Gas Transport Notes


Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Gas Transport essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Gas Transport:

Oxygen binding capacity and oxygen content

Ventilation-perfusion ratios and V/Q mismatch


Oxygen-hemoglobin dissociation curve


Carbon dioxide transport in blood

Regulation of pulmonary blood flow

Zones of pulmonary blood flow

Pulmonary shunts

NOTES NOTES GAS TRANSPORT OXYGEN BINDING CAPACITY & OXYGEN CONTENT MEASURES OF OXYGEN AVAILABILITY O2 binding capacity ▪ Maximum amount of O2 bound to hemoglobin when 100% saturated (per blood volume) ▫ More hemoglobin → more oxygen (per blood volume) ▪ Measurement ▫ Expose blood to air with high PO2 → complete hemoglobin saturation ▫ Hemoglobin’s oxygen affinity → 1g of hemoglobin A binds 1.34mL of O2 ▫ Normal hemoglobin A concentration in blood → 15g/100mL ▫ O2 binding capacity = hemoglobin concentration × hemoglobin’s affinity for oxygen ▪ Example: O2 binding capacity = 15g/100mL × 1.34mL O2/g hemoglobin = 20.1mL O2/100mL blood Oxygen content (CaO2) ▪ Oxygen (mL) per 100mL of blood ▪ CaO2 = O2 binding capacity × % saturation + oxygen dissolved in solution ▫ Correction for dissolved O2 → solubility of O2 in blood → 0.003mL O2/100mL blood per mmHg ▪ CaO2 = hemoglobin concentration (g/100mL blood) × hemoglobin oxygen affinity (mL O2/g) × SaO2 (arterial oxygen saturation) + partial pressure of oxygen (mmHg) × solubility of O2 in blood (mL O2/ blood/mmHg) ▪ CaO2 (ml O2/100mL blood) = ([Hb] × 1.34 x SaO2) + (PaO2 × 0.003) O2 DELIVERY TO TISSUES ▪ Dependent on blood flow (determined by cardiac output), blood’s oxygen content ▪ O2 delivery = cardiac output × oxygen content OXYGEN TRANSPORT ▪ Majority of oxygen in blood bound to hemoglobin, remainder dissolved in solution Dissolved O2 ▪ Free in solution (1.5% of total blood O2 content) ▪ Only free O2 contributes to partial pressure → drives O2 diffusion ▪ O2 solubility in blood = 0.003mL O2/100mL blood per mmHg → at normal PaO2 of 100mmHg → concentration of dissolved O2 is 0.3mL O2/100mL blood ▪ Normal consumption of O2 = 250mL O2/ minute ▪ Only dissolved O2 delivered to tissues (cardiac output 5L/min) × dissolved O2 concentration → 15mL O2/min → incompatible with life ▪ Hemoglobin increases amount of O2 carried by blood Hemoglobin bound ▪ Hemoglobin → greater concentrations of O2 carried to tissues by blood ▪ 98.5% of O2 in blood bound to hemoglobin OSMOSIS.ORG 611
▪ Four subunits of hemoglobin molecule ▫ Each subunit contains heme moiety: iron-binding porphyrin, polypeptide chain (alpha/beta) ▫ Adult hemoglobin subunits (α2β2): two alpha chains, two beta chains → each contains one iron molecule (Fe2+) → binds one O2 molecule → four molecules of O2 per molecule of hemoglobin → oxyhemoglobin ▫ Deoxygenated hemoglobin → deoxyhemoglobin Figure 71.1 Each of the four hemoglobin subunits contains a heme group capable of binding one oxygen molecule. ▪ Heme binds oxygen in lungs → oxyhemoglobin ▫ Oxygen diffuses from alveoli → across single cell thick alveolar walls → diffuses into blood → through red blood cell (RBC) membrane → interacts with heme → oxyhemoglobin (bright red blood) ▪ Oxygen binding to hemoglobin → conformational shift in heme structure → ↑ oxygen binding affinity → sigmoidal (S-shaped) oxygen-binding affinity/ dissociation curve ▪ At tissue level: association process reversed ▫ O2 released → deoxyhemoglobin (dark red blood) ▫ 20% of dissolved CO2 → binds with globin amino acids (not heme group) of deoxyhemoglobin → carbaminohemoglobin Fetal oxygen transport ▪ Fetal blood requires higher affinity for oxygen to facilitate movement of O2 from maternal to fetal blood ▪ Fetal variant hemoglobin (hemoglobin F) ▫ Contains two alpha chains, two gamma chains (α2γ2) → greater affinity for oxygen