Heart Failure Flashcards
an impairment of the contraction of the left ventricle. SV is reduced. EF is reduced (<45%)
systolic dysfunction
heart failure with preserved left ventricular systolic function
diastolic dysfunction
ventricular filling rate and extent of filling (EDV) are reduced. Normal EF is maintained
diastolic dysfunction
CO=?
CO=HRxSV
left ventricular end diastolic pressure
preload
systemic vascular resistance
afterload
Causes of ischemic heart failure
coronary artery disease (myocardial ischemia and infarction)
causes of non-ischemic heart failure
HTN, primary myocardial muscle dysfunction, valvular abnormalities, structural damage to valvular walls, dilated cardiomyopathy
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)
direct toxic effects of NE and AT2
arrhythmias, apoptosis
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
Symptoms include weight gain, transient ankle swelling, abdominal distention, anorexia, nausea. Signs include JVD, edema, hepatomegaly, ascites, and maybe hepatojugular reflux
RVF
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
this diuretic can be useful if GFR > 30 ml/min and work on the distal tubule
thiazides
these diuretics work on the ascending LOH and are more of a DOC for HF
loops
what should you monitor for a pt on diuretics
K, Mg, BUN, SCr
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
Hemodynamic effects in HF include increased CO, decreased wedge pressure, and increased LVEF
digoxin
neurohormonal effects in HF include vagomimetic action, improved baroreceptor senitivity, decreased NE, decreased RAAS activation, direct sympathoinhibitory effect
digoxin
this drug results in increased sympathetic CNS outflow at high doses, decreased cytokine concentration, and increased release of ANP and BNP
Digoxin
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
a low dose of this drug is sufficient. Inotropic effects can be seen at low concentrations, but women may not derive benefit
digoxin
this drug inhibits ATPase pump which acts to increase intracellular calcium leading to increased contractility
digoxin
Conditions likely to alter serum concentrations of this drug include changing renal function, drug interactions, and hypokalemia
digoxin
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
