Heart Failure - Comprehensive Notes

Heart Failure: A Quick Review

Basic Concepts

• Definition: Heart failure occurs when cardiac output is inadequate for the body's needs.

• Prevalence: Affects 1-3% of the general population, rising to ~10% among elderly patients.

• Key Classifications:

  • Systolic Failure (HFrEF):

    • Ventricle's inability to contract normally, leading to reduced cardiac output.

    • Ejection Fraction (EF) is <40%.

    • Causes include Ischemic Heart Disease (IHD), Myocardial Infarction (MI), and cardiomyopathy.

  • Diastolic Failure (HFpEF):

    • Ventricle's inability to relax and fill properly, resulting in increased filling pressures.

    • Typically, EF is >50%.

    • Causes include ventricular hypertrophy, constrictive pericarditis, tamponade, restrictive cardiomyopathy, and obesity.

    • Note: Systolic and diastolic failure often coexist.

Definition and Types of Heart Failure

• Definition: Heart failure is a complex clinical syndrome resulting from functional or structural heart abnormalities. This impairs the ventricle's ability to eject blood (tissue perfusion) or fill adequately.

• Diagnostic Criteria: Clinical syndrome presents with typical symptoms and signs.

  • Systolic Heart Failure (HFrEF):

    1. Typical Symptoms

    2. Typical Signs

    3. Reduced Left Ventricular Ejection Fraction (LVEF)

  • Heart Failure with Preserved LVEF (HFpEF):

    1. Typical Symptoms

    2. Typical Signs

    3. Normal or slightly decreased LVEF; Non-dilated LV

    4. Structural heart disease (LVH; LAH) and/or diastolic dysfunction

• LVEF Calculation:
  LVEF = \frac{Stroke Volume}{End-Diastolic Volume} = \frac{End-Diastolic Volume - End-Systolic Volume}{End-Diastolic Volume}

• Compensatory Mechanism: When LVEF is decreased, stroke volume is maintained by increasing end-diastolic volume (eccentric LVH).

Heart Failure Classification by Ejection Fraction

• HFrEF (Heart Failure with Reduced Ejection Fraction):

  • LVEF < 40%

  • Symptoms and Signs are present.

• HFmrEF (Heart Failure with Mid-Range Ejection Fraction):

  • LVEF 40-49%

  • Symptoms and Signs are present.

  • Elevated levels of natriuretic peptides required.

  • At least one additional criterion:

    • Relevant structural heart disease (LVH and/or LAE).

    • Diastolic dysfunction.

• HFpEF (Heart Failure with Preserved Ejection Fraction):

  • LVEF ≥50%

  • Symptoms and Signs are present.

  • Elevated levels of natriuretic peptides required.

  • At least one additional criterion:

    • Relevant structural heart disease (LVH and/or LAE).

    • Diastolic dysfunction.

• Natriuretic Peptide Levels:

  • BNP >35 pg/mL and/or NT-proBNP >125 pg/mL.

Symptoms and Signs of Heart Failure

• Symptoms:

  • Dyspnea

  • Orthopnea

  • Paroxysmal Nocturnal Dyspnea (PND) - 1-2 hours after going to bed, resolves in 15-30 min

  • Reduced exercise tolerance

  • Tiredness

  • Lower limb edema

  • Peripheral edema

  • Nocturnal cough

  • Wheezing

  • Weight gain

  • Loss of appetite

  • Right Upper Quadrant (RUQ) pain

  • Nocturia

• Signs:

  • Cachexia

  • Hypotension; Orthostatic Hypotension (OH); Narrow pulse pressure

  • Pulsus alternans; Decreased Pulse amplitude

  • Tachycardia

  • Tachypnea

  • Cheyne-Stokes breathing

  • Jugular Venous Distension (JVD); Hepatojugular Reflux (HJ reflux)

  • Lateralized and widened apex

  • Left parasternal heave / Signs of Pulmonary Hypertension (PHT)

  • Decreased S1

  • S3 - S4 (± palpable)

  • Atrioventricular (AV) valve regurgitation

  • Crackles

  • Wheezing

  • Signs of pleural effusion

  • Hepatomegaly (± pulsatile)

  • Peripheral edema (leg edema; scrotum; presacral; ascites)

  • Cold extremities

  • Confusion / Decreased level of consciousness

Forms of Heart Failure

• Acute vs. Chronic Heart Failure:

  • Clinical manifestations depend on the rate of syndrome development.

