Leading causes
The above-mentioned vagal response is a cause of cardiovascular collapse during laparoscopy. This pathophysiology is usually self-limiting in a healthy patient. By releasing the pneumoperitoneum and supporting the patient while the sympathetic nervous system resets, normal cardiopulmonary physiology can usually be reestablished. Additionally, antimuscarinic agents (either glycopyrrolate or atropine) are often administered by the anesthesia team to combat bradycardia, interrupting the vagal signaling arc and decreasing the incidence of bradycardia. Glycopyrrolate has a longer duration of action and does not cause central anticholinergic syndrome, but is the slower-onset of the two commonly-used antimuscarinics. Occasionally, sympathomimetics (ephedrine or epinephrine) are needed to raise the heart rate if unresponsive to atropine. The other two leading causes of cardiovascular collapse can be much more malignant and require more intervention. These are accidental vascular injury and/or carbon dioxide embolism caused in relation to the formation of the pneumoperitoneum.
The rate of vascular injury is 0.03%-0.06%3. An Australian study reported a rate of 7/10,000 for vascular injury with a 23-56% mortality rate resulting9. The most common injured major blood vessels are the abdominal aorta followed by the common iliac vessels however mesenteric and all other intraabdominal vessels are at risk. The injury of these large vessels leads to exsanguination and resulting hemorrhagic sock. This condition is diagnosed first by a flash of blood through the insufflating device followed by tachycardia and hypotension. These are the hallmarks of acute blood loss. Cardiovascular collapse ensues when intravascular volume and pressure are lost and the heart, as well as other organs, are no longer perfused.
The incidence of carbon dioxide embolism during laparoscopy is much more elusive. Trans-esophageal echocardiogram during routine laparoscopy has shown gas bubbles present in the right heart in 6.25 to 100% of all cases10,11. Granted, the majority of these emboli are asymptomatic. It is estimated that clinically relevant emboli occur in 0.001% of laparoscopies of which 28% are fatal10. Dog and pig studies have demonstrated that it would take greater than 70 cc/minute of direct injection of intravascular carbon dioxide to cause cardiovascular collapse4,11. Normal laparoscopic low flow rates should only introduce 5% of that volume10. Carbon dioxide embolism causes gas bubbles to be trapped and occlude the pulmonary vasculature. This results in a V-Q mismatch which causes hypoxia and hypercapnia. This loss of oxygen and respiratory acidemia results in decreased oxygenation and acidosis of the heart and other organs and organ failure. Carbon dioxide embolism is diagnosed by cyanosis, bradycardia and hypotension. End tidal carbon dioxide, measured during ventilation, rapidly increases then drops off dramatically. The pathognomonic mill-wheel murmur is heard as trapped gas bubbles are heard in the right heart. Precordial Doppler has been used in the past to also recognize this trapped gas. While rare, carbon dioxide may also cross a patent foramen ovale and cause arterial occlusion. This is considerably less dangerous than arterial air given the solubility of carbon dioxide in blood, but nonetheless is a potential cause of embolic stroke.