Chapter 12 Gas Exchange PDF

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CuriousPlaytpus

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San Joaquin Valley College - Visalia

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gas exchange oxygen transport alveoli physiology

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This document provides a detailed overview of gas exchange within the human body, covering alveolar gas tensions, diffusion mechanisms, and the factors affecting oxygen loading and unloading. It also discusses ventilation/perfusion ratios, and factors influencing oxygen transport and hemoglobin saturation. The document will be useful for students, particularly in the fields of physiology and medicine.

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Terminology pH: Measures the balance of acids and bases in the blood. Normal: 7.35 - 7.45. PaO2: Measures the partial pressure of O2 in the blood. PAO2: Measures the partial pressure of oxygen in the alveoli. PaCO2: Measures the partial pressure of Carbon dioxide in the blood. SaO2: The calculated...

Terminology pH: Measures the balance of acids and bases in the blood. Normal: 7.35 - 7.45. PaO2: Measures the partial pressure of O2 in the blood. PAO2: Measures the partial pressure of oxygen in the alveoli. PaCO2: Measures the partial pressure of Carbon dioxide in the blood. SaO2: The calculated arterial oxygen saturation. Determinants of Alveolar Gas tensions Alveolar Carbon Dioxide: PACO2 Varies directly with the body’s production of carbon dioxide (CO2) and inversely with alveolar ventilation (VA). Normal: 34-45 mmHg. What will happen? ​ PACO2 will increase above normal if CO2 production increases while alveolar ventilation remains constant. ​ Increase in dead space (ventilation w/o perfusion) can lead to increase PACO2. ​ PACO2 decreases if CO2 production decreases or alveolar ventilation increases. ​ If CO2 production increases, ventilation automatically increases in order to maintain the PACO2 within normal range. Alveolar air Equation (PAO2) ​ Gas fully saturated with water vapor at BTPS is 47 mmHg ​ Moving into the alveoli, the PO2 is less because it contains water vapor and CO2 ​ Healthy PCO2: 35-45 mmHg ​ O2 diffuses out of the alveoli faster than CO2 diffuses into it. ​ Constant FIO2, PAO2 varies inversely with PACO2 ​ Prime determinant of PACO2 is VA (Ventilate more) Mechanisms of Diffusion Diffusion occurs along pressure gradients Barriers to diffusion, A/C membrane has 3 main barriers: ​ Alveolar epithelium ​ Interstitial space and its structures ​ Capillary endothelium RBC membrane Fick’s law: The greater the surface area, diffusion constant, and pressure gradient, the more diffusion will occur. Mechanism of gas diffusion Given that the area of and distance across the alveolar-capillary membrane are relatively constant in healthy people, diffusion in the normal lungs depends on gas pressure. Pulmonary diffusion gradients: Diffusion occurs along pressure gradients. Time limits to diffusion: ​ Pulmonary blood is normally exposed to alveolar gas for 0.75 (takes this much to diffuse), during exercise may fall 0.25 second. ​ Normally equilibrium occurs in 0.25 second. ​ With diffusion limitation or blood exposure time of less than 0.25 seconds, there may be inadequate time for equilibration. Under normal resting conditions, blood moves through the alveolar capillary membrane in approx. 