Heart Failure Flashcards
Define Heart Failure
-clinical syndrome or condition caused by heart’s inability to generate enough cardia output to meet body’s metabolic demands
Pathophysiology (Signs and Sxs) of HF
- intravascular and interstitial volume overload: SOB, rales, edema
- manifestations of inadequate tissue perfusion (fatigue, poor exercise tolerance)
5 Year Mortality Rate HF
> 50%
Causes of HF
- coronary artery disease
- HTN
- idiopathic dilated cardiomyopathy
Preload
amount of venous return to heart
Afterload
resistance against which the ventricle must pump
Contractility
force of contraction
What effect do positive inotrope medications have on contractility?
positive inotropes increase contractility
Sxs of Heart Failure
- dyspnea, orthopnea, SOB, PND, exercise intolerance, tachypnea
- cough
- fatigue, weakness, lethargy
- nocturia, polyuria
- hemoptysis
- abdominal pain, anorexia, nausea, bloating, ascites
Signs of Heart Failure
- rales, S3 gallop
- pleural effusion
- tachycardia
- cardiomegaly
- peripheral edema
- JVD
- hepatojugular reflex, hepatomegaly
Lab Tests for HF
- BNP > 100 pg/mL
- EKG
- SCr
- CBC
- CXR
- echocardiogram
Stage A HF
- pts at high risk of developing HF but w/o structural heart dz or sxs of HF
- eg pts w/ HTN, DM, obesity, metabolic syndrome, atherosclerotic dz
Stage B HF
- pts with structural heart dz but w/o signs or sxs of HF
- eg pts w/ previous MI, LVH, low EF
Stage C HF
- pts with structural heart dz with current or prior sxs of HF
- eg pts w/ known structural heart dz and SOB, fatigue, reduced exercise tolerance
Stage D HF
- pts with refractory HF requiring specialized interventions
- eg pts with marked sxs at rest despite maximal medical therapy
NY Functional Class I
-pts w/ cardiac dz but w/o limitations of physical activity
NY Functional Class II
-pts with cardiac dz that results in slight limitations of physical activity (ordinary activity results in fatigue, palpitation, dyspnea and angina)
NY Functional Class III
-pts with cardiac dz that results in marked limitation of physical activity
NY Functional Class IV
-pts with cardiac dz that results in an inability to carry on physical activity without discomfort
Drugs that May Precipitate/Exacerbate HF
- negative inotropic effect (anti-arrhythmics, BB, CCB, terbinafine)
- cardiotoxic: doxorubicin, daunomycin, imatinib, ethanol, amphetamines
- Na and water retention: NSAIDs, COX2 inhibitors, glucocorticoids, androgens, estrogens, salicylates (ASA)
Treatment Principles for HF
- optimize preload
- reduce afterload
- increase contractility
ACE-I Effect on Ventricular Workload
-decrease preload and afterload
ACE-I Benefits for HF
- reduce morbidity and mortality
- reduce hospitalizations in HFrEF
- slow dz progression: decrease or prevent ventricular remodeling
ACE-I Recommended for which HF Pts?
- all pts with reduced EF to prevent HF
- all pts with HFrEF unless CI (2/3 tri preg, angioedema, renal artery stenosis, hyperkalemia)
Beta Blockers that Are Used in HF
-carvedilol, metoprolol, bisoprolol
BBs Effect on Ventricular Workload
-decrease preload and afterload; decrease HR and antiarrhythmic
Benefits of BBs in HF
- reduce morbidity and mortality
- reduce hospitalizations
- cause “reverse modeling” of L ventricle; return heart to more normal size, shape, function
BBs Recommended for which HF Pts?
- all pts with reduced EF to prevent HF
- all STABLE pts with HF unless CI (eg asthma)
How should pharm therapy be initiated with BB for HF?
- start at low doses
- titrate slowly up to target dose and monitor closely
Monitoring for BB for HF
- BP
- HR
- fluid status
Aldosterone Antagonists MOA
-decrease sodium retention
Aldosterone Antagonists Effect on Ventricular Workload
decrease preload
Aldosterone Antagonists Benefits in HF
- reduce morbidity and mortality
- reduce hospitalizations
Aldosterone Antagonists Recommended for which HF Pts?
- patients with NYHA class II-IV who have LVEF < 35%
- pts after acute MI with LVEF <40% w/ sxs of HF or DM
Aldosterone Antagonists Monitoring
- BP
- K+
- renal function (baseline, 3 days, 1 week, qmonth x3 for spironolactone)
Diuretics Effect on Ventricular Workload
-decrease preload
Diuretics Benefit in HF
-relieve congestive sxs (systemic edema)
Diuretics Recommended in which HF Pts?
Also say which diuretic for mild, mod, severe
-pts with HFrEF with fluid retention
+mild overload = thiazide
+moderate = loop
+severe = IV furosemide
Diuretics Monitoring
- BP
- serum K+
ARBs MOA
- block angiotensin II receptor, but do not affect bradykinin
- effect is vasodilation and inhibition of ventricular remodeling
ARBs Recommended for which HF Pts?
- pts w/ HFrEF who are ACE-I intolerant
- alternative to ACE-I as first line therapy in HFrEF
- consider in persistently symptomatic pts with HFrEF on guideline directed med therapy
Hydralazine/Isosorbide MOA
- hydralazine: direct acting vasodilator = decrease SVR, increase SV and CO
- nitrates: venodilation = decreased preload, may inhibit ventricular remodeling
Hydralazine/Isosorbide Recommended for Which HF Pts?
- African Americans with NYHA class III-IV HFrEF
- pts with HFrEF who cannot have ACE-I or ARBs
Hydralazine/Isosorbide AEs
- HA
- palpitations
- nasal congestion
Digoxin MOA
-positive inotrope = increase contractility
Digoxin Benefits in HF
- antiarrhythmic for pts with afib
- alleviates sxs and improves clinical status in pts with HFrEF (decrease hospitalizations)
When should dig be used in HF pts?
-add for pts who remain symptomatic despite optimized tx
Signs of Digoxin Toxicity
- anorexia
- N/V/D
- tiredness, weakness
- decrease HR
- yellow/green halo vision
- confusion, HA
Digoxin Drug Interactions
- verapamil
- captopril
- diuretics
- amiodarone, dronedarone
- clarithromycin, erythromycin
Managing Decompensated HF
- hospitalize
- IV loop diuretic for pts w/ sig fluid overload
- IV dobutamine to increase renal blood flow and diuresis
- if symptomatic HoTN is absent, IV NTG, nitroprusside or nesiritide may be considered
B-type Natriuretic Peptide Indication
-IV tx of pts with acutely decompensated HF with dyspnea at rest or with minimal activity
B-type Natriuretic Peptide MOA
- smooth muscle relaxation
- dilates veins and arteries
- dose dependent decrease in wedge pressure and systemic arterial pressure
B-type Natriuretic Peptide Half Life
18 minutes
B-type Natriuretic Peptide Elimination
- cell surface clearance receptors
- proteolytic cleavage
- renal filtration
- clearance proportional to body weight
B-type Natriuretic Peptide Monitoring
-monitor BP and decrease dose if HoTN develops
