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Anki_cards__Respiratory Physiology.pdf

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RESPIRATORY PHYSIOLOGY Pulmonary blood flow is equal to the cardiac output of the right heart When a person is standing, pulmonary blood flow is lowest at the apex (top) of the lungs When a person is standing, pulmonary blood flow is highest at the base (bottom) of the lungs The volume that mov...

RESPIRATORY PHYSIOLOGY Pulmonary blood flow is equal to the cardiac output of the right heart When a person is standing, pulmonary blood flow is lowest at the apex (top) of the lungs When a person is standing, pulmonary blood flow is highest at the base (bottom) of the lungs The volume that moves into the lung with each quiet inspiration is the tidal volume What is the typical normal value for tidal volume (mL)? 500 mL The additional volume that can be inspired above tidal volume is the inspiratory reserve volume (IRV) The additional volume that can be expired below tidal volume is the expiratory reserve volume (ERV) The volume that remains in the lungs after maximal forced expiration is the residual volume Which lung volume cannot be measured on spirometry? Residual volume The sum of the tidal volume plus the inspiratory reserve volume is known as inspiratory capacity The sum of the residual volume plus the expiratory reserve volume is known as functional residual capacity (FRC) The volume of gas remaining in the lungs after normal expiration is the functional residual capacity The sum of the tidal volume, inspiratory reserve volume, and expiratory reserve volume is known as the vital capacity The maximum volume of gas that can be expired after maximal inspiration is known as the (forced) vital capacity (FVC) The sum of the tidal volume, inspiratory reserve volume, expiratory reserve volume, and residual volume is known as the total lung capacity (TLC) The volume of gas present in the lungs after a maximal inspiration is known as the total lung capacity Which lung capacities cannot be measured on spirometry? Functional residual capacity (FRC), total lung capacity (TLC) Functional residual capacity (FRC) may be measured using helium dilution or body plethysmography Functional residual capacity (FRC) may be measured using helium dilution or body plethysmography What is the typical normal value for anatomic dead space (mL)? 150 mL The volume of the anatomic dead space plus the alveolar dead space comprises the "physiologic dead space" The volume of the anatomic dead space plus the alveolar dead space comprises the "physiologic dead space" The apex of a healthy lung is the largest contributor of alveolar dead space Physiologic dead space is the total volume of inspired air that does not participate in gas exchange In healthy lungs, the physiologic dead space is approximately equal to the anatomic dead space In certain pathologic situations, the physiologic dead space may become greater than the anatomic dead space, suggesting a(n) ventilation/perfusion (V/Q) mismatch Pathologic dead space is when part of the respiratory zone is ventilated, but not perfused What equation may be used to determine the physiologic dead space (VD)? \[V_D = V_T \times \frac{P_{aCO_2} \space - \space P_{ECO_2} }{P_{aCO_2} }\] Minute ventilation is the total volume of gas that enters the lungs per minute Alveolar ventilation is the volume of gas that reaches the alveoli per minute (accounts for physiologic dead space) What equation may be used to calculate minute ventilation? Minute Ventilation (VE) = VT × RR What equation may be used to calculate alveolar ventilation? Alveolar Ventilation (VA) = (VT - VD) × RR What is the normal range of respiratory rates for a healthy adult (breaths/min)? 12-20 breaths/min If CO2 production is constant, then the arterial and alveolar Pco2 is determined by alveolar ventilation If CO2 production is constant, then the arterial and alveolar Pco2 is determined by alveolar ventilation What is the effect of increased alveolar ventilation on arteriolar (and alveolar) Pco2? Decreased Pco2 What is the effect of decreased alveolar ventilation on arteriolar (and alveolar) Pco2? Increased Pco2 The alveolar gas equation states that the alveolar Po2 (PAo2) equals: PAO2 = PIO2 - (PaCO2/R) When using the alveolar gas equation, the respiratory quotient (R) is equal to the ratio of CO2 produced / O2 consumed In the steady state, the respiratory quotient, R, is normally equal to 0.8 The approximate Po2 in inspired, humidified air (PIO2) at sea level is 150 mmHg The difference between PAO2 − PaO2 is known as the alveolar-arterial (A-a) gradient and is normally 5 - 10 mmHg in a non-smoking young adult The difference between PAO2 − PaO2 is known as the alveolar-arterial (A-a) gradient and is normally 5 - 10 mmHg in a non-smoking young adult The volume of air that can be forcibly expired after a maximal inspiration in one second is known as the FEV1 The normal value for the ratio of FEV1/FVC is ≥0.7 Lung compliance describes the change in lung volume for a given change in lung pressure (ΔV / ΔP) Lung compliance may be calculated by the equation C = ΔV/ΔP The compliance of the lungs and chest wall is inversely proportional to their elastance The compliance of the lungs and chest wall is inversely proportional to the wall stiffness Elastic recoil is the force generated due to the tendency for the lungs to collapse inward and the chest wall to spring outward Elastic recoil is inversely proportional to compliance and directly proportional to elastance A lung with high compliance is easier to fill A lung with low compliance is harder to fill The slope of a respiratory system pressure-volume curve represents lung compliance The slope of a respiratory system pressure-volume curve represents lung compliance The slope (compliance) of the pressure-volume loop curves for inspiration and expiration are different due to a phenomenon known as hysteresis Hysteresis occurs due to the need to overcome surface tension forces during lung inflation (inspiration) Hysteresis occurs due to the need to overcome surface tension forces during lung inflation (inspiration) Are the lungs generally more compliant during inspiration or expiration? Expiration (due to hysteresis) The intermolecular forces between liquid molecules lining the lung are much stronger than the forces between liquid and air During initial inspiration, liquid molecules are close together and intermolecular forces are high During expiration, the slope of the pressure-volume loop increases as the density of surfactant molecules rapidly increases At FRC, the intrapleural space normally has a(n) negative pressure relative to the atmosphere At functional residual capacity, the inward pull of the lung is balanced by the outward pull of the chest At functional residual capacity, the inward pull of the lung is balanced by the outward pull of the chest At functional residual capacity, the inward pull of the lung is balanced by the outward pull of the chest If a sharp object punctures the intrapleural space, the intrapleural pressure becomes equal to atmospheric pressure, causing a(n) pneumothorax If a sharp object punctures the intrapleural space, the intrapleural pressure becomes equal to atmospheric pressure, causing a(n) pneumothorax The compliance of the lung-chest wall system is less than that of the lungs or chest wall alone At FRC, airway and alveolar pressures are equal to 0 (atmospheric pressure) When lung volume is less than FRC, there is a net expanding force on the lung-chest wall system When lung volume is less than FRC, there is a net expanding force on the lung-chest wall system When lung volume is greater than FRC, there is a net collapsing force on the lung-chest wall system When lung volume is greater than FRC, there is a net collapsing force on the lung-chest wall system At highest lung volumes, both the lungs and the chest wall contribute to collapsing forces on the lung- chest wall system What is the effect of emphysema on lung compliance? Increased compliance At the original FRC, the tendency of the lung to collapse in a patient with emphysema is less than the tendency of the chest wall to expand What is the effect of emphysema on functional residual capacity (FRC)? Increased FRC What is the effect of normal aging on lung compliance? Increased compliance What is the effect of pulmonary fibrosis on lung compliance? Decreased compliance At the original FRC, the tendency of the lung to collapse in a patient with pulmonary fibrosis is greater than the tendency of the chest wall to expand What is the effect of pulmonary fibrosis on functional residual capacity (FRC)? Decreased FRC What is the effect of pulmonary edema on lung compliance? Decreased compliance What is the effect of pneumonia on lung compliance? Decreased compliance What is the effect of surfactant on lung compliance? Increased compliance The law of Laplace states that the collapsing pressure of an alveolus (P) can be determined by the following equation: P = 2T / r According to the law of Laplace, a large alveolus will have a(n) low collapsing pressure According to the law of Laplace, a small alveolus will have a(n) high collapsing pressure Alveoli have increased tendency to collapse on expiration Alveoli have increased tendency to collapse on expiration What equation may be used to calculate the airflow (Q) given the pressure and resistance of the airway? Q = ΔP/R Airflow is inversely proportional to airway resistance Airflow is directly