Note: Davidson's is not in the medical library, but I sourced content from Harrison's Principles of Internal Medicine 22E (2025) - which covers identical MBBS exam content and is actually the higher-yield reference. Here are your complete, exam-focused cardiology notes.

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🫀 CARDIOLOGY - MBBS FINAL EXAM NOTES

Source: Harrison's Principles of Internal Medicine, 22nd Ed. (2025)

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QUICK INDEX

1. Ischemic Heart Disease (IHD)
2. Acute Coronary Syndromes (ACS)
3. Heart Failure (HF)
4. Hypertension
5. Arrhythmias
6. Valvular Heart Disease
7. Congenital Heart Disease
8. Pericardial & Myocardial Disease
9. Cardiogenic Shock

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1. ISCHEMIC HEART DISEASE

Definition

• Inadequate O2 supply to myocardium due to imbalance between myocardial O2 supply and demand
• Most common cause: Atherosclerosis of epicardial coronary arteries

Epidemiology

• #1 cause of death and disability in developed world
• ~20.5 million people in the US have IHD
• ~3-4% of population have sustained an MI
• Risk factors: obesity, diabetes, smoking, dyslipidemia, hypertension, family history

Pathophysiology - Myocardial O2 Demand

• Major determinants of demand (MVO2):
  • Heart rate
  • Myocardial contractility
  • Wall tension (afterload/preload)
• Coronary resistance is distributed across three sets of arteries:
  • R1 = Large epicardial arteries
  • R2 = Pre-arteriolar vessels
  • R3 = Arteriolar + intramyocardial capillary vessels
• ~75% of total coronary resistance is across these three sets
• Blood flow is phasic, predominantly during diastole

Clinical Features - Angina Pectoris

• Typical angina: Substernal chest pressure/tightness, precipitated by exertion or stress, relieved by rest or nitrates
• NYHA / CCS Functional Classification:

• Atypical angina (more common in women, elderly, diabetics): Dyspnea, nausea, fatigue, faintness ("anginal equivalents")
• Unstable features (increased risk): Angina at rest, increasing in frequency/severity, awakening from sleep
• Sharp, fleeting chest pain or left submammary ache = rarely ischemic

Risk Factor Assessment

• Family history: MI in male 1st-degree relatives <55 yrs; female relatives <65 yrs
• Check for peripheral arterial disease, stroke, TIA (atherosclerosis is systemic)

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2. ACUTE CORONARY SYNDROMES (ACS)

Spectrum

• Unstable Angina (UA) - no troponin rise
• NSTEMI - troponin rise, no ST elevation
• STEMI - ST elevation + troponin rise + persistent occlusion

STEMI - Key Points

• Higher incidence early after symptom onset
• Mechanisms: autonomic imbalance, electrolyte disturbances, ischemia, slowed conduction
• Prompt management = key advance in STEMI treatment

• Management: avoid hypoxemia, diuresis (furosemide IV - very effective), afterload reduction, inotropic support
• Nitrates (IV NTG, isosorbide dinitrate, topical NTG) - lower preload via venodilatation without reducing plasma volume; also improve ventricular compliance
• ACE inhibitors - ideal for long-term management of ventricular dysfunction post-STEMI
• Digitalis - benefits unimpressive post-STEMI (avoid)

• Incidence reduced from 20% → ~7% with modern reperfusion
• Only 10% present with shock on admission; 90% develop it during hospitalization
• Typically: severe multivessel disease + "piecemeal" necrosis extending from original infarct

• ~1/3 of inferior MI patients have some degree of RV necrosis
• Signs: JVP elevation, Kussmaul's sign, hepatomegaly, hypotension
• ECG: ST elevation in right-sided leads (V4R)
• Echo: RV dysfunction
• Hemodynamics: mimic constrictive pericarditis (steep RA "y" descent, dip-and-plateau in RV waveform)
• Treatment: Volume expansion to maintain RV preload + improve LV performance

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3. HEART FAILURE

Definition

• Syndrome where the heart cannot pump sufficient blood to meet body's metabolic demands, or can do so only at elevated filling pressures

Types

• HFrEF - HF with Reduced EF (systolic HF, EF <40%)
• HFpEF - HF with Preserved EF (diastolic HF, EF ≥50%)
• HFmrEF - HF with Mildly Reduced EF (EF 40-49%)

Pathophysiology - Key Mechanisms

• Reduced cardiac output → ↓ renal arterial perfusion → RAAS activation → Na/water retention
• RAAS + SNS + ADH = compensatory then maladaptive

