- cool extremities - tachycardia - low pulse pressure

- meds end in -olol (metoprolol, carvedilol, bisoprolol) - effects: antagonize effects of sympathetic system (B adrenergic blockage), dec. contractility, best for mild to mod sx of HF - side effects: negative inotrope (fluid retention, hypotension, dec. cardiac output), bronchoconstriction - good for HFrEF

- reverses fluid retention (Na Loss) - most common HF therapy - can be use chronically or acutely - side effects- dehydration, hypokalemia, sulfa, tinnitis - good for HFrEF and HFpEF

- arterial vasodilation- dec. LV afterload, dec. cardiac work, dec. mitral regurg, dec preload and afterload - hydralazine/isosorbide dinitrate in HFrEF in pts of african descent (can cause drug induced lupus side effect) - vasodilation- dec. preload - nitro

Unit 1 Day 5 Flashcards by Danielle Eves

Major Symptoms Associated with Heart Failure

dec. cardiac output = -fatigue, sleepiness, wasting, reduced urine output
inc. pulmonary venous pressure = dyspnea, orthopnea, paroxysmal nocturnal dyspnea
inc. central venous pressure = edema, ascites

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NYHA Function Classifications

-based on what people can do functionally
1 = asymptomatic
2= can walk up stairs with few symptoms
3= walk up stairs with symptoms
4 = symptomatic at rest

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Signs of Low Flow

cool extremities
tachycardia
low pulse pressure

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Signs of Inc. Left Sided Pressure

rales
hypoxia
tachypnea
sitting bolt upright

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Signs of Inc. Right Sided Pressure

edema
hepatic congestion/hepatomegaly
JVD

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Heart Failure Tests and Imaging Studies

chest radiography (CXR)- enlarged cardiac silhouette, acute pulmonary edema
natriuretic peptides (BNP or NT-proBNP)- secreted by myocardium in response to ventricular stretch
EKG- no direct diagnosis of HF
cardiac imaging for LVEF- ultrasound, nuclear, MRI, CT
right heart catheterization- measures pressure in various areas

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ACE Inhibitors (Angiotensin Converting Enzyme)

meds in in -pril (lisinopril, enalapril, benazepril)
block conversion of angiotensin1 to angiotensin 2
effects: direct vasodilation, dec. aldosterone activation, salt/water excretion, most effective in sicker pts
side effects: hypotension, worsening renal function, cough, hyperkalemia, angioedema
drug interactions: lithium, NSAIDs, salt substitutes, loop diuretics, K+ spakring diuretics
contraindications: pregnancy, bilateral renal artery stenosis, renal failure, angioedema, hyperkalemia
antiremodeling
prevents ACE breakdown of bradykinin (BK is a vasodilator)

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ARBs (Angiotensin Receptor Blockers)

meds end in -sartan (valsartan, candesartan, losartan)
effect: block receptor of angiotensin 2, salt/water excretion, potassium retention
clinical use: equivalent to ACE1, ACE + ARB combo may provide added benefit, generally used when pts develop cough due to ACE
side effects: ARBs, do not produce cough, similar side effects to ACE (hypotension, worse renal function, hyperkalemia, angioedema)
contraindications: over-producers of uric acid, pregnancy, volume depletion, renal arterial stenosis, hyperkalemia
no difference between ACE and ARB in all cause mortality

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Beta Blockers

meds end in -olol (metoprolol, carvedilol, bisoprolol)
effects: antagonize effects of sympathetic system (B adrenergic blockage), dec. contractility, best for mild to mod sx of HF
side effects: negative inotrope (fluid retention, hypotension, dec. cardiac output), bronchoconstriction
good for HFrEF

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Diuretics

reverses fluid retention (Na Loss)
most common HF therapy
can be use chronically or acutely
side effects- dehydration, hypokalemia, sulfa, tinnitis
good for HFrEF and HFpEF

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Neurohormonal Antagonists if HFrEF

