Respiratory alkalosis is the primary reduction of PCO2 with or without a compensatory decrease in HCO3–; The pH is elevated or almost normal. The causes lie in the increased frequency or depth of breathing (hyperventilation). The condition can be acute or chronic. The chronic form has no symptoms, while the acute one causes haze, confusion, paresthesias, cramps and syncope. There is hyperpnea or tachypnea with carpopedal spasms. The clinical diagnosis is confirmed by blood gas analysis and serum electrolyte findings. Treatment is causal.

Etiology and pathophysiology

Respiratory alkalosis is a reflection of the primary decrease in PCO2 (hypocapnia) due to hyperventilation. Mostly in response to hypoxia, metabolic acidosis, and increased metabolic demands (eg fever), it is found in many serious conditions. In addition, pain, anxiety and some CNS disorders increase the number and depth of respirations without a physiological background.

Alkalosis can be acute or chronic, and the difference is in the degree of metabolic compensation. Excess HCO3– is neutralized by extracellular H + in a few minutes, but basic compensation occurs after 2–3 days as the kidneys reduce H + excretion.

     Pseudorespiratory alkalosis is a condition of low PCO2 and high pH in the arterial blood of patients with severe metabolic acidosis due to systemic hypoperfusion (eg cardiogenic shock, cardiopulmonary resuscitation); occurs when mechanical ventilation (often hyperventilation) eliminates accumulated CO2 from the alveoli. High concentrations of CO2 in the alveoli during gas analysis of arterial blood create a clinical picture of respiratory alkalosis, but systemic hypoperfusion and cellular ischemia cause cellular and later blood acidosis. The diagnosis is confirmed by evidence of a large arteriovenous difference in PCO2 and pH and a high lactate concentration, and treatment consists of repairing hemodynamics.

Clinical image

     The clinical picture depends on the degree and rate of PCO2 downregulation. Acute respiratory alkalosis leads to haze, confusion, peripheral and circulatory paresthesias, spasms, and syncope, resulting in changes in brain flow and pH. Often the only symptoms are tachypnea or hyperpnea, in more severe cases, carpopedal spasms occur. Chronic respiratory alkalosis is most often asymptomatic.

Diagnosis and treatment

Recognition of respiratory alkalosis and appropriate renal compensation rests on blood gas analysis and the finding of serum electrolytes. Mild hypophosphatemia and hypokalemia may also be found due to cell migration, as well as a decrease in Ca ++ due to increased calcium binding to proteins.

Most causes are revealed by a good history and physical examination. Since hypoxia does not have to accompany pulmonary embolism, it should be ruled out in hyperventilating patients before the cause is attributed to anxiety. Hypoxia and increased alveolar-arterial O2 difference, i. inhaled PO2 – (arterial PO2 + 5/4 arterial PCO2) suggest finding a hidden cause.

Treatment is focused on the underlying problem. Respiratory alkalosis is not life-threatening, so interventions to raise pH are not justified. The inhalation concentration of CO2 is often increased by re-inhaling the exhaled air (eg with a paper natron bag), which can be dangerous in some people with CNS disease where the pH of the CSF is already lowered.


AMQAT Health Analysis – A Non-Invasive Method for Early Detection of Potential Diseases. However, depending on your symptoms and other information your doctor collects, additional tests may be performed. If you have diabetes, your glucose and ketone levels can be tested. If you have taken ethylene glycol or methylene, you may pass an osmolality test from a morning urine sample or during a 24-hour diuresis.

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