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| Norepinephrine | |
| Receptor binding | α‐1, β‐1, β‐2 |
| Pharmacology | Less β receptor activity than epinephrine α receptor predominant at higher doses |
| Dosing range | 0.01–3 μg/kg/min (for 70 kg adult, that is 0.7–210 μg/min) |
| Clinical scenarios to consider use | Septic shock (first line) Cardiogenic shock (first line) Vasoplegia after cardiac surgery |
| Clinical pearls | If norepinephrine requirements are increasing, evaluate volume status and pH Norepinephrine has been demonstrated to be equivalent to other vasopressor agents, including dopamine, with less adverse events, including tachyarrhythmias In cardiogenic shock, mortality was lower with norepinephrine than with dopamine. This has led to use of norepinephrine as first line agent for cardiogenic shock, including shock from an acute myocardial infarction The Surviving Sepsis Campaign guidelines recommend norepinephrine as the first line agent for septic shock |
| Dopamine | |
| Receptor binding | α‐1, β‐1, β‐2, D1 |
| Pharmacology | Binds DA receptors at low doses, promoting vasodilation particularly in the splanchnic circulation Binds adrenergic receptors at higher doses, leading to vasoconstriction |
| Dosing range | 0.5–3 μg/kg/min, predominantly D1 agonism 3–10 μg/kg/min, weak β‐1 agonism; promotes norepinephrine release >10 μg/kg/min, increasing α‐1 receptor agonism: Vasodilation of capillary beds (low dose)Increased contractility and chronotropy (medium dose)Vasoconstriction (high dose) |
| Clinical scenarios to consider use | Cardiogenic shock complicating acute myocardial infarction with moderate hypotension(SBP 70–100 mmHg); however, this has largely been replaced by norepinephrine Symptomatic bradycardia (temporizing measure) |
| Clinical pearls | While often used as a vasopressor agent that can be used peripherally while central access is being set up, extravasation of dopamine is not benign Renal dosing of dopamine for acute kidney injury was hypothesized to be of use due to vasodilation and improved blood flow to the splanchnic circulation at lower doses (1–3 μg/kg). However, clinical trials have not shown a benefit and it is currently not recommended for this use |
| Dobutamine | |
| Receptor binding | β‐1, β‐2, minor α‐1 |
| Pharmacology | Synthetic catecholamine with preferential β‐1 agonism (3:1 ratio of β‐1 to β‐2), inotropic effect β‐2 activity causes vasodilation, which makes dobutamine an inodilator Progressive α‐1 agonism at high doses causes vasoconstriction |
| Dosing range | 2–40 μg/kg/min Dose in ICU for cardiogenic shock rarely exceeds 10 μg/kg/min |
| Clinical scenarios to consider use | Acute decompensated systolic heart failure Refractory septic shock associated with low cardiac output (also known as ‘hypodynamic’ or ‘cold’ sepsis, a relatively small subset of patients) Pharmacologic stress testing (e.g. for ischemia, viability, aortic stenosis severity) |
| Clinical pearls | Tolerance develops after a few days of therapy Ventricular arrhythmias can occur at any dose Dobutamine significantly increases myocardial oxygen demand so do not use in patients with acute coronary syndromes, severe and unstable coronary disease, or ongoing ischemia Dobutamine has inotropic properties that increase myocardial contractility and cardiac output, while the vasodilatory effects further improve cardiac output by reducing afterload. This makes dobutamine an ideal agent in decompensated heart failure. Remember to use an agent such as norepinephrine as the initial agent if shock and hypotension are present |
| Milrinone | |
| Receptor binding | PDE‐3 |
| Pharmacology | PDE‐3 inhibitor PDE‐3 inhibition increases intracellular cAMP concentrations, enhancing contractility and promoting vascular smooth muscle relaxation Relatively long half‐life (2–4 hours) Renal elimination |
| Dosing range | 0.125–0.75 μg/kg/min (renal adjust) |
| Clinical scenarios to consider use | Acute decompensated systolic heart failure Right ventricular failure |
| Clinical pearls | Fewer arrhythmogenic and chronotropic side effects compared with catecholamines, but vasodilatory effects can worsen hypotension that limits the use of milrinone in patients with shock Can be useful if adrenergic receptors are downregulated or desensitized in setting of chronic heart failure, or after chronic β‐agonist administration Potent pulmonary vasodilator so can be useful in right ventricular (RV) failure by lowering pulmonary vascular resistance (RV afterload) Long half‐life (2–4 hours); hypotension can persist for longer so short‐term infusions may be more beneficial than continuous infusions |
| Phenylephrine | |
| Receptor binding | α‐1 |
| Pharmacology | Pure α‐1 agonism Minimal inotropic and chronotropic effect Rapid onset, short half‐life |
| Dosing range | 0.4–9.1 μg/kg/min (for 70 kg adult, that is 28–637 μg/min) Bolus administration possible, usually 0.1–0.5 mg every 5–15 minutes |
| Clinical scenarios to consider it | Dynamic intracavitary gradient: ‘suicide ventricle’ after transcatheter aortic valve replacement (TAVR), anteroapical STEMI, hypertrophic cardiomyopathy with systolic anterior motion of the mitral valve and LV outflow obstruction, and Takotsubo cardiomyopathy Inadvertent combination of sildenafil and nitrates Hypotension during PCI or anesthesia‐related hypotension Hypotension in the setting of atrial fibrillation with rapid ventricular rate Aortic stenosis with hypotension Vagally mediated hypotension during percutaneous diagnostic or therapeutic procedures |
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