Prep For Clinical Practice Flashcards
-Absorbed dose
total amount of radiation absorbed by an object (International System of unit or SI unit: Gray (Gy)).
Equivalent dose
absorbed dose x radiation weighing factor, to account for how harmful a type of radiation is to biological tissues (SI unit: Sievert (Sv)).
Effective dose:
equivalent dose x tissue weighing factor, to account for the radiosensitivity of different organs and the increased risk of the patient developing stochastic (see below) effects (SI unit: Sievert (Sv)).
Direct damage:
results in break of molecular bonds within cells (eg DNA).
Indirect damage
esults in interaction with water leading to creation of free radicals, which in turn can break molecular bonds within cells.
Deterministic effects
they occur at a specific dose threshold and represent tissue reactions; the severity of these effects is dose-dependent. Rapidly dividing cells are most sensitive and radiation sickness reflects body systems affected (eg dermatitis, burns, cataract, gastrointestinal disturbance or changes in blood). The latter are known as somatic effects.
Stochastic effects
represent effects that have no threshold and occur randomly. The severity of the effects is not dose-dependent, but the probability for the effects to occur is dose-dependent.
Carcinogenic effect: tumors may be induced decades after the radiation exposure Genetic effects: mutations may occur in the chromosomes of germ cells in the ovaries or testes, with potential effects in the offspring.
ALARP
he main goal is to keep the radiation dose As Low As Reasonably Practicable (Achievable) at all times
Doses are kept lower than the threshold for deterministic effects. As there is no threshold for stochastic effects, doses should always be kept as low as possible.
Too high kVp will lead to
increased scatter production by the patient, increased scatter in the radiography room and reduced image contrast
oo low kVp may lead to
increased exposure time, with a likelihood of motion artifacts and a need for repeat examination.
Use a grid for subjects greater than
10 cm thick.
Methods of protection against scatter radiation
time, distance, shielding
Dosimetry
Measurement of radiation exposure
Compton absorption
photon of electromagnetic energy interacts with a loosely bound electron in the outer shell of an atom.
The photon displaces the loosely bound electron which can ionize other atoms.
The photon is diverted and continues in a different direction with a lower energy ’Scattered radiation.
Increases with increasing energy.
As energy increases more of scattered radiation is directed in a forward direction, ie more likely to reach x-ray film.
Independent of atomic number of tissue.
Production of scatter
catter is produced when x-rays interact with matter.
Lower energy than primary beam.
Travel in any direction.
Very important inlarge animal radiography.
At high kV less of the primary beam is converted to scatter but more scattered radiation is moving forward towards the film.
Increases with increasing volume of tissue irradiated.
ncreases radiation exposure to personnel.
Increases radiation dose to patient.
Reduces film contrast (increases overall film density in a non-specific way).
how is scatter reduced?
collumation
Compress patient
Reduces volume of tissue irradiated. Can be achieved using Bucky band - a webbing strap which can be tightened around the body (particularly abdomen).
Reduce kVReduce scatter affecting filmGrids
Placed between film and patient to absorb scatter. Most scatter is travelling in an oblique direction and therefore is unable to pass through grid. Results in increased exposure factors required. Grid lines can appear on film.
Alternative filtration devices
Air gap between patient and film:
Radiation travelling obliquely misses film.
Important in large animal radiography where film is often some distance from object.
Air gap increases magnification and reduces image sharpness.
Filter between patient and film:
Lead backing to film cassettes
Reduce effects of scatter on film
Intensifying screens (particularly rare earth) intensify primary photons more than scatter. Screens also increase gamma so that film contrast is enhanced and effect of scatter is reduced.
When compiling an exposure chart as many variables as possible should be kept constant: what variables are these
Film focal distance.
Object film distance.
Processing
Film type
Intensifying screen type Radiography
Use of grid use.
Line mains compensation.
Variable kV
This is used if:
Machine allows variation in kVp of 1-2. Due to the variation in dog size and shape selecting an exposure based on dogs weight may be inaccurate. Breed variability in conformation can be overcome by basing exposure on tissue thickness. Keep mAs constant and as high as possible and alter kV based on tissue thickness. A grid should be used if tissue depth is >10 cm and may be useful in smaller obese animals.
Grids
If using a grid the exposure will need to be increased.
Multiply grid factor by mAs to obtain new mAs.
X-rays
electromagnetic radiation.
Their usefulness stems from a number of properties:
Travel in straight lines. Can pass through a vacuum. Travel at constant speed. Variably absorbed by body tissue. Affect photographic film to produce a latent image ause certain substances to fluoresce (emit visible light)
X-rays are produced when electrons are rapidly deccelerated
Kilovoltage (kV) control
Alters the potential difference applied across the tube head during exposure.
Alters the speed and energy with which electrons hit the target and hence the pentrating power of the subsequent x-ray beam.
In some machines it is linked to mA so that if high mA is selected, kV must be reduced.
Milliamperage (mA) control
Controls the heating of the filament and hence the number of electrons released by the cathode.
This directly affects the quantity of x-rays produced.
Timer (x rays)
The time for which the exposure is applied affects the number of x-rays produced.
The quantity is usually measured as a combination of amperage and time, ie mAs.
The longer the exposure the more chance there is of a patient moving so it is preferable to use the highest mA permissible with a given kV and reduce the exposure time accordingly.
Older machines had clockwork timers but new machines have electronic timers which are quieter and more accurate.
Portable x ray machines
Stationary anode (heat lost by convection and conduction).
Self or half wave rectified.
Often fixed mA
Occasionally fixed kV.
Run from domestic supply (13 amp).
Cheaper than mobile/3-phase machines to buy and maintain.
Can be dismantled and used for domicillary examinations.
mobile x ray machines
Rotating anode (heat lost by radiation)
Usually full wave rectified - 2-pulse.
May be capacitor discharged.
High and variable mA facilitating shorter exposure times.
Higher output allows grid and grid use to be used more readily.
More expensive to buy and maintain than portable machines.
Limited to use within the practice unless van or trailer used!
3-phase x ray machines
Rotating anode.
Full wave rectified - 6 pulse.
High and variable mA and kV.
Very high exposures and short exposure times possible.
Expensive to buy and service.
Fixed installation ’ dedicated room needed.
Medium frequency (high frequency) x-ray machines
An invertor increases the frequency of the electrical supply so that with vastly increased number of pulses the ripple factor is negligible and the generator is equivalent to a constant potential unit.
Used in some mobile machines which may use a battery supply and some fixed machines which run off a 13 amp supply.
Pharmacokinetics
what the body does to the drugp
Pharmacodynamics (PD)
What the drug does to the body
ADME
Absorption (administration), distribution, metabolism and elimination; ADME
Given the heterogonous structure of bodies, on top of its target a drug will inevitably interact with more than one element (side effects possible).
Understanding the ADME (absorption/distribution/metabolism/excretion) of a compound is central to any therapy.
A - Routes of Administration
Enteral routes:
Directly into the gastrointestinal tract
Sublingual
Swallowing
Rectal
Parenteral routes:
Topical admin.
Intradermal admin.
Subcutaneous admin.
Intramuscular admin.
Intravascular admin.
Inhalation
Intravascular administration
Mostly used when there is a need to control accurately the body concentration of drugs. Typically used when compounds have narrow margins of safety between therapeutic and toxic index (e.g. induction agents/anticancer drugs).
Drawback:
Drug injected cannot be recalled . A slow infusion administration is needed to avoid side effects.
Inhalation administration
Gas and aerosols:
Rapid systemic effect but dependent on:
1- the tidal volume
2- the size of the aerosol particle (not true for gas). The smaller the more likely to reach alveolar ducts and sacs. Otherwise get stacked in bronchi.
D - Distribution
Distribution around the body occurs after drug reaches circulation
It must then penetrate tissues to act
consider Movement of drugs across membranes- passive, active, ionic
Active transport / Carrier mediated transport
In general, compounds that rapidly cross membranes have:
a. Low degree of ionization b. High lipid/water partition in the non ionized form c. Relatively low MW < 1000 d. A biological affinity with transporters/facilitated diffusion (e.g. cephalporins are absorbed by a transporter for dipeptides)
Effect of ionization on drugs crossing membranes
Must be neutral to cross the membrane (if too charged they would associate with many other molecules which would impair their ability to diffuse).
Many drugs are weak acids or weak bases
Recall that weak acids (HA) donate (H+) to form anions: HA↔H++A-
Recall that weak bases (B) accept a proton (H+) to form cations: BH+ ↔B+ H+
Recall Henderson-Hasselbalch equation:
pH=pKa+log[nonprotonated/protonated]
pH=pKa: protonated form equal to nonprotonated concentration
pHpKa: vice versa
(dont need to know this just understad concept)
An example!
Effects of ionization on the macrolide antibiotic erythromycin
Erythromycin pka = 8.8
Plasma pH = 7.4. Milk pH = 6.5
Given pH = pka + log non-ionized/ionized
In milk, 199.5 ionized to every non-ionized, in plasma 25 parts ionized to every nonionized = ION TRAPPING
Chemical Properties of Drugs- isomers
constitutional isomers
setrioisomers- diastereomers (cis/trans)- conformers, rotamers
enantomers
M - Drug metabolism
Lipophilic drugs must follow a very special treatment to become hydrophilic (polar), often inactive, and then be excreted.
The drug transformation may be a two phase reaction (but the phase I may be sufficient to inactive and excrete the drug)
In the liver the major drug metabolising enzymes act in the Smooth
Endoplasmic Reticulum of Liver Cells (hepatocytes)
aneamia can effect
drug metabolism
Metabolism and CYPs
The majority of CYPs are found in the liver, but certain CYPs are also present in the cell wall of the intestine.
The mammalian CYPs are bound to the endoplasmic reticulum, and are therefore membrane bound
CYP 3A4, CYP 2D6, and CYP 2C9 are especially involved in the metabolism of xenobiotics and drugs in humans (and probably veterinary species)
Metabolism & Glucuronidation
The major phase II drug metabolising family of enzymes are the Uridine Diphosphate Glucuronyl Transferases (UGTs)
Cats are deficient in UGTs
– Limited ability to perform glucuronidation
– Paracetamol toxicity
Metabolites known as glucuronide conjugates
– Excreted in bile and urine
– Limited stability and can hydrolyse in the gut
– Undergo enterohepatic recirculation
major routs of Drug excretion
renal
billary- faeces
pulminoary
minor routs of excretion
mammary
salivary
Biliary excretion
Parent drug or metabolites may either be excreted in bile and eliminated via the GI tract or recycle several times before entering the systemic circulation (the drug follows bile salts)
Specific liver transporters are involved in the biliary excretion of metabolized drugs
Drugs can be very long lasting (e.g. Antibiotics)
renal excretion
passive filtration, secretion and reabsorbtion
Pharmacokinetic Drug-DrugInteractions
Tissue/plasma levels of one drug altered by another one
– Absorption
• Change in gastric pH
• Alteration in bacterial flora
• Decreased gastric emptying – metaclopramide
– Excretion
• Sodium bicarbonate makes urine more alkaline – increases excretion of weak acids (why?)
• Probenecid reduces renal excretion of penicillins
– Some drugs reduce circulation and may therefore reduce
• Clearance
• Elimination
– Eg alpha-2 agonists
– Metabolism
• Enzyme inhibition/induction
Quantitative Pharmacokinetics (PK)
Changes in plasma/tissue drug concentration with time
Quantitative Pharmacodynamics (PD)
– Changes in biological response with time
Absorption kinetics
IV infusion = zero order kinetics (straight line on grph)
IM/SC/oral = tend to follow first order kinetics. (increasing line on graph) Absorption rate from oral administration tends to be proportional to amount of drug (first order)
Amount of drug at administration site decreases with time therefore, rate of absorption decreases
Drug Elimination Rate
The amount of parent drug eliminated from the body per unit time – occurs after distribution
Volume of water in glass tank is analogous to the volume of blood plus interstitial fluid (body water) also described as the initial volume of distribution (Vi)
Concentration of contaminant in water = 100 mg / 10 L = 10 mg / L
This is analogous to drug concentration in blood immediately after
IV bolus dosing
Contaminant stuck on glass is in equilibrium with contaminant in solution
Concentration of contaminant in solution = 30 mg / 10 L = 3 mg / L
This is analogous to the concentration of a drug in blood after distribution
to tissue
Volume of distribution
Vd usually given in litres/kg
TBW approx. 0.6LKg
ECF approx. 0.1-0.3L/Kg
Vd of 0.1-0.3L/Kg drug most likely water soluble and mainly in ECF. E.g., midazolam or NSAIDs Vd high (2L/Kg +) drug accumulates in another site – e.g., fentanyl in fat
Properties of X-rays and Gamma Rays:
No charge and no mass
Invisible and cannot be felt
Travel at speed of light
Travel in straight line
Penetrate all matter to some degree
Cause some substances to fluoresce
Expose photographic emulsion
Ionise atoms
X-rays are produced by the interaction of electrons with an atom
2 types:
Characteristic
Bremsstrahlung (braking)
Cathode
coiled tungsten wire
The cathode in an X-ray tube generates a stream of electrons via thermionic emission
Potential difference applied across the X-ray tube accelerates the electrons towards the positively charged anode
These hit and interact with the atoms within the target area of the anode resulting in the release of X-rays
Radiodensity (or radiopacity)
is opacity to the radio wave and X-ray portion of the electromagnetic spectrum: that is, the relative inability of those kinds of electromagnetic radiation to pass through a particular material.
Scatter
The effect of the X-ray beam striking another atom
Lower energy radiation produced in the patient’s body tissues - Compton Effect
Amount depends on:
Density/atomic no. of the patient/tissue
Increases in kV- higher penetration higher dose- may stay in tissues- domino effect of ionisation
Larger area (collimation)
As the size of the field increases, the amount of scatter will increase
Properties
May travel in any direction
Image degradation
Ionisation in tissues
Radiation dose – patient, YOU!
Harmful effects of X-rays
Genetic effects
Increased risk of DNA mutation and inherited abnormalities with ionising radiation
Somatic effects
Skin erythema, BM hypoplasia, abortion..
Carcinogenic effects- Rapidly dividing cells most susceptible
Persons under 18
Pregnant women (foetus)
Bone marrow
Gonadal tissue/repro organs
Germinal layers of skin (and gut)
legilation on radiation saftey
Ionising Radiations Regulations 2017 (IRR17)
BVA Guidance Notes for the Safe use of Ionising Radiations in Veterinary Practice
Must appoint a Radiation Protection Advisor and a Radiation Protection Supervisor
Must define and identify a controlled area
Must draw up and follow Local Rules
Radiation Protection Advisor
External to practice
Advanced knowledge of radiation (e.g. Radiation Physicist or Veterinary Diploma holder)
Must hold a RPA Certificate of Competence
Initially helps design and setup radiography facilities (or when any significant changes)
Establishes Local Rules
Annual visits to advise on:
Room design
Layout and shielding
Siting and use of equipment
Local Rules
Dosimetry
Radiation Protection Supervisor
Member of staff within practice
Responsible for day-to-day supervision and enforcement of rules
Makes sure local rules are followed
Keeps local rules and other paperwork up to date
Understand legal requirements
Ensures radiation doses are kept to a minimum
Manage radiation emergencies
Consults with RPA where necessary
Local Rules
(for x-ray
Code of conduct for performing radiography
Should be in an easily visible place
Should be read and understood by every member of staff involved in radiography
Detail equipment, procedures and access restrictions
List RPA, RPS and any staff involved in radiography
Define controlled areas (in practice and for mobile work)
Includes written arrangements for making radiographs, including restraint, record keeping and protective clothing
Controlled Area
(for x-ray)
Area where there is risk of significant radiographic exposure
Determined by Radiation Protection Advisor
Should be clearly defined with warning signs
Primary beam stopped by 4½ inches of brick (double thickness) or 1mm of lead
Scattered radiation stopped by single brick thickness
Radiation not stopped by wood or glass (lead glass and lead lining may be used in protective doors)
Creating controlled area (for x-rays) in the field
Don’t take radiographs in the stable
Too confined
Cant visualise behind stable wall
Stay in open area/yard with good line of sight in the direction of the primary beam
Work on 20 metre control zone
Based on Inverse Square Law, at that distance, the dose from a single diagnostic radiograph will be negligible
Double the distance reduces the exposure risk 4-fold
Dose Monitoring
Film badges or TLDs (thermoluminescent dosimeters) most commonly used
Must be worn by all staff involved in radiography on a regular basis
Must be regularly checked (usually every 1-3 months, depending on practice)
The badge must be OVER the lead, not underneath it
Worn on the chest/neck area
Film-focal Distance
The closer the x-ray tube to the film or plate, the more “concentrated” the x-ray beam and vice versa
The exposure varies according to the inverse square law
Particularly in-field radiography
Maintain source-image distance (SID) for the radiograph itself
Controlling Scatter
- To reduce scatter produced:
Adequate collimation
Use lowest kV compatible with a diagnostic image - To reduce amount of scatter reaching the plate:
Use of a grid
Functions:
Absorb secondary scattered radiation
Allows primary beam to pass through to form the useful image on the film
Used when x-raying patient/part >10cm thick
Grid factor – when a grid is used, the amount of exposure required increases.
The exposure factors increased is the mAs
- Reduce effect of scatter on personnel
Milliampere-seconds (mAs)
The number of electrons generated at the cathode is determined by the mA (milliamperes) and exposure time
mA relates to the tube current
Milliampere-seconds (mAs) is the product of mA and time in seconds
The mA governs the current applied to the filament and this is applied for a specific time (= sec.)
Increased mA = Increased tube current -> Increased number of electrons ->
Greater number of x-rays are produced
HOWEVER
The energy of the x-rays is unchanged
mA x sec = mAs
mAs is a measure of the number of X-rays produced
the kV (kilovolts)
Potential difference applied across the X-ray tube
Aka The energy of the electrons striking the anode is determined by the kV (kilovolts) applied (sometimes called kVp = kilovolt peak)
Increase kV..
Increased energy of electrons
Increasing kV = Increased electron acceleration Increased energy of electrons =
Greater number of x-rays are produced
AND
X-rays have increased energy = increased penetrating power
Quality (x ray)
penetrating power of the beam
Intensity (xray)
amount of radiation in the beam
mA affects intensity only
3 basic things for Xray production:
Source of electrons (through thermionic emission)
A means of accelerating those electrons (kV)
A means of decelerating the electrons (slamming into the anode)
Attenuation
Reduction in intensity of the X-ray beam as it passes through the matter
Due to absorption or scatter or both!
Absorption
The energy from X-ray photon transferred to atoms of absorber.
As more energy is absorbed, the number of X-rays reaching the film reduces – and therefore affects the appearance of the radiograph!
So tissues are seen on a radiograph in various shades of grey according to how much they absorb.
