General Knowledge

Cushing's triad

• Irregular respirations

• Hypertension with widening pulse pressure

• Bradycardia

AEIOUTIPS

• Alcohol/Drugs, Acidosis, Arrhythmias

• Epilepsy (seizures / post-ictal), Electrolytes

• Encephalopathy (brain conditions)

• Insulin (diabetic emergency)

• Oxygen / Overdose

• Underdose (withdrawal), Uremia

• Trauma (head), Temperature, Thiamine (B1)

• Infection (delirium),

• Urinary Odors

• Psychiatric, Pain, Poisoning

• Stroke, Shock, Syncope, Space Occupying Lesion

7 Seizure types

Generalized Seizures (Affect both hemispheres of the brain)

• Tonic-Clonic (Grand Mal) Seizure – Loss of consciousness, muscle rigidity (tonic phase), followed by rhythmic jerking movements (clonic phase).

• Absence (Petit Mal) Seizure – Brief loss of awareness (staring spell), often seen in children, with no convulsions.

• Myoclonic Seizure – Sudden, brief muscle jerks, usually affecting both sides of the body.

• Tonic Seizure – Sudden muscle stiffness or rigidity, often causing falls.

• Clonic Seizure – Repetitive jerking movements, usually rhythmic.

• Atonic (Drop Attack) Seizure – Sudden loss of muscle tone, causing the person to collapse.

• Status, seizure lasts >5 minutes or multiple seizures occur without full recovery between them.

Stroke Mimics

• Hypoglycemia

• Brain Tumor

• Post-ictal state (following a seizure)

• Migraine

• Electrolyte imbalance

• Overdose (toxicity-related neurological impairment)

• Head Trauma

• Transient Ischemic Attack (TIA)

Stroke Treatment

• 45 degrees (Positioning the patient with the head elevated)

• Antiemetics (To manage nausea and vomiting)

• IV fluids (For hydration and circulatory support)

• O₂ if hypoxic (Supplemental oxygen if oxygen saturation is low)

• NIHSS-8 (National Institutes of Health Stroke Scale score of 8)

Sepsis Signs & Risk factors

• HR > 90 (Elevated heart rate)

• RR > 22 (Increased respiratory rate)

• Temperature > 38°C or < 36°C (Fever or hypothermia)

• BGL > 7 (Elevated blood glucose, possible stress response)

• SpO₂ < 94% (Low oxygen saturation)

• Diabetes (Risk factor for sepsis)

• Steroids (Immunosuppression can increase risk)

• Chemotherapy (Weakened immune response)

• Decreased urination (Possible sign of organ dysfunction)

Syncope (3 classes) + common causes

Orthostatic (Ortho) – Blood pressure drops when standing due to inadequate automimic compensation.

• hypovolemia

• medications (hypertensives, diuretics)

• Autonomic dysfunction (can stem from underlying conditions like diabetes, Parkinson's, infections)

• Prolonged bed rest

Neural

• vasovagal (stress, pain, fear, sees blood)

• situational (defecation, coughing, vomiting, straining)

• Carotid sinus hypersensitivity (shaving, turning head, tight collar)

Cardiac

• arrythmias

• structural heart disease

• Ischemia/ACS

Anaphylaxis process

• Exposure to Allergen → The immune system mistakenly identifies a harmless substance (e.g., food, insect sting) as a threat and triggers an immune response.

• B Cells Produce IgE Antibodies → B cells are immune cells that create IgE antibodies, which are specialized proteins designed to recognize and attach to specific allergens.

• IgE Antibodies Bind to Mast Cells → Mast cells are immune cells that store inflammatory chemicals like histamine. IgE antibodies attach to mast cells, making them hypersensitive to the allergen.

• Re-exposure to Allergen → When the allergen enters the body again, it binds to the IgE-coated mast cells, causing them to activate.

• Mast Cell Degranulation → Activated mast cells release histamine, heparin, and other inflammatory chemicals into the bloodstream, triggering widespread immune effects.

• Histamine Causes Blood Vessel Leakage → This leads to swelling (angioedema), redness, hives, and a sudden drop in blood pressure (shock) due to fluid leaking from blood vessels.

• Bronchoconstriction & Mucus Production → Airways tighten, and excessive mucus is produced, causing wheezing, difficulty breathing, and potential airway obstruction.

• Eosinophils Worsen Inflammation → These white blood cells leave the bloodstream and move to the reaction site, damaging tissues and increasing inflammation, making symptoms worse.

