HEART FAILURE
Mark Tuttle 2014
EPIDEMIOLOGY: Most common admitting diagnosis for patients 65 and older in USA12 PROGNOSIS: Mortality after diagnosis is 10.4% at 30 days, 22% at 1 yr, and 42.3% at 5 yrs1, worse than many cancers. DEFINITION: Clinical syndrome of dyspnea and fatigue resulting from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. “Heart failure” is the preferred term. “Congestive heart failure” suggests decompensation. Definitions of heart failure1 LVEF Proportion of patients HFrEF: Heart failure with reduced ejection fraction ≤40% ½ HFpEF: Heart failure with preserved ejection fraction ≥50% ½ ● HFpEF, borderline: LVEF 41-49% ● HFpEF, improved: LVEF > 40% previously <40% PATHOPHYSIOLOGY ● Neurohumoral: ↑ norepinephrine, renin, angiotensin, aldosterone, vasopressin ● Cytoskeletal: Fibrosis, sarcomere alteration ● Metabolic: Oxidative stress, apoptosis/necrosis, calcium overload ● Electrical: Conduction disease, arrhythmias ● Geometric: Dilation, ↑ wall stress, functional regurgitation
THERAPY FOR COMPENSATED HEART FAILURE BY STAGE Stage
Population Goals Drugs ● Treat risk factors (ex. ● ACE-I/ARB: if HTN, DM, A: At risk, but no ● Hypertension ● CAD HTN, HLD, DM, atherosclerosis structural ● DM obesity) abnormalities or ● Obesity ● Exercise symptoms ● Cardiotoxins ● Quit E tOH, smoking, ● Fam Hx of CM drugs ● Prior MI ● Same a s stage A ● ACE-I/ARB: If ↓ LVEF B: Structural ● LV remodeling: ● β-blocker: If history of MI or ↓ disease, but no Low E F o r L VH LVEF signs/symptoms ● Asymptomatic valvular ● Statin: If history of MI/ACS disease ● Avoid: NSAIDs, CCBs (except amlodipine), TZDs ● Structural heart disease ● Same as stage A+B ● Same as stages A+B C: Structural AND dyspnea, fatigue, ↓ ● Reduce symptoms ● Diuretics: If congestion disease with exercise tolerance ● Improve QOL ● Aldosterone antagonist: current OR PRIOR + ● Na r estriction LVEF ≤35% OR symptoms LVEF ≤40% and MI, DM ● Hydralazine/nitrates: if AA and LVEF ≤40% ● Digoxin:Can be considered ● Marked rest sx ● Same as A-C ● Same as stages A-C D: Refractory ● Repeat hospitalizations ● End of life care ● Palliative inotropes despite optimal tx ● Intolerance of meds Caveats for compensated heart failure with preserved ejection fraction (HFpEF)1 ● Unlike with HFrEF, no trials have demonstrated mortality benefit for drug therapy in HFpEF ● Management strategies ○ Comorbid hypertension: beta-blocker, ACE inhibitor, or ARB ○ ARBs may decrease hospitalizations ○ Revascularization if CAD contributing to symptoms
GRADING SYMPTOMS
Devices ● No role for devices
● ICD: If LVEF ≤ 30%, 40+ days after MI, NYHA 1y ● ICD: As above but can have LVEF ≤ 35% ● BiV Pacer: QRS > 150, LBBB, NYHA II+
Mechanical support: VAD, BiVAD, TAH Transplant ICD deactivation?
