1. Evan Hardegree, MD Cardiology Fellow, PGY-5
Congestive Heart Failure
Evan Hardegree, MD
Cardiology Fellow, PGY-5

2. Congestive Heart Failure
CHF is an imbalance in pump function in which cardiac output is inadequate to meet the body’s demands
CHF occurs when the heart cannot generate sufficient cardiac output to meet the needs of the body while maintaining low filling pressures

3. Impact of Heart Failure
Over 5.8 million people (2.6% of adults)
670,000 new cases annually in people >45
283,000 deaths annually with HF as cause or contributor
Most common Medicare discharge diagnosis
1.11 million hospitalizations with HF as first diagnosis
Total 3-4 million with HF as contributing diagnosis
Mean hospital stay >4 days

4. Rehospitalizations in CHF
Rehospitalizations in Heart Failure
Roger J Am Coll of Cardiol, 2009; 54: 1698

5. Estimated Costs of CHF in U.S.

6. Survival Following a 1st Admission For HF, MI and 4 Most Common Cancers
5 yr survival in HF patients compared with cancer patients following a first admisstion to any Scottish Hospital in 1991 for HF, MI and the 4 most common sites of cancer specific to women and men
From Stewart S et al, Eur Heart J 2001;3:315.
Stewart et al, Eur Heart J 2001;3:315.

7. “Effective arterial blood volume” (EABV)

8. RAAS: Renin-Angiotensin-Aldosterone System
Enhances the retention of sodium
Excretion of magnesium and potassium
Vasoconstriction
Increases myocardial energy requirements
Myocardial and vascular fibrosis
Parasympathetic inhibition
Baroreceptor dysfunction
Vascular damage and hinders arterial compliance

9. EF among CHF patients in Cardiovascular Health Study

10. HFrEF (systolic) vs. HFpEF (diastolic)
Systolic (HFrEF)
Diastolic (HFpEF)
EF <40%
EF >40-45%
Impaired contraction
Diastolic dysfunction
Most common causes: ischemic HD, HTN
Most commonly related to HTN and LVH

11. Clinical Management Establish Stage/Class Define LV function
Assess symptoms
Severity
Congestion vs low output
Define LV function
Consider etiologies
Tailored therapy

12. History and Physical Examination
Assessment of functional status
NYHA Class
Activities of daily living
Assessment of congestion or low output

13. New York Heart Association (NYHA) CHF Classification
Class I – no limitations
Class II - symptoms with routine activity (i.e., moderate exertion)
Class III - symptoms with less than routine activity (i.e., mild exertion)
Class IV - symptoms at rest

14. Stages of Heart Failure and Treatment Strategies

15. CHF: Symptoms Left heart Right heart shortness of breath (SOB) cough
dyspnea on exertion (DOE)
orthopnea
paroxysmal nocturnal dyspnea (PND)
Right heart
abdominal swelling
right upper quadrant (RUQ) pain
pedal edema
nausea
anorexia

16. CHF: Signs Left heart failure rales
dullness to percussion (pleural effusion)
S3, S4
holosystolic murmur (MR)
Right heart failure
JVD
right-sided S3, S4
holosystolic murmur (TR)
hepatomegaly
ascites
pedal edema

17. CHF: Signs Low output state tachycardia low blood pressure
narrow pulse pressure
cool, clammy extremities
cyanosis
somnolence, obtundation

18. Etiology & Risk Factors
Identify cardiac (e.g. CAD) or non-cardiac potential causes of heart failure
Risk factors for cardiovascular disease
HTN, DM, smoking, obesity, known CAD
Other risk factors for heart failure
Alcohol, cocaine, chemotherapy agents, radiation, family history, OSA, tachycardia, endocrine disease (pheochromocytoma, hypo or hyperthyroidism)

19. Initial Testing Serum labs (lytes, CBC, TFT, HgbA1c, BNP) 12-lead EKG
AP and lateral CXR
Echocardiogram
Assess LV ejection fraction
Assess valvular disease
Coronary angiography if presenting with ischemia or angina and CAD status unknown

