gasping type of respiratory pattern. The presence of a silent chest andbradycardia in such patients is an ominous sign. These findings imply extensivemucus plugging and impending suffocation. These symptoms may occur for the first time at any age, and may be episodicor persistent. Patients with episodic asthma are usually asymptomatic betweenexacerbations, which occur during viral respiratory tract infections or after exposureto allergies. This pattern is seen in children or young adults who are atopic. Patients with persistent asthma, chronic wheeze and breathlessness are seen.This pattern is more common in older patients with adult onset asthma who are non-atopic and typifies intrinsic asthma. Posture is characteristic in Asthmatic patients. The problem is worse in lyingposture, better in standing position, fixing the shoulder girdle (hunched shoulder) toassist the accessory muscles of respiration. 81
  • 82. Asthma symptoms show a characteristic pattern of diurnal variability ofworsening during night and early morning. Circadian variations in bronchomotor toneand bronchial activity reach their nadir between 3am and 4am, increasing symptomsof broncho constriction. 82
  • 83. TAMAKA SWASA BHEDAS In general Swasa vyadhi is of 5 types basing of hetu & linga bhedas:1) Maha Swasa: Uddhuyamana vata, swasa with dukha, swasa with loud sound like a mattarishabha, and can be heard from long distance, pranasta gnana and vignana, vibhranta lochana, vivrutakshi, vivrutanana, baddha mutra & varcha, viseernavak, and deena are the lakshanas. It is asadhya140.2) Urdhwa Swasa: Deergha urdhwa swasa, adhaswasa is difficult, sleshmavruta mukha and srotases, discomfort due to provoked vata, urdhwa drushti & vibhranta aksha looking here and there, pramoham due to severe vedana, suklaasya, arati, tamas and when urdhwa swasa is more adha swasa is obstructed. It is asadhya141.3) Chinna Swasa: Vicchinna swasa or ceased swasa due to sarva prana peeda, ruk like marma cheda, anaha, sweda, murcha, vasti daha, viplutaksha, pariksheena, and raktaika lochana as the manifestation of the disease, vicheta, parisushkasya, vivarna and pralapa are seen. It is also asadhya142.4) Kshudra Swasa: This occurs from ruksha ahara & vihara sevana and ayasa. There is no athyartha dukha or anga prabadha, it doesn’t interfere with bhojana or pana and causes no discomfort to indriyas143.5) Tamaka Swasa: The symptomatology of Tamaka swasa was explained else where. Though Tamaka Swasa is a single disease entity, it has two types of manifestations basing on different pathologically considerable conditions. They are: 1. Pratamaka Swasa 2. Santamaka Swasa. 83
  • 84. Acharya Charaka, Madhava Nidanakara & Yogaratnakara explained bothtypes while susruta, Ashtanga sangraha & Hridayakaras, and Bhavaprakasakaraexplains only Pratamaka Swasa. Pratamaka Swasa: If Tamaka Swasa is associated with Jwara & Murcha, it is called Pratamaka. Udavarta, Rajas, Ajeerna, Klinnakaya & Veganirodha are the etiological factors attributed. According to Vagbhata this type of Swasa subsided by giving Seetala Upachara144. Santamaka Swasa: This type aggravates due to tamas and alleviates with Seetala upachara. The patient with this condition feels as being submerged in tamas. The translators of Charaka Samhita of Jamnagar are of the opinion that this type is a Cardiac Asthma145. On modern lines the disease Bronchial Asthma is traditionally divided into 2types based on the stimuli initiating the disease. They are:1) Extrinsic (Allergic/ Atopic/ Reagin-mediated) a) Allergic b) Occupational c) Allergic Bronchopulmonary Aspergillosis.2) Intrinsic (Idiosyncratic/ Non-atopic) 84
  • 85. Table No. 19 EXTRINSIC ASTHMA INTRINSIC ASTHMAExtrinsic Asthma is initiated by Type – Intrinsic Asthma is initiated by diverse,I Hypersensitivity immune reaction non-immune mechanism.induced by exposure to extrinsicantigen. CLINICAL FEATURESIt is most common type. Less common type.Usually begins in childhood or in early Develops later in life, in adults over 35adult life (Teenage) yrs or more.Positive family history of atopy is No family history.common, and asthmatic attacks areoften preceded by allergic rhinitis,urticaria or eczema.Attacks are related to specific antigens Attacks are related to infection,like household dust, pollen, animal exercise, stress etc.,dander, moulds & particular foodsetc.,Intermittent attacks Often persistent asthma.Attacks are acute but usually self- Attacks are more fulminant and severe.limiting.Asthma is not Aspirin sensitive. Aspirin-sensitivity is present.Nasal polyps are occasional. Nasal polyps are frequent.Occupational asthma stimulated byfumes, gases, organic & chemical dustsis a variant of extrinsic asthma.Allergic broncho-pulmonaryAspergillosis is also a variant ofextrinsic asthma. INVESTIGATIONSSkin test is usually positive with Skin test is usually negative.immediate wheal & flare by specificoffending inhaled antigen.Ig E is frequently raised. Ig E is usually normal or low. 85
  • 86. SAMPRAPTI The process of manifestation of a disease, along with the characteristicfeatures of the dosha which are exhibited during the course of establishment of thedisease is SAMPRAPTI146. The way the dosha dusti occurs due to nidana and the way the vyadhi arambhaor nivrutti takes place is SAMPRAPTI147. ‘Jati’ & ‘Agati’ are the paryayas of samprapti148. According to the swasa vyadhi samprapti, Pranavaha, Udakavaha & Annavahasrotases and amasaya / pitta sthana are the organ systems affected in the pathogenesisof the disease149 due to the vitiation of Vata and Kapha.VATA: The role of vata in Tamaka swasa samprapti can be established based on thefollowing factors: ‘Kshepta bahir malanam’ – prakupita vata pitta kaphas which are harmful to the sareera are considered as malas by Charaka150. Hence in this context the dusta kapha produced is considered as mala and it is the function of the vata to expel it outside. Prakopa of Vata occurs due to Dhatu kshaya and Margavarana151. The amasaya sthita Vata when vitiates causes ruja of Hrudaya, Nabhi, Parshwas & Udara,and also causes Trishna, Udgara, Visuchika, Kasa, Kantha shosha, Asya shosha and Swasa152.Prana Vata: The following are the factors supporting the role of Prana vata in TamakaSwasa: Sthanas of Prana Vata are the sthanas of Prana vaha Srotas itself which is the adhishthana of Tamaka swasa. According to Chakrapani Prana vata moves through Prana Vaha srotases153. Swasa is one of the prakruta karmas of Prana Vata154. Sarangadhara’s description of Prana vata clearly indicates the functions of respiration (Deha Preenana and Jeevana of jatharanala), which are affected in Tamaka Swasa155. 86
  • 87. The lakshanas of Prana vaha sroto dushti are abnormalities of swasa like Ati srushta, Ati baddha, Kupita, Alpalpa, Abhikshna and Swasa with Shabda and Soola156. According to Susruta it generally causes the diseases Hicca and Swasa. The Chikitsa indicated in Prana vaha srotodushti is that of swasa. This statement is a good evidence for the relationship between swasa and Pranavaha srotases157. In Kaphaavruta Prana also swasa is seen as a lakshana158.Udanta Vata:The following factors establish the role of Udana vata in swasa: Vakpravrutti, prayatna, urja, maintenance of bala and Varna are the functions of udanavata, which are all disturbed in swasa vyadhi159. Srotopreenana is another function mentioned in Astanga sangraha which is absolutelyhampered in swasa160. Vikruti of Udanavata causes urdhwa uatrugata vyadhis like hicca, swasa, kasa etc. Vijaya Rakshita and Gangadhara used the term ‘Udana vahasrotases’ in swasa samprapti. In pranaavruta Udana, Sirograha, pratisyaya, Nisswasochwasa sangraha, Hridroga and Mukhasosha161 are seen and in Udanaavruta Apana Chardi, swasa etc., are seen162.KAPHA:This is stated as pradhana dosha in Tamaka swasa. The following factors establish itsrole: Kapha is said to be ‘Tamo guna bhuyishtha’163, and the name Tamaka swasa itself contains ‘Tamaka’ sabda which indicates the role of Kapha. The avarana of pranavata with kapha is a factor responsible for swasa164. The avarodha of srotases with kapha is a factor is swasa165. The Kapha situated in the uras is udeerita (aroused) in shwasa166. Increase of kapha can cause swasa167.Kapha also exists in five forms among those Avalambaka and kledaka play a key rolein swasa.Avalambaka Selshma:The involvement of avalambaka sleshma is swasa is appreciated by the followingfactors: Uras, the seat for avalambaka sleshma is also the seat for swasa168. 87
  • 88. Puppusas which are involved in swasa are supported and protected by avalambaka sleshma. Kaphaavruta Prana Vata also causes swasa169. Here the Kapha can be considered as Avalambaka.Kledaka Kapha:The role of Kledaka kapha can be established based on the following factors: The sthana of kledaka kapha is amasaya, which is also the udbhava sthana for swasa170. Kledaka kapha aids in the sukha jarana of ahara by its oudaka guna, and its vriddhi causes Agni vaishamya as seen in swasa171. Kledaka kapha protects the other seats of sleshma by udaka karmas through its prabhava, and its vikruti causes vikruti of other kaphas172.UDHBHAVASTHANA: The udbhava sthana of swasa is mentioned as Pittasthana by Charaka173 andAmasaya by vaghbhata174. According to Charaka Amasaya is visesha sthana forPitta175 and Chakrapani comments that Pittasthana denotes Amasaya.Amasaya:Amasaya is one of the koshtangas, situated in between nabhi and sthana176.Its involvement in the causation of swasa can be enunciated based on the followingpoints: Amasaya is the moola for Anna vaha srotases, which is primarily affected in Tamaka swasa177. Visesha sthana for Pitta according to Charaka178. Seat for Sleshma according to Susrutha179. Kapha locates in urdhwa bhaga and Pitta in adhobhaga180. Sambhavasthana for Sleshma181. Seat for Kledaka Sleshma and Ranjaka Pitta182. Samana Vata moves in it183. Kapha is produced at the beginning of paka and Pitta produced at the pachyamanavastha184. Shwasa vyapara is mentioned as the pravrutti of amasaya by Indu in his Sasilekha commentary. 88
  • 89. ADHISTANA:Uras is said as the adhishtana for swasa185, because of the following reasons: Puppusas which are the organs for swasa are located in uras186. Prana Udana vatas and Avalambaka kapha are located in the Uras187. Hridaya is also situated in the uras, sosha of which occurs by the effect of swasa188.SROTASES: ‘Srotas’ denotes a channel, and the entire body is composed of innumerablesrotases which are classified into Antarmukha and Bahirmukha. Though Antarmukhasrotases are innumerable, bahirmukha srotases are only 9 in number. In view ofkayachikitsya, Acharya Charaka explained 13 srotases, while Susruta explains 11pairs of srotases in view of shalyatantra.The srotases are divided into 3 main categories depending on the material theytransport: 1. Srotases which transport Ahara dhatus 2. Srotases which transport Asthayee dhatus 3. Srotases which transport Mala dhatus Those which transport Ahara dhatus include pranavaha, udakavaha &annavaha srotases which are related to and affected by swasa vyadhi. Hence, thepatients of swasa vyadhi are presented with improper nourishment leading to thesoshana of Hridaya and Rasadi dhatus189.Prana vaha srotas:The role of Prana vaha srotas in Tamaka swasa samprapti: Sroto Dusti Lakshanas like Atisrista swasa, Atibaddha swasa, Kupita swasa, Alpa swasa, Adhika swasa, Sasabdha swasa, Sasula swasa etc are related to swasa vyadhi 190. The treatment given in swasa chikitsa is mainly indicated in treating pranavaha sroto dusti. 191Udakavaha srotas: The role of Udaka vaha srotases in Tamaka swasa samprapti: Tamodarsana, trishna and asyasosha are some of the lakshanas of Udaka vaha sroto dushti, which are seen in Tamaka swasa192. Water balance is one of the important functions of respiration193. 89
  • 90. Annavaha srotas:The role of Annavaha srotases in Tamaka swasa samprapti: Amasaya which is moola for Annavaha srotases is also the udbhava sthana for swasa194. Ahara viharas which causes anna vaha sroto dushti also cause swasa195. Kledaka kapha involved in swasa samprapti is located in Amasaya196. Some of the Annavaha sroto dushti lakshanas such as bhakta dwesha, asya vairasya, anaha, etc., are seen as purva roopas in Tamaka Swasa197. Some other lakshanas of Annavaha sroto dushti like aruchi, vami etc. are seen as roopa in Tamaka Swasa198. The chikitsa advised in Anna vaha sroto dushti, i.e., ama dosha chikitsa is also advised in Tamaka Swasa199.ROLE OF PITTA IN SWASA SAMPRAPTI: Pitta performs pachana and thereby ‘Sajateeyeekarana’ of the ahara that enters the body. This is the intention in saying that Amasaya or Pitta sthna is the udbhava sthana of Swasa vyadhi, where the prakopa of Vata & Kapha occurs by the intake of specific prakopakra ahara. Kapha vilayana occurs due to the presence of pitta, without which the Kaphasrava cannot occur. This supports the role of inflammation in the manifestation of Bronchial Asthma.SAMANYA SAMPRAPTI OF SWASA: According to Ashtanga Hridaya, the prakupita or dushta vata located in theuras, is obstructed by dushta kapha and moves all over the uras causing dushti ofpranavaha, Udaka vaha and Annavaha Srotases, thus causing swasa, which isAmasaya Samudhbhavam200. According to Susruta, vata leaving its Prakruti moves along with Kapha inupward direction causing Swasa Vyadhi201. 90
  • 91. TYPES OF SAMPRAPTITable No 20 TYPE OF SAMPRAPTI RELATIVE PLACE OF TAMAKA SWASASankhya 5 types:Maha, Urdhwa,Chinna,Tamaka,KshudraPradhanya. KaphaPradhana.Vidhi Tamaka Swasa.Vikalpa Amshas of Kapha and Vata.Bala Based on Nidana, Purva roopa etc.,Kala Varsha & Vasanta rutu, Ratri. PATHOLOGY OF BRONCHIAL ASTHMA Bronchial asthma is a disease characterized by hyper-reactive airways leadingto episodic, reversible bronchoconstriction, owing to increased responsiveness of thetracheobronchial tree to various stimuli. Asthma results from a state of persistent subacute inflammation of airwayswhere the airway epithelium is both the target and a contributor to the inflammatorycascade, which can be initiated by a variety of different factors in different patients. Though the Asthmatics are divided clinically into Extrinsic and Intrinsic type,the pathological features of both types are identical. The pathology of Asthma can be better understood by studying the mostcommon type i.e., Atopic asthma, where the pathogenesis is mediated by Ig E. 91
