1.3 Heart Failure & Cardiomyopathy

Heart Failure & Cardiomyopathy

PANCE High-Yield Focus: Heart failure is heavily tested on the PANCE, particularly the pharmacological management of systolic heart failure. Memorize the four pillars of Guideline-Directed Medical Therapy (GDMT) that provide a mortality benefit in HFrEF. Be prepared to identify the physical exam signs of heart failure (such as S3 and S4 gallops) and the distinct clinical presentations, dynamic murmur changes, and diagnostic profiles of dilated, hypertrophic, and restrictive cardiomyopathies.

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Heart Failure Classifications & Pathophysiology

Heart failure is a complex clinical syndrome resulting from any structural or functional impairment of ventricular filling or ejection of blood.

• Heart Failure with Reduced Ejection Fraction (HFrEF / Systolic HF): Defined by an ejection fraction (EF) <=40%. It is characterized by inadequate myocardial contractility, leading to eccentric ventricular remodeling. Common etiologies include ischemic heart disease (post-MI), dilated cardiomyopathy, and chronic volume overload.
• Heart Failure with Preserved Ejection Fraction (HFpEF / Diastolic HF): Defined by an ejection fraction (EF) >=50%. It is characterized by impaired ventricular relaxation and decreased compliance during diastole, preventing proper filling. Common etiologies include concentric ventricular hypertrophy (driven by long-standing hypertension), restrictive cardiomyopathy, and aging.

ACC/AHA Stages vs. NYHA Functional Classes

• ACC/AHA Stages (Progressive, objective staging - Patients cannot move backward):
  • Stage A: High risk for heart failure but no structural heart disease or symptoms.
  • Stage B: Structural heart disease present, but without symptoms of heart failure (e.g., asymptomatic low EF).
  • Stage C: Structural heart disease with current or prior symptoms of heart failure.
  • Stage D: Advanced refractory heart failure requiring specialized interventions (e.g., transplant, LVAD, continuous inotropes).
• NYHA Functional Classes (Symptom-based classification - Can change dynamically with therapy):
  • Class I: No limitation of physical activity.
  • Class II: Slight limitation. Comfortable at rest, but ordinary activity causes dyspnea, fatigue, or palpitations.
  • Class III: Marked limitation. Comfortable at rest, but less-than-ordinary activity causes symptoms.
  • Class IV: Inability to carry out physical activity without discomfort; symptoms may be present at rest.

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Diagnostic Workup of Heart Failure

A comprehensive workup combines biomarkers, imaging, and clinical evaluation:

• B-type Natriuretic Peptide (BNP) and NT-proBNP: Released by ventricles in response to increased wall stretch and volume overload. Highly useful for differentiating cardiac dyspnea from pulmonary dyspnea in acute settings. PANCE Tip: BNP levels can be falsely elevated in renal failure (due to decreased clearance) and falsely low in obese patients.
• Echocardiography: The single most useful diagnostic tool. It establishes the ejection fraction, evaluates chamber sizes, wall thickness, valvular function, and diastolic filling parameters.
• Clinical Auscultation:
  • S3 Gallop: Low-pitched diastolic sound occurring during rapid passive ventricular filling. Pathognomonic for systolic heart failure (HFrEF), reflecting a large volume of blood filling a dilated, compliant ventricle.
  • S4 Gallop: Low-pitched late diastolic sound occurring during active atrial contraction. Pathognomonic for diastolic heart failure (HFpEF), reflecting atrial contraction against a stiff, non-compliant ventricle.

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Guideline-Directed Medical Therapy (GDMT) for HFrEF

Pharmacotherapy for HFrEF is focused on blocking chronic neurohumoral overactivation (the sympathetic nervous system and RAAS) that drives adverse ventricular remodeling. Four drug classes make up the "four pillars" of GDMT that reduce mortality:

1. Angiotensin Receptor-Neprilysin Inhibitor (ARNI): Sacubitril/Valsartan is preferred over ACEi or ARBs. Sacubitril inhibits neprilysin, preventing the breakdown of beneficial natriuretic peptides (which promote vasodilation and natriuresis), while Valsartan blocks the AT1 receptor.
   • Clinical Rule: A 36-hour washout period is mandatory when switching from an ACEi to an ARNI to prevent life-threatening angioedema. A washout is not required when transitioning from an ARB.
2. Beta-blockers: Only three beta-blockers have a proven mortality benefit in HFrEF: Carvedilol, Metoprolol succinate (long-acting), and Bisoprolol. PANCE Warning: Do not start or titrate beta-blockers in patients with acute decompensated heart failure (fluid overload). The patient must be hemodynamically stable and dry first.
3. Aldosterone Antagonists (Spironolactone or Eplerenone): Indicated for patients with NYHA Class II-IV and EF <=35%. They reduce cardiac fibrosis. Monitor potassium and renal function closely; contraindicated if K+ > 5.0 mEq/L or creatinine >2.5 mg/dL (men) / >2.0 mg/dL (women).
4. SGLT2 Inhibitors (Dapagliflozin or Empagliflozin): Originally developed for diabetes, these agents reduce cardiovascular mortality and heart failure hospitalizations in HFrEF, regardless of glycemic status.

Symptomatic Control: Loop Diuretics (Furosemide, Bumetanide) are the cornerstone for managing volume overload and congestion (pulmonary rales, peripheral edema). They improve symptoms but do not provide a mortality benefit.

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Cardiomyopathy Types

Cardiomyopathies are diseases of the heart muscle that cause mechanical or electrical dysfunction.

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PANCE Clinical Traps

• HCM Murmur Differentiation: The murmur of HCM sounds identical to Aortic Stenosis (AS). Differentiate them using dynamic auscultation:
  • Valsalva/Standing: Decreases preload. This increases the HCM murmur (a smaller LV chamber allows the septum and mitral leaflet to come closer, increasing outflow obstruction) but decreases the AS murmur (less volume passing through a fixed stenotic valve).
  • Squatting/Passive Leg Raise: Increases preload. This decreases the HCM murmur (larger LV chamber pushes the septum away from the mitral leaflet, reducing obstruction) but increases the AS murmur (more blood volume across the valve).
• Avoid in Severe HCM: Never prescribe diuretics, nitrates, CCBs (dihydropyridines), or digoxin in patients with obstructive HCM. Diuretics and nitrates decrease preload, which worsens LVOT obstruction, while digoxin increases contractility, bringing the septum closer to the valve and worsening the blockage.