Accuracy of the ultrasonic cardiac output monitor in healthy term neonates during postnatal circulatory adaptation

Background Echocardiography is regarded as a gold standard for measuring hemodynamic values. The ultrasonic cardiac output monitor （USCOM） is a new method for measuring hemodynamics and could provide non-invasive point of care guidance. So far, there are no published USCOM reference values for neonates, nor has USCOM＇s accuracy been established in this population. We aimed to determine the accuracy and clinical utility of the USCOM in healthy neonates relative to published echocardiographic data, to establish normal hemodynamic parameters that it measures, and to assess the possible role of USCOM as an alternative to echocardiography as a trend monitor. Methods Right and left heart hemodynamics of 90 normal neonates were measured during circulatory adaptation over the first three days of life using the USCOM and automated oscillotonometry. Results Heart rate showed a significant decline from days one to three, from 126 to 120 （P〈0.001）. Systolic, diastolic and mean arterial pressures all increased significantly from 66 to 71 mmHg, 33 to 38 mmHg and 44 to 49 mmHg, respectively （P 〈0.001 in each case）. Right ventricular cardiac index （RV-CI） showed no change with a mean of 5.07 L.minl.m2. Left ventricular cardiac index （LV-CI） declined from 3.43 to 3.00 L.minl.m2 （P 〈0.001）. RV-CI exceeded LV-CI on all three days by a mean of 61%. The systemic vascular resistance index （SVRI）, based on LV-CI, increased significantly over the three days from 1083 to 1403 dyne.sec.cm5.m2 （P 〈0.001）. Conclusions Normal neonatal hemodynamic values, as indicated by USCOM, were established. LV-CI measurement showed excellent agreement with published echocardiographic studies. RV-CI was constant and exceeded LV-CI for all three days of this study. It may be falsely high due to flow velocity measurement errors arising from the pulmonary branch arteries, and may represent a limitation of the USCOM method. The progressive rise of arterial pressure and SVRI despite a declining LV-CI may indicate functional closure of the ductus arteriosus, with the greatest change occurring within the first 24 hours. Evidence of closure of the foramen ovale was not observed.

Cardiopulmonary Response to Exercise at High Altitude in Adolescents with Congenital Heart Disease

Objective:To extend our knowledge on tolerance of acute high-altitude exposure and hemodynamic response to exercise in adolescents with congenital heart disease(AscCHD)without meaningful clinical or functional restriction.Methods:A symptom limited cardiopulmonary exercise stress test and a non-invasive cardiac output measurement during steady state exercise were performed at 540 m and at 3454 m a.s.l.Symptoms of acute mountain sickness were noted.Results:We recruited 21 healthy controls and 16 AscCHD(59%male,mean age 14.7±1.1 years).Three subjects(2 controls,1 AscCHD)presented light symptoms of acute mountain sickness(dizziness and headache).During the symptom limited exercise test at lowland,control subjects showed a significantly higher power to weight index(3.5±0.6 W/kg vs.3.0±0.7 W/kg,p<0.001),heart rate(188.8±10.41/min vs.179.4±13.11/min,p<0.050)and ventilation(92.8±22.9 l/min vs.75.4±18.6 l/min,<0.050).At altitude,power to weight index only remained significantly higher in the control group(2.8±0.6 W/kg vs.2.6±0.6 W/kg,p<0.001).Pulmonary blood flow(PBF)at lowland showed no difference between the control and the AscCHD group,neither at rest(5.4±0.8 l/min vs.5.1±0.9 l/min,p=0.308),nor during the steady state test(10.6±2.4 l/min vs.10.5±2.0 l/min,p=0.825).At high altitude,PBF increased by 110%and 112%,respectively(12.8±2.32 l/min vs.12.5±3.0 l/min;intergroup difference:p=0.986).Conclusions:High altitude exposure was well tolerated in an unselected group of AscCHD.No significant difference in the cardio-pulmonary adaptation to a control group was noted during a steady state exercise.Symptoms of minor acute mountain sickness did occur,which should however not be misinterpreted as signs of hemodynamic maladaptation.