prep for clinical practice spot exam Flashcards
Total body water =
2/3 body weight
Aims of fluid therapy
Maintenance of normal physiology – e.g. during anaesthesia
Improvement of organ function e.g. kidney, heart, liver
The correction of electrolyte disturbances
The correction of hypovolaemia
The correction of acid base disturbances
(Total parenteral nutrition (TPN) - usually partial parenteral nutrition (PPN) used in animals)
what is the fluid defecit of a patient with tacky muscous membranes
5-6%
what is the fluid defecit of a patient with skin tenting and shrunked eyes
6-8%
what is the fluid defecit of a patient with increased pulse rate and colde peripheries
8-10%
what is the fluid defecit of a patient with weak pulses
10-12%
what is the fluid defecit of a patient with collapse
12-15%
What is the daily maintenance rate for an animal?
≈2.5ml/kg/hour
≈60ml/kg/day
{Or (30 x Kg) + 70 ???}
Types of fluid
Crystalloids (hypotonic, isotonic, hypertonic)
Colloids
Blood products
HBOCS (hemoglobin-based oxygen carrying solutions) –££ & problems….
Crystalloids- Isotonic-Lactated Ringer’s solution (LRS) aka Hartmann’s
If in doubt, choose Hartmann’s!
Inadequate potassium for long term therapy
Good for shock, diuresis, during anesthesia & can use for maintenance (can add other things to it)
Only 25% remains in vascular space after 12 minutes
Na+ 130 mEq/l , Cl– 109mEq/l
Buffered, contains lactate as a bicarbonate precursor
Crystalloids- Hypotonic
0.18% NaCl
0.18% NaCl + 5% glucose
Do you really want to use this ???
Hypotonic losses occur when the type of fluid being lost has a higher concentration of water than plasma, such as with diabetes insipidus and panting.
Hypotonic crystalloids are useful for treating patients with hypotonic fluid losses that result in hypernatremia or patients that have renal disease and cannot excrete the salt load of balanced isotonic solution
Crystalloids- Hypertonic saline
Draws water from interstitial space
Transient effect (10-15 mins)
Rapid restoration of MAP, increased myocardial contractility, CO & oxygen delivery
2ml/kg over 10 min, can repeat once but must follow with isotonic fluids
More commonly used in large animals (e.g. prior to colic surgery) but can be used in dogs and cats (carefully)
Also used in severe life-threatening raised ICP
used during resuscitation in hypovolemic shock and to decrease intracranial pressure.
colloids
Colloid solutions contain large molecules (>10,000 Da) and tend to remain in the intravascular space longer than crystalloids
Support circulating blood volume
e.g. severe hypovolaemia, haemorrhage, hypoproteinaemia
Exert a colloid osmotic pressure
More rapid initial re-expansion of volume
Only 1/4 of crystalloid administered remains in circulation in 40 mins
Support circulation longer than crystalloids
Types
HES solutions are thought to be most effective in treating hypovolemia because the colloid should theoretically remain in the intravascular space
includes-
artificial -gelatins, dextrans, starches, HBOCs
Oxypolygelatin
Dextran 40
Pentastarch
Hetastarch
Albumin
Whole blood
Plasma
artificial -gelatins, dextrans, starches, HBOCs
natural colloids e.g. albumin, plasma
However, no evidence of clinical superiority
over crystalloids
Colloids – Gelatins (ntk)
Oxypolygelatins
Plasma half life 2-4 hours (manufacturer data)
Weight average 30,000 D -pulls an equivalent volume of water from interstitial space
No need for concurrent crystalloid but often do give both
Produces osmotic diuresis
No direct coagulation effects
15 ml/kg total
Colloids – starches (ntk)
Plasma half life 25 hours (hetastarch) - due to molar substitution
Initial elimination by tissue uptake
Excretion by metabolism - serum amylase rises
Volume expanded by volume given
Reversal of microvascular permeability
?anti inflammatory effect ?
Direct coagulation effects
Increased APT in dogs (factor VIII precipitation)
Anaphylaxis in 0.0005-0.085% human patients
Nausea and vomiting in cats - slow administration
Up to 40 ml/kg/day
blood products
Natural’ colloids
Chosen according to clinical requirement
Whole blood
pRBCs
Ffp
Cryoprecipitate
Match the fluid to the loss
Oxyglobin Solution
Oxyglobin is a solution for infusion (drip into a vein). What is Oxyglobin used for? Oxyglobin is used to increase the oxygen content of the blood in dogs with anaemia (low red-blood-cell count). Oxyglobin should be used for at least 24 hours.
