Reach me cardiovascular and respiratory system medicine completely
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That is your complete, structured medical-student-level guide to both systems. Here is a quick orientation to what was covered:
What Was Covered
🫀 Cardiovascular System (Part 1)
PART 1 - Anatomy: Gross anatomy, cardiac skeleton, chambers, valves, coronary anatomy (RCA, LAD, LCx), conduction system (SA → AV → His-Purkinje), action potential phases
PART 2 - Physiology: Cardiac cycle (systole/diastole), heart sounds (S1-S4), Frank-Starling law, preload/afterload/contractility, Laplace's law, excitation-contraction coupling, molecular sarcomere proteins (myosin, actin, troponin complex), coronary blood flow regulation
PART 3 - Pathology:
- Heart failure (HFrEF vs HFpEF, GDMT - ARNI, beta-blockers, MRA, SGLT2i)
- Ischemic heart disease / ACS (STEMI/NSTEMI, ECG localization, MI complications)
- Hypertension (classification, target organ damage, management)
- Arrhythmias (AF, VT/VF, heart blocks, Torsades de Pointes)
- Valvular disease (AS, AR, MS, MR - murmurs, signs, management)
- Infective endocarditis (Duke criteria, organisms, peripheral signs)
- Pericardial disease (pericarditis, tamponade, constrictive)
- Cardiomyopathies (dilated, HCM, restrictive, ARVC)
- Aortic dissection (Stanford A vs B)
PART 4 - Pharmacology: Antihypertensives (ACEi, ARB, ARNI, diuretics, CCBs, beta-blockers), antiarrhythmics (Vaughan-Williams classification), anticoagulants (warfarin, heparin, DOACs with reversals), antiplatelets, statins
PART 5 - Clinical Skills: History-taking, examination approach, ECG reading
🫁 Respiratory System (Part 2)
PART 1 - Anatomy: Upper/lower tract, tracheobronchial tree generations, right vs left bronchus differences, alveolar structure (Type I vs II pneumocytes, surfactant), blood-gas barrier
PART 2 - Physiology: Lung volumes/capacities (VT, TLC, FRC, RV), spirometry (obstructive vs restrictive), compliance, surfactant/LaPlace's law, airway resistance (Poiseuille's law), V/Q matching (West zones), 5 mechanisms of hypoxemia, A-a gradient, Hb-O₂ dissociation curve (shifts), CO₂ transport, control of breathing (central/peripheral chemoreceptors), acid-base
PART 3 - Diseases:
- COPD (Blue Bloater vs Pink Puffer, GOLD classification, emphysema types, step-up therapy, exacerbation management, LTOT)
- Asthma (pathophysiology, triggers, step-up therapy, biologics, status asthmaticus)
- Pneumonia (CAP/HAP/atypical, CURB-65, antibiotic regimens, Legionella)
- Tuberculosis (primary vs reactivation, RIPE regimen, drug toxicities)
- Pulmonary embolism (Wells score, S1Q3T3, CTPA, thrombolysis)
- Pleural diseases (Light's criteria, pneumothorax types, tension pneumothorax management)
- ILD/IPF (UIP pattern, pirfenidone/nintedanib)
- Lung cancer (SCLC/NSCLC, paraneoplastic syndromes, Pancoast/Horner's, SVC syndrome, targeted therapy)
- Cystic fibrosis (ΔF508, Trikafta, management)
- OSA (CPAP)
- Mechanical ventilation (ARDSnet protocol, lung protective ventilation)
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🫀 CVS - Scroll up to find:
- Anatomy - Gross anatomy, valves, coronary arteries, conduction system
- Physiology - Cardiac cycle, heart sounds, preload/afterload, sarcomere proteins
- Pathology - Heart failure, ACS/STEMI, hypertension, arrhythmias, valvular disease, IE, pericarditis, cardiomyopathies, aortic dissection
- Pharmacology - Antihypertensives, antiarrhythmics, anticoagulants, antiplatelets, statins
- Clinical - ECG reading, cardiac examination
🫁 Respiratory - Scroll up to find:
- Anatomy - Airways, alveoli, Type I/II pneumocytes
- Physiology - Lung volumes, spirometry, V/Q matching, O₂/CO₂ transport, control of breathing
- Diseases - COPD, Asthma, Pneumonia, TB, PE, Pleural diseases, ILD/IPF, Lung cancer, CF, OSA, Mechanical ventilation
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🫀 CARDIOVASCULAR SYSTEM - Complete Medical Student Guide
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🫀 CARDIOVASCULAR SYSTEM - Complete Medical Student Guide
PART 1: CARDIAC ANATOMY
Gross Anatomy
The heart is a phasic, electrically self-actuated, variable-speed hydraulic pump composed of two dual-component elastic muscular chambers - each with an atrium and a ventricle. It simultaneously delivers equal volumes of blood to the pulmonary and systemic circulations.
The Cardiac Skeleton:
The annulus of the valves, the aortic and pulmonary roots, the central fibrous body, and the left/right fibrous trigones form the heart's cartilaginous skeleton. Located at the base of the heart, it:
- Supports the four valves
- Resists forces of developed pressure and blood flow
- Provides insertion sites for superficial subepicardial muscle
An interstitial collagen fiber network + elastin provides structural support, flexibility, and elasticity.
The Four Chambers
| Chamber | Wall Thickness | Key Features |
|---|---|---|
| Right Atrium (RA) | Thin | Receives SVC, IVC, coronary sinus |
| Right Ventricle (RV) | ~3-5 mm | Crescent-shaped; low-pressure circuit |
| Left Atrium (LA) | Thin | Receives pulmonary veins |
| Left Ventricle (LV) | ~8-12 mm | Ellipsoid; generates ~120 mmHg systolic |
The LV is composed of three myocardial layers:
- Outer layer: counterclockwise spiral fibers
- Middle layer: circumferential fibers (responsible for most shortening)
- Inner layer: clockwise fibers
This three-dimensional fiber architecture produces both shortening and twisting (torsional) motion during systole.
Cardiac Valves
| Valve | Type | Cusps | Separates |
|---|---|---|---|
| Tricuspid | AV | 3 leaflets | RA → RV |
| Pulmonary | Semilunar | 3 cusps | RV → Pulmonary artery |
| Mitral (Bicuspid) | AV | 2 leaflets | LA → LV |
| Aortic | Semilunar | 3 cusps | LV → Aorta |
Mitral valve apparatus: anterior and posterior leaflets attached to papillary muscles via chordae tendineae. Rupture of papillary muscles (e.g., post-MI) causes acute mitral regurgitation.
