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General Medicine Long Notes - BDS 3rd Year (University Exam Pattern)

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QUESTION 1: MYOCARDIAL INFARCTION

Describe Myocardial Infarction - Etiology, Pathogenesis, Clinical Features, Investigations, Management

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DEFINITION

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ETIOLOGY

• Age (males >45 years, females >55 years)
• Male sex
• Positive family history (first-degree relative with MI before age 55 in males / 65 in females)
• Genetic predisposition

• Hypertension (HTN)
• Hyperlipidemia (elevated LDL, low HDL)
• Diabetes mellitus
• Cigarette smoking
• Obesity and physical inactivity
• Metabolic syndrome

• Coronary artery spasm (Prinzmetal's angina)
• Coronary arteritis (e.g., Kawasaki disease, SLE)
• Cocaine use (causes vasospasm + thrombosis)
• Embolism to coronary artery (from prosthetic valves, IE)
• Severe anemia with reduced oxygen delivery
• Congenital coronary artery anomalies

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PATHOGENESIS

• Platelet adhesion to exposed subendothelial collagen via von Willebrand factor and GP Ib receptors
• Platelet activation and release of ADP, thromboxane A2, serotonin (amplification)
• Platelet aggregation via GP IIb/IIIa receptors + fibrinogen
• Activation of coagulation cascade forming fibrin clot
• Result: Occlusive thrombus in the coronary lumen

• Complete occlusion stops blood flow distal to the obstruction
• Small collateral flow is insufficient to prevent necrosis
• Cardiac muscle requires ~1.3 mL O2/100g/min just to remain alive
• In the central core of infarction (zero collateral flow): cells die within 20-40 minutes
• Subendocardial muscle is most susceptible because it has higher O2 consumption and vessels are compressed during systole

• ATP depletion, anaerobic glycolysis, lactic acid accumulation
• Intracellular Na+ and Ca2+ overload
• Cell swelling, membrane disruption
• Irreversible cell death (coagulative necrosis) - starts at 20-40 min, complete by 4-6 hours
• Release of cardiac enzymes (Troponin, CK-MB) into bloodstream

• Zone of necrosis (core): dead myocytes
• Zone of injury (periphery): stunned, potentially salvageable
• Zone of ischemia (outer): ischemic but viable

• STEMI (ST Elevation MI): Full-thickness (transmural) infarct - complete occlusion
• NSTEMI (Non-ST Elevation MI): Partial thickness (subendocardial) - incomplete occlusion

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CLINICAL FEATURES

1. Chest pain - The cardinal symptom
   • Severe, crushing, constricting, or squeezing
   • Retrosternal in location
   • Radiates to left arm (most classic), jaw, neck, epigastrium, or right arm
   • Duration: >30 minutes (distinguishes from angina which is <20 min)
   • NOT relieved by nitrates (unlike angina)
2. Sweating (diaphoresis) - profuse, cold, clammy
3. Nausea and vomiting - due to vagal stimulation
4. Dyspnea - due to LV failure/pulmonary edema
5. Sense of impending doom (angor animi)
6. Palpitations - due to arrhythmias

1. Arrhythmias (most common): VF (leading cause of early death), VT, AF, heart block (especially in inferior MI - RCA occlusion)
2. Cardiogenic shock: BP <90 mmHg, cold clammy skin, urine output <20 mL/hr
3. Left ventricular failure / pulmonary edema
4. Mechanical complications: Papillary muscle rupture (acute MR), VSP (VSD), free wall rupture, cardiac tamponade
5. Pericarditis: Day 1-3 (early fibrinous); Dressler syndrome: 2-10 weeks post-MI (immune-mediated)
6. Ventricular aneurysm: Persistent ST elevation, thrombus, heart failure
7. Re-infarction

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INVESTIGATIONS

• Hyperacute T waves: First change (minutes to hours) - tall peaked T waves
• ST segment elevation (>1mm in limb leads, >2mm in chest leads): Indicates acute transmural injury
• Pathological Q waves: Width >0.04 sec, depth >25% of R wave - indicates transmural necrosis (develops over hours to days)
• T wave inversion: Develops as injury evolves