0 ml per kilogram body weight, administered at a rate of up to 10 ml/kg per hour. The most appropriate dose depends on the severity of the anaemia and how long the dog has been anaemic, as well as the desired duration of the medicine’s effect. Oxyglobin is intended for a single use only. Oxyglobin does not need to be matched to the dog’s blood type
Intravenous access for fluid therapy
Commonest route used
Relatively simple to master
Consider the different veins that can be used e.g. cephalic, saphenous, jugular, auricular, lateral thoracic
Select large bore cannula (flow α r 4)
Complications can & do occur:
Extravasation
Thrombosis
Thrombophlebitis
Infection
Emboli
Exsanguination
burette
will deliver 60 drops per ml (more accuratethan giving set) for fluid therapy
giving set
it will deliver 15 or 20 drops per ml (check on the packet)
for fluid therapy
less accurate than burrette
how to calculate Volume and rate of fluid therapy
Calculate total deficit (% fluid deficit + losses )
Add on maintenance fluids
Acute (replace ½ total deficit over first 1-2 hours) then consider rate thereafter (over 24 or 48 hours) – keep monitoring ins and outs
In cases of shock can give 60-90ml/kg/hr (<1hr though, and MUCH less in cats)
Chronic losses – replace over 3-4 days
OR BASE RESPONSE ON CLINICAL SIGNS!!
Why Give Fluids during anesthesia?
maintain circulating volume to ensure adequate perfusion and oxygen delivery to organs
Allows an ‘open vein’
Ancillary drugs/PIVA
Emergency situations
Fluid deficits caused by peri-operative fasting
Vasodilatory effects of anaesthetic drugs leading to a relative hypovolaemia
Acepromazine, isoflurane
Losses from the respiratory tract (worsened by endotracheal intubation)
Use HME’s, low flow anaesthesia if appropriate
Stranguria
difficulty/straining to urinate
Generally disorders of:
The lower urinary tract (bladder or urethra)
The genital tract (prostate, vagina)
Both
Two processes have potential to cause stranguria:
Non-obstructive stranguria
Mucosal irritation/inflammation of lower urinary/genital tract
Obstructive stranguria
Obstruction or narrowing of the urethra/bladder neck
Stranguria + large bladder may be obstructed = emergency!
Dysuria
difficult +/or painful urination
Pollakiuria
abnormally frequent urination (little & often)
Haematuria
present of blood in urine
Haematuria causes:
Iatrogenic haematuria
Pathological haematuria
Genital sources (if voided)
Do they have clinical signs associated with LUTD?
Has bleeding been noticed from other sites?
Trauma?
Rodenticides?
Blood in faeces?
Pattern to urine pigmentation?
Look for haemorrhage at other sites
Abdomen, thorax, mucosae (especially mouth, axillae, groin)
Palpate and assess kidneys for size, symmetry, discomfort
Examine the external genitalia
Gross “pigmenturia”
red, brown or black urine
- Urinalysis: positive haem
3 possible causes:
Haematuria
Haemoglobinuria
Myoglobinuria
Gross haematuria:
>150 RBCs/hpf
Occult haematuria:
Positive Hb on dipstick
>5 RBCs/hpf but not visibly pink
Care re: interpretation if catheterised/cysto
Both can be accompanied by clinical signs (stranguria, dysuria, pollakiuria)
Periuria
urination at inappropriate sites
Anuria
failure of urine production by the kidneys
Oliguria
reduction in urine production
Polyuria
Increase urine production
Pigmenturia
The presence of a component that imparts an abnormal colour to urine.
Haemoglobinuria
pink-red urine
Intravascular lysis of RBCs
Lysis of RBCs within the urinary excretory pathway e.g. USG <1.008, pH>7
Myoglobinuria
rare in dogs and cats (seen more in horses)
Extensive skeletal muscle damage/myopathies
Creatinine Kinase
tests for the function of the distile tubule and loop of henle
Urine Specific Gravity
tests for the function of the proximal tubes
Dipstick
tests for the function of the Glomerular function
Biochemistry
Dipstick
dog urine specific gravity
1.015 to 1.045
cat urine specific gravity
1.035 to 1.060
what does a dipstick test for
Protein
pH
Blood/Haem
Ketone
Bilirubin
Glucose
also measures Leucocytes
Nitrite
Urobilinogen
USG
but these should not be used
Renal Tubular Casts
Proteinaceous plugs of dense, mesh-like mucoprotein +/- cells accumulate in distal portion of nephron
Low number (<2/HPF) can be normal
Increased number relates to tubular disease
Try to identify associated cells, e.g. epithelial, WBC, RBC
pyuria
pus in your pee
Leucocytes
Cystocentesis sample - <3/HPF
<8/HPF catheter/voided
High counts = pyuria
+/- bacteria
Magnesium ammonium phosphate
struvite
Most commonly seen in dogs and cats
Neutral-alkaline urine
UTI’s
Diet
thin long, pyramidal
Cystine
Hexagonal
Acidic Urine
Abnormal finding
Inherited defect in proximal renal tubular transport of AA’s
Concentrated, acidic urine
Radiolucent
Calcium oxalate dihydrate
Cross-striations, “envelope”
Acidic urine
Can be seen in clinically normal animals or storage artefact
Or urolithiasis, hypercalcuria, hyperoxaluria..
