Overview from standard sources miller, morgan with reference of pediatric anesthesia, viva ty0e during a case of pediatric anesthesia for adenoyonsillectomy

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Pediatric Anesthesia for Adenotonsillectomy: Viva Overview

Sources: Miller's Anesthesia 10e, Morgan & Mikhail's Clinical Anesthesiology 7e, Barash/Stoelting's Clinical Anesthesia 9e

1. INDICATIONS FOR ADENOTONSILLECTOMY

Q: What are the indications for adenotonsillectomy in children?
  • Recurrent/chronic tonsillitis (most common) - typically defined as >7 episodes/year or >5/year for 2 consecutive years
  • Peritonsillar abscess
  • Tonsillar/adenoidal hyperplasia with airway obstruction
  • Obstructive Sleep Apnea Syndrome (OSAS) - most important anesthetic concern
  • Failure to thrive, speech disorders, dental abnormalities from chronic obstruction
  • Cardiac valvular disease with recurrent streptococcal bacteremia
  • Malignant disease (lymphoma - important caveat for dexamethasone use)
(Barash 9e, p.4079)

2. PREOPERATIVE EVALUATION - KEY VIVA POINTS

Q: What is your preoperative focus for this child?
A - Airway assessment:
  • Size of tonsils and adenoids
  • Degree of nasopharyngeal obstruction
  • Mouth opening, neck mobility
B - Screen for OSAS:
  • Snoring, witnessed apneas, restless sleep, daytime somnolence, nocturnal enuresis, behavioral changes
  • The "gold standard" is polysomnography (PSG)
  • Apnea-Hypopnea Index (AHI): severe OSA = AHI >10 AND oxygen saturation nadir <80%
  • Barash: "Despite only mild-to-moderate tonsillar enlargement, these patients have upper airway obstruction while awake and apnea during sleep - do not underestimate severity based on tonsillar size alone"
C - Cardiac comorbidities from chronic OSAS:
  • Cor pulmonale - right ventricular hypertrophy, cardiomegaly
  • Pulmonary hypertension, systemic hypertension
  • ECG for RVH; CXR for cardiomegaly
  • Each apneic episode spikes pulmonary artery pressure further
D - Recent URTI:
  • Active fever or productive cough = grounds for postponement
  • Recent URTI within 2-4 weeks increases risk of laryngospasm, bronchospasm
E - Coagulation status:
  • History of bleeding, family bleeding history
  • Platelet count, clotting screen if indicated
F - Obesity:
  • Obese children: especially high risk for OSA, opioid sensitivity, respiratory arrest post-op (Miller 10e, Morgan 7e, Barash 9e)

3. PEDIATRIC AIRWAY - ANATOMICAL DIFFERENCES (VIVA FAVORITE)

Q: How is the pediatric airway different from adult?
FeaturePediatricClinical Implication
HeadProportionately largerSniffing position - less neck extension needed
TongueLarger relative to oral cavityHigher risk of obstruction
LarynxAnterior and cephalad (C3-C4 vs C4-C5 in adult)More anterior - view can be difficult
EpiglottisLonger, floppy, U-shapedUse straight blade (Miller) for better lift
Narrowest pointCricoid ring (<5 years) vs glottis in adultsUncuffed tube may leak; cuffed tubes now safe if chosen correctly
TracheaShorterHigher risk of endobronchial intubation
Nasal breathersUntil ~5 monthsObligate nasal breathers - blocked nose = respiratory distress
FRCReduced (chest wall very compliant)Rapid desaturation during apnea
(Morgan & Mikhail 7e, p.1671; Barash 9e)
Q: What is the formula for uncuffed ETT size?
  • (Age/4) + 4 for uncuffed; (Age/4) + 3.5 for cuffed
  • Confirm with air leak at 15-20 cmH2O (uncuffed) or cuff pressure <20 cmH2O

4. ANESTHETIC INDUCTION

Q: How would you induce anesthesia?
Inhalational induction (preferred in children):
  • Sevoflurane is the agent of choice - greater therapeutic index than halothane
  • MAC of sevoflurane is highest in infants (2.5%) vs adults (2.0%)
  • Inhalational induction followed by IV cannulation
  • Glycopyrrolate 10 mcg/kg IV after IV access - reduces secretions, attenuates bradycardia
IV induction (if IV access present or older child):
  • Propofol 3-4 mg/kg + fentanyl 1-2 mcg/kg
  • Ketamine useful if haemodynamically compromised
Q: What is important about MAC in pediatric patients?
  • MAC is highest in infants (not neonates), decreasing with age
  • Exception: sevoflurane MAC shows no difference between neonates and infants
  • Physiological reason: higher alveolar ventilation/FRC ratio, greater cardiac output to vessel-rich group = faster wash-in of volatile agents (Morgan & Mikhail 7e)

5. AIRWAY DEVICE

Q: ETT or LMA for adenotonsillectomy?
Options:
  1. Oral RAE (Ring-Adair-Elwyn) preformed ETT - most commonly used; taped in the midline to mandible; keeps tube out of surgical field; risk of kinking with mouth gag
  2. Wire-reinforced (armored) ETT - resistant to kinking
  3. Flexible LMA - used in some centers; kinking/displacement with Boyle-Davis gag is a concern; requires experienced team; advantage of avoiding laryngoscopy
Key points:
  • Tube taped in midline of mandible (not corner of mouth)
  • After gag placement: always recheck tube position - kinking or displacement is not uncommon
  • ETT cuff inflation pressure must be checked after position change (neck extension for surgery)
  • Throat pack placement by surgeon - mandatory documentation, must be removed before extubation (Miller 10e, p.9812; Barash 9e)

6. MAINTENANCE OF ANESTHESIA

Q: What agents do you use for maintenance?
  • Either volatile (sevoflurane/isoflurane) or TIVA (propofol infusion) - both acceptable
  • TIVA preferred by some due to reduced PONV, no theatre pollution, cleaner emergence
  • Opioids: Fentanyl or morphine (use cautiously in OSA - reduce dose by up to 50%)
  • Dexamethasone 0.15-0.5 mg/kg IV: reduces PONV, reduces postoperative swelling, improves oral intake
    • CONTRAINDICATED if lymphoma is suspected - may cause lethal hyperkalemia from tumor lysis
  • NSAIDs (e.g., ketorolac, ibuprofen): good evidence for analgesia without increased bleeding risk, though some surgeons avoid
  • Paracetamol/acetaminophen: inadequate alone for tonsillectomy pain
  • Ondansetron for PONV prophylaxis
  • Local anaesthetic infiltration to tonsillar bed (with or without epinephrine) by surgeon - caution: injection into tonsillar vessels beneath tonsillar bed can cause seizures or cerebral infarction (Miller 10e; Barash 9e, p.10647)
Q: Why avoid NSAIDs in some centers?
  • Theoretical concern about platelet dysfunction and post-tonsillectomy haemorrhage
  • Evidence: bleeding rate NOT significantly increased with NSAIDs; most guidelines support their use
  • Individual surgeon/institutional preference governs

