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TOPIC 1: RESIDUAL NEUROMUSCULAR BLOCKADE (RNMB)

Definition

Note: The threshold was revised from <0.7 (pre-1990s) to <0.9 (late 1990s) as studies showed pharyngeal dysfunction persists even at TOF ratios of 0.7-0.9.

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Incidence

• Reported in 20-40% of patients in most studies
• One study found 56% incidence on PACU arrival in the pre-sugammadex era (Miller's Anesthesia, 10e)
• Up to 40-60% of patients who received neostigmine reversal still have RNMB at extubation (Barash, 9e)
• Even with intermediate-acting NMBDs (vecuronium, rocuronium, atracurium), a significant proportion recover incompletely

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Why RNMB is Dangerous - Pathophysiology

Key Concept: Differential Muscle Recovery

• The diaphragm recovers from NMB before the pharyngeal muscles
• This means adequate tidal volume and ETCO2 can be present while the upper airway is still compromised
• A patient may appear to ventilate adequately through an ETT but cannot protect the airway after extubation

Clinical Consequences at Various TOF Ratios

Adverse Effects at TOF < 0.90 (Awake Volunteer Studies)

• Impaired pharyngeal and upper esophageal sphincter function
• Increased risk of aspiration of gastric contents
• Upper airway obstruction
• Impaired hypoxic ventilatory response
• Unpleasant sensations of diplopia, blurred vision, facial weakness, and generalized weakness (Miller's, 10e)

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Factors Contributing to Prolonged/Residual NMB

Drug-Related Factors

• Inhaled anesthetic agents (potentiate NMB)
• Local anesthetics (lidocaine)
• Cardiac antiarrhythmics (procainamide)
• Antibiotics: polymyxins, aminoglycosides, clindamycin, metronidazole, tetracyclines
• Calcium channel blockers
• Corticosteroids
• Dantrolene

Metabolic and Physiologic States

• Hypermagnesemia - inhibits ACh release at NMJ
• Hypocalcemia
• Hypothermia - decreases metabolism and elimination of NMBDs, also impairs twitch monitoring
• Respiratory acidosis - limits ability of anticholinesterases to reverse NMB
• Hepatic or renal failure (altered pharmacokinetics)
• Myasthenia gravis / Lambert-Eaton syndrome

Cholinesterase-Related

• Reduced plasma cholinesterase activity (prolongs succinylcholine and mivacurium)
• Atypical (dibucaine-resistant) pseudocholinesterase variants
• Disease states causing reduced cholinesterase: hepatic disease, uremia, malnutrition, pregnancy

Patient Factors

• Advanced age (reduced renal/hepatic clearance)
• NMBD overdose
• Long-acting NMBDs (pancuronium) vs. intermediate-acting (rocuronium, vecuronium, atracurium)

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Detection of RNMB

Why Clinical Tests Fail

• Clinical tests (5-second head lift, hand grip, tongue depressor test) are unreliable - they require only 33% receptor occupancy to be performed adequately
• Subjective (qualitative) TOF fade cannot be detected by touch or vision until TOF ratio falls below 0.30-0.40
• Therefore, a patient may have significant residual block (TOF 0.40-0.89) with no clinically detectable fade (Miller's, 10e)

Gold Standard: Quantitative Monitoring

• EMG (Electromyography) - most accurate; safe to extubate at TOF > 0.9
• MMG (Mechanomyography) - research gold standard; TOF > 0.9
• AMG (Acceleromyography) - most commonly used in clinical practice; extubate at TOF > 1.0 (normalized) due to systematic overestimation
• Quantitative monitoring is the only reliable method to confirm full recovery and guide reversal drug dosing

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Reversal of RNMB

Anticholinesterases (Neostigmine)

• Mechanism: inhibit acetylcholinesterase → increased ACh at NMJ → competes with NDNMB
• Most effective when TOF count = 4 with no fade (minimal block)
• Neostigmine dose: 20-70 mcg/kg
• Limitations:
  • Ceiling effect - cannot reverse deep block
  • Muscarinic side effects require glycopyrrolate/atropine co-administration
  • Paradoxical "neostigmine weakness" at high doses (desensitization block)