Calcium oxalate monohydrate
Picket fence
Abnormal in cats/dogs
Ethylene glycol ingestion
Not 100% sensitive
Can be seen in normal horse
Calcium Carbonate
Alkaline Urine
Yellow-brown or colourless
Common in equine
Not seen in dogs and cats
Bilirubin in the urine
Orange-reddish brown
Low number routinely observed in dogs
Ammonium biurate Crystals
Acidic urine
Abnormal finding in most breeds
Routine finding in Dalmations
Amorphous Crystals
Aggregates/no defining shape
Urates - acidic
Phosphates – alkaline
Xanthene
Urolith
A calculus (stone) in the urinary tract
Single or multiple
Cystolith, ureterolith, nephrolith…
Remember – Crystals do NOT = Urolith
Recognised in all species
Common urolith types vary with species
Calcium carbonate – horses, rabbits
Magnesium ammonium sulphate, calcium oxolate – dogs, cats
One mineral normally predominates
Renomegaly – uni/bilateral +/- pain
Renal failure if bilateral
“big kidney-little kidney” cats
Nephroliths
Kidney stones
Asymptomatic
Incidental finding on x-rays
Associated with pyelonephritis
Pain, pyuria, pyrexia
Eupnoea
Normal respiration
Tachypnoea
Increased respiratory rate (not necessarily depth)
Primary cardiac disease
Neurological disease- Damage to respiratory control centre
Pain
Stress
Hyperthermia- Cooling mechanism
Metabolic disease
Acidosis/alkalosis
Increased PaCO2
Abdominal discomfort
Restricted movement of diaphragm
Primary respiratory disease
Apnoea
Absence of respiration
Hypoventilation and Hyperventilation are both…
Alterations in ventilation at the alveolar level
Hypercarbia
Increased CO2 in blood
Hypoventilation
Inc prodn of CO2
Primary drive for respiration
Hypoxaemia
Decreased O2 in blood
Poor O2 intake
Hypoventilation
Increased O2 consumption
Decreased O2 carrying capacity
STRIDOR
noisy breathing that occurs due to obstructed air flow through a narrowed airway.
as compared to stertor, which sounds like a snore, stridor is a high-pitched sound that results from rigid tissue vibrations. It is typically associated with laryngeal or tracheal disease. Laryngeal paralysis and tracheal collapse are two common presentations in companion animal practice.
STERTOR
This term implies a noise created in the nose or the back of the throat. It is typically low-pitched and most closely sounds like nasal congestion you might experience with a cold, or like the sound made with snoring
Upper RT Obstruction respiritory pattern
Causes marked inspiratory effort
Dynamic collapse of soft tissues due negative pressure associated with inspiration
Inspiratory STRIDOR or STERTOR
Lower RT Obstruction
Thickening, inflammation and mucus
Causes increased expiratory effort
Small airways held open during inspiration
Early collapse during expiration
Restrictive Respiratory Pattern
Expansion of the thorax restricted
Decreased tidal volume
Tachypnoea / short-shallow breaths
Hypoventilation
Paradoxical Respiratory Pattern
Paradoxical movement of the chest wall
Trauma – “Flail” chest
Terminal respiratory failure – fatigue of muscles
serous nasal discharge
Inc. nasal secretions
Allergic rhinitis
Acute Inflammation
Viral infection
mucoid nasal discharge
Inc. mucus prodn
Chronic disease
puralent nasal discharge
Bacterial infection
1o or opportunistic
pathogen
haemorraghic nasal discharge
Trauma
Clotting disorder
Vascular disease
unilateral nasal discharge can be from
Nasal cavity
Paranasal sinuses
Guttural Pouch (horses)- sometimes bilateral
Nasopharyngeal- sometoimes bilateral
bilateral nasal discharge can be from
URT Origins-
Guttural Pouch (horses)
Nasopharyngeal
Trachea
LRT Origins-
Bronchoalveolar space
Oedema, Pneumonia
Pulmonary vasculature
Haemorrhage
Laryngeal Hemiplagia (recurrent laryngeal neuropathy
a disease that affects the upper airway in horses. It causes a decrease in airflow to the lungs and can cause exercise intolerance. Horses with the disease are called “roarers” because they make a characteristic respiratory noise that sounds like “roaring” when exercised
Common cause of poor performance in race horses
Also occurs in dogs, in association with hypothyroidism
Radiographic Patterns- Interstitial
Interstitium is the space between the alveoli and capillaries
Interstitium becomes more prominent
Air still present in alveoli and normal vessels seen
Diffuse (unstructured) - e.g. oedema/ diffuse lymphoma
Nodular – e.g. soft tissue mass ie neoplasia/abscess
Underexposure, expiration or obesity can look similar – often misdiagnosed
Radiographic Patterns- Bronchial
Thickened bronchi
Infiltration/mineralisation of bronchial walls or due to peribronchial changes
thickning/ mineralisation of the brochial walls or peribrochial changes result in Classical ‘donuts’ or ‘tramlines’
Bronchi may be more obvious in the periphery of the lungs where normally wouldn’t be seen
Radiographic Patterns- Alveolar
Consolidation or collapse of alveoli
Air in alveoli is replaced by fluid (oedema/haemorrhage) or cells
Air bronchogram is commonly seen
Can be focal or diffuse
Examples; bronchopneumonia, aspiration pneumonia, oedema, haemorrhage, neoplasia, lung lobe collapse or torsion
