Condensed anaesthesia

General anaesthesia

Reversible controlled drug induced intoxication of the central nervous system in which the patient, neither perceives nor recalls noxious or painful stimuli

Liverpool triad

General anaesthesia requirements of analgesia, narcosis and muscle relaxation

Balanced/ multi-modal anaesthesia

Combination of different drugs each with a specific effect (acting at different levels/ receptors) to produce the desired objective → ideally makes anaesthesia safer

For example: inhalation anaesthesia + TIVA or regional anaesthesia + GA

Minimum alveolar concentration (MAC)

The alveolar concentration required to prevent muscular movement in response to a painful stimulus in 50% of subjects

Want it to be lower so you can use less of it

MAC sparing

The ability of a secondary drug to reduce the amount of inhaled general anaesthetic required to keep a patient unconscious and immobile

Effective osmolality (tonicity)

The concentration of solutes that cannot freely cross cell membranes (primarily sodium and glucose), dictating water movement into or out of cells

Starling’s forces

The forces that control the movement in and out of blood vessels (include hydrostatic pressure and colloid oncotic pressure)

Hydrostatic pressure

Pressure of the blood on the vessel walls into the ISF

Colloid oncotic pressure

Generated by large plasma protein, pulling fluid back into the blood vessel

Glycocalyx

The thin layer of proteins and carbohydrates lining the luminal surface of the vascular endothelium, separating the intravascular and interstitial space, regulating fluid flow

Perfusion parameters

Heart rate, blood pressure, capillary refill time, mucous membranes, femoral pulse

Minute Ventilation (MV L/min) =

Respiratory Rate (per min) X Tidal Volume (Vt ml or L)

Circuit for up to 4kg animal

Non-rebreathing - bain

Circuit for a 4 to 10-12kg animal

Re-breathing - paediatric

Circuit for a 12 to 25-35kg animal

Re-breathing - F circuit

Circuit for a 35kg+ animal

Re-breathing - circle circuit

Non-rebreathing circuit

Does not recycle exhaled gases

Allows a constant flow of fresh gas, allowing rapid changes

Rebreathing circuit

Recirculates a portion of the patient's exhaled anaesthetic gases and oxygen (CO2 absorber - sodalime)

Allows natural heating, increases resistance

Bag size =

50mL/ kg - allows a reservoir for subsequent inhalations

Stage 1 anaesthesia

Voluntary excitement, increased HR/ RR, excessive salivation, voiding of faeces and urine, struggling

Stage 2 anaesthesia

Involuntary excitement, cortical depression, narcosis. Some reflex struggling, pupils dilate/ nystagmus

Induction agents aim to ‘drift through’ stage 1 and stage 2

Stage 3 anaesthesia

Surgical anaesthesia → loss of reflexes, increased CV/ respiratory depression, increased muscle relaxation

Plane 1

Light plane, some surgical procedures can be carried out

Plane 2

Level required for most patients, most surgical procedures can be carried out

Plane 3

Too deep for most patients, deeper than required for most procedures

Stage 4 anaesthesia

Respiratory arrest, cardiac arrest

ASA classification 1

Normal healthy patient

ASA classification 2

Mild systemic disease

ASA classification 3

Severe systemic disease that is not incapacitating

ASA classification 4

Disease is a constant threat to life

ASA classification 5

Moribund, will live no more than a day without intervention

ASA classification E

Emergency surgery

Quicker induction with:

1. Increased vaporiser concentration

2. Higher fresh gas flow (more oxygen) → more anaesthetic vapour at the alveolar interface

3. Increased respiratory rate

4. B/G coefficient → less soluble the agent, faster the formation of equilibrium, factor the induction (and recovery)

5. Decreased cardiac output

6. Lung pathology (V/Q mismatch)

Monitoring goal

Maintain the patient in a physiological state that is as close as possible to ‘normal’ whilst allowing a surgical procedure to be carried out

