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Effects of CV Drugs on Hemodynamics: Which Drug When?

Robin Donohoe Dennison, DNP, APRN, CCNS, CNE

copyright Robin Donohoe Dennison 2015

Objectives

• describe the hemodynamic effects of select CV drugs

• select the appropriate CV drug in a clinical situation

• explain rationale for use of one drug over another drug

To increase:

treatment of cause

parasympatholytics:

atropine

sympathomimetics:

epinephrine

pacemaker

To decrease:

treatment of cause

antidysrhythmics

I: procainamide,

quinidine, lidocaine

II: beta-blockers

III: amiodarone,

ibutilide, dofetilide

IV: calcium channel

blockers

Misc: adenosine,

digoxin

vagal maneuvers

cardioversion

overdrive pacing

defibrillation

Heart RatePalpable Pulse

Herlihy, 2007

by fluids by diuretics, venous vasodilators

by vasopressors by arterial vasodilators, IABP

Volume

Pressure

Optimal preload

Understretched

Normal but suboptimal

Optimal

Overstretched

PreloadRV: RAP

LV: LAP (PAOP)

To decrease:

venous

vasodilators:

morphine; NTG

diuretics

ACE inhibitors or

ARBs

To increase:

crystalloids: NS,

LR

colloids: albumin,

hetastarch,

dextran

blood and blood

products

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AfterloadRV: PVRI

LV: SVRI

To decrease:

· arterial vasodilators:

NTP, NTG > 1 mcg/

kg/min; hydralazine

· ACE inhibitors or

ARBs

· IABP

RV specifically

· oxygen

· pulmonary

vasodilators:

aminophylline,

epoprostenol

(Flolan), bosentan

(Tracleer), nitric

oxide

To increase:

· vasopressors:

phenylephrine,

norepinephrine,

dopamine,

vasopressin

ContractilityRV: RVSWI

LV: LVSWI

To increase:

cardiac glycosides:

digoxin

sympathomimetics:

dobutamine

PDE inhibitors:

milrinone

To decrease:

beta-blockers

calcium channel

blockers

Inotropic Agents • Cardiac glycosides: digoxin

• Sympathomimetic (adrenergic) agents

– Epinephrine

– Dopamine

– Dobutamine

• Phosphodiesterase inhibitors

– Inamrinone

– Milrinone

Hemodynamic effects of inotropic agents

Drug CO/CI MAP PAOP SVR Heart rate

Digoxin

Dobutamine or

Dopamine

Inamrinone/

Milrinone

Sympathomimetics Drug Alpha Beta1 Beta2

Phenylephrine ++++ 0 0

Norepinephrine ++++ ++ 0

Epinephrine ++++ ++++ ++

Dopamine +++ +++ +

Dobutamine + ++++ ++

Isoproterenol 0 ++++ ++++

Inotropes

___chronic LVF

___acute LVF

___calcium channel blocker toxicity

___beta-blocker toxicity

___end-stage refractory LVF

a. Dobutamine

b. Milrinone

c. Digoxin

d. Glucagon

e. Calcium

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Vasodilators

Vasodilators

Venous dilators to decrease preload

Arterial dilators to decrease afterload

Vasoactive effects of selected drugs DRUG ARTERIES VEINS

Morphine sulfate no yes

Nitroglycerin (Tridil) only if > 1 mcg/kg/min yes

Hydralazine (Apresoline) yes no

Minoxidil (Loniten) yes no

Fenoldopam mesylate (Corlopam) yes no

Clevidipine butyrate (Cleviprex) yes no

Milrinone (Primacor) yes yes

Nicardipine (Cardene) yes yes

Nifedipine (Procardia) yes yes

Nesiritide (Natrecor) yes yes

Nitroprusside (Nipride) yes yes

Phentolamine (Regitine) yes yes

Prazosin (Minipress) yes yes

Effects of calcium channel blockers

Type of Calcium Channel

Blocker

Coronary

Arterial

Dilation

Peripheral

Arterial

Dilation

AV Nodal

Depression

SA Nodal

Depression

Effect on LV

Contractility

Dihydropyridine type

(e.g., nifedipine)

+ +++ 0 0 0

Diphenylalkylamine type

(i.e., diltiazem)

+ ++

Benzothiazepine type

(i.e., verapamil)

+ +

Copyright Dennison, R. D. (2013). Pass CCRN! (4 ed). Philadelphia: Elsevier.

