List of important emergency medicine emergencies like necrotising fasc

List of important emergency medicine emergencies like necrotising fasciitis

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Now let me search the medical library for emergency medicine topics in parallel:

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Now let me get the Rosen's Emergency Medicine table of contents to find the key emergencies covered:

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Good - I have Tintinalli's Emergency Medicine in the library too. Let me get the key content from Tintinalli's and Rosen's to compile the best list:

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I now have enough information from the textbooks to compile a comprehensive, well-organized answer. Let me also fetch the NF image:

Here is a system-by-system list of important emergency medicine emergencies, modelled on the clinical severity and time-sensitivity profile of necrotising fasciitis. Each condition is immediately life-threatening without prompt recognition and treatment.

Surgical / Soft-Tissue Emergencies

1. Necrotising Fasciitis

Rapidly spreading infection causing necrosis of subcutaneous tissues and overlying skin; caused by beta-haemolytic streptococci, S. aureus, or polymicrobial (Bacteroides, Clostridium, Pseudomonas, Klebsiella)
Presentations: dusky blue/black skin, severe pain out of proportion, bullae, fever, septic shock; mortality approaches 70% without aggressive treatment
Management: ICU admission, IV high-dose penicillin G + broad-spectrum antibiotics (cephalosporins + metronidazole), emergency surgical debridement - the cornerstone; daily wound revision; hyperbaric oxygen as adjunct
Special forms: Fournier's gangrene (perineum), Meleney's gangrene (abdominal wall)
Bailey and Love's Short Practice of Surgery 28th Edition

Cardiovascular Emergencies

2. Acute Myocardial Infarction (STEMI)

Full-thickness myocardial ischemia from coronary artery occlusion; ST elevation on ECG
Time is myocardium: door-to-balloon time target <90 minutes
Management: aspirin + P2Y12 inhibitor, anticoagulation, primary PCI (preferred) or thrombolysis

3. Aortic Dissection

Tear in the intima of the aorta; Stanford Type A (ascending) requires emergency surgery; Type B may be managed medically
Classic presentation: tearing/ripping chest/back pain, unequal BP/pulses, widened mediastinum on CXR
Immediate BP control with IV beta-blockers (target SBP 100-120 mmHg)

4. Cardiac Tamponade

Fluid accumulation in pericardial sac compresses cardiac chambers; Beck's triad: hypotension, JVD, muffled heart sounds
ECG: electrical alternans; Echo is diagnostic
Treatment: immediate pericardiocentesis (needle drainage)

5. Hypertensive Emergency

Severe hypertension (usually >180/120) with acute end-organ damage (encephalopathy, AKI, ACLE, aortic dissection)
Controlled BP reduction by 20-25% in first hour with IV labetalol or nicardipine; not a rapid drop
ROSEN's Emergency medicine

Respiratory Emergencies

6. Tension Pneumothorax

Lung collapse with mediastinal shift; air trapped under pressure compresses great vessels
Presents with hypoxia, hypotension, absent breath sounds, tracheal deviation (late sign), raised JVP
Do not wait for CXR - immediate needle decompression (2nd ICS, mid-clavicular line) followed by chest drain
Bailey and Love's; Roberts and Hedges' Clinical Procedures in Emergency Medicine

7. Pulmonary Embolism (Massive)

Haemodynamically significant PE causes right heart failure and circulatory collapse
Presentations: hypoxia, pleuritic chest pain, tachycardia, syncope; ECG shows S1Q3T3 (classic but non-specific)
CT pulmonary angiography is diagnostic gold standard; treatment: systemic thrombolysis or catheter-directed therapy for massive PE

8. Acute Severe Asthma (Near-Fatal)

Status asthmaticus: bronchospasm unresponsive to initial bronchodilators
Silent chest is an ominous sign (no air movement)
Management: continuous nebulized salbutamol, IV magnesium sulfate, IV corticosteroids; intubation as last resort (high risk)

9. Acute Respiratory Distress Syndrome (ARDS)

Diffuse alveolar damage from direct/indirect lung injury; bilateral infiltrates, hypoxia (PaO2/FiO2 <200)
Management: lung-protective ventilation (low tidal volume 6 mL/kg, PEEP titration), prone positioning

Neurological Emergencies

10. Status Epilepticus

Continuous seizure activity >5 minutes or recurrent seizures without recovery of consciousness
Management: benzodiazepines first-line (lorazepam/diazepam), then second-line agents (levetiracetam, valproate, phenytoin); refractory SE requires anaesthetic agents (propofol, midazolam, thiopental)
Tintinalli's Emergency Medicine; ROSEN's Emergency Medicine

11. Acute Ischaemic Stroke

"Time is brain" - 1.9 million neurons die per minute during occlusion
IV alteplase (tPA) within 4.5 hours of symptom onset; mechanical thrombectomy for large vessel occlusion up to 24 hours in selected patients
Rule out haemorrhage with CT before giving thrombolytics

12. Subarachnoid Haemorrhage (SAH)

"Worst headache of my life" (thunderclap headache); caused by ruptured aneurysm in ~85% of cases
CT head non-contrast first; if negative, LP for xanthochromia
Neurosurgical consultation urgently; nimodipine for vasospasm prevention