HEART FAILURE
Mark Tuttle 2014
NYHA FUNCTIONAL CLASS26 Class Symptoms I No limitation of activity II Ordinary activity results in fatigue, palpitation, or dyspnea III Less than ordinary activity results in fatigue, palpitation, or dyspnea IV Unable to carry out any physical activity without discomfort 27 Criticisms : ● Variable benchmark of “ordinary activity”: Stairs, walk distance, walking to local landmarks, around house ● Self-reported exercise tolerance is a poor metric of actual exercise tolerance ● Interobserver variability: Study of 50 patients assessed by 2 cardiologists agreed on class just 54% of time ● Used widely in clinical research despite the above limitations (15% of papers in Circulation cite NYHA)
IMPACT OF GUIDELINE-DIRECTED MEDICAL THERAPY (GDMT) ( AHA 2013) GDMT ACEi/ARB Beta blocker Aldosterone antagonist Hydralazine/nitrate
RR reduction in mortality 17% 34% 30% 43%
NNT (mortality @ 36 mo) 26 9 6 7
RR reduction in HF hospitalization 31% 41% 35% 33%
Risk modifier models: Seattle Heart Failure Model
INITIAL EVALUATION28
Past medical history ● Hypertension ● Diabetes ● Dyslipidemia ● Valvular heart disease ● CAD/PVD ● Myopathy (ex. muscular dystrophy) ● Rheumatic fever ● Mediastinal radiation ● Sleep disordered breathing ● Exposure to cardiotoxins (anthracyclines, transtuzimab, cocaine) ● EtOH, illicits, smoking ● STDs ● Thyroid disorder ● Pheochromocytoma
Family history ● MI ● Stroke ● PVD ● Sudden cardiac death ● Myopathy ● Conduction disease (PPM) ● Arrhythmia ● Cardiomyopathy Lab evaluation ● CBC, electrolytes, Cr, U/A ● BNP, NT-proBNP ● Fasting lipids, HbA1c ● LFTs ● TSH ● HIV if at risk ● Sleep study in select ● Hemochromatosis in select
Imaging ● Electrocardiogram ● Echocardiography Repeat if change in clinical status or have recovered from event or received treatment which may have impacted function Cardiac cath/nuclear imaging ● ALL patients unless not a candidate for revascularization Endomyocardial biopsy ● New-onset unexplained HF with hemodynamic compromise
HEART FAILURE
Mark Tuttle 2014
DIAGNOSING ACUTE DECOMPENSATED HEART FAILURE (ADHF)
PROGNOSIS: After hospitalization for ADHF, 50% readmission rate in 6 months and 25-35% 1-year mortality. ASSESS FOR CONGESTION AND PERFUSION ● Congestion: Easier to see if acute. ○ History: Orthopnea, PND, weight changes, dietary changes, medication adherence, chest pain Symptom/History24 Sensitivity Specificity PLR NLR
○
Fatigue
Common
Nonspecific
N/A
N/A
Dyspnea on exertion
84%
34%
1.3
0.48
Orthopnea
50%
77%
2.2
0.65
Paroxysmal nocturnal dyspnea
41%
84%
2.6
0.7
History of myocardial infarction 40% 87% 3.1 6.9 Physical exam: Heart rate, pulse pressure, jugular venous distension (see below), rales, cardiac wheeze, edema, ascites, hepatosplenomegaly, weight gain, murmurs, Cheyne-Stokes respirations Physical Finding24 Sensitivity Specificity PLR NLR S3
13%
99%
11
0.88
Abdominojugular reflux
24%
96%
6.4
0.79
39%
92%
5.1
0.66
Crackles (Rales)
60%
78%
2.8
0.51
Jugular venous distension
○
○
