Friday, May 27, 2016

Acute Respiratory Distress, Hypoxia, and a Large Right Ventricle on Bedside Ultrasound

A 50-something presented in acute hypoxic respiratory failure, alert and in respiratory distress.  She required Bilevel positive pressure ventilation.

Pulse was 139 and BP 99/75.  She was diaphoretic.

A bedside ultrasound was done immediately:

Notice the very large RV and very small, but well functioning, left ventricle.

What do you think?
















There were also B-lines (not shown).

Here is here initial ECG:
What do you think?













There is sinus tach.  There is a large S-wave in lead I.  There is a Q-wave in III.  Do these indicate acute right heart strain, typical of pulmonary embolism?











No!

First, there is no full S1Q3T3 (no T-wave inversion in lead III; for significance of S1Q3T3, see notes at the bottom).

More importantly, there is also a large R-wave in lead V1.  This combined with the right axis deviation (S greater than R in lead I) is all but diagnostic of RV hypertrophy (in contrast to acute right heart strain) which is a chronic condition.  Notice there are also large upright P-waves in right precordial leads (though not in lead II).  These are also suggestive of right atrial hypertrophy, which often accompanies right ventricular hypertrophy.

Seeing this, the probability of PE was greatly diminished.  The B-lines on lung ultrasound was also very strong evidence against PE.

She turned out to have chronic pulmonary fibrosis and acute pulmonary edema.  The RV enlargement was chronic.

A previous formal echo was found:
Pulmonary hypertension. The estimated peak systolic PA pressure is 60 mmHg
plus RA pressure and diastolic pressure 13 mmHg plus RA pressure.   Right ventricular enlargement with distortion of the position of the interventricular septum consistent with right ventricular pressure
overload.  Decreased right ventricular systolic performance. The left ventricular is relatively small with decreased systolic performance. The estimated left ventricular ejection fraction is 39 %.
There are no convincing regional wall motion abnormalities.


After therapy for pulmonary edema, she improved.

Learning Points:

In the context of hypoxic respiratory failure and a large RV on echo, the ECG can help to differentiate acute right heart strain (which can be due to acute hypoxia, especially from pulmonary embolism) from chronic RV hypertrophy.

The presence of a large R-wave in lead V1 well differentiates acute right heart strain from chronic RV hypertrophy.



S1Q3T3


This is a paper worth readingMarchik et al. studied ECG findings of PE in 6049 patients who had clinical findings suspicous of PE, 354 of whom had PE.  They found that S1Q3T3 had a Positive Likelihood Ratio of 3.7, inverted T-waves in V1 and V2, 1.8; inverted T-waves in V1-V3, 2.6; inverted T-waves in V1-V4, 3.7; incomplete RBBB 1.7 and tachycardia, 1.8. Finally, they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE. 

What is an S1Q3T3?  Very few studies define S1Q3T3.  It was described way back in 1935 and both S1 and Q3 were defined as 1.5 mm (0.15 mV).  In the Marchik article, (assuming they defined it the same way, and the methods do not specify this), among patients with suspicion for PE, S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.


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