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2012-03-11 18:33:20
Acid Base Cooper Lung

Acid Base Cooper Lung
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  1. ´╗┐Acid-Base Regulation
    • A vital function of Ve is to regulate arterial pH at, or close to, normal.
    • This can be accomplished if PaCO2 is controlled to remain in proportion to the current [HCO3-] level.
    • The law of mass action enables us to calculate blood pH:
    • pH = pK'+ log ([HCO3-]/(alpha*PCO2))
    • pK' is a constant with a value of 6.1 in plasma
    • alpha is the solubility coefficient, relating PCO2 in mm Hg to [CO2] in mM/L, having a value in plasma at 37*C of 0.03.
    • This equation means that pH will be defined by the ratio of HCO3- to alpha*PCO2.
    • Any normal ratio of HCO3- to alpha*PCO2 will give a normal pH regardless of whether both HCO3- and alpha* PCO2 are normal, both are proportionally low, or both are proportionally high.
    • The normal ratio of [HCO3-] to alpha*PCO2 is 20:1, i.e., normal plasma [HCO3-] is 24 mM per L, PCO2 is 40 mm Hg and CO2 solubility alpha is 0.03 mM/L/mm Hg.
  2. Metabolic Acidosis
    • An acute metabolic acidosis, caused, for example, by a sudden, exercise-induced increase in [lactic acid], results in a reduction of arterial [HCO3-].
    • The consequent fall in pH leads to a rapid stimulation of Ve, causing PaCO2 to decrease, ideally until the ratio [HCO3-] / PaCO2 is returned to normal and pH is therefore restored.
  3. Metabolic Alkalosis
    Similarly, for an acute metabolic alkalosis (i.e., pH acutely increased, causing [HCO3-] to rise), Ve should be reduced sufficiently to cause PaCO2 to rise until [HCO3-] / PaCO2 is returned towards normal.
  4. Respiratory Acidosis
    • Arterial pH may also be affected by respiratory acid-base disturbances; i.e., resulting from ventilatory control mechanisms.
    • If, for example, PaCO2 is caused to rise owing to alveolar hypoventilation, [HCO3-] / PaCO2 - and hence pH - will be low.
    • This condition is an acute respiratory acidosis, and is compensated for by renal retention of HCO3- (a process that may take several days to complete).
  5. Respiratory Alkalosis
    • Similarly, acute reduction in PaCO2 - consequent, for example, to hypoxemia or voluntary hyperventilation - induces an acute respiratory alkalosis.
    • Renal mechanisms compensate by increasing the excretion of HCO3-, thereby reducing blood [HCO3-] and restoring [HCO3-] / PaCO2 towards normal.
  6. Chronic Lung Disease
    • Some patients with chronic lung disease exhibit a compensated respiratory acidosis with chronic hypoxemia, hypercapnia, renal HCO3- retention and a relatively normal blood pH.
    • These patients can become insensitive to the chronically elevated PaCO2 so that their ventilation is predominantly stimulated by hypoxia.
    • Giving oxygen to correct the hypoxia can reduce ventilatory drive leading to a further increase in PaCO2.
    • This type of patient typically develops pulmonary hypertension in response to hypoxemia which can lead on to right-sided heart failure (cor pulmonale).

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