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What I Can Help You With

• Drugs, dosages, mechanisms of action, side effects
• Disease diagnosis, pathophysiology, and management
• Anatomy, physiology, and lab values

• Understanding clinical cases and presentations
• Interpreting investigations (ECG, X-ray, labs, imaging)
• Procedures and patient management protocols

• Breaking down complex topics (pharmacology, pathology, surgery, medicine)
• Quick summaries of conditions you encounter on the ward
• Exam prep (MBBS finals, PG entrance, USMLE, etc.)

• Searching the latest clinical evidence and guidelines (PubMed)
• Understanding journal articles and studies

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• "What's the management of diabetic ketoacidosis?"
• "Explain the mechanism of beta-blockers"
• "What does a raised troponin mean?"

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Pulmonary Embolism (PE) - Complete Guide for Your Internship

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1. What Is It?

• Murray & Nadel's Textbook of Respiratory Medicine: "PE is a life-threatening feature of venous thromboembolism and most frequently originates from deep venous thrombosis in the lower extremities."

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2. Pathophysiology - Why Is It Dangerous?

Respiratory failure

• The blocked lung segment gets ventilated but NOT perfused - creating dead space (V/Q mismatch)
• Hypoxia results from shunting and atelectasis
• Surfactant loss can cause pulmonary infarction in peripheral emboli

Cardiovascular collapse

• Obstruction of the pulmonary vasculature increases right ventricular afterload suddenly
• The right ventricle (RV) is a thin-walled chamber - it is not built for high pressure
• RV dilation causes the interventricular septum to bow into the left ventricle (LV), reducing LV filling and cardiac output
• This leads to systemic hypotension and shock - the "obstructive shock" of massive PE

A large PE can obstruct the entire right ventricular outflow system, causing sudden cardiovascular collapse and cardiac arrest. About 25% of sudden cardiac deaths are thought to be due to PE. (Rosen's Emergency Medicine)

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3. Risk Factors - Virchow's Triad

• Murray & Nadel's: "Three predisposing factors - hypercoagulability, stasis, and venous injury or inflammation (Virchow's triad) - may each contribute to a clot that becomes clinically evident as DVT or PE."

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4. Clinical Presentation

Symptoms

Signs

• Tachycardia (most common sign)
• Tachypnoea
• Low O2 saturations
• Hypotension (in massive PE only)
• Signs of DVT: unilateral leg swelling, redness, warmth
• Fever is usually low-grade; >38.6°C (101.5°F) suggests infection instead

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5. Diagnosis

Step 1 - Estimate Pre-test Probability (PTP)

• Score >4: High probability - go straight to imaging
• Score ≤4: Low/moderate - test D-dimer first

Step 2 - PERC Rule (to avoid unnecessary testing)

1. Age < 50
2. Pulse < 100
3. SaO2 > 94%
4. No unilateral leg swelling
5. No hemoptysis
6. No recent trauma or surgery
7. No prior PE/DVT
8. No hormone use

Step 3 - D-Dimer

• Sensitivity 95-98%, specificity only 40-55%
• A negative D-dimer rules out PE in low/moderate probability patients
• A positive D-dimer is NOT diagnostic - requires imaging
• Age-adjusted D-dimer threshold: age × 10 ng/mL (for patients >50 years) - increases the number of patients who can be ruled out without imaging by 10-20%

Step 4 - Imaging

• CTPA (CT Pulmonary Angiography) - gold standard, most commonly used
• V/Q scan - when CTPA contraindicated (contrast allergy, pregnancy, renal failure)
• Echocardiography - useful in unstable patients to assess RV strain
• Chest X-ray - often normal; classic signs:
  • Hampton's Hump (wedge-shaped pleural opacity from infarction)
  • Westermark sign (oligaemia distal to embolus)
  • Fleischner sign (enlarged pulmonary artery)
• ECG - most common finding is sinus tachycardia. The classic S1Q3T3 pattern (S in lead I, Q wave + T-wave inversion in lead III) suggests acute right heart strain - not sensitive but specific when present

