Acid-Base Physiology

6.4   Respiratory Alkalosis - Metabolic Effects

[Important Note: The distinction between hypocapnia & respiratory alkalosis has been made in Section 6.1. The metabolic effects mentioned here are those of hypocapnia rather than respiratory alkalosis per se.]

Effects of Hypocapnia

1. Neurological effects

  • Increased neuromuscular irritability (eg paraesthesias such as circumoral tingling & numbness; carpopedal spasm)
  • Decreased intracranial pressure (secondary to cerebral vasoconstriction)
  • Increased cerebral excitability associated with the combination of hypocapnia & use of enflurane
  • Inhibition of respiratory drive via the central & peripheral chemoreceptors

2. Cardiovascular effects

  • Cerebral vasoconstriction (causing decreased cerebral blood flow) [short-term only as adaptation occurs within 4 to 6 hours]
  • Cardiac arrhythmias
  • Decreased myocardial contractility

3. Other effects

  • Shift of the haemoglobin oxygen dissociation curve to the left (impairing peripheral oxygen unloading)
  • Slight fall in plasma [K+]


  • Most of these effects decrease with time. A chronic hypocapnia is associated with few symptoms because of the compensation that occurs.
  • The underlying cause will also have effects other than hyperventilation & these may dominate the clinical picture - for example, the adverse effects of hypoxaemia

The reduction in cerebral blood flow is marked.

Cerebral blood flow (CBF) decreases quite markedly with hypocapnia: a decrease of 4% per mmHg reduction in pCO2. For example, an acute drop in pCO2 from 40 down to 25mmHg will decrease CBF by about 60%. In awake subjects this can cause light-headedness and even confusion. Patients with sickle cell anaemia may be very adversely affected by the decrease in cerebral blood flow (eg development of cerebral thrombosis). 

Hypocapnia causes neuromuscular irritability.

The patient may complain of paraesthesias (incl circumoral numbness & tingling). Tetany may also occur and may manifest as carpopedal spasm. This is a well known problem in patients with anxiety-hyperventilation syndrome and the symptoms can be relieved by rebreathing into a paper bag (with precautions to avoid hypoxaemia of course).

Particular Effects of Hypocapnia in Anaesthetised Patients
  • Decreased cerebral blood flow (CBF) [This effect may be beneficial]
  • Depression of myocardial contractility
  • Cardiac arrhythmias
  • Cerebral excitability may occur in association with high levels of enflurane
  • Shift of the oxygen dissociation curve to the left (impairing oxygen unloading peripherally)
  • Fall in plasma potassium (usually slight only)
  • Obligatory hypoventilation at end of the operation (This is exacerbated by residual drug effects as well)

It has been argued that these adverse effects of hypocapnia are significant enough that the Anaesthetist should aim to maintain normocapnia throughout the duration of anaesthesia in most cases. There are some situations where intraoperative hyperventilation and hypocapnia is specifically useful eg to acutely reduce increased intracranial pressure (ICP) in neuroanaesthesia. In this situation, a therapeutic respiratory alkalosis is useful. These effects are short-lived (hours rather then days) as bicarbonate equilibration occurs across the blood-brain barrier and CBF and ICP returns to normal. This is now a dangerous situation as any increase in pCO2 towards normal will cause a rise in CBF. Hyperventilation to reduce ICP is useful because of its rapid onset but as the effect only lasts for 4 to 6 hours. The main role of acute therapeutic hypocapnia is to provide acute reduction in ICP so that surgical treatment of intracerebral mass lesions can be facilitated.

One argument for routine intraoperative use of hypocapnia  is to use the induced cerebral vasoconstriction to counteract the cerebral vasodilator effects of volatile anaesthetic agents. A particular disadvantage of this is the hypoventilation at the end of the operation which delays recovery from general anaesthesia.

The clinical picture is often dominated by the signs and symptoms of the underlying disorder.