  • Acute Heart Failure: Often describes patients with acute-onset dyspnea and pulmonary edema; can also refer to cardiogenic shock (hypotension and oliguria). Compensatory mechanisms are not yet fully operative.

  • Acute deterioration can result from myocardial infarction (MI), arrhythmia, or acute valve dysfunction (e.g., endocarditis).

• Right vs. Left Heart Failure:

  • These terms indicate whether the patient primarily experiences systemic venous congestion (right heart failure) or pulmonary venous congestion (left heart failure).

  • These terms do not necessarily indicate the most severely affected ventricle.

• Fluid Retention:

  • In heart failure, fluid retention arises from reduced Glomerular Filtration Rate (GFR) and activation of the renin-angiotensin-aldosterone and sympathetic systems.

  • Swollen ankles can result from causes other than heart failure (gravitational issues, venous thrombosis/obstruction, varicose veins, hypoproteinemia, lymphatic obstruction).

• High-Output vs. Low-Output Heart Failure:

  • High-Output Failure: Can be caused by thyrotoxicosis, Paget's disease, beriberi, and anemia. Characterized by warm extremities and normal or widened pulse pressure.

  • Low-Output Failure: Characterized by cool, pale extremities, cyanosis (due to systemic vasoconstriction), and low pulse volume.

  • Mixed venous oxygen saturation (marker of oxygen delivery to tissues) is abnormally low in low-output states but normal or high in high-output states.

NYHA Functional Classification

• NYHA I: No limitation in ordinary physical activity (≥ 7 METS). Examples: climbing stairs with groceries, shoveling snow, bicycling, skiing, jogging/walking (8 kph).

• NYHA II: Slight limitation during physical activity; ordinary physical activity causes symptoms (5-7 METS). Examples: climbing stairs without stopping, brisk walking (6.5 kph), gardening, dancing.

• NYHA III: Marked limitation during physical activity; comfortable at rest; less than ordinary activity causes symptoms (2-5 METS). Examples: showering/dressing without breaks, brisk walking (4 kph), making a bed, bowling, golf.

• NYHA IV: Inability to carry on any physical activity without discomfort; symptoms at rest (< 2 METS). Unable to perform NYHA III activities.

Etiologies of Heart Failure

• Arrhythmia (AV Block)

• CAD (Ischemic Heart Disease)

• Cardiomyopathy & Myocarditis

• Hypertension

• Valvular Heart Disease

• Pericardial Disease

• Congenital Heart Disease

• Hypervolemic State (Renal Failure; Iatrogenic)

• High Output State (Anemia; Sepsis; Hyperthyroidism; Paget's disease; AV fistula; Beriberi)

• Pulmonary Disease (Cor Pulmonale)

Conditions Mimicking Heart Failure

• Obesity

• Chest disease (lung, diaphragm, chest wall)

• Venous insufficiency in lower limbs

• Drug-induced ankle swelling (dihydropyridine calcium blockers)

• Drug-induced fluid retention (NSAIDs)

• Hypoalbuminemia

• Intrinsic renal disease

• Intrinsic hepatic disease

• Pulmonary embolic disease

• Depression and/or anxiety disorders

• Severe anemia

• Thyroid disease

• Bilateral renal artery stenosis

Pathophysiology of Heart Failure

• Initial injury leads to:

  • Fluid retention

  • Decreased contractility

  • Tachycardia

  • Vasoconstriction

• Neurohormonal Activation:

  • Renin-Angiotensin-Aldosterone System Activation

  • Sympathetic System Activation

• Compensated Phase:

  • Body attempts to compensate for initial injury.

• Chronic Neurohormonal Activation:

  • Increased Wall Stress

  • Increased O₂ Demand

  • Mitral Regurgitation (MR)

  • Dyssynchrony

  • Decreased Pump Efficiency

• Decompensated Phase:

  • Remodeling

  • Fibrosis

  • Apoptosis

• Progressive LV Dysfunction:

  • Decreased Cardiac Output

  • Increased Filling Pressures (congestion)

• Target Organ Damage:

  • Renal Failure

  • Liver Congestion

  • Pulmonary Hypertension (PHT)

  • Right Ventricular (RV) Failure

• LV Wall Stress Equation:
  LV Wall Stress = \frac{P \times r}{2 \times LV Wall Thickness}, where P is pressure and r is the radius of the left ventricle.

