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Induction — Critical Care

40 diseases · 64 criteria · structured C/P · Inves · Mng

C/P — Clinical Presentation
Inves — Investigations
Mng — Management
Special — Pathognomonic / disease-unique

Shock & Sepsis Syndromes

12 entries
1

Haemorrhagic / Hypovolaemic Shock

C/P
  • Brain hypoperfusion: anxiety (initial) → diminished consciousness (later)
  • Renal: reduced urine output
  • Skin: pale, cold, clammy (sympathetic overactivity)
  • Capillary refill >2s (prolonged)
  • Pulse: thready
  • Associated: thirst, air hunger
  • Tachycardia, tachypnea, hypotension in setting of acute blood loss
  • ATLS 4-stage classification (% blood loss / cap refill / peripheries / HR / BP / RR / urine output / consciousness):
    • Stage 1: <15% / <2s / warm / <100 / normal / 14–20 / >30 / slightly anxious
    • Stage 2: 15–30% / >2s / cool / >100 / normal or narrow pulse pressure / 20–30 / 20–30 / agitated
    • Stage 3: 30–40% / 5s / colder / >120 / low / 30–40 / 5–15 / confused/lethargic
    • Stage 4: >40% / >5s / coldest / >140 / very low / >35 / negligible / unresponsive
  • Compensation sequence: peripheral vasoconstriction → tachycardia → postural hypotension → recumbent hypotension
Inves
  • ABGs + lactate (gauge severity, response): metabolic acidosis, base deficit, high lactate (anaerobic metabolism)
  • Tachypnoea drives compensatory respiratory alkalosis
  • Hb/Hct not useful acutely (transcapillary refill + IV fluids must occur first before drop is appreciable)
  • Blood group & cross-match (secure compatible blood for replacement)
Mng
  • Two principles: stop the bleed + replace the loss
  • Wound compression
  • Two wide-bore peripheral IV lines
  • IV fluids until blood components available
  • Low-volume resuscitation + early blood component therapy (minimise coagulopathy of trauma)
  • Permissive hypotension (raising BP may induce rebleeding)
  • Don't over-fluid (dilutes coagulation factors)
  • Blood component ratio PRBC:FFP:Platelets = 1:1:1
  • Exclude associated head injury before suturing scalp wounds
  • Antibiotics, tetanus prophylaxis, analgesia as indicated
  • Reassess vitals + repeat ABGs
  • Do NOT give vasopressors/inotropes in hypovolaemia — they squeeze an empty heart; without adequate preload this precipitates irreversible shock (↓ coronary perfusion in diastole + depletion of myocardial stores → pump destruction). Volume first, pressors after
Special
  • BP is the LAST parameter to drop — normal BP does NOT rule out significant blood loss
  • Major Haemorrhage Protocol triggers: replacement of entire blood volume in 24h; >8–10 RBC units in 24h; >50% blood volume in 3h; loss ≥150 ml/min; ≥4 RBC units in 1h with ongoing bleeding; predicted need ≥8 RBC units in 2h
  • TXA: give ASAP, 1g bolus over 10 min then 1g infusion over 8h; every 15-min delay decreases survival by 10%
  • Lethal triad — hypothermia + acidosis + coagulopathy
physiology · background · low-yield
Physiology
  • Hypothyroid (low thyroxine) and adrenal-insufficiency (low cortisol) patients cannot mount a proper sympathetic response — adrenergic receptors fail without permissive thyroxine/cortisol → predisposed to shock
Other
  • ATLS absolute blood-loss volumes (70-kg adult): Class I <750 mL, Class II 750–1500 mL, Class III 1500–2000 mL, Class IV >2000 mL
2

Sepsis / Septic Shock

C/P
  • Classical Sepsis 1: infection + SIRS → severe sepsis (organ dysfunction) → septic shock (CV collapse needing vasopressors)
  • SIRS criteria (≥2): T ≥38 or ≤36; HR ≥90; RR ≥20 or PaCO₂ ≤32; WBC ≥12,000 or ≤4,000 or ≥10% bands
  • Sepsis 3 (2016) definition: life-threatening organ dysfunction caused by dysregulated host response to infection
  • qSOFA (≥2 of 3): RR >22; altered mental status; SBP <100 — bedside screen
  • Septic shock (Sepsis 3): vasopressors needed for MAP >65 + lactate >2.0 despite adequate fluid resuscitation
  • Classic appearance: unwell, hypotensive, flushed cheeks, warm peripheries, bounding pulses (early "warm" shock; SVR ↓, CO ↑)
  • Late distributive shock: cool skin, hypotension (despite distributive aetiology)
Inves
  • Blood cultures BEFORE antibiotics (do not delay therapy)
  • Lactate (resuscitation marker, target normalisation)
  • SOFA score: PO₂/FiO₂, platelets, bilirubin, MAP/vasopressors, GCS, creatinine/urine output; SOFA ≥2 = ≥10% mortality
  • Imaging to identify source
  • Rapid antigen assay if fungal suspected
Mng
  • Sepsis Six bundle (within first hour): supplemental O₂; IV access + crystalloid; urinary catheter; blood cultures before antibiotics; empirical antibiotics; lactate level
  • O₂: high flow 15 L/min via non-rebreathe, target sats >94%
  • Fluids: crystalloid 30 ml/kg (or 20 ml/kg boluses 0.9% saline or Hartmann's, max 60 ml/kg if hypotensive)
  • Ensure Hb >7 g/dl
  • Source control as soon as possible (e.g., ERCP for cholangitis)
  • Surviving Sepsis Campaign quantitative targets: CVP ≥8 mmHg; MAP ≥65 mmHg; urine output ≥0.5 ml/kg/h; ScvO₂ ≥70%; normalise lactate
  • Vasopressors if hypotensive despite fluids
  • First-line vasopressor: centrally-administered noradrenaline
  • Dobutamine if myocardial dysfunction
  • Dopamine NOT for "renal protection"
  • Phenylephrine NOT recommended
  • IV hydrocortisone if hypotension responds poorly to fluids+vasopressors (max ≤300 mg/d)
  • Tidal volume target 6 ml/kg; plateau pressure ≤30 cmH₂O; PEEP to avoid lung collapse
  • Glucose upper target 180 mg/dl
  • Stress ulcer ppx: PPI or H2 blocker
  • DVT ppx: LMWH or unfractionated heparin
  • 7.6% mortality increase per hour delay in antibiotics
Special
  • Sepsis 3 abandoned SIRS criteria and "severe sepsis" term
  • qSOFA has poor sensitivity for early sepsis screening
  • Lactic acidosis causes: microcirculatory lesions; hypotension; mitochondrial injury; decreased hepatic clearance
  • US: ~750,000 cases/year, ~30% mortality
  • Mixed-venous O₂ (SvO₂) HIGH despite tissue hypoxia — AV shunting + extraction defect; contrasts with LOW SvO₂ in cardiogenic/hypovolaemic shock (one number, opposite meaning)
  • Severe sepsis/septic shock drives DIC (tissue factor ↑, fibrinolysis inhibited) → microvascular occlusion + large-vessel thrombosis → MODS
physiology · background · low-yield
Mechanism
  • Triphasic course: (1) vasodilation → relative hypovolaemia; (2) capillary leak → inadequate BP despite normal/high CO; (3) myocardial depression — heart becomes hypodynamic and the picture starts to resemble cardiogenic shock
Physiology
  • Chronic ACE-inhibitor patients have low plasma vasopressin → predisposed to vasodilatory shock during open-heart surgery
3

Anaphylactic Shock

C/P
  • Rapid onset of shock after known allergen exposure
  • Airway: dyspnea, wheezing, swollen face/lips, stridor
  • BP low, HR high
  • No fever
  • Wheezes on auscultation = airway involvement / bronchospasm
  • Classic triggers: drug intake (penicillin, iodine-containing contrast) or hydatid cyst fluid (surgical spillage)
  • Distinguishing peripheral profile: urticarial rash, warm skin, sweating ABSENT, capillary refill normal-to-rapid (vasodilation dominates) — opposite of the cold, sweaty, slow-refill picture of hypovolaemic/cardiogenic shock
Inves
  • Primarily clinical
  • Monitor sats, vitals, GCS/AVPU, rashes/oedema
Mng
  • ABCDE approach
  • Oxygen + consider early intubation (laryngeal oedema can progress rapidly)
  • IV crystalloids
  • IM adrenaline (life-saving)
  • IV corticosteroids
  • Antihistamines
Special
  • Distributive shock category
  • Always consider early intubation before airway compromise becomes impossible
physiology · background · low-yield
Mechanism
  • Neurogenic shock (distributive, like anaphylaxis): loss of sympathetic tone → vasodilation + venous pooling; profile CI ↑, SVR ↓, CVP ↓, SvO₂ ↓
4