OXYGEN-HEMOGLOBIN DISSOCIATION CURVE ▪ Proportion of saturated hemoglobin plotted against partial pressure of oxygen ▪ Illustrates how blood carries, releases oxygen as partial pressures vary ▫ Hemoglobin: primary oxygen transporter in blood ▫ Amount of oxygen bound to hemoglobin at any given time determined by environmental partial pressure of oxygen (high in lungs, lower in tissue 612 OSMOSIS.ORG capillary beds) → hemoglobin binds to oxygen in lungs, releases at tissue level ▫ Oxyhemoglobin dissociation curve: determined by hemoglobin affinity for oxygen; rate hemoglobin acquires, releases oxygen into surrounding fluid; plots SO2 against PO2
Chapter 71 Respiratory Physiology: Gas Transport Figure 71.2 Each hemoglobin molecule can bind four O2 molecules, but each hemoglobin isn't always 100% saturated, or bound, by O2. A hemoglobin molecule with no O2 bound (0% saturation) is called deoxyhemoglobin. SIGMOIDAL SHAPE ▪ Oxyhemoglobin dissociation curve is sigmoidal ▫ Positive cooperativity → each successive oxygen molecule binding to heme group → ↑ affinity ▫ Approaches maximum saturation limit → few binding sites remain → little additional binding possible → curve levels off → large ↑ in oxygen partial pressure → no effect on hemoglobin saturation beyond saturation point ▫ Partial pressures ↓ at tissue level → oxygen release → with each successive oxygen molecule release, subsequent release eases → rapid oxygen unloading at low partial pressures P50 ▪ P50: partial pressure of oxygen in blood when hemoglobin 50% saturated (e.g. 26.6mmHg) ▪ Conventional measure of hemoglobin affinity for oxygen ▪ Physiological/disease processes may shift dissociation curve to left/right, alter P50 ▫ Left shift → lower P50 → ↑ oxygen affinity ▫ Right shift → raised P50 → ↓ oxygen affinity RIGHT SHIFT ▪ Right shift → lower oxygen affinity → 50% saturation occurs at higher PO2 → oxygen unloading ↑ PCO2, ↓ pH ▪ ↑ metabolic activity of tissues → ↑ CO2 → ↑ H+ concentration → ↓ pH → ↓ hemoglobin oxygen affinity → oxygen unloading in metabolically active tissues ▪ Effect of PCO2, pH on oxygen-hemoglobin dissociation curve → Bohr effect ↑ temperature ▪ Very metabolically active tissue (e.g. active muscle → ↑ heat production → ↓ hemoglobin oxygen affinity) Figure 71.3 The oxygen-hemoglobin dissociation curve. O2 saturation is influenced by the PO2 of the blood. P50 indicates the partial pressure at which hemoglobin proteins are 50% saturated. ↑ 2,3-diphosphoglycerate (2,3-DPG) concentration ▪ 2,3-DPG (glycolysis byproduct) → binds deoxyhemoglobin beta chains → ↓ oxygen affinity → binds to hemoglobin beta chains → oxygen unloading ▪ 2,3-DPG production ↑ under hypoxic conditions (e.g. living at high altitude) → OSMOSIS.ORG 613
hypoxemia → 2,3-DPG production in red blood cells → greater oxygen delivery to tissues LEFT SHIFT ▪ Left shift → higher oxygen affinity → 50% saturation occurs at lower PO2 → impairs oxygen unloading ↓ PCO2, ↑ pH ▪ ↓ tissue metabolism → ↓ CO2 production → ↓ H+ concentration → ↑ pH → left shift → O2 tightly bound to hemoglobin ↓ temperature ▪ ↓ tissue metabolism → ↓ heat production → ↓ O2 unloading ↓ 2,3-DPG concentration ▪ ↓ tissue metabolism → ↓ 2,3-DPG concentration → ↓ O2 unloading Hemoglobin F ▪ Alternate molecular structure → ↑ oxygen affinity → left shift ▪ 2,3-DPG doesn’t bind strongly to HbF gamma chains Carbon monoxide (CO) ▪ Causes left shift, ↓ maximum saturation possible (curve levels off at lower PO2) ▪ CO binds to hemoglobin with 250x affinity of O2 (at partial pressure; 1/250 O2, = O2; CO bound to hemoglobin) → forms carboxyhemoglobin (longer-living molecule than oxyhemoglobin) ▪ CO binding to heme → confirmation shift → ↑ remaining heme molecules’ affinity for oxygen (reducing oxygen release efficiency) → CO poisoning reduces blood’s absolute oxygen-carrying capacity, impairs oxygen release → hypoxic injury Figure 71.4 Summary of factors that can shift the oxygen-hemoglobin dissociation curve to the left (↑ hemoglobin's affinity for O2) and to the right (↓ hemoglobin's affinity for O2). 614 OSMOSIS.ORG
