Respiratory Physiology

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Respiratory Physiology : 

Respiratory Physiology Presenter: Dr. Manjula Sudhakar Rao Moderator: Dr. Linga Raju Y. K

Respiratory System : 

Respiratory System

Introduction : 

Introduction The term respiration includes 3 separate functions: Ventilation: Movement of air in and out of the lungs Gas exchange: Between alveoli and capillaries in the lungs. Between systemic capillaries and tissues of the body. 0xygen utilization: Cellular respiration.

Respiratory System Functions : 

Respiratory System Functions Gas exchange: Oxygen enters blood and carbon dioxide leaves Regulation of blood pH: Altered by changing blood carbon dioxide levels Voice production: Movement of air past vocal folds makes sound and speech Olfaction: Smell occurs when airborne molecules drawn into nasal cavity Protection: Against microorganisms by preventing entry and removing them

Non-Respiratory Lung Functions : 

Non-Respiratory Lung Functions Reservoir of blood: available for circulatory compensation Filter for circulation: thrombi, microaggregates etc Metabolic activity: activation: angiotensin III inactivation: noradrenaline bradykinin 5 H-T some prostaglandins Immunological: IgA secretion into bronchial mucus

The Respiratory Defense System : 

The Respiratory Defense System Consists of a series of filtration mechanisms Removes particles and pathogens Components of the Respiratory Defense System Goblet cells and mucous glands: produce mucus that bathes exposed surfaces Cilia: sweep debris trapped in mucus toward the pharynx (mucus escalator) Filtration in nasal cavity removes large particles Alveolar macrophages engulf small particles that reach lungs

Ventilation : 

Ventilation Mechanical process that moves air in and out of the lungs. [O2] of air is higher in the lungs than in the blood, O2 diffuses from air to the blood. C02 moves from the blood to the air by diffusing down its concentration gradient. Gas exchange occurs entirely by diffusion: Diffusion is rapid because of the large surface area and the small diffusion distance. Insert 16.1

Intrapulmonary Pressure : 

Intrapulmonary Pressure Also called intra-alveolar pressure Is relative to Patm In relaxed breathing, the difference between Patm and intrapulmonary pressure is small: about —1 mm Hg on inhalation or +1 mm Hg on expiration

Intrapleural Pressure : 

Intrapleural Pressure Intrapleural pressure ranges from -5.6 mmHg on inspiration to -2.6 mmHg on expiration It is less negative at the bottom than top During a strong inspiratory effort with closed glottis pressure upto -40mmHg is recorded During forced expiratory effort with closed gloti it is 50mmHg

Transpulmonary Pressure : 

Transpulmonary Pressure Transpulmonary pressure = Alveolar pressure* – Pleural pressure *With no air movement and an open upper airway, mouth pressure equals alveolar pressure

Pulmonary Pressures : 

Pulmonary Pressures

The Mechanics of Breathing : 

The Mechanics of Breathing Inhalation: always active Exhalation: active or passive

3 Muscle Groups of Inhalation : 

3 Muscle Groups of Inhalation Diaphragm: contraction draws air into lungs 75% of normal air movement External intercostal muscles: assist inhalation 25% of normal air movement Accessory muscles assist in elevating ribs: sternocleidomastoid serratus anterior pectoralis minor scalene muscles

Muscles of Active Exhalation : 

Muscles of Active Exhalation Internal intercostal and transversus thoracis muscles: depress the ribs Abdominal muscles: compress the abdomen force diaphragm upward

Boyle’s Law : 

Boyle’s Law Changes in intrapulmonary pressure occur as a result of changes in lung volume. Pressure of gas is inversely proportional to its volume. Increase in lung volume decreases intrapulmonary pressure. Air goes in. Decrease in lung volume, raises intrapulmonary pressure above atmosphere. Air goes out.

Alveolar Pressure Changes : 

Alveolar Pressure Changes

Inspiration : 

Inspiration Active process – requires ATP for muscles contraction

Expiration : 

Expiration Passive process –muscles relax

Physical properties that affect lung function : 

Physical properties that affect lung function Compliance. Elasticity. Surface tension

Lung compliance: : 

Lung compliance: Is the change in volume per unit change in pressure Types: Static compliance=Corrected tidal volume Plateau pressure-PEEP Dynamic compliance = corrected tidal volume Peak inspiratory pressure-PEEP

Elasticity : 

Elasticity Tendency to return to initial size after distension. High content of elastin proteins. Very elastic and resist distension. Elastic tension increases during inspiration and is reduced by recoil during expiration.

