Respiratory System PhysiologyDr. Amjed Hassan lecture 2



Compliance of the Respiratory SystemLung ComplianceLung compliance expresses the dispensability of the lungs, that is, how easily the lungs expand when trans-pulmonary pressure increases. It is expressed by the following equation:C = ΔV/ΔPwhereC = lung complianceΔV = increase in lung volume (mL)ΔP = increase in trans-pulmonary pressure (mm Hg).– Compliance is inversely related to stiffness.– Compliance is inversely related to the elastic recoil, or elastance, of the lung. Recoil causes the lungs to return to their previous volume when stretching ceases following an increase in trans-pulmonary pressure. It is mediated by surface tension in the alveoli and by elastic fibers in thelung connective pliance of the Lung–Chest Wall CombinationBecause the lungs and chest wall expand and contract together, the overall compliance of the respiratory system is that of the lung–chest wall combination. The compliance of the lung–chest wall combination is lower than the compliance of the lungs alone or chest wall alone.– The compliance of the lung–chest wall combination varies with lung volume. Compliance is highest at the normal resting volume (functional residual capacity [FRC]) and decreases at both very low and very high volumes.– At low volumes, compression of the chest wall reduces compliance.– At high volumes, the increased stretch of elastic tissues in the lung parenchyma causes the lungs to get stiffer (less compliant). High trans-pulmonary pressure is required to drive this increase in volume, but it is not responsible for the decrease in compliance.Changes in lung compliance in disease states– Lung compliance is decreased in pulmonary fibrosis because the interstitium surrounding the alveoli becomes infiltrated with inelastic collagen.– Lung compliance is increased in emphysema because many small alveoli are replaced by fewer but larger coalesced air spaces that have less elastic recoil.Surface Tension in the AlveoliSurface tension is due to the cohesive forces between water molecules at the air–water interface in the alveoli of lungs. It acts to contract the alveoli and is a major contributor to the force of elastic recoil of the lung.If there were no opposing force, surface tension would cause the alveoli to collapse (atelectasis).However, the collapsing force is opposed by trans-pulmonary pressure, which is always positive, allowing the alveoli to remain open.According to the law of Laplace, the trans-pulmonary pressure P (in dynes/cm2) required to prevent collapse of an alveolus is directly proportional to surface tension T (in dynes/cm), and inverselyproportional to alveolar radius r (in cm), as expressed byP = 2T/r– All alveoli in a given region of the lungs have about the same trans-pulmonary pressure. If they all had the same surface tension, the Laplace relationship predicts that the smaller alveoli would collapse and force their volume into larger alveoli. However, surface tension is reduced bypulmonary surfactant, and the reduction is greater in small alveoli than in larger ones because small alveoli concentrate the surfactant. Thus, the increased tendency to collapse because of small radius is just balanced by a greater reduction in surface tension.SurfactantSurfactant is a complex substance, consisting of proteins and phospholipids (mainly dipalmitoyl lecithin), that is produced in type II pneumocytes. It lines alveoli and lowers surface tension by the same mechanism as detergents and soaps (i.e., it coats the water surface and reduces cohesiveinteractions between water molecules).As an extension of its role in lowering surface tension, surfactant also produces the following effects:– It increases compliance at all lung volumes, which allows for easier lung inflation and greatly decreases the work of breathing.