Cardiogenic Shock

C/P
  • Primarily a differential in:
    • Elderly trauma patient with chest pain post-MVC (tension pneumothorax, tamponade, or MI causing the crash)
    • Post-op patient with oliguria + hypotension (rule out MI)
  • Flat neck veins ↔ excludes cardiogenic shock (helps differentiate)
  • Peripheries: pale, cold, possibly cyanosed; sweating present; capillary refill slow — same 'cold' peripheral picture as hypovolaemic shock
Inves
  • 12-lead ECG, cardiac enzymes, troponin
  • Bedside ultrasonography (caval filling for volume status)
  • CVP, urinary output
Mng
  • Exclude hypoxia and hypovolaemia
  • High flow O₂
  • ABG, Hb, troponin
  • Seek senior advice
  • Definitive treatment: inotropic drugs (↑ myocardial contractility) + intra-aortic balloon pump (IABP)
  • Named drug of choice — DOBUTAMINE (inodilator: β1 inotrope + mild β2 vasodilator) matched to the low-cardiac-output deficit
Special
  • Elderly with beta-blocker therapy → lack of tachycardia may falsely reassure
  • Normal BP in chronically hypertensive elderly may represent severe relative hypotension
  • Haemodynamic profile: cardiac index ↓↓, SVR ↑↑, CVP/PCWP ↑ (fluid backs up into heart/lungs), mixed-venous O₂ (SvO₂) LOW — slow flow allows maximal tissue extraction
5

SIRS / MODS

C/P
  • SIRS = systemic manifestations of inflammation: fever (or hypothermia), elevated WBC, tachycardia, tachypnea
  • MODS: sequential failure of distant organs — pulmonary (ARDS), hepatic, intestinal, renal, cardiac
  • SIRS is not always infective — four initiating insults: trauma, infection, inflammation, ischaemia/ischaemia-reperfusion injury (e.g., acute pancreatitis triggers the same dysregulated response)
Inves
  • As per sepsis workup
Mng
  • Early enteral feeding + adequate resuscitation to maintain gut mucosal barrier and prevent translocation
  • Treat underlying source
  • MODS prevention: rapid resuscitation + early definitive treatment of major injuries; good surgical technique; appropriate prophylactic/therapeutic antibiotics; early diagnosis/treatment of infective complications; early thorough excision of necrotic/infected tissue; optimise O₂ delivery (correct metabolic acidosis)
Special
  • "Gut is the motor of critical illness"
  • Gut failure pathway: gut-associated lymphoid tissue failure + villous atrophy → colonisation by aerobic gram-negative bacilli → endotoxin translocation across gut wall → mesenteric lymph node macrophage activation → massive IL-6 + TNF release → SIRS + MODS
  • Sepsis 3 (2016) abandoned the "severe sepsis" term
physiology · background · low-yield
Epidemiology/Risk
  • MODS/MOF first recognised as an entity in the mid-1970s; now the most common reason for surgical patients to stay >5 days in intensive care
6

Toxic Shock Syndrome (Wound TSS)

C/P
  • Acute onset multi-organ illness resembling severe scarlet fever
  • ~50% post-surgical cases present within 48h of operation
  • Initial: diarrhoea, vomiting
  • Initial signs: high fever, diffuse skin redness, hypotension
  • Late (1–2 days): diffuse desquamation
  • Surgical wound itself often looks unremarkable
  • Multi-organ pattern: shock, renal failure, coagulopathy, liver disease, respiratory distress, generalised erythematous rash, soft tissue necrosis at infection site
Inves
  • Clinical; wound culture
Mng
  • Wound drainage
  • Antibiotics — clindamycin (inhibits exotoxin production)
Special
  • Most common organism: S. aureus expressing TSS toxin-1, enterotoxin B, enterotoxin C
  • Rare: S. pyogenes (group A streptococci)
  • Originally classic in menstruating women (tampons); increasingly seen in post-surgical wounds
  • Superantigen mechanism: binds conserved MHC + TCR β chain → stimulates up to 20% of T lymphocytes → massive cytokine release (TNF, IL-1)
7

Tetanus

C/P
  • Lockjaw / trismus (jaw)
  • Neck spasm/rigidity
  • Risus sardonicus (sardonic smile — facial spasm)
  • Back spasms so intense they can cause spontaneous vertebral fractures
  • Laryngospasm and/or respiratory muscle spasm → respiratory failure
  • Incubation 7–8 days (range 3–21)
Inves
  • Clinical diagnosis only
  • No characteristic labs; wound/blood culture unhelpful
Mng
  • Human tetanus immunoglobulin
  • Airway protection (early tracheostomy)
  • IV magnesium (spasm prevention)
  • High-calorie replenishment
  • Benzodiazepines
  • Active immunisation as condition stabilises (natural disease confers NO immunity)
Prophylaxis (tetanus-prone wound criteria — any of)
  • Sustained >6h before surgery; significant devitalised tissue; puncture injury; soil/manure contact; associated clinical sepsis, foreign body, or compound fracture
  • Up to date + standard wound: no further vaccine
  • Up to date + high risk (e.g., manure): + immunoglobulin
  • Not up to date + tetanus-prone: reinforcing Td/IPV + immunoglobulin
  • Not up to date + non-prone: reinforcing Td/IPV only
  • Immunoglobulin standard 250 IU IM; high risk / >24h elapsed / heavy contamination / burns: 500 IU
Special
  • Clostridium tetani — gram-positive anaerobic spore-forming rod
  • Two exotoxins: tetanolysin, tetanospasmin
  • Tetanospasmin: neurotoxin blocking inhibitory neurotransmitter release → unopposed muscle contraction; acts at peripheral motor end plates, spinal cord, sympathetic nervous system
  • Infectious but NOT contagious (no person-to-person spread)
8

Malignant Hyperthermia

C/P
  • Rare, life-threatening response to inhaled anaesthetics or some muscle relaxants
  • Core temperature >40°C
  • Trismus, hypercapnia, tachycardia, tachypnea, hypertension, cardiac dysrhythmias, metabolic acidosis, hypoxaemia, myoglobinuria/coagulopathy
Inves
  • Clinical
Mng
  • Halt anaesthetic
  • Dantrolene over 48 hours
  • Sodium bicarbonate
  • Active cooling
Special
  • Autosomal dominant with variable penetrance
  • Mechanism: abnormal calcium metabolism in skeletal muscle → heat generation
9

Endocrine shock

Special
  • Endocrine shock - named as one of the 5 categories (Summary box 2.1: hypovolaemic, cardiogenic, obstructive, distributive, endocrine); mentioned at survey level only, no further detail given in the lecture
10

Traumatic Shock

Special
  • Special type: combination of hypovolaemia (blood loss) + activation of the inflammatory cascade by tissue injury
  • Like septic shock — produces a systemic inflammatory response directly
11

Septic Shock

Special
  • 1) extensive vasodilatation → relative hypovolaemia; 2) widespread endothelial damage → ↑capillary permeability + massive interstitial fluid leak (inadequate BP despite normal/↑ cardiac output); 3) depression of myocardial contractility
  • Cardiac output and neck veins/CVP/PCWP INCREASED in the hyperdynamic stage, DECREASED in the hypodynamic stage
  • Downregulates the natural anticoagulant alpha-1-antitrypsin, upregulates tissue factor (procoagulant), inhibits fibrinolysis → DIC
  • Oxygen-EXTRACTION defect: heterogeneous microcirculatory impairment (intraparenchymal shunting) and/or impaired mitochondrial oxidative phosphorylation; haemorrhagic shock restores O2 consumption, septic shock shows persistent regional dysoxia
12

SIRS / MODS (Systemic Inflammatory Response & Multi-Organ Dysfunction)

Special
  • Proinflammatory phase (restore tissue function + eradicate microorganisms) and anti-inflammatory / counter-regulatory phase (prevent excessive proinflammatory activity + restore homeostasis)
  • IL-1α/β, IL-2, IL-6, IL-8, interferon, TNF, PAF
  • IL-4, IL-10, IL-13, prostaglandin E2, TGF-β
  • 'DaNang lung' / 'shock lung' — emerged as a new cause of death after aggressive Vietnam-War-era fluid resuscitation (once renal failure became survivable); now a component of the MODS spectrum
  • Systemic hypoperfusion → accumulation of acid + potassium load + activated cellular/humoral elements (complement, neutrophils, microvascular thrombi); on restoring circulation, flush-back causes (1) direct myocardial depression + vascular dilatation → further hypotension and (2) endothelial injury to distant organs → multi-organ failure. Attenuated only by reducing extent/duration of tissue hypoperfusion
  • Endothelial swelling, dysfunction and leukocyte/platelet recruitment cause capillary occlusion that persists after resuscitation → further ischaemic injury; experimentally, neutrophil depletion gives fewer no-reflow capillaries and lower mortality in haemorrhagic shock

