34. Cardiovascular Effects of CO2

34. Cardiovascular Effects of CO

Pneumoperitoneum

Lee L. Swanström, M.D., F.A.C.S.

Any surgical procedure elicits a physiologic response from the patient. This response is both acute, occurring during the procedure, and of intermediate dura- tion, during the healing/recovery phase. The causes of the host response are mul- tifactorial and include the psychological stress induced by the need for surgery, the effects of medication and anesthetic agents, the hormonally mediated stress response to the surgical insult, and mechanical effects peculiar to the procedure.

These mechanical effects include, but are not limited to, volume shifts from positioning, compression from retraction and exposure, induced transient organ ischemia, hypovolemia from blood and fluid loss, hypothermia, and a myriad of other factors. Perioperative surgical stress can affect any of the major organ systems. Of primary concern is its impact on the cardiovascular system, as this can be difficult to control and may be potentially dangerous for the patient.

Minimally invasive surgical techniques, as defined by access via small inci- sions, operative imagery by videoscopy, and exposure by instillation of insuf- flated gas, offer some physiologic advantage to patients (e.g., a lessened surgical stress response) at the cost of introducing other unique cardiovascular variables.

Cardiovascular changes in minimally invasive surgery can be categorized as those resulting from patient positioning, neurologically mediated responses, hypothermia, and absorption of insufflated gas as well as the pressure effects of insufflating a body compartment.

A. Effects of Positioning

In minimally invasive surgery, organ retraction and manipulation are com- promised by the small size of laparoscopic instruments. This drawback is, to a large extent, overcome by creative and sometimes radical positioning of the patient during surgery. In effect, the laparoscopic surgeon uses gravity to retract solid organs, viscera, or lungs away from the operative field. Various positions are described for different procedures and include Trendelenburg, reverse Tren- delenburg, lateral decubitus, and even prone. Some procedures such as colon resections may even require several changes of position during a single case.

These unusual position changes result in significant fluid shifts that are frequently amplified by positive-pressure insufflation. These position-related alterations should be foreseen and compensated for by the anesthetist.

For the most part, patients in exaggerated reverse Trendelenburg position have a decreased cardiac preload and subsequent decreased cardiac output (CO).

This should primarily be treated with volume replacement, although simple com-

pression stockings or sequential pneumatic compression devices have been pos- tulated to help as well. Patients in steep Trendelenburg position have the oppo- site problem, with dramatically increased right heart pressures secondary to increased central venous pressure. This can lead to right heart failure in sus- ceptible patients and should be treated with fluid restriction and even afterload reduction (nitrates, nitroprusside) in severe cases. Acute intraoperative changes are best handled initially by simply decreasing the acute angle of the position- ing, even if additional access ports need to be inserted to maintain exposure.

B. Neurologically Mediated Cardiac Effects

Although rare, cardiac output can be affected indirectly by pneumoperi- toneum via central nerve stimulation. The most common cause is a vasovagal reaction to peritoneal stretch. Although this is usually benign and self-limited, on occasion it can lead to profound bradycardia and even asystole and cardio- vascular collapse. Treatment consists of immediate desufflation of the abdomen, atropine administration, and CPR if necessary. A rarer cause of bradycardia is the increased intracranial pressure associated with pneumoperitoneum. In head- injured patients, this effect can result in a Cushing’s response in which the heart rate decreases but blood pressure increases. This can be further compounded by the acidosis associated with CO2 insufflation, which indirectly contributes to brain swelling and can even lead to cerebral herniation. For these reasons, a CO2

pneumoperitoneum should probably be avoided in patients with increased intracranial pressure.

C. Hypothermia

Unless insufflated gas is heated and humidified, it invariably induces hypothermia. Total body cooling can be surprisingly rapid because of the large area of exposed serosa and peritoneum as well as the vasodilation that occurs from the increased PCO2. If the core temperature drops below 34°, marked cardiac alterations such as bradycardia and decreased cardiac output may develop. These cardiac responses are attributed to direct myocardial depression as well as to the contradictory effects of peripheral vasoconstriction (the body’s compensatory response to hypothermia) and venous dilation (related to the sys- temic acidosis caused by the CO2 pneumoperitoneum). These cardiovascular alterations can be corrected by restoring the normal body temperature. It is best to avoid hypothermia by using warm blankets, “bear huggers,” and by warming and humidifying the CO2gas used to create the pneumoperitoneum.

D. Biologic Effect of Insufflated Gas

Although some have advocated the use of abdominal wall lifting devices (isobaric exposure techniques), positive-pressure pneumoperitoneum has long been recognized as the most effective and widely applicable method of abdom-

inal exposure. Thoracoscopy, on the other hand, because of the bony chest, can be carried out without positive-pressure insufflation although some surgeons prefer low-pressure pneumothorax. The most commonly used insufflation gas is CO2. CO2is inexpensive, inhibits combustion, is readily available, and is rapidly absorbed and metabolized by the patient. It is this rapid absorption and metab- olism that gives CO2its safety profile. It takes large amounts of intravascular CO2gas to cause an embolic event because the body has a large buffering capa- bility and is able to excrete excess absorbed CO2. These same biologic factors can also impact the cardiovascular system, however, and can lead to anesthesia management problems. CO2 is rapidly absorbed into the intravascular space because of its high solubility quotient.

