No abstract

Pulmonary hypertensive disease is assessed by quantification of pulmonary vascular resistance. Pulmonary total arterial compliance is also an indicator of pulmonary hypertensive disease. However, because of difficulties in measuring compliance, it is rarely used. We describe a method of measuring pulmonary arterial compliance utilizing magnetic resonance (MR) flow data and invasive pressure measurements. Seventeen patients with suspected pulmonary hypertension or congenital heart disease requiring preoperative assessment underwent MR-guided cardiac catheterization. Invasive manometry was used to measure pulmonary arterial pressure, and phase-contrast MR was used to measure flow at baseline and at 20 ppm nitric oxide (NO). Total arterial compliance was calculated using the pulse pressure method (parameter optimization of the 2-element windkessel model) and the ratio of stroke volume to pulse pressure. There was good agreement between the two estimates of compliance (r = 0.98, P < 0.001). However, there was a systematic bias between the ratio of stroke volume to pulse pressure and the pulse pressure method (bias = 61%, upper level of agreement = 84%, lower level of agreement = 38%). In response to 20 ppm NO, there was a statistically significant fall in resistance, systolic pressure, and pulse pressure. In seven patients, total arterial compliance increased >10% in response to 20 ppm NO. As a population, the increase did not reach statistical significance. There was an inverse relation between compliance and resistance (r = 0.89, P < 0.001) and between compliance and mean pulmonary arterial pressure (r = 0.72, P < 0.001). We have demonstrated the feasibility of quantifying total arterial compliance using an MR method.

No abstract

Background-After the Norwood operation, a patient's suitability for proceeding to a bidirectional cavopulmonary connection (BCPC) is assessed by a combination of echocardiography and diagnostic cardiac catheterization. In this study, we describe the results of 37 patients who underwent cardiovascular magnetic resonance (MR) assessment before BCPC. Methods and Results-Cardiovascular MR and echocardiography were performed in 37 infants with hypoplastic left heart syndrome before BCPC, and the findings were compared with surgical findings. MR assessment of ventricular function and valvar regurgitation were compared with echocardiography. MR exhibited high sensitivity and specificity for identification of neoaortic (sensitivity 86%, specificity 97%) and left pulmonary artery (sensitivity 100%, specificity 94%) obstruction. Echocardiography exhibited poor sensitivity for identification of vascular stenosis. The mean right ventricular ejection fraction calculated from the MR data was 50Ϯ10%.

Medical examiners' use of objectively measurable risk factors, such as obesity, history of hypertension, and/or diabetes, rather than symptoms, may be more effective in identifying undiagnosed OSA in commercial drivers during the commercial driver medical examinations.

No abstract

A potential morbidity of incomplete re-warming following hypothermic cardiopulmonary bypass (CPB) is cardiac arrest. In contrast, attempts to fully re-warm the patient can lead to cerebral hyperthermia. Similarly, rigid adherence to 37.0 degrees C during normothermic CPB may also cause cerebral overheating. The literature demonstrates scant information concerning the actual temperatures measured, the sites of temperature measurement and the detailed thermal strategies employed during CPB. A prospective, randomized, controlled study was undertaken to investigate the ability to manage perfusion temperature control in a group of hypothermic patients (28 degrees C) and a group of normothermic patients (37 degrees C). Eighty patients presenting for first-time, elective coronary artery bypass graft surgery (CABG) were randomly allocated to the hypothermic and normothermic groups. All surgery was performed by one surgeon and the anaesthesia managed by one anaesthetist. Temperature measurements were made at the nasopharyngeal (NP) site, as well as in the arterial line of the CPB circuit. The hypothermic group had the arterial blood temperature lowered to 25.0 degrees C to maintain the NP temperature at 28.0-28.5 degrees C. During re-warming, the arterial blood was raised to 38.0 degrees C. Meanwhile, in the normothermic group, the arterial blood temperature was raised to a maximum of 37.0 degrees C to maintain NP temperature at 36.5-37.0 degrees C. Despite strict guidelines, some patients transgressed the temperature control limits. Two patients in the hypothermic group failed to reach an NP temperature of 28.5 degrees C. Twenty-six patients were managed entirely within the control limits. During rewarming in both groups, control of both arterial and NP temperature was well managed with only 25% patients breaching the respective upper control limits. During the re-warming phases of CPB, we were unable to make any correlation between NP temperature and arterial blood temperature, using body weight or body mass index as predictors. Based on the results obtained, we recommend that strict criteria should be implemented for the management of temperature during CPB, in conjunction with more emphasis being placed on monitoring arterial blood temperature as a marker of potential cerebral hyperthermia. We should, therefore, not rely on NP temperature measurement alone during CPB.

The TEG(®) FF does not produce results equivalent to those of the Clauss fibrinogen regardless of platelet count.