Radiographic Patterns- Vascular
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 effusion
Fluid in the pleural space
Transudate, exudate, haemorrhage, chyle
lung edges to move away from the thoracic wall
Pneumothorax
Air in the pleural space
TRACHEAL WASH
Sampling of tracheal mucus
Trans-endoscopic
Trans-tracheal
Representative of tracheal secretions and ascending lower airway secretions
Cytology + Culture
BRONCHALVEOLAR LAVAGE
Sampling of bronchoalveolar space
Trans-endoscopic
Blind
Cytology on
TYPES OF SYNCOPE
Neurocardiogenic
Cardiogenic
neurocardiogenic syncope
Bradyarrhythmia and vasodilation
- Vasovagal- occurs when you faint because your body overreacts to certain triggers,
- Tussive- known also as laryngeal vertigo or laryngeal epilepsy, is a. syndrome in which fainting and vertigo with or without convulsions follows. a paroxysm of coughing
- Situational- when a patient faints in response to a specific trigger, or a specific situation. Some triggers can include: Swallowing. Coughing. Prolonged periods of straining
cardiogenic syncope
Hypotension-inducing arrhythmias
- Sinus arrest
- V Tach
- AV block
Combination of structural heart disease & less hypotensive inducing arrhythmias +/- excitement/ exertion
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
SVT is an umbrella term
AF, accessory pathways, atrial flutter…
Regular SVT less common cause of syncope
Ventricular tachycardia
Boxers and Dobermanns
Can drop CO dramatically
Sudden death – more so when abnormal function of LV
Cyanosis
Blue or grey skin or lips (cyanosis) happens when there’s not enough oxygen in your blood,
Right parasternal long-axis view
displays the right ventricular outflow tract which is usually a third of the normal left ventricle.
Right parasternal short-axis view
e define several short-axis views, each cutting the heart at a different level between the base and the apex. The entire heart can be scanned using these short-axis views
Fractional Shortening
FS (%) = (Left ventricular internal diameter during diastole – Left ventricular internal diameter during systole)/ LVDd
calculated by measuring the percentage change in left ventricular diameter during systole. It is measured in parasternal long axis view (PLAX) using M-mode. The end-systolic and end-diastolic left ventricular diameters are measured.
if there are no abnomalities fractional shortening correlates with ejection fraction- the amount of blood that the heart pumps each time it beats
FS% is affected by many external factors therefore has its limitations
Cornell formula
Left ventricular internal diameter during diastole
cm/Body Weightˆ0.294
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
E-point to septal separation (EPSS)
Using Echocardiography, the mitral Valve E-Point to Septal Separation (EPSS) is a straightforward approach that roughly corresponds to the status of left ventricular (LV) function, but its use has been limited to echocardiography and without solid quantitative correlation to left ventricular ejection fraction (LVEF)
he minimal distance between the anterior leaflet of the mitral valve and the septal endocardium over several cardiac cycles.
Bacterial causes of farm animal respiritory disease
Mannheimia haemolytica
Pasturella multocida
Histophilus somnus
Mycoplasma spp.
Others
parasitic causes of respiritory disease in farm animals
Parasitic bronchitis, commonly known as husk, is caused by lungworm, Dictyocaulus vivaparus, invasion. Unlike most respiratory disease, which tends to be seen in winter months, this disease is only seen from late spring until early autumn. Like other parasitic diseases, its aetiology is dictated by its lifecycle. Once infection occurs by ingestion the infective larvae penetrates the gut wall, migrating through the body to the lung where it reaches adulthood and begins egg laying. The eggs are coughed up, swallowed and pass out through faeces
Fog fever
Trypthophan toxicity
respiritory disease in cattle
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
an allergic reaction to the inhalation of fungal spores usually from mouldy silage
Differential diagnosis – bovine pneumonia
Enzootic calf pneumonia
Pneumonic pasteurellosis (shipping fever)
Mycoplasma bovis
IBR
RSV
PI3
Verminous pneumonia
Fog Fever
Farmers lung
Aspiration pneumonia
Embolic pneumonia (vena caval abcess)
?Stridor - Calf diptheria (Fusobacterium necrophorum)
?Tachypnoea - Septicaemia (eg salmonella Dublin)
What is heart disease vs. failure?
Heart disease is any condition affecting the cardiovascular system
- chronic in nature e.g. cardiomyopathy
- acute in nature e.g. myocarditis
- may or may not have clinical signs associated with it e.g. syncope, exercise intolerance
- abnormalities on physical examination usually present e.g. heart murmur
Heart failure is a syndrome where the heart can no longer meet the metabolic demand of the body
- Usually acute onset
- Clinical signs present e.g. exercise intolerance, syncope, lethargy, anorexia etc.
- Physical examination abnormalities present e.g. fluid thrill, dyspnoea, crackles, jugular pulsation etc.