  • 92. TYPE I HYPERSENSITIVITY Type I reactions are mediated by Ig E antibodies. An allergen stimulates β lymphocyte production of Ig E, principally at themucosal site of entry of the antigen and in the draining lymph nodes – through TH2subset of CD+ helper T cells assistance. Ig E antibodies formed will have a strong tendency to attach to mast cells andbasophils, which have high-affinity receptors for the Fc portion of Ig E. When a mast cell or basophil, armed with cytophilic Ig E antibodies, is reexposed to the specific allergen, a series of reactions takes place, leading eventually tothe release of a variety of powerful mediators responsible for the clinical expressionof type I hypersensitivity reaction.PRIMARY MEDIATORS: These are contained within Mast cell granules. Thesecan be divided into 4 categories:1) BIOGENIC AMINES: ‘Histamine’ – Intense bronchial smooth muscle contraction Increased vascular permeability Increased secretion of Nasal, Bronchial & Gastric glands. ‘Adenosine’ – Enhances mast cell mediator release Broncho constriction Inhibits platelet aggregation.2) CHEMOTACTIC MEDIATORS: “ Eosinophil Chemotactic Factor” (ECF) “ Neutrophil Chemotactic Factor” (NCF)3) ENZYMES: (These are contained in the granule matrix) Proteases – Chymase Tryptase Acid Hydrolases – The enzymes lead to the generation of kinins and activated components of complement (eg. C3a) by acting on their precursor proteins. 92
  • 93. 4) PROTEOGLYCANS: ‘Heparin’SECONDARY MEDIATORS: 2 Classes of compounds.1) LIPID MEDIATORS: These are generated by sequential reactions in the mast cell membranes that lead to activation of “PHOSPHOLIPASE A2”, an enzyme that acts on membrane phospholipids to yield “ARACHIDONIC ACID”. Arachidonic acid is the parent compound from which “LEUKOTRIENES” and “PROSTAGLANDINS” are derived by “5-LIPOXYGENASE” and “CYCLOOXYGENASE” pathways.a) ‘Leukotrienes’: Leukotrienes C4, D4 & E4 are the most potent vasoactive and spasmogenic agents. They are several thousand times more active than histamine in increasing vascular permeability and causing bronchial smooth muscle contraction. Leukotriene B4 is highly chemotactic for Neutrophils, Eosinophils & Monocytes.b) ‘Prostaglandin D2’ – Intense bronchospasm & increased mucus secretion.c) ‘Platelet-activating factor’ (PAF) – It is not a product of Arachidonic acid metabolism. It is formed from Membrane phospholipids. Its functions are: Platelet aggregation Release of Histamine Bronchospasm Increased vascular permeability VasodilatationProinflammatory actions: Chemotatic to neutrophils and eosinophils. At higherconcentrations, it activates the newly elicited inflammatory cells, causing them toaggregate and degranulate.2) CYTOKINES: (IL-1, IL-3, IL-4, IL-5, IL-6, TNF-α & GM –CSF)These are the polypeptides produced by Mast cells.These have ability to recruit and activate inflammatory cells. TNF-α is an important mediator of Ig E dependant cutaneous reactions. 93
  • 94. It is a potent proinflammatory cytokine that can attract neutrophils and eosinophils, favour their transmigration through the vasculature and activate them in the tissues. IL – 4 is important for the recruitment of eosinophils. Inflammatory cells that accumulate at the site of reactions are additional sources of cytokines and histamine releasing factors that cause further mast cell degeneration.Ig E mediated hypersensitivity reaction elicits an ‘Acute immediate response’ and a‘Late phase reaction’.a) ACUTE IMMEDIATE RESPONSE: This occurs with in minutes after stimulation, and mainly causes release of mediators leading eventually to bronchoconstriction. In addition, direct stimulation of sub epithelial vagal (parasympathetic) receptors provokes bronchoconstriction through both central and local reflexes.b) LATE-PHASE REACTION: This starts 4-8 hours later and may persist for 12- 24 hours. This is mediated by swarm of leucocytes which are recruited and activated bychemotactic factors and cytokines, thereby perpetuating the chronic inflammatoryreaction. HISTOLOGICAL FINDINGS OF PATHOGENESISThe occlusion of bronchi & bronchioles by thick and tenacious mucus plugs. Thesemucus plugs contain whorls of (twisted strips) normal or degenerated shed respiratoryepithelium called CURSCHMANN’S SPIRALS.Sputum usually contains CHARCOT-LEYDEN CRYSTALS which are made up ofEosinophil membrane protein.Bronchial wall shows: Thickened basement membrane of bronchial epithelium. Edema and inflammatory infiltrate or exudates in the bronchial wall consisting of lymphocytes, plasma cells with prominence of eosinophils. Submucosal oedema. Hypertrophy of submucosal glands. 94
  • 95. Hypertrophy of bronchial smooth muscle, a reflection of prolonged broncho constriction. Emphysematous changes sometime occur, and if chronic bacterial infection has supervened, bronchitis may appear.In the more severe forms, the progressive hyperinflation may eventually produceemphysema. Superimposed bacterial infection may lead to chronic persistentbronchitis, bronchiectasis or pneumonia. In some cases, corpulmonale and Heartfailure eventually develop. PATHOPHYSIOLOGYThe pathophysiologic hallmark of asthma is: Broncho constriction Vaso dilatation Vascular congestion Increased vascular permeability Increased Bronchial secretion/Mucus Oedema of Bronchial wall Impaired muco-ciliary transport These effects results in: Increase in airway resistance. Decrease in FEV and flow rates. Hyperinflation of lungs and Thorax. Increased work of breathing. Alteration in respiratory muscle function. Changes in elastic recoil. Abnormal distribution of both ventilation and pulmonary blood flow with mismatched ratios. Altered arterial blood gas concentration. FEV1 and / or PEFR is typically less than 40% of predicted. Residual volume frequently approaches 400% of normal, in acute patients. Functional Residual capacity doubles. Hypoxia is a universal finding during acute exacerbations. 95
  • 96. Most asthmatics have hypocapnia and a respiratory alkalosis Presence of metabolic acidosis in acute asthma signifies severe obstruction. Cyanosis is a very late sign.With the increasing severity and the chronicity of the disease remodeling of theairway occurs, leading to fibrosis of the airway wall, fixed narrowing of the airwayand a reduced response to medication.PATHOGENESIS OF OCCUPATIONAL ASTHMA:Occupational asthma result from 2 mechanisms:1. Immunologic: This Occupational Asthma occurs upon exposure to an agent after alatent period of immune sensitization. The mechanism is Ig E mediated.2. Non Immunologic: This occupational Asthma may or may not occur after alatency period of exposure to an agent(s) which doesn’t induce immune sensitization. 96
  • 97. VYAVACCHEDAKA NIDANA Tamaka Swasa can be confirmed by differentiating it from other types ofSwasa. They are:1. Maha Swasa: Uddhuyamana vata, swasa with dukha, swasa with loud sound like amattarishabha, and can be heard from long distance, pranasta gnana and vignana,vibhranta lochana, vivrutakshi, vivrutanana, baddha mutra & varcha, viseernavak, anddeena are the lakshanas. It is asadhya.2. Urdhwa Swasa: Deergha urdhwa swasa, adhaswasa is difficult, sleshmavrutamukha and srotases, discomfort due to provoked vata, urdhwa drushti & vibhrantaaksha looking here and there, pramoham due to severe vedana, suklaasya, arati, tamasand when urdhwa swasa is more adha swasa is obstructed. It is asadhya.3. Chinna Swasa: Vicchinna swasa or ceased swasa due to sarva prana peeda, ruklike marma cheda, anaha, sweda, murcha, vasti daha, viplutaksha, pariksheena, andraktaika lochana as the manifestation of the disease, vicheta, parisushkasya, vivarnaand pralapa are seen. It is also asadhya.4. Kshudra Swasa: This occurs from ruksha ahara & vihara sevana and ayasa. Thereis no athyartha dukha or anga prabadha, it doesn’t interfere with bhojana or pana andcauses no discomfort to indriyas. Kasa, Kshaya, Sosha and Yakshma are the different conditions which are to be considered to confirm the diagnosis of Swasas. Swasa is found as lakshana swaroopa in Yakrutodara, Hridroga and Yakshma vyadhis, as Upadrava Swaroopa in Pandu and Vataja Kasa. 97
  • 98. DIFFERENTIAL DIAGNOSIS: The differentiation of asthma from other diseases associated withdyspnoea and wheezing is usually not difficult, particularly if the patient is seenduring an acute episode. An extremely common feature of asthma is nocturnalawakening with dyspnoea and for wheezing.Disorders that mimic asthma typically fall into one of the 3 categories: 1) Upper & Lower airway disorders 2) Systemic Vasculitides 3) Psychiatric disordersTable No. 21 1) Upper & Lower airway disordersUpper airway disorders Lower airway disordersVocal cord paralysis Non asthmatic COPD (Chronic bronchitis &Vocal cord dysfunction emphysema)syndrome BronchiectasisForeign body aspiration TuberculosisGlottic dysfunction Allergic bronchopulmonary mycosisLaryngotracheal masses Cystic fibrosisLaryngeal edema Eosinophilic pneumoniaTumor Bronchiolitis obliteransTracheal narrowing NeoplasmsTracheomalacia Recurrent pulmonary emboliAirway edema Carcinoid tumors Allergic alveolitis (Farmer’s lung Bird breeder’s lung Bagassosis Weaver’s cough etc., )2) Systemic Vasculitides: CHURG – STRAUSS Syndrome etc.,3) Psychiatric disorders: Conversion disorders like Functional asthma, Emotional laryngeal wheezing, Episodic laryngeal dyskinesis. 98
  • 99. Table No 22 ASTHMA COPDHISTORYAllergy or asthma in patient’s Yes NofamilyCough and sputum Often recent Over many yearsOnset of breathlessness Sudden GradualVariable breathlessness Much SlightAttack of breathlessness atrest Common UncommonCough at night Awakens coughing Wakes, then coughsINVESTIGATIONSImproved in PEFR afterbronchodilator i.e., reversible Usually Little or moreobstruction ‘Morning dip’Daily variations in PEFR increases day to day LittleTable No 23 BRONCHIAL ASTHMA TROPICAL EOSINOPHILIAHISTORY Usually starts before 3Age years of age Any ageDuration of symptoms Long duration Short duration Dyspnoea more thanCough & Dyspnoea Paroxysmal cough more cough. Breathlessness than dyspnoea particularly after bout of coughFever Rare CommonLoss of Weight Seldom Fairly common Disproportion between Compatible with degree cough and breathlessnessAuscultatory signs of cough and and signs. breathlessness 99
  • 100. Table No 24 BRONCHIAL ASTHMA CARDIAC ASTHMAAge of onset At any age from childhood to Onset usually after 40 about 30 years yearsTime of attack About 3-5 a.m. Midnight – about 12-2 a.m. Precipitated by any of the May be precipitated byMode of onset Causative factors exertion Starts with dyspnoea Couch and dyspnoea almost simultaneous.Symptoms Expectoration of thick Cough associated with tenacious mucous. watery expectoration Paroxysm ceases when Cough which increases in becomes more. intensity towards the end of attack Accessory muscles of Not active Respiration active. Usually expiration is prolonged Both the phases ofSigns respiration are prolonged No signs of cardiac involvement Signs of cardiac involvement present B.P. – normal or low B.P. raised Eosinophils, Charcot-Leyden No Eosinophilia. crystals & Curshmann’s spirals Copious and frothy ifSputum present. pulmonary oedema is presentOther conditions considered for differential diagnosis of Asthma: ‘Munchausen Syndrome’ or malingering may rarely explain the patient’s complaints. Advanced Chronic Nephritis. Severe Anaemia. 100
  • 101. INVESTIGATIONS & LABORATORY FINDINGSFollowing laboratory findings and investigations can be made use for the diagnosis ofBronchial asthma: Positive wheal-and-flare reactions to skin tests can be demonstrated to various allergens. Rise in the eosinophilic count of sputum or peripheral blood. (Eosinophilia in the range of 5-15% of TLC is found. During exacerbation, it increases). An increased serum level of total or allergen – specific Ig E (Radio Allergo Sorbent Test – RAST) may be helpful. Measurement of FEV1/VC ratio or PEF provides a fairly reliable indication of the degree of airflow obstruction. These parameters are used to examine whether asthma is provoked by exercise, hyperventilation or occupational exposure. In asthma there is usually a marked diurnal variation in PEF, the lowest values being recorded in the mornings – ‘Morning dipping’. The chest radiograph (Chest x-ray) is not significant, but show hyper-inflation in an acute attack of asthma. It reveals complications of severe asthma such as ribfracture, pneumothorax and pneumomediastinum. It may be rarely show mediastinal, pericardial, or subcutaneous emphysema in patients with acute severe asthma. Arterial blood gas analysis (of PaO2 & PaCO2) is indispensable in the management of patients with acute severe asthma. Lung volumes such as Residual Volume (RV) and Total Lung Capacity (TLC) are increased. CO diffusion capacity is also increased in asthmatics. Pulse Oximetry shows readings less than 92%. 101
  • 102. UPASAYA – ANUPASAYAS Charakacharya mentioned Upasayaanupasayas of Tamaka Swasa as:UPASAYA:These are the factors which induce relief and are desirous by the patient.1. Sleshma Mokshanam: This is the expectoration of the Phlegm produced during productive cough. As the excess mucus production in the lungs obstructs the passages and causes difficulty in breathing, its expulsion makes the passages clear and patient feels free to breath.2. Aasanam: This is the sitting posture which is comfortable because in this posture the diaphragm will be at the lowest level allowing the lungs to expand (inferiorly) and thus help in easy breathing.3. Ushna Ahara: These are the hot food and other eatables which are desirable by the patient as they keep the viscosity of the mucus very low thus assisting in easy propulsion of the phlegm to the exterior.4. Ushna Vihara: These are the warm climatic conditions and habitual factors which are very conducive to the patient as they keep the respiratory system warm and all the passages clear and open, allowing easy respiration.ANUPASAYA:These are the factors which aggravate the symptoms and are undesirable to the patient.1. Sleshma Amokshna: This is the stagnation of the Phlegm in the lungs thus imparting extreme difficulty to the patient in breathing.2. Sayanam: This is the lying posture which aggravates the condition of breathlessness due to the alignment of diaphragm at the higher level thus restricting the expansion of the lung during inspiration, and hence causing difficulty in breathing.3. Megha, Ambu, Seeta, Pragvata: These are the cloudy atmosphere, cold water and weather and the cool breeze from the east which is particularly very cold and discomfortable to the patient. These factors cause the constriction of respiratory passages and increases the viscosity of the mucus thus restricting the easy breathe.4. Sleshmala Ahara: These are the foods which are cold, oily and heavy for digestion. These mainly increase ama condition in the body.5. Sleshmala Vihara: These are the atmospheric, behavioral and habitual factors which are provocative to the symptoms of the disease. 102
  • 103. SADHYA – ASADHYATA Chronicity of the disease plays important role in planning the treatment for adisease. Of all the types of Swasa, Maha swasa, Urdhwa swasa, Chinna swasa areAsadhyas and shall not be considered for treatment. Kshudra swasa is Sadhya.Tamaka Swasa is Kricchra Sadhya in nature202. Tamaka swasa is said to be asadhya ifafflicted a weak person or if it prolongs for more than 1 year duration. Asadhya is oftwo types viz., Yapya and Anupakramya and Tamaka swasa falls into Yapya type ofAsadhya vyadhi. Yapya diseases are those which are deep rooted, affecting multiple dhatus,having lodges in marmas, with frequent recurrence and chronic periodicity. Modern medicine has an edge over the Asthma excepting some conditionswhere the paroxysms of attack leads to ‘status asthmaticus’, where in the prognosis isfatal. 103