• Identifies wall motion abnormalities (hypokinesis, akinesis, dyskinesis)
• Assesses EF, pericardial effusion, mechanical complications
• Bedside echo is invaluable in emergency setting

• CBC: Leukocytosis (neutrophilia) within 24-48 hours
• ESR, CRP: Elevated (inflammatory response)
• Blood glucose (hyperglycemia common)
• Lipid profile (taken at admission - levels fall after 24 hrs)
• Renal function (before thrombolysis/contrast)
• Coagulation profile (PT, aPTT)

• Cardiomegaly (if pre-existing LV dysfunction)
• Pulmonary venous congestion, Kerley B lines, pulmonary edema
• May be normal early on

• Definitive investigation to identify culprit vessel
• Performed urgently for STEMI (door-to-balloon time <90 min)
• PCI performed at same sitting

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MANAGEMENT

A. IMMEDIATE / EMERGENCY MANAGEMENT ("MONA" + "REACT")

• Aspirin 300 mg stat (chewed) - antiplatelet
• Clopidogrel/Ticagrelor - P2Y12 inhibitor (dual antiplatelet therapy)
• Morphine 2-4 mg IV - pain relief, reduces preload, allays anxiety
• Oxygen - only if SpO2 <94% (avoid hyperoxia in non-hypoxic patients)
• Nitrates (GTN sublingual) - for pain relief if SBP >90 mmHg; avoid in inferior MI with RV involvement
• 12-lead ECG and cardiac monitoring
• IV access, blood samples

B. REPERFUSION THERAPY (for STEMI - most critical intervention)

• Treatment of choice if available within 90 min of first medical contact
• Balloon angioplasty + stenting of culprit artery
• Superior to thrombolysis
• Door-to-balloon time should be <90 min

• Streptokinase 1.5 million units IV over 60 min
• tPA (Alteplase), Tenecteplase - more fibrin-specific
• Contraindications: recent surgery, stroke, active bleeding, uncontrolled HTN

C. ANTICOAGULATION

• Heparin (LMWH - enoxaparin, or UFH) - prevents re-thrombosis
• Fondaparinux - in NSTEMI/UA

D. ADDITIONAL MEDICAL THERAPY

E. LONG-TERM MANAGEMENT (Secondary Prevention)

• Dual antiplatelet therapy (aspirin + P2Y12 inhibitor) for 12 months
• Statin indefinitely
• ACE inhibitor / ARB
• Beta-blocker (especially if EF reduced)
• Lifestyle modification: smoking cessation, diet, exercise, weight loss, BP and DM control
• Cardiac rehabilitation

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QUESTION 2: INFECTIVE ENDOCARDITIS + ANTIBIOTIC PROPHYLAXIS

Write in Detail about Infective Endocarditis + Antibiotic Prophylaxis

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DEFINITION

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CLASSIFICATION

• Acute IE: Aggressive, rapid onset (days) - often due to S. aureus; destroys normal valves
• Subacute IE (SBE): Indolent course over weeks to months - often viridans streptococci; occurs on abnormal valves

• Native Valve IE (NVE): On normal or diseased native valves
• Prosthetic Valve IE (PVE): On artificial valves
  • Early PVE: <60 days after surgery
  • Late PVE: >60 days
• IVDU-associated IE: Right-sided (tricuspid valve most common) - S. aureus

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EPIDEMIOLOGY AND PREDISPOSING CONDITIONS

• Rheumatic heart disease (developing countries - most common predisposing condition)
• Congenital heart disease (VSD, PDA, bicuspid aortic valve)
• Mitral valve prolapse with regurgitation
• Degenerative valvular disease (elderly)
• Prosthetic cardiac valves (highest risk)
• Previous IE
• Hypertrophic cardiomyopathy

• IV drug use (IDU)
• Indwelling central venous catheters / hemodialysis access
• Poor dental hygiene
• Immunosuppression (HIV, diabetes, malignancy)
• Recent dental/surgical/urological procedures