Interaction of X-rays with tissues
The five basic densities:
Metal – White (all x-rays absorbed)
Bone – nearly white
Soft tissue/Fluid – mid grey
Fat – dark grey
Gas – very dark/black (few x-rays absorbed)
The optimal radiograph
Well positioned
Good collimation, centring
Good definition, no film faults
A wide range of well differentiated shades of grey
This means a balance of kV and mAs to ensure there is enough penetration of the patient with sufficient X-rays passing through
Exposure charts help obtain consistent results!
Pink Camels Collect Extra Large Apples
positioning
centering
collumation
expousure
labling
artifacts
Positioning
Position the area of interest as close as possible to the cassette
Anatomical distortion
Rotation
Standard radiographic positions
Use a reference text for standard views
Described in detail in later lectures and in CS booklets
Centring
Centre the primary beam over the area of interest
Can lead to distortion on the image
Centre in middle of area of interest AND middle of the cassette
Collimation
Scatter contributes to image opacity
And increases radiation hazard
Collimate beam to minimum size necessary
But include enough!
The primary beam should ALWAYS be contained within the area of the cassette
Is it collimated sufficiently?
Safety
Describe the number of unexposed borders seen within the boundary of the film/cassette.
0% 25% 50% 100% for 1,2,3,4 sides seen
Exposure
underexposed- too white
overexposed- too dark
Contrast
Difference between radiographic densities
Seen as shades of grey
Ideal is with extremes of black and white
To improve contrast, must adjust the penetration of the X-ray beam.. How?
… This will change the amount of the x-ray beam absorbed by the tissues and therefore the shades of grey
Labelling
abelling:
Patient details and date
Exposed onto film, digital (embedded)
Side markers – should always be exposed onto the image
Side of body/recumbency (L/R)
Artefacts:
Things that shouldn’t be there!
Sandbags, troughs, driplines, collars!
radiographic quality
Blurring
Magnification
Distortion
Scatter
Good definition?
Any film faults?
Pink Camels..
Blurring
(xray)
Movement
Involuntary e.g. breathing
Voluntary e.g. conscious
How do we overcome this?
Chemical restraint, positioning aids
Magnification/Distortion
(xray)
Primary beam diverges with distance from the tube
Can also lead to geometric distortion if object is positioned obliquely to the beam
Beam intensity
Amount of radiation (number of X-ray photons) in beam
affected by mAs and KV
Beam quality
Beam quality
Penetrating power of beam
affected by KV
Density of the image
Amount of blackening of the image
Affected by mAs and KV (film)
Contrast of the image
The range of shades of grey in the image
Affected by KV (film)
The Ultrasound Machine
(Ultra) Sound Waves
Medium required (liquid, solid, gas) for propagation
Piezoelectric crystals oscillate = sound waves
Reflected differently by different tissue types
Picked up by transducer = image
Piezoelectric crystals – an electric voltage is applied to the crystals which causes them to oscillate which is then transmitted as an ultrasound wave into the body. The wave hits something, bouncing back as an echo. The crystals converts the receiving echo into electricity which is then converted into a real-time image on the screen
The transmitted sound waves pass through the thin layer of skin, but bounce off fluids, tissues and internal organs. These reflected waves are received by the probe, which converts them into electric signals which is the converted into an image
Gain- ultrasound
overall brightness
TGC (Time Gain Compensation)
selectively adjusting the gain at different depths
Near field vs far field
accounts for diffrent layers
Focus zones and position
The pulse of ultrasound can be manipulated to be at its narrowest at a particular depth, the focal position.
Maximise image quality
The focal zone is typically positioned at or just below the object you are evaluating.
like a zoom on a tissue
Depth
“zooms in” in 1cm graduations. Higher the depth, lower the image quality.
Depth = the time it takes for the echo to return from the organ
Frequency
- image resolution at the level of the object being evaluated.
highest frequency for a superficial object (in the near field).
lowest frequency for a deeper object
Higher frequency (ultrasound)
decreased penetration but with increased resolution
lower frequency (ultrasound)
Lower frequency = better penetration with decreased resolution
Echogenicity
Echogenicity is a measure of acoustic reflectance, i.e. the ability of a tissue to reflect an ultrasound wave.
Or “how many echoes are bounced back”
The source of echogenicity is impedance mismatching between tissues
Hyperechoic
= tissues that produce strong echoes
Fat, bone, stones, air
Bright/white as ultrasound is reflected
Hypoechoic
tissues that produce few echoes
Soft tissue, muscle
Grey as some ultrasound passes through the tissue, some is reflected
Anechoic
structures that produce no echoes
Fluid
Dark as no ultrasound waves are reflected
Reverberation echo:
Produced by a pulse bouncing back and forth between two interfaces
Transducer:Tissue or tissue:tissue
More likely to occur from highly reflective surfaces like gas and bone
Homogenous
uniform
Heterogenous
non-uniform
Shadowing
Complete reflection of the sound beam
Zone deep to structure will be anechoic
Bone, gas, calculi
Mirror Image
A strongly reflective, obliquely orientated surface may reflect the sound beam distally instead of returning it to the transducer
Takes longer for the sound waves to return, the image will appear deeper to the structure it is reflecting
drug volume=
(weight x dosage)/ drug concentration
drug dosage=
(mg/kg) /weight
Flow rate =
Volume (ml) / Time (hours) Drop Rate
Total Body (Blood) Clearance
the volume of blood plasma cleared of parent drug per time unit
or
a constant relating to the rate of elimination to the blood/plasma concentration
Bioavailability
how much of the drug taken orally that actually gets to the blood plasma
one compartment model
body is seen as one single compartment
two compartment model
bosy is seen as teo compartments
vessel rich group and then to other tissues in the brain heart and kidneys
vessel rich group
Lung, brain, heart, and major organs (liver, kidney) have a relatively high blood flow (vessel-rich group [VRG]) compared with muscle and fat and are more susceptible to anesthetic drug-related effects
theraputic window
the plasma concentration at which the drug is effective
Tmax
the point on the curve where the drug is most active in the body
Constant rate infusions
a loading dose is given and then a low, constant rate of the drug i given to keep within theraputic window
multiple dosing
giving multiple dosing to keep drug level in theraputic range
can lead to overdose
loading dose
A loading dose is an initial higher dose of a drug that may be given at the beginning of a course of treatment before dropping down to a lower maintenance dose
A loading dose is most useful for drugs that are eliminated from the body relatively slowly, i.e. have a long systemic half-life
Without an initial higher dose, it would take a long time for the concentration of these drugs to reach therapeutic levels
Examples include ketamine and fentanyl
what type of biological molecules can drugs interact with
most often proteins
e.g
Enzymes (e.g. ACE inhibitors, aspirin, neostigmine)
Carrier Molecules (e.g. flavonoid – Pgp antagonist, digoxin)
Ion channels (e.g. verapamil - L-type calcium channel antagonist)
Receptors (e.g. benzodiazepine – GABA receptor agonist, adrenoceptor agonists and antagonists )
Structural proteins (e.g. Taxol – Tubulin “agonist”)
DNA (e.g. anti cancer agents like Doxorubicin) (dont need to memorise)
Lipophilicity (Hydrophobicity)
drugs that are hydrophobic may stay in cell membrane and dissrupt cell membrane
this is how inhaled anathetic drugs have a CNS effect
vey lipid soluble molecules take only low doses to produce an anethetic effect
receptors
Protein molecules whose function is to recognise and respond to endogenous chemical signals.
– Chemicals which mimic the endogenous signals (i.e. drugs) will also elicit an effect. Drugs need to bind to receptors with high affinity and high specificity However…drugs generally lack complete specificity
Dose response curves
how do we know a drug is doing what we want
shaped graphs x axis= concentration y axix= effect of drug
shows at a low does there is little effect
rapid increase in the theraputic window
platues at high does- this could be where you see side effects
Potency
amount of drug required to produce 50% of its maximal effects.
Used to compare drugs within a chemical class (usually expressed in milligrams/kg). Example: if 5 mg/kg of drug A relieves pain as effectively as 10 mg/kg of drug B, drug A is twice as potent as drug B.
Efficacy
the maximum therapeutic response that a drug can produce (example: morphine vs buprenorphine)
the tendency of a drug to activate the receptor once bound
Agonism
an agonist produces a responce in a receptor
a full agonist
If the activation is 100%, namely each time a drug interacts with its
target there is a response then the agonist is said to be a “full agonist”
If the activation is <100%, the agonist is said “partial agonist”. Partial
agonists have lower efficacy than full agonists – even with maximal occupancy of receptors.
An agonist has affinity and efficacy – therefore elicits a biological response
Affinity
the tendency of a drug to bind to the receptor
Antagonism
Antagonist: molecule/drug that binds a receptor without activation
Antagonist have affinity but zero efficacy (as they block the target activity)
Main types of antagonism:
• Competitive
• Non-competitive
• Irreversible
competative antagonists
Competitive agonists compete with agonists for the receptor binding site.
The chemical structure of the agonist and competitive antagonist are often similar (lock and key hypothesis).
Antagonist binds to receptor in such a way as to prevent agonist binding
Competitive antagonism is surmountable – additional agonist can overcome the receptor blockade.
Addition of a competitive antagonist shifts the dose response curve of the agonist to the right (e.g. methadone/naloxone)- more drug will have to be given to overcome the block
decrece potency but not efficacy
Non-competitive Antagonism
Non-competitive antagonists either bind to a different receptor site, blocking the desired receptor
OR
Block the chain of events “post” binding - acting “downstream” of the receptor.
ketamine is an example of this
decrese potency and efficacy
Irreversible Antagonism
Antagonist dissociates from the receptor only very slowly or not at all.
The antagonist forms covalent bonds with the receptor.
Irreversible antagonism is insurmountable – additional agonist cannot overcome the receptor blockade.
Often used in drug discovery, rarely in practice – risky
asprin and omeprozol, anticancer drugs
Inverse agonism
drug that reduces the activation of a receptor with constitutive activity (example: GABAA receptor)- these receptors fire without stimulation
Can be regarded as drugs with negative efficacy.
Therapeutic index =
toxic dose (or LD50) ÷ effective dose (or ED50)
EC50: Effective concentration. The dose required for an individual to experience 50% of the maximal effect.
ED50: Effective dose. The dose for 50% of the population to obtain the therapeutic effect
EC50:
Effective concentration. The dose required for an individual to experience 50% of the maximal effect.
ED50:
Effective dose. The dose for 50% of the population to obtain the therapeutic effect.
Would an ideal drug have a small or large therapeutic index?
large!
ideally you want a large toxic dose and small effective dose
Drug receptor types
Ion channel cell surface transmembrane receptor- things tha topen up to let ions in and out of cells to change polarity and make them less or more likley to fire- drugs can open and close these channels
Ligand regulated enzyme- brings molecules toghther to form active catalitic domain
G-protein coupled receptors
Protein synthesis regulating receptor- can upregulate or decrease. acth stimulation test
Tachyphylaxis (“rapid protection”).
Reduction in drug tolerance which develops after a short period of repeated dosing. Not common. Often due to a lack of a co-factor. the bosy runs out of the effect the drug asks it to produce
happens in mainly IV drugs- addrenaline
not self antagonism
Self-Antagonism
When a drug becomes antagonistic to its own effects
Loss of target sensitivity
Change in receptors- become resistant to drug stimulation/conformational changes
Loss of receptors - endocytosis
Exhaustion of mediators- degradation/low re-expression level
Increased metabolic degradation- higher concentration of drugs are needed
Physiological adaptation- crosstalk between body systems, one takes over
Drug transporters- drug removed from receptor sites
Drug-drug interactions
Potential outcomes of drug-drug interactions:
• Action of one or more drugs is ENHANCED
• Development of totally NEW EFFECTS
• INHIBITORY effects on one drug on the other
• NO CHANGE
ligand regulated enzyme
the binding of an extracellular ligand causes enzymatic activity on the intracellular side
G-protein coupled receptors
integral membrane proteins that are used by cells to convert extracellular signals into intracellular responses
activated by agonists
When a ligand binds to the GPCR it causes a conformational change in the GPCR, which allows it to act as a guanine nucleotide exchange factor (GEF). The GPCR can then activate an associated G protein by exchanging the GDP bound to the G protein for a GTP. The G protein’s α subunit, together with the bound GTP, can then dissociate from the β and γ subunits to further affect intracellular signaling proteins or target functional proteins directly depending on the α subunit type
GPCRs are an important drug target
CRI
constant rate infusion
the use of low levels of agents to maintain theraputic dose
CD
controlled drug
TIVA
total intravenous anaesthesia
PO/SC/IM/IV are all …
dosing routes
describe the diffrent sites analgesia may act on
They may act at the site of injury and decrease the pain associated with an inflammatory reaction (e.g. NSAIDs)
They may alter nerve conduction (e.g. local anaesthetics)
They may modify transmission in the dorsal horn (e.g. opioids & some antidepressants)
They may affect the central component and the emotional aspects of pain (e.g. opioids & antidepressants)
Opioids
Natural (opiate) and synthetic (opioid) drugs
Endogenous opiates
Opioid receptors identified; mu(most important), delta, kappa (important in birds), nociceptin
Effect depends on dose, route, species, stimulus etc
CVS effects, pruritis, urinary retention, ileus, pancreatic duct, temperature, miosis, mydraisis, vomiting & nausea, mania & respiratory depression?- MOSTLY IN PEOPLE, side effects limited in vet species
decrease the likly hood that pain signals will be firesd at primary and secondary neurons- work a t a numebr of sites
Morphine
The most efficacious opioid at relieving pain
It is a full agonist at mu, delta and kappa receptors
Not licensed. (CD II)
Nevertheless still used widely
CRIs and epidurals plus horses
Methadone
opiate
A synthetic mu agonist (full) & affinity for NMDA receptor
Has effects as a norepinephrine and serotonin reuptake inhibitor
Following IV - duration of action is approximately 4 hours (can be longer with sc)
Vomiting – not usually
Use as premed, for sedation, intra op (v slow IV), on recovery, and as CRI
Poor oral availability
Licensed for dogs and cats. CD II
Pethidine (Meperidine)
Synthetic agonist at the mu receptor
Also shown to block sodium channels
Agonist at alpha 2 B subtypes
Negative inotropic effects but tends to increase heart rate
NOT IV- Can induce histamine release, im only
Pethidine should not be administered to dogs receiving selegiline
Monoamine oxidase inhibitor + pethidine ≡ serotonin syndrome
CD II (licensed for dogs, cats, horses)
Spasmodic colic
DOA (duration of action) ≈ 90 minutes- short acting
Fentanyl
Fentanyl is a highly lipid soluble short acting mu opioid agonist. CD II
Uses:
Intraoperatively as bolus, with peak analgesic effects occurring in 3-5 minutes
At induction with a benzodiazepine
For compromised patients, fentanyl + benzodiazepine may be sufficient for intubation
CRIs are very effective
Transdermal fentanyl patches
Respiration slows or may cease following a bolus
Bradycardia can be significant
Fentanyl ‘spot on’ licensed for dogs (Recuvyra)
Codeine
has been used in dogs (often with paracetamol) for mild to moderate pain (post op) but…..
Oxycodone
has also been advocated for use in dogs (post op), but little information is currently available
Naloxone
for antagonism of pure mu opioids
Tramadol
Tramadol is popular! But there is a lack of data in dogs, better in cats
It is commonly prescribed to humans – now licensed in dogs
It is a synthetic analogue of codeine; it is a low potency mu selective partial agonist PRODRUG with LIMITED metabolism in dogs
It has an alpha 2 adrenergic effect and inhibits 5HT reuptake
CDIII
Very limited value in dogs but useful in cats
Buprenorphine
a partial agonist with a strong affinity for mu receptors (mild kappa antagonist)
Highly potent but not as efficacious as pure opioids
Peak effect IV admin 45-60mins- long wait time
Mild to moderate pain, good sedation, long duration of action, preservative in multi dose vials
Licensed for dogs and cats and horses
OTM route works v well (cats>dogs)
- Better than butorphanol for analgesia but as it is a partial agonist you cannot increase the effect by giving more- occupies and blocks the receptors for about 6 hours
Allows patients a night sleep and is good for mild to moderate pain
OTM route
oral trans mucosal
Butorphanol
Only mixed one!
is a kappa opioid agonist and mu antagonist (short-medium duration)
Its actions differ to that of the other opioids
Available as oral form (Torbutrol)
Useful in combination with acepromazine for sedation e.g. cardiac patients
Licensed for dogs, cats & horses
Antitussive- suppresses cough
LIMITED ANALGESIA- Blocks mu receptors for up to 6 hours! But only 10 mins of analgesia and prevents use of other opiod analgesis
Alfentanil, sufentanil and remifentanil
can be used during anaesthesia to blunt sympathetic stimulation
All have context sensitive half lives shorter than fentanyl
Remifentanil is metabolized by plasma esterases
Remifentanil always given by CRI
Given as low dose (for analgesia) or higher doses as part of TIVA
MAC reduction of these opioids has been shown in dogs and cats
None licensed for dogs and cats
Local Anaesthetic (LA) Agents
block the sodium channels in nerve fibers, blocking transmission
the unionised local anethetic enters cell, becomes ionised and is then able to block the sodium channel
it can also affect eh membrane directly
LAs are weak bases and largely ionised at physiological pH. - Problem in inflamed tissue
Their speed of onset is inversely related to their degree of ionization. -Longer to start working in inflamed tissue
Their duration of effect is directly related to their degree of protein-binding.
Their potency is related to their lipid solubility.
Lidocaine
Prilocaine (+lidocaine)
Bupivicaine
Mepivicaine
Ropivicaine
Etidocaine
Amethocaine
Proparacaine
Cocaine
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
Inhibit prostaglandin production by interfering with cyclo-oxygenase (COX)- COX 1, 2
Now thought also to have a spinal action
Synergistic with other drugs
iv, im, sc, po
non sterodials vlock the production of cyclooxygenase and therfore the production of PGG2- steriods also act earlier of this pathway so they should not be used toghter- gastric ulcration
Some licensed for pre-operative use
Carprofen and meloxicam have revolutionized perioperative pain management in UK in last 3 decades
Traditional NSAIDs are contraindicated in patients with:
Renal or hepatic insufficiency
Hypovolaemia
Congestive heart failure & pulmonary disease
Coagulopathies, active haemorrhage
Spinal injuries
Gastric ulceration
Concurrent use of steroids
Shock, trauma (esp head trauma)
Pregnancy
COX 1
NSAI block the production of this enzyme
Prostaglandin (PG) synthesis attributable to COX 1 along length of GIT
PGs play a role in regulating renal blood flow, reducing vascular resistance & enhance organ perfusion
COX 1 is found in neurones and in the foetus, amniotic & uterine tissue
Blood platelets contain COX 1
Cox 1 = ‘housekeeping’?
