A-fib RVR and CHF

RocketMedic

RocketMedic

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76 y/o male, 130kg, pale skin, wet and wheezy lungs, ejection fraction of 28% with an AICD, renal dysfunction, CHF, hypertension and an MI for history. Four days of progressively worsening dyspnea, first with exertion, then at rest, and fluid retention, progressing until today when he reports weakness, profound shortness of breath and increased work of breathing and tachycardia. Initial vitals 150/90, pulses irregular and thready at radials, rate around 130ish, room-air sats 84% with 30 breaths a minute, ECG a fib rvr without other acute findings. Capnograph waveform normal but hypocapnic at 25. Lung sounds present with rales to all fields and inspiratory wheezing to upper lobes.

I thought about the traditional nitro course for him, but opted a different way instead due to the sustained tachycardia. CPAP at 7.5cm H2O fixed the breathing and maintained sats, and I hung 25mg of diltiazem in 100mL NS over 4 minutes with conversion of the RVR into relatively regular atrial fibrillation at around 70. With this, his pressure actually increased somewhat, at which point I put in 2 doses of nitro with pressure reduced to 136/90. Lung sounds got better, skin improved, but then his pressure tanked in the ED for a few minutes down to 70/40 before edging its way back up. No LOC.

Was I right to treat it as a rate problem causing CHF instead of the other way around?
 
Short answer: yes, my money is on the (chronic?) CHF that contributed to the cascade of events that appeared to have unfolded before your very eyes.
 
Sounds like what you did worked.

That type of call, with AF + RVR thrown into the mix, gets complicated.

By the way, you can't trust the ETCO2. The only thing you know is that the true CO2 level was at least 25 mm Hg, but it could've been much higher too.
 
Yes. Thats typically the route I take with A-fib RVR and CHF exacerbation mixed in together. The A-fib may or may not be causing the fluid back up but it certainly isnt helping.

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Sounds to me like acute CHF exacerbation 2* fluid retention 2* CKD (and this patient almost certainly had PHtn w fluid on the lungs from that) until there was enough volume overload to trigger Afib due to atrial stretching.... then loss the atrial kick in a heart already on the wrong side of the starling curve and add in increased myocardial demand of the RVR... and possible catecholemine response for compensation.

Does this pt take their heart meds and are they on carvedilol? Bblocker? been taking them? Compensatory or normal pressure... or lower than normal?

LIke treating the rate problem with dilt if tolerated.
Like the CPAP.
Agree with zzyzx that etCO2 is a poor proxy for PaCO2 in this pt.
I'm not sure I like the nitro, I mean, seems shocky, but what else ya got?

Stat lasix and/or dialysis depending on CKD staging.
CXR, ABG, trops
Admit ICU.
Echo
If doing well, can continue medical mgmt with dilt loading or try amio load. Pt could easily end up with cardioversion
 
Most of the time when CHF patients have issues with pulmonary edema, especially associated with hypertension, it is because of diastolic dysfunction and nitro is very beneficial. Even with a low EF and slightly shock presentation I would still be giving it and is very conservative compared to some places APE protocols in which they bolus insane doses of IV nitro.
 
You had me with the CPAP and CCB. I think the NTG was gilding the lily a bit in the "the enemy of good is better" category.

Having the luxury of the retrospectoscope , as opposed to operating in real time like you had to do, Rocket Medic, I'd have avoided it for 2 reasons. The first is that I think you had the guy dialed in pretty well for transport. Stable SaO2 and ventricular rate. BP was perfectly acceptable. As time went on, I think you could have expected the MAP to fall even more as the dilt moves toward it's peak effect of about 2 hours.

But here's the deal with an EF of 25%...paradoxically, and as inefficient as it was, the guy might have needed the preload that was coming out of the lungs to load his LV enough to maintain a stroke volume compatible with life (no help from the atria)

This guy in this situation needed the volume he had to maintain his cardiac out put even though it was causing problems in his lungs. We only know that now because he didn't tolerate the CCB with the NTG.

While your dilt slowed the HR and therefore increased LV fulling, the combination of NTG and CCB seems to have unloaded him enough to drop his stroke volume and cause the fall in cardiac output.

I can't say I wouldn't have done the same thing as you, but what I would say, as a result of your story and having been burned enough times myself, is to pick one drug that will help and wait. Improvement? Let it ride.
 
I'm loving this thread, guys.

Carry on...
 
That makes sense. He was on carvedilol, lisinopril, lasix, plavix, potassium, atorvastatin and flomax, no official A fib Dx and no beta-blockers. Did have prior CHF exacerbations and familiar with the symptoms and treatments.
 
RocketMedic said:
That makes sense. He was on carvedilol, lisinopril, lasix, plavix, potassium, atorvastatin and flomax, no official A fib Dx and no beta-blockers. Did have prior CHF exacerbations and familiar with the symptoms and treatments.
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You mean he was on a beta blocker, the carvedilol. I wonder what the Plavix was all about? My first guess would be a coronary stent, but could have been for LV thrombus prophylaxis with such a low EF.

