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- cAMP:
- cyclic adenosine monophosphate
- cGMP:
- cyclic guanosine monophosphate
- ECMO:
- extracorporeal membranous oxygenation
- eNOS:
- endothelial nitric oxide synthase
- iNO:
- inhaled nitric oxide
- LV:
- left ventricular
- NO:
- nitric oxide
- OI:
- oxygenation index
- PAP:
- pulmonary arterial pressure
- PBF:
- pulmonary blood flow
- PCWP:
- pulmonary capillary wedge pressure
- PDA:
- patent ductus arteriosus
- PDE:
- phosphodiesterase
- PFO:
- patent foramen ovale
- PPHN:
- persistent pulmonary hypertension of the newborn
- PVR:
- pulmonary vascular resistance
- RV:
- right ventricular
- SaO2:
- saturation of arterial oxygen
- SAP:
- systemic arterial pressure
- SVR:
- systemic vascular resistance
Abstract
Failure of the normal transition from in utero to ex utero physiology leads to “persistent” pulmonary hypertension of the newborn (PPHN). PPHN is frequently associated with low systemic blood pressure and low cardiac output because of increased right ventricular afterload and myocardial dysfunction. The general management of newborns with PPHN is geared toward maintenance of normothermia, normal serum electrolytes, normal intravascular volume, correction of acidosis, adequate sedation/analgesia, adequate ventilation and oxygenation with optimal lung recruitment, and avoidance of hyperoxia. Inotropic and vasoactive agents are commonly initiated early to increase cardiac output, maintain adequate systemic blood pressure, and enhance oxygen delivery to the tissue. Unfortunately, there is not much evidence on the choice, timing of initiation, dosing, monitoring, and titrating of vasoactive agents in this patient population. In this review, we will discuss the pathophysiology of PPHN and review the use of inotropic, lusitropic, and vasoactive agents in the management of PPHN, with particular attention to milrinone.
- Copyright © 2020 by the American Academy of Pediatrics
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