Book Text

Increase in the Partial Pressure of Arterial Carbon Dioxide

During uneventful CO₂ pneumoperitoneum, the increase in partial pressure of arterial carbon dioxide (PaCO₂ ) progressively increases to reach a plateau 15 to 30 minutes after the beginning of CO₂ insufflation in patients under controlled mechanical ventilation during gynecologic laparoscopy in the Trendelenburg position^[19] or laparoscopic cholecystectomy in head-up position^[20] ^[21] ( Fig. 57-2 ). Any significant increase in PaCO₂ after this period requires a search for a cause independent of or related to CO₂ insufflation, such as CO₂ subcutaneous emphysema. The increase in PaCO₂ depends on the IAP.^[22] During laparoscopy with local anesthesia, PaCO₂ remains unchanged, but minute ventilation significantly increases.^[23] However, during general anesthesia with spontaneous breathing, the compensatory hyperventilation is insufficient to avoid hypercapnia because of anesthetic-induced ventilatory depression and increased work of breathing from the decreased thoracopulmonary compliance. Because it takes 15 to 30 minutes for PaCO₂ to plateau, anesthetic techniques using spontaneous breathing should be limited to short procedures at low IAPs.^[24] ^[25]

Capnography and pulse oximetry provide reliable monitoring of PaCO₂ and arterial oxygen saturation in healthy patients and in the absence of acute intraoperative disturbances (see Fig. 57-2 ).^[17] ^[20] ^[21] Although mean gradients (Δa-ETCO₂ ) between PaCO₂ and the end-tidal carbon dioxide tension (PETCO₂ ) do not change significantly during peritoneal insufflation of CO₂ , individual patient data regularly show variations of this difference during pneumoperitoneum.^[26] ^[27] PaCO₂ and Δa-ETCO₂ increase more in ASA class II and III patients than ASA class I patients ( Fig. 57-3 ).^[28] ^[29] These findings have been documented in patients with chronic obstructive disease (COPD)^[30] and in children with cyanotic congenital heart disease.^[31] These data therefore highlight the lack of correlation between PaCO₂ and PETCO₂ in sick patients, particularly those with impaired CO₂ excretion capacity, and in otherwise healthy patients with acute cardiopulmonary disturbances. Consequently, arterial blood sampling is recommended when hypercapnia is clinically suspected, even in the absence of abnormal PETCO₂ . Postoperative intra-abdominal CO₂ retention results in increased respiratory rate and PETCO₂ of patients breathing spontaneously after laparoscopic cholecystectomy as compared with open cholecystectomy.^[32]

During CO₂ pneumoperitoneum, the increase of PaCO₂ may be multifactorial: absorption of CO₂ from the peritoneal cavity; impairment of pulmonary ventilation and perfusion by mechanical factors such as abdominal

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Figure 57-2 Ventilatory changes (pH, PaCO₂ , and PETCO₂ ) during carbon dioxide pneumoperitoneum for laparoscopic cholecystectomy. For 13 American Society of Anesthesiologists (ASA) class I and II patients, minute ventilation was kept constant at 100 mL/kg/min with a respiratory rate of 12 per minute during the study. Intra-abdominal pressure was 14 mm Hg. Data are given as the mean ± SEM.*, P < .05 compared with time 0.

distention, patient position, and volume-controlled mechanical ventilation; and depression of ventilation by premedicant and anesthetic agents in the case of spontaneous breathing ( Table 57-1 ). The observation of an increase in PaCO₂ when CO₂ , but not nitrous oxide (N₂ O) or helium, was used as the insufflating gas suggests that the main mechanism of the increased PaCO₂ during CO₂ pneumoperitoneum is absorption of CO₂ rather than the mechanical ventilatory repercussions of increased IAP.^[33] ^[34] ^[35] Accordingly, direct measurement of CO₂ elimination (V̇CO₂ ) using a metabolic monitor combined with investigation of gas exchange showed a 20% to 30% increase of V̇CO₂ without significant changes in physiologic dead space in healthy patients undergoing pelvic laparoscopy

Figure 57-3 Ventilatory changes as a function of patient physical status. The partial pressure of arterial carbon dioxide (PaCO₂ ) and end-tidal carbon dioxide tension (PETCO₂ ) were measured before and during carbon dioxide insufflation. Patients were grouped according to ASA classification: group 1 (open circles), ASA I (n = 20); group 2 (red circles), ASA II–III (n = 10). (Data from Wittgen CM, Andrus CH, Fitzgerald SD, et al: Analysis of the hemodynamic and ventilatory effects of laparoscopic cholecystectomy. Arch Surg 126:997, 1991.)

