Congestive Heart Failure -- ie, CHF
    Source: NEJM, and MAYO reviews (attached) and MKSAP16 

    Definition

    • A complex clinical syndrome, resulting from almost any cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.

    Etiology

    Two forms:

     

    Reduced Ejection Fraction

    • Impaired LV contraction reduces LVEF (<40%) and decreases flow.  

      • Echo Grading:
        •  

          Left Ventricular Ejection Fraction (LVEF)

          • Grade I (EF >60%) Normal
          • Grade II (EF = 40-59%)
          • Grade III (EF = 21-39%)
          • Grade IV (EF ≤ 20%)

           

      • Best Tests for evaluating Ejection Fraction:
        • Cardiac MRI
        • Nuclear Imaging
        • Echocardiography (most common)
        • Contrast Ventriculogram

     

    • Causes: 

      • Ischemic (CAD) 

      • Non-ischemic (HTN, DM, EtOH, myocarditis, dilated cardiomyopathy, anthracycline chemo)

    Preserved Ejection Fraction

    • Definition:
    • Often called HF-PEF - Heart Failure with Preserved Ejection Fraction
    • HF in setting of normal EF --> almost always assumed to be diastolic HF.
    • Now recognized as a broader condition (not just poor relaxation), but other factors such as cardiorenal interactions  and miscmatch between ventricular and arterial impedance.  (causes may not be specific to the heart)
    • Diastolic Dysfunction:

      • Asymptomatic patient with LVH and Echo findings of normal LVEF, abnormal LV filling.

    • Diastolic Heart Failure

      • Clinical syndrome of heart failure (volume overload, dyspnea, exertional intolerance) is associated with evidence of diastolic dysfunction (by cardiac catheterization, echo, or cardiac biomarkers).

     

    • Mechanism:

      • Abnormal relaxation of the LV causing decreased ventricular filling.

      • LV Diastolic Pressure curve shifted up and left:

      • Diastolic Heart Failure.png

      • Relatively small increase in central venous blood volume or venous tone / arterial stiffness can cause in increased left atrial and pulmonary venous pressures --> ACUTE PULMONARY EDEMA.

      • Large percentage of diastolic heart failure patients have LOW STROKE VOLUME and a reduced CARDIAC OUTPUT despite NORMAL EJECTION FRACTION.

        • Cannot increase cardiac output during exercise.

        •  

          Alternative explanation is that cardiac output is normal because the body retains salt+water to maintain high diastolic filling pressures, to keep a normal cardiac output.  Rapid diuresis can cause hypotension as the filling pressure drops, the heart rapidly drops output. 

    • Incidence: (33-55%) (About 1/3 of HF have diastolic dysfunction)

      • Incidence increases in age and higher in women.

    • Causes:

      • Increased resistance of diastolic filling:

        • Intrinsic to myocardium:

          • Myocardial hypertrophy (HTN, Aortic stenosis, hypertrophic cardiomyopathy)

          • Fibrosis,

          • Ischemia

          • Iniltrative cardiomyopathies such as amyloidosis

        • Extrinsic to myocardium:

          • Acute mitral regurgitation

          • Constrictive pericarditis

          • Pericardial effusion

          • Mechanical Ventilation

      • Risk Factors: older age, female, HTN, obesity, DMII, CAD, CKD.

    • Considerations:

      • Exercise Intolerance due to:

        • 1. Elevated pulmonary pressure --> Decreased lung compliance.

        • 2. Inadequate cardiac output during exercise --> fatigue of legs and accessory respiratory muscles.

      • Aggressive diuresis can result in serious hypotension in pts with diastolic heart failure due to steep curve for LV diastolic pressure/volume.

      • Tachycardia reduces ventricular relaxation time and filling time --> increasing diastolic pressure --> and worsens hypotension/HF.  (Esp if new onset rapid Afib)

        • Control rate.

      • BNP is lower compared to systolic heart failure.