7. OSA AND OPIOID SENSITIVITY - CRITICAL VIVA POINT

Q: Why are OSA children sensitive to opioids?
  • Chronic intermittent hypoxemia upregulates central opioid receptors
  • Altered CO2 response curves - blunted hypercapnic drive
  • Risk of post-op respiratory arrest even with standard doses
  • Reduce opioid dose by up to 50% in OSA patients (Barash 9e, Key Point 3)
  • Maximize non-opioid multimodal analgesia

8. EXTUBATION - DEEP vs. AWAKE

Q: When do you extubate - deep or awake?
Awake extubation (more common, safer overall):
  • Patient regains protective airway reflexes
  • Reduces risk of airway obstruction post-extubation
  • Risk: coughing/bucking on tube may trigger bleeding from surgical site
Deep extubation:
  • Smoother emergence, less coughing/straining
  • Reduces bleeding risk from Valsalva-like maneuvers
  • Risk: airway obstruction - must be managed in high-dependency environment
  • Only appropriate if very experienced team and environment capable of rapid detection/management of obstruction
Adjuncts for smooth emergence (awake route):
  • Lignocaine (lidocaine) 1.5 mg/kg IV or topical down ETT (cuff deflated)
  • Light remifentanil infusion during emergence
  • Suction oropharynx thoroughly + remove throat pack before extubation
  • Pass orogastric tube to decompress stomach (swallowed blood/secretions) (Miller 10e, p.9812)

9. COMPLICATIONS

A. Post-Tonsillectomy Haemorrhage (PTH) - MOST FEARED COMPLICATION

Q: How do you manage a child with post-tonsillectomy haemorrhage?
Primary (within 6 hours): often from inadequate surgical haemostasis Secondary (days 5-10): usually infective sloughing of eschar
Anaesthetic management - key principles:
  1. Volume resuscitate first - IV access, fluids, blood if needed; hypovolemia reduces induction drug requirement - consider etomidate
  2. Treat as full stomach - significant swallowed blood in stomach
  3. Rapid sequence induction (RSI) with cricoid pressure - mandatory
  4. Prepare for difficult airway - bleeding + swelling + anxious child = previously easy laryngoscopy can quickly become impossible
    • Have multiple laryngoscope sizes/blades available
    • Videolaryngoscope on standby
    • Have smaller ETT sizes ready
    • Vigorous suction needed during laryngoscopy
  5. Surgeon must be present and scrubbed before induction
(Miller 10e, p.9812; Barash 9e, Key Point 4)

B. Laryngospasm

  • Most common airway complication in pediatric anesthesia
  • Risk factors: light anesthesia, secretions/blood, recent URTI
  • Treatment: CPAP, jaw thrust, deepen anesthesia (propofol 0.5-1 mg/kg), suxamethonium 1-2 mg/kg IV (or 4 mg/kg IM) if complete

C. Negative Pressure Pulmonary Edema (NPPE)

  • Occurs after sudden relief of chronic upper airway obstruction
  • Mechanism: high negative intrapleural pressures (-30 cmH2O in obstruction vs. -10 cmH2O normally) increase venous return and disrupt pulmonary microvasculature
  • Frothy pink fluid in ETT, SpO2 drop, bilateral interstitial infiltrates on CXR
  • Prevention: apply moderate CPAP during induction to allow circulatory adaptation
  • Treatment: supportive - oxygen, CPAP/PEEP, diuretics; usually resolves within 24 hours (Barash 9e, p.4094-4095)

D. Post-operative Nausea & Vomiting (PONV)

  • Very common - multimodal prophylaxis essential
  • Dexamethasone + ondansetron + TIVA where possible

E. Airway Obstruction Post-extubation

  • Especially with residual tonsillar tissue, edema, or in OSA children
  • Lateral "tonsil position" (lateral decubitus) for recovery

10. OSA - POSTOPERATIVE DISPOSITION

Q: Who needs overnight admission after adenotonsillectomy?
Admit to hospital (Barash Table 48-1) if ANY of:
  • Age <3 years
  • Severe OSA (AHI >10, SpO2 nadir <80%)
  • Cor pulmonale / cardiac abnormality
  • Failure to thrive / poor oral intake
  • Craniofacial abnormality
  • Neuromuscular disorder
  • Obesity (BMI >95th percentile)
  • Sickle cell disease
  • Post-op SpO2 <80% in recovery
  • Bleeding concerns
  • Lives far from hospital / no reliable carer
Day-surgery discharge criteria: no active bleeding, PONV controlled, adequate analgesia, adequate oral intake of fluids, SpO2 acceptable on room air for >1 hour, appropriate carer/distance.

11. PHARMACOLOGY REMINDERS (VIVA SPECIFICS)

DrugDoseNotes
Sevoflurane MAC~2.5% (infant)Higher than adult (2.0%)
Propofol induction3-4 mg/kgReduce in OSA/hypovolemia
Fentanyl1-2 mcg/kgReduce 50% in OSA
Dexamethasone0.15-0.5 mg/kg (max 8mg)Avoid if lymphoma suspected
Ondansetron0.1 mg/kg (max 4mg)PONV prophylaxis
Glycopyrrolate10 mcg/kgAnti-sialagogue, attenuates bradycardia
Suxamethonium (laryngospasm)1-2 mg/kg IV; 4 mg/kg IMBeware bradycardia in children
Lignocaine (smooth emergence)1.5 mg/kg IVOr topical via deflated cuff

12. SURGICAL SETUP - VIVA POINTS

  • Position: supine, head ring, neck extended (shoulder roll)
  • Mouth gag: Boyle-Davis gag - risk of ETT/LMA displacement, kinking; ALWAYS recheck after placement
  • Throat pack: surgeon places; anaesthetist must document and ensure removal before extubation ("count" system)
  • Shared airway: requires constant communication between surgeon and anaesthetist

SUMMARY ALGORITHM FOR THE CASE

Pre-op: Screen for OSA severity → Echo/ECG if cor pulmonale → Check coags → Postpone if active URTI/fever
Induction: Inhaled sevoflurane → IV access → glycopyrrolate → RSI if full stomach/PTH
Airway: Oral RAE ETT (midline taped) or flexible LMA
Maintenance: Volatile or TIVA + reduced-dose opioids (OSA) + dexamethasone + paracetamol + NSAID
Intraop: Check ETT after gag placement; monitor EtCO2, SpO2, temp
End of case: Remove throat pack + suction oropharynx + OGT to empty stomach
Extubation: Awake preferred; deep only if skilled team; lateral recovery position
Post-op: Multimodal analgesia; PONV prophylaxis; admit if OSA criteria met
Complication readiness: PTH → RSI protocol; Laryngospasm → sux protocol; NPPE → CPAP/PEEP

References:

With anesthesia, age, weight of patient, height of patient, circuits. Drugs, cannulae, mabl , ebv to be used

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Pediatric Adenotonsillectomy: Complete Practical Anesthesia Reference

All calculations shown for three representative age groups for viva readiness

STEP 1 - WEIGHT ESTIMATION (If actual weight unknown)

AgeFormulaExample
1-5 years(Age × 2) + 84 yr = 16 kg
6-12 years(Age × 3) + 78 yr = 31 kg
Older (APLS)Age × 310 yr = 30 kg
Most adenotonsillectomies are done in 3-10 year olds (peak 4-8 years). Use three worked examples: 4 yr/16 kg, 6 yr/22 kg, 10 yr/32 kg.