Decompensated Heart Failure Pathophysiology

• Decompensated Heart Failure: Results from the interplay of precipitating factors and underlying substrate.

• Precipitating Factor: Can be intracardiac or extracardiac.

• Substrate: Consists of the absence of structural disease (Stage A), asymptomatic structural heart disease (Stage B), or compensated heart failure (Stage C).

• Amplification:

  • Neurohormonal activation.

  • Persistent heart damage/ischemia.

• Decompensated Heart Failure Manifestations:

  • Decreased cardiac output.

  • Increased filling pressures.

Causes of Worsening Heart Failure

• Noncardiac:

  • Noncompliance (lifestyle changes, medication).

  • Newly prescribed drugs.

  • Renal dysfunction.

  • Infection.

  • Pulmonary embolus.

  • Anemia.

• Cardiac:

  • Atrial fibrillation.

  • Other tachyarrhythmias.

  • Bradycardia/heart block.

  • Worsening valve disease.

  • Myocardial ischemia (including infarction).

Precipitating Factors in Acute Deterioration

• Acute Deterioration:

  • Tachyarrhythmia

  • Bradyarrhythmia - Blocks

  • Acute coronary syndrome / Ischemia

  • Mechanical complication of MI

  • Valvular heart disease (e.g.: ischemic MR)

  • Pulmonary embolism

  • Hypertensive crisis

  • Cardiac tamponade

  • Aortic dissection

  • Surgery

  • Hemorrhage

  • Endocarditis

• Subacute Deterioration:

  • Infection

  • COPD exacerbation / Asthma

  • Acute Renal Failure (ARF)

  • Nonadherence to treatment

  • Nonadherence to restrictions

  • Drugs (NSAID; corticosteroids; Pregabalin)

  • Arrhythmias - Blocks

  • Uncontrolled Hypertension (HTN)

  • Hypothyroidism / Hyperthyroidism

  • Alcohol - Illicit drugs

  • Anemia

  • Left Bundle Branch Block (LBBB)

  • Progression of heart disease

Figure 5.2 Pathophysiology of Heart Failure

• Starling effect.

• Decreased Stroke volume.

• Decreased Arterial perfusion.

• Increased Wall stress.

• Remodeling.

• Neuroendocrine activation.

• Compensated: Normalised wall stress, restoration of stroke volume, limited volume shape change.

• Non-compensated: Persistant increase in wall stress, persistant neuroendocrine activation, increased LV volume and decreased LVEF.

Stages of Heart Failure

• Stage A: At Risk for Heart Failure

  • Patients at high risk for HF but without structural heart disease or symptoms of HF.

  • Examples: Hypertension, atherosclerotic disease, obesity, metabolic syndrome, using cardiotoxins, family history of cardiomyopathy.

  • Therapy Goals: Treat hypertension, encourage smoking cessation, treat lipid disorders, encourage regular exercise, discourage alcohol/drug use, control metabolic syndrome.

  • Drugs: ACEI or ARB in appropriate patients for vascular disease or diabetes.

• Stage B: Structural Heart Disease

  • Structural heart disease but without signs or symptoms of HF.

  • Examples: Previous MI, LV remodeling (LVH and low EF), asymptomatic valvular disease.

  • Therapy Goals: All measures under Stage A.

  • Drugs: ACEI or ARB, Beta-blockers in appropriate patients.

  • Devices: Implantable defibrillators in selected patients.

• Stage C: Clinical Heart Failure

  • Structural heart disease with prior or current symptoms of HF.

  • Examples: Known structural heart disease with shortness of breath, fatigue, reduced exercise tolerance.

  • Therapy Goals: All measures under Stages A and B, dietary salt restriction.

  • Drugs for Routine Use: Diuretics for fluid retention, ACEI, Beta-blockers.

  • Drugs in Selected Patients: Aldosterone antagonist, ARBs, Digitalis, Hydralazine/Nitrates, Biventricular pacing, implantable defibrillators.

• Stage D: Refractory Heart Failure

  • Refractory HF requiring specialized interventions.

  • Examples: Marked symptoms at rest despite maximal medical therapy, recurrent hospitalizations, inability to be safely discharged without specialized interventions.