Surface Tension : 

Surface Tension Force exerted by fluid in alveoli to resist distension. Lungs secrete and absorb fluid, leaving a very thin film of fluid. This film of fluid causes surface tension. Fluid absorption is driven (osmosis) by Na+ active transport. Fluid secretion is driven by the active transport of Cl- out of the alveolar epithelial cells. H20 molecules at the surface are attracted to other H20 molecules by attractive forces. Force is directed inward, raising pressure in alveoli.

Surface Tension : 

Surface Tension Law of Laplace: Pressure in alveoli is directly proportional to surface tension; and inversely proportional to radius of alveoli. Pressure in smaller alveolus would be greater than in larger alveolus, if surface tension were the same in both. Insert fig. 16.11

Surfactant : 

Surfactant Phospholipid produced by alveolar type II cells. Lowers surface tension. Reduces attractive forces of hydrogen bonding by becoming interspersed between H20 molecules. Surface tension in alveoli is reduced. As alveoli radius decreases, surfactant’s ability to lower surface tension increases. Disorders: RDS. ARDS. Insert fig. 16.12

Volumes Versus Capacities. : 

Volumes Versus Capacities. There are four volume subdivisions which: do not overlap. can not be further divided. when added together equal total lung capacity. Lung capacities are subdivisions of total volume that include two or more of the 4 basic lung volumes.

Pulmonary Volumes : 

Pulmonary Volumes Tidal volume Volume of air inspired or expired during a normal inspiration or expiration Inspiratory reserve volume Amount of air inspired forcefully after inspiration of normal tidal volume Expiratory reserve volume Amount of air forcefully expired after expiration of normal tidal volume Residual volume Volume of air remaining in respiratory passages and lungs after the most forceful expiration

Pulmonary Capacities : 

Pulmonary Capacities Inspiratory capacity Tidal volume plus inspiratory reserve volume Functional residual capacity Expiratory reserve volume plus the residual volume Vital capacity Sum of inspiratory reserve volume, tidal volume, and expiratory reserve volume Total lung capacity Sum of inspiratory and expiratory reserve volumes plus the tidal volume and residual volume

Slide 29: 

Respiratory volumes

Graph of Lung Volumes/Capacities : 

Graph of Lung Volumes/Capacities

Clinical significance : 

Clinical significance Vital capacity reduced in Alterations in muscle power- any drug that depresses the activity of ventilatory mechanism Cerebral tumour, polio myelitis.raised ICT, NMJ disorders Pulmonary disease Chronic bronchitis.pneumonia,asthma,atelectasis Space occupying lesions in the chest neurofibroma, pleural effusion, pericardial effusion,chyphoscoliosis,pneumothorax Abdomonal tumours Abdominal pain/splinting Alterations in the posture

Postural variation : 

Postural variation Percentage of reduction in vital capacity in different postures

Dead space : 

Dead space Anatomic- conducting airways. Estimated to be about 1ml per pound of ideal body weight Alveolar- normal lung volume that has become unable to take part in gas exchange because of reduction in pulmonary blood flow Eg. Pulmonary embolism Physiologic- Sum of anatomic and alveolar dead space volumes

Gravity Dependent distribution of pulmonary Perfusion : 

Gravity Dependent distribution of pulmonary Perfusion

Slide 35: 

Zone I corresponds to a region in which alveolar pressure exceeds vascular pressure, which results in essentially no perfusion. Zone II is characterized by pulmonary artery pressure exceeding alveolar pressure, which in turn exceeds venous pressure. The driving pressure will then be arterial minus alveolar pressure.