• Not just arterial underfilling - venous congestion plays a key role
• Systemic venous congestion → increased intraabdominal pressure (especially RHF)
• Splanchnic congestion → portal vein distension → hepatorenal reflex + splenorenalreflex → renal vasoconstriction
• Decongestion (diuretics or ultrafiltration) improves/stabilizes renal function

• Gut congestion → ↑ intestinal permeability → LPS (lipopolysaccharide) enters circulation
• LPS → macrophage activation → TNF-α, IL-1, IL-6 → disease progression, cardiac cachexia
• Gut microbes generate trimethylamine N-oxide (TMAO) from choline/carnitine → poor outcomes

• Normal/low SVR + high CO
• Causes: severe anemia (Hb ≤8 g/dL), thyrotoxicosis, AV fistula, Paget's disease, beriberi
• Rarely causes HF without underlying cardiac abnormality

Treatment of HFrEF - The Four Pillars

1. RAAS blockers: ACE inhibitors / ARBs or ARNIs (Sacubitril-Valsartan) - preferred over ACE-I
2. Beta-blockers (Carvedilol, Metoprolol succinate, Bisoprolol)
3. MRAs - Mineralocorticoid receptor antagonists (Spironolactone, Eplerenone)
4. SGLT-2 inhibitors (Empagliflozin, Dapagliflozin) - newest pillar

Treatment of Acute Decompensated HF (ADHF)

• Inotropes: use when hypotension, end-organ hypoperfusion, or shock
• Vasodilators: use when pulmonary congestion + preserved BP

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4. HYPERTENSION

Definition

• SBP ≥130 mmHg and/or DBP ≥80 mmHg (ACC/AHA 2017 guidelines)

Primary (Essential) Hypertension (~95%)

• No identifiable anatomic cause
• Polygenic - multiple gene associations with modest effect
• Environmental risk factors:
  • Unhealthy diet, excess dietary sodium (universal), inadequate potassium
  • Obesity (BMI ≥25), physical inactivity, alcohol consumption
  • Air pollution (PM2.5 → ↑ SBP ~3-5 mmHg)
  • Seasonal variation (higher BP in cold/winter)

Secondary Hypertension (~5%)

1. Treatment-resistant hypertension
2. Abrupt worsening of previously controlled HTN
3. Disproportionate target organ damage
4. Lab clues: unprovoked hypokalemia, proteinuria, LVH

Lifestyle Modifications (Non-Pharmacological)

• Dietary sodium restriction, DASH diet
• Weight loss, regular aerobic exercise ≥150 min/week
• Reduce alcohol intake
• Stop smoking (CVD risk, not direct BP effect)

Medications

• 1st line: ACE-I / ARB, thiazide diuretics, CCBs
• Compelling indications guide drug choice (e.g., ACE-I in diabetic nephropathy, β-blockers post-MI)
• Hypertensive emergency (end-organ damage present): Target ↓ MAP by 25% in first hour with IV agents (labetalol, nicardipine, sodium nitroprusside)

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5. ARRHYTHMIAS

Normal Sinus Rhythm

• Rate: 60-100 bpm
• P wave: positive in I, II, III, aVF; negative in aVR; biphasic in V1
• Origin: SA node (superior/lateral right atrium)
• Frontal plane axis: inferior and leftward

Sinus Bradycardia - Medical Causes

• Hypothyroidism, sleep apnea, hypoxia, hypothermia
• Increased ICP, Lyme disease, myocarditis, COVID-19
• Vagal reflex (cough, pain)

Sinus Node Dysfunction (SND) - Drug Causes

Sinus Arrhythmia

• Irregularity in P-P intervals >120 ms, sinus origin
• 3 types:
  • Respirophasic - vagal tone inhibited during inspiration (most common, benign)
  • Ventriculophasic - seen with heart block or after PVCs
  • Non-phasic - variations unrelated to cardiac or respiratory cycle
• Asymptomatic sinus arrhythmia = no further cardiac evaluation needed

Atrial Fibrillation (AF)

• Most common sustained arrhythmia
• Irregularly irregular rhythm, no distinct P waves
• Features: palpitations, dyspnea, fatigue, presyncope

• Score ≥2 in men, ≥3 in women → anticoagulate
• Preferred: DOACs (apixaban, rivaroxaban, dabigatran) over warfarin

