Characteristics of single isovolumic left-ventricular pressure waves of dog hearts in situ.
By fitting isovolumic phases of an ejecting beat with a model-wave function, one can predict source pressure of the ejecting beat (Sunagawa et al. Trans Biomed Eng 1980; 27:299-305), this being a major determinant of systolic performance. Prior applications of this principle have involved two assumptions: (1) that the isovolumic pressure wave is shaped like an inverted cosine wave, and (2) that duration of an isovolumic beat is the same as that of an ejecting beat. The first assumption might cause overestimation of source pressure, since an isovolumic pressure wave begins declining before the midpoint of the wave. The second assumption might cause underestimation of source pressure, since an ejecting beat is always shorter than an adjacent isovolumic beat at the ejecting beat's end-diastolic volume. Although the two errors tend to cancel, it would be more rational and accurate to use a realistic model wave shape and a realistic isovolumic beat duration. To acquire the information necessary for this, pressure and volume time courses were measured during ejecting beats and adjacent isovolumic beats in dogs under the following steady-state conditions: basal, atrial pacing at various rates, infusion of dobutamine, infusion of verapamil, coronary ligation(s), and ventricular pacing at various sites. These conditions affected the amplitude and duration of isovolumic pressure waves substantially but did not affect the shape of the waves significantly. The duration of each isovolumic beat exceeded that of the previous ejecting beat to a degree which corresponded approximately to the ejecting beat's normalized pressure reserve (source pressure minus peak ejection pressure)/(source pressure). A more accurate source-pressure prediction should be possible by use of a realistic isovolumic pressure-wave shape and by taking account of the effect of pressure reserve on contraction duration.
Regen
D M
DM
Vanderbilt University School of Medicine, Department of Molecular Physiology and Biophysics, Nashville, TN 37232-0615.
Howe
W C
WC
Peterson
J T
JT
Little
W C
WC
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology; D002304:Cardiac Pacing, Artificial; D003198:Computer Simulation; D004280:Dobutamine / Q000494:pharmacology; D004285:Dogs; D005583:Fourier Analysis; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D017202:Myocardial Ischemia / Q000503:physiopathology; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology*; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology*; D014700:Verapamil / Q000494:pharmacology
D004280:Dobutamine; D014700:Verapamil