6.4: Metabolic Effects
- Page ID
- 10901
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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 |
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2. Cardiovascular effects |
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3. Other effects |
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NOTES
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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).
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.