Hypercarbia is associated with multiple cardiovascular alterations (Table 34.1). In general, CO2excess is well managed by humans because of the inher- ent buffering system of the intravascular and extravascular spaces. In addition, the pulmonary exchange mechanism whereby CO2is exchanged for oxygen via transalveolar diffusion is incredibly efficient. This ability to compensate, however, can be compromised in several instances.

CO2pneumoperitoneum has direct and indirect cardiovascular effects. These effects and alterations are amplified in patients whose homeostatic protective mechanisms are compromised (Table 34.2).

Once absorbed, CO2 combines with H2O to form carbonic acid, which dissociates into bicarbonate (HCO3-) and hydrogen ions (H⁺). The body’s impressive buffering capability helps limit the acidosis that ensues. CO2is also efficiently eliminated from the body by the lungs; however, the pneumoperi- toneum impairs ventilation to a varying extent. Furthermore, the acidosis results in profound vasodilation, which lowers the systemic vascular resistance and ele- vates the pulmonary vascular resistance. These alterations typically result in a lower blood pressure and an increased cardiac output. These effects are balanced by the sympathomimetic response that occurs as a result of peritoneal stretch and irritation and other alterations associated with pneumoperitoneum.

Table 34.1. The cardiovascular effects of absorbed CO2 from abdominal or thoracic insufflation.

Parameter Metabolic acidosis

Cardiac output Increased from lowered systemic vascular resistance Decreased from myocardial depression and elevated

pulmonary vascular resistance Net effect = slight decrease

Blood pressure Slight decrease from diminished cardiac output and vasodilation

Stroke volume Decreased due to myocardial depression Pulmonary vascular

resistance Increased

E. Cardiovascular Effects of Positive-Pressure Pneumoperitoneum

Positive-pressure insufflation provides the best exposure for intraabdominal and thoracic procedures as well as for operations where CO2is intentionally insufflated into subcutaneous tissue planes (e.g., for inguinal hernia repair). The size or, more correctly stated, the volume of the intracorporeal operative field to a large extent varies directly with the insufflation pressure (the higher the pres- sure, the better the exposure). Unfortunately, the untoward physiologic manifes- tations of CO2pneumoperitoneum (both gas- and pressure related) also directly correlate with the insufflation pressure. In general, pneumoperitoneum in excess of 15 mmHg has deleterious effects on the cardiovascular system. The pneu- moperitoneum compresses the vena cava and thus decreases venous return to the heart; this results in blood pooling in the lower half of the body and a decrease in cardiac output. Higher insufflation pressures also further impair ventilation by pushing up on the diaphragms. Last, the higher insufflation pressures also increase the systemic absorption of CO2. Under these circumstances the sys- temic acidosis worsens and, ultimately, the cardiac output decreases. This can, in extreme cases (in compromised patients or with very high insufflation pres- sures), lead to cardiovascular collapse or death.

Saffran et al. documented a 15% decrease in cardiac output and a 30%

increase in mean arterial pressure in patients undergoing CO2 pneumoperi- toneum at 15 mmHg pressure. Clinically, this studied patient population showed no adverse outcomes from pneumoperitoneum.

In normal patients, the effect of positive-pressure pneumoperitoneum or pneumothorax relates directly to decreased pulmonary efficiency and gas exchange. This, in turn, leads to an increase in acidosis with its well-known cardiac effects. Higher insufflation pressures can also compress the vena cava, which decreases venous return to the right heart and leads to a decreased cardiac output. The pressures generated by insufflation can therefore amplify the bio- logic activity of the absorbed CO2.

Table 34.2. Patients who are at increased risk of cardiovascular complications with standard CO2

pneumoperitoneum.

• Pulmonary hypertension

• Congestive heart failure or gross fluid overload

• ^Sepsis

• Hypovolemia/anemia (chronic or acute)

• Myocardiopathy

• Pulmonary dysfunction (chronic or acute)

F. Conclusion

In general, CO2pneumoperitoneum and pneumothorax are well tolerated.

The cardiac depressive effects of acidosis, decreased preload, and decreased sys- temic vascular resistance are usually mitigated by the sympathomimetic effects of surgical intervention and by anesthesia management (primarily hyperventila- tion and intravascular volume replacement). The net effect in a normal patient is therefore negligible. This homeostatic balance can be easily upset, however, by underlying patient disease: acidosis from other causes, respiratory failure, hypovolemia, or hypothermia. In such cases insufflation with CO2can lead to marked hypotension, decreased cardiac output, and even death. Awareness of the physiologic effects of CO2pneumoperitoneum and pneumothorax on cardiovas- cular function is critical for the surgeon. Such awareness allows for the safe application of this important surgical tool in appropriate patients.

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