Mount Sinai Expert Guides. Группа авторов

Mount Sinai Expert Guides

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
Clincial pearls	Phenylephrine increases MAP by raising SVR (afterload), and therefore is particularly useful when SVR <700 dyn·s/cm⁵ Increased afterload can result in decreased stroke volume and cardiac output in patients with pre‐existing cardiac dysfunction
	Contraindicated in patients with SVR >1200 dyn·s/cm⁵, which is most patients with cardiogenic shock Lower concentration (20 μg/mL) available which can be infused peripherally while awaiting central line placement Generally not recommended for septic shock unless serious arrhythmias happen with norepinephrine Can cause reflex bradycardia

Vasopressin
Receptor binding	V1, V2
Pharmacology	Agonism of V1 receptors on smooth muscle causes vasoconstriction Agonism of V2 receptors in nephron induces translocation of aquaporin water channels to plasma membrane of collecting duct cells
Dosing range	Fixed dose: 0.04 units/min
Clinical scenarios to consider it	When avoiding β agonism is desired (e.g. left ventricular outflow obstruction, tachyarrhythmia) or when trying to reduce dose of first line agent Hypotension accompanied by severe acidosis Second line agent in refractory vasodilatory/septic shock
Clinical pearls	Vasoconstrictive effect is relatively preserved despite conditions of hypoxia and acidosis (which can attenuate effects of catecholamines) Doses above 0.04 units/min have been associated with coronary and mesenteric ischemia and skin necrosis Rebound hypotension often occurs after withdrawal of vasopressin. To avoid this, the dose is slowly tapered by 0.01 units/min every 30 minutes

Reading list

1 Bangash MN, Kong M‐L, Pearse RM. Use of inotropes and vasopressor agents in critically ill patients. Br J Pharmacol 2012; 165:2015–33.

2 Bellomo R, Chapman M, Finfer S, Hickling K, Myburgh J. Low‐dose dopamine in patients with early renal dysfunction: a placebo‐controlled randomised trial. Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group. Lancet 2000; 356:2139–43.

3 De Backer D, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med 2010; 362:779–89.

4 Dellinger RP, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012. Intensive Care Med 2013; 39:165–228.

5 Hollenberg SM. Vasoactive drugs in circulatory shock. Am J Respir Crit Care Med 2011; 183:847–55.

6 Holmes CL. Vasoactive drugs in the intensive care unit. Curr Opin Crit Care 2005; 11:413–17.

7 Jentzer JC, Coons JC, Link CB, Schmidhofer M. Pharmacotherapy update on the use of vasopressors and inotropes in the intensive care unit. J Cardiovasc Pharmacol Ther 2015; 20:249–60.

8 Overgaard CB, Dzavik V. Inotropes and vasopressors: review of physiology and clinical use in cardiovascular disease. Circulation 2008; 118:1047–56.

9 Unverferth DA, Blanford M, Kates RE, Leier CV. Tolerance to dobutamine after a 72 hour continuous infusion. Am J Med 1980; 69:262–6.

10 Vincent JL, De Backer D. Circulatory shock. N Engl J Med 2013; 369:1726–34.

Additional material for this chapter can be found online at:

www.wiley.com/go/mayer/mountsinai/criticalcare

This includes multiple choice questions.

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