Changes in the carbon dioxide partial pressure

Chapter 23 Changes in the carbon dioxide partial pressure




KEY POINTS



image Hypocapnia occurs when alveolar ventilation is excessive relative to carbon dioxide production and usually results from hyperventilation due to hypoxia, acidosis or lung disease.

image Hypercapnia most commonly occurs because of inadequate alveolar ventilation from a multitude of causes, or more rarely from increased carbon dioxide production.

image Arterial Pco2 affects the cerebral circulation – hypocapnia may cause potentially harmful vasoconstriction whilst vasodilatation from hypercapnia may increase intracranial pressure.

image Hypercapnia, and the resulting acidosis, both have depressant effects on the cardiovascular system, but these are opposed by the stimulant effects of catecholamine release.

Routine monitoring of end-expiratory and arterial Pco2 means it should now be possible to avoid both hypo- and hypercapnia under almost all clinical circumstances. However, interest in hypercapnia has continued over recent years for two reasons. First, changes in the approach to artificial ventilation in severe lung injury have led to the use of ‘permissive hypercapnia’ (page 457). In order to minimise pulmonary damage, minute volume of ventilation is maintained deliberately low, and the arterial Pco2 is allowed to increase. Secondly, a massive expansion of laparoscopic surgical techniques, mostly using carbon dioxide for abdominal insufflation, has led to the anaesthetist having to control arterial Pco2 under conditions of significantly increased pulmonary carbon dioxide output (page 347).


Before describing the effects of carbon dioxide on various physiological systems, this chapter will briefly outline the causes of changes in arterial Pco2.



Causes of Hypocapnia1


Hypocapnia can result only from an alveolar ventilation that is excessive in relation to carbon dioxide production. Low values of arterial Pco2 are commonly found, resulting from artificial ventilation with an excessive minute volume or from voluntary hyperventilation due to psychological disturbance such as hysteria. A low arterial Pco2 may also result simply from hyperventilation during arterial puncture. Persistently low values may be due to 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 Po2 below about 8 kPa (60 mmHg). Hypocapnia secondary to hypoxaemia opposes the ventilatory response to the hypoxaemia (page 73).


Metabolic acidosis produces a compensatory hyper-ventilation (air hunger), which minimises the fall in pH that would otherwise occur. This is a pronounced feature of diabetic ketoacidosis; arterial Pco2 values below 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 the vagus, resulting in moderate reduction of the Pco2. Thus conditions such as pulmonary fibrosis, pulmonary oedema and asthma are usually associated with a low to normal Pco2 until the patient passes into type 2 respiratory failure (page 393).


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 occurs following head injury or subarachnoid haemorrhage.



Causes of Hypercapnia


It is uncommon to encounter an arterial Pco2 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 attained by breath holding. It is difficult for the healthy subject to exceed this level by any respiratory manoeuvre other than by breathing mixtures of carbon dioxide in oxygen.


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


Increased concentration of carbon dioxide in the inspired gas. This iatrogenic cause of hypercapnia is uncommon but it is dangerous and differs fundamentally from the other causes listed below. 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. The latter is now very rare as a supply of carbon dioxide is not provided on modern anaesthetic machines. Hypercapnia from rebreathing is more common, but fortunately its severity is limited by the rate at which the Pco2 can increase. If all the carbon dioxide produced by metabolism is retained and distributed in the body stores, arterial Pco2 can increase no faster than about 0.4–0.8 kPa.min−1 (3–6 mmHg.min−1).

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.

Though not strictly an increase in production, absorption of carbon dioxide from the peritoneum during laparoscopic surgery has the same respiratory effects and is described on page 347.


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).

Increased dead space. This rare cause of hypercapnia is usually diagnosed by a process of exclusion when a patient has a high Pco2, with a normal minute volume and no evidence of a hypermetabolic state or inhaled carbon dioxide. The cause may be incorrectly configured breathing apparatus, or an excessively large alveolar dead space (page 130). This might be due to pulmonary embolism or a cyst communicating with the tracheobronchial tree and receiving preferential ventilation.


Effects of Carbon Dioxide on the Nervous System


A number of special difficulties hinder an understanding of the effects of changes in Pco2 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 below).


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


image It is a major factor governing cerebral blood flow.

image It influences the intracerebral pressure through changes in cerebral blood flow.

image 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.

image 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.

image It influences the excitability of certain neurones, particularly relevant in the case of the reticuloactivating system.

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



Effects On Consciousness


Carbon dioxide has long been known to cause unconsciousness in dogs entering the Grotto del Cane in Italy, where carbon dioxide issuing from a fumarole forms a layer near the ground. It has been widely used as an anaesthetic for short procedures in small laboratory animals. Inhalation of 30% carbon dioxide is sufficient for the production of anaesthesia in humans, but is complicated by the frequent occurrence of convulsions.2 In patients with ventilatory failure, carbon dioxide narcosis occurs when the Pco2 rises above 12–16 kPa (90–120 mmHg).3

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Jun 12, 2016 | Posted by in RESPIRATORY | Comments Off on Changes in the carbon dioxide partial pressure

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