  • Therapy Goals: Appropriate measures under Stages A, B, and C, decision regarding appropriate level of care.

  • Options: Compassionate end-of-life care/hospice, extraordinary measures (heart transplant, chronic inotropes, permanent mechanical support, experimental surgery/drugs).

Assessment and Work-Up

• Initial Work-Up:

  • Complete Blood Count (CBC)

  • Electrolytes (including Ca²⁺/Mg²⁺)

  • Creatinine - Blood Urea Nitrogen (BUN)

  • Liver Function Tests (LFTs)

  • Blood glucose

  • HbA1c

  • Thyroid-Stimulating Hormone (TSH)

  • Urinalysis

  • Lipids

• If Necessary:

  • Creatine Kinase (CK)

  • Iron assessment

  • HIV test

  • Anti-Nuclear Antibody (ANA)

  • Rheumatoid Factor (RF)

  • Urine metanephrines

  • Serum Protein Electrophoresis (SPEP) - Urine Protein Electrophoresis (UPEP)

  • Uric acid

  • C-Reactive Protein (CRP)

  • Troponin

  • Polysomnography

• ECG Findings:

  • Sinus tachycardia

  • Arrhythmia (AF; Premature Ventricular Contractions (PVCs); Non-Sustained Ventricular Tachycardia (NSVT))

  • Conduction disorder / Left Bundle Branch Block (LBBB)

  • Left Ventricular Hypertrophy (LVH)

  • Left Atrial Hypertrophy (LAH)

  • Q waves

  • Ischemia

  • Low voltage QRS

• AV Block Causes:

  • Drug-induced

  • Myocardial infarction

  • Myocarditis

  • Sarcoidosis

  • Familial cardiomyopathy (LMNA; SCN5A)

  • Lyme disease

• Chest X-Ray (CXR) Findings:

  • Prominent hila

  • Kerley B lines (fine horizontal linear opacities extending to the pleura)

  • Peribronchial edema

  • Interstitial / alveolar edema

  • Redistribution to apices

  • Pleural effusion

  • Fluid in the fissure

  • Cardiomegaly

  • Other causes of dyspnea

CXR Findings in Left Ventricular Failure

• ABCDE:

  • Alveolar edema (perihilar 'bat's wing' shadowing).

  • Kerley B lines (septal lines attributed to interstitial edema).

  • Cardiomegaly (cardiothoracic ratio >50% on PA film).

  • Dilated prominent upper lobe veins (upper lobe diversion).

  • Pleural Effusions.

Additional Diagnostic Tests

• Transthoracic Echocardiogram (TTE ± Contrast):

  • Chamber dimensions

  • LVH

  • Systolic and diastolic function

  • LVEF (Simpson's method)

  • Valve assessment

  • Pulmonary Artery Pressure (PAP)

  • Thrombus detection

  • Cardiac output (Left Ventricular Outflow Tract Velocity Time Integral - LVOT VTI)

• Radionuclide Ventriculography:

  • LVEF; Right Ventricular Ejection Fraction (RVEF)

• Cardiac MRI:

  • Cardiac structure and function

  • LVEF

  • Tissue characterization

  • Evaluation of cardiomyopathy/myocarditis

• Coronary Angiography (± FFR):

  • Rule out significant Coronary Artery Disease (CAD)

  • Noninvasive evaluation (MIBI-P; stress echocardiography; coronary CT angiography) if few risk factors / low pre-test probability / low impact of the result on management

Stress Testing and Functional Evaluation

• Stress Test / 6-Minute Walk Test (6MWT) / VO₂max:

  • Objective evaluation of functional class.

  • Rule out ischemia.

  • Pre-transplant evaluation (VO2max).

  • Prescription of exercise.

  • Prognosis.

  • Distinguish cardiac from pulmonary cause.

• VO2max:

  • VO2max < 12 mL O2/kg/min is associated with poorer survival compared to patients receiving a heart transplant.

• 6MWT:

  • Normal > 600 m

  • < 350 m roughly equivalent to NYHA III

BNP and NT-proBNP

• BNP (B-type Natriuretic Peptide):

  • Released by the failing heart or in response to hemodynamic stress.

  • Reflects wall stress and filling pressures.

  • Increases with age; decreases with obesity.