Coronary Anatomy
Right Coronary Artery (RCA):
- Supplies SA node (~60%), AV node (~80-90%), RV, inferior LV
- Terminates as PDA in right-dominant circulation (~85% of people)
Left Coronary Artery (LCA):
- Left main → divides into:
- LAD: anterior LV, anterior septum, apex, RBB, anterior LBB fascicle
- LCx: lateral/posterior LV, SA node in ~40%
Clinical Pearl: LAD occlusion = "widow maker" → anterior STEMI, ST elevation V1-V4.
Conduction System
SA Node (pacemaker, 60-100 bpm)
↓ internodal tracts
AV Node (delay ~0.12 sec; backup 40-60 bpm)
↓
Bundle of His
↓
Right Bundle Branch + Left Bundle Branch
(LBB → Anterior fascicle + Posterior fascicle)
↓
Purkinje Fibers → Ventricular myocardium
Action Potential (Ventricular):
| Phase | Ion movement | Effect |
|---|---|---|
| Phase 0 | Fast Na⁺ in | Rapid depolarization |
| Phase 1 | K⁺ out | Early repolarization |
| Phase 2 | Ca²⁺ in + K⁺ out | Plateau (unique to cardiac muscle) |
| Phase 3 | K⁺ out | Rapid repolarization |
| Phase 4 | Na⁺/K⁺ ATPase | Resting membrane potential |
The plateau phase (Phase 2) creates a long refractory period, preventing tetany.
PART 2: CARDIAC PHYSIOLOGY
The Cardiac Cycle
Systole:
- Isovolumetric contraction - AV valves close (S1), pressure rises, no volume change
- Ejection phase - semilunar valves open, blood ejected
Diastole:
3. Isovolumetric relaxation - semilunar valves close (S2), pressure falls, no volume change
4. Rapid filling - AV valves open; 70% of filling occurs here
5. Slow filling - passive
6. Atrial kick (presystole) - active atrial contraction adds last 20-30%
Loss of atrial kick (e.g., AF) reduces CO by 20-30% in stiff ventricles.
Heart Sounds
| Sound | Timing | Cause |
|---|---|---|
| S1 | Start of systole | Closure of mitral + tricuspid valves |
| S2 | End of systole | Closure of aortic + pulmonary valves |
| S3 | Early diastole | Rapid ventricular filling; normal in children; suggests HF in adults |
| S4 | Late diastole | Atrial contraction into stiff ventricle; always pathological |
Splitting of S2:
- Physiologic: Widens on inspiration (normal)
- Wide fixed splitting: ASD
- Paradoxical splitting: LBBB, severe AS (P2 before A2)
Determinants of Cardiac Performance
CO = Heart Rate × Stroke Volume (Normal: 4-8 L/min)
1. Preload - LVEDV/LVEDP; Frank-Starling Law: increased stretch → increased force
2. Afterload - SVR (left heart); Laplace's Law: T = P × r / (2 × wall thickness)
3. Contractility - Increased by catecholamines, Ca²⁺; decreased by beta-blockers, acidosis, hypoxia
Contractile Apparatus - Molecular Mechanism
Sarcomere proteins:
- Myosin (thick filament): Globular heads with ATPase activity; hinge rotation drives contraction
- Titin: Elastic spring anchoring myosin to Z-lines; contributes to diastolic stiffness
- Actin (thin filament): Activates myosin ATPase via reversible binding
- Tropomyosin: Inhibits actin-myosin interaction at rest
- Troponin complex:
- TnC: Ca²⁺ binding - when Ca²⁺ binds, moves tropomyosin, exposes actin
- TnI: Inhibitory subunit (clinical biomarker for MI)
- TnT: Binds to tropomyosin
Excitation-Contraction Coupling:
- Action potential → T-tubule depolarization
- L-type Ca²⁺ channels open
- Ca²⁺-induced Ca²⁺ release (CICR) from SR via ryanodine receptors
- Ca²⁺ binds TnC → tropomyosin shifts → actin exposed
- Myosin-actin cross-bridge cycling → contraction
- Relaxation: Ca²⁺ pumped back into SR (SERCA2a) + Na/Ca exchanger
Coronary Blood Flow Physiology
- LV receives blood only during diastole (systolic compression occludes vessels)
- Normal flow: ~250 mL/min (5% of CO)
- O₂ extraction by LV is near-maximal (~70-80%) at rest → increased demand MUST be met by increased flow
Regulation:
| Mechanism | Details |
|---|---|
| Metabolic | CO₂, adenosine → vasodilation (most important) |
| Endothelium | NO (vasodilator), endothelin (vasoconstrictor) |
| Autoregulation | Constant flow over 60-130 mmHg perfusion pressure |
| Autonomic | α₁: vasoconstriction; β₂: vasodilation |
PART 3: CARDIAC PATHOLOGY
Heart Failure (HF)
Definition: Unable to eject blood sufficient to meet metabolic demands OR unable to fill adequately without elevated filling pressure.