  • 104. UPADRAVAS Though there is no description of Upadravas for Tamaka Swasa, modernliterature contributes few complications for Bronchial asthma.COMPLICATIONS OF BRONCHIAL ASTHMA: Complications of asthma include exhaustion, dehydration, airway infection,tussive syncope. Acute hypercapnic and hypoxic respiratory failure occurs in severedisease.1) RESPIRATORY:a) From mucus plugs – i) Atelectasis lobar or lobular ii) Bronchiectasisb) From cough – i) Subcutaneous emphysema ii) Mediastinal emphysema iii) Spontaneous pneumothorax iv) Cystic degeneration of lungs v) Spontaneous rib fracture.c) From infection – Recurrent bronchitis and pneumonia.d) From uneven ventilation and pulmonary perfusion – Respiratory failure and corpulmonale.2) CARDIAC:a) Dysrhythmias from hypoxia and stress of asthma, compounded by bronchodilatortherapy with a β-agonist and theophylline.b) Myocardial infarction rarely occurs in acute severe asthma.3) HYPOKALEMIA: Due to high-dose corticosteroids, high dose β-agonists,respiratory alkalosis of hypocapnia.4) OTHER COMPLICATIONS:a) Nausea and vomiting from theophylineb) Acute myopathy due to high-dose I.V. steroids. This can lead to respiratory muscleweakness. 104
  • 105. ARISHTA LAKSHANAS Arista lakshanas are the signs and symptoms which suggest the certainity of death.Swasa itself is an arista in diseases like Sannipata Jwara, Gulma, Hridroga, Vatarakta,Yakshma, Medovriddhi, Pleehodara, Yakritodara and Jalodara. The arishta lakshanasof swasa vyadhi are: The patient taking long expiration followed by short inspiration and then faints. The patient whose expiration is either abnormally long or short and gives sugandha or dugandha smell. The rogi with Heena Varna, bala kshaya and sleshmadhika ahara developing urdhwa swasa.. The rogi losing ushnata from the body, whose mutra & pureesha are grathitha and feels pain in vankshana, while suffering from swasa. The balavaan rogi suffering from atisweda, atidaha, hikka along with swasa. The rogi suffering from trishna, siro roga, moha, dourbalya, antrakoojana and sakrut bheda along with swasa. A durbala rogi with ghurghuruka, praswasa, saithilya, atisara, pipasa and mukha sosha. The appearance of Atisara, Jwara, Hikka, Andagranthi and Medhra Sopha as complications in swasa or kasa. Swasa rogi dreaming as if he is walking. It should be understood from these arista lakshanas that the ultimate prognosisof swasa vyadhi could be fatal if not dealt within time. This understanding is for goodpractice by a clinician who is intelligent and reputed enough. 105
  • 106. TAMAKA SWASA CHIKITSA All the five types of swasa are teevra and asukari in nature and of which Mahaswasa, Urdhwa Swasa and Chinna Swasa are Asadhyas and Kshudra swasa is sadhya.Tamaka Swasa is said to be sadhya within one year of onset and yapya after that. Charakaacharya enunciates that the treatment should be administeredimmediately for both Sadhya and yapya types. If the treatment is delayed, it destroysthe patient’s Sareera as is the destruction of dry grass by the fire203. Charaka204 classified the patients into 4 categories viz., balavan,Durbala, Kaphadhika & Vatadhika. These can be categorized into two groups basingon their similarity i.e., Kaphadhika & Balavan, Vatadhika & Durbala. Kaphadhika & Balavan: These patients should first be given anupa and varija mamsa rasas followed by sneha & sweda karmas before proceeding to shodhana therapy. After Samshodhana, the patients should be given Pathya ahara, swasahara dhooma pana & avalehyas205 etc., Vatadhika & Durbala: The patients having vatadhikyata and Ruksha shareera and who are durbala,baala or vriddha should be treated with samskrita jangala or anupa mamsa rasas,snehas and yushas possessing vata samaka gunas. Sodhana procedures such as vamana or virechana should not be administeredto those patients whose kapha dosha is not aggravated and to whom swedanaprocedure was not performed. Sodhana chikitsa is to be done only to strong patients,and the weak are to be treated with samanoushadhis such as Kashayas, Lehyas,Snehas and Brimhana dravyas206. Charakacharya also advocates Brimhana and Samana chikitsas irrespective ofsodhana procedure being done to them207. 106
  • 107. In Swasa Vyadhi, as the vitiated Kapha and Vata doshas will be of samestrength, the treatment should not aim at any single dosha. Though Samana is thetreatment for Kapha and Brimhana is for Vata, administering one treatment willalleviate one dosha and may aggravate other dosha and hence both the treatmentprocedures should be given alternately in order to maintain a homeostatic therapeuticeffect.SPECIFIC TREATMENT FOR TAMAKA SWASA:A. THE CONCEPT OF RASAYANA Charakacharya advocated Rasayana therapy in addition to the panchakarmaprocedures in the pathological conditions which occur among large populationsimultaneously, involving environmental factors as aetiology. Considering Tamaka Swasa as the manifestation due to industrial pollutants,the treatment through Rasayana oushadha as mentioned in Janapadodhwamsa chikitsais planned, giving the disease a status of epidemic and Industrial hazard. Rasayana chikitsa is a disease modifying and prophylactic therapy, whichaims at fortifying the ultimate natural resistance of an individual i.e., the innateimmunity. The concept and practical implication of the Rasayana was well elucidated byCharaka208, Susruta209, Vagbhata210, Yogaratnakara211, Bhaishajya Ratnavali212,Bhava Prakasha213, Vangasena214, Hareetha Samhita215, Rasa Ratna Samucchayam216and Gada Nigraha217. Rasayana therapy has multidimensional and positive impact on the health ofan individual. It promotes health, prevents disease, delays ageing & develops youth. Ithas its effect both on mind and body. The Rasayana oushadha performs thesefunctions by improving the qualitative nourishment to the Rasadi saptha dhatus,ultimately rendering immunity to the body. 107
  • 108. While all the Authors explained the general adaptability of Rasayana, Susrutaacharya elucidated the disease specific Rasayana therapies under the name of‘Naimittika Rasayana’218, which performs the actions of both Samsamana andSamsodhana, thus combating the disease on the whole.B. TREATMENT PRINCIPLE IN PRESENT STUDY The manifestation of the disease ‘Tamaka Swasa’ involves varied contributoryfactors leading to different consequences where the treatment approaches should bemore meticulous considering the pathophysiological states of the disease.Different aetiological factors forming nidana to Tamaka swasa will be sufficientenough in rendering pitta sthana to become more vulnerable in triggering the basicsamprapthi ghatakas viz Kapha & Vata, thereby establishing they vyadhi. The consequential occurrence of agni dourbalya leads to improper digestionand metabolism of the ingested food thereby disturbing the equilibrium of Kapha &Vata doshas resulting into vitiated and aggravated Kapha & Vata. The cumulative effect of this basic pathology propagates the altered regulationof Vata i.e., the pratilomagati, against to its natural anuloma gati. The undesirablepropagation of Vata, being supported and obliterated by aggravated kapha creates thedisturbance in Prana vata & Udana vata functions and vitiates the prana vaha, UdakaVaha and Annavaha Srotases yielding the symptomatology from a prodromal stage,pinasa to an established stage of Tamaka Swasa. The whole depiction of the disease goes purely by the citation as told byDridhabala – ‘Kapha Vatatmakavetau pittasthana samudbhavau219’ where it explainsthat the root cause of the origin of the disease is pittasthana leading to the vitiationand perversion of Kapha & Vata doshas, the ultimate culprits which victimize thePranavaha, Udakavaha & Annavaha srotases and disturbs the Prana vata & Udanavata functions. 108
  • 109. Thus the complete pathophysiology sets in 3 stages, first being the disturbancein Agnivyapara due to undesirable aetiological factors which hinders the capacity ofagni causing agnimandhya thereby producing ama thus initiating a pathologic stage,next being the undermetabolism and underassimilation of Vata & Kapha doshasappearing as an after effect of the first stage and, the consequent vitiation of whichultimately leads to the final stage of pratiloma gati of vata affecting the said srotases.With this elucidative samprapthi, it is to be understood that the treatment modalities todeal the condition should be planned considering the 3 stages viz., Agni Dourbalya(Agni vikruti), Kapha vata dosha vitiation & Pratiloma vayu.The drug ‘Sri Bahusala Gudam’ considered for the present study is a compoundpreparation where the ingredient drugs possess those properties which clearly nullifythe samprapti ghatakas. The inherent property of the ingredient drugs like Chitraka, Trikatu, Vidanga,Hareetaki, Danti, Gavakshi, Ela, Lavanga & Guda performs the functions of Deepana,Pachana, Pittasarana and Rechana. Other drugs like Bhallataka, Trikatu, Vidanga, Chitraka, Jyothismati,Vriddhadaru, and Sooranakanda are consistent with Kapha vata hara property. Trivrit, Danti, Gavakshi, Sooranakanda possesses a safe vatanulomanaproperty. The whole of these drugs, with their specified functions are compounded intothe lehya preparation with Madhurarasa base thus imparting the Rasayana effect to thedrug. This is being fortified through the drugs like Pippali, Hareetaki, Musta andJyotismati which are potential enough in neutralising the effects of ama formed due toagnidourbalya and in detoxifying the endotoxins. Thus the drug can be conveniently concluded as a ‘Naimittika Rasayana’ adisease specific Rasayana as told by Susrutacharya, encompassing the functions ofSodhana, Samana and Rasayana with a basic control over Agni vyapara. 109
  • 110. C. LINE OF TREATMENT IN TAMAKA SWASA1) Sneha and Sweda: Tila taila mixed with Saindhava lavana is boiled and applied on uras asabhyanga followed by swedana with Snigdha dravyas using Nadi, prastara & Sankaratypes of sweda. This process causes Kapha Vilayana and Sroto mardavam thusrestoring vata sanchara220.2) Sodhana: There may be prakopa of doshas even after treated by langhana & pachana,but when treatd with sodhana, there will be no recurrence of vitiation of doshas. Theprinciple holds good for Swasa Chikitsa, as sodhana causes samprapti vighatanathereby preventing the possibilities of punarudbhava. In Tamaka Swasa all the urdhwa and adhosodhanas can be done exceptingsneha vasti.a) Vamana: It is the pradhana chikitsa for aggravated Kapha dosha and is particularlyindicated in Swasa vyadhi. The dusta Kapha accumulated in the body which was brought to Koshta bySneha & Sweda Karma is expelled by Vamana, causing Sroto suddhi and allowingvata sanchara. Thus the pathology is said to be tackled.b) Virechana: This process eliminates doshas through adhomarga. This is a pradhanasodhana Chikitsa for pitta dosha, but it is also useful in Kapha yukta pitta or pittasthana gata kapha. Amasaya is the sthana for pitta as well as for Kledaka kapha which areinvolved in Swasa Samprapti. Virechana is indicated in general in Swasa and in particular in Tamaka Swasa.In this disease the virechana dravya should possess Vata Kapha nasaka properties.This process is to be done after vamana and Samsarjana karma. 110
  • 111. In case of Tamaka swasa associated with adhmana and udavarta, virechanaoushadha made with madeephala rasa and saindhava lavana and is hot is to beadministered. Thus Sroto sodhana and vatanulomana are achieved221.3) Dhooma Pana: It is done to eliminate the leena doshas. This is particularly indicatedwhen the doshas are left unexpelled and when Vata & Kapha are obstructed in theSwasa marga. Dhooma pana should be done after vamana karma or after sneha & sweda butnever after virechana. 111
  • 112. PATHYA – APATHYAAll the nidana factors act as apathya and thus should be avoided. The oushadhas,ahara & vihara which are conducive to the patient and acting against the aetiology ofthe disease are considered as pathya222.PATHYAS:1) Aahara:Table No.25Suka dhanya Purana shashtika dhanya, Rakta Sali dhanya, Yava, GodhumaSimbi dhanya Kulutha, MudgaSakas Patola, Pushkaramula, Vartaka, Sati, Lasuna, Hareetaki,Bimbi, Vasthuka, Amla vetasa, TanduleeyakaPhalas Amla rasa pradhana phalas, Madeephala, Jambheera, Dadima, Draksha, Amalaki, BilwaJantava Dravyas Purana Sarpis, Samskruta ksheeras, Ksheera paka, Aja ksheera, Samskrita takra, Yusha yukta dadhi, Gomutra, MadhuMamsas Mayura, Suka, Tittira, Kukkuta, Lavaka and other jangala mamasSamskara dravyas Trikatu, Saindhava, Sauvarchala & bida lavana, Ela, Jeeraka, Hingu, Yava kshara2) Vihara: Diva Swapna3) Paneeya: Madira Sura Sauveera Madhu Ushnodaka4) Karma: Virechana Swedana Dhoomapana 112
  • 113. APATHYAS: All the nidana factors specific for the disease and to the individual are to beconsidered apathya. 1) Ahara: Vidahi Vishtambi Kapha vardhaka Ruksha, Seeta, guru guna ahara Taila bharjita nishpava Aja ghritam Ksheeram Dusta jalam Anupa mamsa Sarshapa Masha etc. 2) Vihara: Mutra, Udgara, Chardi, Trishna, Swasa & Kasa Vegavarodha Danta dhavana with Danta kashta Srama Adhwagamana Bharavahana Maithuna Prakvayu Aatapa Rajas Dhuma 3) Karma: Nasya Vasthi Raktamokshana 4) Others: Chinta Shoka & other Manasika karanas 113
  • 114. DRUG REVIEW & CRITERIA‘SRI BAHUSALA GUDAM’: The drug ‘Sri Bahusala Gudam’, selected for the present study is a compoundpreparation in lehya form. The drug has its reference in ‘Sahasrayogam’ (lehyavarga), Chakradatta (Arsho roga Chikitsa), and Bhaishajya Ratnavali etc. These textsare comprehensive and contemporary enough. Though mentioned in Arshovyadhi Chikitsa, the drug has gotmultidimensional therapeutic effects in the body. From the disorders of Head andNeck to those of Anorectal regions, the pathologies of all the organ systems are dealtwithin the pharmaco therapeutics of the drug. Above all, the drug is a best Rasayanaand Medhajanana. When the drug is considered in view of present study, many strong supportingfeatures are to be undertaken: The drug, involves in its indications, apart from others, Pinasa & Pratisyaya,the primary and prodromal symptoms of Swasa, Rajayakshma the ultimatecomplication of Tamaka Swasa. These indications are the extreme pathologicalconditions related to respiratory system, and henceforth drug is highly expected todeal with commonest pathologies of the lung, the important being Bronchial Asthma. When the drug, its ingredients and their actions are observed, they clearlyexplain the drug properties which are highly attributable for Samprapti Vighatana,thus alleviating the vitiated doshas. The Rasayana property of the drug can be more specific as ‘NaimittikaRasayana’. Susrutaacharya, in Chikitsa sthana explains Naimittika Rasayana as adisease specific Rasayana. Such Rasayana is supposed to perform its functions eitherby Sodhana or by Samana. The drug ‘Sri Bahusala Gudam’ completely supports thisexplanation by performing its functions through both sodhana and samana actions. 114