BUT
Earlier NSAIDS also inhibit COX1
COX 2
NSAIDs with a more favourable GIT profile were being sought before COX 2 was discovered
When COX 2 was discovered in 1991 it was shown that 3 drugs (carprofen, etodolac & meloxicam) with an enhanced GIT protective profile inhibited COX 2
Then assumed that COX 2 selective NSAIDs were the answer…
This has not been shown to hold true
Deracoxib & firocoxib – problems in humans, not all coxibs have problems!
COX 2 induction in heliobacter pylori gastritis, IBD & bacterial infections
Therefore COX 2 inhibition may exacerbate the situation…
Supported by transgenic studies
COX 2 may have a role in GI defence
In summary do not equate COX 2/COX 1 inhibition ratios to overall in vivo safety!
Licensed NSAIDs for horses
Phenylbutazone
Suxibuzone
Firocoxib
Meloxicam
Flunixin meglumine
Vedaprofen
Carprofen
Grapiprant (Galliprant)
New class of piprant NSAIDs- Non-cyclooxygenase inhibiting non-steroidal anti-inflammatory drug- blocks EP4 further down in pathway instead
Licenced for treatment of mild to moderate osteoarthritis pain and inflammation in dogs
Has been called ‘next step’ when ‘traditional’ NSAIDs are not tolerated
Approved for use in dogs from 9 months of age and favourable safety profile
Once daily administration (chewable tablet) – 2mg/kg
Adverse events include vomiting, diarrhoea, decreased appetite and tiredness.
Often dogs will adjust but washout between NSAIDs essential
Not for use in cats
What is paracetamol?
Paracetamol: 10-15 mg/kg PO two to three times daily. Is it a NSAID?
Analgesic & antipyretic
Mechanism of action unknown!
Thought to inhibit COX-3(??) but recent data suggest there may be another site
Alpha-2 Adrenoceptor Agonists
good sedatives
between opiates and nonsteriodals
Bind to alpha 2 receptors
Receptors widespread
Drugs have other actions (sedation, ↓HR etc)
Systemic, epidural, peripherally
Synergism with LA’s
Dogs/cats
Medetomidine (45 minutes)
Dexmedetomidine (45 minutes)
Horses
Xylazine (30 minutes)
Detomidine (45 minutes)
Romifidine (60-70 minutes)
Cattle
Xylazine
Detomidine
Very useful drugs
Sedative action
Analgesic (& reduce MAC)
Compatible with other drugs & potential to antagonise (atipamezole),
IV, IM, epidurally, buccally (detomidine)
Small volume
Alpha 2 receptors:
3 subtypes (4) A,B,C
Diverse sites: CNS & PNS
Side effects-
Hyper (B) then normo/hypotension (A)
Decreased CO & HR, increased SVR
Respiratory depression
Increased urine production
Decreased GI motility
Decreased surgical stress response
Hyperglycaemia, GH enhanced
Thermoregulation affected
Sweating
NMDA Antagonists
Ketamine
As induction agents
As analgesics peri op
Ketamine for fractious cats (sprayed in mouth)
Very versatile
Will improve the patient’s post op comfort
Ketamine
It has been shown that at low doses ketamine can prevent the ’wind up’ and sensitisation of dorsal horn cells
0.5mg/kg after induction
Can be used in the pre-med
CRI e.g. Add 60mg ketamine to 1L LRS and administer at 10ml/kg/hr to dogs intra op (10mcg/kg/min)
NMDA Antagonists
As induction agents
As analgesics peri op
Ketamine for fractious cats (sprayed in mouth)
Very versatile
Will improve the patient’s post op comfort
Premed combinations
Acepromazine + opioid
Alpha 2 agonist + opioid or BZD or ketamine
BZD + Ket
Opioid + BZD
Alpha 2 + BZD + opioid
Post operative period in regards to anelgesic drugs
How long should we provide analgesia for?
24-72 hours for routine ops
Involve the owner
Rescue analgesia (what is yours?)
What options do we have available?
NSAIDs (daily, oed, monthly)
Opioids (patch, long acting formulations, oral forms (tramadol, morphine, OTM buprenorphine)
LA blocks
Adjuncts for chronic pain (amantadine, gabapentin etc)
side effects of antibiotics
Direct toxicity – aminoglycosides
Drug interactions – sulphonamides and alpha-2 agonists
May reduce normal protection – gut flora
May cause tissue site necrosis (tetracyclines)
Chloramphenicol has been shown to cause a reduced immune response
Some can cause reduced metabolism
Potential residues in food producing animals
RESISTANCE
Hypersensitivity
Anaphylactoid reactions
What Influences Success of antibiotics
Bacterial susceptibility
Pharmacokinetics and tissue penetration
Most tissues – concentration is perfusion limited
Free drug concentration in plasma is related to, or equal to that in tissue
In some tissues – concentration is permeability limited where non inflamed
CNS
Eye
Lung
Prostate
Mammary gland
Local factors
Abscess - pus - necrosis – inactivates aminoglycosides and sulphonamides
Foreign material – bacterial glycocalix
Slowed bacterial growth – less susceptible to cephalosporins and penicillins
Low pH/low oxygen – erythromycin, fluoroquinolones
Haemoglobin - penicillins
Wound cleansing and drainage
Compliance
Factors Affecting Choice of antibiotic
Presence of infection (Gram stain culture and sensitivity)
Spectrum
Habitual reliance on broad spectrum indicates low standard of diagnosis
Bacteriocidal versus bacteriostatic
Cost
Toxicity
Concurrent disease
Pregnancy
Habit…..!
Dosage and frequency
Route
Duration and re-evaluation
Acute versus chronic infection
Immunocompromise
Septic arthritis
Osteomyelitis
Combination therapy
Not bacteriostat + bacteriocide
Peptidoglycan is unique to bacteria, making it ….
good antibiotic target
Amoxicillin-clavulanate
Penicillin based – -lactamase inhibitor
Staphs, streps
Gram negatives
Escherichia and Klebsiella spp variable
Pseudomonas enterobacter resistant
Lincosamides
Penicillin based – -lactamase inhibitor
Usually bacteriostatic
GI irritation –do not use in horse except foals, never in rabbits
Basic drugs – ion trapping in milk
Fluoroquinolones
Penicillin based – -lactamase inhibitor
Reserve for serious gram-negative systemic infections
Do not use routinely and non-selectively
If used, use the correct dose!
Potentiated sulphonamides
Penicillin based – -lactamase inhibitor
Old but useful – resistance growing
Aminoglycosides
Penicillin based – -lactamase inhibitor
Gentamicin – gram-negative aerobes
Adjuncts
Probiotics?
Anti-tetanus toxin
Foaming agents –foot rot
prophylactic use of antibiotics
Not indicated for routine, clean surgery where no inflammation is present, GI system not invaded and aseptic technique has not been broken
But do use for:
Dental procedures
Leukopenia
Contaminated surgery
Where infection would be disastrous – orthopaedic
Administer before procedure and within 3-5 hours of contamination
Slow IV
Appropriate to contaminating pathogen
licensed antifungals
Ketoconazole Fungiconazol 200 mg tablets for dogs – dermatphytosis. Used off licence for systemic infections.
Itraconazole oral solution for cats and birds, e.g. Itrafungol 10 mg/ml Oral Solution (treats M. Canis). Used off licence for systemic infections.
Miconazole. In various shampoos and ear drop preparations.
Nystatin ear drops - Canaural
Terbinafine – in various ear drops for dogs
Clotrimazole- in various ear drops for dogs
Enilconazole. Imaverole Concentrate for Cutaneous Emulsion – cattle, horses and dogs vs dermatophytosis
Bovilis® Ringvac MSD Animal Health UK Limited vaccination for cattle
unlicnened antifunglas
Amphotericin b
Climbazole
Fluconazole
Silver sulfadiazine
Tiabendazole
treatment of ringworm
Clipping of the hair coat, especially small animals, removes infected hairs, stimulates new hair growth and hastens recovery
Systemic ketoconazole (dogs), itraconazole (cats) plus a topical treatment (e.g. miconazole)
Treatment with ketoconazole suppresses testosterone concentrations and increases progesterone concentrations and may affect breeding effectiveness in male dogs during and for some weeks after treatment
Treatment of dermatophytosis should not be limited to treatment of the infected animal(s)
Measures to prevent introduction of M.canis into groups of cats may include isolation of new cats, isolation of cats returning from shows or breeding, exclusion of visitors and periodic monitoring by Wood’s lamp or by culturing for M.canis
Bovilis® Ringvac reduces clinical signs of ringworm caused by Trichophyton verrucosum (prophylactic dose) and shortens the recovery time of infected cattle showing clinical signs of ringworm (therapeutic dose)
Initially the whole herd should be vaccinated (two vaccinations 10-14 days apart).
Subsequently, (closed herds) only young calves require revaccination at around 2 weeks of age, followed by a second injection 10-14 days later. New animals should receive a full vaccination course. No subsequent doses are required.
Can be used during pregnancy (?lactation).
Administration is by intramuscular injection.
Aspergillosis treatment
First line treatment = topical clotrimazole formulated in a polyethylene glycol base
Indwelling tubes trephined into the frontal sinuses or via the nares as a single infusion.
The infused solution is left in place for 1 hr, during which the dog’s position is changed periodically
~80% success rate
Also reports of enilconazole (bid for 7–14 days), via tubes implanted surgically into the frontal sinuses
Systemic treatments of ketoconazole, itraconazole, fluconazole, voriconazole, and Posaconazole reported
In horses, surgical exposure and curettage have been used for guttural pouch mycosis.
Topical natamycin and oral potassium iodide have been reported effective
Itraconazole (3 mg/kg, bid for 84–120 days) has been reported effective in Aspergillus rhinitis in horses
aspergiliosis diagnosis
Imaging (radiographs/CT) of the nasal cavity can show turbinate tissue destruction
Visualization of fungal plaques by rhinoscopy together with serologic and either mycologic or radiographic evidence of disease is gold standard .
Culture result alone is not appropriate (ubiquitous and can be isolated from the nasal cavities of healthy patients)
Systemic disease is usually diagnosed by culture of the organism, often from urine
Two pharmacological approaches to viral control
effective vaccines or antiviral therapy
licensed Antiviral agents
One licensed agent
Virbagen Omega
Contains recombinant omega interferon of feline origin
For cats (sc) and dogs (iv)
Licenced for treatment of canine parvovirus, feline leukaemia virus (FeLV), and feline immunodeficiency virus (FIV)
Interferons increase the cell’s resistance to a virus
unlicenced antiviral agents
Aciclovir
Famciclovir
Ganciclovir
Lamivudine
Zidovudine
Oseltamivir for treatment of viral diseases in dogs (parvovirus and parainfluenza) has also been reported
Biochemistry/haematology/serology of FIP
Hypergammaglobulinaemia; raised bilirubin without liver enzymes being raised, lymphopenia; non-regenerative anaemia, high antibody titre to FCoV
FIP treatment
Feline interferon omega (Virbagen Omega) or human interferon alfa-2b have been used – limited success
Stimulate body’s response
Immunosuppressive and anti-inflammatory drugs reduce inflammation. Commonest immunosuppressive drug used in FIP is prednisolone (corticosteroid) but no placebo-controlled trials showing prednisolone to be better than other anti-inflammatories
GS-441524 is a nucleoside analogue
Two published studies from UC Davis in 2018 and 2019. Results were 100% (10/10) recovery rate reported in experimentally infected cats and 84% (25/31) recovery rate in naturally infected cats. Of the recovered cats, owners reported that they returned to “near normal” within two weeks of treatment
The 2019 study proposed the optimized treatment protocol for GS-441624 use as 4.0 mg/kg given as a subcutaneous injection once daily for at least 12 weeks
can only buy it for research currently
Equine vaccines
Routinely equine flu, tetanus, equine herpes virus, equine rotavirus and now strangles
Following 2019 equine flu outbreak in the UK some governing bodies moved from annual to six-monthly requirements
All vaccination records should be kept up to date in the horse’s passport document
Up-to-date vaccination record is a requirement of many sporting governing bodies for horses competing under their rules
Cattle vaccines – what’s available?
Bovine viral diarrhoea
Very common disease in the UK. About 60% of cattle in the EU test positive for exposure to the BVD virus. Timings for all BVD vaccines are to aim for full protection to occur at least two to three weeks prior to service.
Infectious bovine rhinotracheitis
Live and inactivated vaccines are available. Live vaccines have rapid onset of immunity and are of use in the face of an outbreak to reduce clinical signs and improve the immunity quickly but inactivated vaccines appear to be better at producing longer-term immunity
Leptospirosis
Two vaccines are available in the UK for leptospirosis control. In both cases a primary course of two doses four to six weeks apart, followed up with annual boosters, is preferably given in the spring before the period of highest risk.
Calf enteric disease – rotavirus, coronavirus and Escherichia coli
A number of vaccines are available for immunising pregnant cows and heifers to raise antibodies to rotavirus, coronavirus and Escherichia coli. After birth, the calves gain protection in their gut from drinking the colostrum and milk that is fortified with these antibodies.
Some minor differences exist in the timing of the various vaccines.
Pneumonia vaccines
Calf pneumonia vaccines are available for infectious bovine rhinotracheitis, parainfluenza type three, bovine respiratory syncitial virus, Pasteurella, Mannheimia haemolytica and Histophillus somni, and many combinations are available depending on what protection is needed.
It is important to identify the common diseases present and the age calves become infected
Lungworm
The only lungworm vaccine available uses irradiated live lungworm larvae that create an immune response from the animal, but the larvae do not continue to reproduce, so do not cause clinical disease. The vaccine is a two-dose programme given approximately four weeks apart to youngstock at the beginning of their first grazing season. The second dose should be given at least two weeks before turnout, and vaccinated and unvaccinated stock should not be mixed for at least two weeks after the second dose has been given.
It is preferable for calves to be exposed to low levels of lungworm larvae throughout the grazing season to stimulate and maintain this immunity. If the worming protocol on the farm is too effective, there may be small exposure of the calves to lungworm, allowing very little natural immunity to build up, and this leads to insufficient long-term immunity in adult cattle, which can develop the disease in subsequent grazing years.
Clostridial diseases
Vaccinations against clostridial diseases are routinely given to sheep, but the uptake is much less in the cattle sector. A number of products exist on the market.
Ringworm
Mastitis
STARTVac, covers the main mastitis causing pathogens, E coli, Coliforms, Staph aureus and Coagulase-Negative Staphylococci (CNS), but does not protect against Strep uberis. It involves a complicated programme and is quite expensive
Salmonella
In the face of a Salmonella outbreak on farm, a fluid vaccine can be used to improve immunity to S. enterica serovar Dublin and S enterica serovar Typhimurium
Bluetongue
Not routinely used in UK but two vaccinations are available
Pig vaccines – what’s available?
Porcine parvovirus
Porcine reproductive and respiratory syndrome
E.coli
Clostridia
Erysipelas
Mycoplasma hyopneumoniae
Lawsonia intracellularis
Atrophic rhinitis
Glasser’s Disease
Aujeszky’s Disease
Salmonella typhimurium
Also relatively new intramuscular vaccine to control ileitis in pigs
The bacterial disease is present on most pig farms in the UK and causes widespread digestive health problems
There are often no visible signs of ill health, but an infection with the bacterium Lawsonia intracellularis can lead to poor feed conversion ratios (FCR) and reduced growth rates
More serious infection levels also cause diarrhoea and result in increased herd mortality rates.
Sheep vaccines – what’s available?
Vaccines available in the UK for sheep
Clostridial diseases, e.g. lamb dysentery, pulpy kidney, tetanus, braxy, blackleg
Pasteurellosis
Ovine abortion, e.g. toxoplasmosis and enzootic abortion
Louping ill
Contagious pustular dermatitis (Orf)
Footrot
Dog Core vaccines in the UK
Canine Distemper Virus (D)
Canine Adenovirus/Infectious Canine Hepatitis (H)
Canine Parvovirus (P)
Leptospirosis (L). Please be advised that vaccines are multivalent; preparations are available containing different Leptospira strains.
Core vaccines
protect animals from severe, life-threatening diseases that have global distribution and which ALL dogs and cats, regardless of circumstances or geographical location, should receive. Non-core vaccinations protect from disease where the animal’s geographical location, lifestyle or environment puts them at risk, e.g. rabies vaccination before overseas travel. (
Dog non-core vaccines in the UK
Bordetella bronchiseptica +/- Canine parainfluenza virus (“Kennel Cough” vaccine): vaccination should be considered for dogs before kennelling or other situations in which they mix with other dogs (e.g. dog shows, training classes)
Rabies: legal requirement for dogs travelling abroad / returning to the UK
Canine Herpes Virus: for breeding bitches
Leishmaniasis: before travelling to endemic areas
Borrelia burgdorferi (Lyme disease): for dogs at high risk of exposure
Cat core vaccines in the UK
Feline enteritis (feline parvovirus) (P)
Cat flu (feline calicivirus (C) and herpes virus (H)
Cat non–core vaccines in the UK
Feline leukaemia vaccine (FeLV) (this may be considered a core vaccine for all cats that go outdoors or are in contact with cats which go outdoors).
