Performance comparison of ventricular and arterial dP/dtmax for assessing left ventricular systolic function during different experimental loading and contractile conditions

García, Manuel Ignacio Monge; Jian, Zhongping; Settels, Jos J.; Hunley, Charles; Cecconi, Maurizio; Hatib, Feras; Pinsky, Michael R.

doi:10.1186/s13054-018-2260-1

Cited by 66 publications

(67 citation statements)

References 37 publications

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“…However, it is unclear what level of VAC, its duration, or level of exogenous catecholamines are necessary to create this detrimental effect. Recently, animal studies demonstrate that NE can impair LV ejection by increasing the magnitude of arterial pressure reflected waves during ejection, which also becomes manifest as VAC uncoupling without increasing coronary perfusion pressure [23]. As was also seen in patients with postoperative vasoplegia [11], we observed that only patients with higher Ees and normalized VAC increased CO during NE (Fig.…”

Section: Discussionsupporting

confidence: 78%

Cardiovascular determinants of resuscitation from sepsis and septic shock

2019

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Background We hypothesized that the cardiovascular responses to Surviving Sepsis Guidelines (SSG)-defined resuscitation are predictable based on the cardiovascular state. Methods Fifty-five septic patients treated by SSG were studied before and after volume expansion (VE), and if needed norepinephrine (NE) and dobutamine. We measured mean arterial pressure (MAP), cardiac index (CI), and right atrial pressure (Pra) and calculated pulse pressure and stroke volume variation (PPV and SVV), dynamic arterial elastance (Ea dyn ), arterial elastance (Ea) and left ventricular (LV) end-systolic elastance (Ees), Ees/Ea (VAC), LV ejection efficiency (LVeff), mean systemic pressure analogue (Pmsa), venous return pressure gradient (Pvr), and cardiac performance (Eh), using standard formulae. Results All patients were hypotensive (MAP 56.8 ± 3.1 mmHg) and tachycardic (113.1 ± 7.5 beat min −1 ), with increased lactate levels (lactate = 5.0 ± 4.2 mmol L −1 ) with a worsened VAC. CI was variable but > 2 L min −1 M −2 in 74%. Twenty-eight-day mortality was 48% and associated with admission lactate, blood urea nitrogen (BUN), and creatinine levels but not cardiovascular state. In all patients, both MAP and CI improved following VE, as well as cardiac contractility (Ees). Fluid administration improved Pra, Pmsa, and Pvr in all patients, whereas both HR and Ea decreased after VE, thus normalizing VAC. CI increases were proportional to baseline PPV and SVV. CI increases proportionally decreased PPV and SVV. VE increased MAP > 65 mmHg in 35/55 patients. MAP responders had higher PPV, SVV, and Ea dyn than non-responders. NE was given to 20/55 patients in septic shock, but increased MAP > 65 mmHg in only 12. NE increased Ea, Ea dyn , Pra, Pmsa, and VAC while decreasing HR, PPV, SVV, and LVeff. MAP responders had higher pre-NE Ees and lower VAC. Dobutamine was given to 6/8 patients who remained hypotensive following NE. It increased Ees, MAP, CI, and LVeff, while decreasing HR, Pra, and VAC. At all times and all steps of the protocol, CI changes were proportional to Pvr changes independent of treatment. Conclusions The cardiovascular response to SSG-based resuscitation is highly heterogeneous but predictable from pre-treatment measures of cardiovascular state. Electronic supplementary material The online version of this article (10.1186/s13054-019-2414-9) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 78%

Cardiovascular determinants of resuscitation from sepsis and septic shock

2019

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“…Blood pressure recordings were analyzed for systolic blood pressure (SBP) and the maximum rate of systolic pressure increase (dP/dt max ) as a measure of myocardial contractility. Measurement of dP/dt max from the femoral artery has been shown to provide good tracking of left ventricular contractility (Monge Garcia et al, 2018). To establish evenly sampled series, any beats for which ARI, SBP or dP/dt max measurements could not be determined were replaced by linear interpolation between the surrounding beats.…”

