Respiratory alkalosis is a medical condition in which increased respiration (hyperventilation) elevates the blood pH (a

condition generally called alkalosis).

• Acute respiratory alkalosis occurs rapidly. During acute respiratory alkalosis, the person may lose consciousness
where the rate of ventilation will resume to normal.
• Chronic respiratory alkalosis is a more long-standing condition. For every 10 mM drop in pCO2 in blood, there is a
corresponding 5 mM of bicarbonate ion drop. The drop of 5 mM of bicarbonate ion is a compensation effect which
reduces the alkalosis effect of the drop in pCO2 in blood. This is termed metabolic compensation.

Respiratory alkalosis generally occurs when some stimulus makes a person hyperventilate. The increased breathing
produces increased alveolar respiration, expelling CO2 from the circulation. This alters the dynamic chemical equilibrium of
carbon dioxide in the circulatory system, and the system reacts according to Le Chatelier's principle. Circulating hydrogen
ions and bicarbonate are shifted through the carbonic acid (H2CO3) intermediate to make more CO2 via the enzyme
carbonic anhydrase

Physical
Physical examination findings in patients with respiratory alkalosis are usually nonspecific and are related to the underlying
illness or cause of the respiratory alkalosis. Note the following:
• Many patients with hyperventilation syndrome appear anxious and are frequently tachycardic. Understandably,
tachypnea is a frequent finding.
• In acute hyperventilation, chest wall movement and breathing rate increase. In patients with chronic
hyperventilation, these physical findings may not be obvious.
• Positive Chvostek and Trousseau signs may be elicited.
• Patients with underlying pulmonary disease may have signs suggestive of pulmonary disease, such as crackles and
rhonchi. Cyanosis may be present if the patient is hypoxic.
• If the underlying pathology is neurologic, the patient may have focal neurologic signs or a depressed level of
consciousness.
• Cardiovascular effects of hypocapnia in healthy and alert patients are minimal, but in patients who are anesthetized,
critically ill, or receiving mechanical ventilation, the effects can be more significant. Cardiac output and systemic
blood pressure may fall as a result of the effects of sedation and positive-pressure ventilation on venous return,
systemic vascular resistance, and heart rate.
• Cardiac rhythm disturbances may occur because of increased tissue hypoxia related to the leftward shift of the
hemoglobin-oxygen dissociation curve.
The differential diagnosis of respiratory alkalosis is broad; therefore, a thorough history, physical examination, and
laboratory evaluation are helpful in limiting the differential and arriving at the diagnosis.
Central nervous system causes are as follows:
• Pain
• Hyperventilation syndrome
• Anxiety
• Psychosis
• Fever
• Cerebrovascular accident
• Meningitis
• Encephalitis
• Tumor
• Trauma
Hypoxia-related causes are as follows:
• High altitude
• Severe anemia
• Right-to-left shunts
Drug-related causes are as follows:
• Progesterone
• Methylxanthines
• Salicylates
• Catecholamines
• Nicotine
Endocrine-related causes are as follows:
• Pregnancy
• Hyperthyroidism
Pulmonary causes are as follows:
• Pneumothorax/hemothorax
• Pneumonia
• Pulmonary edema
• Pulmonary embolism
• Aspiration
• Interstitial lung disease
• Asthma
• Emphysema
• Chronic bronchitis
Miscellaneous causes are as follows:
• Sepsis
• Hepatic failure
• Mechanical ventilation
• Heat exhaustion
• Recovery phase of metabolic acidosis
• Congestive heart failure
Laboratory Studies
The following laboratory studies may be helpful:
• Arterial blood gas determinations: Alkalemia is documented by the presence of an increased pH level (>7.44) on
arterial blood gas determinations. The presence of a decreased PCO2 level (<36 mm Hg) indicates a respiratory
etiology of the alkalemia.
• Serum chemistries: Acute respiratory alkalosis causes small changes in electrolyte balances. Minor intracellular
shifts of sodium, potassium, and phosphate levels occur. A minor reduction in free calcium occurs due to an
increased protein-bound fraction. Compensation for respiratory alkalosis is by increased renal excretion of
bicarbonate. In acute respiratory acidosis, the bicarbonate concentration level decreases by 2 mEq/L for each
decrease of 10 mm Hg in the PaCO2 level. In chronic respiratory acidosis, the bicarbonate concentration level
decreases by 5 mEq/L for each decrease of 10 mm Hg in the PaCO2 level. Plasma bicarbonate levels rarely drop
below 12 mm Hg secondary to compensation for primary respiratory alkalosis.
• Complete blood cell count: An elevation of the WBC count may indicate early sepsis as a possible etiology of
respiratory alkalosis. A reduced hematocrit value may indicate severe anemia as the potential cause of respiratory
alkalosis.
• Liver function test: Findings may be abnormal if hepatic failure is the etiology of the respiratory alkalosis.
• Cultures of blood, sputum, urine, and other sites: These should be considered, depending on information obtained
from the history and physical examination and if sepsis or bacteremia are thought to be the cause of the respiratory
alkalosis.