Classification by EF
| Type | EF | Mechanism | Causes |
|---|---|---|---|
| HFrEF (systolic) | < 40% | Reduced contractility, dilated ventricle | IHD, dilated CM, myocarditis |
| HFmrEF | 40-49% | Intermediate | |
| HFpEF (diastolic) | ≥ 50% | Impaired relaxation, stiff ventricle | HTN, HCM, aging, DM, obesity |
Pathophysiology:
- ↓ CO → ↓ tissue perfusion
- RAAS activation → Na⁺/H₂O retention → volume overload
- Sympathetic activation → compensatory initially, then harmful (remodeling)
- Ventricular remodeling: dilation, hypertrophy, fibrosis
Clinical Features:
- Left HF: Dyspnea, orthopnea, PND, pulmonary crackles, S3 gallop
- Right HF: JVD, peripheral edema, hepatomegaly, ascites
NYHA Classification:
- I: No symptoms with ordinary activity
- II: Mild symptoms with moderate exertion
- III: Symptoms with minimal exertion
- IV: Symptoms at rest
GDMT for HFrEF (4 pillars):
| Drug class | Examples | Benefit |
|---|---|---|
| ACEi / ARB | Enalapril, Losartan | ↓ preload/afterload, antiremodeling |
| ARNI | Sacubitril-Valsartan | Superior to ACEi; ↓ mortality |
| Beta-blockers | Carvedilol, Metoprolol succinate, Bisoprolol | ↓ HR, antiremodeling, ↓ mortality |
| MRA | Spironolactone, Eplerenone | ↓ fibrosis, diuresis |
| SGLT2i | Dapagliflozin, Empagliflozin | ↓ HF hospitalizations, ↓ mortality |
| Loop diuretics | Furosemide | Symptom relief only |
| ICD | EF < 35% | Prevent sudden cardiac death |
| CRT | EF < 35% + LBBB | Resynchronization |
Ischemic Heart Disease (IHD)
Pathogenesis:
Endothelial injury → LDL oxidation → macrophage foam cells → fatty streak → fibrous plaque → vulnerable plaque (thin cap, lipid core) → rupture → thrombosis → ACS
Angina Pectoris
| Type | Mechanism | ECG | Relief |
|---|---|---|---|
| Stable | Fixed stenosis, demand ↑ | ST depression on exertion | Rest/nitrates |
| Unstable | Plaque rupture, partial occlusion | ST depression/T-inversion at rest | Hospitalization, antithrombotic |
| Variant (Prinzmetal) | Coronary vasospasm | ST elevation at rest | Nitrates/CCB |
Acute Coronary Syndrome (ACS)
STEMI:
- Complete occlusion → transmural infarction
- ECG: ST elevation in contiguous leads; new LBBB
- Sequence: Hyperacute T waves → ST elevation → Q waves → T inversion
- Management: Primary PCI within 90 min (door-to-balloon time)
NSTEMI:
- Partial occlusion → subendocardial infarction
- ECG: ST depression, T-wave inversion (no ST elevation, no Q waves)
- Troponin elevated
- Management: Antiplatelet + anticoagulation + early invasive strategy
Localization by ECG:
| Territory | Vessel | Leads |
|---|---|---|
| Anterior | LAD | V1-V4 |
| Lateral | LCx | I, aVL, V5-V6 |
| Inferior | RCA | II, III, aVF |
| Posterior | RCA/LCx | ST depression V1-V3; confirm V7-V9 |
| Septal | LAD (septal perforators) | V1-V2 |
Complications of MI:
- Hours: Arrhythmias (VF - most common early death), heart block (inferior MI)
- Days (3-5): Free wall rupture, VSD, papillary muscle rupture → acute MR
- Weeks: Dressler syndrome, LV aneurysm, mural thrombus
Hypertension
Classification (ACC/AHA 2017):
| Stage | BP |
|---|---|
| Normal | < 120/80 |
| Elevated | 120-129 / < 80 |
| Stage 1 HTN | 130-139 / 80-89 |
| Stage 2 HTN | ≥ 140 / ≥ 90 |
| Hypertensive Crisis | > 180 / > 120 |
Secondary HTN causes:
- Renal artery stenosis, CKD
- Primary hyperaldosteronism (Conn syndrome)
- Pheochromocytoma, Cushing syndrome
- OSA, hyperthyroidism
- Drugs: NSAIDs, OCP, cocaine, steroids
Target organ damage: LVH, diastolic dysfunction, HF, IHD, stroke, CKD, hypertensive retinopathy, aortic dissection
Management:
- Lifestyle: DASH diet, Na restriction, weight loss, exercise
- First-line drugs: ACEi/ARB + thiazide diuretics + CCBs
- Hypertensive emergency: IV nitroprusside, labetalol, nicardipine
Cardiac Arrhythmias
Supraventricular
Atrial Fibrillation (AF):
- Irregularly irregular; absent P waves; narrow complex
- Causes: HTN, HF, valve disease, hyperthyroidism, alcohol
- Risk: Stroke (LA appendage thrombus)
- CHA₂DS₂-VASc for stroke risk; anticoagulate if ≥ 2 (men) / ≥ 3 (women)
- Rate control: Beta-blocker, diltiazem, digoxin
- Rhythm control: Cardioversion, antiarrhythmics, ablation
SVT (AVNRT/AVRT):
- Narrow complex, regular, abrupt onset/offset
- Treatment: Vagal maneuvers → Adenosine → CCB/beta-blocker → cardioversion
Ventricular
| Arrhythmia | Rate | QRS | Treatment |
|---|---|---|---|
| PVCs | Variable | Wide, bizarre | Beta-blockers if symptomatic |
| VT | > 100 bpm | Wide > 120 ms | Stable: amiodarone; Unstable: DC cardioversion |
| VF | Chaotic | Irregular | Immediate defibrillation + CPR |
Torsades de Pointes:
- Polymorphic VT; causes: Long QT (drugs), hypokalemia, hypomagnesemia
- Treatment: IV Magnesium sulfate + remove causative agent
Heart Block
| Degree | Features | Management |
|---|---|---|
| 1st | PR > 200 ms; all P waves conduct | None |
| 2nd Mobitz I | Progressive PR lengthening until P drops | Observe |
| 2nd Mobitz II | Constant PR; sudden dropped QRS | Pacemaker |
| 3rd (Complete) | P and QRS dissociated | Pacemaker |
Valvular Heart Disease
Aortic Stenosis (AS)
- Classic triad: Syncope, Angina, Heart Failure (SAD)
- Murmur: Crescendo-decrescendo systolic ejection murmur; right upper sternal border; radiates to carotids
- Pulse: Pulsus parvus et tardus
- Severe: Valve area < 1.0 cm², mean gradient > 40 mmHg
- Management: TAVR or surgical AVR when symptomatic or EF < 50%
Aortic Regurgitation (AR)