  • Differential Diagnosis (DDx): Chronic Renal Failure (CRF); arrhythmia; Acute Coronary Syndrome (ACS); pulmonary embolism; severe COPD / PHT; sepsis; cirrhosis.

  • Indications: Identify the cause of dyspnea (cardiac versus non-cardiac); Prognosis.

• Acute Heart Failure Likelihood:

  • BNP < 100 pg/mL: Unlikely

  • BNP > 500 pg/mL: Probable

  • NT-proBNP < 300 pg/mL (NPV 98 %): Acute heart failure unlikely

  • NT-proBNP > 450 pg/mL (< 50 years), > 900 pg/mL (50-75 years), > 1800 pg/mL (> 75 years): Acute heart failure probable.

  • Change of > 30% in BNP level should call for more intensive follow-up / treatment.

Algorithm for Diagnosis of Heart Failure (Figure 5.3)

• Suspect heart failure due to history, symptoms, and signs.

• Exclude heart failure through 12-lead ECG and/or natriuretic peptides (BNP or NT-proBNP, where available).

• Other recommended tests: chest X-ray, blood tests (U&Es, creatinine, FBC, TFTs, LFTs, glucose, and lipids), urinalysis, peak flow or spirometry.

• Both Normal: Heart failure unlikely. Consider alternative diagnoses.

• One or More Abnormal:

  • Imaging by echocardiography.

  • No Abnormality Detected: Heart failure unlikely, but consider diastolic dysfunction and specialist referral if diagnostic doubt persists.

  • Abnormal: Assess HF severity, etiology, precipitating and exacerbating factors, and type of cardiac dysfunction. Identify correctable causes. Consider referral.

Framingham Criteria for Congestive Cardiac Failure (CCF)

• Diagnosis requires the simultaneous presence of at least 2 major criteria or 1 major criterion in conjunction with 2 minor criteria.

• Major Criteria:

  • Paroxysmal nocturnal dyspnea

  • Crepitations

  • S3 gallop

  • Neck vein distention

  • Acute pulmonary edema

  • Hepatojugular reflux

  • Cardiomegaly (cardiothoracic ratio >50% on chest radiography)

  • Increased central venous pressure (>16cmH20 at right atrium)

  • Weight loss >4.5kg in 5 days in response to treatment

• Minor Criteria:

  • Bilateral ankle edema

  • Dyspnea on ordinary exertion

  • Tachycardia (heart rate >120/min)

  • Nocturnal cough

  • Hepatomegaly

  • Pleural effusion

  • Decrease in vital capacity by 1/3 from maximum recorded

Prognosis

• Seattle Heart Failure Model: http://depts.washington.edu/shfm

• Heart Failure Survival Score

• Prognostic Factors:

  • Demographics

  • Etiology

  • Comorbidities

  • NYHA class

  • Hemodynamics (LVEF; PAP; Wedge; Cardiac index; Transpulmonary gradient)

  • Exercise stress test (BP; 6MWT; VO2max; Anaerobic threshold; Ve/VCO₂ slope > 35)

  • Anemia

  • Hyponatremia

  • QRS duration

  • BNP

  • Troponin…

Systolic Heart Failure Management

• Objectives:

  • Quality of Life: Decrease symptoms, decrease hospitalizations, improve functional class.

  • Quantity of Life: Increase survival, prevent disease progression.

Primary Prevention of Sudden Death

• Ischemic Heart Disease:

  • NYHA I: LVEF ≤ 30%, > 40 days post-myocardial infarction.

  • NYHA II-III: LVEF ≤ 35 %, adequate treatment, 3 months post-revascularization, life expectancy > 1 year.

• Nonischemic Cardiomyopathy: NYHA II-III, LVEF ≤ 35 %, adequate treatment, life expectancy > 1 year.

• Defibrillator (± resynchronization) indicated.