COPD Signs and Symptoms

Chronic Obstructive Pulmonary Disease (COPD) ✅ Signs and Symptoms:

• Pursed lips breathing (self-PEEP)

• Tripod position

• Responds to supplemental oxygen

• History of COPD or chronic lung disease

• Use of CPAP

• Use of accessory respiratory muscles

• Chronic smoker

• Barrel chest (especially in emphysema)

• Yellow or green sputum

• Peripheral oedema / "blue bloater" (chronic bronchitis)

• Thin, wiry frame / "pink puffer" (emphysema)

📈 Common ECG Changes in COPD:

• Right Axis Deviation (RAD)

• P pulmonale (peaked P waves in lead II from right atrial enlargement)

• Right Ventricular Hypertrophy (RVH)

• Poor R wave progression (V1–V6)

• Low voltage QRS (especially in limb leads due to hyperinflation)

• Multifocal atrial tachycardia (MAT) in severe cases

APO Signs and Symptoms

Acute Pulmonary Oedema (APO) ✅ Signs and Symptoms:

• Sudden onset of dyspnoea (especially at night)

• Orthopnoea (SOB worse when lying flat)

• Feeling of suffocation

• Severe hypoxia that may not improve with oxygen

• Cyanosis (late sign)

• Tachycardia

• Hypertension early, hypotension late

• Crackles on auscultation (usually bilateral)

• Pink frothy sputum

• Commonly on diuretics

📈 Common ECG Changes in APO:

• Left Ventricular Hypertrophy (LVH)

• Left Bundle Branch Block (LBBB)

• Left Atrial Enlargement (LAE) — broad, notched P waves (P mitrale)

• Atrial Fibrillation (AF) — common in CHF-related APO

• ST segment depression or T wave inversion in lateral leads if ischemia triggered

• Signs of recent or ongoing MI if cardiac cause

what are ACE inhibitors + examples

• Suffix: -pril (e.g., enalapril, ramipril, perindopril)

• Blocks ACE with creates Angiotensin II with is vasodilator

• Lowers BP by vasodilation (↓ afterload)

• Protects the kidneys by lowering high blood pressure and reducing pressure within the kidney's tiny filters

• Can cause hypotension, Syncope hyperkalaemia, dry cough, or angioedema

• They slow kidney disease but can cause kidney impairment & AKI

• Used in heart failure and post-MI patients

Cushings/TBI/ICP

Key Clinical Signs:

• Wide pulse pressure

• Initial hypertension, progressing to bradycardia and irregular respirations as coning (brain herniation) develops

• Late-stage hypertension due to brainstem compression

• Bradycardia and irregular breathing reflect brainstem dysfunction

ECG Changes Associated with Raised ICP:

• Global ST-segment changes

• T wave inversions

• Prolonged QT interval

ARBs (Angiotensin II Receptor Blockers)

Suffix: -sartan (e.g., losartan, candesartan, irbesartan)

↓ BP via vasodilation,

no cough or angioedema (unlike ACE inhibitor)

Can cause hypotension, hyperkalaemia, renal effects

May be used if ACE inhibitors not tolerated

Beta Blockers

• Suffix: -olol (e.g., metoprolol, atenolol, propranolol)

• blocks adrenalin & noradrenaline from binding to β-receptors

• slows heart rate, reduces force of contraction, relaxes blood vessels

• ↓ HR, BP, and myocardial oxygen demand

• May blunt tachycardia in shock/sepsis

• Watch for bradycardia, hypotension, bronchospasm (esp. in asthmatics)

• Common in hypertension, post-MI, arrhythmias

• makes Anaphylaxis refectory to Adrenaline

• Glucagon needed in anaphylaxis with B-Blocker

Alpha & Beta receptors

• Alpha-1: (vessel dilation)

  Found in most sympathetic organs; causes smooth muscle contraction (e.g., blood vessel constriction, pupil dilation). 

• Alpha-2:

  Located on nerve terminals; inhibits further release of norepinephrine and insulin. 

• Beta-1: (increases heart rate)

  Primarily in the heart and kidneys; increases heart rate, force of contraction, and renin release. 

• Beta-2: (bronchodilation)

  In lungs, blood vessels, and smooth muscles; causes dilation (e.g., bronchioles, arteries to skeletal muscle) and relaxation. 

• Beta-3:

  In fat tissue; stimulates fat breakdown (lipolysis). 

Calcium Channel Blockers

• Suffix: dipine

• Dihydropyridines: -dipine (e.g., amlodipine, nifedipine) ↓ BP (vasodilation) Minal effect on HR

• Non-dihydropyridines: verapamil, diltiazem (no consistent suffix) strong cardiac effects, ↓ HR and contractility

• Verapamil & Diltiazem particularly toxic, overdose can cause bradycardia and cardiogenic shock

• Watch for hypotension, bradycardia, peripheral oedema, heart block

• Used in **hypertension, angina, arrhythmias (especially SVT AF and Atrial flutter (Non-dihydropyridines))

• Calcium Gluconate for verapamil or diltiazem overdose

• CCB overdose can cause Bradycardia, Heart block, Hypotension, cardiogenic shock, seizures, coma, hyperglycemia, metabolic acidosis.

• Consider adrenaline

• Consider atropine

• Consider pacing

Refractory anaphylaxis (3x IM adrenaline) with persistent wheeze.

What medications will you give?

