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Assessment of Diastolic Function of the Heart: Background and Current Applications of Doppler Echocardiography. Part I. Physiologic and Pathophysiologic.

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Presentation on theme: "Assessment of Diastolic Function of the Heart: Background and Current Applications of Doppler Echocardiography. Part I. Physiologic and Pathophysiologic."— Presentation transcript:

1 Assessment of Diastolic Function of the Heart: Background and Current Applications of Doppler Echocardiography. Part I. Physiologic and Pathophysiologic Features*   RICK A. NISHIMURA, M.D.  Mayo Clinic Proceedings  Volume 64, Issue 1, Pages (January 1989) DOI: /S (12) Copyright © 1989 Mayo Foundation for Medical Education and Research Terms and Conditions

2 Fig. 1 Diagram depicting various definitions of diastole that have been proposed, based on left ventricular pressure and volume curves throughout the cardiac cycle. Original definition by Wiggers consisted of time period from mitral valve opening to mitral valve closure. Clinical definition of diastole encompasses a period beginning at aortic valve closure and extending to mitral valve closure. A new physiologic definition of diastole reported by Brutsaert and associates25 proposes two phases for the cardiac cycle. In systolic phase, both active contraction (Con) and relaxation (Relax) occur. Diastasis (D) is a passive phase dependent on filling properties of the heart. EKG = electrocardiogram; IC = isovolumic contraction (mitral closure to aortic valve opening); EP = ejection period (aortic valve opening to aortic valve closure); IR = isovolumic relaxation (aortic valve closure to mitral valve opening); RF = rapid filling; SF = slow filling; AC = atrial contraction. (Modified from Brutsaert and colleagues.25 By permission of the American Heart Association, Inc.) Mayo Clinic Proceedings  , 71-81DOI: ( /S (12) ) Copyright © 1989 Mayo Foundation for Medical Education and Research Terms and Conditions

3 Fig. 2 Diagram of myocardial contraction and relaxation at cellular level. Simplified depiction shows major movements of calcium ions in mammalian ventricular myocardium. After electrical excitation, calcium ions are released (1) from sarcoplasmic reticulum (SR), enter myocardial cells (2) through sarcolemma (SL), bind to regulatory protein (troponin C) on thin filaments (3), and allow myosin to interact with actin to form force-generating cross-bridges and contraction to develop. Calcium ions dissociate from troponin C (4) and are sequestered back to the SR (4) or are removed from the cell (5), and myocardial relaxation proceeds. Mayo Clinic Proceedings  , 71-81DOI: ( /S (12) ) Copyright © 1989 Mayo Foundation for Medical Education and Research Terms and Conditions

4 Fig. 3 Analogy between velocity of lengthening of isolated papillary muscle and Doppler flow signal. Upper three tracings represent shortening of muscle length (L), velocity of shortening (Lmax/s), and force (F) as a function of time of two superimposed physiologically sequenced twitch contractions of an isolated papillary muscle. The afterload in contraction b is higher than in contraction a. The phases of contraction are as follows: development of force, isotonic shortening, decline of force at the end-systolic length, and isotonic lengthening; this sequence mimics the contraction-relaxation cycle in the intact heart. At transition of isometric force decline and onset of lengthening, there is a small electronic artifact, which, for the sake of clarity, has been removed from the velocity tracing (second from top). Phase of rapid lengthening simulates rapid filling of ventricle. In bottom tracing, velocity of lengthening has been displayed upside down, to illustrate analogy of lengthening velocity signals with Doppler flow traces. An increase in afterload (b) causes a later onset of lengthening and a smaller peak velocity. Original tracings of right ventricular papillary muscle of a ferret (temperature, 30°C; stimulus interval, 4 seconds). Mayo Clinic Proceedings  , 71-81DOI: ( /S (12) ) Copyright © 1989 Mayo Foundation for Medical Education and Research Terms and Conditions

5 Fig. 4 Schematic diagram of calculation of time constant of myocardial relaxation (tau). Pressure is plotted on y-axis, and time is plotted on x-axis. Pressure is measured by high-fidelity, manometer-tipped catheters. Pressure from time of aortic valve closure (upper dot) to mitral valve opening (lower dot) is fitted to a monoexponential equation. Time constant of relaxation (T) is obtained from equation as demonstrated, e = natural logarithm; p = pressure; t = time; T = tau. Mayo Clinic Proceedings  , 71-81DOI: ( /S (12) ) Copyright © 1989 Mayo Foundation for Medical Education and Research Terms and Conditions

6 Fig. 5 Pressure-volume relationships during cardiac cycle. Pressure is plotted on y-axis, and volume is plotted on x-axis. In each loop, left vertical border represents isovolumic relaxation and right vertical border represents isovolumic contraction. Filling of heart is represented by inferior border of each loop. A, There is a larger change in pressure per change in volume (ΔP1/ΔV1) in comparison with baseline state (ΔP/ΔV). This result occurs when myocardial stiffness increases. B, Increase in ΔP1/ΔV1 is also evident when pressure-volume curve shifts rightward, and a larger end-diastolic volume is obtained. This outcome is due to curvilinear nature of relationship between pressure and volume during diastole. Mayo Clinic Proceedings  , 71-81DOI: ( /S (12) ) Copyright © 1989 Mayo Foundation for Medical Education and Research Terms and Conditions


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