# A-fib RVR and CHF



## RocketMedic (May 1, 2017)

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?


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## VentMonkey (May 1, 2017)

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.


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## zzyzx (May 1, 2017)

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.


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## GMCmedic (May 1, 2017)

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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## Summit (May 1, 2017)

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


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## VFlutter (May 1, 2017)

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.


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## E tank (May 1, 2017)

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.


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## EpiEMS (May 1, 2017)

I'm loving this thread, guys.

Carry on...


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## RocketMedic (May 1, 2017)

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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## E tank (May 1, 2017)

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.



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.


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## RocketMedic (May 1, 2017)

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.


Yes. Attention was diverted by puppies lol.


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## EpiEMS (May 1, 2017)

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



Do you have a BP threshold for nitro administration?


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## VFlutter (May 1, 2017)

EpiEMS said:


> Do you have a BP threshold for nitro administration?



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.


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## E tank (May 1, 2017)

Chase said:


> . May have been just a little too aggressive with the CCB + Nitro in quick succession



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.


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## hometownmedic5 (May 1, 2017)

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.


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## Carlos Danger (May 2, 2017)

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.


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## Handsome Robb (May 3, 2017)

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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## Alan L Serve (May 4, 2017)

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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## VFlutter (May 4, 2017)

Alan L Serve said:


> Give IV Amlodipine right away.



Either a typo or you just killed this patient.


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## NomadicMedic (May 4, 2017)

Chase said:


> Either a typo or you just killed this patient.



Seems like he's confused his CCBs.


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## Carlos Danger (May 4, 2017)

It isn't a typo or confusion, he's intentionally trolling


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## Alan L Serve (May 5, 2017)

Chase said:


> Either a typo or you just killed this patient.


Big typo. That's what I get for working a 72h shift. Yes, I definitely would have killed this patient. I meant to write give IV Diltiazem (a non-dihydropyridine) and not Amlodipine (a dihydropyridine). No I am not trolling, either.


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## Carlos Danger (May 5, 2017)

Alan L Serve said:


> Big typo. That's what I get for working a 72h shift. Yes, I definitely would have killed this patient. I meant to write give IV Diltiazem (a non-dihydropyridine) and not Amlodipine (a dihydropyridine). No I am not trolling, either.



So you know enough about the CCB's to know which classes these common ones belong to, yet you aren't aware that IV amlodipine doesn't exist? Interesting.

FWIW, amlodipine would not kill this patient. It wouldn't do anything at all to them. Assuming optimal absorption, it takes 6 hours just to start working, and close to 24 to reach full effect.


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## Alan L Serve (May 5, 2017)

Remi said:


> So you know enough about the CCB's to know which classes these common ones belong to, yet you aren't aware that IV amlodipine doesn't exist? Interesting.
> 
> FWIW, amlodipine would not kill this patient. It wouldn't do anything at all to them. Assuming optimal absorption, it takes 6 hours just to start working, and close to 24 to reach full effect.



IV Amlodipine doesn't exist? Interesting.

https://www.ncbi.nlm.nih.gov/pubmed/12021583


> *Effects of intravenous amlodipine on coronary hemodynamics in subjects with angiographically normal coronary arteries.*


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## Carlos Danger (May 5, 2017)

Alan L Serve said:


> IV Amlodipine doesn't exist? Interesting.



No, outside of a research setting, it does not exist in the US. 

Try finding some on formulary somewhere to give to someone in rapid AF and get back to me.


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## Chimpie (May 6, 2017)

*Thread cleaned up and reopened. Keep it on topic and civil.*


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## RocketMedic (May 6, 2017)

Talked with our senior clinical guy, he's OK with it but would _personally_ go with a cardioversion in this particular case due to the preexisting heart damage. All's well that ends well though and he agreed that the rate needed fixing.


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## VFlutter (May 6, 2017)

RocketMedic said:


> Talked with our senior clinical guy, he's OK with it but would _personally_ go with a cardioversion in this particular case due to the preexisting heart damage. All's well that ends well though and he agreed that the rate needed fixing.



I have to disagree. Cardioverting this guy with a low EF and in A fib with unknown duration not on anticoagulation (more than just plavix)  is a horrible idea. Especially since symptoms started days ago.


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## RocketMedic (May 6, 2017)

Chase said:


> I have to disagree. Cardioverting this guy with a low EF and in A fib with unknown duration not on anticoagulation (more than just plavix)  is a horrible idea. Especially since symptoms started days ago.