Level I monitoring

Basic monitoring → requirement for all animals under anaesthesia

Observation of reflexes, assessment of muscle tone, respiration (depth and rate)

Mucous membrane colour

Heart rate, rhythm, strength of pulse and capillary refill time

Temperature

Level 2 monitoring

Routine use recommended for some/ all patients

Arterial blood pressure measurement (indirect or direct)

Electrocardiograph

Pulse oximetry

Capnography, urine output, blood glucose, PCV/ protein

Level 3 monitoring

Specific patients/ problems

Anaesthetic gas analyser

Blood gas machine

Cardiac output, central venous pressure

Peripheral nerve stimulator

What to monitor resiratory system

What goes in → inspired gas and equipment

What goes out → functional ventilation

Efficacy of gas exchange

Agent monitoring

How to monitor inspired gas and equipment

Check oxygen delivery, volatile agent/ nitrous oxide delivery and inspired CO2

Pre-anaesthetic machine checks reduce risk, but direct monitoring such as FiO₂ and agent monitoring is more reliable

How to monitor functional ventilation

Spontaneous and mechanical ventilation

• Ideally use capnography (monitors end-tidal CO2, which reflects alveolar ventilation, pulmonary blood flow and metabolism)

How to monitor spontaneous ventilation

Watch respiratory rate, chest movement and tidal volume estimate

How to monitor mechanical ventilation

Monitor respiratory rate, tidal volume/ inspiratory pressure and ventilator settings

How to monitor efficacy of gas exchange

Pulse oximetry estimates oxygen saturation and is non-invasive/ continuous, but is less accurate with movement, poor perfusion, irregular pulses or severe anaemia

Subjective assessment via MM colour

How to monitor agent

Inspired and expired volatile agent → end-tidal agent reflects alveolar/ blood/ brain concentration

Gold standard for respiratory monitoring

Blood gas monitoring

Arterial → direct assessment of gas exchange, but invasive, intermittent, expensive

CVS monitoring goal

Maintain oxygen delivery (DO2) to tissues

DO2 = Qt x [O2 per mL of blood]

CVS what to monitor

Heart rate

Blood pressure

Temperature

Mucous membrane colour

CRT

Pulse quality

Normal heart rate

Small dogs 80-160 bpm

Large dogs: 60-120bpm

Cats: 120-220 bpm

Normal blood pressure

SAP: 90-160

DAP: 55-90

MAP: 60-100

Normal temperature

Dogs: 38.3 – 39.2

Cats: 37.5 – 39.2

Normal mucous membranes

Pink, 1-2 second capillary refill time

Pale/ white mucous membranes

Anaemia/ vasoconstriction

Cyanotic mucous membranes

Severe hypoxaemia

Injected mucous membranes

Vasodilation/ shock/ hypercapnia

How to monitor HR

Pulse oximeter, stethoscope, pulses

ECG for electrical activity (not perfusion)

Non-invasive blood pressure measurement

Doppler: ultrasound waves from a probe create an audible sound of blood flow

Oscillometric: detection of oscillations (doesn’t work with irregular/ weak pulse or severe bradycardia)

Easy but intermittent and less accurate

Invasive blood pressure measurement

Cannula directly into peripheral artery

Invasive and technically difficult but continuous and highly accurate

How to monitor pulse quality

Palpate peripheral pulse → weak pulse = poor perfusion/ low stroke volume

NIBP cuff width

30-40% of limb circumference at level of the heart

• Too wide = false decrease in measures BP, too narrow = false increase in measured BP

• Above heart = lower BP, below heart = higher BP

Monitoring fluid balance

Monitor fluid in (IV fluids, boluses, blood products) and fluid out (urine, blood loss, surgical losses)

Normal urine output

0.8-2 mL/ kg/ hr

Low urine output under anaesthesia

Can reflect poor renal perfusion/ low CO, but also be mindful of drug effects

Opioids decrease urine output by increasing ADH

Alpha-2 agonists increase urine output by decreasing ADH

Patient high-risk anaesthetic factors

Age (neonates and geriatric)