Chlamydophila felis (Chlamydia)
Rabies: legal requirement for cats travelling abroad / returning to the UK
Bordetella bronchiseptica
Rabbit vaccines
Myxomatosis
Two forms of Rabbit Viral Haemorrhagic Disease (RHD) caused by RHDV-1 and RHDV-2 strains where local risks and individual veterinary advice indicate the need
ferret vaccines
Rabies: legal requirement for ferrets travelling abroad / returning to the UK
Distemper: No vaccine currently licensed for use in ferrets in the UK, some owners ask for canine distemper vaccines in discussion with their vet
what is the mode of action and target of penicillin
inhibits cells wall synthesis
gram postitive bacteria
what is the mode of action and target of ampicillin
inhyibits cell wall syntheisis
broad spectrum
what is the mode of action and target of Bacitracin
inhibits cell wall syntheisis
gram positive bacteria (applied as skin ointment)
what is the mode of action and target of cephalosporin
inhibits cell wall syntheisis
gram positive bacteria
what is the mode of action and target of tetracycline
inhibits protien synthesis
broad spectrum
has wide spread, plasmid mediated imunity
what is the mode of action and target of streptomycin
inhibits protien synthesis
gram neg
tuberculosis
what is the mode of action and target of sulfa drug
inhibits cell motabolism
bacterial meningitis
urinary tract infections
what is the mode of action and target of rifampicin
inhibits RNA synthesis
gram positive bacteria
gram negative bacteria
what is the mode of action and target of quinolones
inhibits DNA synthesis
urinary tract infections
what is the mode of action of polyenes
(amphotericin, B Nystatin)
interacts with sterols in cell membrane to cause cellular leak
what is the mode of action of antibiotics (against antifungals)
griseofulvin
inhibits mitosis (via the microtubules)
what is the mode of action of azoles
fluconazole
itraconazole
ketoconazole ect
inhibits ergosterol synthesis (inhibits cell membrane)
what is the mode of action of allylamines
terbinafine
inhibits ergosterol (cell membrane)
what is the mode of action of thicocarbamate
tolnaftate
inhibits ergostero (cell membrane)
what is the mode of action and target of antimetabolite
flucytosine
inhibits dna and rna synthesis
what is the mode of action and target of profens
flurbiprofen
ibuprophen
directly damages the fungal cytoplasmic membrane
what are the components of a surgical theatre
Surgical environment should have several distinct areas:
Changing area
Surgical prep/induction
Scrub area
Operating theatre
Recovery
Utility
Skin disinfectants
Chlorhexidine 2% with or without 70% isopropyl alcohol
Not suitable for broken skin, wounds, mucous membranes
Povidone iodine 7.5%
Suitable for contact with mucous membranes
Non-povidone iodine (alcohol free)
For use with ocular surgery
Equally effective at reducing bacterial counts
Chlorhexidine has greatest residual action
what class of antibiotis inhibit cell wall synthesis
penicillin
ampicillin
bacitracin
cephalosporin
what class of antibiotis inhibit protein synthesis
tetracyclin
streptomycin
what class of antibiotis inhibit cell metabolism
sulfa drug
what class of antibiotis inhibit RNA synthesis
rifampicin
what class of antibiotis inhibit DNA synthesis
Quinolones
comon bacterial agents of Bite wounds, trauma and contaminated wounds
Staphylococcus spp, Streptococcus spp, Pasteurella spp, anaerobes
comon bacterial agents of Osteomyelitis
Staphylococcus spp, Streptococcus spp, Proteus, Pseudomonas (cat/dog), anaerobes
Septic arthritis
Staphylococcus spp, Streptococcus spp, coliforms
What is General Anaesthesia?
Controlled, reversible depression of the CNS so as to produce lack of awareness of painful inputs (nociception)
Minimal depression of hind brain functions – cardiovascular centres
What is Local Anaesthesia/analgesia?
Local anaesthesia (local analgesia) – not aiming for CNS depression
what are the components of the anethetic triad
unconciousness
muscle relaxation
analgesia
one drug does not do all of these therefore we need a cocktail
The less anaesthetic you give…
…the better for the patient’s physiology
Less cell and organ damage
Quicker recoveries
Quicker return to normal appetite
Better functioning immune systems
Balanced Anaesthesia
Using multiple drugs to minimise the dose and the side-effects of any one of them
Results in lower doses of potent anaestheticsless CNS depression
Better achievement of the goal of anaesthesia
Hypnosis
artificially induced sleep
analgesia
Anti-nociception
Muscle relaxation
From the same agent producing hypnosis or
From a centrally acting muscle relaxant - diazepam or
From a specific neuromuscular junction blocking agent - curare
modern stages of anesthesia
Conscious
Anaesthetised
Dead
Unconsciousness is an all or nothing thing
Level of CNS depression
Specific signs related to muscle relaxation
Signs related to brain stem depression
Respiratory rate
Heart rate
Blood pressure
Minimising anesthesia risk
Support
Oxygen
Fluids
Warmth
Monitoring
During anaesthesia
Recovery
Anaesthesia record sheet
Legal record
The trained anaesthetist
Tranquilisation
relief of anxiety
Sedation –
central depression, drowsiness
Narcosis
drug induced sleep produced by narcotics - opium like drugs
Dissociative anaesthesia
induced by drugs such as ketamine that dissociate the thalamo-cortical and limbic systems
The Anaesthetic Process
IDENTICAL for all species
History and examination
The anaesthetic plan
Place iv cannula
Premedicate, allow to settle
Induce anaesthesia – injectable agent
Once intubated do ABC
AIRWAY, BREATHING, CIRCULATION
Connect to anaesthetic machine and supply volatile anaesthetic in oxygen (or us total injectable with top ups)
Alter inspired concentration in response to physical signs
Supply analgesia separately
Recover following anaesthesia
Continue to monitor until patient comfortable/discharged
Why are combinations of agents used for anesthesia?
One agent could be used to induce and produce all 3 desired effects of the triad (unable to perceive painful stimuli, relaxed muscles, unconsciousness) but with massive physiological depression
Eg isoflurane, sevoflurane
But usually injectable agents are used in combination
“Balanced anaesthesia”
E.g. ketamine: if used alone, poor muscle relaxation
Add medetomidine: improved analgesia and muscle relaxation
Why is Airway Management Important?
Allows delivery of oxygen and inhaled anaesthetic gas
Most anaesthetics cause respiratory depression
Loss of airway reflexes = prone to airway obstruction
Brachycephalics obstruct
All the above cause hypoxia- high mortality
Allows scavenging and environmental protection
Allows intermittent positive pressure ventilation (IPPV)
Allows ventilator support in ICU setting
‘Protects the airway’
Under normal anaesthesia
Reflux 40-60% in anaesthetised dogs
Most of this is silent – may not be witnessed
When carrying out oral/pharyngeal procedures
E.g. Dental work and associated debris
Allows airway management during bronchoscopy
Allows one lung ventilation
Pre-Anaesthetic Fasting?
Recommended in adult dogs/cats 3-6 hours, water until premed
<3 = food present. >6 = stomach pH drops so reflux is damaging
Neonates = from 0.5 to 3 hours – monitor glucose
Horses withdraw concentrate overnight (to reduce gas distension) – controversial
Ruminants withdraw 6 hours and reduce concentrates ( to reduce gas distention) 12-24 hours
Small exotics/furries – shorter times depending on species
intubation methods
Endotracheal tubes
Supraglottic airway devices
V-gels (rabbits)/I-gels (cats)
Laryngeal mask airways
Face masks
Others
(Tracheostomy tubes)
(Arndt endobronchial blockers)
Endotracheal Tubes (ETT)
Various types available
Most are cuffed with a visible pilot balloon
Inflate to ~25mmHg – use manometer if possible
Murphy, Magill or Cole
Use of laryngoscope advisable
Flow = ∆𝑃𝜋𝑟4/8∩𝐿
Go as large as possible
What size shall I place?
Selection based on nasal septal width = 21% accurate
Selection based on tracheal palpation = 46% accurate
Best technique = visualise larynx using laryngoscope
Spray lidocaine (only cats as the have larygneal spazm) and WAIT
Try largest but have a range available
Cut to length – minimise dead space
Not possible with armoured tubes
Red Rubber ETT
Red rubber in common use
Crack over time + non-repairable
Prone to kinking
Irritant
Not possible to visualise blockages
Low volume high pressure cuff
Can lead to tracheal trauma but good seal
Difficult to recommend
PVC and Silicone ETT
More popular than rubber
Disposable but reused, silicone tubes repairable
Less prone to kinking compared to rubber
Non-irritant
Allows visualisation of blockages
Usually high volume low pressure cuff
Less risk of tracheal trauma but relatively good seal
Recommended
Armoured Endotracheal Tubes
Wire coil embedded in wall
Resist kinking but more difficult to place without stylet
If bitten may permanently obstruct
Useful in ophthalmic cases
Impossible to reduce dead space
Contraindicated in MRI
Cole Pattern Tubes
Designed for emergency use in paediatric anaesthesia
The shoulder of the tube should impact in the larynx to provide a gas-tight seal
However movement or IPPV tends to dislodge the tube
Still quite useful for exotic animal anaesthesia- snake ect
Supraglottic Airway Devices (SADs)
Developed originally for human anaesthesia
Major cardiovascular and laryngospasm problems in humans
ETT remain ‘gold standard’
veterinary specific LMAs achieving popularity for short uncomplicated procedures
Increasing evidence of their effectiveness in veterinary patients
Veterinary Specific SADs
V-gels are veterinary specific (rabbits and cats)
2 species where ETT placement can be challenging
Designed to anatomical standards
Can be used to protect the airway the same as an ETT
IPPV is possible
Channels to divert regurgitation can be incorporated
Very useful for short procedures and for bronchoscopy
Always use capnography
Face Masks for anesthesia
Should cover nose and mouth
Not whole head
Avoid eyes
Beware of dead space – choose the shape
Transparent masks preferable
Ensure a good seal using rubber diaphragms
Have been used for anaesthetic induction – NOT recommended
Stage 2 excitement and no airway protection
Very useful for provision of supplemental oxygen
Complications of Airway Management
High pressure/low volume (red rubber and some silicone ETT) exert pressure on a small part of the tracheal mucosa.
May see tracheitis or pressure necrosis
This can lead to tracheal strictures
Extreme cases may see tracheal rupture
Post-op subcutaneous emphysema in cats – but still recommended to use a cuff
ALWAYS disconnect from breathing system when changing position whenever a change in recumbency is needed
Especially with dental cases where head and neck movement is common
Always inflate carefully preferably with manometer
Or listen for leaks
ETT over insertion – carefully measure
Should be at level of thoracic inlet
Too long potential one lung ventilation
Cleaning and storage of ETT and LMAs
Usually stored on wall brackets ideally keep covered to avoid contamination
Common cause of tracheitis is insufficient rinsing of ETT tubes
LMAs need to be thoroughly dried after cleaning or tend to degrade
What Type Of Intravenous Cannula?
‘Over the needle’
24-10 gauge, 1.9-13.3 cm long
Relatively stiff material
‘Through the needle’
Large bore insertion needle
Cannula passed through the needle
Central veins
Not used commonly
Peel away – place through an over the needle cannula
Seldinger/over the wire cannula
placment of cannula
Cephalic
Most used site as animals easiest to restrain
Start distally (can then use the higher site)
Saphenous Veins
Requires more assistance
Medial or lateral saphenous
Use vein on caudal aspect of leg as it ascends
Medial easier in cat – straighter
Good choice in brachycephalics
Jugular- horse
Useful for long term therapy & regular sampling
Well tolerated
Multilumen cannulae available
right (straighter in the dog)
The Auricular Veins
Useful in animals with large or floppy ears, rabbits, ruminants too
EMLA cream can help to reduce discomfort
What size of cannula should u use?
22g (blue) for v small patients
20g (pink) or greater for most patients including cats
>20kg dogs use 18g
Very large dogs use 16g or 14g
maintinance of a placed intravenous cannula
Check cannula regularly and flush q 6 hours with heparinised saline (1IU/ml); does this help ????
Normal cannulae can be maintained for up to 3 days after which they should be replaced (exceptions do occur)
Swab ports prior to injection
Replace giving sets, bungs and T ports after 3 days
complications a cannula
Extravasation
Thrombosis (where do the thrombi occur)
Thrombophlebitis
Infection
Emboli (air, catheter)
Exsanguination
What would you do in these situations?
what are the functions of an anesthetic machine?
Delivery of oxygen / nitrous oxide at known rate.
Delivery of known concentration of IAA.
Removal of exhaled gases from patient.
Recirculation or removal of exhaled gases.
Facilitate IPPV/ CPR.Delivery of oxygen / nitrous oxide at known rate.
Delivery of known concentration of IAA.
Removal of exhaled gases from patient.
Recirculation or removal of exhaled gases.
Facilitate IPPV/ CPR.
Gas Source of an enesthetic machine function?
Molybdenum steel cylinders
Specific yokes and Bodok seal
Colour coded (e.g. oxygen = black/white top). Also piped gas from large cylinders. Usual sizes = E,G,F
Oxygen ; pressure = contents
Nitrous oxide ; liquid with vapour above. Therefore volume of gas in cylinder = (Wt. Cylinder – Empty Wt. Cylinder) x 534
Needle valve and flowmeter.
Regulate flow into low pressure side of machine. Flowmeter = graduated glass tube with floating bobbin/ball. Can stick. Read at TOP of bobbin/middle of ball. Rotate.
Back bar
Horizontal part of the anaesthetic machine circuit between the rotameter block and the common gas outlet
Vaporisers are mounted on the back bar, enabling volatile agents to be added to the fresh gases. The pressure in the back bar is approximately 1 kPa at the outlet end, and may be 7–10 kPa at the rotameter end
Contains a ‘blow off’ or pressure relief valve at the outlet end plus safety features to only allow one vaporiser in use
Intermittent positive pressure ventilation (IPPV)
Intermittent manual – ‘sighing’. A good habit! Close valve + short inspiration up to 20cm water. Chest supra-maximal. OPEN VALVE AGAIN.
Continuous manual. Repeated sighing. Can be tiring. Will allow breathing control but turn down vaporiser.
Mechanical. Ventilator. TV – 10-20ml/kg. Use large TV with slow rates. Various types. Frees anaesthetist and regular rhythm.
Soda Lime
USA – baralime.
90% = calcium hydroxide;
Ca(OH)2 +CO2 -> CaCO3 + H2O + Heat. Therefore gas warmed and humidified.
Colour change – usually to purple but NOT permanent so change if needed at end of anaesthetic.
Dust. Tracking of gas. Dead space. Resistance. Hyperthermia.
Exhaustion – colour change, no heat, increased heart/resp rate and bp, wound ooze, red mms.
Gas storage safety aspects
Oxygen/nitrous support combustion – naked flames/heat/electrical sparks.
Puncture cylinders – rocket effect; chain/ secure well. Move with carts. Store upright in dedicated area.
Keep tops dust free – plastic and blow dust off briefly before attachment.
Clearly label full/in use/empty.
Inhaled anaesthetic agent storage safety
Ether – highly flammable.
Halothane/Isoflurane/Sevoflurane.
Store upright in cool cupboard and avoid breakages.
Fill vaporisers at end of each day.
Recap bottles when empty.
If spill – open windows, wear gloves/mask and use absorbent into airtight container.
Scavenging
Prolonged exposure to anaesthetic gases potentially detrimental
Some anaesthetic are ozone gases
Legal requirement to control pollution
Control of substances hazardous to health
(COSHH)
Need to vent waste anaesthetic gases
Recommended max concentrations (UK)
* 100 ppm Nitrous oxide * 50 ppm isoflurane * 10 ppm halothane
Excess gas vented via pressure relief
(pop-off valve/APL valve)
Disc held by weak
spring
Connected to wide –bore
scavenge tubing
Types of scavenging
Charcoal cannister e.g. Cardiff aldasorber
Passive
- window
- hole in wall
- vent to outside
Active
- pumped outside
Charcoal canister
Cardiff aldasorber
Charcoal absorbs halogenated anaesthetics
Does not absorb nitrous oxide
Increasing weight indicates exhaustion
Heating causes release of gases
Active scavenging
Collecting & transfer system
Receiving system
- valveless open-ended reservoir
- bacterial filter
Pump to generate vacuum
Scavenging systems and safety
IMPORTANT – long term exposure to IAAs/nitrous possibly associated with;
Abortion/congenital problems.
Halothane hepatotoxicity.
Neurological problems – memory.
Bone marrow suppression/anaemia (nitrous).
?renal toxicity with methoxyflurane.
Therefore;
Cuffed tubes
Closed breathing systems
Wear gloves and fill vaporisers at end of day in fume hood
Key filling system
Turn on gas flows only if animal connected
Avoid mask induction and ventilate room – 20 air changes an hour
Monitor and inspect equipment
Oxygen failure alarm
Nitrous cut-off or oxygen failure protection device: if oxygen pressure is lost then the other gases can not flow past their regulator
Hypoxic-mixture alarms (hypoxy guards or ratio controllers) to prevent gas mixtures which contain less than 21-25% oxygen being delivered to the patient
Often chain linked (link 25 system). Located on the rotameter assembly, unless electronically controlled.
Ventilator alarms, which warn of low or high airway pressures.
Interlocks between the vaporizers preventing inadvertent administration of more than one volatile agent concurrently
Pin Index Safety System on gas cylinders
Pipeline gas hoses have non-interchangeable Schrader valve connectors, which prevents hoses being accidentally plugged into the wrong wall socket
Ambulatory infusion:
An animal is freely moving without need for a tether to connect with the catheter. This is normally only possible with larger animals that can be fitted with jackets to carry an infusion pump and compound reservoir. Totally implanted pumps can sometimes be used in rodents but have size limitations.
Atraumatic:
Minimal tissue injury is caused during the procedure
Biocompatibility:
Good toleration of implants by animal tissues after implantation.
Biofilm
A coating which develops on implanted materials derived from the animal’s own tissue fluids and cells
Catheter/cannula:
Flexible tube inserted into body cavities or organs for medical or experimental procedures
Dehiscence:
Bursting open or splitting along natural or sutured lines.
Haematogenous spread
Spread of microbial infection through the blood stream
Thrombogenic:
Property of causing or promoting blood clotting (thrombosis).
Breathing system requirements
Supply fresh gas & anaesthetic to patient
Allow removal of carbon dioxide
Allow scavenging
Enable positive pressure ventilation
Easy to use & clean
Inexpensive to buy and use
Re-breathing systems
Expired gas is ‘scrubbed’ of CO2
Chemical CO2 absorber
Low fresh gas flow
Economical
Expensive to buy
Large and cumbersome
Conserves heat and moisture
Increases resistance to breathing
Only suitable for larger animals
e.g. > 10 kg
Large animal systems available
formula Working out gas flow requirements for rebreathing systems
Minimum requirement is metabolic oxygen demand
i.e. 10 ml/ kg/ minute
However, must supply minimum vaporizer flow
e.g.Penlon sigma (sevoflurane) 0.25 Lmin-1
Denitrogenation
With any rebreathing system where carrier gas is oxygen
Use higher flows for ~10 minutes- 2l or 3 l per minute
Risk of alveolar hypoxia
N.B also after short disconnections – movement between theatres etc
can also increase to deliver more anethesia
Non-rebreathing systems
High gas flow requirements
Loss of heat and moisture
Cheap to purchase, expensive to run
Low resistance to respiration
Suitable for very small patients
formula for Working out gas flow requirements for non rebreathing systems
Based on multiples of minute volume, where minute volume is;
Respiratory rate x Tidal volume
OR
200 ml per kg
Magill non rebreathing system
Reservoir bag at fresh gas inlet
Awkward to use
1 x Vm (Vm = Vt x RR) or (Vm =200ml/kg)
no ippv
Lack non rebreathing syste
Co-axial Magill
1 x minute volume
Damage to inner limb results in rebreathing
no ippv
Mini Lack non rebreathing system
Alternative to T-piece for patients under 10 kg
Bodyweight range 1-10kg
1 x minute volume
No bag twist hazard
Very low resistance
Easy to clean smooth bore tubing
no ippv
T-piece
Suitable for very small patients, < 8 kg
2-3 x Vm- half as efficent at lck or magill
Suitable for IPPV
Bain non rebreathign system
Co-axial T-piece
Suitable for 7 – 10 kg
2- 3 X Vm
Beware – damage to inner tub
Humphrey ADE
3 different modes
- lever upright (lack)
- lever down (T-piece)
- circle
Versatile, suitable for 4 kg - >20 kg
Pros
Compact
Well designed
Scavenge at machine end
Straightforward conversion to IPPV (Nb increase flow)
Applies PEEP
Increases FRC
Prevents microatalectasis
Lowers work of breathing in human infants
Cons
Cost
Very heavy – strain on common gas outlet
Flows of 50ml/kg/min in lever up (lack) not substantiated in animals
Relies on 3 human references
Unquantified resistance from inspiratory/expiratory valves
Hoses pinch at valve end and start to crack
Colour codes misleading (S. African)
Excessive (unquantified) mechanical dead space
Surprising lack of veterinary controlled trials
Soda lime canister capacity 690ml
Filled with soda lime capacity 345ml
This intergranular volume falls as anaesthesia progresses as soda lime is used up
Expired volume must not exceed this or expired breath will not be completely scrubbed of carbon dioxide
This leads to maximum limit of 29kg dog with tidal volume of 12ml/kg
Morphology of necrosis
Continued swelling and hypereosinophilia
Nuclear changes:
Pyknosis = shrinkage
Karyorrhexis = fragmentation
Karyolysis = dissolution
Inflammation
Pyknosis
shrinkage or condensation of a cell with increased nuclear compactness or density
Karyorrhexis
the destructive fragmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm.