Dependent pitting edema 50% 78% 2.3 0.64 Chest X-ray: ■ Redistribution (PCWP 12-18): Cephalization of vessels, broadening of vascular pedicle, ↑ artery:bronchus size (normally is 1:1) ■ Interstitial edema (PCWP 18-25): Kerley B lines (at periphery), bronchial cuffing (thickening), perihilar haze (loss of definition) ■ Alveolar edema (PCWP > 25): Cottonwool, air bronchogram (bronchus looks dark on lighter edematous background), pleural effusion Labs: BNP, lactate, CBC, chem-10, troponin, TSH, LFTs, urinalysis in all patients ■ Zebras: HIV, hemochromatosis, amyloidosis, pheochromocytoma if clinically suspected ■ Natriuretic peptides: B-type (BNP) or N-terminal pro-BNP (NT-proBNP) ● Recommended in suspected HF when diagnosis is uncertain1,12 (AHA 2013) ● Can be used as a target to direct therapy in stable outpatients ( AHA 2013) ● ProBNP released by stretched myocardium, cleaved to BNP and inert NT-proBNP ● Falsely low: Lower in obese patients22 (cleared by adipose), normal EF ● Falsely high: Chronic kidney disease, pHTN, sepsis, AF ● NT-proBNP: Standardized assay, BNP: Assays widely differ ⇒ Breathing not properly (BNP) study23: BNP>100 is 90% sensitive, 76% specific for ADHF Adapted from data in reference 24 ○ Echocardiogram: Assesses LVEF, diastolic function, valves, pericardial effusion, RWMA (ischemia) ■ Indications (AHA 2013) ● Initial evaluation ● Significant change in clinical status ● Experienced or recovered from a clinical event (ex. STEMI) ● Received treatment which may have had an impact on cardiac function ● If a candidate for device therapy (ex. ICD, CRT) ■ Diagnose HFpEF12,33 Clinical HF WITH 1+ of: LVH, left atrial enlargement (without AF), doppler evidence, exclusion of non myocardial (ex. valvular, pericardial) causes ● E/A ratio < 1: E (early filling velocity) A (atrial systole filling velocity) in HFpEF ● E/e’ > 8: e’ is velocity of mitral annulus during early diastole
HEART FAILURE
Mark Tuttle 2014
Coronary angiography: ALL new-onset HF or if ACS suspected & candidate for PCI/CABG ( AHA 2013) Endomyocardial biopsy: Indicated when histologic diagnosis would dictate management ■ Indications25 ● New-onset unexplained HF (<2 weeks) with hemodynamic compromise ● New-onset unexplained HF (2 weeks - 3 months) and ↓LVEF, VT, 2° Mobitz II, CHB, or failure to respond to usual care within 1-2 weeks. ○ Hemodynamic monitoring: Pulmonary artery catheter (Swan-Ganz catheter) ■ Indications (AHA 2013) ● Respiratory distress/↓ perfusion + clinical exam inconclusive re: congestion (Class I) ● Persistent symptoms despite standard therapies (Class IIa), and: ○ Uncertain fluid status, perfusion, SVR, PVR ○ Renal function worsening with therapy ○ Requiring vasoactive agents, or ○ May need mechanical support or transplantation 30 ⇒ ESCAPE trial : No effect on mortality vs usual care. Caveat: not all patients required inotropes. Assess perfusion: Impairment suggests cardiogenic shock and need for CCU/inotropes ○ ↓UOP, acute kidney injury ○ Cool extremities ○ ↑ lactate ○ Altered mental status ○ Narrow pulse pressure: if pulse pressure is < 25% of SBP, 91% sensitive, 83% specific for CI < 2.232 ○ Cheyne-Stokes: tachypnea/hyperpnea alternate with apnea due to prolonged circulation time ○ Resting tachycardia Two-minute hemodynamic profile19,20 No congestion (dry) Congestion (wet) ○ ○
●
Good perfusion (warm)
Bad perfusion (cold) Need ICU
Warm and dry PCWP normal CI normal
Warm and wet PCWP ↑ CI normal
Outpatient management
Diuretics ± vasodilators
Cold and dry PCWP normal CI ↓
Cold and wet PCWP ↑ CI ↓
Inotropes ± advanced therapies
Inotropes + diuretics/aquaretics
27% of patients 11% 6 mo mortality
4% of patients 17% 6 mo mortality
49% of patients 22% 6 mo mortality
20% of patients 40% 6 mo mortality
INITIAL THERAPY IN ACUTE DECOMPENSATED HEART FAILURE ●
●