Sugammadex (Selective Relaxant Binding Agent)

• Mechanism: encapsulates rocuronium/vecuronium (aminosteroid NMBDs) forming a water-soluble complex - no receptor-level effect
• Can reverse even deep block (PTC 1-2)
• Dose:
  • Deep block (PTC 1-2): 16 mg/kg
  • Moderate block (TOF 1-2): 4 mg/kg
  • Shallow block (TOF ≥ 2): 2 mg/kg
• Preferred agent in high-risk patients (obese, COPD, myasthenia gravis)
• Does not work for benzylisoquinolinium NMBDs (atracurium, cisatracurium, mivacurium)

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Management in PACU

• Any patient who received NMBDs and presents with respiratory distress/agitation - suspect RNMB first
• Re-administer quantitative monitoring
• If confirmed: administer sugammadex (or neostigmine if AMG monitoring is available and block is minimal)
• Supportive airway measures until reversal confirmed

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TOPIC 2: NEUROMUSCULAR MONITORING (NM Monitoring)

Purpose

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Peripheral Nerve Stimulator (PNS) - Setup

Standard Setup

• Nerve stimulated: Ulnar nerve (stimulate at wrist, monitor adductor pollicis)
• Alternative sites: Facial nerve (orbicularis oculi - correlates with laryngeal/diaphragm, earlier recovery), posterior tibial nerve
• Electrode placement: Two surface electrodes over the ulnar nerve at the wrist
• Current: 10-60 mA supramaximal stimulus (20% above threshold to ensure all fibers are activated)

Why Adductor Pollicis?

• Easy to monitor
• Recovery at adductor pollicis closely reflects recovery of pharyngeal muscles
• Laryngeal and diaphragmatic muscles recover faster than adductor pollicis
• Therefore: TOF ≥ 0.9 at adductor pollicis = pharyngeal recovery adequate (Miller's, 10e)

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Stimulation Patterns

1. Train-of-Four (TOF) Stimulation

• 4 supramaximal stimuli at 2 Hz (0.5 second intervals)
• TOF count: Number of responses (1-4) - used during deep block
• TOF ratio (T4/T1): Used to quantify shallow/residual block
  • T4/T1 = 1.0 → no block
  • T4/T1 < 0.9 → RNMB
  • T4/T1 = 0 with T1 still present → 75-92% receptor occupancy

2. Single Twitch Stimulation

• Single stimuli at 0.1 Hz or 1 Hz
• Compares height of twitch response to baseline control
• Useful for onset and deep block monitoring
• T1 (first twitch of TOF) = T1% control height

3. Tetanic Stimulation

• 50 Hz or 100 Hz sustained stimulation for 5 seconds
• Detects fade during partial block
• Painful - only used in anesthetized patients
• Followed by post-tetanic facilitation

4. Post-Tetanic Count (PTC)

• After 50 Hz tetanus (5 s) → wait 3 seconds → deliver single stimuli at 1 Hz
• Count number of responses
• Used when no TOF responses are present (deep block, intubating conditions)
• PTC 1-2 = intense/deep block; PTC > 10 → expect first TOF twitch within minutes

5. Double-Burst Stimulation (DBS)

• Two short (60 ms) bursts of 50 Hz tetanic stimuli, 750 ms apart
• More sensitive than TOF for detecting fade manually
• Fade with DBS = TOF ratio < 0.6 approximately
• Still inferior to quantitative monitoring

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Types of Neuromuscular Monitors

Qualitative (Subjective) Monitors

• Peripheral Nerve Stimulator (PNS)
• Provides tactile/visual assessment only
• Cannot detect fade when TOF ratio > 0.3-0.4
• Not acceptable as sole monitor for confirming full recovery (Miller's, 10e)

Quantitative Monitors

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Depth of Block Classification

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Key Clinical Points for the Resident

1. Always use quantitative monitoring - qualitative PNS alone is insufficient to confirm recovery
2. Calibrate/normalize the AMG before NMBD administration (baseline T1 = 100%)
3. Time neostigmine administration when TOF count = 4 (minimal block) for maximum efficacy
4. Sugammadex can reverse any depth of aminosteroid block and should be the first choice when in doubt
5. Respiratory acidosis (common in PACU) limits neostigmine efficacy by decreasing motor nerve terminal ACh release

