Congestive Heart Failure

- Mini-Lecture-Kristopher Huston MD, PGY2

Ali Ashtiani MD, PGY2Arash Taghavi MD, PGY1

Heart Failure-Definition“a complex clinical syndrome that can result

from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.”

HFrEF or Systolic HFEF<40%Aim of majority of therapies

HFpEF or Diastolic FailureEF>50%Exclusion of other noncardiac causes of symptoms

Definition

Classification Systems NYHA Functional Class

I: No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF (fatigue, palpitations, dyspnea or angina)

II: Comfortable at rest, slight limitation of physical activity III: Comfortable at rest. Marked limitation, less than ordinary

activity

causes discomfort IV: Discomfort at rest

ACCF/AHA Stages A = No structural heart disease, risk factors for HF B = Structural heart disease, no HF symptoms C = Structural heart disease, with prior or current HF symptoms D = Refractory HF requiring frequent interventions

The Major CausesCAD (~70% of cases)

Hypertension

Valvular disease

Diabetes Mellitus cardiomyopathy and progression of CAD

Less Common Causes Myocarditis

Tachyarrhythmia

Congenital Heart Defects (HOCM)

Cardiomyopathy Stress-induced Toxins: Drugs (Cocaine, Methamphetamine, Chemotherapy, Radiation),

Alcohol

Pulmonary: OSA

Rheumatologic: Sarcoidosis, SLE

Infiltrative: Hemochromatosis, Amyloidosis

Chronic Disease DM, HIV, Thyroid Disorders

How patients present

Clinical SymptomsDyspnea (100% sensitivity)PNDSwelling/Dependent edema Fatigue, Weight gain

Risk Factors:Obesity, smoking, physical inactivity, lower

socioeconomic status factors.

Physical Exam Pulmonary: Respiratory distress, Rales

Cardiac: Bradycardia/Tachycardia, Displaced PMI, JVD, S3 gallop rhythm.

Abdomen: Ascites, Hepato-jugular Reflux

Extremities: cool, dependent edema, cyanosis, pallor

DiagnosisEKG (check for MI, PE, Arrhythmia, LVH)

CXRPulmonary venous congestion, interstitial edema Cardiomegaly, pleural effusions

LabsCBC, CMP, Troponin, ABG, Thyroid function tests

Echocardiography: evaluate severity, causes, characterization

Coronary Angiogram in setting of STEMI/NSTEMI

DiagnosisBNP, NT-proBNP

Equally good sensitivity/specificity in diagnosing CHF BNP = < 100 unlikely CHF and > 400 likely CHF Increases with age, renal disease/arrhythmia, sepsis,

CAD, Women, African-Americans Decreased in obesity In acute HF, predictor of mortality and cardiovascular

events when >200. Limited evidence in serial monitoring in outpatient

setting Support clinical decision making Establish prognosis and disease severity

Management Lifestyle Modification

Vaccines: Pneumococcal and Flu Low Sodium (<2-3 g daily) Alcohol and Tobacco cessation Medications to avoid

NSAIDs (reduce GFR, worsen response to diuretics and ACE) Recommended to use ASA only for CAD Thiazolidinedione (fluid retention), Metformin (increased risk for LA) Phosphodiesterases (PDE3 and 4, data for PDE5 is not as convincing)

MORTALITY REDUCTION! ACE-I/ARB, Beta-Blocker, Aldosterone Antagonist, Hydralazine

plus Isosorbide Nitrate

ManagementACE-Inhibitors

Decrease MORTALITY and hospitalizations

Initial baseline treatment in all patients with heart failure, regardless of NYHA classEnalapril Initial: 2.5 mg PO BID (Target:10-20 mg

BID)Captopril Initial: 6.25 mg PO TID (Target: 50-100mg

TID)Lisinopril Initial: 5 mg PO Daily (Target: 20- 40 mg

Daily)

**ARB’s have comparable mortality reduction, used when ACE-I not tolerated**

ManagementBeta-Blockers

These BB decrease MORTALITY in patients with heart failure who already are taking an ACE inhibitor and/or a diuretic. start low and go slow (double every 2-4 weeks)