     

    • HFPEF.png

     

     

    • Management Points:

     

    • 1. Acute: Reverse consequences of diastolic dysfunction:
      • Diuretics (Reduce pulmonary venous congestion).
      • Pulmonary edema:
        • Oxygen
        • Morphine
        • Parenteral diuretics
        • Nitroglycerin
      • If HTN and not responding --> IV nitroprusside (or nitroglycerin if myocardial ischemia)
        • (1-50 ug/min - venous vasodilation, >50 ug/min - arterial vasodilation)
      • Treat tachycardia
        • B-blockers or non-dihydropyridine CCB (no data to support either).
    • 2. Long-Term:  Reduce/Eliminate factors responsible
      • 1. B-blockers or rate-lowering CCB (slow rate)
      • 2. Diuretics (to control/prevent edema)
      • 3. ACEi (treat hypertension and maybe regress LVH)
      • 4. Treat Ischemia (??)
         
      • Literature Summary (based on NEJM 2004 revew)
        • Very little literature as of 2013.  Some evidence of candesartan (CHARM-Preserved study).
          • Candesartan --> fewer hospitalizations, weak evidence of improving cardiac death.
        • Some studies: CCB and ACE/ARB may improve exercise tolerance in HTN +/- CAD patients.
        • Another study: Treatment with propranolol --> decreased mortality.
        • PCI:
          • ONLY if ischemia is a significant contributor.  However, high HF recurrence rate.  Tell us that diastolic heart failure has likely a combination of ischemic/non-ischemic causes.
    • -------------------------------------------------------------------
    • Another approach to diastolic HF management is:
      • 1. Aggressive BP control
        • (systolic and diastolic) control to prevent further hypertrophy.
      • 2. Coronary Revascularization
        • (only if CAD b/c myocardial ischemia can cause impaired relaxation)
      • 3. Control of ventricular rate
        • (esp if arrhythmias to increase ventricular filling time and coronary perfusion)
      • 4. Control of fluid overload
        • (while being cautious of dose b/c diastolic HF pts are sensitive to preload reduction). 

    Causes

    • Systolic Dysfunction Diastolic Dysfunction
      • Coronary Disease
      • Cardiomyopathies
        • Viral Syndrome
        • Other Infections
        • EtOH, cocaine
        • Chemotherapy
        • Connective Tissue Disease
      • Endocrinopathies
        • Nutritional Deficiencies
      • Valvular Disease
        • Aortic regurgitation
        • Mitral regurgitation

       

      (See CAUSES for additional approach)

      • Hypertension
      • Ischemia (heart can't relax)
      • Cardiomyopathies
        • Restrictive
        • Hypertrophic
      • Valvular Disease
        • Aortic stenosis
        • Mitral stenosis
      • Pericardial Disease

        (See CAUSES for additional approach)

     

    5 most common causes of heart failure:

     

        (1) Coronary Artery Disease
        (2) HTN
        (3) Idiopathic
        (4) valvular
        (5) Alcohol

     

    Clinical Features:

     

    • Dyspnea
    • Edema
    • Ascites
    • Orthopnea
    • PND
    • Fatigue, weakness
    • Resting sinus tachycardia
    • Narrow pulse pressure
    • Diaphoresis
    • Increased JVP
    • Pulsus alternans (pathognomic of LV failure)

     

    • None of the signs are very sensitive or specific.  A few notes:
      • Pulmonary crackles: (higher sensitivity)
      • S3 gallop (most specific)
      • JVP distension, Ascites (also quite specific).
      • HJR (Hepatojugular reflux) - also very specific but insensitive.

     

     

    NYHA Functional Class

    • NYHA Class  
      Class I No Limitation - (ordinary physical activity does not cause symptoms of HF)
      Class II Slight Limitation w/ physical activity - (comfortable at rest, ordinary physical activity results in symptoms)
      Class III

      Limited ordinary activities - (marked limitation of ordinary activity; less than

                                                 ordinary physical activity results in symptoms)

         (IIIA - symptoms with less than ordinary activity

         (IIIB - symptoms with minimal exertion)

      Class IV

      Unable to carry on any physical activity without symptoms

         (inability to carry out any physical activity without discomfort, symptoms may be present at rest)

     

    Investigations:

     

