Hospital Medicine

Respiratory alkalosis

I. Problem/Condition.

Respiratory alkalosis is produced by a primary reduction in the partial pressure of carbon dioxide.

A. What is the differential diagnosis for this problem?

  • A decrease in the partial pressure of carbon dioxide (PaCO2) could be due to respiratory alkalosis or could be a compensatory response to metabolic acidosis.

  • An elevated arterial pH could be due primarily to respiratory alkalosis or metabolic alkalosis.

B. Describe a diagnostic approach/method to the patient with this problem

  • The most important and first step in the evaluation of a patient with suspected respiratory alkalosis is measurement of arterial blood gases (ABG). The presence of an alkaline pH (pH > 7.40) combined with a decreased PaCO2 (PaCO2 <37 millimeters mercury [mmHg]) confirms the presence of respiratory alkalosis.

  • The etiology of respiratory alkalosis can be divided into central nervous system causes, hypoxemia, iatrogenic causes, endocrine causes, pulmonary causes and complications of other medical conditions.

  • Central nervous system causes include pain, fear, anxiety, psychosis, fever, cerebrovascular accidents, meningitis, encephalitis, tumor, trauma or voluntary hyperventilation.

  • Hypoxemia can be due to lung disease or decreased atmospheric oxygen tension (e.g., high altitude), severe anemia or right-to-left cardiac shunts.

  • Iatrogenic causes of respiratory alkalosis include medications like progesterone, methylxanthines (e.g., theophylline), salicylates (also cause primary metabolic acidosis), catecholamines and nicotine as well as excessive minute ventilation provided by mechanical ventilation (especially in chronic obstructive pulmonary disease [COPD] or obstructive sleep apnea/obesity hypoventilation syndrome OSA/OHS patients who have chronic respiratory acidosis).

  • Pulmonary causes include reduced lung volume (e.g., due to pneumothorax or pleural effusion), pneumonia, pulmonary edema, pulmonary embolism, interstitial lung disease, asthma, chronic obstructive pulmonary disease on mechanical ventilation as above.

  • Medical conditions associated with respiratory alkalosis include pregnancy (due to progesterone), hyperthyroidism, sepsis (due to cytokines), chronic liver disease, heat exhaustion, congestive heart failure and recovery from metabolic acidosis.

1. Historical information important in the diagnosis of this problem.

Respiratory alkalosis is most commonly a physiologic response to hypoxemia, metabolic acidosis or increased metabolic demands (e.g., due to fever, pain or anxiety).

Mixed acid base disorders with respiratory alkalosis should alert clinician to look for other causes (major ones being sepsis and salicylate toxicity).

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

  • Signs of underlying condition.

  • Positive Chvostek and Trousseau signs may be present (because of calcium binding).

  • Cardiovascular effects can include reduced cardiac output and cardiac arrhythmias.

  • Mechanical ventilation mode and minute ventilation rate.

3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.

For every 10 mmHg drop in PaCO2, plasma bicarbonate decreases by about 2 milliequivalents/liter [mEq/liter] in the acute setting and about 4-5 mEq/liter in the chronic setting which is usually after 3-5 days.

Or for each decrease of 1mmHg in the PaCO2, the plasma bicarbonate concentration decreases by 0.4 millimoles/liter (mmol/L). For the first 1-2 days after the development of respiratory alkalosis, the serum bicarbonate level will not decline below 15-18 mmol/L; after this time, it can decline to 12mmol/L. For each decrease of 1mmHg in the PaCO2, the pH decreases by 0.4. For the first 1-2 days, pH is expected to increase by 0.008 x (40-PaCO2); after that pH increases by 0.017 x (40-PaCO2).

Acute respiratory alkalosis causes a reduction in serum levels of potassium and phosphate due to intracellular shifts. A reduction in ionized calcium can occur due to increased binding to albumin. Hyponatremia and hypochloremia may also be present.

C. Criteria for Diagnosing Each Diagnosis in the Method Above.

Evaluation is dictated by the clinical findings. Basic evaluations include complete blood count (CBC) with differential, blood chemistries and chest x-ray. Findings will dictate whether further testing is indicated (e.g., computed tomography [CT] scan of the brain or chest, lumbar puncture, toxicology screen, cultures of blood, urine or cerebrospinal fluid).

D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem.

Venous blood gas is not useful for the evaluation of respiratory alkalosis since passage through the tissues will increase the bicarbonate concentration and PaCO2.

A. Management of respiratory alkalosis.

Management of respiratory alkalosis requires a reduction in the minute ventilation: respiratory rate or tidal volume. This can be accomplished acutely with analgesics or anxiolytic agents. Ventilation into a paper bag will increase the concentration of CO2 in inspired air so will increase the PaCO2 acutely. These manoeuvres are effective in hyperventilation syndrome and management of CNS causes of respiratory alkalosis.

Correction of the underlying cause should be the principal management, the most important clinical one being hypoxia and treatment directed toward correction of hypoxia.

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem

Most patients with respiratory alkalosis have underlying disorders which require treatment. Reduction of the minute ventilation may require mechanical ventilation to temporarily reverse the alkalosis mainly in situations where hypoxia is a driving factor.

What's the evidence?

Madias, NE:. "Renal acidification responses to respiratory acid-base disorders.". J. Nephrol. vol. 23. 2010. pp. S85-91.

Dubin, A,, Masevicius, FD:. "Improving acid-abse evaluation: The proper use of old tools.". Intensive Care Med. vol. 36. 2010. pp. 371.

McNamara, J,, Worthley, LI. "Acid-base balance: part II. Pathophysiology.". Crit Care Resusc. vol. 3. 2001. pp. 188-201.

Laffey, JC,, Kavanagh, BP:. "Hypocapnia.". NEJM. vol. 347. 2002. pp. 43-53.

Androgue, HJ,, Madias, NE:. "Medical progress: Management of life-threatening acid-base disorders.". NEJM. vol. 338. 1998. pp. 107-11.

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