Those were my thoughts as well.


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## E tank (May 6, 2017)

Chase said:


> I have to disagree. Cardioverting this guy with a low EF and in A fib with unknown duration not on anticoagulation (more than just plavix)  is a horrible idea. Especially since symptoms started days ago.



Agreed.. I'd be pretty surprised if he formed was able to form thrombus on Plavix. The risk for thrombus formation in untreated a fib is about 5% a year (cumulative) and unless a large part of his heart were dead, even very low EF patients don't need thinners.


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## MackTheKnife (May 7, 2017)

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.


Or the Plavix for the A-fib vice Coumadin.

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## VFlutter (May 7, 2017)

http://emedicine.medscape.com/article/2172597-overview#a1


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## E tank (May 8, 2017)

MackTheKnife said:


> Or the Plavix for the A-fib vice Coumadin.
> 
> Sent from my XT1585 using Tapatalk



Very unusual for Plavix to be used for thrombus prophylaxis in afib. As far as his CHADS score goes, his risk is less than 6% yearly untreated, given what is given.  Doesn't sound like chronic afib, though.


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## VFlutter (May 8, 2017)

Agreed but even in a lower risk patient I would not be very agresssive trying to cardiovert prehospital unless that patient was crashing. Talking specifcally about new onset a fib with unknown duration without therapeutic anticoagulation. The standard of care is usually TEE prior to cardioversion and I think it's prudent to try chemical rate control and let it ride till the hospital.


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## TomB (May 10, 2017)

In my opinion you should always start with NTG and CPAP with decompensated heart failure. The rate typically comes down on its own with increased SpO2 and decreased work of breathing. In fact this is one of the reasons we removed diltiazem from the trucks.


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## RocketMedic (May 10, 2017)

TomB said:


> In my opinion you should always start with NTG and CPAP with decompensated heart failure. The rate typically comes down on its own with increased SpO2 and decreased work of breathing. In fact this is one of the reasons we removed diltiazem from the trucks.



I take it that your agency cardioverts malignant tachydysrhythmias somewhat more often, then? I have found that nearly all of my diltiazem uses have been fairly clear-cut tachydysrhythmias (a-fib RVR and SVT refractory to adenosine); this was actually the first time I've given it in the context of a CHF exacerbation.


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## TomB (May 10, 2017)

RocketMedic said:


> I take it that your agency cardioverts malignant tachydysrhythmias somewhat more often, then? I have found that nearly all of my diltiazem uses have been fairly clear-cut tachydysrhythmias (a-fib RVR and SVT refractory to adenosine); this was actually the first time I've given it in the context of a CHF exacerbation.



Shouldn't we all be cardioverting "malignant" tachydysrhythmias?


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## Handsome Robb (May 10, 2017)

TomB said:


> Shouldn't we all be cardioverting "malignant" tachydysrhythmias?



Depends on how you're defining "malignant". 


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## VentMonkey (May 10, 2017)

Handsome Robb said:


> Depends on how you're defining "malignant".


Not benign.


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## RocketMedic (May 10, 2017)

Things that need fixin'


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## Handsome Robb (May 10, 2017)

VentMonkey said:


> Not benign.



Funny guy!



RocketMedic said:


> Things that need fixin'



A symptomatic tachydysrhythmia needs fixin' but does necessarily need Edison medicine. 


Personally someone would have to be peri-arrest for me to cardiovert AF with RVR unless there was a very clear cut recent onset. Our MD has been known to order cardizem in a drip over 10 minutes with a drip of calcium as well in hypotensive AF c/ RVR patients when they're in that grey area between actively trying to die and "stable". 



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## VentMonkey (May 10, 2017)

Handsome Robb said:


> Funny guy!








...carry on.


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## RocketMedic (May 10, 2017)

I personally think around the same, I would rather try a CCB (diltiazem) for a symptomatic, acute, currently stable A-Fib than cardio version as a first line.


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## TomB (May 12, 2017)

If your criterion for diltiazem is symptomatic but hemodynamically stable AF/RVR with symptom onset < 48 hours (as it should be) then it can wait.

Let the docs decide whether or not they want to perform an echo or give heparin prior to conversion. There's simply no rush.

If the patient's in heart failure NTG and CPAP goes a long way to relieving symptoms.

