Ventricular Contractility Assessment (dP/dt))

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The rate (dP/dt max) of left ventricle (LV) pressure rise in early systole is one of the oldest measures of LV global contractility. The greater the contractile force exerted, the greater the rate of increase in left ventricular pressure. This rate can be measured invasively, using high-fidelity micromanometer catheters inside the LV, as well as non-invasively, from a continuous wave Doppler examination of mitral regurgitation jet. Mitral regurgitation jet velocity is dependent on the pressure gradient between the left ventricle and the left atrium. During isovolumic contraction (IVCT, interval between mitral valve closure and aortic valve opening), there is no significant change in left atrial (LA) pressure. Therefore, mitral regurgitation velocity changes during this period reflect LV pressure changes.


Contents

How to measure dP/dt

To perform a dP/dt measurement, recording of the mitral regurgitation spectral profile at a high sweep speed (typically 100mm/sec) is necessary. The time interval between the points at which the velocity is 1 m/s and 3 m/s is measured. According to the Bernoulli equation, the pressure increase in the left ventricle between these points is 32 mm Hg (ΔP = 4 X V2² - 4 x V1² = 4 x 3² - 4 x 1²). Thus, dP/dt (in mm Hg/sec) is calculated from the following formula: LV dP/dt max = 32 mmHg / time (sec) [Fig. 1].


Clinical applications

Several studies have demonstrated a good correlation between the noninvasive Doppler-derived and catheter-derived dP/dt [1] [2]. Normal value of dP/dt max is 1000-1200 mmHg/sec or more. In addition, LV dP/dt max may be useful in predicting postoperative systolic function in patients with severe mitral valve regurgitation [3], but more clinical applications of dP/dt require further investigation.

Similarly, an increase in diastolic relaxation (lusitropy) of LV causes a rapid decrease in LV pressure and increased dP/dt min (-dP/dt) during isovolumic relaxation period (IVRT). Hence, dP/dt min can be used as a valuable tool in the evaluation of diastolic function of LV. Either a reduced dP/dt max or dP/dt min carries significant prognostic implications.

The rate of pressure rise in right ventricle (RV) reflects RV contractility, and can be derived in an analogous manner from the tricuspid regurgitation jet, except that the interval between 1 m/s and 2 m/s should be used [Fig. 2]. Therefore, RV dP/dt max = 12mmHg / time (sec) [(4 x 2²- 4 x 1²)/ time].



Limitations of dP/dt

The calculation of dP/dt can be performed only when a recordable mitral regurgitation jet is present.

Eccentric MR jets may not reflect true velocity and will result in underestimation of dP/dt, unless careful colour Doppler examination of the jet is made to minimize angulation error.

DP/dt max is also influenced by preload, afterload, heart rate and myocardial hypertrophy [4]. Maximum dP/dt rises with increases in afterload and preload. A normal dP/dt maybe present in hypertension and aortic stenosis even with impaired LV function.

In the presence of marked mechanical dyssynchrony (as typified by left bundle branch block), dP/dt may be reduced, not due to intrinsically decreased myocardial contractility, but rather as a consequence of contractile dyssynchrony and overall pump inefficiency.

References

  1. 1. Bargiggia GS, Bertucci C, Recusani F, Raisaro A, de Servi S, Valdes-Cruz LM, Sahn DJ, Tronconi L. A new method for estimating left ventricular dP/dt by continuous wave Doppler-echocardiography. Validation studies at cardiac catheterization. Circulation. 1989 Nov;80(5):1287-92.
  2. 2. Chung N, Nishimura RA, Holmes DR Jr, Tajik AJ. Measurement of left ventricular dp/dt by simultaneous Doppler echocardiography and cardiac catheterization. J Am Soc Echocardiogr. 1992 Mar-Apr;5(2):147-52.
  3. 3. Leung DY, Griffin BP, Stewart WJ, Cosgrove DM 3rd, Thomas JD, Marwick TH. Left ventricular function after valve repair for chronic mitral regurgitation: predictive value of preoperative assessment of contractile reserve by exercise echocardiography. J Am Coll Cardiol. 1996 Nov 1;28(5):1198-205.
  4. 4. Grossman W, Haynes F, Paraskos J et al. Alterations in preload and myocardial mechanics. Circ. Res 1972;31:83
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