Pathophysiology of newborn hypotension outside the transitional period

https://doi.org/10.1016/j.earlhumdev.2005.03.007Get rights and content

Abstract

Hypotension is a common diagnosis in neonatal intensive care units. Although there are epidemiological data for normative blood pressure values in preterm and term infants, the ranges of normal blood pressure where adequate organ perfusion is ensured for different gestational and postnatal ages remain unclear. An understanding of the developmentally regulated differences in the physiology and pathophysiology of the neonatal cardiovascular system in comparison to that of mature subjects is important to formulate an appropriate treatment strategy in neonates with circulatory compromise. This article reviews the current understanding of pathophysiology of hypotension and shock in the neonate beyond the transitional period, focusing on hypovolemia, myocardial dysfunction, abnormal peripheral vasoregulation, and relative or absolute adrenal insufficiency with potentially associated down regulation of adrenergic receptors.

Section snippets

Normal blood pressure

Although the exact gestational- and postnatal-age dependent autoregulatory blood pressure range has not been defined for the neonatal patient population [1], findings of recent studies on organ blood flow and its autoregulation have provided some novel information in this area [2]. However, several theoretical and clinical aspects of developmental cardiovascular pathophysiology relevant to neonatal shock remain unclear [3]. One area where the available information certainly needs further

Definition and phases of neonatal shock

Shock is a state of cellular energy failure caused by the inability of tissue oxygen delivery to satisfy tissue oxygen demand. Shock presents in phases of advancing severity characterized by specific pathological alterations in cardiovascular, renal and neuroendocrine function [1], [6]. In the initial compensated phase, vital organ (brain, heart and adrenal glands) perfusion and blood pressure are maintained by neuroendocrine compensatory mechanisms via redistribution of blood flow from the

Definition and clinical relevance of neonatal hypotension

Although there is some prospectively collected information on the relationship between blood pressure and organ blood flow in the transitional period especially in the VLBW patient population, very little data exist for the post-transitional neonatal period (from the 2nd to the 28th postnatal days). Except for the VLBW neonate during the first 24 postnatal hours, the general assumption is that the laws of cardiovascular physiology as we know from studies on mature animals and humans govern the

Hypovolemia

Although in the pediatric patient population absolute hypovolemia is the most frequent primary cause of hypotension, in neonates, abnormal peripheral vasoregulation with or without myocardial dysfunction is the most frequently encountered primary etiological factor [1]. The lack of a relationship between blood volume and blood pressure and the finding that dopamine is more effective in normalizing blood pressure than is volume administration support that absolute hypovolemia is a less frequent

Key guidelines

  • The normal postnatal increase in blood pressure is primarily the result of increase in peripheral vascular resistance.

  • Prompt recognition of neonatal shock in the compensated phase is difficult.

  • Unlike older children, the most common cause of hypotension in preterm and term infants is dysregulation of vascular tone with or without myocardial dysfunction rather than hypovolemia.

  • The structural and functional immaturity of the myocardium makes neonates, especially preterm infants, vulnerable to the

Research directions

  • Prospective clinical trials to define the gestational and postnatal age-specific normal blood pressure based on organ blood flow autoregulation during well-being and disease.

  • Prospective clinical trials to study the hemodynamic changes in different forms of neonatal shock and in response to different treatment modalities.

References (14)

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