OXYGEN: If hypoxic or in respiratory distress (nasal cannula or NPPV) ⇒ Avoid morphine sulfate: ↑ mechanical ventilation, ↑ LOS, ↑ in-hospital mortality34 ⇒ NPPV: Meta analyses show ↓ in-hospital mortality, ↓ mechanical ventilation in pulmonary edema35 OPTIMIZE VOLUME STATUS: IV diuresis ○ Give outpatient oral dose as IV or furosemide 40mg x creatinine ○ If incomplete response in 2 hours, give double prior dose ○ If inadequate response after up-titration, consider adding thiazide diuretic (ex. metolazone) ⇒ No difference in sx with bolus dosing vs. gtt (DOSE trial9, but no bolus given before gtt) ○ If soft blood pressures, consider gtt, but always bolus x 1 before starting gtt to get to steady state
HEART FAILURE ● ● ● ● ● ● ● ●
Mark Tuttle 2014
○ If still inadequate diuresis, consider low-dose inotrope (ex. dopamine) DIET: Sodium (2g/day) and fluid restriction (2L/day) LABS: Monitor electrolytes BID (especially K, Mg) and replete HOLD BETA BLOCKER if decompensated1 ○ Restart beta blocker when no longer congested and off IV agents (AHA 2013) VASODILATORS: Nitroprusside, nitroglycerin, nesiritide ○ Consider if HTN, acute pulmonary edema, or added to IV diuresis1,12. Avoid in hypotension. INOTROPES: If evidence of impaired perfusion. See above for assessment of perfusion. See below for dose. ULTRAFILTRATION: Can be considered if refractory to above1,12 VASOPRESSIN ANTAGONISTS: If hypervolemic hyponatremia not responsive to fluid restriction1,12 ESTABLISH AND TREAT ETIOLOGY OF DECOMPENSATION ○ Noncompliance (most common): Medications, diet, fluid restriction ■ Identify barriers to adherence: education, cost ○ Addition of detrimental medication ■ Non-amlodipine calcium channel blocker (ex. verapamil, nifedipine, etc) ■ NSAIDs: Cause renal sodium retention and thus hypervolemia ○ Arrhythmia ■ If atrial fibrillation, may need to cardiovert or ablate ■ If pacemaker/ICD is present, interrogate device to determine if arrhythmia caused ADHF ○ Myocardial infarction: Often missed in heart failure ○ Valvular disease (ex. mitral regurgitation, aortic stenosis) ○ Infection (sepsis, UTI, pneumonia, viral illness) ○ Metabolic (ex. hyper/hypothyroid) ○ Acute kidney injury ○ Anemia: Transfuse ○ Pulmonary embolism ○ Toxins: Alcohol, cocaine, chemotherapy ○ Hypertensive crisis ○ Stress-induced (takotsubo) cardiomyopathy
PREVENT READMISSION
WHY DOES THIS MATTER? ● ~25% of patients are readmitted within 30 days. Costs $39 billion/year ● Patients readmitted frequently have a higher mortality ● Performance metric measured by Centers for Medicare & Medicaid Services (CMS) ● Patient Protection and Affordable Care Act (ObamaCare): Penalizes hospitals with high 30-day readmission IMPROVE TRANSITIONS OF CARE (Agency for Healthcare Research & Quality [AHRQ]) ● Pre-discharge: Med reconciliation, appointment scheduled before discharge, patient/caregiver education ● Post-discharge: Home visits, heart failure specialty, telemedicine, support hotline ● Bridging: HF-specific case management, increase provider continuity (same provider inpatient/outpatient)
ASSESSMENT OF JUGULAR VEINS ●
Inspection of neck veins: Used as a marker for elevated filling pressures by estimating CVP ○ Identify internal jugular vein on right side ■ Place patient head of bed between 30-45° and ask patient to rotate their head left ■ Anatomy: IJ runs from between two heads of SCM in straight line to just anterior to the ear ● Avoid confusion with external jugular vein which is more lateral. Elevated EJ pressures may not reflect elevated CVP since it contains valves. ■ Venous pulsations: need to differentiate from carotid artery pulsation ● Palpate radial pulse as you are looking at neck veins ● Using a pen light may help identify pulsation ● Venous pulsations will have a and v components (biphasic), may look like flickering
