---

🫀 AORTIC REGURGITATION (AR)

Simple Definition

---

SYMPTOMS of AR

Acute AR (sudden onset) - think emergency:

• Sudden severe breathlessness
• Chest pain (if aortic dissection is present)
• Rapidly developing heart failure, pulmonary edema, and cardiogenic shock

Chronic AR (slow onset) - patient tolerates for years:

• Asymptomatic for 10-15 years - patient feels fine for a long time
• Palpitations - especially on lying down; patient feels the heart beating hard, often described as "head pounding"
• Exertional dyspnea - first symptom of deterioration; breathlessness on effort, then later at rest (orthopnea, PND)
• Angina pectoris - chest pain even WITHOUT coronary artery disease. Why?
  • Low diastolic BP → less blood to coronary arteries (coronary flow is mainly in diastole)
  • Increased myocardial oxygen demand due to LV hypertrophy
  • This angina does NOT respond well to sublingual nitroglycerine
• Congestive heart failure
• Sudden cardiac death

---

PERIPHERAL SIGNS OF AR

📌 Easy Way to Remember: These signs all result from HIGH systolic + LOW diastolic pressure (wide pulse pressure)

PULSES

Famous Named Signs of Wide Pulse Pressure (Rare but Examinable):

• De Musset's sign - Head nodding with each heartbeat
• Quincke's sign - Visible pulsation in fingernail capillaries
• Duroziez's sign - To-and-fro murmur over femoral artery on compression
• Traube's sign - "Pistol shot" sound over femoral artery
• Müller's sign - Uvula pulsation
• Corrigan's pulse - Bounding carotid pulsation

INSPECTION AND PALPATION FINDINGS

• Prominent neck pulsations and thrill in carotids
• Apex beat displaced - inferiorly and toward the axilla (because LV is enlarged)
• Apex may be diffuse or hyperdynamic
• Diastolic thrill - palpable along left sternal border (in thin-chested patients - Erb's maneuver)
• Systolic thrill - palpable in suprasternal notch, goes up along carotids

AUSCULTATION (Heart Sounds)

• S1 (first heart sound): May be soft
• A2 (aortic closure sound):
  • Soft in rheumatic AR
  • Loud like a "tambour" (drum sound) in syphilitic AR
  • May be narrowly split, single, or paradoxically split
• S3 (third heart sound): Present if LV dysfunction exists
• S4 (fourth heart sound): Prominent in LV hypertrophy

MURMURS in AR

• Immediately after A2
• High-pitched, blowing, decrescendo sound
• Loudest at LEFT sternal border
• Best heard: End of expiration + sitting + leaning forward
• Important: Duration of murmur = better indicator of severity than loudness

• When the AR diastolic murmur is heard mainly in the LEFT AXILLA (instead of left sternal border)
• Happens when regurgitation is caused by dilatation of the valve

• Heard at the cardiac apex in SEVERE AR
• It is a LOW-PITCHED, MID-DIASTOLIC RUMBLING murmur
• Mimics mitral stenosis murmur but there is NO mitral stenosis
• Why does it occur? The AR jet hits the anterior mitral leaflet (AML):
  1. AR jet forces down the AML, narrowing the mitral opening
  2. Turbulence when AR jet meets the mitral inflow jet
  3. AML flutters due to the AR jet
  4. LV endocardial vibrations from the AR jet
• Cooing Dove Murmur - if murmur is musical, it means eversion or perforation of aortic cusp

Maneuvers to Remember:

• Sustained handgrip intensifies AR murmur (increases systemic vascular resistance)

---

INDICATORS OF SEVERITY OF AR (Box 1.43)

1. Duration of murmur >2/3 of diastole + murmur becomes holodiastolic and rough
2. Bisferiens pulse (double-peaked pulse)
3. S3 gallop
4. Positive Hill's sign >60 mmHg (popliteal BP minus brachial BP is >60 in severe AR)
5. Cardiomegaly - apical impulse displaced down and out
6. Austin Flint murmur
7. A2 soft
8. Marked peripheral signs

---

ACUTE AR vs CHRONIC AR - Key Differences (Important for exam)

