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Rockford Cardiology ConferenceMarianne Pop, Pharm.D., BCPS2/24/2018
Describe the pathophysiology of cardiogenic shock
Identify inotropes and vasopressors used in the management of cardiogenic shock
Recognize adjunct agents used in the management of cardiogenic shock
Differentiate between the inotropes and vasopressors used in the management of cardiogenic shock
Speaker has nothing to disclose.
Cardiomyopathy Acute exacerbation of heart failure Myocardial infarction Cardiac arrest Myocarditis
Arrhythmias Atrial and ventricular Bradyarrhythmias
Mechanical Severe aortic or mitral valve insufficiency Acute valvular defects
BP = CO x SVRCO= HR x SV
↓ Systolic blood pressure ↓ Cardiac index
↑ Left ventricular diastolic pressure
Inadequate tissue oxygenation
Tachycardia to overcompensate for poor stroke volume and cardiac output
Multiple organ dysfunction
Irreversible cell destruction
Pump FailureDecreased
Tissue Perfusion
Shock Response
Receptor Location Action Effect
α1 Systemic Vasculature Vasoconstriction ↑ SVR
β1 Myocardium↑HR
↑contractility ↑CO
D KidneySplanchnic Vasculature
Renal & Mesenteric Vasodilation
↑UOP
V1 Systemic Vasculature Vasoconstriction ↑ SVR
BP = CO x SVRCO= HR x SV
α = SVR β = CO
Isoproterenol
Dobutamine
Dopamine
Epinephrine
Phenylephrine
Norepinephrine
Milrinone
PDE inhibitor =
CO + SVR
Distributive shock
Hypovolemic shock
Code situation
Cardiogenic shock
Cardiomyopathy
Vasopressin
V 1 = SVR
Inotropes: increase cardiac contractility
Vasopressors: induce vasoconstriction and elevate mean arterial pressure (MAP)
Indications: patients with decreased perfusion resulting in end-organ dysfunction due to
Decrease >30 mmHg from baseline or SBP < 90 mmHg
MAP <65 for > 30 minutes
Pharmacology: Primarily a β1 agonist with minimal α activity contractility > HR
Dose: 2.5 – 20 mcg/kg/min titration provider specific
Pearls: Max of 40 mcg/kg/min per manufacturer not guidelines Can lead to tachycardia Primarily used in decompensated HF to CO Vasodilation can cause hypotension myocardial oxygen demand High risk for arrhythmias (especially at higher doses)
Pharmacology: Phosphodiesterase enzyme inhibitor
▪ contractility = CO, vasodilation = SVR
Dose: 0.2-0.5 mcg/kg/min titration provider specific Using a loading dose increases risk for hypotension
Pearls: Primarily used in decompensated HF patients
Long half-life (~2.5 hrs) = prolonged vasodilation
High risk for arrhythmias
Pharmacology: Pure β agonist; contractility and HR = CO
Dose: 2 – 10 mcg/min titration provider specific Onset: immediate, duration: 10 – 15 minutes
Pearls: May cause hypotension (β2 activity)
Increases HR in patients refractory to atropine
Useful in bradyarrhythmias, AV block, and torsades
Pharmacology: Potent α agonist with some β1 effects Vasoconstriction (SVR & MAP) + modest increase in
HR (CO)
Dose: 0.5-30 mcg/min titrate 1 mcg/min every 15 minutes or 0.05 to 0.4 mcg/kg/minute
Pearls: Only causes a modest increase in HR Lower arrhythmia risk
Pharmacology: Equal α and β activity, β1 > β2
SVR (vasoconstriction), contractility and HR = CO
Dose: 1-10 mcg/min titrate 1 mcg/min every 15 minutes or 0.01 to 0.5 mcg/kg/minute
Pearls: 1st line therapy for anaphylactic shock, cardiac arrest
May decrease splanchnic blood flow
Increase serum lactate
Can lead to tachycardia before BP rises