Gallop sounds
audible s3 and s4 sounds
Normally heard in dogs and cats;
Occur during systole
S1
‘lub’
Closure of AV valves
S2
‘dub’
Closure of semilunar valves
Not normally heard in dogs and cats
Gallop sounds (occur in diastole)
S3
Early diastolic filling
Not heard in compliant ventricle
Systolic dysfunction
S4
Atrial contraction
Forceful atrial ejection into a noncompliant ventricle
Hypertrophic/ restrictive cardiomyopathy
describe the grades if a heart murmer
1 – barely audible, need quiet room
2 – audible but quieter than heart sounds
3 – clearly audible and as loud as heart sounds
4 - louder than heart sounds
5 – THRILL (PALPATION) present
6 – Audible with stethoscope lifted off chest
Mild/ moderate/ loud/ thrilling (Ljungvall 2014)
Apical systolic murmurs
Mitral regurgitation-
Grade can correlate with severity (MMVD not DCM)
Pansystolic worse (MMVD)
Can be musical/ whooping
Often radiates to right
a type of heart valve disease in which the valve between the left heart chambers doesn’t close completely, allowing blood to leak backward across the valve.
Tricuspid regurgitation-
Difficult to distinguish from radiating left sided murmurs
Vary with respiration
Tricuspid valve dysplasia
Pulmonary hypertension
Degeneration of valve
occurs when the valve’s flaps (cusps or leaflets) do not close properly.
Basilar systolic murmurs
Harsh sounding
Radiate widely to thoracic inlet
Low grade are difficult to distinguish from physiologic/ innocent
(Cats – HOCM dynamic)
The valve between the lower left heart chamber and the body’s main artery (aorta) is narrowed and doesn’t open fully.
Pulmonic stenosis
Left heart base
Radiate dorsally
he narrowing of the pulmonary valve, which controls the flow of blood from the heart’s right ventricle into the pulmonary artery
Innocent/ functional murmurs
Innocent-
Puppies and kittens
No structural heart disease
Grade 1-3
Systolic
Left heart base
Don’t radiate widely
Functional-
Associated with disease process
Anaemia
Hyperthyroidism
Fever
Hypertension
Pregnancy
No structural heart disease
Grade 1-3
Systolic
Left heart base
Don’t radiate widely
Ventricular septal defect (VSD)
Usually left to right
Smaller defect louder murmur
Right sternal border
Increased right side pressure
Quieter
Bi-directional
Right to left
Absent
Atrial septal defect (ASD)
Murmur not directly related to ASD
Only large defects
Increased blood flow
Relative pulmonic stenosis
Left heart base
Differentials for heart disease
Respiratory disease – cyanosis, dyspnoea/ tachypnoea, muffled heart sounds, crackles, dull percussion, cough, syncope
Neoplasia – ascites, muffled heart sounds, dyspnoea/tachypnoea, dull percussion, weakness
Hypoproteinaemia – ascites, muffled heart sounds
Neurological disease – paresis, paralysis, weakness, syncope
Metabolic disease – syncope, weakness, tachypnoea
clinical signs of heart disease
Heart murmur (dog vs cats)
Arrhythmia (dogs vs cats)
Gallop sound
Cat with cold hindlimbs
Cyanosis
Presence of goitre
Retinal detachment
Some neurological signs
clinical signs of heart faliure
Dyspnoea/ tachypnoea
Crackles in lungs
Ascites (fluid thrill)
Jugular distension
Significant jugular pulsation
Muffled heart or lung sounds
Positive hepatojugular reflux
Pulsus alternans/ paradoxus
Peripheral oedema
Plus usually signs of heart disease
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)
cardiac faliure aetiologies
Chronic Myxomatous
Mitral Valve Dz/CMVD
- Dilated
Cardiomyopathy/DCM
- Hypertrophic
Cardiomyopathy/HCM
- Pericardial Effusion/PE
- Restrictive
Cardiomyopathy/RCM
Patent Ductus
Arteriosus
* Mitral Valve Dysplasia
* Tricuspid Valve
Dysplasia
* Pulmonic Stenosis
diagnosing congestive
heart failure
horacic rads with echo are the gold standard
Echocardiography will also diagnose the underlying disease, provide
chamber size (prognosis) and identify any effusions
VHS
vertebral heart scale measured on VD and DV radiographs
a method for measuring heart size in thoracic radiograph
8.5 – 10.5 in dog
7.5 in cat
NT-proBNP
diagnostic test for heart failure and its management. It has a very high diagnostic sensitivity for HF
Non-cardiac causes of rraised NT-proBN-
Systemic hypertension
Hyperthyroidism
Renal failure
What is LA (left atrium) to AO (aorta) ratio?
