Anaesthesia - condensed

general anaesthesia definition

reversible controlled drug induced intoxication of the CNS in which the patient, neither perceives nor recalls noxious stimuli

liverpool triad definition

general anaesthesia reuqirements of analgesia, narcosis and muscle relaxation

balanced/multimodal analgesia definition

combination of different drugs each with a specific effect (Acting at different levels/receptors) to produce the desired objective —> ideally make anaesthesia safer
e.g. inhalation anaesthesia + TIVA

e.g. Regional anaesthesia + GA

minimum alveolar concentration (MAC) definition

the alveolar concentration required to prevent muscle movement in response to painful stimulus in 50% of patients (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 reuqired to keep a patient unconscious and immobile

effective osmolality (tonicity) definition

the concentration of solutes that cannot move freely across cell membranes (primarily sodium and glucose), directly affecting water movement into or out of cells

starling’s forces

the forces that control the movement in and out of blood (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

glycolax

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 perameters

HR, BP, CRT, MM, femoral pulse

minute ventilation (MV L/min)

respiratory rate / min x tidal volume (Vt mL or L)

what circuit do you use for up to 4kg animal?

bain, non-rebreathing

what circuit do you use for 4 to 10-12kg animal?

paediatric circle, re-breathing

what circuit do you use for 12 to 25-35kg animal?

F circuit, re-breathing

what circuit do you use for +35kg animal?

circle circuit, re-breathing

what does non-rebreathing circuit allow

allows for constant flow of fresh gas, allowing rapid changes

what does rebreathing circuit allow

natural heating, but increased resistance and have a CO2 absorber

bag size

6 x (10xBW)

ET tube size

Dog: (BW/4) + 4 (size down for brachycephalic)

Cat: 3-3.5—>4

stage one of anaesthesia

voluntary excitement, increased HR/RR, excess salivation, voiding of faeces/urine, struggling

stage two of anaesthesia

involuntary excitement, cortical depression, nacrosis. some reflex struggling, pupils dilate/nystagmus —> induction agents aim to drift through stages 1 and 2

stage 3 of anaesthesia (include planes)

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 formost surgical procedures

stage 4 of anaesthesia

too deep - respiratory and cardiac arrest

surgical plane reflexes

absent palpebral reflex, loose jaw tone, ventral medial eyeball position, corneal reflex present, anal tone absent/lax

ASA classifications (5)

1. normal healthy patient
2. mild systemic disease
3. severe systemic disease that is not incapacitating
4. disease is a constant threat to life
5. moribund, will live no more than a day without intervention

E = emergency surgery

quicker induction with (6 things)

1. Increased vaporiser concentration

2. higher fresh gas flow (more oxygen) —> more anaesthetic vapour at alveolar interface

3. increased RR

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

5. decreased CO

6. lung pathology (V/Q mismatch)

goal of monitoring

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

level 1 monitoring

basic monitoring —> requirement for all animals under GA

• observation of reflexes, assessment of muscle tone, respiration rate and depth

• MM colour

• HR, rhythm, strength of pulse, CRT

• temperature

level 2 monitoring

routine use recommended for some/all patients

• arterial blood pressure measurement (indirect or direct)

• electrocardiography

• pulse oximetry

• capnography, urine output, blood glucose, PCV/protein

level 3 monitoring

specific patient/problems

• anaesthetic gas analyser

• blood gas machine

• cardiac output, central venous pressure

• peripheral nerve stimulator

respiratory monitoring of inspired gas and equipment (what goes in)

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

respiratory monitoring of functional ventilation (what goes out)

spontaneous ventilation —> watch RR, chest movement, Vt estimate

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

mechanical ventilation —> monitor RR, Vt/inspiratory pressure and ventilator settings

respiratory monitoring - efficiency of gas exchange

pulse oximetry estimates o2 saturation and is non-invasive/continuous, but is less accurate with movement, poor perfusion, irregular pulses or severe anaemia.

subjective assessment via MM colour

respiratory monitoring - agent monitoring

inspired and expired volatile agent —> end tidal agent reflects alveolar/blood concentration

gold standard for respiratory monitoring?

blood gas monitoring

arterial —> direct assessment of gas exchange, but invasive, intermittent and expensive

CVS monitoring goal

main goal is to maintain O2 delivery (DO2) to tissues
DO2 = Qt x [O2/mL of blood]

what is included in CVS monitoring

HR, BP, temperature, MM colour, CRT, pulse quality

normal HR perameters

large dog: 60-120bpm
small dog: 80-160bpm
cat: 120-220bpm

how to monitor HR

pulse oximeter, stethoscope, pulses
ECG for electrical activity not perfusion

normal BP perameters

SAP: 90-160mmHg
DAP: 55-90mmHg
MAP: 60-100mmHg

how to monitor BP

NIBP

• doppler - ultrasound waves from a probe create an audible sound of blood flow

• oscillometric - detectio of oscillations

IBP: cannula directly into peripheral artery

normal temperature perameter

dog: 38.3-39.2
cat:37.5-39.2

MM colour assessment

pink = normal

pale/white = anaemia/vasoconstriction

cyanotic = severe hypoxaemia

injected = vasodilation/shock/hypercapnia

pulse quality measurement

palpate peripheral pulse —> weak pulse = poor perfusion/low stroke volume (expect strong, regular pulses)

