Use of vasopressors and inotropes 2011 09 28

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Use of vasopressors and inotropes 2011. 09. 28 신장내과 R 1 김소라

Use of vasopressors and inotropes 2011. 09. 28 신장내과 R 1 김소라

Introduction • Vasopressors – Induce vasoconstriction and elevate mean arterial pressure • Inotropes –

Introduction • Vasopressors – Induce vasoconstriction and elevate mean arterial pressure • Inotropes – Increase cardiac contractility • Many drugs have both effects

Introduction • Shock – Significant reduction of systemic tissue perfusion -> Decreased oxygen delivery

Introduction • Shock – Significant reduction of systemic tissue perfusion -> Decreased oxygen delivery to the tissues -> Derangement of critical biochemical processes at the cellular v level, which can progress to the systemic level – Types

Receptor physiology • Alpha-1 adrenergic – Vascular walls : Vasoconstriction – Heart : Increase

Receptor physiology • Alpha-1 adrenergic – Vascular walls : Vasoconstriction – Heart : Increase the duration of contraction • Beta-1 adrenergic – Heart : Increase the inotropy and chronotropy • Beta-2 adrenergic – Vascular walls : Vasodilation • Dopamine – Renal, splanchinic, coronary, cerebral vascular beds : Vasodilation – Second subtype : Vasoconstriction

Practical issues • Volume resuscitation – Crucial prior to the initiation of vasopressors –

Practical issues • Volume resuscitation – Crucial prior to the initiation of vasopressors – Septic shock require at least 2 L – Fluids may be withheld in patients with ARDS or HF • Selection and titration – Selection : etiology of shock – Titration : urine output or mentation • Route of administration – CVC : rapid delivery to heart, eliminates the risk of extravasation • Subcutaneous delivery of medications – Bioavailability can be reduced due to cutaneous vasoconstriction – Change to an IV form

Adrenergic agents • Phenylephrine – Purely alpha-adrenergic : vasoconstriction – Use • Hyperdynamic sepsis

Adrenergic agents • Phenylephrine – Purely alpha-adrenergic : vasoconstriction – Use • Hyperdynamic sepsis • Neurologic disorders • Anesthesia-induced hypotension – Contraindication • SVR > 1200 dynes x sec/cm 5

Adrenergic agents • Norepinephrine – Alpha-1 adrenergic : vasoconstriction Beta-1 adrenergic : increase CO

Adrenergic agents • Norepinephrine – Alpha-1 adrenergic : vasoconstriction Beta-1 adrenergic : increase CO – Increased MAP -> reflex bradycardia ->HR unchanged/decreases – Use • Septic shock • Cardiogenic shock

Adrenergic agents • Epinephrine – Beta-1 adrenergic : increase CO – Low dose :

Adrenergic agents • Epinephrine – Beta-1 adrenergic : increase CO – Low dose : Alpha-1 < Beta-2 : vasodilation High dose : Alpha-1 > Beta-2 : vasoconstriction – Use • Anaphylaxis • 2 nd line agent in septic shock • Hypotension following CABG

Adrenergic agents • Ephedrine – Alpha-1, Beta-2 adrenergic : less potency – Leading to

Adrenergic agents • Ephedrine – Alpha-1, Beta-2 adrenergic : less potency – Leading to release of endogenous NE – Use (rare) • Post-anesthesia-induced hypotension

Adrenergic agents • Dopamine – Purely alpha-adrenergic : vasoconstriction – 1~2 mcg/kg/min • Dopamine-1

Adrenergic agents • Dopamine – Purely alpha-adrenergic : vasoconstriction – 1~2 mcg/kg/min • Dopamine-1 : renal, mesenteric, cerebral, coronary vasodilation – 2~5 mcg/kg/min • Variable effects – 5~10 mcg/kg/min • Beta-1 adrenergic : increase SV -> increase CO – >10 mcg/kg/min • Alpha-1 adrenergic : vasoconstriction

Adrenergic agents • Dopamine – Usual dose range : 2~20 mcg/kg/min – 130 mcg/kg/min

Adrenergic agents • Dopamine – Usual dose range : 2~20 mcg/kg/min – 130 mcg/kg/min have been employed – Use • Septic shock • Cardiogenic shock -> Start at 2 mcg/kg/min

Adrenergic agents • Dobutamine – Beta-1 adrenergic : increase CO Alpha-1, Beta-2 adrenergic :

