In order to obtain surgical exposure, carbon dioxide is insufflated into the abdomen. This leads to a number of physiologic changes affecting different organ systems that the anesthesiologist must be aware of. These changes tend to be insufflation pressure-dependent, such that the greater the insufflation pressure, the greater the effect on various organ systems. At this time, it is recommended to maintain insufflation pressures below 15 mmHg if possible and below 12 mmHg in cases of steep Trendelenburg [6].

Insufflation has several effects on the cardiovascular system. There can be many reactions to initial insufflation, including tachycardia and hypertension . Response to insufflation includes release of catecholamines and vasopressin with renin-angiotensin activation [7]. Also of great concern is the potential for a vasovagal reaction resulting in severe bradycardia and hypotension, which may be significant enough to lead to asystole and cardiac arrest. This may respond to anticholinergic agents such as glycopyrrolate or in more severe cases atropine or vasopressors such as ephedrine. In cases of hemodynamic instability, the surgeons should be notified to desufflate the abdomen immediately and allow the patient time to recover prior to reinsufflation. Following treatment with anticholinergic agents and adequate recovery time, insufflation can be attempted again slowly; usually subsequent attempts do not lead to such significant hemodynamic consequences. Other complications associated with initial insufflation include hemorrhage due to blood vessel injury during trocar placement and carbon dioxide embolism, resulting in cardiovascular collapse. The latter complication has been shown to occur with a much higher frequency than would be thought, though the incidence of clinically significant embolism is low [8]. The diagnosis can be made by transesophageal echocardiography, along with a high degree of suspicion from the timing of events.

Venous return is altered during insufflation. While initially there is an increase in venous return due to compression of the splanchnic circulation, subsequently there is a decrease, due to interference of venous flow from the lower extremities, ultimately leading to a drop in cardiac output and potential hypotension. Patients who are already intravascularly depleted are more at risk for this complication.

Transesophageal echo evaluation during pneumoperitoneum has shown conflicting results with regard to left ventricular ejection fraction (EF). Though some studies have shown no overall effect on EF, a more recent study documented an initial decrease felt to be related to increased afterload followed by a subsequent recovery, often facilitated by positioning in the Trendelenburg position [9]. The author has noted direct distortion of the cardiac profile during pneumoperitoneum, with compression of the right ventricle and rotation of the cardiac axis. Though usually tolerated, this may be of significance in a patient with already compromised cardiac function. The release of catecholamines secondary to the pneumoperitoneum may add stress to patients with preexisting coronary artery disease and, combined with increased afterload and tachycardia in the presence of diastolic dysfunction, may lead to ischemia and cardiac decompensation [9].

Many aspects of the respiratory system are affected during robotic procedures. Functional residual capacity, already compromised by anesthesia, undergoes further reduction as a result of the pneumoperitoneum, causing diaphragmatic elevation, lung compression, and decreased pulmonary compliance. This in turn can lead to high peak pressures and an increased risk of barotrauma. Carbon dioxide is used to create the pneumoperitoneum, which is absorbed by patients to a varying degree and leads to a variable rise in PaCO₂, necessitating increased minute ventilation. It is estimated that between 14 and 48 mL/min of CO₂ is absorbed during laparoscopic procedures [10]. Just over 5% of the time, PaCO₂ rises at a greater rate than can be removed and severe hypercapnia results. This in turn results in a significant respiratory acidosis. The use of bicarb is contraindicated here due to the ultimate rise in CO₂. Though patients often tolerate some degree of respiratory acidosis well, rises in potassium can be seen with this technique and can be significant [11]. One also must bear in mind the effects of hypercarbia on pulmonary artery pressures, especially in those with preexisting pulmonary hypertension . It is important to remember that as PaCO₂ rises, PetCO₂ can become a less reliable reflection of PaCO₂ (difference increases) due to increased dead space or V/Q mismatch, or both.