Hydrocortisone

Adult - (doubel dose 200mg)

Paed - 4mg/kg (max 100mg)

Salbutamol

Adult - 5mg Neb (no max dose)

Paed - (1-5 years) 2.5mg (no max dose).

>6 years = Adult For salbutamol

Refractory anaphylaxis (3x IM adrenaline) with persistent hypotension

what medications will you give?

Glucagon1mg IM/IV

Adult - 1mg single dose

Pead >25kg 1mg

Paed <25kg 0.5mg

Normal Saline

Adult- (titrate as needed)

Paed - 10-20ml/kg (Max 60ml/kg)

Refractory anaphylaxis with stridor

Adrenaline Neb 5mg (5 vials)

Medications Causes of long QT

Medication causes

Common drugs that prolong QT:

Antiarrhythmics

Amiodarone

Sotalol

Procainamide

Flecainide

Psychotropics

SSRIs (citalopram, escitalopram)

Antipsychotics (haloperidol, droperidol, quetiapine, risperidone)

Antibiotics

Macrolides (azithro, erythro)

Fluoroquinolones (ciprofloxacin, moxifloxacin)

Antiemetics

Ondansetron

Domperidone

Others

Methadone

Lithium

Hydroxychloroquine

Some antihistamines (older ones)

Electrolytes & Metabolic/physiological causes of long QT

Electrolyte causes

Anything that reduces myocardial stability:

Hypokalaemia

Hypomagnesaemia

Hypocalcaemia

Metabolic/physiological causes

Bradycardia

Hypothermia

Myocardial ischaemia

Raised ICP

Endocrine disorders (e.g., hypothyroidism)

Anorexia/ prolonged malnutrition

Long QT management

2 lead look for Q-Tc >500ms

Look for triggers & reversible causes:

-Medications known to prolong QT

-History of anorexia/malnutrition, electrolyte disturbances (hypokalaemia, hypomagnesaemia, hypocalcaemia)

-Bradycardia (pause‐dependent rhythms)

-Recent re-feeding or metabolic disturbance

Patient at high risk of TdP (no amiodarone!)

TdP = Magnesium Sulfate (consult)

Hospital will treat with Magnesium Sulfate

Hs & Ts (Hs Causes, Signs and Treatment)

Hypoxia = choking, drowning, overdose CPR, ventilations, O2

Hypovolemia = bleeding, trauma, vomiting/diarrhoea, dehydration, shock, flat neck veins, Saline

H+ Acidosis = DKA, Sepsis, Pt may have been hyperventilating (Hx Kussmaul resps) QRS wide, arrest will likely be PEA > Asystole ETCO2 will likely be low <10mmHg CPR, ventilations, Sodium bicarbonate, saline, calcium gluconate

Hyper/Hypokalemia

Hyperkalemia
Hx renal disease, missed dialysis, Crush Syndrome/Rabo (red urine/ strenuous exercise/ long lies),

Overdose (∧Hx) CKD, renal impairment., dehydration, sepsis, dose escalation, multi therapies,

• ACE inhibitors, & ARBs, (pril, sartan)

• K+ sparing diuretics, Spironolactone ^(offender), Amiloride, Eplerenone

• NSAID

• Trimethoprim-sulfamethoxazole (TMP/SMX, Bactrim and Septra) combination antibiotic for bacterial, fungal, and protozoal infections.

• Heparin (∧H x) diabetic

Flattened P waves > Peaked T waves > wide QRS > sinusoidal waves.

Calcium gluconate, salbutamol 20mg neb adult, 5mg child, sodium bicarbonate.

Hypokalemia

Hx of diuretic use(loop/thiazide), vomiting, diarrhoea, muscle cramps, weakness, seizure, poor intake, magnesium deficiency.

Overdose

• β₂-Agonists (bronchodilators)

• insulin

palpitations prior to arrest
Potassium chloride IV

magnesium sulfide if TDP or prolonged QT

Flatted T waves, ST depression, prominent U waves, prolonged QT, PVC, TdP risk

K+ replacement and Mg+ if Mg+ is low (K+ won’t stay if Mg+ is out)

Hypoglycemia

150 mL of 10% (15 g of glucose), paediatric 0.25 g/kg (2.5 mL/kg) of 10%

Hypothermia (not dead till your warm and dead)

active rewarming during CPR is critical, 3 shocks then wait till >30°, no adrenaline, amiodarone till >30°, remove wet clothing, warm torso, insulate from ground, heat packs groin, neck, axillae.

