The haemodynamic effects of propofol, given as a single dose of 2 mg kg-1 immediately followed by a continuous infusion of 6 mg kg-1 h-1, were studied in 10 elderly patients premedicated with lorazepam 1 mg i.v. All patients breathed room air spontaneously. Unconsciousness was successfully induced in all patients and persisted during the 60 min of the infusion. Statistically significant decreases in systolic and diastolic arterial pressures were observed 2 min after induction (28% and 19%, respectively) and during infusion (30% and 25%, respectively) and were related to decreases in systemic vascular resistance (21% following induction and 30% during infusion). Cardiac output was not affected at any time nor were stroke volume and heart rate. We conclude that the arterial hypotension associated with the induction and infusion of propofol is mainly a result of a decrease in afterload without compensatory increases in heart rate or cardiac output.

CTED represents an intermediate clinical phenotype. Exercise imaging unmasks cardiovascular dysfunction not evident at rest and identifies hemodynamically significant disease that results from reduced contractile reserve or increased vascular load.

Background Patients with a Fontan circulation achieve lower peak heart rates ( HR ) during exercise. Whether this impaired chronotropic response reflects pathology of the sinoatrial node or is a consequence of altered cardiac hemodynamics is uncertain. We evaluated the adequacy of HR acceleration throughout exercise relative to metabolic demand and cardiac output in patients with a Fontan circulation relative to healthy controls. Methods and Results Thirty subjects (20 healthy controls and 10 Fontan patients) underwent cardiac magnetic resonance imaging with simultaneous invasive pressure recording via a pulmonary and radial artery catheter during supine bicycle exercise to near maximal exertion. Adequacy of cardiac index, stroke volume, and HR reserve was assessed by determining the exercise‐induced increase (∆) in cardiac index, stroke volume, and HR relative to the increase in oxygen consumption ( VO 2 ). HR reserve was lower in Fontan patients compared with controls (71±21 versus 92±15 bpm; P =0.001). In contrast, increases in HR relative to workload and VO 2 were higher than in controls. The change in cardiac index relative to the change in VO 2 (∆cardiac index/∆ VO 2 ) was similar between groups, but Fontan patients had increased ∆ HR /∆ VO 2 and reduced ∆ stroke volume/∆ VO 2 compared with controls. There was an early and marked reduction in stroke volume during exercise in Fontan patients corresponding with a plateau in cardiac output at a low peak HR . Conclusions In Fontan patients, the chronotropic response is appropriate relative to exercise intensity, implying normal sinoatrial function. However, premature reductions in ventricular filling and stroke volume cause an early plateau in cardiac output beyond which further increases in HR would be physiologically implausible. Thus, abnormal cardiac filling rather than sinoatrial node dysfunction explains the diminished HR reserve in Fontan patients.

Functional cardiac evaluation during exercise is a promising tool in differentiating healthy athletes with borderline LVEF from those with an underlying cardiomyopathy. Excellent exercise capacity does not exclude significant LV damage.

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