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Dehydration: Unrecognized Cause of Left Ventricular Outflow Tract Premature Ventricular
Contraction
Levina Tri Ratana1, Hizkia1, Michael Jonatan1, Arif Ridha2 Arinta Setyasari3, Prihati Pujowaskito4
1
Cardiology Intern at Dustira Hospital, 2General Practitioner at Dustira Hospital , 3Cardiologist at
Dustira Hospital, 4Head of Cardiology Department at Dustira Hospital
Introduction
Premature Ventricular Contraction (PVC) has been linked to several cardiac structural
abnormalities. Miscellanous systemic causes of PVCs are frequently overlooked.
Case
A 56 year-old woman came to our hospital with chief complain of palpitation and breathlessness.
On physical examination, her blood pressure was 150/80, heart rate was 68 beat/minute with
irregularly irregular pattern, respiration was 32 times/minute, and oxygen saturation was 96%.
There was elevated jugular venous pressure, clear lung on auscultation, and pretibial edema. On
laboratory examination, her hemoglobin was 17.4, hematocrite was 52.7, and other parameter
within normal limit. ECG showed atrial fibrillation with ventricular rate of 64 bpm, anteroseptal
old myocardial infarction, and bigeminal PVC. Holter monitoring, echocardiography, and coronary
angiography were not executed due to financial issues. She was treated with injection of
Furosemide 1x20 mg, Valsartan 1x80 mg, Bisoprolol 1x5 mg, warfarin 1x2 mg, Isosorbide
trinitrate 3x1, Aspilet 1x80 mg, Clopidogrel 1x75 mg, and Atorvastatin 1x20 mg. On the second
day of hospitalization, her palpitation increased. Second day ECG showed atrial fibrillation with
ventricular rate of 56 bpm, anteroseptal old myocardial infaction, and multiple multifocal PVCs.
Second day laboratory examination revealed Hb 18.1 and Ht 54.9, suggestive of
hemoconcentration. The patient was rehydrated and diuretic and beta blocker was discontinued.
Thereafter, PVCs disappeared and clinical condition of the patient improved. After 1 more day of
observation, the patient’s condition stabilized and she was then discharged home.
Discussion
Dehydration could cause PVC by means of increasing subaortic pressure gradient. Subaortic
pressure gradient could be caused by 2 mechanisms: decreased ventricular volume (e.g
administration of nitroglycerin and dehydration), and increased ventricular contractility (e.g
dobutamine administration and exercise). Furosemide reduced the ventricular volume and further
increased the patient’s subaortic gradient, thus aggravated PVCs in this patient. Bisoprolol also
reduced the patient’s ventricular rate and precipitate a compensatory mechanism in form of PVCs.
Rehydration and discontinuation of furosemide and bisoprolol eliminated PVC in this patient.
Conclusion
PVC could be an unusual sign of dehydration. Proper and immediate correction of volume status
could terminate ECG abnormalities