Computationally Managed Bradycardia Improved Cardiac Energetics While Restoring Normal Hemodynamics in Heart Failure

We were already capable of restoring automatically blood pressure, cardiac output, and left atrial pressure by an inotropic, a vasodilator, and volume infusion/a diuretic. Countermeasures for cardioprotection, however, should be integrated to improve the long-term outcomes. We established a full control of heart rate and examined if such a control was useful for decreasing cardiac oxygen consumption. Based on a simulation result, we conducted an animal experiment. In 7 dogs with acute heart failure, we treated hemodynamics, and then lowered heart rate. Compared to the treatment for hemodynamics alone, the addition of bradycardia decreased cardiac oxygen consumption. It was possible to maintain hemodynamics without sacrificing cardiac oxygen consumption.

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“…We reproduced a similar condition as the previous simulation and examined if the same results would be obtained in an animal experiment [5].…”

Section: Animal Experimentssupporting

confidence: 52%

Reduction of myocardial oxygen demand by controlling heart rate and hemodynamics simultaneously by novel circulatory model

Sugimachi

Uemura

Kawada

et al. 2011

2011 Annual International Conference of the IEEE Engineering in Medicine and Biology Society

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“…2b , 4b , and 5b ). S is related to R, left ventricular end-systolic elastance (E es , an index of LV contractility), heart rate (HR) and diastolic myocardial stiffness (κ) by the following formula [ 10 , 11 , 13 ], …”

Section: Discussionmentioning

confidence: 99%

Computer-controlled closed-loop drug infusion system for automated hemodynamic resuscitation in endotoxin-induced shock

et al. 2017

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BackgroundHemodynamic resuscitation in septic shock requires aggressive fluid replacement and appropriate use of vasopressors to optimize arterial pressure (AP) and cardiac output (CO). Because responses to these drugs vary between patients and within patient over time, strict monitoring of patient condition and repetitive adjustment of drug dose are required. This task is time and labor consuming, and is associated with poor adherence to resuscitation guidelines. To overcome this issue, we developed a computer-controlled closed-loop drug infusion system for automated hemodynamic resuscitation in septic shock, and evaluated the performance of the system in a canine model of endotoxin shock.MethodsOur system monitors AP, CO and central venous pressure, and computes arterial resistance (R), stressed blood volume (V) and Frank-Starling slope of left ventricle (S). The system controls R with noradrenaline (NA), and V with Ringer’s acetate solution (RiA), thereby controlling AP and CO. In 4 dogs, AP and CO were measured invasively. In another 4 dogs, AP and CO were measured less invasively using clinically acceptable modalities, aiming to make the system clinically feasible. In all 8 dogs, endotoxin shock was induced by injecting Escherichia coli lipopolysaccharide, which significantly decreased AP from 95 (91–108) to 43 (39–45) mmHg, and CO from 112 (104–142) to 62 (51–73) ml·min−1·kg−1. The system was then connected to the dogs, and activated. System performance was observed over a period of 4 h.ResultsOur system immediately started infusions of NA and RiA. Within 40 min, RiA increased V to target level, and NA maintained R at target level, while S was concomitantly increased. These resulted in restoration of AP to 70 (69–71) mmHg and CO to 130 (125–138) ml·min−1·kg−1. Median of absolute performance error, an index of precision of control, was small in AP [2.5 (2.1–4.5) %] and CO [2.4 (1.4–5.5) %], which were not increased even when the variables were measured less invasively.ConclusionsIn a canine model of endotoxin shock, our system automatically improved and maintained AP and CO at their target values with small performance error. Our system is potentially an attractive clinical tool for rescuing patients with septic shock.Electronic supplementary materialThe online version of this article (10.1186/s12871-017-0437-9) contains supplementary material, which is available to authorized users.

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“…Therefore, in this investigation, we developed a framework to quantitatively predict the impact of baroreflex on dynamic circulatory equilibrium and arterial pressure. To achieve this goal, we applied the framework of ventricular-arterial coupling (end-systolic pressure-volume relationship) to the circulatory equilibrium as reported previously (30). We demonstrated that the framework we developed quantitatively reproduces baroreflex-induced dynamic changes in circulatory equilibrium.…”

Section: Contribution Of Ventricular and Vascular Properties To Barormentioning

confidence: 79%

Changes in vascular properties, not ventricular properties, predominantly contribute to baroreflex regulation of arterial pressure

Sakamoto

Kakino

Sakamoto

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Baroreflex modulates both the ventricular and vascular properties and stabilizes arterial pressure (AP). However, how changes in those mechanical properties quantitatively impact the dynamic AP regulation remains unknown. We developed a framework of circulatory equilibrium, in which both venous return and cardiac output are expressed as functions of left ventricular (LV) end-systolic elastance (Ees), heart rate (HR), systemic vascular resistance (R), and stressed blood volume (V). We investigated the contribution of each mechanical property using the framework of circulatory equilibrium. In six anesthetized dogs, we vascularly isolated carotid sinuses and randomly changed carotid sinus pressure (CSP), while measuring the LV Ees, aortic flow, right and left atrial pressure, and AP for at least 60 min. We estimated transfer functions from CSP to Ees, HR, R, and V in each dog. We then predicted these parameters in response to changes in CSP from the transfer functions using a data set not used for identifying transfer functions and predicted changes in AP using the equilibrium framework. Predicted APs matched reasonably well with those measured (r2=0.85-0.96, P<0.001). Sensitivity analyses indicated that Ees and HR (ventricular properties) accounted for 14±4 and 4±2%, respectively, whereas R and V (vascular properties) accounted for 32±4 and 39±4%, respectively, of baroreflex-induced AP regulation. We concluded that baroreflex-induced dynamic AP changes can be accurately predicted by the transfer functions from CSP to mechanical properties using our framework of circulatory equilibrium. Changes in the vascular properties, not the ventricular properties, predominantly determine baroreflex-induced AP regulation.

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Computationally Managed Bradycardia Improved Cardiac Energetics While Restoring Normal Hemodynamics in Heart Failure

Cited by 8 publications

References 33 publications

Reduction of myocardial oxygen demand by controlling heart rate and hemodynamics simultaneously by novel circulatory model

Reduction of myocardial oxygen demand by controlling heart rate and hemodynamics simultaneously by novel circulatory model

Computer-controlled closed-loop drug infusion system for automated hemodynamic resuscitation in endotoxin-induced shock

Changes in vascular properties, not ventricular properties, predominantly contribute to baroreflex regulation of arterial pressure

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