Respiratory Failure & Acid-Base

12 entries
13

Type 1 Respiratory Failure

C/P
  • Hypoxaemia (PaO₂ <60 mmHg) with normocapnia (PaCO₂ <45 mmHg)
Inves
  • ABG (per definition)
Mng
  • O₂; treat underlying cause
Special
  • Causes listed: pneumonia, ARDS, pulmonary embolus, lactic acidosis
14

Type 2 Respiratory Failure

C/P
  • Hypoxaemia (PaO₂ <60 mmHg) with hypercapnia (PaCO₂ >45 mmHg)
Inves
  • ABG (per definition)
Mng
  • O₂ (cautiously)
  • NIV (BiPAP for ventilation; CPAP for oxygenation/alveolar splinting)
Special
  • Causes listed: opiate toxicity, obstructive sleep apnea, opiate overdose
15

Metabolic Acidosis

C/P
  • ↓ pH, ↓ HCO₃⁻, ↓ CO₂ (with respiratory compensation)
  • Mixed respiratory + metabolic acidosis: ↓ pH, ↑ CO₂, ↓ HCO₃⁻ → cardiac arrest, multi-organ failure in severe sepsis
Inves
  • ABG: base deficit (<-2 mmol/L)
  • Anion gap
  • Anion gap = (Na⁺ + K⁺) − (Cl⁻ + HCO₃⁻); normal 10–14 mmol/L
  • Winter's formula (checks respiratory compensation): expected PaCO₂ = 1.5 × HCO₃ + 8 (±2) — actual below range = respiratory alkalosis element, above range = respiratory acidosis element, within range = pure metabolic acidosis
Mng
  • Treat underlying cause
Special
  • ROME mnemonic: Respiratory Opposite, Metabolic Equal (pH and CO₂ move in same direction in metabolic disorder)
  • HCO₃⁻ = renal/metabolic contribution to pH control
  • Two mechanisms: anion-gap MA = gain of H⁺; non-anion-gap MA = loss of HCO₃⁻ (replaced by Cl⁻ in plasma)
  • Raised anion-gap causes: ketoacidosis (DKA, starvation), lactic acidosis, salicylate overdose, renal failure, rhabdomyolysis
  • Normal anion-gap causes: diarrhoea, renal tubular acidosis, ureterosigmoidostomy, acetazolamide, Addison's disease
physiology · background · low-yield
Other
  • Corrected Na⁺ in hyperglycaemia = measured Na⁺ + (glucose / 4) (all mmol/L) — a falsely low Na⁺ makes the anion gap look smaller than it truly is; normal glucose 3.9–5.8 mmol/L
Physiology
  • Normal ABG values: pH 7.35–7.45; PaCO₂ 35–45 mmHg (4.7–6.0 kPa); PaO₂ 80–100 mmHg (11–13 kPa); HCO₃⁻ 22–28 mEq/L; O₂ sat 96–100% (kPa × 7.5 = mmHg)
  • pH buffers: plasma proteins + bicarbonate (extracellular); proteins, phosphate, ammonia (intracellular). H⁺ excreted by the kidney, CO₂ by the lungs
16

Metabolic Alkalosis

C/P
  • ↑ pH, ↑ HCO₃⁻, ↑ CO₂ (with respiratory compensation)
  • Mixed respiratory + metabolic alkalosis: ↑ pH, ↓ CO₂, ↑ HCO₃⁻ → liver cirrhosis with diuretic use, hyperemesis gravidarum, excessive ventilation in COPD
Inves
  • ABG: base excess (>+2 mmol/L)
Mng
  • Treat underlying cause
Special
  • —
  • Causes: excessive vomiting, diuretic use, bicarbonate administration, Conn's syndrome (hyperaldosteronism), Liddle syndrome, liquorice
17

Respiratory Acidosis

C/P
  • ↓ pH, ↑ CO₂, HCO₃⁻ normal (acute) or ↑ (compensated)
Inves
  • ABG
Mng
  • Treat underlying cause; ventilatory support if needed
Special
  • Causes: respiratory depression (opiates), Guillain-Barré (paralysis), asthma, interstitial lung disease, COPD, iatrogenic (incorrect mechanical ventilation settings)
18

Respiratory Alkalosis

C/P
  • ↑ pH, ↓ CO₂, HCO₃⁻ normal (acute) or ↓ (compensated)
Inves
  • ABG
Mng
  • Treat underlying cause
Special
  • Causes "WASH OUT" (anxiety/panic, pregnancy, early sepsis, mechanical ventilation at excessive rate/volume)
19

Acute Kidney Injury (AKI)

C/P
  • Anuria/oliguria, post-op
  • Urosepsis, urinary tract bleeding
Inves
  • Fluid chart
  • Regular U&E
  • Renal tract ultrasound
  • Urgent urology/nephrology referral
Mng
  • Treat underlying cause; renal replacement therapy if indicated
  • RRT indications: symptomatic uraemia; creatinine >600 µmol/L (6.8 mg/dl); refractory hyperkalaemia; severe acidosis; significant oliguria/anuria; fluid management (overload)
Special
  • Pre-renal: hypovolaemia, hypotension, excessive vasoconstriction (vasopressors)
  • Intrinsic: acute tubular necrosis (drugs/toxins), glomerulonephritis, rhabdomyolysis
  • Post-renal: renal calculi, blocked catheter, neuropathic bladder
20

Acid-Base Physiology (ABG Basics)

Special
  • pH = logarithmic scale of [H+]; inversely proportional to [H+] - more H+ = more acidity
  • Closely controlled 7.35-7.45 by buffering + excretion of acids
  • Extracellular: plasma proteins + bicarbonate; Intracellular: proteins, phosphate, ammonia
  • H+ excreted via the kidney; CO2 excreted via the lungs
  • CO2 + H2O <-> H2CO3 <-> HCO3- + H+ (carbon dioxide + water <-> carbonic acid <-> bicarbonate + hydrogen ion)
  • pH survival range 6.8-8.0 (normal 7.35-7.45)
  • A normal pH does NOT rule out respiratory/metabolic pathology - always check all values (compensated or mixed disorder possible)
21

Normal ABG Values (Reference)

Special
  • pH: 7.35-7.45
  • PaCO2: 35-45 mmHg (4.7-6.0 kPa)
  • PaO2: 80-100 mmHg (11-13 kPa)
  • HCO3-: 22-28 mEq/L
  • O2 saturation: 96-100%
  • kPa x 7.5 = mmHg
22

Compensation (Acid-Base)

Special
  • Attempt of respiratory/renal systems to restore pH; compensation ALWAYS goes in the same direction as the primary problem
  • paCO2 up -> HCO3- up; paCO2 down -> HCO3- down
  • HCO3- up -> paCO2 up; HCO3- down -> paCO2 down
  • To decide pure metabolic vs pure respiratory vs mixed disorder
23

Milk-alkali syndrome

C/P
  • severe nausea + weakness
  • past peptic-ulcer disease, self-treating recurrent pain
  • large intake of milk + calcium carbonate (antacid) over a week
  • Ca 11.5 mg/dL (hypercalcaemia), creatinine 1.4 (mild renal impairment)
Inves
  • Room-air ABG (Case 11): pH 7.46, PaCO2 49, PaO2 70, HCO3 34-35, Na 139, Cl 95
  • 6-step read: pH alkalosis, PaCO2 up, HCO3 up = metabolic alkalosis; compensation = CO2 retention (hypoventilation)
Special
  • Excess calcium carbonate + milk drives a metabolic alkalosis with hypercalcaemia (milk-alkali syndrome); ABG shows raised HCO3 and compensatory CO2 retention
  • Triad: hypercalcaemia + metabolic alkalosis + renal impairment (raised creatinine)
24

Same ABG, two diagnoses - clinical correlation

Inves
  • ABG: pH 7.39, PaCO2 49, HCO3 30 (Case 17, 'Cherry on top')
Special
  • Identical numbers can be EITHER compensated respiratory acidosis (COPD / Type 2 failure retaining CO2 with HCO3 compensation) OR compensated metabolic alkalosis (vomiting -> acid loss with hypoventilation to compensate)
  • Key principle: 'never treat the blood gas alone' - assess the clinical picture first and correlate it with the ABG; the clinical context, not the numbers, decides