Slide 36: 

Zone III, both arterial pressure and venous pressure exceed alveolar pressure. The difference between arterial and venous pressure creates the driving force through this zone. Zone IV In the bottom of the lung there is a decrease in blood flow that is explained by increasing interstitial pressure compressing extra-alveolar vessels

Hypoxic Pulmonary Vasoconstriction : 

Hypoxic Pulmonary Vasoconstriction compensatory mechanism aimed at reducing blood flow in hypoxic lung regions Alveolar hypoxia Vasoconstriction Reduction in blood flow in hypoxic area Diversion of blood to the oxygenated area Normal arterial oxygen saturation maintained

Clinical implications of HPV : 

Clinical implications of HPV High altitude: Decrease in FIO2 increases Ppa which increases perfusion at the apices, recruiting unused vessels. A-a gradient is less than that at the sea level. Minimizes transpulmonary shunting: Diverts blood from areas of hypoventilation such as atelectasis or unventilated lung in one lung ventilation Normalizes regional VA/Q Pulmonary vasodilators: In patients with COPD, Asthma, pneumonia, mitral stenosis, vasodilators decrease PVR and PaO2 by increasing right to left transpulmonary shunt Inhibits protective nature of HPV

PULMONARY VASCULAR RESISTANCE : 

PULMONARY VASCULAR RESISTANCE INCREASED REDUCED hypoxia alpha-blockers a-sympathomimetic b-sympathomimetic B blockers prostaglandins E1,2 Protamine acetylcholine Histamine aminophylline Serotonin alkalaemia Acidemia Na Nitroprusside Cyclopropane Diethyl ether

Ventilation and perfusion : 

Ventilation and perfusion Gravity causes vertical intrapleural pressure difference which in turn causes regional alveolar volume, compliance and ventilation differences.The lung has ¼ the density of water and its height is 30 cms.Thus Ppl increases by 3/4=7.5cms of H2O from top to bottom of the lung Since the PA is same throught the lung, Ppl gradient causes regional variations in the transpulmonary distending pressure. Since the Ppl is most positive (least negative) at the dependent basilar lung region, alveoli in this region are more compressed and considerably smaller compared to the non compressed alveoli of the apical region. If the regional differences in the alveolar volume are translated into a pressure volume curve, for normal lung, the dependent small alveoli are in the mid portion and the non dependent alveoli are in the top flat portion of the curve

Ventilation-Perfusion ratio : 

Ventilation-Perfusion ratio VA/Q Both ventilation and perfusion increase down the lung due to gravity However, perfusion increases at a more rapid rate than ventilation. Hence the ratio decreases. 3.3 at the apices Over ventilated but underperfused 0.6 at the base Over perfused but underventilated Mean is 0.8

VA/Q inequalities : 

VA/Q inequalities PAO2 decreases from 132 to 89 mmHg from apex to the base while PaCO2 increases from 28 to 42mmHg from top to bottom PAO2 and PaO2 gradients are large with ventilation perfusion mismatches, while PACO2 and PaCO2 gradients are small Blood perfusing an overventilated alveoli can eliminate excess of CO2 to compensate for the underventilated alveoli That same blood cannot proportionately increase the O2 uptake secondary to the flatness of the oxygen hemoglobin dissociation curve in the region

Gas Exchange in the Lungs : 

Gas Exchange in the Lungs Dalton’s Law: Total pressure of a gas mixture is = to the sum of the pressures that each gas in the mixture would exert independently. Partial pressure: The pressure that an particular gas exerts independently. PATM = PN2 + P02 + PC02 + PH20= 760 mm Hg. 02 is humidified = 105 mm Hg. H20 contributes to partial pressure (47 mm Hg). P02 (sea level) = 150 mm Hg. PC02 = 40 mm Hg.

Partial Pressures of Gases in Inspired Air and Alveolar Air : 

Partial Pressures of Gases in Inspired Air and Alveolar Air Insert fig. 16.20

Significance of Blood P02 and PC02 Measurements : 

Significance of Blood P02 and PC02 Measurements At normal P02 arterial blood is about 100 mm Hg. P02 level in the systemic veins is about 40 mm Hg. PC02 is 46 mm Hg in the systemic veins. Provides a good index of lung function.

