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🫀 VALVULAR HEART DISEASE

Quick Mental Framework

Think of valvular lesions in 2 categories:

• Stenosis = valve won't open properly → pressure overload upstream
• Regurgitation = valve won't close properly → volume overload of the receiving chamber

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1. AORTIC STENOSIS (AS)

Pathophysiology in one line

Causes

Grading (by valve area)

Classic Symptom Triad (SAD = Syncope → Angina → Dyspnea)

• Syncope (especially exertional) — worst prognosis signal (mean survival 3 yrs)
• Angina — mean survival 5 yrs
• Dyspnea / Heart Failure — mean survival 2 yrs
• Also: sudden cardiac death (~5%), TIAs from calcium emboli, GI bleeding (Heyde's syndrome)

Clinical Signs

• Slow-rising, small-volume pulse (pulsus parvus et tardus) — carotid delayed
• Narrow pulse pressure
• Heaving, undisplaced apex beat (concentric hypertrophy)
• Ejection systolic murmur — harsh, crescendo-decrescendo, at aortic area (2nd right ICS), radiates to carotids
• Single or paradoxically split S2 (severe AS)
• S4 gallop (stiff LV)

Investigations

• LVH (Sokolow-Lyon criteria: S in V1 + R in V5/V6 > 35 mm)
• Left axis deviation
• ST depression, T-wave inversion (strain pattern)

• Normal heart size initially (concentric hypertrophy, not dilation)
• Post-stenotic dilatation of ascending aorta
• Calcification of aortic valve (seen on lateral CXR)
• Pulmonary congestion in late stages

• Doppler gradient across valve (mean gradient >40 mmHg = severe)
• Valve area calculation (continuity equation)
• LV wall thickness, function, LVEF
• Monitoring schedule: every 3–5 yrs (mild), 1–2 yrs (moderate), 1 yr (severe)

• Direct pressure measurement (when echo is inconclusive)
• Coronary angiography before AVR if CAD suspected (mandatory >40 yrs)

⚠️ Exercise testing is contraindicated in symptomatic severe AS

Management

• Treat HF conservatively (diuretics cautiously — preload-dependent)
• Statins do NOT slow progression
• Balloon aortic valvuloplasty: temporary bridge in very elderly/high surgical risk; does NOT provide sustained benefit

1. Symptomatic severe AS (Class I)
2. Asymptomatic severe AS + LVEF <50%
3. Severe AS undergoing other cardiac surgery
4. Rapid progression + very severe AS

• For high/intermediate surgical risk patients
• Now increasingly used even in lower risk patients

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2. AORTIC REGURGITATION (AR)

Pathophysiology

Causes

Symptoms

• Chronic AR is long asymptomatic (LV compensates)
• Eventually: exertional dyspnea, orthopnea, PND
• Palpitations (hyperdynamic circulation)
• Angina (increased myocardial O₂ demand + low diastolic pressure)
• Acute AR = emergency: sudden pulmonary edema, cardiogenic shock

Clinical Signs — The "Peripheral Signs" of AR (all from wide pulse pressure)

Investigations

• Cardiomegaly (enlarged LV)
• Dilated ascending aorta
• In acute AR: pulmonary edema without cardiomegaly

• LV dimensions (end-diastolic, end-systolic diameters)
• LVEF
• Regurgitant fraction/jet size
• Aortic root dimensions

Management

• Vasodilators (nifedipine, hydralazine, ACE inhibitors) — reduce afterload, reduce regurgitant fraction; especially in those with symptoms/hypertension who are not yet surgical candidates
• Avoid bradycardia (worsens AR — more time for backflow)

1. Symptomatic severe AR
2. Asymptomatic severe AR + LVEF ≤50% or
3. Asymptomatic + LV severely dilated (LVESD >50 mm)
4. Acute severe AR = surgical emergency

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3. MITRAL STENOSIS (MS)

Pathophysiology

Cause

Symptoms

• Exertional dyspnea (most common)
• Hemoptysis (pink frothy sputum, or rust-colored from alveolar hemorrhage)
• Atrial fibrillation (LA dilation) → palpitations, systemic emboli, stroke
• Hoarseness — Ortner's syndrome (enlarged LA compresses left recurrent laryngeal nerve)
• Signs of pulmonary hypertension and right heart failure (late)