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MICROBIOLOGY

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PATHOGENESIS

1. Endothelial damage: Turbulent blood flow (from valvular disease, congenital defects) damages the endothelium
2. Non-bacterial thrombotic endocarditis (NBTE): Sterile platelet-fibrin thrombus deposits at the site of injury
3. Bacteremia: Organisms enter the bloodstream during dental procedures, catheterization, IV drug use, or even routine activities (chewing, brushing teeth)
4. Bacterial adherence: Organisms adhere to the NBTE via surface adhesins (fibronectin-binding proteins in S. aureus, dextran in viridans streptococci)
5. Vegetation formation: Bacteria proliferate within the fibrin-platelet matrix, protected from host defenses and antibiotics; further fibrin deposition enlarges the vegetation
6. Consequences: Vegetation fragments embolize; local valve destruction; immune complex deposition causing remote organ damage

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CLINICAL FEATURES

• Fever (most common symptom - present in >90%)
• Chills, rigors, night sweats
• Fatigue, malaise, anorexia, weight loss
• Dyspnea (due to valvular regurgitation / heart failure)
• Arthralgia, myalgia

• New or changing heart murmur (most important sign - present in ~85%)
  • Aortic regurgitation (soft decrescendo diastolic murmur)
  • Mitral regurgitation (pansystolic murmur at apex)
• Signs of heart failure (elevated JVP, crepitations, S3 gallop)
• Pericardial rub (pericarditis)

• Stroke / TIA (left-sided IE - brain embolism)
• Splenic infarct (pain in left hypochondrium)
• Renal infarct (hematuria, loin pain)
• Pulmonary embolism (right-sided IE - S. aureus, IVDU)
• Mycotic aneurysm (weakening of arterial wall by septic emboli)

• Immune complex glomerulonephritis (hematuria, proteinuria)
• Focal embolic glomerulonephritis

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DIAGNOSIS: DUKE CRITERIA

1. Positive blood cultures: Typical organisms (viridans streptococci, S. bovis, HACEK, S. aureus, enterococci) from two separate cultures; OR persistently positive (>12 hours apart)
2. Evidence of endocardial involvement on echocardiography:
   • Oscillating vegetation on valve or supporting structures
   • Abscess
   • New partial dehiscence of prosthetic valve
   • New valvular regurgitation

1. Predisposing heart condition or IV drug use
2. Fever >38°C
3. Vascular phenomena: arterial emboli, Janeway lesions, septic pulmonary infarcts, mycotic aneurysm
4. Immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots, positive RF
5. Positive blood culture not meeting major criteria
6. Positive echocardiogram not meeting major criteria

• Definitive IE: 2 major, OR 1 major + 3 minor, OR 5 minor criteria
• Possible IE: 1 major + 1 minor, OR 3 minor criteria

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INVESTIGATIONS

1. Blood cultures (most important):
   • 3 sets from 3 different venepuncture sites, before antibiotics
   • Aerobic and anaerobic bottles
   • 45-minute intervals between each
   • Positive in ~90% of cases
2. Echocardiography:
   • TTE (transthoracic echo): First line; sensitive for large vegetations
   • TEE (transoesophageal echo): More sensitive (>90%); for prosthetic valves, TTE-negative cases, intracardiac abscess
3. CBC: Normocytic normochromic anemia, leukocytosis, elevated ESR, CRP
4. Urinalysis: Hematuria, proteinuria, red cell casts (glomerulonephritis)
5. Renal function: Creatinine may be elevated
6. Rheumatoid factor: May be positive in subacute IE
7. Serology: For culture-negative organisms (Coxiella, Bartonella)
8. Chest X-ray: Cardiomegaly, pulmonary edema, or septic emboli
9. ECG: New heart block (aortic root abscess spreading to AV node)

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MANAGEMENT

• Must be bactericidal, prolonged (4-6 weeks IV)
• Blood cultures must be obtained before starting
• Empirical therapy adjusted according to culture results

