Clinical Images

12-lead ECG showing inferior myocardial infarction

📷 ECG: ST elevation in leads II, III, aVF · tap to expand

Inferior MI + AV Block

Why right-dominant RCA occlusion can hit the inferior wall, AV node, and RV, why this looks like GI trouble, and why giving nitroglycerin can kill your patient.

CLINICAL SCENARIO

A 69-year-old man is brought in by his wife after developing epigastric pain and nausea while gardening. "Probably just heartburn," he says. He looks pale and soaked in sweat.

BP 90/50 HR 55 RR 30 SpO2 94%

Exam: distended neck veins, lungs clear to auscultation. EKG shows P waves and QRS complexes firing completely independently of each other at a ratio of about 2:1. ST elevation in leads II, III, and aVF. ST depression in leads I and aVL.

What is the FIRST thing you should do?

Give sublingual nitroglycerin for chest pain

IV fluid bolus + prepare for pacing

Give IV morphine for pain control

Start diuresis for heart failure

IV fluids + prepare for pacing. This man has an inferior MI with complete heart block AND right ventricular infarction (JVD + hypotension + clear lungs). His RV is starved of preload. Giving nitro would drop his preload further and tank his blood pressure. Morphine drops preload too. Diuresis would be catastrophic. He needs fluids to fill that struggling RV, and his AV node is dead so pacing is next if atropine fails.

THE ANATOMY

Why Right-Dominant RCA Lesions Hit Multiple Targets

Tap any region to learn what it supplies and what breaks when it occludes

Patient rightAnterior viewPatient left

Right Coronary Artery (RCA)

The RCA comes off the right aortic sinus and runs in the patient's right AV groove. In a right-dominant heart, it wraps posteriorly and gives the posterior descending artery (PDA), which supplies the inferior LV wall and posterior septum. It also gives the acute marginal branch to the RV free wall.

Dominance is the key. Right dominance means RCA gives the PDA. Left dominance means LCx gives the PDA. So the RCA does not magically own both left and right sides; in the usual right-dominant pattern, one proximal RCA lesion can hit the PDA territory, the AV node, and the RV branch.

Left Coronary Artery (LCA)

The left main splits into LAD and LCx on the patient's left. LAD supplies anterior wall and septum. LCx supplies lateral LV and, in left-dominant hearts, can wrap around to give the PDA and inferior territory.

Board distinction: Most boards assume right dominance unless told otherwise. So inferior ST elevation plus AV block points to RCA. If the stem says left-dominant anatomy, then LCx can be the inferior-wall culprit.

AV Node

Sits in the right atrium at the inter-atrial septum. Controls the ventricular rate. The AV nodal artery usually comes from the dominant coronary artery and is most often RCA-derived. When a right-dominant RCA goes down, the AV node can lose its blood supply. Ischemia causes progressively worse conduction: 1st degree, 2nd degree, or complete heart block.

PASS textbook says it directly: "Right Coronary infarct clue: Heart Block."

The AV node uses slow calcium channels (Phase 0). This is why calcium channel blockers, beta blockers, and adenosine cause AV block, and why atropine (blocks vagal slowing) helps in the acute setting.

SA Node

The SA nodal artery comes from the RCA in most people, but a large minority receive it from the LCx. Ischemia here causes sinus bradycardia or sinus pauses. In inferior MI, the dramatic exam pattern is often AV nodal slowing plus vagal activation.

Inferior Wall (Leads II, III, aVF)

The inferior wall of the LV faces downward toward the diaphragm. Leads II, III, and aVF look at it from below. In right-dominant circulation, the PDA comes from RCA and supplies this inferior LV/posterior septal territory. When inferior wall cells die, those leads show ST elevation in II, III, aVF.

Reciprocal changes: Leads I and aVL are on the opposite side (lateral wall), so they see the damage from the other direction, giving ST depression in I and aVL. This is normal and expected, not a separate ischemic territory.

Right Ventricle (RV Infarction)

The acute or right marginal branch of the RCA supplies the RV free wall. A proximal RCA occlusion can therefore create inferior MI plus RV infarction. That is a branch-pattern problem, not the RCA being drawn on both sides of the heart.

