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 – expanded to include suppression of reflexes (motor and autonomic) plus unconsciousness/ amnesia

Balanced 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 combining inhalation + intravenous + regional anaesthesia

Stage 1 of anaesthesia

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

Induction agents aim to ‘drift through’ this

Stage 2 of anaesthesia

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

Induction agents aim to ‘drift through’ this

Stage 3 of anaesthesia

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

Plane I – light

Plane 2 – medium

Plane 3 – deep

Stage 4 of 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

Why do we monitor patients?

Monitoring provides early warning of life-threatening disorders - complications can occur even in healthy patients in all stages of anaesthesia

Monitoring in poor risk patients should be incorporated earlier than normal and continue after the conclusion of anaesthesia

Anaesthetic records are an important legal document

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

Premedication

Prepares patient and provides optimum conditions for surgery/ anaesthesia

Relieves anxiety/ fear/ resistance to induction of anaesthesia

Potentially counters unwarranted side effects such as vomiting, salivation, bradycardia

Acepromazine premed pros

Minimal respiratory depression

MAC sparing (reduces amount of volatile agent required)

Antiarrhythmic effects

Long acting, dose dependent

Acepromazine premed cons

Needs to be combined with an opioid for analgesia → most commonly used with methadone

Vasodilation/ hypotension

Hypothermia

Priapism/ paraphimosis

No reversal

Diazepam premed pros

CV and respiratory parameters well maintained

Midazolam premed pros

Water soluble

Effective and well tolerated as IM

Diazepam premed cons

Poorly water soluble

Painful injection

Reduces MAC

Midazolam premed cons

Shorter acting than diazepam

Alpha 2 agonist premed pros

Potential for reversal, although not generally used due to potential excitatory effects

Alpha 2 agonists premed cons

Vasoconstriction - hypertension - bradycardia - CO falls

Bad for animals with heart problems

Don’t use in last trimester - uterine stimulation

Barbiturates as induction agents

Respiratory depressants with poor analgesia

Propofol as an induction agent

Pharmacokinetics make it very suitable for TIVA → poor analgesia

Anaesthesia and hypnosis occur in a circulation time → initial recovery is due to redistribution but then is rapidly metabolised by the liver

Dose dependent cardiovascular and respiratory depression

Alfaxalone as an induction agent

Rapidly metabolised in the liver, short acting, non-cumulative and suitable as TIVA

CV and respiratory parameters quite stable at recommended dosages

Ketamine as an induction agent

Produces a cataleptic or dissociated state, complete analgesia with superficial sleep - needs to be combined with a muscle relaxant

Distribution is rapid and initial recovery through redistribution

CV well maintained, increased HR and myocardial O2 consumption

Minimum alveolar concentration

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

MAC is reduced by:

Other drugs, neonates, geriatrics, hypothermia, pregnancy, disease process, hyponatremia

Distribution of inhalations

During inspiration, inhalationals are taken up by the blood and tissues

Uptake continues until equilibrium is reached

Quicker induction with:

1. Increased vaporiser concentration

2. High fresh gas flow (more oxygen)

3. Increased respiratory rate

4. B/ G coefficient - less soluble the agent, faster the formation of equilibrium

5. Decreased cardiac output

6. Lung pathology (V/Q mismatch)

Isoflurane

Halogenated ether, non-flammable liquid

High volatility and relatively low solubility in blood tissues - quick inductions and recoveries

Significant respiratory depression, little cardiac depression

Poor analgesia, moderate muscle relaxation

Goal of monitoring

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

Heart rate

Determinant of cardiac output

Affects blood pressure and perfusion

Blood pressure

Arterial hydrostatic pressure compared with atmospheric pressure

Result of cardiac output and peripheral resistance

Systolic arterial pressure

Pressure in the arteries during systole

Determined primarily by stroke volume and arterial compliance

Systolic = squeezing (contraction of the myocardium)

Diastolic arterial pressure

Pressure in the arteries when heart is relaxed

Determined primarily by circulating blood volume and vasomotor tone

Diastolic = drawing (blood into the ventricles)

Mean arterial pressure

Average of the area under the pulse pressure wave form

Below 60 mmHg vital organ perfusion likely to be inadequate as autoregulation fails

Temperature

Decrease in temperature very common in small animals

Anaesthetic drugs inhibit thermoregulation - inhibition of vasoconstriction/ vasodilation and shivering

Pulse oximeter

Red and infrared light transmitted through a thin layer of tissue back to a receiver in the probe → Hb bounds to O2 absorbs more infrared, unbound Hb absorbs more red light

Thickness of tissue, presence of pigment/ hair can lead to signal failure as can ambient light and movement

