and animals. While 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 [41–45]. 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 [33, 46, 47]. The decrease in cardiac output tends to parallel decreases 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 [41, 42, 48]. These effects seem to be enhanced in the reverse Trendelenburg position while less pronounced in the Trendelenburg position, likely due to gravity further influencing venous return [49]. 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 [32, 42, 43, 45, 48]. This increase in resistance is thought at least in part to be the result of abdominal aortic compression and neuroendocrine effects during peritoneal stretch resulting from insufflation [31, 42,49–51]. Plasma levels of norepinephrine, epinephrine, cortisol, vasopressin, atrial naturetic peptide, renin, and aldosterone have been shown to be elevated during pneumoperitoneum [52]. The anesthetist is cautioned not to become complacent when recording normal blood pressure values, as 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 10–15 mmHg, hepatic, renal, and mesenteric blood flows are decreased. In studies with pigs, intra‐abdominal pressures greater than 10 mmHg were associated with significant reductions in hepatic artery and splanchnic blood flow [53, 54]. In dogs intra‐abdominal pressures in the range of 16–20 mmHg decreased portal venous and mesenteric arterial flow [55, 56]. 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 [42, 54, 57]. Oliguria is reported with pressures in the 15–20 mmHg range and anuria may be seen when pressures exceed this ranges [42, 57, 58]. The decrease in renal blood flow leads to an increase in renin and aldosterone levels [59]. In dogs, renal blood flow and glomerular filtration were decreased by over 75% with intra‐abdominal pressures of 20 mmHg, and anuria was observed when abdominal pressures reached 40 mmHg [42, 58]. Similar findings were reported in pigs, where oliguria was observed with pressures over 15 mmHg [57]. Albeit uncommon, patients with chronic kidney disease may be at higher risk for acute kidney injury during laparoscopic surgery [60–62].
Interestingly, in a single study in healthy cats, pneumoperitoneum up to an intra‐abdominal pressure of 16 mmHg with carbon dioxide as the insufflation gas did not significantly influence cardiovascular parameters, albeit ventilation seemed to be negatively impacted; regional blood flow was not evaluated [63]. While 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 the type of insufflation gas.
Figure 7.3 Dog prepared for laparoscopic intervention in Fowler position (reverse Trendelenburg).
For example, head up – also known as Fowler or reverse Trendelenburg – (Figure 7.3) positioning can compromise venous return and cardiac output due to gravitational effects. This is of greater consequence during anesthesia due to the blunting of baroreceptor reflexes. During Trendelenburg positioning, there is an increase in venous return from the pelvic limbs. However, cardiac output again decreases, but the reasons differ and include decreases in heart rate and vasomotor tone [64, 65]. In anesthetized dogs, both body positions have further compromised cardiac output during pneumoperitoneum, with the reverse Trendelenburg position having the most significant impact [47]. There is also increasing concern regarding changes in intracranial pressure, which will compound those seen with carbon dioxide pneumoperitoneum. A recent study has shown a correlation between laparoscopic insufflation pressures and intracranial pressure in human patients undergoing laparoscopic ventriculoperitoneal shunt placement [66]. While unlikely to be serious in healthy patients, this could be of great significance in patients with intracranial disease.
Peritoneum distension due to abdominal insufflation may increase vagal tone and cause bradyarrhythmias, with a reported incidence between 14 and 27% in healthy young humans [67, 68]. Bradycardia should be addressed quickly as it may be an early indication of cardiac arrest [69, 70].
Respiratory Effects
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 [42, 48,71–73]. Hence, it is not surprising that the effects tend to be proportional to insufflation pressures as is shown in young swine [74] and adult dogs [48, 75]. In spontaneously breathing dogs, respiratory rate remained unchanged with abdominal insufflation, but a significant reduction in tidal volume was reported [75]. With volume‐controlled ventilation maintenance of tidal volume results in an increase in peak inspiratory pressure [48], 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 carbon dioxide are proportional to increasing insufflation pressure and the negative impact lasts longer in animals exposed to the higher pressures [75]. This reflects fatigue on the part of the patient and has led to the common recommendation for mechanical ventilation in patients in whom the procedure is anticipated to last longer than 15–30 minutes.
The inability for a patient 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 blood stream 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) [76–78]. An increase in arterial CO2 tensions may initially be cardiovascularly supporting [41, 76], but will ultimately result in a concurrent decrease in blood pH which in turn has a potential to impact cellular metabolic processes. The cardiac rhythm may also be affected by the increase in CO2 tensions and resulting acidosis and increased sympathetic tone, which can lead to tachycardia, premature ventricular contractions, and in rare occasions ventricular tachycardia and fibrillation [79].
Elevated CO2 tensions are also associated with increased cerebral blood flow [80, 81], but additional mechanisms may exist [82]. 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 mmHg have anesthetic effects in their own right [83].
As for the cardiovascular system, additional factors such as positioning may further impact respiratory effects [32, 71, 72, 84]. Both Trendelenburg and reverse Trendelenburg positions have a negative impact on