Gentle handling movement can cause VF/VT,

Hs & Ts (Ts Causes, Signs and Treatment)

Tension Pneumothorax

Trauma, absent breath sounds on one side, distended neck veins, difficult ventilation, tracheal deviation, subcutaneous emphysema, chest pain sudden and pleuritic, increased work of breathing

Decompress chest, high flow O2

Tamponade (Cardiac)

Penetrating chest trauma, JVD, hypotension unresponsive to fluids, low voltage alternating QRS, pulsus, paradoxus (>10mmhg fall in systolic during inspiration) arrect likely PEA

Rapid transport, continue CPR

Toxins (Overdose/Poisoning) examples, suffixes

Drug paraphernalia, medication packets, pinpoint or dilated pupils, known history, ventilate, consider naloxone early

Poor ventilation, cherry red skin engines running, could indicate CO

• Opioids, bradycardia, Pinpoint pupils, Naloxone, Vent, one, ine

• Benzos, Vent, aspiration risk from sedation, pam, lam

• TCAs, wide QRS, long Q-T Sodium bicarbonate, triptyline, paramine

• Paracetamol, N-acetylcysteine in hospital

• β-blockers, bradycardia, Glucagon IV, olol

• Ca+ channel blockers, +ACE or β-blockers = high risk, bradycardic, Calcium gluconate, adrenaline, atropine, pacing, amil, tiaz, zem, Verapamil & Diltiazem(worst)

• SSRI, antipsychotics, methadone, Long Q-T, MgSO₂

Thrombosis – Cardiac (MI)

History of chest pain, known cardiac disease, ECG pre-arrest (if available)

pre-alert hospital, pPCI referral OR thrombolysis

S-T elevation in 2 continual leads (.2mm limb, >1mm chest), QRS<0.12ms,

Thrombolysis

• Tenecteplase IV,50mg in 10ml saline,1ml solution per 10kg, max 50mg

• Enoxaparin IV 30mg

• Clopidogrel Oral 300mg (4 tablets)

• Enoxaparin sub-cut 1mg/kg, max 100mg, after 15 min

pPCI

• Heparin IV,5000 IU single dose

• Ticagrelor IV 30mg OR Clopidogrel Oral 600mg (8 tablets)

Thrombosis – Pulmonary (PE)

Hx dyspnea beforehand, pleuritic chest pain, swollen leg, long immobilisation (e.g., post-op, long haul flight) tachy & hypotensive.

Hypoxic and refectory to O2,

Right heart strain, RBBB, S1Q1T3, poor R>S progression, Right axis (I=neg, aVF=pos)

Supportive care only prehospital – good CPR, consider PE in handover

Risk factors. (DVT), Recent surgery (especially pelvic, abdominal, or orthopaedic), Cancer (especially metastatic or on chemotherapy), Trauma or fractures (especially to lower limbs or pelvis), Prolonged immobility (e.g. bed rest, long travel, hospitalisation), pregnancy/post-partum, hormone therapy.

• O2,

• cautions fluids (to support RV preload) too much fluid > RV dilation > septal shift > reduced LV preload, targes MAP 65 or sys 90.

• noradrenaline to main same BP targets

• tPA tissue plasminogen activator, (PE is fibrin rich clot, instead of platelet rich, tPA is used for fibrin rich clots)

• tPA, 50mg IV during CPR, repeat @ 15 min, continue CPR for 90 min.

Trauma

Blunt or penetrating injury, visible wounds, obvious signs of major trauma

Control bleeding, decompress chest if indicated, rapid extrication and transport, keep warm, consider pelvic binder if significant mechanism. Traction long bones, pack junctional bleeds, tourniquets, proactive warming.

normal Q-Tc

Men <440 (Borderline441-460) (prolonged >460) (TdP risk >500)

Women <460 (Borderline461-480) (prolonged >480) (TdP risk >500)

Pathological Q waves

A Q wave is pathological if any of the following apply in ≥2 contiguous leads (same anatomical territory):

1. Duration

• ≥ 0.04 seconds (≥ 40 ms)
  (one small ECG box wide)

2. Depth

• ≥ 2 mm deep, or

• ≥ 25% of the height of the following R wave

3. Lead-specific rules

• Any Q wave in V1–V3 is pathological
  (Q waves are normally absent here)

📍 Contiguous lead groupings

To count, Q waves must appear in anatomically related leads:

• Inferior: II, III, aVF

• Lateral: I, aVL, V5–V6

• Anterior: V1–V4

• Septal: V1–V2

Cardiac Tamponade S&S

·        Hypotension

·        Raised JVP (distended neck veins)

·        Muffled heart sounds

·        Narrow Pulse pressure

·        Pulsus paradoxus (>10 mmHg SBP drop on inspiration, if measurable)

·        Chest trauma + unexplained hypotension

·        Low voltage QRS

·        Electrical alternans (swinging heart)

DVT > PE factors and S&S

Venous stasis

·        Immobility, long travel, paralysis, heart failure

Endothelial injury

·        Trauma, surgery, IV lines, inflammation

Hypercoagulability

·        Cancer, pregnancy/post-partum, OCP/HRT, thrombophilias, dehydration

 

