title: End-systolic pressure as a balance between opposing effects of ejection.
abstract: Ejection has previously been thought to exert only negative effects on end-systolic left ventricular pressure, via mechanisms like shortening deactivation and the force-velocity relation. Whether ejection also exerted a positive influence on pressure generation was tested by comparing two successive beats: 1) the last beat of steady-state ejection versus 2) a totally isovolumic contraction at the end-systolic volume. In 12 isolated, blood-perfused canine hearts loaded with a simulated arterial system, ejecting end-systolic pressure exceeded isovolumic pressure by approximately 10 mm Hg when ejection fraction was 0.3. With both higher and lower ejection fractions, the excess of ejecting end-systolic pressure was smaller; beyond an ejection fraction of roughly 0.5, the trend reversed so that ejecting end-systolic pressure fell below isovolumic pressure. The maximum excess in ejecting end-systolic pressure was quite variable (1-17 mm Hg), but the pattern of its variation with ejection fraction was consistent. A correlate of the positive effect of ejection on ventricular pressure was found in the timing of end systole. For an ejection fraction of 0.4, the systolic duration of ejecting beats was approximately 45% longer than in isovolumic beats (range, 23-67%). Potentially, a positive effect of ejection might be due to a residual influence of the stronger activation of cardiac myofilaments early in ejecting systole during which the sarcomeres were at longer lengths than in the isovolumic beat at end-systolic volume (length-dependent activation). A hypothetical model based on this mechanism reproduced both of the positive effects of ejection that were observed: excess end-systolic pressure and prolonged duration of systole. Thus, the approximate load independence of end-systolic pressure could result from the counter balance between opposing influences of ejection.
authors.affiliation: Department of Biomedical Engineering, Johns Hopkins Medical School, Baltimore, Maryland 21205.
authors.forename: W C
authors.initials: WC
authors.lastname: Hunter
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D004285:Dogs; D006321:Heart / Q000502:physiology*; D009200:Myocardial Contraction; D013318:Stroke Volume; D013599:Systole; D013997:Time Factors