Bradycardia after nitro administration

[Nova1300]

I find atropine to be rather sneaky. In some patients it brings about a modest increase in HR at low doses. In others, they skyrocket. Also, if I were to use it in this patient it would be worked in very slowly -- but therein lies another problem, the so called " paradoxic effect" of low dose atropine.

If I was going to raise this patients HR with drugs, it would likely be with robinul, to keep the anticholinergic out of the brain and because I'm more comfortable with its effects.

But I still like electricity. And I'm stubborn.

 

[Veneficus]

Whether or not it's desirable to treat sinus bradycardia and marginal blood pressure in the setting of acute inferior/posterior STEMI is situational and always controversial when discussed although Braunwald talks about the desirability of using atropine when the patient is showing signs of shock and states that ST-elevation even resolves somewhat after 0.5 mg atropine.

I first disclaim I do not like cardiology.

But looking at this statement, it makes perfect sense. If a patient has clinical evidence of shock, there is a failure of delivery of O2. Assuming, no anemia, good heme saturation, and no hemorrhage, with a catecholamine response to stress, it would likely minimize the effects of loss of vascular capilary tone, with any dilation from NTG (GTN) in the venous system.

Increasing cardiac output, theorhetically should increase venous return right?

So from the logical point Q=SV x HR,

increasing HR is more easily achieved than stroke volume in injured cardiac tissue.

I see the argument of increasing demand, but also in a bit of logic, the tissue most likely injured because of increased demand is behind the block. Not receiving direct blood supply (with atropine) but maybe some from collateral circulation.

The Actual tissue with metabolic increase still should have intact blood supply. Which I would expect to be able to meet its increased demands by the increased output.

One of the most devastating parts of shock is when the heart cannot meet its own circulatory demands. More output will intervene in that.

But I highlighted what I think to be the key phrase to the whole argument.

It doesn't stipulate showing bradycardia, or low BP, it directly talks about inadequete tissue perfusion of such extent to produce clinical signs.