STEP 2 - HEIGHT & BSA (Quick Reference)

AgeApprox HeightBSA (Mosteller)
4 yr~102 cm~0.67 m²
6 yr~116 cm~0.82 m²
10 yr~138 cm~1.10 m²
BSA formula (Mosteller): √(Ht cm × Wt kg / 3600)

STEP 3 - BREATHING CIRCUITS

This is a classic viva topic. Choice is based purely on weight (< or >20 kg rule):

< 20 kg → Mapleson F (Jackson-Rees modification of Ayres T-piece)

  • Why: Low resistance, no valves, suitable for small tidal volumes, allows IPPV and spontaneous breathing
  • Fresh Gas Flow (FGF) for spontaneous breathing: 2-3 × Minute Volume (or ~200-300 mL/kg/min)
  • FGF for IPPV: 1000 mL + 100 mL/kg/min
  • Minute volume in child = 100-150 mL/kg/min (TV 8-10 mL/kg × RR 20-30)
Example - 4 yr/16 kg child:
  • Tidal Volume = 8 mL/kg = 128 mL
  • Respiratory rate = 22/min
  • Minute volume = ~2.8 L/min
  • FGF (spontaneous) = 3 × 2.8 = ~8-9 L/min
  • FGF (IPPV) = 1000 + (100×16) = 2600 mL/min = 2.6 L/min minimum

> 20 kg → Circle System (Paediatric/Adult Circle Absorber)

  • CO2 absorber (soda lime) used; lower FGF acceptable (1-2 L/min)
  • Can use adult circle with smaller tidal volumes

Summary Rule:

WeightCircuitFGF
<5 kgMapleson F (T-piece)3× MV
5-20 kgMapleson F / Jackson-Rees2-3× MV
>20 kgCircle absorber1-2 L/min
(Barash Clinical Anesthesia 9e; Miller's Anesthesia 10e)

STEP 4 - AIRWAY EQUIPMENT (Age/Weight Based)

Endotracheal Tube Size

Formula4 yr6 yr10 yr
Uncuffed ETT (ID mm)(Age/4) + 45.05.56.5
Cuffed ETT (ID mm)(Age/4) + 3.54.55.06.0
For adenotonsillectomy: Oral RAE tube preferred (preformed, keeps tube out of surgical field). Order size of RAE = same formula. Always have 0.5 mm smaller available.
Cuffed vs Uncuffed:
  • Cuffed ETT is now standard and safe in children >1 year (Microcuff low-pressure cuff)
  • Confirms cuff pressure <20 cmH2O
  • Advantage for adenotonsillectomy: protects against blood/secretion aspiration from surgical field

ETT Depth (Oral)

  • (Age/2) + 12 cm at lips
  • Confirm with bilateral auscultation + CXR if uncertain

Laryngoscope Blade

AgeBlade
<1 yrStraight (Miller 0 or 1)
1-8 yrStraight (Miller 1) or Curved (Macintosh 2)
>8 yrMacintosh 2-3

LMA Size (if used)

WeightLMA SizeMax Cuff Volume
5-10 kg1.57 mL
10-20 kg210 mL
20-30 kg2.514 mL
30-50 kg320 mL

STEP 5 - IV CANNULA SIZE

Weight/AgeIV CannulaGaugeNotes
<10 kg24G (yellow)24GDorsum of hand, wrist
10-20 kg22G (blue)22GMost 4-6 yr olds
20-40 kg20G (pink)20GStandard for >20 kg
>40 kg18G (green)18GAs adult
Rule of thumb for viva: "In children <20 kg, we use a 22G or 24G cannula; in children >20 kg, we upsize to 20G. For adenotonsillectomy, a single IV access is usually sufficient, but 2 IV lines are prudent in OSA children or anticipated difficult cases."

STEP 6 - ESTIMATED BLOOD VOLUME (EBV) & MABL

EBV by Age Group

(Barash Clinical Anesthesia 9e, p.3759)
Age GroupEBV
Premature neonate95-100 mL/kg
Term neonate (0-1 month)85-90 mL/kg
Infant (1-12 months)75-80 mL/kg
Child (1-12 years)70-75 mL/kg
Adult male70 mL/kg
Adult female65 mL/kg

MABL Formula

(Barash 9e, p.3759)
MABL = EBV × (Starting Hct - Target Hct) / Starting Hct
  • Target Hct for healthy children = 20-25% (i.e., Hb ~7-8 g/dL)
  • Use 25% as target for OSA children (higher O2 carrying capacity needed)

Worked Examples:

Example 1: 4-year-old, 16 kg, Hct 36%, Target Hct 25%
  • EBV = 70 × 16 = 1120 mL
  • MABL = 1120 × (36-25)/36 = 1120 × 0.306 = ~342 mL
Example 2: 6-year-old, 22 kg, Hct 38%, Target Hct 25%
  • EBV = 70 × 22 = 1540 mL
  • MABL = 1540 × (38-25)/38 = 1540 × 0.342 = ~527 mL
Example 3: 10-year-old, 32 kg, Hct 38%, Target Hct 25%
  • EBV = 70 × 32 = 2240 mL
  • MABL = 2240 × (38-25)/38 = 2240 × 0.342 = ~766 mL
For adenotonsillectomy: blood loss is usually 50-100 mL, well within MABL. MABL becomes critical in post-tonsillectomy haemorrhage (PTH) where significant concealed loss (swallowed blood) has already occurred before the child reaches theatre.

STEP 7 - FLUID MANAGEMENT (4-2-1 Rule)

Maintenance Fluids (Holliday-Segar / 4-2-1 Rule)

Body WeightRate
First 10 kg4 mL/kg/hr
Next 10 kg2 mL/kg/hr
Every kg after 20 kg1 mL/kg/hr
Worked Examples:
  • 16 kg child: (4×10) + (2×6) = 40 + 12 = 52 mL/hr
  • 22 kg child: (4×10) + (2×10) + (1×2) = 40 + 20 + 2 = 62 mL/hr
  • 32 kg child: (4×10) + (2×10) + (1×12) = 40 + 20 + 12 = 72 mL/hr

Fluid deficit (from NPO period)

Deficit = Maintenance rate × hours of fasting Give 50% in first hour, then 25%/25% over next 2 hours

Fluid choice:

  • Isotonic balanced crystalloid (Hartmann's / Lactated Ringer's) = standard
  • Normal saline AVOIDED as first choice (hyperchloremic acidosis risk)
  • Dextrose-containing fluids only in neonates/infants at risk of hypoglycemia

STEP 8 - DRUG DOSES (Complete Viva Chart)

A. INDUCTION AGENTS

DrugDoseRoute16 kg22 kg32 kg
Propofol3-4 mg/kgIV48-64 mg66-88 mg96-128 mg
Thiopentone5-7 mg/kgIV80-112 mg110-154 mg160-224 mg
Ketamine1-2 mg/kgIV16-32 mg22-44 mg32-64 mg
Sevoflurane6-8% inductionInhalational---

B. MUSCLE RELAXANTS

DrugDoseRoute16 kg22 kg32 kg
Suxamethonium (intubation/RSI)1.5-2 mg/kgIV24-32 mg33-44 mg48-64 mg
Suxamethonium (laryngospasm)4 mg/kgIM64 mg88 mg128 mg
Atracurium0.5 mg/kgIV8 mg11 mg16 mg
Rocuronium0.6 mg/kgIV9.6 mg13.2 mg19.2 mg
Vecuronium0.1 mg/kgIV1.6 mg2.2 mg3.2 mg
Note: Adenotonsillectomy does not routinely require muscle relaxants - most cases done with spontaneous breathing or IPPV using volatile ± remifentanil.

