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Explore the complexities of hypoxia and respiratory failure including classifications, mechanisms, consequences, and factors determining oxygenation. Learn about the interplay of oxygen transport, CO2 exchange, and the disturbed gas exchange in respiratory disorders.
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HYPOXIARESPIRATORY FAILURE M. Tatar
glucose 38 ATP Krebs´s cycle O2 CO2 H2O glucose 2 ATP lactate pyruvate
The aim of oxygen transport to preserve high PO2 gradient between capillaries andmitochondria Q x Hb conc. x (SaO2 – SvO2) O2 c circulation respiration ADP Hb afinity to O2 microcirculation erythropoiesis VO2 m
Classification of hypoxia (1) • Hypotonichypoxemichypoxia - PaO2, CaO2;Q . Hb . ( SaO2– SvO2) - carotid body stimulation, hyperventilation - pulmonaryhypertension in chronicform - respiratoryfailure 2. Izotonichypoxemichypoxia - normal PaO2, CaO2; Q . Hb . ( SaO2 – SvO2) - chemoreceptors are notstimulated, lack of dyspnea - anemia, carboxyhemoglobin
Hb concentration and CaO2 interrelationship 300 100 polycythemia Hb = 20 200 100 normal Hb = 15 CaO2 (ml/l) 150 SaO2 (%) 100 anemia Hb = 10 20 60 100 120 PaO2 (mmHg)
Classification of hypoxia (2) 3. Hypoextractive hypoxia - increased Hb afinity to O2 - Q . Hb . (SaO2 – SvO2) 100 released O2 SaO2 (%) 50 pH = 7,4; t = 37 °C pH 7,4; t 37 °C 614 PaO2 (kPa)
Classification of hypoxia (3) 4. Hypocirculatory hypoxia - Q . Hb . (SaO2 – SvO2) - ischemic, congestive; local, general 5. Overutilization hypoxia - demand of tissues for O2 excesses the available supply - angina pectoris, epilepsy (fatigue and cerebral depression) 6. Histotoxic hypoxia - disturbed ATP production, blocked oxidative phosphorylation - Q . Hb . (SaO2 – SvO2) - cyanide
Definition Syndrome characterized by disturbed exchange of oxygen and carbon dioxide in lung Consequences: PaO2 60 mmHg (8.0 kPa) with or without PaCO2 > 50 mmHg (6.7 kPa) - under resting condition - breathing atmospheric air at sea level Classification: 1. Hypoxemic (hypoxemia with normal or PaCO2) 2. Hypercapnic (hypoxemia and hypercapnia)
Factors determining oxygenation and CO2 exchange are different PaCO2 must be regarded as a function of ventilation of the entire lung (overall alveolar ventilation), without regard to local inequalities of distribution of ventilation and perfusion PaO2, on the other hand, depends not only on the amount of alveolar ventilation but also on the matching of ventilation and perfusion in individual compartments
Mechanisms responsible for gas exchange disorders A. intrinsic lung disorders (airways, lung parenchyma) 1. Ventilation/perfusion (V´/Q´) mismatch 2. Venous admixture 3. Diffusion impairment B. extrinsic lung disorders (respiratory centre, nerve pathways, respiratory muscles, thoracic cage, pleural space) 1. Alveolar hypoventilation (overall)
ventilatory drive 100 40 50 50 PaO2 PaCO2 120 30 70% chemoreceptors SaO2 100% hypoxemia normocapnia hypoxemia hypercapnia
Mechanisms of hypoxemia 1. alveolar hypoventilation 2. compartments with low V´/Q´ ratio 3. right-to-left shunting of blood in compartments with zero V´/Q´ratio 4. diffusion impairment due to thickening of the alveolar-capillary membrane
Diffusion impairment – oxygen saturation of arterial blood normal PcO2 12 impaired kPa exercise rest PvO2 4 0.8 s Er contact time with A-c membrane
Mechanisms enhancing hypoxemia Pure oxygen breathing - weakened hypoxic pulmonary vasoconstriction - resorptive atelectasis ( PAN2, resorption of O2) - central inspiratory drive
Mechanisms of hypercapnia 1. overall alveolar hypoventilation 2. critical amount of the compartments with low V´/Q´ ratio overall ventilation have to be increased to maintain effective alveolar ventilation (normal CO2 exchange) limits of effective alveolar ventilation - work of breathing - respiratory muscle fatigue - dead space ventilation