Ventilation and Perfusion in different zones of lungs.Gyaltsen Gurung
This powerpoint presentation will make you explore about the Perfusion and Ventilation in different zones of lungs with its co-relation with pulmonary tuberculosis.
lecture 5: it's good for as to take a breif about how does atmospheric air will pass to our lungs then to blood, for transportation and utilization of oxygen and excretion of carbon dioxide. Many issue are related when gas exchange is performed.
Gas exchange between the alveoli and the pulmonary capillary blood occurs by diffusion, as will be discussed in the next chapter. Diffusion of oxygen and carbon dioxide occurs passively, according to their concentration differences across the alveolar-capillary barrier. These concentration differences must be maintained by ventilation of the alveoli and perfusion of the pulmonary capillaries.
Alveolar ventilation brings oxygen into the lung and removes carbon dioxide from it. Similarly, the mixed venous blood brings carbon dioxide into the lung and takes up alveolar oxygen. The alveolar Image not available. and Image not available. are thus determined by the relationship between alveolar ventilation and pulmonary capillary perfusion. Alterations in the ratio of ventilation to perfusion, called the Image not available., will result in changes in the alveolar Image not available. and Image not available., as well as in gas delivery to or removal from the lung.
Alveolar ventilation is normally about 4 to 6 L/min and pulmonary blood flow (which is equal to cardiac output) has a similar range, and so the Image not available. for the whole lung is in the range of 0.8 to 1.2. Image not available. However, ventilation and perfusion must be matched on the alveolar-capillary level, and the Image not available. for the whole lung is really of interest only as an approximation of the situation in all the alveolar-capillary units of the lung. For instance, suppose that all 5 L/min of the cardiac output went to the left lung and all 5 L/min of alveolar ventilation went to the right lung. The whole lung Image not available. would be 1.0, but there would be no gas exchange because there could be no gas diffusion between the ventilated alveoli and the perfused pulmonary capillaries.
Oxygen is delivered to the alveolus by alveolar ventilation, is removed from the alveolus as it diffuses into the pulmonary capillary blood, and is carried away by blood flow. Similarly, carbon dioxide is delivered to the alveolus in the mixed venous blood and diffuses into the alveolus in the pulmonary capillary. The carbon dioxide is removed from the alveolus by alveolar ventilation. As will be discussed in Chapter 6, at resting cardiac outputs the diffusion of both oxygen and carbon dioxide is normally limited by pulmonary perfusion. Thus, the alveolar partial pressures of both oxygen and carbon dioxide are determined by the Image not available. If the Image not available. in an alveolar-capillary unit increases, the delivery of oxygen relative to its removal will increase, as will the removal ...
Ventilation and Perfusion in different zones of lungs.Gyaltsen Gurung
This powerpoint presentation will make you explore about the Perfusion and Ventilation in different zones of lungs with its co-relation with pulmonary tuberculosis.
lecture 5: it's good for as to take a breif about how does atmospheric air will pass to our lungs then to blood, for transportation and utilization of oxygen and excretion of carbon dioxide. Many issue are related when gas exchange is performed.
Gas exchange between the alveoli and the pulmonary capillary blood occurs by diffusion, as will be discussed in the next chapter. Diffusion of oxygen and carbon dioxide occurs passively, according to their concentration differences across the alveolar-capillary barrier. These concentration differences must be maintained by ventilation of the alveoli and perfusion of the pulmonary capillaries.
Alveolar ventilation brings oxygen into the lung and removes carbon dioxide from it. Similarly, the mixed venous blood brings carbon dioxide into the lung and takes up alveolar oxygen. The alveolar Image not available. and Image not available. are thus determined by the relationship between alveolar ventilation and pulmonary capillary perfusion. Alterations in the ratio of ventilation to perfusion, called the Image not available., will result in changes in the alveolar Image not available. and Image not available., as well as in gas delivery to or removal from the lung.
Alveolar ventilation is normally about 4 to 6 L/min and pulmonary blood flow (which is equal to cardiac output) has a similar range, and so the Image not available. for the whole lung is in the range of 0.8 to 1.2. Image not available. However, ventilation and perfusion must be matched on the alveolar-capillary level, and the Image not available. for the whole lung is really of interest only as an approximation of the situation in all the alveolar-capillary units of the lung. For instance, suppose that all 5 L/min of the cardiac output went to the left lung and all 5 L/min of alveolar ventilation went to the right lung. The whole lung Image not available. would be 1.0, but there would be no gas exchange because there could be no gas diffusion between the ventilated alveoli and the perfused pulmonary capillaries.