C. ANALGESICS

DrugDoseRoute16 kg22 kg32 kg
Fentanyl1-2 mcg/kgIV16-32 mcg22-44 mcg32-64 mcg
Fentanyl (OSA child)0.5-1 mcg/kg (50% reduction)IV8-16 mcg11-22 mcg16-32 mcg
Morphine0.05-0.1 mg/kgIV0.8-1.6 mg1.1-2.2 mg1.6-3.2 mg
Paracetamol IV15 mg/kg (max 1g)IV240 mg330 mg480 mg
Paracetamol rectal20 mg/kgPR320 mg440 mg640 mg
Ibuprofen5-10 mg/kgIV/PO80-160 mg110-220 mg160-320 mg
Ketorolac0.5 mg/kg (max 15 mg)IV8 mg11 mg15 mg

D. ANTIEMETICS

DrugDoseRoute16 kg22 kg32 kg
Ondansetron0.1 mg/kg (max 4 mg)IV1.6 mg2.2 mg3.2 mg
Dexamethasone0.15-0.5 mg/kg (max 8 mg)IV2.4-8 mg3.3-8 mg4.8-8 mg

E. ANTICHOLINERGICS / ANTISIALAGOGUES

DrugDoseRoute16 kg22 kg32 kg
Atropine (bradycardia)0.02 mg/kg (min 0.1 mg, max 0.6 mg)IV0.32 mg0.44 mg0.6 mg
Glycopyrrolate0.005-0.01 mg/kgIV0.08-0.16 mg0.11-0.22 mg0.16-0.32 mg

F. EMERGENCY DRUGS

DrugDoseIndication16 kg22 kg32 kg
Adrenaline (cardiac arrest)0.01 mg/kg (1:10,000)PEA/VF/asystole0.16 mg = 1.6 mL of 1:10,0000.22 mg0.32 mg
Adrenaline (anaphylaxis)0.01 mg/kg IM (1:1000)Anaphylaxis0.16 mL of 1:10000.22 mL0.32 mL
Suxamethonium (laryngospasm IM)4 mg/kg IMLaryngospasm64 mg88 mg128 mg
Propofol (laryngospasm)0.5-1 mg/kgPartial laryngospasm8-16 mg11-22 mg16-32 mg
Glucose 10%2-5 mL/kgHypoglycemia32-80 mL44-110 mL64-160 mL

G. MAINTENANCE INFUSIONS

DrugInfusion RateNotes
Propofol TIVA6-12 mg/kg/hr induction → 3-6 mg/kg/hr maintenanceGood for PONV reduction
Remifentanil0.05-0.2 mcg/kg/minSmooth emergence; titrate to response
Dexmedetomidine0.2-0.5 mcg/kg/hrOpioid-sparing; useful in OSA

STEP 9 - COMPLETE WORKED EXAMPLE (Viva Model Answer)

"6-year-old girl, 22 kg, 116 cm, presenting for adenotonsillectomy for OSA"
ParameterCalculationValue
Weight6 yr: (6×3)+725 kg (actual: 22 kg - use actual)
HeightEstimated116 cm
BSA√(116×22/3600)0.84 m²
Circuit<20 kgJackson-Rees (Mapleson F)
FGF (IPPV)1000+(100×22)3.2 L/min
ETT (cuffed oral RAE)(6/4)+3.55.0 mm ID
ETT depth(6/2)+1215 cm at lips
IV cannula10-20 kg22G
EBV70 mL/kg1540 mL
MABL (Hct 38% → 25%)1540×(13/38)~527 mL
Maintenance fluids4-2-162 mL/hr
Propofol induction3 mg/kg (OSA: reduce)~55-66 mg
Fentanyl (OSA - 50% reduction)1 mcg/kg22 mcg
Paracetamol IV15 mg/kg330 mg
Dexamethasone0.3 mg/kg6.6 mg
Ondansetron0.1 mg/kg2.2 mg
Atropine (if bradycardia)0.02 mg/kg0.44 mg
Suxamethonium (laryngospasm IM)4 mg/kg88 mg
Adrenaline (arrest)0.01 mg/kg0.22 mg

STEP 10 - MONITORING SETUP

MonitorComment
SpO2Pre-induction (pre-ductal in neonates)
ECGStandard 3-lead
NIBPAppropriate cuff = 2/3 width of upper arm; >1/2 to <2/3 arm length
EtCO2 (capnography)Mandatory; assess ventilation
TemperatureAxillary/rectal/oesophageal - prevent hypothermia
Precordial stethoscopeUseful in <10 kg
Peripheral nerve stimulatorIf NMB used
NIBP Cuff Sizes:
WeightCuff
NeonateNeonatal (4 cm)
InfantInfant (6 cm)
Child 1-5 yrChild (9 cm)
Child 6-12 yrChild large (12 cm)

QUICK-RECALL CARD (Exam Summary)

WEIGHT:  (Age×2)+8 for <5 yr; (Age×3)+7 for 6-12 yr
CIRCUIT: <20 kg → Jackson-Rees (Mapleson F); >20 kg → Circle
ETT:     Uncuffed = (Age/4)+4; Cuffed = (Age/4)+3.5
DEPTH:   (Age/2)+12 cm at lips
LMA:     <10 kg=1.5; 10-20 kg=2; 20-30 kg=2.5; 30-50 kg=3
CANNULA: <10 kg=24G; 10-20 kg=22G; >20 kg=20G
EBV:     Neonate=90 mL/kg; Infant=80 mL/kg; Child=70-75 mL/kg
MABL:    EBV × (start Hct - target Hct) / start Hct
FLUIDS:  4 mL/kg for 1st 10 kg + 2 for 2nd 10 kg + 1 beyond
FENTANYL: 1-2 mcg/kg (HALVE in OSA)
SUXAMETHONIUM: 1.5-2 mg/kg IV; 4 mg/kg IM (laryngospasm)
DEXAMETHASONE: 0.15-0.5 mg/kg (AVOID if lymphoma suspected)
ATROPINE: 0.02 mg/kg (min 0.1 mg)
Sources: Barash/Stoelting Clinical Anesthesia 9e (p.3759); Miller's Anesthesia 10e; Morgan & Mikhail Clinical Anesthesiology 7e

