Right Ventricular Infarction – Part 1

Right ventricular infarction. What is it and why should you care?

Depending on what you read, right ventricular infarct may complicate up to 40 or 50% of all inferior MIs.

Remember, when we say inferior MI or anterior MI we’re talking about the inferior wall of the left ventricle or the anterior wall of the left ventricle.

If you look at the typical patient’s coronary anatomy, the right coronary artery comes off of the aortic root and runs down the right side of the heart, supplying the right atrium, right ventricle, and the inferior wall of the left ventricle.

That’s why the right coronary artery (RCA) is usually the culprit artery for an inferior wall MI.

But where in the RCA is the occlusion located?

If it’s a proximal occlusion (high up in the RCA) then the occlusion may actually be affecting the right ventricle and the inferior wall of the left ventricle.

Why is this a problem? Simple.

Look at this cross section of the heart.

heart cross section

When compared to the left ventricle (which is essentially a muscular tube) the right ventricle is thinner and attaches to the left ventricle like a pocket.

Remember, the right ventricle is only responsible for pulmonary circulation (lower pressure) where as the left ventricle (higher pressure) has to pump blood to the entire body and back.

In the setting of right ventricular infarction, the right ventricle can become “stunned” and fail to pump blood effectively. It essentially becomes a conduit through which blood flows. When this occurs, the patient becomes highly dependent on central venous pressure to maintain adequate cardiac output.

Sometimes, this is referred to as being “pre-load dependent” which is a term that I find amusing. In the first place, it’s become a catch phrase, but more importantly, raise your hand if you’re not pre-load dependent!

Because patients with a stunned right ventricle are dependent on central venous pressure to maintain cardiac output, it can be dangerous to give these patients nitroglycerin, which is a potent vasodilator. Morphine can cause problems for the same reason.

Patients with right ventricular infarction (almost always associated with inferior wall MI) tend to start out with borderline blood pressures. This is due in part to right ventricular stunning, but also because inferior MI often stimulates the Bezold-Jarisch reflex, which leads to a state of hypervagotonia. It’s no accident that sinus bradycardia is the most common arrhythmia associated with inferior MI!

Granted, it’s possible for a proximal occlusion of the RCA to upset the blood supply to the SA node, which could cause sinus bradycardia, but the percentage of inferior MIs that present with sinus bradycardia is far higher than this phenomenon could explain.

It’s also worth mentioning that varying degrees of AV block are known to occur with inferior MI, usually with a narrow complex escape rhythm.

So how do you know if a patient with inferior MI has an associated right ventricular infarct? After all, it might change your treatment! Or should it?

In Part 2 we’ll discuss how to identify right ventricular infarction on the 12 lead ECG, and in Part 3 I’ll share my thoughts as to whether or not it’s necessary to apply electrodes to the right side of the patient’s chest.

See also:

Right ventricular infarction Part 1

Right ventricular infarction Part 2

Right ventricular infarction Part 3

Check out our video-based 12-lead ECG course at ECG Medical Training!


  • Tazambo says:

    Sounds good.Bring on part IIRegardsDave

  • SoCal Medic says:

    To answer your question I have been taught two different ways, the first by obtaining V4R and evaluating that for ST Segment changes and the second by comparing Lead II to Lead III. Surprsingly, so far in my career, I have had more Inferior Wall MI’s with RVI, then LVI’s.

  • Tom B says:

    Remember, inferior wall MI is a left ventricular infarction! (I know you meant anterior). You know, I had a run of inferior STEMIs for a while, and I started to wonder! Then I had a run of anterior STEMIs.It all works out in the end. 🙂

    • Gregory Conner says:

      Regarding CVP in RV MI: as the RV becomes ischemic its pump capability (ability to generate contractile/stroke pressure) decreases and blood flow slows through the right-sided circulation. Increasing preload (CVP) increases RV filling and contractility. In RV MI hypotension results from decreased flow arriving to the left ventricle, thus decreased blood ejected during LV systolic contraction. Remember, the heart is extremely well-perfused with collateral circulation. The RV is perfused primarily by the RCA but also by the LAD (little) and by the Circumflex. The RCA is dominant in 80% of the population. In patients with a dominant circumflex, RV MI may complicate a 12-lead picture of an Inferolateral and Posterior MI. LV pump failure usually results from Proximal LAD occlusion and Left Main occlusion, with the latter being quickly fatal if not corrected immediately. The bread and butter points are: suspect RV MI when EKG changes involve the inferior, lateral and posterior walls, when the patient is hypoeensive with clear lungs, and if there is an “excessive” BP drop with NTG, albeit a relative /judgement call. The treatment should focus on large volume fluid supplementation (4-8 liters) as well as immediate reperfusion.

  • Medic1477 says:

    Could you further explain the relation of central venous pressure and RVI?

    I guess Im confused that we want to maintain or improve CVP but through a failing RV the CVP is being increased on its own. In my mind I would think the CVP would decrease with failure of the heart since less blood return and contractility would result in less pressure (CVP).

    Calrification is always appreciated 🙂

  • Ian says:

    Can you give me a little more info on hypervagotonia? I googled around for some info but there doesn’t seem to be much info and it’s a term I’ve never heard before. Thanks!

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