Pacing question

I can see what you are saying about the shorter have life of some vasopressors and also being able to titrate then, but if im seeing a narrow complex bradycardia, then atropine is the most obvious candidate. All you are doing is reducing the vagal tone on the heart, whereas with a vasopressor you are messing with so much more, like increasing the afterload. It is like taking your foot off the brake rather as opposed to mashing on the gas. Rember the simple concept of cardiac output equalling stroke volume x rate. When you see bradycardia and hypotension, atropine seems like a no brainer to me. Also consider that ischemia of the SA node could well be the reason for the hypotension, especially if this is an inferior MI
 
zzyzx said:
I can see what you are saying about the shorter have life of some vasopressors and also being able to titrate then, but if im seeing a narrow complex bradycardia, then atropine is the most obvious candidate. All you are doing is reducing the vagal tone on the heart, whereas with a vasopressor you are messing with so much more, like increasing the afterload. It is like taking your foot off the brake rather as opposed to mashing on the gas. Rember the simple concept of cardiac output equalling stroke volume x rate. When you see bradycardia and hypotension, atropine seems like a no brainer to me. Also consider that ischemia of the SA node could well be the reason for the hypotension, especially if this is an inferior MI
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So, you are correct that cardiac output is stroke volume x hr. However, they are both equally important. And while atropine is going to give you a boost in HR, it is generally going to hurt you in terms of stroke volume.

Infarcting ventricles do not contract well and they do not fill well. And yes, increasing the heart rate will increase cardiac output to a point. But once you get past that point you will decrease the fill time of the ventricle, and thus decrease the stroke volume.

This is also a dynamic process. As the infarct develops and ventricular wall motion worsens, the heart which liked a rate of 85 a few minutes ago may now perform better with a longer fill time of 70 bpm. You can titrate a pacer to find the rate your patient likes best as the infarct evolves. Once you give a dose of atropine, you are stuck.

That is why I, personally, would not elect for atropine in this clinical scenario.


Lastly, one more point- increasing afterload in a failing heart does seem counterintuitive. However, don't forget that most of the perfusion of the left ventricle myocardium happens during diastole and is thus dependent on the diastolic blood pressure. If the diastolic blood pressure is low, you are only allowing the infarct to worsen. Sometimes you have to drive the BP up to perfuse the coronaries, even at the expense of higher afterload. It is a very delicate balance.
 
@Nova1300 who are you? You should post more... I like the way you explain things.
 
Nova1300, I like your explanation too, and I look forward to hearing more from you.
I am going to ask some of the cardiologist that I see in the ER for their opinion on atropine vs vasopressors in this scenario. I'll try to ask a few of them so that I get different perspectives, and I'll come back to post in a few weeks and let you guys know what their opinions are.
 
Doctor. Anesthesia+CCM. Work 100% ICU. Split my time between CT surgery ICU, neuro ICU and extracorporeal LS.

And I'm a paramedic. Its why I got here.


Over time I have come to realize that much of my knowledge has been gained from quietly watching and listening to other providers, of many levels. So, I come here to learn. And sometimes to argue.

As a disclaimer, take what I say with a grain of salt. If there is anything this road has taught me, it's that I'm frequently still wrong.
 
I searched the site today for pacing vs. Dopamine and came across this thread and figured this is a good spot to ask this question...
I came across a case today a fellow Advanced Care Paramedic student had where a ~70 y/o male was having a massive right sided STEMI. Rate was in the 30's and pressure around 60/30.

Our three treatment options are atropine, pacing and dopamine if the patient does not respond to a 10ml/kg NaCl bolus.

I understand that atropine will increase the MVO2 of the myocardium, will dopamine not have this same effect? I know that they are two completely separate actions but both are chemically increasing the rate. We have standing orders for dopamine at 5ug/kg/min increasing Q5min to a max of 20ug/kg/min for cardiogenic shock. Is the better option to call for a pacing order (no standing order) in a right sided MI?
 
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