Anaesthesia Flashcards
ASA* score is a subjective assessment of a patient’s overall health:
I Completely healthy, fit, patient.
II Mild systemic disease.
III Severe systemic disease that is not incapacitating.
IV Incapacitating disease that is a constant threat to life
V Not expected to live 24 hours
E. Emergency surgery, E is placed after the Roman numeral.
Premedication:
Prepares patient and provides optimum conditions for surgery/anaesthesia.
Relieves anxiety/ fear/ resistance to induction of anaesthesia.
MAC sparing / decrease amount of volatiles
Counters unwarranted side effects such as vomiting, salivation, bradycardia.
Contributes to peri -anaesthetic analgesia.
Tranquilizers and Sedatives
Phenothiazines
Butyrophenones
Benzodiazepines
Alpha 2 agonists
Opioids
Guaiphenesin (*Centrally acting muscle relaxants)
Phenothiazines:
Acepromazine
Acepromazine activity:
Dopamine receptor antagonism responsible for most of sedation properties.
Alpha1 adrenergic receptor antagonism mediates the vasodilation/decrease in blood pressure seen with acepromazine. This antagonism also at least partly responsible for decrease in thermoregulatory control.
Acepromazine
Dose rates:
SA & LA: 0.02-0.05 mg/kg
IV/ IM/ SC/ oral routes
List some phenothiazines:
Acepromazine
Perphenazine enanthate
Fluphenazine
Butyrophenones:
Primary action dopamine antagonist
Azaperone - pigs
Fluanisone/ Droperidol
Benzodiazepines
GABA receptor within CNS - primary inhibitory neurotransmitter.
Diazepam and Midazolam (most common)
- Zolazepam
- Zolitil (wildlife)
- Climazolam
Diazepam
Poorly water soluble
Painful injection especially IM
Unreliable sedation as a sole agent in fit and healthy individuals (not recommended).
Effective in sick or older patients and can be used in foals (0.2 mg/kg) to achieve recumbency.
CV and respiratory parameters well maintained.
Main role in anaesthesia in combination with drugs such as ketamine/ tiletamine (reduces excitatory effects and provides muscle relaxation). Reduces MAC.
Ant- convulsant
Midazolam
Water soluble, effective - well tolerated as IM injection
Shorter acting than diazepam
metabolised in the liver
Unpredictable sedative (agitation and excitement in SAs and ataxia in horses).
Co-administered with other agents (ketamine) and to reduce the dosages of induction agents (alphaxalone/propofol).
Use in triple drip formulations in horses with xylazine (alpha 2 agonist) and ketamine as an alternative to guaiphenesin
Dissociative anaesthetics + Benzodiazepine used for wildlife:
Zoletil
(Tiletamine combined with Zolazepam)
Anticholinergic agents
Use to block the effects of acetylcholine (muscarinic receptors) at parasympathetic postganglionic nerve endings.
Atropine and glycopyrrolate are the most widely used.
Main beneficial actions include treatment of anaesthetic induced (opioid) bradycardia, excessive salivation and respiratory secretions and blockage of vasovagal reflexes.
Alpha 2 (adrenergic receptor)
agonists
Xylazine, Detomidine, Medetomidine,
Dexmedetomidine, Romifidine.
Alpha 2 receptors are widespread throughout the body, in neural tissue, organs, vascular tissue and platelets = variety of ± effects
Alpha 2 agonists
Mode of action:
Central sedation effects caused by binding of presynaptic ∝ 2 receptors
(negative feedback loop)
Analgesia from binding of receptors centrally and within dorsal horn of the spinal cord (pre- and postsynaptic)
alpha 2 agonists have some impact at ∝1 receptors
Clinical aspects of alpha 2 drugs:
Bradycardia, initially a reflex baroreceptor response to peripheral induced vasoconstriction (↑ SVR) but major reason is suppression of CV centre and decreased sympathetic drive.
GI motility is reduced
Urine production increases (central inhibition of ADH)
Reduced renin and insulin secretions → hyperglycaemia
Potential for reversal
Opioid
Receptor types and MOA:
mu(µ), kappa(K) and delta(𝛿).