NIBP cuff requirements

cuff width 30-40% of limb circumference
too wide or above the heart = falsely decrease BP
too tight or below the heart = falsely increase BP

NIBP doppler vs oscillometric

NIBP measurement depends on cuff size relative to limb circumference, position above/below heart

oscillometric doesn’t work with irregular/weak pulse or severe bradycardia

IBP vs NIBP

IBP is invasive and technically difficult but continuous and highly accurate
NIBP is easy but intermittent and less accurate

monitoring fluid balance

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

normal urine output = 0.8-2mL/kg/hr

what does low urine output indicate

can reflect poor renal perfusion/low CO BUT keep in mind effect of drugs

• opioids = decreased urine output by increasing ADH

• alpha-2 agonists = increased urine output by decreased ADH

factors for high risk anaesthetic

patient: age, ASA classification I-V, breed, extremes of size
drug factor: use of certain drugs, TIVA vs gaseous GA
procedure factors: length of procedure, experience, emergency

when to intervene for hypotension

SAP <90mmHg
MAP <60-65mmHg

normal end tidal CO2 level

ETCO2 = 35-45mmHg

when to intervene for hypercapnia

ETCO2 around 60mmHg

when to intervene for hypocapnia

ETCO2 around 30mmHg

normal O2 levels

PaO2 90-100mmHg
SpO2 95-100%

when to intervene for hypoxaemia

SpO2 <90%

when to intervene for hypoxia

PaO2 < 60mmHg

when to intervene for hypothermia

<35°C

causes of hypotension

decreased CO ± decreased SVR

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

consequence of hypotension

MAP <60mmHG = loss of autoregulation and risk of organ dysfunction

hypotension fix

treat the cause

reduce anaesthetic if possible

low HR = atropine

normal/fast HR = dopamine

suspect hypovolaemia = IV fluid bolus

hypertension cause

pain, too light GA, vasoconstriction, a2 agonists, preexisting disease

hypertension consequence

mild/moderate not acute life threatening

inadequate depth = awareness ± 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 = atropin, reduce anaesthetic depth

with normotension and regular rhythm = no treatment

tachycardia cause

too light, pain, hypovolaemia, hypoxia, electrolyte abnormaliteis

tachycardia consequence

increased myocardial work and O2 demand

tachycardia fix

increase anaesthetic depth and administer analgesia
hypovolaemia = IV fluid bolus

arrhythmias cause

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

arrhythmia consequence

impaired perfusion

arrhythmia fix

treat if perfusion affected —> defib ± CPR

cardiopulmonary arrest cause

respiratory or cardiac failure leading to hypoxia

cardiopulmonary arrest consequence

death

cardiopulmonary arrest fix

CPR

hypoventilation cause

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

hypoventilation consequence

hypercapnia —> tachycardia, respiratory acidosis, CV depression, arrhythmia

hypoventilation fix

decrease anaesthetic depth, administer IPPV or controlled mechanical ventilation

hypoxia cause

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

hypoxia consequence

tissue damage and death

hypoxia fix

1. start or increase oxygen therapy

2. check for obstruction

3. check breathing —> if not, IPPV

4. manage hypoventilation (increase RR ± Vt)

5. improve pulmonary function —> PPV, bronchodilators, pulmonary vasodilators

hypercapnia cause

hypoventilation, high FiCO2 (inspired)

hypercapnia consequence

acidosis

hypercapnia fix

hypoventilation —> increase MV (RR ± Vt)

FiCO2 —> remove dead space, replace soda lime, increase fresh gas flow rate

hypothermia causes

anaesthesia inhibits thermoregulation + vasodilation + heat loss

hypothermia consequences

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

hypothermia fix

prevention

active rewarming

hyperthermia cause

drug reactions or malignant hyperthermia

hyperthermia consequence

death

hyperthermia fix

management of cause

dantrolene for malignant hyperthermia

regurgitation cause

drugs, reduced sphincter tone, positioning, abdominal surgery, long GA

regurgitation consequence

oesophagitis, strictures, aspiration

regurgitation fix

prevention —> cuffed ET tube, fasting, positioning

GIT meds (metoclopramide)

myopathy cause

prolonged pressure + hypotension, especially large animals

myopathy consequence

muscle damage

myopathy fix

adequate padding

intra-op blood loss monitoring

monitor with swabs/lap sponges, drapes and flooransuction

intra-op blood loss consequences

DO2 capacity lost, hypotension, death