(IAP of 12 to 14 mm Hg) in the head-down position^[16] ^[19] ^[36] or laparoscopic cholecystectomy in the head-up position.^[19] ^[37] The time courses of the increase in V̇CO₂ and PaCO₂ are superposable. The absorption of a gas from the peritoneal cavity depends on its diffusibility, the absorption area, and the perfusion of the walls of that cavity. Because CO₂ diffusibility is high, absorption of large quantities of CO₂ into the blood and the subsequent marked increases in PaCO₂ would be expected to occur. The limited rise of PaCO₂ actually observed can be explained by the capacity of the body to store CO₂ ^[38] and by impaired local perfusion due to increased IAP.^[22] During desufflation, CO₂ accumulated in collapsed peritoneal capillary vessels reaches the systemic circulation, leading to a transient increase in PaCO₂ and V̇CO₂ . ^[6]

Respiratory changes during the laparoscopic procedure may contribute to increasing CO₂ tension. Mismatching of ventilation and pulmonary perfusion can result from

TABLE 57-1 -- Causes of increased PaCO₂ during laparoscopy

1. Absorption of carbon dioxide (CO₂ ) from the peritoneal cavity

2. V̇A/ mismatch: increased physiologic dead space

Abdominal distention

Position of the patient (e.g., steep tilt)

Controlled mechanical ventilation

Reduced cardiac output

These mechanisms are accentuated in sick patients (e.g., obese, American Society of Anesthesiologists class II or III)

3. Increased metabolism (e.g., insufficient plane of anesthesia)

4. Depression of ventilation by anesthetics (e.g., spontaneous breathing)

5. Accidental events

CO₂ emphysema (i.e., subcutaneous or body cavities)

Capnothorax

CO₂ embolism

(Selective bronchial intubation)

**TABLE 57-1** -- Causes of increased PaCO₂ during laparoscopy
1. Absorption of carbon dioxide (CO₂ ) from the peritoneal cavity
2. V̇A/ mismatch: increased physiologic dead space
Abdominal distention
Position of the patient (e.g., steep tilt)
Controlled mechanical ventilation
Reduced cardiac output
These mechanisms are accentuated in sick patients (e.g., obese, American Society of Anesthesiologists class II or III)
3. Increased metabolism (e.g., insufficient plane of anesthesia)
4. Depression of ventilation by anesthetics (e.g., spontaneous breathing)
5. Accidental events
CO₂ emphysema (i.e., subcutaneous or body cavities)
Capnothorax
CO₂ embolism
(Selective bronchial intubation)

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the position of the patient and the increased airway pressures associated with abdominal distention.^[23] ^[39] Lister and colleagues^[22] investigated the relationship between V̇CO₂ and intraperitoneal CO₂ insufflation pressure in pigs. For an IAP up to 10 mm Hg, increased V̇CO₂ accounts for the increased PaCO₂ . At higher IAP, the continued rise of PaCO₂ without a corresponding increase in V̇CO₂ results from an enlargement of respiratory dead space, as reflected by a widening of the Δa-ETCO₂ gradient.^[22] If controlled ventilation is not adjusted in response to the increased dead space, alveolar ventilation will decrease, and PaCO₂ will increase. In healthy patients, absorption of CO₂ from the abdominal cavity represents the main (or the only) mechanism responsible for increased PaCO₂ , ^[40] but in patients with cardiorespiratory problems, ventilatory changes also contribute significantly to increasing PaCO₂ . ^[28] PaO₂ values and intrapulmonary shunting do not change significantly during laparoscopy. ^[20] ^[28] ^[40]

Although increased PaCO₂ may be well tolerated by young, otherwise healthy patients, the extent to which hypercapnia is acceptable has not been determined and probably varies according to the patient's physical status. It is wise to maintain PaCO₂ within physiologic ranges by adjusting controlled mechanical ventilation. Except in special circumstances, such as CO₂ subcutaneous emphysema, correction of increased PaCO₂ can be easily achieved by a 10% to 25% increase in alveolar ventilation.