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Chronic Right Ventricular Hypertrophy, or Acute Right Heart Strain? The ECG Helps Make the Diagnosis.

Posted Oct 02 2012 9:39am
A middle-aged, obese, non English speaking man presented as a walk-in with SOB and leg swelling. His O2 saturations were 59% on room air.  Systolic BP was in the 170's.  He appeared to be mildly dyspneic, in no great distress, and was speaking in almost full sentences.  Breath sounds were slightly distant but seemed to be clear.  Pulses were full and extremities warm, but with bilateral leg edema.  The patient was put on Bilevel Positive Airway Pressure [BiPAP (R)] and an immediate ED cardiac ultrasound was performed (there are 2 clips here; the RV is on the left and LV on the right of the screen)

rvh 2 from HQMedEd on Vimeo .

RVH 5 from HQMedEd on Vimeo .



These ultrasounds were interpreted to show a very large right ventricle (RV) and also left ventricular hypertrophy.  The differential included acute right heart strain (such as pulmonary embolism) and chronic right ventricular hypertrophy (RVH).  A high quality ultrasound could tell the difference between these two, but in the ED at that moment, only a bedside ultrasound without Definity contrast was available.

However, an ECG was immediately recordedThere is a large S-wave in lead I and a very large R-wave in V1.  This is diagnostic of RV hypertrophy, not of acute right heart strain.

Now the suspicion was that this patient has chronic hypoxia, such that he is not in great distress from a saturation of 59%.  He likely has any one of a number of problems that cause chronic hypoxia, pulmonary hypertension, and RV hypertrophy.  The possibility of a septal defect, or other defect, with right to left shunting (Eisenmenger's syndrome) was entertained.

On BiPAP with 100% O2, the O2 saturation came up to 97%, suggesting that if a right to left shunt were present, it could not be very large.  Obstructive sleep apnea, with chronic hypoventilation, with hypoxia and hypercarbia and resulting RV hypertrophy, was also high on the differential diagnosis.

Finally a BP of 170/100 was obtained by manual blood pressure.  The hemoglobin returned at 20g/dl, confirming chronic hypoxia.  The total CO2 returned at 33, suggesting chronic hypercapnia.  A venous blood gas returned with pCO2 of 66, confirming present hypercapnia.

Further history thru an interpreter was obtained: the patient had been SOB for months, worse recently, and much worse in the last day.  He had no medical history and was on no medications.

Bedside ED Ultrasound of the lower legs was done and confirmed no DVT.

The patient was much better after the nitroglycerine dose reached 200 mcg/min and the BP was down to 130 systolic.  Furosemide was also given.

A rapid d dimer was obtained which was only minimally elevated, effectively ruling out pulmonary embolism.

Subsequent testing revealed a previously undiagnosed congenital heart defect, with right to left shunting and Eisenmenger's syndrome, complicated by acute heart failure.

The ECG was instrumental in differentiating chronic RV hypertrophy from acute right heart strain, and helped guide therapy towards left heart failure (nitroglycerine) which could be dangerous in pulmonary embolism.
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