• Native valve: Amoxicillin + Flucloxacillin + Gentamicin IV
• If MRSA suspected/nosocomial: Vancomycin + Gentamicin
• Prosthetic valve: Vancomycin + Gentamicin + Rifampicin

• Heart failure due to severe valvular regurgitation (most common indication)
• Persistent bacteremia/fever despite 5-7 days of appropriate antibiotics
• Perivalvular abscess (aortic root abscess)
• Prosthetic valve endocarditis with dehiscence
• Large mobile vegetations (>10mm) with high embolic risk
• Fungal endocarditis
• Recurrent emboli despite treatment

• Daily clinical assessment, repeat blood cultures
• Weekly CRP, CBC, renal function
• Repeat echo if clinical deterioration

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ANTIBIOTIC PROPHYLAXIS FOR IE

1. Prosthetic cardiac valves (mechanical or bioprosthetic)
2. Transcatheter prosthetic valves
3. Cardiac valve repair with devices (annuloplasty rings, clips)
4. Previous IE
5. Congenital heart disease:
   • Unrepaired cyanotic CHD (including palliative shunts)
   • Completely repaired CHD with prosthetic material/device in first 6 months
   • Repaired CHD with residual defects at the prosthetic patch site
6. Cardiac transplant recipients who develop cardiac valvulopathy
7. Left ventricular assist devices (LVADs)

• Uncomplicated ASD, VSD, PDA (after complete repair)
• Isolated MVP without regurgitation
• Coronary artery disease
• Implanted pacemakers/defibrillators
• Previous CABG

• Dental procedures involving gingival tissue manipulation
• Manipulation of periapical region of teeth
• Perforation of oral mucosa (extractions, scaling)
• Respiratory tract procedures with incision/biopsy of respiratory mucosa
• Procedures on infected skin/musculoskeletal tissue

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QUESTION 3: RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE

Pathogenesis and Features

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DEFINITION

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EPIDEMIOLOGY

• Most common in children aged 5-15 years; no sex predilection
• Prevalent in developing countries (~100 cases/100,000 children/year)
• Associated with overcrowding, poverty, poor sanitation
• Occurs primarily in cooler months (mirroring streptococcal pharyngitis epidemiology)
• 1/3 of patients have mild or asymptomatic preceding streptococcal infection
• Recurrence is common without prophylaxis; risk decreases with time

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PATHOGENESIS

• S. pyogenes (Group A beta-hemolytic streptococcus) infects the pharynx
• Specific "rheumatogenic" M protein types (types 1, 3, 5, 6, 18) are responsible
• Important: Only pharyngeal infection (NOT skin infection) triggers RF

• 2-4 weeks after pharyngitis, the immune response goes awry
• Streptococcal M protein antigens share structural similarity with human heart tissue proteins:
  • Cardiac myosin
  • Sarcolemmal membrane proteins
  • Laminin (heart valve endothelium)
• Antibodies produced against streptococcal antigens (anti-streptolysin O, anti-M protein) cross-react with cardiac proteins
• CD4+ T cells also cross-react with cardiac antigens
• This autoimmune inflammation causes damage to the heart

• Fibrinous pericarditis
• Pericardial friction rub
• "Bread and butter" pericarditis appearance

• Aschoff bodies = pathognomonic lesion of RF
  • Focal areas of fibrinoid necrosis surrounded by
  • Large macrophages with owl-eye nuclei ("Anitschkow cells" / caterpillar cells)
  • Lymphocytes and plasma cells
  • Located in perivascular regions of myocardium
• Myocardial dysfunction, heart block

• Inflammation along the valve leaflets
• Small (1-2 mm), flat, firm, wartlike vegetations along the lines of valve closure
• Mitral valve most commonly affected (75%), then aortic (25%)
• Order of valve involvement: Mitral > Aortic > Tricuspid > Pulmonary ("MATP")

• Repeated episodes of valve inflammation cause:
  • Leaflet thickening and fibrosis
  • Commissural fusion
  • Chordae tendineae shortening, thickening, and fusion
  • Calcification (in advanced disease)
• Result: Predominantly Mitral Stenosis (MS) - "fish-mouth" valve appearance
• Also: Mitral regurgitation, aortic stenosis, aortic regurgitation