  • 115. The pharmacokinetics of the drug is evidence based as many of the ingredientdrugs viz., Tejovati, Chitraka, Vriddhadaru, Sunti etc., have Kapha-vata samanaproperty, a samana rupa chikitsa for tamaka swasa as these two doshas (Vata &Kapha) form fundamental samprapti ghatakas of the disease. The actions of theingredient durgs include swasahara, kasahara & sleshmaghna etc., thus supporting thesamana property of the selected drug. The ingredient drugs viz., Trivrit, Danti etc., are proved purgatives, inducingvirechana, (sodhana rupa chikitsa) in the swasa rogi, thus supporting the treatmentprinciple, ‘Tamaketu Virechanam’. The drug, in addition to samana and sodhana rupa chikitsa, also regulatesJataragni, thus maintaining equilibrium of tridoshas. The cumulative effect of the drug ‘Sri Bahusala Gudam’ thus reveals thetherapeutic and Rasayana properties related to the swasa vyadhi establishing confidentcriteria for the selection. 115
  • 116. METHOD OF PREPARATION: Step 1. Trivrit, Tejovati, Danti, Swadamstra, Chitraka, Sati, Gavakshi, Musta, Viswahwa, Vidanga --------- Each 1 pala Suddha Arushkara - 8 pala Vriddha daru - 6 pala Surana Kandha - 16 pala Water - 2 drona The above drugs are to be boiled as Kashaya paka till ¼ th remains. Step 2. Then filter the above preparation, add Guda 3 times to the kashaya and heat thoroughly to make lehya paka. Step 3. To this paka, add the churnas of Trivrit, Tejovati, Danti, Chitraka each 2 pala; Ela, Twak, Maricha, Gajapippali each 6 pala.Mix properly and store safely for a timely administration.Dosage: 10 gms twice daily, after food followed by a cup of milk.The present study used the drug collected from ‘IMPCOPS’ pharmacy, a Chennaibased trusted manufacturing unit which prepared ‘Sri Bahusala Gudam’, based on thecompilation ‘Vaidyayoga Ratnavali’, taking the reference from ‘BhaishajyaRatnavali’. 116
  • 117. 1.TRIVRIT - Operculina Turpethum 2. TEJAVATI – Zanthoxylum alatum3. DANTI – Baliospermum axillare 4.CHITRAMULA – Plumbago zeylanica 5.GOKSHURA – Tribulus terrestris6. SATI – Hedychium spicatum 117
  • 118. 1. TRIVRITBotanical Name: Operculina TurpethumFamily: ConvolvulaceaeGanas: Bhedaniya (Charaka) Syamadi (Susruta)Synonyms: Trivrit, Sarvanubhuti, Sarala, Rechani, Tribhandi, Suvaha, Triputa, Palindi, Ardhachandra, Sushenika, Nishotha, SaaraVernacular Names: Sanskrit : Trivrit Hindi : Nisoth, Tarbut Kannada : Sigada Malayalam : Trikolpakkonna, Triputa, Sivata Tamil : Sivatai, Kumbham Telugu : Tegada English : Indian Jalap, Turpeth.Chemical constitution : TurpenthinProperties: Rasa : Tikta, katu Guna : Laghu, Ruksha, tikshna Veerya : Ushna Vipaka : KatuAction : Kapha, Pitta Hara, Rechana, Bhedana, LekhanaIndications:- Jwara, Sotha, Udara, Pandu, Kamala, Arshas, Vatarakta, Ama vata, Kasa, Swasa etc.,Useful Part: Mula TwakDose : 1 – 3 gmsOther Therapeutic Properties:- The root is purgative, carminative, bechic,expectorant, useful in Bronchitis, diseases of brain, pains, ascitis, leucoderma, itch,ulcers, inflammation, anaemia, fevers, biliousness, piles, erysipelas, tumours,jaundice, opthalmia, hepatic disorders & heart diseases. 118
  • 119. 2. TEJOVATIBotanical Name: Zanthozylum alatumFamily: RutaceaeGanas: Sirovirechana, katukaskandha (charaka)Synonyms: Tejovati; Tejaswani; Tumbura; Sourabha; Vanaja; parijata; Valkali; Suvarnanakuli; Bidalaghni; Sutejasi.Vernacular names: Sanskrit : Tejaswini Hindi : Tumru; Tejphal Bengal : Nepali thaniya Malayam : Tumpunal; Tumpuni Tamil : Tumpunalu Kannada : Tumburudu, Dhiva Telugu : Gandhalu; Malkangini English : Tooth ache treeChemical constituents: Berberine (Bark wood)’ Dictamine – Magnoflorine –Xanthoplanine (Stembark, root, wood); skimmianine – spilanthol (root); β- sitosterol– Pinoresinol dimethylether (aerial parts); Thujene, monoterpenetriol, xanthoxyleneetc.,Properties: Rasa : Katu; Tikta Guna : laghu; ruksha; Tikshna Veerya : Ushna Vipaka : katuActions: Kapha-vata hara; Deeepana; Pachana; Kanthya; Pittavardhaka; Swedajanana; Kushtagna.Indications: Kasa; Swasa; Pratisyaya; Krimi; Arshas; Hridroga; Udaravyodi; Agnimanadya; Hikka; Sula; Jwara; ENT disorders;Useful parts: Twak; PhalaDose: Churna: 1 – 2 gmsOther Therapeutic Properties:Fruit is useful as appetizer and in headache; heaviness; asthma; cough; dyspnoea;stomatitis; Seeds:- Carminative; All parts:- Carminative; Stomachic & in generaldebility. 119
  • 120. 3. DANTIBotanical Name: Baliospermum axillareFamily: EuphorbiaceaeGanas: Rechana; Mulini (Charaka) Syamadi; Adhobhagahara (Susruta)Synonyms: Danti; Nikhumba; Udumbaraparni; Erandaphala; Visalya; Makulaka; Varahangi; Ghanapriya; Shyenaghanta; ShigraVernacular names: Sanskrit : Danti Hindi : Danti Bengali : Danti Tamil : Niradimuttu Kannada : Kaduharalu Malayam : Nagandadi; Danti Telugu : Adaviamudam; Kondamudam.Chemical constituents: Seeds: Axillarenic acid; Seed oil Roots: Baliospermin; Montanin, StarchProperties: Rasa : Katu Guna : Guru; Tikshna Veerya : Ushna Vipaka : katuAction: Kapha -Vata hara; Deepana; pachana; Krimigna; Vedanasthapana; Yakrituttejakam.Indications: Swasa; Arshas; Sula; Kushta; Kandu; Asmari; Sotha; Udara; KrimiUseful parts: Mula, Beeja; Patra. (Root; Seed; Leaf)Dose: Root powder: 1-3 gms; Seed powder:- 125-250 mgOther Therapeutic Properties:Decoction of the leaves is useful in Asthma; Dropsy & piles; Bronchitis.Root is pungent, purgative; anthalmintic; diuretic; alexiteric, useful in skin, abdomendisorders; piles; wounds; splenomegaly; itching; inflammation; anaemia; leucoderma;Jaundice. 120
  • 121. 4. CHITRAMULABotanical Name: Plumbago zeylanicaFamily: PlumbaginaceaeGanas: Deepaneeya; Sulaprasamana; Bhedaniya; Arshohara; Lekhaniya (Charaka); Pippalyadi; Mustadi; Amalakyadi; Varunadi; Aragwadadi (susruta)Synonyms: Anala; pithi; Dahana; Vahnisanjnaka; Vyala; UshanaVernacular names: Sanskrit : Agni; Agnimata; Agnisikha Hindi : Chita; Chitruk; Sufaid Malayam : Tumpukotuveli Tamil : Adigarradi; Akkini; Angodiveli; anilam; Karimai; Kodiveli Telugu : Agnimata; Chitramula English : Ceylon leadwort.Chemical constituents:- Root : Plumbagin.Properties: Rasa : Katu Guna : Laghu; Ruksha; Tikshna Veerya: Ushna Vipaka: KatuActions: Kapha – vata hara; Deepana; pachana; grahi; Rasayana; Krimighna; SwedajananaIndications: Kasa; Jeernapratisyaya; Grahani; Arsas; Sula; Krimi; Udara vyadhi; Pandu.Useful part: RootbarkDose: 1-2 gmsOther Therapeutic Properties: Root is laxative, expectorant; carminative; astringentto bowels; anthalmintic; useful in bronchitis; laryngitis of cough; antiseptic;rejuvenating. Leaves are Aphrodisiac. 121
  • 122. 5. GOKSHURABotanical Name: Tribulus terrestrisFamily: ZygophyllaceaeGanas: Mutravirechaniya; Sothahara; Krimighna (charaka) Vidarigandadi; Veeratarvadi; Laghu panchamuladi (Susruta)Synonyms: Gokshura; Trikantaka; Swadamastra; Ikshugandhika; Swadukantaka; Palankasha; Swaji; VanasringatakaVernacular names: Sanskrit : Gokshura Bangali : Gokshura Hindi : Chhotagokhru Tamil : Nerinji Telugu : Palleru Kannada : Negalu; Sennanegalu Malayalam : Nerinni English : Land Caltrops; Puncture wine.Chemical constituents: Fruits – Chlorogenin; Rhamnose; Rutin Fruits & Flowers – Diosgenin; Gitogenin Flowers –Neogitogenin; quercetin Flowers & Root – Stigmasterol Seed – HarmineProperties: Rasa : Madhura Guna : Guru; Snigdha Veerya : Sheeta Vipaka : MadhuraActions: Vata pitta hara; deepana; Hridrogahara; Vastishodana; Rasayana; Vedanasthapana; Kaphanihsarana.Indications: Kasa; swasa; arshas; asmari; Pramcha; Mutrakricchra; HridrogaUseful part: Fruit; RootDose: Fruit powder: 3-6 gms Kwatha 1 -50 - 100 mlOther Therapeutic Properties: The root & fruit are sweetish, cooling, tonic,aphrodisiac, and anti-inflammatory. Useful in Cough, Asthma, Heart diseases; piles;leprosy etc. Laxative; Expectorant. 122
  • 123. 6. SATIBotanical Name: Hedychium spicatumFamily: ZingiberaceaeGanas: Swasahara; Hikkanigrahana (Charaka)Synonyms: Gandhamulika; palasi; karchura; vedamukha; Dravida; Kalpaka; Gandhasara; Jatala; DurlabhaVernacular names: Sanskrit : Amlaharidra; Amlanisha; Durva Tamil : Simaikkichilikkilhangu Bengal : Ada; Ama; Gandhashati Hindi : Gandha palashi; Kapurakachari Marati : Kapurakachari; sonatakka Telugu : KacchuramulaChemical constituents: Starch; cellulose; Mucilage; albumin; saccharine; acid resin; fixed oil; Methyl paracumarin acetate.Properties: Rasa : Katu; Tikta; Kashaya Guna : Laghu; Tikshna Veerya : Ushna Vipaka : KatuActions: Kapha-vatahara; Grahi; Deepana; Vidanasthapana; Sulaprasamana; Raktasodhaka; Durgandhanasaka.Indications: Kasa; Swasa; Pratisyaya; Hikka; Sula; JwaraUseful part: KandhaDose: Ch: 1-3 gmsOther Therapeutic Properties: Useful in Bronchial asthma and eosinophilia;bronchitis; vomiting; inflammation etc., Root stock is carminative; tonic; stomachic &stimulant. 123
  • 124. 7. GAVAKSHI – Citrullus colocynthis 8. MUSTAKA – Cyperus rotundus 9. SUNTI – Zingiber officinale 10.HARITAKI – Terminalia chebula11.VIDANGA – Embelia ribes 12.BHALLATAKA – Semecarpus anacardium 124
  • 125. 7. GAVAKSHI (INDRAVARUNI)Botanical Name: Citrullus ColocynthisFamily: CucurbitaceaeGanas: Rechana; Mulini (Charaka) Adhobhagahara; Syamadi (Susruta)Synonyms: Indri; Chitra-Chitraphala; Galvakshi; Visala; Gavadani; Gaja chermita; Mrigairvaru; Bhara; PitamkotiVernacular names: Sanskrit : Indravaruni Hindi : Indrayan Bengali : Indrayan Tamil : Peykkumutti Telugu : Chedupuccha English : Bitter apple; ColocynthChemical constituents: Pulp – Colocynthin (bitter principle) – a glucoside, Colocynthin; Colocynthetin; Pectin; Gum & Ash.Properties: Rasa : Tikta Guna : Laghu Tikshna Veerya : Ushna Vipaka : KatuActions: Kapha – pitta hara; rechana, Ruksha Garbhapatana; Kapha nihsarana; Rakta shodhaka; Vranasothahara;Indications: Kasa; Swasa; Jaundice; Udaravyadhi; Krimi; Kusta; Prameha; Vrana; Mudhagarbha; Sandhivata; GandamalaUseful part: Fruit, RootDose: Fruit Powder: - 1/8 – ½ gms Root Powder: - 1-3 gmsOther Therapeutic Properties: In small doses it is expectorant & alternative; usefulin cough and asthma of children. Fruit is bitter, pungent, purgative, anthelmintic;antipyretic; carminative; cures tumours; Ascitis; Asthma; Bronchitis. 125
  • 126. 8. MUSTAKABotanical Name: Cyperus rotundusFamily: CyperaceaeGanas: Lekhaniya; Trishna nigrahana; Kandughna; sthanyashodhana (Charaka); Mustadi; Vachadi (Susruta)Synonyms: Varida; Kodreshta; Hima; Sugandhi; Kaseruka; Gangeya; AbhranamakaVernacular names: Sanskrit : Musta Hindi : Nagarmotha; motha Tamil : Korai Telugu : Tungamusta Malayalam : Muttanna Kannada : Tungegadda; Tungahalli; Badramusti English : NutgrassChemical constituents: Essential oils, albuminous matter, starch, fibre, ash, Trace alkaloid, fat, sugar, gum, carbohydratesProperties: Rasa : Tikta, Katu, Kashaya Guna : Laghu; Ruksha Veerya : Sheeta Vipaka : KatuActions: Kapha – pitta Hara; Deepana; pachana; Grahi; Legkhana; Sthanyashodhana; Kimighna; Kphaghna; Mutrala.Indications: Kasa; Swasa; Jwara; Trishna; Atisara; KrimiUseful part: KandhaDose: Churna: 3-6 gms Kwatha: 50-100 mlOther Therapeutic Properties: Root is diuretic; immiegogue; anthelmintic;stomachic; carminatic; diaphoretic; anti-inflammatory; Small tubers act on the lungs& liver. Useful in cough and bronchitis. 126
  • 127. 9. SUNTIBotanical Name: Zingiber officinaleFamily: ZingiberaceaeGanas: Trupthighna; Arshoghna; Deepaneeya; Sulaprasamana; Trishna nigrahana (Charaka) Pippalyadi; Trikatu (Susruta)Synonyms: Aardraka; Aardrika; Sringaveram; Katubhadra; Nagara; Vishwabheshaja;Ushana; Mahaushada; BheshajaVernacular names: Sanskrit : Aardrakam Tamil : Inci Telugu : Allam, Aardrakam Malayalam : Inci, Erukkilannu Hindi : Adarak Kannada : Harisunti; Ardraka English : GingerChemical constituents: Aromatic volatile oil which contains Camphene,Phellandrene, Zingiberine, Cineol, borneol, gingerol, an oleo-resin, ‘Gingerin’; resins;Starch; ;K-oxalate etc., Protein, Calcium; Phosphorus; Iron, Vit – A,B,CProperties: Rasa : Katu Guna : Laghu; Snigdha Veerya : Ushna Vipaka : MadhuraAction: Kapha-Vata hara, Deepana; Bhedana; pachana; Sulaprasamana; Rakta shodhaka; VrishyaIndication: Kasa; Swasa; Hikka; Chardi; Arsas; Hridroga; Sotha; Slupada; Anaha; Sula; UdaravyadhiContra – Indication: Kusta; pandu; Mutrakricchra; Rakta pitta; Vrana; Jwara; Daha; Grishma; Sharad RutuUseful part: KandhaDose: Swarasa: 5 – 10 ml Churna : 1-2 gmsOther Therapeutic Properties: It is appetizer; laxative; stomachic; aphrodisiac,Carminative; useful in diseases of heart & throat, dyspepsia; Bronchitis; Asthma;snake bite; Scorpion sting. 127
  • 128. 10. HARITAKIBotanical Name: Terminalia chebulaFamily: CombretaceaeGanas: Jwaraghna; Arshoghna; Kasaghna; kushtaghna; prajasthapana (Charaka) Amalakyadi; Parushakadi; Triphala (Susruta)Synonyms: Pathya; abhaya; amrita; vayastha; kayastha; puthana; Haimavati; avyatha; chetaki; sreyasi; siva vijaya; Jeevanti; Rohini etc.,Vernacular names: Sanskrit : Haritaki Bengali : Haritaki Hindi : Harra, Harad, Harara, Hara Tamil : Kadukkai Malayalam : Katukka Kannada : Harra, Karakkayi Telugu : Karakkaya English : Chebulic myrabolanChemical constituents: Anthraquinone, glycoside, chebulinic acid, Tannic Acid, Gallic Acid, Terchebin; Vit – C; arachidic; behemic, linoleic, Oleic, Palmatic, Stearic acids; Chebulin in flowers.Properties: Rasa : Pancha Rasa (lavana varjita; kashya pradhana) Guna : Laghu; Ruksha Veerya : Ushna Vipaka : MadhuraActions: Vatta – pitta – kapha Hara; Anulimana; Deepana; Pachane; Medhya; Rasayana; Chakshushya; Brimhana; PrajasthapanaIndications: Kusta; pramcha; krimi; sotha; Hridroga; Tamaka swasa; Kasa; Chardi; Hikka; Vatarakta; Mutrakricchra; Asmari; pandu; Kamala; Grahani; Vishama Jwara.Useful part: FruitDose: Churna 3-6 gmsOther Therapeutic Properties: Purgative; expectorant; used in fevers; cough;asthma; urinary disorders; worm infestations; Rheumatism. Hepato & Splenomegaly;Diarrhoea & Dysentry. 128
  • 129. 11. VIDANGABotanical Name: Embelia ribesFamily: MyrsinaceaeGanas: Krimighna; Kushtanghna; Tripthighna (Charaka) Surasadi; Pippalyadi (Susruta)Synonyms: Tandula; Chitratandula; Krimighna; Vella; Amogha; Jantunasaka;Vernacular names: Sanskrit : Vidangam Hindi : Vay vidang; Bhabhirang Tamil : Vayu vilamga Malayam : Vilal Kannada : Vayuridanga Telugu : Vayuvidangamu English : EmbeliaChemical constituents: Embelin; Embelic acid; Christembine; Volatile and fixed oils.Properties: Rasa : Katu, Kashaya Guna : Laghu; Ruksha; Tikshna Veerya : Ushna . Vipaka : KatuActions: Kapha – vata hara; Deepana; Krimighna; Vishahara; Sirovirecha; pachana; Anulomana; RaktasodhakaIndications: Krimi; Sula; Adhmana; Kushta; UdaravyadhiUseful part: FruitDose: 5-10 gmsOther Therapeutic Properties: Fruit is Carminative; anthelmintic; rejuvenating;laxative, useful in asthma; bronchitis etc., 129
