Heart Failure Heart failure is a clinical syndrome in which the heart is unable to pump blood adequately to meet the body’s metabolic needs, or can do so only with elevated filling pressures.

• Not a single disease → it’s the end result of many cardiovascular disorders (e.g., ischemic heart disease, hypertension, valvular disease, cardiomyopathy).
• Can result from systolic dysfunction (impaired contraction) or diastolic dysfunction (impaired relaxation).
• Leads to reduced cardiac output, neurohormonal activation (RAAS, sympathetic), and fluid retention.

1. Heart
Failure

2. What is Heart Failure ?
A complex clinical syndrome characterized by,
•Structural or Functional impairment of ventricular filling or ejection of blood.
•Resulting in, Inadequate cardiac output to meet metabolic demands of the body and/or elevated
intracardiac pressures at rest or during stress.
Key Concepts:
•Ejection Fraction (EF): Central to classification.
▪HFrEF (HF with reduced EF): EF ≤ 40%
▪HFmrEF (HF with mildly reduced EF): EF 41-49%
▪HFpEF (HF with preserved EF): EF ≥ 50%
•Compensatory Mechanisms: Initially helpful, ultimately harmful.
▪Neurohormonal activation (SNS, RAAS)
▪Ventricular dilation & hypertrophy (remodeling)

3. Causes and Aetiologies
Underlying Causes (What initiates the problem?):
* Coronary Artery Disease / Myocardial Infarction (Most common in developed countries)
* Hypertension (A major cause of HFpEF)
* Cardiomyopathies (Dilated, Hypertrophic, Restrictive)
* Valvular Heart Disease (Stenosis or Regurgitation)
* Toxins: Alcohol, Chemotherapy (e.g., Doxorubicin)
* Arrhythmias (e.g., Chronic Tachycardia, Atrial Fibrillation)
* Congenital Heart Disease

4. Causes and Aetiologies - continues
Precipitating Factors (What causes acute decompensation?):
* Infection (e.g., Pneumonia)
* Non-adherence to medication or diet
* Myocardial Ischemia/Infarction
* Arrhythmias (new-onset AF, Bradycardia)
* Uncontrolled Hypertension
* Renal Impairment
* Drugs: NSAIDs, corticosteroids, negative inotropes (e.g., verapamil)

5. Pathophysiology
Preload: The stretch on the ventricular myocardium
at the end of diastole (related to end-diastolic
volume).
Afterload: The resistance the ventricle must
overcome to eject blood (largely determined by
systemic vascular resistance and aortic pressure).
Contractility: The intrinsic force of contraction of the
heart muscle, independent of preload and afterload.
▪HF fundamentally represents a failure of the
heart as a pump, disrupting these forces.

6. •What starts the process? Any condition that causes:
▪Loss of viable myocardium: Myocardial Infarction (most common)
▪Chronic pressure overload: Hypertension, Aortic Stenosis
▪Chronic volume overload: Valvular regurgitation (e.g., Mitral regurgitation)
▪Direct myocardial damage: Cardiomyopathies, Myocarditis, Toxins (e.g., chemotherapy)
•The body detects a drop in cardiac output (CO) and/or blood pressure (BP).
•It activates three key short-term compensatory systems to maintain perfusion to vital organs (brain,
heart):
1)The Frank-Starling Mechanism
2)Neurohormonal Activation: Sympathetic Nervous System (SNS) & Renin-Angiotensin-Aldosterone
System (RAAS)
3)Myocardial Hypertrophy

7. Compensatory Mechanism 1: Frank-Starling Law
•Principle: Increased preload (ventricular filling) leads to increased stroke volume (up to a
point).
•In HF: The failing heart operates on a depressed Frank-Starling curve.
•To achieve the same stroke volume as a healthy heart, it requires a much higher filling
pressure.
•Consequence: This increased pressure backs up into the lungs (dyspnea) and systemic
circulation (edema)

8. Compensatory Mechanism 2: Neurohormonal Activation - SNS & RAAS
✓Sympathetic Nervous System (SNS):
•Trigger: ↓ CO → ↓ Baroreceptor activity.
•Action: ↑ Heart rate, ↑ contractility, vasoconstriction (to maintain BP).
•Short-term: Helpful. Long-term: ↑ Cardiac workload, arrhythmogenic, promotes
remodeling.
✓Renin-Angiotensin-Aldosterone System (RAAS):
•Trigger: ↓ Renal perfusion → Renin release.
•Action: Angiotensin II → potent vasoconstriction & Aldosterone release → sodium/water
retention.
•Short-term: ↑ Blood volume & BP. Long-term: ↑ Preload & Afterload, promotes fibrosis.