Progressive Approach to Heart Failure Management

• Stage A: At Risk

  • Risk factor reduction: HTN, Lipids, DM, Obesity, Smoking

  • ACE inhibitors

• Stage B: Asymptomatic Structural Lesion

  • ACE inhibitors (± BB) + ACE inhibitors

• Stage C: Clinical HF (NYHA II to IV)

  • Diuretics

  • ACE inhibitors + BB + Mineralocorticoid Receptor Antagonists (MRA)

  • Ivabradine and/or Sacubitril/Valsartan if eligible

  • Refer to heart failure clinic

  • Defibrillator and resynchronization

• Stage D: Advanced HF

  • Palliative

  • Left Ventricular Assist Device (LVAD); Transplant

  • Inotropes

  • ± Hydralazine / Nitrates; Digoxin

Treatments for Heart Failure with LVEF < 40%

• Beta-Blockers (BB): MERIT-HF, CIBIS

• Mineralocorticoid Receptor Antagonists (MRA): RALES, EMPHASIS-HF

• Sacubitril/Valsartan: PARADIGM-HF, replace ACEI or ARB

• Resynchronization - CRT (± ICD): COMPANION, CARE-HF, RAFT, MADIT-CRT

• Hydralazine / Nitrates: V-HeFT, A-HeFT

• Digoxin

• LVAD: Palliative or transplant

Dosing of Heart Failure Medications

• ACE Inhibitors:

  • Captopril: 6.25 mg TID, Target 50 mg TID

  • Enalapril: 1.25 mg BID, Target 10-20 mg BID

  • Lisinopril: 2.5 mg QD, Target 20-40 mg QD

• Beta-Blockers:

  • Bisoprolol: 1.25 mg QD, Target 10 mg QD

  • Carvedilol: 3.125 mg BID, Target 25-50 mg BID

  • Metoprolol succinate XL: 12.5-25 mg QD, Target 200 mg QD

• Angiotensin Receptor Blockers (ARBs):

  • Candesartan: 4 mg QD, Target 32 mg QD

  • Valsartan: 20-40 mg BID, Target 160 BID

• Neprilysin Inhibitor:

  • Sacubitril / Valsartan: Start 50 (24/26) - 100 (49/51) mg BID, Target 200 (97/103) mg BID

• IF Channel Inhibitor:

  • Ivabradine: 5 mg BID, Target 7.5 mg BID

• Loop Diuretics:

  • Furosemide: 20-40 mg QD or BID (adjusted to renal function), max 600/24h

• Mineralocorticoid Receptor Antagonists (MRAs):

  • Spironolactone and Eplerenone: CrCl > 50 mL/min: 25 mg QD

• Thiazide Diuretics:

  • Hydrochlorothiazide: 25 mg QD or BID, max 200/24h

• Digoxin:

  • 0.125 mg, adjusted to renal function

• Hydralazine / Nitrates:

  • Hydralazine: 10-25 mg TID, Target 75 mg TID

  • Isosorbide dinitrate: 10 mg TID, Target 40 mg TID

Angiotensin-Converting Enzyme (ACE) Inhibitors Studies and Guidelines

• Mortality, Hospitalization, Stabilizes remodeling, Symptoms

• ADVERSE EFFECTS: ARF; hyperkalemia; hypotension; cough (secondary to bradykinins); angioedema

• CONTRAINDICATIONS: angioedema; bilateral renal artery stenosis; pregnancy

Beta-Blockers (BB) Studies and Guidelines Studies and Guidelines

• 
  studies

• Mortality, Hospitalization, Stabilization of Remodeling, Symptom Relief:

• ADVERSE EFFECTS: decompensated heart failure; bronchospasm; bradycardia / block; hypotension; tiredness; depression; nightmares; erectile dysfunction; glucose intolerance

• CONTRAINDICATIONS: active decompensated heart failure (continue BB if already used predecompensation); shock - hypoperfusion; asthma; 2nd or 3rd degree AV block; severe PAD (ischemia at rest)

Mineralocorticoid Receptor Antagonists (MRA)

• Mortality; Hospitalization; Symptoms

• ADVERSE EFFECTS: hyperkalemia; ARF; gynecomastia - impotence libido - menstrual irregularities (Spironolactone)

• CONTRAINDICATIONS: CRF (creatinine > 221 µmol/L in males or > 177 µmol/L in females or GFR < 30 mL/min); hyperkalemia > 5 mmol/L

Diuretics

• Symptoms Management.
  Target dry weight and lowest possible dose

• ADVERSE EFFECTS: ARF; hypovolemia; hypokalemia; hyponatremia (thiazides); hypomagnesemia; metabolic alkalosis; hyperuricemia; ototoxicity
  CAUTION: CRF; hypokalemia; hypotension

Sodium Excretion of Diuretics

Loop diuretics (25%), Thiazides (5-10 %), Mineralocorticoid (1-2 %), Vasopressin (0%)