---

INVESTIGATIONS OF CHRONIC AR

Chest X-ray

• Cardiomegaly - LV enlarged in inferior + leftward direction
• Ascending aorta also dilated (looks prominent on X-ray)
• In syphilitic AR: calcification of ascending aorta
• Late stage: features of left heart failure (pulmonary edema pattern)

ECG

1. LV hypertrophy: Tall R waves + deeply inverted T waves in left chest leads (V5-V6)
2. Left axis deviation
3. Left atrial enlargement
4. LV volume overload pattern: Prominent Q waves in I, aVL, V5-V6; small r waves in V1
5. LV conduction defects (late sign)

Echocardiography (ECHO) - Most important

• Assess valve structure (bicuspid vs tricuspid, flail leaflet, thickening)
• Look for vegetations (endocarditis)
• Quantitative measurements: regurgitant volume, fraction, orifice area
• LV function: LVEF, LVEDD, LVESD
• Fluttering of anterior mitral leaflet (Austin Flint mechanism visible)

Other tests:

• Cardiac MRI - quantifies regurgitant volume
• Coronary angiography - before surgery if patient has CAD risk factors
• VDRL + TPHA - if syphilis suspected
• RA factor, ANA, ESR, CRP - to exclude connective tissue disorders

---

TREATMENT OF AR

Acute Severe AR (Short note question)

• Medical bridge to surgery:
  • Dobutamine - to increase cardiac output and shorten diastole
  • Sodium nitroprusside - to reduce afterload (in hypertensive patients)
• Usually needs urgent surgical intervention

Chronic AR - Medical Treatment

• Vasodilator therapy - useful in patients with systolic hypertension
  • Sodium nitroprusside, Hydralazine, Nifedipine, Felodipine
  • These reduce PVR, increase forward output, reduce regurgitant volume
  • Decrease end-diastolic volume (EDV) and increase ejection fraction (EF)
• In normotensive patients, vasodilators may NOT be useful

Surgical Treatment

• Aortic valve replacement (AVR) with prosthetic valve - main treatment
• TAVR/TAVI (transcatheter aortic valve replacement/implantation) - valve-sparing option

Types of valves:

When to operate? (Management flowchart to remember):

1. Significant ascending aorta enlargement → Surgery directly
2. Severe AR + Symptoms → Surgery
3. Severe AR + No symptoms, but LVEF ≤50% or LVEDD >70mm or LVESD >50mm → Surgery
4. Otherwise → Follow-up

Aortic Root Dilation causing AR (e.g., Marfan syndrome):

• Treated by encircling suture, subcommissural annuloplasty, or aortic graft + prosthetic valve

---

---

🫀 TRICUSPID STENOSIS (TS)

Simple Definition

Causes (Etiology)

• Rheumatic (most common - usually with mitral/aortic involvement)
• Carcinoid syndrome (causes both TS and TR)
• Congenital
• Infective endocarditis
• Anorectics (fenfluramine - a weight loss drug)
• Fabry disease

Pathophysiology (Simple)

Symptoms

• Usually masked by associated mitral stenosis symptoms
• Right heart failure symptoms: abdominal pain/hepatic discomfort, leg swelling (edema), ascites
• Little or NO dyspnea (important - because problem is on right side, lungs are not congested)
• Fatigue common

Signs

• JVP raised with giant 'a' waves and slow y-descent (no rapid ventricular filling)
• Mid-diastolic murmur: rumbling, high-pitched (higher than MS murmur), with presystolic accentuation
  • Best heard at LOWER LEFT sternal border
  • Gets LOUDER on inspiration = De Carvallo's sign
• Tricuspid Opening Snap (OS): occasionally heard
• Right heart failure signs: hepatomegaly with presystolic pulsation, ascites, edema

Investigations

• Chest X-ray: prominent right atrial bulge
• ECG: enlarged right atrium (tall P waves in lead II = P pulmonale)
• Echocardiogram: thickened, immobile tricuspid valve

Treatment

• Medical: Diuretics + salt and fluid restriction
• Surgical: Tricuspid valve replacement