PE S&S

·        Sudden dyspnoea

·        Pleuritic chest pain

·        Unexplained tachycardia

·        Syncope or near-syncope

·        Hypoxia with clear lungs

1.       Vertigo – sudden, severe, episodic (minutes–hours)

2.       Fluctuating unilateral sensorineural hearing loss

3.       Tinnitus ± aural fullness (pressure in the ear)

What’s likely condition

Ménière’s disease

excess inner-ear fluid → vestibular + cochlear dysfunction

History clues

Recurrent attacks with full recovery between episodes

Unilateral ear symptoms

Known diagnosis or previous similar episodes

 

Exam clues

Horizontal/rotatory nystagmus during attack

Normal limb power/sensation

No focal neurological deficit

 

🚨 Red flags — think NOT Ménière’s

If any of the following are present, prioritise stroke work-up:

First-ever vertigo in older patient

Persistent vertigo >24 h without improvement

Focal neuro signs (ataxia, dysarthria, weakness)

New severe headache

Vertical or direction-changing nystagmus

➡ Posterior circulation stroke can mimic Ménière’s.

These are the symptoms you see:

• Confusion / altered mental state

• Unsteady gait (ataxia), frequent falls

• Nystagmus or other abnormal eye movements

• May appear “intoxicated” without clear intoxication

This is the patient history:

• Chronic alcohol use or poor nutrition

• Prolonged vomiting / not eating

• Homelessness, social neglect, eating disorder, or post-bariatric surgery

• Recent illness with reduced intake

Likely condition:

Wernicke encephalopathy (thiamine deficiency) B1

These are the symptoms you see:

• Episodic severe headaches

• Profuse sweating

• Tachycardia / palpitations

• PVCs or other catecholamine-driven arrhythmias

• May have anxiety, tremor, pallor, or hypertension during episodes

This is the patient history you may find:

• Recurrent sudden attacks with complete recovery between episodes

• Known or episodic hypertension

• Attacks triggered by stress, exertion, surgery, or certain medications

• Possible family history of endocrine tumours (MEN syndromes)

Likely condition:

Pheochromocytoma (catecholamine-secreting adrenal tumour)

4 types of Vasopressor

Levophed (Norepinephrine)

This medication gently tightens blood vessels and helps the heart pump more effectively. It raises blood pressure so blood can reach vital organs. It’s often the first choice for severe low blood pressure.

 

 Vasopressin

Vasopressin helps the body hold onto fluid and narrows blood vessels. It works differently than other medications and is often used alongside Levophed to improve blood pressure.

 

 Epinephrine (Adrenaline)

Epinephrine helps increase heart rate, blood pressure, and heart strength. It’s commonly used in emergencies like cardiac arrest, severe allergic reactions, or shock.

Phenylephrine

This medication raises blood pressure by tightening blood vessels without increasing heart rate as much. It’s helpful when blood pressure is low but heart rate is already high.

AAA

Pain

Signs

Exam Clues

Risk factors

Pain — what does the pain feel like?

• Sudden onset abdominal, back, flank, or groin pain

• Severe, deep, tearing, ripping, or “worst ever” pain

• May start mild or intermittent before rapid deterioration

• Can radiate to the back, flank, or legs

Signs — what might I observe?

• Syncope or near-syncope

• Hypotension (often late)

• Tachycardia

• Pale, clammy, diaphoretic

• Shock or reduced level of consciousness

Exam clues — what might I find (or not find)?

• Minimal abdominal tenderness

• Soft abdomen despite severe pain

• Pulsatile abdominal mass often absent

• Rapid haemodynamic deterioration

Risk factors — who is high risk?

• Age >65

• Male

• Smoking history

• Known AAA

• Hypertension

• Atherosclerotic or vascular disease

• Family history of AAA

Ectopic Pregnancy

Pain

Signs

Exam Clues

Risk factors

Pain — what does the pain feel like?

• Lower abdominal or pelvic pain

• Often unilateral initially

• Sudden worsening if rupture occurs

Signs — what might I observe?

• PV bleeding or spotting

• Shoulder tip pain (referred diaphragmatic irritation)

• Dizziness, syncope

• Hypotension and shock if ruptured

Exam clues — what might I find (or not find)?

• Lower abdominal tenderness

• Signs of shock disproportionate to visible bleeding

• Abdominal exam may appear relatively benign early

Risk factors — who is high risk?

• Female of reproductive age

• Missed or abnormal period

• Previous ectopic pregnancy

• IUD in situ

• Fertility treatment or assisted reproduction

Mesenteric Ischaemia

Pain

Signs

Exam Clues

Risk factors

Pain — what does the pain feel like?

• Sudden, severe, diffuse abdominal pain

• Constant, non-colicky

• Pain out of proportion to exam

Signs — what might I observe?

• Nausea and vomiting

• Diarrhoea (may become bloody late)

• Tachycardia

• Hypotension (late finding)

Exam clues — what might I find (or not find)?

• Early: soft abdomen with minimal tenderness

• Late: peritonism, guarding, rigidity

• Shock once bowel necrosis occurs

Risk factors — who is high risk?

