Mechanisms of Hypercapnia and Hypocapnia during Anesthesia

Hypercapnia

Hypoventilation, increased dead space ventilation, increased CO₂ production, and inadvertent switching off of a CO₂ absorber can all cause hypercapnia ( Fig. 17-40 ).

Hypoventilation

Patients spontaneously hypoventilate during anesthesia because it is more difficult to breathe (abnormal surgical position, increased airway resistance, decreased compliance) and they are less willing to breathe (decreased respiratory drive because of anesthetics). Hypoventilation results in hypercapnia (see Fig. 17-22 and Fig. 17-23 ).

Increased Dead Space Ventilation

A decrease in Ppa, as during deliberate hypotension,^[196] may cause an increase in zone 1 and alveolar dead space ventilation. An increase in airway pressure (as with PEEP) may also cause an increase in zone 1 and alveolar dead space ventilation. Pulmonary embolism, thrombosis, and

Figure 17-40 Schematic diagram of the causes of hypercapnia during anesthesia. An increase in carbon dioxide (CO₂ ) production (V̇CO₂ ) will increase PaCO₂ with a constant minute ventilation (V̇E). Several events can increase alveolar dead space: a decrease in pulmonary artery pressure (Ppa), the application of positive end-expiratory pressure (PEEP), thromboembolism, and mechanical interference with pulmonary arterial flow (ligatures and kinking of vessels). A decrease in V̇E causes an increase in PaCO₂ with a constant V̇CO₂ . It is possible for some anesthesia systems to cause rebreathing of CO₂ . Finally, the anesthesia apparatus may increase the anatomic dead space, and inadvertent switching off of a CO₂ absorber in the presence of low fresh gas flow can increase PaCO₂ . (Redrawn with modification from Benumof JL: Anesthesia for Thoracic Surgery, 2nd ed. Philadelphia, WB Saunders, 1995, Chapter 8.)

The anesthesia apparatus increases total dead space (VD/VT) for two reasons. First, the apparatus simply increases the anatomic dead space. Inclusion of normal apparatus dead space increases the total VD/VT ratio from 33% to about 46% in intubated patients and to about 64% in patients breathing through a mask.^[197] Second, anesthesia circuits cause rebreathing of expired gases, which is equivalent to dead space ventilation. The rebreathing classification by Mapleson is widely accepted. The order of increasing rebreathing (decreasing clinical merit) during spontaneous ventilation with Mapleson circuits is A (Magill), D, C, and B. The order of increasing rebreathing (decreasing clinical merit) during controlled ventilation is D, B, C, and A. There will be no rebreathing in system E (Ayre's T-piece) if the patient's respiratory diastole is long enough to permit washout with a given fresh gas flow (common event) or if the fresh gas flow is greater than the peak inspiratory flow rate (uncommon event).

The effects of an increase in dead space can usually be counteracted by a corresponding increase in the respiratory V̇E. If, for example, the V̇E is 10 L/min and the VD/VT ratio is 30%, alveolar ventilation will be 7 L/min. If a pulmonary embolism occurred and resulted in an increase in the VD/VT ratio to 50%, V̇E would need to be increased to 14 L/min to maintain an alveolar ventilation of 7 L/min (14 L/min × 0.5).

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Increased Carbon Dioxide Production

All the causes of increased O₂ consumption also increase CO₂ production: hyperthermia, shivering, catecholamine release (light anesthesia), hypertension, and thyroid storm. If V̇E, total dead space, and V̇A/ relationships are constant, an increase in CO₂ production will result in hypercapnia.

Inadvertent Switching Off of a Carbon Dioxide Absorber

Many factors, such as patient ventilatory responsiveness to CO₂ accumulation, fresh gas flow, circle system design, and CO₂ production, determine whether hypercapnia will result from accidental switching off or depletion of a circle CO₂ absorber (see Chapter 9 ). However, high fresh gas flows (>-5 L/min) minimize the problem with almost all systems for almost all patients.

Hypocapnia

The mechanisms of hypocapnia are the reverse of those that produce hypercapnia. Thus, all other factors being equal, hyperventilation (spontaneous or controlled ventilation), decreased VD ventilation (change from a mask airway to an endotracheal tube airway, decreased PEEP, increased Ppa, or decreased rebreathing), and decreased CO₂ production (hypothermia, deep anesthesia, hypotension) will lead to hypocapnia. By far the most common mechanism of hypocapnia is passive hyperventilation by mechanical means.