the most commonly used method to evaluate left atrial (LA) size in dogs
Normal LA dimension was defined as an LA/Ao ratio <1.6
appearence of the diaphram on a vetrodorsal thoratic x ray
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
Normal Heart Size - Dog
Normal width (DV)
○ < 2/3 width of thorax
* Normal width (lateral)
○ 2.5 – 3.5 intercostal spaces wide Significant breed variation
* Normal height (lateral – 5th rib)
○ 2/3 height of thorax
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
norma; cardiac silhouette
O’Clock:
Aortic Arch = 11-1
Right Atrium = 9-11
Main PA = 1-2
Left aurical = 2-3
Left ventricle = 2-5
Right Ventricle = 5-9
Pink Camels collect extra large apples
- Assess technical quality
Good technique is essential to obtain diagnostic radiographs
Positioning
Centring
Collimation
Exposure factors
Labelling
Artefacts
what are the uses for different radiograph views
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
Right lateral radiograph
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
Lateral view:
Centre beam slightly caudal to caudal border of scapula
Collimate to thoracic inlet, thoracic spine, sternum and diaphragm (cranial abdomen)
ventral dorsal radiograph
Heart rotates to one side and distorts shadow
May produce better pulmonary detail
Can see more of the lung fields
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.
dorsal ventral radiograph
Safer in dyspnoeic patient
Heart lies in anatomically correct position – easier to interpret cardiac silhouette
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
Equine Premedication
Aim to produce a horse ‘sedated enough’ for ketamine induction
Healthy horses often receive ACP I/M
Associated with improved outcome and better oxygenation
Place IV cannula
Alpha-2 agonist IV
Xylazine shortest acting and can ‘top up’ - ? Good choice with colics
Detomidine intermediate action (45 minutes), small volumes
Romifidine longest acting (up to 90 minutes) and ? Less ataxia – standing sx?
Less common technique – infuse GGE until ‘knuckling’ then induce
Centrally acting muscle relaxant
Infused immediately prior to induction until horse is ataxic & as part of TIVA often called ‘Triple Drip’
Currently licensed and produced by Dechra
Best to use to 5% or 10% solution
Can substitute benzodiazepines (BZD) midazolam, diazepam (zolazepam)
Used in combination with induction agents to improve relaxation
Good in foals alone, don’t use in adults alone
Guaifenesin (GGE)
Centrally acting muscle relaxant
Infused immediately prior to induction until horse is ataxic & as part of TIVA often called ‘Triple Drip’
Currently licensed and produced by Dechra
Best to use to 5% or 10% solution
Can substitute benzodiazepines (BZD) midazolam, diazepam (zolazepam)
Used in combination with induction agents to improve relaxation
Good in foals alone, don’t use in adults alone
Equine Induction Agents
Ketamine - Dissociative anaesthetic
Excellent anaesthesia combined with other drugs
Must not be used alone (seizures)
Eyes remain open and central, less cumulative than thiopentone
Can be used as ‘top ups’ (don’t exceed induction dose)
Takes up to 2 minutes to ‘go down’
Used in combination with acepromazine, alpha 2 agonists, BZDs or guaifenesin (GGE)
Example Recipe forfeild anesthesia in a horse
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)
Ketamine iv top ups q 8-15 mins (0.1-0.2mg/kg) OR ‘triple drip’ (GGE, ketamine, alpha-2)
Add ¼ dose detomidine after 4/5 doses if using ketamine alone
DO NOT leave until horse standing
Field recoveries usually smoother than hospital
Advice to owner and arrange follow up
Flies
Bleeding
Swelling
Example recipe for General equine Anasthetic 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
Anaesthesia of Ruminants
LEGAL ASPECTS – check licenced drugs
Many procedures done standing
Induction of anaesthesia usually achieved iv (calves can be masked induced)
Some cows may drink chloral hydrate…
pig anaesthesia
Can be achieved with drugs given im (deep), iv or via mask with inhalant
Ketamine, alfaxalone, propofol
Ketamine combinations
Malignant hyperthermia (rare condition of pigs will manifest itself soon after exposure to inhalant usually), rapidly fatal, can be treated with dantrolene
Common anaesthetic problems
Hypotension-
Reduce IAA, fluid boluses, pressors/anticholinergics
Inadequate anaesthesia and poor recovery-
Is usually inadequate analgesia and premedication!
Anaesthetic overdose-
Use of alpha-2s, adding CRIs and not reducing vaporiser
Equipment/monitor issues-
Check first!
Hypothermia – delayed recovery and arrhythmias
Maintain body temp (warming devices)
Low glucose
Cardiac dysrhythmias-
Bradycardia: Alpha-2s, hypothermia, anaesthetic overdose
Tachycardia: Nociception, hypovolaemia, drugs
what happens when the pop off valve is closed
Increased intra-thoracic pressure
Gas flow from flowmeters has nowhere to escape
Increased intra-thoracic pressure as lungs inflate
Increased alveolar pressure causes:
Compression (collapse) of pulmonary capillaries (reduced preload)
Compression of heart chambers (decreased filling)
Compression of aorta (increased afterload)
=> Dramatic reduction in cardiac output
Circulatory arrest
Alveolar damage / rupture
subcutaneous emphysema
air becoming trapped in tissues beneath the skin. The condition is rare, but it can occur as a result of trauma, injury, infection, or certain medical procedures. Doctors sometimes refer to subcutaneous emphysema as crepitus, tissue emphysema, or subcutaneous air.