    • Electrolytes, BUN, Creat, Glucose, Mg, Fasting Lipids, CBC, Albumin, Uric Acid
      • Liver Chemistries, Urinalysis, thyroid function studies. 
      • BNP (helps distinguish HF from lung pathology like COPD) [lack of sensitivity of physical exam findings].
        • If <100 (excludes HF)
        • But chronic HF can have normal up to 500.
        • Currently studied if BNP monitoring helps titrate medications
    • ECG (Prior MIs, rapid HR, low voltage [effusion/emphysema/obesity?], ventricular dyssynchrony, QT interval)
    • CXR (pulmonary edema? often lymphatics get better in chronic HF, less pulm. edema).
    • Echocardiography --> essential for HF, and etiology. (+ prognostic information)
      • Distinguishes types of HF (Preserved-Systolic or Systolic dysfunction)
      • Valve abnormalities
      • Infiltrative causes
    • Echo Grading:
      • Grade I (EF >60%) Normal
      • Grade II (EF = 40-59%)
      • Grade III (EF = 21-39%)
      • Grade IV (EF ≤ 20%)
    • Execise tsting, Cardiac MRI (best method for ejection fraction).
    • Ischemic testing:
      • Sometimes a reversible cause of LV systolic dysfunction. 
      • Angiography - if high pre-test probability of CAD.
      • In first-time HF, angiography may be reasonable (if no prior assessment).

     

    Principles of prevention:

    1. symptomatic measures (elevate head of bed, oxygen in hospital)
    2. lifestyle measures (diet, exercise, DM control, smoking cessation, decrease ETOH, patient education, sodium and fluid restriction)
    3. multidisciplinary heart failure clinics for individuals at higher risk

     

    Precipitants of heart failure:

     

    • H-HTN
    • E-endocarditis/environment
    • A-anemia
    • R-rheumatic heart disease
    • T-thyrotoxicosis
    • F-failure to take meds
    • A-arrythmia
    • I-infection/ischemia/infarction
    • L-lung problems
    • E-endocrine
    • D-dietary indiscretions

     

    Principles of management:

    Acute treatment (symptoms):

    • L-lasix, 40-500mg IV
      • Lowest dose of diuretic to achieve edema-free "dry weight" is used.
      • Measure weights daily.
      • Can combine loop diuretic (lasix) with thiazide (metolazone), and aldosterone blocker (Spironolactone) for sequential nephron blockade, but need to carefully monitor electrolytes.
      • IV therapy REQUIRED due to decreased absorption secondary to bowel edema.
    • M-morphine 2-4mg, IV
    • N-nitroglycerin.. options:
      • nitro spray 0.4 mcg/spray 3x q5min until pain disappears
      • nitroglycerin patch 0.4 mg/hr SC (q12h otherwise tachyphylaxis develops)
      • nitroglycerin infusion
        • (1-50 ug/min - venous vasodilation, >50 ug/min - arterial vasodilation)
      • nitroprusside (0.3-2 ug/kg/min) - more potent vasodilator, but issue with cyanide toxicity (do not use in CAD, can produce coronary steal syndrome).
    • O-oxygen
    • P-positive airway pressure (CPAP/BiPAP)
    • P-position (sit up with legs hanging down)

     

    • Diuretic therapy is key to acute HF
    • Sometimes higher doses of lasix required and a synergistic agent such as metolazone.
    • Ultrafiltration
      • Lower rate of recurrent hospitalization
    • If Hyponatremia develops, can use two ADH-antagonists:
      • conivaptam (non-selective V1a/V2a receptor blocker).
      • Tolvaptam (oral V2a receptor blocker)
        • They do help hyponatermia, but unknown if helps outcomes. 
        • Usually in HF and very severe hyponatremia (often feel better)

    Chronic treatment:

    Conservative measures

    1. symptomatic measures (elevate head of bed, oxygen in hospital)
    2. Lifestyle (diet, exercise, DM control, smoking cessation, patient education, sodium & fluid restriction)
      • Studies show exercise effective.  However intensive intervetions were used.
    3. Daily Weights + double diuretic dose + call MD if acute increase in weight > ****

