45. Acute and chronic alveolar hyperventilation
There are some reasons someone might hyperventilate to cover physiological needs, like during exercise. This hyperventilation is compensatory due to increased CO2 production, and is necessary to keep the pCO2 levels normal.
However, these cases are not alveolar hyperventilation. By definition, alveolar hyperventilation is when alveolar ventilation exceeds the need, being out of proportion to the pCO2 production. Clinically, we see this as arterial pCO2 below 36 mmHg (hypocapnia).
Because alveolar hyperventilation leads to hypocapnia, it leads to respiratory alkalosis as well. As such, alveolar hyperventilation and respiratory alkalosis are actually two sides of the same coin (making this topic useless as there’s a separate topic for respiratory alkalosis).
Etiology
The causes are as follows:
- Acute alveolar hyperventilation
- Metabolic acidosis (causes Kussmaul breathing)
- Neurological and physiological disorders
- CNS lesions
- Anxiety
- Fear
- Pain
- Drugs
- Fever
- Sepsis
- Pulmonary disorders
- Pneumonia
- Fibrosis
- Pulmonary oedema
- Pulmonary embolism
- Bronchial asthma
- Decompensated heart failure
- Hypotension
- Chronic alveolar hyperventilation
- Hypoxaemia
- High altitude (> 3000 m)
- Cardiac shunt
- Hypoxaemia
Dyspnoea of pulmonary origin and dyspnoea of cardiac origin (cardiac dyspnoea) have different consequences. Cardiac dyspnoea induces alveolar hyperventilation while pulmonary dyspnoea doesn’t.
There’s some data that visiting a physician can evoke hyperventilation (like fear does perhaps?). This hyperventilation can explain some of the symptoms seen in the office.
Alveolar hyperventilation is a chronic compensatory mechanism in cases of chronic hypoxaemia, like living at high altitudes or having a cardiac shunt. In these cases, hyperventilation is required to maintain normoxaemia.
Pathophysiological consequences
Alveolar hyperventilation leads to respiratory alkalosis, which is what causes the pathophysiological consequences. See topic 79.