Assignment: 1. Cardinal symptoms of Rs n CVS in order of appearance 2. Chest pain causes 3. Rs n CVS causes of hemoptysis 4. Rs dyspnea grading (mmrc) 5. Define, clinical features, investigation, treatment, complications of all spotters

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Here is the complete assignment covering all five points:

RS & CVS - Complete Assignment


1. Cardinal Symptoms of RS and CVS (In Order of Appearance)

Respiratory System (RS) - Cardinal Symptoms

OrderSymptomNote
1CoughUsually the earliest and most common presenting symptom
2Dyspnea (Breathlessness)Appears as disease progresses
3Chest painPleuritic or non-pleuritic
4HemoptysisCoughing up blood
5WheezeHigh-pitched whistling sound on breathing
6CyanosisCentral (lips, tongue) - late sign of hypoxia
7Fever / Constitutional symptomsInfection-related - weight loss, anorexia

Cardiovascular System (CVS) - Cardinal Symptoms

OrderSymptomNote
1Dyspnea (Breathlessness)Earliest symptom - exertional initially
2Chest pain / AnginaCentral, crushing, radiates to left arm/jaw
3PalpitationsAwareness of heartbeat - arrhythmias
4Syncope / Pre-syncopeTransient loss of consciousness
5EdemaDependent pitting edema (ankle/sacral)
6FatigueReduced cardiac output
7CyanosisCentral (cardiac shunts) or peripheral
8HemoptysisClassically in mitral stenosis

2. Causes of Chest Pain

Chest pain has a broad differential - organized by system:

A. Cardiac Causes

  • Ischemic: Stable angina, Unstable angina, Myocardial Infarction (STEMI/NSTEMI)
  • Pericarditis - sharp, positional, worse on lying flat, relieved leaning forward
  • Myocarditis
  • Cardiac tamponade
  • Aortic dissection - tearing/ripping pain radiating to back (life-threatening)

B. Pulmonary Causes

  • Pulmonary Embolism (PE) - pleuritic chest pain + dyspnea
  • Pneumothorax - sudden onset unilateral pleuritic pain + dyspnea
  • Pleurisy / Pleuritis - sharp, stabbing, worse with breathing
  • Pneumonia - pleuritic, with fever, productive cough
  • Pleural effusion
  • Lung cancer - dull, persistent, non-pleuritic

C. Gastrointestinal Causes

  • GERD / Acid reflux - burning, retrosternal, post-meal
  • Esophageal spasm - can mimic cardiac chest pain
  • Peptic ulcer disease
  • Hiatus hernia

D. Musculoskeletal Causes

  • Costochondritis (Tietze syndrome) - reproducible tenderness on palpation
  • Rib fracture
  • Intercostal muscle strain

E. Other Causes

  • Herpes Zoster (Shingles) - dermatomal, burning
  • Anxiety / Panic attack - functional chest pain
  • Mediastinitis
Mnemonic for life-threatening chest pain: PATCH MD - PE, Aortic dissection, Tension pneumothorax, Cardiac tamponade, MI, Dissection (esophageal rupture)

3. RS and CVS Causes of Hemoptysis

Definition: Expectoration of blood originating from the lower respiratory tract (below the glottis).

RS (Respiratory) Causes - By Category

Airway Disease:
  • Bronchiectasis (most common cause in developing countries)
  • Chronic bronchitis
  • Lung cancer / Bronchogenic carcinoma
  • Bronchial adenoma (carcinoid)
  • Foreign body
  • Tracheobronchitis
  • Cystic fibrosis
Parenchymal / Infection:
  • Tuberculosis (major cause - 15-25% in high TB-prevalence areas)
  • Pneumonia (bacterial, fungal, viral)
  • Lung abscess
  • Septic emboli
  • Aspergilloma ("fungus ball" - classically causes massive hemoptysis)
Vascular - Pulmonary:
  • Pulmonary embolism with infarction
  • Arteriovenous malformation (AVM)
  • Pulmonary artery pseudoaneurysm (Rasmussen's aneurysm - in TB)
  • Hereditary hemorrhagic telangiectasia (HHT)
  • Diffuse alveolar hemorrhage (Goodpasture syndrome, Wegener's, SLE)
Drugs / Iatrogenic:
  • Anticoagulants, antiplatelet agents
  • Cocaine inhalation
  • Post-lung biopsy

