A respiratory alkalosis is a primary drop in PCO2 with or without compensatory waste of bicarbonate (HCO3-). The pH can be high or almost normal. The cause is an increase in respiratory rate and / or tidal volume (hyperventilation). A respiratory alkalosis can be acute or chronic. The chronic form is asymptomatic, but the acute form may cause dizziness, confusion, paresthesias, cramps and syncope cause. The clinical signs are Hyperpnea or tachypnea and Karpopedalspasmen. The diagnosis is clinical and with ABG and measurement of serum electrolytes. The treatment depends on the particular cause.

See also acid-base regulation, acid-base disorders, and hyperventilation syndrome.)

A respiratory alkalosis is a primary drop in PCO2 with or without compensatory waste of bicarbonate (HCO3-). The pH can be high or almost normal. The cause is an increase in respiratory rate and / or tidal volume (hyperventilation). A respiratory alkalosis can be acute or chronic. The chronic form is asymptomatic, but the acute form may cause dizziness, confusion, paresthesias, cramps and syncope cause. The clinical signs are Hyperpnea or tachypnea and Karpopedalspasmen. The diagnosis is clinical and with ABG and measurement of serum electrolytes. The treatment depends on the particular cause. See also acid-base regulation, acid-base disorders, and hyperventilation syndrome). Etiology A respiratory alkalosis is a primary drop of PCO2 (hypocapnia) by an increase in respiratory rate and / or tidal volume (hyperventilation). An increase of the ventilation (at height z. B.), metabolic acidosis and increased metabolic requirements usually occurs as a physiological response under hypoxia (eg. B. fever) and can be observed at as many serious disorders. In addition, pain and fear and some diseases of the central nervous system can increase breathing without physiological needs. Pathophysiology respiratory alkalosis can be acute therapy Chronic The distinction is based on the degree of metabolic compensation. Excess HCO3- is buffered by extracellular H + within minutes, but a more extensive compensation occurs within 2-3 days, when the kidneys reduce the H + excretion. Pseudorespiratorische alkalosis A pseudorespiratorische alkalosis is a low arterial PCO2 and a high pH in mechanically ventilated patients with severe metabolic acidosis in a systemic hypoperfusion (z. B. in cardiogenic shock, during cardiopulmonary resuscitation). The pseudorespiratorische alkalosis occurs when by a mechanical ventilation (often hyperventilation) larger amounts of alveolar Carbondioxid (CO2) is exhaled as normal. The expiration of large quantities of CO2 causes respiratory alkalosis in the arterial blood (and thus in the ABG-measurements), but the poor systemic perfusion and cellular ischemia produce a cellular acidosis leading to acidosis in the venous blood. The diagnosis is made by detecting a significant difference between arterial and venous PCO2 and pH and by the increased lactate levels in patients whose respiratory alkalosis show ABG. The treatment consists of the improvement of systemic hemodynamics. Symptoms and signs The symptoms and discomfort depend on the speed and extent of PCO2 waste. Acute respiratory alkalosis causes dizziness, confusion, and peripheral and perioral paresthesia, cramps and syncope. As mechanism it is believed a change in cerebral blood flow and the pH. Tachypnea or Hyperpnea is often the only clinical sign. Karpopedalspasmen can occur (brought into the cells in exchange for hydrogen ions [H +]) due to fallen Mirroring of ionized calcium in the blood in severe cases. Chronic respiratory alkalosis is usually asymptomatic and has no typical symptoms. Clinical calculator: Arterial blood gas interpretation TreeCalc diagnosis ABG and serum electrolytes When hypoxia is present, are urgently needs to search for the cause, the diagnostic criteria for respiratory alkalosis and the corresponding renal compensation (acid-base disorders: diagnostic) require ABG and the measurement of serum electrolytes. A slight hypophosphatemia and hypokalemia by intracellular shifts and reduced values ??for ionized calcium (Ca ++) by an increase in protein binding may occur. there is hypoxia or increased alveolar-arterial (A-a) OO2 gradient (inspiratory PO2 [arterial PO2 + 5/4 arterial PCO2]), the cause must be clarified. Other causes are often revealed by the history or physical examination. As a pulmonary embolism occurs very frequently without hypoxia, pulmonary embolism must be excluded before accepting anxiety as a cause for a patient hyperventilating yet. Clinical calculator: A-a gradient treatment of the underlying disease treatment, the treatment depends on the underlying disorder. A respiratory alkalosis is not life threatening, so that no measures for reducing the pH are necessary. An increase in the inspiratory CO2 by rebreathing (z. B. with a paper bag) is a common measure, but can also, particularly in some patients with CNS disorders in which the pH in the CSF may already have been below normal, be dangerous , Summary An respiratory alkalosis is accompanied by an increase in respiratory rate and / or tidal volume (hyperventilation). Hyperventilation usually occurs in response to hypoxia, metabolic acidosis and increased metabolic demands (eg. As fever), pain or fear. Do not assume that fear the cause of hyperventilation is, were excluded to more serious conditions. The treatment depends on the underlying cause. A respiratory alkalosis is not life threatening, so that no measures for reducing the pH are necessary.

Health Life Media Team

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