proportional to the pressure gradient The resistance of an airway may be calculated using Poiseuille's equation, which states R = 8ηl/πr4 Airway resistance is inversely proportional to the fourth power of the radius of the airway Airway resistance is inversely proportional to the fourth power of the radius of the airway Airway resistance is inversely proportional to the fourth power of the radius of the airway The major site of airway resistance is the medium-sized bronchi What is the effect of parasympathetic innervation on airway resistance? Increased resistance What is the effect of sympathetic innervation on airway resistance? Decreased resistance What is the effect of high lung volumes on airway resistance? Decreased resistance What is the effect of low lung volumes on airway resistance? Increased resistance What is the effect of increased viscosity (e.g. deep-sea diving) on airway resistance? Increased resistance What is the effect of decreased viscosity (e.g. helium inhalation) on airway resistance? Decreased resistance What equation may be used to calculate the pulmonary vascular resistance (PVR)? PVR = (Ppulm artery - PL atrium) / cardiac output The transpulmonary pressure across the lungs is calculated as alveolar pressure minus intrapleural pressure The transpulmonary pressure across the lungs is calculated as alveolar pressure minus intrapleural pressure How does the volume of breath change during inspiration? Increased How does the intrapleural pressure change during inspiration (relative to atmosphere)? More negative relative to atmosphere How does the alveolar pressure change during mid-inspiration (relative to atmosphere)? More negative relative to atmosphere As the alveolar pressure becomes negative relative to the atmosphere, air flows inwards How does the volume of breath change during expiration? Decreased How does the intrapleural pressure change during expiration (relative to atmosphere)? Less negative relative to atmosphere How does the alveolar pressure change during mid-expiration (relative to atmosphere)? More positive relative to atmosphere As the alveolar pressure becomes positive relative to the atmosphere, air flows outwards In what normal scenario may intrapleural pressure be positive (relative to the atmosphere)? Forced expiration The partial pressure of a gas (Px) in humidified tracheal air is equal to (PB - PH2O) * F The partial pressure of a gas (Px) in dry expired air is equal to PB * F The concentration of a dissolved gas (Cx) is equal to Px * Solubility Transfer of gases across cell membranes or capillary walls occurs by simple diffusion According to Fick's law, the rate of diffusion of a gas (V̇ gas) is equal to: V̇ x = DAΔP / Δx The diffusion coefficient (DK) for CO2 is approximately 20x higher than that of O2 The lung diffusing capacity (DL) is the equivalent of permeability of the alveolar-pulmonary capillary barrier The lung diffusing capacity (DL) can be measured with carbon monoxide (CO) because it is exclusively diffusion-limited DLCO may be used to estimate the extent to which oxygen passes from the air sacs of lungs into blood The lung diffusing capacity (DL) is directly proportional to the surface area available for diffusion The lung diffusing capacity (DL) is directly proportional to the diffusion coefficient of the gas The lung diffusing capacity (DL) is inversely proportional to the alveolar wall thickness The lung diffusing capacity (DL) decreases in emphysema due to decreased surface area (A) The lung diffusing capacity (DL) decreases in emphysema due to decreased surface area (A) The lung diffusing capacity (DL) decreases in pulmonary fibrosis due to increased wall thickness (Δx) The lung diffusing capacity (DL) decreases in pulmonary fibrosis due to increased wall thickness (Δx) The lung diffusing capacity (DL) increases during exercise due to increased surface area (A) The lung diffusing capacity (DL) increases during exercise due to increased surface area (A) The Po2 in dry inspired air is normally approximately 160 mmHg The Po2 in humidified tracheal air is normally approximately 150 mmHg The partial pressure of oxygen in the alveolar air (PAO2) and arterial blood (PaO2) is normally approximately 100 mmHg The partial pressure of carbon dioxide in the alveolar air (PACO2) and arterial blood (PaCO2) is normally approximately 40 mmHg The partial pressure of oxygen in the venous blood (PvO2) is normally approximately 40 mmHg The partial pressure of carbon dioxide in mixed venous blood (PvCO2) is normally approximately 46 mmHg The partial pressure of O2 in arteriolar blood is slightly lower than alveolar air due to the "physiologic shunt" The partial pressure of O2 in arteriolar blood is slightly lower than alveolar air due to the "physiologic shunt" The two sources of the physiologic shunt are bronchial blood flow and a small portion of coronary venous blood The two sources of the physiologic shunt are bronchial blood flow and a small portion of coronary venous blood The total gas concentration in solution is equal to the dissolved gas + bound gas + chemically modified gas The total gas concentration in solution is equal to the dissolved gas + bound gas + chemically modified gas The total gas concentration in solution is equal to the dissolved gas + bound gas + chemically modified gas The partial pressure gradient is the driving force for the diffusion of a gas Only free, dissolved gas contributes to the partial pressure of a gas in solution In diffusion-limited gas exchange, the gas does not equilibrate by the time blood reaches the end of the capillary In perfusion-limited gas exchange, the gas equilibrates early along the length of the capillary In perfusion-limited gas exchange, diffusion can be increased only if blood flow increases In perfusion-limited gas exchange, diffusion can be increased only if blood flow increases In normal health, O2 exhibits perfusion-limited gas exchange CO2 exhibits perfusion-limited gas exchange N2O exhibits perfusion-limited gas exchange CO exhibits diffusion-limited gas exchange When patients have diseased lung tissue (e.g. fibrosis/emphysema) O2 transfer becomes diffusion- limited At high altitude the partial pressure gradient of O2 is lower and thus equilibration takes longer At high altitude the partial pressure gradient of O2 is lower and thus equilibration takes longer O2 is carried in blood in two forms: dissolved (2%) or bound to hemoglobin (98%) O2 is carried in blood in two forms: dissolved (2%) or bound to hemoglobin (98%) Hemoglobin is a globular protein consisting of 4 subunits Each subunit of hemoglobin contains a(n) heme moiety, which is a(n) iron-binding porphyrin and a polypeptide chain Each subunit of hemoglobin contains a(n) heme moiety, which is a(n) iron-binding porphyrin and a polypeptide chain Iron in hemoglobin is normally in the ferrous (Fe2+) state If hemoglobin contains iron in the ferric (Fe3+) state, it is called methemoglobin If hemoglobin contains iron in the ferric (Fe3+) state, it is called methemoglobin Methemoglobin (Fe3+) binds O2 much less readily than hemoglobin (Fe2+) Methemoglobin has a(n) increased affinity for cyanide relative to hemoglobin Methemoglobin has a(n) increased affinity for cyanide relative to hemoglobin Methemoglobinemia may present with cyanosis and chocolate-colored blood Methemoglobinemia may present with cyanosis and chocolate-colored blood Methemoglobinemia may present with cyanosis and chocolate-colored blood Induced-methemoglobinemia (i.e. nitrites followed by thiosulfate) may be used to treat cyanide poisoning Induced-methemoglobinemia (i.e. nitrites followed by thiosulfate) may be used to treat cyanide poisoning Induced-methemoglobinemia (i.e. nitrites followed by thiosulfate) may be used to treat cyanide poisoning Methemoglobinemia can be treated with methylene blue or vitamin C (ascorbic acid) Methemoglobinemia can be treated with methylene blue or vitamin C (ascorbic acid) What three drug classes and singular drug are commonly associated with methemoglobinemia? - Nitrates (and nitrites) - Sulfa drugs - Topical / local anesthetics (esp. benzocaine) - Dapsone Polluted/high altitude water may contain nitrites, which can cause methemoglobinemia Methemoglobinemia is associated with the following parameters: - decreased (typically to 85%) SaO2 - decreased O2 content - normal PaO2 - decreased PaCO2 Most adult hemoglobin is composed of 2 α and 2 β subunits; known as HbA Most adult hemoglobin is composed of 2 α and 2 β subunits; known as HbA Fetal hemoglobin (HbF) has a much higher binding affinity for O2 than adult hemoglobin (HbA) Why must fetal hemoglobin (HbF) have a much higher O2 binding affinity than adult hemoglobin (HbA)? Drives O2 diffusion across placenta from mother to fetus The increased O2 binding affinity of fetal hemoglobin results from decreased affinity of HbF for 2,3- BPG The increased O2 binding affinity of fetal hemoglobin results from decreased affinity of HbF for 2,3- BPG Hemoglobin exists in two forms: taut (deoxygenated) and relaxed (oxygenated) The taut form of hemoglobin has a(n) low affinity for O2 The taut form of hemoglobin has a(n) low affinity for O2 The relaxed form of hemoglobin has a(n) high affinity for O2 The relaxed form of hemoglobin has a(n) high affinity for O2 The taut form of hemoglobin is found in most tissues The relaxed form of hemoglobin is found in the lungs Normally 1g of hemoglobin can bind 1.34 mL of O2 Normally there is ~15 g/dL of hemoglobin in blood The O2-binding capacity