Hemodynamic changes and complications result from many factors, including surgical intervention as previously mentioned, patient position, anesthesia, and variations in carbon dioxide (CO₂) tension. A body of literature indicates that peritoneal insufflation, regardless of the gas used, alters hemodynamics in both human beings and animals. Although variability is reported, the most consistent changes are those to cardiac output and vascular resistance. A decrease in cardiac output and concomitant increase in systemic vascular resistance are the most typical changes associated with increased abdominal pressure.^27-31 This occurs despite the frequently observed slight increase in heart rate with insufflation. The decrease in cardiac output has been measured using many different tools (e.g., pulmonary artery catheterization, esophageal Doppler echocardiography) and interestingly is seen in human and veterinary patients regardless of whether they are in a head-up or head-down position.^20,32,33 The decrease in cardiac output tends to parallel a decrease in venous return, which is believed to occur as a result of caval compression (with increasing insufflation pressure), pooling of blood in the caudal extremities, and changes in venous resistance.^27,28,34 It is interesting that despite a decrease in cardiac output, blood pressure changes are not consistent. In fact, blood pressure is often elevated in healthy patients with the increase in systemic vascular resistance offsetting the decrease in cardiac output.^{19,28,29,31,34} This increase in resistance is thought at least in part to be the result of vasopressin release during peritoneal stretch resulting from insufflation.^27,34,35 The anesthetist is cautioned not to become complacent when recording normal blood pressure values because there is evidence that tissue perfusion to abdominal organs is progressively decreased with increases in abdominal insufflation pressures.

As insufflation pressures increase into the range of 10 to 15 mm Hg, hepatic, renal, and mesenteric blood flows are decreased. In studies with pigs, intraabdominal pressures greater than 10 mm Hg were associated with significant reductions in hepatic artery and splanchnic blood flow.^36,37 In dogs, intraabdominal pressures in the range of 16 to 20 mm Hg decreased portal venous and mesenteric arterial flow.^38,39 Impairment of blood flow in other vessels (e.g., celiac artery) and to the intestinal mucosa is also reported for both dogs and pigs in this similar pressure range.^28,37,40 Oliguria is reported with pressures in the 15 to 20 mm Hg range, and anuria may be seen when pressures exceed this ranges.^37,40,41 (In dogs, renal blood flow and glomerular filtration rate were decreased by more than 75% with intraabdominal pressures of 20 mm Hg, and anuria was observed when abdominal pressures reached 40 mm Hg.^28,41 Similar findings were reported in pigs, in which oliguria was observed with pressures over 15 mm Hg.⁴⁰ Interestingly, in a single study in healthy cats, pneumoperitoneum up to an intraabdominal pressure of 16 mm Hg with CO₂ as the insufflation gas did not significantly influence cardiovascular parameters; regional blood flow was not evaluated.⁴²

Although healthy cats did not show changes in measured parameters during peritoneal insufflation, it is important to remember that cardiovascular function may be further influenced by the patient’s health status, positioning during anesthesia and surgery, duration of the procedure, and type of insufflation gas.

Respiratory function is also altered during laparoscopic intervention. The increase in abdominal pressure and volume limits diaphragmatic excursion and reduces pulmonary compliance, functional residual capacity, and vital capacity of the lung and may lead to ventilation/perfusion mismatch.^28,34,46-48 Hence, it is not surprising that the effects tend to be proportional to insufflation pressures as is shown in young swine⁴⁹ and adult dogs.^34,50 In spontaneously breathing dogs, the respiratory rate remained unchanged with abdominal insufflation, but a significant reduction in tidal volume was reported.⁵⁰ With volume-controlled ventilation, maintenance of tidal volume results in an increase in peak inspiratory pressure,³⁴ and hypercapnia and hypoxemia might still occur. Similarly, when using pressure-controlled ventilation, the peak inspiratory pressure must be increased to overcome the decrease in lung compliance and avoid a reduction in tidal volume. The resulting positive pressure in the chest has an additional impact on reducing venous return, and thus cardiac output could be further compromised.

In spontaneously breathing animals, the decrease in tidal volume and increase in end-tidal CO₂ are proportional to increasing insufflation pressure, and the negative impact lasts longer in animals exposed to the higher pressures.⁵⁰ This reflects fatigue on the part of the patient and has led to the common recommendation for mechanical ventilation in patients when the procedure is anticipated to last longer than 15 to 30 minutes.

The inability for patients to compensate for the elevation in CO₂ by adjusting their ventilation is even more notable when CO₂ is used as the insufflation gas as is common practice. This is because CO₂ is highly diffusible and enters the bloodstream, contributing to a rise in arterial tension. Hence, the impact on ventilation is greater than insufflation with an inert gas such as helium or with other gases such as nitrous oxide (N₂O) or air (albeit those gases have other disadvantages).^51-53 An increase in arterial CO₂ tensions may initially be cardiovascularly supporting^27,51 but will ultimately result in a concurrent decrease in blood pH, which in turn has a potential to impact cellular metabolic processes. Elevated CO₂ tensions are also associated with increased cerebral blood flow,^54,55 but additional mechanisms may exist.⁵⁶ In compromised patients or those breathing a low inspired oxygen tension, excessive CO₂ ­levels may contribute to hypoxemia. In addition, CO₂ tensions greater than 90 mm Hg have anesthetic effects in their own right.⁵⁷

As for the cardiovascular system, additional factors such as positioning may further impact respiratory effects.^19,46,47,58 Both the Trendelenburg and reverse Trendelenburg positions have a negative impact on lung expansion because of increased lung and chest wall impedance.⁵⁹ The observed decrease in lung compliance and volumes, such as functional residual capacity and total and vital lung capacity^46,47,60,61