Heart failure caused by propranolol treatment in a newborn infant

Heart failure caused by propranolol treatment in a newborn infant

Case report

Supraventricular tachycardia developed at 34 weeks of gestation after an uneventful pregnancy. Fetal echocardiogram showed a structurally normal heart and an optically normal ventricular function. There were no signs of hydrops except for minimal pericardial and pleural effusions. The mother was started on digoxin with conversion of the tachycardia into a normal sinus rhythm. The digoxin therapy was continued until delivery.
A baby boy was delivered by cesarean section at 38 weeks of gestation with an Apgar score of 8-8-8 and a birthweight of 3150g (P 25-50). The baby was in sinus rhythm with a heart rate of 120 to 130 per minute. He developed respiratory distress and was admitted to the neonatal unit with Fi02 of 60%. At the time of admission he was tachypnoeic (80 per minute), had sternal retractions, nasal flaring and grunting. Chest X-ray showed a cardiothoracic index of 0.55 and hyperinflated lungs compatible with wet lungs. The baby improved rapidly and supplemental oxygen was reduced to 25% by the end of the first day of life. Digoxin measurement in cord blood (0.5nmol/l) was below the therapeutic level.
On the first day of life cardiac assessment was performed. Auscultation of the heart was totally normal. ECG (figure) showed a normal sinus rhythm with a heart rate of 130-140 per minute, tall P waves suggesting atrial hypertrophy, and no evidence of Wolff-Parkinson-White syndrome; echocardiography showed a 2mm persistent arterial duct with bidirectional shunting confirming pulmonary hypertension, patent foramen ovale with left-to-right shunt, and otherwise a structurally normal heart. Both atria were enlarged. The measurement of systolic ventricular function was normal but there was a mild diastolic dysfunction and the ventricular filling appeared to be slightly impaired.

After evaluation of the situation with the paediatric cardiologists it was decided to put the baby on propranolol, which was started on the first day of life at a dose of 1mg/kg/day and increased gradually up to 3mg/kg/day on day three. The baby never showed supraventricular tachycardia but his heart rate slowed to about 90-100 per minute. Further, the baby was extremely quiet and showed very poor feeding.
Following the initial improvement on the first day of life, the baby deteriorated steadily and developed signs of heart failure. On the fourth day of life he presented suddenly with marked tachypnoea of 120 per minute. He was hypercapneic, required 40% of supplemental oxygen and was placed on nasal CPAP. In addition he had several episodes of apnoea and bradycardia. Further examination revealed a pale infant with diminished peripheral perfusion; clinical signs of right-sided heart failure like edema, puffy eyelids, or enlargement of the liver were absent. Heart auscultation was still normal without gallop rhythm; blood pressure was normal. ECG was not performed at this stage, on chest X-ray there was cardiomegaly (cardiothoracic index 0.65) and signs of pulmonary venous congestion. Echocardiography showed cardiomegaly with ventricular and atrial dilatation and a mild reduced ventricular contractility; the arterial duct had closed spontaneously. Our hypothesis was that the heart failure was the consequence of propranolol treatment. The drug was discontinued and a low dose of diuretics was given. The baby improved rapidly and supplemental oxygen as well as nasal CPAP could be stopped within 12 hours. He started to feed and was increasingly active. The diuretics were stopped after 2 days of treatment. The antibiotics started at the time of clinical deterioration were stopped after obtaining negative blood cultures. On control echocardiography at the age of seven days the systolic ventricular function was normal. Propranolol was restarted at the age of ten days begining with a small dose of 0.5mg/kg/d and was increased daily. This time it was well tolerated without development of heart failure. Holter ECG was normal and the baby was discharged from hospital at the age of 15 days. Ambulatory follow up at the paediatric cardiology unit showed an uneventful course with no further episodes of tachycardia.

Discussion

Intrauterine supraventricular tachycardia can lead to heart failure and hydrops within a short time and therefore requires rapid treatment. Among the many possibilities of prenatal treatment digoxin given to the mother is often the first choice and was successful in the present case with rapid conversion into sinus rhythm.
It is nowadays well established that newborns having had fetal supraventricular tachycardia in utero should be treated prophylactically during the first year of life. Beta blockers are popular drugs and propranolol is usually used as the first line of treatment because it is easily applicable, usually well tolerated, and has a low incidence of complications. Side effects are described, among them the negative inotropic and chronotropic effect of the beta blockers which can accentuate heart failure. Other side effects are bradycardia and other arrhythmias, arterial hypotension, diminished peripheral perfusion, apneic episodes, bronchospasms, allergic skin reactions, and reduced activity.
Our patient presented postnatally with sinus rhythm and a normal systolic function on echocardiogram. Despite the normal shortening fraction, ejection fraction and cardiac output, echocardiogram showed diastolic dysfunction which led to the suspicion of mild heart failure during the tachypnoeic epidose. In this patient the measurement of cardiac function was normal but the cardiac reserve was poor and this was underestimated. Furthermore, the baby had respiratory distress after birth, which accentuated his cardiac overload. Propranolol was started at that stage and this led to a deterioration of the cardiac function within four days as well as to pulmonary hypercirculation and edema. The negative chronotropic and inotropic effect of propranolol accentuated the reduction of cardiac output and led to congestive heart failure, which could not be compensated by an elevation of the heart rate as this adrenergic response was blocked by propranolol. Heart failure was however limited to the left side in this case and it is unclear why right-sided failure was not observed.

Conclusion

Propranolol is an effective drug and is usually well tolerated. However caution is required in the case of a poor cardiac reserve or in conditions which may produce cardiac overload, for example, respiratory distress in the newborn. If this is the case, another antiarrhythmic drug or delay in starting the treatment should be considered.