Biomarkers

• Troponin - elevated in massive/submassive PE due to RV strain; indicates high risk for mortality
• BNP/NT-proBNP - elevated with RV dysfunction
• D-dimer - as above

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6. Classification by Severity

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7. Management

Immediate stabilisation

• O2 supplementation (target SaO2 >94%)
• IV access, cardiac monitoring
• Fluid resuscitation cautiously (excessive fluids worsen RV dilation)
• Vasopressors (noradrenaline) if haemodynamically unstable

Anticoagulation - the mainstay of treatment

• LMWH (Low Molecular Weight Heparin, e.g., enoxaparin) - drug of choice for most patients
• Unfractionated heparin (UFH) IV - preferred if thrombolysis planned or severe renal impairment

• DOACs (Direct Oral Anticoagulants) - e.g., rivaroxaban, apixaban - now first-line for most patients
• Warfarin - still used in certain cases (e.g., antiphospholipid syndrome, mechanical valves)

Thrombolysis (systemic or catheter-directed)

• Indicated in massive PE with haemodynamic instability (the patient is in shock or cardiac arrest)
• Drugs: alteplase (tPA), streptokinase
• Risk: major bleeding, including intracranial haemorrhage - so used only when risk of death outweighs bleeding risk
• Murray & Nadel's: "Primary difference between prophylaxis and treatment is the dosages of anticoagulants; treated patients receive a higher dosage."

Surgical embolectomy

• Reserved for massive PE when thrombolysis fails or is contraindicated

IVC filter

• When anticoagulation is absolutely contraindicated (e.g., active major bleed)

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8. Special Scenarios to Know

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9. Complications

• Pulmonary hypertension - if PE recurs or goes untreated, chronic clot can scar the pulmonary arteries
• Chronic Thromboembolic Pulmonary Hypertension (CTEPH) - occurs in 1-4% after PE
• Right heart failure
• Post-PE syndrome - persistent dyspnea and reduced exercise tolerance after an index PE

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Quick Memory Aid

• C - Cancer
• L - Long trips / immobility
• O - OCP / hormones / Obesity
• T - Trauma / surgery / Thrombophilia
• S - Surgery / Stasis / previous clot

• S - Sudden dyspnea
• A - Acute chest pain (pleuritic)
• D - DVT signs in leg

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Syncope - Complete Guide for Your Internship

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1. Definition

• Abrupt onset
• Short duration
• Spontaneous and complete recovery

• Tintinalli's Emergency Medicine: "A brief loss of consciousness associated with inability to maintain postural tone that spontaneously resolves without medical intervention."

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2. Pathophysiology

~10 seconds of complete disruption of blood flow to both cerebral cortices or to the brainstem reticular activating system, OR a 35-50% reduction in cerebral perfusion pressure

• Tintinalli's: "Cerebral perfusion and consciousness are restored by the supine position, autonomic autoregulatory response, or restoration of a perfusing cardiac rhythm."

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3. Classification and Causes

A. Reflex-Mediated / Neural (Most Common - ~21%)

1. Trigger (e.g., pain, fear, prolonged standing)
2. Prodrome: nausea, pallor, sweating, lightheadedness, tunnel vision, yawning
3. Loss of consciousness (brief, usually <1 minute)
4. Recovery: fatigue, nausea for hours after

B. Orthostatic Hypotension (~9%)

• Dehydration / blood loss / vomiting
• Medications: antihypertensives, diuretics, nitrates, alpha-blockers
• Autonomic neuropathy (diabetes, Parkinson's disease)
• Elderly (blunted baroreceptor response)
• Prolonged bed rest

C. Cardiac Syncope (~10%) - THE DANGEROUS ONE

• Bradycardias: Sick sinus syndrome, high-degree AV block, pacemaker malfunction
• Tachycardias: Ventricular tachycardia (VT), Ventricular fibrillation (VF), SVT
• Channelopathies: Long QT syndrome, Brugada syndrome, WPW syndrome