  • 130. 12. BHALLATAKABotanical Name: Semecarpus anacardiumFamily: AnacardiaceaeGanas: Deepaniya; Bhedaniya; Kustaghna; Mutra sangrahana (Charaka) Nyagrodhadi; Mustadi (Susruta)Synonyms: Arushkara; Agnimukhi; Sophakrit; Veeravruksha; Agnika; Bhalla;ArushkaVernacular names: Sanskrit : Bhallataka Hindi : Bhela Bengali : Bhallataka Tamil : Shenkottai; Erimugi Malayalam : Ceru; Alakkuceru Kannada : Goddugeru; Karigeri; Bhallika Telugu : Bhallataka; Jeedi English : Marking – Nut tree.Chemical constituents: Bhilwanol; Semecarpol; Nuts – Biflavanoids A, B, C; Nallaflavone Nutshell – Gullaflavanone; Jeedi flavanone Anacardic acid; Aromatic amines; Leaves – Amentoflavone Kernel Oils – Linoleic; mysistic; oleic; palmitic & stearic oils.Properties: Rasa : Katu; Tikta; Kashaya Guna : Laghu; Snigdha; Tikshna Veerya : Ushna Vipaka : MadhuraActions: Kapha – vata hara; Deepana; Bhedana; Medhya; Rasayana; Vrishya; Mutrasangrahana.Indications: Kapha vyadhi; Arshas; Grahani; Gulma; Krimi; Kusta etc.,Useful part: FruitDose: Kalka: 3-6 gm Tailam: 10-20 dropsOther Therapeutic Properties: Fruit is aphrodisiac;anthelmintic; useful in Asthma; bronchitis; leprosy, epilepsy, paralysic, Rheumatism.Kernel is nutritive, appetizer, carminative; cardiac tonicl general respiratory stimulant. 130
  • 131. 13. VRIDDHADARU – Argyreria speciosa 14.SURANA KANDA – Amorphophallus comp. 15.TWAK – Cinnamomum zeylanicum 16. ELA – Ellataria cardamum 17. MARICHA – Piper nigrum 18. PIPPALI – Piper longum 131
  • 132. 13. VRIDDHA DARUBotanical Name: Argyreia speciosaFamily: ConvolvulaceaeSynonyms: Avegi; Chagantri; VrishyagandhikaVernacular names: Sanskrit : Vriddha daru Tamil : Samuttirappaccai; Samuttirappalai Telugu : Chandrapada Malayalam : Marikkunni; Marututari; Samudrappacca Kannada : Chandrapada Hindi : Samandar-ka-pat; Samudrasos English : Elephant creeperChemical constituents: Tannin, amber coloured acid resin soluble in ether, benzoland alkalies.Properties: Rasa : Katu; Tikta; Kashaya Guna : Laghu; Snigdha Veerya : Ushna Vipaka : MadhuraActions: Kapha – Vata hara; Vrishya; Medhya; Rasayana; Deepana; pachana; Kaphaghna; KanthyaIndications: Kasa, Amavata; Sotha; Arsas; PramehaUseful part: RootDose: Churna: 3-6 gmsOther Therapeutic Properties: Root is aphrodisiac, diuretic; carminative; aperient;anti-inflammatory; expectorant; rejuvenating; useful in cough, bronchitis; diseases ofCNS; Rheumatism, wounds etc., 132
  • 133. 14. SURANA KANDABotanical Name: Amorphophallus companulatusFamily: AraceaeSynonyms: Arshoghna; Kandala; Ola; kandha; suvrutha; TivrakantaVernacular names: Sanskrit : Surana Hindi : Iluram; Jamikand Tamil : Karunaikkilanku Malayalam : Cena Kannada : Suranagadda Telugu : Kandagadda English : Elephant foot yamChemical constituents: Albuminoids; soluble carbohydratesProperties: Rasa : Katu; Kashaya Guna : Laghu; Ruksha; Tikshna Veerya : Ushna Vipaka : KatuActions: Kapha-vata hara; sothahara; Deepana; Pachana; Vedanasthapana; Vrishya; Rasayana; VatanulomanaIndications: Krimi; Gulma; Shula; Arshas; Swasa; Kasa; PlehodaraUseful part: KandhaDose: Churna 3-6 gmsOther Therapeutic Properties: Tuber is Anti inflammatory; expectorant;Carminative; aphrodisiac; rejuvenating; useful in Asthma & Bronchitis. 133
  • 134. 15. TWAKBotanical Name: Cinnamomum zeylanicumFamily: LauraceaeSynonyms: Twak; Darusheeta; Varanga; Svadvi; TanutwakVernacular names: Sanskrit : Twak; Chocham; Darusheeta Hindi : dalchini; Darucini Tamil : Lavangam; Karuva Malayalam : Lavangam; Elavangam; Karuva; Vayara Kannada : Dalchini Telugu : Dalchini chekka English : CinnamonChemical constituents: Cinnamic acid; Resin; Tannin; Cinnamyl acetateProperties: Rasa : Katu; Tikta; Madhura Guna : Laghu; Ruksh; Tikshna Veerya : Ushna Vipaka : KatuActions: Vata-kapha hara; Deepana; Pachana; Varnya; Sukrala; Grahi;Raktashodhaka; OjovardhakaIndications: Kasa; Swasa; Agnimandya; Aruchi; Hrillasa; Adhmana; Arshas; Pinasa; Krimi; Hridroga; Trishna; MukhasoshaUseful part: Twak; TailamDose: Twak Churnam – 1-3 gms Tailam - 2-5 dropsOther Therapeutic Properties: Bark is aphrodisiac; Carminative; Stimulant;anthelmintic; antispasmodic, useful in bronchitis & Asthma; Expectorant; Elexiteric;emmenagogue. 134
  • 135. 16. ELABotanical Name: Ellateria cardamumFamily: ZingiberaceaeGanas: Swasahara; Angamardaprasamana; Katukaskanda (Charaka) Eladi (Susruta) Trijataka; Chaturjataka (Vagbhata)Synonyms: Ela; triputa; Dravidi; Korangi; Truti; ThuthaVernacular names: Sanskrit : Ela Hindi : Elachi Tamil : Elam Malayalam : Elam, Cittalam Kannada : Elakki Telugu : Elakkayalu English : CardamomChemical constituents: Terpinyl acetate; cincole; limoneneProperties: Rasa : Katu, madhura Guna : Laghu; Ruksha Veerya : Sheeta Vipaka : MadhuraActions: Kaphavata hara; Hridya; Deepana; Pachana; Rochana; Sukranasa; Trishnanigrahana; MukheshodanaIndications: Swasa; Kasa; Mutrakricchra; Vastisula; Hridroga; Arshas; Chardi; SirahsulaUseful part: SeedDose: Churnam: ½ -1 gmOther Therapeutic Properties: Seeds are useful in Asthma; bronchitis; piles;expectorant; carminative; Anti inflammatory; useful in diseases of liver; chest andthroat. 135
  • 136. 17. MARICHABotanical Name: Piper nigrumFamily: PiperaceaeGanas: Deepaneeya; sulaprasamana; Krimighna (Charaka) Pippalyadi; Triyushana (Susruta)Synonyms: Maricha; Vellaja; Ushana, Krishna; DharmapattanaVernacular names: Sanskrit : Maricha Hindi : Kalimirchi Tamil : Milaku; Marisam Malayalam : Kurumaluka Kannadaa : Ollimonasu Telugu : Miriyalu English : Black pepperChemical constituents: piperine; piperidine; charicinProperties: Rasa : Katu Guna : Laghu; Tikshna Veerya : Ushna Vipaka : KatuActions: Kapha-vata-hara; Deepana; pachana; AartavajananaIndications: Kasa; Swasa; Vishamajwara; PratisyayaUseful part: FruitDose: ½ - 1 gm ChurnamOther Therapeutic Properties: Fruit is Carminative; aphrodisiac, purgative; usefulin diseases of Asthma, liver & spleen; throat etc., 136
  • 137. 18. PIPPALIBotanical Name: Piper longumFamily: PiperaceaeGanas: Deepaneeya; sulaprasamana; kasahara; Hikkanigrahana (Charaka) Pippalyadi; Urdhwabhagahara (Susruta)Synonyms: Magadhi; Krishna; Vaidehi; Chapala; kana; Kola; TeekshnatandulaVernacular names: Sanskrit : Pippali Hindi : Pipli, Pipal Kannada : Hipli Tamil : Pippili, Tippili Malayalam : Tippali Telugu : Pippallu English : Indian long pepperChemical constituents: Resin; volatile oil; starch; gum; piperineProperties: Rasa : katu Guna : Laghu; snigdha; tikshna Veerya : Anushna sheeta Vipaka : MadhuraActions: Kapha vata samaka; Medhya; Mutrala; Krimighna; Sulaprasamana; Vatanulomana; Rasayana; Vrishya; Rechana; DeepanaIndications: Swasa; Kasa; Hikka; Kshya; Yakshma; Udara; Prameha; KushtaUseful part: Fruit; RootDose: Churnam: ½ - 1 gmOther Therapeutic Properties: Root is laxative; anthelmintic; carminative.Fruit is aphrodisiac; useful in diseases like asthma; bronchitis; tuberculous glands;Expectorant; useful in liver & spleen disorders etc., 137
  • 138. CLINICAL STUDYAIM: The main aim is to study the Naimittika Rasayana effect of the drug ‘SriBahusala gudam’ in the disease ‘Tamaka Swasa’ considering it as an industrialhazard.OBJECTIVES: To assess the efficacy of the drug in Asthmatics due to Industrial pollutant. To evaluate the Naimittika Rasayana effect of the drug. 138
  • 139. MATERIAL & METHODS:a) SUBJECTS: A total of 30 patients were considered for the study who were divided into 2groups (Gr A, Gr B) with 15 patients (subjects) each. The subjects were selectedmainly from chemical and cotton industries with 15 subjects from each type ofindustry. After a series of medical camps 15 subjects (Gr A) were selected fromchemical industries located in Industrial Development Authority area of Bollaram,and Khazipalli, Medak Dist, and 15 subjects (Group B) were selected from a cottonindustry in Bhongir, Nalgonda Dist. The two industrial areas were located within theconsiderable vicinity of Govt. Ay. College, Hyderabad. The selected subjects are with ages ranging from 15 – 60 yrs and irrespectiveof sex & religion.b) SELECTION: Inclusion criteria: 1. Subjects with classical symptomatology and with elevated Ig E values were only selected for the study. 2. All the subjects who were in the latent period of the disease. 3. All the subjects who have occupational aetiology for their disease. Exclusion Criteria: 1. Acute attacks of Asthma 2. Tuberculosis 3. Lung malignancies 4. Smokers 5. Uncontrolled Diabetes mellitus 6. Asthma due to other systemic origin. 139
  • 140. A complete and disease specific proforma was prepared, including subjective &objective parameters thus enabling a detailed record of observations, upon the consentand examination of the patients.c) DESIGN OF THE STUDY: The present study is a Randomized Clinical Trial (RCT) & Open trial, selected tominimize the bias.30 subjects were selected randomly and made into 2 Groups (Group A & Group B)depending on the industry from which they are selected i.e., Chemical Industry(Group A, 15 subjects) and Cotton Industry (Group B, 15 subjects).Duration of the Study:The total duration of the study was for 90 days including a follow up period of 45days.Mode of Administration:The drug is administered in the dose of 10 gms with a cup of cold milk to be takentwo times a day after food i.e., after breakfast & after dinner.d) PARAMETERS: Subjective: Out of all the clinically presented symptoms, only the following subjective parameters (variables) which were found common in all were selected and considered as the criteria for results. Pinasa Kanta Asya Uddhwamsa Ghurghuruka Kricchra Bhasitam Teevra Vega Swasa Anidra Pratamyati Abala Trit Kasa 140
  • 141. Four gradations were given to these parameters (except Kasa) according to theirseverity. Grade 3 – Severe Grade 2 – Moderate Grade 1 – Mild Grade 0 – NormalFor KASA, the gradations are: Grade 3 – Cough with Severe Expectoration Grade 2 – Cough with Mild Expectoration Grade 1 – Dry Cough Grade 0 – Normal Objective Parameters: Ig E was the only parameter considered for theassessment of the result and effect of the drug as Naimittika Rasayana.e) DATA COLLECTION: Values of a single selected variable (Selected subjective parameter) wererecorded in 3 periods viz., B.T (Before Treatment), D.T (During Treatment) & A.T(After Treatment) of all 15 subjects in each group, like wise for all the selected 10variables in each group.Values of all the selected variables (10 selected subjective parameter) for a singlesubject (single patient) were recorded in 3 periods (B.T, D.T & A.T), like wise for allthe 15 subjects in each group.The values of Ig E were recorded for all the subjects of both Groups in B.T & A.Tperiods. 141
  • 142. DATA OF INDIVIDUAL VARIABLE IN ALL THE SUBJECTS OF GROUP ATable No. 26S.no Sym. Period 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 BT 2 2 2 1 1 1 2 1 2 1 2 2 1 1 21 Pi DT 2 2 1 2 1 1 1 1 1 1 2 1 1 1 1 AT 1 1 1 2 2 0 0 0 0 1 1 0 0 1 1 BT 2 2 2 1 1 2 2 1 2 1 1 2 1 1 12 Gh DT 2 2 2 1 2 2 2 1 2 1 1 1 1 2 1 AT 1 2 1 1 2 1 1 2 1 1 1 1 1 2 1 BT 2 2 2 1 1 2 2 1 2 1 2 1 1 1 23 TVS DT 1 3 1 1 2 1 2 1 2 1 2 1 1 2 1 AT 1 2 1 2 2 1 1 2 1 0 1 2 1 2 1 BT 2 1 1 1 1 2 2 1 1 1 1 1 1 1 14 Pr DT 1 1 0 1 1 1 1 1 0 0 0 0 1 0 0 AT 1 2 0 1 2 0 1 1 0 0 0 0 2 0 0 BT 2 2 2 2 2 2 2 1 2 2 2 1 1 1 25 Tr DT 1 2 1 1 1 1 1 1 1 1 1 0 1 0 1 AT 1 1 0 0 0 0 1 0 1 0 0 0 0 1 0 BT 2 2 1 1 2 1 2 1 1 2 1 1 1 1 16 KAU DT 1 2 1 1 2 1 1 1 1 2 1 1 1 2 1 AT 0 2 0 2 2 1 1 2 1 1 1 0 1 2 1 BT 2 1 2 2 1 1 2 1 2 1 1 1 1 1 27 KB DT 1 1 1 1 1 0 1 1 1 1 1 1 1 1 1 AT 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 BT 2 1 2 2 2 2 2 2 2 2 2 2 2 2 28 An DT 2 2 2 2 1 1 2 1 1 2 1 1 1 2 1 AT 1 1 1 1 0 0 1 1 0 1 1 1 1 1 1 BT 1 2 1 1 1 2 1 2 1 1 1 1 1 1 29 Ab DT 1 1 1 1 1 2 1 2 1 1 1 0 1 0 1 AT 1 1 0 1 0 1 0 2 0 1 0 1 1 0 0 BT 2 1 2 1 1 2 1 1 2 1 1 1 1 1 110 Ka DT 2 1 2 0 2 2 1 1 2 1 0 1 2 2 1 AT 1 1 1 1 1 1 1 1 1 2 1 1 2 1 2(1 – 15 are the Names of the Respective subjects in Group – A)Pi – Pinasa KAU – Kanta Asya UddhwamsaGh – Ghurghuruka KB – Kricchra BhasitamTVS – Teevra Vega Swasa An – AnidraPr – Pratamyati Ab – AbalaTr – Trit Ka – Kasa 142
  • 143. DATA OF ALL VARIABLES IN INDIVIDUAL SUBJECT OF GROUP – ATable No.27S.No NAME Pi Gh TVS Pr Tr KAU KB An Ab Ka1 Julie BT 2 2 2 2 2 2 2 2 1 2 DT 2 2 1 1 1 1 1 2 1 2 AT 1 1 1 1 1 0 0 1 1 12 Bheema rao BT 2 2 2 1 2 2 1 1 2 1 DT 2 2 3 1 2 2 1 2 1 1 AT 1 2 2 2 1 2 0 1 1 13 Shilpa BT 2 2 2 1 2 1 2 2 1 2 DT 1 2 1 0 1 1 1 2 1 2 AT 1 1 1 0 0 0 0 1 0 24 Pushpa BT 1 1 1 1 2 1 2 2 1 1 DT 2 1 1 1 1 1 1 2 1 0 AT 2 1 2 1 0 2 0 1 1 15 Latha BT 1 1 1 1 2 2 1 2 1 1 DT 1 2 2 1 1 2 1 1 1 2 AT 2 2 2 2 0 2 0 0 0 16 Krishna dev BT 1 2 2 2 2 1 1 2 2 2 DT 1 2 1 1 1 1 0 1 2 2 AT 0 1 1 0 0 1 0 0 1 17 Murali mohan BT 2 2 2 2 2 2 2 2 1 1 DT 1 2 2 1 1 1 1 2 1 1 AT 0 1 1 1 1 1 0 1 0 18 Damodar BT 1 1 1 1 1 1 1 2 2 1 DT 1 1 1 1 1 1 1 1 2 1 AT 0 2 2 1 0 2 0 1 2 19 Yadagiri BT 2 2 2 1 2 1 2 2 1 2 DT 1 2 2 0 1 1 1 1 1 2 AT 0 1 1 0 1 1 0 0 0 110 Vishwanath BT 1 1 1 1 2 2 1 2 1 1 DT 1 1 1 0 1 2 1 2 1 1 AT 1 1 0 0 0 1 0 1 1 211 Azam bee BT 2 1 2 1 2 1 1 2 1 1 DT 2 1 2 0 1 1 1 1 1 0 AT 1 1 1 0 0 1 0 1 0 112 Saroja BT 2 2 1 1 1 1 1 2 1 1 DT 1 1 1 0 0 1 1 1 0 1 AT 0 1 2 0 0 0 0 1 1 113 Srinivas BT 1 1 1 1 1 1 1 2 1 1 DT 1 1 1 1 1 1 1 1 1 2 AT 0 1 1 2 0 1 0 1 1 214 Rajesh singh BT 1 1 1 1 1 1 1 2 1 1 DT 1 2 2 0 0 2 1 2 0 2 AT 1 1 2 0 1 2 0 1 1 115 Mohan BT 2 1 2 1 2 1 2 2 2 1 DT 1 1 1 0 1 1 1 1 1 1 AT 1 1 1 0 0 1 0 1 0 2 143
  • 144. DATA OF INDIVIDUAL VARIABLE IN ALL THE SUBJECTS OF GROUP BTable No. 28S.no Sym. Period 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 BT 2 2 2 1 1 2 2 2 1 1 2 2 1 1 21 Pi DT 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 AT 0 0 0 0 0 0 1 0 0 0 1 0 0 0 1 BT 3 3 3 3 3 2 2 2 2 2 2 2 2 2 22 Gh DT 2 2 2 2 2 1 1 1 1 1 1 1 1 2 1 AT 1 1 1 1 0 0 0 0 0 0 0 0 1 1 1 BT 3 2 3 2 2 2 2 2 2 2 2 3 3 2 23 TVS DT 2 1 2 1 2 1 1 1 1 1 1 2 2 1 1 AT 1 0 1 0 1 0 0 0 0 0 0 1 1 0 0 BT 2 1 2 1 1 1 1 1 1 1 1 2 2 1 14 Pr DT 1 1 1 0 0 0 1 1 0 1 0 1 1 0 0 AT 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 BT 2 1 2 1 2 2 2 1 1 1 1 2 2 1 15 Tr DT 1 0 1 0 1 1 1 0 1 1 0 1 1 0 0 AT 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 BT 2 2 2 2 2 1 1 2 2 1 1 2 2 2 26 KAU DT 1 1 1 1 1 1 0 1 1 0 0 1 1 1 1 AT 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 BT 2 2 1 2 2 1 2 2 1 1 1 2 2 2 17 KB DT 0 1 0 0 1 1 1 0 1 0 0 1 1 1 1 AT 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 BT 2 2 2 2 2 2 2 3 3 3 3 2 2 2 28 An DT 1 1 1 1 1 1 1 2 2 1 1 1 1 1 1 AT 1 1 0 0 0 1 0 1 1 1 1 0 0 0 0 BT 2 2 2 2 2 2 2 2 2 2 2 2 2 2 29 Ab DT 1 1 1 1 1 1 1 1 0 0 0 2 1 1 1 AT 0 0 0 0 0 1 1 1 0 0 0 1 0 0 0 BT 2 3 2 2 2 2 2 3 2 2 2 2 2 2 210 Ka DT 1 2 1 1 1 1 1 2 1 1 1 2 1 1 1 AT 0 1 0 0 0 0 0 1 0 0 1 1 1 0 0( 1 – 15 are the Names of the Respective subjects in Group – B )Pi – Pinasa KAU – Kanta Asya UddhwamsaGh – Ghurghuruka KB – Kricchra BhasitamTVS – Teevra Vega Swasa An – AnidraPr – Pratamyati Ab – AbalaTr – Trit Ka – Kasa 144
  • 145. DATA OF ALL VARIABLES IN INDIVIDUAL SUBJECT OF GROUP – BTable No.29S.No NAME Pi Gh TVS Pr Tr KAU KB An Ab Ka1 Venkat reddy BT 2 3 3 2 2 2 2 2 2 2 DT 1 2 2 1 1 1 0 1 1 1 AT 0 1 1 0 0 0 0 1 0 02 Shyamala BT 2 3 2 1 1 2 2 2 2 3 DT 1 2 1 1 0 1 1 1 1 2 AT 0 1 0 0 0 0 0 1 0 13 Manamma BT 2 3 3 2 2 2 1 2 2 2 DT 1 2 2 1 1 1 0 1 1 1 AT 0 1 1 0 0 0 0 0 0 04 Veeramma BT 1 3 2 1 1 2 2 2 2 2 DT 1 2 1 0 0 1 0 1 1 1 AT 0 1 0 0 0 0 0 0 0 05 Kotesh BT 1 3 2 1 2 2 2 2 2 2 DT 1 2 2 0 1 1 1 1 1 1 AT 0 0 1 0 0 0 0 0 0 06 Raheematulla BT 2 2 2 1 2 1 1 2 2 2 DT 1 1 1 0 1 1 1 1 1 1 AT 0 0 0 0 0 0 0 1 1 07 Rehena begum BT 2 2 2 1 2 1 2 2 2 2 DT 1 1 1 1 1 0 1 1 1 1 AT 1 0 0 0 0 0 0 0 1 08 Chauhan BT 2 2 2 1 1 2 2 3 2 3 DT 1 1 1 1 0 1 0 2 1 2 AT 0 0 0 0 0 0 0 1 1 19 Asif BT 1 2 2 1 1 2 1 3 2 2 DT 1 1 1 0 1 1 1 2 0 1 AT 0 0 0 0 0 0 0 1 0 010 Narsing BT 1 2 2 1 1 1 1 3 2 2 DT 1 1 1 1 1 0 0 1 0 1 AT 0 0 0 0 0 0 0 1 0 011 Chandrakanth BT 2 2 2 1 1 1 1 3 2 2 DT 1 1 1 0 0 0 0 1 0 1 AT 1 0 0 0 0 0 0 1 0 112 Suramma BT 2 2 3 2 2 2 2 2 2 2 DT 1 1 2 1 1 1 1 1 2 2 AT 0 0 1 0 0 0 0 0 1 113 Bayyamma BT 1 2 3 2 2 2 2 2 2 2 DT 1 1 2 1 1 1 1 1 1 1 AT 0 1 1 0 0 0 0 0 0 114 Sukkumani BT 1 2 2 1 1 2 2 2 2 2 DT 1 2 1 0 0 1 1 1 1 1 AT 0 1 0 0 0 0 0 0 0 015 Suresh BT 2 2 2 1 1 2 1 2 2 2 DT 1 1 1 0 0 1 1 1 1 1 AT 1 1 0 0 0 0 0 0 0 0 145