- Causes: Bicuspid AV, rheumatic, IE, Marfan, syphilis
- Murmur: Early diastolic decrescendo; left sternal border; leaning forward
- Signs: Water-hammer pulse, wide pulse pressure, De Musset's sign, Quincke's sign, Austin Flint murmur
- Management: ACEi/ARBs; surgery when severe/symptomatic
Mitral Stenosis (MS)
- Almost always rheumatic
- Murmur: Low-pitched diastolic rumble at apex; opening snap; loud S1
- Severe: MV area < 1.5 cm²
- Complications: AF, pulmonary HTN, right HF, emboli
- Management: Diuretics, rate control, anticoagulation; PBMV or MVR
Mitral Regurgitation (MR)
- Causes: MVP, rheumatic, ischemia, IE, dilated CM
- Murmur: Holosystolic high-pitched at apex; radiates to axilla
- Surgery: When severe with EF < 60% or LVESD > 40 mm
Infective Endocarditis (IE)
Duke Criteria - Major:
- Positive blood cultures (≥2 typical organisms)
- Echo: vegetation, abscess, new valvular regurgitation
Duke Criteria - Minor:
- Predisposing condition/IVDU
- Fever ≥ 38°C
- Vascular phenomena (Janeway lesions, emboli)
- Immunologic phenomena (Osler's nodes, Roth spots, +RF)
- Single positive blood culture
Definite IE: 2 major / 1 major + 3 minor / 5 minor
Organisms:
| Patient | Organism |
|---|---|
| Native valve (community) | Streptococcus viridans (most common) |
| IV drug user | Staphylococcus aureus; right-sided (tricuspid) |
| Prosthetic valve (early) | Staph epidermidis, Staph aureus |
| Colon cancer | Streptococcus bovis → do colonoscopy! |
Peripheral signs:
- Janeway lesions: Painless, hemorrhagic (palms/soles) - septic emboli
- Osler's nodes: Painful, nodular (fingers/toes) - immune complex
- Roth spots: Retinal hemorrhages with pale centres
- Splinter hemorrhages
Pericardial Disease
Acute Pericarditis
- Causes: Viral (Coxsackie B), TB, autoimmune, post-MI (Dressler)
- Clinical: Sharp pleuritic pain, relieved sitting forward; friction rub
- ECG: Diffuse saddle-shaped ST elevation + PR depression (no reciprocal changes)
- Management: NSAIDs + Colchicine (reduces recurrence)
Cardiac Tamponade
- Beck's Triad: Hypotension + JVD + Muffled heart sounds
- Pulsus paradoxus > 10 mmHg
- ECG: Electrical alternans
- Management: Emergency pericardiocentesis
Constrictive Pericarditis
- Causes: TB (most common worldwide), radiation, viral
- Features: Kussmaul's sign, pericardial knock, "square root sign"
- Management: Pericardiectomy
Cardiomyopathies
| Type | Pathology | Key Features | Management |
|---|---|---|---|
| Dilated CM | Enlarged, thin-walled; systolic dysfunction | Most common CM; causes: ischemic, alcoholic, viral, peripartum | GDMT for HFrEF |
| HCM | Asymmetric septal hypertrophy; diastolic dysfunction; LVOT obstruction | Most common cause of SCD in young athletes; SAM of MV; murmur increases with Valsalva/standing | BB/CCB; ICD; myectomy or alcohol ablation |
| Restrictive CM | Stiff ventricle; normal cavity | Causes: Amyloidosis, sarcoidosis, hemochromatosis, eosinophilic | Treat underlying cause |
| ARVC | Fibro-fatty RV replacement | Epsilon waves on ECG; VT/VF risk | ICD; beta-blockers |
Aortic Dissection
- Intimal tear → blood enters media → false lumen
- Risk: HTN (most common), Marfan, bicuspid AV, cocaine
- Stanford A: Ascending aorta → Emergency surgery
- Stanford B: Descending only → Medical management (BB + vasodilators); endovascular if complicated
- Clinical: Tearing/ripping chest pain radiating to back; unequal BP in arms
- Diagnosis: CT angiography (gold standard)
PART 4: CARDIOVASCULAR PHARMACOLOGY
Antihypertensives
| Class | Examples | MOA | Side Effects |
|---|---|---|---|
| ACE Inhibitors | Enalapril, Ramipril, Lisinopril | Block ACE → ↓ AngII | Dry cough (bradykinin), angioedema, hyperkalemia, teratogenic |
| ARBs | Losartan, Valsartan | Block AT1 receptor | Angioedema (rare), hyperkalemia, teratogenic |
| ARNI | Sacubitril-Valsartan | Neprilysin inhibition + AT1 block | Angioedema (DO NOT combine with ACEi), hypotension |
| Thiazides | HCTZ, Chlorthalidone | Block NCC in DCT | Hypokalemia, hyperuricemia, hyperglycemia, hypercalcemia |
| Loop Diuretics | Furosemide, Bumetanide | Block NKCC2 in TAL | Hypokalemia, ototoxicity, metabolic alkalosis |
| K-sparing Diuretics | Spironolactone, Amiloride | Block aldosterone/ENaC | Hyperkalemia; spironolactone: gynecomastia |
| DHP CCBs | Amlodipine, Nifedipine | L-type Ca²⁺ block (vessels) | Peripheral edema, reflex tachycardia, flushing |
| Non-DHP CCBs | Diltiazem, Verapamil | Ca²⁺ block (heart + vessels) | AV block, constipation, worsens HF |
| Beta-blockers | Metoprolol, Carvedilol, Atenolol | Block β1 (±β2) | Bradycardia, bronchospasm, masks hypoglycemia |
Antiarrhythmics (Vaughan-Williams)
| Class | Mechanism | Drugs | Uses |
|---|---|---|---|
| Ia | Na⁺ block (moderate); ↑ QT | Quinidine, Procainamide | AF, VT |
| Ib | Na⁺ block (fast); ↓ QT | Lidocaine, Mexiletine | VT, digoxin toxicity |
| Ic | Na⁺ block (slow); no QT change | Flecainide, Propafenone | AF (no structural heart disease) |
| II | Beta-blockers | Metoprolol, Esmolol | AF, SVT, post-MI |
| III | K⁺ block; ↑ QT | Amiodarone, Sotalol | VT, VF, AF |
| IV | Non-DHP CCBs | Diltiazem, Verapamil | SVT, AF rate control |
| Misc | - | Adenosine | SVT (half-life 10 sec) |
| Misc | - | Digoxin | AF rate control; narrow TI |
Amiodarone toxicities (long t½ ~40-55 days):
Pulmonary fibrosis, thyroid (hypo/hyper), hepatotoxicity, corneal microdeposits, photosensitivity, blue-grey skin, peripheral neuropathy, bradycardia, ↑ QT
