scholarly journals Comparative Study between Ivabradine Versus Bisoprolol Effects for Heart Rate Control on Hemodynamics and Clinical Outcomes in Patients with Septic Shock

2021 ◽  
pp. 58-68
Author(s):  
Omnia Ali El-Miseery ◽  
Hesham Elsaid Elashry ◽  
Magdy Elsaid Elbably ◽  
Magdy Elsaid Elbably ◽  
Ahmed Mohammed Hamed
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Septic Shock ◽  
Cardiac Output ◽  
Clinical Outcomes ◽  
Nasogastric Tube ◽  
Rate Control ◽  
Conventional Therapy ◽  
The Other ◽  
Heart Rate Control

Background: Septic shock is associated with excessive sympathetic outflow, high plasma catecholamine levels, myocardial depression, vascular hypo-reactivity, and autonomic dysfunction. Typically, patients have a low resistance, high cardiac output circulation with tachycardia and arterial hypotension that may be poorly or even nonresponsive to exogenous catecholamine vasopressors. The aim of the present study was to compare the effect of ivabradine vs bisoprolol for heart rate control on the hemodynamics and clinical outcomes in patients with septic shock. Methods: The study was carried out on 90 patients, aging from 18 to 60 years of both sex presented with septic shock in ICU. Patients were randomly classified into 3 equal groups each of 30 patients. Group I (Control group) received conventional therapy. Group II (Bisoprolol group) received conventional therapy plus bisoprolol 5 mg once daily & one placebo pill on 12 hrs interval via nasogastric tube for 7 days. Group III (Ivabradine group) received conventional therapy plus ivabradine 5 mg twice daily on 12 hrs interval via nasogastric tube for 7 days. Results: Both bisoprolol and ivabradine effectively lowered heart rate in septic shock patients but ivabradine was more effective than bisoprolol. Both bisoprolol and ivabradine did not affect mean blood pressure, with ivabradine being more effective in maintaining blood pressure than bisoprolol. Noradrenaline dose was lower in ivabradine group in comparison with the other two groups. As regard to stroke volume & cardiac output, there was improvement in ivabradine group in comparison with bisoprolol and control groups. As regard to serum lactate level, there was improvement in ivabradine group in comparison with the other two groups. Both bisoprolol & ivabradine resulted in reduction in LOS & 28-day mortality with no significant difference between both groups. Conclusions: Controlling heart rate in septic shock patients with either bisoprolol or ivabradine improves outcomes. Ivabradine is better than bisoprolol in maintaining hemodynamics and improving tissue perfusion parameters.

scholarly journals Heart Rate Control during Experimental Sepsis in Mice

2020 ◽  
Vol 132 (2) ◽  
pp. 321-329
Author(s):  
Alexandre Bedet ◽  
Guillaume Voiriot ◽  
Julien Ternacle ◽  
Elisabeth Marcos ◽  
Serge Adnot ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Rate Control ◽  
Transthoracic Echocardiography ◽  
Systolic Function ◽  
Left Ventricular Systolic Function ◽  
Left Ventricular ◽  
Heart Rate Control ◽  
Ventricular Systolic Function

