Right ventricular infarction – Part II

Let’s look at a case study that demonstrates the potential danger associated with right ventricular infarction.

EMS is called to the residence of a 68 year old female with chest pain.

On arrival, the patient is anxious, cool, pale, and diaphoretic.

Vital signs are assessed.

Resp: 20
Pulse: 68
BP: 105/55
SpO2 95 on RA

A 12 lead ECG is captured showing acute inferior STEMI.

“Time is therapy” for STEMI patients, so the most important issue to consider is how this patient is going to be reperfused.

The other issue to consider is how you’re going to manage the patient.

The paramedic in charge of the call wisely suspected the possibility of right ventricular involvement and decided to capture another 12 lead ECG using modified lead V4R.

Basically, this is lead V4 moved over to the right side of the chest (hence the addition of the letter ‘R’ which stands for ‘right’).

When lead V4R shows at least 1 mm of ST segment elevation in the presence of inferior STEMI, it’s a highly sensitive marker for right ventricular involvement.

Does this mean that every patient with right ventricular involvement will develop the hypotensive syndrome? No. But it means the patient is at risk and drugs like nitroglycerin and morphine should be used with caution!

Here is the 12 lead ECG with lead V4 in the position of V4R.

Is there at least 1 mm of ST segment elevation in lead V4R?


Even if there wasn’t quite 1 mm of ST segment elevation in this lead, because the QRS complex is so small, you’d want to consider the amount of ST segment elevation relative to the size of the QRS complex (thanks for this tip Dr. Smith).

To fully appreciate this point, look at the same cardiac cycle in lead V4R “stretched” vertically, which makes it easier to see the ST segment elevation relative to the size of the QRS complex.

This is the inverse of the rule for LBBB (and LVH) where the deeper the S wave, the higher the ST segment.

So we have a patient with acute inferior STEMI with right ventricular involvement.

Now what?

Place the patient on oxygen, start an IV, and give the patient a fluid bolus!

These patients can handle a lot of fluid, and it helps maintain their pressure, especially if you’re even thinking about a trial of nitroglycerin!

The paramedic on this call gave the patients a bolus of 500 ml 0.9% NS which brought the patient’s pressure up to 124/68.

A single dose of SL NTG brought the patient’s pressure down to 90/48.

Can you imagine what would have happened had the paramedics not performed a preemptive fluid bolus?

The paramedics withheld NTG for the remainder of the transport and repeated the fluid bolus of 500 ml 0.9% NS which brought the patient’s pressure back to 110/55 (almost what they started with).

On arrival at the hospital, the lead paramedic gave a report to the on duty ED physician, who was completely dismissive when the paramedic showed her the 12 lead ECG with lead V4 in the position of V4R.

Please note, I have the highest respect for the medical profession. I have nothing against emergency physicians. I’m just telling it like it was.

The physician immediately ordered NTG and morphine.

The paramedic sat down to write the report, and within 5 minutes he heard a nurse yell out “I need help in here!”

The patient was crashing. Fast.

Here is a 12 lead ECG that was captured after the patient’s pressure plummeted (I never found out how low it went).

Do you notice anything about the ST segment elevation?

Suffice it to say, we are not doing our patients a favor when we put them into uncompensated cardiogenic shock.

The patient was stabilized after several tense minutes and sent up to the cardiac cath lab.

Here is an ECG taken before the intervention.

Here is an ECG taken after.

As far as I know, the patient made a full recovery.

See also:

Right ventricular infarction Part I

Right ventricular infarction Part II

Right ventricular infarction Part III


  • Shaggy says:

    I work in a busy ED and one day the medics brought in a hypotenisive patient with an inferior wall MI on their 12 lead. I asked the attending if she wanted me to do a 12 lead with V4R. Her answer which I heard from others was if it is inferior and hypotensive, consider it right sided and treat as such. However, after reading this post, I see the importance of checking the right side on a normotensive patient with an inferior MI. I am glad you are around. I just wish I didn’t have to keep reviewing your posts.

  • Tom B says:

    I actually agree the your attending, and I’ll be discussing this in the Part III.I would simply suggest that you include marginal blood pressures in your calculus.Thanks for the comment, Shaggy! :)

  • Bob Jester says:

    My practice, and what I teach anyone who asks is to move V3, V4, V5 and V6 over to the right chest at the same anatomical landmarks. Am I going for overkill or does the single lead provide adequate confirmation? What are your thoughts on treating IWMI/RVMI patients with a small does of IV nitroglycerin after the fluid bolus? My thinking is that the IV dose is more titratable (if that is a word), and at a 30 to 40 mcg dose might not cause as profound a hypertension.

  • Anonymous says:

    Tom, good case review on this one. It is a shame the patinet decomp on arrival at the ER, was Dr.Death working that day?Scottm

  • Tom B says:

    Scott – Thanks for reading my blog, brother! No comment! :)

  • Tom B says:

    Bob – I have read that lead V4R is a sensitive enough marker all by itself (I’ll see if I can find the supporting documentation so I can cite a source for you).Your point about IV NTG sounds logical to me, but I don’t have any experience with it! It seems to me you should be okay if you perform a preemptive fluid bolus and augment the pressure prior to a trial dose of SL NTG.Thanks for the comment!

  • Anonymous says:

    I really enjoyed every detail of this case. put down very nice.

  • Tom B says:

    Thank you, anonymous!

  • Anonymous says:

    I am an ALS paramedic working in Australia. We have only 3 lead ECG capability. Just seeking clarification….. Inf MI should raise alarms for RVI, particularly with hypotension, clear lung fields and raised JVP.RCA involvement is approx 50%, circumflex is approx 10%….can anyone tell me how the rest is made up?

  • Tom B says:

    Anonymous – I would say that 90% are RCA and 10% are LCX.Depending on the patient’s coronary anatomy, it’s possible for the LCX to supply the RV, but it’s not common.Thanks for the comment! Tom

  • Anonymous says:

    You don't need a right sided ekg. If you lok at the ST Elevations, and the highest elevation is in Lead III, you have an RV infarct and should treat it as such.RV infarct should never receive nitro, morphine, beta blockers, or anything taht could cause a drop in pressure.RV infarct require usually 15-20 liters of 0.9 NS to survive without sequelea of kidney damage, brain damage, heart damage, and other hypotensive damage. They may also require dopamine in teh meantime.I would get two large bore IVs and start giving them 2 Liters at the same time. How do you know you have given them enough fluid? Until you hear it in their lungs, or they need more oxygen. You have to flood them. 98% of patients will require between 15-20 liters. Don't be shy with fluids.Great case, great write up!

  • suba hsj says:

    i receive alot of inferior mi presenting with hypotensions with evidence of RV infarcts in my ED…i agree that we should increase the pre-load by running fluids but i still don't get some colleagues who still refuse for fluids but starts the inotropes in order to avoid pulmonary edema especially those with bibasal crepts.

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