Chest Compressions for Bradycardia during Neonatal Resuscitation-Do We Have Evidence?

Abstract

The International Liaison Committee on Resuscitation (ILCOR) recommends the initiation of chest compressions (CC) during neonatal resuscitation after 30 s of effective ventilation if the infant remains bradycardic (defined as a heart rate less than 60 bpm). The CC are performed during bradycardia to optimize organ perfusion, especially to the heart and brain. Among adults and children undergoing cardiopulmonary resuscitation (CPR), CC is indicated only for pulselessness or poor perfusion. Neonates have a healthy heart that attempts to preserve coronary and cerebral perfusion during bradycardia secondary to asphyxia. Ventilation of the lungs is the key step during neonatal resuscitation, improving gas exchange and enhancing cerebral and cardiac blood flow by changes in intrathoracic pressure. Compressing the chest 90 times per minute without synchrony with innate cardiac activity during neonatal bradycardia is not based on evidence and could potentially be harmful. Although there are no studies evaluating outcomes in neonates, a recent pediatric study in a hospital setting showed that when CC were initiated during pulseless bradycardia, a third of the patients went into complete arrest, with poor survival at discharge. Ventilation-only protocols such as helping babies breathe are effective in reducing mortality and stillbirths in low-resource settings. In a situation of complete cardiac arrest, CC reinitiates pulmonary flow and supports gas exchange. However, the benefit/harm of performing asynchronous CC during bradycardia as part of neonatal resuscitation remains unknown.

Keywords: bradycardia; chest compressions; neonatal resuscitation.

Figure 1

Effective strategies that could prevent neonatal bradycardia. Copyright Satyan Lakshminrusimha.

Figure 2

Effect of positive pressure ventilation (PPV) on pulmonary and systemic hemodynamics during neonatal bradycardia. Aeration of lung increases pulmonary blood flow facilitating gas exchange, maintaining left ventricular preload, and enhancing cerebral blood flow during systole and coronary blood flow during diastole. The pressure gradients caused during PPV enhance venous return, maintaining right ventricular preload and pulmonary circulation. (LV-left ventricle, RV- right ventricle). Copyright Satyan Lakshminrusimha.

Figure 3

Hemodynamic changes during asphyxia-induced bradycardia and subsequently during chest compressions. The BIOPAC snapshot shows the aortic pressure and carotid and coronary flows. (A) During asphyxia-induced bradycardia (HR 50 bpm) with peak systolic carotid and peak diastolic coronary flows. (B) When CC is performed during bradycardia, note the retrograde flows. Also note the inherent perfusing rhythm between CCs. Copyright Praveen Chandrasekharan

Figure 4

The illustration shows the effect of external cardiac compression during the “diastolic phase” of neonatal bradycardia. The coronary flow and ventricular filling occurs during diastole. Performing asynchronous external chest compressions could interfere with coronary perfusion and impair ventricular filling. (PA—pulmonary artery, PDA—patent ductus arteriosus). Copyright Satyan Lakshminrusimha.

Figure 5

The BIOPAC snapshot shows the aortic pressure and carotid, pulmonary, and ductal flows during chest compressions (CC). Note the initial inherent heart activity in between CCs is lost while CC is continued with cardiac arrest. In addition, the pulmonary flow is reduced along with ductal shunting. Copyright Praveen Chandrasekharan.