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Heart Failure Lecture Notes
Jul 10, 2024
Heart Failure Lecture Notes
Introduction
Topic: Heart Failure within Clinical Medicine section
Types: Left heart failure, right heart failure, high output failure
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Pathophysiology
Types of Heart Failure
Left Heart Failure
Most common type
Subtypes: Systolic and Diastolic
Right Heart Failure
High Output Failure
Left Heart Failure
Systolic Heart Failure (HFrEF)
Cause
: Reduction in contractility of LV myocardium
Common Causes
:
Myocardial infarction (MI) -> fibrosis
Dilated cardiomyopathy
Myocarditis (less common)
Mechanism
:
Contractility ↓, Left ventricular ejection fraction (LVEF) ↓
EF < 40% -> Heart Failure with Reduced Ejection Fraction (HFrEF)
Cardiac output ↓ due to poor forward flow
Diastolic Heart Failure (HFpEF)
Cause
: Issues with filling of the heart
Common Causes
:
Chronic hypertension
Aortic stenosis
Mechanism
:
Stroke volume = preload + contractility + afterload
Afterload ↑ -> blood hard to pump out
LV hypertrophy (left ventricular hypertrophy – LVH)
LV filling ↓, but LVEF preserved
EF > 40% -> Heart Failure with Preserved Ejection Fraction (HFpEF)
Right Heart Failure
Systolic Right Heart Failure
Cause
:
Right ventricular MI
Mechanism
:
Contractility ↓, Right ventricular ejection fraction ↓
Low right ventricular cardiac output
Diastolic Right Heart Failure
Cause
:
Pulmonary hypertension (various types)
Mechanism
:
Right ventricular hypertrophy
Right ventricular filling ↓, but RV ejection fraction preserved
High Output Heart Failure
Cause
: Uncommon, includes conditions like sepsis, thiamine deficiency (beriberi), thyrotoxicosis, severe anemia
Mechanism
:
Massive vasodilation -> systemic vascular resistance (SVR) ↓,
Compensatory mechanism: cardiac output ↑ but still fails to meet tissue demands
Results in low blood pressure, activation of sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS)
Compensatory Mechanisms in Heart Failure
Low Cardiac Output
:
Activates baroreceptors -> Sympathetic nervous system activation
Increased heart rate, peripheral vasoconstriction
Renin-Angiotensin-Aldosterone System (RAAS)
:
Low cardiac output -> renin release -> angiotensin II formation -> aldosterone and ADH release -> increased preload and afterload
Problem: Worsens heart failure by increasing afterload and preload, increasing edema
Atrial Natriuretic Peptide (ANP)
:
Counter-regulatory hormone released in response to atrial stretch
Goal: Inhibit Angiotensin II, reduce RAAS activity
Complications of Heart Failure
Left Heart Failure
Pulmonary Edema
: Increased pulmonary capillary wedge pressure (PCWP)
Symptoms: Dyspnea, orthopnea, paroxysmal nocturnal dyspnea
Severe Complications
:
Acute decompensated heart failure -> severe pulmonary edema, V/Q mismatch, hypoxia
Cardiogenic shock: MI, tachyarrhythmia -> systemic perfusion ↓
Symptoms: Cold extremities, pallor, organ malperfusion (brain, heart, kidneys, GIT), lactic acidosis
Right Heart Failure
Systemic Congestion
: Jugular venous distension (JVD), pitting edema
Liver Congestion
: Hepatic congestion leading to liver failure
Ascites
: Increased portal pressure -> fluid leakage into abdomen
Cardiogenic Shock
: Septal shift causing left ventricular filling ↓ and systemic malperfusion
Diagnosis
Clinical Examination
Physical Examination
: JVD, pitting edema, crackles on lung auscultation
Imaging & Tests
Chest X-ray
: Look for cardiomegaly, pulmonary edema, pleural effusions
BNP Levels
: Helps rule out/exclude heart failure in acute settings (high levels suggest CHF)
Echocardiogram
: Assess heart function, LV ejection fraction, and wall movements
Right Heart Catheterization
: Pulmonary capillary wedge pressure > 18 mmHg confirms left heart failure
Treatment
Reduce Sympathetic Nervous System Activity
Beta Blockers
: Metoprolol, Carvedilol
SGLT2 Inhibitors
: Empagliflozin
Reduce RAAS Activity
ACE Inhibitors
Angiotensin Receptor Neprilysin Inhibitor (ARNI)
: Sacubitril/Valsartan
ARB
Aldosterone Antagonists
: Reduce sodium and water retention
Symptomatic Management
Diuretics
: Loop and thiazide diuretics for edema
Additional Therapies
: Hydralazine and Isosorbide dinitrate for African-Americans, Ivabradine (if in normal sinus rhythm and maxed beta-blockers)
Device Therapy
Cardiac Resynchronization Therapy (CRT)
: For LVEF < 35% and LBBB
Automatic Implantable Cardioverter Defibrillator (AICD)
: For LVEF < 35%, preventing VT/VF
Left Ventricular Assist Device (LVAD) and Transplant
: For advanced heart failure
Acute Management
Inotropes
: Dobutamine, milrinone for acute decompensation
Mechanical Circulatory Support
: Intra-aortic balloon pump (IABP), Veno-Arterial Extracorporeal Membrane Oxygenation (VA-ECMO)
Non-invasive Ventilation (BiPAP)
: Helps reduce pulmonary edema and improve cardiac output
Summary Treatment Approach
Initial Management
:
ACE inhibitor or ARB + beta blocker
Symptom-based Additions
:
Diuretics for congestion
Aldosterone antagonists, SGLT2 inhibitors
ARNI for further symptom control
Special considerations: Hydralazine + isosorbide dinitrate, ivabradine
Advanced Strategies
:
CRT or AICD if indicated
Inotropes and mechanical support for refractory cardiogenic shock
Final Strategy
:
LVAD or heart transplant in end-stage cases
Conclusion
Summary of key points: Differentiation between types of heart failure, treatment approach, complications, diagnostic strategy
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