CVS (Cardiovascular) Causes

CauseMechanism
Mitral stenosisElevated left atrial pressure -> pulmonary venous hypertension -> rupture of bronchial veins / pulmonary capillaries
Left ventricular failure / Pulmonary edemaRaised pulmonary venous pressure causing "pink frothy" sputum
Pulmonary arterial hypertensionHigh pressure damages pulmonary vessels
Eisenmenger syndromeRight-to-left shunt with pulmonary hypertension
Pulmonary veno-occlusive disease
Aortic aneurysm rupture into bronchusMassive, life-threatening
Pulmonary artery catheter perforation (iatrogenic)
Note: 90% of hemoptysis arises from the bronchial circulation (high-pressure system); only 10% from pulmonary circulation. - Murray & Nadel's Textbook of Respiratory Medicine
Frequency order (decreasing): Bronchiectasis > Adenoma > Tracheobronchitis > Tuberculosis > Mitral stenosis > Foreign body (KJ Lee's Essential Otolaryngology)

4. Respiratory Dyspnea Grading - mMRC Scale

Modified Medical Research Council (mMRC) Dyspnea Scale
GradeDescription
0Not troubled with breathlessness except with strenuous exercise
1Troubled by shortness of breath when hurrying on the level or walking up a slight hill
2Walks slower than people of the same age on the level because of breathlessness, OR has to stop for breath when walking at own pace on level
3Stops for breath after walking about 100 yards (~90 m) or after a few minutes on the level
4Too breathless to leave the house OR breathless when dressing/undressing
Source: Fishman's Pulmonary Diseases and Disorders - Data from ATS/ERS Task Force (Celli BR, MacNee W. Eur Respir J. 2004)
Clinical use: mMRC ≥2 indicates significant dyspnea. It is one of the four components of the BODE Index in COPD prognostication (Body mass index, Obstruction, Dyspnea, Exercise tolerance).

5. RS and CVS Spotters


RS SPOTTERS


A. CLUBBING

Definition: Bulbous enlargement of the terminal phalanges of fingers (and toes) due to proliferation of fibrovascular tissue, with loss of the normal angle between the nail and nail-bed (Lovibond angle >180°).
Grades of Clubbing (Schamroth's / Grades 1-4):
GradeFeatures
ISoftening/fluctuation of nail bed
IILoss of angle between nail and nail fold (Lovibond angle obliterated)
IIIIncreased curvature of nail (beak-like/parrot-beak appearance)
IVHypertrophic pulmonary osteoarthropathy (HPOA) - periosteal new bone formation
Schamroth's sign: Normally a diamond-shaped window is visible when the dorsal surfaces of the terminal phalanges of the same finger of both hands are placed together. In clubbing, this window is obliterated.
Clinical Features:
  • Fluctuant nail bed (early sign)
  • Loss of nail fold angle (most reliable early sign)
  • Increased nail curvature
  • Drumstick appearance of fingers
  • In HPOA: painful swollen wrists/ankles, periosteal reaction on X-ray
RS Causes:
  • Lung cancer (most common in adults)
  • Bronchiectasis
  • Lung abscess / Empyema
  • Fibrosing alveolitis (IPF)
  • Cystic fibrosis
  • Mesothelioma
  • TB (less common)
CVS Causes: Cyanotic congenital heart disease (Fallot's tetralogy, Eisenmenger), Infective endocarditis, Atrial myxoma
GI Causes: Cirrhosis, Crohn's disease, Ulcerative colitis, Celiac disease
Investigations:
  • CXR (primary lesion)
  • CT chest (mass, bronchiectasis, ILD)
  • PFTs (restrictive/obstructive pattern)
  • Bone scan (HPOA)
  • Echocardiography (if CVS cause suspected)
Treatment: Treat the underlying cause. Clubbing itself may partially regress when cause is treated (e.g., post-lobectomy for lung cancer). HPOA: NSAIDs, bisphosphonates.
Complications: Depends on underlying cause. HPOA causes significant joint pain and disability.

