Sympathectomies and atropine

charles-thor · Oct 14, 2005

This is such a great topic, but I’m probably bias as this was the focus of my research requirement for school. Bradycardia leading to cardiac arrest with spinal anesthesia is probably a more common problem than many people believe with an estimated incidence of somewhere between around 7/10,000 spinal anesthetics.

Originally bradycardia and subsequent cardiac arrest during sab was believed to be directly related to over sedation leading to hypoxia and cardiovascular instability. Today, however, we know this in fact not the case. Although there is no universally agreed upon answer as to why this occurs, its mechanism is believed to originate from 2 sources:

1.) An unopposed vagal tone secondary to sympathectomy. This sympathectomy occurs 2-6 dermatomes higher than sensory block, so that a sensory block of T6 can conceivably inhibit all of the sympathetic innervation to the heart.

2.) The Bezold-Jarisch reflex – which may be widely under appreciated phenomenon. You’ll be surprised how many clinicians are not well versed in this essential physiology.

Sympathectomy → reductions in venous tone → profound decreased venous return. This activates mechanoreceptors embedded within the walls of the myocardium → stimulating vagal afferents → vasomotor center of medulla → increased vagal tone to the heart, thus slowing or stopping the heart entirely to allow enough filling time to generate an effective stroke volume. At first glance, this point seems counter intuitive, however ask yourself -what good is reflexively increasing HR in the relative absence of blood to pump forward?

I could go on and on here, but I’ll stop and answer Kat’s questions.

Atropine is largely ineffective for bradycardia in this situation, as it removes parasympathetic tone, but has no DIRECT action on the myocardium. If you have chemically dennervated the heart, than you have little to no (depending on the level of block and dose of atropine) autonomic influence to the heart. This does not necessarily result in asystole, because the SA node and the rest of the conduction system demonstrate automaticity. Think of the heart transplant patient.

Many will argue the early use of atropine (glycopyrolate is a much weaker chronotrope) or ephedrine, but if these don’t work VERY EARLY, you should promptly switch to epinephrine. This will offer ino/chronotropic support and more importantly restore venous tone/return and support, which was the original cause of the problem.

Here are 2 great articles:

Caplan et al. Unexpected cardiac arrest during spinal anesthesia. Anesthesiology. 1988;68:5-11.

Campagna JA, Carter C. Clinical relevance of the Bezold-Jarisch reflex. Anesthesiology. 2003 May;98(5):1250-60.

Appreciating the potential height of the sympathectomy, maintaining preload, and prompt intervention with epinephrine for bradycardia during sab are thus essential to prevent ensuing cardiac arrest.

versatile_kat · Oct 14, 2005

This is such a great topic, but I'm probably bias as this was the focus of my research requirement for school. Bradycardia leading to cardiac arrest with spinal anesthesia is probably a more common problem than many people believe with an estimated incidence of somewhere between around 7/10,000 spinal anesthetics.
Originally bradycardia and subsequent cardiac arrest during sab was believed to be directly related to over sedation leading to hypoxia and cardiovascular instability. Today, however, we know this in fact not the case. Although there is no universally agreed upon answer as to why this occurs, its mechanism is believed to originate from 2 sources:
1.) An unopposed vagal tone secondary to sympathectomy. This sympathectomy occurs 2-6 dermatomes higher than sensory block, so that a sensory block of T6 can conceivably inhibit all of the sympathetic innervation to the heart.
2.) The Bezold-Jarisch reflex - which may be widely under appreciated phenomenon. You'll be surprised how many clinicians are not well versed in this essential physiology.
Sympathectomy → reductions in venous tone → profound decreased venous return. This activates mechanoreceptors embedded within the walls of the myocardium → stimulating vagal afferents → vasomotor center of medulla → increased vagal tone to the heart, thus slowing or stopping the heart entirely to allow enough filling time to generate an effective stroke volume. At first glance, this point seems counter intuitive, however ask yourself -what good is reflexively increasing HR in the relative absence of blood to pump forward?
I could go on and on here, but I'll stop and answer Kat's questions.
Atropine is largely ineffective for bradycardia in this situation, as it removes parasympathetic tone, but has no DIRECT action on the myocardium. If you have chemically dennervated the heart, than you have little to no (depending on the level of block and dose of atropine) autonomic influence to the heart. This does not necessarily result in asystole, because the SA node and the rest of the conduction system demonstrate automaticity. Think of the heart transplant patient.
Many will argue the early use of atropine (glycopyrolate is a much weaker chronotrope) or ephedrine, but if these don't work VERY EARLY, you should promptly switch to epinephrine. This will offer ino/chronotropic support and more importantly restore venous tone/return and support, which was the original cause of the problem.
Here are 2 great articles:
Caplan et al. Unexpected cardiac arrest during spinal anesthesia. Anesthesiology. 1988;68:5-11.
Campagna JA, Carter C. Clinical relevance of the Bezold-Jarisch reflex. Anesthesiology. 2003 May;98(5):1250-60.
Appreciating the potential height of the sympathectomy, maintaining preload, and prompt intervention with epinephrine for bradycardia during sab are thus essential to prevent ensuing cardiac arrest.

You rock ...

NCgirl · Oct 14, 2005

You do indeed rock! I've wondered the same thing myself.

Lorus · Oct 15, 2005

Thanks thor - great post