9. The Counter-Regulatory System: Natriuretic Peptides
•ANP (Atrial) & BNP (B-type/Brain): Released from stretched cardiac chambers.
•Actions: Promote vasodilation, natriuresis (sodium excretion), and inhibit RAAS and SNS.
•The Problem in HF: Although levels are high, their effects are overwhelmed by the powerful SNS and
RAAS systems. Measuring BNP is a key diagnostic tool.
Compensatory Mechanism 3: Myocardial Hypertrophy
•The heart muscle thickens in response to increased wall stress (Laplace's Law).
•Goal: To normalize wall stress.
•Types:
▪Concentric Hypertrophy: (Pressure overload, e.g., HTN) - New sarcomeres in parallel → wall
thickening.
▪Eccentric Hypertrophy: (Volume overload, e.g., Mitral regurgitation) - New sarcomeres in series →
chamber dilation.

10. The Turning Point: From Compensation to Decompensation -
VENTRICULAR REMODELING
•Definition (Robbins): "Alterations in mass, dimensions, and
shape of the heart (geometric remodeling) and molecular and
cellular phenotypic changes (biological remodeling) in response
to injury."
•This is the central pathological process in progressive HF.
•Features: Myocyte death (apoptosis), fibroblast proliferation,
interstitial fibrosis, abnormal gene expression, and chamber
dilation.
•Result: The heart becomes less efficient, more arrhythmogenic,
and geometrically worse at pumping—a vicious cycle.

11. The Vicious Cycle of Heart Failure (Summary Diagram)
Initiating
Injury (e.g.,
MI)
↓ Cardiac
Output / ↑
Filling
Pressures
Activation of
Compensatory
Mechanisms
(SNS, RAAS,
Hypertrophy)
Short-Term
Improvement
Long-Term
Consequences:
Vasoconstrictio
n, Fluid
Retention,
Remodeling
Worsening
Cardiac
Function (↑
Preload, ↑
Afterload,
more injury)

12. Clinical Correlates: Forward vs. Backward Failure
✓Forward Failure: Symptoms due to low cardiac output.
•Fatigue, weakness, confusion, oliguria (low urine output), cool peripheries.
✓Backward Failure: Symptoms due to elevated filling pressures (congestion).
•Left Heart: Pulmonary congestion → Dyspnea, orthopnea, pulmonary edema.
•Right Heart: Systemic congestion → Elevated JVP, hepatomegaly, peripheral edema, ascites.
•Most patients have elements of both.

13. Clinical Presentation - Symptoms & Signs
Symptoms (Driven by fluid congestion and low output):
* Dyspnoea: Exertional → Orthopnoea → Paroxysmal Nocturnal Dyspnoea (PND) → Rest dyspnoea.
* Fatigue & Weakness: Due to reduced cardiac output and skeletal muscle hypoperfusion.
* Fluid Retention: Peripheral oedema (ankles, sacrum), weight gain, ascites.
* Others: Nocturnal cough, wheezing, loss of appetite, cognitive impairment.
Signs (On Examination):
* General: Tachypnoea, pallor, cyanosis.
* CVS: Tachycardia, elevated JVP, displaced apex beat, third heart sound (S3 gallop), murmurs.
* Respiratory: Bibasal fine crepitations (rales), pleural effusion.
* Systemic: Peripheral pitting oedema, hepatomegaly, ascites.
* Chronic Low Output: Cachexia, cardiac cachexia.

14. Investigations
To Confirm the Diagnosis:
* Blood Tests:
* Natruiretic Peptides (BNP or NT-proBNP): Cornerstone. Elevated levels support a diagnosis of HF (high
sensitivity, rules out HF if normal). Levels correlate with severity.
* Electrocardiogram (ECG): Rarely normal. May show MI, LVH, arrhythmia (e.g., AF), conduction defects.
* Chest X-Ray:
* Cardiomegaly (Cardiothoracic ratio > 50%)
* Pulmonary venous congestion (Upper lobe blood diversion)
* Pulmonary oedema (Kerley B lines, peri-hilar bat's wing shadowing)
* Pleural effusions

15. Investigations - continues
To Identify Aetiology and Assess Physiology:
✓Echocardiogram:The key investigation.
* Assesses Ejection Fraction (EF) – critical for classification.
* Evaluates chamber sizes, wall thickness and motion
* Identifies valvular disease, pericardial effusion, and regional wall motion abnormalities.
✓Blood Tests (Further):
* FBC: Anaemia as a cause/precipitant.
* U&Es, eGFR: Renal function (crucial for guiding therapy).
✓LFTs, TFTs: To exclude other causes.
* Cardiac Troponins: To detect acute coronary syndrome.
✓Coronary Angiography: If underlying coronary artery disease is suspected.