    Pharmacological

    1. ACE Inhibitors (1st line).  ARBs (2nd line)
      • Hemodynamic benefit: afterload reduction + neurohormonal benefit (blocks RAAS)
        • Reduces risk of death by 30-40% in CHF vs. placebo. (progressive HF).
        • Reduces rate of hospitalization, progression of LV dysfunction, and development of LV dysfunction after MI.
        • High dose vs. low dose has not been shown to affect survival (but reduces hospitalizations!)
      • Initiate at diagnosis, continue indefinitely.
      • All patients with decreased systolic function should be on ACEi regardless of cause.
      • Benefits:
        • Reduce ventricular size
        • increase ejection fraction
        • Reduce symptoms.
        • Decrease MI risk
        • CONSENSUS & SOLVD Trials: Enalapril: (with diuretics + digoxin) => less hosp admission, RRR for death was 16-40%.
        • 1992 Trial: Enalapril reduced risk of heart failure in pts with systolic dysfunction but NYHA Class I.
      • All ACEi appear to work, not drug specific! (unlike B-blockers)
    2. Angiotensin Receptor Blocker
      • Efficacy similar to ACE (based on single candesartan trial CHARM-Alternative)
      • Generally: Mortality benefit comparable to ACEi
      • Less ACEi cough, and other S/E, but more expensive.
      • Two (placebo, randomized) trials - valsartan or candesartan addition (to ACE and B-blocker) in patients who are still symptomatic (NYHA II-IV) despite optimal therapy decreased hosp for HF by 17-22%, and CVS mortality by 16%.
      • ARBs are non-inferior to ACEi in all-cause mortality  or hospitalizations. 
      • ARBs + ACEi studied (better RAAS blockade), but found higher renal failure, hyperK, etc..
    3. Beta-Blockers
      • (At one point considered a contra-indication for heart failure, but now known benefit!!)
      • Along with ACEi, they are also FIRST LINE regardless of systolic dysfunction cause.
      • Benefits:
        • Reduces symptoms.
        • Increases ejection fraction by 5-10%.
        • Reduces hospitalizations
        • Reduces mortality by 34% (when added to ACEi, digoxin, diuretic in NYHA II-IV).
          • Reduces both sudden death and from HF.
      • Notes:
        • Do not start in acute decompensated HF.  Start before leaving hospital.
        • If already on B-blocker, do not discontinue (unless hemodynamic instability).
        • Advise patients of fatigue that may last days to weeks until they adapt.
      • NOT All b-blockers work.
        • Survival Benefit: metoprolol, bisoprolol (renal/hepatic clearance), carvedilol (for stable CHF only).
        • B-blockers that don't work: xamoterol, bucindolol (both have intrinsic sympathetic activity).
    4. Aldosterone Antagonists
      • Spironolactone
        • See RALES trial (below).  30% reduction in mortality with severe systolic HF (Class III IV) in addition to diuretic, digoxin, and ACEi.
        • Careful in renal failure!!! (excluded Cr > 221)  Risk of hyperkalemia.  Risk higher if K+ > 4.5.
        • NOTE: Adding to ACE inhibitor: Either Aldosterone antagonist or ARB, but not both!!! (+++ AKI, hyperkalemia)
      • Eplerinone
        • Specific aldosterone antagonist.
        • No gynecomastia, mastaglia.
      • Now indicated for:
        • NYHA III-IV
          • And probably for NYHA class II with LVEF ≤35%
        • Serum K+ < 5 mEq/L
        • Serum Creat < 221 (<2.5mg/dL)
    5. Hydralazine and Isosorbide Dinitrate
      • Used in African-American patients (on top of other therapies)
      • ACEi aren't as effective in blacks, but hydralazine and Isosorbide Dinitrate worked better (than in whites).
      • AA-HFT Study: hydralazine-isosorbide dinitrate added to ACEi, BB, and (sometimes) aldo antagonist in black patients with NYHA class III or IV (and on maximal medical therapy)
        • reduced rate of hospitalization for HF
        • improved quality of life
        • increased survival.
      • Mechanism: alters oxygen deliver to myocardium (antioxidant effects)
    6. Others: Digoxin
      • Trial: Digoxin, added to diuretic, ACEi, no effect on mortality but reduced rate of hosp for HF by 28% and reduced symptoms.
        • Withdrawal of digoxin in stable patients can precipitate heart failure decompensation.
        • When used to treat heart failure, digoxin should be dosed at low levels (serum level 0.5-0.8 ng/mL).
          • (most labs say theraputic range is 1-2)
        • Higher serum levels = increased risk for mortality.
        • Unlike ACE inhibitors and diuretics, digoxin is not useful in the treatment of patients with acutely decompensated heart failure.
        • Renally cleared and must be used with caution in patients with kidney disease.
      • Trial: 1g of n-3 polyunsaturated fatty acid /day --> small reduction in CVS complications & death.
      • Aspirin, Statin, erythropoesis-stimulators are of uncertain benefit..
      • Harmful: thiazolidinediones, NSAIDs, antiarrhythmics
      • Pneumococcal/Influenza vaccinations recommended.