---

---

🫀 TRICUSPID REGURGITATION (TR)

Simple Definition

De Carvallo's Sign

Causes

• Rheumatic heart disease
• Endocarditis (especially IV drug abusers)
• Ebstein's anomaly
• Carcinoid syndrome

• Right ventricular dilatation due to chronic LEFT heart failure
• Right ventricular infarction, inferior wall MI
• Pulmonary hypertension (cor pulmonale)
• Cardiomyopathy

Clinical Features

• Usually nonspecific - tiredness from reduced forward flow
• Right heart failure: edema, ascites, hepatomegaly with systolic pulsation (liver pulses with each heartbeat)
• Valvular regurgitation increases right atrial and systemic venous pressure

• JVP raised with prominent "giant v waves" (cv wave replaces normal x descent)
• Lancisi's sign - earlobe pulsation (in severe TR)
• Blowing pansystolic murmur at lower-left sternal border
  • Increases on inspiration, decreases on expiration = De Carvallo's sign
• P2 may be loud (due to pulmonary hypertension)
• RV S3 may be heard
• Severe TR: Right jugular venous thrill + RV impulse at left lower sternal border
• Can lead to atrial fibrillation (AF)
• Echocardiogram: dilated right ventricle + thickened valve

Treatment

• Functional TR: Treat the underlying cause (usually left heart failure). Diuretics + vasodilators for CCF.
• Organic TR:
  • Severe organic TR with normal PA pressure - usually well tolerated
  • Annuloplasty (repair) or plication or valve repair
  • Tricuspid valve replacement occasionally needed
  • In IV drug addicts with endocarditis - surgical removal of valve (to eradicate infection)

---

---

🫀 PULMONARY STENOSIS (PS)

Simple Definition

Causes

• Congenital (most common) - may be isolated OR part of Fallot's tetralogy. Associated with rubella during pregnancy.
• Acquired (rare):
  • Rheumatic (very uncommon)
  • Carcinoid syndrome

Types

• Valvular (most common)
• Subvalvular/infundibular (below the valve)
• Supravalvular (above the valve)

Symptoms

• Mild PS: Asymptomatic
• Moderate/Severe PS:
  • Fatigue, syncope (fainting), dyspnea
  • Right heart failure symptoms
  • Angina or syncope = indicator of SEVERE PS

Signs

• Best heard at LEFT UPPER STERNUM in 2nd intercostal space
• Radiates to left shoulder
• Harsh, gets louder + peaks later as severity increases
• Best heard on INSPIRATION
• Usually preceded by an ejection click (especially in valvular PS)

• In mild valvular PS - heard before the murmur
• Paradoxically becomes more prominent in EXPIRATION (unusual - opposite of what you'd expect)
• Why? During inspiration, RV end-diastolic pressure rises and opens the valve earlier (in late diastole) → no click in systole

• High-pitched early diastolic murmur after a prominent P2
• Heard in pulmonary regurgitation SECONDARY to pulmonary hypertension
• Found in patients with severe PS who develop pulmonary hypertension

• RV S4 + prominent jugular venous 'a' wave

1. Loud, harsh murmur
2. P2 inaudible
3. Increased RV heave
4. Prominent 'a' waves in jugular pulse
5. RV hypertrophy on ECG
6. Chest X-ray: post-stenotic dilatation of pulmonary artery

Investigations

• ECG: Right ventricular + right atrial hypertrophy
• Chest X-ray: Prominent pulmonary artery (post-stenotic dilatation, extends into left pulmonary artery branch)
• Doppler Echocardiography: Definitive investigation
• Cardiac catheterization: Measures pressure gradient

Treatment

• Mild PS: No specific treatment; only infective endocarditis prophylaxis
• Moderate-Severe PS (resting gradient >50 mmHg with normal cardiac output):
  • Percutaneous balloon valvotomy - first choice (non-surgical)
  • Surgical valvotomy - if balloon not available
  • Note: After treatment, pulmonary regurgitation may develop - but it is benign

---

QUICK EXAM SUMMARY TABLE

---

KEY NAMED SIGNS CHEAT SHEET

---