CHF

Heart Failure

Introduction and Overview: 

Heart failure is one of the most common medical conditions I see and deal with at work and so, I wanted to research and write on it.

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

1. Modify risk factors

2. Start ACEi/ARB + β-blocker

3. Add diuretics if congested

4. Add aldosterone antagonist + SGLT2 inhibitor

5. Switch to ARNI if appropriate

6. Consider hydralazine/nitrates when indicated

7. Add CRT for electrical dyssynchrony

8. Use inotropes if unstable

9. Mechanical support if refractory

10. 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