Anticoagulants
| Drug | Target | Monitoring | Reversal |
|---|---|---|---|
| Warfarin | Vit K epoxide reductase → ↓ II,VII,IX,X | INR (target 2-3) | Vitamin K, FFP, 4-factor PCC |
| UFH | Antithrombin → inhibits IIa, Xa, IXa | aPTT | Protamine sulfate |
| LMWH | Mainly anti-Xa | Not routine | Partial: protamine |
| Dabigatran | Direct thrombin (IIa) inhibitor | ECT/dTT | Idarucizumab |
| Rivaroxaban/Apixaban | Direct Factor Xa inhibitors | Not routine | Andexanet alfa |
Antiplatelets
| Drug | MOA | Uses |
|---|---|---|
| Aspirin | Irreversible COX-1 inhibition → ↓ TXA2 | ACS, stroke prevention, post-PCI |
| Clopidogrel | P2Y12 ADP antagonist (prodrug, CYP2C19) | ACS, post-PCI (DAPT) |
| Ticagrelor | Reversible P2Y12 (not prodrug) | ACS (PLATO trial - preferred over clopidogrel) |
| Prasugrel | Irreversible P2Y12 (prodrug) | ACS with PCI; avoid in prior stroke |
Statins
- Block HMG-CoA reductase → ↓ LDL synthesis + ↑ LDL receptors
- Pleiotropic: ↓ inflammation, plaque stabilization
- High intensity: Atorvastatin 40-80 mg, Rosuvastatin 20-40 mg
- Side effects: Myopathy, rhabdomyolysis (rare), transaminase ↑
PART 5: CVS CLINICAL SKILLS
ECG Systematic Reading
Rate → Rhythm → Axis → P waves → PR → QRS → QT → ST/T → Assessment
Normal values:
- HR: 60-100 bpm
- PR interval: 120-200 ms
- QRS: < 120 ms
- QTc: < 440 ms (M), < 460 ms (F)
- Axis: -30° to +90°
Axis deviation:
- Left axis: LBBB, LAHB, LVH, inferior MI
- Right axis: RBBB, RVH, pulmonary HTN, lateral MI
🫁 RESPIRATORY SYSTEM - Complete Medical Student Guide
PART 1: RESPIRATORY ANATOMY
Upper Respiratory Tract
- Trachea: Starts at C6; 10-15 cm; bifurcates at carina (T4/sternal angle)
- Larynx: C3-C6; vocal cords; epiglottis protects airway during swallowing
Tracheobronchial Tree
| Zone | Generations | Purpose |
|---|---|---|
| Conducting (dead space ~150 mL) | 0-16 | Air conduction only; no gas exchange |
| Respiratory | 17-23 | Gas exchange (respiratory bronchioles → alveolar sacs) |
- Right bronchus: Shorter, wider, more vertical → foreign bodies lodge in right lower lobe
- Left bronchus: Longer, narrower, more horizontal
Lungs:
- Right: 3 lobes (upper, middle, lower); 10 bronchopulmonary segments
- Left: 2 lobes (upper, lower) + lingula; 8-10 segments
Alveoli - Gas Exchange Unit
- ~300-500 million alveoli; surface area ~70-80 m²
- Type I pneumocytes (~95% surface area): Gas exchange; flat, squamous
- Type II pneumocytes (~5%): Produce surfactant (DPPC/lecithin); progenitor cells; host defense proteins
- Alveolar macrophages: First-line immune defense
- Blood-gas barrier: Alveolar epithelium → basement membrane → capillary endothelium = ~0.3-0.5 µm
PART 2: RESPIRATORY PHYSIOLOGY
Lung Volumes and Capacities
| Volume/Capacity | Normal | Definition |
|---|---|---|
| Tidal Volume (VT) | 500 mL | Volume per breath |
| IRV | 3000 mL | Max extra inspiration above VT |
| ERV | 1200 mL | Max extra expiration below VT |
| Residual Volume (RV) | 1200 mL | Air after maximal expiration |
| Vital Capacity (VC) | 4800 mL | IRV + VT + ERV |
| FRC | 2400 mL | ERV + RV; end-quiet-expiration volume |
| TLC | 6000 mL | All volumes combined |
RV, FRC, and TLC cannot be measured by spirometry - need helium dilution, N₂ washout, or body plethysmography.
Spirometry - Obstructive vs Restrictive
| Pattern | FEV1 | FVC | FEV1/FVC | TLC | Causes |
|---|---|---|---|---|---|
| Obstructive | ↓↓ | Normal/↓ | < 0.70 | Normal/↑ | COPD, Asthma, Bronchiectasis |
| Restrictive | ↓ | ↓↓ | Normal or ↑ | ↓ | IPF, Pleural effusion, NMD, Obesity |
| Mixed | ↓ | ↓ | < 0.70 | ↓ | Sarcoidosis, some COPD |
Respiratory Mechanics
Compliance
C = ΔVolume / ΔPressure (Normal lung ~200 mL/cmH₂O)
| ↓ Compliance (stiff) | ↑ Compliance (floppy) |
|---|---|
| Pulmonary fibrosis, ARDS, pulmonary edema, NRDS | Emphysema, aging |
Surfactant:
- Produced by Type II pneumocytes
- Lowers surface tension (LaPlace's law: P = 2T/r; prevents alveolar collapse)
- Deficient in premature infants (<32 weeks) → NRDS
- Treatment: Antenatal betamethasone; exogenous surfactant (beractant)
Airway Resistance
Poiseuille's Law: R = 8ηL / πr⁴ (resistance inversely proportional to 4th power of radius)
- Medium bronchi (3rd-4th generation) contribute most resistance
- ↑ Resistance: bronchospasm, mucosal edema, secretions, foreign body
Gas Exchange
V/Q Ratio
- Normal overall V/Q = 0.8 (ventilation ~4 L/min; CO ~5 L/min)
Regional differences (upright):
| Region | V/Q | Features |
|---|---|---|
| Apex (Zone 1) | > 1 | Low perfusion; high O₂, low CO₂ |
| Middle (Zone 2) | ~0.8 | Normal |
| Base (Zone 3) | < 1 | High perfusion; low O₂, high CO₂ |
West Zones:
- Zone 1: PA > Pa > Pv → No flow (not normally present; occurs in hemorrhage or PPV)
- Zone 2: Pa > PA > Pv → Flow = Pa - PA
- Zone 3: Pa > Pv > PA → Continuous flow (most blood flow)
V/Q Mismatch → Hypoxemia:
- Low V/Q: Hypoxemia (responds to O₂)
- True shunt (V/Q = 0): Hypoxemia NOT corrected by 100% O₂ (atelectasis, consolidation)
- High V/Q: Dead space → mainly hypercapnia
5 Mechanisms of Hypoxemia:
- Hypoventilation - ↑ CO₂ displaces O₂; A-a gradient normal
- Diffusion impairment - IPF; worsens on exercise
- V/Q mismatch - Most common; responds to O₂
- True shunt - Does NOT respond to 100% O₂
- Low FiO₂ - High altitude
A-a gradient = PAO₂ - PaO₂; Normal < 10-15 mmHg; elevated in V/Q mismatch, shunt, diffusion impairment; normal in hypoventilation.