B. BARREL CHEST

Definition: Increased AP diameter of the chest equal to or exceeding the transverse diameter, with a horizontal (rather than sloping) rib orientation and elevated sternum, resembling a barrel.
Clinical Features:
  • Increased AP:transverse diameter ratio (normally 1:2; in barrel chest approaches 1:1)
  • Horizontal ribs
  • Widened intercostal spaces
  • Hyperresonance on percussion
  • Reduced chest expansion bilaterally
  • Decreased breath sounds
  • Prolonged expiration with expiratory wheeze
  • Use of accessory muscles of respiration
Causes:
  • COPD (emphysema) - most common
  • Severe chronic asthma
  • Air trapping from any cause
Investigations:
  • CXR: Hyperinflation, flat diaphragms, increased retrosternal air space, >6 anterior ribs visible above diaphragm in mid-clavicular line
  • CT chest: Emphysematous bullae, air trapping
  • Spirometry: Obstructive pattern (FEV1/FVC <0.7), increased RV and TLC, decreased DLCO (in emphysema)
  • ABG: May show hypoxemia, hypercapnia (type II respiratory failure)
Treatment:
  • SABA (Salbutamol), LABA, LAMA (tiotropium) bronchodilators
  • Inhaled corticosteroids
  • Pulmonary rehabilitation
  • O2 therapy (target SpO2 88-92% in COPD)
  • LTOT (long-term oxygen therapy) if PaO2 <55 mmHg
  • Lung volume reduction surgery / Bullectomy in selected cases
  • Lung transplantation (severe cases)
Complications: Cor pulmonale, Respiratory failure (Type II), Pneumothorax (bullae rupture), Frequent exacerbations, Death.

C. TRACHEAL DEVIATION

Definition: Displacement of the trachea from its normal midline position, detected by palpating the trachea in the suprasternal notch.
Clinical Features:
  • Trachea palpated off-centre in suprasternal notch
  • "Tracheal tug" may be present (downward movement of trachea with each heartbeat - in aortic arch aneurysm) or with forced inspiration in COPD
Causes:
DirectionCause
Away from lesion (pushed)Tension pneumothorax, Large pleural effusion, Large unilateral goitre
Toward lesion (pulled)Pulmonary fibrosis (upper lobe), Collapse/Atelectasis, Post-pneumonectomy, Apical fibrosis (TB)
Investigations:
  • CXR (PA): Best initial test
  • CT chest: Detailed assessment
  • Spirometry (if fibrosis/COPD)
Treatment: Treat underlying cause:
  • Tension pneumothorax: Immediate needle decompression (2nd intercostal space, midclavicular line), then chest drain
  • Pleural effusion: Thoracocentesis
  • Lung fibrosis: Antifibrotics (pirfenidone, nintedanib for IPF)
Complications: Respiratory failure, mediastinal shift complications, cardiovascular compromise (especially tension pneumothorax).