HEART FAILURE
○
○
○
Mark Tuttle 2014
○ Will not see a wave in atrial fibrillation ● Hepatojugular reflux will increase IJ pressure but not carotid Measure the vertical distance above the sternal angle (angle of Lewis) to the height of the IJ ■ Add 5 cm if head of bed at 30-45° and add 10 cm if patient is vertical ■ Yields JVP in cm H2O, > 8 is elevated. ● Divide by 1.36 to get pressure in mmHg (1.36 cm H2O = 1.0 mm Hg) Test characteristics ■ 47-92% sensitive, 93-96% specific, positive likelihood ratio 9.018 ● Less sensitive since patients anatomy, distance of RA below angle of Lewis) varies among individuals and positionally. Differential diagnosis of elevated JVP: Heart failure, lung disease, pHTN, tricuspid stenosis/regurg
PHARMACOTHERAPY ACE-I/ARB: Class effect. Do not use both ACE and ARB concurrently. ● Benefits: ↓ mortality, ↓ hospitalization, ↓ symptoms, ↑ clinical status, ↑ overall sense of well-being. ● Mechanism: ↓ neurohormonal activation ● Indications: ○ HFrEF Stage B-D: All patients (AHA 2013) ⇒ SOVLD trial5: enalapril vs. placebo ↓ mortality (35% vs. 40%) at 48 months ○ HFpEF Stage A-D: Consider if comorbid hypertension. Role is less clear without HTN. ○ STEMI: Within 24 hours in all patients (AHA, 2013) ⇒ SAVE trial5: captopril vs. placebo ↓ mortality (20% vs. 25%) at 42 months ● Contraindications: Angioedema, pregnancy, hypotension, AKI/CKD (sometimes) β-blocker: metoprolol succinate, carvedilol, or bisoprolol ONLY. ● Benefits: ↓ mortality, ↓ sudden death, ↓ hospitalization, ↓ LVH. ● Indications ○ HFrEF Stage B-D: All patients (AHA 2013) ⇒ MEFIT-HF13: Metoprolol XL vs. placebo ↓ mortality (7% vs 11%) @ 1 year w/EF ≤40% & NYHA II+ ⇒ COPERNICUS14: Carvedilol vs. placebo ↓ mortality (13% vs. 20%) @10 mo w/EF < 25% & NYHA III-IV ⇒ CIBIS-II16: Bisoprolol vs. placebo ↓ mortality (12% vs. 17%) @ 1.3 yr w/EF ≤35% & NYHA III-IV ○ HFpEF Stage A-D: Consider if comorbid hypertension. Role is less clear without HTN. ● Contraindications: ADHF, shock, reactive airway disease, hypotension, 1° AV delay > 0.24 s, or 2° AV block Aldosterone antagonists: Spironolactone, eplereone ● Indications: ○ HFrEF Stage C-D: Added to ACE-I/ARB w/LVEF ≤35% OR LVEF ≤40% and history of MI, DM (A HA 2013)1 ⇒ RALES trial2: Spironolactone ↓ mortality (35% vs. 46% @ 2 yr) in pts with ↓ LVEF after MI and NYHA III-IV ○ After acute MI: with NYHA II or DM (AHA 2013)1 ⇒ EPHESUS3: Eplerenone ↓ mortality (14% vs. 17% @ 14 mo) in pts w/↓ LVEF after acute MI and NYHA II-III ● Contraindications ○ Cr ≥ 2.5, K ≥ 5.0, or unable to follow BMP ○ Not recommended without concurrent loop diuretic therapy. ⇒ TOPCAT trial36: In patients with HFpEF, no diff in death from cardiovascular causes, aborted cardiac arrest, or hospitalization for the management of heart failure @ 3.3 years in spironolactone vs. placebo (18.6% vs. 20.4%, p=0.14) ● Check renal function at 3 days, 1 week, and monthly x 3 months after initiating therapy. K-sparing Diuretics Spironolactone (PO) Eplerenone (PO) Amiloride (PO) Triamterene (PO) Metabolism/excretion Hepatic/renal Hepatic/renal Hepatic/renal Hepatic Onset of action 1 day 1.5 hours < 2 hours 2-4 hours Duration of action 3-5 days 24 hours 6-24 hours 8-12 hours