Hb-O₂ Dissociation Curve
Shift RIGHT (↓ O₂ affinity, ↑ delivery to tissues):
↑ Temperature, ↑ 2,3-DPG, ↑ CO₂, ↓ pH (Bohr effect), exercise
Shift LEFT (↑ O₂ affinity, ↓ delivery):
↓ Temperature, ↓ 2,3-DPG, ↓ CO₂, ↑ pH, HbF, CO poisoning, methemoglobin
O₂ Content: CaO₂ = (Hb × 1.34 × SaO₂) + (0.003 × PaO₂)
CO₂ Transport
- 70%: As HCO₃⁻ (carbonic anhydrase in RBCs) - Chloride shift
- 23%: Carbaminohaemoglobin (bound to Hb)
- 7%: Dissolved in plasma
Haldane Effect: Deoxygenated Hb binds more CO₂ → facilitates CO₂ unloading at lungs.
Control of Breathing
Respiratory centres (brainstem):
- Pre-Bötzinger complex (medulla): Rhythm generator
- Dorsal Respiratory Group (NTS): Inspiration
- Pneumotaxic centre (upper pons): Limits inspiration
- Apneustic centre (lower pons): Sustained inspiration (overridden by pneumotaxic)
Central chemoreceptors (ventral medulla):
- Respond to ↑ PCO₂ → ↓ CSF pH
- Primary drive to breathe in normal individuals
- Slow response; insensitive to PO₂
Peripheral chemoreceptors (carotid + aortic bodies):
- Carotid bodies most important (CN IX → NTS)
- Respond to: ↓ PaO₂ (< 60 mmHg), ↑ PCO₂, ↓ pH
- Fast response (seconds)
COPD Clinical Pearl: Chronic CO₂ retention desensitizes central chemoreceptors → "hypoxic drive" via peripheral chemoreceptors. High-flow O₂ suppresses this → CO₂ retention risk.
Acid-Base - Respiratory Component
| Disorder | pH | PaCO₂ | HCO₃⁻ | Compensation |
|---|---|---|---|---|
| Respiratory Acidosis | ↓ | ↑ | ↑ | Acute: +1 mEq/L per 10 mmHg ↑ CO₂; Chronic: +3.5 mEq/L |
| Respiratory Alkalosis | ↑ | ↓ | ↓ | Acute: -2 mEq/L per 10 mmHg ↓ CO₂; Chronic: -5 mEq/L |
Causes Respiratory Acidosis: COPD, sedatives/opioids, NMD, severe asthma, pneumothorax
Causes Respiratory Alkalosis: Anxiety, pregnancy, salicylates (early), high altitude, mechanical ventilation, sepsis (early)
PART 3: RESPIRATORY DISEASES
COPD
Definition: Persistent, largely irreversible airflow limitation; FEV1/FVC < 0.70 post-bronchodilator
| Chronic Bronchitis ("Blue Bloater") | Emphysema ("Pink Puffer") | |
|---|---|---|
| Mechanism | ↑ mucus, airway inflammation, narrowing | Alveolar wall destruction, ↓ elastic recoil |
| Cause | Smoking; cough ≥3 months/yr for ≥2 yrs | Smoking; α1-antitrypsin deficiency (young, panacinar) |
| Hypoxia | Severe, early cyanosis | Mild; compensatory hyperventilation |
| CO₂ retention | Common | Rare until late |
Emphysema subtypes:
- Centrilobular: Smoking; upper lobes
- Panacinar: α1-antitrypsin deficiency; lower lobes
- Paraseptal (distal acinar): Young adults; associated with spontaneous pneumothorax
GOLD Classification (FEV1 % predicted):
- GOLD 1 (Mild): ≥ 80%
- GOLD 2 (Moderate): 50-79%
- GOLD 3 (Severe): 30-49%
- GOLD 4 (Very Severe): < 30%
Stable COPD Management:
- Smoking cessation (most important - only intervention reducing mortality)
- Bronchodilators: SABA → SAMA → LABA → LAMA (tiotropium)
- ICS: Add for frequent exacerbations; ICS + LABA combination
- Triple therapy: ICS + LABA + LAMA
- Pulmonary rehabilitation
- LTOT: PaO₂ ≤ 55 mmHg (or ≤ 60 mmHg with polycythemia/cor pulmonale) → ≥ 15 hrs/day → ↓ mortality
- Influenza + pneumococcal vaccines
- Roflumilast (PDE4 inhibitor): Severe + chronic bronchitis
COPD Exacerbation Management:
- O₂: Target SpO₂ 88-92%
- Nebulized SABA + ipratropium
- Systemic corticosteroids (prednisolone 40 mg × 5 days)
- Antibiotics if purulent sputum
- NIV (BiPAP): If pH < 7.35 + ↑ CO₂ → ↓ intubation, ↓ mortality
Asthma
Definition: Chronic inflammatory airway disease with episodic, reversible airflow obstruction and bronchial hyperresponsiveness
Pathophysiology:
- Allergen → IgE-mediated mast cell degranulation → histamine, leukotrienes → bronchoconstriction
- Th2 inflammation (eosinophils, mast cells)
- Airway remodeling in chronic/severe asthma
Triggers: Allergens, cold air, exercise, NSAIDs (aspirin-exacerbated), beta-blockers, smoke, viral URTI
Step-up Therapy:
| Step | Treatment |
|---|---|
| 1 | SABA PRN |
| 2 | Low-dose ICS + SABA PRN |
| 3 | Low-dose ICS + LABA |
| 4 | Medium-high ICS + LABA |
| 5 | High ICS + LABA ± LAMA ± oral corticosteroids |
| Severe (Biologic) | Anti-IgE (Omalizumab), Anti-IL5 (Mepolizumab), Anti-IL4/13 (Dupilumab) |
Acute Severe Asthma (Status Asthmaticus):
- Life-threatening signs: Silent chest, bradycardia, confusion, normal/↑ PaCO₂ (should be LOW in asthma - if normal = very severe)
- Management: O₂ (SpO₂ 94-98%), nebulized SABA q20 min, ipratropium, IV/oral steroids, IV Magnesium sulfate 2g over 20 min, IV aminophylline, intubation if deteriorating
Pneumonia
Classification:
| Type | Common Pathogens |
|---|---|
| CAP | S. pneumoniae (most common), Mycoplasma, Legionella, H. influenzae |
| HAP (> 48 hrs) | Gram-negatives (Pseudomonas, Klebsiella), S. aureus (MRSA) |
| Aspiration | Anaerobes, mixed flora |
| Atypical ("walking") | Mycoplasma, Chlamydophila, Legionella |
Typical vs Atypical:
| Feature | Typical (S. pneumoniae) | Atypical (Mycoplasma) |
|---|---|---|
| Onset | Acute, sudden | Gradual |
| Fever | High, rigors | Low-grade |
| CXR | Lobar consolidation | Diffuse/bilateral patchy |
| Sputum | Purulent, productive | Non-productive |
| Treatment | Amoxicillin | Macrolide, Doxycycline |