Pharmacologic effects are dose dependent: Low dose (1-5 mcg/kg/min): renal blood flow, UOP Moderate dose (5-10 mcg/kg/min): HR, CO High dose (>10 mcg/kg/min): BP, vasoconstriction
Dose: 2-20 mcg/kg/min titrate 1-2 mcg/kg/min every 30 minutes
Pearls: Can lead to tachycardia and arrhythmias myocardial oxygen demand
Pharmacology: V1 = Vasoconstricts vascular smooth muscle = SVR
V2 = Reabsorbs H2O from renal collecting duct = UOP
Dose: 0.02 – 0.04 units/minute titration provider specific
Pearls: myocardial & peripheral ischemia at higher doses
Effects preserved during hypoxic or acidotic conditions
Increases vascular sensitivity to norepinephrine
Typically added for shock refractory to fluids/pressors
•Norepinephrine•Dobutamine
Cardiogenic
Shock
Vasopressor/Inotrope
α1 β1 β2 D V1/V2
Norepinephrine ++++ ++ + Ø Ø
Epinephrine +++ +++ ++ Ø Ø
Dopamine ++ +++ + ++++ Ø
Vasopressin Ø Ø Ø Ø +++
Dobutamine + +++ + Ø Ø
Milrinone Ø +++ Ø Ø Ø
Isoproterenol Ø ++++ +++ Ø Ø
Agent Class Dose Action Benefits Contraindications
Nitroglycerin (Tridil) IV
Nitrate 10-20 mcg/minute, titrate (10-20mcg/minute every 5-15 minutes) up to 200 mcg/minute
Vasodilator that relaxes smooth muscle
Dilation of both venous and arterial blood vessels
Hypotension; compensatory tachycardia
Nitroprusside(Nitropress) IV
Nitrate 5-10 mcg/minute; titrate (every 5 minutes) to achieve desired hemodynamic effect; usual dosage range: 5-300 mcg/minute
Dilates veins and arteries
Dilation of both venous and arterial blood vessels
Acute heart failure associated with reduced peripheral vascular resistance
Nesiritide(Natrecor) IV
Natriuretic peptide
2 mcg/kg (bolus optional); continuous infusion at 0.01 mcg/kg/minute
Dilates veins and arteries
Reduces pulmonary capillary wedge pressureand improves dyspnea
Hypotension
Agent Class Dose Action Benefits Contraindications
Furosemide(Lasix)IV/PO
Loop diuretic
Patient dependent40 mg
Inhibits reabsorption of sodiumand chloride
↑ water, sodium, chloride, magnesium,and calcium excretion to decrease edema
Severe electrolyte depletion
Bumetanide (Bumex)IV/PO
Loop diuretic
Patient dependent1 mg
Inhibits the sodium-potassium ATPasepump; blocks reabsorption of chloride
Induces diuresis in renal insufficiency; treatmentfor edema associated with heart failure
Anuria, severe electrolyte depletion
Torsemide(Demadex)IV/PO
Loop diuretic
Patient dependent10 mg
Inhibits the sodium, potassium, chloridecarrier system in the loop of Henle
↑ urinary excretion of sodium chloride and water without significantly altering the GFR
Known hypersensitivity to sulfonylureas;caution with hepatic disease
Metolazone(Zaroxolyn)PO
Loop diuretic
2.5-20 mg Inhibits the sodium, potassium, chloridecarrier system in the loop of Henle
↑ diuretic effect when given concurrentlyWITH Furosemide
Anuria, known hypersensitivity
Ethacrynic acid (Edecrin) IV/PO
Loop diuretic
50-200 mg/day
Inhibits reabsorption of filteredsodium
Known sulfa allergy; renal insufficiency
Severe electrolyte depletion
Spironolactone (Aldactone)PO
Potassiumsparing diuretic
12.5-50 mg/day
Competes with aldosterone receptor sitesto increase sodium and water excretion
Potassium sparing Renal failure
Agent Class Dose Action Benefits Contraindications
Ticagrelor(Brilinta)PO
Cyclopentyltriazolo-pyrimidine
180 mg load for PCI Reversibly inhibits the P2Y12platelet receptor
Short half-life and reversible antiplatelet effect