D. PLEURAL EFFUSION

Definition: Abnormal accumulation of fluid in the pleural space (normally 10-20 mL).
Clinical Features:
  • Reduced/absent chest movement on affected side
  • Stony dull percussion (most characteristic sign)
  • Reduced/absent breath sounds
  • Reduced vocal resonance/fremitus
  • Bronchial breathing and aegophony above the effusion level (at the fluid meniscus)
  • Tracheal deviation away (large effusion)
Causes - Transudate (protein <30g/L):
  • Heart failure (bilateral)
  • Nephrotic syndrome
  • Liver cirrhosis
  • Hypothyroidism
  • Hypoalbuminemia
Causes - Exudate (protein >30g/L) - Light's Criteria:
  • Pneumonia (parapneumonic)
  • Malignancy (mesothelioma, metastatic)
  • TB
  • Pulmonary embolism
  • Connective tissue disease (SLE, RA)
  • Pancreatitis (left-sided)
Investigations:
  • CXR: Meniscus sign, blunting of costophrenic angle (>200mL needed)
  • USS chest: Confirms effusion, guides aspiration
  • CT chest: Detects underlying cause
  • Diagnostic aspiration (pleural tap): Protein, LDH, pH, glucose, cytology, culture, Light's criteria
  • Light's Criteria (exudate if ANY): Pleural protein/serum protein >0.5; Pleural LDH/serum LDH >0.6; Pleural LDH >2/3 upper limit serum LDH
Treatment:
  • Transudate: Treat underlying cause (diuretics for CCF, albumin for cirrhosis)
  • Exudate: Treat cause + therapeutic thoracocentesis
  • Malignant: Pleurodesis (talc), indwelling pleural catheter
  • Parapneumonic: Antibiotics ± chest drain
  • Empyema: Chest drain + antibiotics ± VATS decortication
Complications: Respiratory failure, Empyema, Fibrothorax, Trapped lung, Pneumothorax (post-aspiration), Mediastinal shift.

E. PNEUMOTHORAX (as RS spotter - may present with hyperresonance, absent breath sounds)

Definition: Presence of air in the pleural space.
Types:
  • Spontaneous: Primary (young, tall, thin male, no lung disease) or Secondary (underlying lung disease - COPD, TB, asthma, CF)
  • Traumatic
  • Iatrogenic (post-procedure)
  • Tension pneumothorax (medical emergency)
Clinical Features:
  • Sudden onset pleuritic chest pain + dyspnea
  • Reduced chest movement on affected side
  • Hyperresonance on percussion (vs stony dull in effusion)
  • Reduced/absent breath sounds
  • Tracheal deviation AWAY (tension pneumothorax only)
  • Tension PTX: Tachycardia, hypotension, JVD, tracheal deviation - haemodynamically unstable
Investigations:
  • CXR: Visible lung edge with absent vascular markings peripheral to it
  • CT chest: Gold standard (especially for small/recurrent)
  • ABG: Hypoxemia
Treatment:
  • Small primary (<2cm): Observation ± aspiration
  • Large (>2cm): Needle aspiration or chest drain (Seldinger technique)
  • Tension PTX: IMMEDIATE needle decompression (2nd ICS MCL), then chest drain
  • Recurrent: Pleurodesis or VATS bullectomy
Complications: Tension pneumothorax, Recurrence (20-50%), Haemopneumothorax, Re-expansion pulmonary edema, Respiratory failure, Death.

F. CONSOLIDATION / LOBAR PNEUMONIA

Definition: Replacement of alveolar air by fluid (exudate, pus, blood) resulting in a solid-appearing lung segment on CXR.
Clinical Features:
  • Fever, productive cough (rusty sputum in pneumococcal)
  • Pleuritic chest pain
  • Reduced chest expansion
  • Dull percussion
  • Bronchial breathing (hallmark)
  • Increased vocal resonance / whispering pectoriloquy
  • Crepitations
Causes: Streptococcus pneumoniae (most common), Klebsiella (upper lobe, diabetics), Staphylococcus, Legionella, Mycoplasma
Investigations:
  • CXR: Homogeneous opacity with air bronchogram, lobar distribution
  • Sputum culture, Blood culture
  • FBC: Leukocytosis
  • Urinary antigen (Legionella, Pneumococcal)
  • ABG if severe
Treatment (Community-acquired - CURB-65 guided):
  • CURB-65 0-1: Amoxicillin PO (Penicillin G)
  • CURB-65 2: Co-amoxiclav ± Macrolide, consider hospitalization
  • CURB-65 3-5: IV broad-spectrum (co-amoxiclav + clarithromycin), ICU if severe
  • Atypical: Macrolide or Doxycycline
CURB-65: Confusion, Urea >7mmol/L, Respiratory rate ≥30, BP systolic <90 or diastolic ≤60, Age ≥65 (1 point each; score 3+ = severe)
Complications: Empyema, Lung abscess, Septicemia, ARDS, Respiratory failure, Pleuritis.

