Oxygen Transport Studies PDF
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Tamethia Perkins
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These lecture notes cover oxygen transport, including factors influencing total oxygen delivery, arterial-venous oxygen content difference, oxygen consumption, oxygen extraction ratio, and mixed venous oxygen saturation. This document also discusses pulmonary shunting, shunt-like effects, and oxygen transport-related clinical cases. They are suitable for medical or respiratory therapy students.
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OXYGEN TRANSPORT Tamethia Perkins MS, RRT-NPS, RRT-ACCS RT 3005/6005 OXYGEN TRANSPORT STUDIES Oxygen Transport Studies ◼ Total oxygen delivery ◼ Arterial-venous oxygen content difference ◼ Oxygen consumption ◼ Oxygen extraction ratio ◼ Mixed venous oxygen saturati...
OXYGEN TRANSPORT Tamethia Perkins MS, RRT-NPS, RRT-ACCS RT 3005/6005 OXYGEN TRANSPORT STUDIES Oxygen Transport Studies ◼ Total oxygen delivery ◼ Arterial-venous oxygen content difference ◼ Oxygen consumption ◼ Oxygen extraction ratio ◼ Mixed venous oxygen saturation ◼ Pulmonary shunting TOTAL OXYGEN DELIVERY ◼ Depends on: ◼ Body’s ability to oxygenate the blood. ◼ [Hb] ◼ Q ◼ DO2 = QT x (CaO2 x10) = ◼ 5 L/min x (20 vol% x 10)=1000 mL O2/min C (a-v)O2 ◼ CvO2 is normally computed from a PAC. ◼ C(a-v)O2 = CaO2 – CvO2 ◼ Normal = 20 vol% - 15 vol% = 5 vol%. ◼ 5 mL of oxygen are extracted from each 100 mL of blood for tissue metabolism (50mL O2/L). ◼ Q= 5L/min =250 mL of oxygen are extracted from the blood in a minute. OXYGEN CONSUMPTION ◼ Amount of oxygen extracted by the tissues in one minute. (VO2) ◼ VO2 = QT [C(a-v)O2 x 10] ◼ VO2 = 5L/min x 5 vol% x 10 ◼ VO2 = 250 mL O2/min ◼ VO2 is normally indexed to consider patient’s BSA. ◼ Normal average: 125-165 mL O2/m2. OXYGEN EXTRACTION RATIO (O2ER) ◼ Amount of O2 extracted by the tissues divided by total O2 delivered to the tissues. ◼ Also called oxygen coefficient ratio. ◼ O2ER = C(a-v)O2/CaO2 ◼ O2ER = 5 vol%/20 vol% ◼ O2ER =.25 ◼ Under normal circumstances, Hb returns to the alveoli approximately 75% saturated with O2. ◼ For 1L of DO2, 250 mL are metabolized by the tissues and 750 mL return to the lungs O2ER Clinical Case ◼ If a patient has a CaO2 of 10 vol% and a CvO2 of 5 vol%: ◼ C(a-v)O2 = 5 vol% ◼ O2ER = 5 vol%/10 vol% ◼ O2ER = 50% vs. 25% normal ◼ Dangerous oxygen transport status. MIXED VENOUS O2 SATURATION ◼ Changes in SvO2= early indicator of changes in patient’s C(a-v)O2. VO2, and O2ER. ◼ Normal SVO2: 75%, but >65% is acceptable. MECHANISMS OF PULMONARY SHUNTING ◼ Pulmonary shunting: ◼ Portion of the cardiac output that enters the L side of the heart without gas exchange (true shunt) or ◼ Blood that exchanges gases but does not obtain a normal PaO2 (shunt-like effect). ◼ Physiologic effect of shunt: HYPOXEMIA. True Shunt ANATOMIC ◼ 2-5% of cardiac output. ◼ Bronchial, pleural and Thebesian veins. ◼ Abnormalities that cause anatomic shunting: ◼ Congenital heart disease ◼ Intrapulmonary fistula ◼ Vascular lung tumors True Shunt CAPILLARY ◼ Caused by: ◼ Alveolar collapse or atelectasis ◼ Alveolar fluid accumulation ◼ Alveolar consolidation ◼ SUM OF ANATOMIC AND CAPILLARY SHUNTS = TRUE OR ABSOLUTE SHUNT= REFRACTORY TO O2 THERAPY Shunt-Like Effect ◼ When capillary perfusion exceeds alveolar ventilation. ◼ Common causes: ◼ Hypoventilation ◼ Bronchospasm or mucus plugging ◼ ACM diffusion defects ◼ CONDITIONS CORRECTED WITH O2 THERAPY VENOUS ADMIXTURE ◼ It is the end result of pulmonary shunting. SHUNT EQUATION ◼ Qs/Qt:Cco2-Cao2/Cco2-Cvo2 ◼ Necessary