– It reduces the otherwise highly negative pressure in the interstitial space, which reduces the rate of filtration from pulmonary capillaries. This assists in maintaining lungs without excessive water.Failure of surfactant production and/or excessive surfactant breakdown occurs in neonatal respiratory distress syndrome (RDS).Effect of Alveolar Radius on the Pressure Caused by SurfaceTension. Note from the preceding formula that the pressure generated as a result of surface tension in the alveoli is inversely affected by the radius of the alveolus, which means that the smaller the alveolus, the greater the alveolar pressure caused by the surface tension. Thus, when the alveoli have half the normal radius (50 instead of 100 micrometers), the pressures noted earlier are doubled. This is especially significant in small premature babies, many of whom have alveoli with radii less than one quarter that of an adult person.Further, surfactant does not normally begin to be secreted into the alveoli until between the sixth and seventh months of gestation, and in some cases, even later than that. Therefore, many premature babies have little or no surfactant in the alveoli when they are born, and their lungs have an extreme tendency to collapse, sometimes as great as six to eight times that in a normal adult person. This causes the condition called respiratorydistress syndrome of the newborn. It is fatal if not treated with strong measures, especially properly applied continuous positive pressure breathing.The work of inspiration can be divided into three fractions: (1) that required to expand the lungs against the lung and chest elastic forces, called compliance work or elastic work; (2) that required to overcome the viscosityof the lung and chest wall structures, called tissue resistance work; and (3) that required to overcome airway resistance to movement of air into the lungs, called airway resistance work.Energy Required for Respiration. During normal quiet respiration, only 3 to 5 per cent of the total energy expended by the body is required for pulmonary ventilation. But during heavy exercise, the amount of energy required can increase as much as 50-fold, especially if the person has any degree of increased airway resistance or decreased pulmonary compliance. Therefore, one of the major limitations on the intensity of exercise that can be performed is the person’s ability to provide enough muscle energy for the respiratory process alone.Airflow through the Bronchial TreeAirflow through the bronchial tree obeys the same principles as blood flow through blood vessels except that the viscosity of air is much lower than that of blood. Airflow is related to the driving pressure and the resistance to flow byQ = ΔP/Rwhere Q is airflow (mL/min), ΔP is pressure gradient between the mouth/nose and alveoli (cm H2O),and R is airway resistance (cm H2O/mL/min).– Airflow is directly proportional to the pressure difference between the mouth/nose and the alveoli and inversely proportional to airway resistance.Airway ResistanceResistance is derived from Poiseuille’s equation as expressed byR = 8ηL/πr4where R is airway resistance, r is radius of the airway (cm), η is viscosity of air, and L is length of the airway.– Like the circulatory system, the length of the bronchial tree is relatively constant, as is the viscosity of inspired air. Therefore, any changes in resistance to airflow are mainly due to changes in the radius of the airways. Because resistance is inversely proportional to the airway radius to the fourth power, small changes in diameter cause large changes in resistance.– The large airways offer little resistance to airflow. The small airways individually have high resistance, but their enormous number in parallel reduces their combined resistance to a small value. Therefore, the sites of highest resistance in the bronchial tree are normally in the mediumairways.Regulation of Airway Resistance. Airway resistance is primarily regulated by modulation of airway radius by the parasympathetic and sympathetic nervous systems.– Parasympathetic nervous system: Vagal stimulation releases acetylcholine that acts on muscarinic (M3) receptors in the lungs, leading to bronchoconstriction. This increases the resistance to airflow.– Sympathetic nervous system: Postganglionic sympathetic nerves release norepinephrine that act on β2 receptors, leading to broncho-dilation. This decreases the resistance to airflowLung Volumes and Capacities– Lung volumes are a way to functionally divide volumes of air that occur during different phases of the breathing cycle (Fig. 12.5). They are all measured by spirometry, except for residual volume.They vary with height, sex, and age.– Lung capacities are the sums of two or more lung volumes.– Tidal, inspiratory, and expiratory reserve volumes and inspirational and vital capacities are used in basic pulmonary function tests.Lung Volumes– Tidal volume (TV) is the volume of air that moves in or out of the lungs during one normal, resting inspiration or expiration.