Article repost: high dose IV NTG post cardiac arrest

8jimi8

8jimi8

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Never heard this before.

Doesn't surprise me though. I have long advocated treating the cause of a cardiac arrest would lead to better outcomes.

Identifying that cause is the trick though. It seems in this instance the doctor made a effort at the end to treat a reversible cause with a therapy that might work rather than jst run the ACLS algorhytm and call it a day.

I don't think it would work all the time, but if it helps some people, it can't be that bad.

Of course some evidence based medicine extremist could argue that it works in so few cases that there is no statistically significant evidence it helps and therefore should not be attempted.
 
It's interesting to read, but it's just a case report. It's a single instance where the proposed novel therapy (in this case a large bolus dose of NTG), was associated with a good outcome.

With a single patient, it's impossible to know if the ROSC occurred because of a beneficial effect of the NTG bolus, despite a negative affect of the NTG, or whether the NTG being administered had nothing at all to do with it. The ROSC could have been a result of the prior standard ACLS treatment, or could represent a failure of the resuscitation team to identify ROSC when they terminated resuscitative efforts.

They report one other instance 26 years ago, where NTG was used under similar circumstances, and then go on to discuss acute heart failure / pulmonary edema patients. They don't really have any real numbers (in terms of the total number of patients).

Assuming that the NTG caused the ROSC because it was given beforehand, is a "post hoc ergo hoc" logical fallacy. Just because the NTG was given before ROSC, doesn't mean that it caused the ROSC. And the authors seem to recognise that -- they're just suggesting this as a possible hypothesis to investigate further in a real trial. Not that anyone cares what I think, but they've failed to convince me.
 
I doubt any sciencist would be convinced by two anecdotal case studies. This article was reposted for discussion.

You can whittle away at their reproducability or lack of controls, but the fact remains that an interesting piece of medicine is what was reported.

Are you at all interested in the pathophysiology they discussed concerning the large bolus of IV NTG?

*I don't even know who these DRs are, i have no dog in this hunt, other than interest in the subject and willingness to participate should there ever be a study.*
 
8jimi8 said:
Are you at all interested in the pathophysiology they discussed concerning the large bolus of IV NTG?
Click to expand...

Very much so. From the article:

"A possible explanation for the hemodynamic benefit of NTG in our patients is increased cardiac output produced by rapid vasodilatation in a heart operating at the extreme of the Frank-Starling curve. Vasodilators in heart failure with or without acute myocardial infarction have been proven to decrease left ventricular filling pressure and systemic vascular resistance while increasing cardiac index [7]. The more severe the failure, the more beneficial the effect of vasodilators [13]."
7:Bayley S, Valentine H, Bennett ED. The haemodynamic responses to incremental doses of intravenous nitroglycerin in left ventricular failure. Intensive Care Med. 1984;10:139–145. doi: 10.1007/BF00265803. [PubMed] [Cross Ref]
13:Flaherty JT. Comparison of intravenous NTG and sodium nitroprusside in acute MI. Am J Med. 1983;74:53–60. doi: 10.1016/0002-9343(83)90855-0. [PubMed] [Cross Ref]

I'm also wondering if the extreme?, amount of vasodilation of the coronary vasculature opens up some collateral circulation thereby improving the O2 delivery to the myocardium and aiding in the mechanics of a beating/ dying/ failing heart?

Interesting article!
 
Sam Adams said:
Very much so. From the article:

"A possible explanation for the hemodynamic benefit of NTG in our patients is increased cardiac output produced by rapid vasodilatation in a heart operating at the extreme of the Frank-Starling curve. Vasodilators in heart failure with or without acute myocardial infarction have been proven to decrease left ventricular filling pressure and systemic vascular resistance while increasing cardiac index [7]. The more severe the failure, the more beneficial the effect of vasodilators [13]."
7:Bayley S, Valentine H, Bennett ED. The haemodynamic responses to incremental doses of intravenous nitroglycerin in left ventricular failure. Intensive Care Med. 1984;10:139–145. doi: 10.1007/BF00265803. [PubMed] [Cross Ref]
13:Flaherty JT. Comparison of intravenous NTG and sodium nitroprusside in acute MI. Am J Med. 1983;74:53–60. doi: 10.1016/0002-9343(83)90855-0. [PubMed] [Cross Ref]

I'm also wondering if the extreme?, amount of vasodilation of the coronary vasculature opens up some collateral circulation thereby improving the O2 delivery to the myocardium and aiding in the mechanics of a beating/ dying/ failing heart?

Interesting article!
Click to expand...

More likely just decreased the peripheral resistance so what was left of the myocardium could overcome the back pressure I think.
 
Veneficus said:
More likely just decreased the peripheral resistance so what was left of the myocardium could overcome the back pressure I think.
Click to expand...


I think of it as letting the tires out of a semi wedged under a bridge.
 
Last edited by a moderator:
8jimi8 said:
I doubt any sciencist would be convinced by two anecdotal case studies. This article was reposted for discussion.

You can whittle away at their reproducability or lack of controls, but the fact remains that an interesting piece of medicine is what was reported.

Are you at all interested in the pathophysiology they discussed concerning the large bolus of IV NTG?
Click to expand...

Absolutely. I love physiology. Sorry if I came across as rude... I didn't mean to.

*I don't even know who these DRs are, i have no dog in this hunt, other than interest in the subject and willingness to participate should there ever be a study.*
Click to expand...

Me too.

All the best.
 
No biggie, Friend. Sometimes i'm a little automatically defensive...

stupid vicariously acquired defense mechanisms...
 
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