G. BRONCHIECTASIS

Definition: Permanent, abnormal dilatation of the bronchi (>1.5x diameter of accompanying pulmonary artery) due to destruction of bronchial wall elastic and muscular components.
Clinical Features:
  • Chronic productive cough with large volumes of purulent sputum (3-layered sputum: mucoid top, mucopurulent middle, purulent bottom)
  • Recurrent chest infections
  • Hemoptysis (common, may be massive)
  • Clubbing
  • Coarse crepitations on auscultation
  • Wheeze
Causes:
  • Post-infective: TB, Pertussis, Measles, Pneumonia
  • Immunodeficiency
  • Cystic fibrosis (commonest genetic cause)
  • Kartagener syndrome (ciliary dyskinesia)
  • ABPA (allergic bronchopulmonary aspergillosis)
  • Obstruction (foreign body, tumour)
  • Yellow nail syndrome
Investigations:
  • HRCT chest: Gold standard - "signet ring" appearance (bronchus > pulmonary artery), "tram-track" lines
  • CXR: Tram-tracking, ring shadows, crowded lung markings
  • Spirometry: Obstructive or mixed pattern
  • Sputum culture (Pseudomonas, H. influenzae, Staph. aureus in CF)
  • Sweat chloride test (if CF suspected)
  • Serum immunoglobulins
  • ABPA screen (IgE, aspergillus precipitins)
Treatment:
  • Chest physiotherapy (postural drainage) - cornerstone
  • Antibiotics: Guided by sputum culture (Amoxicillin, Ciprofloxacin for Pseudomonas)
  • Bronchodilators (SABA, LABA)
  • Inhaled corticosteroids (if ABPA or asthma-overlap)
  • Mucolytics (hypertonic saline, DNase in CF)
  • Surgery: Lobectomy/segmentectomy for localized disease unresponsive to medical Rx
Complications: Massive hemoptysis, Respiratory failure, Cor pulmonale, Amyloidosis (AA type - secondary), Brain abscess (hematogenous spread), Empyema.

H. PNEUMOTHORAX (see above)


CVS SPOTTERS


A. MITRAL FACIES (Malar Flush)

Definition: A purplish-red flush over the malar prominences (cheeks) and nose, seen classically in mitral stenosis, due to reduced cardiac output causing peripheral vasodilatation and venous stasis in the facial skin.
Clinical Features:
  • Bilateral malar flush (purplish-red discoloration of cheeks)
  • Signs of mitral stenosis: Dyspnea, orthopnea, hemoptysis, palpitations
  • Low-volume pulse
  • Tapping apex beat (palpable S1)
  • Loud S1, Opening snap (OS), Mid-diastolic rumble with presystolic accentuation at apex
  • Signs of pulmonary hypertension: Loud P2, RV heave
  • AF (later complication)
Investigations:
  • ECG: P-mitrale (bifid P wave), AF
  • CXR: Enlarged left atrium (double shadow, splaying of carina), pulmonary venous congestion, Kerley B lines
  • Echocardiography (TTE/TEE): Gold standard - valve area <1 cm² (severe), gradient across valve, commissural fusion
  • Cardiac catheterisation (if echo inconclusive)
Treatment:
  • Medical: Diuretics, beta-blockers/digoxin (rate control in AF), anticoagulation (warfarin if AF, history of embolism)
  • Percutaneous Mitral Balloon Valvuloplasty (PMBV) / Balloon Commissurotomy: Preferred intervention (pliable, non-calcified valve without MR)
  • Surgical: Open mitral commissurotomy or Mitral valve replacement (MVR) - calcified/regurgitant valve
  • Antibiotic prophylaxis: No longer routinely recommended except in highest-risk groups (prosthetic valve, prior IE)
Complications: Atrial fibrillation, Systemic embolism/stroke, Pulmonary hypertension, Cor pulmonale, Infective endocarditis, Pulmonary edema, Right heart failure.