Oxygen is delivered to the alveolus by alveolar ventilation, is removed from the alveolus as it diffuses into the pulmonary capillary blood, and is carried away by blood flow. Similarly, carbon dioxide is delivered to the alveolus in the mixed venous blood and diffuses into the alveolus in the pulmonary capillary. The carbon dioxide is removed from the alveolus by alveolar ventilation. As will be discussed in Chapter 6, at resting cardiac outputs the diffusion of both oxygen and carbon dioxide is normally limited by pulmonary perfusion. Thus, the alveolar partial pressures of both oxygen and carbon dioxide are determined by the Image not available. If the Image not available. in an alveolar-capillary unit increases, the delivery of oxygen relative to its removal will increase, as will the removal ...
Regulation of respiration (the guyton and hall physiology)Maryam Fida
Normal respiration is spontaneous and unconscious.
There are 4 groups of neurons on each side in the Pons and medulla oblongata which are involved in regulation of respiration. These include
1. Medullary centers
Dorsal respiratory group of neurons
Ventral respiratory group of neurons
2. Pontine centers
Pneumotaxic centre
Apneustic centre.
It contains “I”neurons which are inspiratory neurons.
It’s located in dorsal portion of medulla oblongata.
It also includes the nucleus of tractus solitarius which is the sensory termination of afferent fibers in 9th ( GLOSSOPHARYNGEAL NERVE) and 10th (VAGUS NERVE) cranial nerves.
They receive impulses from peripheral chemoreceptors, carotid and aortic baroreceptors and also other receptors in the lungs.
In this group inspiratory ramp signals are produced spontaneously.
If we cut the medulla oblongata from other parts of brain and also the afferent nerves which enter the medulla, still inspiratory ramp signals are produced which indicate it’s the inherent property of medulla.
Initially the signal is weak and then it progressively increases and then fades away.
Each ramp signal’s duration is 2 sec and then for 3 seconds there is no ramp signal.
So each cycle lasts for 5 seconds and there are 12 cycles /minute which is the respiratory rate.
Significance of the signal in the form of ramp is that it causes progressive expansion of the lungs. After production, these ramp signals are transmitted to the contra lateral motor neurons supplying the inspiratory muscles.
Rate and duration of inspiratory ramp signals is controlled by impulses from the Pneumotaxic centre and impulses from the lungs via vagi.
Ventilation perfusion ratio (The guyton and hall physiology)Maryam Fida
Ventilation perfusion ratio is :
“The ratio of alveolar ventilation and the amount of blood that perfuse the alveoli”.
FORMULA
It is expressed as VA/Q.
VA is alveolar ventilation
Q is the blood flow (perfusion)
Normal value of ventilation perfusion ratio is about
0.8
VA is 4.2 L /min
Q is 5.5 L/min (Same as Cardiac output)
So VA/Q = 4.2/5.5 = 0.8
If VA becomes zero ratio becomes zero
If Q becomes zero ratio becomes infinite.
If ratio becomes zero or infinite then there is no gaseous exchange. So this ratio indicates the efficiency of gaseous exchange in lungs.
In standing or sitting position this ratio is not uniform in all parts of the lungs.
In standing position, in upper parts of lungs there is almost no blood flow so normally in upper parts of lungs the ratio is higher may be near 3.
In lower part of lungs, there is more blood flow so the ratio is decreased may be 0.6.
In certain diseases the VA/Q ratio is higher which means perfusion is inadequate i.e. in some parts of lungs the alveoli are non functional or partially functional. This is seen in cases of pulmonary thrombosis or embolism.
When there is higher VA/Q ratio, PO2 and PCO2 in the alveolar air resembles the values in the inspired air.
When exchange is not occurring because of lack of perfusion, inspired air goes to alveoli, as there is no exchange occurring so the same values of PCO2 and PO2 as in inspired air.
Like heartbeat, breathing must occur in a continuous, cyclic pattern to sustain life processes.
Inspiratory muscles must rhythmically contract and relax to alternately fill the lungs with air and empty them.
