STEMI best seen in PVC

Here is a patient who had a cardiac arrest. Only approximately 25% of our atraumatic cardiac arrest patients have a STEMI, so the diagnosis of STEMI by the ECG is critical for the reperfusion decision. Here is the ECG:


The rhythm is atrial fibrillation. The QRS complex is wide, with a right bundle branch block but only subtle ST elevation in III and aVF, with very subtle reciprocal depression in lead aVL. The second complex in the ECG is a PVC, and is seen in leads I, II, and III. In leads II and III, in which the QRS of the PVC is predominantly negative (S-wave), there is marked discordant (opposite to QRS) ST elevation in leads II and III (inferior), far out of proportion to the preceding S-wave. In lead I there is a positive QRS (R-wave) and reciprocal depression that is similarly discordant to the QRS and out of proportion. These PVC findings confirm the diagnosis of inferior wall STEMI in this otherwise difficult ECG.

The patient had an RCA occlusion.

Probable Left Main coronary artery occlusion/obstruction, with STE in aVR, alternating BBB, and arrest

This 59 yo male had sudden chest and abdominal pain and dyspnea. He called 911. Paramedics found him in profound distress, stating "I can't breathe". He had this prehospital ECG recorded at 0953:
There is sinus tach and a wide QRS, not quite 120 ms, with wide upright R-waves in lateral leads; this is consistent with incomplete Left Bundle Branch Block. There is concordant ST depression in V2-V4, excessively discordant ST depression in I, aVL, V4-V6, and extremely excessively discordant ST elevation in aVR. ST elevation in aVR is one sign of high grade Left Main obstruction. This is STEMI. This confirms that acute coronary syndrome is the etiology of his illness and that cath lab activation is indicated. This was done.

He arrived in the Emergency department at 10:13 in severe distress. He was agitated, cool, and mottled with a weak pulse and O2 saturation of 44%. The following ECG was recorded at 10:15.
There is again sinus tach, but this time with Right Bundle Branch Block and a long PR interval. Alternating Right and Left BBB is a sign of impending complete heart block below the bundle of HIS, which would lead to asystole or ventricular escape (wide and slow complex). There is persistent ST elevation in aVR and ST depression in lateral leads.

Heart rate dropped to 36 with BP 53/30. Bedside ultrasound showed a normal right ventricle but very poor LV function. After stating "I can't breathe", the patient collapsed and could not be resuscitated. No autopsy was done, so left main obstruction cannot be proven, but this is the classic clinical and ECG presentation of such pathophysiology.

Though this is STEMI, it went entirely unrecognized by the computer algorithm. The medics and physicians knew what they were dealing with but the patient died too quickly for resuscitation.

Should this patient go to the cath lab while undergoing CPR? It is the only hope for survival, and there are case reports of survival in similar situations.

ST depression, hypertension, pulmonary edema -- what was the inciting factor?

This patient, with a history of CVA and hypertension, presented with a two hour onset of pulmonary edema and chest pressure, severely elevated blood pressure, and very tachycardic. His prehospital BP was 280/150, and it was 230/150 in the ED. He had not been taking his antihypertensives He was speaking in 1-2 word sentences and had diffuse rales. Chest xray confirmed pulmonary edema. The initial EKG follows:

This shows horizontal ST depression in V4-V6 diagnostic of ischemia. There is no LVH. The ST depression is not secondary to LVH, but due to ischemia. There is also ST elevation in aVR, which may be a sign of severe acute left main ischemia.

The important diagnostic question is: what initiated this ischemia? There are two primary possibilities. First, the patient has hypertension which worsened, increasing afterload, leading to some pulmonary edema and demand ischemia and worsening in a vicious cycle. Second, he had an acute coronary syndrome which initiated the increase in end diastolic pressure, leading to pulmonary edema, increased catecholamine output, increased BP and HR, with a different kind of vicious cycle.