  • 146. Ig E VALUES OF GROUP ATable No.30S.NO NAME IgE BFORE Tx (IU/ml) IgE AFTER Tx (IU/ml) 1 Julie 190 187 2 Bhima Rao 240 240 3 Shilpa 163 148 4 Pushpa 178 182 5 Latha 172 168 6 Krishna Dev 238 218 7 Murali Mohan 162 162 8 Damodar 182 184 9 Yadagiri 153 153 10 Vishwanath 184 184 11 Azam Bee 202 202 12 Saroja 152 142 13 Srinivas 174 174 14 Rajesh singh 169 169 15 Mohan 162 156 Ig E VALUES OF GROUP BTable No.31S.NO NAME IgE BFORE Tx (IU/ml) IgE AFTER Tx (IU/ml) 1 Venkat Reddy 172 144 2 Shyamala 168 168 3 Manamma 256 184 4 Veeramma 155 140 5 Kotesh 192 142 6 Raheematulla 203 182 7 Rahena Begum 240 164 8 Chauhan 151 150 9 Asif 183 141 10 Narsing 224 174 11 Chandrakanth 156 154 12 Suramma 156 136 13 Bayyamma 202 174 14 Sukkumani 287 174 15 Suresh 160 160 146
  • 147. f) DATA ANALYSIS: Statistical Analysis was done in 3 ways: Individual Analysis: a. Individual Variable Analysis: Values of individual selected variable of 15subjects in each Group obtained in 3 periods B.T, D.T & A.T were averaged (takenMean).The Mean data was subjected to Paired‘t’ test (two tailed) to assess the significantdifference between B.T & D.T; B.T & A.T periods. b. Individual Subject Analysis: Values of all the selected variables of a singlesubject (For total 15 subjects) in each Group obtained in 3 periods B.T, D.T & A.Twere averaged (taken Mean). The Mean data was subjected to Paired‘t’ test (two tailed) to assess thesignificant difference between B.T & D.T; B.T & A.T periods. c. Ig E Analysis: The collected values of Ig E of all subjects in both Groups wereaverage (Mean) and subjected to Paired‘t’ test. Percentage Difference: Percentage of difference after treatment was analyzed as the following:After collecting the Mean data of individual variables & individual subjects of eachGroup in B.T & A.T periods, their Mean difference was taken. With this meandifference, % of change in each variable and each subject after treatment wascalculated by MD/B.T x 100. (MD = B.T – A.T)Data Analysis of Ig E: The Ig E Mean data of all the subjects in both Groups in B.T &A.T periods is used to attain Mean difference. With this mean difference, % of changein each subject after treatment was calculated. 147
  • 148. Result Gradation:Complete result – 100%.Marked result – 75% & aboveModerate result – 50% to 75%Mild result – 25% to 50%No result – Zero Internal Comparison:Percentage of change in individual variable after treatment, of Group A & Group Bwas compared within.% of change in Ig E values after treatment of both Groups was compared within. Mean data of individual variables in before treatment & after treatmentperiods of both Groups was subjected to Paired‘t’ test and obtained ‘P’ values werecompared among Group A & Group B . 148
  • 149. OBSERVATIONS & RESULTS A) DISTRIBUTION ACCORDING TO INCIDENCE DISTRIBUTION ACC.TO AGEGraph No.1 50 45 40 35 30 25 20 15 10 5 0 Gr-A % Gr-B % Total % 15-30 6 40 5 33.33 11 36.67 31-45 5 33.33 7 46.67 12 40 46-60 4 26.67 3 20 7 23.33Data Table No.32Out of 30 Subjects selected for the study 11 subjects (36.67%) belong to the ageGroup of 15 – 30 yrs, 12 subjects (40%) belong to the age Group of 31 – 45 yrs, 7subjects (23.33%) belong to the age Group of 46 – 60 yrs.In Group – A, Out of 15 subjects, 6 subjects (40%) belong to the age Group of 15 –30 yrs, 5 subjects (33.33%) belong to the age Group of 31 – 45 yrs, 4 subjects(26.67%) belong to the age Group of 46 – 60 yrs.In Group – B, Out of 15 subjects 5 subjects (33.33%) belong to the age Group of 15 –30 yrs, 7 subjects (46.67%) belong to the age Group of 31 – 45 yrs, 3 subjects (20%)belong to the age Group of 46 – 60 yrs. 149
  • 150. DISTRIBUTION ACCORDING TO SEX:Graph No.2 60 50 40 30 20 10 0 Gr-A % Gr-B % Total % MALE 9 60 8 53.33 17 56.67 FEMALE 6 40 7 46.67 13 43.33Data Table No.33Out of 30 Subjects selected for the study 17 subjects (56.67%) are males and 13subjects (43.33%) are females.In Group A, Out of 15 Subjects, 9 subjects (60%) are males and 6 subjects (40%) arefemales.In Group B, Out of 15 subjects, 8 subjects (53.33%) are males and 7 subjects(46.67%) are females. 150
  • 151. DISTRIBUTION ACCORDING TO SOCIO - ECONOMIC STATUSGraph No.3 70 56 42 28 14 0 Gr-A % Gr-B % Total % LIG 9 60 10 66.67 19 63.33 MIG 6 40 5 33.33 11 36.67Data Table No.34Out of 30 subjects considered for the study, 19 subjects (63.33%) belong to lowincome group and 11 subjects (36.67%) belong to middle income group.In Group A, Out of 15 subjects considered for the study, 9 subjects (60%) belong tolow income group and 6 subjects (40%) belong to middle income group.In Group B, Out of 15 subjects considered for the study, 10 subjects (66.67%) belongto low income group and 5 subjects (33.33%) belong to middle income group. 151
  • 152. DISTRIBUTION ACCORDING TO DIETGraph No.4 70 56 42 28 14 0 Gr-A % Gr-B % Total % MIXED 9 60 10 66.67 19 63.33 VEG 6 40 5 33.33 11 36.67Data Table No.35Out of 30 subjects considered for the study, 19 subjects (63.33%) belong to mixeddiet group and 11 subjects (36.67%) belong to vegetarian diet group.In Group A, Out of 15 subjects considered for the study, 9 subjects (60%) belong tomixed diet group and 6 subjects (40%) belong to vegetarian diet group.In Group B, Out of 15 subjects considered for the study, 10 subjects (66.67%) belongto mixed diet group and 5 subjects (33.33%) belong to vegetarian diet group. 152
  • 153. DISTRIBUTION ACCORDING TO PRAKRITIGraph No.5 60 50 40 30 20 10 0 Gr-A % Gr-B % Total % VP 1 6.67 2 13.33 3 10 PK 8 53.33 5 33.33 13 43.33 VK 6 40 8 53.33 14 46.67Data Table No.36Out of 30 subjects considered for the study, 3 subjects (10%) were of Vata – PittaPrakriti, 13 subjects (43.33%) were of Pitta – Kapha Prakriti, 14 subjects (46.67%)were of Vata – Kapha Prakriti.In Group A, Out of 15 subjects considered for the study, 1 subject (6.67%) was ofVata – Pitta Prakriti, 8 subjects (53.33%) were of Pitta – Kapha Prakriti, 6 subjects(40%) were of Vata – Kapha Prakriti.In Group B, Out of 15 subjects considered for the study, 2 subjects (13.33%) were ofVata – Pitta Prakriti, 5 subjects (33.33%) were of Pitta – Kapha Prakriti, 8 subjects(53.33%) were of Vata – Kapha Prakriti. 153
  • 154. DISTRIBUTION ACCORDING TO HERIDITYGraph No.6 80 64 48 32 16 0 Gr-A % Gr-B % Total % PRESENT 3 20 4 26.67 7 23.33 ABSENT 2 80 11 73.33 23 76.67Data Table No.37Out of 30 subjects selected for the study, 7 subjects (23.33%) possess hereditary causeas Genetic predisposition to Asthma and 23 subjects (76.67%) did not possess anyhereditary cause.In Group A, Out of 15 subjects selected for the study, 3 subjects (20%) possesshereditary cause as Genetic predisposition to Asthma and 12 subjects (80%) did notpossess any hereditary cause.In Group B, Out of 15 subjects selected for the study, 4 subjects (26.67%) possesshereditary cause as Genetic predisposition to Asthma and 11 subjects (73.33%) didnot possess any hereditary cause.This observation implies that the most of the selected subjects were Asthmaticsmainly because of the pollutants in their occupation and not due to hereditary cause. 154
  • 155. DISTRIBUTION ACCORDING TO CHRONICITYGraph No.7 40 35 30 25 20 15 10 5 0 Gr-A % Gr-B % Total % 1-5yra 6 40 5 33.33 11 36.67 6-10yrs 4 26.67 5 33.33 9 30 11-15yrs 5 33.33 5 33.33 10 33.33Data Table No.38Out of 30 subjects considered for the study, 11 subjects (36.67%) have the chronicityof 1 – 5 yrs, 9 subjects (30%) have chronicity of 6 – 10 yrs and 10 subjects (33.33%)have the chronicity of 11 – 15 yrs.In Group A, Out of 15 subjects considered for the study, 6 subjects (40%) have thechronicity of 1 – 5 yrs, 4 subjects (26.67%) have chronicity of 6 – 10 yrs and 5subjects (33.33%) have the chronicity of 11 – 15 yrs.In Group B, Out of 15 subjects considered for the study, 5 subjects (33.33%) have thechronicity of 1 – 5 yrs, 5 subjects (33.33%) have chronicity of 6 – 10 yrs and 5subjects (33.33%) have the chronicity of 11 – 15 yrs. 155
  • 156. B) EFFECT OF THE TREATMENT COMPARISON OF P VALUES OF INDIVIDUAL VARIABLES IN BOTH GROUPS Table No.39S. PAIRED t TEST variable Group n BT DT ATno MD SD SEM t p Re M M M Bt-Dt 0.27 0.60 0.15 1.74 0.052 NS GroupA 15 1.53 1.26 0.731 Bt-At 0.80 0.94 0.24 3.29 0.002 S Pinasa Bt-Dt 0.60 0.51 0.13 4.58 0.000 S GroupB 15 1.60 1.00 0.20 Bt-At 0.40 0.51 0.13 10.7 0.000 S Bt-Dt 0.00 0.53 0.14 0.00 0.500 NS GroupA 15 1.46 1.46 1.262 Ghughur Bt-At 0.20 0.77 0.20 1.00 0.167 NS uka Bt-Dt 0.93 0.26 0.06 14.0 0.000 S GroupB 15 2.33 1.40 0.46 Bt-At 1.87 0.52 0.13 14.0 0.000 S Bt-Dt 0.00 0.65 0.17 0.00 0.500 NS Teevra GroupA 15 1.53 1.53 1.463 Bt-At 0.67 0.88 0.22 0.30 0.387 NS vega Bt-Dt 0.27 2.57 0.66 0.40 0.347 NS swasa GroupB 15 2.26 2.00 0.33 Bt-At 1.93 0.25 0.06 29.0 0.000 S Bt-Dt 0.67 0.48 0.12 5.30 0.000 S GroupA 15 1.20 0.53 0.674 Pratamya Bt-At 0.53 0.91 0.24 2.25 0.200 S ti Bt-Dt 0.73 0.46 0.12 6.21 0.000 S GroupB 15 1.26 0.53 0.00 Bt-At 1.26 0.46 0.12 10.7 0.000 S Bt-Dt 0.80 0.41 0.10 7.48 0.000 S GroupA 15 1.73 0.93 0.33 Bt-At 1.40 0.63 0.16 8.57 0.000 S5 Trit Bt-Dt 0.86 0.35 0.09 9.53 0.000 S GroupB 15 1.46 0.60 0.00 Bt-At 1.47 0.52 0.13 11.0 0.000 S Kanta Bt-Dt 0.80 0.41 0.10 7.48 0.000 S GroupA 15 1.73 0.93 0.33 asya Bt-At 1.40 0.63 0.16 8.57 0.000 S6 udhwams Bt-Dt 0.93 0.26 0.06 14.0 0.000 S GroupB 15 1.73 0.80 0.00 a Bt-At 1.73 0.46 0.12 14.6 0.000 S Bt-Dt 0.46 0.52 0.13 3.50 0.002 S GroupA 15 1.40 0.93 0.00 Kricchra Bt-At 1.40 0.50 0.13 10.7 0.000 S7 bhasitam Bt-Dt 1.06 0.60 0.15 6.95 0.000 S GroupB 15 1.60 0.53 0.00 Bt-At 1.60 0.51 0.13 12.2 0.000 S Bt-Dt 0.46 0.64 0.16 2.80 0.007 S GroupA 15 1.93 1.46 0.73 Bt-At 1.20 0.56 0.14 8.30 0.000 S8 Anidra Bt-Dt 1.13 0.35 0.09 12.4 0.000 S GroupB 15 2.26 1.43 0.46 Bt-At 1.80 0.41 0.11 16.8 0.000 S Bt-Dt 0.26 0.45 0.12 2.25 0.020 S GroupA 15 1.26 1.00 0.66 Bt-At 0.60 0.63 0.16 3.67 0.001 S9 Abala Bt-Dt 1.20 0.41 0.10 11.2 0.000 S GroupB 15 2.00 0.80 0.20 Bt-At 1.80 0.41 0.10 16.8 0.000 S Bt-Dt 0.66 0.60 0.15 0.43 0.335 S GroupA 15 1.26 1.33 1.20 Bt-At 0.66 0.70 0.18 0.36 0.351 S10 Kasa Bt-Dt 1.00 0.37 0.09 10.2 0.000 S GroupB 15 2.13 1.13 0.33 Bt-At 1.80 0.56 0.14 12.4 0.00 S 156
  • 157. Assessment of Individual selected variable in Three Periods (BT, DT & AT) of bothGroups:1. Pinasa – In Group A the Mean value of Pinasa, before treatment is 1.53, duringtreatment is 1.26 and after treatment is 0.73. The P value of BT – AT variable is0.0025 (<0.05). In Group B the the Mean values of BT, DT & AT are 1.60, 1.10 &0.20 respectively. The P value of BT – AT variable is 0.00 (<0.05). It shows that theresults in both the Groups are significant as their P values are less than 0.05.2. Ghurghuruka – In Group A the Mean values, before treatment is 1.46, duringtreatment is 1.46 and after treatment is 1.26. The P value of BT – AT variable is 0.167(>0.05). In Group B the Mean values of BT, DT & AT are 2.33, 1.40 & 0.46respectively. The P value of BT – AT variable is 0.00 (<0.05). It shows that the resultsin Group B are significant as their P values is less than 0.05, those Group A are nonsignificant as their P values is > 0.05. This suggest that the symptom is less effectedby the drug in Group A subjects who are workers of Chemical Industry.3. Teevra Vega Swasa – In Group A the Mean values, before treatment is 1.53, duringtreatment is 1.53 and after treatment is 1.46. The P value of BT – AT variable is 0.387(>0.05). In Group B the Mean values of BT, DT & AT are 2.26, 2.20 & 0.33respectively. The P value of BT – AT variable is 0.00 (<0.05). It shows that the resultsare significant in Group B than Group A.4. Pratamyati – In Group A the Mean values, before treatment is 1.20, duringtreatment is 0.53 and after treatment is 0.67. The P value of BT – AT variable is 0.020(<0.05). In Group B the Mean values of BT, DT & AT are 1.26, 0.53 & 0.00respectively. The P value of BT – AT variable is 0.00 (<0.05). It shows that the resultsin both the Groups are significant as their P values are less than 0.05 and thesignificance is more in Group B than in Group A.5. Trit – In Group A the Mean values, before treatment is 1.73, during treatment is0.93 and after treatment is 0.33. The P value of BT – AT variable is 0.00 (<0.05). InGroup B the Mean values of BT, DT & AT are 1.46, 0.60 & 0.00 respectively. The Pvalue of BT – AT variable is 0.00 (<0.05). It shows that the results in both the Groupsare significant as their P values are less than 0.05. 157
  • 158. 6. Kanta Asya Uddhwamsa – In Group A the Mean values, before treatment is 1.73,during treatment is 0.93 and after treatment is 0.73. The P value of BT – AT variableis 0.00 (<0.05). In Group B the Mean values of BT, DT & AT are 1.73, 0.80 & 0.00respectively. The P value of BT – AT variable is 0.00 (<0.05). It shows that the resultsin both the Groups are significant as their P values are less than 0.05.7. Kricchra Bhasitam – In Group A the Mean values, before treatment is 1.40, duringtreatment is 0.93 and after treatment is 0.00. The P value of BT – AT variable is 0.00(<0.05). In Group B the Mean values of BT, DT & AT are 1.60, 0.53 & 0.00respectively. The P value of BT – AT variable is 0.00 (<0.05). It shows that the resultsin both the Groups are significant as their P values are less than 0.05.8. Anidra – In Group A the Mean values, before treatment is 1.93, during treatment is1.46 and after treatment is 0.73. The P value of BT – AT variable is 0.04 (<0.05). InGroup B the Mean values of BT, DT & AT are 2.26, 1.13 & 0.46 respectively. The Pvalue of BT – AT variable is 0.00 (<0.05). It shows that the results in both the Groupsare significant as their P values are less than 0.05 with more significance in Group B.9. Abala – In Group A the Mean values, before treatment is 1.26, during treatment is1.00 and after treatment is 0.66. The P value of BT – AT variable is 0.001 (<0.05). InGroup B the Mean values of BT, DT & AT are 2.00, 0.80 & 0.20 respectively. The Pvalue of BT – AT variable is 0.00 (<0.05). It shows that the results in both the Groupsare significant as their P values are less than 0.05.10. Kasa – In Group A the Mean values, before treatment is 1.26, during treatment is1.33 and after treatment is 1.20. The P value of BT – AT variable is 0.35 (>0.05). InGroup B the Mean values of BT, DT & AT are 2.13, 1.13 & 0.33 respectively. The Pvalue of BT – AT variable is 0.00 (<0.05). It shows that the results in Group B aresignificant and those in Group A are non-significant. 158