Everything about pulse oximetry and capnography

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Pulse Oximetry & Capnography: Complete Viva Reference

Sources: Miller's Anesthesia 10e, Barash/Stoelting Clinical Anesthesia 9e, Morgan & Mikhail 7e

PART A: PULSE OXIMETRY


1. DEFINITION & PRINCIPLE

Q: What is pulse oximetry?
Pulse oximetry is a continuous, non-invasive measurement of the functional arterial oxygen saturation (SpO2) of hemoglobin, using the differential light absorption of oxygenated (O2Hb) and deoxygenated (deO2Hb) hemoglobin.
  • The value measured is called SpO2 (from pulse oximetry) to distinguish from SaO2 (directly measured arterial blood gas)
  • Accuracy: SpO2 is within ±2-3% of SaO2 over the range of 70-100% (Miller's Anesthesia 10e, p.5456)

2. PHYSICS & HOW IT WORKS

Q: Explain the Beer-Lambert Law as applied to pulse oximetry
Beer-Lambert Law: The intensity of light transmitted through a substance decreases exponentially with the concentration of the absorbing substance and the path length.

Two wavelengths used:

WavelengthAbsorbed more byColour
660 nm (red)Deoxygenated Hb (deO2Hb)Red light
940 nm (infrared)Oxygenated Hb (O2Hb)Infrared light
Why these two wavelengths? At 660 nm, deO2Hb absorbs ~10× more than O2Hb. At 940 nm, O2Hb absorbs more than deO2Hb. The difference is maximised - this gives the best discrimination between the two species.

AC/DC Separation - the key innovation:

Light absorption by tissue is divided into:
  • DC component (non-pulsatile, "direct current"): Venous blood, capillary blood, tissue, bone, pigment - all constant
  • AC component (pulsatile, "alternating current"): Arterial blood only - changes with each heartbeat
The ratio R is calculated:
R = (AC660/DC660) / (AC940/DC940)
This ratio R is then looked up on an empirically derived calibration curve (built by having volunteers breathe hypoxic mixtures across SpO2 70-100%) to yield SpO2.
(Miller's Anesthesia 10e, p.5456-5457)

Physical construction:

  • Two LEDs (660 nm + 940 nm) that flash sequentially
  • One photodetector on opposite side (transmission) or same side (reflectance)
  • When both LEDs off: ambient light subtracted from signal automatically

3. FIVE SPECIES OF HAEMOGLOBIN (Critical Viva Point)

Q: Why is standard pulse oximetry a two-wavelength device a limitation?
Standard pulse oximetry measures functional saturation - only O2Hb and deO2Hb:
Functional SaO2 = O2Hb / (O2Hb + deO2Hb) × 100
But there are 5 species of Hb in blood:
SpeciesNormal %Notes
O2Hb (oxyhaemoglobin)~97%Absorbs 940 nm more
deO2Hb (deoxyhaemoglobin)~2%Absorbs 660 nm more
COHb (carboxyhaemoglobin)<1% (smoker: up to 10%)Absorbs 660 nm same as O2Hb → falsely HIGH SpO2
MetHb (methaemoglobin)<1%Absorbs equally at both wavelengths → SpO2 drifts toward 85% regardless of true SaO2
SHb (sulphaemoglobin)<1%Rare, causes SpO2 to read low
Pulse co-oximetry (e.g., Masimo Rad-7) uses 8 wavelengths and can measure COHb and MetHb directly.
(Miller's Anesthesia 10e, p.5449-5462)

4. THE OXYHEMOGLOBIN DISSOCIATION CURVE (OHC)

Q: What is the clinical significance of the shape of the OHC for pulse oximetry?
The OHC is sigmoid (S-shaped):
SpO2 (%)
100 |----___
 98 |       \
 90 |        \   ← STEEP PART: small ΔPO2 = big ΔSpO2
 75 |         \
 50 |          |  P50 = 27 mmHg
    |__________|___
              PaO2 (mmHg)
Clinical implications:
  1. Flat upper portion (PaO2 >70 mmHg): SpO2 cannot detect hyperoxia - dangerous in premature neonates (retinopathy of prematurity risk)
  2. Steep lower portion: Once SpO2 starts falling rapidly, PaO2 is already critically low - pulse oximetry gives late warning
  3. SpO2 of 90% corresponds to PaO2 ~60 mmHg (onset of respiratory failure)
  4. SpO2 of 75% corresponds to PaO2 ~40 mmHg (mixed venous level)
Shifts of the curve:
Shift LEFT (↑ affinity, ↓ O2 release)Shift RIGHT (↓ affinity, ↑ O2 release)
↓ Temperature↑ Temperature
↓ CO2 / alkalosis↑ CO2 / acidosis
↓ 2,3-DPG↑ 2,3-DPG
Fetal Hb (HbF)Sickle cell disease
COHb, MetHbExercise, anaemia

5. PHOTOPLETHYSMOGRAPHY - BONUS VIVA POINT

The pulse oximeter trace is also a photoplethysmograph (PPG):
  • Shows arterial blood volume changes with each heartbeat
  • Respiratory variation in PPG amplitude (ΔPOP / PVI) predicts fluid responsiveness in mechanically ventilated patients
  • PVI (Pleth Variability Index) - commercially available on Masimo devices
  • More reliable in mechanically ventilated than spontaneously breathing patients (Miller's Anesthesia 10e, p.5461)

6. PROBE SITES

SiteNotes
Finger (standard)Most common; affected by vasoconstriction, nail polish
Ear lobeFaster response time (~6 sec); good during vasoconstriction
Forehead (reflectance)Best during hypotension/vasoconstriction/hypothermia - least responsive to catecholamines
NoseAlternative site
Toe/footPost-ductal in neonates (different from right hand pre-ductal)
Palm/wristNeonates
In vasopressor-dependent patients: use ear or forehead probe - less vasoconstriction at these sites compared to fingers (Miller's Anesthesia 10e, p.5469-5470)

7. LIMITATIONS & SOURCES OF ERROR

This is the most popular viva topic:

A. Causes of FALSELY HIGH SpO2 (reads higher than true SaO2)

CauseMechanism
Carbon monoxide poisoning (COHb)COHb absorbs 660 nm same as O2Hb; SpO2 reads near 100% even in severe CO poisoning
Methaemoglobinaemia (early)MetHb initially drives SpO2 up before plateau

B. Causes of FALSELY LOW SpO2 (reads lower than true SaO2)

CauseMechanism
Methaemoglobinaemia (established)Regardless of true SaO2, SpO2 drifts toward 85%
Dyes (methylene blue, indocyanine green, indigo carmine)Absorb at 660 nm - cause transient drop in SpO2
Nail polish (blue/black/green)Absorbs 660 nm; dark colours more problematic
Severe jaundice (bilirubin >20 mg/dL)Absorbs at 460 nm - minimal clinical effect in adults

C. Causes of INACCURATE or NO READING

CauseMechanism
Vasoconstriction / poor perfusionReduced pulsatile component (AC signal too small)
HypothermiaPeripheral vasoconstriction
Hypotension / shockWeak peripheral pulse
Movement artefactMost common cause of false alarms; next-generation signal processing (e.g., Masimo SETS) mitigates this
Ambient light interferenceBright theatre lights; resolved by shielding probe
Venous pulsationTricuspid regurgitation, high venous pressure → venous "pulsation" misread as arterial
Anaemia (severe)At very low Hb, insufficient absorbing molecules; generally accurate unless Hb <5 g/dL
Melanin (dark skin)May cause slight overestimation of SpO2 - subject of recent concern and regulatory review
KEY VIVA POINT - Racial bias: Studies (including Sjoding et al., NEJM 2020) showed pulse oximeters overestimate SpO2 in patients with dark skin by ~3.5%, potentially masking hypoxemia. This is an active area of regulatory review by FDA.

