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What are the cardiovascular changes associated with laparoscopic surgery?
Although laparoscopic surgery is tolerated well by most, it may produce adverse consequences in those with limited cardiac reserve. The hemodynamic changes occurring during laparoscopy result from the combined effects of:
· Systemic absorption of CO2
· Patient positioning
Cardiovascular changes are proportional to the intra-abdominal pressure (IAP) attained. Peritoneal insufflation to IAPs >10 mmHg induces significant alterations in hemo-dynamics. As IAP increases, the cardiovascular changes associated with the pneumoperitoneum are biphasic in nature. Cardiac output decreases to 50% of preoperative levels 5 minutes after the onset of CO2 insufflation and then gradually increases back toward baseline 10 minutes after the onset of insufflation.
Increased IAP causes compression of the abdominal arterial and venous vessels. Aortic compression contributes to an increase in systemic vascular resistance (SVR), which may result in a decrease in cardiac output. A second cause of increased SVR is compression of the splanchnic circula-tion, in both the venous and arterial systems. The effect of an increase in SVR on cardiac output is dependent upon the patient’s volume status. A modest fall is seen in normo-volemic patients, with a more pronounced fall in hypo-volemic patients. Neurohumoral factors, such as circulating catecholamines, renin/angiotensin, and vaso-pressin, may also influence the cardiovascular response to the pneumoperitoneum.
Venous compression causes a decrease in venous return, and a consequent decrease in preload. Paradoxically, central venous pressure (CVP) and pulmonary capillary occlusion pressure (PCOP) rise during insufflation. This increase is secondary to a cephalad shift of the diaphragm due to increased intra-abdominal contents and pressure. This translates into increased intrathoracic pressures. Consequently, pressures obtained by transvenous catheters may not be reflective of true volume status. Increasing the circulating volume prior to establishment of the pneumo-peritoneum may attenuate the decreases in venous return and cardiac output.
Dysrhythmias, more commonly bradycardias or asystole, occur most often during early insufflation. This may be the result of sudden stretching of the peritoneum with an abrupt increase in vagal tone. If treatment is necessary, vagolytic drug therapy and decreasing the IAP are often helpful.
The induction of the pneumoperitoneum has the least consequences if done with the patient in the level, supine position.
The absorption of CO2 has effects at various sites in the body, often with opposing results. The direct effects are ini-tially inhibitory causing decreases in heart rate, contractility, and SVR. Counteracting these effects is the stimulation of the sympathetic nervous system, causing increases in heart rate, contractility, and SVR. If acidosis should develop, the parasympathetic effect may be enhanced.
Tachycardias and premature ventricular contractions resulting from CO2 are usually benign, yet in the presence of severe hypercapnia, may be fatal. This hypercapnia may potentiate the vagal stimulation associated with peritoneal insufflation and can produce bradydysrhythmias or asystolic arrest.
The site of surgery determines the patient’s position dur-ing laparoscopic surgery. The Trendelenburg position is used for pelvic and inframesocolic procedures (e.g., ovarian cystectomy or appendectomy); the reverse Trendelenburg position is used for supramesocolic operations (e.g., chole-cystectomy). These positions may contribute to the hemo-dynamic changes associated with laparoscopic procedures.
The cardiovascular effects of the Trendelenburg posi-tion are multifactorial. The changes associated with this position are related to the degree of head-down tilt, patient’s age, intravascular volume status, associated car-diac disease, ventilation techniques and anesthetic drugs. In the healthy patient, the Trendelenburg position favors venous return and improves cardiac output. If intact baro-receptor responses are maintained, compensatory responses are activated, and there is a decrease in heart rate and vaso-dilation. With all reflexes intact, the overall effect of the Trendelenburg position is insignificant. However, in patients with coronary artery disease, the increase in central blood volume is associated with a deleterious increase in myocar-dial oxygen demand as the ventricular volume is increased.
The reverse Trendelenburg position results in a decrease in venous return that is reflected as a decrease in mean arterial pressure and cardiac output. In healthy patients, the reduction in cardiac output is insignificant. In those with pre-existing cardiac disease, these changes may not be benign. The already diminished cardiac output may be lessened further, reducing already compromised end-organ perfusion.
The lateral tilt has minimal hemodynamic effects. It may occasionally counteract the adverse effects of the reverse Trendelenburg position. Extreme right lateral positioning may obstruct the vena cava, decreasing venous return.
In summary, the alterations in cardiovascular function are dependent on the patient’s status (intravascular volume, pre-existing disease, neurohumoral factors) and surgical factors (IAP, patient position, CO2 absorption, ventilation strategy, nature and duration of the procedure).
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