Without evidence of benefit, an intervention should not be presumed to be beneficial or safe.

- Rogue Medic

Comments on High-Dose NTG for CHF


There are a couple of important comments to Unreasonable Fear of Hypotension and High-Dose NTG – Part I. In one, Brooks Walsh writes –

50 NTG tabs for 1 patient? Holy cow, that sounds labor intensive!


This would have been labor intensive.


There are 52 NTG tabs in that picture. The study protocol mentioned tabs, but I was using NTG spray.

If I had been using tabs, the patient might have ended up being treated for thrush, or for a seizure, due to the white paste in his mouth, rather than CHF.

Even with all of the not expired, still potent, NTG spray, his systolic blood pressure never dropped below 200 mm/Hg.

Did you have to have another ALS unit intercept to re-supply you with more little brown bottles?


Medium-size red spray bottles.


The spray level did descent like a low MPG fuel gauge.

In the other comment, JJ Greulich writes –

We were just talking about this today in Medic class.


This is a topic that seems to require a lot more time than most others, but after seeing large doses dramatically improve outcomes without any significant side effects, the concept seems to be easier to grasp.

I was curious as to why it is alright to give NTG or another Nitrate every 3-5 minutes without worrying about the BP tanking, but didn’t have time to ask. Can you elaborate on this a little for me?


I do not worry about why. Failed treatments are often supported by claims that the mechanism is _________. Those are the failed treatments.

Similarly, misplaced endotracheal tubes are often accompanied by the words – I saw it go through the cords.

We have known since the 1970s that most CHF patients are not fluid overloaded, but people continue to claim that we need to remove the imaginary fluid overload with furosemide (Lasix). That’s a reasonable explanation, but it’s lousy medicine.

Expect explanations to be wrong.

High-dose NTG works. The improvement in outcomes is repeatable, predictable, and results in many fewer deaths and many fewer intubations.

Pathophysiology can be years behind research, because pathophysiology is derived from research, the conclusions of which may be extrapolated well beyond what is reasonable. Pathophysiology tends to lead us to believe that we know more than we do.

This can lead to excessive caution, which is dangerous, or to recklessness, which can be just as dangerous as excessive caution being too safe.

Based on research, we could probably save half of the patients who will die due to acute CHF, if we would only stop trying to be safe.

We are killing our patients with caution and congratulating ourselves on how careful we are.

CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure) patients seem to be resistant to nitrates.

This may be similar to giving morphine to someone who has been taking regular doses of an opioid. To treat the patient’s pain, we need to give a much larger dose than would be needed for pain management for an opioid naive patient (no recent opioid use) with similar pain. The same is true for addicted patients, since tolerance is one part of what changes with addiction.

In-hospital treatment with nitrates can include nitrate holidays – temporary removal (holiday) of the nitrate to allow the tolerance to decrease.

The pathophysiology appears to be that high-dose NTG – especially when given as an IV Bolus – has much more of an effect on afterload (the resistance that the heart is pushing against and part of what is causing the failing heart to fail), than on anything else.

Large IV bolus doses of NTG to reduce afterload, even for hypotensive patients, may be the most beneficial drug treatment for acute CHF.

Go listen to the very first EMCrit podcast.

In under 10 minutes Dr. Weingart explains how to save the lives of crashing CHF patients.