G protein coupled receptors, closure of Ca2+ gated channels, cellular hyperpolarization and reduced cAMP production= inhibition of neurotransmitters
Reversal possible = naloxone
List of Opioids:
Buprenorphine
Butorphanol (poor analgesic)
Fentanyl
Methadone
Guaifenesin
Centrally acting muscle relaxant
Interferes with polysynaptic transmission
No analgesia
Largely replaced by benzodiazepines
Injectable (induction) anaesthetic
agents (list):
Barbiturates
Propofol
Alfaxalone
Ketamine or Tiletamine
Barbiturates
Phenobarbitol
thiopental, and methohexital
long acting and anticonvulsant
All exert their effects at the GABA receptor
Respiratory depressants with poor analgesia
Metabolised via the liver
Thiopental/ thiopentone
Short-acting barbiturate
Perivascular injections - irritable, significant tissue damage.
Hypovolaemic states lead to reduced redistribution= ↑ clinical effect.
Poor analgesic
(Beware use in neonates, caesarean section, Sighthounds)
Propofol
Anaesthesia/hypnosis occurs
Rapidly metabolised by the liver
Dose-dependent CV and respiratory depression
Poor analgesia
I/V induction agent of choice in humans
Steroid anaesthetics
Alfaxalone
Rapidly metabolised in the liver, short acting, non cumulative
Suitable as total IV anaesthesia
Premedicated:
dogs, 2mg/kg, I/V (slowly)
cats up to 5mg/kg
Can be used as CRI, beware of respiratory depression= ventilatory support
Dissociative agents
MOA:
Ketamine/ Tiletamine
Non competitive antagonists at the NMDA - receptor preventing the excitatory neurotransmitter glutamate from binding.
Cataleptic or dissociated state, complete analgesia - superficial sleep. Many reflexes are maintained (pharyngeal/ laryngeal), hypertonus is present, eyes remain open.
Dissociative agents need complementary drugs to ameliorate these side effects and to improve muscle relaxation.
Ketamine/ Tiletamine
Metabolised by:
CV effects:
NS effects:
1: liver, excreted via the kidneys
2: CV is usually well maintained
indirect sympathomimetic action, ↑HR and myocardial O2 consumption.
Beware in certain patients with severe CV disease i.e. cardiomyopathies
3: ↑ CBF and ICP, avoid in seizuring patients/ head trauma
Volatile agents/ Inhalational agents
Halothane
Isoflurane
Sevoflurane
Desflurane
Nitrous Oxide - (most analgesia)
MAC:
Minimum Alveolar Concentration (MAC), a measurement of the
relative potencies of inhalational agents and can guide in the
concentration required for a given clinical situation.
MAC is reduced by:
Other drugs, premedications, N20
Age, neonates and geriatrics
Hypothermia
Pregnancy (progesterone)
Disease processes, hyponatraemia
Arterial BP < 50 mmHg
PaO2 <40mmHg
PaCO2 > 95mmHg
ET tube sizing:
weight/4 + 4 = ET tube size
e.g. 20kg/4 = (4) + 4 = 9
Inhalationals: Mode of Action
Likely to be multiple sites within the CNS (both brain and spinal cord)
Some potentiation of inhibitory GABA receptors likely as well as
inhibition of NMDA receptors
Isoflurane
Halogenated ether
High volatility and relatively low solubility in blood and tissues, means relatively quick inductions and recoveries
Dose dependent depression of CV system BP↓ SVR↓ but little cardiac depression and HR is maintained (at MAC levels). CO and blood flow largely preserved.
Respiratory depression significant. Ventilation recommended especially in horses.
Poor analgesia, moderate muscle relaxation.
Less than 1% metabolised.
What are the 3 H (common anaesthetic complications):
Hypotension
Hypothermia
Hypoventilation
Blood pressure = CO x SVR
SAP 125 – 160mmHg
MAP 90 – 110mmHg
DAP 75 – 95mmHg
Intervention is required if the MAP is:
< 60-65mm Hg; SAP < 90mmHg
Spey clinic surgical fluid rate =
5mg/kg/h
Hypotension with possible hypovolemia treatment:
Assess fluid responsiveness:
Administer test bolus 5-10ml/kg of isotonic crystalloids over 5-10 minutes.
if improves/resolves consider increasing fluid rate.
Hypotension without hypovolemia - treatment:
MAC-sparing analgesia bolus or CRI and reduce isoflurane
Commence dopamine CRI (5-15ug/kg/min)
Hypotension with bradycardia treatment:
Administer anticholinergic -
Atropine 0.02-0.04mg/kg IV
Hypoxaemia = PaO2
?mmHg
<60mmHg
Types of heat loss:
Convection - heat transfer from body surface to air or water moving past the animal. E.g. laminar air flow from cooling or heat loss from blood inside vessels
Conduction – heat transfer across a surface. E.g. patient in contact with surgical table
Evaporation – moisture in contact with skin or respiratory tract dissipates into air. E.g. open body cavity
Radiation – exchange of heat between body & objects in environment that are NOT in contact with skin.
