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Hemodynamic analysis in infants with late‐onset circulatory collapse
Author(s) -
Washio Yosuke,
Uchiyama Atsushi,
Nakanishi Hidehiko,
Totsu Satsuki,
Masumoto Kenichi,
Kusuda Satoshi
Publication year - 2013
Publication title -
pediatrics international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.49
H-Index - 63
eISSN - 1442-200X
pISSN - 1328-8067
DOI - 10.1111/ped.12114
Subject(s) - medicine , circulatory collapse , shock (circulatory) , hemodynamics , afterload , cardiology , oliguria , circulatory system , gestational age , blood pressure , cardiac output , blood flow , anesthesia , renal function , pregnancy , biology , genetics
Background Late‐onset circulatory collapse ( LCC ) is a disorder in which blood pressure decreases and oliguria suddenly occurs in preterm infants who have survived the acute stage, leading to shock, without contributing underlying factors. In order to evaluate hemodynamic changes during LCC , the correlation between myocardial functions and organ blood flow was investigated with echography. Methods Seven very‐low‐birthweight infants were given a diagnosis of LCC during the study period. Cardiovascular and organ flow parameters of the infants were recorded prospectively, once a week, and compared with eight control very‐low‐birthweight infants with matching gestational age. Echographic study was performed before LCC , at the onset of LCC , and after LCC among infants with LCC . Results A significant increase in ejection fraction and a significant decrease in end systolic wall stress were observed in infants with the LCC condition. At the same time, the mean blood flow velocity increased significantly in the superior mesenteric artery, while it decreased in the anterior cerebral artery. Systolic blood flow velocity increased and mean velocity was maintained in the renal artery during LCC . Conclusion LCC is a distributive shock, characterized by a hyperdynamic state and decreased afterload. Echographic examination of organ flow during LCC is useful in understanding the pathophysiology of the disorder.