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Inotropes and Vasopressors

Inotropes et vasopresseurs

Les vasopresseurs induisent une vasoconstriction et augmentent la pression artérielle moyenne (PAM). Les inotropes augmentent la force contractile cardiaque (contractilité). Plusieurs agents endogènes et synthétiques existent et sont fréquemment combinés pour atteindre le résultat hémodynamique souhaité. La plupart des agents présentent à la fois des effets vasopresseurs et inotropes (Figure 1). Ci-dessous suit un manuel des médicaments à utiliser dans l’USC (unité de soins coronariens), l’USI (unité de soins intensifs) ou les urgences. Une surveillance électrocardiographique et hémodynamique attentive avec ECG, cathéter veineux central et cathéter intra-artériel (A-line) est nécessaire.

Aperçu des vasopresseurs et inotropes

Inotropes et vasopresseurs.
Inotropes et vasopresseurs.

Tableau 1. Manuel des médicaments pour les inotropes et vasopresseurs

Drug Indications Dose α1 effect β1 effect β2 effect D1/D2 effect Result Side Effects
Dopamine – low dose Rarely used Low dose: 0.5-3.0 μg/kg/min + + + +++++ Low dose dopamine stimulates D1 receptors and induces vasodilation in coronary, renal, cerebral, and mesenteric vessels. Few
Dopamine – medium dose Cardiogenic shock
Vasodilatory shock
Heart failure (HF), acute
Heart failure (HF), chronic
Bradycardia (second-line alternative)		 Medium dose: 3.0-10.0 μg/kg/min. + ++++ + +++++ Medium dose dopamine activates β1, releases norepinephrine, and thus increases contractility, chronotropy, and mild increase in SVR. Ventricular arrhythmias
Myocardial ischemia Tissue ischemia (high doses or extravasation)
Dopamine – high dose Cardiogenic shock
Vasodilatory shock
Heart failure (HF), acute
Heart failure (HF), chronic
Bradycardia (second-line alternative)		 High dose: 10.0-20.0 μg/kg/min. ++++ ++++ ++ +++++ High dose dopamine additionally induces α1 stimulation and thus vasoconstriction and pronounced increase in SVR. As medium dose, and additionally severe hypertension (caution if patient on nonselective beta-blockers).
Dobutamine Cardiogenic shock
Bradycardia (second-line therapy)
Stress testing (due to induced increase in myocardial O2 consumption)		 Regular: 2.0–20 μg/kg/min
Max: 40 μg/kg/min		 + +++++ +++ 0 Potent inotrope with slight chronotropic effect. Doses <5 μg/kg/min induce mild vasodilation.
Doses >5 μg/kg/min induce vasoconstriction, which dominates at dosages >15 μg/kg/min.		 Tachycardia
Increased ventricular rate in AF
Ventricular arrhythmias
Cardiac ischemia Hypertension (in patients on nonselective β-blocker)
Tolerance after a few days
    Norepinephrine Shock (any)
Hypotension (any)		 0.01–3.0 μg/kg/min

Safe for peripheral use

 +++++ +++ ++ 0 Potent vasoconstrictor with mild inotropic effect. Increases systolic pressure, diastolic pressure, and pulse pressure with minimal effect on CO. Minimal chronotropic effect. Increases coronary blood flow. Atrial or ventricular arrhythmias
Bradycardia
Peripheral (digital) ischemia
Hypertension (especially nonselective β-blocker patients)
Prolonged use may be cardiotoxic.
Epinephrine Shock (any)
Cardiac arrest
Bronchospasm
Anaphylaxis
Bradycardia (second-line alternative)		 Infusion: 0.01 to 0.10 μg/kg/min
Bolus: 1 mg IV every 3 to 5 min (max 0.2 mg/kg) IM: (1:1000): 0.1 to 0.5 mg (max 1 mg)
Safe for peripheral use		 +++++ ++++ +++ N/A Beta-effect more pronounced at low doses. Alpha-effect pronounced at higher doses. Coronary flow enhanced.
Pulmonary vasoconstriction.
Increased pulmonary blood flow.		 Ventricular arrhythmias Severe hypertension resulting in cerebrovascular hemorrhage Cardiac ischemia Sudden cardiac death
Prolonged use may be cardiotoxic.
Isoproterenol Bradycardia (first-line therapy)
Bradycardia causing torsade de pointes
Brugada syndrome		 2.0–10.0 μg/min
Safe for peripheral use		 0 +++++ +++++ 0 Powerful chronotropic and inotropic effect. Potent systemic vasodilation. Mild pulmonary vasodilation. No effect on CO. Ventricular arrhythmias Cardiac ischemia Hypertension Hypotension
    Phenylephrine Typically used as emergency bolus to correct acute hypotension.
Hypotension (any)
Used to increase MAP during hypotension in aortic stenosis.
Used to decrease LVOT gradient in HCM
Used to correct hypotension caused by the simultaneous ingestion of sildenafil and nitrates		 Bolus: 0.1 to 0.5 mg IV every 10 to 15 min
Infusion: 0.4 to 9.1 μg/kg/min