Coreg 3.125 mg PO BID (Target: 25 to 50 mg BID) Metoprolol Succinate 12.5 mg PO daily (Target: 200 mg daily) Bisoprolol 1.25 mg PO daily (Target: 5 to 10 mg PO daily) COMET (2003): NYHA classes II-IV treated with Coreg had greater

reduction in mortality than those treated with metoprolol, although hypotension was increased in Coreg group

Relative Contraindications Symptomatic Hypotension or pressor requirement HR < 60, 2nd or 3rd degree AV block, PAD with ischemia

ManagementAldosterone receptor antagonist

(Spironolactone)NYHA Class II-IV, LVEF of 35% or less

Reduce morbidity and mortalityMonitor renal function, BMP

Creatinine 2.5mg/dl or less Potassium 5.0 mEq/L or less

Hydralazine and Isosorbide African Americans. NYHA Class III-IVOptimal ACE-I and BBReduce morbidity and mortality

ManagementDigoxin

Symptom relief in absence of arrhythmias decreases hospitalization

Diuretics improve the symptoms and exercise tolerance

Anticoagulation In the setting of Afib and additional cardio-embolic

risk factors

ManagementFish Oil

Conflicting evidence for this, however, not harmfulConsider 1g daily supplementation with OTC

StatinsNo evidence for benefit in CHF

CCBPeripheral vasodilators (Amlodipine, Felodipine)

safe to use in HFNo benefit, and possible harm, with Diltiazem or

Verapamil like drugs

Management ICD

Primary Prevention Prior MI (<40 days) and EF <30% NYHA Class II, EF <35% Have been on maximal medical therapy > 3 months Syncope with structural heart disease and sustained VT/VF on EP

study

Cardiac Resynchronization GRADE 1A Indication

1. SR, QRS > 150 ms, LBBB, EF < 35%, NYHA > III with optimal therapy

GRADE 1B Indication 1. SR, QRS > 150 ms, LBBB, EF < 30%, NYHA > II with ICD

placement

Nonpharmalogic Treatment

Multidisciplinary ApproachPatient education and instruction

Appropriate hospital follow-up (within 7 days)Management of comorbidities Decreases hospitalizations and quality of life

Moderate Exercise in chronic stable HFDecrease mortality Improves hospitalizations and quality of life

References KING, M, KINGERY, J and CASEY, B. “Diagnosis and Evaluation of Heart Failure” Am Fam

Physician. 2012 Jun 15;85(12):1161-1168.

MCCONAGHY, J. “Outpatient Treatment of Systolic Heart Failure” Am Fam Physician. 2004 Dec 1;70(11):2157-2164.

Nishimura, RA et al. “2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.” Circulation. 2014 Jun 10;129(23):2440-92. doi: 10.1161/CIR.0000000000000029. Epub 2014 Mar 3.

MKSAP Question 1A 74-year-old man is evaluated in the emergency department for a 7-day history of progressive exertional dyspnea associated with a dry cough, increasing orthopnea (from two to four pillows), and inability to buckle his belt. He has a 20-year history of hypertension treated with diltiazem.

On physical exam, blood pressure is 162/86 mmHg, pulse rate is irregularly irregular at 84/min, and respiration rate is 18/min. Estimated central venous pressure is 14 cm H2O. Cardiac examination reveals an irregularly irregular rhythm and an S4. Bibasilar crackles are heard on auscultation of the lungs. His liver is enlarged 2 cm below the costal margin. His extremity examination reveals bilateral pitting edema.

Serum electrolyte levels and kidney function tests are normal. Serum B-type natriuretic peptide level is 2472 pg/mL. ECG shows atrial fibrillation. Echocardiogram shows a left ventricular ejection fraction of 60%, septal wall thickness of 1.5 cm, and posterior wall thickness of 1.4 cm. Chest radiograph shows hazy bilateral infiltrates.

Which of the following is the most appropriate next step in management?

(A) B-Blocker

(B) Cardioversion

(C) Furosemide

(D) Spironolactone

Manage heart failure with preserved ejection fraction with diuretics.

Answer: C Furosemide

This patient should be admitted to the hospital and given IV furosemide. His presentation is characteristic for heart failure with preserved ejection fraction (HFpEF). He has volume overload manifested by increasing abdominal girth, increased exertional dyspnea, and progressive orthopnea. His left ventricular ejection fraction is normal, but he has mild left ventricular hypertrophy and a long history of hypertension. Additionally, he has a markedly elevated B-type natriuretic peptide level. The etiology of his acute exacerbation into heart failure is most likely acute atrial fibrillation, but because he is already on diltiazem and has a normal heart rate, he may have been in atrial fibrillation for some time and not noticed it.