13. Raised Intracranial Pressure (ICP) / Brain Herniation

Cushing's triad: bradycardia, hypertension, irregular breathing
Immediate: head elevation 30°, hyperventilation (transient), IV mannitol or hypertonic saline, neurosurgery

Abdominal / GI Emergencies

14. Ruptured Abdominal Aortic Aneurysm (rAAA)

Classic triad: hypotension, pulsatile abdominal mass, back/flank pain
Mortality >80% without surgery; bedside FAST ultrasound confirms; immediate theatre
No time for CT if haemodynamically unstable

15. Acute Mesenteric Ischaemia

Occlusion of superior mesenteric artery causes bowel infarction; "pain out of proportion to examination"
Causes: arterial embolism (50%), arterial thrombosis, venous thrombosis, non-occlusive
CT angiography diagnostic; surgical/endovascular revascularization; bowel resection if infarcted
Schwartz's Principles of Surgery

16. Perforated Viscus (Perforated Peptic Ulcer)

Free air under diaphragm on erect CXR; peritonitis on examination
Surgical emergency: IV resuscitation, broad-spectrum antibiotics, urgent laparotomy/laparoscopy

17. Bowel Obstruction with Strangulation / Sigmoid Volvulus

Closed-loop obstruction causes rapid bowel ischemia and gangrene
CT abdomen is diagnostic; emergency surgery when strangulation suspected

Infectious / Sepsis Emergencies

18. Septic Shock

Life-threatening organ dysfunction from infection; MAP <65 mmHg despite fluid resuscitation
Hour-1 bundle: blood cultures, broad-spectrum antibiotics, IV fluid bolus (30 mL/kg crystalloid), vasopressors (norepinephrine), measure lactate
ROSEN's Emergency Medicine

19. Toxic Shock Syndrome (TSS)

Staphylococcal or streptococcal superantigen-mediated multi-organ failure
Diffuse macular erythroderma ("sunburn rash"), desquamation, fever, hypotension
Management: source control, clindamycin (toxin suppression), IV fluids, IVIG in severe cases

20. Bacterial Meningitis

Triad: fever, neck stiffness, altered consciousness; do not delay antibiotics for CT
Immediate: IV dexamethasone + ceftriaxone + vancomycin; add ampicillin if Listeria risk
Lumbar puncture after antibiotics if CT required

21. Ludwig's Angina

Rapidly spreading cellulitis of the floor of the mouth causing airway compromise
Immediate airway management (awake fibreoptic intubation preferred - avoid blind intubation); surgical drainage; IV antibiotics

Endocrine / Metabolic Emergencies

22. Diabetic Ketoacidosis (DKA) / Hyperosmolar Hyperglycaemic State (HHS)

DKA: anion gap metabolic acidosis, ketones, hyperglycaemia; HHS: extreme hyperglycaemia (>600 mg/dL), hyperosmolarity, no ketosis
Management: IV fluids, insulin infusion, electrolyte replacement (especially K+); HHS needs very slow correction

23. Adrenal Crisis (Addisonian Crisis)

Profound hyponatraemia, hyperkalaemia, hypoglycaemia, hypotension in adrenal insufficiency
Immediate: IV hydrocortisone 100 mg bolus, aggressive IV saline, glucose; do not wait for cortisol results

24. Thyroid Storm

Extreme hyperthyroidism; fever, tachycardia, heart failure, altered consciousness
Management: propylthiouracil (blocks synthesis), Lugol's iodine (blocks release), beta-blockers, dexamethasone, cooling

Obstetric Emergencies

25. Ruptured Ectopic Pregnancy

Intraperitoneal haemorrhage from fallopian tube rupture; hypovolaemic shock; positive urine hCG
FAST ultrasound shows free fluid; resuscitate and take to theatre immediately - surgical emergency

26. Eclampsia

Seizures in pregnancy/postpartum + hypertension; can cause stroke, placental abruption, multi-organ failure
Immediate: IV magnesium sulfate (4 g loading dose), antihypertensives (hydralazine/labetalol), urgent delivery

27. Amniotic Fluid Embolism

Catastrophic obstetric collapse: hypoxia, cardiac arrest, DIC
Resuscitation per ACLS protocols; manage DIC aggressively

Toxicological Emergencies

28. Organophosphate / Nerve Agent Poisoning

SLUDGE syndrome (salivation, lacrimation, urination, defecation, GI distress, emesis) + bronchospasm, miosis, seizures
Atropine (in large doses), pralidoxime (oxime reactivator), benzodiazepines for seizures

29. Tricyclic Antidepressant (TCA) Overdose

QRS widening (>100 ms), arrhythmia, seizures, hypotension
IV sodium bicarbonate is the treatment (alkalinizes plasma to reduce drug binding to Na channels)

30. Carbon Monoxide Poisoning

Cherry-red skin (unreliable sign); headache, confusion, coma; SpO2 is falsely normal
100% O2 via non-rebreather mask; hyperbaric oxygen for severe cases (COHb >25%, neurological signs, cardiac involvement)