Doppler NIBP

Ultrasound waves emitted from one of two piezoelectric crystals in probe = incident signal

Second crystal receives the reflected signal from moving cells

Frequency difference between incident and reflective signal = audible sound of blood flow

Oscillometric BP monitor

Detection of oscillations, firstly at the SAP, maximal amplitude at MAP, decreasing at DAP

Stage III Plane I

Light plane, some surgical procedures can be carried out

Central eyeball position, palpebral reflex present, lots of jaw tone

Stage III Plan 2

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

Rotated medial ventral eyeballs, no palpebral reflex, some jaw tone

Stage III Plane 3

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

Rotated medial ventral eyeballs, no palpebral reflex, little jaw tone

Ideal surgical plane reflexes

No palpebral reflex

Loose jaw tone

Ventral medial pupils

Corneal reflex presnet

Anal tone absent, lax

Intervention of hypotension

SAP <90 mmHg

MAP <60-65 mmHg

If autoregulation fails → inadequate organ perfusion

Intervention of hypercapnia

ETCO2 ~ 60 mmHg

Severe respiratory depression

Intervention of hypocaemia

PaO2 < 60 mmHg

Tissue damage, death

Intervention of hypothermia

<35 ºC

Effects on CV function, metabolism, recovery

High risk patient factors

Age (neonates and geriatric), ASA classification I-V, breed, extremes of size

High risk drug factors

Use of certain drugs (ACP? In certain scenarios), TIVA vs gaseous anaesthesia

High risk procedure factors

Length of procedure, fatigue, emergency procedures, experience level of staff

What causes hypotension under GA

Drugs

Equipment

Mechanical → position, IPPV, abdominal distension (low venous return)

Patient factors → hypovolaemia, azotaemia, CNS depression, sepsis, haemorrhage

Cardiac → decreased contractility (arrhythmias), decreased rate (bradycardia). Primary cardiac disease.

Respiratory → IPPV, pleural space disease

Allergic → reaction to medications and histamine release

Pathophysiology of hypotension under GA

Blood pressure = CO x SVR

Indirect indicator of haemodynamic status

MAP <60-65 mmHg leads to loss of autoregulation and risk of organ dysfunction

Correction of hypotension under GA

Treat the CAUSE

Assess anaesthetic depth & reduce if possible

IV fluid therapy

Pharmacological intervention:

- Atropine if HR low

- Dopamine if HR normal/ high (inotropic support)

What causes hypoventilation under GA

Due to effects of general anaesthesia (direct drug effects)

Also indirect effects: recumbency, atelectasis, heavy/distended abdominal viscera, body composition, thoracic trauma or pleural space disease, abnormal breathing patterns, airway obstruction

Pathophysiology of hypoventilation under GA

Reduced alveolar ventilation → hypercapnia (increased PACO₂ increases)

Hypercapnia causes tachycardia ± ↑ BP or hypotension, respiratory acidosis, ↑ intracranial pressure, CV depression, arrhythmias

Correction of hypoventilation under GA

Provide intermittent positive pressure ventilation (IPPV) or controlled mechanical ventilation

What cause hypoxia under GA

Caused by low inspired O2, hypoventilation or venous admixture

Pathophysiology of hypoxia under GA

PaO₂ < 60 mmHg

↓ O₂ delivery → tissue damage, DEATH

Early signs: ↑ RR, ↑ BP, ↑ HR

Late signs: cyanotic mucous membranes, cardiac arrest

Correction of hypoxia under GA

Provide oxygen, improve ventilation, mechanical ventilation (RMs, PEEP)

Drugs (Salbutamol), position change

Causes of hypothermia under GA

Due to anaesthetic induced:

Inhibition of thermoregulation

Vasodilation

Inability to respond behaviourally (e.g. shivering)

Heat loss via conduction, convection, radiation and evaporation

Pathophysiology of hypothermia under GA

Decreased core temperature

Causes bradycardia, arrhythmias, hypoventilation, reduced metabolism and drug clearance, decreased MAC, impaired immunity, coagulopathies, poor recovery

Correction of hypothermia under GA

PREVENT heat loss → insulation, minimise clipping, warm environment, warmed fluids

Active rewarming → heated IV fluids, humidified O2, air blankets, heated systems

What causes hyperthermia under GA?

Caused by drug interactions (ketamine/tiletamine/opioids in cats) or malignant hyperthermia (genetic, triggered by inhalational agents, succinylcholine)

Pathophysiology of hyperthermia under GA

Increased temperature with ↑ RR, ↑ CO₂, metabolic acidosis, tachycardia, hypertension, arrhythmias → death

↑ calcium release → ↑ muscle contracture and metabolism

Correction of hyperthermia under GA

Management of underlying cause

What causes arrhythmias under GA?