16. Management - General & Pharmacological (HFrEF)
→Non-Pharmacological (Foundation of care):
* Patient education and self-management (daily weight monitoring).
* Salt and fluid restriction.
* Regular, tailored physical activity (Cardiac rehabilitation).
* Vaccination (Influenza, Pneumococcal).
→Pharmacological Therapy for HFrEF (The "Four Pillars"):
1. ACE Inhibitors (or ARNI): First-line. Antagonize the harmful RAAS system. Reduce mortality and
hospitalizations. Sacubitril/Valsartan (ARNI) is now preferred over ACE-i in many patients who remain
symptomatic.
2. Beta-Blockers : (Bisoprolol, Carvedilol, Nebivolol). Antagonize harmful sympathetic nervous system
activation. Must be started low and titrated up slowly.

17. 3. Mineralocorticoid Receptor Antagonists (MRAs): (Spironolactone, Eplerenone). Potent anti-fibrotic
and diuretic effects. Further reduce mortality.
4. SGLT2 Inhibitors : (Dapagliflozin, Empagliflozin). A new pillar. Proven to reduce CV death and HF
hospitalizations regardless of diabetes status.
Additional Drugs:
▪Diuretics: (Furosemide). For symptom relief of congestion. Do not improve prognosis alone.
▪Ivabradine: If heart rate remains high despite beta-blockade.
▪Digoxin: For rate control in AF or for symptomatic relief in sinus rhythm.

18. Management - Device & Surgical Therapy
Device Therapy:
* ICD (Implantable Cardiverter Defibrillator): For primary or secondary prevention of sudden
cardiac death in patients with HFrEF and life expectancy >1 year.
* CRT (Cardiac Resynchronization Therapy): For patients with HFrEF (EF ≤35%) and a broad QRS
complex (≥150ms) on ECG. Improves symptoms and mortality by coordinating ventricular
contraction.
Surgical Options:
* Revascularization (CABG): If coronary artery disease is the cause.
* Valve Surgery/Intervention: For severe primary valvular disease.
* Heart Transplantation: Final option for selected end-stage patients.
* LVAD (Left Ventricular Assist Device): "Destination therapy" for those ineligible for transplant or
as a "bridge to transplant".

19. Management of HFpEF:
* Focuses on treating the cause (e.g., aggressive BP control).
* Diuretics for symptom relief.
* SGLT2 inhibitors now have a role. No other disease-modifying drugs have
proven mortality benefit.

20. Complications & Prognosis
Common Complications:
* Renal Impairment (Cardiorenal Syndrome): Worsening renal function due to low cardiac output or
diuretic overuse.
* Cardiac Arrhythmias: Atrial Fibrillation (common), Ventricular Tachyarrhythmias (can cause sudden
death).
* Thromboembolism: Risk of stroke and PE due to stasis in dilated chambers (especially in AF).
* Hepatic Dysfunction: Due to chronic venous congestion.
* Cardiac Cachexia: Severe weight loss and muscle wasting due to chronic catabolic state.
Prognosis:
* Remains serious. Mortality compares to many cancers.
* Poor prognostic indicators: Advanced age, low ejection fraction, low systolic BP, renal impairment,
elevated natriuretic peptides, frequent hospitalizations.
* Modern evidence-based pharmacotherapy has significantly improved survival and quality of life.

21. Summary & Key Takeaways
* Heart Failure is a clinical syndrome, not a single disease.
* Classification by EF (HFrEF vs. HFpEF) is critical for guiding management.
* BNP/NT-proBNP and Echocardiography are the key diagnostic tests.
* Management of HFrEF is based on four pillars of disease-modifying therapy: ACE-i/ARNI, Beta-
Blocker, MRA, SGLT2i.
* Diuretics are for symptom relief; they do not improve survival alone.
* Device therapy (ICD/CRT) plays a vital role in selected patients.
* Identifying and treating the underlying cause is essential.