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TOPIC 3: INVASIVE PRESSURE MONITORING (Invasive Arterial Blood Pressure)

Indications

• Current or anticipated haemodynamic instability (major vascular, cardiac, thoracic surgery)
• Beat-to-beat BP regulation required (end-organ disease, haemorrhage risk)
• Need for frequent arterial blood gas or blood sampling
• Use of potent vasoactive drugs (vasopressors, nitroprusside, volatile agents for deliberate hypotension)
• Patient with severe HTN, pulmonary hypertension, or cardiac failure
• Procedures in extreme positions (prone, sitting)

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Sites of Arterial Cannulation

Allen's Test

• Pre-cannulation assessment of ulnar collateral flow to the hand
• Method: exsanguinate hand, compress both arteries, release ulnar, watch flushing of thumb
  • < 5 sec: adequate collateral - safe to cannulate radial
  • 5-10 sec: equivocal

  • 10 sec: inadequate - do NOT cannulate radial

• Limitation: Allen's test is unreliable and many practitioners routinely avoid it; Doppler/pulse oximetry-based collateral assessment is preferred (Morgan's, 7e)

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The Catheter-Tubing-Transducer System

Principle

• Arterial pulse wave is transmitted via fluid-filled tubing to a strain-gauge transducer (Wheatstone bridge)
• Mechanical energy (pressure wave) → electrical signal
• Requires adequate frequency response and damping

Key Physical Concepts

Natural Frequency (Resonant Frequency)

• The system must have a natural frequency exceeding the highest harmonics of the arterial waveform (approximately 16-24 Hz)
• The arterial waveform contains harmonics up to 10-15 Hz
• Most transducers have natural frequencies >200 Hz, but tubing, stopcocks, and air reduce this

Damping Coefficient (β)

• Optimal: β = 0.6-0.7 (critical/optimal damping)
• Underdamped (β < 0.6): Resonance/overshoot → falsely high systolic, falsely low diastolic (MAP relatively accurate)
• Overdamped (β > 0.7): Sluggish system → falsely low systolic, falsely high diastolic (MAP relatively accurate)

Causes of Overdamping

• Air bubbles in the tubing
• Blood clot at catheter tip
• Kinking of catheter or tubing
• Excessive tubing length or multiple stopcocks

How to Optimize the System

• Use short, stiff, low-compliance tubing
• Minimize stopcocks
• Remove all air bubbles
• Flush catheter regularly (pressurized bag at 300 mmHg)
• Perform fast-flush (square wave) test to assess system dynamic response

Zeroing and Levelling

• Transducer levelled at the phlebostatic axis (4th intercostal space, mid-axillary line) = right atrium level
• For neurosurgery/sitting position: level at external auditory meatus (Circle of Willis)
• Re-zero to atmospheric pressure before each set of measurements

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Arterial Waveform Interpretation

Normal Waveform Components

• Anacrotic notch - brief notch on upstroke (aortic valve opening)
• Systolic peak - ventricular ejection
• Dicrotic notch - aortic valve closure (represents systole/diastole transition)
• Diastolic run-off - diastolic decay

Waveform Changes with Position

• Systolic pressure increases peripherally (radial > brachial > aortic) due to reflected waves
• MAP is relatively constant throughout the arterial tree
• Brachial artery provides least distorted waveform of peripheral sites (Morgan's, 7e)

Pulse Pressure Variation (PPV) and Stroke Volume Variation (SVV)

• Derived from arterial waveform during controlled mechanical ventilation
• PPV > 13% or SVV > 10-13% predicts fluid responsiveness (requires regular rhythm, TV ≥ 8 mL/kg)

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Complications of Arterial Cannulation

• Thrombosis (most common) - distal ischemia
• Haematoma at insertion site
• Infection - bacteraemia, septic arteritis
• Pseudoaneurysm - especially femoral
• Arteriovenous fistula
• Nerve injury - especially axillary/brachial
• Accidental intra-arterial drug injection - catastrophic; causes vasospasm and distal ischaemia
• Retrograde air embolism (especially axillary - can reach cerebral circulation)