• Aortic stenosis (syncope on exertion = very ominous sign)
• Hypertrophic obstructive cardiomyopathy (HOCM)
• Pulmonary embolism
• Cardiac tamponade
• Pulmonary hypertension
• Atrial myxoma (tumour obstructing mitral valve)

D. Other Causes

• Neurologic (~4%): Seizures (not true syncope, but mimics it), transient ischaemic attack (TIA) of posterior circulation
• Metabolic: Hypoglycaemia, hypoxia, anaemia
• Medications: Beta-blockers, antihypertensives, antidepressants
• Unknown: 37-50% of cases remain unexplained even after workup

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4. Key Clinical Features - History Is Everything

Before the event

• What were you doing? (exertion = cardiac; prolonged standing = vasovagal)
• Any prodrome? (nausea/sweating = vasovagal; NO prodrome = cardiac/arrhythmic)
• Any palpitations before? (arrhythmia)
• Any recent illness, vomiting, blood loss? (orthostatic)
• New medications?

During the event

• Witnessed? Duration?
• Limb jerking? (brief jerks can occur in syncope from hypoperfusion, but prolonged rhythmic jerking = seizure)
• Tongue biting? Incontinence? (seizure rather than syncope)
• Colour: Pale = vasovagal/cardiac; Blue = cyanotic/respiratory/arrhythmic

After the event

• How quickly did they recover? (<1 min = syncope; prolonged confusion = seizure - "postictal phase")
• Headache? Focal neurological deficit? (TIA/stroke)
• Chest pain? (ACS, PE, aortic dissection)

Red flag features suggesting cardiac cause

• Syncope during exertion (not after)
• Syncope when lying down or sitting (arrhythmia)
• No prodrome - sudden collapse
• Family history of sudden cardiac death or channelopathy
• Known structural heart disease
• Palpitations just before syncope
• Age >65 years
• Abnormal ECG

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5. Examination

• Vital signs: BP in both arms (aortic dissection), HR, postural BP and HR (lying vs. standing 1 and 3 min)
• Cardiovascular: Murmurs (aortic stenosis, HOCM), signs of heart failure, carotid bruits
• Neurological: Any focal deficits? Tongue laceration?
• Skin: Pallor, cyanosis, diaphoresis

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6. Investigations

Always do:

ECG - what to look for in syncope:

• Long QT (risk of Torsades de Pointes VT)
• Brugada pattern (right bundle branch block + saddle-shaped ST elevation in V1-V3)
• Delta waves (WPW - pre-excitation, risk of fast AF)
• S1Q3T3 (PE)
• Complete heart block / high-degree AV block
• Left bundle branch block (new LBBB = very high-risk)
• Right bundle branch block

If cardiac syncope suspected:

If orthostatic suspected:

• Tilt-table test (gold standard for vasovagal and orthostatic syncope)

If neurological cause suspected:

• CT/MRI brain - only if focal neuro signs or post-ictal state
• EEG - if seizure suspected

Important: Routine CT brain, EEG, or carotid Doppler are NOT recommended in isolated syncope with no neurological features.

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7. Risk Stratification - Who Needs Admission?

Admit / High-risk if ANY of:

• Abnormal ECG
• History of structural heart disease or heart failure
• Age >65
• Syncope during exertion
• Syncope supine or without prodrome
• New-onset cardiac murmur
• Positive troponin
• SBP <90 mmHg on arrival
• Family history of sudden cardiac death

Can consider discharge / Low-risk if:

• Young patient
• Clear vasovagal trigger with prodrome
• Normal ECG
• No cardiac history
• Normal vital signs

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8. Treatment - Based on Cause

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9. Syncope vs. Seizure vs. Cardiac Arrest - The Key Differential

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10. Mortality Risk by Cause (Framingham Heart Study)

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Quick Memory Aid

• C - Cardiac history (structural or arrhythmia)
• R - R on T / abnormal ECG findings
• A - Age >65 or Arrhythmia-related
• S - Sudden (no prodrome), Supine
• H - Haemodynamic instability (hypotension, dyspnea)

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Vital Signs - Complete Guide for Your Internship

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What Are Vital Signs?