0.75 seconds. During exercise, or stress, total transit time for blood through the alveolar capillary membrane is less than normal. When rate of diffusion is decreased because of alveolar thickening, oxygen equilibrium likely will not occur. Shunting (Perfusion without ventilation) Ventilation and perfusion is not perfect in the normal lungs. PaO2 is normally 5-10 mmHg less than PAO2 because of shunts: condition where deoxygenated blood bypasses gas exchange in the lungs, resulting in a reduction of oxygen in the blood ​ Anatomical (Right to left shunts) -​ Bronchial venous drainage -​ Thebesian venous drainage A-a gradient (PAO2-PaO2) or P(a-a)O2 Measures the difference between Alveolar and arterial PO2; How well oxygen is moving from the alveoli to the blood. The normal A-a gradient is less than 20 mmHg It can help determine the cause of hypoxemia. ​ It indicates the efficiency of gas exchange. ​ Estimates the degree of hypoxemia and shunting: 5-10 mmHg on 21% = Normal 25 - 65 mmHg = V/Q Mismatch > 300 mmHg = Shunt PAO2-PaO2 : If increased, then there is an abnormal O2 exchange: ​ A small difference between alveolar and arterial O2 is due to the small number of veins carrying deoxygenated blood that bypasses the lungs and empties into arterial circulation. Normal Variations from Ideal Gas Exchange Ventilation / Perfusion ratio: Ideal is 1, where VQ is in perfect balance Areas with ventilation and NO blood flow is called dead space: ​ Alveolar dead space causes increases in PE (pulmonary embolism, partial destruction of the pulmonary vasculature, destroyed pulmonary vasculature (like in COPD) and reduced cardiac output. ​ Anatomic dead space which is the portion of VT that never reaches the alveoli for gas exchange. If ventilation and blood flow are mismatched (V/Q Mismatch): Impairment of both O2 and CO2 transfer occurs. -​ If VENTILATION exceeds perfusion: V/Q is greater than 1 -​ If PERFUSION exceeds ventilation: V/Q is less than 1 -​ Ventilation with 0 blood flow = Alveolar dead space (Increases PO2 and lowers alveolar PCO2) -​ Lower alveolar PO2 increased PaCO2: Perfusion but no ventilation -​ Decreased ventilation causes: Hypoxic vasoconstriction in pulmonary capillary -​ Ventilation is decreased to the affected lobe with Pneumonia To sum it up: -​ Physiological dead space = Ventilation with reduced perfusion. Causes: Pulmonary embolism, Pulmonary arteritis, Necrosis or Fibrosis (Loss of capillary bed) -​ Normal = Ventilation and perfusion -​ Physiological Shunt = Perfusion with ventilation reduces. Causes: Airway limitation (Asthma and COPD), Lung collapse or consolidation, Loss of elastic tissue (emphysema) Disease of the chest wall. Oxygen Transport Oxygen is transported into 2 forms: dissolved and bound. ​ Dissolved: Physically dissolved in plasma: Gaseous oxygen enters blood and dissolves. Henry’s law allows calculation of amount dissolved: Dissolved O2 (ml/dl) = PO2 x 0.003 ​ Chemically bound to hemoglobin (Hb): A majority is carried here. Each gram of Hb can bind 1.34 ml of oxygen. 70 times more O2 transported than dissolved. ​ Hemoglobin saturation: Saturation is % of Hb that is carrying oxygen compared to total Hb: Normal is 95-100% -​ SaO2 = (HbO2/total Hb) x 100 O2 HB curve LEFT RIGHT Increase affinity. Decreased Affinity Increase PH (Alkalosis). Decrease Acidosis Decrease PaCO2. Increase PaCO2 Decrease Body Temperature. Increase Temperature Decrease 2-3 DPG. Increase 2-3 DPG Affinity: Whether or not the Hb holds onto or releases oxygen from the Hb either associates or dissociates. An increased hemoglobin’s affinity for oxygen; O2 strongly binds to hemoglobin and is less available to the tissues. Decrease in hemoglobin’s affinity for O2: Allows hemoglobin to easily off-load O2 to the peripheral tissues. Factors affecting O2 loading and unloading ​ HbO2 curve ​ pH (Bohr effect): Describes the effect pH has on Hb affinity for O2. pH alters position of HbO2 curve (Low pH shifts curve to right, high pH shifts to left). It enhances o2 transport: at tissue, pH is 7.37 more O2 unloaded. At lungs, pH 7.4 shift back left, enhancing O2 loading. ​ Body temperature: When body temperature is higher, right