ASA classification I-V

Breed

Extremes of size

High risk anaesthetic drug factors

Use of certain drugs (ACP? In certain scenarios)

TIVA vs gaseous anaesthesia

High risk anaesthetic procedure factors

Length of procedure

Fatigue

Emergency procedures

Experience level of staff

Normal ETCO2

35-45mmHg

Normal PaO2

90-110mmHg

Normal SpO2

95-100%

Hypotension when to intervene

SAP <90 mmHg

MAP <60-65 mmHg

Hypercapnia when to intervene

ETCO2 ~ 60 mmHg (CO2 >> 45mmHg = acidosis (pH <7.4))

Hypocapnia when to intervene

ETCO2 ~ 30 mmHg (CO2 << 35mmHg = alkalosis (pH >7.4))

Hypoxia/ hypoxaemia when to intervene

SpO2 <90% or PaO2 < 60mmHg

Hypothermia when to intervene

<35 ºC

Hypotension cause

Decreased CO and/ or decreased SVR

Usually from anaesthetic drugs, hypovolaemia, haemorrhage, bradycardia, IPPV/ positioning

Hypotension consequence

MAP <60 mmHg leads to loss of autoregulation and risk of organ dysfunction

Hypotension fix

Treat the cause

Reduce anaesthetic if possible

Low HR = atropine

Normal HR = dopamine

Suspect hypovolaemia = IV fluid bolus

Hypertension cause

Pain, too light, vasoconstriction, a2 agonists, preexisting disease

Hypertension consequence

Mild/ moderate not acute life threatening

Inadequate depth = awareness and/ or movement

Hypertension fix

Assess anaesthetic depth

Bradycardia cause

Dose dependent drugs, high vagal tone, electrolyte abnormalities

Bradycardia consequence

Reduced CO → hypotension → organ injury → death

Bradycardia fix

With hypotension = atropine, reduce anaesthetic depth

With normotension and regular rhythm = no treatment

Tachycardia cause

Too light, pain, hypovolaemia, hypoxia, electrolyte abnormalities

Tachycardia consequence

Increased myocardial work and O2 demand

Tachycardia fix

Increase anaesthetic depth/ administer analgesia

Hypovolaemia = IV fluid bolus

Arrhythmias cause

Drugs, hypoxia, hypercapnia, electrolyte/ acid-base issues, cardiac disease

Arrhythmias consequence

Impaired perfusion

Arrhythmias fix

Treat if perfusion affected → defib and/ or CPR

Cardiopulmonary arrest cause and fix

Respiratory or cardiac failure leading to hypoxia - CPR

Hypoventilation cause

Anaesthetic drugs, recumbency, airway obstruction, abdominal pressure, thoracic disease

Hypoventilation consequence

Hypercapnia → tachycardia, respiratory acidosis, CV depression, arrhythmias

Hypoventilation fix

Decrease anaesthetic, provide intermittent positive pressure ventilation (IPPV) or controlled mechanical ventilation

Hypoxia cause

Low inspired O2, hypoventilation, V/Q mismatch, atelectasis, shunt

Hypoxia consequence

Tissue damage + death

Hypoxia fix

1. Start or increase oxygen therapy

2. Check for obstructions

3. Check breathing → if not, PPV

4. Manage hypoventilation (increase RR and/ or increase Vt)

5. Improve pulmonary function → PPV, bronchodilators, pulmonary vasodilators

Hypercapnia cause

Hypoventilation, high FiCO2 (inspired)

Hypercapnia consequence

Acidosis

Hypercapnia fix

Hypoventilation → increase MV (RR and/ or Vt)

FiCO2 → remove dead space, RB replace sodalime, NRB increase fresh gas flow rate

Hypothermia cause

Anaesthesia inhibits thermoregulation + vasodilation + heat loss

Hypothermia consequence

Bradycardia, arrhythmias, hypoventilation, reduced drug clearance, poor recovery