B. JUGULAR VENOUS PULSE (JVP) - RAISED JVP

Definition: The JVP is the visible pulsation in the neck (internal jugular vein) that reflects right atrial pressure. Normally the JVP is measured at <4 cm above the sternal angle (45° position).
JVP Waveform:
  • a wave: Atrial systole (absent in AF, giant in tricuspid stenosis, cannon waves in complete heart block)
  • c wave: Tricuspid valve closure (often not visible)
  • x descent: Atrial relaxation
  • v wave: Venous filling when tricuspid is closed (giant v wave in tricuspid regurgitation)
  • y descent: Tricuspid opens, blood flows to RV
Causes of Raised JVP:
  • Right heart failure (most common)
  • Cardiac tamponade (raised JVP + hypotension + muffled heart sounds = Beck's triad)
  • Constrictive pericarditis (Kussmaul's sign: JVP rises on inspiration)
  • Superior vena cava obstruction (non-pulsatile raised JVP)
  • Fluid overload
  • Tension pneumothorax
Investigations:
  • ECG
  • CXR
  • Echocardiography (RA pressure, pericardial effusion)
  • CT chest/abdomen (SVC obstruction)
Treatment: Treat underlying cause - diuretics for right heart failure, pericardiocentesis for tamponade.

C. PEDAL EDEMA (Dependent Pitting Edema)

Definition: Abnormal accumulation of interstitial fluid in the feet and ankles due to increased capillary hydrostatic pressure, reduced oncotic pressure, or lymphatic obstruction.
Grading:
  • Grade 1: Ankle edema only
  • Grade 2: Pitting edema up to knee
  • Grade 3: Pitting edema up to thigh/genitalia
  • Grade 4: Anasarca (total body edema)
Clinical Features:
  • Pitting edema (finger pressure leaves a pit)
  • Bilateral (cardiac/systemic) vs Unilateral (DVT, lymphedema)
  • Associated signs: Raised JVP, S3 gallop, hepatomegaly, ascites (right heart failure)
Causes:
  • Cardiac: Right heart failure, Constrictive pericarditis, Cardiomyopathy
  • Renal: Nephrotic syndrome, Renal failure
  • Hepatic: Cirrhosis, hypoalbuminemia
  • Venous: DVT, chronic venous insufficiency
  • Lymphatic: Lymphedema
  • Drugs: CCBs (amlodipine), NSAIDs, corticosteroids
Investigations:
  • FBC, U&E, LFTs, Albumin, BNP/NT-proBNP
  • CXR, Echocardiography
  • Urinalysis (proteinuria for nephrotic), 24-hr urine protein
  • Doppler ultrasound (DVT)
Treatment:
  • Diuretics (furosemide) - first-line for cardiac cause
  • Leg elevation
  • Compression stockings (if no arterial disease)
  • Fluid restriction
  • Treat underlying cause
Complications: Skin breakdown/ulceration, Infection (cellulitis), DVT, Pulmonary edema, Pleural effusion.

