Hypotensive CHF

jcroteau

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What is the best way to treat a hypotensive CHF patient?

Our normal course of action here for a normotensive patient would be nitro (SL,IV or patch) and CPAP (both which could reduce pressure even further).

If they are hypotensive we can start a Dopamine drip and talk about CPAP with a doctor.

My main question is, if you use Dopamine to increase their pressure, would it then be acceptable to go back to nitro and CPAP? Cause that's what they need in the end ya?
 
What is the best way to treat a hypotensive CHF patient?

Our normal course of action here for a normotensive patient would be nitro (SL,IV or patch) and CPAP (both which could reduce pressure even further).

If they are hypotensive we can start a Dopamine drip and talk about CPAP with a doctor.

My main question is, if you use Dopamine to increase their pressure, would it then be acceptable to go back to nitro and CPAP? Cause that's what they need in the end ya?

Yes. Could also think about levophed instead, if you have it. CPAP can reduce BP, but it's usually minimal. That minimal drop in BP might be worth it, because CPAP should hopefully reduce their breathing rate, which can lead to better systemic perfusion. Also can have some beneficial outcome on the preload.

The prognosis of this patient is crap.
 
I assume you mean a patient whose pulmonary congestion is secondary to LV failure? The fix is to improve cardiac output by giving an inotrope and if necessary, an afterload reducer, such as nitroprusside. I'm not quite as up on this stuff as I used to be so there may be something newer out there, but to my knowledge dobutamine and the PDE inhibitors are still the best single drugs to use, because they increases inotropy while also giving some after load reduction, which is exactly what you want. Dobutamine can cause tachycardia though, which is bad.

CPAP might help the pulmonary congestion but if they are already hypotensive, I'd be very careful with it. The higher pulmonary pressures that exist in pulmonary congestion make the patient more susceptible to the hypotensive effects of increases airway pressures.
 
So I ask you, what kind of CHF? And what is going wrong in each type of CHF? Can you tell them apart in a prehospital patient?

You have two circuits, each with a pump.
For each you think, Preload Afterload Contractility!

Usually in CHF, in at least one circuit, there is some combination of:
Too much preload
Too much afterload
Not enough contractility

Think really hard about what vasoactive medications do!!!
Why do we give something like nitro?
What does Norepi do to afterload? Is it a good drug in CHF?
What does Dopamine do to afterload and contractility and in what dose ranges?
What are other drugs that the patient might be on and how do they work? What about dig?
What is Dobutamine? How does it work and what are its effects?
What is Milrinone and what does it do?
 
The overall answer is to correct what is causing their left ventricular failure. The most common cause of exacerbated LVF is dysrhythmia (e.g. VT or STEMI).

Inotropes are only a temporising measure until the underlying problem is treated. Sometimes the underlying problem is not completely reversible for example a pt with dilational cardiomyopathy or LVH where the EF has become increasingly poor as the heart is so damaged it simply won't contract enough. I have seen pts with EF as low as 15 or 20% and they are essentially permanently in their chair in the lounge or in bed because their SOBOE is so bad

In somebody with heart failure where GTN is contraindicated due to their hypotension, even if I got their pressure up with fluids or inotrope I wouldn't be overly keen on giving them GTN. There is no specific guidance in the CPGs on this but to me it seems like a bad idea.
 
A quick answer from a doc;

Dobutamine
Dopamine
Nitro drip.
 
A quick answer from a doc;

Dobutamine
Dopamine
Nitro drip.

This... A lot of people will swap out Dopamine for Levophed, that's how our protocols look. Hypotensive heart failure = cardiogenic shock. These patient have crap prognosis and are some of the most difficult to manage as well. We would also inquire about volume already given, and likely give a small 250ml bolus and obtain a lactate level at bedside. Epi infusion is also way down the line if all else is failing... Although the studies shown they don't decrease morbidly or mortality, these patients will likely buy themselves a balloon pump as a temporary bridge / assist....


I have know also seen some ED docs give push bolus of Phenyl while they are trying to order labs and infusions. Problem with that is it will increase your SVR. Although it will make your monitor numbers look great it will result in less cardiac output.
 
I have know also seen some ED docs give push bolus of Phenyl while they are trying to order labs and infusions. Problem with that is it will increase your SVR. Although it will make your monitor numbers look great it will result in less cardiac output.
Wouldn't Levo essentially do the same thing, considering Levo has little beta crossover.
 
Wouldn't Levo essentially do the same thing, considering Levo has little beta crossover.

The goal in managing heart failure is to increase CO by improving inotropy and decreasing SVR. As a pure vasoconstrictor that does nothing to help contractility and in fact often reduces CO, phenylephrine does pretty close to exactly the opposite of what you are trying to achieve in managing heart failure.

Norepinephrine actually has plenty of beta1 effects, I think it's like 30% of its action at lower doses and more at higher doses. It is often preferred to epi primarily because it causes less tachycardia.

I see far more dobutamine and amrinone used than levo or epi.
 
At my service we start levo then add dobutamine and titrate down the levo. As dobutamine has a tendency to initially lower the BP
 
The goal in managing heart failure is to increase CO by improving inotropy and decreasing SVR. As a pure vasoconstrictor that does nothing to help contractility and in fact often reduces CO, phenylephrine does pretty close to exactly the opposite of what you are trying to achieve in managing heart failure.

Norepinephrine actually has plenty of beta1 effects, I think it's like 30% of its action at lower doses and more at higher doses. It is often preferred to epi primarily because it causes less tachycardia.

I see far more dobutamine and amrinone used than levo or epi.

I think this is often one of those 5 cardiologists will manage things slightly different and with different agents.

Dopamine increases myocardial oxygen demand much more then Dobutamine, and also normally results in more tachycardia then Dobutamine and Levo combination.

So what Tx said above about titrating Dobutamine and Levo makes sense.

Levophed also isn't perfect because it can increase afterload and filling pressures, subsequently decreasing CO at higher doses.

So I don't believe there is one right answer, and often why we see so many different opinions and approaches.
 
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