In contrast to patients with a reduced ejection fraction, no drugs have been shown to reduce mortality rates in patients with HFpEF. Instead, guidelines emphasize controlling blood pressure and volume. Patients with HFpEF are often volume sensitive, and careful use of diuretics to maintain euvolemia is important. This patient is not already taking a diuretic, and starting with a low dose of furosemide is a reasonable approach. Patients with HFpEF should be encouraged to monitor their weight closely, as small differences in volume can quickly cause volume overload and subsequent hospital admissions.

B-blocker therapy is relatively contraindicated in this patient with acute decompensated heart failure as it may exacerbate his heart failure. Once his heart failure is successfully treated with diuretics, this patient may benefit from B-blocker therapy to manage his heart rate and blood pressure.

Despite the fact that the patient is currently in atrial fibrillation, cardioversion at this point is incorrect. Because he is hemodynamically stable with good rate control, there is no indication for immediate cardioversion.

Several small trials have suggested that aldosterone antagonists may improve diastolic function in patients with HFpEF. However, a recent trial comparing spironolactone with placebo showed a reduction in heart failure hospitalizations but no difference in mortality rates or all-cause hospitalizations in patients with HFpEF, and spironolactone was associated with significant increases in serum creatinine and potassium levels.

Key point: Patients with HFpEF are often volume sensitive, and careful use of diuretics to maintain euvolemia is important.

Question 2A 56-year-old man with heart failure is admitted to the hospital with a 2-week history of increasing exertional dyspnea and fatigue. He also has type 2 diabetes mellitus. Medications are metformin, lisinopril, carvedilol, furosemide, metolazone, and digoxin.

On physical examination, blood pressure is 88/60 mmHg, pulse rate is 95/min, and respiration rate is 20/min. He is somewhat confused and inattentive. Jugular venous distension is present to the angle of the jaw while sitting. Cardiac examination reveals an S3. There are bibasilar crackles on pulmonary examination. He has edema to the mid-thighs. Extremities appear mottled and are cool to the touch.

Serum creatinine level is 3.1 mg/dL; baseline value was 1.1 mg/dL. Serum sodium level is 133 mEq/L. ECG shows no evidence of ischemia. Chest radiograph shows cardiomegaly and vascular congestion.

In addition to intravenous diuresis, which of the following is the most appropriate management?

(A) Dobutamine

(B) Intra-aortic balloon pump

(C) Milrinone

(D) Right heart catheterization

Answer: A Dobutamine

This patient should be started on dobutamine for probable cardiogenic shock. Cardiogenic shock is present when there is systemic hypotension and evidence for end-organ hypoperfusion, primarily due to inadequate cardiac output. Cardiogenic shock usually requires treatment intravenous vasoactive medications and, in severe cases, device-based hemodynamic support.  

In this patient, initiating inotropic therapy is reasonable. Both dobutamine and milrinone are used to increase cardiac output; however, in the setting of kidney dysfunction, dobutamine would be the appropriate choice because milrinone is metabolized by the kidneys. Also, milrinone is a vasodilator, which could exacerbate his hypotension.

Mechanical therapy for cardiogenic shock should be considered in patients with end-organ dysfunction that does not rapidly show signs of improvement (within the first 12-24 hours) with IV vasoactive medications and correction of volume overload. It is premature to consider mechanical therapy for this patient.

Right heart catheterization can be helpful to guide therapy if volume status or cardiac output is uncertain. However, it has not been shown to improve outcomes in patients hospitalized with heart failure. Placement of a right heart catheter is not necessary prior to initiating inotropic therapy.

Question 3A 66-year-old woman is evaluated prior to discharge. She has ischemic cardiomyopathy and was admitted to the hospital 5 days ago for worsening symptoms of heart failure. She skipped taking her diuretics during a recent business trip. Today, she feels well and is able to walk around the ward twice without any symptoms.