Oxygen & Hypoxia

5 entries
25

Hypoxia (clinical syndrome)

C/P
  • Symptoms: light-headedness, euphoria (more likely to laugh when hypoxic), tiredness, ataxia, confusion, nausea, tingling, coma
  • Signs: tachycardia, low saturations, cyanosis
Special
  • Relative/absolute deficiency of cellular O2 — increased demand (seizures, pyrexia), decreased supply (anaemia, CCF, IHD), abnormal usage (cyanide poisoning)
26

Carbon monoxide (CO) poisoning

Special
  • Hb has a higher affinity for CO than O2
  • Left-shifts it — increased affinity, impaired O2 unloading
  • Anaemic / histotoxic hypoxia
27

Cyanide poisoning

Special
  • Histotoxic hypoxia = 'abnormal usage' of O2 — cellular/cytochrome oxidase utilisation blocked despite adequate delivery
28

Type 2 Respiratory Failure (O2 in COPD)

Mng
  • High index of suspicion in COPD
  • Start low O2 concentration via Fixed Performance (Venturi/HAFOE) mask 24-28%
  • Serial arterial blood gases
  • Monitor for signs of rising CO2 (CO2 narcosis)
Special
  • Peripheral vasodilatation/bounding pulse, coarse flapping tremor/twitching, confusion → drowsiness → coma
29

Type 1 Respiratory Failure (mechanisms)

Special
  • Low inspired O2 (FiO2), alveolar hypoventilation, impaired pulmonary diffusion, V/Q mismatch/shunt (intrapulmonary e.g. shunt; extrapulmonary e.g. pulmonary embolism)

Fluids & Electrolytes

5 entries
30

Dehydration / fluid-deficit (volume depletion)

C/P
  • Symptoms: thirst, fatigue, headache, nausea
  • Signs: decreased skin turgor, dry mucosae, pallor
  • Raised HR, low BP, oliguria, low CVP
Inves
  • Raised haematocrit, urea, albumin
  • Urine SG >=1.02, osmolality >500
  • Urine [Na+] <=15
Special
  • History (dehydration symptoms) + examination (signs of reduced perfusion) + investigation (blood + urinalysis)
31

Third-space fluid sequestration (transcellular water)

Special
  • CSF; gut (ileus); bladder (retention); serous cavities (effusions)
  • Can account for huge 'unseen' losses; counts as both a pre-existing deficit and an ongoing loss
32

Post-operative surgical stress response

Special
  • Stress-induced release of ADH, aldosterone and cortisol
  • Net effect: retention of water and Na+, with K+ and N (nitrogen) loss
33

Haemorrhagic / Hypovolaemic Shock (fluid replacement)

Mng
  • Initially replace with a salty crystalloid e.g. Hartmann's at 3x the estimated loss
  • Large/acute losses replaced with colloid e.g. gelofusine
  • Much larger losses replaced by blood; Hb <8 g/dL is the general trigger to transfusion
34

Sepsis / Septic Shock (fluid resuscitation)

Mng
  • Oesophageal Doppler / stroke-volume-guided resuscitation: give just enough fluid to maintain intravascular filling without giving excess
  • Optimal-filling curve: too little / just right / too much
Special
  • Titrate to stroke volume via oesophageal Doppler rather than fixed static dosing

Critical Care / ICU

3 entries
35

Post-Intensive Care Syndrome (post-ICU psychological morbidity)

C/P
  • 50% of ICU survivors suffer psychological harm
  • Clinical depression
  • Anxiety
  • PTSD
  • Hallucinations, flashbacks, nightmares (delusional ICU memories)
Mng
  • ICU follow-up clinics now increasingly common
36

Sepsis / Septic Shock — cardiovascular support

Mng
  • Cardiovascular support = inotropes vs vasopressors
  • Agents taught: noradrenaline, adrenaline, dobutamine
  • Delivered via central access
Special
  • β1 = inotropy + chronotropy (heart); α1 = vasoconstriction; β2 = vasodilatation (peripheral vasculature)
  • Profound capillary vasoconstriction → end-organ hypoperfusion, ischaemic injury (digital/peripheral gangrene), arrhythmias
37

SIRS / MODS — multi-organ failure

Special
  • Mortality rises with each additional failing organ system (MOF); reaches ~100% with ≥4 organ-system failures

Pre-op Assessment

3 entries
38

Preoperative Investigations — Indications & Special Tests

Inves
  • Full blood count — >60 yrs; known/suspected anaemia; risk of intra-op blood loss (group & save)
  • Kidney function tests — >60 yrs; known/suspected renal disease; major intraoperative fluid shifts
  • Liver function & coagulation profile
  • ECG — >50 yrs (>40 yrs if diabetic or hypertensive); previous MI / suspected ischaemic heart disease; palpitations, SOB or chest pain on exertion
  • CXR — rarely indicated (e.g. severe COPD, thoracic surgery, COVID)
  • Sickle cell testing — all patients with family history of homozygous disease or heterozygous trait; any patient of African / Afro-Caribbean background whose sickle status is unknown
  • Special investigations — exercise ECG; 24-hour tape (Holter monitoring); echocardiography; pulmonary function tests
Special
  • General condition; co-morbidities; nature of surgery
  • Exercise ECG precluded by his lower-limb (hip) fracture
39

General Perioperative Risks

Special
  • General → Morbidity → Mortality
  • Bleeding (++); cardiac arrhythmias / cardiac arrest; blood transfusion; uncontrolled heart failure; intraoperative myocardial ischaemia
40

Preoperative Assessment — Aim (WHY) & Anaesthetist's Explanation

Special
  • Screen for unknown conditions; optimise medical problems; assess possible risks; anticipate complications; reduce risks to a minimum
  • Choice of the safer anaesthetic technique; need for invasive monitoring (arterial & central venous lines); the postoperative analgesia plan; justification for admitting to ICU / high-dependency unit (HDU)

Sepsis & Infection

7 entries
1

Sepsis 1 vs Sepsis 3 Definitions

Use: Classify infection-related illness severity.

Sepsis 1 (1991) — classical spectrum
  • Sepsis = identifiable source of infection + SIRS
  • Severe sepsis = sepsis + organ dysfunction
  • Septic shock = sepsis + cardiovascular collapse (requiring vasopressor support)
Sepsis 3 (2016) — new definition
  • Sepsis = life-threatening organ dysfunction caused by a dysregulated host response to infection
  • Septic shock = vasopressors needed for MAP >65 mmHg + lactate >2.0 mmol/L despite adequate fluid resuscitation
  • Abandoned: SIRS criteria for identifying sepsis; "severe sepsis" term
2

SIRS Criteria (Sepsis 1)

Use: Identify systemic inflammatory response. ≥2 criteria required.

  • Temperature: ≥38°C or ≤36°C
  • Heart rate: ≥90 bpm
  • Respiratory rate: ≥20/min OR PaCO₂ ≤32 mmHg (or mechanical ventilation)
  • WBC: ≥12,000/µL OR ≤4,000/µL OR ≥10% band forms
3

qSOFA Score

Use: Bedside screening tool to identify patients at risk of poor outcome from infection. Score ≥2 → start sepsis care pathway.

  • Respiratory rate >22/min
  • Altered mental status
  • Systolic BP <100 mmHg

Limitation: Poor sensitivity — likely excludes its use as an early sepsis screening tool on its own.

4

SOFA Score

Use: Predicts mortality risk for ICU patients based on lab and clinical data. A score of ≥2 is associated with a 10% or greater increase in mortality.

SystemParameter
RespiratoryPO₂ / FiO₂
CoagulationPlatelets / mm³
LiverBilirubin (mg/dl)
CardiovascularMAP and requirement for vasopressors (Dopamine, Epinephrine, Norepinephrine)
CNSGlasgow Coma Scale
RenalCreatinine (mg/dl) and Urine output (ml/d)
5

Sepsis Six Bundle

Use: Within the first hour of sepsis recognition. Key stat: 7.6% mortality increase for every hour delay in giving antibiotics.

  • Supplemental Oxygen (high flow 15 L/min via non-rebreathe, target sats >94%)
  • Establish IV access and start crystalloid (30 ml/kg)
  • Insert a urinary catheter (hourly output monitoring)
  • Draw a blood culture before starting antibiotics
  • Administer empirical antibiotics
  • Determine a lactate level

Ensure Hb >7 g/dl. Consider vasopressors if hypotensive after fluid resuscitation. Control the source of sepsis.