Sick dude.
 
E tank said:
You mean he was on a beta blocker, the carvedilol. I wonder what the Plavix was all about? My first guess would be a coronary stent, but could have been for LV thrombus prophylaxis with such a low EF.

Sick dude.
Click to expand...
Yes. Attention was diverted by puppies lol.
 
Chase said:
it is because of diastolic dysfunction and nitro is very beneficial. Even with a low EF and slightly shock presentation I would still be giving it
Click to expand...

Do you have a BP threshold for nitro administration?
 
EpiEMS said:
Do you have a BP threshold for nitro administration?
Click to expand...

It depends on the situation but generally SBP > 100 in the field. I prefer an IV drip vs sublingual in these types of patients since you can start low and titrate up as well as quickly stop if needed.

Here is a quick article. I like how it breaks down the categories.
https://lifeinthefastlane.com/collections/ebm-lecture-notes/acute-pulmonary-oedema/

Acute heart failure syndrome (AHFS) spectrum can be divided into 5 groups as regards therapeutic management:
  • (i) Dyspnoea + /- congestion with elevated systolic blood pressure (SBP)>140 mmHg, usually with abrupt onset APO (most frequent type)
  • (ii) Dyspnoea + /- congestion with normal SBP 100-140 mmHg, usually with gradual onset predominant systemic oedema and milder APO
  • (iii) Dyspnoea + /- congestion with low SBP <100 mmHg, with predominant cardiogenic shock or end-stage cardiac failure (most fatal type)
  • (iv) Dyspnoea + /- congestion with signs of ACS such as chest pain
  • (v) Isolated RV failure usually without APO.
This guy sounds pretty sick with a low EF however I do think he is more category I/II then he is III. I agree with E Tank that he may be preload sensitive but I do not think Nitro was necessarily a bad choice given the presentation. May have been just a little too aggressive with the CCB + Nitro in quick succession. Unfortunately given the various types of heart failure without knowing the exact type or having the luxury of a swan/echo it is a lot of guess work.
 
Chase said:
. May have been just a little too aggressive with the CCB + Nitro in quick succession
Click to expand...

Very much this ^ ... When I approach any hemodynamic instability, it is a deliberate stepwise approach with a little patience thrown in between the steps because, as Chase says, there is a lot of guesswork in this setting and the other thing is that the goal is to create a more stable situation, not necessarily solve the problem in the short time with the patient.

So my steps are addressing the problems associated with:
1.HR
2.Rhthym
3. preload (volume)
4. afterload (vasomotor tone)
5. contractility (inotrope)

In that order, not skipping anything until it is clear to me that it isn't a problem anymore or at all. Some things can be dealt with simultaneously, some not.

This is really useful when the picture is muddy.

So dealing with the RVR first here was the absolute correct thing to do, IMO. Preload happened to be an issue as well, but he found out the hard way.
 
I would have left the rate alone for the time being. Pt has a stable blood pressure, adequate mentation and no chest pain. He can live at 130 for the moment.

How, the impending respiratory failure, that we cant sit idly by and hope it gets better. CPAP naturally and excellent choice. his pressure is absolutely high enough for some nitro. As we start to see some improvement from there, we can consider how to proceede, but that's enough to get the wheels turning in the direction of the hospital. Depending on transport time, further management may be necessary, but its a start.

I would not have gone with the cardizem for exactly the reasons you encountered. You fixed the rate, then dog piled ntg on top of it. When the cardizem really went to work, he boxed and now you're buried with few options to get out of it. You cant jam him with fluids or you'll be right back where you started. I dont know what your situation is regarding pressors in the field, but even if you have a free hand, its an aggressive solution that could have been avoided.
 
First, good job, @RocketMedic. It is always hard to figure out what is going on with these patients. Which came first, the chicken or the egg?

For initial resuscitation, I still think in terms of the basic a A-B-C approach to most patient management situations:

A/B: Fixing hypoxemia is top priority. CPAP is usually a good place to start with CHF, no matter the etiology of the exacerbation.
C: Rate control is always a high priority in someone with with a sick heart. Good choice with the diltiazem.

Beyond that, you just have to move slowly with further interventions (especially vasoactive meds) until you get a better picture of what is going on. Without an echo and labs, you aren't doing much more than guessing.
 
From the looks of it this PT would've been prime for a tridil drip rather than 400mcg blasts of SL NTG. With that said I think you made some good choices with CPAP and controlling the rate, very possible that with rate control their ventricular emptying will improve and reduce pressure in the pulmonary vasculature allowing the edema to be absorbed back into the blood stream.


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You need to slow down his exceeding high rate. That will help immensely with his fluid build up. Give IV Amlodipine right away.
 
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