Why it looks weird: The RV is a one-way pump. It depends on volume (preload) to push blood through the pulmonary circuit to the LV. When the RV is infarcted, it can't squeeze. Blood backs up (JVD), but the lungs stay clear because the RV isn't pushing enough forward. Classic triad: JVD + hypotension + clear lungs.

Diagnose with right-sided leads: ST elevation in V4R is the key finding. Get them in any inferior MI.

THE MECHANISM

Why This Presentation Makes Perfect Sense

Once you see the chain, you can never unsee it

1. Why does it feel like stomach pain?

The inferior wall of the heart sits right on top of the diaphragm. The phrenic nerve (C3-C5) and the vagus nerve both run nearby. When the inferior wall ischemes, it irritates the vagus nerve, which refers pain to the epigastric region. The patient and his wife think it's heartburn. The ER thinks it's an ulcer. clinical medicine want you to know it's a heart attack.

The tell: diaphoresis (profuse sweating) and nausea with epigastric pain in a risk-factor patient. Heartburn does not cause you to sweat through your shirt in your garden.

2. The Bezold-Jarisch Reflex 🔑Bezold-Jarisch = Brad and Just-stop (bradycardia + hypotension). The heart hits the vagal panic button.

Think of the inferior wall as having a hidden emergency alarm. When it ischemes, it fires off a massive vagal signal. Vagus nerve activation does two things at once: drops the heart rate (bradycardia) and drops the blood pressure (vasodilation). This is the Bezold-Jarisch reflexA cardioinhibitory reflex: inferior MI stimulates vagal afferents in the LV wall, triggering bradycardia, hypotension, and nausea. The heart is essentially pulling a fire alarm on itself..

You end up with HR 55 and BP 90/50 not just because the heart muscle is damaged, but because the nervous system is actively hitting the brakes. This is why atropine (which blocks vagal slowing) is often the first drug tried for inferior MI bradycardia.

3. Complete Heart Block: What P waves independent of QRS means

In a normal heart, every P wave (SA node fires, atria contract) is followed by a QRS (ventricles contract). They work together like a two-person rowing crew. In 3rd degree AV blockComplete AV dissociation. The AV node is infarcted. P waves and QRS complexes have NO relationship. Atria fire at their own rate (~60-100/min), ventricles escape at their own rate (~30-40/min). Both are independent. ALL need a pacemaker emergently per PASS textbook., the AV node is dead. The rowers stopped listening to each other. Atria fire at 70+/min from the SA node. Ventricles fire at 30-40/min from an escape rhythm in the Purkinje fibers. Two separate rhythms. No coordination.

On the EKG you see P waves marching along at one rate and QRS complexes at a completely different, slower rate. They occasionally line up by coincidence, but they have zero relationship. The PR interval keeps changing because there IS no PR relationship.

📋 PASS textbook: "3rd degree = complete infarct of AV node. ALL must have a pacemaker emergently."

PATTERN RECOGNITION

EKG Pattern Game

Four rhythm strips. Name what you see before the clue runs out.

EKG STRIP

COMPARISON

LV vs RV Infarction: The Key Split

A proximal right-dominant RCA lesion can hit inferior LV territory and the RV branch. Each behaves differently.

Feature	LV Inferior MI	+ RV Infarction
JVD	Absent or mild	Present (blood backs up)
Lungs	May have crackles if LV fails	CLEAR (RV not pushing forward)
Hypotension	Variable	Marked (CO is dropped)
Response to fluids	Neutral to harmful	HELPS (fills the RV)
Nitro/Morphine	Use with caution	AVOID (drops preload, kills CO)
Diuretics	Use if congested	AVOID (removes the preload it needs)
Diagnosis	Standard 12-lead	V4R ST elevation (right-sided leads)

THE PLAYERS

Inferior MI: The Five Signatures

Tap each card to flip. Each one is a distinct board-testable finding that comes with RCA occlusion.

📈

ST Elevation II/III/aVF

Inferior territory · RCA

tap to flip →

Board Signature

ST elevation in leads II, III, and aVF with reciprocal ST depression in I and aVL. The depression in I/aVL is a mirror image, NOT a second MI.

Leads II, III, aVF look at the inferior wall from below. When inferior cells die, those leads see elevation. Leads I/aVL (lateral wall) see the opposite side of the same event.