Chapter 71 Respiratory Physiology: Gas Transport ERYTHROPOIETIN (EPO) ▪ Glycoprotein cytokine secreted by kidney (cellular hypoxia response) → stimulates erythropoiesis → RBCs RENAL INDUCTION OF EPO SYNTHESIS ▪ ↓ O2 delivery to kidneys (↓ hemoglobin concentration/PaO2) → increased production of alpha subunit of hypoxiainducible factor 1 (HIF1) ▪ Hypoxia-inducible factor 1-alpha (HIF1A) → acts on fibroblasts in renal cortex, medulla → upregulation of EPO messenger RNA (mRNA) → increased EPO synthesis ▪ EPO → promotes proerythroblast differentiation → mature to form erythrocytes (maturation not EPOdependent) RENAL SENSING OF HYPOXIA ▪ To effectively regulate EPO secretion, kidneys must distinguish between following: Decreased blood flow ▪ → ↓ O2 availability ▫ ↓ renal blood flow → ↓ glomerular filtration → ↓ sodium (Na+) filtration/ reabsorption → ↓ O2 consumption (Na+ resorption closely linked to O2 consumption in kidney) ▫ O2 delivery, consumption remain matched → EPO production not triggered Decreased arterial blood O2 content ▪ → ↓ O2 availability ▫ Renal blood flow remains normal → normal glomerular filtration → normal Na+ filtration/reabsorption → reduced oxygen availability for given metabolic demand → stimulus for EPO secretion CARBON DIOXIDE TRANSPORT IN BLOOD ▪ Carried as dissolved carbon dioxide (CO2), carbaminohemoglobin (bound to hemoglobin), bicarbonate (HCO3-) DISSOLVED CO2 ▪ Small fraction of CO2 dissolved in blood (similar to oxygen) ▪ Henry’s law: CO2 concentration in blood = partial pressure x solubility of CO2 ▪ Solubility: 0.07mL CO2/100mL blood per mmHg ▪ Partial pressure: 40mmHg ▪ Concentration = 2.8mL CO2/100mL blood (5% of total CO2 content of blood) CARBAMINOHEMOGLOBIN ▪ CO2 binds to terminal amino groups on proteins (e.g. albumin, hemoglobin) ▪ CO2 bound to hemoglobin → carbaminohemoglobin (3% of total blood CO2) ▫ CO2 binding to hemoglobin at different site than oxygen → conformational shift of protein structure → ↓ oxygen affinity OSMOSIS.ORG 615
→ right shift in dissociation curve ▫ Haldane effect: less O2 bound to hemoglobin → ↑ CO2 affinity BICARBONATE ▪ 90% of CO2 in blood ▪ Tissue level: CO2 produced by aerobic metabolism → driven by partial pressure gradient → CO2 diffuses across cell membrane, capillary wall → enters RBCs RBC blood pH regulation ▪ RBCs regulate blood pH via interaction with CO2 in blood ▪ RBCs contain enzyme, carbonic anhydrase → catalyzes conversion of CO2, water → carbonic acid (also catalyzes reverse reaction) ▪ Carbonic acid dissociates into bicarbonate, hydrogen ion in blood ▫ CO2 + H2O ⇌ H2CO3 ⇌ HCO3- + H+ ▫ Mass action drives reaction to right as tissues continuously supply CO2 ▪ H2CO3 dissociates → H+, HCO3▪ H+ remains in RBCs → buffered by deoxyhemoglobin ▫ If H+ remains free in solution → acidifies RBCs, venous blood → H+ must be buffered ▫ H+ buffered by deoxyhemoglobin, carried in venous blood (deoxyhemoglobin more efficient buffer than oxyhemoglobin) ▫ H+ production favors oxyhemoglobin conversion → deoxyhemoglobin (Bohr effect) ▪ HCO3- transported into plasma (exchanged for chloride) ▫ Band 3 protein facilitates anion exchange of Cl- for HCO3- (chloride shift) ▫ HCO3- carried in plasma to lungs Respiratory system blood pH regulation ▪ Respiratory system further regulates blood pH ▫ Controls CO2 elimination rate → CO2 elimination ↑ pH by shifting equation to left ▫ RBCs, carbonic anhydrase allow rapid reaction in lungs → reverse processes in blood at tissue level Figure 71.5 CO2 transport in the form of bicarbonate. CO2 undergoes a chemical reaction with H2O to form carbonic acid, which then dissociates into hydrogen ions and bicarbonate ions. This reaction can occur in the plasma, but is sped up in red blood cells by the presence of carbonic anhydrase enzymes. Ionic exchange of bicarbonate ions and chloride occurs via facilitated diffusion to ensure charges stay balanced. Bicarbonate then travels to the lungs in the plasma. 616 OSMOSIS.ORG