20. Tx: Inotropes & Diurese
Hemodynamic Assessment
Congestion at Rest? No
Yes
Warm
& Dry
& Wet
Cool No
Low Perfusion at Rest?
No treatment
Tx: Diurese
Yes
Tx: Inotropes, IVF’s
Tx: Inotropes & Diurese

21. Treatment of Acute Decompensated CHF
Correct underlying exacerbating factors
Ischemia
Anemia
Infection
Arrhythmia
Acute valvular insufficiency/shunt

22. Initial Treatment of Acute Decompensated HF
Monitor O2 sat, V/S, telemetry, UOP, get basic labs
Supplemental O2 for hypoxia  NIPPV or MV if severe resp. distress, persistent hypoxia/resp acidosis
Give IV Diuretic (Lasix 40 to 80 mg IV)
If severely hypertensive  hydralazine, NTG gtt (20+ mcg/min)
If hypotensive AND signs of shock  consider inotropes (think ICU…), IABP
Think about etiology

23. Treatment of Acute Decompensated CHF
Monitor I&O’s, daily weights
Sodium/volume restriction
Diuretic – dosing based on response!!
Oxygen – may need NIPPV
Vasodilators/afterload reduction
Inotropes
Avoid beta blockers and vasoconstrictors
Control ventricular rate if atrial fibrillation present

24. Treatment of Acute Decompensated Systolic CHF
Diuretic (IV)
loop diuretic: furosemide (40-80mg), bumetanide (1mg) or torsemide (10-20mg)
chlorothiazide (500mg) or PO metolazone (5-10mg) for loop-diuretic resistance
Vasodilator/Afterload reduction IV
Nitroglycerin (5 to 10 mcg/min initially, ↑in increments of 5 to 10 mcg/min every 3 to 5 minutes as required and tolerated ; dose range mcg/min)
Nitroprusside
Oral
ACE (preferred)
ARB (for ACE intolerant pts)
Inotropic Agent
Milrinone
Dobutamine
Mechanical assist device (IABP, Impella or LVAD)

25. Treatment of Chronic CHF
Beta Blockers
ACEI or ARB
Diuretics
+/- Digoxin
+/- Inotropes
Fluid/salt restriction, education
Treatment of comorbidities