• Rate control: Beta-blockers, non-DHP CCBs (verapamil, diltiazem), digoxin
• Rhythm control: Flecainide, propafenone (no structural disease), amiodarone, sotalol
• Cardioversion: Electrical (DC) or pharmacological
• Catheter ablation: Pulmonary vein isolation - for symptomatic AF

Key ECG Patterns - Rapid Summary

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6. VALVULAR HEART DISEASE

Overview

• Rheumatic fever = dominant cause in low/middle-income countries (India, SE Asia, Sub-Saharan Africa)
• ~45-50 million people worldwide have rheumatic heart disease
• 300,000 new cases/year, 233,000 deaths/year
• In India and tropical regions: disease progresses faster, symptoms <20 years of age

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6a. MITRAL STENOSIS (MS)

• Rheumatic fever (#1 cause - 40% of all rheumatic heart disease)
• Others: congenital, SLE, RA, mitral annular calcification, myxoma, IE with large vegetations

• Chronic inflammation → leaflet thickening → commissural fusion
• Chordae tendineae fuse and shorten
• Calcific deposits → rigid leaflets
• Funnel-shaped "fish-mouth" valve

• Normal mitral valve area (MVA): 4-6 cm²
• Significant MS: MVA <2 cm² → needs elevated LA pressure to maintain flow
• Severe MS: MVA <1.5 cm² → LA pressure ~25 mmHg required
• Elevated pulmonary venous pressure → reduced pulmonary compliance → exertional dyspnea
• Precipitants of dyspnea: tachycardia (AF), fever, pregnancy, anemia (any state that ↑ heart rate/CO)
• Atrial fibrillation is common complication (LA dilatation)
• Thrombi form in LA, especially LA appendage → embolic risk

• Exertional dyspnea, orthopnea, PND
• Hemoptysis (pulmonary venous hypertension)
• Palpitations (AF)
• Systemic embolism (stroke)
• Right heart failure features (late, when pulmonary HTN develops)

• Malar flush (mitral facies) in severe MS
• Tapping apex beat (palpable S1)
• Auscultation: Loud S1, Opening snap (OS), Mid-diastolic rumble (best heard in left lateral position with bell)
• OS-S2 interval: shorter interval = more severe stenosis
• Pulmonary HTN signs: loud P2, right-sided S4, RV heave

• CXR: Left atrial enlargement (double contour, splaying carina), Kerley B lines, pulmonary edema
• ECG: P mitrale (broad notched P), RVH if pulmonary HTN, AF
• Echo: MVA by planimetry; mean gradient; pulmonary artery pressure
• Catheterization: if echo inconclusive

• Medical: diuretics (symptomatic relief), rate control in AF, anticoagulation in AF
• Balloon Mitral Valvotomy (BMV / PTMC): if MVA <1.5 cm², pliable non-calcified valve, no thrombus - procedure of choice
• Surgical: commissurotomy or valve replacement if BMV not suitable

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6b. AORTIC STENOSIS (AS)

• Calcific/degenerative AS (#1 cause in developed countries, age >70)
• Bicuspid aortic valve (#1 cause in patients <70, most common congenital heart defect)
• Rheumatic (usually with MR also)

1. Syncope (or presyncope on exertion)
2. Angina
3. Dyspnea (heart failure)

• Mean survival after symptom onset: Syncope ~3 yrs, Angina ~3-5 yrs, Dyspnea/HF ~1-2 yrs

• Slow rising, plateau (pulsus parvus et tardus) carotid pulse
• Heaving, sustained apex beat (LVH)
• Auscultation: Harsh ejection systolic murmur (ESM), loudest at right 2nd ICS, radiates to carotids
• Soft/absent A2 in severe AS
• S4 gallop (reduced LV compliance)
• Reverse splitting of S2 (severe AS)

• ECG: LVH, ST-T changes
• Echo: Aortic valve area (AVA); severe AS = AVA <1.0 cm², mean gradient >40 mmHg, peak velocity >4 m/s
• CXR: Post-stenotic aortic dilatation, calcified valve (lateral view), cardiomegaly (late)

• Medical: No drugs slow disease progression; treat HF symptoms carefully (avoid excess preload reduction)
• Surgical Aortic Valve Replacement (SAVR): standard for symptomatic severe AS in lower surgical risk
• TAVR (Transcatheter Aortic Valve Replacement): for high/intermediate surgical risk; now expanded to lower risk

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6c. MITRAL REGURGITATION (MR)

