Heart Failure: High-Output States & Classification

• Heart Failure (HF) is a clinical syndrome with structural or functional cardiac abnormality.
• HF is corroborated by elevated natriuretic peptide levels, objective evidence of pulmonary or systemic congestion.
• BNP levels are elevated with pulmonary or systemic congestion.

High-Output States

• High-output states increase strain on the heart, leading to heart failure in the presence of underlying structural heart disease.
• Metabolic disorders can cause high-output states.
• Thyrotoxicosis can cause high-output states.
• Nutritional disorders, such as beriberi or B1 vitamin deficiency, can cause high-output states.
• Excessive blood flow requirements can cause high-output states.
• Systemic arteriovenous shunting can cause high-output states.
• Chronic anemia can cause high-output states.

Different Paradigms of HF

• HF classification includes functional class (NYHA I-IV) and physiological stage (ACC/AHA A-D).
• HF can affect the right ventricle (RV), left ventricle (LV), or both (biventricular).
• HF presentation includes decreased exercise tolerance, volume overload, and incidental findings.
• HF types include HF with preserved ejection fraction (diastolic dysfunction), HF with diminished ejection fraction (systolic dysfunction), and mixed systolic/diastolic dysfunction.
• HF etiology and duration are new onset HF, chronic HF, and acute decompensation (ADHF).

NYHA Functional Classification

• Class 1: Asymptomatic.
• Class 2: Symptoms with moderate activity e.g., long-distance walking, climbing two flights of stairs).
• Class 3: Symptoms with minimal exertion e.g., short-distance walking, climbing one flight of stairs).
• Class 4: Symptoms at rest.

ACC/AHA HF Stage

• Stage A involves being at high risk for heart failure but asymptomatic.
• Stage B is pre-heart failure, asymptomatic, but with some abnormality evidence on echo.
• Stage C is symptomatic heart failure.
• Stage D is advanced heart failure with marked symptoms at rest, despite maximal medical therapy, needing transplant or hospice.

RV Failure

• Left ventricular failure is the most common cause of right ventricular failure.
• Coronary artery disease (ischemia) can cause RV failure.
• Pulmonary hypertension can cause RV failure.
• Right valvular disease can cause RV failure.
• Pulmonary embolism can cause RV failure.
• Chronic pulmonary disease can cause RV failure.
• Neuromuscular disease can cause RV failure.
• Pure RV failure symptoms include elevated jugular venous pressure (JVP) and edema.

Right Heart Failure

• Right heart failure increases central venous pressure, increasing resistance to portal flow, causing hepatomegaly.
• In RV failure, increased venous pressure leads to fluid transudation, causing ankle, sacral edema, ascites, and elevated jugular venous pressure.

LV Failure

• Important causes of LV failure are coronary artery disease (ischemia) and left valvular disease.
• Symptoms of left ventricle failure include dyspnea on exertion (DOE).
• Paroxysmal nocturnal dyspnea (PND) is a symptom of left ventricle failure.
• Orthopnea (needing to prop up with pillows) is a symptom of left ventricle failure.
• Pulmonary edema is a symptom of left ventricle failure
• Low output HF results in a mixture of right and left heart failure symptoms.

Congestive Heart Failure

• Decreased LV output with exercise causes dyspnea on exertion (DOE).
• Increased end-diastolic volume leads to cardiac dilation.
• LV failure increases pulmonary venous pressure, leading to fluid transudation and pulmonary edema.
• Increased venous return exacerbates pulmonary vascular congestion, potentially leading to orthopnea.

Signs of Heart Failure

• Pulmonary crackles (rales) and wheezing (cardiac wheezes) are lung sounds associated with HF.
• An S3 heart sound in indicates left ventricular failure (systolic dysfunction).
• An S4 heart sound indicates decreased LV compliance (diastolic dysfunction).
• Acute pulmonary edema can occur.
• Cyanosis can occur due to pulmonary shunting.
• Hypotension indicates cardiogenic shock.
• Poor cerebral and renal perfusion can occur.

CXR Findings in CHF

• Cardiomegaly is a finding in CHF.
• Vascular redistribution (redistribution of flow to apices) in CHF.
• Pulmonary venous congestion (white areas) in CHF.
• Kerley B lines indicate chronic elevation of LA pressure and thickening of intralobular septa from edema.
• Pleural effusions are typically small and bilateral (usually transudative).

B-Type Natriuretic Peptide/Brain Natriuretic Peptide (BNP)

• BNP is synthesized and released by the heart.
• Elevated BNP levels are associated with reduced LVEF, LV hypertrophy, elevated LV filling pressures, acute MI, and ischemia.
• BNP is used in combination with clinical evaluation to distinguish dyspnea from HF from other causes.
• BNP level < 50 pg/ml has a negative predictive value of 96%.
• BNP level > 500 pg/ml is predictive of CHF.
• BNP levels of 100-500 pg/ml may indicate CHF, or pulmonary embolus PE, primary pulmonary hypertension, chronic pulmonary disease, end-stage renal disease, cirrhosis or hormone replacement.