– Inspiratory reserve volume (IRV) is the volume of air that can be inspired beyond a normal inspiration.– Expiratory reserve volume (ERV) is the volume of air that can be expired beyond a normal expiration.– Residual volume (RV) is the volume of air left in the lungs and airways after maximal expiration.Table 12.1 contains the normal approximate lung volumes and expresses them as a percentage of total lung capacity (TLC).Lung Capacities– Inspirational capacity (IC) is the maximum volume of air that can be inspired with a deep breath following a normal expiration. It is the sum of TV and IRV.– Functional residual capacity (FRC) is the volume of the lungs after passive expiration with relaxed respiratory muscles. It is the sum of ERV and RV.– Vital capacity (VC) or forced vital capacity (FVC): is the maximum volume of air that can be expired in one breath after deep inspiration. It is the sum of TV, IRV, and ERV.– Total lung capacity (TLC) is the total volume of air that can be contained in the lungs and airways after a deep inspiration. It is the sum of all four lung volumes: TV, IRV, ERV, and RV.Note: TLC and FRC cannot be measured by spirometry because residual volume is needed for their calculation.Table 12.2 contains the normal lung capacity volumes.Forced Expiratory Volume (FEV1) is the volume of air that can be forcibly expired in the first second following a deep breathIt is usually > 70% of the FVC (FEV1/FVC > 70%).– In obstructive lung disease (e.g., asthma and COPD), FEV1is reduced proportionally more than FVC; therefore, FEV1 /FVC < 70%.– In restrictive lung disease (e.g., fibrosis), both FEV1 and FVC are reduced. This means that FEV1 /FVC is normal or increased.Figure: old spirometry techniqueFigure: lung volumes and capacitiesDead SpaceDead space is volume within the bronchial tree that is ventilated but does not participate in gas exchange.– Anatomical dead space is the volume of the conducting airways (pharynx, trachea, and bronchi) that do not contain alveoli and therefore cannot participate in gas exchange. It is ~150 to 200 mL.– Physiological dead space is the total volume of the bronchial tree that is ventilated but does not participate in gas exchange.Fig. 12.6 Volume exhaled versus time during a forced exhalation.The total volume exhaled is the forced vital capacity (FVC), and the volume exhaled in the first second is the forced expiratory volume (FEV1).– In healthy lungs, physiological dead space is approximately equal to anatomical dead space.However, physiological dead space may be increased in lung diseases where there are mismatches between ventilation (V) and perfusion (pulmonary blood flow [Q]).– Physiological dead space can be calculated using Bohr’s equation. This calculation assumes that the partial pressure of CO2(Paco2) in the alveoli is the same as that in systemic arterial blood.Ventilation RateMinute ventilation refers to the total ventilation per minute. It is expressed asMinute ventilation = TV × breaths/minAlveolar ventilation refers to ventilation of alveoli that participate in gas exchange per minute. It isexpressed as Alveolar ventilation = (TV – physiological dead space) × breaths/min.Distribution of Pulmonary Blood FlowWhen a person is upright, the force of gravity affects the distribution of pulmonary blood flow within the lungs (but not the total amount of blood flow) because vascular pressures progressively fall at locations above the heart. This distribution of blood flow is described in terms of “zones” of the lung.Zone 1: Lung Apex. If pulmonary artery pressure is not high enough to support the column of bloodfrom the right ventricle all the way to the apices of the lungs, the uppermost blood vessels collapse, and there is no flow in this region. This does not normally occur in healthy lungs but may occur if right ventricular pressure is extremely low (e.g., due to hemorrhage). Also, if alveolar pressure isincreased to the point where it exceeds vascular pressure, blood vessels collapse (e.g., due to positive pressure ventilation).Zone 2: Middle of the Lung. In zone 2, blood flow is intermittent. Pulmonary artery pressure drives blood flow at its peak during systole, but not during the rest of the cardiac cycle.Zone 3: Lung Base. Zone 3 has no gravitational impediment to blood flow because regions located below the heart always have vascular pressures greater than alveolar pressure. Therefore, blood flowis