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1. Temperature

Normal

Abnormal values and their names

Clinical pearls

• Fever pattern matters: intermittent (malaria), remittent (typhoid), continuous (lobar pneumonia)
• Elderly and immunocompromised patients may NOT mount a fever even in serious infection - a normal temp does NOT rule out sepsis in these groups
• In PE, fever is usually low-grade (<38.6°C); temperature above this suggests infection
• Fever + rigors = bacteraemia until proven otherwise

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2. Heart Rate (Pulse)

Normal

Abnormal values

What to assess with pulse

• Rate: fast, normal, slow
• Rhythm: regular, irregularly irregular (AF), regularly irregular
• Volume: full/bounding (sepsis, CO2 retention) vs. weak/thready (shock, low cardiac output)
• Character: collapsing pulse (aortic regurgitation), slow rising (aortic stenosis)

Clinical pearls

• Shock index = HR / SBP - if >1.0, patient is in haemodynamic compromise
• A patient with PE who has HR > systolic BP is approaching cardiac arrest
• Pulsus paradoxus (exaggerated drop in BP >10 mmHg on inspiration) = cardiac tamponade / severe asthma
• Persistent tachycardia in an "apparently stable" patient is always concerning - find the cause

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3. Blood Pressure

Normal (Adults)

Key derived values

• Pulse pressure = Systolic - Diastolic (normal 40 mmHg)
  • Wide (>60): aortic regurgitation, aortic stiffness, CO2 retention, sepsis
  • Narrow (<25): aortic stenosis, cardiac tamponade, shock
• Mean Arterial Pressure (MAP) = Diastolic + (Pulse pressure / 3) - normal 70-100 mmHg; MAP >65 is the target in resuscitation

Abnormal states

Clinical pearls

• Always measure BP in both arms - >15 mmHg difference = aortic dissection or subclavian artery stenosis until proven otherwise
• Correct cuff size matters - too small a cuff = falsely high reading
• Auscultatory gap - Korotkoff sounds disappear and reappear in some hypertensive patients; can cause underestimation of BP
• In children: hypotension = SBP < 70 + (2 × age in years)

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4. Respiratory Rate

Normal

Abnormal values

Breathing patterns to recognise

Clinical pearls

• RR is the most sensitive early warning sign of clinical deterioration - often the first vital to change before everything else crashes
• RR is also the most commonly under-recorded vital sign on wards - many nurses write "18" on every patient without counting
• Count for a full 60 seconds at the bedside - do not estimate
• Tachypnoea + fever + productive cough = pneumonia until proven otherwise
• Tachypnoea + pleuritic chest pain = PE / pneumothorax

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5. Oxygen Saturation (SpO2)

Normal

Clinical pearls

• SpO2 measures peripheral oxygen saturation via pulse oximetry (infrared light through fingertip)
• Limitations - falsely normal in: carbon monoxide poisoning (carboxyhaemoglobin reads as oxyhaemoglobin), methaemoglobinaemia
• Falsely LOW with: nail varnish (esp. dark colours), poor perfusion/cold extremities, severe anaemia, motion artefact
• SpO2 is a late sign of respiratory failure - by the time it falls, the patient is already significantly hypoxic on the oxygen-haemoglobin dissociation curve
• In COPD patients: target SpO2 88-92% - high-flow O2 can suppress hypoxic drive and cause CO2 retention

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Quick Abnormal Vitals Summary Table

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The ABCDE Approach - How Vitals Fit In

A - Airway         → Is it patent?
B - Breathing      → RR, SpO2, work of breathing
C - Circulation    → HR, BP, capillary refill, skin
D - Disability     → GCS, blood glucose
E - Exposure       → Temperature, check whole body

• Always reassess vitals after any intervention
• Early Warning Scores (EWS/NEWS2) use all 6 parameters to flag deteriorating patients - learn your hospital's system

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Memory Aid - TPBRO2

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