information: ◼ PB ◼ PaO2 ◼ PaCO2 ◼ PvO2 ◼ Hb ◼ PAO2 ◼ FiO2 ◼ SaO2 ◼ SvO2 CASE STUDY ◼ 38 yom on volume-cycled ventilation. ◼ PB mmHg ◼ FiO2.70 ◼ Hb: 13g% ◼ PaO2: 50 mmHg (SaO2 85%) ◼ PaCO2: 43 mmHg ◼ PvO2: 37 mmHg (SvO2 65%) ◼ PAO2:438.35 mmHg ◼ CcO2: (Hbx1.34)+(PAO2x0.003) ◼ 18.73 vol% ◼ CaO2:14.43 vol% ◼ CvO2:11.43 vol% ◼ Qs/Qt= 18.73-14.95/18.73-11.43 ◼.517 = 52% shunt CLINICAL SIGNIFICANCE ◼ Normal shunt: 30%: potentially life- threatening. TABLES FOR REVIEW Factors that Increase the C(a-v)O2 Decreased Cardiac Output Periods of Increased O2 consumption * Exercise * Seizures * Shivering * Hyperthermia Factors that Decrease the C(a-v)O2 Increased Cardiac Output Skeletal relaxation Certain poisons Hypothermia Factors that Increase O2 Consumption Exercise Seizures Shivering Hyperthermia Factors that Decrease the O2 consumption Increased Cardiac Output Skeletal relaxation Certain poisons Hypothermia Factors that Increase the O2ER Decreased Cardiac Output Periods of Increased O2 consumption * Exercise * Seizures * Shivering * Hyperthermia Anemia Decreased arterial oxygenation Factors that Decrease the SVO2 Decreased Cardiac Output Periods of Increased O2 consumption * Exercise * Seizures * Shivering * Hyperthermia Factors that Increase the SVO2 Increased Cardiac Output Skeletal relaxation Certain poisons Hypothermia TISSUE HYPOXIA ◼ Inadequate level for cellular metabolism. ◼ Four types: ◼ Hypoxic hypoxia ◼ Anemic hypoxia ◼ Circulatory hypoxia ◼ Histotoxic hypoxia Hypoxic Hypoxia ◼ hypoxemic hypoxia. ◼ PaO2 and CaO2 are abnormally low. Hypoxic Hypoxia ◼ It can develop from pulmonary shunting and from: ◼ Low PAO2 ◼ Hypoventilation ◼ High altitudes ◼ Breathing gas mixtures with < than 21% O2. ◼ Diffusion impairment ◼ Interstitial fibrosis, alveolar consolidation, interstitial and/or alveolar edema. ◼ Ventilation/Perfusion Mismatch (V/Q) ◼ Capillary blood flow is in excess of alveolar ventilation. Shunt-like effect. Anemic Hypoxia ◼ Normal PaO2, but O2 carrying capacity of the blood is inadequate. ◼ It can develop from: ◼ Low Hb ◼ Deficiency in the ability of Hb to carry O2 (CO poisoning). ◼ Main compensatory mechanism for anemic hypoxia: increase cardiac output. Circulatory Hypoxia ◼ Normal PaO2 and CaO2 but inadequate blood flow. ◼ Main causes: ◼ Stagnant hypoxia ◼ Arterio-venous shunting ◼ STAGNANT HYPOXIA ◼ Peripheral capillary blood flow is slow such as in decreased cardiac output, vascular insufficiency. It causes a decrease in SvO2. ◼ ARTERIO-VENOUS SHUNT ◼ Blood bypasses tissue cells and moves into the venous system. ◼ No O2 delivery to the tissues. Histotoxic Hypoxia ◼ Any condition that impairs the ability of tissue cells to utilize O2. ◼ Cyanide poisoning. ◼ PaO2 and CaO2 are normal but tissue cells are hypoxic. ◼ PvO2, CvO2 and SvO2 are elevated because oxygen is not utilized. CYANOSIS ◼ In cases of severe hypoxemia. ◼ Purplish discoloration seen on mucous membranes, fingertips, and toes. ◼ Present when blood has at least 5g% of reduced Hb. ◼ Normal Hb 14-15g%, PaO2 97-100 mmHg, 20 vol%. CYANOSIS ◼ In a cyanotic patient with 5g% of reduced Hb, PaO2 will be 30 mmHg, and there will be 13vol% of O2 in the blood. ◼ In a polycythemic patient, cyanosis may be present at a PaO2 above 30 mmHg since the amount of reduced Hb is greater than 5g% and CaO2 is usually 20vol%. POLYCYTHEMIA ◼ Abnormal increase in the RBC number. ◼ Pulmonary disorders that induce chronic hypoxemia. ◼ Erythropoietin responds stimulating bone marrow to increase RBC production. ◼ Increased viscosity of the blood, higher P to overcome R = L or R ventricular hypertrophy = failure.