continuous.Gas Exchange and TransportPartial PressuresIn a gas mixture, each gas species exerts a pressure, the partial pressure of that gas. The sum of the partial pressures of the gases in a mixture equals the total gas pressure.Partial pressure for an individual gas = the fraction of that gas in the gas mixture × total gas pressure Calculation of Partial Pressure of Oxygen (Po2) in Dry Inspired Air O2 comprises 21% of air; total gas pressure = 760 mm Hg (at sea level)At high altitude, the Po2 is reduced because barometric pressure is lower.Correction of Po2 for the Presence of Water VaporDry air entering the lungs becomes completely saturated with water as air passes through moist airways. This displaces some of the other gases and slightly reduces their partial pressures.Partial pressure of water vapor (PH2o) is 47 mm Hg at body temperature.Total pressure of gases other than water = 760 mm Hg ? 47 mm Hg= 713 mm HgTherefore, the Po2 in warm, humidified inspired air isGas ExchangeDiffusion of GasesO2 and carbon dioxide (CO2 ) diffuse between alveolar gas and pulmonary capillary blood according to standard physical principles– The total amount moved per unit of time is proportional to the area available for diffusion and to the difference in partial pressure between alveolar gas and pulmonary capillary blood, and inversely proportional to the thickness of the diffusion barrier.– Gas will diffuse from the alveoli (higher partial pressures) to the pulmonary capillaries (lower partial pressures) until they equilibrate and no partial pressure gradient exists. As a result, blood entering the pulmonary veins from the pulmonary capillaries has virtually the same partialpressures as gases in the alveoli.– The diffusion barrier, composed of alveolar epithelial cells (type I pneumocytes) and capillary endothelial cells, is very thin, which ensures that the diffusion distance between alveolar gas and pulmonary capillary blood is very short. This allows blood in the pulmonary capillaries to equilibrate with alveolar gas during the short time (< 1 sec) that the blood is in the capillaries.Figure . Ultra structure of the respiratory membrane where diffusion occurs.Partial Pressure Changes of Oxygen and Carbon DioxideFollowing Gas ExchangePartial Pressure Changes of Oxygen– The Po2 of humidified inspired air is 150 mm Hg.– The Po2 of alveolar air is 100 mm Hg. This is due to the diffusion of O2from alveolar air into pulmonary capillary blood.– The Po2 of systemic arterial blood is 95 mm Hg. It is almost the same as the Po2 of alveolar air because the partial pressure of pulmonary capillary blood equilibrates with alveolar air. However, ~2% of the cardiac output bypasses the pulmonary circulation, which accounts for the slight discrepancy in partial pressures.– The Po2 of venous blood is 40 mm Hg because O2 has diffused from arterial blood into the tissues.Partial Pressure Changes of Carbon Dioxide– The Pco2 of humidified inspired air is almost zero.– The Pco2 of alveolar air is 40 mm Hg because CO2 from venous blood entering the pulmonary capillaries diffuses into alveolar air.– The Pco2 of systemic arterial blood is 40 mm Hg because pulmonary capillary blood equilibrates with alveolar air.– The Pco2 of venous blood is 46 mm Hg. It is higher than systemic arterial blood due to the diffusion of CO2 from the tissues into venous blood following cellular respiration.Ventilation and Perfusion Ratios for Optimum Gas ExchangeVentilation/perfusion ratio is the ratio of alveolar ventilation V to perfusion (pulmonary blood flow)Q.– In healthy lungs, the V/Q ratio is close to 1:1, resulting in optimum gas pressures and oxygenation in systemic arterial blood.Distribution of V/Q RatiosThere are regional differences in alveolar ventilation and blood flow in the upright individual.– Alveolar ventilation is higher at the base of the lungs than the apices because the base is more compliant and changes more in volume during each breathing cycle.– Blood flow is very low at the apex of the lung and very high at the base due to the effects of gravity.The differences in regional blood flow are greater than the differences in regional ventilation. This creates different V/Q ratios at various levels of the lung. Typical values are as follows:– Apex V/Q is ~3:1.– Middle of lungs (heart level) V/Q is ~1:1.– Base of lungs V/Q is ~1:2. ................
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