Diuretic Resistance

• Mechanisms: A) Post-sodium excretion stimulation of RAA / sympathetic systems (rebound sodium absorption); B) Drug absorption (edema of intestinal wall); C)Decreased Cardiac output (renal perfusion therefore tubular secretion of the diuretic); D) Hypertrophy of distal tubule; E) ARF or cardiorenal syndrome
  Management:

• Strict water/NaCl restriction

• Increase the dose of the loop diuretic or increase the frequency of administration
  Addition of an mineralocorticoid receptor antagonist

• Combination of loop diuretic and metolazone (temporary measure; daily assessments)

• Continuous Lasix infusion (sustained sodium excretion):
  20-40 mg IV bolus then infusion 5-40 mg/h (400 mg/100 mL NS)

• Inotropes: Dopamine (renal effect) or Dobutamine or Milrinone

• Ultrafiltration: refractory patient (( slow continuous veno-venous method, no benifit))

Angiotensin Receptor Blockers (ARB)

• Intolerance to ACE inhibitors (cough; angioedema)
  Combining with ACE inhibitors if intolerant to mineralocorticoid receptor antagonists and persistent symptoms.

Neprilysin Inhibitor

• Active natriuretic peptides

• Sacubitril + Valsartan vs Enalapril; decrease Mortality and Hospitalization; improvement Symptoms; risk of Hypotension Angioedema (sacubitril/valsartan) .
  Dosing:
  stop ACEI 36 h before; start with 50 (24/26) or 100 (49/51) mg bid; double the dose after 2-4 weeks; target dose of 200 (97/103) mg bid if tolerated

Ivabradine

• Inhibits the sinoatrial node.

• Decrease the rate of Hospitalization; improvement of Symptoms and Remodeling., risks are Bradycardia and Phosphenes.

Digoxin

• Inhibits the Sodium-Potassium-ATPase pump.

• Persistent symptoms despite standard treatment;

• AF (rate control)
  Adjustment according to renal function and serum digoxin levels target Digoxin level 0.5 to 0.9 ng/mL.

• ADVERSE EFFECTS: atrial / junctional / ventricular arrhythmias combined with blocks; visual disorders; confusion; Gl symptoms.

• CONTRAINDICATIONS: CRF; bradycardia - blocks.

• Serum Digoxin levels: Amiodarone; Verapamil; Nifedipine; Diltiazem; Quinidine;Propafenone; Captopril; Carvedilol; Spironolactone; Cyclosporine; Macrolides.

Hydralazine / Isosorbide Dinitrate

• Reduction of Mortality in Afro-Americans

• Improvement of Hospitalization and Symptoms
  INDICATIONS:
  Intolerance to ACE inhibitors and ARB, patient persist sintoms despite BB - ACE inhibitors - MRA (particularly in Afro-Americans)

• ADVERSE EFFECTS: headache; hypotension; nausea; arthralgia; asymptomatic ANA; drug-induced lupus

Complications of Drugs used in Heart Failure

• Diuretics: electrolyte imbalance (hypokalemia; hypomagnesemia; hyponatremia); arrhythmia

• ACE inhibitors: cough, angioedema

• B-Blockers: asthmatic attack, heart block

• Spironolactone: hyperkalemia

• Digoxin: life-threatening arrhythmias

• Amiodarone: sleep disturbance, thyrotoxic storm, pulmonary, or hepatic fibrosis

• Intropes: arrhythmia, cardiotoxicity

Self-Surveillance

• Weight: Daily, on waking, before getting dressed, post-voiding increase the dose of diuretics or notify if weight increase.

• Sodium: Restriction of (<2-3 g per day)

• Fluids Restriction ( <2 liters per day)

• Vaccination: influenza (annually); pneumococcus (every 5 years)

• TREATMENTS TO BE AVOIDED: A) Thiazolidinediones; B) Non-dihydropyridine CCBS; C) NSAIDS;
  D) Certain AAD: Dronedarone, Class I AAD and E) Alpha-blockers

Exercise

Regular isotonic exercise increase symptoms and improve functional capacity Prescription: (30-45 min; 60-70% of peak heart rate)

Implantable Cardiac Defibrillator (ICD)

dfibilator indicated and avoid NYHA IV due death secondary to progressive heart failure

Cardiac Resynchronization Therapy (CRT)

*

• LV lead