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CLINICAL FEATURES

Diagnostic Criteria: REVISED JONES CRITERIA (2015 AHA)

• Pancarditis affecting all 3 layers
• Most serious manifestation (only one that causes permanent damage)
• Murmurs: New murmur - mitral regurgitation (pansystolic at apex, most common), Carey-Coombs murmur (mid-diastolic - due to mitral valvulitis)
• Signs of heart failure (tachycardia, elevated JVP, hepatomegaly, pulmonary congestion)
• Pericardial friction rub
• Tachycardia out of proportion to fever
• Conduction abnormalities (prolonged PR interval)

• Migratory, fleeting arthritis
• Large joints mainly: knees, ankles, wrists, elbows
• Hot, swollen, tender joints
• Shifts from joint to joint (migratory)
• Very painful (exquisitely tender)
• Resolves completely without deformity
• Responds dramatically to aspirin (this response is so characteristic it is "diagnostic")

• Also called St. Vitus' dance
• Involuntary, purposeless, non-repetitive movements of the face, limbs
• Emotional lability
• Muscular weakness
• Late manifestation (2-6 months after streptococcal infection)
• Pure chorea alone is sufficient for diagnosis of RF (single major criterion)
• Self-limiting, resolves in weeks to months

• Pink/red macular rash with serpiginous (wavy) borders
• Clear center (rings) - margin extends outward
• Seen on trunk and proximal limbs (NOT the face)
• Non-pruritic, evanescent (comes and goes)
• Specific for RF (though uncommon)

• Hard, painless, freely movable nodules
• Located over bony prominences and tendons: elbows, knees, wrists, spine, scalp
• 3mm to 2cm in size
• Associated with severe carditis
• Similar histologically to Aschoff bodies

1. Fever (>38.5°C)
2. Elevated ESR (>60 mm/hr), CRP (>3 mg/dL)
3. Prolonged PR interval on ECG
4. Arthralgia (only if arthritis is not used as major criterion)

• Elevated or rising ASO (antistreptolysin O) titer - most commonly used
• Elevated anti-DNase B, anti-hyaluronidase
• Positive throat culture for GAS
• Positive rapid antigen test

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INVESTIGATIONS

1. Throat culture for Group A Streptococcus
2. ASO titer (Anti-Streptolysin O) - elevated in ~80%; useful retrospectively
3. Anti-DNase B - more sensitive for skin strains
4. CBC - leukocytosis, normocytic anemia
5. ESR, CRP - markedly elevated
6. ECG - prolonged PR interval (1st degree AV block), ST changes
7. Chest X-ray - cardiomegaly, pulmonary congestion
8. Echocardiography - subclinical carditis, valvular lesions; most sensitive for RHD

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MANAGEMENT

1. Antibiotic therapy (eradicate GAS):
   • Benzathine Penicillin G 1.2 million units IM single dose (gold standard)
   • OR Penicillin V oral 10 days
   • Amoxicillin 250 mg TID x 10 days (preferred in children)
   • If penicillin-allergic: Erythromycin 250 mg QID x 10 days
2. Anti-inflammatory therapy:
   • Arthritis without carditis: Aspirin 80-100 mg/kg/day in 4-5 doses (dramatic response expected)
   • Carditis (moderate-severe): Corticosteroids (Prednisolone 2 mg/kg/day, max 80 mg) for 2-4 weeks, then taper
3. Heart failure management: Digoxin, diuretics, ACE inhibitors
4. Sydenham's chorea: Haloperidol or valproate; penicillin prophylaxis
5. Bed rest: During acute phase

• Benzathine Penicillin G 1.2 million units IM every 3-4 weeks - most effective (drug of choice)
• Penicillin V 250 mg orally BD
• Sulfadiazine 1g daily (adults)
• If penicillin-allergic: Erythromycin 250 mg BD

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QUESTION 4: CONGESTIVE CARDIAC FAILURE (CCF)