Phases of heat loss:
Phase 1 (first hour) – initial rapid
decrease in core temperature
Phase 2 (2 – 3 hours) – slow, linear
reduction in core temperature due to
heat loss exceeding production.
Significant reduction in metabolism and heat production
Phase 3 (3 – 4 hours) – body
temperature reaches a plateau where loss = production
Hypothalamus is responsible for
thermoregulation
Thermoreceptors throughout the body → afferent input to CNS → thermoregulation
Efferent responses are instigated as required
‘Interthreshold range’ very narrow ± 0.2ºC
Cardiac output (CO) =
Cardiac output (CO) (volume of blood pumped per min) = stroke volume (volume from LV) x heart rate (bpm)
Mean Arterial Pressure =
Mean Arterial Pressure = CO x SVR (systemic vascular resistance - blood pressure (bp))
Chronotropy
Speed of heart rate
Inotropy
Strength of contractility
Preload
how much blood can you have before the heart ejects it (prior to systole)
Alpha2 agonists such as medetomidine (used in all cats), shouldn’t be used in animals with heart disease because:
increase in afterload
increase in vasoconstriction and increase BP, barrow receptor will then decrease HR decreased HR will decrease cardiac output (CO)
Arrest rhythms include:
Asystole, ventricular fibrillation, pulseless ventricular tachycardia &
pulseless electrical activity
If there is known blood loss and the patient has hypotention, tavhicardia (or normal HR):
we can bolus for 15 minutes but don’t give more than 1 blood volume of isotonic crystalloids
90ml/kg in dog
50-60ml/kg in a cat
stop fluid bolus after 2-3 attempts if no resolution - try colloids
Advantages of Regional Anaesthesia
- Simple to perform & minimal equipment
- Highly effective analgesia
- Low risk of complications (with precautions)
- ‘Standing Surgery’
- Adjunct to general anaesthesia
MOA for local anaesthesia:
Block sodium channels (blocks progressive depolarisation) in sensory nerves preventing signal conduction.
Bupivacaine is more sensitive than lignocaine what are the different overdose effects?
Lignocaine CNS signs
Bupivacaine CVS depression and cardiac arrest occur first.
Onset of Action vs duration of locals:
– Lignocaine Fast (5 min)
lasts 60-90 minutes
– Bupivacaine Slow (up to 20 min)
lasts 180-360 minutes
Supraorbital nerve
forehead and upper eyelid
sensory
Infraorbital nerve
rostral part of the upper jaw and nose
Retrobulbar Block
Enucleation
Auriculopalperbal
nerve (motor)
motor for the upper eyelid
Cornual nerve
dehorning - supplies most of the nerve add with local at the back of the horn
vertebrae involved in a para vertebral regional anaesthesia
Dorsal - T13, L1 & L2
Lateral - T13, L2 & L3
what percentage of the body is water?
70%
2/3 intracellular
1/3 extracellular
- interstitial fluid
- plasma
Electrolytes in the body:
Extracellular
- Na
- Cl
- bicarbonate
Intracellular
- K
Crystalloids
Water
small molecules:
- NaCl
- other electrolytes
- Glucose
Most commonly used IV fluids (crystalloids)
Hartman’s solution
Sodium chloride
Hypotonic fluids:
Less substances than blood - mostly water
Isotonic fluids:
Same concentration as blood
Hypertonic fluids:
Much more substances- higher concentration than blood
Uses for crystalloids:
Maintenance fluids (hypo or iso and given slowly)
Replacement fluids (iso or hyper tonic - can be given rapidly)
Special
Maintenance fluid rate:
2-3 ml/kg/h
Peri-operative fluid rate:
5 ml/kg/h
Typical (resting) oxygen requirements:
2-3 ml/kg/min
Hypercapnia:
(CO2»_space; 45mmHg) = acidosis (pH <7.4)
Hypocapnia:
CO2:
pH:
(CO2 «_space;35mmHg) = alkalosis (pH >7.4)
Common respiratory depressant drugs:
Volatile agents
Acepromazine
Propofol/Alfaxalone (strong)
Ketamine (mild)
Opioids (mu = strongest)
Benzodiazepines (mild)
Atelectasis
Alveolar collapse
Loss of ventilated surface area for gas exchange
Spontaneous Ventilation
Minute ventilation =
Minute Ventilation = RR x Vt
Oxygen Saturation
Oxygen binding to Haemoglobin
Proportion of Haemoglobin (Hb) saturated with oxygen
Capnography
CO2
in alveolar gas
How does the plus optometry work?
