Heart Failure Flashcards by Lauren Ames

an impairment of the contraction of the left ventricle. SV is reduced. EF is reduced (<45%)

systolic dysfunction

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heart failure with preserved left ventricular systolic function

diastolic dysfunction

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ventricular filling rate and extent of filling (EDV) are reduced. Normal EF is maintained

diastolic dysfunction

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CO=?

CO=HRxSV

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left ventricular end diastolic pressure

preload

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systemic vascular resistance

afterload

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Causes of ischemic heart failure

coronary artery disease (myocardial ischemia and infarction)

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causes of non-ischemic heart failure

HTN, primary myocardial muscle dysfunction, valvular abnormalities, structural damage to valvular walls, dilated cardiomyopathy

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what are compensatory mechanisms for heart failure

increased SNS activity (increase HR, BP)
Frank starling (increase preload= increase SV)
Activation of RAAS
myocardial remodeling (concentric and eccentric hypertrophy)

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direct toxic effects of NE and AT2

arrhythmias, apoptosis

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Symptoms include SOB, DOE, orthopnea, cough, PND, fatigue and weakness, memory loss and confusion, anorexia. Signs include tachy, rales, diaphoresis, S3 and S4 gallops

LVF

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Symptoms include weight gain, transient ankle swelling, abdominal distention, anorexia, nausea. Signs include JVD, edema, hepatomegaly, ascites, and maybe hepatojugular reflux

RVF

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this class of drugs has no data regarding morb or mort of HF. Class I- indicated in pts with current or prior symptoms of HF and reduced LVEF w evidence of fluid retention (level of evid- C)

diuretics

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this diuretic can be useful if GFR > 30 ml/min and work on the distal tubule

thiazides

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these diuretics work on the ascending LOH and are more of a DOC for HF

loops

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what should you monitor for a pt on diuretics

K, Mg, BUN, SCr

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this drug is class IIa and can be beneficial in pts with current or prior symptoms of HF and reduced LVEF to decrease hospitalization for HF (level of evidence B)

Digoxin

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Hemodynamic effects in HF include increased CO, decreased wedge pressure, and increased LVEF

digoxin

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neurohormonal effects in HF include vagomimetic action, improved baroreceptor senitivity, decreased NE, decreased RAAS activation, direct sympathoinhibitory effect

digoxin

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this drug results in increased sympathetic CNS outflow at high doses, decreased cytokine concentration, and increased release of ANP and BNP

Digoxin

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electrophysiological effects of this drug include slowing sinus rate (SA node), slowed conduction (AV node), decreased refractory period (atrium) and no effects of the ventricles and Purkinje fibers

digoxin

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a low dose of this drug is sufficient. Inotropic effects can be seen at low concentrations, but women may not derive benefit

digoxin

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this drug inhibits ATPase pump which acts to increase intracellular calcium leading to increased contractility

digoxin

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Conditions likely to alter serum concentrations of this drug include changing renal function, drug interactions, and hypokalemia

digoxin

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amniodarone and quinidine increase clearance of this drug (empirically by 50%)

digoxin

Drug interaction include diltiazem, verapimil, abx, azole antifungals, propafenone- all of these decrease clearance of the drug. Also interacts with furosemide

digoxin

pt comes in with ventricular arrhythmias, heart block. also complaining of visual changes, anorexia, N/V/D, abdominal pain, confusion, and HA

digoxin toxicity

treat digoxin toxicity

digoxin immune Fab

these classes are recommended for all pts with current or prior symptoms of HF and LVEF class I LOE A

ACE I | beta blockers

how is dosing of ACEI different for HTN and HF

higher for HF

what should you monitor when someone is on ACEI

SCr, K, BP, symptoms

this drug may interfere with the efficacy of ACEI

aspirin

side effects of this class include renal impairment, hyperkalemia, hypotension, and cough

