Thursday, September 1, 2016

Syncope, Hypotension, and a Large Right Ventricle -- What is the ECG Diagnosis?


A 60-something woman had syncope and was unconscious for a few minutes.  It was not a seizure.  EMS found her lethargic and short of breath but without chest pain.  Pulse was 103, BP 100/60, and O2 saturation on room air 98%.

She was brought to the ED, where her SpO2 was 93%, BP 88/48, pulse 100.

On arrival in the ED, she underwent an immediate bedside cardiac ultrasound:

What do you see?

There is a very large RV and very poor LV filling; the LV ejection fraction is nearly 100%.  It is easy to jump to the conclusion that this patient has a pulmonary embolism (hypotension, tachycardia, low O2 saturations, syncope, large RV).

An ECG was recorded:
What do you see?

At first glance, this ECG also suggests pulmonary embolism.  It shows an S1Q3T3.  One might think this is then highly specific for pulmonary embolism.  However, S1Q3T3 has a very limited (+) and (-) likelihood ratio for PE; it is seen in only 8.5% of patients with PE and 3.3% of patients who are evaluated for PE but do not have it.  See this post for detailed information.

This ECG has quite a bit more information: it shows sinus tachycardia with right axis deviation, a large wide R-wave in V1 (but without complete RBBB), and ST depression with T-wave inversion in V2-V6.  This is a typical ECG of right ventricular hypertrophy.

Further history

Further history revealed that the patient had poor po intake and vomiting.   Review of records revealed "chronic cor pulmonale" and a review of a previous formal echo showed:
--Pulmonary hypertension .
--Cor pulmonale, severe.
--Normal estimated left ventricular ejection fraction.
--Right ventricular enlargement Marked.

--Decreased right ventricular systolic performance severe 
--pulmonary artery pressure: 75 mmHg (normal 15-25)

People with right ventricular hypertrophy due to pulmonary hypertension may have severely decreased RV function and are very susceptible to low preload.  Any condition which lowers intravascular volume (such as vomiting and poor po intake) may lead to hypotension and syncope.

In these patients, can volume be assessed with ultrasound imaging of the inferior vena cava (IVC), as is often done in the ED?  

No!  The pulmonary hypertension will result in a "plump" IVC even with severe volume depletion.  The pulmonary hypertension requires high filling pressures (plump IVC) for adequate RV filling.

Physical exam tip: In patients who can stand up, a better measure of volume than IVC is to check orthostatic vital signs and symptoms.  In patients who are young and not on beta blockers or calcium channel blockers, the change to an upright position will result in a rise in heart rate to more tachycardic.  Older patients or those on such medications will have a drop in BP.  If symptomatic, it is pretty specific for volume depletion.   The exact numbers are more difficult to specify and beyond the scope of this post, but correction with volume repletion is very good evidence of relative volume depletion.  

Case continued

The first troponin returned at 0.090 ng/mL (normal, up to 0.030).

I had just seen this ECG in a stack and knew it was RVH.  I had not seen the history yet when the treating physicians sought me out to show me the ECG.   Due to the ST depression, echo, and troponin, they were worried about posterior MI or pulmonary embolism.   I pointed out that it represents typical findings of chronic RVH due to chronic pulmonary hypertension, not of pulmonary embolism or acute MI.   I suggested that this would be typical for an acute exacerbation of severe pulmonary hypertension due to dehydration.

Suggested evaluation: Check orthostatics, do thorough chart review and review of previous ECGs (these showed RVH) and echos (which showed RVH).  Give some fluids and check a d dimer (this was not done).

The patient did get a CT pulmonary angiogram for other reasons (suspicion of AV malformation), and  it was negative for pulmonary embolism.

Troponin peaked at 0.289 ng/mL.  The patient was rehydrated and discharged after a short stay in the hospital.

Although acute coronary syndrome (type 1 Non-STEMI) was not absolutely ruled out, the clinical presentation is typical for dehydration in the setting of pulmonary hypertension and I agree that an angiogram is not necessary.


So this episode of volume depletion in the setting of RVH resulted in a type II MI.

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