Section: Discussionmentioning

confidence: 99%

Complex Interaction Between Low-Frequency APD Oscillations and Beat-to-Beat APD Variability in Humans Is Governed by the Sympathetic Nervous System

et al. 2020

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Background: Recent clinical, experimental and modeling studies link oscillations of ventricular repolarization in the low frequency (LF) (approx. 0.1 Hz) to arrhythmogenesis. Sympathetic provocation has been shown to enhance both LF oscillations of action potential duration (APD) and beat-to-beat variability (BVR) in humans. We hypothesized that beta-adrenergic blockade would reduce LF oscillations of APD and BVR of APD in humans and that the two processes might be linked. Methods and Results: Twelve patients with normal ventricles were studied during routine electrophysiological procedures. Activation-recovery intervals (ARI) as a conventional surrogate for APD were recorded from 10 left and 10 right ventricular endocardial sites before and after acute beta-adrenergic adrenergic blockade. Cycle length was maintained constant with right ventricular pacing. Oscillatory behavior of ARI was quantified by spectral analysis and BVR as the short-term variability. Betaadrenergic blockade reduced LF ARI oscillations (8.6 ± 4.5 ms 2 vs. 5.5 ± 3.5 ms 2 , p = 0.027). A significant correlation was present between the initial control values and reduction seen following beta-adrenergic blockade in LF ARI (r s = 0.62, p = 0.037) such that when initial values are high the effect is greater. A similar relationship was also seen in the beat-to beat variability of ARI (r s = 0.74, p = 0.008). There was a significant correlation between the beta-adrenergic blockade induced reduction in LF power of ARI and the witnessed reduction of beat-to-beat variability of ARI (r s = 0.74, p = 0.01). These clinical results accord with recent computational modeling studies which provide mechanistic insight into the interactions of LF oscillations and beat-to-beat variability of APD at the cellular level.

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“…Animals were initially resuscitated with colloids (Voluven R , 130/0.4, Fresenius Kabi Deutschland GmbH, Bad Homburg, Germany) until no further increase in CO. Then they were allowed to stabilize for at least 10 min. Stability was defined as heart rate and MAP variation <5% (Monge Garcia et al, 2018). The study protocol consisted of three consecutive stages with two opposite interventions: changes in afterload (phenylephrine and nitroprusside), preload (bleeding and fluid bolus), and contractility (esmolol and dobutamine).…”

Section: Experimental Protocolmentioning

confidence: 99%

Dynamic Arterial Elastance as a Ventriculo-Arterial Coupling Index: An Experimental Animal Study

García¹,

Jian

Hatib

et al. 2020

Front. Physiol.

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Dynamic arterial elastance (Ea dyn), the ratio between arterial pulse pressure and stroke volume changes during respiration, has been postulated as an index of the coupling between the left ventricle (LV) and the arterial system. We aimed to confirm this hypothesis using the gold-standard for defining LV contractility, afterload, and evaluating ventricular-arterial (VA) coupling and LV efficiency during different loading and contractile experimental conditions. Twelve Yorkshire healthy female pigs submitted to three consecutive stages with two opposite interventions each: changes in afterload (phenylephrine/nitroprusside), preload (bleeding/fluid bolus), and contractility (esmolol/dobutamine). LV pressure-volume data was obtained with a conductance catheter, and arterial pressures were measured via a fluid-filled catheter in the proximal aorta and the radial artery. End-systolic elastance (Ees), a load-independent index of myocardial contractility, was calculated during an inferior vena cava occlusion. Effective arterial elastance (Ea, an index of LV afterload) was calculated as LV end-systolic pressure/stroke volume. VA coupling was defined as the ratio Ea/Ees. LV efficiency (LV eff) was defined as the ratio between stroke work and the LV pressure-volume area. Ea dyn was calculated as the ratio between the aortic pulse pressure variation (PPV) and conductance-derived stroke volume variation (SVV). A linear mixed model was used for evaluating the relationship between Ees, Ea, VA coupling, LV eff with Ea dyn. Ea dyn was inversely related to VA coupling and directly to LV eff. The higher the Ea dyn , the higher the LV eff and the lower the VA coupling. Thus, Ea dyn , an easily measured parameter at the bedside, may be of clinical relevance for hemodynamic assessment of the unstable patient.

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Performance comparison of ventricular and arterial dP/dtmax for assessing left ventricular systolic function during different experimental loading and contractile conditions

Cited by 66 publications

References 37 publications

Cardiovascular determinants of resuscitation from sepsis and septic shock

Cardiovascular determinants of resuscitation from sepsis and septic shock

Complex Interaction Between Low-Frequency APD Oscillations and Beat-to-Beat APD Variability in Humans Is Governed by the Sympathetic Nervous System

Dynamic Arterial Elastance as a Ventriculo-Arterial Coupling Index: An Experimental Animal Study

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