D. Calibration limit

  • Calibration curves only validated down to SpO2 70% - accuracy below 70% is unknown

8. CLINICAL APPLICATIONS

  • Intraoperative monitoring (mandatory standard ASA/AAGBI)
  • Sedation monitoring (procedural sedation, endoscopy, ICU)
  • PACU / ward monitoring
  • Transport monitoring
  • Newborn screening for critical congenital heart disease (detects pre-ductal vs post-ductal difference)
  • Pulse oximetry during COVID-19: enabled remote monitoring
  • Fluid responsiveness assessment (via PPG waveform variation)


PART B: CAPNOGRAPHY


1. DEFINITIONS

TermDefinition
CapnometryNumerical measurement of CO2 concentration in a gas sample
CapnographyContinuous graphical display of CO2 concentration over time (waveform = capnogram)
End-tidal CO2 (EtCO2 / PETCO2)CO2 concentration at the end of tidal exhalation (approximates alveolar CO2)
Volumetric capnographyCO2 plotted against exhaled volume (rather than time)
Normal EtCO2 = 35-45 mmHg (or 4.7-6.0 kPa)

2. PHYSICAL PRINCIPLE

Infrared (IR) spectroscopy:
  • CO2 absorbs infrared radiation at 4.28 μm wavelength
  • The amount of IR absorbed is proportional to CO2 concentration (Beer-Lambert Law)
  • A light source emits IR; the detector measures transmission; CO2 concentration calculated from absorption

Two system types:

TypeDescriptionPros/Cons
Sidestream (aspirating)Gas sample drawn from circuit via fine tubing to analyser outside the airwayPro: lightweight probe, works with LMA/mask; Con: 5-10 sec delay, sampling tube can block with water/secretions
Mainstream (non-aspirating)Sensor sits directly in the breathing circuitPro: no delay, no sampling tube blockage; Con: heavy sensor on circuit, adds dead space, sensor can get hot
(Miller's Anesthesia 10e, p.11316)

3. THE CAPNOGRAM WAVEFORM - FOUR PHASES

This is the most tested viva topic on capnography:
CO2
(mmHg)
45  |        __________D
    |       /          \
    |      /C           \
    |     /              \
  0 |____/A   B           \E___
    |←expiration→|←inspiration→|
      I  II  III              IV
PhaseNameWhat it represents
Phase I (A-B)Inspiratory baselineDead space gas - no CO2; should be at zero
Phase II (B-C)Expiratory upstrokeMixture of dead space + alveolar gas; rapid CO2 rise
Phase III (C-D)Alveolar plateauMostly alveolar gas; slight upslope due to ongoing CO2 diffusion from different lung units
Point DEnd-tidal CO2The peak CO2 at end of exhalation = EtCO2
Phase IV (D-E)Inspiratory downstrokeFresh gas displaces CO2; rapid return to zero
Normal angle (alpha angle): Junction of Phase II and Phase III; normally ~100°. Widened in obstructive disease.
Beta angle: Junction of Phase III and Phase IV (downstroke); normally ~90°. Increased in rebreathing.

4. PaCO2 - EtCO2 GRADIENT

Q: What is the normal PaCO2 - EtCO2 gradient? What does it mean?
  • Normal gradient = 2-5 mmHg (PaCO2 slightly higher than EtCO2)
  • EtCO2 is always ≤ PaCO2 in healthy lungs
  • Why? Because EtCO2 represents a mixture of gas from different alveoli including those with V/Q mismatch and dead space
The gradient INCREASES when dead space increases:
  • Pulmonary embolism (major cause - reduced perfusion, high V/Q)
  • Pulmonary hypotension
  • Overdistended alveoli (high PEEP)
  • Low cardiac output
  • Haemorrhage / hypovolaemia
Alveolar Dead Space Fraction:
AVDSf = (PaCO2 - EtCO2) / PaCO2
(Miller's Anesthesia 10e, p.11316)

5. CAUSES OF CHANGES IN EtCO2 - COMPLETE TABLE

A. INCREASED EtCO2

CauseMechanism
Hypoventilation↓ minute volume → CO2 accumulates
RebreathingExhausted soda lime, incompetent inspiratory valve
Malignant hyperthermiaMassive ↑ CO2 production - often first/most sensitive sign
Fever / sepsis / shivering↑ metabolic rate → ↑ CO2 production
Tourniquet releaseSudden flush of accumulated CO2
NaHCO3 administrationCO2 released from buffering
Thyrotoxicosis↑ metabolic rate
Laparoscopy (CO2 insufflation)Absorption of CO2 from peritoneum
Light anaesthesia (pain/response)↑ sympathetic activity, ↑ metabolism

B. DECREASED EtCO2

CauseMechanism
Hyperventilation↑ CO2 elimination
Pulmonary embolism↑ dead space → less alveolar CO2
Cardiac arrest / circulatory collapseNo pulmonary perfusion → near-zero EtCO2
Hypothermia↓ metabolic rate, ↓ CO2 production
Severe haemorrhage / hypovolaemia↓ pulmonary perfusion
Air embolism↑ dead space
Pulmonary hypoperfusion (any cause)↑ V/Q mismatch

C. ABSENT EtCO2

CauseMechanism
Oesophageal intubationMost critical - no CO2 from stomach (though transient CO2 from carbonated drinks)
Complete circuit disconnectNo gas sampling
Complete circuit obstructionNo gas flow
Cardiac arrestNo pulmonary blood flow
Blocked sidestream sampling tubeWater/secretions

6. ABNORMAL WAVEFORM PATTERNS - VIVA FAVOURITES

Pattern 1: Slanted / shark-fin upstroke (Phase II-III slope increased)

     /\
    /  \
   /    \
  /      \___
  • Obstructive airway disease (asthma, COPD, bronchospasm)
  • Different lung units empty at different rates → prolonged, sloping plateau
  • Increased alpha angle

Pattern 2: Elevated baseline (Phase I not returning to zero)

     _____
    /     \
___/       \_____  ← does not return to 0
  • Rebreathing of exhaled CO2
  • Exhausted soda lime
  • Stuck/incompetent inspiratory valve
  • Insufficient fresh gas flow (esp. Mapleson circuits)