Echocardiogram

• 2D echocardiogram with Doppler flow studies is used to look for ejection fraction, structural abnormalities of the left ventricle, abnormalities of the myocardium, valvular heart disease, abnormalities of the pericardium.

Summary of Recommended Work-Up

• A thorough history and physical exam should be conducted.
• Lab tests should be done.
• A 12 lead ECG & CXR should be conducted.
• An echocardiogram should be performed
• Determine if the etiology is caused by ischemia, valvular heart disease, Hypertension, Cardiomyopathies, toxins (ETOH, Drugs)

Diastolic vs Systolic Dysfunction

• Diastolic dysfunction is a filling problem called HFpEF.
• Systolic dysfunction is an ejection problem called HFrEF.

Ejection Fraction

• Ejection Fraction (EF) = (SV / EDV) × 100%, Stroke Volume (SV) = EDV – ESV
• Normal EF: >50-60%
• Both diastolic and systolic dysfunction decrease stroke volume.

Classification of HF by Pathophysiologic Mechanism Types

• HF with preserved EF (HFpEF): LVEF of at least 50
• HF with mildly reduced EF (HFmrEF): LVEF of 41-49%.
• HF with reduced EF (HFrEF): LVEF of up to 40%.
• HF with improved EF (HFimpEF): baseline LVEF of 40% or less, an increase of at least 10 points from baseline LVEF, and a second measurement of LVEF of greater than 40%.
• HF with preserved Ejection Fraction also known as Diastolic .
• HF with diminished Ejection Fraction (formerly known as Systolic
• Mixed systolic/diastolic.

HFpEF Diagnosis

• Clinical signs or symptoms of HF, evidence of preserved or normal LVEF, evidence of abnormal LV diastolic dysfunction.

Etiologies of Diastolic Dysfunction

• Pathologic hypertrophy from secondary causes (hypertension or obstructive valvular disease such as Aortic Stenosis).
• Primary (hypertrophic cardiomyopathies).
• Restrictive cardiomyopathy
• Infiltrative disorders (amyloidosis.
• Storage diseases (hemochromatosis.
• Fibrosis (from myocardial ischemia/infarction).
• Aging
• Endomyocardial disorders
• Metabolic disorder

Pathophysiology of diastolic dysfunction in HTN

• The left ventricle hypertrophies in response to hypertension and increased afterload.
• Concentric hypertrophy, directed inwardly, encroaches on the LV cavity (cLVH).
• Stiff, fibrotic LV muscle does not relax in diastole.
• Left ventricle doesn't fill enough, the reduced end diastolic volume.
• Ejection maintained.

Restrictive Cardiomyopathy Etiologies

• Amyloidosis-Overproduction of Protein
• Sarcoidosis-non-caseating granulomas
• Hemochromatosis: “bronze diabetes"

Restrictive Cardiomyopathy

• Presents like constrictive pericarditis
• A cardiac Biopsy is useful for diagnosis
• Treatment underlying cause

Hypertrophic Cardiomyopathies

• Etiologies congenital or familial
• Hypertrophy of IVS results in decreased LV outflow with or without obstruction

Hypertrophic Cardiomyopathy

• Dypnea
• Chest pain
• Snycope
• Ventrical arrhythmia is sudden
• Brisk carotid upstroke with pulsus bisferiens, Loud S4, Loud systolic murmur at the left sternal border Increases with valsalva or standing abruptly (decreased filling increases the obstruction), Decreases with squatting (increased filling decreases the obstruction) and handgrip (increased afterload decreases obstruction) distinsigh Aortic Stenosis

Hypertrophic Cardiomyopathy

• Best study - Echocardiogram findings, Asymmetrical Septal Hypertrophy Septum > 1.3 x thickness of LV posterior wall, LV contractile function excellent with small end -systolic volume, Systolic Anterior Motion of the Mitral Valve
• treat with first line Beta blockers, second line Verapamil, Antiarrhythmic agents may suppress atrial & ventricular arrhythmias, Treat primary or secondaryprevention sudden cardiac Contraindicated Digoxin.overload,and

Hypertrophic Cardiomyopathy

• In the event of surgery Surgical Myomectomy

Hypertrophic Cardiomyopathy

• Long exercise or heavy lifting avoid HF w/
• Echocardiogram DX, Contractility is preserved
• Treatment of underlying cause

Treatment

• Restrictive Cardiomyopathies already detailed earlier and detailed again: Amyloidosis ,Sarkoidosis. Hemochromatosis

Treatment

• Hypertrophie Cardiomyopathies - BETA blockers or Verapamilis the route, surgical Myomectomy if fails Antiarrlythnuieagents prevent suddeuscar Contraindicated: Digonino,overluereis.and