Safe for peripheral use		 +++++ 0 0 N/A Immediate and pronounced increase in MAP. Reflex bradycardia Hypertension (especially with nonselective β-blockers)
Severe peripheral and visceral vasoconstriction Tissue necrosis with extravasation
Milrinone (Phosphodiesterase Inhibitor) Heart failure, acute
Heart failure, decompensated chronic.		 Bolus: 50 μg/kg bolus over 10 to 30 min
Infusion: 0.375 to 0.75 μg/kg/min.		 0 0 0 0 PDI (Phosphodiesterase Inhibitor).
Potent inotrope.
Induces vasodilation.
Results in reduced preload, afterload, and SVR.		 Ventricular arrhythmias Hypotension
Myocardial ischemia
Torsade des pointes
Accumulates in renal failure (dose adjustment necessary)
Amrinone Heart failure, acute
Heart failure, decompensated chronic		 Bolus: 0.75 mg/kg over 2 to 3 min Infusion: 5 to 10 μg · kg−1 · min−1 0 0 0 0 PDI (Phosphodiesterase Inhibitor). Rarely used due to side effects. Arrhythmias, enhanced AV conduction
Hypotension Thrombocytopenia Hepatotoxic
Vasopressin Shock (any)
Cardiac arrest		 Infusion: 0.01–0.1 U/min (common fixed dose 0.04 U/min)

Bolus (IV): 40 U

 0 0 0 0 Vasopressin stimulates V1 receptors (vascular smooth muscle) and V2 (renal). V1 stimulation induces vasoconstriction, and V2 increases renal water reabsorption. Vasopressin increases SVR with no significant effect on CO. Vasopressin potentiates the vascular effect of norepinephrine. Arrhythmias Hypertension Decreased CO (at doses >0.4 U/min) Cardiac ischemia Severe peripheral vasoconstriction causing ischemia (especially skin) Splanchnic vasoconstriction
Levosimendan Heart failure, decompensated chronic Loading dose: 12–24 μg/kg over 10 min
Infusion: 0.05–0.2 μg/kg/min		 0 0 0 0 Levosimendan is a calcium sensitizer that
enhances ventricular contractility and induces peripheral arteriolar and venous vasodilation.		 Enhanced AV conduction
Hypotension
CO = cardiac output, AF = atrial fibrillation, SVR = systemic vascular resistance, MAP = mean arterial pressure.

Récepteurs des catécholamines

  • Récepteurs adrénergiques alpha-1 : exprimés dans les cellules musculaires lisses vasculaires, leur activation entraîne une vasoconstriction et une augmentation de la résistance vasculaire systémique (SVR).
  • Récepteurs adrénergiques bêta-1 : exprimés dans le myocarde ; leur excitation entraîne une augmentation de la force contractile (contractilité) et une augmentation de la chronotropie.
  • Récepteurs adrénergiques bêta-2 : exprimés dans les cellules musculaires lisses vasculaires et entraînent une vasodilatation.
  • D1 et D2 (récepteurs de la dopamine) : L’excitation des récepteurs dopaminergiques D1 et D2 dans le rein et la vasculature splanchnique induit une vasodilatation rénale et mésentérique.

NB : Les altérations rapides de la pression artérielle peuvent induire des réponses autonomes réflexes qui affectent le résultat hémodynamique final.

La dobutamine est une catécholamine synthétique.

Références

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Updated on 2025-04-09
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