Elevation in II/III/aVF + depression in I/aVL = inferior territory. Default culprit: right-dominant RCA unless the stem says left dominance.

🫀

RV Infarction

V4R · JVD + clear lungs

tap to flip →

Board Signature

ST elevation in V4R (right-sided lead). Clinically: JVD, hypotension, clear lungs. RV cannot pump forward; blood backs up into neck veins but does not reach lungs.

Treatment: IV fluids (preload). AVOID nitrates, morphine, diuretics. All three drop preload and crash cardiac output.

JVD + hypotension + clear lungs = RV infarct. Fluids, no nitro.

⚠

Complete AV Block

3rd degree · pacemaker stat

tap to flip →

Board Signature

P waves and QRS complexes fire at completely independent rates. No PR relationship. Atria at ~70/min, ventricles at ~35/min. Two separate pacemakers with zero coordination.

The AV nodal artery usually comes from the dominant coronary artery, most often the RCA. When a right-dominant RCA occludes, the AV node can become ischemic and conduction can fail completely.

3rd degree block = emergent pacemaker in ALL cases per PASS textbook

🔲

Bezold-Jarisch Reflex

Vagal bradycardia + hypotension

tap to flip →

Board Signature

Inferior wall ischemia fires a massive vagal signal. Result: bradycardia (HR 55) + hypotension (BP 90/50) + nausea. The heart pulls its own fire alarm via the vagus nerve.

First-line treatment: atropine (blocks the vagal brake). If structural AV node damage, atropine fails and transcutaneous pacing is next.

Inferior MI + bradycardia + hypotension = Bezold-Jarisch. Atropine first.

🤮

Epigastric Masquerade

Looks like heartburn

tap to flip →

Board Signature

Inferior wall ischemia irritates the vagus nerve, which refers pain to the epigastric region. Nausea, vomiting, and "heartburn" in a 60-70-year-old with risk factors + diaphoresis.

The tell: diaphoresis (sweating through shirt) does NOT happen with true heartburn. Sweating + epigastric pain + risk factors = get an EKG first.

Epigastric pain + diaphoresis + risk factors = inferior MI until proven otherwise

📷 12-lead ECG · inferior STEMI II/III/aVF

📷 Color-coded ST elevation · territory map

2nd degree AV block Mobitz I Wenckebach ECG

📷 Wenckebach · progressive PR then dropped QRS

TREATMENT

The Management Algorithm

Tap each step to expand. Order matters.

Call a Code: Airway, Access, Monitor

O2 if hypoxic IV access x2 Continuous cardiac monitor 12-lead EKG

Get RIGHT-SIDED LEADS (place V3R-V6R on right side of chest). If V4R shows ST elevation, the RV is infarcted and the rest of your management changes dramatically.

Antiplatelet + Anticoagulation

Aspirin 325mg (chewed) P2Y12 inhibitor (ticagrelor or clopidogrel) Heparin

These go early. Dual antiplatelet therapy opens the clot from the inside. Works synergistically with whatever reperfusion strategy you choose.

Fix the AV Block: Atropine First

Atropine 0.5-1mg IV Transcutaneous pacing if atropine fails Transvenous pacing if persistent

The AV block from inferior MI is often temporary and vagally mediated (the Bezold-Jarisch reflex). Atropine blocks the vagus and can restore conduction. If the AV node is actually infarcted (3rd degree block), atropine may not work and you need to pace.

Complete heart block = emergent pacemaker per PASS textbook. No exceptions.

If RV Infarct: IV Fluids

Normal saline bolus (500mL-1L) NO nitrates NO morphine NO diuretics

The RV is preload-dependent. Think of it like a water wheel that only spins when there's enough water coming in. An infarcted RV can still pump IF you give it enough volume to work with. Fluids fill the RV, increase its stroke volume, and raise cardiac output. Anything that drops preload (nitrates, morphine, diuretics) cuts off the water and the wheel stops.

Reperfusion: Primary PCI is the Goal

Primary PCI (preferred, goal <90min) Thrombolytics if PCI not available within 120min

Open the artery. Everything else is temporizing. The sooner the RCA is opened, the more of the inferior wall, AV node, and RV you save. Door-to-balloon time under 90 minutes is the standard. If you're in a facility without a cath lab and transfer time exceeds 120 minutes, lytics are given.