Karyolysis
he complete dissolution of the chromatin of a dying cell due to the enzymatic degradation by endonucleases.
Causes of necrosis - anoxia
Reduction or cessation of ATP production due to hypoxia or anoxia respectively will result in loss of function on energy-dependent cell pumps: -Na+/K+ pumps
Results in cell swelling due to osmotic pressure
ONCOTIC NECROSIS- Cell swelling is the typical feature and distinguishes it from apoptosis
-Calcium efflux pumps
are also affected
resulting in accumulation of intracellular calcium
describe membrane damage as a Cause of necrosis –
Membranes can be directly damaged by:
Pore-forming infectious agents/toxins- One of the best examples of membrane damage by pore-forming toxins are those produced by Clostridium perfringens
Reactive oxygen species (ROS)
Phospholipase activation
Protease activation- cytoseletal damage
Viruses can damage cell membranes as they leave the host cell.
Enveloped viruses require incorporation of host cell membrane to form part of their envelope
Viruses that bud off from the outer cell membrane (retroviruses) do so quietly, leaving an intact host cell
Those that bud from the golgi or RER (flavi, corona, arteri, bunya), and those that bud from nuclear membrane (herpes) lyse the cell as they go
Non-enveloped viruses can also only leave the host cell upon lysis
Additionally, viruses may causes cell lysis due to disruption of the cytocavitary network and other homeostatic mechanisms when they “hijack” intracellular processes for replication
Viruses will also induce apoptosis
how do viruses cause cell membrae damage
Viruses can damage cell membranes as they leave the host cell.
Enveloped viruses require incorporation of host cell membrane to form part of their envelope
Viruses that bud off from the outer cell membrane (retroviruses) do so quietly, leaving an intact host cell
Those that bud from the golgi or RER (flavi, corona, arteri, bunya), and those that bud from nuclear membrane (herpes) lyse the cell as they go
Non-enveloped viruses can also only leave the host cell upon lysis
Additionally, viruses may causes cell lysis due to disruption of the cytocavitary network and other homeostatic mechanisms when they “hijack” intracellular processes for replication
Viruses will also induce apoptosis
describe free radicals as a Cause of necrosis –
Free radicals are any molecule with a free electron
Reactive oxygen species (ROS) and reactive nitrogen species (NO)
Produced by oxidative metabolism, therefore most frequently made by mitochondria, but will also damage the mitochondria if cannot be removed.
Vitamin E and selenium are important co-factors in the neutralisation of free radicals
Programmed cell death - apoptosis
Apoptosis is normal- Embryological, Physiological
May be due to a pathological process:
Organ not receiving stimulus- portosystemic shunt
Cell contains infectious agent
Cell is irreparably damaged
DNA is irreparably damaged
Cell is cancerous
Two main mechanisms of apoptosis
Intrinsic- due to something within the cells. meachanism within the cell tell cellt to die
Extrinsic- more complex. binding of death ligand with cell receptor
morphology of apoptosis compared to necrosis
Morphology differs to necrosis:
Cell is shrunken
No/minimal inflammation- only a few inflamatory cells coming to clean up dead cell
Chromatin condensation around nuclear periphery (most characteristic)-
Formation of cytoplasmic blebs = apoptotic bodies as oposed to bursting out as in Karyorrhexis,
Karyolysis
There are different types of programmed cell death
Fresh Gas Flow Calculations
• To calculate fresh gas flow calculations we first need to calculate the animals minute volume (MV).
• All our non-rebreathing systems require 1-1.5 or 2-3 times the minute volume to run effectively and efficiently. This is know as the circuit or system factor.
• To calculate the minute volume (MV) we need to know the volume of air inspired or expired in one breath (tidal volume) and over a minute (minute volume)
• Minute Volume (MV) = Tidal Volume (TV) x Respiration Rate (RR)
• Tidal Volume (TV) = 10-15ml/kg
• We then multiply this amount with the system/circuit factor.
• Alternatively, the MV can be estimated using 200ml/kg/min.
fgf= MV x CF
A 4 year old Male Entire Staffordshire Bull Terrier presents at your practice for a dental descale and polish (routine). His Pre-op bloods and physical exam are normal. He weighs 19.8kg.
- Which of the following would be a suitable choice of breathing system for this patient? If not, why not?
a. Bain
b. Parallel Lack
c. Circle
d. T-piece
b
Aims of premedication
Sedation and anxiolysis (The reduction of anxiety by means of sedation or hypnosis) facilitating handling of the animal
Reduction of the stress for the animal- reduce adrenaline, prevent cardiac problems
Reduction the amount of other anaesthetic agents
Provision of a balanced anaesthesia technique
Provision of analgesia
Counter the effects of other anaesthetic agents to be administered during the anaesthesia procedure e.g. atropine to prevent an opioid mediated bradycardia
Contribute to a smooth, quiet recovery after anaesthesia
ideal Properties of drugs of pre med drugs
Reliable sedation and anxiolysis
Have minimal effects on the cardiovascular system
Cause minimal respiratory depression –animals will not be intubated following premedication until induction of anaesthesia, therefore they should breathe spontaneously after premedication
Provide analgesia, e.g. Opioid component
Be antagonisable: The ability to antagonise the effects of premedication may be desirable to hasten recovery from anaesthesia
Alpha2 Adrenoceptor Agonists (Alpha-2s) as premeds
Potent sedative and analgesic drugs- keeps patient really sedated. very good for very sick patients post op as anelgesia
Xylazine was the first a2 agonist to be used in veterinary practice
Superseded by medetomidine & dexmedetomidine (cats & dogs), both lasting about 45 minutesas xylazine is assosiated with death
Xylazine (30minutes), detomidine (45 minutes)and romifidine (60 minutes, less ataxia) used in horses- only real difference is leanth of action
Xylazine and detomidine used in cattle- licenced for food animals
The superior selectivity of dexmedetomidine makes it the theoretical a2 agonist of choice for use in small animals
work on alpha 2 receptiors on presynaptic neurons- widly distributed on cns- alpha 2s activate alpha 2 receptors and provides negative feedback and reduces release of neurotransmitor
Sedation is profound & dose related
Alpha 2 agonists provide good analgesia through an agonist effect at spinal cord A2 receptors
The duration of analgesia provided by a 10 µg/kg dose of dexmedetomidine is approximately 1 hour
Intra-op analgesia improved
The dose of induction and maintenance agents required after alpha 2 agonists are dramatically reduced in small animals- be careful of this
Intravenous induction agents must be given slowly and to effect (vein to brain circulation time is slowed)
Alpha 2 agonists produces a biphasic effect on blood pressure (initial increase followed by a return to normal or slightly below normal values)
Heart rate is decreased throughout the period of a2 agonist administration HR 45-60bpm dogs and 100-120 bpm cats
Alpha2agonists cause a reduction in cardiac output & in healthy animals.
Urine production is increased due to a reduction in vasopressin and renin secretion
avoid these drugs in patients with heart issues
Endogenous insulin secretion is reduced leading to a transient hyperglycaemia- do not test for diabetes after administration of these drugs
Both liver blood flow and the rate of metabolism of other drugs by the liver are reduced
Peripheral vasoconstriction tends to reduce peripheral heat loss
As a consequence it can be easier to maintain normothermia during the peri-operative period compared to animals given acepromazine
Small ruminants are quite sensitive to alpha 2 agonists
Alpha 2 sedation and analgesia is rapidly antagonised by the administration of atipamezole, a specific alpha2 adrenergic receptor antagonist- wont always antagonise cardiovascular effects
Reversal is advantageous because the recovery period is noted to be a high risk time for anaesthetic complications
IM atipamezole produces smooth and good quality recoveries
IV atipamezole produces a very rapid, excitable recovery from anaesthesia and this route of administration is not recommended
It is important to ensure that analgesia is supplemented with different classes of drugs
Atipamazole rarely used in horses and cattle
Phenothiazines
Acepromazine commonest/only licensed one
Sedation and anxiolysis that is initially dose dependent- less flat out sedation
can last 46 hours- lasts through recovery
With larger doses the duration of action is more prolonged
The quality and reliability of sedation can be improved by combination with an opioid (neuroleptanalgesia)
Addition of an opioid also provides analgesia, advantageous since acepromazine itself is not analgesic
To maximise sedation the animal should be left undisturbed for 30-40 minutes after administration
Less reliable sedation cf dexmedetomidine
Acepromazine (ACP) is an antagonist of a1 adrenoreceptors and can cause peripheral vasodilation and a fall in arterial blood pressure- will bleed more
Avoid in animals with marked cvs disease or animals in shock
Acepromazine is long lasting & non-reversible(!) so avoid in hypotensive animals
Acepromazine has anti-arrhythmic properties which may be advantageous during anaesthesia- decreses central arythmia, very potent at this
Reduction in body temperature occurs due to a resetting of thermoregulatory mechanisms combined with increased heat loss due to peripheral vasodilation
No evidence to suggest that acepromazine alters seizure threshold despite what some say
Giant breeds of dog may be “more sensitive” to the effects of acepromazine
Some boxer dogs are sensitive to even small doses of acepromazine, which has been attributed to acepromazine induced orthostatic hypotension or vasovagal syncope in this breed
Although acepromazine is not contraindicated in boxers, it is not the premedicant of choice in this breed - a very low dose (≤0.01 mg/kg) is recommended and animals should be monitored carefully after administration
Acepromazine is a dopamine antagonist- Anti-emetic
Contraindicated in breeding stallions- causes repro problems
comes in gell for horses and tablet ofr dogs and cats as well as injectable
neuroleptanalgesia
combination of opiod and Phenothiazines (ACP)
Benzodiazepines
Midazolam or diazepam (MA coming for midazolam, diazepam has MA in France)
Benzodiazepines alone produce minimal or no sedation in healthy cats and dogs
May even cause excitation due to loss of learned “inhibitory” behaviour
Benzodiazepines are therefore given in combination with other sedatives
In dogs benzodiazepines often combined with opioids because both classes of drugs are cardiovascularly stable and the combination can provide reliable sedation
In cats benzodiazepine and opioid is not very sedative, so benzodiazepine is most commonly combined with ketamine
These drugs have minor effects on cardiorespiratory systems
Therefore these drugs tend to be used as premedicants in animals with cardiovascular compromise.
Benzodiazepines are commonly used to manage convulsions, particularly as a first line intervention for animals presenting in status epilepticus
Premedication drug combinations (dogs and cats)
Acepromazine + opioid
Alpha 2 agonist + opioid
Alpha 2 agonist + BZD
Alpha 2 agonist + Ketamine
BZD + Ketamine
Opioid + BZD
Alpha 2 agonist + BZD + opioid
how to choose premeds for anethesia
Reason for anaesthesia or sedation
Duration of sedation required
Procedure to be carried out
Degree of pain expected from the procedure
Species and breed of the patient
Age of the patient
ASA classification of the patient
Injectable Induction,Why choose it?
Can be injected:
direct from needle/syringe (IM, SC, IV)
via IV cannula/syringe (IV only)
Renders patient unconscious by drug reaching brain directly via blood - rapid and smooth
Injectable Induction Agents in Common Use – Small Animals
Propofol
Alphaxalone
Dissociative agent & benzodiazepine
Inhalant Induction
Simple
Choice of agent critical
Speed
Pungency
Not generally recommended – VERY POOR for the patient and associated with higher mortality
distressing for animal
propofol
pros- Quick recovery with no hangover
cons-Apnoea if given too quickly
Propofol (‘milk of amnesia’)
Most commonly used anaesthetic in UK (dogs and cats)
Alkyl phenol, white emulsion 10mg/ml
Soyabean oil, glycerol, egg lecithin, no preservative, NaOH (changes pH)
Supports bacteria and endotoxin
Use within 24 hours
A multi-dose vial with preservative was available (‘Propoflo Plus’ – Zoetis) 28d shelf life
Rapid onset of action -rapid uptake by CNS
Short period of unconsciousness (5-10 mins)
Large volume of distribution (lipophilic)
Rapid smooth emergence due to redistribution & efficient metabolism (hepatic and extra hepatic) metabolites inactive
good for patietn swith hepatic problems as it is alos metabolised in the lungs
Respiratory depression (apnoea) - IPPV - Speed of injection should be slow, less needed if given over longer period
Cardiovascular depression
Rapid and smooth recovery
Suitable for top ups or TIVA
Muscle relaxation usually ok- can cause extention and rigisity of legs, wait it out or give muscle relaxant
Anticonvulsant
Not irritant, pain reported
not Analgesic
↓ ICP (patients with raised and normal ICP)
problems-
Rigidity, twitching
Apnoea
Profound bradycardia
Care in hypoproteinaemia
Heinz body anaemia in cats
??? Use for patients with pancreatitis / hyperlipoproteinaemia or diabetic hyperlipidaemia
Pain on injection ?
Local reaction (clear formulation, discontinued)
Alfaxalone
Is suitable for cats and dogs (& other spp)
Alfaxalone is a clear colourless neuroactive steroid
Causes anaesthesia by activating the GABA (inhibitory) receptor
has a short plasma elimination half life and is cleared from the body relatively quickly
Alfaxalone can be give as repeated boluses or as TIVA to maintain anaesthesia
Premedication is preferable
Anaesthesia induction is smooth, and the injection is given slowly over 60 seconds.
Occasional apnoea is seen and IPPV may be necessary (more than propofol)
The drug has good cardiovascular stability, causes no histamine release and produces good muscle relaxation
Animals should not be disturbed during recovery as excitement can occur
Dissociative Agents
Ketamine (also Tiletamine in Europe/USA)
Weak organic base pH 3.5
Racemic 10% solution (100mg/ml)
IV, IM, SC, IP, PO, epidural
Dissociative state
Used in many species for induction and analgesia
What is ‘dissociative anaesthesia’?
Dissociative anaesthesia = detached from surroundings- Patient may have their eyes open and make reflex movements during surgery
In recovery the patient may be agitated- Hallucinations are associated with human ketamine anaesthesia, Can be reduced by premedication with benzodiazepines
Ketamine increases the intracranial pressure- causes rigitity, give other meds along side this
Ketamine
Can be combined with BZD, alpha 2 agonists, acepromazine, opioids
Versatile induction agent and wide safety margin
Invariably needs to be combined with something
Rapid induction
Respiratory effects are mixed – bronchodilation and RR usually preserved but my stop!
GOOD ANALGESIA
CVS effects depend on dose
Muscle tone ↑ and jerky movements
Salivation and lacrimation ↑
Ketamine can be diluted with sterile water or physiological saline
Stormy recovery if disturbed or not adequately premedicated
Depth assessment is different (eyes open)
Corneal drying - use ‘Lacrilube’ or similar tears
Vomiting common with alpha 2 combinations avoid in patients with GI obstruction
Avoid in patients with ↑ Intra ocular pressure, ocular surgery, fever, hyperthyroidism
schedual 2 control drugs- records important
MAC
Minimal Alveolar Concentration (MAC)
The alveolar concentration (at 1 atm) producing immobility in 50% of patients in response to a noxious stimulus
i.e. Potency
MAC is for healthy, un-premedicated patients
MAC affected by
Age, N2O, hypotension, hypoxia, anaemia, opioids, sedatives , LAs, pregnancy
premeds reduce mac- not nsaids though
MAC not affected by
Stimulation, duration, species, sex, CO2, NSAIDs
Concentration of agent rises in plasma at a rate that depends upon
Ventilation
Concentration of agent in carrier gas
Cardiac output (inversely)
Solubility of agent in the body (inversely)- the more soluble the slower the effect
Blood:gas partition coefficient =
Solubility
This is the ratio of the amount of anaesthetic in blood and gas when the two phases are of equal pressure and volume
The LESS soluble agents (low coefficient) are washed away less quickly therefore the alveolar concentration rises FASTER
Blood: gas partition coefficient
The LESS soluble agents (low coefficient) are washed away less quickly therefore the alveolar concentration rises FASTER
a fat animal will recover from anethesia slower than a thin one. why?
Recovery is the reverse of induction, so dependant on blood solubility, redistribution will have occurred into the fat, which then acts as a depot of anaesthetic so (depending on fat solubility) a fat animal will recover slower than a thin one….
ideal anasthetic agent
Stable
No preservatives
Non-inflammable
Cheap
Ozone friendly
Non metabolised
Non-toxic
No CVS effects
Analgesic
What are negative effects of inhaled agents?
To the animal-
Cardiorespiratory depression
Formation of carbon monoxide with soda lime
(Formation of other toxic gases)
To the anaesthetist-
Little or no evidence apart from nitrous oxide
Bone marrow suppression
Teratogenesis
Nitrous oxide – becoming obsolete (why?)
H and S issues
Expensive
Analgesic
Min CVS & resp effects
V high MAC > 100%
Isoflurane
Lower solubility
Different CV depression
‘SAFER’ in dog
CEPSAF
summerise the considerations made with anethetic agents
Most anaesthetics induced by injection and maintained by an inhalational agent.