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TOPIC 4: SpO₂ (PULSE OXIMETRY)

Definition

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Physical Principles

Beer-Lambert Law

• The absorbance of light by a solution is proportional to the concentration of the absorbing substance and the path length through the solution
• Oxyhaemoglobin (HbO₂) and deoxyhaemoglobin (Hb) have different absorption spectra

Two Wavelengths of Light

• Two LEDs transmit light through a pulsatile vascular bed (finger, earlobe, forehead)
• A photodetector on the opposite side measures transmitted light
• The ratio of red to infrared absorption is calculated

Pulsatile Signal Discrimination

• The device distinguishes:
  • AC component (pulsatile arterial blood) - this is what is measured for SpO₂
  • DC component (venous blood, tissue, bone) - this is subtracted as background
• This is why a pulsatile waveform is essential for oximetry function (Barash, 9e)

Empirical Calibration

• Pulse oximeters are calibrated against healthy volunteers with known SaO₂ (from co-oximetry) across a range of 70-100%
• Below 70%, the calibration is extrapolated and less reliable

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Clinical Use

Normal Values

• SpO₂ ≥ 95% considered normal
• SpO₂ 90-94% = mild desaturation, warrants attention
• SpO₂ < 90% = significant hypoxaemia (PaO₂ ≈ 60 mmHg - on the steep part of ODC)
• SpO₂ < 85% = severe hypoxaemia requiring urgent intervention

Correlation with Oxyhaemoglobin Dissociation Curve

• SpO₂ is a good indicator of hypoxaemia on the steep part of the curve (SaO₂ 70-90%)
• On the flat part (SaO₂ > 95%, PaO₂ > 80 mmHg), SpO₂ changes minimally despite large PaO₂ changes - SpO₂ cannot detect hyperoxia
• Acidosis, hypercapnia, hyperthermia → right shift → decreased SaO₂ for given PaO₂ (Barash, 9e)

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Limitations of Pulse Oximetry (VERY HIGH YIELD)

1. Motion Artifact

• Patient movement creates a spurious AC signal
• Causes false low or fluctuating readings

2. Poor Peripheral Perfusion

• Vasoconstriction (hypothermia, shock, vasopressors) - no adequate pulsatile signal
• During CPB - continuous non-pulsatile flow → oximeter fails
• Ventricular assist devices (VADs) with continuous flow → probe may fail

3. Dysfunctional Haemoglobins (Most Clinically Important Limitation)

• To detect dysfunctional haemoglobins: use co-oximetry (ABG analysis with CO-oximeter measures HbO₂, HHb, COHb, MetHb separately)

4. Dyes and Pigments

• Methylene blue → falsely low SpO₂ (transiently, 1-2 minutes)
• Indocyanine green, indigo carmine → may cause transient falsely low readings
• Nail varnish (especially blue/green/black) → may falsely lower SpO₂
• Dark skin pigmentation → slight overestimation at lower saturations in some studies

5. Ambient Light Interference

• High-intensity surgical lights, fluorescent lights can interfere
• Solution: cover probe with opaque material

6. Anaemia

• Does NOT cause falsely low SpO₂ directly - oximetry measures saturation, not content
• However, severe anaemia with normal SpO₂ can still mean critically low oxygen delivery (DO₂ = CO × CaO₂)

7. Late Indicator of Apnoea/Hypoventilation

• In a patient breathing supplemental oxygen, apnoea may continue for several minutes before SpO₂ falls
• This is the most clinically dangerous limitation
• SpO₂ is a poor indicator of ventilation adequacy - use capnography for that (Barash, 9e)

8. Venous Pulsation

• Tricuspid regurgitation, constrictive pericarditis → venous pulsation → contamination of AC signal

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SpO₂ vs SaO₂

• SpO₂ from pulse oximetry ≈ SaO₂ from ABG co-oximetry within ±2% in normal conditions
• Divergence occurs with: dysfunctional Hb, poor perfusion, pigmentation issues

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TOPIC 5: NON-INVASIVE CARDIAC/CARDIAC OUTPUT MONITORING

Overview

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Classification of CO Monitoring

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1. Pulse Contour/Pulse Wave Analysis