⚠ DO NOT GIVE THESE IN RV INFARCTION

Nitroglycerin

Drops venous preload. The RV's only lifeline is volume. Remove it and cardiac output crashes. Blood pressure can tank within minutes.

Morphine

Causes venodilation, dropping preload. Same problem as nitro. Also linked to worse outcomes in ACS generally (though debated). Hard avoid when RV is involved.

Diuretics (furosemide)

Looks like heart failure because of JVD, but it's NOT volume overload. Diuresing this patient removes the preload the failing RV desperately needs.

Beta-blockers (acute)

Already bradycardic with AV block. Beta-blockers slow conduction further and can worsen or complete the block. Hold until rhythm stabilizes and HR improves.

⚡

BOARD TRAP #1: JVD + Hypotension + Clear Lungs = Reach for Fluids, Not Lasix

This triad looks like right heart failure, which you might instinctively treat with diuretics. But in the setting of inferior MI, this is RV infarction, a preload-dependent state. Lasix kills this patient. JVD here is a sign of RV that can't pump forward, NOT volume overload. Flood the RV with saline.

⚡

BOARD TRAP #2: Epigastric Pain in an Older Man with Risk Factors = Get an EKG

Inferior MI is the great masquerader. Vagal stimulation from inferior wall ischemia creates nausea, vomiting, and epigastric pain that looks exactly like GI pathology. The board will show you a 60-70-year-old with "indigestion" and sweating. Diaphoresis is the red flag. Heartburn does not make you sweat through your shirt.

⚡

BOARD TRAP #3: ST Depression in I and aVL is NOT a Second MI

When you see ST elevation in II/III/aVF with ST depression in I/aVL, the depression is reciprocal change, not a lateral wall MI. It's the mirror image of the inferior elevation seen from leads looking at the opposite wall. There is one culprit artery. Do not be distracted into thinking this is multivessel disease.

GAME TIME

Differential Diagnosis Elimination

Four patients just walked in. One has inferior MI + AV block. Eliminate the others one clue at a time.

Inferior MI + AV Block

RCA occlusion

Anterior MI

LAD occlusion

Upper GI Bleed

Hematemesis + hypotension

Massive PE

Saddle embolism, RV strain

Loading clue...

DECISION TREE

RV Infarct: Check the Chain

Inferior MI just landed. Walk through the RV infarct decision pathway before you give anything.

📈

Your EKG shows ST elevation in leads II, III, and aVF with reciprocal depression in leads I and aVL.

What territory is infarcting?

Inferior wall, right-dominant RCA territory

Anterior wall, LAD territory

Lateral wall, LCx territory

🔍

Confirmed inferior MI. You examine the patient: JVD present, lungs clear to auscultation, BP 88/52.

What do you do NEXT to confirm RV infarction?

Give furosemide for the JVD

Place right-sided leads and check V4R for ST elevation

Give sublingual nitroglycerin for hypotension

✅

Right-sided leads placed. V4R shows 2mm ST elevation.

This confirms RV infarction. What is the FIRST treatment?

IV normal saline bolus 500mL

Sublingual nitroglycerin 0.4mg

Furosemide 40mg IV

IV morphine for pain

⚡

Fluids running. Monitor shows P waves at 80/min completely independent of QRS at 32/min with no consistent PR interval.

What rhythm and what is the immediate treatment?

Wenckebach (Mobitz I): observe and monitor only

3rd degree AV block: atropine first, then transcutaneous pacing if needed

Junctional rhythm: give adenosine to reset

💊

Atropine given, pacing in place, fluids running. BP improving to 100/60.

What is the definitive treatment?

Primary PCI of the RCA (goal door-to-balloon <90 min)

Continue medical management and monitor indefinitely

Emergency CABG immediately

PROVE IT

Clinical Vignettes

Six patients just rolled in. All have different pieces of this puzzle. Don't let any of them down.

clinical Walkthrough

Original clinical vignettes. Shuffled, never-repeat, full explanations for every choice.

Medically reviewed by Kaitlyn Cocuzzo, MD and Fatima Ali, DO · Last updated July 1, 2026 at 10:03 PM ET

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