Recovery faster with a less soluble agent such as sevoflurane but MAC is higher
MAC is altered in states such as pregnancy and with other drugs
Scavenging is important although little evidence for problems
All inhalants are CV depressants
Evidence supports use of isoflurane over halothane
No data supporting further reduction of risk with sevoflurane
methods other than vapors to maintain anaesthesia
TIVA = total intravenous anaesthesia
PIVA = partial intravenous anaesthesia
Often used in horses but increasingly in small animals
Offer environmental advantages
TIVA
total intravenous anaesthesia
Can be used for short procedures in small animals/aggressive patients
E.g. ‘quad’ anaesthesia for cat neuters
The Cat Group
Routinely used for field procedures in horses
E.g. ‘GGE, ketamine, alpha-2 agonist – so called triple drip
Various ‘recipes’
GGE (Guaifenesin, a centrally acting skeletal muscle relaxant with little or no analgesic properties)
Supplied as 5% guaifenesin in 5% dextrose and infused to effect until signs of ataxia are seen, at which time IV bolus of ketamine is given
Maintained with infusion given to effect
However, always remember
Protect the airway – regurgitation risk (which species?)
Supply oxygen
Have a means to ventilate
PIVA
partial intravenous anaesthesia
Goals of PIVA
Reduce MAC
Reduce cardiopulmonary depression
Provide additional analgesia
Improve environmental impact
(Improve plane of anaesthesia)
Reduced cardiopulmonary depression, and less inhalant can be used
Analgesia provision
Less pollution & organ toxicity
Improved intra operative conditions
Improved outcome?
We don’t know yet
Evidence based medicine
Cardiopulmonary depression will still occur
Most IV drugs accumulate over time
Additional equipment required
the ideal drug-
MAC reduction
Analgesic
Minimal toxicity
Minimal effects on the body
Short context sensitive half life
Compatible with other drugs
NO single drug meets these requirements
Hence the need for combinations
combinations for PIVA
Inhalant+
Lidocaine- Analgesic
MAC reduction (25%)- not for cats !!!
Ketamine-
Often given as boluses during anaesthesia
Ketamine CRI (30% MAC reduction)
Alpha 2 agonists (not licensed as CRIs)- Xylazine, detomidine, medetomidine and dexmedetomidine can be given as small (tiny) boluses
Bradycardia !
Can also be given as CRIs
Opioids – various commonly used
Combinations may be the key
Remember most drugs accumulate over time
Lidocaine + ketamine have been shown to improve cardiovascular stability during isoflurane anaesthesia
Many combinations are possible and again we must used evidence based medicine to recommend the recipes
what can be measured on a monitor during anesthesia
Capnograph- The term capnography refers to the noninvasive measurement of the partial pressure of carbon dioxide (CO2) in exhaled breath expressed as the CO2 concentration over time.
Blood pressure
ECG
Pulse oximeter
Cardiac output
What Should We Monitor in a patient under anesthesia?
CNS depression- Eye position, jaw tone, EEG, BIS, etAA
Physiology and homeostasis-
Respiratory: Oesophageal stethoscope, capnograph, pulse oximeter
Cardiovascular : Blood pressure (MAP), pulse, ECG
Delivery of oxygen = how much oxygen is being carried to the tissues by how much blood pressure
Temperature under anesthesia
Anaesthetised, sedated and critical patients unable to regulate temperature
Measure temperature using rectal thermometer (may under read) or oesophageal thermoprobe (gold standard)
Core-periphery differences
Use bubble wrap, socks, hot water beds, lamps, low flow anaesthesia, warm theatre, heated pads, blankets, themovents/HMEs
Temperature affects many aspects of anaesthesia
Increased pain
Increased wound infections
Delayed recovery
Core temperature support?-
Consider warm saline irrigation
Circle systems (rebreathing system)
Consider warm water enemas
Hypothermia during anaesthesia
Temperature falls due to
Reduced shivering
Vasodilation
Reset thermoneutral point- opiods
Open body cavity
Cold gases
Dry gases
Wetting and prep
monitoring pule during anethesia
Use peripheral pulses
Get used to palpating pulses at different sites
Femoral artery
Dorsal metatarsal artery
Lingual artery
Auricular artery
Compare dorsal metatarsal artery and femoral artery
With hypotension dorsal metatarsal artery disappears
use fingertips to locate artery
Pulse Oximetry
Displays percentage oxygen saturation of haemoglobin
Accuracy is affected by
poor circulation (common in critical patients)
ambient light
movement of the probe
chow-chows
Limitations- High/low heart rates
Probe design
Useful post-op
saturating on room air?
Early warning?
Cyanosis – crude estimation
But ‘On a cliff edge
How is the haemoglobin saturation SPO2% (reading from pulse oximeter) related to PaO2 (partial pressure of oxygen in the blood)?
Oxygen content is dependent on both SaO2 and PaO2
Oxygen content
= (1.39 x Hb x SPO2%) + (0.003 x PaO2)
SPO2%
the haemoglobin saturation
PaO2
amount of oxygen disolved in the plasma
drives SPO2%
Cyanosis
not enough oxygen in the blood
Hb of 15g/dL (PCV 45%)
Cyanosis may start to manifest at SpO285% - no other signs
Haemoglobin of 9 g/dL (PCV 27%)
The threshold SaO2 level for cyanosis is lowered to about 73% (PaO2 38 mm Hg), the patient would certainly have other signs
Oxygen Content
Blood gas analysis-
pH
HCO3
PCO2
PO2
Arterial blood gases- the most accurate
Capnography – a good alternative for (PACO2)
Electrocardiogram (ECG)
ECG analysis does not give information about the mechanical activity of the heart
Important for arrhythmia diagnosis and monitoring response to treatment
Various arrhythmias may be seen
Tachycardia (sinus) may be the result of
Nociception- pulling on ovaries
Hypercapnia
Hypovolaemia
Hypokalaemia
And many more…
ECG may show characteristic changes depending on the underlying cause
Bradycardia (less common)
Drugs (e.g. alpha-2 agonists, opioids)
Hypothermia
Electrolyte disturbances e.g. severe hyperkalaemia
Knowledge of the patient is vital to determine treatment;
Alpha-2 agonist-induced bradycardia with second degree AV blocks
treatment is antagonism of the original dose
Opioid-induced bradycardia
treatment is the administration of an anticholinergic (contraindicated following alpha-2 agonist administration)
Capnography
Capnography (carbon dioxide measurement) conveys information relating to both respiratory and cardiac function
The end tidal carbon dioxide concentration is measured from the alveolar plateau and should remain constant with unchanged ventilation and cardiac output
Main-stream (measured directly in the box) and side-stream machines (measured via a water trap are available
need to be scavenged from!
Normal ET CO2 = 35–45 mm Hg
Hyperventilation – Decreased ETCO2
Hypoventilation - Increased ETCO2
obstructive pattern- sharks fin pattern:
asthma
kinked endotrachial tube
not reaching baseline- rebreathing:
sodalime has run out
non rebreathing apperatus has inadiquate flow
Other indicators
Oesophageal intubation
Leak at cuff/Patient disconnection
Adequacy of resuscitation
Normal variation – cardiac oscillations
Arterial Blood Pressure Monitoring methods
Non-invasive blood pressure (NIBP) monitoring, sphygmomanometry, oscillometric ( & HDO)
Doppler
Invasive blood pressure monitoring
Finger on pulse?
NO (Systolic 90-150 feels the same)
Monitoring Blood Pressure- Doppler
Set up takes a few minutes
Piezoelectric crystal placed over artery (clip fur, use gel)
Locate artery with distinct noise of arterial pulse
Cuff placed proximal to probe
Cuff size must be accurate
Audible signal v useful
Systolic pressure only (cats?)
Non-invasive blood pressure (NIBP) monitoring- oscillometric
Cuff size must be accurate- must go 1/3 of the way around
small cuff size makes reading high- large cuf size makes reading low
Unreliable in cats & small dogs
Quite expensive
More accurate methods available
High definition oscillometric devices– the future?, fast can cope with high HR & poor perfusion but clinically poor
Invasive blood pressure monitoring- Artery cannulation
Direct arterial pressure via an arterial cannula “gold standard”
Usually placed in the dorsal pedal artery
Auricular and facial arteries also used
Cannula is attached via saline-filled non-distensible tubing to an electrical transducer which gives continuous ‘beat to beat’ diastolic, mean and systolic arterial pressures
Must label cannula, line & flush regularly (hep saline)
Never inject any other drugs
Tubing must be narrow bore and non-compliant to amplify signal
Causes of decreased blood pressure include
Intravascular fluid loss (haemorrhage, third space losses)
Failing myocardial function
Sepsis
Relative hypovolaemia (vasodilation – drugs/sepsis)
determining renal perfusion
Although blood pressure monitoring is important it does not tell us directly about organ perfusion
Assessing urine output may be of equal value in determining renal perfusion
Aim for 1-2ml/kg/hr intraoperatively
treatment of Hypothermic patient with bradycardia and low blood pressure
Anticholinergic treatment and warming to raise heart rate and subsequently blood pressure
treatment of Septic patient with tachycardia but poor blood pressure
Intravenous fluid therapy to improve status
Patients with advanced sepsis require pressor support
Noradrenaline
Dopamine
Phenylephrine
Central Venous Pressure (CVP)
Used as an approximation of right atrial filling pressure (late guide) but of limited clinical value in anaesthesia
?Acts as a guide to correct fluid therapy (late guide)
May aid in detection of tricuspid valve problems
Central Nervous System Monitoring
Aims -Adequate ‘depth’ for procedure undertaken
Electroencephalogram (EEG)
Experimentally – Bispectral index (BIS)
Electroencephalogram (EEG)
Raw signal data
Spectral edge frequency
Auditory evoked potentials
Very limited clinical value
Anaesthesia Recovery
The process of allowing a patient to regain consciousness after anaesthesia
Recovery is the most common time for an anaesthetic-related death
Recovery Involves-
inhalant- Turn off inhalant.
Remain on oxygen.
Allow inhalant to be breathed off.
injectable-Turn off infusion/stop top-ups.
Drugs are metabolised/re-distributed.
Goal of recovery is to ensure patients return to the physiological norm as quickly as possible
Key points:
Heat loss leading to hypothermia
Extubation
Only perform when patient can swallow and has control of airway
Care with brachycephalic breeds
IV access
Leave cannular in for 1 hour after patient appears stable for patients not on longer term IV fluids
causes and solutions to prolonged recovery
Hypothermia
Excessive pre-med use
Patient too deep during maintenance
Hypoglycaemia
Choice of inhalant
Choice of induction agent
solutions-
Heat supplementation
Reconsider premed use
Closer monitoring to give as little anaesthetic as possible
IV fluids
Use faster acting inhalant
Use shorter acting induction agent
causes and solutions of airway instructions
Debris or gauze left
after dental procedures
Body fluids eg vomit,
blood
solutions-
Clear oral cavity then extubate after patient gains control of swallow reflex
causes and solutions of agitated recovery
Inadequate use of premeds or analgesics
solutions-
Reconsider premed and analgesic protocol and dose rates
Recovery in BOAS Patients
Sedation (acepromazine followed by alpha-2 agonist or vice versa)
Don’t forget analgesia (NSAIDS* +/- opioids)
*caution if steroids
Oxygen supplementation
Monitoring plan
Leave IV cannula in situ
Check for regurgitation prior to extubation
EXTUBATE LATE - after the head is raised
Very well tolerated!
Be prepared to re-intubate
Have a full dose of induction agent ready
Tracheostomy
When to re-intubate?
SPO2 consistently low on room air
If reading 80 something then consider oxygen / re-intubation
Pulling tongue out assists readings
Obvious effort/distress
Cyanosis
Paradoxical breathing
Post operative analgesia
Untreated pain leads to;
Chronic pain states
Wound infection
Wound breakdown and interference
Occasional reports of diabetes mellitus
Catabolic states (insulin resistance)
Welfare concerns
Unhappy owners
Will anything given pre or intraoperatively last into recovery period?
What is the predicted degree of pain post operatively?
Is it a requirement that the animal is fully conscious rapidly post operatively ?
Is a slower recovery required?
What is the preferred route of administration?
Enteral – oral , rectal, transmucosal
Parentral – intravenous, intramuscular, subcutaneous, transdermal
How long is the predicted length of analgesic requirement?
Intermittent bolus
Continuous rate infusion
How Can We Apply Local Anaesthetic Techniques in addition to general anethesia?
Somatic infiltration generally reliable & safe
Multiple intradermal (or s/c) injections
Usually administered in sedated/anaesthetised animals
Lidocaine spray – ‘Intubeaze’ (2%)
Lidocaine jelly (2%) for catheterising the urethra
Lidocaine & prilocaine cream (EMLA) useful for IV cannula placement
Proparacaine 0.5% and butacaine 2% topical on cornea (10-20 minutes)
can improve recovery
How Do We Use Local Anaesthetic?
Intravenous route- Only use lidocaine IV
More benefit in soft tissue pain??
Can be used in both dogs and horses
Decreases MAC and reduces opioid requirements
Can also be useful post-op
AVOID in cats- very sensitive
Somatic infiltration generally reliable & safe
Multiple intradermal (or s/c) injections
Usually administered in sedated/anaesthetised animals
Lidocaine spray – ‘Intubeaze’ (2%)
Lidocaine jelly (2%) for catheterising the urethra
Lidocaine & prilocaine cream (EMLA) useful for IV cannula placement
Proparacaine 0.5% and butacaine 2% topical on cornea (10-20 minutes)
Small animals
Splash blocks
Epidurals
Dental blocks
Limb nerve blocks
Intraoperative articular blocks
Farm animals
Cornual block
Caudal epidural
Inverted L-block
IVRA
Paravertebral
Horses
Diagnostic nerve blocks
Epidural
Eye and dental blocks
Intraoperative + intraarticular
small animal anesthetic techniques
Splash blocks
Epidurals
Dental blocks
Limb nerve blocks
Intraoperative articular blocks
Farm animals anesthetic techeniques
Cornual block
Caudal epidural
Inverted L-block
IVRA
Paravertebral
Horse anesthetic techniques
Diagnostic nerve blocks
Epidural- caudal
Eye and dental blocks
Intraoperative + intraarticular
Local Blocks
Revise anatomy!
Place local anaesthetic in region of the nerve
Nerve Location Techniques- Nerve stimulator, Ultrasound of femoral triangle
Head/Dental Blocks
infraorbital n.- upper lip, nose, roof of nose, skin rosral to canal
maxillary n. - maxilla, upper teeth, nose upper lip
rigeminal n.- akinesia of globe, desensitises eye and orbit
mental n,- lower lip, incisors
mandibular n.- mandible, teeth, akin, mucosa
Infraorbital Block
upper lip, nose, roof of nose, skin rosral to canal
Transbuccal
Transdermal
Place needle into canal
Maxillary Block
Tmaxilla, upper teeth, nose upper lip
ransorbital approach
Transdermal approach
Ventral to notch in zygomatic arch
Transmucosal – cannula into infra-orbital canal
Mental Block
lower lip, incisors
Mandibular nn
Mental foramen
Mandibular Block
Medial mandible
Just rostral to angular process
Or transmucosal – medial aspect mandible
mandible, teeth, akin, mucosa
Ophthalmic Blocks
Auriculopalpebral
Supraorbital
3 point
Petersen block
Retrobulbar
Forelimb Blocks
Brachial plexus
Median
Radial and ulnar
(RUMM block)
Digital
Hindlimb Nerve Blocks
Sciatic
Femoral
Tibial
Fibular
Digital
Motor- ok in small animals but bad in large animals- flighty horse will be stressed by loss of use of limbs
Sensory
Forelimb Blocks
Brachial plexus
Median
Radial and ulnar
(RUMM block)
Digital
Intercostal Blocks
Useful for:
Rib fractures & flail chests
Chest drains
Thoracic surgery
‘Soaker’ Cathetersv
Useful for analgesia for total ear canal ablations (TECA), limb amputations & extensive reconstructive surgery
Relatively large bore (6-12 French) catheters with very tiny holes
Allow distribution of local anesthetic into the surgical site
Placed just before closing incision and secured to the skin at the end of the surgery
Intravenous Regional Anaesthesia (IVRA)
Esmarch bandage applied and tourniquet proximal
After removal of the bandage 0.25-0.5% lidocaine (2.5mg-5mg/kg) injected using a vein distal to tourniquet
Tourniquet can be left in place for up to 90 minutes
Used in conjunction with GA or heavy sedation
Common in cattle -digit amputation
Paravertebral Anaesthesia
Predominantly used in farm animals – traditionally!
Inject L.A around spinal nerves emerging from vertebral canal
Advantages
Desensitizes large area
Good muscle relaxation - motor
Reduced I/abdominal pr
?simple/quick
Less L.A required than infiltration
Epidural Analgesia
Indications
Abdominal and hind quarter surgery in small animals under light GA
Post operative analgesia
Standing surgery in farm animals and horses
Post operative analgesia for above surgeries or injuries
Caudal Epidural Analgesia
Commonest technique in large animals
Inject slowly over 5-10sec
Iml/100kg 2% lidocaine
Max effect in 10 min - lasts c. 60 min
Useful in small animals – tail amputations, perineal surgery
Epidural Analgesia Complications
Accidental vascular injection
Haematoma formation
Subarachnoid injection
Infection
Hypotension
Respiratory depression due to cephalad spread
Nerve damage
Pruritis
Urinary retention
Motor dysfunction
Hypothermia
Supporting Anaesthetised Patients
Influence on outcome – evidence base
Ethical considerations
Common sense….
Supporting oxygenation: Indications
During all anaesthetics
Pre-induction
Recovery
Increased FIO2-
Methods
Flow by
Intranasal
Intratracheal
Tracheostomy
Incubator
Mask
Hypothermia during anaesthesia:
Hypothermia causes
Increased pain
Wound infection
Delayed recovery
Temperature falls due to
Reduced shivering
Vasodilation
Reset thermoneutral point
Behavioural modification
Open body cavity
Cold gases
Dry gases
Wetting and prep
Core temperature support
Active warming
Minimise heat loss
Circle systems (rebreathing system)
Pre-clip
Warm environment
Minimise wetting
Aim for short anaesthesia time
Drug choices?
Support of renal function during anesthesia
Fluids during anaesthesia
5 x maintenance.. Why?