Chapter 71 Respiratory Physiology: Gas Transport REGULATION OF PULMONARY BLOOD FLOW ▪ Regulated by altering arteriole resistance → controlled by arteriolar smooth muscle tone ▪ Regulatory changes mediated by local vasoactive substance concentrations PULMONARY VASOACTIVE SUBSTANCES & STATES Nitric oxide (NO) ▪ Retains similar function on pulmonary vascular beds (compared to systemic) → vasodilation ▪ Nitric oxide (NO) synthase inhibition → hypoxic vasoconstriction enhancement ▪ Inhaled NO → reduction in/prevention of hypoxic vasoconstriction Thromboxane A2 ▪ Product of arachidonic acid metabolism via cyclooxygenase pathway (macrocytes, leukocytes, endothelial cells) ▪ Lung injury → potent vasoconstrictor of pulmonary arterioles, veins Prostaglandin I2 (prostacyclin) ▪ Product of arachidonic acid metabolism via cyclooxygenase pathway (endothelium) ▪ Potent local vasodilator Leukotrienes ▪ Product of arachidonic acid metabolism via lipoxygenase pathway ▪ Potent airway constrictor LUNG VOLUME ▪ Pulmonary blood vessels → alveolar capillaries that surround alveoli, extraalveolar vessels which do not (arteries, veins) Increased lung volume ▪ Crushes alveolar capillaries → ↑ resistance to blood flow ▪ Intrapleural pressure becomes more negative (↓ resistance) → pulls open extra alveolar vessels ▪ Total pulmonary vascular resistance: sum of alveolar, extra-alveolar resistance → increased lung volume effect dependent on larger effect ▫ Low lung volumes (extra-alveolar vessels dominate) → ↑ volume → extra-alveolar vessels pulled open → ↓ resistance ▫ High lung volume (alveolar capillaries dominate) → ↑ lung volume → alveolar vessels crushed, sharp ↑ resistance Figure 71.6 Blood vessel resistance associated with increased lung volume. OSMOSIS.ORG 617
ZONES OF PULMONARY BLOOD FLOW POSITIONAL EFFECT ▪ Supine gravitational effect largely uniform ▪ Upright distribution of blood flow (perfusion), ventilation throughout lungs not uniform ▪ Blood flow favors gravity-dependent lung regions → ↑ pulmonary arterial hydrostatic pressure moving inferiorly → blood flow in inferior (basal) regions > superior (apical) regions ▪ Ventilation favors apices → ventilation ↓ with move towards bases of lungs LUNG ZONES ▪ Lungs divided into three vertical sections (based on pressure differences between compartments) ▪ PA generally = atmospheric pressure; can be overcome by low-pressure lung circulation ▪ Positive pressure ventilation → PA > Pa in apices of lung → blood vessels collapse → physiological dead space (ventilated, not perfused) Zone II ▪ Pa > PA > pulmonary venous pressure (PV) ▪ Capillary compression not problematic ▪ Perfusion driven by difference between Pa, PA (not Pa, PV; as in systemic vascular beds) Zone III ▪ Majority of healthy lung volume ▪ No external resistance to blood flow ▪ Flow determined by Pa - PV (both exceed PA) Zone I ▪ Unobserved in healthy lung: pulmonary arterial pressure (Pa) > alveolar pressure (PA) in all parts of lung Figure 71.7 Relationships between PA, Pa, and Pv in the three lung zones. 618 OSMOSIS.ORG
