Hemodynamic changes and evaluation during hypoxic-ischemic encephalopathy and therapeutic hypothermia

Multiorgan damage is a hallmark of hypoxic-ischemic encephalopathy and cardiovascular and hemodynamic changes during asphyxia contribute significantly to the brain damage. The main insult to the heart is myocardial damage and associated ventricular dysfunction, which is manifested by reduced preload and afterload. The immature myocardium reacts to asphyxia by bradycardia and reduced contractile capacity. Pulmonary hypertension aggrevates cardiac dysfunction. Hypothermia is the only effective treatment for HIE but it may also affect the heart and peripheral vascular system leading to bradycardia and peripheral vasoconstriction. In fact, these effects might be cardioprotective also. Rewarming after hypothermia may increase the heart rate and cardiac metabolism, augmenting the cardiac output. Monitoring of patient with HIE during and after hypothermia is possible by using near-infrared spectroscopy, echocardiography and electrocardiography. Cerebral effects may be monitored by magnetic resonance imaging also. Management should include the physiological status of the patient and appropriate treatments, including inotropes, vasopressors or rarely fluid boluses. Dopamine should not be used unless absolutely necessary. Drugs like melatonin and magnesium are under investigation. All treatments should be evidence-based and targeted echocardiography should be used more often in these vulnerable infants. •Cardiovascular and hemodynamic changes in perinatal asphyxia contribute to the mortality and morbidity of these patients.•Myocard performance is severely affected in perinatal asphyxia and contribute to impaired cerebral circulation.•Targeted echocardiography and near-infrared spectroscopy should be integrated to the monitoring of asphyxiated infants.•Inotropes and vasopressors should be evidence based and tailored to the underlying physiology.