Causes, Clinical Features, Management

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DEFINITION

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CLASSIFICATION

• Left heart failure: Reduced forward output + pulmonary congestion
• Right heart failure: Systemic venous congestion
• Biventricular (congestive) failure: Both sides involved

• HFrEF (Heart Failure with reduced EF, EF <40%): Systolic dysfunction - ventricle cannot contract adequately
• HFpEF (Heart Failure with preserved EF, EF >50%): Diastolic dysfunction - ventricle cannot relax/fill adequately

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CAUSES

1. Ischemic Heart Disease (most common cause in Western countries):
   • Myocardial infarction (acute or chronic)
   • Coronary artery disease with chronic ischemia
2. Hypertension (most common cause globally):
   • Pressure overload leads to LV hypertrophy, then failure
   • Diastolic dysfunction initially
3. Valvular Heart Disease:
   • Aortic stenosis/regurgitation (pressure/volume overload)
   • Mitral regurgitation (volume overload)
   • Mitral stenosis (impaired LV filling)
4. Cardiomyopathies:
   • Dilated cardiomyopathy (systolic dysfunction)
   • Hypertrophic cardiomyopathy (diastolic dysfunction)
   • Restrictive cardiomyopathy (diastolic dysfunction)
5. Myocarditis (viral, autoimmune)
6. Arrhythmias: Chronic AF, VT

1. Left heart failure (most common cause of RHF) - backed-up pressure from LHF
2. Pulmonary hypertension (primary or secondary)
3. Cor Pulmonale: RHF due to lung disease (COPD, pulmonary fibrosis)
4. Pulmonary stenosis / regurgitation
5. Tricuspid valve disease
6. RV infarction (inferior MI)
7. ASD, VSD, large PDA (congenital left-to-right shunts)

• Severe anemia
• Thyrotoxicosis
• Arteriovenous fistula
• Paget's disease of bone
• Beriberi (thiamine deficiency)
• Pregnancy

• Infection (especially pneumonia)
• Myocardial infarction
• Arrhythmias (especially fast AF)
• Non-compliance with medications or diet (excessive salt/fluid intake)
• Pulmonary embolism
• Hypertensive crisis
• Anemia
• Thyrotoxicosis
• Pregnancy
• NSAIDs (cause fluid retention)

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PATHOPHYSIOLOGY

1. Frank-Starling mechanism: Increased preload (ventricular filling) → increased stroke volume; but eventually the overstretched ventricle fails
2. Neurohormonal activation:
   • Sympathetic Nervous System (SNS): Increased catecholamines → tachycardia, increased contractility, vasoconstriction; short-term beneficial but long-term toxic to myocardium, causes arrhythmias
   • RAAS (Renin-Angiotensin-Aldosterone System): Reduced renal perfusion → renin → angiotensin II → vasoconstriction, aldosterone release → Na+/H2O retention → increased preload; long-term causes cardiac fibrosis and hypertrophy
   • ADH (vasopressin): Water retention → hyponatremia (dilutional), edema
3. Ventricular Remodeling:
   • LV dilation and eccentric hypertrophy (volume overload)
   • Concentric hypertrophy (pressure overload)
   • Progressive loss of myocytes, fibrosis, collagen deposition
   • Reduced EF, further cardiac dysfunction - a vicious cycle

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CLINICAL FEATURES

LEFT HEART FAILURE

1. Dyspnea on exertion (DOE): Earliest and most common symptom; initially on exertion, later at rest
2. Orthopnea: Dyspnea on lying flat; relieved by sitting up; caused by redistribution of blood from legs to central circulation; graded in terms of pillows
3. Paroxysmal Nocturnal Dyspnea (PND): Patient wakes from sleep after 1-3 hours with severe breathlessness; sits up, opens window; due to re-absorption of peripheral edema + reduction in adrenergic drive during sleep
4. Cardiac Asthma: Bronchospasm due to pulmonary congestion
5. Acute Pulmonary Edema: Severe form - frothy, pink-tinged sputum; extreme distress
6. Fatigue and weakness: Reduced cardiac output
7. Nocturia: Nocturnal fluid redistribution from periphery; renal perfusion improves at night

