POST GRADUATE TRAINING AND RESEARCH UNIT             DEPARTMENT OF KAYACHIKITSA   Dr. B.R.K.R GOVT. AYURVEDIC COLLEGE & HO...
ACKNOWLEDGEMENTS       I owe an enormous debt to my parents who have been a constantpsychololgical support and backup thro...
I’m fortunate enough to have friends like D.Dinesh Chakravarthy,Dr.L.Srinivas and Miss.Sana, for their inestimable and inv...
INDEXS.No                   TITLE              Pg. No I     INTRODUCTION                         1 II    HISTORICAL REVIEW...
IV    CLINICAL STUDY       1   Aims & Objectives        126       2   Material & Materials     127       3   Observations ...
LIST OF TABLESS.No                                    TITLE                    Pg.No 1     Solubility Coefficients        ...
29   Data of all variables of individual subject in Gr.B                      13330   IgE Values of Gr.A                  ...
LIST OF GRAPHSS.No                                    TITLE                                     Pg.No 1     Distribution o...
INTRODUCTION       Ayurveda, the science of life is the supreme theory with unerring factors basedon Tridosha and Panchabh...
the Industrialization in the developing countries where an additional causative factorin the form of Industrial Pollutant ...
HISTORICAL REVIEW       Swasa vyadhi reveals its evolution through ages, with origin in Vedic age,existence in medieval ag...
PURANAS:Garuda Purana allotted an entire chapter for the description of Swasa.The disease has been mentioned in Vishnupura...
HIPPOCRATES (460-367 B.C), Father of Medicine, was the first to use the term inreference to the medical condition – in his...
GALEN said that many cure Asthma with owl’s blood given in wine.In 17th Century, BERNARDINO RAMAZZINI, Father of Occupatio...
Found in Egypt in 1870s, the ‘GEORG EBERS PAPYRUS’ contains a writtenevidence of Asthma.In 1873 CHARLES HARRISON BLACKLEY ...
In 1940 KELLAWAY and TRETHWIE showed the release of a substance now calledas Slow Reacting Substance in anaphylaxis (SRS-A...
RACHANA SHAREERA       The Swasa Kriya is performed by the cumulative effect of different organsincluded under Swasana sam...
Susrutha mentioned the presence of 8 asthis27 and one sandhi in Nasa28, and 2 asthisnear Kaninika29.Ghrana mula is the ter...
Nasal septum has 3 parts:    1. The bony part: - Formed by the vomer, and the perpendicular plate of the        ethmoid.  ...
e) Nasal Conchae: These are curved bony projections directed downwards andmedially. They are 3 in number: 1. Inferior, 2. ...
It is a wide muscular tube, situated behind the nose, the mouth and the larynx.The upper part transmits only air, the lowe...
Venous Drainage:The venous plexus on the posterolateral aspect of the pharynx receives blood frompharynx, soft palate and ...
3. EpiglotticPaired Cartilages: - 1. Arytenoids                    2. Corniculate                    3. CuneiformArterial ...
Gala nalaka is the term used by Dalhana for Swara yantra & trachea and GalaNalakasthis is used for hyoid, thyroid and Cric...
Arterial Supply: Inferior thyroid arteries.Venous Drainage: Into the left branchiocephalic vein.Nerve supply: Parasympathe...
LUNGS:       These are a pair of respiratory organs situated in the thoracic cavity. Each lunginvaginates the correspondin...
5. Bronchial veins    6. Anterior and posterior pulmonary plexuses of nerves    7. Lymphatics of the lung.    8. Bronchopu...
BRONCHIAL TREE:        Trachea divides at the level of the lower border of 4th thoracic vertebra into 2principle bronchi, ...
SEGMENTS:Right Lung: Upper Lobe     1. Apical                           2. Anterior                           3. Posterior...
HISTOLOGY OF THE RESPIRATORY TRACTNOSE:        The vestibule of the nasal cavity is lined by skin continuous with that on ...
LUNGS:       As the bronchi become smaller the epithelium first becomes simple ciliatedcolumnar, then non-ciliated columna...
KRIYA SHAREERA       The Nirgama and pravesa of prana vayu by nasika and gala marga is calledswasa. The roga in which avar...