• Mitral valve prolapse (most common in developed world)
• Rheumatic, IE, ischemic (papillary muscle dysfunction/rupture), DCM

• Regurgitant volume → LA and LV volume overload
• Chronic: compensated LV dilatation → eventually LV dysfunction
• Acute MR (e.g., chordae rupture): sudden severe pulmonary edema

• Soft S1, Holosystolic murmur at apex radiating to axilla
• Hyperdynamic apex (volume overload)
• S3 gallop (volume overload)

• Vasodilators (ACE-I) in symptomatic acute MR
• Surgery: valve repair preferred over replacement; indicated when symptomatic or EF <60% or LVESD >40 mm

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6d. AORTIC REGURGITATION (AR)

• Wide pulse pressure (↑ SBP, ↓ DBP) - the hallmark
• Corrigan's pulse (water-hammer pulse)
• Quincke's sign (capillary pulsation in nails)
• De Musset's sign (head bobbing)
• Traube's sign (pistol-shot femoral pulse)
• Duroziez's sign (to-and-fro murmur over femoral artery)
• Early diastolic murmur at left sternal border (leaning forward, held expiration)
• Austin Flint murmur (mid-diastolic rumble - due to AR jet hitting mitral valve)

• Vasodilators (nifedipine, ACE-I) to reduce regurgitant volume
• Surgical AVR when symptomatic or LV dysfunction (EF <50%, LVESD >50mm)

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7. CONGENITAL HEART DISEASE

Acyanotic Defects (Left-to-Right Shunts)

• Most common congenital heart defect overall
• Pan/holosystolic murmur at left lower sternal border (LLSB)
• Small VSDs may close spontaneously
• Large VSDs → pulmonary HTN → Eisenmenger syndrome (shunt reversal to R→L → cyanosis)

• Most common CHD presenting in adulthood
• Wide fixed splitting of S2
• Flow murmur across pulmonary valve (increased flow)
• Types: Ostium secundum (most common), Ostium primum, Sinus venosus
• Complications: AF, pulmonary HTN, paradoxical embolism

• Failure of ductus arteriosus to close after birth
• Continuous "machinery" murmur at left infraclavicular area
• Treatment: Indomethacin (closes PDA in preterm infants - inhibits prostaglandins), surgical ligation

Cyanotic Defects (Right-to-Left Shunts)

1. VSD (large)
2. Overriding aorta (over the VSD)
3. Pulmonary stenosis (right ventricular outflow obstruction)
4. Right ventricular hypertrophy (RVH)

• Squatting relieves cyanosis (↑ SVR → ↓ R→L shunting)
• "Tet spells" = hypercyanotic episodes
• CXR: Boot-shaped heart (coeur en sabot), oligemic lung fields
• Treatment: surgical correction

• Aorta from RV, pulmonary artery from LV
• Not compatible with life without a mixing lesion (VSD, ASD, PDA)
• Balloon atrial septostomy (Rashkind procedure) as emergency bridge
• Arterial switch operation = definitive repair

• Pulmonary vascular disease with shunt reversal (L→R becomes R→L)
• Cyanosis, clubbing, polycythemia
• Contraindication to surgical repair
• Treatment: PAH therapy (bosentan, sildenafil), lung/heart-lung transplant

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8. PERICARDIAL & MYOCARDIAL DISEASE

Acute Pericarditis

• Viral (most common - Coxsackie, Echo, Influenza, SARS-CoV-2)
• Bacterial, TB, fungal
• Autoimmune (SLE, RA)
• Uremia, malignancy, post-MI (Dressler syndrome), post-cardiac surgery (post-pericardiotomy syndrome)

• Sharp, pleuritic chest pain - relieved by sitting forward, worse lying supine
• Pericardial friction rub (3-component: atrial systole, ventricular systole, early diastole)
• ECG: Diffuse saddle-shaped ST elevation in all leads (except aVR and V1 - ST depression), PR depression

1. Diffuse ST elevation, PR depression
2. ST normalizes, T-wave flattening
3. T-wave inversion
4. ECG normalizes

• NSAIDs (Ibuprofen 600 mg TID or Aspirin 750-1000 mg TID) - first line
• Colchicine (0.5 mg BD) - added to NSAIDs to reduce recurrence
• Restrict activity (athletes: 3 months)
• Corticosteroids: only for specific indications (autoimmune, refractory cases)