Principle

• CO is derived from analysis of the arterial pressure waveform (requires arterial catheter)
• Based on ventriculo-arterial coupling: pulse pressure and contour are determined by LV stroke volume and arterial impedance
• By integrating the systolic area (beginning of systole to dicrotic notch) divided by aortic impedance → stroke volume → CO

Types by Calibration

• Externally calibrated (transpulmonary thermodilution - PiCCO; lithium dilution - LiDCO): more accurate, require periodic recalibration
• Internally calibrated (using biometric/demographic data): e.g., FloTrac/Vigileo
• Uncalibrated (PRAM - Pressure Recording Analytical Method): uses waveform morphology alone

Additional Variables Derived

• Pulse Pressure Variation (PPV) - predicts fluid responsiveness
• Stroke Volume Variation (SVV) - predicts fluid responsiveness
• Valid only in controlled mechanical ventilation, TV ≥ 8 mL/kg, regular rhythm

Limitations

• Inaccurate with arrhythmias, aortic regurgitation, IABP, severe vasoconstriction, over/underdamped traces
• PPV/SVV invalid in spontaneously breathing patients, AF, or low lung compliance (Miller's, 10e)

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2. Esophageal Doppler Monitor (EDM)

Principle

• Doppler probe inserted ~35 cm into esophagus
• Measures Doppler frequency shift of blood flow in descending thoracic aorta
• Aortic blood flow velocity integrated over time → stroke distance → stroke volume → CO

Key Variables

• FTc (Corrected Flow Time): Duration of systolic flow corrected for heart rate; normal 330-360 ms; ↓ in hypovolaemia
• Peak Velocity (PV): Reflects contractility
• Stroke Volume / CO

Limitations

• Measures only descending aorta flow (~70% of total CO) → correction factor applied (×1.4)
• Factor inaccurate in pregnancy, aortic cross-clamping, post-CPB
• Aortic diameter assumed constant (not measured continuously)
• Position-sensitive - probe movement = measurement error
• Requires intubated/sedated patient (Miller's, 10e)

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3. Thoracic Bioimpedance / Bioreactance

Principle

• Small alternating current passed through the thorax via surface electrodes
• Changes in thoracic electrical impedance with each heartbeat reflect changes in aortic blood volume
• Bioreactance (newer): measures phase shifts of the AC signal rather than impedance changes - less sensitive to respiratory artifact

Limitations

• Affected by: pleural effusions, pulmonary oedema, electrode placement, arrhythmias, obesity, movement artifact
• Least accurate of CO monitoring methods in critically ill patients

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4. Finger Cuff Photoplethysmography (Nexfin / ClearSight / CNAP)

Principle

• Finger cuff with built-in LED light source continuously tracks arterial BP waveform using volume-clamp method
• From continuous BP waveform, CO is derived using pulse contour analysis
• Completely non-invasive

Limitations

• Inaccurate in severe vasoconstriction, peripheral vascular disease, peripheral oedema, circulatory shock, high-dose vasopressors (Miller's, 10e)

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5. Transthoracic Echocardiography (TTE) / Transesophageal Echocardiography (TEE)

Principle

• Doppler-based CO: CO = LVOT velocity-time integral × LVOT area × HR
• TEE additionally provides: direct visualisation of cardiac chambers, wall motion abnormalities, filling, pericardial effusion, valve function

Advantages of TEE in Anaesthesia

• Gold standard for intraoperative cardiac assessment
• Assesses preload (LV end-diastolic area), contractility, regional wall motion
• Detects air embolism, aortic dissection, hypovolaemia vs. cardiac failure

Limitations of TTE

• Operator-dependent
• Intermittent, not continuous
• Poor windows in obese, COPD, post-sternotomy patients

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6. Partial CO₂ Rebreathing (NICO)

• Uses the Fick principle for CO₂ instead of O₂
• Periodic brief dead-space increase induces partial rebreathing; change in ETCO₂ used to calculate CO
• Measures pulmonary capillary blood flow (not total CO - requires shunt correction)
• Requires intubation; relatively contraindicated in raised ICP or pulmonary hypertension (Miller's, 10e)

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Summary Table: Non-Invasive CO Monitoring Comparison

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