HEART FAILURE Hydralazine/Nitrates ● Benefits: ↓ afterload, ↓ mortality in African-Americans ● Indications: African-American patients with ↓ LVEF and NYHA III-IV ⇒ A-HeFT31: ↓ mortality (10.2% vs. 6.2%, p=0.02) at mean follow-up of 10 months ● Contraindications: PDE-inhibitors (ex. sildenafil) Loop Diuretics ● Benefits: ↓ JVP, ↓ pulm edema, ↓ peripheral edema, ↑ CO, ↑ exercise tolerance ● Mechanism of action: Inhibit Na-K-Cl transporter at the luminal side of ascending Loop of Henle. ○ ↑ FENa 20-25%, ↑ free H2 O clearance, effective GFR < 40 ○ Furosemide also has unique venodilatory effect; may explain effect in pulmonary edema7 ● Pharmacokinetics: protein-bound and secreted (not filtered). Must reach lumen to exert effects. ○ In AKI/CKD, organic anions compete for secretor channels, ↓ drug delivery. ○ Need to be dosed BID to avoid rebound sodium retention ● Indications: ○ Acute decompensated heart failure ⇒ Small Cochrane meta-analysis showed mortality benefit (10.7% vs 2.8%) at 4-14 weeks4 ⇒ DOSE trial9: Bolus vs. gtt, No difference in symptoms @ 72 h. ● However, they did not give an initial load before starting the drip ○ Chronic heart failure ⇒ ↓ readmission rate (17% vs 32%) for HF with torsemide vs. furosemide at 1 year11 ● Contraindications: Hypotension, ototoxicity (worst w/ethacyrinic), sulfa allergy (except ethacrynic) Loop diuretics8 Furosemide Bumetanide Torsemide Ethacrynic Acid Bioavailability (%) 10-100 (avg 50) 80-100 80-100 ~100 Equipotent dose 80mg PO/ 40mg IV 2 mg 40 mg 100 mg Affected by food Yes Yes No No Metabolism 50% renal 50% hepatic 80% hepatic hepatic Onset (PO) 30-60 min 30-60 min 30-60 min 30-60 min Onset (IV) 5 min 2-3 min unavailable 5 min t1/2 (healthy) 1.5-2 h 1 h 3-4 h 1 h t1/2 (heart failure) 2.7 h 1.3 h 6 h unavailable
Mark Tuttle 2014
HEART FAILURE
Mark Tuttle 2014
Thiazide diuretics ● ↑ FENa 5-10%, ↓ free H2O clearance, ineffective at GFR < 40, greater antihypertensive effect ● Indications: Progressive resistance of loop diuretics ○ Sequential nephron blockade10: Combination w/loop ↓ chronic adaptations of nephrons.
Thiazide diuretics Equipotent dose Metabolism/excretion Onset of action Duration of action
HCTZ (PO) 25 mg Renal 2 hours 6-12 hours
Metolazone (PO) 2.5 mg 80% renal 1 hour 24 hours
Chlorthalidone (PO) 25 mg Renal 2-6 hours 24-72 hours
Chlorothiazide (IV) 250 mg Renal 15 min 6 hours
Aquaretics: conivaptan, tolvaptan ● Benefits: ↓ body weight, ↑ serum sodium ● Mechanism of action: Vasopressin receptor antagonists, inhibit reuptake of water in collecting ducts ● Indications: Hyponatremia despite water restriction and risk of cognitive impairment (AHA 2013) ⇒ EVEREST trial29: tolvaptan vs. placebo, no mortality benefit ● Dosing: ○ Conivaptan: 20mg IV x 1, then 20-40mg over 24 hours, or 20-40mg PO BID ○ Tolvaptan (PO): 30-90mg QD Digoxin ● Mechanism of action: Inhibits Na-K ATPase ○ ↑ inotropy ○ Sensitizes vagal afferent fibers, ↓ symp outflow. ○ ↓ renal sodium reabsorption ● Benefits: ↓ symp outflow, ↑ inotropy, ↓ symptoms, ↓ hospitalizations for ADHF ● Indications ○ Stages B-D: Consider use in patients with current or prior symptoms and ↓ LVEF (AHA 2013, IIa) ⇒ DIG trial15: Digoxin vs. placebo. ↓ hospitalization (27% vs 35%) @ 2-5 years. No mortality benefit. ○ Comorbid atrial fibrillation as a rate control agent ● Bottom line: Improves symptoms, reduces hospitalizations, but no effect on mortality ● Caveat: There may be ↑ mortality risk in women and outside the narrow therapeutic window (> 0.8 ng/ml) Calcium Channel Blockers ● Amlodipine ○ The only CCB to have a neutral effect on mortality in HF (PRAISE)21. ○ Can be used for comorbid stable angina, hypertension Inotropes1 ● Benefits: ↑ CO, ↑ tissue perfusion ● Indications (AHA 2013) ○ Cardiogenic shock ○ Bridge to transplant or mechanical cardiovascular support (ex. LVAD) ○ Palliative