D. INFECTIVE ENDOCARDITIS (IE) - Peripheral Stigmata

Definition: Infection of the endocardium (usually heart valves) by microorganisms, most commonly bacteria.
Classic Peripheral Signs (Clinical Spotters):
SignDescriptionLocation
Osler's nodesPainful, tender, red nodulesFinger/toe pads
Janeway lesionsPainless hemorrhagic maculesPalms/soles
Splinter hemorrhagesLinear red-brown linesUnder nails
Roth spotsOval retinal hemorrhages with pale centreRetina
ClubbingLate findingFingers
PetechiaeSmall capillary hemorrhagesConjunctiva, skin
Duke Criteria (Definite IE = 2 Major OR 1 Major + 3 Minor OR 5 Minor):
  • Major: Positive blood cultures (2 of typical organisms), Positive echo (vegetation, abscess, new valve regurgitation)
  • Minor: Predisposing cardiac condition/IVDU, fever >38°C, vascular phenomena, immunologic phenomena, microbiologic evidence not meeting major
Investigations:
  • Blood cultures x3 (before antibiotics, from different sites)
  • FBC (leukocytosis, anemia), ESR/CRP raised
  • Urinalysis (microscopic hematuria)
  • CXR
  • ECG (AV block = septal abscess)
  • Echocardiography: TTE first, TEE if negative/inconclusive (more sensitive)
Treatment:
  • Viridans streptococci (native valve): Benzylpenicillin + Gentamicin (2 weeks)
  • Staphylococcus aureus (native valve): Flucloxacillin ± Gentamicin (4-6 weeks)
  • Prosthetic valve: Vancomycin + Rifampicin + Gentamicin (6 weeks)
  • Surgery indications: Heart failure, Persistent bacteraemia, Perivalvular extension, Embolic events, Large vegetations (>10mm)
Complications: Embolic (stroke, splenic/renal infarct), Perivalvular abscess, Heart block, Heart failure (acute MR/AR), Mycotic aneurysm, Metastatic infection, Death.

E. CARDIAC CACHEXIA / CYANOSIS (Central - CVS cause)

Definition (Central Cyanosis): Blue discolouration of mucous membranes (tongue, lips) due to >5g/dL deoxygenated Hb in blood or abnormal Hb. In CVS, it implies right-to-left shunting.
Clinical Features:
  • Blue tongue and lips (central cyanosis)
  • Clubbing (in chronic cases)
  • RV heave, Loud P2 (pulmonary hypertension)
  • Single S2 (Fallot's) or loud P2 (Eisenmenger's)
  • Murmurs of underlying cardiac defect
Causes (CVS):
  • Tetralogy of Fallot (most common cyanotic CHD after neonatal period)
  • Eisenmenger syndrome
  • Transposition of great arteries (TGA)
  • Tricuspid atresia
  • Total anomalous pulmonary venous return (TAPVR)
  • Pulmonary hypertension with right-to-left shunt
Investigations:
  • SpO2 (reduced, <95%)
  • ABG: PaO2 reduced, does not fully correct with 100% O2 (vs RS cause)
  • CXR: Cardiomegaly, pulmonary plethora or oligemia
  • ECG: RVH, RAD
  • Echocardiography: Defines structural defect
  • Cardiac catheterisation: Pressures, shunt calculation (Qp:Qs ratio)
Treatment:
  • Fallot's: Total surgical correction (right ventriculotomy + VSD patch + RVOT relief)
  • Eisenmenger: Pulmonary vasodilators (sildenafil, bosentan), Heart-lung transplant
  • Supportive: Avoid dehydration, polycythemia management (venesection if PCV >0.65)
Complications: Polycythemia, Paradoxical embolism, Brain abscess, Endocarditis, Arrhythmias, Pulmonary hemorrhage, Death.