  • 159. P VALUES OF INDIVIDUAL SUBJECTS OF GROUP ATable No.40 S NAME MEAN PAIRED t TEST .no MD SD SEM T P RE Julie BT 1.90 Bt-Dt 0.60 0.52 0.16 3.67 0.002 S 1 DT 1.30 Bt-At 1.10 0.56 0.18 6.12 0.000 S AT 0.80 2 Bhima Rao BT 1.60 Bt-Dt 0.01 0.56 0.17 0.55 0.295 NS DT 1.70 Bt-At 0.30 0.67 0.21 1.40 0.096 NS AT 1.30 3 Shilpa BT 1.70 Bt-Dt 0.50 0.52 0.16 3.00 0.007 S DT 1.20 Bt-At 1.10 0.56 0.18 6.12 0.000 S AT 0.60 4 Pushpa BT 1.30 Bt-Dt 0.20 0.63 0.20 1.00 0.171 NS DT 1.10 Bt-At 0.20 1.13 0.36 0.55 0.295 NS AT 1.10 5 Latha BT 1.30 Bt-Dt 0.01 0.74 0.23 0.42 0.339 NS DT 1.40 Bt-At 0.20 1.23 0.38 0.51 0.309 NS AT 1.10 6 Krishna Dev BT 1.70 Bt-Dt 0.50 0.53 0.16 3.00 0.007 S DT 1.20 Bt-At 1.20 0.63 0.20 6.00 0.000 S AT 0.50 7 Murali Mohan BT 1.80 Bt-Dt 0.50 0.53 0.16 3.00 0.007 S DT 1.30 Bt-At 1.10 0.56 0.18 6.12 0.000 S AT 0.70 8 Damodar BT 1.20 Bt-Dt 0.01 0.31 0.01 1.00 0.171 NS DT 1.10 Bt-At 0.01 0.87 0.27 0.36 0.263 NS AT 1.10 9 Yadagiri BT 1.70 Bt-Dt 0.50 0.53 0.16 3.00 0.007 S DT 1.20 AT 0.50 Bt-At 1.20 0.63 0.20 6.00 0.084 S 159
  • 160. 10 Vishwanath BT 1.30 Bt-Dt 0.20 0.42 0.13 1.50 0.025 NS DT 1.10 Bt-At 0.60 0.84 0.27 2.25 0.018 S AT 0.70 11 Azam Bee BT 1.40 Bt-Dt 0.40 0.52 0.16 2.45 0.001 S DT 1.10 Bt-At 0.80 0.63 0.20 4.00 0.002 S AT 0.60 12 Saroja BT 1.30 Bt-Dt 0.60 0.52 0.16 3.67 0.012 S DT 0.70 Bt-At 0.70 0.82 0.26 2.68 0.000 S AT 0.60 13 Srinivas BT 1.10 Bt-Dt 0.00 0.47 0.15 0.00 0.500 NS DT 1.10 Bt-At 0.20 0.78 0.25 0.80 0.221 NS AT 0.90 14 Rajesh Singh BT 1.00 Bt-Dt 0.20 0.92 0.29 -0.68 0.254 NS DT 1.20 Bt-At 0.00 0.67 0.21 0.00 0.500 NS AT 1.00 15 Mohan BT 1.60 Bt-Dt 0.70 0.48 0.15 4.58 0.000 S DT 0.90 Bt-At 0.90 0.99 0.31 2.86 0.009 S AT 0.70Assessment of Results in Individual Subjects of Group A:In Group A i.e., in the patients of chemical industry P values of 6 subjects were morethan 0.05 suggesting that the results of these subjects are non significant with the drugSri Bahusala Gudam. 160
  • 161. P VALUES OF INDIVIDUAL SUBJECTS OF GROUP B Table No.41S NAME MEAN PAIRED t TEST.no MD SD SEM t P RE Venkat Reddy BT 2.20 Bt-Dt 1.30 0.50 0.15 8.51 0.000 S1 DT 0.90 Bt-At 1.90 0.31 0.01 19.00 0.000 S AT 0.302 Shyamala BT 2.00 Bt-Dt 1.10 0.31 0.10 11.00 0.000 S DT 0.90 Bt-At 1.70 0.50 0.15 11.12 0.000 S AT 0.303 Manamma BT 2.10 Bt-Dt 1.20 0.42 0.13 9.00 0.000 S DT 0.90 Bt-At 1.90 0.31 0.01 19.00 0.000 S AT 0.204 Veeramma BT 1.80 Bt-Dt 1.10 0.56 0.17 6.12 0.000 S DT 0.70 Bt-At 1.70 0.50 0.15 1.12 0.000 S AT 0.105 Kotesh BT 1.90 Bt-Dt 0.80 0.42 0.13 6.00 0.000 S DT 1.10 Bt-At 1.80 0.63 0.20 9.00 0.000 S AT 0.106 Raheematullah BT 1.70 Bt-Dt 0.80 0.42 0.13 6.00 0.000 S DT 0.90 Bt-At 1.50 0.52 0.16 9.00 0.000 S AT 0.207 Rahena Begum BT 1.80 Bt-Dt 1.10 0.56 0.17 6.12 0.000 S DT 0.70 Bt-At 1.60 0.51 0.16 9.80 0.000 S AT 0.208 Chauhan BT 2.00 Bt-Dt 1.00 047 0.15 6.70 0.000 S DT 1.00 Bt-At 1.70 0.48 0.15 11.12 0.000 S AT 0.309 Asif BT 1.70 Bt-Dt 0.80 0.63 0.20 4.00 0.001 S DT 0.90 AT 0.10 Bt-At 1.60 0.51 0.16 9.79 0.000 S 161
  • 162. 10 Narsing BT 1.60 Bt-Dt 0.90 0.73 0.23 3.85 0.002 S DT 0.70 Bt-At 1.50 0.52 0.16 9.00 0.000 S AT 0.1011 Chandrakanth BT 1.70 Bt-Dt 1.20 0.42 0.13 9.00 0.000 S DT 0.50 Bt-At 1.40 0.51 0.16 8.60 0.000 S AT 0.3012 Suramma BT 2.10 Bt-Dt 0.80 0.42 0.13 6.00 0.00 S DT 1.30 Bt-At 1.80 0.42 0.13 13.50 0.00 S AT 0.3013 Bayyamma BT 2.20 Bt-Dt 0.90 0.31 0.10 9.00 0.00 S DT 1.10 Bt-At 1.70 0.50 0.15 11.12 0.00 S AT 0.3014 Sukkumani BT 1.70 Bt-Dt 0.90 0.31 0.10 9.00 0.00 S DT 0.80 Bt-At 1.50 0.52 0.17 9.00 0.00 S AT 0.2015 Suresh BT 1.70 Bt-Dt 0.90 0.31 0.01 9.00 0.00 S DT 1.80 Bt-At 1.50 0.52 0.16 9.00 0.00 S AT 0.20Assessment of Results in Individual Subjects of Group B:In Group B i.e., in the patients of Cotton Industry of all the Subjects yieldedsignificant results with the Drug Sri Bahusala Gudam. 162
  • 163. MEANS & PERCENTAGE DIFFERENCE OF INDIVIDUAL SELECTED VARIABLE IN ALL SUBJECTS OF GROUP- ATable No.42 BT DT AT %S.NO SYMPTOM MEAN MEAN MEAN MD DIFF. 1 Pinasa 1.53 1.26 0.73 0.80 52.28758 2 Ghughuruka 1.46 1.46 1.26 0.20 13.69863 3 Teevra Vega Swasa 1.53 1.53 1.46 0.67 43.79085 4 Pratamyati 1.20 0.53 0.67 0.53 44.16667 5 Trit 1.73 0.93 0.33 1.40 80.92486 Kanta Asya 6 Uddhwamsa 1.73 0.93 0.33 1.40 80.92486 7 Kricchra Bhashitam 1.40 0.93 0.00 1.40 100 8 Anidra 1.93 1.46 0.73 1.20 62.17617 9 Abala 1.26 1.00 0.66 0.60 47.61905 10 Kasa 1.26 1.33 1.20 0.06 4.671905It is assessed that in Group A, among 10 selected variables, Ghughuruka & Kasareduced marginally (0-25%),Teevra Vega Swasa, Pratamyati and Abala were reduced mildly (25-50%)Pinasa and Anidra were reduced moderately (50-75%)Trit and Kanta Asya Uddhwamsa were reduced markedly (above 75%)Kricchra Bhashitam was relieved completely (100%)( Mean data of individual variable is represented by Line graph.)( % difference of individual variable is represented by Bar graph.) 163
  • 164. MEANS OF INDIVIDUAL VARIABLE IN ALL SUBJECTS OF GROUP AGraph No.8 2.5 2 1.5 1 0.5 0 Pi Gh TVS Pr Tr KAU Kb An Ab Ka BT Mean 1.53 1.46 1.53 1.2 1.73 1.73 1.4 1.93 1.26 1.26 DT Mean 1.26 1.46 1.53 0.53 0.93 0.93 0.93 1.46 1 1.33 AT Mean 0.73 1.26 1.46 0.67 0.33 0.33 0 0.73 0.66 1.2 % DIFFERENCE OF INDIVIDUAL VARIABLE IN ALL SUBJECTS OF GROUP AGraph No.9 100 90 80 70 60 50 40 30 20 10 0 Pi Gh TVS Pr Tr KAU Kb An Ab Ka % DIFFERENCE 52.28 13.69 43.79 44.16 80.92 80.92 100 62.17 47.61 4.67 164
  • 165. MEANS & PERCENTAGE DIFFERENCE OF ALL THE SELECTED VARIABLES IN INDIVIDUAL SUBJECT OF GROUP- A Table No.43 BT DT AT NAME MD % DIFF. S.NO MEAN MEAN MEAN 1 1.90 1.30 0.80 1.10 57.89474 Julie 2 1.60 1.70 1.30 0.30 18.75 Bhima Rao 3 1.70 1.20 0.60 1.10 64.70588 Shilpa 4 1.30 1.10 1.10 0.20 15.38462 Pushpa 5 1.30 1.40 1.10 0.20 15.38462 Latha 6 1.70 1.20 0.50 1.20 70.58824 Krishna dev 7 Murali 1.80 1.30 0.70 1.10 61.11111 Mohan 8 1.20 1.10 1.10 0.01 0.833333 Damodar 9 1.70 1.20 0.50 1.20 70.58824 Yadagiri 10 1.30 1.10 0.70 0.60 46.15385 Vishwanath 11 1.40 1.00 0.60 0.80 57.14286 Azam Bee 12 1.30 0.70 0.60 0.70 53.84615 Saroja 13 1.10 1.10 0.90 0.20 18.18182 Srinivas 14 1.00 1.20 1.00 0.00 0.00 Rajesh Singh 15 1.60 0.90 0.70 0.90 56.25 Mohan In Group A, by observing % differences in each individual, it is assessed that 6subjects got marginal or no result (0-25%); 1 subject got mild relief (25-50%); 8subjects got moderate result (50-75%) by the end of the study. Mean data of all selected variables in each subject were recorded in line graph. % differences of all selected variables in each subject were recorded in bargraph. 165
  • 166. MEANS OF ALL SELECTED VARIABLES IN INDIVIDUAL SUBJECT OF GROUP AGraph No.10 2 1.5 1 0.5 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 BT Mean 1.9 1.6 1.7 1.3 1.3 1.7 1.8 1.2 1.7 1.3 1.4 1.3 1.1 1 1.6 DT Mean 1.3 1.7 1.2 1.1 1.4 1.2 1.3 1.1 1.2 1.1 1 0.7 1.1 1.2 0.9 AT Mean 0.8 1.3 0.6 1.1 1.1 0.5 0.7 1.1 0.5 0.7 0.6 0.6 0.9 1 0.7 % DIFFERENCE OF ALL SELECTED VARIABLES IN INDIVIDUAL SUBJECT OF GROUP AGraph No.11 80 70 60 50 40 30 20 10 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 % DIFFERENCE 57.9 18.8 64.7 15.4 15.4 7.58 61.1 0.83 70.6 46.2 57.1 53.8 18.2 0 56.3 166
  • 167. MEANS & PERCENTAGE DIFFERENCE OF INDIVIDUAL SELECTED VARIABLE OF ALL SUBJECTS IN GROUP B Table No.44 BT DT AT S.NO SYMPTOM MEAN MEAN MEAN MD % DIFF 1 Pinasa 1.60 1.00 0.20 1.40 87.50 2 Ghurghuruka 2.33 1.40 0.46 1.87 80.25751 Teevra Vega 3 Swasa 2.26 2.00 0.33 1.93 85.39823 4 Pratamyati 1.26 0.53 0.00 1.26 100 5 Trit 1.46 0.60 0.00 1.47 100 Kanta Asya 6 Uddhwamsa 1.73 0.80 0.00 1.73 100 Kricchra 7 Bhashitam 1.60 0.53 0.00 1.60 100 8 Anidra 2.26 1.13 0.46 1.80 79.64602 9 Abala 2.00 0.80 0.20 1.80 90.00 10 Kasa 2.13 1.13 0.33 1.80 84.50704 In Group B, there was a marked reduction (75% & above) in the symptoms ofPinasa, Ghurghuruka, Teevra Vega Swasa, Anidra, Abala & Kasa and there was acomplete relief (100%) in symptoms of Pratamyati, Trit, Kanta Asya Uddhwamsa &Kricchra Bhasitam. 167
  • 168. MEANS OF INDIVIDUAL VARIABLE IN ALL SUBJECTS OF GROUP BGraph No.12 2.5 2 1.5 1 0.5 0 Pi Gh TVS Pr Tr KAU Kb An Ab Ka BT Mean 1.6 2.33 2.26 1.26 1.46 1.73 1.6 2.26 2 2.13 DT Mean 1 1.4 2 0.53 0.6 0.8 0.53 1.13 0.8 1.33 AT Mean 0.2 0.46 0.33 0 0 0 0 0.46 0.2 0.33 % DIFFERENCE OF INDIVIDUAL VARIABLE IN ALL SUBJECTS OF GROUP BGraph No.13 100 80 60 40 20 0 Pi Gh TVS Pr Tr KAU Kb An Ab Ka % DIFFERENCE 87.5 80.25 85.39 100 100 100 100 79.64 90 84.5 168
  • 169. MEANS & PERCENTAGE DIFFERENCE OF ALL SELECTED VARIABLES IN INDIVIDUAL SUBJECT OF GROUP- B Table No.45 BT DT AT % S.NO NAME MEAN MEAN MEAN MD DIFF. 1 Venkat reddy 2.20 0.90 0.30 1.9 86.36364 2 Shyamala 2.00 0.90 0.30 1.70 85 3 Manamma 2.10 0.90 0.20 1.90 90.47619 4 Veeramma 1.80 0.70 0.10 1.70 94.44444 5 Kotesh 1.90 1.10 0.10 1.80 94.73684 6 Raheematulla 1.70 0.90 0.20 1.50 88.23529 7 RehenaBegum 1.80 0.70 0.20 1.60 88.88889 8 Chauhan 2.00 1.00 0.30 1.70 85 9 Asif 1.70 0.90 0.10 1.60 94.11765 10 Narsing 1.60 0.70 0.10 1.50 93.75 11 Chandrakanth 1.70 0.50 0.30 1.40 82.35294 12 Suramma 2.10 1.30 0.30 1.80 85.71429 13 Bayyamma 2.00 1.10 0.30 1.70 85 14 Sukkumani 1.70 0.80 0.20 1.50 88.23529 15 Suresh 1.70 0.80 0.20 1.50 88.23529.. In Group B, it is assessed that all the 15 subjects got marked relief (75 - 100%)of the selected variables. 169
  • 170. MEANS OF ALL SELECTED VARIABLES IN INDIVIDUAL SUBJECT OF GROUP BGraph No.14 2.5 2 1.5 1 0.5 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 BT Mean 2.2 2 2.1 1.8 1.9 1.7 1.8 2 1.7 1.6 1.7 2.1 2 1.7 1.7 DT Mean 0.9 0.9 0.9 0.7 1.1 0.9 0.7 1 0.9 0.7 0.5 1.3 1.1 0.8 0.8 AT Mean 0.3 0.3 0.2 0.1 0.1 0.2 0.2 0.3 0.1 0.1 0.3 0.3 0.3 0.2 0.2 % DIFFERENCE OF ALL SELECTED VARIABLES IN INDIVIDUAL SUBJECT OF GROUP BGraph No.15 100 75 50 25 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 % DIFFERENCE 86.4 85 90.5 94.4 94.7 88.2 88.9 85 94.1 93.8 82.4 85.7 85 88.2 88.2 170
  • 171. INTERNAL COMPARISIONA) COMPARISION OF PERCENTAGE DIFFERENCE: After completion of the study with the drug Sri Bahusala Gudam, 30 subjectswho were divided into 2 groups (Group A & Group B) of 15 subjects each, where thegrouping was based on the type of the industry in which the subjects work, now, thepercentage of changes observed in the 10 selected subjective parameters among bothgroups was compared. INTERNAL COMPARISION BETWEEN INDIVIDUAL PARAMETERS OF TWO GROUPSGraph No.16 100 90 80 70 60 50 40 30 20 10 0 Pi Gh TVS Pr Tr KAU KB An Ab Ka GROUP A % Difference 52.28 13.69 43.79 44.16 80.92 80.92 100 62.17 47.61 4.76 GROUP B % Difference 87.5 80.25 85.39 100 100 100 100 79.64 90 84.5 It is observed that the percentage of changes in selected variables are more inGroup B than in Group A which confers encouraging results in Group B who are thesubjects from cotton industry. 171
  • 172. B) COMPARISION OF P VALUES: The obtained Mean data of individual selected subjective parameter in BT &AT periods was subjected to Paired‘t’ test to compare the results among two Groups.It was observed that the obtained ‘p’ value of Group A is 0.02 (<0.05) and Group B is0.00 (<0.05) suggesting significant results in both the Groups, with more significancein Group B than in Group A.C) RESULTS OF OBJECTIVE PARAMETER AMONG BOTH THE GROUPS: The collected Mean data of all the subjects in both Groups is averaged in B.T& A.T periods and the Mean values are subjected to paired ‘t’ test. The ‘p’ value of IgE in all the subjects of Group A is 0.0435 (<0.05). The ‘p’value of Ig E in all thesubjects of Group B is 0.001. The percentage difference of Ig E in all the subjects of Group A & Group Bare calculated by MD/BT x 100, where the Group A percentage difference is1.764057 and that of Group B is 17.83022, which signifies that there is a moresignificant change in Ig E values after the treatment in Group B than in Group A i.e.,Group B is almost 10 times more responding to the drug than Group A shown bymarked changes in the values of Ig E in Group B. 172
  • 173. DISCUSSIONIn the present study, among 30 subjects considered for the research, the incidence ofthe occupational asthma was more (40%) in the age Group of 31-45 yrs (Middle ageGroup). The incidence of the disease is comparatively more in males (56.67%). This ispartly due to more number of male workers in the industrial arena. The criteria of socio-economic status involved most of the subjects who werein the low income Group (63.33%). Most of the involved subjects were under mixed diet Group (63.33%). The ‘Prakruti (temperament) of nearly half of the subjects considered is Vata-Kaphaja (46.67%) which is an important physical factor playing vital role in thePathogenesis of Tamaka Swasa vyadhi. The factor of genetic predisposition though a common one was observed less(76.67%) among the subjects of the present study who were mainly considered fromthe industrial sectors. This implies that the pollutant factor played a more importantrole in initiating the disease. The Chronicity was observed more in those with a period of 1-5 yrs (36.67%).It conveys that the pollutants to which the subjects were being exposed were potentialenough in causing the disease within a short span. Though multiple symptoms were involved in the manifestation of the disease,only 10 most common & important symptoms observed among all the subject(subjective parameters) were considered to assess the result and efficacy of the drugused for the treatment. 173
  • 174. The response of individual subjective parameter and individual subjectdiffered between the chemical industry (Group A) and Cotton industry (Group B)workers. The symptoms like Ghurghuruka, Teevra Vega Swasa and Kasa in the subjectsof Group ‘A’ have not responded to the drug yielding the ‘P’ values >0.05 which is anon significant result. Other symptoms like Pratamyati and Anidra have respondedonly to a limited extent with less significant ‘P’ values which are close to 0.05. The % differences of symptoms in Group A subjects showed a marginal (0-25%) relief of the symptoms Ghurghuruka & Kasa, Mild (25-50%) relief of thesymptoms Teevra Vega Swasa, pratamyati & Abala, Moderate (50-75%) relief ofPinasa & Anidra, the symptoms mainly related to upper respiratory tract, like Trit,Kanta Asya Uddhwamsa were relieved markedly (75% & above) and KricchraBhasitam, completely (100%). The parallel study in Group B, with the same drug yielded completelysignificant results where all the symptoms responded to the maximum extent withtheir p-values much <0.05. In Group B, almost all the subjective parameters have responded well with amarked relief (75% & above) in Pinasa, Ghurghuruka, Teevra Vega Swasa, Anidra,Abala & Kasa and complete relief (100%) in the symptoms Pratamyati, Trit, KantaAsya Uddhwamsa & Kricchra Bhasitam. In Group A, the % difference of the result in the individual subjects showedthat 6 subjects got Marginal (0-25%) relief, 1 subject got Mild (25-50%) relief and 8subjects got Moderate (50-75%) relief. In Group B, the % differences showed that all the 15 subjects got Marked(above 75%) relief in their subjective parameters. By the end, the total study involving the data collection & data analysis ofindividual Variable (Subjective parameter) and individual subject by estimating the 174
