Heart Failure
Introduction and Overview
The video opens with an introduction to heart failure, also known as congestive heart failure (CHF), framed within the context of clinical medicine. The presenter emphasizes that understanding heart failure begins with mastering its pathophysiology, terminology, and major classifications.
Heart failure is presented not as a single disease, but as a clinical syndrome resulting from impaired cardiac function.
Types of Heart Failure
Heart failure is broadly categorized into:
Left heart failure
Right heart failure
High-output heart failure (less common)
Left Heart Failure
Left heart failure, the most common form, is divided into:
1. Systolic Heart Failure (HFrEF)
Systolic failure results from reduced contractility of the left ventricle.
Common causes include:
Myocardial infarction (fibrosis replacing functional myocardium)
Dilated cardiomyopathy (thin, weakened ventricular walls)
Myocarditis (less common)
Key mechanism:
Decreased contractility
→ Reduced left ventricular ejection fraction (LVEF)
When LVEF < 40%, this is termed:
Heart Failure with Reduced Ejection Fraction (HFrEF)
Consequences:
Decreased cardiac output
Impaired forward blood flow
2. Diastolic Heart Failure (HFpEF)
Diastolic failure involves impaired ventricular filling, not pumping.
Common causes include:
Chronic hypertension
Aortic stenosis
These conditions increase afterload, leading to:
Left ventricular hypertrophy (LVH)
Thickened ventricular walls
Reduced filling space
Key mechanism:
Decreased preload
→ Preserved ejection fraction
When LVEF ≥ 40–50%, this is termed:
Heart Failure with Preserved Ejection Fraction (HFpEF)
Important note:
Both systolic and diastolic failure reduce cardiac output, but through different mechanisms.
Compensatory Mechanisms
A fall in cardiac output leads to reduced blood pressure:
BP = CO × SVR
To compensate, the body increases:
Systemic vascular resistance (SVR)
Sympathetic nervous system activity
Renin–angiotensin–aldosterone system (RAAS) activation
Sympathetic Activation
Triggered by baroreceptors sensing low blood pressure:
Norepinephrine & epinephrine release
β₁ stimulation → Increased heart rate
α₁ stimulation → Vasoconstriction
Short-term benefit: Maintains perfusion
Long-term harm:
Increased afterload → Worsened hypertrophy
Increased preload → Ventricular dilation
RAAS Activation
Reduced renal perfusion stimulates renin release:
Renin → Angiotensin I → Angiotensin II (via ACE)
Effects of Angiotensin II:
Vasoconstriction
Aldosterone release → Sodium & water retention
ADH secretion → Water retention
Result:
Increased preload
Fluid overload
Edema
Counter-Regulation: ANP
Atrial Natriuretic Peptide (ANP) is released from stretched atria:
Promotes natriuresis
Causes vasodilation
Inhibits RAAS
This mechanism attempts to limit heart failure progression.
Right Heart Failure
Right heart failure shares similar principles.
Systolic Dysfunction
Caused by:
Right ventricular myocardial infarction
Leads to:
Reduced contractility
Dilated right ventricle
Reduced RVEF
Diastolic Dysfunction
Most commonly due to pulmonary hypertension, which increases afterload.
Causes of pulmonary hypertension include:
Idiopathic
Left heart disease
Lung disease
Chronic thromboembolism
Systemic diseases
Leads to:
Right ventricular hypertrophy
Impaired filling
Reduced cardiac output
High-Output Heart Failure
A rare condition where:
Cardiac output is elevated but still insufficient
Primary mechanism:
Massive peripheral vasodilation
→ Markedly reduced SVR
Causes include:
Sepsis (most common)
Thiamine deficiency (beriberi)
Thyrotoxicosis
AV fistulas
Severe anemia
Despite increased heart rate and stroke volume, tissue demands remain unmet.
Complications of Heart Failure
Left Heart Failure
Pulmonary congestion & edema:
Elevated left atrial pressure
Increased pulmonary venous pressure
Elevated pulmonary capillary wedge pressure (PCWP)
Symptoms:
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Severe cases → Acute decompensated heart failure
Cardiogenic Shock
Markedly reduced cardiac output → Systemic hypoperfusion
Clinical signs:
Cold, pale extremities
Mottling
Organ dysfunction
Possible consequences:
Encephalopathy
Myocardial ischemia
Acute kidney injury (cardiorenal syndrome)
Mesenteric ischemia
Lactic acidosis
Right Heart Failure
Due to elevated central venous pressure:
Jugular venous distension
Peripheral edema
Hepatic congestion
Ascites
Rarely → Cardiogenic shock via septal shift
Diagnosis
1. Chest X-ray
May show:
Cardiomegaly
Pulmonary edema
Pleural effusions
B-lines
2. BNP / NT-proBNP
Low levels → HF unlikely
High levels → Supports diagnosis
3. Echocardiogram
Essential for:
LVEF assessment
Differentiating HFrEF vs HFpEF
Detecting valvular disease
4. Physical Exam
Helps distinguish:
Right vs left heart failure
5. Right Heart Catheterization
Gold standard for PCWP
PCWP > 18 mmHg → Strongly suggests left heart failure
Treatment
Management focuses on neurohormonal modulation.
Core Therapies
β-blockers (metoprolol, carvedilol):
Reduce sympathetic activation
Improve remodeling
ACE inhibitors / ARBs / ARNIs:
Suppress RAAS
Reduce remodeling & mortality
Aldosterone antagonists:
Reduce fluid retention
Improve outcomes
SGLT2 inhibitors:
Promote diuresis
Provide cardiovascular benefits
Alternative Vasodilator Therapy
For selected patients:
Hydralazine + Isosorbide dinitrate
Symptom Control
Diuretics:
Relieve congestion
Reduce preload
Device Therapy
CRT → For LVEF < 35% with LBBB
AICD → Prevent sudden cardiac death
Advanced Support
LVAD → Bridge to transplant
Inotropes (dobutamine, milrinone) → Short-term support
IABP
VA ECMO
Acute Decompensation
BiPAP → Reduces preload & afterload
Oxygenation support
Systematic Treatment Algorithm
Modify risk factors
Start ACEi/ARB + β-blocker
Add diuretics if congested
Add aldosterone antagonist + SGLT2 inhibitor
Switch to ARNI if appropriate
Consider hydralazine/nitrates when indicated
Add CRT for electrical dyssynchrony
Use inotropes if unstable
Mechanical support if refractory
LVAD / Transplant for end-stage disease
Key Insights
Heart failure is a syndrome, not a single disease
Systolic and diastolic dysfunction differ mechanistically
Compensatory systems initially help but ultimately worsen HF
Diagnosis integrates imaging, biomarkers, and hemodynamics
Treatment targets neurohormonal pathways, volume status, and cardiac mechanics
Understanding pathophysiology is essential for:
Clinical reasoning
Treatment selection
Exam preparation