Chapter 71 Respiratory Physiology: Gas Transport PULMONARY SHUNTS ▪ Shunts occur when blood flow redirected from expected route, bypassing circulatory conduit PHYSIOLOGICAL SHUNTS (ANATOMICALLY NORMAL) ▪ Bronchial blood flow: fraction of pulmonary blood which bypasses alveoli to supply bronchi ▪ Coronary blood flow: thebesian venous network allows for alternative myocardium drainage directly into left ventricle (not reoxygenated) LEFT-TO-RIGHT SHUNTS ▪ More common ▪ Blood shunted from left to right heart ▫ Due to septal defects (e.g. trauma, patent ductus arteriosus) ▪ Blood intended for systemic circulation directly circulated back to lungs → pulmonary blood flow exceeds systemic blood flow → fraction of blood does reach systemic circulation fully oxygenated → no hypoxia Figure 71.8 Physiologic shunts. OSMOSIS.ORG 619
RIGHT-TO-LEFT SHUNTS ▪ Defect in wall between right, left sides of heart → blood shunted from right to left side of heart ▪ Allows for large cardiac output fraction to be shunted (approx. 50%) → bypasses lungs → oxygenated blood diluted with shunted deoxygenated blood → hypoxemia ▪ Not responsive to high PO2 gas treatment → complete pulmonary blood saturation doesn’t improve shunted blood oxygenation ▪ Causes minimal PaCO2 change → central chemoreceptors responsive to small PaCO2 increases (shunted blood not available for gas exchange) → ↑ ventilation rate → extra CO2 expired ▪ Central O2 receptors significantly less sensitive than CO2 receptors → only ↑ ventilation once PaO2 < 60mmHg Shunt fraction equation ▪ Oxygenation bypass of venous blood in lung capillaries ▪ QS/QT = (CCO2 - CAO2)/(CCO2 - CVO2) ▪ QS: blood flow through right-to-left shunt (L/min) ▪ QT: cardiac output (L/min) ▪ CCO2: oxygen content of nonshunted pulmonary capillary blood ▪ CaO2: oxygen content of systemic arterial blood ▪ CVO2: oxygen content of venous blood Figure 71.9 Pathologic shunts occurring in the left-to-right (more common) and right-to-left directions. 620 OSMOSIS.ORG
Chapter 71 Respiratory Physiology: Gas Transport VENTILATION PERFUSION RATIOS & V Q MISMATCH ▪ Ratio of amount of air to amount of blood reaching alveoli per minute (V̇ /Q̇ ratio) IDEAL SCENARIO ▪ Oxygen provided saturates blood fully → ratio of 1 NORMAL SCENARIO ▪ Average across entire lung → ratio of 0.8 (apex higher, bases lower) ▪ Normal breathing rate, tidal volume, cardiac output DEFECTS ▪ Mismatching between ventilation, perfusion → abnormal gas exchange Dead space ▪ Ventilation of lung regions not perfused ▪ No gas exchange (no blood to facilitate gas exchange) ▪ Alveolar gas same composition as humidified inspired air (PAO2 = 150mmHg, PACO2 = 0) ▪ Pulmonary embolism High V̇/Q̇ ▪ High ventilation relative to perfusion (ventilation wasted) ▪ Usually due to ↓ blood flow (limited blood flow → limited gas exchange) ▪ Relatively high ventilation → pulmonary capillary blood with high PO2, low PCO2 ▪ Emphysema Low V̇/Q̇ ▪ Low ventilation relative to perfusion (perfusion wasted) ▪ Usually due to ↓ ventilation → pulmonary capillary blood with low PO2, high PCO2 ▪ Asthma, chronic bronchitis, pulmonary edema, etc. Right-to-left shunt ▪ Perfusion of lung regions not ventilated ▪ No gas exchange occurs (no gas available to exchange) ▪ Same blood composition as mixed venous blood (PaO2 = 40mmHg, PaCO2 = 46mmHg) ▪ Airway obstruction, right-to-left cardiac shunts, etc. Figure 71.10 Normal V̇ /Q̇, Pa, and PA compared to pulmonary embolism and airway obstruction. OSMOSIS.ORG 621
HYPOXEMIA & HYPOXIA HYPOXEMIA ▪ Decrease in arterial PaO2 High altitude ▪ Barometric pressure is decreased → decrease in PO2 of inspired air → decreased PAO2 ▪ Equilibration of alveolar air, pulmonary capillary blood (normal) ▪ Systemic arterial blood achieves same (lower) PO2 of alveolar air ▪ Normal alveolar–arterial (A–a) gradient ▪ High altitude breathing supplemental O2 → raised inspired PO2 → raised PAO2 → raised PaO2 Hypoventilation ▪ Less inspired fresh air → decrease in PAO2 ▪ Normal equilibration → pulmonary capillary blood achieves same (lower) PAO2 as A–a gradient ▪ Hyperventilation: breathing supplemental O2 → raised PAO2 → raised