ENT / Head and Neck Emergencies

31. Epiglottitis

Rapidly progressive supraglottic inflammation; "tripod position," drooling, stridor, muffled voice
Do not examine the throat in children - can precipitate complete obstruction
Immediate anaesthetic/ENT team; controlled intubation in theatre; IV ceftriaxone

32. Retropharyngeal Abscess

Deep neck space infection extending to mediastinum (descending mediastinitis); high mortality
CT neck + chest; surgical drainage + IV antibiotics

Orthopaedic / Vascular Emergencies

33. Compartment Syndrome

Raised pressure in a closed fascial compartment causing tissue ischaemia; the 6 P's: Pain (especially with passive stretch), Pressure, Paresthesia, Pallor, Paralysis, Pulselessness (late)
Emergency fasciotomy - do not delay

34. Acute Limb Ischaemia

Sudden arterial occlusion; the 6 P's again: Pain, Pallor, Pulselessness, Paresthesia, Paralysis, Poikilothermia (cold)
Embolectomy or bypass within 6 hours to prevent irreversible muscle/nerve damage

Key Principle: "Time-Critical" Emergencies

The emergencies above share one feature with NF: delay = death or permanent disability. The most time-critical include:

Emergency	Time Window
STEMI	PCI within 90 min
Ischaemic stroke	Thrombolysis within 4.5 h
Acute limb ischaemia	Revascularization within 6 h
Septic shock	Antibiotics within 1 h
Necrotising fasciitis	Debridement within hours
Tension pneumothorax	Needle decompression immediately
Ruptured AAA	Theatre without delay
Eclampsia	Magnesium + delivery

Sources: Bailey and Love's Short Practice of Surgery 28th Edition; ROSEN's Emergency Medicine; Tintinalli's Emergency Medicine: A Comprehensive Study Guide; Roberts and Hedges' Clinical Procedures in Emergency Medicine; Schwartz's Principles of Surgery 11th Edition

Explain me a normal 12 lead ECG with normal axis and where would you normally find inverted t waves

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normal 12 lead ECG with axis and waveform labels

A standard 12-lead electrocardiogram (ECG) recording displayed on a red-lined grid paper. The image represents diagnostic cardiology imaging from a post-operative follow-up. The tracing demonstrates normal sinus rhythm characterized by consistent P waves preceding every QRS complex, normal PR intervals, and regular R-R intervals. The 12 leads (I, II, III, aVR, aVL, aVF, V1-V6) are organized into four columns, with a long rhythm strip of Lead II at the bottom. Waveform morphologies show appropriate axis and progression, including positive P waves in leads I and II, an inverted aVR, and normal R-wave progression across the precordial leads (V1-V6). QRS complexes and T waves appear within normal limits for duration and amplitude, with no evidence of acute ischemia, significant ST-segment deviation, or conduction abnormalities. This clinical photograph serves as an educational example of baseline cardiac electrical activity and post-surgical recovery monitoring.

A standard 12-lead diagnostic resting electrocardiogram (ECG) displayed on a grid. The tracing includes the standard limb leads (I, II, III), augmented limb leads (aVR, aVL, aVF), and precordial leads (V1-V6), with a long rhythm strip of lead II at the bottom. The visual demonstrates a normal sinus rhythm characterized by consistent P-wave morphology preceding every QRS complex, regular R-R intervals, and a heart rate within normal physiological limits (approximately 80-85 bpm). Waveform analysis shows normal axis, absence of ST-segment elevation or depression, and normal T-wave morphology across all leads, indicating no acute ischemic changes at rest. Technical parameters visible at the top specify a paper speed of 25 mm/s, a gain (voltage scale) of 10 mm/mV, and the application of artifact and baseline filters. This diagnostic image serves as a baseline comparison for clinical cardiac assessment and the evaluation of coronary artery disease.

This diagnostic image is a standard 12-lead electrocardiogram (ECG) recorded on a pink grid background. The tracing displays the limb leads (I, II, III), augmented limb leads (aVR, aVL, aVF), and precordial leads (V1-V6) arranged in a traditional four-column format, with a continuous rhythm strip of lead II at the bottom. The horizontal axis represents time at a standard speed (25 mm/sec) and the vertical axis represents voltage (10 mm/mV). The ECG shows a regular sinus rhythm with narrow QRS complexes and distinct P and T waves. Notable morphology includes a normal R-wave progression in the precordial leads, characterized by increasing R-wave amplitude from V1 through V6. In lead V1, the QRS complex is primarily negative (rS pattern), transitioning to a primarily positive deflection by V5-V6. This visual material is used in clinical cardiology education to teach baseline cardiac rhythm analysis, waveform recognition, and lead-specific morphological variations.

This diagnostic image shows a standard 12-lead electrocardiogram (ECG) displayed on a red-ruled grid. The chart is organized into four rows: the top three rows represent the standard limb leads (I, II, III), augmented limb leads (aVR, aVL, aVF), and precordial leads (V1–V6) in a three-channel format, while the bottom row provides a continuous rhythm strip of Lead II. Each lead demonstrates clear P waves, narrow QRS complexes, and T waves, indicating a normal sinus rhythm. The grid follows standard calibration where the vertical axis represents voltage (10 mm = 1 mV) and the horizontal axis represents time (25 mm = 1 s). Notable morphology includes normal R-wave progression from V1 through V6 and typical negative deflections in aVR. The image serves as a clinical reference for assessing cardiac electrical activity and is used in medical education to teach lead placement, waveform identification, and cardiac rhythm interpretation.