6

Surviving Sepsis Campaign Bundles (2012)

Within 3 hours
  • Measure lactate level
  • Obtain blood cultures prior to administration of antibiotics
  • Administer broad-spectrum antibiotics
  • Administer 30 ml/kg crystalloid for hypotension or lactate ≥4 mmol/L
Within 6 hours
  • Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation) to maintain MAP ≥65 mmHg
  • In persistent hypotension despite volume resuscitation or initial lactate ≥4 mmol/L: measure CVP and central venous oxygen saturation (ScvO₂)
  • Remeasure lactate if initial lactate was elevated
Quantitative resuscitation targets
  • CVP ≥8 mmHg
  • MAP ≥65 mmHg
  • Urine output ≥0.5 ml/kg/h
  • ScvO₂ ≥70%
  • Normalisation of lactate
7

LRINEC Score (NSTI)

Use: Supports clinical suspicion of necrotising soft tissue infection. Score ≥6 → high suspicion (PPV 92%, NPV 96%).

6 variables
  • Total WBC count
  • Haemoglobin
  • Sodium
  • Glucose
  • Serum creatinine
  • C-reactive protein
Suggestive lab thresholds
  • WBC ≥15,400/µL
  • Serum sodium <135 mEq/L

Limitation: Failed to distinguish those with or without septic shock/death — should not be solely relied on for diagnosis.

Trauma & Shock

9 entries
8

ATLS Haemorrhage Classification (4-Stage)

Use: Classify severity of haemorrhagic shock by physiological parameters.

ParamStage 1Stage 2Stage 3Stage 4
% Blood loss<15%15–30%30–40%>40%
Cap refill<2s>2s5s>5s
PeripheriesWarmCoolColderColdest
Heart rate<100>100>120>140
Blood pressureNormalNormal or narrow pulse pressureLowVery low
Resp rate14–2020–3030–40>35
Urine output (ml/hr)>3020–305–15Negligible
ConsciousnessSlightly anxiousAgitatedConfused/lethargicUnresponsive

Compensation sequence: peripheral vasoconstriction → tachycardia → postural hypotension → recumbent hypotension

BP is the LAST parameter to drop — normal BP does NOT rule out significant blood loss.

9

Major Haemorrhage Protocol Triggers

Use: Activate massive transfusion protocol (e.g., dial 2222). Communication via SBAR. Nominate a coordinator/scribe.

  • Replacement of entire blood volume in 24 hours
  • Total transfusion >8–10 packed RBC units in 24 hours
  • Replacement >50% blood volume in 3 hours
  • Blood loss ≥150 ml/min
  • Transfusion of ≥4 RBC units in 1 hour with ongoing haemorrhage
  • Patient predicted to need ≥8 packed RBC units within 2 hours

Component ratio PRBC : FFP : Platelets = 1:1:1. Use permissive hypotension. Don't over-fluid (dilutes coagulation factors).

TXA (Tranexamic Acid): 1g bolus over 10 min then 1g infusion over 8h. Every 15-min delay decreases survival by 10%.

10

ABCDE Primary Survey

Use: Vertical approach for trauma resuscitation. For multiple trauma patients, use a horizontal approach (simultaneous, team-based task execution with delegated roles).

  • A — Airway
  • B — Breathing
  • C — Circulation
  • D — Disability (neurological assessment — GCS, pupils, lateralising signs, blood glucose)
  • E — Exposure / Environment (remove clothing, logroll, prevent hypothermia, keep dignity, remove spine board ASAP)

Adjuncts: e-FAST, CXR, PXR, ± lateral cervical spine, ± whole-body CT, ± angiography/IR; analgesia (pharmacological, psychological, physical).

Planning round (STOP): all life-threats identified? all investigations done? analgesia given? what is the Plan? non-essential team disbanded? relatives informed?

11

AMPLE History (Secondary Survey)

Use: Concise medical history during trauma secondary survey, performed only when all immediately life-threatening conditions have been treated.

  • A — Allergies
  • M — Medications
  • P — Past medical history
  • L — Last meal
  • E — Events leading to presentation
12

Classification of shock - Summary box 2.1 (5 categories)

Use: Bailey & Love umbrella classification of shock into 5 categories, with causes of the main types

5 categories (Summary box 2.1)
  • Hypovolaemic
  • Cardiogenic
  • Obstructive
  • Distributive
  • Endocrine
Causes of the main types
  • Cardiogenic - primary: infarction, arrhythmia, myocardial depression
  • Cardiogenic - secondary (obstructive): cardiac tamponade, pulmonary embolism
  • Hypovolaemic - loss of blood, plasma or extracellular fluid
  • Distributive (low resistance) - vasogenic septic: endotoxin release + activation of cellular and humoral immune components
  • Distributive (low resistance) - neurogenic: failure of sympathetic outflow (bradycardia)
  • Distributive (low resistance) - anaphylactic: histamine release
13

Class of haemorrhagic shock (I-IV)

Use: Estimate blood-loss volume and severity of haemorrhagic shock from clinical parameters (Class I-IV)

Parameters by class
  • Blood loss (mL): I up to 750; II 750-1500; III 1500-2000; IV >2000
  • Blood loss (% blood volume): I up to 15; II 15-30; III 30-40; IV >40
  • Pulse rate (per minute): I <100; II 100-120; III 120-140; IV >140
  • Blood pressure: I normal; II normal; III decreased; IV decreased
  • Pulse pressure (mmHg): I normal or increased; II decreased; III decreased; IV decreased
  • Respiratory rate (per minute): I 14-20; II 20-30; III 30-40; IV >35
  • Urine output (mL/hour): I >30; II 20-30; III 5-15; IV negligible
  • CNS / mental status: I slightly anxious; II mildly anxious; III anxious, confused; IV confused, lethargic
14

Modified Early Warning Score (MEWS)

Use: Bedside physiological deterioration score for surgical patients; a modification of the Early Warning Score

Parameters (each scored 0–3)
  • Respiratory rate — e.g. <9 or ≥30
  • Heart rate — <40 or ≥130
  • Systolic BP — <70 or ≥200
  • Temperature — <35 or ≥38.5
  • AVPU (conscious level)
Cut-offs
  • Score ≥3 = needs urgent assessment
  • Score ≥5 = likely critical care / HDU / ICU
15

Three-Stage Model of Shock (Compensation → Decompensation → Irreversible)

Use: Clinical staging of shock progression

  • Stage I — Compensation: skin + splanchnic vasoconstriction; signs minimal but recognisable
  • Stage II — Decompensation: mechanisms fail to sustain tissue perfusion despite working at full capacity; urgent intervention needed
  • Stage III — Essentially irreversible: prolonged shock → severe major-organ damage
16

Haemodynamic Responses Across Shock Types

Use: Compare cardiac index, SVR, venous capacitance, CVP/PCWP and SvO2 across shock types

Hypovolaemic
  • Cardiac index ↓
  • SVR ↑
  • Mixed venous O2 saturation (SvO2) low
  • Base deficit high
Cardiogenic
  • Cardiac index ↓
  • SVR ↑
  • Mixed venous O2 saturation low
  • Base deficit high
Septic
  • Cardiac index ↑ in hyperdynamic, ↓ in hypodynamic stage
  • CVP/PCWP ↑ in hyperdynamic, ↓ in hypodynamic stage
  • Mixed venous O2 saturation high
  • Base deficit high
Neurogenic
  • Cardiac index ↑
  • SVR ↓
  • Venous capacitance unchanged
  • CVP/PCWP ↓
  • SvO2 ↓

Pre-op Assessment

12 entries
17

NCEPOD Classification of Intervention Urgency

Use: Classify timing of surgical intervention. NCEPOD = National Confidential Enquiry into Patient Outcome and Death.

ClassDefinition & timingExample
ImmediateLife/limb/organ saving; resuscitation simultaneous with surgery; within minutesRapid bleeding (trauma, aneurysm)
UrgentLife/limb/organ threatening; within hoursPerforated bowel or less urgent bleeding
ExpeditedEarly surgery within a day or twoLarge bowel obstruction, closed long bone fracture
ElectiveTiming to suit patient and hospitalJoint replacement, unobstructed hernia repair, cataract
18

ASA Classification & Mortality

Use: American Society of Anesthesiologists physical status classification.

ClassDefinitionMortality
IA normally healthy patient0.05%
IIMild systemic disease, not limiting activity0.4%
IIISevere systemic disease that limits activity but not incapacitating4.5%
IVIncapacitating systemic disease, constant threat to life25%
VMoribund; not expected to survive 24h with or without operation50%
19

POSSUM Score

Use: Risk stratification for surgical patients. POSSUM = Physiological and Operative Severity Score for the enUmeration of Mortality and Morbidity.

Composition: 12 physiological + 6 operative parameters.

