A-fib with RVR + sepsis + hypotension = conundrum

How do we slow the rate without lowering the BP? Will slowing the rate even help the BP? How do we raise the BP without speeding up the rate?

The patient who inspired this post came in for a bowel obstruction. Cards was initially consulted for possible new a-fib, but there really wasn’t much to do from a cardiac standpoint. THEN he perforated his bowel and went for emergency surgery, where he required pressors and went into a-fib with RVR. He was packed open and taken to the SICU, where he was hypotensive to SBP 70s, tachycardic to 160s, and intermittently hypoxic.

If you want to skip my thoughts on the case and head straight for the facts, here is an interesting article about a-fib in critically ill patients. It talks about the various options for management and the pros/cons of each.

If expert opinion is more your style, try this.

Of course, there is also controversy around slowing down a-fib when it is caused by sickness. Should we let the body do its thing to try and compensate? Here’s one article that suggests maybe we shouldn’t get so hung up on rate control in sick people.

Now back to the case. The surgery resident and I were of the mind that slowing the rate and organizing the rhythm should help with cardiac output. There are several reasons why this logic still seems to be in the majority.

– With a-fib you lose atrial kick. That little extra oomph from the atrium may not seem like a big deal, but it can have a significant impact on cardiac output. Here’s a fun article from 1965 that shows a 53% increase in cardiac output from converting a-fib to sinus (using quinidine because 1965). The results have obviously been redemonstrated in more recent studies, but how often do you get to reference quinidine? Not that often.

– Diastolic filling is important for stroke volume. With any tachyarrhythmia, less diastolic filling time means lower stroke volume. However people who do “math” would argue that increasing the rate would likely keep cardiac output about the same. This logic holds up with regular rhythms, but studies show that irregular rhythm decreases cardiac output compared to regular rhythm. Here’s one such study.

– In real life, we went for amiodarone and electrical cardioversion. From the a-fib in critical care article above, it seems like that’s still the best option.
Here’s a good article I wish I had read before embarking on a cluster of a cardioversion. P.S. Put the pads on correctly. Anterior-posterior pads definitely worked better for this 350 pound patient. Anterior pads = fail x3. AP pads = success!

– It’s worth noting that this is not one of the scenarios when you’re worrying about giving someone a stroke with cardioversion. This guy’s risk of death was much greater than his risk of stroke.

Another consideration for this situation was the choice of pressors. Eventually the patient ended up maxed on pretty much all pressors, but that may not always be the case.

Surviving Sepsis guidelines are all about Levophed as a first line pressor, which is usually a great option. But guidelines are just guidelines. How many of our patients are otherwise 100% healthy and just have a little sepsis? Not that many.

– In this case, I think phenylephrine may have been a better first option. Pure alpha agonist activity vasoconstricts without Levophed’s cardiac effects, which probably didn’t do us any favors with the RVR.

– Based on the EMCrit blog above it also seems like phenylephrine might have allowed us to use a beta blocker without worrying about blocking the effects of the pressor or a calcium channel blocker without exacerbating hypotension. Thoughts?

– Anyone have other ideas about pressors in this scenario?

There was a lot more to the case after that, but this post has already ended up way longer than I intended. In the end, it was a 350 pound unhealthy guy with a less than ideal heart, so unfortunately, his family ended up withdrawing care. I doubt anything we could have done would have changed his outcome, but maybe there’s something to learn from it that will help someone else someday. I’ve talked to several people about this case and gotten different opinions from each one, so I figure why not open it up for a few more opinions to really confuse clear things up.

The elusive S1Q3T3

So this is a case I thought was interesting that I had in the department back in May. We all know that the most common EKG finding in the setting of PE is sinus tach, however the pimp question that is also asked is the finding of S1Q3T3. While I can easily recite the alphabetic-numeric code S1Q3T3 by heart at the drop of a hat, I had never seen one and honestly thought I never would. I thought finding S1Q3T3 was likely as rare as surviving a ED thoracotomy (OK maybe not that rare).  So on to the case.

39 year old female presents to the ED complaining of SOA and cough for the past two weeks. Cough was productive of green sputum, no fevers, and she does complain of some chest pain which sounds pleuritic in nature. Initial vitals HR 118 BP 111/73 RR 16 O2 97% room air. As I get into her PMH she says she has a history of multiple PEs with an IVC filter placed 1 yr ago because apparently she wasn’t very good at remembering to take her coumadin. She has had a hypercoagulability workup which was negative, no recent travel, no estrogen use.

So at this point with a history of multiple PEs, tachycardia, SOA, and pleuritic chest pain I am thinking I am going to scan this lady. Even though she had a IVC placed a year ago, she is still saying all the right things for PE. So while the CTPE protocol was cooking I got an EKG and there it was, S1Q3T3!

