Heart Failure - Clinical Cardiology

Notes for MGR University BPT Exam 2026 (15 Marks)

DEFINITION

• Goldman-Cecil Medicine
• Robbins & Kumar Basic Pathology

EPIDEMIOLOGY

• At least 1 in 5 adults will develop heart failure in their lifetime
• In the US, 6.5 million people have heart failure
• Heart failure is a leading cause of morbidity and mortality, especially in the elderly
• Nearly half of patients have preserved ejection fraction (HFpEF)
• Coronary artery disease (with prior MI) accounts for ~70% of HF cases in developed countries

ETIOLOGY / CAUSES

CLASSIFICATION

1. By Ejection Fraction (EF)

2. By NYHA Functional Classification

3. ACC/AHA Staging (Progression-based)

PATHOPHYSIOLOGY

Cardiac Compensatory Mechanisms

1. Cardiac Hypertrophy:
   • Pressure overload (hypertension, aortic stenosis): new sarcomeres added in parallel → concentric hypertrophy → increased wall thickness
   • Volume overload (regurgitation, shunts): sarcomeres added in series → eccentric hypertrophy → ventricular dilatation
   • Hypertrophic myocardium has increased O2 demand but inadequate capillary expansion → vulnerable to ischemia; independent risk factor for sudden cardiac death
2. Neurohumoral Activation:
   • Decreased cardiac output → reduced renal perfusion → activation of Renin-Angiotensin-Aldosterone System (RAAS)
   • Increased aldosterone → sodium and water retention → increased preload
   • Sympathetic nervous system activation → tachycardia, increased contractility (initially compensatory, eventually detrimental)
   • Arginine vasopressin (AVP) secretion → water retention
   • Natriuretic peptides (ANP, BNP) secreted as counter-regulatory hormones
3. Frank-Starling Mechanism: Increased preload stretches ventricle → initially augments contractility; eventually overwhelmed

CLINICAL FEATURES

LEFT-SIDED HEART FAILURE

• Dyspnea on exertion - earliest and most significant symptom
• Orthopnea - dyspnea on lying flat; relieved by sitting up; patients sleep semi-seated
• Paroxysmal Nocturnal Dyspnea (PND) - dramatic breathlessness at night; wakes patient from sleep with extreme dyspnea bordering on suffocation
• Cough - due to fluid transudation into air spaces
• Fatigue and weakness (reduced cardiac output)

• Cardiomegaly
• Tachycardia
• Third heart sound (S3 gallop) - rapid passive ventricular filling
• Fine basal rales (crepitations) - opening of edematous alveoli
• Mitral regurgitation murmur (papillary muscle displacement from ventricular dilation)
• Atrial fibrillation (from left atrial stretch) - irregular pulse
• Pulmonary edema (severe): frothy sputum, cyanosis

RIGHT-SIDED HEART FAILURE

• Peripheral pitting edema - dependent; feet and lower legs (presacral in bedridden patients) - hallmark
• Hepatomegaly (congestive hepatomegaly, tender)
• Nutmeg liver - centrilobular congestion on cut section
• Cardiac cirrhosis - in long-standing severe cases
• Splenomegaly (congestive splenomegaly)
• Ascites (portal hypertension + hepatic congestion)
• Pleural effusion (bilateral in combined failure)
• Raised Jugular Venous Pressure (JVP)
• No significant pulmonary symptoms in pure right HF

BIVENTRICULAR FAILURE

• Combination of both right and left features
• Cyanosis, metabolic acidosis from diminished tissue perfusion
• Organ failure: prerenal azotemia (kidneys), hypoxic encephalopathy (brain - irritability, confusion, stupor, coma)

INVESTIGATIONS

TREATMENT

Non-pharmacological

• Salt restriction (<2g/day sodium)
• Fluid restriction in severe cases
• Daily weight monitoring (detect fluid retention)
• Exercise training (improves functional capacity)
• Smoking cessation, alcohol restriction
• Treat underlying cause

Pharmacological Management (HFrEF)

Device Therapy

• ICD (Implantable Cardioverter Defibrillator): EF ≤35%, NYHA II-III; prevents sudden cardiac death
• CRT (Cardiac Resynchronization Therapy): EF ≤35% + LBBB + wide QRS; biventricular pacing
• VAD (Ventricular Assist Device): Bridge to transplant or destination therapy
• Heart Transplantation: End-stage (Stage D) HF; last resort