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Tachycardia is a hallmark of sepsis. An elevated heart rate could impair ventricular filling and increase myocardial oxygen demand. β-Blockers and ivabradine (a selective inhibitor of If channels in the sinoatrial node) are both able to control sinus tachycardia, with the latter drug being devoid of negative inotropic effect. This work aimed at assessing the hemodynamic effects of ivabradine as compared with a β-blocker (atenolol) during murine peritonitis. Methods Ivabradine (3 μg/g), atenolol (3 μg/g), or placebo was administered intraperitoneally 2 h after induction of peritonitis (cecal ligation and puncture) in male C57BL6 mice. The authors used invasive (left ventricular catheterization) and noninvasive (transthoracic echocardiography) monitoring to assess hemodynamics 20 h after surgery, including heart rate, blood pressure, left ventricular systolic, and diastolic function (n = 10 mice/group). The authors also assessed overall mortality 30 and 60 h after surgery in a distinct subset of animals (n = 20 mice/group). Descriptive data are presented as median (25th to 75th percentile). Results As compared with placebo (601 beats/min [547 to 612]), ivabradine (447 beats/min [430 to 496]) and atenolol (482 beats/min [412 to 505]) blunted sepsis-induced tachycardia assessed by transthoracic echocardiography in awake animals (P < 0.001 and P = 0.004, respectively). Unlike ivabradine, atenolol reduced cardiac output, systolic blood pressure, and left ventricular systolic function (as assessed by ejection fraction, maximal left ventricular pressure rise, and anterior wall strain rate) as compared with septic mice receiving placebo. There was no difference in survival 60 h after sepsis induction with ivabradine (6 of 20, 30%) or atenolol (7 of 20, 35%), as compared with placebo (5 of 20, 25%; P = 0.224). Conclusions Heart rate control could be similarly achieved by ivabradine or atenolol, with preservation of blood pressure, cardiac output, and left ventricular systolic function with the former drug.

Effect of Heart Rate Control With Esmolol on Hemodynamic and Clinical Outcomes in Patients With Septic Shock

JAMA ◽  
2013 ◽  
Vol 310 (16) ◽  
pp. 1683 ◽  
Author(s):  
Andrea Morelli ◽  
Christian Ertmer ◽  
Martin Westphal ◽  
Sebastian Rehberg ◽  
Tim Kampmeier ◽  
...  
Keyword(s):  
Heart Rate ◽  
Septic Shock ◽  
Clinical Outcomes ◽  
Rate Control ◽  
Heart Rate Control

scholarly journals An Enantiomerically Pure Formulation of Esmolol Attenuates Hypotension and Preserves Heart Rate Control in Dogs

2014 ◽  
Vol 121 (6) ◽  
pp. 1184-1193
Author(s):  
Jeffrey S. McKee ◽  
Barrett E. Rabinow ◽  
Justin R. Daller ◽  
Benjamin D. Brooks ◽  
Bernhard Baumgartner ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Adverse Event ◽  
Cardiac Output ◽  
Rate Control ◽  
Cardiovascular Function ◽  
Left Ventricular ◽  
Heart Rate Control ◽  
Enantiomerically Pure ◽  
Developed Pressure

Abstract Background: Esmolol is marketed as a racemate (RS-esmolol) with hypotension being the most frequently reported adverse event. Previously, it has been shown that the S-enantiomer (S-esmolol) possesses all of the heart rate (HR) control. The authors studied whether S-esmolol alone mitigates hypotension at similar degrees of HR control compared with RS-esmolol. Methods: The effects of RS- and S-esmolol on blood pressure (BP) were compared at multiple infusion rates producing similar HR control in dogs (N = 21). Differences in BP were further interrogated by monitoring global cardiovascular function and included the R-enantiomer (R-esmolol) (N = 3). Results: S-esmolol at half the rate (μg kg−1 min−1) of RS-esmolol provided the same degree of HR control over all infusion rates. RS-esmolol lowered BP by 3, 6, 11, 20, and 38 mmHg at 90, 300, 600, 1,000, and 2,000 μg kg−1 min−1, compared with 2, 4, 5, 10, and 16 mmHg at 45, 150, 300, 500, and 1,000 μg kg−1 min−1 for S-esmolol. Decreased BP with RS-esmolol was attributed to decreases in left ventricular developed pressure (LVDP) (−34 mmHg), LVdP/dt+max (−702 mmHg/s), and cardiac output (−1 l/min). R-esmolol also decreased BP (−10 mmHg), LVDP (−10 mmHg), LVdP/dt+max (−241 mmHg/s), and cardiac output (to −0.2 l/min). S-esmolol reversed these trends toward pre-esmolol values by increasing BP (+13 mmHg), LVDP (+12 mmHg), LVdP/dt+max (+76 mmHg/s), and cardiac output (+0.4 l/min). Conclusions: R-enantiomer provided no HR control, but contributed to the hypotension with RS-esmolol, which appears to be due to negative inotropy. Thus, an S-enantiomer formulation of esmolol may provide similar HR control with less hypotension.

Autonomic mechanisms underlying area postrema stimulation-induced cardiovascular responses in rats

1991 ◽  
Vol 261 (1) ◽  
pp. R1-R8 ◽  
Author(s):  
A. V. Ferguson ◽  
P. Smith
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rate Control ◽  
Area Postrema ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Blocking Agent ◽  
Adrenergic Blockade ◽  
Neural Pathways ◽  
Heart Rate Control

Experiments were designed to examine the autonomic mechanisms underlying the decreases in blood pressure and heart rate elicited by electrical stimulation in the rat area postrema (AP). Vagotomy was found to significantly reduce the bradycardia observed in response to AP stimulation (control -123.5 +/- 23.5 beats/min; vagotomized -7 +/- 5.4 beats/min; P less than 0.001) but was without significant effect on blood pressure responses. Hexamethonium significantly reduced both heart rate (control -225.5 +/- 11.9 beats/min; hexamethonium -5.5 +/- 2.8 beats/min; P less than 0.001) and depressor (control -35.4 +/- 4.7 mmHg; hexamethonium -6.4 +/- 0.8 mmHg; P less than 0.001) responses to such stimulation, whereas combined alpha- and beta-adrenergic blockade was without effect. The muscarinic blocking agent atropine also abolished both blood pressure (control -22.0 +/- 4.3 mmHg; atropine 2.8 +/- 4.4 mmHg; P less than 0.01) and heart rate (control -187.0 +/- 41.9 beats/min; atropine 8.8 +/- 2.6 beats/min; P less than 0.01) responses to AP stimulation. These data suggest that AP stimulation influences two separate neural pathways eliciting distinct cardiovascular responses. It would appear that activation of one of these pathways results in activation of vagal efferents to the heart and thus bradycardia. A second parallel pathway influenced by AP stimulation apparently elicits depressor response through actions on cholinergic muscarinic receptors.

Mechanism of circulatory responses to systemic hypoxia in the anesthetized dog

1965 ◽  
Vol 209 (2) ◽  
pp. 397-403 ◽  
Author(s):  
Hermes A. Kontos ◽  
H. Page Mauck ◽  
David W. Richardson ◽  
John L. Patterson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
The Other ◽  
Arterial Flow ◽  
Arterial Blood ◽  
Systemic Hypoxia ◽  
Anesthetized Dogs ◽  
Spontaneously Breathing

The possibility that mechanisms secondary to the increased ventilation may contribute significantly to the circulatory responses to systemic hypoxia was explored in anesthetized dogs. In 14 spontaneously breathing dogs systemic hypoxia induced by breathing 7.5% oxygen in nitrogen increased cardiac output, heart rate, mean arterial blood pressure, and femoral arterial flow, and decreased systemic and hindlimb vascular resistances. In 14 dogs whose ventilation was kept constant by means of a respirator pump and intravenous decamethonium, systemic hypoxia did not change cardiac output, femoral arterial flow, or limb vascular resistance; it significantly decreased heart rate and significantly increased systemic vascular resistance. In seven spontaneously breathing dogs arterial blood pCO2 was maintained at the resting level during systemic hypoxia. The increase in heart rate was significantly less pronounced but the other circulatory findings were not different from those found during hypocapnic hypoxia. Thus, mechanisms secondary to increased ventilation contribute significantly to the circulatory responses to systemic hypoxia. Hypocapnia accounts partly for the increased heart rate, but not for the other circulatory responses.

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