Risk of bleeding; history of intracranialhemorrhage; liver impairment
Prasugrel(Effient)PO
Thienopyridine 60 mg load for PCI Reversibly inhibits the ADP P2Y12platelet receptor to block platelet activation
Faster onset of action, higher levels of plateletinhibition, lower incidence of resistance
↓ liver function, history of pathological bleeding
Clopidogrel(Plavix)PO
Thienopyridine 600 mg load for PCI Reversibly inhibits the ADP P2Y12platelet receptor to block platelet activation
Platelet inhibition Hold 7 d before surgery to decrease risk of bleeding;genetic resistance; ineffective in some patients
Cangrelor(Kengreal)IV
Non-thienopyridine 30 mcg/kg IV bolus prior to percutaneous coronary intervention (PCI), then 4 mcg/kg/min IV infusion for at least 2 hours or for the duration of PCI
Reversibly inhibits the ADP P2Y12platelet receptor to block platelet activation and aggregation
IV formulation Bleeding
Agent Class Dose Action Benefits Contraindications
Aspirin Antiplatelet 325 mg for PCI Inhibits platelet cyclooxygenase and conversion of arachidonicacid to prostaglandins andthromboxane A2
↓ myocardial infarction and cardiac mortalityin first month
Bleeding
Abciximab(ReoPro)
Antiplatelet 0.25 mg/kg bolus administered 10-60 minutes before PCI, infusion of 0.125 mcg/kg/minute (max: 10 mcg/minute) for 12 hours
Inhibits GP IIb/IIIareceptorsresponsible for platelet aggregation
Adjunct to percutaneous transluminal coronaryangioplasty for the prevention of abruptclosure of arteries in high-risk patients
Bleeding, thrombocytopenia
Eptifibatide(Integrilin)
Antiplatelet 180 mcg/kg bolus (max: 22.6 mg) immediately before PCI, continuous infusion of 2 mcg/kg/minute (max: 15 mg/hour). A second 180 mcg/kg bolus (max: 22.6 mg) 10 minutes after the first bolus
Reversibly binds to GP IIb/IIIato inhibit platelet aggregation
Prevents platelets from binding with fibrinogen
Kidney dysfunction
Tirofiban(Aggrastat)
Antiplatelet Bolus 25 mcg/kg administered over 5 minutes PCI; Maintenance infusion: 0.15 mcg/kg/minute
Reversibly binds to GP IIb/IIIato inhibit platelet aggregation
Prevents platelets from binding with fibrinogen
Reduce dose in kidney dysfunction
Some patients may require fluids
Delicate balance of medications needed to maintain adequate perfusion
Monitor effects of medications Hypoxia and acidosis may blunt the effects of vasopressors and
inotropes
Epinephrine and dopamine most likely to cause tachycardia
Milrinone and dobutamine most arrhythmogenic
Monitor intake and output
Rockford Cardiology ConferenceMarianne Pop, Pharm.D., BCPS2/24/2018
Cardiogenic Shock. National Heart Lung and Blood Institute, U.S. Department of Health and Human Services, www.nhlbi.nih.gov/health-topics/cardiogenic-shock Accessed 21 February 2018.
Management of Cardiogenic Shock: AHA Scientific Statement.” American College of Cardiology, www.acc.org/latest-in-cardiology/ten-points-to-remember/2017/10/06/11/36/contemporary-management-of-cardiogenic-shock Accessed 21 February 2018.
Reynolds, Harmony R., and Judith S. Hochman. “Cardiogenic Shock.” Circulation, American Heart Association, Inc., 5 Feb. 2008, circ.ahajournals.org/content/117/5/686 Accessed 21 February 2018.
Warise L. Understanding cardiogenic shock: a nursing approach to improve outcomes. Dimens Crit Care Nurs. 2015 Mar-Apr;34(2):67-78.
Warise, L. Understanding Cardiogenic Shock. Dimens Crit Care Nurs. 2014;34(2):67-78.