The Pressure-Volume Loop Revisited

Aghajani, Ebrahim; Müller, Stig; Kjørstad, Kjell E.; Korvald, Christian; Nordhaug, Dag; Revhaug, Arthur; Myrmel, Truls

doi:10.1097/01.shk.0000209521.20496.7a

Cited by 19 publications

(3 citation statements)

References 29 publications

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“…Hypothermia-induced bradycardia contributes to fewer ESPVR points during occlusions, another factor that may affect the accuracy of the slope. Furthermore, E es has been proven to be an unreliable contractility index in itself in experimental heart failure, as significant increases in E es were encountered in a pig model of stunning, acute ischemic and endotoxemic heart failure despite obvious other indications (significant decreases in CO, dP/dt max and MAP) of depressed myocardial function [34]. The increases in E es were accompanied with significant increases in V 0 , which apparently resulted in steep E es slopes [34].…”

Section: Discussionmentioning

confidence: 99%

Post-hypothermic cardiac left ventricular systolic dysfunction after rewarming in an intact pig model

et al. 2010

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IntroductionWe developed a minimally invasive, closed chest pig model with the main aim to describe hemodynamic function during surface cooling, steady state severe hypothermia (one hour at 25°C) and surface rewarming.MethodsTwelve anesthetized juvenile pigs were acutely catheterized for measurement of left ventricular (LV) pressure-volume loops (conductance catheter), cardiac output (Swan-Ganz), and for vena cava inferior occlusion. Eight animals were surface cooled to 25°C, while four animals were kept as normothermic time-matched controls.ResultsDuring progressive cooling and steady state severe hypothermia (25°C) cardiac output (CO), stroke volume (SV), mean arterial pressure (MAP), maximal deceleration of pressure in the cardiac cycle (dP/dtmin), indexes of LV contractility (preload recruitable stroke work, PRSW, and maximal acceleration of pressure in the cardiac cycle, dP/dtmax) and LV end diastolic and systolic volumes (EDV and ESV) were significantly reduced. Systemic vascular resistance (SVR), isovolumetric relaxation time (Tau), and oxygen content in arterial and mixed venous blood increased significantly. LV end diastolic pressure (EDP) remained constant. After rewarming all the above mentioned hemodynamic variables that were depressed during 25°C remained reduced, except for CO that returned to pre-hypothermic values due to an increase in heart rate. Likewise, SVR and EDP were significantly reduced after rewarming, while Tau, EDV, ESV and blood oxygen content normalized. Serum levels of cardiac troponin T (TnT) and tumor necrosis factor-alpha (TNF-α) were significantly increased.ConclusionsProgressive cooling to 25°C followed by rewarming resulted in a reduced systolic, but not diastolic left ventricular function. The post-hypothermic increase in heart rate and the reduced systemic vascular resistance are interpreted as adaptive measures by the organism to compensate for a hypothermia-induced mild left ventricular cardiac failure. A post-hypothermic increase in TnT indicates that hypothermia/rewarming may cause degradation of cardiac tissue. There were no signs of inadequate global oxygenation throughout the experiments.

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Section: Discussionmentioning

confidence: 99%

Post-hypothermic cardiac left ventricular systolic dysfunction after rewarming in an intact pig model

et al. 2010

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“…The slope of ESPVR, also referred to as E es , is an index of end-systolic elastance, an index that provides information on contractile function ( 134 ). The degree to which E es is load dependent is under discussion ( 3 ). Ventriculoarterial coupling, which reflects the interaction of the heart and its afterload, can also be assessed using the ratio of E es /arterial elastance.…”

Section: Hemodynamicsmentioning

confidence: 99%

Guidelines for measuring cardiac physiology in mice

Lindsey

Kassiri

Virag

et al. 2018

American Journal of Physiology-Heart and Circulatory Physiology

263

194

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Cardiovascular disease is a leading cause of death, and translational research is needed to understand better mechanisms whereby the left ventricle responds to injury. Mouse models of heart disease have provided valuable insights into mechanisms that occur during cardiac aging and in response to a variety of pathologies. The assessment of cardiovascular physiological responses to injury or insult is an important and necessary component of this research. With increasing consideration for rigor and reproducibility, the goal of this guidelines review is to provide best-practice information regarding how to measure accurately cardiac physiology in animal models. In this article, we define guidelines for the measurement of cardiac physiology in mice, as the most commonly used animal model in cardiovascular research.Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/guidelines-for-measuring-cardiac-physiology-in-mice/.

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“…Specifically, the activation energy estimated from the VO 2 -PVA relation has since been used to study the effects of intravenous Ca 2+ infusion (Ohgoshi et al, 1992;Matsushita et al, 1995;Hata et al, 1998) or perfusion (Wannenburg et al, 1992), Ca 2+ overload (Tsuji et al, 2001), positive (Wu et al, 1989;Takeuchi et al, 2001) or negative (Nakayama et al, 1997) inotropic interventions that target Ca 2+ -specific receptors, ryanodine-treated hearts having Ca 2+ -leaky sarcoplasmic reticula (Takasago et al, 1993), and inhibition of the sarcoplasmic reticular Ca 2+ -ATPase (Misawa et al, 2001). It has also been used in studies of cardiac diseases that inferred impaired energy utilisation for intracellular Ca 2+ handling in hyperthyroid hearts (Goto et al, 1990), hypertensive-hypertrophied hearts (Kameyama et al, 1998;Morii et al, 1998), acute endotoxemia (Aghajani et al, 2004), diabetes…”

Section: Introductionmentioning

confidence: 99%

Resolving an inconsistency in the estimation of the energy for excitation of cardiac muscle contraction

Han,

Pham,

Taberner

et al. 2023

Front. Physiol.

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In the excitation of muscle contraction, calcium ions interact with transmembrane transporters. This process is accompanied by energy consumption and heat liberation. To quantify this activation energy or heat in the heart or cardiac muscle, two non-pharmacological approaches can be used. In one approach using the “pressure-volume area” concept, the same estimate of activation energy is obtained regardless of the mode of contraction (either isovolumic/isometric or ejecting/shortening). In the other approach, an accurate estimate of activation energy is obtained only when the muscle contracts isometrically. If the contraction involves muscle shortening, then an additional component of heat associated with shortening is liberated, over and above that of activation. The present study thus examines the reconcilability of the two approaches by performing experiments on isolated muscles measuring contractile force and heat output. A framework was devised from the experimental data to allow us to replicate several mechanoenergetics results gleaned from the literature. From these replications, we conclude that the choice of initial muscle length (or ventricular volume) underlies the divergence of the two approaches in the estimation of activation energy when the mode of contraction involves shortening (ejection). At low initial muscle lengths, the heat of shortening is relatively small, which can lead to the misconception that activation energy is contraction mode independent. In fact, because cardiac muscle liberates heat of shortening when allowed to shorten, estimation of activation heat must be performed only under isometric (isovolumic) contractions. We thus recommend caution when estimating activation energy using the “pressure-volume area” concept.

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The Pressure-Volume Loop Revisited

Abstract: The Ees is particularly load dependent and will reflect load interventions more than the inotropic state of the cardiac muscle. A VCO-generated Ees increase could be an unmasking of a pronounced preload sensitivity in failing myocardium.

Cited by 19 publications

References 29 publications

Post-hypothermic cardiac left ventricular systolic dysfunction after rewarming in an intact pig model

Post-hypothermic cardiac left ventricular systolic dysfunction after rewarming in an intact pig model

Guidelines for measuring cardiac physiology in mice

Resolving an inconsistency in the estimation of the energy for excitation of cardiac muscle contraction

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