HEMODYNAMIC PROBLEMS DURING LAPAROSCOPY

Hemodynamic changes observed during laparoscopy result from the combined effects of pneumoperitoneum, patient position, anesthesia, and hypercapnia from the absorbed CO₂ . In addition to these pathophysiologic changes, reflex increases of vagal tone and arrhythmias can develop.

Hemodynamic Repercussions of Pneumoperitoneum in Healthy Patients

Peritoneal insufflation to IAPs more than 10 mm Hg induces significant alterations of hemodynamics.^{[71] [72] [73] [74] [75]} These disturbances are characterized by decreases of cardiac output, elevations of arterial pressure, and increases of systemic and pulmonary vascular resistances. Heart rate remains unchanged or increases only slightly. The decrease in cardiac output is proportional to the increase in IAP.^{[76] [77]} Cardiac output has also been reported to be increased^[78] or unchanged during pneumoperitoneum. ^{[79] [80] [81]} These discrepancies may be caused by differences in rates of CO₂ insufflation, IAP,^[82] steepness of patient tilt, time intervals between insufflation and collection of data, techniques used to assess hemodynamics, and anesthetic techniques. However, most studies have shown a fall of cardiac output (10% to 30%) during peritoneal insufflation whether the patient was placed in the head-down^{[83] [84] [85]} or head-up position.^{[86] [87] [88]} These adverse hemodynamic effects of pneumoperitoneum have been confirmed by studies using pulmonary artery catheterization,^{[85] [86] [88]} thoracic electrical bioimpedance,^{[84] [87]} esophageal echo-Doppler,^[89] and transesophageal echocardiography.^{[90] [91] [92]} Normal intraoperative values of venous oxygen saturation (SVO₂ ) and lactate concentrations suggest that changes in cardiac output occurring during pneumoperitoneum are well tolerated by healthy patients.^{[79] [88]} Cardiac output, which decreases shortly after the beginning of peritoneal insufflation, subsequently increases, probably as a result of surgical stress.^{[87] [88]} Hemodynamic degradation occurs mainly at the beginning of peritoneal insufflation.

The mechanism of the decrease of cardiac output is probably multifactorial ( Fig. 57-5 ). A decrease in venous return is observed after a transient increase in venous return seen at low IAPs (<10 mm Hg).^{[76] [82] [93] [94]} Increased IAP results in caval compression,^[95] pooling of blood in the legs,^[96] and an increase in venous resistance.^[93] The decline in venous return, which parallels the decrease in cardiac output,^{[76] [77]} is confirmed by a reduction in left ventricular end-diastolic volume measured using transesophageal echocardiography.^[90] Cardiac filling pressures, however, rise during peritoneal insufflation.^{[76] [85] [86] [88]} The paradoxical increase of these pressures can be explained by the increased intrathoracic pressure associated with pneumoperitoneum.^{[76] [86] [87] [97]} Right atrial pressure and pulmonary artery occlusion pressure can no longer be considered reliable indices of cardiac filling pressures during pneumoperitoneum. The fact that atrial natriuretic peptide concentrations remain low despite increased pulmonary capillary occlusion pressure during pneumoperitoneum further suggests that abdominal insufflation interferes with venous return.^[98] The reduction in venous return and cardiac output can be attenuated by increasing circulating volume before the pneumoperitoneum^{[93] [99]} ( Fig. 57-6 ). Increased filling pressures can be achieved by fluid loading or tilting the patient to a slight head-down position before peritoneal insufflation, by preventing pooling of blood with intermittent sequential pneumatic compression device,^[100] or by wrapping the legs with elastic bandages.^[101]

Although inotropism is difficult to assess,^[91] the ejection fraction of the left ventricle assessed by echocardiography does not appear to decrease significantly when IAP increases to 15 mm Hg.^{[90] [102]} However, all studies reported describe an increase in systemic vascular resistance during pneumoperitoneum. This increase in afterload cannot be considered simply to be a reflex sympathetic response to

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Figure 57-5 Schematic representation of the different mechanisms leading to decreased cardiac output during pneumoperitoneum for laparoscopy.

Figure 57-6 Changes in the cardiac index and systemic vascular resistance during laparoscopy in two groups of patients. For group 1 (controls, n = 10, filled bars), pneumoperitoneum was induced with patients in a 10-degree head-up position. Group 2 (volume loaded, n = 10, open bars) patients received 500 mL of lactated Ringer's solution before anesthesia induction and were insufflated in the supine position. Data are presented as the mean ± SEM.

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The increase in systemic vascular resistance is considered to be mediated by mechanical and neurohumoral factors.^[72] The return of hemodynamic variables to baseline is gradual and takes several minutes, suggesting the involvement of neurohumoral factors.^{[84] [86] [103]} Catecholamines, the renin-angiotensin system, and especially vasopressin are all released during pneumoperitoneum and may contribute to increasing afterload.^{[87] [88] [97] [98] [106] [107]} However, only the time course of vasopressin release parallels that of systemic vascular resistance. ^{[87] [88] [107]} Increases in plasma vasopressin concentrations have been correlated with changes in intrathoracic pressure and transmural right atrial pressure.^[97] Mechanical stimulation of peritoneal receptors also results in increased vasopressin release,^[108] systemic vascular resistance, and arterial pressure.^[109] However, whether increasing IAP to 14 mm Hg is sufficient to stimulate these receptors is unknown. The increase in systemic vascular resistance also explains why the arterial pressure increases, whereas the cardiac output falls.^{[72] [73] [75]} Use of α₂ -adrenergic agonists, such as clonidine or dexmedetomidine,^{[88] [110] [111] [112]} and of β-blocking agents^[113] significantly reduces hemodynamic changes and anesthetic requirements. Use of high doses of remifentanil almost completely prevents the hemodynamic changes.^[81]