• Atrial fibrillation

• Recent myocardial infarction

• Known atherosclerotic disease

• Elderly patients

• Embolic or thrombotic disease

Bowel Obstruction / Perforation

Pain

Signs

Exam Clues

Risk factors

Pain — what does the pain feel like?

• Colicky, cramping pain initially

• Becomes constant with strangulation or perforation

Signs — what might I observe?

• Vomiting (bilious or faeculent)

• Abdominal distension

• Absolute constipation (no stool or flatus)

• Fever (late), tachycardia

Exam clues — what might I find (or not find)?

• Distended, tympanic abdomen

• Localised or generalised tenderness

• Guarding or rigidity if perforated

• Peritonism indicates late disease

Risk factors — who is high risk?

• Previous abdominal surgery (adhesions)

• Hernias

• Malignancy

• Elderly

• Chronic constipation

Acute Pancreatitis

Pain

Signs

Exam Clues

Risk factors

Pain — what does the pain feel like?

• Severe epigastric pain

• Radiates through to the back

• Worse lying supine

• Relieved by leaning forward

Signs — what might I observe?

• Persistent nausea and vomiting

• Tachycardia

• Hypotension in severe cases

• Low-grade fever

Exam clues — what might I find (or not find)?

• Epigastric tenderness

• Abdominal distension in severe pancreatitis

• Signs of systemic inflammatory response if severe

Risk factors — who is high risk?

• Heavy alcohol use

• Gallstones

• Recent binge drinking

• Previous episodes of pancreatitis

Inferior Myocardial Infarction (abdominal pain mimic)

Pain

Signs

Exam Clues

Risk factors

Pain — what does the pain feel like?

• Epigastric discomfort or indigestion-like pain

• Pressure, burning, or vague ache

• May radiate to chest, jaw, neck, or back

Signs — what might I observe?

• Nausea and vomiting

• Diaphoresis

• Dyspnoea

• Bradycardia or hypotension (inferior MI pattern)

Exam clues — what might I find (or not find)?

• Normal abdominal exam

• Unexplained abnormal vitals

• ECG changes on 12-lead

Risk factors — who is high risk?

• Older age

• Diabetes

• Known ischaemic heart disease

• Hypertension

• Smoking

• Dyslipidaemia

PE ECG

S1Q3T3 Pattern: This classic PE sign is where you see an S wave in lead I, a Q wave in lead III, and a T-wave inversion in lead III.

Right Axis Deviation: The heart’s electrical axis shifts to the right, suggesting the right ventricle is working harder.

Right Ventricular Strain: T-wave inversions in the right precordial leads (V1–V3) and possibly V4R, indicating strain on the right side of the heart.

Right Ventricular Hypertrophy: A larger R wave in V1, right axis deviation, and sometimes a strain pattern with ST depression in the right-sided leads.

Right Bundle Branch Block: A new RBBB can appear, showing that the right ventricle is under stress.

Second Degree SA block, Type II

• Intermittent P waves “drop out” of the rhythm, while subsequent P waves arrive “on time”.

• distance from one p wave to the other is the same

Second Degree SA block, Type I

The distance between P waves shortens until a P wave is dropped.

You have a wide complex tachycardia is it VT or SVT with Aberrancy

what ECG findings indicate VT

1. AV dissociation

p waves seen in amongst the QRS,s occurring out of sync

1. Fusion and capture beats

normal QRS or strange narrow looking QRS in the wide QRS,s

1. Lack of RBBB or LBBB morphology

wide QRS but no BBB morphologies

V1,V2 are positive (RBBB) but monophasic no rSR, RSR patterns (no M shape) and V6 is all Negative (QS patters)

V1,V2 are negative (LBBB) but there is a q wave in V6,   or in V1,V2

• r onset to S nadir > 60ms (1.5 small boxes)

• notched downstroke

• initial r > 30 ms

1. Chest Lead concordance

all chest leads pointing same way

1. slower initial ventricular activation velocity and faster later velocity

forward shark fin = VT

Backwards shark fun = SVT with aberrancy

list as many ACS red flags or risk factors as you can

·        Age >45M, >55F (Males more likely but females’ worse outcomes)

·        Family Hx Cardiovascular Disease 1^st Degree relative <45M, <55F

·        CAD

·        Pervious MI / ACS / OCI / CABG

·        Smoker

·        Hypertension

·        Diabetes

·        Dyslipidaemia LDL, HDL

·        Obesity / Central Adiposity

·        Sedentary lifestyle

·        Poor diet

·        Excess alcohol

·        Psychosocial Stress

·        Kidney Disease

·        Cocaine / Stimulant use

·        Pressure, Tight, Heavy, Crushing     

·        Radiation Arms, Jaw, Neck, Back

·        Ongoing 10+ min

·        Provinciated Positional, Palpation, Breathing

·        Diaphoresis

·        Nausea / Vomiting

·        Dyspnoea

·        Pallor

·        Anxiety

·        Syncope / near syncope

·        Elderly, Female, Diabetic

Dyspnoea, Indigestion, Fatigue, Syncope

NEXUS criteria

Patella relocation

cervical thoracic and lumbar

Suicide Risk questions

Means - is method available

Method - is method lethal? level of detail?