Due to autonomic imbalance, drugs, electrolyte imbalances or pre-existing disease

Correction of arrhythmias under GA

Treat if perfusion is affected

Non-perfusing rhythms require defibrillation and CPR, asystole/ PEA require CPR

What causes cardiopulmonary arrest under GA

Results from respiratory or cardiac failure leading to hypoxia

Causes include hypoxaemia, hypoventilation, hypotension, hypovolaemia, arrhythmias, hypothermia, drug overdose or equipment failure

Pathophysiology of cardiopulmonary arrest under GA

Loss of effective circulation and respiration → brain and heart dysfunction

Signs include loss of pulse, apnoea, and progressive deterioration in vital parameters

What causes regurgitation under GA

Caused by anaesthesia-related changes (positioning, drugs, reduced sphincter tone)

Risk increased with certain species/breeds, GIT disease, age, longer anaesthesia, and abdominal surgery

Pathophysiology of regurgitation under GA

Movement of fluid from stomach/duodenum into oropharynx

May lead to oesophagitis, strictures, aspiration

Correction of regurgitation under GA

PREVENTION! Cuffed ET tube, appropriate fasting (dogs/cats 12h food, 2h water; ruminants 24h food, 12h water), correct positioning, careful drug selection, GIT meds

What causes myopathy under GA

Hypotension and prolonged compression of tissues during surgery

Correction of myopathy under GA

Adequate padding essential

Advantages of local and regional anaesthesia

Simple, inexpensive and requires minimal equipment

Reduced risk of complications and allows ‘standing surgery’

Useful adjunct to general anaesthesia

MOA of local anaesthetic (lignocaine/ bupivicaine)

Act via sodium channel blockades in sensory nerves - this prevents signal conduction and therefore prevents transmission of painful stimuli

Lignocaine

Most commonly used local anaesthetic in ruminants

Diffuses more widely through tissues

Lignocaine onset and duration

Rapid onset - approximately 5 minutes, lasts for approximately 90-180 minutes

Lignocaine toxicity

Excessive dosages cause increased systemic absorption

CNS signs occur first with toxicity

Bupivicaine onset and duration

Slow onset - approximately 20-30 minutes, but lasts for 180-360 minutes

Bupivicaine toxicity

Excessive doages cause increased systemic absorption

Cardiovascular signs occur first with toxicity

Factors affecting local anaesthetic efficacy

Onset - affected by concentration of drug and proximity of injection site to the nerve

Absorption - prolonged when combined with adrenaline, shortened in highly vascular tissues

Inflammation reduces efficacy because tissue pH changes reduce drug effectiveness

Local vs regional anaesthetic

Local - small area, simpler techniques, larger areas require large volumes, may not desensitise all layers

Regional - entire region blocked, more complex techniques, smaller volumes required, desensitises all layers

Direct infiltration

Local anaesthetic infiltrated directly along incision line

Direct infiltration advantages

Simple and requires limited equipment

Direct infiltration disadvantages

Requires large volume of anaesthetic, shorter duration, delayed wound healing, no muscle relaxation, deeper layers are not anaesthetised

Inverted L block

Local anaesthetic infiltrated in an inverted L around the surgical site

Commonly used for laparotomy/ flank surgery

Inverted L block advantages

Simple and requires limited equipment

Does not interfere with ambulation

Injection away from incision reduces oedema and haematoma, improving surgery and healing

Inverted L block disadavantages

Does not completely anaesthetise or relax deeper structures

Requires larger doses

Increased risk of overdose

Proximal (Cambridge) paravertebral block

Desensitises dorsal and ventral nerve roots of T13, L1 and L2

Blocks nerves as they emerge from intervertebral foramina

Distal (Cornell) paravertebral block

Desensitises dorsal and ventral rami of T13, L1 and L2

Injected at distal ends of transverse processes in a fan-shaped pattern

Advantages of paravertebral blocks

Small doses required, wide and uniform analgesia, good muscle relaxation, decreased intra-abdominal pressure, no local anaesthetic at surgical margins

Disadvantages of paravertebral blocks

Scoliosis towards desensitised side

Difficult landmarks in obese/ heavily muscle animals

Requires greater skill and practice

Intravenous regional anaesthesia

Tourniquet applied proximally

Local anaesthetic injected intravenously distal to tourniquet

Ring blocks, line blocks proximal to surgical site or peripheral nerve blocks

Epidural anaesthesia

S5-Co1 or Co1-Co2

Confirmed with popping sensation, hanging drop technique or loss of resistance