HEART FAILURE Drug Dopamine
Dobutamine Milrinone
Dose mcg/kg/min 0.2-2 “renal” 2-5 5-10 2.5-5 5-20 0.125-0.75
Mark Tuttle 2014
Mechanism D1, D2 β1, D1 β1, α1 β1, β2 β1, β2 , α1 PDE3 inhibitor
t½ 2-20 min Increased 2-3 min 2.5 hours
CO ↑ ↑ ↑ ↑ ↑
HR ↑ ↑ ↑ ↑ ↑
SVR PVR Adverse effects ↓ - Tissue necrosis, arrhythmia (AF, VT) ↑ ↓ - Hypersensitivity ↓ ↓ ↓ BP, renally dosed
CARDIAC RESYNCHRONIZATION THERAPY ● ●
●
Pathophysiology: When the LV septum and free wall contract dyssynchronously (ie. one wall contracts and begins relaxing as other wall contracts), cardiac output is impaired. How it works: Pacer leads in venous system placed in RV (near septum) and coronary sinus (toward LV free wall) and paced synchronously. Patient should have intrinsic sinus pacemaker suppressed with beta blockers to increase effectiveness of CRT. Goal should be pacing > 90% of the time. Indications (AHA 2013) ○ Optimal medical therapy, NYHA III-IV, LBBB, LVEF < 35%, QRS > 150 ○ As above, but QRS ≤ 150 AND have echocardiographic evidence of dyssynchrony ⇒ Echocardiography Guided Cardiac Resynchronization Therapy (EchoCRT) trial17 showed that CRT in patients with QRS <130 did not reduce mortality, or hospitalization for heart failure.
MECHANICAL CARDIOVASCULAR SUPPORT: See advanced heart failure chapter SOURCES 1. Writing Committee, M., et al. (2013). "2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines." Circulation 128(16): e240-319. 2. Pitt B, et al. "The effect of spironolactone on morbidity and mortality in patients with severe heart failure". New England Journal of Medicine. 1999. 341:709-717 3. Pitt B, et al. "Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction". The New England Journal of Medicine. 2003. 348(14):1309-21. 4. Diuretics for heart failure (Cochrane Review). Cochrane Database Syst Rev. 2012 Feb 15;2:CD003838 5. Pfeffer MA, et al. "Effect of Captopril on Mortality and Morbidity in Patients with Left Ventricular Dysfunction after Myocardial Infarction — Results of the Survival and Ventricular Enlargement Trial". The New England Journal of Medicine. 1992. 327(10):669-677. 6. Yusuf S, et al. "Effect of Enalapril on Survival in Patients with Reduced Left Ventricular Ejection Fractions and Congestive Heart Failure". The New England Journal of Medicine. 1991. 325(5):293-302. 7. The acute vascular effects of furosemide in heart failure. Br J Clin Pharmacol. 2000 July; 50(1): 9–13 8. Wargo KA, Banta WM. A comprehensive review of the loop diuretics: should furosemide be first line? Ann Pharmacother. 2009;43:1836-47. 9. Felker GM, et al. "DOSE: Diuretic strategies in patients with acute decompensated heart failure". The New England Journal of Medicine. 2011. 364(9):797-805. 10. Update in Diuretic Therapy: Clinical Pharmacology. Semin Nephrol 31:483-494. 11. Open-label randomized trial of torsemide compared with furosemide therapy for patients with heart failure. Am J Med. 2001 Nov;111(7):513-20. 12. Heart Failure Society of, A., et al. (2010). "HFSA 2010 Comprehensive Heart Failure Practice Guideline." J Card Fail 16(6): e1-194. 13. Fagerberg B, et al. "Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure". The Lancet. 1999. 353(9169):2001-7. 14. Packer M, et al. "Effect of Carvedilol on the Morbidity of Patients With Severe Chronic Heart Failure". C irculation. 2002. 106(17):2194-9.
HEART FAILURE
Mark Tuttle 2014
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