The rhythmic pattern of breathing is established by cyclic neural activity to the respiratory muscles
Altitude physiology typically focuses on people above 2500 m; ∼8000 ft. Altitudes above that are sometimes subdivided into very high (3500–5500 m; ∼11,500–18,000 ft) and extreme (>5500 m; >18,000 ft). An estimated 40 million people travel each year to altitudes >2500 m (∼8000 ft),1 and as many or more travel to altitude for leisure and sports, and work in mines, military or border operations, and the like. Altitude medicine considers the clinical disorders associated with acclimatization by the travelers, workers and migrants, and with adaptation by people with lifetimes or populations with millennia of residence (an estimated 83 million people).
With a hurried ascent, many (∼80%) will report a transient headache (high-altitude headache or [HAH]), and some will develop one of three forms of acute high-altitude illness: acute mountain sickness (AMS) and HAH, high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). AMS and HAH are annoying and interfere with activity and work, however, HACE and HAPE can be fatal with mortality rates approaching 30%. Among some residents, chronic mountain sickness (CMS) and right ventricular hypertrophy develop over months to years of residence at altitude. Birth weights are generally lower and the rate of small-for-gestational-age babies and congenital heart defects are higher than that in lowland populations.
Regulation of respiration (the guyton and hall physiology)Maryam Fida
Normal respiration is spontaneous and unconscious.
There are 4 groups of neurons on each side in the Pons and medulla oblongata which are involved in regulation of respiration. These include
1. Medullary centers
Dorsal respiratory group of neurons
Ventral respiratory group of neurons
2. Pontine centers
Pneumotaxic centre
Apneustic centre.
It contains “I”neurons which are inspiratory neurons.
It’s located in dorsal portion of medulla oblongata.
It also includes the nucleus of tractus solitarius which is the sensory termination of afferent fibers in 9th ( GLOSSOPHARYNGEAL NERVE) and 10th (VAGUS NERVE) cranial nerves.
They receive impulses from peripheral chemoreceptors, carotid and aortic baroreceptors and also other receptors in the lungs.
In this group inspiratory ramp signals are produced spontaneously.
If we cut the medulla oblongata from other parts of brain and also the afferent nerves which enter the medulla, still inspiratory ramp signals are produced which indicate it’s the inherent property of medulla.
Initially the signal is weak and then it progressively increases and then fades away.
Each ramp signal’s duration is 2 sec and then for 3 seconds there is no ramp signal.
So each cycle lasts for 5 seconds and there are 12 cycles /minute which is the respiratory rate.
Significance of the signal in the form of ramp is that it causes progressive expansion of the lungs. After production, these ramp signals are transmitted to the contra lateral motor neurons supplying the inspiratory muscles.
Rate and duration of inspiratory ramp signals is controlled by impulses from the Pneumotaxic centre and impulses from the lungs via vagi.
Ventilation perfusion ratio (The guyton and hall physiology)Maryam Fida
Ventilation perfusion ratio is :
“The ratio of alveolar ventilation and the amount of blood that perfuse the alveoli”.
FORMULA
It is expressed as VA/Q.
VA is alveolar ventilation
Q is the blood flow (perfusion)
Normal value of ventilation perfusion ratio is about
0.8
VA is 4.2 L /min
Q is 5.5 L/min (Same as Cardiac output)
So VA/Q = 4.2/5.5 = 0.8
If VA becomes zero ratio becomes zero
If Q becomes zero ratio becomes infinite.
If ratio becomes zero or infinite then there is no gaseous exchange. So this ratio indicates the efficiency of gaseous exchange in lungs.
In standing or sitting position this ratio is not uniform in all parts of the lungs.
In standing position, in upper parts of lungs there is almost no blood flow so normally in upper parts of lungs the ratio is higher may be near 3.
In lower part of lungs, there is more blood flow so the ratio is decreased may be 0.6.
In certain diseases the VA/Q ratio is higher which means perfusion is inadequate i.e. in some parts of lungs the alveoli are non functional or partially functional. This is seen in cases of pulmonary thrombosis or embolism.
When there is higher VA/Q ratio, PO2 and PCO2 in the alveolar air resembles the values in the inspired air.
When exchange is not occurring because of lack of perfusion, inspired air goes to alveoli, as there is no exchange occurring so the same values of PCO2 and PO2 as in inspired air.
Like heartbeat, breathing must occur in a continuous, cyclic pattern to sustain life processes.