10ml/kg/hr dogs (less for cats)
Estimated output 1-2ml/kg/hr
Measurement
Volume - use of collection systems
specific gravity
Minimal Support for anesthesia
Baseline monitoring
Oesophageal stethoscope
Finger on pulse
Ventilation rate
Monitoring record (BP, capnography, temperature)
Fluids and intravenous access
Oxygen
Analgesia
what breathing system would you use on a 5 kilo patient
a tpiece if you neet to ippv
a lack if not
what breathing system would you use on a 10 kilo or above patient
a rebreathing system
effiecine with lower flows
cant be used for patients lees than ten kilos due to valve and sodalime- resistance
minute volume (MV)
the volume breathed per miniute
on average this is 200ml per kg
risks of equine GA
duration of anesthesia corellates with increased risk
difficult to manage after and hour and a half
factors that effect duration:
-caseload
-skill of surgeon and staff
- current condition of surgeon and staff- time of day or week, have they had a break
why increased risk-
big
flighty
cardiopulmanory depression- nit designed to lie down
- experience with anesthesia- horse thats experienced it before is more acoustomed to it
specific risks- cardiac arrest, fracture (esspecially of a long bone- mares who have recetly had foals most at risk)
feild equine anesthesia
minor procedures
castration, sacrcoid removals ect
Total Intreveneous Anesthesia- TIVA
extra boluses of ketamine to maintain anesthesia
check the feild- stones, watercourses, batteries, holes, slopes, type of fence (barbed wire)- anything that could injusre horse as it goes down
draw up all drugs and palce iv cannula- get all equipment ready
fit horse with padded head collar
have help and a plan
administer drugs and induce anesthesia
position horse- if horse in lateratl, bottom forelimb forward, hind limbs parallel
hospital equine anesthesia
more majour surgery
horse is intubated-same as small animals but cannot visulise the larynx- use gag
endoscope up the nares could be used
dorsal recumbancy is maintianed when using oxygen in isofurane
monitor as usual
pre-oxygen rarly tolerated but used in very sick cases
theater equipmetn must be checked- hoist, inflatable beds
equine premed
aim is to produce a horse sedate enough for ketamine
could use propofol but requires large amount
healthy horses ofter recive acp intramuscularly- only drug assosiated with improved outcome- not good for colic due to vasodilation
iv jugular canula- want to place on uppermost side depending on surgery
alpha 2 agonists also used-
xylazine- quick acting, can top up, good for colics
romifodine- takes 5 to 10 mins, longest acting, less ataxia, could take too long. lasts 45 mins,
detomidine- interediate, lasts 45 mins, small volumes
can tell sedation by knocking on sinuses or indeifference to lip being touched
GGe- used in horses not healthy enough for an Alpha 2 (specifically for cardiovascular problems)- muscle relaxant
infuse IV until horse is “knuckling then give etamine and microdose of APHA 2
equine induction agents
ketamine-
dissociative
good anesthesia
must not be used alone- causes sezures
eyes remain open and central
can be used as top ups (dont exceed induction dose)- every 10-20 mins
takes 2 mins to go down
use head to guide which side horse goes down in
Used in combination with acepromazine, alpha 2 agonists, BZDs or guaifenesin (GGE)
give an example of the “recipe” for a GA eqine feild induction
ACP- wait 30-45 mins
detomidien IV- wait 5 mins, check heart rate (> 20 BPM), chek for adiquate sedation
diazepam/ katamine iv for induction
ketamine iv top ups every 8-15 mins or triple drip (GGE, Ketamine, Alpha 20
add 1/4 doese detomidine after 4/5 doses i using katamine alone
with ketamine continue to give top ups of alpha 2
problems suring equine anesthesia
arterial blood pressure
low PO2
high CO2- vetilate patient
bradycardia- common
tachycardia- rare
aponea
pain
movment
poor recovary
methods of equine hospital recovery
free recovery
rope recovery
anaesthesia of ruminents
licenced drugs for food animals must be considered
many orocedures done standing
usually achived via iv (calves cna be masked)
diffucult cows may drink chloral hydrate
iv cannula placment??
intubation of ruminents
small ruminents -direct visulisation
larger ruminents- intubated by palpation, developed skill
cuffed tubes- regurgitation risk! rumenants have a rumen!!!
induction of anesthesia in pigs
deep im (just behind ear- dont go into back or hindlimb), iv or mask with inhalant
ketamine, alfaxalone, propofol
ketamine combinations
malignant hyperthermia- rare condition of pigs. after exposure to inhalant, rapidly fatal- can be treated with drug
intubation is challenging- larynx is complex
anasthetic risk for rabbits
difficult to intubate- lidocane needed, big fleshy tounge
difficult to handle
lack of familiarity
sublinical disease
small lungs
prone to hypothermia
rabbit premed
if in doubt go low with dose
buprenorphine- 30 40 mins to peak if given Im
maintanence and monitoring or rabbits
difficult to monitor depth
gi support of rabbuts for anestheisa
gut stasis big killer
Why do we Encounter Dysrhythmias?
Older/sick patients
Multiple underlying conditions
Cardiovascular depression
Vasoactive drugs (which?), inhaled anaesthetic agents (effects?)
Hypothermia
Fluid loss
Overstimulation
Nociception
ECG triangle
lead 2 (left leg)- standard lead, most diryhtmias recorded in
lead 1(right arm)
lead 3(left leg)
ecg wave
p wave- atrial depolarisation
qrs complex- ventricular depolarisation
t wave- repolarisation of ventricals
qrs complex is bigger as it is a cordinated movmemt involving punjinke fibres. t wave is doen by individual myocytes
st segment should be at same level as baselinw but is often below- indicates myocardial hypoxia
a big q wave could mean a thickened intraventricular septum
ecg does not tell you anything about the pulse- Pulseless electrical activity can occur- electrical activity without actual beat of the heart
st segment depression indicates…
myocardial hypoxia
Dysrhythmia Interpretation
What is the rate
What is the overall rhythm
Is there a P for every QRS
Is there a QRS for every P
Are there aberrant (usually ventricular) complexes
What do the monitors tell you about the patient?
Sinus arrhythmia
Perfectly normal rhythm
Often seen in fit anaesthetised patients
Sign of high vagal tone?
Be careful of procedures that stimulate vagus such as ocular surgery
(1st degree) and 2nd Degree A-V Block
Occasional p waves with no QRS
Common to see
Can be caused by vagal stimulation or very ‘deep’ anaesthesia
Can be idiopathic
Commonly as a result of alpha-2 agonists
Very rarely HIGH dose opioids
Will be heard as missed heartbeats
Treatment?- do you need to?-
Is treatment necessary?
How would you decide?
If necessary, antagonise the alpha-2 agonist (or administer naloxone?)
Problem with this?
Decrease anaesthetic depth
If still no response and reduced cardiac output?
Consider atropine/glycopyrrolate
3rd degree AV block
P waves and qrs doing own thing
Artial pacemaker cells and avn are not working in sync
Impulse not originating in avn
REAL PROBLEM
Treatment while under anesthesia– Stop further deterioration, ensure all other parameters are normal- depth of anesthesia ect
pacemaker can be places
Atrail Fibrilation and ventricular ectopic
Gap of complexes different
Height of complexes different
No pause after ventricles contract
worring!!!
ventricular ectopic-electric signals in the heart starting in a different place and travelling a different way through the heart.
Treatment?
Stop further deterioration, ensure all other parameters are normal
Recover asap, ?amiodarone
Then cardiology
Rate control if there is underlying heart disease – medical mx
Electrical DC cardioversion may be an option
Ventricular premature complexes (VPCs) plus compensatory pause
Fairly regular but with a few ventricular ectopic beats- strange and occasional variation in size of qrs complex
Is the pause good or bad?
Treatment?
Check physiology – often due to hypoxia or hypercapnia. Sometimes low blood pressure
Add analgesia – may be due to nociception
Possible lidocaine if becoming frequent
Ventricular tachycardia (V tach)
Some normal beats
Others wide, abnormal ventricular beats
Ventricular tachycardia (V tach)
Often a deterioration of SVT – treat underlying cause
Often as a result of sepsis or a major underlying condition
May deteriorate into ventricular fibrillation (often fatal)
Treatment = underlying cause, lidocaine, amiodarone, magnesium
Ensure all other parameters normal
Ventricular escape
Triphasic qrs
Actually quite normal
Ventriclas are firing to restart normal rhythm
Would you treat this?
Possible due to alpha-2 agonists or high dose opioids?
What would you do?
Treat cause otherwise ensure all other physiology is normal- probebly no nead to treat
Whatever the Cause of abnomal ECGs, you should always
Apply First Principles..
Check physiological parameters and correct if possible
Oxygen, carbon dioxide, temperature, heart rate
External factors and correct if possible
Blood loss, surgery, nociception, drug reaction (contrast for example)
Antagonise drugs (or add more – nociception)
Finish surgery as soon as possible – into ICU
Imaging Modalities for imaging the thorax:
Radiography
Widely available
Non-invasive
Time and cost-efficient
Ultrasonography (echocardiography- imaging the heart)
Complementary
First choice for cardiac disease
no good if lungs are full of air
Computed Tomography (CT)
Where radiography and US fail
Higher sensitivity
Assess technical quality
Positioning
Centring/Collimation
Exposure factors
(Inspiratory)
Labelling
No Artefacts
Restraint
methods for imaging the thorax
Chemical
General Anaesthesia-
Avoids voluntary patient movement
Allows control of respiratory movement
Facilitates good oxygenation
Increased atelectasis of the dependent lung
Sedation-
Safer if suspect CVS or pleural disease e.g. butorphanol
Can lead to respiratory depression (so monitor and flow by O2)
No control of respiration
Physical restraint alone – does not mean manual restraint
Difficult to get good quality images
Rabbit burrito/cats in resp distress in a box can work well.
how do you decide which views to take on a radiograph
A minimum of 2 orthogonal views
Beyond that – case dependent!
Routine (inc cardiac) cases – RL and DV
Screening for metastases RL + LL + VD/DV
Specific lung pathology – RL + LL + VD
Appearance unclear on one lateral and DV/VD – take the other lateral
taking a right lateral view
Right lateral preferred
Cardiac silhouette position more consistent
Diaphragm obstructs less lung field
More lung between cardiac silhouette and thoracic wall
Position:
Right lateral recumbency
legs secured cranially, neck extended
foam wedge to prevent rotation
Centering/Collimation
Centre beam slightly caudal to caudal border of scapula
Collimate to thoracic inlet, thoracic spine, sternum and diaphragm (cranial abdomen)
taking a ventral dorsa/ dorsal ventral view
DV/VD centring/collimation
Ensure symmetrical positioning with spine and sternum superimposed (to avoid axial rotation)
Centre beam in midline, at level of caudal border of scapula
Collimate to thoracic inlet, diaphragm and body wall (skin edges) – unless investigation requires otherwise.
vd
Heart rotates to one side and distorts shadow
May produce better pulmonary detail
Can see more of the lung fields
dv
Safer in dyspnoeic patient
Heart lies in anatomically correct position – easier to interpret cardiac silhouette
Timing of exposure when imaging the thorax
Aim for peak inspiration:
Diaphragmatic line straight dorsally – T12/13
Expiration:
Diaphragmatic line domed, increased contact with CS
– T10/11
Avoiding movement blur when imaging the thorax
Good restraint
Good radiographic technique
Exposure time - High kV / low mAs technique
Relevant to film radiography
Low mAs minimises exposure time
High kV reduces the high contrast appearance of the thorax
Less relevant with digital radiography
Use a grid if thickness > 10cm
Controls scattered radiation
Timing of the exposure
At peak inspiration
May need to use the expiratory pause in a conscious panting animal
Radiopacities
The five basic densities:
Metal – White (all x-rays absorbed – most opaque)radiopaque
Bone – nearly white
Soft tissue/Fluid – mid grey
Fat – dark grey
Gas – very dark/black (few x-rays absorbed – most lucent)- radiolucent
Border obliteration
How visible is the border of the structure being evaluated?
Structures of the same opacity which are in contact will appear as one shadow
Border obliteration
(silhouette sign or border effacement)
Mass effect
Displacement of structures due to adjacent space-occupying lesions
e.g. fluid or mass
Interpretation of thoratic Radiology
1.Assess technical quality (Pink Camels..)
- Assess the respiratory system
- Assess the cardiac silhouette
- Assess everything except the heart and lungs
General Principles:
Be consistent!
Ensure you evaluate:
Thoracic boundaries
Pleural space
Lower airways and lung fields
Mediastinum
Heart and blood vessels
Always ask:
Is the radiographic diagnosis consistent with clinical findings?
Is the quality of the radiograph adequate to permit a confident radiographic diagnosis?
Roentgen Signs
Number
Location
Size
Shape
Margination
Radiopacity
Pulmonary Vasculature on imaging
Normal vasculature
Normal pulmonary vessels are clearly visible in central and middle zones
Vessels taper towards the periphery
In lateral view
Artery is dorsal to bronchus and vein
Veins are ventral to bronchus and artery
In DV view
Veins are medial to arteries
so.. veins are ventral and central
Lung Patterns on imaging
Lung disease
different characteristic radiological appearances depending on which component of the lung is affected.
Known as lung patterns:
Bronchial
Alveolar
Vascular
Interstitial
Diffuse
Nodular
lung varitation Dogs vs Cats
In dogs, caudodorsal lungs very close to spine, right up to the tip
In cats, diverge slightly from the spine around caudal T11/cr T12 due to the larger sublumbar muscles
Cardiac Silhouette
Assess the cardiac silhouette
Generalised enlargement
Individual chamber enlargement:
left atrium
right atrium
Left ventricle
Right ventricle
Change in great vessels
VD
Diaphragm often appears as 3 ‘humps’
Distance between diaphragm & heart is greater than for DV
Better visualisation of accessory lobe
Gas should be in the pylorus
Right and ventral
DV
Diaphragm appears as a single dome
Gas should be in the fundus
Left and dorsal
Normal Heart Size - Cat
Cat - Normal width (DV)
< 2/3 width of thorax
Normal short axis (lateral)
= cranial 5th rib to caudal 7th rib
Normal long axis (lateral)
2/3 height of thorax
Vertebral Heart Scores
Leanghth + Width = VHS
Normal values:
Dog = 8.5 – 10.5
Cats = 7.5
Pericardial Effusion on imaging
Cardiac silhouette grossly enlarged
Globoid appearance
Ultrasound = sensitive indicator!
Pneumothorax on imaging
Lung retraction from thoracic wall
Space between heart and sternum
Example recipe for GA Hospital
Acepromazine im, wait approx 30-45 minutes
Detomidine iv, wait 5 minutes, HR>20 bpm, adequate sedation must be apparent
Diazepam/ketamine iv for induction (can use ketamine alone)
Intubate, maintain on isoflurane in oxygen
Monitor depth, keep ABP > 70mmHg, and PCO2 <60mmHg IPPV if necessary. Sedate for recovery
Achieving a secure airway in a rabbit
Obligate nasal breather
need to disengage the soft palate from the epiglottis to visualise larynx
Big fleshy tongue
Narrow gape
cheeks
VERY sensitive larynx
I always use lidocaine spray prior to an ETT
Depth Test - jaw tone??, tongue withdrawal (care), cough when local applied to larynx. Breath holding vs apnoea.
Raise the head and extend the neck to disengage the soft palate
Ideally visualise the larynx to intubate the patient
apply local to larynx
otoscope/laryngoscope
slightly curved ET tube, no cuff
~1 mm diameter for every kg bw
Right parasternal long-axis view
obtained with the transducer in the parasternal window with the transducer index mark pointed toward the patient’s right shoulder (10 o’clock) in the third or fourth intercostal space.
Depth of an ultrasound
this adjusts the field of view (the real-time image should fill the field)
Gain of an ultrasound
power (high gain = white image)
Sector Width of an ultrasound
(the smaller the sector angle, the faster the frame rate and the higher the resolution of the real-time image)
Sector width affects frame rate.
The narrower the width, the higher the frame rate.
Focus of an ultrasound
make sure you place the focal point at the depth level of interest on the image
Right-sided ultrasound views – why do we want them?
Subjective assessment of chamber size and systolic function
Evaluate the mitral and tricuspid valves
Measure chamber size (particularly the left ventricle and left atrium)*
Evaluate some measurements of systolic function
How to perform a basic echo exam
PREPARATION
clip fur
dont sedate when posible
ECG trace – don’t worry about where your ECG clips are. You just want the timing intervals.
Remember your cardiac cycles.
Beginning of the QRS is end-diastole.
End of the T wave is end-systole.
Choose the correct transducer according to patient size.
Palpate the apex beat prior to scanning.
POSTURE – avoid twisting to look at the screen. Use an arm rest. Try to relax and DON’T PRESS TOO HARD! Use more gel….takes a few minutes to soak in.
Try to ultrasound as many patients as possible to get a good technique and develop consistency. PRACTISE!
Understand cardiac pathophysiology well.
make sure image fills screen
obtain Right Parasternal Long-axis Four Chamber View- asses systolic function: Interventricular septum, Interatrial septum, Mitral valve
Watch the left ventricle contract
turn thumb and tip probe till left ventrical is curcular- Right Parasternal Short-axis View (papillary muscle level)
tip transducer upwards ot visulise mitral valve- fish mouth view
tilt it further to visulise the aortic valve
Measurements – How to Make Them on an echocardiogram
As a general rule, measurements should be taken from 3 cardiac cycles then averaged.
Most importantly, ensure that the view is correct and well aligned before taking any measurements. It is best not to make measurements if your image is substandard.
Fractional Shortening
FS (%) = (LVDd – LVDs)/ LVDd
LVDd=Left ventricular internal diameter during diastole
LVDs=Left ventricular internal diameter during systole
FS% is affected by many external factors therefore has its limitations
standard reference ranges can be obained
measure of contractillity and function
can be effected by preload, afterload and contractility
Cornell measurement
When assessing LV diameter, use published breed specific reference ranges when possible, however, these are not always available OR the dog may be a cross breed. What then?
LVDd=Left ventricular internal diameter during diastole
For those dogs which are cross breeds are pure bred dogs with no published reference ranges available, then the “Cornell method” scales the LVDd (cm) to bodyweight (kg).
Cornell formula; LVDd cm/BWˆ0.294
For the “EPIC Study”*, dogs were classified as having enlarged left ventricles when the LVDdALLO was >1.7
E-Point to Septal Separation (EPSS)
an easy measurement to obtain that is accurate in estimating the LVEF. EPSS is measured in the parasternal long axis view (PLAX) of the heart, which gives a view of the left ventricle and is often used to assess its function.
sensitive and specific for ventricular function
Indications for Echocardiography
Investigation of a heart murmur*.
Investigation of breathlessness, cough and/or collapse.
Investigation of an arrhythmia.
Investigation of a gallop rhythm.
Investigation of the presence, significance and cause of pericardial disease.
Investigation of ascites or pleural effusions whereby noncardiac disease has been excluded.
Investigation of unexplained pyrexia.
Breed screening (in particular for preclinical dilated cardiomyopathy).
Assessment pre-chemo.