     

    HeartFailureTargets.png

     

    Devices

    • Implantable Cardioverter-Defibrillator (ICD)
      • 50% of pts with HF die of arrhythmias while the other 50% die from pump failure.
      • Study: ICD implantation, no quality of life difference, but survival benefit after 1 year.
      • Indications/Guidelines:
        • Secondary prevention: patient survives and unprovoked Vfib or sustained Vtach.
        • Primary prevention in
          • EF ≤35% (ischemic or non-ischemic) with NYHA class II-III symptoms.
          • EF ≤30% (ischemic) and NYHA class I-III symptoms
        • (pts in NYHA class II-III with ejection fraction <35% or less despite optimal medical therapy, and expected to survive >1yr with reasonable QOL.)
    • Cardiac-Resynchronization Therapy
      • Potentially correctable problems in HF patients:
             Intraventricular conduction delays QRS >120msec common (1/3 of all systolic function pts) --> dyssynchronous contraction of LV, --> impaired emptying in some pts + mitral regurgitation.
      • Causing Asynchronous contraction of left ventricle --> impaired emptying, mitral regurg.
      • Abnormal A-V coupling (prolonged PR).
      • How?
        • Two leads placed into LV (one on lateral side and the other on septal aspect)
        • Provides simultaneous depolarization of LV
      • Studies: Pts with severe heart failure reduced symptoms, improved functional capacity, reduction in hospitalizations for HF, increased survival.
      • Indications/Guidelines:
        • Pts with SEVERE symptoms NYHA Class III - IV while optimal medical therapy.
        • Ejection fraction < 35%
        • Sinus rhythm
        • LV dys-synchrony on EKG (QRS >120ms)
      • Canadian Guidelines:
        • ​NYHA-II, EF <30%, LBBB+QRS >150ms  
        • Trials: MADIT-CRT-D, RAFT, CARE-HF        
    • ​LV Assist Devices (LVAD)
      • Indications:
        • Awaiting recovery from cardiogenic shock (i.e. Bridge to transplantation).
        • Destination therapy (implanted lvad?)
    • SystolicHFalgorithm.png

    Cardiogenic Shock

    • See Cardiogenic Shock Section
    • Key point: if systemic BP tolerable, use vasodilator-inotropes such as dobutamine and milrinone
    • Key point: if systemic BP is low: use vasoconstrictor inotropes such as dopamine and levophed.

     

    Anticoagulation

    • Warfarin was historically used in very low EF HF.
    • Recent RCT: Warfarin added to very low EF HF --> lower risk of thrombotic and ischemic events, but higher bleeding risk.
      • No literature supporting the use, no longer added to HF therapy without another indication.

    Contraindications

    • Calcium channel blockers (negative inotropes) - no outcomes benefits, implicated in 13% more decompensations. (especially
      • Felodapine and Amlodipine - neutral effects on mortality in pts with systolic HF.  (can treat angina/HTN in CHF).

     

    Follow-up

    • Guidelines: Electroyltes, creatinine q6months.
    • Routine echocardiogram monitoring not indicated.
    • F/U with MD 1 week post-discharge = 10-15% reduction in all-cause readmission.