• Tachycardia (compensatory)
• Displaced apex beat (cardiomegaly, LV dilation) - displaced laterally and inferiorly
• S3 gallop (ventricular filling in dilated LV) - "Ken-tuc-ky" rhythm; indicates systolic failure
• S4 gallop (atrial kick against stiff LV) - diastolic dysfunction
• Mitral regurgitation murmur (functional - due to LV dilation)
• Pulsus alternans (alternating strong and weak beats - severe LV failure)
• Fine basal crepitations (bilateral, due to pulmonary edema; do NOT clear with coughing)
• Pleural effusion (typically bilateral, larger on right)
• Cheyne-Stokes respiration (in severe LV failure - alternating hyperpnea/apnea)

RIGHT HEART FAILURE

• Ankle/leg swelling (pitting edema)
• Abdominal swelling, fullness (ascites, hepatomegaly)
• Anorexia, nausea (hepatic and gut congestion)
• Fatigue

• JVP elevated (most important sign) - raised >3 cm above sternal angle
  • Hepatojugular reflux (HJR) positive - pressing on liver causes JVP to rise
• Pitting edema: Ankle/pretibial (ambulant patients); sacral (bedridden patients); anasarca (generalized edema)
• Tender hepatomegaly: Smooth, pulsatile (if TR present)
• Ascites: Transudate (protein <25g/L)
• Pleural effusion (usually bilateral)
• Raised S2 (P2 component): If pulmonary hypertension present
• Right ventricular heave (parasternal left sternal edge)
• Tricuspid regurgitation murmur (functional)
• Splenomegaly (chronic passive congestion)
• Icterus (jaundice): Cardiac cirrhosis in long-standing RHF

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INVESTIGATIONS

1. ECG:
   • LVH (tall R in V5/V6, deep S in V1, strain pattern)
   • AF (common precipitant and consequence)
   • Old MI, LBBB, RVH
   • Prolonged QRS (LBBB - indicates dyssynchrony, candidate for CRT)
2. Chest X-ray (CXR) - "ABCDE" of CCF:
   • Alveolar edema (bat-wing/butterfly shadows)
   • B-lines/Kerley B lines (horizontal lines at lung bases - interstitial edema)
   • Cardiomegaly (CTR >0.5)
   • Diversion (upper lobe blood diversion/venous prominence in upper zones)
   • Effusions (pleural effusions - blunting of costophrenic angles)
3. Echocardiography (most important investigation):
   • Assesses EF (systolic vs diastolic failure)
   • Identifies cause (valvular, cardiomyopathy, regional wall motion abnormality)
   • LV size, wall thickness
   • Diastolic function (tissue Doppler)
   • Pulmonary artery pressure
4. BNP / NT-proBNP:
   • Most useful biomarker for diagnosis and monitoring of HF
   • BNP >100 pg/mL or NT-proBNP >300 pg/mL = HF likely
   • Elevated due to ventricular wall stress
   • Used to guide therapy and predict prognosis
5. Blood tests:
   • CBC (anemia as cause/aggravant)
   • Renal function (cardiorenal syndrome, pre-treatment)
   • Electrolytes (hyponatremia = poor prognosis; K+ important with diuretics)
   • LFTs (hepatic congestion)
   • TFTs (thyrotoxicosis as cause)
   • Fasting glucose, lipids
   • Troponin (if acute MI suspected)
6. Urinalysis: Proteinuria, microalbuminuria

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MANAGEMENT

A. GENERAL / NON-PHARMACOLOGICAL

• Fluid restriction: <1.5-2 L/day
• Salt restriction: <2g sodium/day
• Daily weight monitoring: Alert if >2 kg gain in 2 days (fluid retention)
• Rest (acute decompensation); graded exercise program (stable CHF - proven to improve outcomes)
• Smoking cessation, alcohol restriction (alcoholic cardiomyopathy)
• Treat underlying cause (revascularization, valve surgery, arrhythmia control)
• DVT prophylaxis (hospitalized patients)

