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Chapter 2 Normal Physiology: Hypoxia

Chapter 2 Normal Physiology: Hypoxia. Topics. Oxygen cascade from air-to-tissue Effects of reduced barometric pressure Alveolar ventilation equation Hyperventilation Acid-base changes Control of ventilation. Case Study #2: Bill. Mountain climber Hyperventilates on exposure to hypoxia

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Chapter 2 Normal Physiology: Hypoxia

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  1. Chapter 2Normal Physiology: Hypoxia

  2. Topics • Oxygen cascade from air-to-tissue • Effects of reduced barometric pressure • Alveolar ventilation equation • Hyperventilation • Acid-base changes • Control of ventilation

  3. Case Study #2: Bill • Mountain climber • Hyperventilates on exposure to hypoxia • What causes this? Is it good? Bad? • Alveolar gas equation • Relationship between PACO2 and PAO2 • pH effects • Oxygen transport • Blood-myocyte O2 exchange

  4. Case Study #2: Bill • Barometric pressure and altitude • Dalton’s law of partial pressures • PiO2 varies with PB • PiO2 = PB * 20.93 • SL: (760-47) * .2093 = 149 mmHg • Mt Everest: (250-47) * .2093 = 42.5 mmHg • 19,200 m: (47-47) * .2093 = 0

  5. Oxygen cascade: air to tissue • Po2 falls as it enters the body and ultimately reaches the tissues • Inspired air: 149 mmHg • Alveolar air: 100 • Arterial blood: ~100 • Capillary blood: 20-40 mmHg • Tissue: 5-20 • Mitochondria: <1

  6. Hyperventilation: secret weapon • Tidal volume is a composite of dead space and alveolar gas • However, all Co2 comes from the alveolar gas • Vco2 = VA * Fco2 • Pco2 = Fco2 * K • Pco2 = [Vco2/VA]*K • Alveolar ventilation eq. • PAO2 = PiO2 – [PACO2/R] • Normal: 149 – [40/0.8] =100 mmHg • Hypoxia: 100 – [40/0.8] = 50 • Hypoxia + hyperventilation: 100 – [20/0.8] = 75

  7. Alveolar and arterial gas • Reasons why arterial gas approaches but does not equal alveolar • Diffusion limitation (esp. at altitude) • Shunt • VA/Q mismatching

  8. Acid-base status • Has respiratory and metabolic components • In other words, the lung can affect acid-base • Henderson-Hasselbalch eq. • H2CO3↔ H+ + HCO3- • Dissociation constant of H2CO3; because H2CO3 and Co2 are proportional KA = [H+] * [HCO3-]/[Co2] Log KA = log [H+] + log [HCO3-]/[Co2] -Log [H+] = - Log KA + log [HCO3-]/[Co2] pH = pKA + log [HCO3-]/[Co2]

  9. Acid-base status • Because CO2 obeys Henry’s law: At a constant temperature, the amount of a given gas dissolved in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid • pH = pKA + log [HCO3-]/{0.03 * Pco2} • pH = 6.1 + log (24/{0.03 * 40}) • pH = 6.1 + log (20) • pH = 6.1 + 1.3 • pH =7.4 • HCO3- typically determined by the kidney • PCO2 by the lung

  10. Acid-base status • Davenport diagram • HCO3- can be raised or lowered • Renal excretion or retention • Renal compensation • Pco2 can be raised or lowered • Hyper or hypo ventilation • Respiratory compensation • Respiratory acidosis, Respiratory alkalosis, metabolic acidosis, metabolic alkalosis

  11. Respiratory alkalosis • Caused by hyperventilation • Altitude, anxiety • Decrease in Pco2 • Elevates pH • Buffer line moves from A to C • Over time kidney compensates by excreting HCO3- • Buffer line moves from C to F • “compensated respiratory alkalosis” • Usu. Not complete • Degree to which it compensates can be derived by the distance betw. Buffer lines A-C and G-F or the base deficit

  12. Respiratory acidosis • Caused by hypoventilation • Drug overdose, chronic COPD • Increase in Pco2 • Reduces pH • Buffer line moves from A to B • Over time kidney compensates by conserving HCO3- • Buffer line moves from B to D • “compensated respiratory acidosis” • Usu. Not complete • Degree to which it compensates can be derived by the distance betw. Buffer lines A-B and D-E or the base excess

  13. Metabolic acidosis • Hco3- falls • Accumulation of lactic acid or diabetes • Move along line A-G • Respiratory compensation • Hyperventilation • Move from G to F • Base deficit will occur

  14. Metabolic alkalosis • Increase in HCO3- • Vomiting • Move along line A to E • Respiratory compenstaion • Hypoventilation • Move along line E to D • Base excess