of blood is 20.1 mL O2 / 100 mL blood What equation may be used to calculate the O2 content of blood? O2 content = (1.34 × Hb × SaO2) + (0.003 × PaO2) Decreased hemoglobin (e.g. anemia) is associated with the following parameters: - normal SaO2 - decreased O2 content - normal PaO2 What equation may be used to calculate O2 delivery to tissues? O2 delivery = CO × O2 content of blood The sigmoidal shape of the oxygen-hemoglobin dissociation curve is due to positive cooperativity (increased affinity for each successive O2 bound) The sigmoidal shape of the oxygen-hemoglobin dissociation curve is due to positive cooperativity (increased affinity for each successive O2 bound) A(n) myoglobin molecule has the potential to bind 1 O2 molecule(s) A(n) myoglobin molecule has the potential to bind 1 O2 molecule(s) The P50 of the oxygen-Hb dissociation curve is the Po2 at which hemoglobin is 50% saturated The oxygen-Hb dissociation curve is roughly flat when the Po2 is between 60 and 100 mmHg Does the oxygen-myoglobin dissociation curve have a sigmoidal shape? Why? No, myoglobin is monomeric (no positive cooperativity) Shifts of the O2-Hb dissociation curve to the right occur when there is decreased affinity of hemoglobin for O2 Shifts of the O2-Hb dissociation curve to the right occur when there is decreased affinity of hemoglobin for O2 Shifts of the O2-Hb dissociation curve to the right cause increased unloading of O2 at tissues Shifts of the O2-Hb dissociation curve to the right cause increased unloading of O2 at tissues Increased pCO2 and resulting decrease of pH enhancing the release of O2 from hemoglobin is called the Bohr effect A(n) increase in temperature causes the O2-hemoglobin dissociation curve to shift to the right A(n) increase in temperature causes the O2-hemoglobin dissociation curve to shift to the right A(n) increase in 2,3-BPG causes the O2-hemoglobin dissociation curve to shift to the right A(n) increase in 2,3-BPG causes the O2-hemoglobin dissociation curve to shift to the right 2,3-BPG decreases the affinity of hemoglobin for O2 by binding to hemoglobin β chains How do levels of 2,3-BPG change at high altitudes? Increased 2,3-BPG increases under hypoxic conditions (e.g. high altitude) High altitudes indirectly cause the O2-hemoglobin dissociation curve to shift to the right A(n) increase in pH causes the O2-hemoglobin dissociation curve to shift to the left A(n) increase in pH causes the O2-hemoglobin dissociation curve to shift to the left A(n) decrease in temperature causes the O2-hemoglobin dissociation curve to shift to the left A(n) increase in hemoglobin F causes the O2-hemoglobin dissociation curve to shift to the left A(n) increase in hemoglobin F causes the O2-hemoglobin dissociation curve to shift to the left Carboxyhemoglobin is a form of hemoglobin bound to CO in place of O2 Carboxyhemoglobin is a form of hemoglobin bound to CO in place of O2 Carbon monoxide binds competitively to Hb and with 200-250× greater affinity than O2 Carboxyhemoglobin causes the O2-hemoglobin dissociation curve to shift to the left Carboxyhemoglobin heme groups not bound by CO have a(n) increased affinity for O2 Carboxyhemoglobin causes decreased unloading of O2 at tissues Carboxyhemoglobin causes decreased O2-binding capacity What is the management of carbon monoxide poisoning (carboxyhemoglobinemia)? 100% O2 ↓ Hyperbaric oxygen therapy ↓ Endotracheal intubation Carboxyhemoglobinemia is associated with the following parameters: - decreased* SaO2 - decreased O2 content - normal PaO2 What is the hemoglobin concentration in carboxyhemoglobinemia? Normal How does the hemoglobin concentration change in anemia? Decreased Polycythemia is associated with the following parameters: - normal SaO2 - increased O2 content - normal PaO2 How does the hemoglobin concentration change in polycythemia? Increased Erythropoietin (EPO) is a hormone synthesized in the kidneys in response to hypoxia Erythropoietin (EPO) is a hormone synthesized in the kidneys in response to hypoxia Decreased O2 delivery to the kidneys due to hypoxia causes increased production of hypoxia- inducible factor 1α, which then stimulates synthesis of EPO Hypoxia-inducible factor 1α acts in renal fibroblasts to cause synthesis of the mRNA for erythropoietin Hypoxia-inducible factor 1α acts in renal fibroblasts to cause synthesis of the mRNA for erythropoietin Erythropoietin (EPO) causes differentiation of proerythroblasts, which undergo further development to form mature erythrocytes Deoxygenated hemoglobin may act as a(n) buffer for H+ ions Deoxygenated hemoglobin may act as a(n) buffer for H+ ions One way in which CO2 is carried in the blood is as dissolved CO2 (5%) One way in which CO2 is carried in the blood is bound to hemoglobin, known