Good results. Now let me read the key textbook sections in parallel:

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T wave inversion normal leads aVR V1 ECG

A standard 12-lead diagnostic electrocardiogram (ECG) printed on pink grid paper, demonstrating significant repolarization abnormalities. The primary visual finding is deep, symmetric T-wave inversions (TWIs) localized to the lateral (lead I) and anteroseptal to lateral precordial leads (V1 through V6). Blue arrows highlight these specific inversions in leads I, V1, V2, V4, and V5. The QRS complexes appear to be of normal duration and morphology with regular R-R intervals, suggesting a sinus rhythm. There is evidence of mild ST-segment depression accompanying the T-wave changes in the precordial leads. In contrast, the inferior leads (II, III, aVF) and augmented limb leads (aVR, aVL) show upright or flat T-wave morphology. Clinically, this pattern of widespread anterior and lateral T-wave inversion is highly significant for myocardial ischemia, such as Wellens' syndrome or non-ST elevation myocardial infarction (NSTEMI), or potentially secondary to hypertrophic cardiomyopathy or pulmonary embolism. The educational focus is on identifying patterns of ischemia and differentiating regional repolarization abnormalities.

A standard 12-lead resting electrocardiogram (ECG) printed on grid paper, displaying limb leads (I, II, III, aVR, aVL, aVF) and precordial leads (V1-V6). The tracing shows a regular rhythm with visible P-waves, QRS complexes, and T-waves. Key clinical features include T-wave inversions specifically in the right precordial leads V1 and V2. In contrast, T-waves in the lateral precordial leads (V3-V6) and the limb leads (I, II, aVF) are upright and demonstrate normal morphology. The corrected QT (QTc) interval is reported at 432 ms, which is within the normal range. The tracing is set at a standard paper speed of 25 mm/s and voltage of 10 mm/mV. This visual is used to demonstrate cardiac repolarization patterns, where T-wave inversion in V1-V2 can be a normal variant or associated with specific cardiomyopathies such as Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) or Mitral Valve Prolapse (MVP) syndromes.

A 12-lead electrocardiogram (ECG) demonstrating the classic 'Type A' Wellens' Syndrome pattern. The recording shows a regular rhythm with normal QRS complexes; however, there is a pathognomonic T-wave morphology in the precordial leads, specifically V2 and V3. These leads exhibit biphasic T-waves characterized by an initial shallow positive deflection followed by a deep, terminal negative deflection. The terminal inversion is more prominent in amplitude than the initial upward phase. Such findings in the context of clinical stability are highly specific for critical stenosis of the proximal left anterior descending (LAD) coronary artery. The ECG also includes standard limb leads (I, II, III), augmented limb leads (aVR, aVL, aVF), and the full precordial series (V1-V6), with rhythm strips for V1, II, and V5 at the bottom. The paper speed is noted at 25mm/s with a sensitivity of 10mm/mV, providing a standard diagnostic reference for ischemic heart disease and acute coronary syndrome (ACS) evaluation.

Now let me get the Harrison's ECG section and the Tintinalli normal ECG intervals section for interval data:

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Let me get the rest of the Harrison's ECG section which covers T waves and axis:

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Let me get the section covering T waves in the normal ECG from Harrison's:

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I now have all the information I need from authoritative textbooks. Let me also fetch the ECG image from the library:

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Excellent - I have rich textbook material and images. Now I can compose a thorough, well-illustrated answer.

The Normal 12-Lead ECG

Here is a complete breakdown of the normal 12-lead ECG, including axis, waveforms, intervals, and where T-wave inversions are physiologically expected.

The 12 Leads - What They "See"

Limb leads (frontal plane)

I, II, III - bipolar; look at the heart in the frontal plane
aVR, aVL, aVF - augmented unipolar limb leads

Precordial leads (horizontal plane)

V1 - right side of the heart (right sternal border, 4th ICS)
V2 - left sternal border, 4th ICS
V3 - between V2 and V4
V4 - mid-clavicular line, 5th ICS
V5 - anterior axillary line
V6 - mid-axillary line

Here is the standard precordial electrode placement (from Harrison's):

Normal ECG Waveforms and Intervals

Each cardiac cycle produces 3 main events on the ECG:

Waveform	What it represents	Normal values
P wave	Atrial depolarization	Duration <120 ms; amplitude <2.5 mm
PR interval	AV conduction time	120-200 ms (3-5 small squares)
QRS complex	Ventricular depolarization	<120 ms (3 small squares)
ST segment	Start of ventricular repolarization	Isoelectric (at baseline)
T wave	Ventricular repolarization	Upright in most leads (see below)
QT interval	Total ventricular electrical activity	QTc <440 ms (male), <460 ms (female)
U wave	Afterdepolarization (Purkinje?)	Small, same polarity as T wave; most visible in V2-V3

ECG paper calibration: Paper speed 25 mm/s; voltage 10 mm/mV. Each small square = 0.04 s horizontally and 0.1 mV vertically.