OXYGEN MIXED VENOUS ARTERIAL : 

OXYGEN MIXED VENOUS ARTERIAL PLASMA 0.13ml % 0.3ml% TENSION 40mm Hg 100mm Hg OXYHb 14ml% 19ml% SATURATION 75% 98%

OXYGEN FLUX : 

OXYGEN FLUX The amount of oxygen leaving the left ventricle per minute in the arterial blood Oxygen flux=cardiac output x arterial oxygen saturation x haemoglobinconcentrationx1.31ml/g =5000ml/min x 98/100 x 15.6/100g/mlx1.31 =1000ml/min 1.31 is the volume of oxygen which combines with one gram of Hb 250ml-used up in cellular metabolism and rest returns to the lungs in mixed venous blood

Hemoglobin and Oxygen Transport : 

Hemoglobin and Oxygen Transport Oxygen is transported by hemoglobin (98.5%) and is dissolved in plasma (1.5%) Oxygen-hemoglobin dissociation curve shows that hemoglobin is almost completely saturated when P02 is 80 mm Hg or above. At lower partial pressures, the hemoglobin releases oxygen. A shift of the curve to the left because of an increase in pH, a decrease in carbon dioxide, or a decrease in temperature results in an increase in the ability of hemoglobin to hold oxygen

Hemoglobin and Oxygen Transport : 

Hemoglobin and Oxygen Transport A shift of the curve to the right because of a decrease in pH, an increase in carbon dioxide, or an increase in temperature results in a decrease in the ability of hemoglobin to hold oxygen The substance 2.3-bisphosphoglycerate increases the ability of hemoglobin to release oxygen Fetal hemoglobin has a higher affinity for oxygen than does maternal

Oxyhemoglobin Dissociation Curve : 

Oxyhemoglobin Dissociation Curve

Significance of Sigmoid Curve 4 Point Curve : 

Significance of Sigmoid Curve 4 Point Curve

Four (+one) Things Change Oxyhemoglobin Affinity : 

Four (+one) Things Change Oxyhemoglobin Affinity Hydrogen Ion Concentration, [H+] Carbon Dioxide Partial Pressure, PCO2 Temperature [2,3-DPG] Special Case: Carbon Monoxide

Effects of pH and Temperature on the Oxyhemoglobin Dissociation Curve : 

Effects of pH and Temperature on the Oxyhemoglobin Dissociation Curve

Transport of Carbon Dioxide : 

Transport of Carbon Dioxide Carbon dioxide is transported as bicarbonate ions (70%) in combination with blood proteins (23%) and in solution with plasma (7%) Hemoglobin that has released oxygen binds more readily to carbon dioxide than hemoglobin that has oxygen bound to it (Haldane effect) In tissue capillaries, carbon dioxide combines with water inside RBCs to form carbonic acid which dissociates to form bicarbonate ions and hydrogen ions

Transport of Carbon Dioxide : 

Transport of Carbon Dioxide In lung capillaries, bicarbonate ions and hydrogen ions move into RBCs and chloride ions move out. Bicarbonate ions combine with hydrogen ions to form carbonic acid. The carbonic acid is converted to carbon dioxide and water. The carbon dioxide diffuses out of the RBCs. Increased plasma carbon dioxide lowers blood pH. The respiratory system regulates blood pH by regulating plasma carbon dioxide levels

Carbon Dioxide Transport : 

Carbon Dioxide Transport Bicarbonate ions Muscle: CO2 + H2O → H2CO3 → H+ + HCO3- Lung: H+ + HCO3- → H2CO3 → CO2 + H2O Dissolved in blood plasma Bound to hemoglobin (carbaminohemoglobin)

CO2 Transport and Cl- Movement : 

CO2 Transport and Cl- Movement

Bohr Effect : 

Bohr Effect Bohr Shift Curve

Bohr effect : 

Bohr effect It is a property of haemoglobin first described by Danish Physiologist Christian Bohr (father of the physicist Niels Bohr) which states that in the presence of CO2 the affinity of O2 to respiratory pigments such as Haemoglobin decreases. Because of bohr effect, an increase in blood CO2 level or decreased pH causes haemoglobin to bind to O2 with less affinity This effect facilitates O2 transport as Hb binds to oxygen in the lungs and then releases it to the tissues, perticularly those tissues in most need of Oxygen. The CO2 is converted to acidic protons and bicarbonate ions by carbonic anhydrase enzyme CO2 + H2O H+ + HCO3-

Haldane effect : 

Haldane effect It is a property of Hb first described by Scottish physician John Scott Haldane. Deoxygenation of the blood increases its ability to carry CO2. This property is Haldane effect This is consequence of the fact that reduced Hb (deoxygenated) is a better accepter of protons than oxygenated Hb In RBCs the the enzyme carbonic anhydrase catelises conversion of dissolved CO2 carbonic acid, which rapidly dissociates into bicarbonate and free proton CO2 + H2O H2CO3  H+ + HCO3-

