Respiratory Alkalosis

Respiratory Alkalosis is an acid base disturbance characterized by elevated arterial pH, hyperventilation resulting in a low pCO2 and a usually compensatory decrease in plasma HCO3- concentration.

Respiratory Alkalosis results from an elevation in alveolar ventilation that causes a fall in the partial pressure of dissolved carbon dioxide. The fall in PCO2 causes a compensatory fall in plasma HCO3- concentration as was decribed previously.

The causes of Respiratory Alkalosis are shown in the table below. It is very commonly induced by what the body or patient perceives as a stressor. The stressor which is often associated with anxiety, pain, and infection stimulates the CNS leading to hyperventilation. Other common causes are hypoxemia, sepsis, liver failure and PE. Aspirin intoxication is an interesting cause of respiratory alkalosis which can also cause an elvated anion gap acidosis.


A) CNS stimulation
          1. pain
          2. Anxiety, Psychosis
          3. Fever
          4. CVA
          5. Meningitis, encephalitis
          6. Tumor, trauma
          7. Drugs: Salicylate (also causes metabolic acidosis), methylaxanthines, theophylline, aminophyllines.  
          8. Pregnancy, progesterone
B) Hypoxemia or tissue hypoxia
          1. High altitude
          2. Pulmonary disease: pneumonia, interstitial fibrosis, PE, pulmonary edema
          3. CHF
          4. Hypotension
          5. Severe anemia
          6. Aspiration     
  C) Chest Receptors stimulation
       1. Flail Chest
       2. Hemothorax
       3. PE
4)  Miscellaneous disorders
        1.Gram negative septicemia (very early clinical sign of septicemia)
        2. Hepatic failure
        3. Mechanical hyperventilation
        4. Heat exposure
        5. Recovery from metabolic acidosis               


Clinical Manifestations

Clinical manifestations of respiratory alkalosis vary according to duration and severity and depend on the underlying disease process.

In acute respiratory alkalosis, acute onset of hypocapnia can cause cerebral vasoconstriction. Therefore, an acute decrease in PCO2 reduces cerebral blood flow and can cause neurologic symptoms, including dizziness, mental confusion, syncope, seizures, paresthesias, numbness around the mouth. This acute drop in PCO2, result in a substantial drop in CSF pH not seen in chronic respiratory alkalosis or metabolic alkalosis. In metabolic alkalosis, the change in CSF pH occurs much slower due to the relative inability of HCO3- to cross the blood brain barrier in comparison to CO2.

In addition some complaints may be unrelated to the change in pH. For example, patients with psychogenic hyperventilation often complain of chest tightness, headache, dyspnea, and other somatic symptoms that may be related to anxiety and not alkalemia.
Acute respiratory alkalosis also causes intracellular shift of potassium and phosphates potentially resulting in hypokalemia and hypophosphatemia. The hypokalemia is usually mild. Hypocalcemia typically results, due to an increase in albumin bound calcium and may lead to tetany and a positive Chvostek or Trousseau sign.



Usually self limited since muscles weakness will suppress ventilation.

If the PaCO2 is corrected rapidly in patients with chronic respiratory alkalosis, metabolic acidosis may develop due to the previous compensatory drop in serum bicarbonate.