A Owen1. 1. Royal Brompton National Heart and Lung Hospital, London, United Kingdom.
Abstract
OBJECTIVE: The aim was to clarify the mechanism of the following observations: (1) left ventricular pressure recordings during diastole have shown that the minimum pressure at the base is greater than that at the apex; (2) echocardiographic measurements of the short axis dimension of the left ventricle during early filling have shown that the maximum rate of increase at the base occurs before that at mid-cavity. These observations cannot be explained on the basis of simple pressure-volume relationships and suggest that diastolic haemodynamics are more complex. METHODS: A numerical (computer) model of early diastolic filling was developed. The model represents the atrium and ventricle as distensible cylinders connected by a valve. Parameters in the model such as ventricular stiffness and rate and duration of relaxation can be varied and the resulting haemodynamic changes observed. RESULTS: Despite the simplicity of the model and the omission of several physiological variables, intracavity pressure gradients and the phase relation of radial wall movements are generated that appear to be similar to those found in the human heart. CONCLUSIONS: The results suggest that these observations can be explained by inflow causing a pressure disturbance at the base which propagates to the apex, and which is reflected back to the base. The time between peak rate of change of short axis dimension at the base and mid-cavity may thus be a practical way of assessing diastolic function independently of loading conditions. These values can easily be measured by M mode echocardiography.
OBJECTIVE: The aim was to clarify the mechanism of the following observations: (1) left ventricular pressure recordings during diastole have shown that the minimum pressure at the base is greater than that at the apex; (2) echocardiographic measurements of the short axis dimension of the left ventricle during early filling have shown that the maximum rate of increase at the base occurs before that at mid-cavity. These observations cannot be explained on the basis of simple pressure-volume relationships and suggest that diastolic haemodynamics are more complex. METHODS: A numerical (computer) model of early diastolic filling was developed. The model represents the atrium and ventricle as distensible cylinders connected by a valve. Parameters in the model such as ventricular stiffness and rate and duration of relaxation can be varied and the resulting haemodynamic changes observed. RESULTS: Despite the simplicity of the model and the omission of several physiological variables, intracavity pressure gradients and the phase relation of radial wall movements are generated that appear to be similar to those found in the human heart. CONCLUSIONS: The results suggest that these observations can be explained by inflow causing a pressure disturbance at the base which propagates to the apex, and which is reflected back to the base. The time between peak rate of change of short axis dimension at the base and mid-cavity may thus be a practical way of assessing diastolic function independently of loading conditions. These values can easily be measured by M mode echocardiography.