Critical Care Medicine

Respiratory alkalosis, hypocapnia

Respiratory alkalosis

Synonym

Hypocapnia

Related conditions

Metabolic alkalosis

Metabolic acidosis

Respiratory acidosis

1. Description of the problem

What every clinician needs to know

Relative hyperventilation tending to make blood more alkaline: increased pH, decreased hydrogen ion concentrations

Can be physiological: pregnancy and high altitude

Pathological associated with relative hyperventilation

Clinical features

Often no specific manifestations. Hyperventilation may be apparent.

Key management points

If pathological, treat underlying condition (eg, asthma or cardiac failure).

In ventilated patients, consider decreasing ventilation.

2. Emergency Management

Treat ABC: airway, breathing, circulation.

In symptomatic psychogenic hyperventilation: use rebreathing (paper bag).

3. Diagnosis

In conscious patients acute respiratory alkalosis can cause neurologic symptoms: dizziness, confusion, syncope, seizures, paresthesias (particularly perioral).

Symptoms and signs may be related to underlying conditions such as ischemic or pleuritic chest pain and unrelated to the change in pH. Patients with psychogenic hyperventilation may have symptoms and signs related to severe anxiety.

Normal lab values

PCO2: 35 to 45 mmHg

pH: 7.35 to 7.45

Standard base excess: -3 to 3 mmol/L

Clinical picture

Arterial blood gas: pH > 7.45, pCO2 < 35 mmHg, Bicarbonate > 24 mmol/L, standard base-excess < 0 mmol/L.

Differential diagnosis

Compensated metabolic acidosis

Confirmatory tests

Check blood gas results for compensation or second disorder. Metabolic compensation will never be complete (pH < 7.40), and will take hours. Therefore, early respiratory alkalosis may appear uncompensated.

Compensation: Metabolic side compensates for respiratory acidosis by decreasing renal chloride excretion, leading to decreased strong-ion difference and decreased bicarbonate.

Measured by bicarbonate or standard base excess (SBE).

In acute respiratory alkalosis : Expected SBE = 0 mmol/L,

Expected bicarbonate mmol/L = 24+ 0.2 x (PCO2 - 40)

For both bicarbonate and base-excess this estimate is about +/- 2 mmol/L.

Underlying change will be renal chloride excretion leading to decreased strong-ion difference.

In chronic respiratory alkalosis there is adaptation (increase of compensatory effect).

Measured by bicarbonate or SBE.

In chronic respiratory alkalosis: Expected SBE = 0.4 x (PCO2 - 40) mmol/L,

Expected bicarbonate mmol/L = 24 + 0.5 x (PCO2 - 40)

4. Specific Treatment

Often no specific treatment. Outcome depends on underlying disorder.

If psychogenic, consider rebreathing ("brown paper bag"); increases inspired CO2.

In mechanically ventilated patients, consider decreasing minute ventilation.

5. Disease monitoring, follow-up and disposition

Expected response to treatment will depend on underlying problem.

When should I suspect an incorrect diagnosis?

Increased base excess or bicarbonate

Follow-up

Management of underlying condition

Pathophysiology

Respiratory alkalosis is secondary to relative hyperventilation. The alveolar partial pressure of carbon dioxide, and arterial pCO2, is related to three factors: 1. inspired CO2 (usually zero but can increase in closed environments); 2. body CO2 production; and 3. (inversely) alveolar ventilation.

PCO2 = inspired CO2 + CO2 production / ventilation.

If inspired CO2 is zero this is simplified to PCO2 = CO2 production / ventilation.

The most common cause of decreased PCO2 is an absolute increase in ventilation. Decreased CO2 production without increased ventilation, such as during anesthesia, can also cause respiratory alkalosis. Decreased partial pressure of carbon dioxide will decrease acidity.

Respiratory Alkalosis

Controlled Mechanical Hyperventilation

CNS stimulation

  • Pain

  • Psychogenic

  • Fever

  • Stroke

  • Meningitis, encephalitis

  • Tumor, trauma

  • Drugs: central nervous system stimulants

  • Hypoxia

  • Pulmonary disease

  • Cardiac failure

  • Shock

  • Severe anemia

  • Altered metabolism

  • Sepsis

  • Liver failure

Physiological

  • Pregnancy

  • High altitude

Epidemiology

Common in ventilated patients.

Prognosis

NA

Special considerations for nursing and allied health professionals.

NA

What's the evidence?

Abelow, B. Understanding Acid-Base. Baltimore, Williams and Wilkins. 1998.

An easy-to-read but comprehensive text that covers both physiology and treatment of acid-base disorders using a bicarbonate-centered view of the non-respiratory side. No mention of base excess.

Gennari, FJ, Adrogue, HJ, Galla, JH, Madias, NE. Acid-base disorders and their treatment. Taylor & Francis. 2005.

A more detailed text that highlights some of the clinical chemistry associations of respiratory acid-base changes. Again bicarbonate-centered.

Kellum, JA, Elbers, PWG. Stewart's Textbook of Acid-Base. AcidBase.Org. 2009.

A re-issue and extended edition of Stewart's landmark text. Detailed explanation of the Stewart and base-excess approaches.
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