Cardiac failure for 10 marks from harrison for mbbs ug

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Cardiac Failure (Heart Failure) - 10 Marks

Harrison's Principles of Internal Medicine, 22nd Edition (2025), Chapter 264

Definition

Heart failure (HF) is a complex clinical syndrome with symptoms and signs resulting from any structural or functional impairment of ventricular filling or ejection of blood. The ESC emphasizes cardinal symptoms (breathlessness, ankle swelling, fatigue) accompanied by signs (elevated JVP, pulmonary crackles, peripheral edema) due to structural/functional cardiac abnormality causing elevated intracardiac pressures and/or inadequate cardiac output at rest or during exercise.

The term "heart failure" is preferred over "congestive heart failure," as some patients present without signs of volume overload.

Epidemiology

~6.7 million American adults treated for HF; >600,000 new cases/year in the US
Globally, an estimated 56.2 million people have HF
Leading cause of hospitalisation in adults over 65 years
5-year mortality rivals that of many cancers

Classification / Phenotypes

Based on left ventricular ejection fraction (LVEF):

Type	LVEF	Description
HFrEF (reduced)	<40%	Systolic dysfunction; responds well to RAAS/beta-blocker therapy
HFmrEF (mildly reduced)	40-49%	Intermediate phenotype
HFpEF (preserved)	≥50%	Diastolic dysfunction predominant; driven by hypertension, obesity, DM

Stages (ACC/AHA):

Stage A: At risk (no symptoms, no structural disease)
Stage B: Pre-HF (structural disease, no symptoms)
Stage C: Symptomatic HF
Stage D: Advanced/refractory HF

Etiology

Common causes:

Ischemic heart disease (most common in developed countries)
Hypertension
Valvular heart disease (aortic stenosis, mitral regurgitation)
Dilated cardiomyopathy (familial/idiopathic)
Diabetes mellitus, obesity
Myocarditis, toxic (alcohol, chemotherapy), infiltrative (amyloidosis, sarcoidosis)

Pathophysiology

1. Compensatory Mechanisms

When cardiac output (CO) falls, three key compensatory mechanisms activate:

a) Frank-Starling Mechanism: Increased ventricular end-diastolic volume (preload) augments stroke volume via the length-tension relationship. Initially compensatory, but leads to ventricular dilatation and pulmonary congestion when exhausted.

b) Neurohormonal Activation:

Sympathetic Nervous System (SNS): Increases heart rate and contractility; causes peripheral vasoconstriction to maintain blood pressure. Chronic SNS activation causes beta-receptor downregulation, arrhythmias, and myocardial toxicity.
Renin-Angiotensin-Aldosterone System (RAAS): Activated by reduced renal perfusion. Angiotensin II causes vasoconstriction; aldosterone causes Na+/water retention - increasing preload. Chronic activation leads to myocardial fibrosis and worsening remodeling.

c) Ventricular Hypertrophy / Remodeling:

Concentric hypertrophy in pressure overload (hypertension, aortic stenosis): increased wall mass relative to volume
Eccentric hypertrophy in volume overload (aortic/mitral regurgitation): increased cavity size
Cellular changes: myocyte hypertrophy, interstitial fibrosis, re-expression of fetal genes (beta-myosin heavy chain), impaired Ca2+-handling proteins, beta-adrenergic desensitisation
Loss of myocytes via necrosis, apoptosis (programmed cell death), and autophagy

2. Counter-Regulatory (Vasodilatory) Hormones

Released to counterbalance RAAS/SNS:

ANP (atrial) and BNP (ventricular): released in response to increased stretch; cause vasodilation, natriuresis, inhibit renin/aldosterone
Bradykinin, prostaglandins (PGE1, PGI2), nitric oxide, adrenomedullin
BNP is inactivated by neprilysin - the basis for sacubitril/valsartan (ARNi) therapy

Clinical Features

Symptoms

Symptom	Mechanism
Dyspnoea on exertion	Elevated pulmonary venous pressure
Orthopnoea	Increased venous return supine → elevated LV filling pressure
Paroxysmal nocturnal dyspnoea (PND)	Same mechanism; redistributed fluid from dependent tissues at night
Fatigue, weakness	Reduced CO and skeletal muscle hypoperfusion
Ankle/pedal oedema	Right heart failure + RAAS-mediated Na+ retention
Nocturia	Improved renal perfusion in supine position
Oliguria	Severe reduction in renal blood flow (advanced HF)
Cardiac cachexia	Advanced HF - cytokine-mediated, poor intake, malabsorption