Tom


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## E tank (May 12, 2017)

TomB said:


> If your criterion for diltiazem is symptomatic but hemodynamically stable AF/RVR with symptom onset < 48 hours (as it should be) then it can wait.
> 
> Let the docs decide whether or not they want to perform an echo or give heparin prior to conversion. There's simply no rush.
> 
> ...



Lot's of ways to skin a cat. Going after the HR and rhythm  here is very defensible, IMO, given the likelihood that they were contributing to the problem was high. If NTG and CPAP is all that is available, great, no argument. Bringing another dimension to the picture with rate control has a benefit too.


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## RocketMedic (May 12, 2017)

TomB said:


> If your criterion for diltiazem is symptomatic but hemodynamically stable AF/RVR with symptom onset < 48 hours (as it should be) then it can wait.
> 
> Let the docs decide whether or not they want to perform an echo or give heparin prior to conversion. There's simply no rush.
> 
> ...



The Plavix/xarelto/warfarin does affect that decision-making somewhat though.


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## VFlutter (May 12, 2017)

RocketMedic said:


> The Plavix/xarelto/warfarin does affect that decision-making somewhat though.



If known therapeutic. I wouldn't trust warfarin without labs. Plavix is debatable


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## TomB (May 14, 2017)

E tank said:


> Lot's of ways to skin a cat. Going after the HR and rhythm  here is very defensible, IMO, given the likelihood that they were contributing to the problem was high. If NTG and CPAP is all that is available, great, no argument. Bringing another dimension to the picture with rate control has a benefit too.



What was the benefit in this case? Looks to me like a clear-cut case of heart failure (it doesn't get any clearer based on the history that was provided). The patient's pressure bottomed out to 70/40. Let the ED attending and cardiologist decide how rate control is best achieved in a patient with a baseline EF of 28%, after lungs are clear and SpO2 is back in the 90s, or be prepared to see several more cases like this one. You can say, "if NTG and CPAP is all that's available, great...." but that is the mainstay of modern prehospital treatment of heart failure, and for good reason.


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## TomB (May 14, 2017)

"Because of their favorable effect on morbidity and mortality in patients with systolic HF, beta-adrenergic blockers are the preferred agents for achieving rate control unless otherwise contraindicated. Digoxin may be an effective adjunct to a beta blocker. The nondihydropyridine calcium antagonists, such as diltiazem, should be used with caution in those with depressed EF because of their negative inotropic effect."

2013 ACCF/AHA Guideline for the Management of Heart Failure


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## E tank (May 14, 2017)

TomB said:


> What was the benefit in this case? Looks to me like a clear-cut case of heart failure (it doesn't get any clearer based on the history that was provided). The patient's pressure bottomed out to 70/40. Let the ED attending and cardiologist decide how rate control is best achieved in a patient with a baseline EF of 28%, after lungs are clear and SpO2 is back in the 90s, or be prepared to see several more cases like this one. You can say, "if NTG and CPAP is all that's available, great...." but that is the mainstay of modern prehospital treatment of heart failure, and for good reason.


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## E tank (May 14, 2017)

TomB said:


> What was the benefit in this case? Looks to me like a clear-cut case of heart failure (it doesn't get any clearer based on the history that was provided). The patient's pressure bottomed out to 70/40. Let the ED attending and cardiologist decide how rate control is best achieved in a patient with a baseline EF of 28%, after lungs are clear and SpO2 is back in the 90s, or be prepared to see several more cases like this one. You can say, "if NTG and CPAP is all that's available, great...." but that is the mainstay of modern prehospital treatment of heart failure, and for good reason.



Sorry for the above misfire... moving thru a couple of airports... anyway... just a couple of points. Be careful about hanging your hat on "mainstays"... they change regularly. As an example, the idea of treating chronic chf with beta blockers is only a couple of decades old.

Secondly, this scenario wasn't a straight forward presentation. The a fib/rvr complicated things a lot. Three things were impairing LV filling.... the cardiomyopathy/low ef, the a fib and the high HR. 

This guy was "pre-load dependent" as they say and unloading the heart at that rate (as opposed to the 70 that he was given NTG) had the potential for disaster as well. Add CPAP to that and it has even worse potential. I think he needed a lower HR to tolerate any NTG. How much and when was the question here.

Even the doc on duty would have addressed the HR with DCCV, so the medic was thinking along the same lines.

As far as using a CCB here, it was a good trade off, I think because all the patient had going on was far worse in the setting of an ef in the high 20's than some diltiazem.


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