Adrenergic agents • Dobutamine – Beta-1 adrenergic : increase CO Alpha-1, Beta-2 adrenergic : overall vasodilation – Use • Severe, medically refractory HF • Cardiogenic shock – Should not be routinely used in sepsis : risk of hypotension – Contraindication • Idiopathic hypertrophic subaortic stenosis

Adrenergic agents • Isoproterenol – Beta-1 adrenergic : increase CO : prominent chronotropic effect

Adrenergic agents • Isoproterenol – Beta-1 adrenergic : increase CO : prominent chronotropic effect Beta-2 adrenergic : vasodilation – Use • Hypotension results from bradycardia

Noradrenergic agents • Vasopressin(antidiuretic hormone) and analogs – Use • Refractory septic shock :

Noradrenergic agents • Vasopressin(antidiuretic hormone) and analogs – Use • Refractory septic shock : higher dose is more effective • Refractory anaphylaxis : total doses ranging from 2~40 IU – Complications • • Coronary and mesenteric ischemia Hyponatremia Pulmonary vasoconstriction Skin necrosis from peripheral infusion

Noradrenergic agents • PDE(Phosphodiesterase) inhibitors – Inamrinone, milrinone – Inotropic and vasodilatory actions •

Noradrenergic agents • PDE(Phosphodiesterase) inhibitors – Inamrinone, milrinone – Inotropic and vasodilatory actions • Limit use in hypotensive patients – Use • Medically refractory heart failure • Nitric oxide synthase inhibitors – Increase in SVR, CI and HR decrease • MAP is minimally augmented

Complications • Hypoperfusion – Excessive vasoconstriction – Commonly occurs in the setting of inadequate

Complications • Hypoperfusion – Excessive vasoconstriction – Commonly occurs in the setting of inadequate CO or volume resuscitation – Findings • Autoamputation of the digits • Renal insufficiency and oliguria • Gastritis, shock liver, intestinal ischemia, translocation of gut flora – Maintenance of MAP with vasopressors may be life-saving despite hypoperfusion

Complications • Dysrhythmias – Chronotropic effects via stimulation of beta-1 adrenergic receptor – Types

Complications • Dysrhythmias – Chronotropic effects via stimulation of beta-1 adrenergic receptor – Types • • Sinus tachycardia (m/c) AF Reentrant atrioventricular node tachycardia Ventricular tachyarrhythmias – Adequate volume loading may minimize the frequency or severity – Dopamine > Norepinephrine

Complications • Myocardial ischemia – Chronotropic and inotropic effects increase myocardial oxygen consumption –

Complications • Myocardial ischemia – Chronotropic and inotropic effects increase myocardial oxygen consumption – To avoid • Daily EKG : Screen for occult ischemia • Excessive tachycardia should be avoided

Complications • Local effects – Peripheral extravasation -> excessive local vasoconstriction -> Skin necrosis

Complications • Local effects – Peripheral extravasation -> excessive local vasoconstriction -> Skin necrosis – To avoid • Vasopressors should be administered via CVC – If occurs • Phentolamine 5~10 mg in 10 cc of NS SC • Hyperglycemia – Due to inhibition of insulin secretion

Choice of agent in septic shock • Dopamine vs Norepinephrine – Mortality rate was

Choice of agent in septic shock • Dopamine vs Norepinephrine – Mortality rate was similar – Dopamine more likely to have dysrhythmias and require a second vasopressor • Vasopressin – Beneficial second-line agent • Hyperdynamic shock – Hypotension, low SVR, high CI – Alpha vasoconstrictor : norepinephrine, phenylephrine – Vasopressin • Hypodynamic shock – Hypotension, low~modestly reduced SVR, low CI – Norepinephrine : 1 st choice

Choice of agent in septic shock

Choice of agent in septic shock

Choice of agent in cardiogenic shock • Norepinephrine – Initial agent • Dobutamine

Choice of agent in cardiogenic shock • Norepinephrine – Initial agent • Dobutamine

Reference • Uptodate : Use of vasopressors and inotropes • Uptodate : Shock in

Reference • Uptodate : Use of vasopressors and inotropes • Uptodate : Shock in adults • Comparison of Dopamine and Norepinephrine in the Treatment of Shock (N Engl J Med 2010; 362: 779 -89)