Pattern 3: Sudden drop to zero

___|||||||||_____  (suddenly flat at 0)
  • Oesophageal intubation (most critical diagnosis)
  • Extubation / disconnection
  • Complete circuit obstruction
  • Cardiac arrest

Pattern 4: Exponential decrease toward zero

     ↓↓↓
   ...becoming smaller
  • Pulmonary embolism (sudden) or decreasing cardiac output
  • Cardiac arrest (gradual decline)

Pattern 5: Suddenly elevated then decreasing

    ↑↑
   ...then slowly falling
  • Malignant hyperthermia onset
  • CO2 insufflation starting (laparoscopy)
  • Tourniquet release
  • NaHCO3 bolus

Pattern 6: Cardiogenic oscillations (notches on plateau)

___/^\__/^\_____
  • Heart motion transmitted to lungs during cardiac surgery
  • Normal variant with slow RR and strong cardiac output

Pattern 7: Cleft/notch during Phase III

  • Patient taking spontaneous breath during IPPV (curare cleft)
  • Indicates neuromuscular block wearing off or patient fighting ventilator

7. CLINICAL USES OF CAPNOGRAPHY

UseDetails
Confirm ETT in tracheaStandard of care - 6 consecutive waveforms confirm tracheal placement; zero waveform = oesophageal
Monitor ventilation adequacyEtCO2 guides ventilator settings
Detect disconnection / circuit failureSudden drop to zero
Detect malignant hyperthermiaUnexplained sudden rise in EtCO2
Pulmonary embolism detectionSudden decrease in EtCO2 with clinical deterioration
CPR quality assessmentEtCO2 during CPR correlates with cardiac output; EtCO2 >10 mmHg suggests adequate CPR
ROSC during CPRSudden rise in EtCO2 during CPR = return of spontaneous circulation (ROSC)
Assess NMB reversalCurare cleft = spontaneous breathing returning
Dead space estimationAVDSf calculation
Fluid responsiveness (volumetric)Changes in Bohr dead space with PEEP titration
Sedation monitoringNon-intubated patients (via nasal/oral sampling cannula)
Rebreathing detectionBaseline elevation

8. EtCO2 IN SPECIAL SITUATIONS

Cardiac Arrest

  • Before ROSC: EtCO2 <10 mmHg = inadequate CPR / very poor prognosis
  • Sudden rise to >40 mmHg during CPR = ROSC (most reliable non-invasive sign)
  • If EtCO2 persistently <10 mmHg after 20 min of good CPR = consider stopping resuscitation (prognostic marker)

Paediatric patients

  • Same principles apply
  • EtCO2-PaCO2 gradient may be slightly larger due to V/Q immaturity in neonates
  • Sidestream capnography preferred in small children (lightweight)
  • Accuracy reduces with very high respiratory rates and small tidal volumes (gas mixing in sidestream tubing)
  • Time-based capnography less accurate at very high RRs (>40/min) - gaps between breaths too short to develop clear plateau

Laparoscopy

  • CO2 absorbs from peritoneum → EtCO2 rises by 5-10 mmHg
  • Increase minute ventilation by 10-15% at start
  • Subcutaneous emphysema → very high EtCO2 even with hyperventilation
  • Steep Trendelenburg → ↑ airway pressure + atelectasis → ↑ EtCO2

Malignant Hyperthermia

  • EtCO2 rise is the earliest and most sensitive indicator - precedes temperature rise
  • Often >80-100 mmHg despite maximal ventilation
  • Treat with dantrolene + cooling + hyperventilation

9. VOLUMETRIC CAPNOGRAPHY

Plots CO2 against exhaled volume (rather than time):
  • Provides direct Bohr dead space measurement
  • Helpful for PEEP optimisation (titrate PEEP to minimise dead space without overdistension)
  • Can demonstrate response to bronchodilator therapy
  • Available on modern ICU ventilators (Miller's Anesthesia 10e, p.11317)

10. TRANSCUTANEOUS CO2 (TcCO2)

  • Probe heats skin → dilates capillaries → CO2 diffuses through skin → measured by IR sensor
  • Continuous non-invasive PaCO2 estimate
  • Useful in high-frequency ventilation where capnography inadequate
  • Requires calibration against blood gas; drift over time
  • Less accurate in: low cardiac output, thick skin/obesity, cyanotic heart disease (Miller's Anesthesia 10e, p.11317)

11. COMPARISON TABLE: PULSE OXIMETRY vs CAPNOGRAPHY

FeaturePulse OximetryCapnography
What it measuresO2 saturation (SpO2)CO2 concentration (EtCO2)
What it monitorsOxygenationVentilation
Normal valuesSpO2 >95% (>92% in COPD)EtCO2 35-45 mmHg
Response time~6 seconds (ear fastest)Sidestream: 5-10 sec; mainstream: near-instant
First sign of hypoventilationLate (SpO2 falls only after significant O2 reserve depleted)Early (EtCO2 rises immediately)
Confirms ETT placementNoYes (6 waveforms)
Detects oesophageal intubationNo (SpO2 takes time to fall)Yes (immediate - no waveform)
Detects MHNoYes (early EtCO2 rise)
Detects PEIndirect (SpO2 fall)Yes (EtCO2 falls)
Detects ROSCIndirectYes (sudden EtCO2 rise)
Circuit disconnectNoYes (EtCO2 → 0)
Main limitationDoes NOT detect ventilation failure until SpO2 fallsEtCO2 ≠ PaCO2 when dead space increased

QUICK-RECALL VIVA CARD

PULSE OXIMETRY
- Wavelengths: 660 nm (red) + 940 nm (infrared)
- AC (pulsatile) = arterial; DC (steady) = everything else
- COHb: falsely HIGH SpO2 (660 nm same as O2Hb)
- MetHb: SpO2 drifts to 85% regardless
- Methylene blue: falsely LOW SpO2
- Vasoconstriction → no signal
- OHC flat top: cannot detect hyperoxia
- SpO2 90% ≈ PaO2 60 mmHg

CAPNOGRAPHY
- Phases: I=dead space, II=upstroke, III=plateau, IV=downstroke
- Normal EtCO2: 35-45 mmHg; gradient PaCO2-EtCO2 = 2-5 mmHg
- Gradient INCREASES with: PE, ↓ cardiac output, overdistension
- Sudden EtCO2 to ZERO: oesophageal intubation / disconnection / cardiac arrest
- Sudden EtCO2 RISE: MH / hypoventilation / laparoscopy / NaHCO3
- Sudden EtCO2 DROP: PE / haemorrhage / ↓ cardiac output
- CPR: EtCO2 >10 = adequate; sudden rise = ROSC
- Shark-fin: obstructive disease
- Elevated baseline: rebreathing (exhausted soda lime / bad valve)
Sources: Miller's Anesthesia 10e (Ch.37, p.5449-5470; Ch.31, p.11316-11317); Barash Clinical Anesthesia 9e; Morgan & Mikhail Clinical Anesthesiology 7e

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Pulse Oximetry & Capnography: Relevant Images with Explanations