can result from ruptured trachea caused by et tube
Intra-vascular injection of local anaesthetic
can cause cardiovascular arrest
Start CPR
Specific treatment for local anaesthetic overdose-
Lipid infusion: Intralipid 20%
Bolus 1 ml/kg over 1 min Q 3-5mins
Total dose 3-4 ml/kg
CRI: 0.25 ml/kg/min “until haemodynamic recovery”
Initial research in dogs
Expt overdose of bupivacaine 10 mg/kg i/v
Cardiac massage unsuccessful for 10 mins
6/6 lipid treated dogs survived; 0/6 untreated dogs survived
Normal sinus rhythm returned w/in 5 mins of lipid infusion
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
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
seen as longer streaches between each PQRST complex
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
multiple p waves without a PQRS complex
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
Treatment?
If necessary, antagonise the alpha-2 agonist (or administer naloxone?)
Decrease anaesthetic depth
If still no response and reduced cardiac output?
Consider atropine/glycopyrrolate
3rd degree AV block
very strange p waves
very deep s waves
large t waves
Treatment – Stop further deterioration, ensure all other parameters are normal
AF and ventricular ectopic
ocational very deep s waves coupled with large t waves
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
occasional very large qrs waves with pause after
Check physiology – often due to hypoxia or hypercapnia. Sometimes low blood pressure
Add analgesia – may be due to nociception
Possible lidocaine if becoming frequent
Supra-ventricular tachycardia (SVT)
very squshed look of whole line
no visibel p waves with frequent qrs complexes and strange t waves
Causes?
Anything that causes tachycardia!
Nociception, hypotension, hypercapnia, hypoxia, hypokalaemia, drugs – which?
Treatment?
Underlying cause
Lidocaine/magnesium/amiodarone
Ventricular tachycardia (V tach)
small pqr
very deep s wave and large t wave
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
qrs without p wave with large qrs complex
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
infraorbital nerve blocks
upperlip, roof of nose, skin rostral to canal
Transbuccal
Transdermal
Place needle into canal
maxillary nerve blocks
maxilla, upper teeth, nose, upper lip
Transorbital approach
Transdermal approach
Ventral to notch in zygomatic arch
Transmucosal – cannula into infra-orbital canal
ophthalmic/ trigeminal nerve block
akinesia of globe, desens, eye and orbit
Auriculopalpebral
Supraorbital
3 point
Petersen block
Retrobulbar
mental nerve block
lower lip, insisors
Mandibular nn
Mental foramen
mandibular nerve block
mandible, teeth,skin mucosa
Medial mandible
Just rostqral to angular process
Or transmucosal – medial aspect mandible
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
Useful post-op
saturating on room air?
Limitations-
High/low heart rates
Probe design
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)
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
Remember, >95% saturation tells us nothing about blood oxygen content- could be anamic
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 and side-stream machines are available
Normal ET CO2 = 35–45 mm Hg
Hyperventilation – Decreased ETCO2
Hypoventilation - Increased ETCO2
Cardiovascular status
CVS depression / arrest
Reduced delivery CO2 to lungs
can also show airway obstruction and rebreathing
Other indicators
Oesophageal intubation
Leak at cuff/Patient disconnection
Adequacy of resuscitation
Minimum 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
MAC not affected by
Stimulation, duration, species, sex, CO2, NSAIDs
Isoflurane 1.28 (dog) 1.63 (cat)
Halothane 0.87 (dog) 1.14 (cat)
Sevoflurane 2.2 (dog) 2.58 (cat)
Desflurane 10.3 (dog) 9.8 (cat)
Nitrous oxide 188-297 (dog) 255 (cat)
TIVA
total intravenous anaesthesia
Can be used for short procedures in small animals/aggressive patients
E.g. ‘quad’ anaesthesia for cat neuters
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
PIVA
partial intravenous anaesthesia
Goals of PIVA
Reduce MAC
Reduce cardiopulmonary depression
Provide additional analgesia
Improve environmental impact
ideal drugs-
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
Scald/Ovine Interdigital Dermatitis
Seen in sheep continuously exposed to wet pasture – often lambs but can be seen in housed ewes when straw becomes wet and warm
Fusebacterium Necrophorum – can be zoonotic – human wounds have been swabbed and F. Necrophorum found – wear gloves when examining lame sheep!
Mild and transient lameness, rapidly resolves with treatment
Dermatitis involving some or all of the skin between the claws of the feet – skin between claws appears red and inflamed with white discharge
V common, less important than footrot/CODD, but associated with pathogenesis of foot abscesses and foot rot
Footrot
Footrot – 90% of lameness in the national flock
Dichelobacter Nodusus (Bacteroides) BUT needs F. necorphorum to facilitate epidermal invasion
D.nodosus – obligate parasite, can’t survive in the environment for more than 1 week
Also requires devitalised skin – chronic exposure to wet conditions and faecal contamination
Fly strike can occur in affected feet
Characterised by lameness which can be severe, often recumbent leading to reduced feeding time, weight loss, poor wool quality
Very effective vaccine against footrot.
