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.