Abstract
Background: Hypothermia is well known to elevate the time constant (whatever model is used) of the isochoric left-ventricular pressure fall. Due to different critera in use, it remained unclear whether prolonged diastole in hypothermia is sufficient for complete relaxation. Detecting and quantifying incomplete relaxation may become a valuable tool to prevent diastolic heart failure in hypothermia.Methods: Left-ventricular pressure decays in isolated guinea pig and rat hearts are analysed by 4-parametric regression at different temperatures, at sinus rhythm and electrical stimulation. Residual contraction (F_RC) is introduced and quantified by extrapolating the model's pressure forecast to end-systole, subtracting the asymptote, and normalising.Resultts: Isochoric pressure decay fits the regression model at all temperatures and heart beat frequencies. Residual contraction is virtually absent at normothermia and remains very small (F_RC<3%) down to 31°C. Lower temperatures or pacing induces higher F_RC. Eventually, the pressure curve becomes considerably elevated and looses its concavity.Conclusions: Despite slower pressure fall, ventricular relaxation remains fairly complete at hypothermia; and depends on considerable autoregulation of the individual heart. It is concluded (not proved) that individual emergence of negative lusitropy may indicate imminent heart failure. Asymptotic pressure rises are interpreted at higher ventricular tonus, independent from velocity of relaxation. Gradual increasing time constants may be attributed to a general slowing of bioreactions as temperature falls. Remarkable curve shape changes may be caused by aftercontractions due to elevated Ca++ sensitivity at hypothermia and high Ca++ load by pacing.
Highlights
Mild hypothermia is a secure and widely used method to reduce cardiac work and metabolism for surgical interventions
Ventricular relaxation remains fairly complete at hypothermia, and depends on considerable autoregulation of the individual heart
Gradual increasing time constants may be attributed to a general slowing of bioreactions as temperature falls
Summary
Mild hypothermia is a secure and widely used method to reduce cardiac work and metabolism for surgical interventions. Experimental hypothermic heart failure only occurs during rapid or extended cooling as a sudden, rapid, and complex process. As little or even positive inotropic effects of mild hypothermia has been surmised [1, 2], the diastolic function (lusitropy, relaxation) of the left ventricle became considered as a trigger of hypothermic heart failure. Due to a recent study [3], cooling renders ventricular relaxation incomplete despite its concomitant negative chronotropy. Such conclusion, depends critically on the soundness of modeling the isochoric (isovolumic) left–ventricular pressure fall and its extrapolation toward the onset of the subsequent systole. Hypothermia is well known to elevate the time constant (whatever model is used) of the isochoric left–ventricular pressure fall. Due to different critera in use, it remained unclear whether prolonged diastole in hypothermia is sufficient for complete relaxation Detecting and quantifying incomplete relaxation may become a valuable tool to prevent diastolic heart failure in hypothermia
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