Saturation measured by recording ratio of light absorption
(red and infra red)
Pulmonary Compliance can be measured by:
some high end ventilators and
spirometers
Severe Lung Trauma can be avoided by using normal parameters
Vt 10-15 ml/kg
PIP normal for species but «_space;40cmH2O
Hypothermia
<36C
Severe hypothermia: <34C
Stages of anesthetic depth:
1: Awake
2: Involuntary excitement - loss of consciousness
3: Surgical anesthesia (3 planes)
4: Overdose - death
Rebreathing system flow rate:
Initially 100ml/kg/min or 2L/m (whatever is greatest)
Maintenance 10ml/kg/min or minimum of 500ml/min
Non-rebreathing flow rate:
500ml/kg/min Constantly
5 peripheral pluse locations:
Femoral
Digital
Lingual
Pedal
Coccygeal
Auricular
Intra-venous regional anaesthesia-REGIONAL
Torniquet, stops blood/LA escaping
Esmarch’s bandage, strips blood out of leg
Starlings law
Fluid movement in/out of blood vessels is controlled by:
- Permeability of capillary wall
- Hydrostatic pressure
-Physical pressure in capillaries relative to pressure in interstitial- higher pressure in capillaries, more fluid moves out
-High interstitial pressure- less fluid movement out
-ALWAYS A NET MOVEMENT OUT - oncotic pressure
-Pressure exerted by dissolved substances- high conc in capillaries, water drawn in
-High conc in interstitial- water drawn out of capillary
Pulse oximetry
Haemoglobin-oxygen saturation – indication of partial pressure of oxygen
Indication of the available oxygen for tissue perfusion.
Doppler
Audible sound of blood flow gives SAP - indicates blood pressure.
Advantages and disadvantages of a rebreathing anaesthetic system
*Lower O2 compared to non-rebreathing systems and therefore less cost and less waste
*Natural humidification of inspired gases reduces heat loss
*Increased resistance to breathing (due to absorber, hoses and valves)
*Circuit concentration is slow to change
*Expense of absorber
*Cannot use with animals <4kg or cats as resistance is higher
Consequences of using of an excessive peak inspiratory pressure (PIP) when mechanically ventilating a small dog during general anaesthesia.
*Barotrauma to the lungs
*Hyperventilation – damage to the airways and lungs
*Excessive delivery of volatile anaesthetic agent
Why is there a higher chance of hyperventilating a cat compared to a 12kg dog?
Lung capacity is much smaller
Squeezing the bag too much (only small squeezes would be needed)
Non-rebreathing circuit has high oxygen flow
More immediate impact of non-rebreathing circuit
Give examples of:
Pre-medication:
Induction:
Maintenance:
Fulid therapies:
Pre-medication: methadone 0.4mg/kg + medetomidine 5ug/kg IM
Induction: alfaxalone 1mg/kg IV
Maintenance: isoflurane in 100% O2
Ancillary therapies: Hartmann’s solution @ 5mL/kg/h
How to pick the bag size:
(BW x 10) x 5
e.g. (20kg x 10) x 5 = 1000mls
(round up) 1L bag
Concerns of a L block on LA for abdominal surgery:
- Excessive dose = increased systemic absorption
- Intra-vascular administration – always draw back + rapid injection = toxicity
- Central nervous system (CNS) signs seen first with lignocaine
- Cardiovascular system (CVS) depression and cardiac arrest seen first with Bupivacaine (long before seizures)
Rebreathing: dogs over 4 kgs circut options:
Paediatric Wye: dogs 4-10 kg
F circuit OR Large Wye: dogs OVER 10kg
Large Wye: dogs over 30-40kg
Non-rebreathing: cats or dogs under 4kg circut:
Bain
USG
Dog: >1.030
Cat: >1.035
-Measures the density of urine compared to pure water (using refractoemetr)
-USG determines the concentration of the urine - gives insight into the hydration status of the animal and functional ability of the renal system
-Renal function is essential to ensure that drugs are metabolized correctly and that damage does not occur
How to measure BP cuff size?
Should be 30-50% of the circumference of limb
If meloxicam is not enough post sx - what to give and how long will it last?
Buprenorphine: 6-8 hours Morphine: 3-6 hours
What drug class is medetomidine?
Alpha 2
What drug class is alphaxalone and what receptor does it bind to?
Neuro-steriod, GABBA
Increased GABBA (inhibitory) activity by increasing cl causing hyperpolarisation and decreased neuronal activity