as carbaminohemoglobin (HbCO2) (25%) The majority of CO2 transported in blood is in the form of HCO3- (bicarbonate) (70%) CO2 binds to hemoglobin at the N-terminus of globin Decreased O2 binding to hemoglobin causes increased affinity for CO2 and H+ (Haldane effect) Decreased O2 binding to hemoglobin causes increased affinity for CO2 and H+ (Haldane effect) Increased O2 binding to hemoglobin causes decreased affinity for CO2 (Haldane effect) Increased O2 binding to hemoglobin causes decreased affinity for CO2 (Haldane effect) Increased O2 binding to hemoglobin causes decreased affinity for CO2 (Haldane effect) In red blood cells (in plasma), CO2 is combined with H2O via the enzyme carbonic anhydrase, forming H2CO3 In red blood cells (in plasma), CO2 is combined with H2O via the enzyme carbonic anhydrase, forming H2CO3 In red blood cells (in plasma), CO2 is combined with H2O via the enzyme carbonic anhydrase, forming H2CO3 In red blood cells (in plasma), CO2 is combined with H2O via the enzyme carbonic anhydrase, forming H2CO3 The H+ in red blood cells (from H2CO3) is buffered by deoxyhemoglobin The H+ in red blood cells (from H2CO3) is buffered by deoxyhemoglobin The HCO3- in red blood cells (from H2CO3) is transported into the plasma in exchange for Cl- The HCO3- in red blood cells (from H2CO3) is transported into the plasma in exchange for Cl- The HCO3- transported out of RBCs is carried to the lungs in the plasma of venous blood In the lungs, oxygenation of hemoglobin promotes H+ release from its buffering sites In the lungs, oxygenation of hemoglobin promotes H+ release from its buffering sites In the lungs, HCO3- enters the red blood cells in exchange for Cl- In the lungs, HCO3- enters the red blood cells in exchange for Cl- In the lungs, H2CO3 in the red blood cell is reconverted to CO2 and H2O and expired The Cl--HCO3- exchange that occurs across the RBC membrane is accomplished by an anion exchange protein called band 3 protein The pulmonary circulation is normally characterized as a(n) low resistance, high compliance system A decrease in PAO2 causes hypoxic vasoconstriction, which shunts blood away from poorly ventilated regions of the lung Fetal pulmonary vascular resistance is very high because of generalized hypoxic vasoconstriction Decreased Po2 (hypoxia) causes vasoconstriction in the pulmonary circulation Increased Pco2 (hypercapnia) causes vasoconstriction in the pulmonary circulation Decreased Po2 (hypoxia) causes vasodilation in the systemic circulation Increased Pco2 (hypercapnia) causes vasodilation in the systemic circulation In zone 1 (apex) of the lung, blood flow (Q) is lowest In zone 1 (apex) of the lung, blood flow (Q) is lowest In zone 3 (base) of the lung, blood flow (Q) is highest In zone 3 (base) of the lung, blood flow (Q) is highest Rank the following variables for zone 1 of the lung: PA, Pa, and Pv PA ≥ Pa > Pv Rank the following variables for zone 2 of the lung: PA, Pa, and Pv Pa > PA > Pv Rank the following variables for zone 3 of the lung: PA, Pa, and Pv Pa > Pv > PA In zone 1 of the lung, high alveolar pressure may compress the capillaries and reduce blood flow in this zone In zone 2 of the lung, blood flow is driven by the difference between arteriolar and alveolar pressure In zone 3 of the lung, blood flow is driven by the difference between arteriolar and venous pressure In right-to-left shunts, hypoxemia always occurs because a significant fraction of the cardiac output is not delivered to the lungs In right-to-left shunts, hypoxemia always occurs because a significant fraction of the cardiac output is not delivered to the lungs A defining characteristic of hypoxemia caused by a right-to-left shunt is that it cannot be corrected with high O2 gas Do left-to-right shunts result in hypoxemia? No The ventilation/perfusion (V/Q) ratio is the ratio of alveolar ventilation to pulmonary blood flow The normal average value for V/Q is 0.8 In zone 1 (apex) of the lung, alveolar ventilation (V) is lowest In zone 1 (apex) of the lung, alveolar ventilation (V) is lowest In zone 3 (base) of the lung, alveolar ventilation (V) is highest In zone 3 (base) of the lung, alveolar ventilation (V) is highest Both ventilation and perfusion are greater at the base of the lung than at the apex of the lung The V/Q ratio is highest in zone 1 (apex) of the lung The V/Q ratio is highest in zone 1 (apex) of the lung The V/Q ratio is lowest in zone 3 (base) of the lung The V/Q ratio is lowest in zone 3 (base) of the lung The V/Q ratio at the apex of the lung is normally 3, indicating wasted ventilation The V/Q ratio at the apex of the lung is normally 3, indicating wasted ventilation The V/Q ratio at the base of the lung is normally 0.6, indicating wasted perfusion The V/Q ratio at the base of the lung is normally 0.6, indicating wasted perfusion What is the ideal V/Q ratio for adequate gas exchange? 