Monitoring during Anaesthesia Flashcards
What is monitored during anaesthesia?
Circulation
- ECG: 3 lead (lead II for rhythm), or 5 lead (lead II + lead V for waveform)
- BP (NIBP, IBP)
- CVP: Normally 3 mmHg; 5-6 in ventilated patients. Proxy for intravascular volume status (fluid status)
- Pulmonary artery catheter: Becoming out of favour, because its function of monitoring cardiac output can be done by CO monitor or IA line (calculating area under graph)
- Cardiac output monitor
- Echocardiogram (2DE – TTE, TEE)
Ventilation
- Capnography 🡪 breathing system disconnection, ventilator failure alarm
- Spirometry
Oxygenation
- O2 gas analyser
- Pulse oximetry (SpO2)
Gas analyser
- O2, anaesthetic gases, N2O
- End tidal vs inspiratory values
Nerve stimulator
(train of four)
- Measures extent of neuromuscular blockade (NMB)
- Should not be twitching
- Can be set at a firing rate, e.g. 4, then monitor for number of twitches
- Some surgeries require 0
Urine output
- Surrogate for mean arterial pressure (MAP)
- Reflective volume status or BP issues
Neurological function
- Mental status
- BIS (bispectral index) EEG – depth of anaesthesia is measured as a single number. Ideal range of sedation is between 40-60. For use in TIVA.
- Somatosensory evoked potential (SSEP), motor evoked potential (MEP)
Temperature
- Nasopharyngeal probe (NP probe), oropharyngeal probe
- Important to prevent hypothermia, which can cause AMI
What is the ECG criteria for diagnosis of ischaemia in anaestised patients?
ST depression (any change > 1 mm is significant): Can be upsloping, horizontal, or downsloping
- upsloping ST segment: 2mm depression, 80ms after J point
- Horizontal ST segment: 1mm depression, 60-80ms after J point
- Downsloping ST segmentL 1mm from PQ junction to top of curve
ST elevation
T wave inversion
What is the intra op management of myocardial ischaemia in anaestised patients?
Increase O2 supply
- RBC transfusion (especially if blood loss is significant)
- Nitrate GTN patch
- ? Increase O2 flow/increase FiO2 (of questionable utility of Hb is sufficient, and not useful if SpO2 is already 100%)
Decrease O2 demand: Reduce HR (by ensuring normotension; check BP to exclude hypotension causing tachycardia)
Reduce operative time (ask surgeon to hurry)
What are sources of error for non -invasive BP?
- Wrong cuff size: large cuff under reads BP, small cuff over reads BP
- Wrong cuff site
- Patient movement/shivering 🡪 prolongs cuff inflation times
- Arrhythmia, especially AFib 🡪 HR too fast + irregular pulse volume measured
What are the sites of intra-arterial cannula (IA Line) inserted to measure invasive BP?
- radial artery: most commonly selected site
- ulnar artery: principal source of blood flow to the hand (not commonly selected)
- brachial artery: near median nerve
- femoral artery: accessible in low flow states, risk for local and retroperitoneal haematoma
- dorsal pedis artery
What are the advantages of invasive BP?
Earlier detection of BP changes (immediate feedback, VS wait 3 mins for BP cuff) 🡪 earlier detection of hypotension (e.g. in IHD pts) or small fluctuations in BP (e.g. in phaeochromocytoma)
Access for frequent blood sampling (e.g. Hb, ABG, PT/PTT if patient was anticoagulated with heparin, etc)
Good in some special situations:
- Morbid obesity
- Burns
- Haemodynamic instability
What are the disadvantages of invasive BP?
Invasive
Transducer has to be kept at level of the heart, so when table is shifted in height (e.g. requested by surgeon), transducer needs to shift in height also
Complications of invasive BP
- Early complications: Infection, bleeding and haematoma, trauma to surrounding structures (e.g. nerves), distal ischaemia
- Late complications: Pseudoaneurysm, thrombosis
What are factors influencing accuracy of pulse oximetry?
- Low blood flow conditions (since relies on pulsatile flow)
- Patient movement
- Ambient light
- Dysfunctional Hb (carboxyHb, metHb)
- Methylene blue (stains plasma 🡪 falsely low SpO2 reading)
- Altered relationship between PaCO2 and SaO2 (shift in oxygen dissociation curve)
What are the causes of high ETCO2?
Increased CO2 delivery/production: Malignant hyperthermia, fever, sepsis, seizure, increased metabolic rate or skeletal muscle activity, HCO3- or medication S/E, laparoscopic surgery, clamp/tourniquet release
Hypoventilation: COPD, neuromuscular paralysis/dysfunction, CNS depression, metabolic alkalosis (if spontaneously breathing), medication S/E
Equipment problems: CO2 absorbent exhaustion, ventilator leak, rebreathing, malfunctioning inspiratory or expiratory valve
What are the causes of low ETCO2?
Decreased CO2 delivery/production: Hypothermia, hypometabolism, pulmonary hypoperfusion, low cardiac output or cardiac arrest, pulmonary artery embolism, haemorrhage, hypotension, hypovolaemia, V/Q mismatch or shunt, auto-PEEP, medication S/E
Hyperventilation: Pain/anxiety, awareness/”light” anaesthesia, metabolic acidosis (if spontaneously breathing), medication S/E
Equipment problems: Ventilator disconnection, oesophageal intubation, bronchial intubation, complete airway obstruction of apnoea, sample line problems (kinks), endotracheal tube (ETT) or laryngeal mask airway (LMA) leaks
What is the normal adult range for urine output?
Adults: 0.5-1 mL/kg/hr
What is the normal children range for urine output?
Children: 1-2 mL/kg/hr
What are the uses of IA line?
- Continuous BP monitoring
- Immediate access for point-of-care testing (POCT) ABG and electrolyte analysis
- IA transducer must be at level of the heart (adjust according to OT table height); if lower than heart, then BP higher than normal
- Damage to radial artery (possibly from IA line) can cause finger ischaemia; SpO2 readings on certain fingers may not be reliable
Where are the potential complications of NIBP?
- nerve damage (ulnar neuropathy)
- petectiae
- compartment syndrome
What are the causes of hyperthermia?
- malignant hyperpyrexia
- fever
- sepsis
- thyroid storm