26. ACE Inhibitors lower morbidity and mortality
Angiotensin-converting enzyme (ACE) inhibitors partially inhibit the conversion of angiotensin I to angiotensin II, and also potentiate the effects of bradykinin by inhibiting its degradation. Multiple clinical trials have demonstrated the ability of ACE inhibitors to reduce mortality and HF hospitalizations in patients with reduced LVEF (Figure 1).2
The first three trials—the CONSENSUS (Effects of Enalapril on Mortality in Severe Congestive Heart Failure) trial,3 the SOLVD Treatment (The Effects of Enalapril on Survival in Patients With Reduced Left Ventricular Ejection Fractions and Congestive Heart Failure-Treatment) trial,4 and the SOLVD Prevention (The Effects of Enalapril on Survival in Patients With Reduced Left Ventricular Ejection Fractions and Congestive Heart Failure-Prevention) trial5—demonstrated benefit in patients with severely symptomatic HF, mildly to moderately symptomatic HF, and absence of clinical HF, respectively. The first two studies showed reduction in mortality by treating patients with enalapril; the last study showed a reduction in the HF hospitalization rate, with a trend toward reduced mortality. Subgroup analysis of the SOLVD trials suggested greater benefit in patients with lower baseline LVEF. As first demonstrated in the SAVE (Survival and Ventricular Enlargement Trial) trial, an investigation of the effects of captopril in patients with reduced LVEF following acute myocardial infarction (MI), ACE inhibitors also been demonstrated to prevent recurrent MIs.6
ACE inhibitors were the first agents shown to reduce the rate of progression of LV remodeling, as evidenced by diminishing or preventing the progressive LV dilation observed in patients following large MIs, and in those with reduced LVEF and LV dilation treated with placebo.7-11 These structural effects-with an alteration in the natural history of the myocardial remodeling process-are likely to play a role in mediating the clinical benefits observed with this class of agents and others.
Few studies have prospectively investigated the relative benefit of different ACE inhibitor doses. The largest trial, the ATLAS (Assessment of Treatment With Lisinopril and Survival) trial, compared low-dose lisinopril (2.5-5 mg daily) to high-dose lisinopril ( mg daily) in patients with HF and LVEF ≤30%.12 The results of this trial showed no difference in the primary endpoint of all-cause mortality, but showed favorability of other endpoints, particularly all-cause mortality or hospitalization for HF (although this endpoint was not prespecified).
Principal adverse effects of renal impairment, hypotension, and hyperkalemia are mediated by withdrawal of angiotensin II effects on the renal glomerular efferent arteriole (with resulting reduction in glomerular filtration pressure), the peripheral arterial bed, and the zona glomerulosa of the adrenal gland (with resulting reduction in aldosterone production), respectively. Slight worsening of renal function, mild blood pressure reduction, and slight increase in serum potassium levels are expected pharmacologic effects, and do not necessitate altering the therapeutic course. More severe changes require dose reduction or cessation of treatment. The frequent adverse effect of cough, and the unusual, but potentially life-threatening adverse effect of angioedema, are believed to be mediated by bradykinin and related substances.
The American College of Cardiology Foundation/American Heart Association (ACCF/AHA) 2009 Focused Update of the 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults, as well as the Heart Failure Society of America (HFSA) 2010 comprehensive heart failure practice guideline both recommend the routine use of ACE inhibitors in symptomatic and asymptomatic patients with HF and LVEF ≤40%.13,14 As with other classes of cardiovascular therapeutic agents, dosing recommendations generally follow the approach and target dose used in clinical trials showing outcome benefits.
Intolerance due to cough represents an indication to switch to an angiotensin-receptor blocker (ARB). Intolerance due to hyperkalemia, hypotension, or renal insufficiency, which does not respond adequately to dose reduction, is likely to be replicated by an ARB, and warrants consideration of switching to the combination of hydralazine and isosorbide dinitrate (ISDN). Development of angioedema warrants immediate discontinuation of the ACE inhibitor. ARB substitution should be considered, although rare cases (much less frequent than with ACE inhibitors) of angioedema have been reported with ARBs as well.
RRR
28%
38%
31%

27. ACE Inhibitors: HFSA Practice Guidelines

28. ARBs: HFSA Practice Guidelines

29. Beta Blockers in CHF – Types and Dosing

30. Beta Blockers in CHF Treatment
Metoprolol - ↓ mortality 34%
Beta Blockers in CHF Treatment
Bisoprolol - ↓ mortality 34%
Carvedilol - ↓ mortality 35%

31. Carvedilol Dose Dependency
Bristow et al. Circulation 1996.

32. Carvedilol vs. Metoprolol Succinate

33. Diuretics Recommended for fluid overload
Loops preferred over Thiazides
May add chlorothiazide or metolazone
Oral torsemide or bumetanide in those with bowel edema/ascites (better absorption)

34. Diuretics

35. Spironolactone: RALES Study
Entry criteria
NYHA III/IV
EF < 35%
ACE, loop diuretic, + digoxin
Primary endpoint - Mortality
Kaplan Meier analysis of the probability of survival in patients in the placebo and treatment groups in the RALES trial with spironolactone
At 36 months, mortality in the spironolactone treatment arm of the RALES trial was significantly less than that in the placebo arm, representing a relative reduction of 30% (relative risk 0.70, 95% CI, 0.60 to 0.82; P<0.001).
Pitt et al, NEJM 1999;341:709
AHA 1998

36. Digoxin
Consider in pts. with EF <40% & Class II-IV to improve symptoms
May improve resting rate control in Afib
Starting dose mg/day – ultimately dosed for body mass, renal function
Level <1.0 ( )

37. Summary Acute exacerbation: Chronic HF:
Diurese, fluid/salt restrict, afterload reduce
Think about etiology
Initiate/titrate meds as appropriate
Close F/U
Chronic HF:
Meds: ACE/ARB, BB, Diuretics, Spironolactone, +/-Digoxin, Hydralazine/nitrates in AA
Treat comorbidities (CAD, Afib, etc)