Changes in the carbon dioxide partial pressure

Causes of hypocapnia

Hypocapnia can result only from alveolar ventilation that is excessive in relation to carbon dioxide production. Low values of arterial P co ₂ are commonly found, resulting from artificial ventilation with an excessive minute volume or from voluntary hyperventilation because of psychological disturbances such as anxiety. A low arterial P co ₂ may also result simply from hyperventilation during arterial puncture. Persistently low values may be because of an excessive respiratory drive resulting from one or more of the following causes.

• Hypoxaemia is a common cause of hypocapnia, occurring in congenital heart disease with right-to-left shunting, residence at high altitude, pulmonary pathology or any other condition that reduces the arterial P o ₂ below about 8 kPa (60 mmHg). Hypocapnia secondary to hypoxaemia opposes the ventilatory response to the hypoxaemia (page 53).

• Metabolic acidosis produces a compensatory hyperventilation (‘air hunger’), which minimizes the fall in pH that would otherwise occur. This is a pronounced feature of diabetic ketoacidosis; arterial P co ₂ values less than 3 kPa (22.5 mmHg) are not uncommon in severe metabolic acidosis. This is a vital compensatory mechanism. Failure to maintain the required hyperventilation, either from fatigue or inadequate artificial ventilation, leads to a rapid life-threatening decrease in arterial pH.

• Mechanical abnormalities of the lung may drive respiration through vagal reflexes, resulting in moderate reduction of the P co ₂ . Thus conditions such as pulmonary fibrosis, pulmonary oedema and asthma are usually associated with a low to normal P co ₂ until the patient passes into type 2 respiratory failure (page 316).

• Neurological disorders may result in hyperventilation and hypocapnia. This is most commonly seen in those conditions that lead to the presence of blood in the cerebrospinal fluid, such as after a head injury or subarachnoid haemorrhage.

Causes of hypercapnia

It is uncommon to encounter an arterial P co ₂ above the normal range in a healthy subject. Any value of more than 6.1 kPa (46 mmHg) should be considered abnormal, but values up to 6.7 kPa (50 mmHg) may be transiently attained by breath holding.

When a patient is hypercapnic, there are only four possible causes:

• 1.

  Increased concentration of carbon dioxide in the inspired gas . This normally iatrogenic cause of hypercapnia is uncommon, but it is dangerous and differs fundamentally from the other causes listed here. It should therefore be excluded at the outset in any patient unexpectedly found to be hypercapnic when breathing via any external equipment. The carbon dioxide may be endogenous from rebreathing or exogenous from carbon dioxide added to the inhaled gases. Hypercapnia from rebreathing is more common, but fortunately its severity is limited by the rate at which the P co ₂ can increase. If all the carbon dioxide produced by metabolism is retained and distributed in the body stores, arterial P co ₂ can increase no faster than about 0.4 to 0.8 kPa.min ⁻¹ (3–6 mmHg.min ⁻¹ ).

• 2.

  Increased carbon dioxide production. If the pulmonary minute volume is fixed by artificial ventilation and carbon dioxide production is increased by, for example, malignant hyperpyrexia, hypercapnia is inevitable. Like the previous category, this is a rare but dangerous cause of hypercapnia during anaesthesia. A less dramatic, but very common, reason for increased carbon dioxide production is sepsis leading to pyrexia, which often results in hypercapnia in artificially ventilated patients. Although not strictly an increase in production, absorption of carbon dioxide from the peritoneum during laparoscopic surgery or pleura during thoracic surgery have the same respiratory effects.

• 3.

  Hypoventilation. An inadequate pulmonary minute volume is by far the commonest cause of hypercapnia. Pathological causes of hypoventilation are numerous and considered in Chapter 27 and Figure 27.2 . In respiratory medicine, the commonest cause of long-standing hypercapnia is chronic obstructive pulmonary disease (COPD).

• 4.

  Increased dead space . This cause of hypercapnia is usually diagnosed by a process of exclusion when a patient has a high P co ₂ despite a normal minute volume and no evidence of a hypermetabolic state or inhaled carbon dioxide. The cause may be incorrectly configured breathing apparatus or a large alveolar dead space (page 97) from a variety of pathological causes.

Effects of carbon dioxide on the nervous system

A number of special difficulties hinder an understanding of the effects of changes in P co ₂ on any physiological system. First, there is the problem of species difference, which is a formidable obstacle to the interpretation of animal studies in this field. The second difficulty arises from the fact that carbon dioxide can exert its effect either directly or in consequence of (respiratory) acidosis. The third difficulty arises from the fact that carbon dioxide acts at many different sites in the body, sometimes producing opposite effects on a particular function, such as blood pressure (see later discussion).

Carbon dioxide has at least five major effects on the brain:

• 1.

  It is a major factor governing cerebral blood flow (CBF).

• 2.

  It influences the intracerebral pressure through changes in CBF.

• 3.

  It is the main factor influencing the intracellular pH, which is known to have important effects on the metabolism, and therefore function, of the cell.

• 4.

  It may be presumed to exert the inert gas narcotic effect in accord with its physical properties, which are similar to those of nitrous oxide.

• 5.

  It influences the excitability of certain neurones, particularly relevant in the case of the reticular activating system.

The interplay of these effects is difficult to understand, although the gross changes produced are well established.

Cerebral blood flow

CBF increases with arterial P co ₂ at a rate of about 7 to 15 mL.100 g ⁻¹ .min ⁻¹ for each kPa increase in P co ₂ (1–2 mL.100 g ⁻¹ .min ⁻¹ per mmHg) within the approximate range 3 to 10 kPa (20–80 mmHg). The full response curve is S-shaped ( Fig. 22.1 ). The response at very low P co ₂ is probably limited by the vasodilator effect of tissue hypoxia, and the response above 16 kPa (120 mmHg) seems to represent maximal vasodilatation. P co ₂ also influences the autoregulation of CBF with both hypocapnia and hypercapnia, reducing the range of cerebral perfusion pressures between which CBF is maintained constant. Finally, the relationship between CBF and P co ₂ has a circadian rhythm, being higher in the morning, and is modified by sympathetic nervous system activity.

Mechanisms

In the intact animal, CBF is increased in response to P co ₂ by a combination of vasodilatation of cerebral blood vessels and an increase in blood pressure (see later). Changes in P co ₂ lead to a complex series of events that bring about vasodilation of cerebral blood vessels. In adults, the effect is initiated by changes in the extracellular pH in the region of the arterioles, which alters intracellular calcium levels both directly and indirectly via nitric oxide production and the formation of cyclic guanosine monophosphate. With prolonged hypocapnia, and to a lesser extent hypercapnia, changes in CBF return towards baseline after a few hours, an effect thought to result from changes in cerebrospinal fluid pH correcting the extracellular acidosis. Sensitivity of the cerebral circulation to carbon dioxide may be lost in a variety of pathological circumstances such as cerebral tumour, infarction or trauma. There is commonly a fixed vasodilatation in damaged areas of brain, which if widespread may cause dangerous increases in intracranial pressure (ICP).

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