The P Wave

Generated by atrial depolarization spreading from the sinus node (right atrium) leftward and inferiorly
This vector points toward lead II (positive) and away from aVR (negative)
Therefore:
- Upright in leads I, II, aVF (sinus P wave)
- Inverted/negative in aVR (always - a key normal finding)
- In V1: may be biphasic - small initial positive component (right atrial depolarization) then small negative component (left atrial depolarization)

- Harrison's Principles of Internal Medicine 22E

The QRS Complex - Ventricular Depolarization

Ventricular depolarization proceeds in two phases (see diagram below from Harrison's):

Ventricular depolarization phases and QRS pattern V1 vs V6

Phase 1 (septal): The septum depolarizes first, from left to right

This small rightward vector creates: a tiny r wave in V1 and a tiny q wave in V6

Phase 2 (ventricular): Left + right ventricles depolarize simultaneously; the LV dominates and the vector points leftward and posteriorly

This creates: a large S wave in V1 (negative - vector away from V1) and a large R wave in V6 (positive - vector toward V6)

R-wave progression across precordial leads:

V1: small r, deep S (rS pattern) - predominantly negative
V2-V3: growing r wave
Transition zone (usually V3 or V4): R and S are roughly equal
V5-V6: tall R, small or absent S (qR pattern) - predominantly positive

- Harrison's Principles of Internal Medicine 22E; Guyton and Hall Textbook of Medical Physiology

Lead-by-Lead Normal QRS Morphology Summary

Lead	Normal QRS
I	Positive (upright R)
II	Positive (tallest P and T wave)
III	Variable
aVR	Predominantly negative (QS or rS)
aVL	Variable
aVF	Positive
V1	rS (small r, deep S)
V2	rS or RS
V3	Transition
V4	RS or Rs (transition)
V5-V6	qR or qRs (positive)

Normal Cardiac Axis

The mean electrical axis describes the net direction of ventricular depolarization in the frontal plane. It is normally oriented from the base toward the apex of the heart.

Normal axis: -30° to +90° (or +100° by some sources)

"The mean electrical axis of the normal ventricles is 59 degrees." - Guyton and Hall Textbook of Medical Physiology

Quick axis check method:

Look at leads I and aVF
If QRS is positive in both I and aVF → normal axis (0° to +90°)
If positive in I, negative in aVF → left axis deviation (>-30°)
If negative in I, positive in aVF → right axis deviation (>+90°)
If negative in both → extreme axis deviation ("northwest axis")

Axis deviations:

Axis	Range	Causes
Normal	-30° to +90°	-
Left axis deviation	More negative than -30°	Left anterior fascicular block, LBBB, inferior MI, LVH
Right axis deviation	More positive than +90°	Right ventricular overload, RBBB, lateral MI, dextrocardia, normal variant in young
Extreme	-90° to +180°	Hyperkalaemia, ventricular rhythms

- Harrison's Principles of Internal Medicine 22E

The T Wave - Normal Physiology

The T wave represents ventricular repolarization. Critically, repolarization travels in the opposite direction from depolarization (epicardium to endocardium, not endocardium to epicardium) - this is why the T wave ends up in the same direction as the QRS rather than being inverted.

"The mean T-wave vector is oriented roughly concordant with the mean QRS vector (within about 45° in the frontal plane). Since depolarization and repolarization are electrically opposite processes, this normal QRS-T-wave vector concordance indicates that repolarization normally must proceed in the reverse direction from depolarization (i.e., from ventricular epicardium to endocardium)." - Harrison's Principles of Internal Medicine 22E

Normal T wave characteristics:

Upright in leads I, II, V3-V6
Amplitude: <5 mm in limb leads; <10-15 mm in precordial leads
Asymmetric: gradual upstroke, rapid downstroke
Always upright in lead II
Normal T wave = concordant with QRS polarity

Normal Leads Where T-Wave Inversion is Expected

This is one of the most clinically important points to know:

Lead	T-wave inversion...	Reason
aVR	Always inverted (normal)	aVR looks at the heart from the right shoulder - QRS is also negative here, so T follows (concordant)
V1	Commonly/normally inverted	V1 faces the right ventricle; the repolarization vector points away from V1
V2	May be inverted, especially in women	Can be a normal variant; more common in women and athletes
III	Can be inverted (normal variant)	Depends on cardiac axis; borderline lead
aVL	Can be inverted (normal variant)	Particularly when axis is rightward

Key clinical rule:

T-wave inversion in aVR = always normal
T-wave inversion in V1 = normal (and in V2 in women/children)
T-wave inversion in V3-V6 = abnormal, suspect ischaemia or other pathology
T-wave inversion in II and aVF = always abnormal, consider inferior ischaemia

Here is an ECG showing T-wave inversions in the right precordial leads (V1-V2 as a normal variant pattern):

Pathological Causes of T-Wave Inversion

When T-wave inversions appear beyond the normal leads, consider:

Pattern	Leads affected	Likely cause
Anterior T-wave inversions	V1-V4	Anterior ischaemia, Wellens' syndrome (LAD stenosis), RVOT pathology
Widespread deep T inversions	V1-V6 + I, aVL	Massive PE, apical HCM, Takotsubo cardiomyopathy, NSTEMI
Inferior T inversions	II, III, aVF	Inferior ischaemia
Lateral T inversions	I, aVL, V5-V6	Lateral ischaemia, LVH ("strain" pattern)
Right-sided T inversions	V1-V3	ARVC (arrhythmogenic right ventricular cardiomyopathy), RVH
Diffuse T inversions + Osborn waves	Multiple	Hypothermia

Here is a normal 12-lead ECG for reference:

Normal 12-lead ECG with normal sinus rhythm

Summary Card

Normal 12-lead ECG at a glance:
- Sinus rhythm: P before every QRS, P upright in I & II, inverted in aVR
- PR interval: 120-200 ms
- QRS: <120 ms, normal axis -30° to +90°
- R-wave progression: small in V1 → tall in V5-V6, transition at V3-V4
- T waves: upright in I, II, V3-V6
- T waves NORMALLY inverted: aVR (always), V1 (common), V2 (in women/children)
- QTc: <440 ms (men), <460 ms (women)

Sources: Harrison's Principles of Internal Medicine 22E; Guyton and Hall Textbook of Medical Physiology; Tintinalli's Emergency Medicine: A Comprehensive Study Guide

Neurological examination??

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neurological examination dermatomes motor sensory diagram

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cranial nerves diagram all 12

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dermatome map spinal nerve distribution body

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I now have all the essential content. Let me compile the comprehensive neurological examination guide.

The Neurological Examination

A complete, systematic neurological examination has 7 major components, performed in this order:

Mental Status
Cranial Nerves (CN I-XII)
Motor System
Reflexes
Sensory System
Coordination
Gait

"Neurological examination starts during the interview. A patient's lack of facial expression (hypomimia) may suggest parkinsonism or depression...the pattern of speech may suggest dysarthria, aphasia, or spasmodic dysphonia." - Bradley and Daroff's Neurology in Clinical Practice

1. Mental Status

Assessed throughout the history-taking, not as a separate formal test unless cognition is in question.

Domain	What to assess
Level of consciousness	Alert, drowsy, confused, comatose
Orientation	Person, place, time
Attention	Serial 7s, digit span
Memory	Immediate recall (repeat 3 words), recent (recall after 5 min), remote
Language	Fluency, comprehension, repetition, naming, reading, writing
Higher functions	Abstract thinking, judgment, visuospatial ability
Mood and affect	Depression, anxiety, irritability

Bedside tests: Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA)

2. Cranial Nerve Examination

Tested in numerical order, except CN III, IV, VI are grouped together (all control eye movements).

CN I - Olfactory

Test only if: history of anosmia, suspected inferior frontal lobe lesion (meningioma), or Parkinson's disease
Ask patient to close eyes, sniff a mild odour (coffee, toothpaste) and identify it - each nostril separately

CN II - Optic

Visual acuity: Snellen chart (with glasses if worn)
Visual fields by confrontation: Face the patient at ~1 m, wiggle a finger in each of the 4 quadrants; compare with your own field
Pupils: Size, symmetry, direct and consensual light reflex; swinging flashlight test for relative afferent pupillary defect (RAPD/Marcus Gunn pupil)
Fundoscopy: Optic disc colour, margins, cup-to-disc ratio; retinal vessels, haemorrhages, exudates

CN III, IV, VI - Oculomotor, Trochlear, Abducens

Pupils: Shape, size, reaction to light and accommodation (near reflex - ask patient to follow finger moving toward nose)
Extraocular movements: Follow finger in an "H" pattern; look for paresis, nystagmus, abnormal pursuit
Ptosis: CN III palsy causes complete ptosis; Horner's syndrome causes partial ptosis
CN III - all movements except down-and-out; also pupil constriction
CN IV - depression of adducted eye (superior oblique)
CN VI - abduction (lateral rectus)

Diplopia should resolve when one eye is closed - true diplopia is always binocular. - Harrison's 22E

CN V - Trigeminal

Sensation: Test light touch and temperature (or pinprick) over all 3 divisions:
- V1 (ophthalmic): forehead
- V2 (maxillary): cheek
- V3 (mandibular): jaw/chin
Corneal reflex: Touch cornea gently with cotton wisp; normal = blink (afferent V, efferent VII)
Motor: Jaw clench - feel masseter and temporalis; jaw opening against resistance (pterygoids)
Jaw deviates toward the side of weakness on opening

CN VII - Facial

Inspect for facial asymmetry at rest and with movement
Test: eyebrow elevation, forehead wrinkling, eye closure (forced), smiling, cheek puff, whistling

Critical distinction:

Finding	Lesion type
Lower 2/3 of face weak; forehead spared	Upper motor neuron (contralateral cortex) - forehead has bilateral cortical representation
Entire face weak on one side	Lower motor neuron (e.g., Bell's palsy, parotid tumour)