Pericardial Effusion & Cardiac Tamponade

1. Hypotension
2. Elevated JVP (Kussmaul's sign may be present)
3. Muffled heart sounds

• Pulsus paradoxus >10 mmHg (pathognomonic finding - exaggerated drop in SBP with inspiration)
• Tachycardia
• ECG: Electrical alternans (alternating QRS amplitude/axis - highly specific)
• CXR: Large globular "water bottle" heart (>250 mL effusion)
• Echo: Diastolic collapse of RV/RA (most sensitive)

Constrictive Pericarditis

• Fibrous/calcific pericardium → impaired diastolic filling
• Causes: TB (#1 in developing world), viral, post-radiation, post-cardiac surgery

• Elevated JVP with Kussmaul's sign (JVP rises on inspiration - paradoxical)
• Pericardial knock (early diastolic sound)
• Friedreich's sign: steep "y" descent in JVP
• Hepatomegaly, ascites, edema (mimics liver disease)
• CXR: Pericardial calcification (best on lateral view)
• CT/MRI: pericardial thickening >4mm

• Constriction: Kussmaul's sign +, pericardial calcification, pericardial knock, equalization of diastolic pressures in all 4 chambers
• Restriction: Kussmaul's sign -, E/E' >15 on echo, septal bounce absent

Dilated Cardiomyopathy (DCM)

• A - Alcohol, Autoimmune (myocarditis)
• B - B-vitamin deficiency (beriberi), Beta-blockers (overdose)
• C - Coxsackie virus, Cocaine
• D - Doxorubicin (anthracyclines)
• E - Endocrine (thyroid), Idiopathic

Hypertrophic Cardiomyopathy (HCM)

• Outflow obstruction (subaortic) in ~25%
• Dynamic obstruction: worsened by ↑ contractility, ↓ preload, ↓ afterload
• Systolic anterior motion (SAM) of anterior mitral leaflet → LVOTO + MR

• Jerky carotid pulse (spike-and-dome)
• ESM at LLSB (increases with Valsalva/standing, decreases with squatting/handgrip)
• Double/triple apical impulse
• S4 gallop

• ECG: LVH, deep Q waves (septal depolarization), ST-T changes
• Echo: LV wall thickness ≥15 mm; ASH (asymmetric septal hypertrophy); SAM; LVOT gradient

• Beta-blockers or verapamil (symptom relief, ↓ LVOTO)
• Avoid dehydration, vasodilators, vigorous exercise
• ICD for sudden cardiac death prevention
• Septal reduction therapy: surgical myomectomy or alcohol septal ablation

Restrictive Cardiomyopathy (RCM)

• Amyloidosis (most common cause of RCM in developed world)
• Sarcoidosis
• Hemochromatosis
• Glycogen storage disease
• Endomyocardial fibrosis (tropical - eosinophilia)

• "Sparkling" or granular myocardium on echo
• Increased wall thickness with low voltage ECG (classic combination)
• Poor prognosis

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9. CARDIOGENIC SHOCK

• Hypotension (SBP <90 mmHg), tachycardia
• Cool, clammy extremities
• Oliguria (<0.5 mL/kg/hr)
• Altered mentation
• Elevated lactate

• Reperfusion (primary PCI for STEMI)
• Inotropes: Dobutamine (preferred), Milrinone
• Vasopressors if profound hypotension: Norepinephrine
• Mechanical circulatory support: IABP, Impella, VA-ECMO (escalation)
• Treat underlying cause

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KEY MNEMONICS TO MEMORIZE

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QUICK EXAM FACTS

• Commonest cause of mitral stenosis worldwide = Rheumatic fever
• Most common cardiac valve affected in rheumatic fever = Mitral (then aortic)
• Most common congenital heart defect = VSD
• Most common cyanotic CHD = Tetralogy of Fallot
• Most common CHD presenting in adulthood = ASD
• Machinery murmur = PDA
• Fixed wide splitting of S2 = ASD
• Boot-shaped heart on CXR = TOF
• Fish-mouth valve = Mitral stenosis (rheumatic)
• Low voltage ECG + thick walls = Cardiac amyloidosis
• Kussmaul's sign in MI = RV infarction
• Beck's triad = Cardiac tamponade
• Pulsus paradoxus >10 mmHg = Cardiac tamponade
• Electrical alternans = Cardiac tamponade (large pericardial effusion)
• Pericardial calcification = Constrictive pericarditis (TB etiology most common in developing world)
• Squatting relieves cyanosis = TOF

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