PULSE OXIMETRY IMAGES


1. Oxyhemoglobin Dissociation Curve (OHC)

(Miller's Anesthesia 10e, Fig. 37.2)
Oxyhemoglobin Dissociation Curve
Key teaching points from this curve:
  • Flat upper portion (PaO2 >70 mmHg): SpO2 cannot distinguish between normal and hyperoxic states - dangerous in neonates (retinopathy risk)
  • Steep lower portion: Once SpO2 starts falling, PaO2 is already critically low - pulse oximetry gives late warning of deterioration
  • SpO2 90% = PaO2 ~60 mmHg (onset of respiratory failure)
  • Left shift (Alkalosis, Hypocarbia, Hypothermia, COHb, Fetal Hb): higher affinity, less O2 release to tissues
  • Right shift (Acidosis, Hypercarbia, Hyperthermia, ↑2,3-DPG): lower affinity, better O2 delivery to tissues

2. Haemoglobin Absorption Spectra - The Physics of Pulse Oximetry

(Miller's Anesthesia 10e, Fig. 37.3A & 37.3B)
Haemoglobin Absorption Spectra
Key teaching points:
  • Panel A (left): All 5 Hb species shown across visible spectrum (500-700 nm)
  • Panel B (right): The two dashed vertical lines = the two wavelengths used by pulse oximeters: 660 nm (red) and 940 nm (infrared)
  • At 660 nm: Reduced (deoxy) Hb absorbs MUCH more than OxyHb - so well-oxygenated blood transmits more red light
  • At 940 nm: OxyHb absorbs more than reduced Hb - infrared discriminates in the opposite direction
  • Critical viva point: At 660 nm, COHb (carboxyhaemoglobin) has nearly the same extinction coefficient as O2Hb (red line ≈ blue line at 660 nm) - this explains why CO poisoning produces falsely high SpO2
  • MetHb (orange) has high absorption at BOTH wavelengths - this drives the R ratio toward 1.0, which on the calibration curve corresponds to ~85% SpO2, regardless of true saturation

3. AC/DC Pulse Principle - How Arterial Blood is Isolated

(Miller's Anesthesia 10e, Fig. 37.4)
AC-DC Pulse Principle
Key teaching points:
  • The DC (non-pulsatile) component = background absorption from tissue, venous blood, capillary blood - constant, ignored
  • The AC (pulsatile) component at the top = absorption that changes with each heartbeat = arterial blood only
  • The pulse oximeter calculates the ratio R = (AC660/DC660) / (AC940/DC940) - this ratio isolates arterial saturation from all background tissue
  • This is why poor peripheral perfusion (shock, hypothermia, vasoconstriction) causes loss of signal - the AC component disappears when there is no pulsatile flow

4. Calibration Curve: R-ratio to SpO2

(Miller's Anesthesia 10e, Fig. 37.5)
SpO2 Calibration Curve
Key teaching points:
  • The R ratio (x-axis) is mathematically derived from AC and DC light absorption at both wavelengths
  • The SpO2 (y-axis) is read off this empirically-derived calibration curve built into each oximeter
  • Dashed lines at R=1.0, SpO2=85%: When R=1 (equal absorption at both wavelengths, as happens with MetHb), SpO2 reads 85% - this is the classic MetHb trap
  • Calibration was performed only in volunteers down to SpO2 70% - accuracy below 70% is unknown and unreliable
  • Each manufacturer has their own proprietary calibration curve

5. Photoplethysmogram (PPG Waveform)

(Miller's Anesthesia 10e, Fig. 37.6)
Photoplethysmogram
Key teaching points:
  • The pulse oximeter trace is also a photoplethysmograph - it shows arterial blood volume changes beat to beat
  • Left section (60s scale): tight, small amplitude = fast heart rate
  • Middle/right (3s scale): larger waves with respiratory variation in amplitude (ΔPOP)
  • Point B: ventilation stopped - respiratory variation disappears
  • Clinical use: Respiratory variation in PPG amplitude predicts fluid responsiveness in mechanically ventilated patients (PVI - Pleth Variability Index)
  • Large respiratory swings in PPG = patient likely fluid-responsive


CAPNOGRAPHY IMAGES


6. Normal Capnogram - Phases Labeled (Simple View)

Normal Capnogram Phases
Phases:
  • Phase 1 (blue, baseline): Inspiration - dead space gas, CO2 = 0
  • Phase 2 (pink, upstroke): Expiratory upstroke - mixing of dead space + alveolar gas
  • Phase 3 (red, plateau): Alveolar plateau - represents alveolar gas CO2
  • EtCO2 (green circle): The peak value at end of exhalation = measured end-tidal CO2
  • Phase 4 (yellow, downstroke): Inspiratory downstroke - fresh gas washes out CO2

7. Normal Capnogram - Detailed Anatomy

(Deranged Physiology)
Capnogram Anatomy
Key teaching points:
  • Transitional part (Phase II): Mixing of dead space and alveolar gas - the upstroke represents washout of anatomical dead space
  • Alveolar plateau (Phase III): Average alveolar CO2 concentration - should be nearly flat (slight upslope is normal)
  • Alpha angle: Transition from Phase II to III - represents the quality of alveolar emptying. Widened (>110°) in obstructive disease (bronchospasm, COPD) because different lung units empty at different times
  • End-tidal CO2: Measured at the peak of Phase III = maximal alveolar CO2 concentration
  • CO2 must return to zero on inspiration - if it does not, there is rebreathing (exhausted soda lime or faulty inspiratory valve)

8. Normal Capnogram with Phase Labels (Classic Textbook Style)

Classic Capnogram Phases I-III
Key teaching points:
  • Phase I: Respiratory baseline at 0 mmHg - dead space gas, no CO2
  • Phase II: Expiratory upstroke - steep rise as alveolar gas begins to exit
  • Phase III: Alveolar plateau - EtCO2 measured at the highest point
  • Phase 0: Inspiratory downstroke - rapid return to zero as fresh gas enters
  • Normal EtCO2 = 35-45 mmHg; Normal PaCO2-EtCO2 gradient = 2-5 mmHg

ABNORMAL WAVEFORM PATTERNS SUMMARY TABLE

PatternWhat it looks likeCause
Shark fin / obstructiveSlanted, prolonged upstroke; Phase III slopes upwardBronchospasm, COPD, asthma
Elevated baselineDoes not return to zero on inspirationRebreathing - exhausted soda lime, faulty inspiratory valve
Sudden drop to zeroFlat line at zeroOesophageal intubation, disconnection, circuit obstruction, cardiac arrest
Sudden rise then high plateauAbrupt EtCO2 increaseMalignant hyperthermia, hypoventilation, tourniquet release, laparoscopy
Gradual decreaseEtCO2 progressively fallsPulmonary embolism, decreasing cardiac output, haemorrhage
Curare cleft (notch in plateau)Notch/dip in Phase III plateauReturn of spontaneous breathing - NMB wearing off
Cardiogenic oscillationsSmall oscillations on plateauHeartbeat transmitted to lungs - strong cardiac output, slow RR
Sudden rise during CPREtCO2 jumps from <10 to >40 mmHgROSC - return of spontaneous circulation

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