12 physiological parameters
  • Age, cardiac, respiratory, ECG, systolic BP, pulse rate, haemoglobin, WBC, urea, sodium, potassium, GCS
6 operative parameters
  • Operation type, number of procedures, operative blood loss, peritoneal contamination, malignancy status, CEPOD (timing)
20

Mallampati Classification

Use: Airway assessment based on visible oropharyngeal structures.

ClassVisible structures
IUvula, fauces, soft palate, pillars visible
IIUvula, soft palate, fauces visible
IIIBase of uvula visible; soft palate visible
IVOnly hard palate visible

Three axes to align for intubation: oral, pharyngeal, laryngeal. Mr Douglas airway-difficulty factors: rheumatoid arthritis; cervical spine surgery; limited mouth opening.

21

Preoperative Airway Score (7 Criteria)

Use: Predict difficulty of intubation. Score range 0–14 (higher = greater predicted difficulty).

Criterion0 pts1 pt2 pts
Interincisor gap>4 cm4 cmCannot open mouth
MallampatiClass IClass IIClass III
Head/neck movement>90°=90°<90°
Buck teethCan prognath or edentulousCan approximate teeth onlyCannot approximate teeth
Thyromental distance>6.5 cm6.0–6.5 cm<6.0 cm
Body weight<90 kg90–110 kg>110 kg
Difficult intubation hxNoneQuestionableDefinite
22

Functional Capacity Assessment

Use: Predict perioperative cardiac risk. Strong predictor.

  • Walking endurance: Can the patient walk a mile?
  • Stair tolerance: Can they climb a flight of stairs?
  • Day-to-day function: Activities of daily living
  • Severity & stability of comorbidities; current medications; previous surgery & anaesthetics (problems? family history?)
23

Preoperative Fasting Times

Intake typeMinimum fasting
Clear liquids (water, clear tea, black coffee, carbonated, fruit juice w/o pulp)2 h
Breast milk4 h
Non-human milk / light meal (infant formula; toast + clear liquids)6 h
Regular or heavy meal (fried/fatty food, meat)8 h
24

Preoperative Preparation Steps

  • Correct the correctable (low Hb, low potassium, high INR)
  • Stabilise/improve medical co-morbidities
  • Explain & sign informed consent
  • Premedication (as appropriate)
  • Cross match & save blood
  • Antibiotic & DVT prophylaxis
  • Check for LATEX allergy

Medication rule: Continue preoperative medications. Exceptions: insulin; oral hypoglycaemics; ACE inhibitors (sometimes); anti-coagulants.

Hip fracture timeframe: Standard time-to-fix = 48 hours. Risks of delay >48h: DVT, pneumonia. Specialist consultation: cardiologist & pulmonologist (goal: optimise).

25

ASA Physical Status Classification & Predicted Mortality

Use: Grade systemic disease severity to determine peri-operative mortality/morbidity risk

Grades (definition · mortality % · worked anchor)
  • Grade I — healthy individual, no systemic disease — 0.05%
  • Grade II — mild systemic disease not limiting activity — 0.4%; e.g. hypertensive on medication, controlled
  • Grade III — severe systemic disease that limits activity but not incapacitating — 4.5%; e.g. same hypertensive but NOT controlled
  • Grade IV — incapacitating systemic disease, constantly life-threatening — 25%
  • Grade V — moribund, not expected to survive 24 hrs with or without surgery — 50%; e.g. big aortic aneurysm (~50% survival with surgery, ~50% mortality without)
26

Preoperative Airway Score (AS)

Use: Point-based prediction of intubation difficulty (range 0–14)

Assessment (0 / 1 / 2 points each)
  • Interincisor gap — >4 cm / <4 cm / cannot open mouth
  • Mallampati — Class I / Class II / Class III
  • Head-neck movement — >90° / =90° / <90°
  • Buck teeth — can prognath or edentulous / can approximate teeth only / cannot approximate teeth
  • Thyromental distance — >6.5 cm / 6.0–6.5 cm / <6.0 cm
  • Body weight — <90 kg / 90–110 kg / >110 kg
  • History of difficult intubation — none / questionable / definite
Interpretation (AS range 0–14)
  • 0 = easy intubation
  • 7 = medium
  • 14 = difficult intubation
27

ICU Levels of Care (Levels 0–3)

Use: Classify the intensity of care a patient requires, from ward-based to intensive care

  • Level 0 — requires hospital admission; ward-based care
  • Level 1 — additional monitoring, clinical input or advice (outreach); or recently discharged from ICU
  • Level 2 — single-organ monitoring and support; advanced monitoring
  • Level 3 — advanced organ support; or two or more organ system failures
28

Surgical Site Infection (SSI) Prevention Bundle

Use: Bundled components used to prevent surgical site infection

Preoperative antimicrobial prophylaxis
  • Antibiotic name
  • Timing of administration
  • Weight-based dose
  • Re-dosing (for longer procedures)
  • Discontinuation
  • Antibiotic stewardship program and committee
Skin antisepsis
  • Ensure pre-operative skin antisepsis
  • Develop standardized peri-operative skin antiseptic practices
Physiological optimisation
  • Standardized procedure to ensure normothermia
  • Protocols to optimise glucose control
  • Supplemental oxygen during pre-, intra- and post-operative periods
  • Screen and/or decolonize selected patients with MRSA
Aseptic technique & governance
  • Adhere to established guidelines (e.g. HICPAC, AORN) to ensure basic aseptic techniques — traffic control, attire, audit
  • Utilize a Safe Surgery Checklist to drive a culture of safety
  • Establish a system where SSI data is analysed and shared

Acid-Base / ABG

6 entries
29

ROME (Acid-Base Direction Mnemonic)

Use: Determine whether the primary acid-base problem is respiratory or metabolic.

  • Respiratory Opposite — pH and CO₂ move in opposite directions
  • Metabolic Equal — pH and CO₂ move in the same direction
DisorderpHCO₂HCO₃
Respiratory acidosis↓↑Normal
Respiratory alkalosis↑↓Normal
Resp acidosis + metabolic compensation↓ / ↔↑↑
Resp alkalosis + metabolic compensation↑ / ↔↓↓

Compensation always goes in the same direction as the primary problem. CO₂ is an acid. Remember: ABG steps = Oxygenation → pH → pCO₂ → HCO₃ → Compensation → Anion Gap.

30

Respiratory Alkalosis Causes (WASH OUT)

Use: Common causes of respiratory alkalosis.

  • Anxiety / panic (including panic attacks)
  • Pregnancy
  • Early sepsis
  • Mechanical ventilation at excessive rate or volumes
31

A-a Gradient (Alveolar-arterial O2 gradient)

Use: Assess cause of hypoxaemia - separates normal-gradient from high-gradient causes

Formula
  • A-a gradient = PAO2 (calculated, alveolar gas eq.) - PaO2 (measured on ABG)
  • PAO2 (mmHg) = (FiO2 x 713) - (PaCO2 x 1.2)
  • PAO2 (kPa) = (FiO2 x 93.8) - (PaCO2 x 1.2)
Normal value
  • Normal A-a gradient 12-20
  • Increases by ~1 mmHg per decade of age
Normal A-a gradient hypoxaemia
  • Low inspired O2 content (low FiO2 or low PiO2)
  • Hypoventilation (drugs or CNS depression)
  • High altitude
High A-a gradient hypoxaemia
  • V/Q mismatch (pulmonary embolism)
  • Atelectasis
  • COPD
  • Pneumothorax
32

Expected PaO2 = FiO2 x 500

Use: Oxygenation-adequacy quick check - is the patient hypoxic for the given FiO2?

  • Expected PaO2 = FiO2 x 500
  • e.g. 100 = 0.2 x 500 (room air)
  • Check SpO2 and PaO2 against FiO2 to decide if patient is hypoxic
33

Sodium Correction for Hyperglycaemia

Use: Correct measured sodium for hyperglycaemia

Formula
  • Corrected Na = measured Na + (glucose / 4) - all values in mmol/L
Reference
  • Normal glucose 3.9-5.8 mmol/L (70-105 mg/dL)
  • mmol x 18 = mg/dL
34

6-Step ABG Approach

Use: Systematic order for interpreting an arterial blood gas

  • 1. Oxygenation
  • 2. pH
  • 3. pCO2 (respiratory component)
  • 4. HCO3 (renal/metabolic component)
  • 5. Compensation
  • 6. Anion gap

Fluids & Electrolytes

12 entries
35

Basal daily maintenance requirements

Use: Baseline daily fluid + electrolyte prescription for a patient with no extra losses.

  • H2O - 30 ml/kg
  • Na+ - 1.5 mmol/kg/day
  • K+ - 1.0 mmol/kg/day
36

Daily water requirement estimation bases

Use: Three interchangeable ways to estimate daily water need.