Plans - Rehearsals? time/date? place?

Intent - Plans to carry through? plans to actually die?

Thoughts - Anxious, turmoil? worthlessness? Hopelessness?

Supports - Friends? Family? Case worker? Social network?

History - Personal/family Hx? Pervious attempts? Other illness?

Autonomic dysreflexia symptoms

Above the level of injury (parasympathetic response):

• Severe headache (very common)

• Flushing/redness

• Sweating

• Nasal congestion

• Blurred vision

• Anxiety / feeling of doom

• Pupils may dilate

Seizure, pathophysiology and causes

uncontrolled excessive electrical activity in the brain, imbalance between GABA and Glutamate

GABA = inhibitory

Glutamate = excitatory

• Reduced GABA (EHOT/Benzo withdrawal)

• Excessive glutamate activity (inflammation)

• structural abnormalities

• Metabolic imbalance

• Hypoxia

• Toxins/drugs

• Fever

• Infection

• Head injury

chronic seizures normally happen due to excessive excitatory/glutamate pathways, normally diagnosed in happens in people over 60 and children

Seizure types, ang useful info to capture, and status

Focal

• one hemisphere, aware or impaired awareness, can progress to genialized

Generalized

• Tonic-Colonic, tonic stiffening + colonic rhythmic jerking

• Tonic, sudden stiffening in arms and legs/ pelvic thrust

• Myoclonic, sudden jerking/electric shock, irregular, single muscle or group

• Colonic, repetitive rhythmic jerking contractions

• Atonic, sudden loss of tone/drop

• Absence, brief staring episodes

Unilateral vs bilateral, type, eye behavior, head turning, automatisms (lip smacking, eye blinking etc.) duration, post-ictal phase, incontinence, tongue biting.

It recommended to film seizures, 20-30% of epileptics are misdiagnosed.

status epileptics = seizure > 5 min or two without full recovery in-between

Seizure treatment escalation and reversable causes, airway and duration concerns

1. benzodiazepines, Midazolam

2. anticonvulsants, levetiracetam

3. anesthetics, Ketamine

Reversable causes

• Hypoglycemia - Glucose

• Eclampsia - Magnesium Sulfate

• Hypoxia - Oxygen and ventilate

• CNS infection - Antibiotics, Cefazolin

• Hyponatremia - 3% hypertonic saline

• Alcohol or Benzo withdraw - Benzos

• Hyperthermia - cooling

airway compromise and aspiration = high risk, Laryngospasm mechanism is compromised during seizure and there will by lots of salivation and possibly tongue biting, Recovery position + NPA

The longer a seizure goes on for the less likely patient will respond to treatment, GABA becomes less responsive (moved into cells) and benzos become less effective, NMDA (with glutamate binds to) moves out of cell so 2nd line also loose effectiveness with time because glutamate pathways become intrenched. Treatment must happen quickly

Stroke, types, Risk factors

Ischemic (clot) embolic (clot travels) thromboembolic (atherosclerotic plaque rupture)

Hemorrhagic (bleed)

TIA

Risk factors include

• hypertension

• AF

• Diabetes

• Obesity

• hyperlipidemia

• age

• previous stroke

• TIA

Stroke symptoms + ischemic stroke management

Facial droop (not including forehead)

Limb weakness

Dysarthria = difficulty producing speech/slurring

Aphasia = language problem (Problem with creating or understanding language)

• Expressive (comprehension preserved, can produce language)

• Receptive (comprehension in pared)

• Global (both)

Dysphagia (difficulty swallowing)

Diplopia (double vision)

Dysmetria (loss of depth perception)

Vertigo

Ataxia (balance)

Vomiting

Visual disturbances

Altered LOC

crossed neurological findings (Face affected on one side + body affected on the other side)

hearing loss/tinnitus

permissive hypertension up to 185 sys (to push around clot)

don’t over oxygenate (causes collateral vasoconstriction in cerebellar and coronary vascular beds) O₂ = ROS (reactive oxygen species) with interact with NO to make ONOO^-, this stops NO being able to act as a vasodilator.