CURB-65 (mortality predictor):
| Criterion | Score |
|---|---|
| Confusion (new) | 1 |
| Urea > 7 mmol/L | 1 |
| RR ≥ 30 | 1 |
| BP < 90 systolic or < 60 diastolic | 1 |
| Age ≥ 65 | 1 |
- 0-1: Outpatient | 2: Inpatient | 3-5: ICU consideration
Legionella pneumophila:
- Gram-negative intracellular; grows in water systems (cooling towers)
- Features: Pneumonia + GI + CNS + hyponatremia + ↑ LDH + lymphopenia
- Diagnosis: Urinary antigen (serogroup 1); culture on BCYE agar
- Treatment: Macrolide or fluoroquinolone (NOT beta-lactams)
Pulmonary Tuberculosis (TB)
Mycobacterium tuberculosis - acid-fast bacillus (Ziehl-Neelsen stain)
Primary TB: Ghon focus (mid-lung) + hilar node = Ghon complex; usually asymptomatic; heals with calcification
Post-Primary (Reactivation): Apical/posterior upper lobes; cavitation, caseation necrosis; symptoms: cough, hemoptysis, weight loss, night sweats, evening fever
Diagnosis:
- AFB smear and culture (Lowenstein-Jensen medium; 6-8 weeks)
- GeneXpert MTB/RIF: Fast + detects rifampicin resistance
- Mantoux (TST): ≥10 mm = positive; ≥5 mm in immunocompromised/HIV
- IGRA: More specific, unaffected by BCG vaccination
- CXR: Apical infiltrates, cavitation, calcification
Standard Regimen:
| Phase | Drugs | Duration |
|---|---|---|
| Intensive (RIPE) | Rifampicin + Isoniazid + Pyrazinamide + Ethambutol | 2 months |
| Continuation | Rifampicin + Isoniazid | 4 months |
| Total | 6 months |
Drug toxicities:
| Drug | Key Side Effects |
|---|---|
| Rifampicin | Orange urine/secretions, hepatotoxicity, enzyme inducer (↓ OCP, warfarin) |
| Isoniazid | Peripheral neuropathy (B6 deficiency → give pyridoxine), hepatotoxicity, drug-induced SLE |
| Pyrazinamide | Hyperuricemia (gout), hepatotoxicity |
| Ethambutol | Optic neuritis (monitor visual acuity monthly) |
Pulmonary Embolism (PE)
Risk Factors (Virchow's Triad):
- Stasis: Immobility, post-surgery, long flights
- Hypercoagulability: Factor V Leiden, antiphospholipid syndrome, malignancy, OCP
- Endothelial injury: Trauma, surgery
Wells Score:
| Criterion | Points |
|---|---|
| DVT symptoms/signs | 3 |
| PE more likely than alternative | 3 |
| HR > 100 | 1.5 |
| Surgery/immobility last 4 weeks | 1.5 |
| Prior DVT/PE | 1.5 |
| Hemoptysis | 1 |
| Active malignancy | 1 |
- Score > 4: High probability → CTPA
- Score ≤ 4: Low probability → D-dimer first
Investigations:
- ECG: Sinus tachycardia (most common); S1Q3T3 (classic but not specific)
- CXR: Often normal; Westermark sign, Hampton's hump
- ABG: Hypoxemia, hypocapnia, respiratory alkalosis, ↑ A-a gradient
- CTPA: Gold standard
- V/Q scan: If CTPA contraindicated
Management:
- Massive PE (hemodynamically unstable): Systemic thrombolysis (alteplase); surgical embolectomy if contraindicated
- Stable PE: Anticoagulation with DOACs (rivaroxaban/apixaban preferred)
- Duration: 3 months (provoked); ≥ 3 months (unprovoked/malignancy)
Pleural Diseases
Pleural Effusion - Light's Criteria
Exudate if ANY one met:
- Pleural protein / serum protein > 0.5
- Pleural LDH / serum LDH > 0.6
- Pleural LDH > 2/3 upper limit of normal serum LDH
| Transudate | Exudate |
|---|---|
| Heart failure (most common) | Pneumonia (parapneumonic) |
| Cirrhosis | Malignancy |
| Nephrotic syndrome | TB |
| Hypoalbuminemia | PE, RA, SLE |
Pneumothorax
| Type | Cause | Features |
|---|---|---|
| Primary spontaneous | Young, tall, thin males; blebs | No underlying disease |
| Secondary spontaneous | COPD (bullae), TB, CF, Marfan | Underlying lung disease |
| Tension | Valve effect traps air | Emergency: trachea deviates AWAY, ↓ breath sounds, hypotension, JVD |
Management:
- Small primary (< 2 cm): Observe; high-flow O₂ (4× absorption rate)
- Large/symptomatic: Needle aspiration or chest tube (ICD)
- Tension: Immediate needle decompression (2nd ICS, MCL) → then chest tube
Interstitial Lung Disease (ILD)
Key features: Restrictive pattern, diffusion impairment, bibasal Velcro crackles, ground-glass opacities on HRCT, clubbing (IPF)
| ILD | Associations | HRCT Pattern |
|---|---|---|
| IPF | Elderly male smokers; poor prognosis (median 2-3 yrs) | UIP: Basal, subpleural honeycombing + traction bronchiectasis |
| NSIP | Autoimmune (scleroderma, SLE, PM/DM) | Ground-glass opacities, basal fibrosis |
| COP | Post-infection/drug | Consolidation + GGO, peribronchovascular |
| Sarcoidosis | Young adults; bilateral hilar lymphadenopathy | Micronodules along lymphatics; upper lobe |
| Hypersensitivity Pneumonitis | Organic dust (farmer's lung - thermophilic actinomycetes; bird fancier's lung) | Acute: GGO; Chronic: fibrosis |
| Asbestosis | Occupational; ↑ mesothelioma risk | Basal fibrosis + pleural plaques |
| Silicosis | Occupational; mining, sandblasting | Upper lobe nodules; "eggshell" calcification of hilar nodes |
Treatment of IPF: Pirfenidone or Nintedanib (anti-fibrotic; slow progression); lung transplant for end-stage
Lung Cancer
Most common cause of cancer death worldwide
| Type | Location | Key Features |
|---|---|---|
| Squamous Cell | Central (hilar) | Cavitates; PTHrP → hypercalcemia; Pancoast tumor |
| Adenocarcinoma | Peripheral | Most common in non-smokers/women; EGFR/ALK mutations; lepidic growth pattern |
