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:
· Pneumoperitoneum
· 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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