COMPLICATIONS

• Acute pulmonary edema
• Cardiogenic shock
• Atrial fibrillation and thromboembolic events (stroke)
• Ventricular arrhythmias and sudden cardiac death
• Renal failure (cardiorenal syndrome)
• Hepatic failure (cardiac cirrhosis)
• Malnutrition / cardiac cachexia

PROGNOSIS

• Heart failure has a poor prognosis; 2-year mortality ~27% in symptomatic patients vs. ~10% in asymptomatic patients with reduced EF
• 5-year mortality approaches that of many cancers
• NYHA Class IV: 1-year mortality >50% without advanced therapy
• GDMT has significantly improved survival over recent decades

SUMMARY MNEMONIC

• H - Hypertension / History of MI (causes)
• E - Ejection fraction (classification)
• A - ACEI / ARB (first-line treatment)
• R - RAAS activation (pathophysiology)
• T - Tachycardia / Third heart sound (signs)
• F - Furosemide (diuresis)
• A - Atrial fibrillation (complication)
• I - ICD / CRT (device therapy)
• L - Left vs. Right sided features

Backward Heart Failure

MGR University BPT Exam Notes

CONCEPT: BACKWARD vs. FORWARD HEART FAILURE

"Inadequate cardiac output - called forward failure - is almost always accompanied by increased congestion of the venous circulation - that is, backward failure."

• Robbins & Kumar Basic Pathology

DEFINITION OF BACKWARD HEART FAILURE

• The failing ventricle → increased end-diastolic volume → increased end-diastolic pressure → elevated back-pressure in the upstream venous system

MECHANISM (Pathophysiology)

Ventricular systolic/diastolic dysfunction
          ↓
Incomplete ventricular emptying
          ↓
↑ End-diastolic volume (EDV) and ↑ End-diastolic pressure (EDP)
          ↓
↑ Atrial pressure → ↑ Venous pressure upstream
          ↓
Blood "dams back" into pulmonary (left) or systemic (right) circulation
          ↓
Transudation of fluid into interstitium and body cavities
          ↓
EDEMA, EFFUSIONS, CONGESTION

BACKWARD FAILURE OF EACH VENTRICLE

LEFT-SIDED BACKWARD FAILURE

• Dyspnea on exertion (earliest symptom)
• Orthopnea (dyspnea lying flat)
• Paroxysmal Nocturnal Dyspnea (PND)
• Cough (fluid in airways)
• Fine basal crepitations (rales)
• Pulmonary edema (severe cases)
• Pleural effusion (bilateral in combined failure)

RIGHT-SIDED BACKWARD FAILURE

• Raised JVP (most important clinical sign)
• Pitting pedal edema (bilateral)
• Hepatomegaly (tender)
• Splenomegaly
• Ascites
• Pleural effusion
• No significant respiratory symptoms (in isolated right HF)

BIVENTRICULAR BACKWARD FAILURE

• Pulmonary congestion + systemic venous congestion
• Most severe form: Cyanosis + acidosis (from diminished tissue perfusion)
• Organs affected: Lungs, liver, kidneys, brain, bowel, skin

BACKWARD FAILURE vs. FORWARD FAILURE - COMPARISON

WHY BOTH THEORIES APPLY SIMULTANEOUSLY

1. ↓ Cardiac output (forward failure) → kidneys sense reduced perfusion → activate RAAS → sodium and water retention → increased blood volume
2. This increased blood volume worsens backward pressure → more venous congestion
3. The compensatory fluid retention that attempts to fix forward failure actually aggravates backward failure

CLINICAL RELEVANCE FOR BPT

• Diuretics (e.g., furosemide) primarily treat backward failure by offloading venous congestion and reducing edema
• Inotropes / ACE inhibitors primarily address forward failure by improving cardiac output and reducing afterload
• Relieving venous back-pressure on the kidneys with diuretics can paradoxically improve renal function in right-sided failure (Cardiorenal Syndrome)
• Striking the right fluid balance is critical - over-diuresis causes hypovolemia (worsens forward failure); under-diuresis perpetuates congestion (worsens backward failure)

SUMMARY

Backward heart failure = venous congestion upstream of the failing ventricle.

• Left-sided → pulmonary congestion (dyspnea, PND, pulmonary edema)
• Right-sided → systemic congestion (edema, JVP, hepatomegaly, ascites)
• Both backward and forward failure coexist in most CHF patients