Skip to content

Archives for inferior-mi

See all posts in the network tagged with inferior-mi

66 year old male CC: Chest pain

24 comments

Here's an interesting case that illustrates the value of the prehospital 12 lead ECG.

A 66 year old male became suddenly ill while playing tennis. Bystanders state that he struck the ball with his racket, staggered a few steps, placed his hand over his chest, and sat down on the tennis court.

9-1-1 was contacted immediately.

Past medical history is significant for hypertension, hyperlipidemia, and a "previous episode of chest pain" for which the patient carries SL NTG which he rarely takes PRN for chest discomfort.

A paramedic from out-of-town was present on scene and gave the patient his own NTG.

On EMS arrival, the patient appears acutely ill. He is diaphoretic and weak, complaining of chest pain.

Vital signs are assessed.

Pulse: 72
Resp: 20
BP: 88/58
SpO2: 98 on RA

The cardiac monitor is attached.

Even in monitor mode, you can see ugly looking ST segment elevation in lead III with reciprocal ST segment depression in lead I.

A 12 lead ECG is captured.

This removes all doubt. The ECG shows acute inferior STEMI. There are Q waves in leads III and aVF with ST segment elevation. There are downsloping ST segments in leads I and aVL which represent reciprocal changes.

The 12 lead ECG was transmitted to the local receiving PCI hospital.

The paramedic in charge of the call (good job Tina H.) placed the patient on oxygen, had the patient chew up 4 baby aspirin, started an IV, gave the patient a fluid bolus, and administered SL NTG and 5 mg of morphine.

Look at the next 12 lead ECG captured less than 10 minutes later.

Where is the ST segment elevation? It's gone. The ECG is now non-diagnositc.

If not for the prehospital 12 lead ECG, there's no telling how long this patient would have sat in the emergency department, infarcting away.

Instead, the patient had a 39 minute door-to-balloon (D2B) time.

If you know any old-school paramedics, medical directors, or administrators who care about patients but still aren't sure prehospital 12 lead ECGs are necessary, be sure to share this case with them!

Posted by on March 13, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , ,

Right ventricular infarction – Part I

10 comments

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.


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 II, we’ll discuss how to identify right ventricular infarct (RVI) on the 12 lead ECG, and in Part III, I’ll share my theory 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 I

Right ventricular infarction – Part II

Right ventricular infarction – Part III

Posted by on February 7, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , ,