Acute Hemodynamic and Hormonal Effects of Central Versus Peripheral Sympathetic Inhibition in Patients with Congestive Heart Failure

Mt, Olivari; Tb, Levine; Jn, Cohn

doi:10.1097/00005344-198609000-00014

Cited by 15 publications

(4 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Progressive sympathetic vasomotor deactivation in capacitance vessels (veins) ( 21 , 117 ) is combined with volume loading, which maintains venous return. ( 109 ) Increased LV compliance ( 17 ) and vasomotor sympathetic deactivation in resistance vessels (arteries) ( 15 , 16 , 118 ) and lowered LV impedance ( 19 , 20 ) maintain the SV. Any hypotension, bradycardia or supraventricular arrhythmia relates to lowered venous return, coronary perfusion pressure or compliance.…”

Section: Switching In Unstable Patientsmentioning

confidence: 99%

How should dexmedetomidine and clonidine be prescribed in the critical care setting?

et al. 2021

View full text Add to dashboard Cite

Section: Switching In Unstable Patientsmentioning

confidence: 99%

How should dexmedetomidine and clonidine be prescribed in the critical care setting?

et al. 2021

View full text Add to dashboard Cite

“…v) reduction in pulmonary hypertension evoked by normalizing the sympathetic hyperactivity [181]. vi) increased left ventricular diastolic compliance [182] and systolic performance [183][184][185][186]. vii) improved micro-circulation [187,188] and lactate clearance [189], reduced vasopressor requirement in the setting of septic shock [24,71] and sepsis [64].…”

Section: ) Working Hypothesis: a New Bundle?mentioning

confidence: 99%

Hypothesis: Fever control, a niche for alpha-2 agonists in the setting of septic shock and severe acute respiratory distress syndrome?

et al. 2018

View full text Add to dashboard Cite

During severe septic shock and/or severe acute respiratory distress syndrome (ARDS) patients present with a limited cardio-ventilatory reserve (low cardiac output and blood pressure, low mixed venous saturation, increased lactate, low PaO2/FiO2 ratio, etc.), especially when elderly patients or co-morbidities are considered. Rescue therapies (low dose steroids, adding vasopressin to noradrenaline, proning, almitrine, NO, extracorporeal membrane oxygenation, etc.) are complex. Fever, above 38.5-39.5 C, increases both the ventilatory (high respiratory drive: large tidal volume, high respiratory rate) and the metabolic (increased O2 consumption) demands, further limiting the cardio-ventilatory reserve. Some data (case reports, uncontrolled trial, small randomized prospective trials) suggest that control of elevated body temperature ("fever control") leading to normothermia (35.5-37 C) will lower both the ventilatory and metabolic demands: fever control should simplify critical care management when limited cardio-ventilatory reserve is at stake. Usually fever control is generated by a combination of general anesthesia ("analgo-sedation", light total intravenous anesthesia), antipyretics and cooling. However general anesthesia suppresses spontaneous ventilation, making the management more complex. At variance, alpha-2 agonists (clonidine, dexmedetomidine) administered immediately following tracheal intubation and controlled mandatory ventilation, with prior optimization of volemia and atrio-ventricular conduction, will reduce metabolic demand and facilitate normothermia. Furthermore, after a rigorous control of systemic acidosis, alpha-2 agonists will allow for accelerated emergence without delirium, early spontaneous ventilation, improved cardiac output and micro-circulation, lowered vasopressor requirements and inflammation. Rigorous prospective randomized trials are needed in subsets of patients with a high fever and spiraling toward refractory septic shock and/or presenting with severe ARDS.

show abstract

“…94 in vivo studies on the patients with chronic heart failure (CHF) following clonidine (150 μg bolus) showed reduced left-filling pressure, bradycardia, and increased stroke volume and cardiac output. 95 These observations were repeated as follows: ( a ) after clonidine 400 μg po 96 or 300 μg/day for 1 week 97 or another α-2 agonist, guanabenz (8-12 mg), 98 NYHA III to IV patients showed lowered pulmonary capillary wedge pressure, bradycardia, increased stroke index, and constant cardiac output. However, systemic hypotension (BP < 90 mm Hg) was observed in 3 patients 96 ; and ( b ) upon arrival in the CCU, clonidine-treated patients who were recovering from coronary bypass surgery presented with higher mixed venous saturation.…”

Section: Effects On Circulation and Side Effectsmentioning

confidence: 99%

Dexmedetomidine and Clonidine

Pichot¹,

Ghignone

Quintin

2011

J Intensive Care Med

View full text Add to dashboard Cite

In the critical care setting, α-2 agonists present a multifaceted profile: sedation combined with arousability, suppression of delirium, preservation of respiratory drive, reduced O(2) consumption, preserved renal function, and reduced protein metabolism. In addition, this review details the reduced arterial impedance, improved left ventricular performance, preserved vascular reactivity to exogenous amines, preserved cardiac baroreflex reactivity, preserved vasomotor baroreflex activity combined with a lowered pressure set point: these features may explain the good tolerance observed when α-2 agonists are used as continuous infusion without any loading dose. Reviewing the literature allows one to suggest that a new management appears possible with arousable sedation. However, it remains to be demonstrated whether this arousable sedation can be combined with the preservation of spontaneous ventilation, in the setting of severe respiratory distress, as opposed to conventional controlled mechanical ventilation combined with conventional sedation. Should such a speculative view be confirmed, then α-2 agonists will move from second-line sedative agents to first-line sedative agents. However, key studies are lacking to demonstrate the effect of α-2 agonists on physiological endpoints and outcome. Presently, the existing body of data suggests a niche for the use of α-2 agonists in the critical care setting.

show abstract

Acute Hemodynamic and Hormonal Effects of Central Versus Peripheral Sympathetic Inhibition in Patients with Congestive Heart Failure

Cited by 15 publications

References 0 publications

How should dexmedetomidine and clonidine be prescribed in the critical care setting?

How should dexmedetomidine and clonidine be prescribed in the critical care setting?

Hypothesis: Fever control, a niche for alpha-2 agonists in the setting of septic shock and severe acute respiratory distress syndrome?

Dexmedetomidine and Clonidine

Contact Info

Product

Resources

About