Abstract
Introduction
Persistent asystole following restoration of mechanical circulation during extracorporeal cardiopulmonary resuscitation (E-CPR) is typically considered fatal. However, in profound hypothermia, electrical silence may not reflect irreversible myocardial injury.
Case Report
A term neonate with severe meconium aspiration syndrome (MAS) was initially supported on veno-arterial ECMO at a regional hospital and transported to a tertiary ECMO facility. Following decannulation, she suffered cardiac arrest. Mechanical circulation was achieved after prolonged E-CPR with central cannulation, but the patient remained asystolic in the context of profound hypothermia (31.2°C). Electrical activity reappeared only after controlled rewarming to 33°C. She was discharged home on day 35 with a good long term neurological outcome.
Discussion
Neonates are particularly prone to rapid hypothermia during resuscitation. Controlled rewarming is essential to determine cardiac viability before establishing futility.
Conclusion
Under profound hypothermia, asystole after restoration of mechanical circulation does not preclude irreversible myocardial damage. Cautious rewarming is mandatory to assess myocardial prognosis.
Introduction
Asystole after restoration of mechanical blood flow during extracorporeal cardiopulmonary resuscitation (E-CPR) often suggests irreversible myocardial injury. However, profound hypothermia can temporarily suppress pacemaker automaticity and electrical conduction, mimicking cardiac standstill despite preserved cellular viability.
Neonates are particularly prone to rapid hypothermia due to a large surface-area-to-mass ratio and limited thermoregulatory capacity. 1 During open-chest procedures or massive transfusion with room-temperature fluids, core temperature can drop precipitously.
This is the first report to date of a neonate with persistent asystole after E-CPR, in whom recovery of cardiac activity was achieved only after correction of hypothermia. The case highlights how hypothermia can confound interpretation of myocardial viability and simultaneously exert neuroprotective effects.
Case description
A 3.5 kg term female was delivered by emergency cesarean section for fetal distress. She developed severe hypoxemic respiratory failure from meconium aspiration syndrome and persistent pulmonary hypertension.
Because of refractory hypoxemia and shock, she was cannulated on cervical veno-arterial ECMO by a mobile team and transferred to a tertiary PICU. Of note, jugular cannulation was complicated with vascular tear requiring in situ surgical repair. Her condition improved with recovery of biventricular function, allowing elective decannulation on ECMO day 4 under stable cardiopulmonary function.
Minutes later, she suffered sudden cardiovascular collapse with pulmonary hemorrhage and progressed to asystole. Despite full transfusion support and high-quality CPR, no spontaneous circulation was achieved. Central cannulation for E-CPR via median sternotomy was performed, and extracorporeal flow was established after 57 min.
Even with full ECMO support (120 ml/kg/min), the patient remained asystolic. Hypothermia with core temperature of 31.2°C was noted. Controlled rewarming via the ECMO heat exchanger increased temperature to 33°C within 1 hour, at which point electrical activity resumed as monomorphic ventricular tachycardia. Epicardial cardioversion converted this to an ectopic atrial tachycardia, and sinus rhythm was restored by day 3 with amiodarone infusion.
The post-E-CPR course was complicated by persistent mediastinal bleeding requiring repeated surgical exploration and massive transfusion, precluding anticoagulation. With progressive myocardial and pulmonary recovery, ECMO was discontinued after 5 days. The patient was extubated to CPAP on day 20 and later discharged home on day 35 with normal neurological examination and brain MRI. On follow-up she has shown age-appropriate milestones.
Discussion
This case exemplifies that persistent asystole after restoration of extracorporeal flow does not always signify irreversible cardiac injury. In this neonate, electrical silence reflected reversible hypothermic depression of myocardial excitability and contractility.
Hypothermia-induced cardiac dysfunction
Experimental data show that hypothermia profoundly impairs myocardial excitation–contraction coupling. Under 32°C, pacemaker activity and conduction velocity fall markedly; below 28°C, the risk of cardiac arrest increases sharply.2,3 Cooling also decreases calcium sensitivity and maximal myofibrillar force, producing severe contractile depression that may persist transiently after rewarming. 2
During rewarming, myocardial function may worsen further—a phenomenon termed “rewarming shock”—due to intrinsic myocardial depression and vasodilation. Neonates, with limited calcium handling and small myocardial reserve, are especially susceptible. Controlled rewarming on ECMO offers hemodynamic and thermal stability, reducing the risk of circulatory collapse. 1
Thermal vulnerability in neonates
Newborns lose heat rapidly because of their high surface-area-to-mass ratio, thin skin, and limited thermogenesis. 1 Open-chest exposure during resuscitation, combined with infusion of unheated fluids and blood products, can precipitate severe hypothermia within minutes. In this patient, these iatrogenic factors likely plummeted core temperature.
Such inadvertent intraoperative hypothermia is common yet underrecognized during prolonged CPR.
Hypothermia and E-CPR outcomes
Hypothermia simultaneously offers myocardial and cerebral protection by reducing metabolic rate and oxygen consumption.1,2 This metabolic suppression partially explains preserved neurological outcomes despite prolonged low-flow or no-flow states. Cases of survival without neurological impairment after several hours of CPR have been documented when hypothermia was present and extracorporeal rewarming used. 4
In cohorts rewarmed with ECMO, survival rates of 47–63% have been reported, underscoring the value of continuous perfusion during rewarming. 3 ECMO provides both circulatory and gas-exchange support, helping prevent pulmonary failure, a frequent complication of rewarming from deep hypothermia. 4
Clinical implications
In neonatal E-CPR, these physiological insights demand caution in prognostication. Persistent asystole in a hypothermic patient should not be equated with cardiac death until the core temperature exceeds 33°C. Rewarming must be gradual to minimize hemodynamic instability.
Central cannulation during ongoing CPR, although technically challenging, can be life-saving when performed by a coordinated team. Use of structured, time-limited communication—such as a “30-s countdown” during each pause—minimizes interruption of flow during surgical cannulation and may enhance outcomes.
This case also illustrates the critical importance of thermoregulation in neonatal ECMO and E-CPR protocols. Temperature monitoring should be continuous, and hypothermia recognized as both a confounder of cardiac assessment and a potential therapeutic ally when managed deliberately.
Finally, the precise ethiopathology of the arrest remains unknown and outside the scope of this report, though temporality with decannulation raises the possibility of pulmonary thromboembolism or air embolism contributing.
Conclusion
Persistent asystole during E-CPR should be interpreted cautiously in the presence of profound hypothermia. Electrical silence may represent reversible thermal suppression rather than irreversible myocardial death. Rewarming to at least mild hypothermia is essential before declaring futility.
Meticulous thermoregulation, controlled rewarming, and continuous temperature monitoring should be integral to post-E-CPR care to optimize myocardial and neurological recovery.
This case demonstrates that even after persistent asystole on ECMO, restoration of cardiac rhythm and normal neurodevelopmental outcome are possible when hypothermia is promptly recognized, corrected, and managed with precision.
Footnotes
ORCID iDs
Ethical considerations
Our institution does not require ethical approval for reporting individual cases or case series.
Consent to participate
Written informed consent to submit the anonymised case report was obtained from the patient’s parents.
Funding
The authors received no financial support for the research, authorship, and/or publication of this article.
Declaration of conflicting interests
The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.