Systemic and metabolic consequences of respiratory alkalosis

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Electrolyte modifications occur in response to changes in blood PCO2 (acidosis or alkalosis), and these modifications take place in opposite directions depending on the primary respiratory acid-base disorder. For instance, slight hyponatremia (a decrease of 2-4 mmol/l) has been observed in acute, but not chronic, respiratory alkalosis. This is probably due to increased water reabsorption in the proximal renal tubule associated with a distal enhancement of the action of ADH. Hyperchloremia of small magnitude, due to the chloride shift and to some degree of contraction of the extracellular space, has been observed. According to classical data, serum potassium decreases during the acute respiratory alkalosis. This is caused by a shift of this electrolyte into the cells with concomitant release of the H + ion (a potassium decrease of 0.1-0.4 mmol/l for each increase of 0.1 in pH). However, the increased catecholamine concentrations associated with voluntary hyperventilation may counteract these mechanisms, and the serum potassium may sometimes be slightly elevated (by about 0.3 mmol/l) in acute respiratory alkalosis. This effect is mediated by enhanced a-adrenergic activity and is partly counteracted by b-adrenergic stimulation. The serum potassium level remains normal in chronic respiratory alkalosis.

Hypophosphatemia (about 0.5-1.5 mg/dl or 0.3-0.8 mmol/l), as well as ionized hypocalcemia, is widely recognized with acute hypocapnia. This accounts in part for the well-known increased risk of tetany and seizures seen with hyperventilation. These changes are due to a shift of phosphate into the cells, probably mediated by the intracelluar alkalosis caused by hypocapnia. The increase in intracellular pH enhances glycolysis, leading to the formation of phosphorylated compounds, such as glucose 6-phosphate and fructose 1,6-diphosphate, and a decrease in free phosphate in both the cells and the extracellular fluid. This phenomenon does not seem to have clinical consequences per se and therefore should not need to be treated. However, the clinician should be aware of its existence in order to interpret the occurrence of hypophosphatemia. In animals, the parathyroid hormone (PTH) plasma level actually increases in chronic respiratory alkalosis; this hormone has been shown to decrease proximal tubular bicarbonate resorption and to cause an increase in the transfer of phosphate from the extracellular to the intracellular compartment. However, in humans, chronic respiratory alkalosis induces some degree of renal PTH resistance, mediated by b-adrenergic receptors, which causes a slight hyperphosphatemia and hypocalcemia.

The cardiovascular system appears to be profoundly affected by respiratory alkalosis. In fact, both respiratory acidosis and respiratory alkalosis may cause a decrease in systemic vascular resistance mediated by a relaxation of the systemic arterial tone. However, these actions are partially counteracted by vasoconstriction mediated by the circulating catecholamines and by an increase of the activity of the sympathetic nervous system. The net clinical effect of respiratory alkalosis is a fall in peripheral vascular resistance and arterial blood pressure, with the magnitude of these effects varying according to the relative importances of these mechanisms. Generally, the decrease in blood pressure and systemic vascular resistance is slight. However, patients with a depressed central nervous system and/or under general anesthesia, particularly when passively hyperventilated by mechanical ventilation, may present major reductions in cardiac output and systemic blood pressure. In addition, these patients may be characterized by various levels of peripheral vascular resistance and different degrees of hyperlactatemia, particularly when in acute respiratory alkalemia. It is of paramount importance to be aware that some regional vascular beds react differently from the overall systemic circulation. One of these is the cerebral circulation. Cerebral blood flow decreases in acute hypocapnia, and, when PaCO2 is severely decreased, this may result in brain hypoxia and increased cerebral lactate output. In addition, acute respiratory alkalosis may be responsible for neurological disorders not only because of the low PCO2, but also because of alkalemia, pH-induced shift of the oxyhemoglobin curve, and electrolyte abnormalities.

The function of the peripheral neuromuscular system is strongly modified by alkalemia. In essence, alkalemia, of either metabolic or respiratory origin, increases the binding of ionized calcium to its transporters, mainly serum albumin. Hence, for each pH increment of 0.1, ionized calcium will be reduced by about 0.2 mg/dl (or 0.05 mmol/l). The clinical consequences of this phenomenon depend not only on the level of serum ionized calcium, but also on the rate at which it decreases. Hence more severe symptoms (paresthesias, tetany, anxiety, cardiovascular changes, etc.) will be observed in acute respiratory alkalosis than in the setting of chronic hyperventilation.

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