| Small Cell (SCLC) | Central | Neuroendocrine; oat cells; paraneoplastic syndromes; highly aggressive |
| Large Cell | Peripheral | Undifferentiated; poor prognosis |
Paraneoplastic syndromes:
| Syndrome | Cancer |
|---|---|
| Hypercalcemia (PTHrP) | Squamous cell |
| SIADH (hyponatremia) | SCLC |
| Ectopic ACTH → Cushing | SCLC |
| Lambert-Eaton Myasthenic Syndrome (anti-VGCC) | SCLC |
| Hypertrophic osteoarthropathy / clubbing | Adenocarcinoma |
| Trousseau's syndrome (migratory thrombophlebitis) | Adenocarcinoma |
SVC Syndrome:
- Compression/invasion of SVC
- Features: Facial/arm/neck edema, JVD, dilated chest wall veins, Pemberton's sign
- Most common cause: SCLC, lymphoma
Pancoast Tumor (Superior Sulcus):
- Apex of lung → invades brachial plexus, subclavian vessels, stellate ganglion
- Horner's syndrome: Ptosis, miosis, anhidrosis, enophthalmos
- Shoulder/arm pain (C8/T1/T2 distribution)
- Treatment: Chemoradiation → surgery
Treatment:
- NSCLC I-II: Surgery (lobectomy) ± adjuvant chemo
- NSCLC III: Concurrent chemoradiation
- NSCLC IV: Platinum chemo; targeted (EGFR: osimertinib; ALK: crizotinib); Immunotherapy (pembrolizumab if PD-L1 +)
- SCLC Limited: Chemo + radiation (cisplatin/etoposide) + PCI
- SCLC Extensive: Chemotherapy + atezolizumab
Cystic Fibrosis (CF)
- Autosomal recessive; CFTR gene (chromosome 7q); most common lethal AR disease in Caucasians
- Most common mutation: ΔF508 (deletion Phe 508)
- CFTR = Cl⁻ channel; defect → thick viscous secretions
Clinical features:
| System | Manifestations |
|---|---|
| Respiratory | Chronic cough, bronchiectasis, recurrent pneumonias (Pseudomonas aeruginosa), pneumothorax, respiratory failure |
| GI/Pancreatic | Meconium ileus, pancreatic exocrine insufficiency, CF-related diabetes |
| Reproductive | Male infertility (CBAVD); ↓ female fertility |
| Other | Sinusitis, nasal polyps, clubbing, salt depletion |
Diagnosis:
- Newborn screening: IRT + CFTR mutation
- Sweat chloride test (gold standard): Cl⁻ > 60 mmol/L = diagnostic
Management:
- Airway clearance: Chest physiotherapy, hypertonic saline, dornase alfa (DNase)
- Antibiotics: Inhaled tobramycin/aztreonam (chronic Pseudomonas); IV for exacerbations
- Pancreatic enzyme replacement (Creon); fat-soluble vitamins (A, D, E, K)
- CFTR modulators:
- Ivacaftor (G551D mutation)
- Elexacaftor + Tezacaftor + Ivacaftor (Trikafta/Kaftrio): ΔF508 - transforms outcomes
- Lung transplant (bilateral): End-stage
Obstructive Sleep Apnea (OSA)
- Repetitive upper airway obstruction during sleep
- Risk factors: Obesity, male, age, retrognathia, tonsillar hypertrophy
- Symptoms: Snoring, witnessed apneas, daytime sleepiness, morning headaches
- Complications: HTN (most common), AF, pulmonary HTN, cor pulmonale, cognitive impairment
- Diagnosis: Polysomnography; AHI: mild 5-14, moderate 15-29, severe ≥ 30
- Management: CPAP (first-line, most effective)
Mechanical Ventilation
Lung Protective Ventilation (ARDSnet):
- Tidal volume: 6 mL/kg ideal body weight
- Plateau pressure: < 30 cmH₂O
- Adequate PEEP
- Permissive hypercapnia (pH > 7.20 acceptable)
- Prone positioning 16 hrs/day for severe ARDS (PaO₂/FiO₂ < 150) → ↓ mortality
NIV (BiPAP) indications:
- COPD exacerbation (pH < 7.35 + ↑ CO₂)
- Cardiogenic pulmonary edema
- Type II respiratory failure
- OSA (CPAP)
QUICK REVISION TABLES
CVS Key Facts
| Topic | Key Point |
|---|---|
| Most common cause of HF | IHD/ischemic cardiomyopathy |
| HFrEF EF threshold | < 40% |
| 4 pillars GDMT | ARNI + Beta-blocker + MRA + SGLT2i |
| STEMI treatment | Primary PCI < 90 min |
| Most common valvular disease (developed world) | Aortic stenosis |
| AS classic triad | Syncope, Angina, Heart Failure |
| Most common cause of MS | Rheumatic fever |
| HCM murmur increases with | Valsalva / standing (↓ preload) |
| Most common IE organism (native valve) | Streptococcus viridans |
| Aortic dissection Type A | Emergency surgery |
| Dabigatran reversal | Idarucizumab |
| Xa inhibitor reversal | Andexanet alfa |
Respiratory Key Facts
| Topic | Key Point |
|---|---|
| Cannot measure by spirometry | RV, FRC, TLC |
| Obstructive spirometry | FEV1/FVC < 0.70 |
| Most common cause of hypoxemia | V/Q mismatch |
| Hypoxemia NOT corrected by 100% O₂ | True shunt |
| COPD most important intervention | Smoking cessation |
| COPD LTOT indication | PaO₂ ≤ 55 mmHg |
| COPD NIV indication | pH < 7.35 + ↑ CO₂ |
| Most common CAP organism | Streptococcus pneumoniae |
| Atypical pneumonia treatment | Macrolide/doxycycline |
| TB total duration | 6 months (2 RIPE + 4 RI) |
| Ethambutol toxicity | Optic neuritis |
| Massive PE treatment | Systemic thrombolysis (alteplase) |
| IPF treatment | Pirfenidone or Nintedanib |
| CF most common mutation | ΔF508 |
| CF CFTR modulator for ΔF508 | Elexacaftor/Tezacaftor/Ivacaftor (Trikafta) |
| OSA first-line treatment | CPAP |
| ARDS protective ventilation TV | 6 mL/kg IBW |
Sources: Barash's Clinical Anesthesia 9e | Braunwald's Heart Disease | Fuster & Hurst's The Heart 15e | Murray & Nadel's Textbook of Respiratory Medicine | Katzung's Basic & Clinical Pharmacology 16e
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