Clinical Signs

• Malar flush (mitral facies) — chronic low CO + peripheral vasodilation
• Tapping apex beat (palpable loud S1)
• Loud S1 (partially open, stiff leaflets snap shut)
• Opening snap (OS) — early in diastole; shorter S2–OS interval = more severe
• Rumbling mid-diastolic murmur at apex (low-pitched, best heard in left lateral position with bell) with presystolic accentuation (due to atrial systole — disappears in AF)
• Signs of pulmonary hypertension: loud P2, RV heave, TR murmur

Investigations

• P mitrale — broad, bifid P wave in lead II (LA enlargement)
• AF (very common)
• RVH if pulmonary hypertension develops (right axis deviation, tall R in V1)

• LA enlargement: double heart shadow, splaying of carina >65°, straightening of left heart border
• Kerley B lines (pulmonary venous hypertension)
• Prominent pulmonary arteries (later)
• Normal-sized or small LV (LV is underfilled)

• Mitral valve area (pressure half-time method or planimetry)
• Wilkins score (guides suitability for balloon valvuloplasty): scores leaflet mobility, thickening, calcification, subvalvular involvement. Score ≤8 = good candidate for PTMC
• LA size, LA thrombus (TEE if LA thrombus suspected before any procedure)
• Pulmonary artery pressure

Management

• Rate control in AF: beta-blockers, digoxin
• Anticoagulation (warfarin) if AF, LA thrombus, or prior embolism
• Diuretics for pulmonary congestion
• No vasodilators (preload-dependent — they cause hypotension)
• Penicillin prophylaxis against rheumatic fever recurrence

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4. MITRAL REGURGITATION (MR)

Pathophysiology

Causes

Symptoms

• Chronic MR → long asymptomatic period
• Exertional dyspnea, fatigue, orthopnea
• Palpitations (AF)
• Acute MR (papillary muscle rupture): acute pulmonary edema, emergency

Clinical Signs

• Displaced, hyperdynamic apex beat (volume overload)
• Soft/absent S1
• Pansystolic (holosystolic) murmur — best at apex, radiates to axilla
• S3 (rapid ventricular filling due to large volume)
• Signs of LHF and RHF in late stages

Investigations

• P mitrale (LA enlargement)
• LVH, AF

• LA and LV enlargement
• Pulmonary venous congestion

• Mechanism of MR (leaflet, chordae, annulus, functional)
• LV size and function (EF can be falsely normal early — LV ejects into low-pressure LA)
• Severity grading (regurgitant volume, effective regurgitant orifice area)
• TEE for surgical planning

Management

• ACE inhibitors/ARBs (reduce afterload, reduce regurgitant fraction)
• Diuretics for congestion
• Beta-blockers for AF/HF
• Anticoagulation if AF

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🩺 DECOMPENSATED CHRONIC LIVER DISEASE (DCLD)

What is DCLD?

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Pathophysiology (The Core Mechanism)

Liver fibrosis → Portal hypertension
                       ↓
         Splanchnic arterial vasodilation (NO mediated)
                       ↓
         Effective arterial blood volume ↓
                       ↓
         Activation of RAAS + SNS + ADH
                       ↓
         ┌─────────────┬──────────────────┐
         ↓             ↓                  ↓
    Na retention   Water retention   Renal vasoconstriction
         ↓             ↓                  ↓
      Ascites    Dilutional hyponatremia   HRS

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Investigations of DCLD

Blood Tests

Scoring Systems

Imaging

Ascitic Fluid Analysis (Diagnostic Paracentesis)

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Complications of DCLD and Their Management

1. Ascites

• Grade 1: mild, detectable only by USG
• Grade 2: moderate, detectable clinically
• Grade 3: large with marked abdominal distention

• Serum Na <125 mEq/L
• AKI
• Hepatic encephalopathy
• K <3 mEq/L (stop furosemide) or K >5.5 mEq/L (stop spironolactone)

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2. Spontaneous Bacterial Peritonitis (SBP)

• IV Cefotaxime 2 g 8-hourly × 5 days (drug of choice)
• IV Albumin 1.5 g/kg at diagnosis + 1 g/kg at day 3 → reduces HRS risk and mortality
• Alternative: Amoxicillin-clavulanate in non-severe cases