The first possibility is made significantly less likely by the absence of LVH. Patients with this syndrome of demand ischemia almost always have LVH on the ECG. If this was all initiated by hypertension, then managing the demand by treating the blood pressure and other physiologic variables such as pulmonary edema, hypoxia, etc. would result in resolution of the ischemia, and could be measured by resolving ST depression on the ECG.

Either way, it is necessary to manage the airway, ventilation and oxygenation, treat the hypertension (high dose intravenous nitrates are a fine method), and normalize other important physiologic variables such as anemia and electrolytes.

However, in the second case, aggressive antiplatelet and antithrombotic therapy is essential. If there is no resolution of ischemia with these aggressive medical measures, then urgent cardiac catheterization is indicated and an interventionalist should be consulted immediately.

In this case, the physiologic derangements were well managed and the patient stabilized without endotracheal intubation, the BP came down with 160 mcg/min of IV nitroglycerine, and 1.25 mg of IV enalapril, but there was no followup ECG before admission.

Very soon after admission, the patient's chest pain increased and the following ECG was recorded 2 hours after the first ECG:

This ECG shows new Right Bundle Branch Block and marked ischemic ST elevation in leads V1-V5, I, and aVL, diagnostic of a proximal LAD occlusion. Emergent angiogram confirmed proximal LAD occlusion proximal to two large diagonal vessels, and severe circumflex disease also, but the left main was widely open. The LAD was opened as the patient was prepared for subsequent CABG. The patient survived but does have a severely decreased ejection fraction. The patient had no LVH on echo.

Learning points:

1) Flash pulmonary edema may be from demand ischemia, especially with hypertension, but it may be due to severe acute coronary syndrome.
2) When due to hypertension, there is almost always LVH on the ECG
3) Ischemic ST depression is associated with very high risk.
4) If ischemic ST depression is refractory to management of hemodynamic variables, hemoglobin, oxygenation (i.e., refractory to management of those variables that contribute to demand ischemia), aggressive medical treatment for ACS must be started.
5) If the ischemia is refractory to maximal medical management, angiogram with possible PCI is indicated.
6) Always repeat the ECG to assess management of ST depression.
7) In ACS, thrombus may be partially occlusive and result in ST depression. It may be fully occlusive, without collaterals, resulting in ST elevation. Or it may start as partly occlusive and extend to complete occlusion, as in this case.
8) New Right Bundle Branch block in the presence of STEMI has a very high mortality.

Severe Right Ventricular Hypertrophy

This 23 year old presented to the Emergency Department with pharyngitis, but also complained of dyspnea on exertion. This ECG was recorded:

The wide complex (QRS 155 ms) may distract your attention from the rhythm, which is simply sinus. There are massive S-waves in lateral leads, with an extreme right axis deviation (180 or -180, same thing). There are massive R' waves of RBBB in the right precordial leads. The combination of wide S-wave in V5 and V6, and large R' wave in lead V1 is diagnostic of RBBB. The precordial voltage is extreme, approximately 60 mm (6.0 mV) in V1.

So this is diagnostic of massive Right ventricular hypertrophy. One might be concerned for ischemia because of the large amount of ST depression and T wave inversion in V1-V3. Some discordant (in the opposite direction of a high voltage or bundle branch block QRS) ST depression and T inversion is usually found at baseline in RBBB, but this is more than usual. However, the voltage is also more than usual. The ratio of the ST depression to QRS voltage is about 4mm to 60 mm, or 0.067, which is normal. The troponin was mildly elevated due to demand ischemia of the RV.

Further history revealed congenital pulmonic stenosis which was dilated at age 7 days. The patient did not have further followup. Echocardiogram revealed an estimated peak systolic pulmonary pressure of 127 mmHg with RV enlargement and severe hypertrophy.

Comment on Posterior STEMI

I had a very good question regarding the post on posterior STEMI, and I wanted to be sure that the answer gets attention:

smallville said...