CN VIII - Vestibulocochlear

Hearing: Whisper test (whisper numbers 2 feet away, mask other ear by rubbing)
Weber test: Tuning fork on vertex; normally heard equally; lateralises to good ear in sensorineural loss, bad ear in conductive loss
Rinne test: Air conduction (fork near ear) vs. bone conduction (fork on mastoid); AC > BC = normal or sensorineural; BC > AC = conductive hearing loss
Vestibular: Nystagmus, Dix-Hallpike test for BPPV

CN IX, X - Glossopharyngeal and Vagus

Observe palate at rest and with phonation ("say Ahh") - uvula deviates away from the affected side
Voice quality - hoarseness (recurrent laryngeal nerve - CN X)
Gag reflex: Stimulate posterior pharynx with tongue blade; CN IX = afferent, CN X = efferent. Note: may be absent in normal individuals
Swallowing - ask patient to swallow water

CN XI - Spinal Accessory

Trapezius: Shoulder shrug against resistance
Sternocleidomastoid: Head rotation to each side against resistance

CN XII - Hypoglossal

Inspect tongue at rest: atrophy, fasciculations?
Protrude tongue - deviates toward the weak side
Strength: push tongue into each cheek against examiner's finger

3. Motor Examination

Step 1: Inspection

Muscle bulk (wasting/atrophy vs. hypertrophy)
Fasciculations (fine twitching at rest - LMN disease)
Involuntary movements:
- Tremor at rest → Parkinson's (pill-rolling)
- Tremor with posture → essential tremor
- Intention tremor (worsens finger-to-nose) → cerebellar
- Chorea, dystonia, myoclonus, tics

Step 2: Tone

Test resistance to passive movement of a relaxed limb:

Upper limb: pronate/supinate wrist, flex/extend elbow and wrist
Lower limb: patient supine - lift knee rapidly; normal = ankle drags along bed first; increased tone = heel lifts immediately

Tone abnormality	Type	Cause
Spasticity	Velocity-dependent resistance; "clasp-knife"	Corticospinal tract (UMN) lesion
Rigidity	Resistance in all directions, all velocities	Extrapyramidal (basal ganglia)
Cogwheel rigidity	Jerky interruptions during passive movement	Parkinsonism
Paratonia (Gegenhalten)	Involuntary variable resistance	Frontal lobe disease
Hypotonia (flaccidity)	Reduced resistance	LMN, cerebellar, acute UMN (spinal shock)

Step 3: Power (MRC Scale)

Grade	Meaning
0	No movement at all
1	Flicker/trace contraction, no joint movement
2	Movement with gravity eliminated
3	Movement against gravity, not against resistance
4-	Against mild resistance
4	Against moderate resistance
4+	Against strong resistance
5	Full power

Screening for upper limb weakness - Pronator Drift Test:

Patient holds both arms extended, palms up, eyes closed for 10 seconds
Pronation or downward drift = contralateral corticospinal tract lesion

Pattern of weakness localises the lesion:

Pattern	Lesion location
Hemiplegia (arm + leg, one side)	Contralateral cortex or internal capsule
Pyramidal pattern (arm extensors + leg flexors weak)	Corticospinal tract
Paraplegia (both legs)	Spinal cord
Proximal > distal weakness	Myopathy
Distal > proximal weakness	Peripheral neuropathy
Fatigable weakness (worse with use)	Neuromuscular junction (myasthenia gravis)

4. Reflex Examination

Deep Tendon Reflexes (DTRs) - Grading Scale

Grade	Meaning
0	Absent
1+	Present but diminished
2+	Normal
3+	Increased (may be normal)
4+	Clonus (always abnormal)

Always compare sides. Use Jendrassik maneuver to reinforce: patient hooks fingers together and tries to pull apart while you test the ankle/knee.

Standard DTRs and Their Root Values

Reflex	Nerve root	Muscle tested
Biceps jerk	C5, C6	Biceps brachii
Supinator/brachioradialis	C5, C6	Brachioradialis
Triceps jerk	C6, C7	Triceps
Finger flexor (Hoffmann)	C8, T1	Finger flexors
Knee jerk (patellar)	L3, L4	Quadriceps
Ankle jerk (Achilles)	S1, S2	Gastrocnemius/soleus

Cutaneous/Superficial Reflexes

Plantar reflex (Babinski):

Stroke lateral sole from heel toward little toe, curving medially across the ball
Normal: plantarflexion of toes
Abnormal (Babinski sign): extension (dorsiflexion) of big toe + fanning of other toes = UMN lesion above S1

"Despite its popularity, the reliability and validity of the Babinski sign for identifying upper motor neuron weakness are limited - it is far more useful to rely on tests of tone, strength, stretch reflexes, and coordination." - Harrison's 22E

Abdominal reflexes:

Stroke each quadrant toward umbilicus; umbilicus should pull toward the stimulus
Absent with UMN lesions
Upper abdominal: T8-T10; Lower abdominal: T10-T12

Cremasteric reflex: Stroke medial thigh → ipsilateral testis rises; mediated by L1-L2. Absent in UMN lesions.