PaO2 622 OSMOSIS.ORG Diffusion defects (fibrosis, pulmonary edema) ▪ Increased diffusion distance/decreased surface area → impaired equilibration ▪ Normal PAO2, decreased PaO2 → ↑ A–a gradient ▪ Breathing supplemental O2 → raised PAO2 → increased driving force for diffusion → raised PaO2 Ventilation/perfusion mismatches ▪ Regions of well-ventilated (high PAO2), poorly-ventilated (low PAO2), well-perfused, poorly-perfused lung ▪ Poor perfusion to well-ventilated areas, adequate perfusion to areas poorly ventilated → low PaO2 ▪ Supplemental oxygen → raised PAO2 in poorly-ventilated areas with adequate perfusion → increase in PaO2 ▪ ↑ A–a gradient
Chapter 71 Respiratory Physiology: Gas Transport Right-to-left shunts (right-to-left cardiac shunts, intrapulmonary shunts) ▪ Shunted blood completely bypasses alveoli, cannot equilibrate ▪ Shunted blood mixes with, “dilutes” blood that did pass through alveoli → ↓ PaO2 (even if PAO2 normal) ▪ ↑ A–a gradient ▪ Limited supplemental O2 effect → raises PAO2, PaO2 of nonshunted blood, does not address underlying shunted blood/ oxygenated blood mixing → larger shunt, less effective supplemental O2 HYPOXIA ▪ ↓ O2 delivery to/utilization by tissues ▪ O2 delivery → determined by cardiac output, O2 content of blood ▪ ↓ cardiac output/localized blood flow → hypoxia ▪ Hypoxemia (any cause) → ↓ PaO2 → ↓ hemoglobin saturation → ↓ oxyhemoglobin concentration in blood → ↓ oxygen delivery to tissues → hypoxia ▪ Anemia (↓ hemoglobin concentration) → ↓ oxyhemoglobin concentration in blood → decreased oxygen delivery to tissues → hypoxia ▪ Carbon monoxide poisoning → irreversible binding with hemoglobin → ↓ oxyhemoglobin concentration in blood → ↓ oxygen delivery to tissues → hypoxia ▪ Cyanide poisoning → interferes with O2 utilization on cellular level HYPOXIC VASOCONSTRICTION ▪ Alveolar partial pressure of oxygen (PAO2) major factor controlling pulmonary blood flow ▪ ↓ PAO2 → vasoconstriction (opposite to systemic vasculature where ↓ in PaO2 → vasodilation) ▫ Vasoconstriction in response to poor oxygenation ensures blood flow coupled to areas of good ventilation → optimal gas exchange ▫ In localized lung disease, areas of poorly-ventilated, diseased lung circumvented → blood directed towards healthy lung OSMOSIS.ORG 623
Alveolar PO2 direct action on vascular smooth muscle → hypoxic vasoconstriction ▪ Pulmonary microcirculation surrounds alveoli ▪ O2 highly lipid soluble → permeable across cell membranes ▪ Normal PAO2 (100mmHg), O2 diffuses from alveoli → arteriolar smooth muscle → maintains relaxation, dilation of arterioles ▪ PAO2 decreases (70–100mmHg) → vascular smooth muscle sense change (hypoxia) → vasoconstriction → ↓ pulmonary blood flow to region ▫ Vasoconstriction mechanism likely due to hypoxia → vascular smooth muscle depolarization → voltage-gated calcium channels open → calcium enters smooth muscle → contraction HIGH ALTITUDE & HYPOXIC VASOCONSTRICTION ▪ Entire lung exposed to ↓ PAO2 (e.g. high altitudes) → global ↑ in pulmonary arteriolar resistance → ↑ pulmonary vascular resistance ▪ Chronic ↑ pulmonary vascular resistance → ↑ right heart afterload → right heart hypertrophy 624 OSMOSIS.ORG FETAL HYPOXIC VASOCONSTRICTION ▪ Fetal circulation must acquire oxygen from maternal circulation via placenta → significantly lower PaO2 → fetal lung vasoconstriction → reduction of blood flow to lungs (15% of cardiac output) ▪ At birth low pressure placenta circuit removed → ↑ systemic blood pressure → first breath after birth → ↑ PAO2 → 100mmHg → ↓ hypoxic vasoconstriction → ↓ pulmonary vascular resistance → pulmonary blood flow begins to normalize

Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Gas Transport essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Gas Transport by visiting the associated Learn Page.