  • Metabolic rate: 1 ml/kcal
  • Body surface area: 1.5 L/m2
  • Weight: 30 ml/kg
37

Paediatric maintenance '4-2-1' rule

Use: Hourly maintenance fluid rate in children by weight.

  • 4 ml/kg/hr for first 10 kg
  • 2 ml/kg/hr for next 10 kg
  • 1 ml/kg/hr subsequently
  • Example (25 kg child): 4x10=40 + 2x10=20 + 1x5=5 = 65 ml/hr
38

Three components of daily fluid requirement

Use: Framework for the total volume to prescribe over 24 h.

  • Total = basal maintenance + pre-existing deficits + ongoing losses
Ongoing losses
  • Haemorrhage, drains, fistulae, NG aspirate, insensible, 3rd space
39

Insensible water loss rule

Use: Estimating water lost that you cannot measure directly.

  • H2O lost by evaporation from skin and lungs
  • Excludes sweat (a salty exocrine secretion)
  • Allow 50 ml/hr in unstressed patients
  • Increases by 10% per degree of pyrexia
40

Fluid compartment volumes

Use: Distribution of total body water across compartments.

  • Total body water 42 L = 60% body weight (range 45-75%)
  • ICF 28 L
  • ECF 14 L
  • - intravascular / plasma 3 L
  • - interstitial / tissue fluid 11 L
41

IV fluid distribution rules (which fluid goes where)

Use: Predicts how much of an infused litre stays in the plasma.

1000 ml 5% dextrose
  • Diffuses to all compartments: 67% -> ICF, 33% -> ECF (333 ml)
  • Of ECF: 2/3 -> ISF, 1/3 stays in plasma = only 111 ml
1000 ml normal saline
  • Confined to ECF: 2/3 -> ISF, 1/3 stays in plasma = 333 ml
42

Composition of body fluids

Use: Match replacement fluid to the fluid being lost (mmol/L Na/K/Cl/HCO3).

[Na+] / [K+] / [Cl-] / [HCO3-]
  • Plasma: 140 / 4 / 100 / 25
  • Saliva: 20 / 10 / 30 / 30
  • Gastric: 20 / 10 / 140 / 0
  • Bile: 150 / 10 / 80 / 35
  • Ileal: 130 / 5 / 100 / 30
43

Crystalloid IV fluid compositions

Use: Reference compositions of the common crystalloids.

Normal saline
  • 150 mmol/L NaCl, isosmotic, pH 5 ('nothing normal about it')
5% glucose
  • Glucose 50 g/L, 200 kcal/L, isosmotic
  • Rapidly metabolised to CO2 + H2O = effectively just water
Hartmann's / Ringer's lactate
  • Na+ 131, K+ 5, Ca2+ 2, Cl- 111, lactate 29 (-> HCO3- in liver)
44

Colloid IV fluid types

Use: Small particles exerting osmotic pressure across endothelium.

Gelatins (polypeptide, degraded animal collagen, MW 30,000)
  • Gelofusine = 4% succinylated gelatin
  • Haemaccel = 3.5% urea-linked gelatin
  • Inexpensive; might cause allergy
Hydroxyethylstarches (amylopectin polymers)
  • MW 250-450K Daltons
  • Can impair coagulation; low incidence of allergy; more expensive
Others
  • Albumin, dextrans
45

Doppler-guided fluid administration algorithm

Use: Titrate fluid to stroke volume (oesophageal Doppler measures blood flow by ultrasound).

  • Measure stroke volume -> give a fluid challenge
  • SV rises? Yes -> repeat the challenge
  • SV rises? No -> monitor SV
  • Monitored SV falls? Yes -> give another challenge
46

General approach to fluid deficit

Use: Structured work-up of a patient with a suspected fluid deficit.

Identify cause / type
  • NBM duration, vomiting, diarrhoea, pyrexia, blood loss, surgery
Assess magnitude
  • History - symptoms of dehydration
  • Examination - signs of reduced perfusion
  • Investigation - blood + urinalysis

Critical Care / ICU

9 entries
47

ICU Levels of Care (Level 0–3)

Use: Classifies intensity of inpatient care by monitoring and organ-support needs

  • Level 0 — requires hospital admission; ward-based care
  • Level 1 — additional monitoring, clinical input or advice (outreach); or recently discharged from ICU
  • Level 2 — single-organ monitoring and support; advanced monitoring
  • Level 3 — advanced organ support; two or more organ-system failures
48

Invasive Ventilation (Intubation) — Indications

Use: When to escalate from non-invasive to invasive (intubation + mechanical) ventilation

  • Life-threatening hypoxaemia
  • Failure of NIV
  • Depressed conscious level — GCS <8
  • Airway protection (e.g. burns)
  • Severe dyspnoea
49

Refractory Hypotension — Haemodynamic Algorithm

Use: Targets vasoactive therapy to the deranged haemodynamic variable

Equations
  • BP = CO × TPR
  • CO = SV × HR
  • ∴ BP = (SV × HR) × SVR
  • Values measured via cardiac-output monitoring
Decision
  • Low SV → fluids
  • Low SVR → vasopressors
  • Low CO despite fluids → inotropes
50

ABCDE approach to the deteriorating / critically-ill patient

Use: Systematic initial assessment of any critically ill patient; underpins the Assess – Treat – Reassess concept

Sequence
  • A – Airway
  • B – Breathing
  • C – Circulation
  • D – Disability
  • E – Exposure
Underlying principles
  • Complete initial assessment
  • Treat life-threatening problems (as you find them, before moving on)
  • Reassessment
  • Assess effects of treatment / interventions
  • Call for help early
First steps of initial assessment
  • Personal safety
  • Patient responsiveness
Concept
  • Assess – Treat – Reassess loop
  • Emphasis on early recognition of the deteriorating patient
51

AVPU rapid consciousness scale (Disability)

Use: Rapid Disability (D) consciousness assessment; alternative to GCS

  • A – Alert
  • V – responds to Voice (verbal)
  • P – responds to Pain
  • U – Unresponsive
52

Disability (D) – recognition & hypoglycaemia treatment threshold

Use: Disability (D) module of ABCDE – assessment and treatment

Recognition
  • AVPU or GCS
  • Pupils
  • Random blood sugar
Treatment
  • ABC
  • Blood glucose – if < 4 mmol/L (70 mg/dl) give glucose
  • Treat underlying cause
  • Check drug chart
53

Airway (A) – assessment & management ladder

Use: Airway (A) step of ABCDE – causes, recognition, management

Causes of obstruction
  • CNS depression
  • Blood
  • Vomit
  • Foreign body
  • Trauma
  • Infection
  • Inflammation
  • Laryngospasm
  • Bronchospasm
Recognition
  • Talking
  • Difficulty breathing, distressed, choking
  • Shortness of breath
  • Noisy breathing – stridor, wheeze, gurgling
  • See-saw respiratory pattern, accessory muscles
Management ladder
  • Airway opening – head tilt, chin lift, jaw thrust
  • Simple adjuncts – oropharyngeal, nasopharyngeal airway
  • Advanced techniques – e.g. LMA, tracheal tube
  • Remember: oxygen and removal of any secretions
54

Breathing (B) – causes + Look-Listen-Feel assessment

Use: Breathing (B) step of ABCDE – causes, recognition, treatment

Causes
  • Decreased respiratory drive – CNS depression
  • Decreased respiratory effort – muscle weakness, nerve damage, restrictive chest defect, pain from fractured ribs
  • Lung disorders – pneumothorax, haemothorax, infection, acute exacerbation COPD, asthma, pulmonary embolus, ARDS
Recognition (Look – Listen – Feel)
  • Look – respiratory distress, accessory muscles, cyanosis, respiratory rate, chest deformity, conscious level
  • Listen – noisy breathing, breath sounds
  • Feel – expansion, percussion, tracheal position
Treatment
  • Airway
  • Oxygen
  • Treat underlying cause – e.g. drain pneumothorax
  • Support breathing if inadequate – e.g. ventilate with bag-mask
  • Establish continuous monitoring – SpO2, respiratory rate, capnography
55

Circulation (C) – causes, recognition & treatment

Use: Circulation (C) step of ABCDE – causes, recognition, treatment

Causes
  • Primary – acute coronary syndromes, arrhythmias, hypertensive heart disease, valve disease, hereditary cardiac diseases
  • Secondary – asphyxia, hypoxaemia, blood loss, hypothermia, septic shock, (drugs), (electrolyte / acid-base abnormalities)
Recognition
  • Pulse – tachycardia, bradycardia, regularity
  • Peripheral perfusion – capillary refill time
  • Blood pressure
  • Organ perfusion – mental state, urine output
  • Bleeding, fluid losses
Treatment
  • Airway, Breathing
  • Oxygen
  • IV/IO access, take bloods
  • Establish ECG monitoring
  • Treat cause
  • Fluid challenge
  • Haemodynamic monitoring
  • Inotropes / vasopressors