ACEI

intolerance to this class includes cough, angioedema

ACEI

two alternatives for pts who cant take ACEI

ARBs or a combo of isosorbide dinitrate and hydralazine

effects of chronic adrenergic activation

myocardial remodeling, apoptosis, arrhythmias, impaired diastolic filling, increased myocardial energy demand

contraindications to the class include documented allergy, RAD, symptomatic bradycardia or > 1st degree heart block, fluid overload or on IV inotropic agents

beta blockers

monitor pts taking this class for HR, BP, weight, symptoms (SOB, edema, DOE, dizziness)

beta blockers

hemodynamic effects of aldosterone in CHF

sodium and water retention increased plasma fluid volume elevated BP

Non hemodynamic effects of aldosterone in CHF

myocardial/vascular fibrosis, impaired arterial compliance, baroreceptor dysfunction, K and Mg excretion, elevated ANP, parasympathetic inhibition

you can ADD this class in selected patients with moderately severe to severe symptoms of HF and reduced LVEF who can carefully be monitored for preserved renal function and normal K

aldosterone antagonists

can only use this class is SCr < 2.5 in men and 2.0 in women, K 30

aldosterone antagonists

this drug reduces the risk of CV events in pts without CHF but has not been demonstrated in CHF patients

ASA

this class reserved for patients with afib or previous TE

anticoagulants

this combo trio is never recommended for patients with HF

ACE I ARB aldosterone antagonists

can combine these two in a persistently symptomatic patient who is already being treated with conventional therapy

ACEI plus ARB

use this drug for post MI patients with LV dysfunction or those with gynecomastia from spironolactone

eplerenone

cardiac index

CI= CO/BSA

pulmonary artery wedge pressure

estimate of left ventricular end diastolic pressure (PRELOAD)

systemic vascular resistance

pressure the left ventricle must overcome to eject its blood volume (AFTERLOAD)

myocardial hypertrophy: systolic failure

excessive elongation of fibers so ventricle is unable to contract effectively

myocardial hypertrophy: diastolic failure

hypertrophy of ventricles affects ability to relax, does not fill properly

this diuretic can be administered for ADHF and acts through venodilation and Na/H2O excretion

Furosemide

this drug is a potent beta 1 and beta 2 receptor agonist and a weak alpha 1 agonist

dobutamine

this drug has positive inotropic and chronotropic effects, which increases CO and vasodilation (thereby decreasing SVR)

dobutamine

monitor vitals, urine output, K, and telemetry when giving these drugs

dobutamine dopamine phosphodiesterase inhibitors epi, norepi, isoproterenol

this drug affects beta, alpha, and dopaminergic (DA1) receptors

dopamine

what dose of dopamine is most often used for HF

MEDIUM (increases CO) | high dose has alpha 1 effects, increase SVR and make you worse

these drugs increase intracellular cAMP, which increases intracellular calcium, which increases contractility and CO

phosphodiesterase inhibitors

this positive inotrope does not reduce incidence of sudden death or prolong survival in patients with CHF

amniodarone

these inotropes increase CO and SVR because they are beta 1, beta 2, and alpha 1 agonists

epi and norepi

this inotrope is a beta 1 and beta 2 agonist. It increases CO and decreases SVR

isoproterenol

this class reduces preload and therefore PCWP. Can cause HA, dizziness, reflex tachycardia, hypotension, thiocyanate toxicity

venodilators (thio tox is with nitroprusside)

this venodilator is preferred when CO is not severely compromised or when other inotropic agents are administered

nitroglycerin

this venodilator is also an arterial vasodilator and is preferred in patients with an increased SVR

nitroprusside

this venodilator reduces preload (PWCP) and reduces heart rate

morphine

taper this venodilator to avoid rebound HTN

nitroprusside

this venodilator is typically used in the early stage of tx esp if the pt has anxiety, restlessness, or dyspnea

morphine

monitor vitals for this class

venodilators

this venodilator increases intracellular cGMP which leads to smooth muscle relaxation

nesiritide

this venodilator promotes vasdilation, naturesis, and diuresis. It reduces PCWP, SVR, and increases CO

nesiritide

this drugs use is controversial, it should be limited to patients presenting to the hospital with ADHF and dyspnea at rest

nesiritide