971 likes | 1.72k Vues
Vasopressor Support What, When, and How Much. Todd Miles, RN, MSN, CNP, ANP-BC, CCRN Avera McKennan Hospital and University Health Center Avera eCare Services. OBJECTIVES. Explain the different classes of vasopressors and current dosing recommendations
E N D
Vasopressor SupportWhat, When, and How Much Todd Miles, RN, MSN, CNP, ANP-BC, CCRN Avera McKennan Hospital and University Health Center Avera eCare Services
OBJECTIVES • Explain the different classes of vasopressors and current dosing recommendations • Educate on the indications for different vasopressors according to current guidelines. • Educate on nursing responsibilities while caring for patients undergoing vasopressor infusions. • frequency of VS, route of administration, extravasation
Hemodynamics MAP = CO x SVR CO = HR x SV Preload Afterload Contractility
Case Study • 64 year old male, change in MS, c/o flank pain • VS • HR: 142 • BP: 70/30 • RR: 36 • TEMP: 101.4 • FOLEY: 200 cc with pus drainage • NS 500 cc bolus x4 with no increase in BP
Why do we use vasopressors? • SHOCK • Generalized state of inadequate perfusion and oxygenation of critical organs • SBP < 90 mmHg OR • SBP reduction > 40 mmHg from baseline • With perfusion abnormalities despite adequate fluid resuscitation • Indication for vasopressor use: • Volume resuscitation fails • MAP 65 mmHg • Organs and tissues remain hypoperfused
Acute Organ Dysfunction as a Marker of Shock Tachycardia Hypotension Altered CVP Altered PAOP Altered Consciousness Confusion Psychosis Tachypnea PaO2 <70 mm Hg SaO2 <90% PaO2/FiO2300 Oliguria Anuria Creatinine Jaundice Enzymes Albumin PT Platelets PT/APTT Protein C D-dimer Balk RA. Crit Care Clin 2000;16:337-52.
Classification of Shock • Cardiogenic: pump failure • Hypovolemic: blood/fluid loss • Distributive: excessive dilatation • Obstructive: blockage • Neurogenic: loss of sympathetic tone, excessive dilatation
Oxygen Delivery Oxygen Consumption Oxygen Balance What is the goal?
Vasopressors • Catecholamines responsible for regulation of vascular and bronchial smooth muscle tone and myocardial contractility • Stimulate adrenergic receptors
Vasopressors • Sympathomimetic’s & Catecholamine’s • Dopamine, Epinephrine, & Norepinephrine are naturally produced in the body to activate the sympathetic nervous system (SNS) by: • Initiate Fight or Flight • Stimulate Alpha & Beta receptors, thus increasing CO, provide vasoconstriction
Receptor Pharmacology Dobutamine Dopamine Epinephrine -1 Norepinephrine Dopamine Phenyephrine Epinephrine -1
Vasopressors & Inotropes • Vasopressors • INCREASE SVR subsequently INCREASE BP • Inotropes • INCREASE CO by an INCREASE in contractility • Dobutamine is an INOTROPE
Fluid Resuscitation • Fluid challenges • Crystalloids (NS): 30 mL/kg in the first 3 hours • Colloids (Albumin): 300–500 mL • Fluid resuscitation goals • CVP 8-12 mmHg • MAP ≥ 65 mmHg • Urine output ≥ 0.5 mL/kg/hr • Svo2 ≥ 70%
Review of Vasopressors and Inotropes • Receptor Site • Indication • Clinical Effect • Usual concentration • Usual dosing • Usual titration • Benefits • Adverse Effects
Norepinephrine (Levophed) • Receptor: 90%-1, 10%-1 • Indication: sepsis, cardiogenic shock, hypotension despite fluid resuscitation • Clinical effect: SVR, CO
Norepinephrine (Levophed) • Usual concentration: • 4 mg in 250mL or 8 mg in 250mL NS or D5W • Usual dosing: • 0.5-30 mcg/min • Usual titration: • 1-2 mcg/min every 5 minutes
Norepinephrine (Levophed) \ • Benefits: • Reverses inappropriate vasodilation • Reverses low global oxygen extraction • Attenuates myocardial depression • coronary blood flow • mesenteric perfusion • Least likely vasopressor to cause arrhythmias • May mortality in septic shock
Norepinephrine (Levophed) Adverse effects Tachycardia Tachydysrrhythmias oxygen consumption *Adverse effects are less likely compared to other vasopressors
Norepinephrine (Levophed) NE vs Dopamine NE more potent at receptor site NE more effective at increasing MAP NE maintains oxygen-transport variables better NE is less likely to cause tachyarrhythmias
Epinephrine • Receptor: • 50%-1 (predominate at higher doses) • 50%-1 (predominate at lower doses) • Indication: • Cardiac Arrest (VF/VT, PEA, Asystole) • Anaphylaxis • Bronchospasm • Symptomatic bradycardia • Septic shock after NE has failed to restore minimal perfusion pressure
Epinephrine • Clinical effect: • CO • SVR (low dose)- some beta 2 effects • SVR (high dose) • Bronchial smooth muscle relaxation • Skeletal vasculature relaxation • Vasodilation • Cerebral, hepatic, coronary vessels
Epinephrine • Adverse effects: • Tachycardia • Dysrrhythmia • Angina • Hyperglycemia • Lactic acidosis • Mesenteric Ischemia • Extravasation: tissue necrosis
Epinephrine • Usual concentration: • 1mg in 250mL or 4mg in 250mL NS or D5W • Usual dosing: • 1-10 mcg/min • Usual titration: • 1 mcg every 5 minutes
Phenylephrine (Neosynephrine) Receptor: 100%-1 (pure alpha) Indications neurogenic shock low SVR (<700) is suspected and CO is not impaired tachycardia or arrhythmias with other agents Minimal efficacy data
Phenylephrine (Neosynephrine) • Usual concentration: • 10 mg in 250mL NS (40 mcg/mL) • May double or quad strength to limit fluid • Usual dosing: • 20-200 mcg/min • Start dose 100-180 mcg/min then titrate • Usual titration: • 20 mcg every 10 minutes
Phenylephrine (Neosynephrine) • Clinical effect • Clinical Effect: SVR • Increase in systolic, diastolic, and MAP • Minimal effect on HR or contractility • Arrhythmia potentiation is minimal
Phenylephrine (Neosynephrine) • Adverse effects: • Reflex bradycardia (rare) • oxygen demand • Coronary ischemia • Decreased renal and mesenteric perfusion
Phenylephrine • Phenylephrine vs Norepinephrine • PE may decrease stroke volume • PE less potent at receptor site • PE reduces renal/mesenteric blood flow • PE requires more volume for infusion
Dopamine Receptor: dopaminergic, alpha-1, beta-1 Indication: cardiogenic shock, neurogenic shock, hypotension despite fluid resuscitation Clinical effect: dose dependent Titrate to desired effect
Dopamine *Limited improvement at doses exceeding 20 mcg/kg/min
Dopamine • Usual concentration: • 400 mg in 250mL D5W • Usual dosing: • 2-20 mcg/kg/min • Start dose 2-5 mcg/kg/min • Usual titration: • 2-5 mcg/kg/min every 5-15 minutes
Dopamine Adverse effects Tachycardia, tachyarrhythmias Arrhythmogenesis Myocardial ischemia Increased pulmonary shunt Increased PCWP Necrotic tissue due to extravasation
Dobutamine Receptor: 10%, 90%-1 INOTROPE Indication: Augmentation of cardiac output Cardiogenic shock: decompensated heart failure due to systolic dysfunction with a normal BP Clinical effect: CO SVR
Dobutamine • Usual concentration: • 500mg in 250 mL NS or D5W (standard) • 1000 mg in 250 mL NS or D5W (double concentrated) • Usual dosing: • 2.5-20 mcg/kg/min • Usual titration: • 2.5 mcg/kg/min every 15 minutes • Many times don’t titrate
Dobutamine Strong positive INOTROPE and chronotropic activity without concomitant vasoconstriction contractility and SVR Reflex sympathetic tone Combined 1 agonism & antagonism 2 stimulation Lower doses more vasodilation
Dobutamine • Adverse effects: • Angina ( myocardial O2 demand) • PVC • Arrhythmogenesis • Intravascularly depleted: • Hypotension and reflex tachycardia
Vasopressin • Receptor: V1R, V2R, V3R • Non-adrenergic vasoconstrictor • Indication: septic shock, adjunctive treatment; shock refractory to all other treatments • Clinical Effect: • SVR • Increased BP • Decreased HR • Retains H2O, decreased Na • No inotropic or chronotropic effects
Vasopressin • Usual concentration: • 20 units in 100 mL NS or D5W • Usual dosing: • 0.01-0.04 units/min • Current Surviving Sepsis Guidelines recommends 0.03-0.04 units/min • Usual titration: • Do NOT titrate
Vasopressin Increases receptor sensitivities to adrenergic catecholamines Mechanism of Action: intracellular calcium & antidiuretic hormone analog Adverse Effects: Coronary and mesenteric vasoconstriction Arrhythmias CO Angina Low serum Na
Why Vasopressin? • Patients with septic shock have increased sensitivity to its pressor effects • Vasopressin restores vascular tone in catecholamine resistant shock by several mechanisms including potentiation of adrenergic agents • Low dose vasopressin increases urine output in septic patients, and increases creatinine clearance
Choosing a Vasopressor • Selection of the appropriate agent should be made on a case by case basis with attention to the UNDERLYING CAUSE • Few large randomized, well-controlled studies available • Use is generally based on data from animal studies & often poorly controlled clinical trials
GRADE SYSTEM(Grading of Recommendations, Assessment, Development and Evaluation) • Guide to recommendations’ strengths and supporting evidence • 1 = strong recommendation • 2 = weak recommendation or suggestion • A = good evidence from randomized trials • B = moderate strength evidence from small randomized trial(s) or multiple good observational trials • C = weak or absent evidence, mostly driven by consensus opinion.