Oxygen & Hypoxia

9 entries
56

Classification of Hypoxia (4 types)

Use: Classify a relative/absolute deficiency of cellular oxygen by mechanism

  • Hypoxaemic — low arterial partial pressure
  • Anaemic — low / abnormal haemoglobin
  • Ischaemic — low cardiac output / interrupted blood supply
  • Histotoxic — e.g. cyanide poisoning, CO
57

Causes of Hypoxaemic (Hypoxic) Hypoxia

Use: Four mechanisms of low arterial PO2

  • Low inspired O2 (FiO2) — O2-depleted environment, dilution of inspired O2, altitude
  • Alveolar hypoventilation
  • Impaired pulmonary diffusion
  • V/Q mismatch / shunt — intrapulmonary vs extrapulmonary (PE, shunt)
58

Alveolar Hypoventilation — Central vs Peripheral

Use: Split causes of hypoventilation by central vs peripheral

Central
  • Drugs
  • Hypocapnia (low CO2)
  • Intracranial pathology — head injury, tumour
  • Removal of hypoxic drive / COPD
Peripheral
  • Airway obstruction
  • Restriction — pain, obesity, ascites, bandaging
  • Muscular / neurological — spinal injury, MND, muscular dystrophy, drugs
  • Mechanical — flail chest, pneumothorax, COPD
59

Causes of Impaired Diffusion

Use: Recall causes of impaired pulmonary diffusion

  • Pulmonary oedema
  • Drowning
  • Pulmonary fibrosis
60

Oxyhaemoglobin Dissociation Curve — shift factors

Use: Predict O2 affinity/unloading from curve shifts

Left shift (increased affinity)
  • Decreased temperature
  • Decreased 2,3-DPG
  • Decreased H+
  • CO
Right shift (reduced affinity)
  • Increased temperature
  • Increased 2,3-DPG
  • Increased H+
Shape
  • Sigmoid curve from positive cooperativity
  • Hb A = 2 alpha + 2 beta chains; each subunit binds 1 O2
61

Oxygen Therapy — how much & when

Use: Match O2 concentration to the clinical setting

  • All emergencies → high concentration
  • Correct hypoxia → known concentration
  • Pre-operative → 100%
  • Post-operative supplement → ~30%
  • Therapeutic hyperoxia → high concentration / hyperbaric (chamber gives higher-than-normal O2 to improve recovery)
62

Oxygen Delivery Devices & FiO2 ranges

Use: Pick delivery device by target FiO2 and performance

  • Nasal prongs — set at 2 L/min, low conc 24-35%
  • Variable-performance oxygen mask — 35-60%
  • HAFOE / Venturi mask — fixed performance, delivers prescribed concentration irrespective of respiratory pattern
  • Hudson + non-rebreathing bag — 60-80+%, short-term
  • Anaesthetic mask & circuit — only way to deliver 100% O2
63

Oxygen Therapy Dangers

Use: Recall the harms of oxygen therapy

  • Oxygen toxicity — lung, brain, eye
  • Respiratory depression / CO2 narcosis
  • Drying effect
  • Fire hazard — facial burns and deaths reported when patients smoke during O2 therapy
64

Oxygen Therapy Monitoring

Use: Detect and monitor inadequate oxygenation

Signs of inadequate oxygenation
  • Increased respiratory rate
  • Increased pulse rate
  • Confusion, agitation or reduced conscious level
  • Cyanosis (unreliable)
Methods of monitoring
  • Observation of clinical state
  • Pulse oximetry
  • Arterial blood gases
65

Analgesia & Pain Management

Use: Structured assessment & multimodal treatment of acute pain. Analgesia = relief from pain; anaesthesia = insensitivity to pain; sedation = reduced level of consciousness.

Pain physiology (4 steps)
  • Transduction — nociceptors detect damage (injury, temperature, chemical, mechanical); sensitised by prostaglandins, K⁺, histamine, bradykinin
  • Transmission — Aδ fibres (fast, sharp) & C fibres (slow, dull)
  • Perception — thalamus, limbic system, cortex
  • Modulation — descending inhibitory pathways (GABA/glycine, brainstem projections); gate control theory at the dorsal horn; sensitisation (peripheral & central) increases excitability
Types of pain
  • Acute (superficial/somatic/visceral) vs chronic (persists >3 months, impacts quality of life)
  • Nociceptive (somatic vs visceral) vs neuropathic (nervous-system lesion/dysfunction — shooting, burning, numbness)
  • Cancer pain — infiltration, obstruction, inflammation, or treatment
Assessment
  • Physiological — autonomic (BP, HR, RR)
  • Patient-reported — verbal (mild/mod/severe), visual analogue scale (10 cm line), verbal numerical rating scale (0–10); record with each set of vital signs
  • FLACC — for non-verbal patients

Untreated pain harms: hyperventilation (resp. alkalosis), ↑O₂ demand (→ metabolic acidosis, MI), impaired lung expansion (post-op chest infection), neuroendocrine stress, immune suppression, delayed mobilisation, ↑DVT risk, longer stay.

WHO analgesic ladder & multimodal approach

Step up: non-opioid (± adjuvant) → weak opioid + non-opioid → strong opioid + non-opioid. Combine drug treatment with regional analgesia, physical methods (TENS, nerve blocks) and psychological methods for an additive, opioid-sparing effect.

Analgesic drugs
DrugMechanismNotes / doseKey side effects
ParacetamolInhibits CNS prostaglandin synthesisAnalgesic + antipyretic; 1 g every 6 h (adult); PO/PR/IVLow incidence — rash; liver impairment in overdose
NSAIDsInhibit COX → ↓ prostaglandinsIbuprofen, diclofenac, naproxen, aspirin, indomethacin; COX-2 selective: celecoxib, meloxicamGI ulceration, renal impairment, asthma (~10% NSAID-sensitive), bleeding (platelet inhibition)
Strong opioidsAgonist at μ/δ/κ opioid receptorsMorphine (gold standard), fentanyl, oxycodone, diamorphine, pethidine, hydromorphone, buprenorphineN&V, sedation, respiratory depression, constipation, pruritus, tolerance/addiction, urinary retention
Weak opioidsPartial receptor binding — ceiling effectCodeine 60 mg qds, dihydrocodeine 30 mg qds, tramadol 50 mg qdsAs opioids (milder)
CompoundParacetamol + weak opioidCo-codamol, co-dydramol, co-proxamolCombined
Local anaestheticsBlock Na channels (stop impulse propagation)Lidocaine, bupivacaine, levobupivacaine, ropivacaine; topical/infiltration/epidural/nerve blockToxicity: early — peri-oral tingling, tinnitus, metallic taste, confusion; late — blurred vision, dysrhythmias, convulsions, arrest
Entonox50% N₂O + 50% O₂Self-administered; short sharp procedures; rapid on/off; strong analgesic, weak anaestheticFew side effects
AdjuvantsVariousNeuropathic: TCA (amitriptyline), anticonvulsant (gabapentin); also ketamine, clonidine, baclofen, buscopan, sumatriptanPer agent

Morphine dosing: <70 y — 10 mg IM/SC, 20 mg oral; >70 y — 5 mg IM/SC, 10 mg oral. Water-soluble; titrate to pain; can be 2-hourly; addiction rarely an issue in acute pain.

Advanced techniques
  • Patient-controlled analgesia (PCA) — post-op/trauma/pancreatitis/failed epidural; morphine 1 mg bolus, 5 min lockout; needs a loading dose; fentanyl if opioid SE or renal failure; no other opioids alongside PCA
  • Epidural — continuous infusion (fentanyl + bupivacaine, or plain bupivacaine); patient-controlled epidural analgesia (PCEA) improves pain relief, lowers cumulative dose & side effects
  • Spinal (intrathecal) — lower volume than epidural; diamorphine good; SE nausea, urinary retention, sedation/respiratory depression
  • Nerve blocks — targeted, opioid-sparing, part of multimodal approach; orthopaedic surgery, rib fractures, gynae, hernias; risk of motor block, sensory loss, nerve damage, LA toxicity
Non-pharmacological

CBT (distraction, education, reassurance, imagery, relaxation, hypnosis); physical (counter-stimulation, mobilisation/immobilisation, hot/cold, massage, TENS, acupuncture).