UMN vs. LMN Signs Summary

Feature	UMN (above spinal cord anterior horn)	LMN (anterior horn, root, nerve)
Tone	Increased (spastic/rigid)	Decreased (flaccid)
Reflexes	Increased (hyperreflexia)	Decreased or absent
Plantar	Extensor (Babinski +)	Flexor (normal)
Atrophy	Mild/disuse only	Significant
Fasciculations	Absent	Present
Distribution	Pyramidal pattern or hemiplegia	Focal, nerve/root distribution

5. Sensory Examination

Test the primary modalities first, then higher (cortical) sensory functions.

Primary Sensory Modalities

Modality	Test method	Pathway
Pain	Pin-prick (disposable neurological pin)	Spinothalamic tract (crosses at spinal cord level)
Temperature	Cold (tuning fork) or hot/cold tubes	Spinothalamic tract
Light touch	Cotton wool or fingertip	Dorsal columns (and spinothalamic)
Vibration	128 Hz tuning fork on bony prominences (big toe, medial malleolus, patella, ASIS)	Dorsal columns (ipsilateral)
Joint position sense (proprioception)	Hold lateral sides of distal phalanx; move up/down; ask direction	Dorsal columns (ipsilateral)

Always compare both sides. Test distal before proximal.

Sensory patterns:

Pattern	Cause
Glove-and-stocking	Peripheral neuropathy (length-dependent)
Dermatomal	Nerve root (radiculopathy)
Sensory level on trunk	Spinal cord
Dissociated loss (pain/temp lost, vibration/JPS intact)	Syringomyelia; Brown-Séquard (ipsilateral dorsal column, contralateral spinothalamic)
Hemisensory loss (face + arm + leg one side)	Thalamus or cortex

Higher (Cortical) Sensory Tests

Test when parietal lobe disease is suspected:

Graphesthesia: Write a number in the palm; patient identifies with eyes closed
Stereognosis: Place a familiar object (coin, key) in hand; patient identifies with eyes closed
Two-point discrimination: Normal fingertip: 3-5 mm
Sensory extinction: Touch both sides simultaneously; patient with parietal lesion "extinguishes" the contralateral stimulus

6. Coordination

Tests cerebellar function.

Test	What to do	Abnormal finding
Finger-nose-finger	Patient alternates touching own nose and examiner's finger	Intention tremor, past-pointing (dysmetria)
Heel-shin test	Patient places heel on opposite knee, slides it down shin	Ataxia, dysmetria
Rapid alternating movements (dysdiadochokinesia)	Rapidly pronate/supinate hand on other hand, or tap index finger on thumb	Slowness, inaccuracy = cerebellar
Rebound test	Examiner resists arm flexion, then suddenly releases; normal = small rebound only	Excessive rebound = cerebellar

Cerebellar signs mnemonic - DANISH:

Dysdiadochokinesia
Ataxia (gait)
Nystagmus
Intention tremor
Scanning dysarthria (staccato speech)
Hypotonia

7. Gait

"Watching the patient walk is the most important part of the neurologic examination. Normal gait requires that multiple systems - including strength, sensation, and coordination - function in a highly integrated fashion." - Harrison's 22E

Observe:

Normal walking
Walking on heels (tests ankle dorsiflexors, L4-L5)
Walking on toes (tests gastrocnemius, S1)
Tandem gait (heel-to-toe along straight line) - sensitive for cerebellar and posterior column disease
Romberg test: Stand feet together; eyes open then closed. Falling with eyes closed (but not open) = dorsal column/proprioceptive loss. If unsteady with eyes open too = cerebellar.

Characteristic gait patterns:

Gait	Appearance	Cause
Hemiplegic	Arm flexed, leg circumducts	Corticospinal tract (stroke)
Parkinsonian	Shuffling, stooped, reduced arm swing, festination, en bloc turns	Basal ganglia
Ataxic (cerebellar)	Wide-based, staggering, lurching	Cerebellum
Sensory ataxic	Wide-based, stomping, worse in dark; positive Romberg	Dorsal columns/peripheral neuropathy
Foot drop (steppage)	High knee lift, slapping foot	Common peroneal nerve (L4-L5)
Waddling	Pelvis drops on swing side	Proximal myopathy, hip girdle weakness
Scissors	Legs cross, spastic	Spastic paraplegia
Apraxic (magnetic)	Feet appear "glued to floor," wide-based, difficulty initiating	Frontal lobe (NPH)

Localisation Summary

This table from Harrison's helps match examination findings to the anatomical level of the lesion:

Level	Key signs
Cerebrum	Altered cognition, seizures, contralateral hemiplegia, visual field defect
Brainstem	Crossed signs: ipsilateral cranial nerve + contralateral limb weakness/sensory loss
Spinal cord	Sensory level on trunk, UMN signs below, sphincter dysfunction
Nerve root	Dermatomal sensory loss, LMN weakness in myotomal distribution, loss of single reflex
Peripheral nerve	Stocking-glove sensory loss, LMN weakness, absent reflexes
Neuromuscular junction	Fatigable weakness, no sensory loss
Muscle	Proximal or distal weakness, no sensory loss

- Harrison's Principles of Internal Medicine 22E; Bradley and Daroff's Neurology in Clinical Practice; Guyton and Hall Textbook of Medical Physiology

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