This was her first hospitalization in 3 years, although she has skipped her diuretics during other business trips without apparent ill effect. She had an implantable cardioverter-defibrillator placed 3 years ago. An echocardiogram 1 month ago showed a left ventricular ejection fraction of 15% (stable for the past 6 years). Medications are captopril, metoprolol succinate, digoxin, furosemide, and spironolactone.

On physical examination, blood pressure is 110/72 mmHg, pulse rate is 56/min, and respiration rate is 14/min. She has no jugular venous distension and no S3. Lungs are clear, and she has no edema. ECG shows sinus rhythm, a QRS interval of 90 ms, and Q waves in V1 through V4. There are no changes compared with the admission ECG recorded 3 years ago.

Which of the following is the most appropriate management?

(A) Discharge and schedule follow-up within 7 days

(B) Measure B-type natriuretic peptide

(C) Obtain echocardiography prior to discharge

(D) Upgrade to biventricular implantable cardioverter-defibrillator

Answer: A Discharge and schedule follow-up within 7 days

This patient should be discharged home, with a follow-up appointment scheduled within 7 days. She has had one heart failure hospitalization in the past 3 years and her nonadherence with her diuretic medication was the most likely cause of the admission.

With any heart failure hospitalization, it is important to reassess several factors before discharge. First, patients must be adequately diuresed prior to discharge. It is important to know that measuring a serum BNP level will not help with that assessment. Patients should be examined for flat neck veins, resolution of peripheral or abdominal edema (if possible), and resolution of the signs and symptoms of acute heart failure. Second, patients should be on appropriate medical therapy for their stage of heart failure. For this patient, appropriate medications include ACE inhibitor or ARB, B-blocker, aldosterone antagonist, and an adequate dosage of diuretic to prevent readmission. Third, it has been demonstrated that a patient seen within 1 week after discharge is associated with a reduction of future heart failure hospitalizations.

An echocardiogram performed 1 month ago demonstrated that the patient’s left ventricular function is stable. There is no suggestion of ischemia or change in valvular function as a precipitant of this hospitalization. If this patient had not had an echocardiogram in at least 6 months, it would be reasonable to repeat the echo.

Patients are candidates for a biventricular pacemaker if they have all of the following indications: on guideline-directed medical therapy, a reduced ejection fraction (<35%), a wide QRS interval (>150 ms) or a left bundle branch block, and New York Heart Association functional class III or IV symptoms. This patient has a narrow QRS interval and therefore would not be a candidate for upgrading to a biventricular implantable cardioverter-defibrillator.

Key point: patients hospitalized for heart failure who are scheduled for a follow-up appointment within 1 week after discharge have a reduced risk of future heart failure hospitalization.

Question 4A 77-year-old man with a 5-year history of idiopathic cardiomyopathy is evaluated for progressive exertional fatigue and dyspnea. He has recently stopped carrying groceries in from the car because of his exertional dyspnea. He had an implantable cardioverter-defibrillator placed 3 years ago. Medical history is also significant for hypertension. Medications are lisinopril 40 mg/d; metoprolol succinate 25 mg/d; furosemide 40 mg/d; and spironolactone 25 mg/d.

On physical examination, blood pressure is 94/60 mmHg and pulse rate is 70/min. Estimated central venous pressure is 5 cm H2O. There is no edema.

Serum electrolyte levels and kidney function are normal. ECG shows normal sinus rhythm, a PR interval of 210 ms, QRS duration of 160 ms, and a new left bundle branch block. His left ventricular ejection fraction 3 months ago was 25%.

Which of the following is the most appropriate next step in management?

(A) Cardiac resynchronization therapy

(B) Dobutamine therapy

(C) Increase furosemide dose

(D) Left ventricular assist device placement

Manage heart failure with cardiac resynchronization therapy

Answer: A Cardiac resynchronization

This patient with symptomatic heart failure and a reduced left ventricular ejection fraction with evidence of significant conduction system disease should undergo placement of a biventricular pacemaker (cardiac resynchronization therapy [CRT]). He has progressive heart failure symptoms while on appropriate medical therapy and has New York Heart Association functional class III symptoms. With his EF less than 35% and left bundle branch block (LBBB), he is a candidate for a biventricular pacemaker, which has been demonstrated to reduce mortality and symptoms in patients with NYHA functional class III and IV heart failure by improving cardiac hemodynamics.