Eupnoea
Normal respiration
Tachypnoea
Increased respiratory rate (not necessarily depth)
Apnoea
Absence of respiration
Hypoventilation Hyperventilation are both examples of
Alterations in ventilation at the alveolar level
Hypercarbia
Increased CO2 in blood•Hypoventilation•Incprodnof CO2Primary drive for respiration
Hypoxaemia
Decreased O2 in blood•Poor O2 intake•Hypoventilation•Increased O2 consumption•Decreased O2 carrying capacity
Differentials for tachypnoea
Primary cardiac disease
Neurological disease- Damage to respiratory control centre
Metabolic disease- Acidosis/alkalosis, Increased PaCO2
Hyperthermia- Cooling mechanism
Stress
Pain
Abdominal discomfort- Restricted movement of diaphragm
Primary respiratory disease
OBSTRUCTIVE RESPIRATORY PATTERNs
LRT Obstruction- Thickening, inflammation and mucus
Causes increased expiratory effort
Small airways held open during inspiration
Early collapse during expiration
e.g asthma
positive pressure of inspiration created allows easire passage of air. experation needs more effort
dont get stertor or sridor with this pattern
URT Obstruction- Causes marked inspiratory effort
Dynamic collapse of soft tissues due negative pressure associated with inspiration
Inspiratory STRIDOR or STERTOR
as animal breathes in, negative pressure is created meaning there will be more effort needed to inspire than expire with this pattern
Restrictive Respiratory Pattern
Expansion of the thorax restricted> Decreased tidal volumeTachypnoea / short-shallow breaths> Hypoventilation
restriction can be in lungs, in pleural space or withing ribs or diaphram.
Paradoxical Respiratory Pattern
results form significant trauma to the ribcage
road traffic accidents
Paradoxical movement of the chest wall: -Trauma –“Flail” chest
-Terminal respiratory failure –fatigue of muscles
SEROUS
Nasal Discharge
Inc. nasal secretionsAllergic rhinitisAcute InflammationViral infection
MUCOID nasal discharge
Nasal Discharge
PURULENT Nasal Discharge
Bacterial infection1o or opportunisticpathogen
HAEMORRHAGIC Nasal Discharge
TraumaClotting disorderVascular diseas
Nasal Discharge
Can be difficult to identify
•Intermittent nature
•Cleaning / Licking of nasal planum
Character of the discharge + Unilateral or Bilateral Presentation + Knowledge of common diseases
URT Origins (usually unilateral)-
•Nasal cavity
•Paranasal sinuses
•Guttural Pouch (horses)- could be bilateral
•Nasopharyngeal - could be bilateral
•Trachea- could be bilateral
LRT Origins ( will be consistantly and evenly bilateral)-
•Bronchoalveolarspace
•Oedema, Pneumonia
•Pulmonary vasculature
•Haemorrhage
Coughing
Upper respiratory tract-
•Harsh, dry, hacking cough
•Tracheitis or tracheobronchitis
•Often productive
Lower Respiratory Tract-
•Soft, chesty cough
•Pneumonia
•Lower airway inflammation
•Cardiogenic
Respiratory Sounds
Normal:
Tracheal / Bronchovesicular-
•Normal air movement through airways
•Increase airflow > Harsh intensity
Abnormal:
Wheezes-
Air passing through narrow airways
Bronchoconstriction
Crackles/Rales- Air passing through fluid
Oedema, harmorrhage, pneumonia
Dull/Absent- No air movement though lung
Pleural rubs Friction between pleural surfaces
Systematic auscultation- larynx, trachea, multiple points thorax: craniodorsa, caudodorsa, Hilus, cranioventra
Accentuating Respiratory Sounds
Adventitious noises can difficult to detect during normal: respiration-
•Subclinical inflammatory airway disease / asthma •Interstitial disease
Re-breathing exam (plastic bag over horses nose) -Increase tidal> volumeIncrease air flow> Accentuate adventitious noise
PERCUSSION- assessing resonance of air-filled structures
Thoracic percussion–Lung Parenchyma•Pulmonary consolidation•Pleural fluid accumulationGenerally used as adjunct to auscultation
Sinus percussion-
•Altered resonance in paranasalsinuses •Fluid / pus
•Cysts / Masses Very useful assessment in horses
what is visualised in an endoscopy
Nasal meati
Nasopharynx
Ethmoid turbinates
Nasomaxillary opening
Guttural Pouches
Trachea
can be done without sedation in horses, and possibly while ridden (dynamic endoscopy)- can diagnose Laryngeal Hemiplagia (recurrent laryngeal neuropathy)
Laryngeal Hemiplagia
(recurrent laryngeal neuropathy)
Common cause of poor performance in race horses
•Also occurs in dogs, in association with hypothyroidism
paralysis of larangel cartilages, usually of the recurrent laryngeal nerve
RHINOSCOPY
used to investigating URT disorders
Restricted access in small animals-
•Rigid rhinoscope
•Narrow-bore flexible endoscope
•Otoscope
Indications-
•Nasal foreign body
•Nasal mass –biopsy
RADIOGRAPHY to Investigate URT disorders
Commonly used to assess paranasal sinuses-
Lateral, dorsoventral and oblique projections
Cheap•Quick•Readily available•Doesn’t usually require GA•Excellent for assessing lung parenchyma
Identification of;
•Fluid accumulation in sinus (sinusitis) (fluid line)
•Soft tissue masses
•Distortion/destruction of normal bony architecture
Nasal / Nasopharyngeal Swab
Not appropriate as a screening tool-
•Wide array of commensal bacterial flora
•Contamination of sample is impossible to avoid
Only use for identification/isolation of specific pathogen(s)-
•Virus identification
•Bacterial isolation
-Streptococcus equi equi, Influenza, herpes, IBR
nvestigating LRT disorders using radiography
Cheap
•Quick
•Readily available
•Doesn’t usually require GA•Excellent for assessing lung parenchyma
1.Ensure good (and safe) positioning
2.Obtain 3 standard views if possible- RL, LL. DV
3.Expose on inspiration
Radiographic Patterns- Interstitial
•Interstitiumis the space between the alveoli and capillaries
•Interstitiumbecomes more prominent
•Air still present in alveoli and normal vessels seen
Diffuse(unstructured) -e.g. oedema/ diffuse lymphoma. the tissue around the broncheoles is more radiodense
Nodular –e.g. soft tissue mass ie. neoplasia/abscess- tissue around bronchi is more radiodense but in a more “smattered” pattern
Underexposure, expiration or obesity can look similar –often misdiagnosed
Bronchial Radiographic Patterns
Thickened bronchi
•Infiltration/mineralisation of bronchial walls or due to peribronchialchanges
•Classical ‘donuts’ or ‘tramlines’
•Bronchi may be more obvious in the periphery of the lungs where normally wouldn’t be seen
Alveolar Radiographic Pattern
Consolidation or collapse of alveoli
Air in alveoli is replaced by fluid (oedema/haemorrhage) or cells
Air bronchogram is commonly seenCan be focal or diffuse
Examples; bronchopneumonia, aspiration pneumonia, oedema, haemorrhage, neoplasia, lung lobe collapse or torsion
Vascular Radiographic Pattern
Any changes to the size, course or opacity of the pulmonary vessels
•Vessels may be larger or smaller than normal or may be tortuous
•Commonly seen associated with cardiac disease
•Tortuous vessels seen with heartworm
•Differentials depend on vessels affected
Pleural Disease
Pleural effusion:
•Fluid in the pleural space
•Transudate, exudate, haemorrhage, chyle
Pneumothorax:
Air in the pleural space
Both cause lung edges to move away from the thoracic wall
investigating LRT disorders- ULTRASONGRAPHY
Cheap
•Very Quick
•Readily available
•Ideal where sedation/GA is contraindicated
Excellent for assessing; •Pleural space
•Pleural effusion
•Diseased lung tissue
RESPIRATORY SECRETION SAMPLING
investigating LRT disorders
TRACHEAL WASH-
Sampling of tracheal mucus
Trans-endoscopic
Trans-tracheal
Representative of tracheal secretions and ascending lower airway secretions- wont tell if left lung/ right lung
Cytology + Culture
BRONCHALVEOLAR LAVAGE-
Sampling of bronchoalveolarspace
Trans-endoscopic
Blind
Cytology only
Syncope
another word for fainting or passing out
Cardiogenic syncope
Intermittent, profound hypotension resulting in marked reduction in blood flow to brain
Estimated blood pressure fall ≤50%
Arrhythmia:
Asystole – sinus arrest or ventricular standstill
Marked reduction in cardiac output – rapid V Tach
Duration 10-30 seconds:
Activity level and presence/ absence structural heart disease
Pulmonary hypertension
Most common cause bradyarrhythmias
Might be intermittent
Pre-syncope/ episodic weakness
Intermittent, profound hypotension resulting in reduction in blood flow to brain
BUT lesser degree of hypotension cf. syncope
Arrhythmia:
Less rapid v tach
SVT
Less profound bradyarrhythmias
Structural heart disease and pulmonary hypertension may exacerbate- Excitement/ exertion
Bradycardias
Disorder of impulse formation and conduction systems of the heart
Dogs <60bpm and cats <100bpm
Bradycardias to consider:
Advanced AV block (High grade 2nd degree and 3rd degree)
Sinus arrest
Atrial standstill due to hyperkalaemia
Persistent atrial standstill
Can be drug induced:
ACP
Opioids
Alpha2-agonists
B-blockers, calcium channel antagonists and potassium channel blockers are all c/i in sinus bradycardia, SSS and AVB greater than 1st degree
Sinus bradycardia usually high vagal tone and does not result in syncope
Tachycardias
Supraventricular and ventricular tachycardias
Dogs >160bpm and cats >200bpm
Supraventricular tachycardia
Most common is atrial fibrillation (AF)- New onset – weakness, collapse or syncope. no consistent p waves
loss of atrial contraction and also variable diastolic filling time reduce CO
SVT is an umbrella term-AF, accessory pathways, atrial flutter…
Regular SVT less common cause of syncope- less syncope because regular rhythm and activation of the heart is normal sequence.
Ventricular tachycardia-
Boxers and Dobermanns
Can drop CO dramatically
Sudden death – more so when abnormal function of LV
drop of CO due to short diastolic filling time, lack of atrial connection, aberrant sequence of ventricular activation
Neurocardiogenic syncope
Also called vasovagal syncope
Profound hypotension due to combination of bradyarrhythmia AND vasodilation
Sudden autonomic nervous system failure
Withdrawal of sympathetic tone
Abrupt increase in vagal tone
Triggering events are variable
Coughing (tussive)
Excitement e.g. excited boxer
Situational e.g. micturition, defecation, vomiting, sneezing…
Exacerbated by structural heart disease (SAS) or concurrent GIT disease
Neurally mediated syncope represents an exaggeration of the CV reflexes that normally control the circulation. Syncope occurs when these reflees intermittently become inappropriate in response to a trigger. It is likely that dogs that suffer this type of syncope have some sort of disorder of autonomic control.
Remember that bradycardia can occur on its own as can vasodilation or they can occur together. The degree to which one predominates over the other will vary and persist to differing degrees.
The medulla is the control centre of the reflex.
Neurocardiogenic syncope is an adrenergically stimulated vagal reflex bradycardia/ Vagal mechanoreceptors (C-fibres) initiate the reflex when stretched- they are found in the in the ventricle, LA and LA-PV junction and Pas
Triggered by fight or flight scenarios
Apparently healthy individuals or predisposed individuals:
Genetics
DCM
High preload
Diagnosis often presumptive
Common situation is exertion/ excitement in small breed dog with advanced MMVD-
Hyperdynamic ventricle – increased by sympathetic surge
Vagal afferents when suddenly stretched trigger reflex
In this cohort it is often a sign of v high preload and impending/ overt CHF
Can also occur on diuretics if preload reduced too much
Diuertics is usually treatment of MMVd and syncope associated with high preload. Although if over diurese can cause syncope due to empty ventricle
Boxers-
Bimodal age at 6-24 months 0r 7-10 years
Triggered by exertion with excitement
Older Boxers also ARVC!
Both can occur in same dog
Situational syncope-
Easily identified trigger e.g. cough
Common in small, middle-aged or elderly dogs
Often associated with tracheal/ bronchial compression or big LA
Tussive syncope – transient bradycardia +/- reduced cardiac output
Cats with HCM- On exertion
Pulmonary hypertension, outflow tract obstruction (pulmonic/ sub-aortic): Severe - exertional syncope due to inability to increase RV output
Impaired right-sided inflow:
Compression, pericardial effusion with tamponade
Hypoxia and hypoglycaemia (insulinoma)
Severe anaemia with exertion
Exercise induced – Labradors, Border collies
Non-syncopal collapse
Wide range of diseases
Difficult to differentiate from cardiogenic/ neurocardiogenic
Neurological conditions
Profound hypoxaemia-
Can also have tussive syncope
Metabolic disorders-
Hypoadrenocorticism
Hypoglycaemia
Diagnostics for syncopy
Blood tests-
Complete blood count
Biochemistry & electrolytes
Cardiac troponin I
NT-proBNP?
Basal cortisol?
Fasted glucose level?
Ammonia/ BAST?
Thyroid panel?
Blood pressure -Especially if present collapsed
ECG- Bradyarrhythmia
Tachyarrhythmia
Thoracic and abdominal imaging-
POCUS
Radiography
Abdominal ultrasound
Echocardiography-
Structure and function
Viral causes of livestock respiritory diseae
In cattle the most common viral causes of pneumonia are Parainfluenza 3 (PI3) and Respiratory Synctial Virus (RSV).
IBR can affect any age of stock but is rarely found in young calves. In the endemic setting it is insidious, causing low grade respirator disease in stock. The real problems are seen when it enters a naive population as it causes severe disease and transmits rapidly. Following infection it becomes latent in the cows cells, recrudescing at times of stress.
Bovine viral diarrhoea virus (BVD) as the name suggests doesn’t cause respiratory disease directly but it significantly affects the immune system opening the door for other pathogens. It is therefore commonly considered as part of the respiratory disease complex.
bacterial causes of livestock respiritory diseae
Mannheimia haemolytica
Pasturella multocida
Histophilus somnus
Mycoplasma spp.
Others
A variety of bacterial pathogens can act as opportunistic pathogens but we commonly recognise four bacterial species as causing respiratory disease in cattle. M.haemolytica is probably the most significant and most severe. It can act as a primary disease agent, particularly at times of stress (shipping fever), but frequently is the sequel of viral infections. This is also true of P.multocida and H.somnus. Mycoplasma is increasingly recognised as a cause of respiratory disease in all ages of stock, both primary and secondary.
As already discussed, these pathogens rarely act in isolation and diagnostic samples (eg post mortem) yielding these pathogens does not necessarily make them the instigating agent. Possibly the greatest significance of the bacterial species involvement is to explain why we use antimicrobials in the treatment of respiratory disease and why we see different response rates to different antimicrobials on different farms.
fog fever
respiritory disease
Trypthophan toxicity
Fog fever is seen rarely in cattle grazing lush pasture. It is due to an excess of tryptophan in the diet which the animal can’t process quickly enough resulting in toxic damage to the lungs
Farmers lung
respiritory disease
Allergic reaction to moulds
Two Main Causes of Coughing
CARDIAC DISEASE
Cardiomegaly causing left mainstem bronchus compression
Congestive heart failure (fulminant pulmonary oedema)
RESPIRATORY DISEASE
Upper airway dz(laryngeal paralysis, BUAS, tracheal collapse)
Lower airway dz(infectious/ inflammatory/ neoplastic)
CLINICAL EXAM IS SO IMPORTANT
HEART FAILURE (HF)
HF = a clinical syndrome where cardiac output and tissue perfusion are maintained at the expense of increased cardiac filling pressures.
-Forward and backward failure
-Right-and left-sided heart failure
-Systolic and diastolic failure
-Acute and chronic heart failure
will cause drop in blood pressure and therefor trigger THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM (RAAS)- causes vasoconstriction and odema
AETIOLOGIES of heart failur
-Chronic Myxomatous Mitral Valve Dz/CMVD -Dilated Cardiomyopathy/DCM-Hypertrophic Cardiomyopathy/HCM-Pericardial Effusion/PE-Restrictive Cardiomyopathy/RCM
AETIOLOGIES•Patent DuctusArteriosus•Mitral Valve Dysplasia•Tricuspid Valve Dysplasia•Pulmonic Stenosis
aCUTE HF: TREATMENT
OXYGEN
IV FUROSEMIDE- im if too stressed
MINIMAL STRESS
PIMOBENDAN- vasodilator, increases contractillity
waht to look for in a radiograph to diagnose heart failure
1.Is there cardiomegaly? vhs greater than 8-10 in dogs
2.Is there left atrial enlargement?
3.Is there tracheal elevation?
4.Is there an abnormal lung pattern?
5.Are the pulmonary vessels normal?
Signs of heart failure
Cough (do not trust this as a sign of HF)
Dyspnoea (not always detected by the owner)
Increased sleeping respiratory rate (SRR)
Exercise intolerance
Non-cardiac causes of NT-proBNP
Systemic hypertension
Hyperthyroidism
Renal failure
Calculating the drip rate
The steps to calculate the drip rate are the following..
Calculate the hourly rate according to the total volume requirement (more on this later)
This is all you need to input if you are using an infusion pump
Calculate the minute rate: divide the hourly rate by 60 minutes
Calculate the drops per minute: multiple the minute rate by the giving set drip factor
Calculate the drops per second (drip rate): divide the drop per min by 60 seconds
Creating a fluid therapy plan
Step 1 – Resuscitation
If shock is present step 1 must be followed first. When the patient no longer shows signs of shock, or if no shock is present, move to step 2.
Step 2 – Rehydration
Is the patient is showing signs of dehydration?
Step 3 – Maintenance
Is the patient is not eating/drinking normally?
Step 4 – Ongoing losses
Does the patient have continuous fluid losses (e.g. vomiting)
To create a fluid therapy plan:
- Deal with Step 1 first if required. Stop when the patient no longer shows signs of shock.
- Work out if Steps 2, 3 and 4 apply to your patient. If they do, calculate the volume of fluids needed in each of the Steps 2, 3 and 4 and then add them together. This total must be administered in 24-48 hours.
Monitor the patient to guide continuity of fluids, identify complications and resolution of clinical signs.
Fluid deficit in dehydration is determined by:
Fluid deficit (litres) = Body weight (kg) x % dehydration (as a decimal)
fluid defecit of a patient with No clinical signs, but patient has history of fluid loss
<5%
fluid defecit of a patient with Tacky mucous membranes, ? Thirst,
5-6%
fluid defecit of a patient with Skin tenting (moderate), dry mm’s, sunken eyes, slightly prolonged CRT
6-8%
fluid defecit of a patient with Skin tenting (moderate), dry mm’s, sunken eyes, slightly prolonged CRT plus Increased pulse rate, cold peripheries
8-10%
fluid defecit of a patient with Skin tenting (moderate), dry mm’s, sunken eyes, slightly prolonged CRT, Increased pulse rate, cold peripheries plus prolonged CRT, Tented skin stands in place, Pulses weak
10-12%