shift facilitates, more oxygen unloads to meet metabolic demands. When lower metabolic demands, curve shifts left, because not much o2 is required. ​ 2-3 DPG (Diphosglycerate): Found in RBCs. Stabilizes deoxygenated Hb, decreasing O2’s affinity for Hb. Without 2-3 DPG, O2 cannot unload. -​ Increase 2-3 DPG, promotes O2 unloading: Alkalosis, Chronic hypoxemia, anemia can increase 2-3 DPG -​ Decrease 2-3 DPG, promotes O2 loading: stored blood loses 2-3 DPG, large transfusion can significantly impair tissue oxygenation. ​ Abnormal hemoglobins: HbS (Sickle cell) leads to hemolysis or destruction of RBC and thrombi. ​ Methemoglobin (metHb): abnormal iron (FE3+) cannot bind with oxygen and alters HbO2 affinity (left shift). Commonly caused by NO, nitroglycerin, lidocaine. ​ Carboxyhemoglobin (HbCO): Hb binds CO, has 200 times >Hb affinity than O2 - Carbon monoxide poisoning. Displaces O2 and shifts curve left: O2 cannot unload; Treated with hyperbaric therapy or 100% O2. Abnormalities of Gas transport Impaired O2 delivery: DO2 = CaO2 x CO (Cardiac Output) -​ DO2 = The rate of O2 delivery in milliliters per minute -​ CO = Cardiac output -​ CaO2 = arterial oxygen content. When DO2 is inadequate, tissue hypoxia ensues: Arterial blood oxygen (CaO2) leads to hypoxemia When Cardiac output or perfusion is decreased it can lead to shock or ischemia.. Hypoxemia: Abnormally low PaO2. Most common cause is V/Q mismatch. Other causes would be hypoventilation, diffusion defect, shunting, and low PiO2. Hemoglobin deficiencies: Anemias can be absolute or relative: -​ Absolute: Hb Deficiency occurs when the Hb concentration is lower than normal. -​ Relative: caused by either the displacement of O2 from normal Hb or the presence of abnormal Hb variants. Reduction in Blood Flow (Shock or Ischemia) -​ Circulatory failure (shock): Tissue O2 deprivation is widespread. Body tries to compensare by directing blood flow to the vital organs. -​ Local reductions in perfusion (ischemia): Can cause localized hypoxia (low blood o2). Can result in anaerobic metabolism, metabolic acidosis, and eventuality of affected tissues. Dysoxia: DO2 is normal but cells undergo hypoxia. Cells are unable to adequately utilize oxygen. -​ Cyanide poisoning prevents cellular use of O2 -​ In sepsis or ARDS o2 debt may occur at normal levels of DO2. Impaired CO2 removal: Disorders that decrease A relative to metabolic need impairs CO2 removal -​ Inadequate E (usually result of drug overdose) -​ Increased dead space ventilation (VD/VT) caused by increased physiologic dead space, as in pulmonary embolus. ​ Hb is a conjugated protein that has 4 linked polypeptide chains (the globin), each combined to a heme. Its shape contributed to its affinity of o2. ​ O2 binds to Hb via the FE+ with complete binding the Hb is converted to HbO2 (oxyhemoglobin) ​ Deoxygenated Hb shows characteristics of being a weak acid which is also used a buffer for H+ -​ Bright red color is arterial -​ Venous blood appears more deep purple. -​ Spectrophotometry (oximetry) we can measure the amount of Hb saturated. Hemoglobin Saturation Saturation is a measure of the proportion of available Hb that is carrying oxygen. ​ SaO2 = (HbO2/total Hb) x 100 (expressed as %) Oxygen transport Formula: CaO2 = (Hb x 1.34 x SaO2) + (PaO2 x 0.003) ​ Measures the oxygen delivered to the tissues or best index of oxygen transport. ​ The first part reflects oxygen bound to Hb ​ Second part reflects how much is dissolved in plasma. ​ Normal value: 17-20% Venous content (O2 Transport) CvO2 (mixed venous oxygen content) Formula: (Hb x 1.34 x SvO2) + (PvO2 x 0.003) Normal value: 14 vol % (12 - 16% Vol) ​ Total amount of oxygen carried in the mixed Venous blood ​ Blood is drawn from the pulmonary artery via the balloon-tip, flow directed (Swan-Ganz catheter)