S1Q3T3

Needless to say I was pretty excited and immediately showed the rotating intern next to me who clearly didn’t share my enthusiasm. When I compared this new EKG to a past EKG a month ago she did not have the S1Q3T3.During her admission a month ago, when she had a normal EKG, she had a CTPE showing a chronic PE. This time when her CTPE came back the read was Acute on Chronic Pulmonary Embolism. So a month ago she had a chronic PE with a normal EKG and at this visit she had an EKG with S1Q3T3 and a acute on chronic PE. Out of curiosity I dug through her medical history a little bit more and found that this patient had multiple prior admissions for PE with multiple CTPE protocols and EKGs. What I found was that whenever this patient had a CT read of Chronic PE she had a normal sinus rhythm EKG. However, whenever she had a read of Acute on Chronic PE (which was 4 times!) she had a EKG showing S1Q3T3, dating all the way back to 2012. Yea, apparently this lady has been hanging out with a chronic PE in her distal right main pulmonary artery since 2012 and every once in a while she will throw a new small PE, even with an IVC filter.

So after doing a little bit of thinking and a little bit of reading it made sense. The EKG finding of S1Q3T3 is indicative of right heart strain, in this case resulting from an acute PE. So this patient’s heart has adapted to her chronic PE, however every time she throws a new PE she has an element of right heart strain which can be seen on her EKG as S1Q3T3.

I just thought this was pretty interesting to actually see the physiologic and mechanical adaption and strain this patient’s heart was undergoing being clearly demonstrated on her EKG. Also I learned that S1Q3T3 is not like a q wave after an MI in that it stays on the patient’s EKG, it is a finding that comes and goes depending on the patient’s presentation.

Anyways I thought this was a pretty cool little case and figured I would share. Hope you all enjoyed.

Stress Test

Another one from Mattu’s Feb review. This article compares psychological stress to physical stress to detect effects on perfusion of the heart. Interestingly mental stress causes ischemia where physical stress does not seem to.

There has always been an intuitive relationship between psychological stress and myocardial ischemia. Bernard Lown, a famous cardiologist, said in EVERY MI patient he had he would find a recent large social stressor in the patient. Of course plenty of hindsight bias occurs here.

Either way, if nothing else with this article remember that emotional stress causing chest pain COUNTS AS exertional ischemic symptoms. The fight with the boyfriend or girlfriend does not allow for blaming the pain on “anxiety.” And perhaps the real stress test in our Chest Pain Center is the 20 hours of sleep deprivation coupled with exposure to yelling, retching and dying that our patients must undergo to make it upstairs for a nice quiet little stroll on the treadmill.

Death of CK-MB?

Hey guys here is a relevant (albeit 7 years old) article supporting my abandonment of the CK-MB. I had heard Mattu talk about this on some podcasts but this article (along with some newer ones) is the evidence to support that practice. At Jewish I do not obtain a CKMB though when I want a total CK I now have to remember up front. On the POC machines at Jewish the Trop alone seems to error far less than when CKs are running with it. Still watch out for the Trop false positives.

Also I would plug Dr Mattu’s new ECG site. Now he charges a small fee (can pay weekly or monthly but I did the $27/year). Still video based (I prefer to just read a blog with pics) but top notch quality. There is a weekly case and a monthly lit review. The above article is in his Feb review. Might make a one month subscription part of the ECG month. ECGs of course are learned over years and decades, not in a month long elective.

AvR

Hey guys a long but important post from Steve Smith on AvR ST elevation in setting of ACS, STEMI.

His main point in posting is to emphasize the point that STE in AvR is concerning for Left Main Disease, but NOT SPECIFICALLY Left Main OCCLUSION.

This highlights a consistent theme on Smith’s blog which is our role in differentiating the patients who HAVE ACUTE OCCLUSION, ie STEMI or STEMI equivalent. These patients need emergent cath where others might be best treated medically prior to pulling the trigger for cath lab.

 

Acute Cardiogenic Pulmonary Edema

Here is nice summary post by FOAMed guru Anand Swaminathan with evidence-based discussion of the role (or lack thereof) for diuretics in acute pulmonary edema. Trust me it works. See also the first Emcrit podcast on the topic.

Bottom line: minimal role for diuretics in the pulmonary edema patient in extremis. This is not the mildly fluid overloaded patient with normal respiratory status, they can use a little diuresis once BUN/Cr are determined.

Wellens’ Or Not?

A middle aged male presented for evaluation of AMS; he had agitation, confusion, and tremors. He has a history of Bipolar disease and schizophrenia as well as HTN.  Vital signs were all stable on presentation and within normal limits.  On exam he was oriented only to name, but not place or time. Neurological exam was normal, with the exception of tremors.  Med list includes Haldol Injection, Lithium, Benztropine, Olanzapine, and Propranolol.  At this point, I was not quite sure what is going on with him, so I had a bit of a shotgun approach.  Initial EKG revealed the EKG below.

20140325_223727

It appears to be similar to Wellens’ syndrome but not consistent with my gentlemen’s symptoms.

A quick literature search revealed a case report showing lithium induced EKG changes, similar to his EKG above.  Further supporting his lithium induced changes in this scenario is no clinical findings to suggest ACS, and a negative troponin 3x.  He was ultimately admitted and treated for lithium toxicity, without any cardiac complications.

EKG changes seen in lithium toxicity:
– ST elevations (1 other single case report)
– QT prolongation
– non-specific ST segment changes/T-wave abnormalities