Slide 61: 

In addition to enhancing removal of CO2 from oxygen consuming tissues, haldane effect promotes dissociation of CO2 from Hb in the presence of oxygen. In the oxygen rich capillaries of the lung, this property causes displacement of CO2 to plasma as the venous blood enters the alveolus, as is vital for the alveolar gas exchange. The general equation for haldane effect is H+ + HbO2 H+.Hb + O2

Chloride Shift at Systemic Capillaries : 

Chloride Shift at Systemic Capillaries H20 + C02 H2C03 H+ + HC03- At the tissues, C02 diffuses into the RBC; shifts the reaction to the right. Increased [HC03-] produced in RBC: HC03- diffuses into the blood. RBC becomes more +. Cl- attracted in (Cl- shift). H+ released buffered by combining with deoxyhemoglobin. HbC02 formed. Unloading of 02.

Carbon Dioxide Transport and Chloride Shift : 

Carbon Dioxide Transport and Chloride Shift Insert fig. 16.38

At Pulmonary Capillaries : 

At Pulmonary Capillaries H20 + C02 H2C03 H+ + HC03- At the alveoli, C02 diffuses into the alveoli; reaction shifts to the left. Decreased [HC03-] in RBC, HC03- diffuses into the RBC. RBC becomes more -. Cl- diffuses out (reverse Cl- shift). Deoxyhemoglobin converted to oxyhemoglobin. Has weak affinity for H+. Gives off HbC02.

Reverse Chloride Shift in Lungs : 

Reverse Chloride Shift in Lungs Insert fig. 16.39

Respiratory Structures in Brainstem : 

Respiratory Structures in Brainstem

Regulation of breathing : 

Regulation of breathing DRG stimulates inspiratory muscles, 12-15 times / minute VRG active in forced breathing Pontine respiration centre: finetuning of breathing / inhibits DRG

Rhythmic Ventilation : 

Rhythmic Ventilation Starting inspiration Medullary respiratory center neurons are continuously active Center receives stimulation from receptors and simulation from parts of brain concerned with voluntary respiratory movements and emotion Combined input from all sources causes action potentials to stimulate respiratory muscles Increasing inspiration More and more neurons are activated Stopping inspiration Neurons stimulating also responsible for stopping inspiration and receive input from pontine group and stretch receptors in lungs. Inhibitory neurons activated and relaxation of respiratory muscles results in expiration.

Factors that influence respiration : 

Factors that influence respiration Hypothalamus (emotions / pain) Cortex (voluntary control) Chemoreceptors: Central (in medulla oblongata): responds to CO2 ↑ CO2 passes blood brain barrier CO2 + H2O H2CO3 H+ + HCO3- H+ stimulates receptors  breathing depth ↑ + rate ↑ Peripheral (in aortic / carotid bodies): responds when O2 < 60 mm Hg  increase ventilation Responds to pH ↓  increase ventilation

Factors Influencing Respiration : 

Factors Influencing Respiration

Herring-Breuer Reflex : 

Herring-Breuer Reflex Limits the degree of inspiration and prevents overinflation of the lungs Infants Reflex plays a role in regulating basic rhythm of breathing and preventing overinflation of lungs Adults Reflex important only when tidal volume large as in exercise

5 Sensory Modifiers of Respiratory Center Activities : 

5 Sensory Modifiers of Respiratory Center Activities Chemoreceptors are sensitive to: PCO2, PO2, or pH of blood or cerebrospinal fluid Baroreceptors in aortic or carotid sinuses: sensitive to changes in blood pressure

Slide 75: 

Stretch receptors: respond to changes in lung volume Irritating physical or chemical stimuli: in nasal cavity, larynx, or bronchial tree Other sensations including: pain changes in body temperature abnormal visceral sensations

Chemoreceptor Reflexes : 

Chemoreceptor Reflexes Respiratory centers are strongly influenced by chemoreceptor input from: cranial nerve IX -The glossopharyngeal nerve: from carotid bodies stimulated by changes in blood pH or PO2 cranial nerve X -The vagus nerve: from aortic bodies stimulated by changes in blood pH or PO2 receptors that monitor cerebrospinal fluid- Are on ventrolateral surface of medulla oblongata Respond to PCO2 and pH of CSF

Slide 77: 

Thank You

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