HINTS + exam

Only relevant for continuous vertigo/dizziness

Head impulse L & R	Corrective saccade	Normal/no corrective saccade
Nystagmus (loo L & R into paper)	Horizontal unidirectional, increases when looking towards nystagmus direction	Horizontal but direction changing with gaze, vertical, torsional/rotational
Test of Skew, paper in front of eye	No skew/deviation	Vertical skew/correction
Rub fingers next to ears Anterior Inferior Cerebellar Artery stroke	No new hearing loss	New hearing loss

Hemorrhagic stroke symptoms & Hx & management

Sudden thunderclap headache

sever hypertension

seizures

vomiting/nausea

unequal pupils/unreactive pupils

decreased GCS

Cushing’s triad

• bradycardia

• hypertension with widening pulse pressure

• irregular respirations

reversal of anticoagulants (if anticoagulated)

BP control (try to get <140) Beat blockers

ICP management, head 30°, neutral neck (avoid veinous obstruction), manage pain, Hypertonic fluids (3% saline)

Neurosurgery

Stroke mimics

Hypoglycemia

Migraines

Seizure post ictal

Bells palsy (affects facial nerves, forehead effected, dry eyes, altered sense off taste)

Intoxication

Inner ear causes of vertigo

BPPV

• Brief spinning episodes triggered by head movement

• Caused by displaced calcium crystals in inner ear

• Dix-Hallpike test (sitting > turn head 45° > lay on back quickly with head off end of bed > wait 30-60 seconds > sit back up repeat on other side (after a few seconds pt should experience a transient vertigo attack, with Nystagmus) whichever side produces more symptom id offendig side

• Epley maneuver (sitting > turn head 45° to offending side > lay on back quickly with head off end of bed > wait 30-60 seconds > rotate head 90° to other side > wait 30-60 seconds > roll body to lateral of the direction pt is facing and with face downwards into bed > wait 30-60 seconds > back to sitting position)

Vestibular neuritis (highest risk posterior stroke mimic)

• sudden severe vertigo lasting days, worsened by movement

• Usually viral inflammation of vestibular nerve

• HINTS, head impulse = catch up saccade, Nystagmus = unidirectional horizontal, no skew deviation, no hearing loss.

• Prochlorperazine (Stemetil)

Labyrinthitis

• similar to vestibular neuritis but also causes hearing loss or ringing, worsened by movement

• inflammation of labyrinths (inner ear), usually viral

• HINTS

• Prochlorperazine (Stemetil)

Meniere’s disease

• Episodes of vertigo (20 min to hours) with hearing loss, tinnitus and ear fullness, worsened by movement

• build up of inner ear fluid

• HINTS

• Prochlorperazine (Stemetil)

Stroke assessments, questions etc.

NIHSS-8     1/24

Modified Rankin Score   0-5

BSL                                         BP

Exact Time of onset?

Last known well?

Wake-up stroke?

Sudden or gradual onset?                            Hrs?

Fluctuation?

Trouble understanding me?

Anomia, Difficulty finding words?

Paraphasia, Using incorrect words?

Vision Changes?

Seizure at onset?                                             Todd’s paresis

Syncope?

Blood thinners?

Previous stroke/TIA?

Atrial fibrillation?

Smoker?

Hypertension?

Diabetes?

Family history stroke/TIA?

Recent Head Strike/fall?

Headache?

Neck pain?

New hearing loss?                           rub hands next to ears

STROKE ( ATYPICAL)

Sudden severe vertigo

Diplopia (double vision)

Dysarthria (slurred speech)

Ataxia (loss of coordination)

Dysmetria (over/undershooting target)

Dysphonia (hoarseness, rasp, strain)

Dysphagia (swallowing)

Occipital headache (back of head)

Positional vertigo                                                        Inner ear

Continuous vertigo                                                        Central

Constant                                                                            Central

Episodic                                                                         Inner ear

Ability to walk

Other Nuro signs

Nystagmus

Head Impulse L and R                             normal = central

Test of skew

New hearing loss?                           rub hands next to ears

types of syncope

Type	Simple mechanism	Common causes	Risk level	Key things to assess
Vasovagal	Nervous system overreacts → BP and HR drop → brain gets less blood	Pain, stress, blood, standing, heat	🟢 Usually low	Trigger? Prodrome (nausea, warmth, tunnel vision)? Recovery quick?
Orthostatic	Standing → blood pools in legs → BP drops	Dehydration, bleeding, sepsis, medications	🟡 Moderate	Orthostatic vitals, hydration, meds, bleeding, Postural BP change
Cardiac	Heart suddenly doesn’t pump enough blood	Arrhythmia, valve disease, PE, structural disease	🔴 Highest concern	ECG, palpitations, exertion, chest pain, FHx sudden death
Neurologic	Brain problem (not usually true syncope)	Stroke, seizure, TIA, autonomic dysfunction	🔴 High if suspected	Neuro exam, FAST/NIHSS-8 confusion, headache, focal signs

Subarachnoid haemorrhage (SAH) — Symptoms

• Sudden severe thunderclap headache

• “Worst headache of life”

• Neck pain / neck stiffness

• Nausea

• Vomiting

• Photophobia

• Collapse

• Loss of consciousness

• Reduced GCS

• Confusion

• Seizure

• Visual disturbance

• Diplopia

• Focal neurological deficits

• Dizziness / vertigo

• Weakness

• Speech changes

• Meningism

• Hypertension (sometimes)