While your blog does an excellent job of highlighting posterior STEMIs that were mistaken, are there any solid criteria to help provide a DDx between anterior or subendocardial ischemia and posterior STEMI? Will posterior ST alteration always be limited to v2-v4?


This is a very good question, and not easily answered because there is very little solid research on this.

First, you should know that when there is precordial ST depression due to subendocardial ischemia, it is not necessarily due to anterior wall ischemia. Data from stress testing shows that subendocardial ischemia DOES NOT LOCALIZE on the ECG, and usually is in leads II, III, aVF and V4-V6. But, again, this does not tell you which artery is involved.

Second, ST depression in V1-V3, vs. V4-V6, is much more likely to be posterior than subendocardial ischemia.

Third, patients at higher risk of NSTEMI (older, more risk factors, h/o angiogram with multivessel disease) are much more likely to have subendocardial disease (vs., for instance, a younger smoker).

Fourth, patients with reasons to have demand ischemia (tachycardia, sepsis, GI Bleed, etc.) are much more likely to have subendocardial ischemia (like in a stress test); those with posterior MI are much more likely to present with onset of chest pain and with normal vital signs.

Fifth, look for tall R-waves in V1-V3 (the analog of Q-waves in other locations).

Sixth, an upright T-wave is much more likely to represent posterior MI, but probably signifies reperfusion of the artery rather than persistent occlusion. An inverted T-wave can be either subendocardial or posterior.

Seventh, placement of posterior leads is very helpful. Take leads V4-V6 and place them at the level of the tip of the scapula, with V4 placed at the posterior axillary line ("V7"), V6 at paraspinal area ("V9"), and V5 ("V8") between them. At lease 0.5 mm of ST elevation in 2 consecutive leads is very accurate for posterior MI.

References on posterior leads:

1) Matetzky S et al. Acute myocardial infarction with isolated ST-segment elevation in posterio chest leads V7-V9: "hidden" ST -segment elevation revealing acute posterior infarction. JACC 1999;34:748-53
2) Matetzky S et al. Significance of ST segment elevations in posterior chest leads (V7-V9) in patients with acute inferior myocardial infarction: application for thrombolytic therapy. JACC 1998;31 506-11.
3) Wung SF et al. New electrocardiographic criteria for posterior wall acute myocardial ischemia validated by a percutaneous transluminal coronary angioplasty model of acute myocardial infarction. Am J Cardiol 2001;87:970-4; A4.

Altered Mental Status, Tachycardia, Hypotension, Hyperglycemia, Ill appearing

This diabetic patient with the ECG below was brought in by medics confused, tachycardic, and hyperglycemic, Kussmauling. The computerized ECG algorithm diagnosed Acute MI (I'm not sure why).

The ECG is diagnostic of hyperkalemia, with QRS of 180 ms. The QRS improved immediately after giving 2 doses of Calcium gluconate. K returned at 7.3, with a pH of 6.91, HCO3 of less than 3. After a total of 5 doses of Ca gluconate, 6 doses of bicarb, 4 liters of fluid, and insulin, this patient with extremely severe diabetic ketoacidosis stabilized. He had some demand ischemia, with maximum troponin of 1.5, but there was no acute coronary syndrome.

His ECG from the next AM is shown below; the QRS is now less than 120 ms.

Left Ventricular Hypertrophy May Result in Profound ST Elevation

This 75 year old man presented with weakness. His blood pressure was 220/80. He was found to have renal failure. He ruled out for MI.

There are 4 mm of ST elevation in leads V2 and V3, but it not out of proportion to the very large (> 50 mm) preceding S-wave. This is typical of severe LVH with repolarization abnormalities.

It would be an unusual EKG for anterior STEMI.

In fact, it is very difficult to find a case of anterior MI with extreme voltage like this; this is probably because profound ischemia of LAD occlusion (STEMI) alters the QRS voltage and attenuates the severity of the electrocardiographic LVH voltage.

If anyone out there has such a case (proven LAD occlusion with very large voltage suggestive of LVH), please send it to me!