Vasodilators ____eclampsia

___hypertension with neurologic injury

___need for afterload reduction in acute MI

___benign prostatic hypertrophy

___hypertension after vascular surgery

___cerebral vasospasm

___autonomic dysreflexia

___heart failure

___coronary artery spasm

___renal hypoperfusion

a. Nifedipine (Procardia) b. Nitroglycerin (Tridil) c. Labetalol (Normodyne) d. Phentolamine

(Regitine) e. Fenoldopam mesylate

(Corlopam)

f. Hydralazine (Apresoline)

g. Carvedilol (Coreg) h. Clevidipine (Cleviprex) i. Nitroprusside (Nipride) j. Doxazosin (Cardura)

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Blood pressure =

Vasopressors

Sympathomimetics Drug Alpha Beta1 Beta2

Phenylephrine ++++ 0 0

Norepinephrine ++++ ++ 0

Epinephrine ++++ ++++ ++

Dopamine +++ +++ +

Dobutamine + ++++ ++

Isoproterenol 0 ++++ ++++

Hormone: Vasopressin

Antidysrhythmics Antidysrhythmics

___blocks potassium channel

___blocks beta receptors

___blocks calcium channel

___blocks sodium channel

___blocks reentry

a. Class I

b. Class II

c. Class III

d. Class IV

e. Miscellaneous

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Diuretics

Diuretics

___heart failure

___hypertension

___oliguria

___rhabdomyolysis

___glaucoma

___metabolic alkalosis

___intracranial hypertension

___cirrhosis

a. Thiazide

b. Loop

c. Osmotic

d. Aldosterone antagonists

e. Carbonic anhydrase

___Digoxin ___Dobutamine ___Dopamine 3-5 mcg/kg/min ___Dopamine 5-10 mcg/kg/min ___Dopamine >10 mcg/kg/min ___Fluid challenge ___Furosemide ___Milrinone ___Nesiritide ___Nitroglycerin ___Nitroprusside ___Phenylephrine ___Propranolol ___Vasopressin

a. Increased heart rate b. Decreased heart rate c. Increased preload d. Decreased preload e. Increased afterload f. Decreased afterload g. Increased contractility h. Decreased contractility

Case Study

ST

segment

elevation

in V1 =

septal

injury

Pathologic Q waves and ST segment

elevation in V2 through V5 =

acute anterior MI

ST

segment

elevation

in V6 =

lateral

injury

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• BP 86/56 mm Hg

• MAP 66 mm Hg

• HR 118 bpm

• RA 8 mm Hg

• PA 44/26 mm Hg

• PAOP 22 mm Hg

• CO 3 liters/minute

• CI 1.3 liters/min/m2

• SV 25 ml/beat

• SVR 1680 dynes/sec/cm-5

• PVR 160 dynes/sec/cm-5

• DO2I 259 ml/min/m2

PCI successful with reperfusion of IRA

(LAD)

References • Bockenstedt, T. L., Baker, S. N., Weant, K. A., & Mason, M. A.

(2012). Review of vasopressor therapy in the setting of vasodilatory shock. Adv Emerg Nurs J, 34(1), 16-23.

• Cooper, B. E. (2008). Review and update on inotropes and vasopressors. AACN Advanced Critical Care, 19(1), 5-13; quiz 14-15.

• Dennison, R. D. [2013]. Pass CCRN! [4 ed]. Philadelphia: Elsevier.

• Hays, A. J., & Wilkerson, T. D. (2010). Management of hypertensive emergencies: A drug therapy perspective for nurses. AACN Advanced Critical Care, 21(1), 5-14.

References • Oba, Y., & Lone, N. A. (2014). Mortality benefit of vasopressor

and inotropic agents in septic shock: A bayesian network meta-analysis of randomized controlled trials. Journal of Critical Care, 29(5), 706-10.

• Ndefo, U. A., Erowele, G. I., Ebiasah, R., & Green, W. (2010). Clevidipine: a new intravenous option for the management of acute hypertension. Am J Health Syst Pharm, 67(5), 351-360.

• Improving vasopressor safety (2014). . Fredericton: Nurses Association of New Brunswick.

• Sviri, S., Hashoul, J., Stav, I., & van Heerden, P. (2014). Does high-dose vasopressor therapy in medical intensive care patients indicate what we already suspect? Journal of Critical Care, 29(1), 157-60.

Which of the following would be appropriate to decrease preload? (more than one may be correct) a. Cleviprex b. Nitroprusside c. Nicardipine d. Nitroglycerin

Which of the following is an advantage of dobutamine over dopamine as an inotropic agent? (more than one may be correct) a. less tachycardia b. decrease in preload and afterload c. less proarrhythmogenesis d. less propensity for hypotension