Imaging Studies
Consider the following imaging studies:
• Chest radiography: Perform chest radiography to help rule out pulmonary disease as a cause of hypocapnia and
respiratory alkalosis. Potential etiologies that may be confirmed based on chest radiography findings include
pneumonia, pulmonary edema, aspiration pneumonitis, pneumothorax, and interstitial lung disease.
• CT scanning: CT scanning of the chest may be performed if chest radiography findings are inconclusive or a
pulmonary disorder is strongly considered as a differential diagnosis. CT scanning is more sensitive for helping
detect disease, and findings may reveal abnormalities not seen on the chest radiograph. Consider spiral CT
angiography of the chest if pulmonary embolism is suggested. Consider CT scanning of the brain if a central cause
of hyperventilation and respiratory alkalosis is suggested. Specific etiologies that may be diagnosed based on brain
CT scan findings include cerebrovascular accident, CNS tumor, and CNS trauma.
• Ventilation perfusion scanning: Consider this scan in patients who are unable to have intravenous contrast to assess
for pulmonary embolism.
• Brain MRI: If a central cause of hyperventilation and respiratory alkalosis is suggested and the initial brain CT scan
findings are negative or inconclusive, an MRI of the brain can be considered. MRIs may reveal abnormalities not
seen on CT scans. Possible etiologies based on MRIs include cerebrovascular accident, CNS tumor, and CNS
trauma.
Medical Care
Treatment of respiratory alkalosis is primarily directed at correcting the underlying disorder. Respiratory alkalosis itself is
rarely life threatening. Therefore, emergent treatment is usually not indicated unless the pH level is greater than 7.5.
Because respiratory alkalosis usually occurs in response to some stimulus, treatment is usually unsuccessful unless the
stimulus is controlled. If the PCO2 is corrected rapidly in patients with chronic respiratory alkalosis, metabolic acidosis may
develop due to the renal compensatory drop in serum bicarbonate.

The tidal volume and respiratory rate may be decreased in mechanically ventilated patients who have respiratory alkalosis.
Inadequate sedation and pain control may be the etiology of respiratory alkalosis in patients breathing over the set ventilator
rate.

In hyperventilation syndrome, patients benefit from reassurance, rebreathing into a paper bag during acute episodes, and
treatment for underlying psychological stress. Sedatives and/or antidepressants should be reserved for patients who have not
responded to conservative treatment. Beta-adrenergic blockers may help control the manifestations of the hyperadrenergic
state that can lead to hyperventilation syndrome in some patients.2

In patients presenting with hyperventilation, a stepwise approach should be used to rule out potentially life-threatening,
organic causes first.

Consultations
Based on the findings from the history, physical examination, laboratory studies, and imaging modalities, the necessity for
assistance from consultants such as pulmonologists, neurologists, or nephrologists can be determined.