B. PHARMACOLOGICAL MANAGEMENT

• Loop diuretics (first choice): Furosemide 20-80 mg/day oral or IV
  • Acts on Na+/K+/2Cl- cotransporter in thick ascending loop of Henle
  • Rapid symptom relief; reduces congestion
  • SE: Hypokalemia, dehydration, ototoxicity
• Thiazide diuretics (metolazone): Added to loop diuretics for diuretic resistance
• Aldosterone antagonists (spironolactone/eplerenone): Added for potassium-sparing and mortality benefit (see below)

• ACE inhibitors: Lisinopril, ramipril, enalapril
  • Block RAAS → reduce angiotensin II → reduce afterload + preload
  • Reduce LV remodeling
  • Reduce mortality by ~25% in HFrEF
  • Start low, titrate up
  • SE: Dry cough (switch to ARB), hyperkalemia, renal impairment, angioedema
• ARBs: Candesartan, losartan, valsartan - if ACE inhibitor intolerant
• ARNI (Sacubitril/Valsartan): Superior to ACE inhibitor in HFrEF; increases natriuretic peptides while blocking RAAS

• Carvedilol, bisoprolol, metoprolol succinate
• Block SNS overactivation → reduce HR, prevent arrhythmias, allow LV remodeling reversal
• Improve EF and reduce mortality by ~35%
• Start at very low dose, titrate slowly
• DO NOT start in acutely decompensated HF
• SE: Bradycardia, hypotension, bronchospasm (avoid in asthma)

• Spironolactone / Eplerenone
• Block aldosterone → reduce fibrosis and adverse remodeling; also K+-sparing
• Add in persistent HFrEF (EF <35%) despite ACE-I + beta-blocker
• Reduce mortality ~30%
• SE: Hyperkalemia, gynecomastia (spironolactone)

• Dapagliflozin, empagliflozin
• Reduce HF hospitalizations and CV mortality in both HFrEF and HFpEF
• Osmotic diuresis; reduce myocardial fibrosis and inflammation
• Now considered "4th pillar" of HFrEF therapy

• Positive inotrope (inhibits Na+/K+ ATPase) + rate control (AV node effect)
• Use in: Symptomatic HFrEF despite optimal therapy; HF with AF for rate control
• Narrow therapeutic window; monitor serum levels
• SE: Arrhythmias, nausea, visual disturbances (yellow vision), bradycardia
• Toxicity worsened by hypokalemia (common with loop diuretics)

• Alternative to RAAS blockade if intolerant (e.g., renal failure, hyperkalemia)
• Particularly beneficial in African-American patients

C. DEVICE THERAPY

• ICD (Implantable Cardioverter-Defibrillator): EF ≤35% despite optimal therapy + expected survival >1 year - for sudden cardiac death prevention
• CRT (Cardiac Resynchronization Therapy): LBBB with QRS >150ms + EF ≤35%; improves LV synchrony, EF, and quality of life
• CRT-D: Combines both

D. MANAGEMENT OF ACUTE DECOMPENSATED HF (Acute Pulmonary Edema)

• Lay patient upright (sitting position - reduces preload)
• Morphine 2-4 mg IV (reduces anxiety, dilates veins)
• Nitrates (IV GTN - powerful vasodilator, reduces preload and afterload)
• Oxygen (high-flow; CPAP/BiPAP in respiratory failure)
• Pump (IV Furosemide 40-80 mg - diuresis)
• Treat precipitating cause (AF → rate control; HTN → IV antihypertensives)
• If cardiogenic shock: Inotropes (dobutamine, dopamine); IABP; urgent revascularization

E. ADVANCED / END-STAGE HF

• Heart transplantation (EF <25%, refractory symptoms, no response to medical therapy)
• Left Ventricular Assist Devices (LVAD): Bridge to transplant or destination therapy
• Palliative care (end-stage)

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SUMMARY TABLE - KEY HIGH-Yield Points for Exam

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