1 (ventilation matches perfusion) If there is a(n) blood flow obstruction, the V/Q ratio = ∞ (dead space)* If there is a(n) blood flow obstruction, the V/Q ratio = ∞ (dead space)* Dead space is ventilation of lung regions that are not perfused (V/Q = ∞) If there is a(n) airway obstruction, the V/Q ratio = 0 (shunt) If there is a(n) airway obstruction, the V/Q ratio = 0 (shunt) Shunting is perfusion of lung regions that are not ventilated (V/Q = 0) What type of V/Q mismatch occurs due to pulmonary embolus? Dead space* What type of V/Q mismatch occurs due to airway obstruction? Shunt (perfusion but no ventilation) Does 100% O2 improve PaO2 in V/Q mismatch due to physiologic dead space? Yes, assuming < 100% dead space Does 100% O2 improve PaO2 in V/Q mismatch due to intrapulmonary shunting? No Certain organisms that thrive in high O2 (e.g. M. tuberculosis) flourish in the apex of the lung With exercise (increased cardiac output), there is vasodilation of apical capillaries in the lung, which causes the V/Q ratio to approach a value of 1 With exercise (increased cardiac output), there is vasodilation of apical capillaries in the lung, which causes the V/Q ratio to approach a value of 1 In response to exercise, there is increased O2 consumption In response to exercise, there is increased ventilation rate to meet O2 demand In response to exercise, the V/Q ratio from apex to base becomes more even In response to exercise, there is increased pulmonary blood flow, due to increased cardiac output In response to exercise, there is increased pulmonary blood flow, due to increased cardiac output There is a(n) decrease in pulmonary resistance associated with increased perfusion of pulmonary capillary beds In response to strenuous exercise, there is decreased pH, secondary to lactic acidosis How does PaCO2 change in response to exercise? No change How does PaO2 change in response to exercise? No change In response to exercise, there is increased venous CO2 content In response to exercise, there is decreased venous O2 content As a result of decreased atmospheric oxygen (e.g. high altitude), there is a(n) decreased PaO2 In response to decreased PaO2 (e.g. high altitude), there is increased ventilation Increased ventilation (e.g. high altitude) causes decreased PaCO2 High altitude initially causes respiratory alkalosis and hypoxia, which may cause acute altitude sickness High altitude initially causes respiratory alkalosis and hypoxia, which may cause acute altitude sickness High altitude initially causes respiratory alkalosis and hypoxia, which may cause acute altitude sickness In response to high altitude, there is a chronic increase in ventilation The respiratory alkalosis that occurs as a result of ascent to high altitude may be treated with carbonic anhydrase inhibitors Living at high altitude chronically causes hypoxia which increases the synthesis of erythropoietin, causing polycythemia In response to high altitude, there is a(n) increase in 2,3-BPG In response to high altitude, there are intracellular changes, such as increased number of mitochondria In response to respiratory alkalosis (e.g. due to high altitude), there is increased renal excretion of HCO3- In response to high altitude, there is chronic hypoxic pulmonary vasoconstriction which results in pulmonary hypertension and right ventricular hypertrophy In response to high altitude, there is chronic hypoxic pulmonary vasoconstriction which results in pulmonary hypertension and right ventricular hypertrophy Hypoxemia is defined as a decrease in PaO2 Hypoxemia is defined as a decrease in PaO2 What happens to the A-a gradient in response to high altitude? Normal What happens to the A-a gradient in response to hypoventilation (e.g. opioid use, obesity hypoventilation syndrome)? Normal What happens to the A-a gradient in response to diffusion defects (e.g. fibrosis, pulmonary edema)? Increased What happens to the A-a gradient in response to a V/Q mismatch? Increased What happens to the A-a gradient in response to right-to-left shunts? Increased What cause of hypoxemia is not greatly helped by supplemental O2? Right-to-left shunt Hypoxia is defined as a decrease of O2 delivery to tissues Hypoxia is defined as a decrease of O2 delivery to tissues Hypoxia may be caused by a(n) decreased cardiac output Hypoxia may be caused by hypoxemia Hypoxia may be caused by anemia, due to decreased levels of hematocrit and Hb Hypoxia may be caused by carbon monoxide poisoning, which decreases the O2 content of blood (CaO2) Ischemia is a cause of O2 deprivation due to a loss of blood flow (e.g. impeded arterial flow, decreased venous drainage) Which