Inspiratory muscles must rhythmically contract and relax to alternately fill the lungs with air and empty them.
The rhythmic pattern of breathing is established by cyclic neural activity to the respiratory muscles
Altitude physiology typically focuses on people above 2500 m; ∼8000 ft. Altitudes above that are sometimes subdivided into very high (3500–5500 m; ∼11,500–18,000 ft) and extreme (>5500 m; >18,000 ft). An estimated 40 million people travel each year to altitudes >2500 m (∼8000 ft),1 and as many or more travel to altitude for leisure and sports, and work in mines, military or border operations, and the like. Altitude medicine considers the clinical disorders associated with acclimatization by the travelers, workers and migrants, and with adaptation by people with lifetimes or populations with millennia of residence (an estimated 83 million people).
With a hurried ascent, many (∼80%) will report a transient headache (high-altitude headache or [HAH]), and some will develop one of three forms of acute high-altitude illness: acute mountain sickness (AMS) and HAH, high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). AMS and HAH are annoying and interfere with activity and work, however, HACE and HAPE can be fatal with mortality rates approaching 30%. Among some residents, chronic mountain sickness (CMS) and right ventricular hypertrophy develop over months to years of residence at altitude. Birth weights are generally lower and the rate of small-for-gestational-age babies and congenital heart defects are higher than that in lowland populations.
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
3. INTRODUCTION
• VENTILATION IS CONSTANTLY
ADJUSTED TO MAINTAIN THE
HOMEOSTASIS OF BLD GASES AND
ARTERIAL pH
• VARIATIONS OF PaO2 <3-4 mm Hg
AND EVEN LESS FOR PaCO2
• TO EXPEND MINIMAL ENERGY IN
THE WORK OF BREATHING
6. STRUCTURE
• 3 TYPES
– TYPE I -GLOMUS CELLS
– TYPE II -SUSTENTACULAR /SHEATH
CELLS
– SENSORY NERVE CELLS
7. CAROTID BODY
• RICH BLOOD SUPPLY(2L/100G/MIN)
• UTILIZES DISSOLVED O2 FROM
BLOOD UNLIKE OTHER TISSUES
• SENSES CHANGES IN Pa O2
• HENCE NOT AFFECTED BY
CONDITIONS IN WHICH PaO2 (N)
– MILD ANEMIA
– CO POISONING
8. CHEMOTRANSDUCTION
•
•
•
•
•
•
O2 BINDS CELL MEMB K+ CHANNEL
CLOSING OF K+ CHANNEL
DEPOLARIZATION OF THE CELL
OPENING OF Ca++ CHANNEL
NEUROTRANSMITTER RELEASE
DEPOLARIZES THE CAROTID SINUS
NERVE
• STIMULATES THE MEDULLA (DRG)
9. CHEMORECEPTORS
• RESPOND TO PaO2 AND H+
CONCENTRATION (pH), PaCO2
• 90% VENTILATORY RESPONSE TO
HYPOXEMIA- CAROTID BODY
• 10% RESPONSE -FROM AORTIC
BODIES
• VE INCREASED TIDAL VOLUME