Prana Vata:   The following are the factors supporting the role of Prana vata:   1) The word Prana is derived from the dha...
The Udana vata, located in Uras, circulates through nasa, nabhi and gala with thespecific functions of Vakravritti, prayat...
Kledaka Kapha:        The role of Kledaka kapha can be established based on the following factors:    1) The sthana of kle...
PHYSIOLOGY OF RESPIRATIONThe physiology of respiration in adult human includes:1. Pulmonary ventilation2. Diffusion of Oxy...
Therefore all the muscles that elevate the chest cage are classified as muscles ofinspiration and those that depress the c...
iv) Residual Volume: This is the volume of air remaining in the lungs after the mostforceful expiration. (RV = 1200 ml)PUL...
There are about 300 million alveoli in the two lungs, and each alveoli has anaverage diameter of about 0.2mm. Between the ...
The partial pressure is directly proportional to the concentration of the gas molecules,and inversely proportional to the ...
Once oxygen has diffused from the alveoli into the pulmonary blood, it is transportedto the peripheral tissue capillaries ...
Under normal resting conditions, an average of 4 ml of CO2 is transported from the    tissues to the lungs in each 100 ml ...
b) Ventral Respiratory Group:           This is located in the ventrolateral part of the medulla about 5mm to the dorsal  ...
and bicarbonate ions. The hydrogen ions then have a potent direct stimulatory effecton respiration.       Oxygen, in contr...
FUNCTIONS OF RESPIRATORY PASSAGES        The air is distributed to the lungs by way of respiratory passages viz., nose,tra...
called respiratory bronchiole, which is mainly pulmonary epithelium and underlyingfibrous tissue plus a few smooth muscle ...
PHYSIOLOGICAL CONCEPT OF RASAYANA        Rasayana is a disease modifying and prophylactic function, which aims atfortifyin...
Acquired Immunity:In addition to these, the human body has the ability to develop extremely powerfulspecific immunity agai...
DEFINITIONS & DERIVATIONS       The word ‘TAMAKA’ is derived from ‘TAMAS’ sabda, which meansAndhakara (Darkness). The word...
Asthma or spasmodic bronchial asthma is a paroxysmal affection. It manifestsitself in attacks of severe respiratory dyspno...
PREVALENCE OF ASTHMA        The disease can start at any age, but in about one half of cases it starts before10 yrs of age...
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....
NIDANANidana is the vyadhi karana96.The ultimate significance of the knowledge of nidana is ‘Nidana parivarjana97, whichpo...
VATA PRAKOPAKARA AHARA           Table No.3 S.No             AHARA         M.N102 C.S103 S.S104 A.S105 A.H106      1      ...
KAPHA PRAKOPAKARA AHARA             Table No. 5           S.No        AHARA           M.N112 C.S113 S.S114 A.S A.H        ...
Tamaka Swasa. From an etiological stand point of modern literature, asthma isa heterogenous disease and multifactorial in ...
GENES CURRENTLY IMPLICATED IN ASTHMA  Table No 7PATHOLOGICAL             CANDITATE             CANDIDATE            NORMAL...
d) ALLERGENS:        Table No 8            AERO-ALLERGENS / INHALANTS                         INGESTANTS:         House du...
c) DRUGS: - (Pharmacological Stimuli)       Aspirin – The prevalence of aspirin sensitivity is 10%.       Typical aspirin ...
Running produces a more severe attack of asthma than walking because of its greaterventilatory cost.Inhalation of cold air...
h) OCCUPATION:   Acute and chronic airway obstructions have been reported to follow exposure to alarge number of compounds...
paraphenyl diamine, henna extract)             beauticians     Fluxes (eg colophony, soft core solder)         Solderers, ...
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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. Ayurvedic College, HYDERABAD

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Tamakaswasa kc006 hyd

  1. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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

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