ACE inhibitors
ARBs
MRAs
beta blockers

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Vasodilators

arterial vasodilation- dec. LV afterload, dec. cardiac work, dec. mitral regurg, dec preload and afterload
hydralazine/isosorbide dinitrate in HFrEF in pts of african descent (can cause drug induced lupus side effect)
vasodilation- dec. preload
nitro

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Electrical Therapies of HFrEF

Implanted cadioverter defibrillator (ICD)
Cardiac resynchronization therapy (CRT)
inc. contractility, HR, so inc. CO

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Positive Inotropic Agents

digoxin
dobutamine
milrinone
used acutely and chronically
inc. contractility

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Mineralocorticoid Receptor Antagonists (MRA)

spironolactone and eplerenone
effects: blcok mineralocorticoid receptor (ACE/ARB aldosterone block is incomplete), Na loss
side effects: hyperkalemia, gynecomastia (spiro)

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Tx for Chronic HFrEF (LVEF <40%)

BB
ACE/ARB
aldosterone antagonist
hydralazine/ISDN
+/- digoxin
ICD/CRT

Tx for Acute HFrEF (LVEF < 40%)

IV diuresis
nitrates (if BP allows)
CPAP/BiPAP (if SOB)
pressors (if dec. CO, shock)

Tx for Chronic HFpEF (LVEF > 40%)

control risk factors (DM, HTN, obesity)

- control volume status (?)

Tx for Acute HFpEF

IV diuresis
nitrates (if BP allows)
CPAP/BiPAP

HF Prevention Goals

hypertension
diabetes
hyperlipidemia
physical inactivity
excessive OH intake
smoking
dietary sodium

Digoxin

mechanism of action: blocks Na/K pump ATPase, inotrope (INC CONTRACTION), slows rate of SA node, SLOWED CONDUCTION of AV node (causes activation of the Na/Ca pathway and causes calcium to enter the cell) (prolongs phase 0 and phase 4)
inc. contraction in HFrEF, and is antiarrhythmic in supraventricular arrhythmias
metabolism: oral or IV administration, renally eliminated, 38 hr half life (steady state 7-10 days)
side effects/toxicity: hypokalemia, hypercalcemia, hypomagnesemia, nausea, vomiting, weakness, confusion, bradycardia, arrhythmia, visual changes
sometimes extreme toxicity includes severe arrhythmia, bradycardia, heart block unresponsive to atropine, inc. K+
drug-drug interactions: quinidine, verapimil, amniodarone, propafinone, itraconazole, macrolide antibiotics
reduces number of pts hospitalized
from foxglove plant
reverse toxicity w/ digoxin immune fab

Dobutamine

mechanism of action: beta1 agonist to inc. contractility, slight peripheral vasodilation
metabolism: 2 min half life
side effects/toxicity: angina, arrhythmia, dysrhythmia
drug-drug interactions: beta 1 agonist- not helpful if also taking beta blockers
not recommended if hypotensive

milrinone

mechanism of action: PDE (phosphodiesterase degrades cAMP) inhibitor, augments Ca utilization, moderate peripheral vasodilation
inotrope, vasodilator
metabolism: 1-3 hr half life
side effects/toxicity: hypotension, thrombocytopenia, tachycardia, arrhythmias, fever, inc. LFTs
drug-drug interactions: recommended if receiving beta blocker

dopamine

mechanism of action: endogenous precursor of norepinephrine directly stimulates adrenergic receptors
causes inotropy
metabolism: dose dependent effect, continuous infusion via pump
proarrhythmic
side effects/toxicity: none listed
drug-drug interactions: none listed

HFrEF

-systolic dysfunction

neprilysin inhibitors

- new - prodrug - inhibits neprolysin - neprilysin normally degrades BNP (BNP is good for tx in HF) - also blocks angiotensin 2 receptor

aldosterone

- activated by angiotensin 2 - causes water retention - inc. HR - activates sympathetic nervous system