11. EFFECT OF PaO2
• CHEMORECEPTORS CONTRIBUTES
LITTLE TO EUPNEIC VENTILATION
(10-15%)
• NO CHANGE CAROTID BODY
ACTIVITY TILL PaO2 < 75mmHg
• VENTILATION MARKEDLY
INCREASED WHEN
PaO2 <50mmHg
15. EFFECT OF PaO2
• CO2 POTENTIATES VENTILATORY
RESPONSE TO HYPOXEMIA
• BOTH HYPOXEMIC AND
HYPERCAPNIC RESPONSES
DECREASE WITH AGEING AND
EXERCISE TRAINING
17. EFFECTS OF PaCO2
• RAPID PHASE- RAPID INCREASE IN
VE WITHIN SECONDS DUE TO
ACIDIFICATION OF CSF
• SLOWER PHASE- DUE TO BUILDUP
OF H+ IONS IN MEDULLARY
INTERSTITIUM
• CHRONIC HYPERCAPNIA- WEAKER
EFFECT DUE TO RENAL RETENTION
OF HCO3 WHICH REDUCES THE H+
19. CLINICAL SIGNIFICANCE
• BILATERAL CAROTID BODY
RESECTION
• CAROTID ENDARTERECTOMY
• REDUCES MIN VENTILATION(VE)
• RESTING PaCO2 2-4 mm Hg
• ELIMINATES VENTILATORY TO
HYPOXIA AT REST AND EXERCISE
• 30% DECREASE IN RESPONSE TO
HYPERCAPNIA
20. CASE
•
•
•
•
•
•
•
•
•
69 Y FEMALE COPD,CVA ( OLD)
CAROTID ENDARTERECTOMY 1YR
ELECTIVE CE (R) DONE
PREOP ABG ON R/A- 7.43/50/48/31
DAY 3 EXTUBATED
O2 3L/MIN
DAY5: SOMNOLENT AND CONFUSED
ABG- 7.28/62/69/31
BiPAP INITIATED
IMPROVED
ABG-7.38/72/54/36
21. CO2 NARCOSIS
COPD WITH HYPERCAPNIA &
WORSENING RESP ACIDOSIS FOLL
OXYGEN THERAPY
– LOSS OF HYPOXIC DRIVE
– WORSENING V/Q MISMATCH
PHYSIOLOGIC DEAD SPACE
– CO2 CARRYING CAPACITY AS
OXYGENATION OF Hb IMPROVES
( HALDANE EFFECT)
23. SLOWLY ADAPTING
RECEPTORS
–HERING BRUER INFLATION REFLEX EXP TIME AND RESP RATE WITH
LUNG INFLATION.
– ACTIVE ONLY IF TV>3L , PREVENTS
OVERINFLATION
–PROLONGS INSP IN CONDITIONS OF
AIRWAY OBSTRUCTN ALLOWING
HIGHER TV TO BE ACHIEVED
24. RAPIDLY ADAPTING
RECEPTORS
•
•
•
•
IRRITANT RECEPTORS (COUGH )
CARINA AND PRINCIPAL BRONCHI
NOXIOUS STIMULI-DUST,SMOKE
CAUSES AUGUMENTED BREATHS
‘SIGHS’ DURING (N) BREATHING TO
PREVENT ATELECTASIS
• SENSATION OF DYSPNEA,CHEST
TIGHTNESS ,RAPID SHALLOW
BREATHING IN ASTHMA
25. BRONCHIAL C RECEPTORS
• UNMYELINATED NERVE ENDINGS
• RESPONSIBLE FOR BRONCHOSPASM
IN ASTHMA
• INCREASED TRACHEOBRONCHIAL
SECRETIONS
• MEDIATORS- HISTAMINE,
PROSTAGLANDINS , BRADYKININ
26. PULMONARY RECEPTORS
• JUXTA CAPILLARY RECEPTORS
LOCATED NEAR CAPILLARY IN ALV
WALLS
• RESPONDS TO HYPERINFLATION &
MEDIATORS IN PULM CIRCULATION
• SENSATION OF DYSPNEA IN HEART
FAILURE DUE TO INTERSTITIAL
EDEMA
27. J RECEPTORS
• PAINTAL ET AL(1970) PROPOSED J
RECEPTORS FUNCTION TO LIMIT
EXERCISE WHEN INTERSTITIAL
PRESSURE INCREASES(J REFLEX)
• MECHANISM: INHIBITION OF RESP
MOTOR NEURONS
29. EFFECT OF VAGOTOMY
• EXPT ANIMAL STUDIES
• VAGOTOMY ABOLISHES INCREASED
RESP RATE AND MIN VENT (VE)
WITH ASTHMA
• RAPID SHALLOW BREATHING
PATTERN IN RESP TO BRONCHSPASM