F. AORTIC STENOSIS (AS) - Classic CVS Spotter Signs

Definition: Narrowing of the aortic valve orifice causing obstruction to LV outflow. Normal valve area 2-4 cm²; severe AS <1 cm².
Clinical Triad (SAD):
  • Syncope
  • Angina
  • Dyspnea (exertional)
Clinical Signs:
  • Slow-rising, low-amplitude pulse (pulsus parvus et tardus)
  • Narrow pulse pressure
  • Sustained, heaving apex beat (not displaced early)
  • Ejection systolic murmur (ESM) at aortic area, radiating to carotids
  • Soft/absent A2
  • S4 gallop (LVH)
Investigations:
  • ECG: LVH with strain
  • CXR: Calcified aortic valve (lateral), post-stenotic dilatation of aorta
  • Echocardiography: Valve area (severe <1 cm²), mean gradient (>40 mmHg = severe)
  • Cardiac catheterization (pre-op in older patients)
Treatment:
  • Medical: Diuretics, ACE inhibitors (cautiously), statins do NOT slow progression
  • Avoid: Vigorous exercise, vasodilators (nitrates, alpha-blockers)
  • Surgical Aortic Valve Replacement (SAVR): Standard in younger, low surgical risk
  • TAVI/TAVR: Transcatheter - moderate-to-high surgical risk patients
  • Indications for intervention: Severe AS + symptoms (any of SAD), LVEF <50%, High-gradient
Complications: Sudden cardiac death, Heart failure, Infective endocarditis, Arrhythmias (AF, heart block if calcification extends to conduction system), Complete heart block.

G. MITRAL REGURGITATION (MR)

Definition: Incompetence of the mitral valve allowing regurgitation of blood from LV to LA during systole.
Causes:
  • Rheumatic heart disease
  • MVP (mitral valve prolapse)
  • Papillary muscle dysfunction (post-MI)
  • Infective endocarditis
  • Dilated cardiomyopathy
  • Marfan syndrome
Clinical Features:
  • Displaced, hyperdynamic apex beat
  • Soft/absent S1
  • Pansystolic murmur at apex radiating to axilla
  • S3 (volume overload)
  • Signs of pulmonary hypertension (loud P2)
Investigations:
  • ECG: P-mitrale, LVH, AF
  • CXR: Cardiomegaly, enlarged LA, pulmonary edema (acute)
  • Echocardiography: Regurgitant jet, LV function, LA size
Treatment:
  • Acute severe MR: Emergency surgery
  • Chronic asymptomatic: Monitor; surgery when LVEF <60% or LVESD >40mm
  • Surgical: Mitral valve repair (preferred) or replacement
  • Medical: ACE inhibitors, diuretics, anticoagulation if AF
Complications: AF, systemic embolism, heart failure, pulmonary hypertension, infective endocarditis.

H. HYPERTENSION - RETINAL CHANGES (Keith-Wagener-Barker Classification)

Definition: Persistent BP >140/90 mmHg causing target organ damage including hypertensive retinopathy.
Grades (Keith-Wagener Classification):
GradeFeatures
IMild narrowing/tortuosity of arteries (silver wiring)
IIAV nipping/nicking (arteriovenous crossing changes)
IIIFlame-shaped hemorrhages, cotton wool spots, hard exudates
IVAll of Grade III + Papilledema (hypertensive emergency)
Clinical Features:
  • Usually asymptomatic until advanced
  • Headache, visual disturbance (Grade III-IV)
  • Papilledema in hypertensive emergency
Investigations:
  • Fundoscopy: Gold standard for grading
  • BP measurements (bilateral arm)
  • Urinalysis, U&E, eGFR (renal damage)
  • ECG, Echo (LVH)
  • 24-hr ambulatory BP monitoring
Treatment:
  • Grade I-II: Target BP <130/80 mmHg with antihypertensives
  • Grade III-IV (Hypertensive emergency): IV labetalol or sodium nitroprusside; aim to reduce MAP by no more than 25% in first hour
  • First-line antihypertensives: ACE inhibitor/ARB, CCB, Thiazide diuretic (ACD rule - Age/ethnicity guided)
Complications: Stroke, MI, Renal failure, Heart failure, Aortic dissection, Blindness (retinal artery/vein occlusion), Hypertensive encephalopathy.

Sources: Murray & Nadel's Textbook of Respiratory Medicine | Fishman's Pulmonary Diseases and Disorders | Frameworks for Internal Medicine | Symptom to Diagnosis (Evidence-Based Guide) | KJ Lee's Essential Otolaryngology | Harrison's Principles of Internal Medicine
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