NYHA Functional Classification:

Class I: No symptoms with ordinary activity
Class II: Slight limitation with ordinary activity
Class III: Marked limitation with less than ordinary activity
Class IV: Symptoms at rest

Physical Examination

Tachycardia, hypotension (low output)
Elevated JVP - best single sign of volume overload
S3 gallop - pathognomonic of volume overload/systolic dysfunction
S4 gallop - seen in stiff, non-compliant ventricle (HFpEF)
Basal crackles (crepitations) - pulmonary oedema
Displaced apex beat - cardiomegaly
Pulsus alternans - alternating strong/weak pulse; marker of severe LV dysfunction
Pleural effusion (more often right-sided or bilateral)
Ascites, hepatomegaly, hepatojugular reflux - right heart failure
Peripheral cyanosis, cool extremities - severe low-output HF

Precipitating Factors (may decompensate stable HF)

Patient-related: Non-adherence to medications/diet, excess sodium intake, heavy alcohol use
Provider-related: NSAIDs (Na+/water retention), negative inotropes (non-DHP CCBs)
HF-related: Uncontrolled hypertension, myocardial ischaemia/infarction, arrhythmias (AF most common), pulmonary emboli
Other: Infection, anaemia, hyperthyroidism, worsening renal failure, sleep apnoea

Investigations

Laboratory

BNP / NT-proBNP: Most useful biomarkers; elevated with volume overload; used for diagnosis, prognosis, and therapy guidance
CBC: Anaemia (precipitant or contributor)
RFTs: Renal impairment (cardiorenal syndrome)
LFTs: Congestive hepatopathy
Serum electrolytes: Hyponatremia (poor prognosis), hypokalaemia (risk of arrhythmia)
TSH: Thyroid disease as underlying cause
Cardiac troponin: Elevated with myocardial injury; prognostic value

ECG

No specific diagnostic pattern
LVH + left atrial enlargement → HFpEF
Q waves → ischemic cardiomyopathy
LBBB → candidate for cardiac resynchronisation therapy (CRT)
AF present in up to 40% of chronic HF patients

Chest X-Ray

Cardiomegaly (cardiothoracic ratio >0.5)
Pulmonary venous congestion ("bat wing" or "butterfly" hilar shadowing)
Kerley B lines (interstitial oedema)
Pleural effusions (typically right-sided)
Peribronchial cuffing

Echocardiography (Most Important Non-invasive Test)

Determines LVEF (classifies HF type)
Assesses wall motion, valvular disease, pericardial effusion, intracardiac thrombi
Doppler: CO, pulmonary artery pressures, diastolic filling patterns
Speckle-tracking strain: incremental prognostic value

Cardiac MRI

Highly accurate for LV mass, volumes, function
Identifies specific aetiology: ischaemic vs. non-ischaemic, myocarditis, amyloidosis, sarcoidosis, haemochromatosis

Diagnosis

Diagnosis is clinical - requires appropriate symptoms AND signs AND evidence of structural/functional cardiac abnormality. BNP/NT-proBNP level supports diagnosis when clinical picture is uncertain. Echocardiography is the definitive investigation.

Framingham Criteria (requires 2 major or 1 major + 2 minor):

Major: PND/orthopnoea, S3 gallop, cardiomegaly on CXR, acute pulmonary oedema, elevated JVP, hepatojugular reflux, weight loss >4.5 kg with treatment

Minor: Bilateral ankle oedema, nocturnal cough, dyspnoea on exertion, hepatomegaly, pleural effusion, tachycardia >120 bpm, reduced vital capacity by 1/3

Quick Summary Box for 10-Mark Answer

Feature	Key Points
Definition	Syndrome of impaired ventricular filling/ejection causing symptoms
Most common cause	IHD, hypertension
Pathophysiology	Frank-Starling, SNS/RAAS activation, ventricular remodeling
Key symptoms	Dyspnoea, orthopnoea, PND, fatigue, oedema
Key signs	Elevated JVP, S3, crepitations, displaced apex, pulsus alternans
Best biomarker	BNP / NT-proBNP
Definitive test	Echocardiography (determines LVEF)
Classification	HFrEF (<40%), HFmrEF (40-49%), HFpEF (≥50%)
Common precipitant	AF, non-compliance, infection, ischaemia

Source: Harrison's Principles of Internal Medicine, 22nd Edition (2025) - Chapter 264: Heart Failure: Pathophysiology and Diagnosis (Givertz & Mehra)

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