• Primary: Norfloxacin 400 mg OD if ascitic protein <1.5 g/dL + Child C or renal impairment
• Secondary (after 1st episode): Norfloxacin 400 mg OD or Ciprofloxacin 500 mg OD (lifelong until transplant)

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3. Hepatic Encephalopathy (HE)

• Transplant contraindications/Trauma/Toxins (alcohol binge, drugs, opioids)
• Infection (SBP, UTI, pneumonia — most common)
• Portal hypertension complications (GI bleed — blood = protein load in gut)
• Sodium/electrolyte imbalance, Sedatives, Surgery, constipation, renal failure

1. General care: Airway (oxygen, NGT if needed), IV access, stabilize BP, ICU if severe
2. Identify and treat precipitants: Cultures, treat infection, stop bleeding, correct electrolytes, stop sedatives/opioids
3. Neurological assessment: Rule out other causes (CT head, glucose, drugs)
4. Pharmacotherapy:
   • Lactulose (1st line): 30 mL 2–4 hourly until 2–3 soft stools/day; mechanism = gut acidification → NH₃ → NH₄⁺ (not absorbed) + osmotic cathartic + modulates gut microbiota
   • Rifaximin 550 mg BD (add-on/maintenance): non-absorbable antibiotic, reduces ammonia-producing gut bacteria; excellent for secondary prophylaxis
   • Nutrition: 35–40 kcal/kg/day, 1.2–1.5 g protein/kg/day (do NOT restrict protein — increases muscle wasting which worsens HE); plant protein > animal protein

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4. Variceal Hemorrhage

1. Resuscitation: 2 large-bore IV, blood transfusion (target Hb 7–8 g/dL — over-transfusion worsens portal pressure)
2. Vasoactive drugs (start immediately, before endoscopy):
   • Terlipressin 2 mg IV 4-hourly (drug of choice) OR Somatostatin/Octreotide
   • Continue for 3–5 days
3. Antibiotics: IV Ceftriaxone 1 g OD × 7 days (reduces bacterial infection + improves outcomes)
4. Urgent endoscopy (within 12 hours):
   • Band ligation (EVL) — treatment of choice for esophageal varices
   • Cyanoacrylate injection — for gastric varices
5. Balloon tamponade (Sengstaken-Blakemore tube): bridge to TIPS/endoscopy if uncontrolled bleeding
6. TIPS: For refractory/recurrent variceal bleeding not controlled by above

• Non-selective beta-blockers: Propranolol or Carvedilol (reduce portal pressure)
• OR EVL (esophageal band ligation)

• NSBBs + EVL (combination is standard of care)

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5. Hepatorenal Syndrome (HRS)

• Terlipressin + Albumin (1st line): vasopressor reverses splanchnic vasodilation, albumin expands effective blood volume
• Norepinephrine + Albumin (ICU alternative)
• TIPS: Bridges to transplant
• Liver transplant: Only definitive cure

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6. Hepatocellular Carcinoma (HCC) Screening

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Summary Table: DCLD Complications at a Glance

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Summary Table: Valvular Heart Disease at a Glance

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How to Use This Guide

• AS and MS = Stenosis = obstruction upstream → pressure overload
• AR and MR = Regurgitation = volume leaks back → volume overload
• Investigations follow the same sequence every time: ECG → CXR → Echo (always key) → Cath if needed
• Surgery/intervention is indicated when symptoms appear OR LV starts to fail (measured by EF and dimensions on echo)

• Portal hypertension + splanchnic vasodilation → RAAS activation → all complications flow from this
• The 6 major complications each have a specific trigger, test, and targeted treatment
• Albumin is the common thread across ascites (post-LVP), SBP (alongside antibiotics), and HRS (with terlipressin)
• Liver transplant is the only definitive treatment for all complications

• SAAG ≥1.1 = portal hypertension
• Ascitic PMN >250 = SBP (treat before culture results)
• Spiro:Furo ratio = 100:40 (2.5:1)
• Lactulose target = 2–3 soft stools/day
• Transfuse to Hb 7–8 in variceal bleed (not higher)