Left Ventricular Ejection Time and End-Systolic Pressure Revisited

To the Editor: Left ventricular ejection time (LVET) measures the period of blood flow across the aortic valve and has a normal value of 0.35 +/- 0.08 s. It is influenced by heart rate, preload, afterload, and contractile state. LVET shortens with mitral regurgitation as well as left ventricular heart failure. In these cases, it primarily reflects decreased forward stroke volume. LVET increases with compensated aortic stenosis and high cardiac output sates. LVET can be calculated noninvasively using three methods, including a) carotid pulse contour (or invasive arterial line), b) M-mode echogram of the aortic valve, and c) transesophageal echocardiography Doppler systolic aortic outflow tracing Figure 1. LVET is used for calculation of mean velocity of fiber shortening (Vcf), according to the following formula: Equation 1 where EDD is left ventricular end-diastolic dimension in centimeters; ESD is left ventricular end-systolic dimension in centimeters, and LVET denotes left ventricular ejection time in seconds. Vcf measures the mean velocity of ventricular fiber shortening (in circumferences per second) at the level of the left ventricular minor axis and thus reflects ventricular contractility. Vcf is highly afterload dependent and relatively preload independent.Figure 1: Methods for measurement of left ventricular ejection time (LVET) and calculation of end-systolic blood pressure (ESP). (From Kolev N, Huemer G, Zimpfer M. Transesophageal echocardiography. A new monitoring technique. New York: Springer, 1995:54-72. Used with permission.) LVET can be measured using three methods, including a) arterial pressure curve, b) M-mode echocardiogram of the aortic valve, and c) pulsed Doppler recording from the aortic valve. ESP = (y/x) (PSP - DP) + DP. In our Figure yamplitude is 1.2 cm and x amplitude is 2.4 cm, and if arterial cuff (or from monitor invasive) blood pressure is 120/80 mm Hg, ESP = (1.2/2.4) times (120 - 80) + 80 = 100 mm Hg. DP = diastolic blood pressure; PSP = peak systolic blood pressure; x = amplitude in mm (or cm) of the peak systolic arterial pressure, y = amplitude in mm (or cm) of the incisura (dicotic notch) of the arterial pressure curve which exactly coincide with the end-systolic pressure, and ECG = electrocardiogram. In the study of Goertz et al. [1], an erroneously obtained LVET was used for calculation of Vcf. "The time interval from the peak of the R wave of the ECG to the minimal left ventricular dimension from the left ventricular M-mode was used to define LVET." This includes the preejection period (time interval between the R wave of the electrocardiogram to the LVET Figure 1, which in pathologic cases is elongated. False augmentation of LVET would lead to underestimation of actual Vcf values. Moreover, with left ventricular M-mode the end of the ejection period cannot be obtained precisely. Use of end-systolic pressure (ESP) versus peak systolic pressure (PSP) is important for calculation of afterload. ESP can be measured noninvasively using calibrated carotid pulse tracings. Calibration of the carotid pulse tracing is performed by simultaneously obtaining upper arm cuff pressure (arterial line pressure) and assigning systolic blood pressure to the peak and diastolic pressure (DP) to the nadir of the tracing by the following formula [2,3]Figure 1: Equation 2 The reason that ESP has gained recent interest is that it is important for calculation of left ventricular afterload or left ventricular meridional end-systolic wall stress (sigma) using the LaPlace relation [2,3]: Equation 3 where sigma = left ventricular meridional end-systolic wall stress (g/cm2), ESP = left ventricular end-systolic pressure replaced by end-systolic arterial pressure in g/cm2 (mm Hg times 1.35 = g/cm2), ESD = left ventricular end-systolic dimension in short-axis cross-section (cm) and h = left ventricular end-systolic wall thickness (cm). Attempts to simplify data acquisition by substituting peak systolic pressure for end-systolic pressure are complicated by numerous theoretical as well as physiologic problems. For example, if one uses a combination of peak-systolic blood pressure and end-systolic left ventricular dimension and wall thickness for calculating wall stress, variables from two different times in the cardiac cycle are incorporated. The result is an apparent wall stress value approximately twofold higher than the actual value for meridional wall stress (typical values of left ventricular wall stress using end-systolic pressure are 44 +/- 12 g/cm2). In the same article by Goertz et al. [1], the mistake of Reichek et al. [4], using peak systolic pressure instead of end-systolic pressure for estimation of end-systolic wall stress, has been repeated. Although many anesthesiologists may be unfamiliar with methods of measuring wall stress using echocardiography and blood pressure, it is important for us to understand the basic physiologic principle of wall stress because of its great utility in clinical applications. Normally, left ventricular wall stress reaches its peak within the first third of the ejection phase and then declines throughout the remainder of systole. This occurs despite rising pressures throughout most of the ejection period and emphasizes the importance of the decline in left ventricular size and the increase in wall thickness as determinants of instantaneous systolic wall stress. The use of wall stress as a measure of myocardial function is based on the principle that, for equilibrium to exist at any point of the cardiac cycle, the forces acting within the ventricular wall must exactly balance the force acting on the wall. When the ventricular function is normal, an elevation in afterload reduces ventricular systolic emptying, thus increasing the end-diastolic volume, i.e., preload. The augmented preload enhances myocardial performance and tends to counteract the effect of increased afterload. In contrast, in a failing, dilated ventricle, myocardial performance cannot be enhanced by increases in preload, so this compensatory mechanism is lost. In such cases, afterload becomes an increasingly important determinant of cardiac performance [3], and an increase in afterload may further reduce cardiac output, while pharmacologic reduction of afterload may be beneficial in elevating stroke volume. Moreover, afterload is a major determinant of myocardial oxygen consumption. Smith et al. [5] reported that an intraoperative increase in systolic wall stress was related to a higher incidence of myocardial ischemia. They concluded that, if afterload is evaluated by arterial pressure alone, myocardial ischemia may be overlooked. Nikolai Kolev, MD Michael Zimpfer, MD Department of Anesthesiology and Intensive Care, University Hospital of Vienna, Vienna, AustriaREFERENCES 1. Goertz AW, Hubner C, Seefeld C, et al. Effect of ephedrine bolus administration on left ventricular loading and systolic performance during high thoracic epidural anesthesia combined with general anesthesia. Anesth Analg 1994;78:101-5. Cited Here | View Full Text | PubMed | CrossRef 2. Lang RM, Briller RA, Neumann A, Borow KM. Assessment of global and regional left ventricular mechanics: applications to myocardial ischemia. In: Kerber RE, ed. Echocadiography in coronary artery disease. Mount Kisco, NY: Futura, 1988:227-31. Cited Here 3. Kolev N, Huemer G, Zimpfer M. Transesophageal echocardiography. A new monitoring technique. New York: Springer, 1995:54-72. Cited Here 4. Reichek N, Wilson J, St. John Sutton M, et al. Noninvasive determination of left ventricular end-systolic stress: validation of the method and initial application. Circulation 1982;65:99-108. Cited Here | View Full Text | PubMed | CrossRef 5. Smith JS, Roizen MF, Cahalan MC, et al. Does anesthetic technique make a difference? Augmentation of systolic blood pressure during carotid endarterectomy: effects of phenylephrine versus light anesthesia and of isofurane versus halotane on the incidence of myocardial ischemia. Anesthesiology 1988;69:846-53. Cited Here | View Full Text | PubMed | CrossRef © 1995 International Anesthesia Research Society