IS MEDIATED THROUGH VAGAL
AFFERENTS
30. CHEST WALL RECEPTORS
• MECHANORECEPTORS - SENSE
CHANGES IN LENGTH ,TENSION AND
MOVEMENT
• ASCENDING TRACTS IN ANT ERIOR
COLUMN OF SPINAL CORD TO RESP
CENTRE IN MEDULLA
31. MUSCLE SPINDLES
• SENSE CHANGES IN MSL LENGTH
• INTERCOSTALS > DIAPHRAGM
• REFLEX CONTRACTION OF MUSCLE
IN RESPONSE TO STRETCH
• INCREASE VENTILATION IN
EARLYSTAGES OF EXERCISE
32. GOLGI TENDON ORGANS
• SENSES CHANGES IN FORCE OF
CONTRACTION OF MSL
• DIAPHRAGM >INTERCOSTALS
• HAVE INHIBITORY EFFECT ON
INSPIRATION
34. CLINICAL SIGNIFICANCE
• SENSATION OF DYSPNEA WHEN
INCREASED RESP EFFORT DUE TO
“LENGTH- TENSION
INAPPROPRTATENESS” - LARGE
PLEURAL EFFUSION
• REMOVAL OF FLUID RESTORES THE
END EXP MSL FIBRE LENGTH
RESTORES THE LENTH TENSION
RELATIONSHIP
RELIEF
35. CENTRAL
CHEMORECEPTORS
• DENERVATION OF PERIPHERAL
CHEMORECEPTORS - VENTILATORY
RESPONSE TO CO2 PERSISTED
• LOCATED CLOSE TO
VENTROLATERAL SURFACE OF
MEDULLA
• SENSITIVE TO CHANGES IN H + CONC
IN CSF & MEDULLARY
INTERSTITIAL FLUID
36. CENTRAL
CHEMORECEPTORS
• ROSTRAL - LATERAL TO PYRAMIDS
MEDIAL TO 7TH AND 10 TH NERVES
• CAUDAL - LATERAL TO PYRAMIDS
MEDIAL TO 12 TH NERVE ROOTS
• INTERMEDIATE - NOT CHEMOSENS,
AFFERENT FIBRES FROM BOTH
ZONES CONVERGE
STIM RESP
CENTRES
37. CENTRAL
CHEMORECEPTORS
• INCREASED INTENSITY AND RATE
OF RISE OF INSP RAMP SIGNAL
• INCREASED FREQUENCY OF RESP
RHYTHM
• SENSING OF pH CHANGES REQUIRES
ENZYME CARBONIC ANHYDRASE
• IMIDAZOLE HISTIDINE IS THE
SENSOR MOLECULE
38. MECHANISM
• H+ IONS ENTER CSF BY DIRECT
DIFFUSION FROM BLD STREAM
• ARTERIAL CO2 RAPIDLY
PENETRATES BBB
• CONVERTED TO CARBONIC ACID
• H2C03
H + HCO3
• H+ DIFFUSES INTO CSF
41. BRAINSTEM CENTERS
• PNEUMOTAXIC CENTER
• APNEUSTIC CENTER
• MEDULLARY CENTERS
– DORSAL RESPIRATORY GROUP
– VENTRAL RESPIRATORY GROUP
42. PNEUMOTAXIC CENTER
• PONTINE RESP GROUP
• NUCL PARABRACHIALIS, KOLLIKERFUSE NUCLEUS IN DORSOLAT PONS
• REGULATES TIMING OF RAMP
SIGNAL BY STIMULATORY INPUTS
TO DRG NEURONS
• HYPOXIA, HYPERCAPNIA, LUNG
INFLATION STIMULATE RESP
43. RAMP SIGNAL
• NERVOUS SIGNAL TRANSMITTED TO
INSPIRATORY MUSCLES AS A BURST
OF ACTION POTENTIALS WHICH
INCREASES IN A RAMP LIKE
MANNER GENERATED BY THE DRG
NEURONS
44. APNEUSTIC CENTER
• LOWER PONS
• FUNCTIONS AS “INSPIRATORY CUT
OFF SWITCH” INHIBITS DRG
• TRANSECTION BELOW PNEMOTAXIC
CENTRE + VAGOTOMY INDUCES
• APNEUSTIC BREATHING HAS
PROLONGED INSP TIME AND SHORT
EXP TIME
45. DORSAL RESP GROUP
– BILATERAL AGGREGATES OF RESP
NEURONS
– DORSOMEDIAL MEDULLA
– ADJACENT TO NUCL OF TRACTUS
SOLITARIUS
– MOST NEURAL ACTIVITY IS
INSPIRATORY