The 2013 American College of Cardiology Foundation/ American Heart Association/ Heart Rhythm Society guideline recommends CRT therapy in patients with an ejection fraction of 35% or below, NYHA functional class III or IV symptoms on guideline-directed medical therapy, and LBBB with QRS duration greater than or equal to 150 ms. This patient already has an implantable cardioverter-defibrillator. Now that he has developed a LBBB and an increase in symptoms, it is reasonable to proceed with placement of a biventricular pacemaker as well.

Inotropic therapy, such as dobutamine, is reserved for patients with end-stage heart failure, either as a bridge to transplantation or for palliative care. Although this patient has progressive symptoms, he has not reached this stage yet, and has no indication for inotropic therapy.

The patient has no evidence of volume overload on examination and a borderline low blood pressure; therefore, increasing his diuretic dose would not be expected to improve his symptoms and may worsen them by lowering his cardiac filling pressures and cardiac output.

The patient is fairly symptomatic but has not yet had optimal therapy, as he has an indication for CRT and has not yet received it. Left ventricular assist devices (LVAD) are reserved for patients with end-stage refractory heart failure as a bridge to heart transplantation or as destination therapy in selected patients who are not candidates for transplantation. However, prior to being considered for either an LVAD or heart transplantation, a patient must be on optimal medical therapy.

Key point: Cardiac resynchronization therapy is recommended in patients with an EF of 35% or below, NYHA functional class III or IV symptoms on guideline-directed medical therapy, and LBBB or QRS duration of 150 ms or greater.

Question 5

A 72-year-old woman is evaluated for progressive heart failure symptoms. She has 10-year history of nonischemic heart failure. She currently experiences exertional dyspnea with climbing one flight of stairs, which she was able to do without shortness of breath 3 months ago. Medical history is significant for hypertension, and her medications are lisinopril, carvedilol, furosemide, digoxin, and spironolactone. The patient is black.

On physical examination, blood pressure is 134/72 mmHg and pulse rate is 66/min. BMI is 35. She has no jugular venous distension. Cardiac examination reveals a grade 1/6 holosystolic murmur but is otherwise normal. There is no lower extremity edema. The remainder of her examination is unremarkable.

Laboratory studies are significant for normal electrolyte levels and a serum creatinine level of 1.5 mg/dL. ECG shows normal sinus rhythm, a QRS duration of 110 ms, and nonspecific ST-T wave changes. Echocardiogram shows a left ventricular ejection fraction of 38% and trace mitral regurgitation.

Which of the following is the most appropriate treatment?

(A) Add hydralazine and isosorbide dinitrate

(B) Add losartan

(C) Add warfarin

(D) Cardiac resynchronization therapy

Treat a black patient with heart failure with hydralazine and isosorbide dinitrate in addition to usual therapy.

Answer: A Add hydralazine and isosorbide dinitrate 

This patient should have hydralazine and isosorbide dinitrate added to her medication regimen for the treatment of her heart failure. She has New York Heart Association functional class III heart failure and is black. Hydralazine and isosorbide dinitrate have been demonstrated to improve symptoms and reduce mortality in patients who are black and who are already on maximal therapy with NYHA class III or IV heart failure symptoms. Adverse effects of this therapy include peripheral edema and headaches, but this regimen should be attempted in these patients.

Optimal therapy for patients with heart failure includes treatment with an ACE inhibitor, B-blocker, and an aldosterone antagonist. The addition of an angiotensin receptor blocker, such as losartan, to this combination is generally not recommended, primarily because of concern for hyperkalemia. Additionally, no benefit to this treatment regimen has been documented.

In patients with heart failure, warfarin treatment is appropriate only for those with another indication, such as atrial fibrillation meeting CHADS-VASc criteria, but not heart failure alone. The routine treatment of patients with heart failure with warfarin is not indicated.

Cardiac resynchronization therapy (CRT) may be an effective therapy in patients with heart failure and a prolonged QRS duration indicating dyssynchrony. Because this patient does not have evidence of dyssynchrony or an ejection fraction of 35% or less, she is not a candidate for treatment.

 

Key point: Hydralazine and isosorbide dinitrate improve symptoms and reduce mortality in patients with NYHA class III or IV heart failure symptoms who are black and are already on maximal therapy.