  15. Control of Ventilation • Basics • Ventilatory system can defend against • Changes in PiO2 • Acid-base disturbances • Precisely controlled • Central controller • Sensors • Effectors

  16. Control of Ventilation • Central Controller • Brainstem • Three main groups • Medullary respiratory center • Just below 4th ventricle • Dorsal (inspiration) and ventral (expiration) respiratory groups • Dorsal group responsible for the rhythmicity of the system • Inspiration can be “cut off” by pneumotaxic center: may help increase rate of breathing

  17. Control of Ventilation • Expiratory center • Becomes active during exercise • Apneustic center • Inspiration • Prolongs insp • Increases depth of breathing • Coordinates switch betw insp and exp • Pneumotaxic center • Switches “off” inspiration • fine-tune respiratory rhythm

  18. Control of Ventilation • Cortex • Breathing is under voluntary control • Can alter basic breathing pattern within limits • Can also help initiate changes in ventilation when exercise commences, “central command”

  19. Control of Ventilation • Effectors • Muscles of respiration we discussed last week • Sensors • Central chemoreceptors • Respond to changes in the chemical composition of the blood or fluid surrounding it • Near the ventral surface of the medulla • Surrounded by ECF (extracellular fluid) and CSF • Respond to Co2 and assoc pH changes • Low buffering capacity of CSF • Responds readily to Co2 • Co2 + H2O →H2CO3→H+ + HCO3-

  20. Control of Ventilation • Peripheral chemoreceptors • Carotid bodies • Aortic bodies • Respond to • ↑Pco2 • ↑H+ • ↓Po2 • Carotid body almost wholly resp. for inc. ventilation in response to hypoxia • Respiratory compensation to metabolic acidosis

  21. Control of Ventilation • Lung receptors • Pulm stretch receptors • Mechanoreceptors • Impulses travel along vagus nerve • Inhibit inspiration • Irritant receptors • In the airways • Respond to noxious gases • Bronchoconstriction and hyperventilation • Juxtracapillary or J receptors • Innervated by Vagus • Respond to engorgement of the capillaries • Pulmonary edema, pulm embolism, pneumonia and baraotrauma • Rapid, shallow breathing; may play a role in the dyspnea assoc with these diseases • Bronchial C fibers • In bronchial mucosa • Rapid, shallow breathing, bronchoconstriction, cough, increased vascular permeability and mucus secretion • Sensitive to chemical stimuli (ozone, cigarette smoke, capsaicin)

  22. Integrated responses • Response to Carbon Dioxide • Normally, the most important determinant in the control of ventilation • Very sensitive • Paco2 does not change by much, even with exercise (maybe 3 mmHg) • Normal rise in vent for an increase in Pco2 is 2-3 L/min/mmHg • For lower PAO2, higher vent for any Pco2 and steeper slope • Ventilatory sensitivity to CO2 varies • Lower in trained athletes and divers • Barbiturates severely depress respiratory centers

  23. Integrated responses • Response to O2 • Doesn’t begin until subject is quite hypoxic • Increased PACO2 increases the sensitivity to hypoxia • Mostly a factor at altitude

  24. Integrated responses • Response to pH • Mostly caused by peripheral chemoreceptors • Acidemia causes increased ventilation • Alkalemia causes reduced ventilation • As the ventilatory changes cause corresponding changes in PaCO2 we call these ventilatory changes hyperventilation or hypoventilation

  25. Integrated responses • Response to Exercise • Ventilation increases up to 25 fold • PaCO2 does not rise (in humans), and usu. Falls • PaO2 may stay the same, rise or fall • pH falls

  26. Acclimatization and High-altitude diseases • Hyperventilation • Hypoxemia stimulates peripheral chemoreceptors; blows off Co2, raises PAO2 • PB 250 mmHg do calculation • Renal compensation reduces HCO3- • Polycythemia • Increased Hct and [Hb] • Increases O2 carrying capacity: draw eq. • EPO form kidney • Other features • Rightward shift in O2-Hb dissociation curve (Leftward at extreme altitude) • Improves off-loading of O2 at the tissues • Caused by ↑2,3 DPG at altitude • Increased capillary-to-fiber volume ratio • Muscle mass drops at altitude

  27. Acclimatization and High-altitude diseases • Acute mountain sickness • Headache, dizziness, palpitations, insomnia, loss of appetite and nausea • Hypoxemia and resp. alkalosis • Chronic mountain sickness • Cyanosis, fatigue, severe hypoxemia, marked polycythemia • High altitude pulmonary edema • Severe dyspnea, orthopnea, cough, cyanosis, crackles and pink, frothy sputum • Life threatening • Associated with elevated Ppa (hypoxic pulm vasoconstriction) • High altitude cerebral edema • Confusion, ataxia, irrationality, hallucinations, loss of consciousness and death • Fluid leakage into brain

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