A 40-Something male with a "Seizure," Hypotension, and Bradycardia

This is by one of our outstanding 3rd year residents, Aaron Robinson, with some edits and comments by Smith

EMS responded to a reported seizure in a 42 year old male. Per bystanders, he went down after some intense sporting activity, and had “shaking” type movement. He reports no personal or familial history of seizures.

One of our EMS Fellows along with a Senior EM Resident were on duty that evening, and arrived on the scene with the Fire Department. When the physicians approached him, he was ashen, diaphoretic, and appeared in shock. Fire was able to obtain a BP of 60/palp and a pulse in the 40s. The physicians quickly recognized that this was not a seizure and likely cardiac in nature. 

When the paramedics arrived, they obtained a 12 lead ECG and confirmed the unstable vital signs. EKG is pictured below:

What do you think? There is an obvious inferior STEMI, but what else? Why is the patient in shock?

Besides the obvious inferior STEMI, there is across the precordial leads also, especially in V1. He was in profound cardiogenic shock. 

Smith comment: I suspect lead reversal of V2 and V3: the STE is high in V1, lower in V2, and high again in V3. This STE is diagnostic of Right Ventricular STEMI (RV MI). In fact, the STE is widespread, mimicking an anterior STEMI. It really is an anterior STEMI, but of the Right Ventricular Anterior Wall, not the LV anterior wall.

When there is inferior and anterior STE, the differential is:
1. inferior + RV MI due to RCA occlusion vs.
2. LAD occlusion in a "wraparound LAD" (wraps around to the inferior wall).
In this case, the inferior STE is the most exaggerated, and the anterior STE is highest in V1 and V2. Both of these features make inferior + RV MI by far the most likely (Pseudoanteroseptal MI is another name for this)

There is also sinus bradycardia and the patient is in shock with hypotension. Although the shock is no doubt partly a result of poor pump function, with low stroke volume, especially of the RV, it should be compensated for by tachycardia. Cardiac output is stroke volume x rate, so this patient needs a higher heart rate.

This is a perfect indication for atropine. Atropine may succeed in increasing the heart rate in any narrow complex bradycardia, especially sinus bradycardia, but also with AV block, as AV block with a narrow complex QRS may be a junctional escape. A narrow complex bradycardia without any P-waves is also likely to respond to atropine, as it may be a junctional rhythm.

RCA ischemia often results in sinus bradycardia from vagal reflex or ischemia of the sinus node. In fact, in inferior MI, sinus bradycardia may be further evidence of Proximal RCA occlusion, which is the occlusion location that results in RV MI. Here is full text of this article.

Case continued

EMS immediately transported, activated the cath lab and gave 324 mg aspirin en route. It was about a 7 minute transport time. EMS  also quickly administered 1L of NS to optimize preload and hopefully boost perfusion. They did not have an ultrasound on the ambulance (some local crews are starting to utilize POC limited US in our service areas). 

EMS obtained a second ECG one minute later:

It appears the patient’s inferior STEMI has reperfused, as there is resolution of the inferior STE.

The patient arrived at the Emergency Dept critical care area and had this ECG recorded:

The sinus bradycardia persists. As you can see, the STE has returned in the inferior leads and there is now ST depression in the anterior leads concerning for posterior involvement. A right sided ECG was not recorded. STE in V1 with an inferior STEMI is moderately sensitive for right-ventricular involvement but this is only if there is no ST depression in V2! If there is STD in V2, the STE in V1 may be artificially normal! See this paper by Smith et al. Of note, despite the classic teaching, ST depression in Lead I is NOT reliable for the diagnosis of R-sided MI.

A bedside cardiac US was performed and showed an overall decrease in systolic function.

Also, the RV appears large and hypokinetic

The patient kept having recurrent syncopal episodes in the ED and was subsequently intubated for stabilization and airway protecting prior to going to the cath lab. Before transport, a final ECG was recorded:

There is, again, inferior reperfusion, but persistent marked anterior STE.

He was taken to the cath lab and underwent emergent intervention:

Thrombotic stenosis of the proximal RCA (95% with evidence of plaque

rupture) is the culprit for the patient's inferoposterior STEMI. He was successfully stented. This also confirms right ventricular infarction (RV MI)

A follow up TTE demonstrated a normal LVEF with a “regional wall motion abnormality-posterolateral hypokinetic mild, probable.” His troponin I peaked at 6.107 ng/mL. He was discharged neurologically intact and did very well. He has a history of sudden cardiac death in his family. The patient never arrested during his time at the hospital and his prognosis is good. 

Learning Points:

1. It is easy to mistake syncopal episodes with associated myoclonus as seizures, so have a high index of suspicion for syncope as the etiology. This patient’s shock state upon arrival didn’t fit with seizures and it was quickly recognized.

2. Recognize Right Ventricular STEMI by inferior MI with shock (and clear lungs), sinus bradycardia, and ST elevation in Lead V1 (but it may also be V2 and beyond, with maximal STE in V1 and V2).

3. STE in V1 in inferior MI is moderately sensitive for RV MI (if there is no posterior MI "pulling the ST segment down"). Plus STE in V1 in inferior MI is very specific for RV MI.

4. If time allows, a right sided ECG may help to recognize RV MI, but even this can be falsely negative in the presence of posterior MI (see below).

5. Give atropine for narrow complex bradycardia with hypotension.

6. Give a moderate fluid bolus for Hypotension in RV MI

7. Give norepinephrine for hypotension in spite of the moderate fluid bolus.

I (the senior resident on scene with the EMS Fellow) had a discussion with Dr. Smith regarding this case. During transport, I had debated giving atropine for his bradycardia and cardiogenic shock, but was worried about making an already profoundly ischemic heart more ischemic, and chose instead to optimize preload with pressure bagging 1L NS. Dr. Smith pointed out that while atropine may may result in slightly more oxygen demand, the increase in cardiac output and in blood pressure would increase overall coronary perfusion and decrease ischemia. This is particularly true of RV MI: LV coronary perfusion is dependent on diastolic pressure because the myocardial pressure is too high for perfusion during systole. But RV systolic pressure is low, so the RV perfuses during BOTH systole and diastole. Higher mean arterial pressure improves RV perfusion. Norepinephrine can be very useful adjunct to shock from RV MI, as hypotension is so detrimental to RV perfusion.

So when I find myself in this position again prehospital, I will administer atropine. 

V4R in Right Ventricular MI

As in the Smith study of lead V1 in RVMI, Kosuge et al. studied lead V4R in the context of posterior involvement and found that RVMI was associated with a high rate of STE in V4R in the absence, but not in the presence, of posterior MI. STE V4R had sensitivities of 34% and 96% (p b 0.001), and specificities of 83% and 82% (NS) in the presence and absence of PWI, respectively. They did not study lead V1. Like our study, they used angiographic criteria for RVMI [13]

Kosuge M, Ishikawa T, Morita S, et al. Posterior wall involvement attenuates predictive

value of ST-segment elevation in lead V4R for right ventricular involvement in

inferior acute myocardial infarction. J Cardiol 2009;54(3):386–93.