    Complications

    Cardiorenal Syndrome

    • Definition:
      • Cardiorenal Syndrome

        Worsening of renal function in patients with acute decompensated heart failure

      • Type 1: Cardiac dysfunction precedes renal impairment
      • Type 3: Renal impairment precedes cardiac dysfunction
    • Treatment:
      • Volume status optimization
      • Inotropic therapy
    • Studies:
      • CARRESS-HF - NEJM 2012 - Ultrafiltration vs. pharmacotherapy for cardiorenal syndrome
        • Pharmacotherapy was superior for preservation of renal function, lower adverse events
        • No difference in weight at 
      • Resources: Ronco et al JACC 2012

    Transplant

    • Symptoms of allograft vasculopathy in transplant pt:
      • Syncope
      • New Heart Failure
      • Reduced Exercise Tolerance
      • Dyspnea
      • varying degrees of heart block
      • (Do not experience angina)

    Specific Topics

    Role of Aldosterone Receptor Antagonists

    • Aldosterone
      • Associated with hypertension
      • Associated with :
        • Myocardial and vascular remodeling
        • Increased collagen deposition
        • Increased myocardial stiffness
        • Hypokalemia
        • arrhythmia.
        • Inhibition of nitric oxide synthesis
        • other effects on cerebral and renovascular actions.
      • Association between high aldosterone and increased mortality in heart failure patients.
      • Blocking ACE was thought to sufficiently inhibit aldosterone synthesis, but later shown to not be true.  There is "aldosterone escape", with incindence of 10-25%.   (made by endothelin stimulation, ACE-independent pathways of production). 
    • Aldosterone Receptor Antagonists:
      • Have been used in the past for ascites and heart failure in HUGE doses 200-400mg/day.
      • Since loop diuretics came out, were deemed more potent, and spironolactone has not been used.
    • New RALES and EPHESUS: (doses of 26mg were used).
      • RALES:
        • Spironolactone on morbidity and mortality in patients with severe heart failure. 
          • Included patients with severe heart failure, LVEF <35%, on ACE, loop diuretic, and digoxin.
          • End point: death from all causes:
          • Trial stopped early after 24mo b/c efficacious!
            • 30% reduction in risk of death. (less progressive heart failure, less sudden death)
    • Advantages:
      • Antihypertensive (even in dosages as low as 50 mg/d)
      • Fluid balance: promotes diuresis.
      • Less arrhythmias: reduces QT dispersion, imrpves.  Decreases frequency of PVC's, non-sustained ventricular tachycardias (shifts K+ and Mg+ into muscles)
      • Significant reduce in LVH in hypertension.
      • Improve cardiac remodeling in chronic post-infarction heart failure.
        • Decreases LV end-diastolic volume, increases ejection fraction, improves LV diastolic function.
      • Decreases inflammatory response to injury.
      • Better exercise tolerance.
    • Disadvantages in spironolactone:
      • Less potency than lasix
      • Perpetuates renal failure (23.3% had doubling of creatinine and 8.3% had serious hyperkalemia)
        • MUST MONITOR CREATININE!
        • Discontinue if creat >353 (in trial)
      • Hyperkalemia (8.3% had serious hyperkalemia).
        • Risk is higher in elderly, renal failure, and high baseline potassium.
        • MUST MONITOR POTASSIUM
          • Studies checked K+ at 1 week, 1 month, q3months x1 year, and then q6mo.
            • Decreased doses by 50% if hyperkalemic and discontinued if K+>6.
    • Practical indications (as per inclusion criteria)
      • Contraindicated of K+ > 5.5 or if CrCl < 30mL/min (RALES exclusion of Cr < 221)
      • Diabetic patients and elderly generally excluded (more vulnerable to adverse effects due to renal failure)
      • Usually start at dose 25mg/d and increase to 50mg/d after 8 weeks if heart failure progresses (after checking K+ and Creat)
    • Bottom line:
      • Use it in select patients, especially chronic CHF or post-infarction heart failure.  Careful with k+ and kidney function.

     

    B​-type Naturetic Peptide

    • Released from cardiac myocytes in response to elevated preload or afterload.

      - nt-ProBNP – N-terminal BNP is a precursor to BNP before it is cleaved.

      - Both elevated in increased ventricular loading.

    • Lower BNP than normal expected in:
      • Obesity (presence of naturetic peptide receptors in adipose tissue
    • Elevated BNP without HF:
      • CKD
      • Older
      • Women
      • Acute Increased Heart Workload: Acute MI, PE, tachycardia
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