Abstract
To non-invasively identify the hemodynamic changes in critically ill children during the first 48 h following initiation of mechanical ventilation by the ultrasound cardiac output monitor (USCOM) method and compare the data in children with pulmonary and non-pulmonary pathology. This was a prospective observational study to evaluate the influence of mechanical ventilation on hemodynamic changes and to describe hemodynamic profiles of mechanically ventilated children. A total of 56 children with respiratory failure were included in the present study. Ventilated patients are divided into two groups. Group A (n=36) includes patients with pulmonary pathology. Group B (n=20) consists of patients with extra pulmonary etiology of respiratory failure. Hemodynamic parameters (cardiac index and systemic vascular resistance index) were evaluated using ultrasound cardiac output monitoring (USCOM 1A) immediately following initiation of mechanical ventilation and again at 6, 12, and 48 h. Pharmacological circulatory support (inotropes, vasopressors, levosimendan and phosphodiesterase III inhibitors) was individually and continuously modified based on real-time hemodynamic parameters and optimal fluid balance. No significant differences in hemodynamic profiles were found between Group A and Group B. The protective strategy of mechanical ventilation was not associated with significant differences in hemodynamic profiles between children ventilated for pulmonary and non-pulmonary pathologies. Hemodynamically unstable children ventilated for pulmonary pathology with the protective strategy of mechanical ventilation had a greater requirement for inotropic and combined inotropic and vasoactive circulatory support than children ventilated for non-pulmonary causes of respiratory failure.
Highlights
Circulatory failure in critically ill children is most often caused by a low circulatory volume and low myocardial contractility or a decrease in systemic vascular resistance
The patients were divided into two groups according to primary pathology; group A (n=36) included children with pulmonary pathology and the group B (n=20) included children ventilated for non-pulmonary pathology
All hemodynamically unstable children included in the present study underwent standard monitoring of vital signs (ECG, invasive arterial blood pressure, central venous pressure, one-hour diuresis) and were examined by transthoracic echocardiography (TTE) to exclude structural defects of the heart
Summary
Circulatory failure in critically ill children is most often caused by a low circulatory volume and low myocardial contractility or a decrease in systemic vascular resistance. Treatment aims to optimize oxygen delivery to peripheral tissues according to the current needs of the child by supporting blood circulation and ventilation. Cardiac output is determined by the heart rate and stroke volume, and blood pressure by cardiac output and systemic vascular resistance. Published studies have clearly shown that a clinical estimation of hemodynamic parameters, such as cardiac index and systemic vascular resistance, does not correspond to invasively measured results in critically ill pediatric or adult patients[3,4]. The interval from first presentation to cardiac output measurement using invasive techniques typically exceeds the 60-minute period recommended by the American College of Critical Care Medicine guidelines for fluid resuscitation and selection of first- and second-line vasoactive and inotropic drugs[1]
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