A 55 year old male with a history of hypertension, dyslipidemia, and diabetes mellitus

presents to the emergency department with substernal chest pain radiating to his left
arm, diaphoresis and shortness of breath. He has vomited twice and now is intermittently
feeling lightheaded.

His temperature is 37.4 ℃ , heart rate 70, blood pressure 110/70, and respiratory rate
24. His physical exam reveals no JVD, mild bibasilar rales on lung exam, his heart sounds
are regularly irregular, and an S4 heart sound is present. His ECG is below.

What are the main findings on the below ECG tracing?

The ECG findings include:

1. Sinus rhythm with 2nd degree type I AV block (Wenkebach)

2. Inferior ST segment elevation MI (leads II, III, and aVF) with reciprocal ST
depression (leads I and aVL)

Based on the ECG, which coronary artery is most likely involved in this
myocardial infarction?

Answer: Right coronary artery

In the ECG, ST elevation is noted in leads (leads II, III, and aVF). These leads represent
the inferior portion of the heart. Recalling the coronary anatomy, the right coronary
artery (RCA) supplies the inferior wall of the myocardium as well as the right ventricle
and posterior wall.

What may be responsible for the conduction abnormality seen on this ECG?

Answer: Enhanced parasympathetic tone and ischemia to the AV nodal artery.

This ECG represents an AV nodal block that can occur with inferior wall myocardial
infarctions, specifically second degree type I AV block (Wenckebach). Enhanced
parasympathetic tone can occur with inferior MIs. The proposed mechanisms include
stimulation of the vagus nerve increasing the parasympathetic nervous system which
causes slowing of the AV node and AV nodal blocks and the Bezold-Jarisch reflex. AV
nodal ischemia may also contribute. Remember that AV blocking medications such as
beta-blockers can cause 1st degree AV block or second degree type I AV block as seen in
this scenario.

Also recall that the right coronary artery (RCA), in addition to supplying the right
ventricle and inferior walls, also supplies the sinoatrial node (SA node) and the
atrioventricular node (AV node). A decrease in blood flow to the AV nodal artery (a
branch of the RCA) can result in AV nodal ischemia and AV conduction abnormalities such
as the 2nd degree type I AV block seen in the ECG. In order to cause SA node
dysfunction, the occlusion in the RCA must be very proximal since the SA nodal artery is
one of the first branches of the RCA. The AV nodal artery, however, is more distal and
this is quite commonly affected in acute coronary syndromes involving the RCA.

A majority of people (90%) are "right coronary dominant" meaning the AV nodal artery
originates from the RCA. In this case, the patient must be right coronary dominant since
the RCA is involved (ST elevation in inferior leads) AND there is AV conduction
abnormalities indicating AV nodal artery ischemia. If the patient was left coronary
dominant (10%), an infarct due to RCA occlusion would not cause AV nodal ischemia.
While the inferior wall can be involved in a left dominant circumflex occlusion, the lateral
wall would likely also be involved.

What would be the treatment indicated in this case?

Answer: Standard acute coronary syndrome (ACS) therapy for the ST elevation
MI and no treatment for the conduction abnormality.

Therapy for any ST elevation myocardial infarction includes aspirin, beta-blockers,

nitrates or morphine for chest pain, oxygen, anticoagulation with heparin, statins, and
eventually ACE-inhibitors. For unstable angina, the above may suffice, however for
NSTEMI, coronary angiography should be performed on an urgent basis (within 24-48
hours). In contrast, for an ST elevation MI (STEMI) such as case #1, emergent
revascularization with coronary angiography and stent placement or thrombolytic therapy
should be performed within 90 minutes of the patient presenting to the emergency room.

The 2nd degree type II AV block does not require any therapy since it is a benign rhythm
and rarely causes symptomatic bradycardia. Once the AV nodal ischemia is treated by
revascularization, the AV block will resolve.

What explains the patient's nausea, vomiting and shortness of breath? What
explains the physical exam findings of a low grade temperature, bibasilar rales,
and a S4 heart sound?

During myocardial ischemia, both the sympathetic (SNS) and parasypathetic nervous
system (PNS) are overactive leading to multiple symptoms.

Sympathetic nervous system over-stimulation leads to cold sweats (diaphoresis),

palpitations (from tachycardia and increased inotropy), cold and clammy skin (from
vasoconstriction) and a feeling of impending doom.

Parasympathetic nervous system over-stimulation leads to nausea, vomiting (via vagal

stimulation) and generalized weakness.

The physical exam findings that can be noted during active myocardial ischemia include:

1. Low grade temperature due to inflammation (remember atherosclerosis is an

inflammatory process)

2. Tachycardia and hypertension from SNS over-stimulation

3. An S4 heart sound. Remember the S4 heart sound ("atrial gallop") occurs when blood
being ejected from the left atrium during atrial contraction (late left ventricular diastolic
filling) strikes a non-compliant left ventricle. During active myocardial ischemia, the left
ventricle is not able to relax (relaxation is an active process requiring ATP) thus making it
non-compliant resulting in an S4 heart sound.

4. A murmur of mitral regurgitation (due to papillary muscle dysfunction).