Key result
Radial and particularly femoral dP/dtmax allowed reasonably good tracking of left ventricular contractility changes as loading and inotropic conditions varied, with Ees being the main determinant of arterial dP/dtmax.
Why the study?
LV dP/dtmax requires LV catheterization, leading to surrogate arterial pressure waveform measures whose interactions with load-independent LV contractility during varying loading and contractile conditions needed evaluation.
Arterial dP/dtmax, particularly femoral, can serve as a surrogate for LV dP/dtmax to track left ventricular contractility changes under varying loading and inotropic conditions.
Answers are grounded in this paper and cite their sources.
Requires human validation before clinical use; leaves open translation of arterial dP/dtmax surrogates from animal models.
Maximal left ventricular (LV) pressure rise (LV dP/dtmax), a classical marker of LV systolic function, requires LV catheterization, thus surrogate arterial pressure waveform measures have been proposed. We compared LV and arterial (femoral and radial) dP/dtmax to the slope of the LV end-systolic pressure-volume relationship (Ees), a load-independent measure of LV contractility, to determine the interactions between dP/dtmax and Ees as loading and LV contractility varied. We measured LV pressure-volume data using a conductance catheter and femoral and radial arterial pressures using a fluid-filled catheter in 10 anesthetized pigs. Ees was calculated as the slope of the end-systolic pressure-volume relationship during a transient inferior vena cava occlusion. Afterload was assessed by the effective arterial elastance. The experimental protocol consisted of sequentially changing afterload (phenylephrine/nitroprusside), preload (bleeding/fluid bolus), and contractility (esmolol/dobutamine). A linear-mixed analysis was used to assess the contribution of cardiac (Ees, end-diastolic volume, effective arterial elastance, heart rate, preload-dependency) and arterial factors (total vascular resistance and arterial compliance) to LV and arterial dP/dtmax. Both LV and arterial dP/dtmax allowed the tracking of Ees changes, especially during afterload and contractility changes, although arterial dP/dtmax was lower compared to LV dP/dtmax (bias 732 ± 539 mmHg⋅s− 1 for femoral dP/dtmax, and 625 ± 501 mmHg⋅s− 1 for radial dP/dtmax). Changes in cardiac contractility (Ees) were the main determinant of LV and arterial dP/dtmax changes. Although arterial dP/dtmax is a complex function of central and peripheral arterial factors, radial and particularly femoral dP/dtmax allowed reasonably good tracking of LV contractility changes as loading and inotropic conditions varied.
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García et al. (2018) studied Healthy (anesthetized pigs) (n=10). Arterial (femoral and radial) dP/dtmax monitoring vs. Left ventricular (LV) dP/dtmax and end-systolic elastance (Ees) was evaluated on Contribution of Ees to femoral dP/dtmax (estimated absolute increase per 0.1 mmHg·ml-1 increase in Ees) (95% CI 236.8-415.5, p=<0.001). Radial and particularly femoral dP/dtmax allowed reasonably good tracking of left ventricular contractility changes as loading and inotropic conditions varied, with Ees being the main determinant of arterial dP/dtmax.
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