– PUMP CELLS (P CELLS): ACTIVATION BY
AFFERENTS IMPULSES FROM LUNG
STRETCH LEADS TO HERING- BREUER
INFLATION REFLEX
46. VENTRAL RESP GROUP
• ROSTRAL VENTROLATERAL
MEDULLA
• LONGITUDINAL COLUMN OF NUCLEI
–
–
–
–
BOTZINGER COMPLEX
PRE-BOTZINGER COMPLEX
ROSTRAL VRG
CAUDAL VRG (N. RETROAMBIGUALIS)
47. INSPIRATORY DRG
NEURONS
– AXONAL PROJECTIONS TO SPINAL
CORD MOTOR NEURONS
– LUNG INFLATION
FACILITATES - I BETA NEURONS
INHIBITS - I ALPHA NEURONS
– EXCITATORY DRIVE TO PHRENIC AND
TO LESSER EXTENT EXTERNAL
INTERCOSTAL MOTORNEURONS FOR
INSPIRATION
48. VENTRAL RESP GROUP
• BOTH INSP AND EXP NEURONS
• EXP NEURONS MAINLY (ROSTRAL
AND CAUDAL AREA)
• INSP NEURONS ARE IN MIDDLE
• NUCL AMBIGUALIS CLOSE TO VRG
INNERVATES THE LARYNGEAL AND
PHARYNGEAL AIRWAY MUSCLES
• FOR RHYTMIC RESP CYCLE RELATED
CONTRACTIONS
49. VENTRAL RESP GROUP
• BOTH I AND E NEURONS PROJECT TO
SPINAL CORD
• BULBOSPINAL NEURONS INHIBIT
PHRENIC MOTOR NEURONS
ACTIVELY DURING EXPIRATION
• PRE BOTZINGER COMPLEX IS THE
SITE FOR RESP RHYTHMOGENESIS
• OUTPUT INCREASES WITH EXERCISE
AND OBSTR AIRWAY DISEASES
50. CHEYNE STOKES
RESPIRATION
• PERIODIC BREATHING PATTERN
WITH CENTRAL APNEAS
• BILATERAL SUPRAMEDULLARY
LESION
• CARDIAC FAILURE
• HIGH ALTITUDE
• SLEEP
51. SPINAL CORD
• DECENDING BULBOSPINAL FIBRES
ARE IN THE VENTRAL AND LATERAL
COLUMNS
• RESP NEURONS ARE IN VENTRAL
HORN(CERV,DORSAL,LUMBAR
SEGMENTS)
• EXP NEURONS -VENTROMEDIAL
• INSP NEURONS- LATERAL
52. SPINAL CORD
• ASCENDING SPINORETICULAR
FIBRES CARRY PROPRIOCEPTIVE
INPUTS TO STIMULATE RESP CENTRE
• BILAT CERVICAL CORDOTOMY
FUNCTION OF RAS LEADS TO
RESPIRATORY DYSFUNCTION (SLEEP
APNEA)
53. PHASES OF RESP RHYTHM
• BASED ON PHRENIC NERVE
RECORDINGS
• INSPIRATION - LUNG INFLATION
• POSTINSPIRATORY INSP
ACTIVITY(E1) - FOR BRAKING THE
AIRFLOW TO MAINTAIN FRC
• EXPIRATION(E2) -ACTIVE
EXPIRATION
56. EXERCISE
• PHASEI - IMMED VE WITHIN
SECONDS,NEURAL IMPULSES MSL
SPINDLES, JOINT PROPRIOCEPTORS
• PHASE II- WITHIN 20-30 SEC VENOUS
BLD FROM MSL,SLOW AND
EXPONEN VE( VENTILATION LAGS
BEHIND CO2)
57. EXERCISE
• PHASE III - PULM GAS EXCHANGE
MATCHES THE METAB RATE TO
MAINTAIN STABLE O2, CO2, pH
• PHASE IV - BEGINS AT ANAOERBIC
THRESHOLD, O2 CONSUMTION> O2
DELIVERY AND LACTIC ACID
ACCUMULATES.
59. DRUGS & RESPIRATION
• CAUSE RESP DEPRESSION –
–
–
–
–
VE
INHALATIONAL ANAESTHETICS
NARCOTICS
BEZODIAZEPINES
ALCOHOL
ESP SEVERE COPD UNDER GA
COPD INACUTE EXCACERBATION
– NALOXONE, FLUMAZENIL IN DRUG
OVERDOSE
61. CONCLUSIONS
• ABNORMALITIES OF RESP DRIVE
ARE OVERLOOKED IN CLIN
PRACTICE
• BREATHING ABNORMALITIES MORE
SEVERE DURING SLEEP AND CAN
HAVE SERIOUS CONSEQUENCES