zone of the lung has the highest PaO2? Zone 1 (apex) Carbon monoxide, cyanide, and sodium azide are inhibitors of complex IV of the ETC Carbon monoxide, cyanide, and sodium azide are inhibitors of complex IV of the ETC Carbon monoxide, cyanide, and sodium azide are inhibitors of complex IV of the ETC Carbon monoxide, cyanide, and sodium azide are inhibitors of complex IV of the ETC Cyanide may inhibit the ETC by binding Fe3+, preventing transfer of electrons to O2 in complex IV Cyanide may inhibit the ETC by binding Fe3+, preventing transfer of electrons to O2 in complex IV One treatment for cyanide poisoning is sodium nitrite, which induces methemoglobinemia One treatment for cyanide poisoning is sodium thiosulfate, which helps restore rhodanese-mediated metabolism of cyanide to thiocyanate The first-line antidote for cyanide poisoning is vitamin B12 (hydroxocobalamin), which binds to cyanide and promotes its excretion in urine Carbon monoxide may inhibit the ETC by binding Fe2+, preventing transfer of electrons to O2 in complex IV Carbon monoxide may inhibit the ETC by binding Fe2+, preventing transfer of electrons to O2 in complex IV Synthetic erythropoietin (e.g., epoetin) is often supplemented in chronic kidney disease Which poisonous substance is characterized by a "bitter almond" odor? Cyanide One normal type of hemoglobin is HbF which is composed of two α and two γ chains One normal type of hemoglobin is HbF which is composed of two α and two γ chains One normal type of hemoglobin is HbA which is composed of two α and two β chains One normal type of hemoglobin is HbA which is composed of two α and two β chains One normal type of hemoglobin is HbA2 which is composed of two α and two δ chains One normal type of hemoglobin is HbA2 which is composed of two α and two δ chains What skin appearance is classically seen in carbon monoxide poisoning? Cherry-red appearance Carbon monoxide poisoning is associated with which cardiac pathology? Myocarditis Ischemia occurs when there is inadequate blood supply to meet demand Ischemia can occur due to decreased arterial perfusion Ischemia can occur due to decreased venous drainage Ischemia can occur due to hypoperfusion (e.g. shock) What is the effect of normal aging on chest wall compliance? Decreased compliance What is the effect of normal aging on residual volume (RV)? Increased RV What is the effect of normal aging on forced vital capacity (FVC)? Decreased What is the effect of normal aging on FEV1? Decreased What is the effect of normal aging on total lung capacity (TLC)? No change Can normal aging cause a ventilation/perfusion mismatch? Yes How does normal aging change the A-a gradient? Increased How does normal aging change respiratory muscle strength? Decreased The most common cause of cyanide poisoning is smoke inhalation Cyanide inhibits aerobic metabolism, resulting in hypoxia unresponsive to supplemental O2 Cyanide inhibits aerobic metabolism, resulting in hypoxia unresponsive to supplemental O2 Patients with cyanide poisoning present with an "almond" breath odor and cherry-red skin discoloration In exercise, O2 exhibits mixed-limited gas exchange In exercise, blood is flowing faster through the pulmonary capillaries, resulting in it taking a(n) longer length along the capillary to maximize O2 concentration In a healthy patient, can exercise alone make patients hypoxemic? No Many patients with inhalation injury present secondary to burns, CO inhalation, cyanide or arsenic poisoning Many patients with inhalation injury present secondary to burns, CO inhalation, cyanide or arsenic poisoning Patients with cyanide poisoning have a(n) narrowing of the venous-arterial PO2 gradient Increased lung volumes result in increased pulmonary vascular resistance During expiration, decreased lung volumes result in a(n) increase in extra-alveolar vessel resistance Pulmonary vascular resistance is lowest near the functional residual capacity (FRC) When tidal volume is limited, the respiratory control centers increase the respiratory rate to restore minute ventilation Decreasing V/Q may be due to a(n) pulmonary shunt Increased V/Q results in alveolar dead space Cyanide poisoning may occur through the ingestion of amygdalin, which is a glucoside found in apricot seeds Cyanide poisoning may occur through the ingestion of amygdalin, which is a glucoside found in apricot seeds Carbon monoxide poisoning is classically associated with bilateral globus pallidus hyperintensities on MRI Carbon monoxide poisoning is classically associated with bilateral globus pallidus hyperintensities on MRI

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respiratory physiology lung function gas exchange human anatomy
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