  • 175. ‘P’ value and % difference of the result obtained revealed a most significant change(improvement) in the symptoms of all the Group B subjects than Group A subjects. An important observation among the subjects during treatment (DT) i.e., after45 days showed some undesirable results with completely nil significance in few andaggravated symptoms in some others. This was attributed to the untimely intake of thedrug or altered dosage of the drug consumed by that particular subject. The total study confer that the chemical pollutant induced asthmatics (GroupA) have not shown remarkable response to the drug, when compared to the cottonpollutant induced Asthmatics (Group B). This shows the prominent role played by thetype of industrial pollutant inducing Asthma, where the chemical pollutants, mostlybeing inorganic & synthetic in nature might not have received much of theneutralizing effect from the organic preparation i.e., Sri Bahusala Gudam. The cottonpollutant might have received a better neutralizing or alleviating effect from the drugused, which is clear from the results obtained in Group B. The Ig E levels which were seen rose in the subjects, due to both chemical andcotton pollutant were observed to have responded to the drug though not completelyreached normalcy. This objective parameter has also shown difference in its resultsamong Group A & Group B subjects, where the chemical (Group A) pollutantinduced Ig E raise has responded 1.764% after treatment, and the cotton pollutant(Group B) induced Ig E raise has responded with a considerable improvement of17.83% after treatment, suggesting the better effect of the drug in cotton pollutantinduced asthmatics. The drug Sri Bahusala Gudam as Naimittika Rasayana appears to have workedmore in combating the symptoms related to upper respiratory tract, like Trit, KantaAsya Udhwamsa, Kricchra Bhasitam and to some extent Pinasa in the Chemicalrelated Asthmatics, while upper & lower respiratory tracts were influenced well incotton related asthmatics. 175
  • 176. On the whole the significant role of the Sri Bahusala Gudam can be attributedto its action in the form of Naimittika Rasayana where by both Sodhana property inthe form of Virechana is observed in almost all the subjects, and Samana property inthe form of alleviating the Vata & Kapha doshas as strongly suggested by the actionsof individual drugs of the compound is seen.SCOPE OF THE STUDY: This study understanding Bronchial Asthma asoccupational asthma considered it as an Industrial hazard.Out of over 250 causative agents of occupational asthma only two types of pollutantsviz., chemical & cotton were studied for the present work with better outcome. In the present research the Rasayana effect was ascertained for a period of 90days yielding improved objective parameter Ig E. Though the levels of Ig E have notreached completely to normal, there is a clear reduction in the elevated levels, aftertreatment. The study scope to assess the Rasayana property of the drug definitelyneeds much more duration to analyze the complete variations of objective parametertaken for the study.The study appears to be first of its kind, and leaves scope for better exploration in thefield. 176
  • 177. CONCLUSION After a detailed research study on 30 patients of Asthma, taken from chemicaland cotton industries, the results were truly expressed being strongly supported by therelevant objective parameter Ig E. An appreciable outcome of Sri Bahusala Gudam as a drug and as a NaimittikaRasayana was proved with significant results through subjective & objectiveparameters. 10 subjective parameters (symptoms) specific to Tamaka Swasa and observedin all the 30 subjects were only considered as the criteria for the result, parallelysupported by the variations in Ig E levels. The efficacy of the drug can be ascertained as significant in all the subjects ofCotton Industry where the % difference was markedly obtained i.e., above 75%.There is less significance in the results obtained in subjects of chemical industrywhere the % difference varied from marginal to moderate only (0-75%). The efficacy of the drug as Naimittika Rasayana also yielded similar inferencewhere the change in the elevated Ig E levels towards normalcy after the treatment wasobserved better in cotton induced asthmatics (Group B) with 17.83% than in chemicalinduced asthmatics (Group A) with 1.764%. In a nutshell, the therapeutic and Rasayana effects of the drug ‘Sri BahusalaGudam’ proved satisfactory in the occupational asthma due to cotton pollution thandue to chemical pollution. 177
  • 178. SUMMARY In developing countries like India, where Industrialization is an economicrevolution, is bound to include Hazards and the most common being Respiratoryindustrial Hazard, the Occupational Asthma. The aetiology of Tamaka Swasa has involved varied environmental factorswhich were also implicated in the causation of Janapadodhwamsa. With thissupportive elucidation, Tamaka Swasa as a Janapadodhwamsa Vyadhi can beconsidered rational to occupational Asthma, an industrial hazard. The study related to Industrial Hazards was really a hard task and industriousjob but yielding very significant information to the mankind. The first and foremost step taken towards the conduction of the study was,gathering information on the industries, their Hazards and the concentration of thepopulation suffering from the Hazard. In this regard, sufficient help was taken fromNational Informatics Centre (NIC), Pollution Control Board (PCB) and informationand survey by Green Peace International Organization. Later the required microplanning was used to survey the industries. This baseline work enabled to conduct medical camps in the campus ofpertaining industries. The survey on almost 480 workers in cotton industry and 372workers of chemical industry helped in ending up with more than required number ofsubjects. After a few dropouts the total number of subjects remained 15 from eachindustrial group who were followed till the end of the project. Complete required data and Blood samples (for objective parameter) werecollected from the subjects before the treatment. They were counseled andadministered with the drug. The duration of the study was 90 days including followups with in. Like wise the data collection included that of Before, During & Aftertreatment (B.T, D.T & A.T) 178
  • 179. The observations drawn were subjected to analysis to assess the result due tothe effect of the drug. The final inference was thus understood by studying ‘P’ values& % differences. The therapeutic and Rasayana properties of the drug were analyzedgraphically, which suggests that chemical pollutant was less dealt than cottonpollutant. The symptomatic relief of the Asthmatics due to chemical pollution yieldedless appreciable results than those of cotton pollution. These facts were wellsupported by the respective changes observed in Ig E levels, a parameter to ascertainthe Rasayana angle of the drug. 179
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  • 181. 24 Su. Su. 35 49 B.G. Ghanekar on Su. Sa.6/11 – 4425 Dalhana on Su. Su. 35 50 Atharvana Veda 9-12-7251 Ch. Sa. 7/15 76 Su. Su. 21/552 Su. Chi. 2/9, A.Hr. Sa. 3/12 77 Sabdasthoma Mahanidhi53 Panineeya Sutram 78 A.Hr.Ni.4/354 Su. Sa. 4/31 79 Chakrapani on Ch. Su. 20/855 Sarangadhara Sam. 5 80 A.Hr.Ni.4/356 A.Hr. Sa. 3/12 81 Ch.Su.20/857 Su. Sa. 4/25 82 Su. Su. 21/458 Su. Ni. 6/16 83 A.H.Su 12/1559 Ch. Samhita – Jamnagar, Pg.327, 84 A.Hr.Su.12/16, 12/17 6th sloka60 Sh.S.5/48,49 85 Su. Su. 21/1261 Ch. Su. 17/118 86 Su. Su. 21/1462 Ch.Chi. 29/34 87 Ayurveda Kriya Sareera by Ranjit Roy Desai63 Ch. Su. 18/49 88 Atharvana Veda – IV.4.564 Sarangadhara Sam. 5/48 89 Sathapatha Brahmana III 33.1865 A.Hr. Sa. 3/84 90 Vachaspatyam, Halayudhakosam, Sabdakalpadrumam66 Ch. Su. 12/8 91 Amarakosa, Dwiteeya kanda, Vanaushadhi varga67 Ch. Su. 12/8 92 Amarakosa, Prathama kanda, Swarga varga68 Vachaspatyam 93 Ch. Samhita, Jamnagar, Pg.327, 6th sloka69 Chakrapani on Ch. Vi. 5/8 94 Su. Ut.51/470 A.Hr.Su.12/4 95 ‘Asthma’ edited by G.Jariwalla71 Vachaspatyam 96 Ch.Ni.1/372 Ch. Chi. 28/7 97 Su.Ut. 1/25 181
  • 182. 73 Sarangadhara Sam. 5/43 98 Ch.Ni. 8/2474 A.H.Su12/5 99 Ch.Ni. 5/1675 A.H.Su12/6 100 Ch.Ni. 5/17101 Ch.Ni. 5/18 126 Ch. Vi. 3/7102 Ma. Ni. 12/1 127 Ma. Ni. 12/16103 Ch. Chi. 17/11-16 128 Ch. Chi. 17104 Su. Ut 51/3 129 Su. Ut 51105 A.S. Ni. 4 130 A.S. Ni. 4106 A.Hr.Ni. 4/1,2 131 A.Hr.Ni. 4/1,2107 Ma. Ni. 12/2 132 K.S. Su. Vedanadyaya 17108 Ch. Chi. 17/11-16 133 Ma. Ni. 12/27-34109 Su. Ut 51/3 134 Ch. Chi. 17/55-62110 A.S. Ni. 4 135 Su. Ut 51/8-10111 A.Hr.Ni. 4/1,2 136 A.S. Ni. 4112 Ma. Ni. 12/2 137 A.Hr.Ni. 4/6-10113 Ch. Chi. 17/11-16 138 Ch. Chi. 17/55 – 62114 Su. Ut 51/3 139 Ma. Ni.115 Ch. Chi. 17/11-16 140 Ma. Ni. 12/18,19,20116 Su. Ut 51/3 141 Ma. Ni. 12/21-23117 A.S. Ni. 4 142 Ma. Ni. 12/24-26118 A.Hr.Ni. 4/1,2 143 Ma. Ni. 12/37-39119 Su. Su. 24/8 144 Ma. Ni. 12/35120 Ch. Chi.14/5 145 Ma. Ni. 12/36121 Ch. Chi. 17 146 Ma. Ni. 1 182
  • 183. 122 Ch. Vi. 3 147 Ma. Ni. 1/10123 Ch. Vi. 3/6 148 Ch. Ni. 1/5124 Ch. Vi. 3/16 149 Ch. Chi. 17125 Ch. Vi. 3/24 150 Ch. Sa. 6/15151 Ch. Chi. 28/58 176 Ch.Su.11/48; Su.Chi. 2/9152 Ch. Chi. 28/27 177 Ch. Vi. 2/17153 Chakrapani on Ch. Vi. 5/8 178 Ch. Su. 20/8154 Ch. Chi. 28/6 179 Su. Su. 21/6155 Sarangadhara Sam. 5/8 180 Chakrapani on Ch. Su. 20/8156 Ch. Vi. 5/7 181 Chakrapani on Ch. Su. 20/8157 Ch. Vi. 5/32 182 A.Hr. Su. 12/12 – 17158 Ch. Chi. 28/222 183 Su. Ni. 1/16159 Ch. Chi.28/7 184 Ch. Chi. 15/7, 8160 A. S. Su. 20/4 185 Ch. Chi. 17/17, A.Hr.Ni. 4/3161 Ch. Chi.28/206 186 Su.Chi. 2/9, Su.Sa. 4/31162 Ch. Chi.28/209 187 Ch. Chi.28/6, 7163 A. S. Su. 20/3 188 Ch. Chi. 17/8164 Ch. Chi.28 189 Ch. Chi. 17/8165 Ch. Chi.28 190 Ch. Vi. 5/7166 Ch. Chi.17/62 191 Ch. Vi. 5/16167 A.S.Su.19 192 A.Sangraha168 Su. Su. 21/4 193 Human Physiology – Chatterjee169 Ch. Chi.28/222 194 Ch.Vi. 5/9170 A.Hr.Su.12/16, 12/17 195 Ch.Vi. 5/18 183
  • 184. 171 Su. Su. 21/12 196 A.Hr. Su. 12/16172 Su. Su. 21/14 197 Ch.Vi. 5/9, Ch.Chi.17/20173 Ch. Chi. 17/8 198 Ch.Vi. 5/9174 A.Hr.Ni. 4/3 199 Ch.Vi. 5/32175 Ch.Su.20/8 200 A.Hr. Ni. 4/3, 4201 Su. Ut. 51/4 212 Bhaishajya Ratnavali 73/1 – 4202 Ma. Ni. 12/40, 41 213 Bhavaprakasa, Uttarakanda, Rasayanadhikara203 Ch. Chi. 17/68, 69 214 Vangasena, Loharasayana, 373 sloka204 Ch. Chi. 17/93 215 Hareetha Samhita, Prathama sthana, 1205 Ch. Chi. 17/89 – 92 216 Rasa Ratna Samucchyam, 26206 A.Hr.Chi. 4/18 217 Gada Nigraha, Vol. 3, Samanya Rasayanadhikara207 Ch. Chi. 17/148-150 218 Su. Chi. 27208 Ch. Chi.1/4 – 16 219 Ch. Chi.17/8209 Su. Chi. 27/1 – 2 220 Ch. Chi. 17/70 – 72210 A.Hr. 39/1 – 4 221 Ch. Chi. 17/121211 Yogaratnakara, Uttarardha, 52 222 Ch. Chi. 17/94-110 184
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  • 189. Dr. B.R.K.R.GOVT. AYURVEDIC MEDICAL COLLEGE & HOSPITAL, S.R.NAGAR, HYDERABAD. POST GRADUATE DEPARTMENT OF KAYA CHIKITSA, N.T.R.U.H.S, VIJAYAWADA THESIS CASE SHEET (RANDOMISED CONTROLLED OPEN THERAPEUTIC CLINICAL TRIAL) _____________________________________________________________________• NAME:• FATHER’S NAME:• AGE:• SEX:• ADDRESS: _____________________________________________________________________ CHIEF COMPLAINTS WITH DURATION: ASSOCIATED SYMPTOMS: HISTORY OF PRESENT ILLNESS: HISTORY OF PAST ILLNESS: FAMILY HISTORY: Patient’s Position Grand Father’s Health Grand Mother’s Health Mother’s Health Father’s Health PERSONAL HISTORY: Health of Wife No. of Children Health of Children Hereditary Disorders if any Cause of recent death if any HABITS: ADDICTIONS: DIET: OCCUPATIONAL HISTORY: Dusty Job Any fumes/Vapours Any protective uniform provided at work Any similar illness to fellow employee Duration of work Nature of work 189
  • 190. INDUSTRIAL INFORMATION:• NAME OF INDUSTRY:• ADDRESS:• TYPE OF HAZARDOUS CHEMICAL USED:• TYPE OF HAZARDOUS WASTE PRODUCED: DASAVIDHA PARIKSHA: PRAKRITI VIKRITI SARA SAMHANANA SATVA SATMYA PRAMANA AHARA VYAYAMA VAYAS SAKTHI SAKTHI ASHTASTHANA PARIKSHA: NADI MUTRA MALA JIHWA SHABDA SPARSHA DRIK AKRUTI SROTO PARIKSHA : PRANAVAHA SROTAS (RESPIRATORY SYSTEM): GENERAL EXAMINATION:• INSPECTION – 1) SHAPE Symmetric Asymmetric 2) MOVEMENTS OF THE CHEST Symmetry Accessory Muscular Action• PALPATION – Tactile Vocal Fremitus• AUSCULTATION -1) BREATH SOUNDS – Vesicular with prolonged Expression2) ADDED SOUNDS – Wheezes Monophonic (Ronchi) Polyphonic 190
  • 191. • SPUTUM - Colour Mucoid Consistency Purulent PRINCIPLE SYMPTOMS: 1) COUGH - Aggrevating during Day/Night Aggrevating Factors Dry/Productive cough Painful/Non-painful 2) SPUTUM PRODUCTION - Quantity of production Time of production 3) BREATHLESSNESS – On Exertion At Rest Time of Attack (Day/Night) 4) WHEEZE: Time of occurrence Constant/Intermittant Provoking factors Particular time of worsening 5) CHEST TIGHTNESS – Due to deep breathing/cough Increasing due to cough/sputum/dyspnoea INVESTIGATIONS A) PATHOLOGICAL BEFORE AFTER DATE VALUE DATE VALUE C.B.P E.S.R. A.E.C. B) SEROLOGICAL BEFORE AFTER DATE VALUE DATE VALUE Ig. E 191
  • 192. NIDANA PANCHAKA1) NIDANA:a) VATA PRAKOPAKA AHARA b) VATA PRAKOPAKAVIHARA 1 Vidahi 1 Sita Sthana 2 Ruksha 2 Rajas 3 Sita Pana 3 Dhuma 4 Sita Asana 4 Atapa 5 Apatarpana 5 Anila 6 Vishamasana 6 Vyayama 7 Samasana 7 Bhara 8 Viruddhasana 8 Adhwa 9 Vegaghata 10 Strisevana/Gramya Dharmac) KAPHA PRAKOPAKA AHARA d) OTHERS 1 Guru 1 Abhighata/Marmaghata 2 Vishtambhi 2 Kshaya/Dourbalya 3 Abhishyandi 3 Anaha 4 Ama Dosha 4 Atiroukshyam 5 Adhyasana 5 Atishodana 6 Nishpava 6 Kanta & Urah Pratighata 7 Masha 7 Sroto Vibandha 8 Pinyaka 9 Tilataila10 Pishta11 Shaluka12 Jalaja Pisita13 Anupa Pisita14 Dadhi15 Ama Kshira16 Sleshmakara Ahara2) PURVA RUPA Prodromal Symptoms 0 Day 45 Days 90 Days 1 Hrit Peeda 2 Parsva Sula 3 Adhmana 4 Anaha 5 Vaktra/Vadana Vairasyam 6 Sankha Nistodam 7 Arati 8 Pranasya Vilomatwam 192
  • 193. 9 Bhakta Dwesham2) ROOPA: Lakshana 0 Day 45 Days 90 Days 1 Pinasam 2 Ghurghurukam 3 Tivravegaswasa 4 Prana Prapeedakam 5 Prathamyathi 6 Trit 7 Sanniruddhyate 8 Kasa 9 Ghoshah Mahatavishta 10 Pramoham Kasamanascha 11 Kanta Udhwamsa 12 Asya Udhwamsa 13 Kricchra Bhasitam 14 Anidra 15 Parswagraham 16 Urah Peeda 17 Ushna Abhinandati 18 Ucchritaksha 19 Lalatena Swidhyata 20 Brhisamartiman 21 Visushkasyam 22 Muhuswasa 23 Muhuschaivavadhamyate 24 Parigrihyam Sirogreevam 25 Aruchi 26 Anna Dwesham 27 Vamadhu 28 Vepadu 29 Abala3) UPASAYA: 1 Sleshmanyamucchyamanetu Dukham 2 Nishtyutante Kshanam Sukhee 3 Suptastamakapiditah 4 Asinolabhate Soukhyam 5 Ushna Ahara & Vihara 6 PathyaTREATMENTDOSAGE: 10 gms B.i.d. with milk, after foodDATE:DURATION: 90 Days 193
  • 194. RESULTa) COMPLETE:b) PARTIAL: MARKED (Relief of 75% & above) MODERATE (Relief of 50% – 75%) MILD (Relief of 25% - 50%) NO (Below 25% & No relief) c) DROP OUT: Signature SignatureP.G. Scholar ASST. PROFESSOR / PROFESSOR / H.O.D CONSENT FORMNAME AGE: M/F REG.NO.I -----------------------------------------------------------D/o, S/o -----------------------------here by give consent in a clear mind to undergo the therapy in the industrial premiseswith the permission of the concerned authority. The nature, effect and complicationsof which here by have been explained to me in my native language / mother tongue(Telugu / Hindi / English). I do not hold the Research Scholar responsible for anyuntoward happening.Date: Signature / Thumb impressionWitness:Name & Address: Name & Address: 194
  • 195. SRI BAHUSALA GUDAM 195

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