Acts as treatment and prevention.
Timing is important
A second injection can be needed 4-6 weeks
One injection will last 6 months.
Diagnosis is essential
CODD
Contagious Ovine Digital Dermatitis
Relatively ‘new’ disease – ongoing research
Bacteria – treponeme species. Some association with cattle with Bovine Digital Dermatitis
Link between CODD and footrot
Usually SEVERE lameness with one claw of one foot affected
Initially ulcers develop on the coronary band which then under-run the hoof, can lead to whole hoof avulsion
Graded 1-5
Can lead to permanent hoof growth problems
Often needs systemic treatment with antibiotic and NSAIDs
White line separation in sheep
Often individual rather than ‘whole flock’ issue
Unknown aetiology – walking on stony ground, nutritional imbalance?
‘Shelley Hoof’
Separation of the hoof wall from the underlying tissues
Lameness caused by dirt packing into space created
Can lead to abscess formation
Toe Granuloma
Painful red swellings caused by:
Over-trimming
Chronic untreated lesions
Chemical irritation
ORF
viral disease usually seen around mouth of ewes/lambs – causes proliferative lesions around coronary band
SFR
– ongoing research into aetiology – can appear similar to orf lesions
Laminitis in sheep
lame in all 4 feet, often after grain gorging or over-fat rams, can lead to longer term hoof deformation
Broken leg bottom left
neuro disease presenting as lameness
spinal abscess as a result of any systemic bacterial infection can initially present as lameness before progressing to ataxia
Joint Ill
Most common = septic arthritis ‘Joint-ill;
Streptococcus Dysgalactiae
Transmission still unknown – cord/tagging/tailing/castrating/oral/vaginal canal?
Swollen joints, ill thrift, death
1-2% of flocks, can be up to 50% of lambs in severe outbreaks
control-
Lamb outdoors!- Reduces bacterial load for newborn lambs
Wear long gloves for each assisted lambing
Maintain clean dry lambing shed and pens
Consider if tailing/castration necessary for the particular system
Check colostrum intake
Research evidence suggests that wearing long disposable gloves for lambing will be the most effective method to reduce the prevalence within a flock
Sole Ulcers
Disruption to horn growth due to pressure on the corium underneath P3
Risk Factors:
Standing time
Surfaces
Foot trimming
Fat mobilisation
Inflammation
Remove pressure
Block
Trim loose horn
NSAID
Prevention:
Cow comfort – minimise standing times
Maximise transition health
Ensure cows aren’t lame in dry yards
Prompt ID and treatment
Foot trimming technique and strategy
Digital Dermatitis
Multifactorial
Strong bacterial component
Treponeme spp
Genetic susceptibility
Hoof hygiene!
Foul in the foot
Bacterial infection of interdigital tissue
F. Necrophorum et al
Painful, swollen ID space
Characteristic fragrance
Treatment
Systemic antimicrobials
NSAID
Local treatments
Prevention
Similar to DD
Minimise risk of interdigital trauma
Heel horn erosion
Prevention:
Hygiene and trimming of loose heel horn
v shaped lesions
Footbathing cows
3-4x/week
Not too strong/acidic (below pH3)
No more than 200 cows
Effective design required
Commonest ingredients – formalin, CuSO4
Denitrogenation
using oxygen to wash out the nitrogen contained in lungs after breathing room air, resulting in a larger alveolar oxygen reservoir.
With any rebreathing system where carrier gas is oxygen
Use higher flows for ~10 minutes
Risk of alveolar hypoxia
N.B also after short disconnections – movement between theatres etc
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
Rebreathing circuits use a carbon dioxide absorber to trap and remove CO2 so the patient can breathe gases that have been recycled through the machine. Non-rebreathing circuits use high gas flows to washout expired CO2 from the circuit before the patient takes its next breath.
t piece
bain
lack
mcgill
Working out gas flow requirements
Based on multiples of minute volume, where minute volume is;
Respiratory rate x Tidal volume
OR
200 ml per kg
Magill
non-rebreathing
Reservoir bag at fresh gas inlet
Awkward to use
circute factor of 1
1 x Vm (Vm = Vt x RR) or (Vm =200ml/kg)
resivour bag is attached to one limbs
>5kg
not sutible fopr ippv
Lack
Co-axial Magill
circut factor is 1
1 x minute volume (tvxrr)
Damage to inner limb results in rebreathing
resivour bag is attached to two limbs
> 10 to <25-30kg
not sutible for ippv
Mini Lack
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
T-piece
Suitable for very small patients, < 8 kg
2-3 x Vm
circute factor is 2-3
Suitable for IPPV
resouvouir back further from gass inlet than lack, attached to one limb, with another limb coming form gass outlet
Bain
Co-axial T-piece
Suitable for 7 – 10 kg
circute factor of 2-3
2- 3 X Vm
Beware – damage to inner tube
like magil but with inner tube
Humphrey ADE
versitile circle unit
has sodalime
can be converted form circle to lack to t- piece
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
Breathing system checks
Inspect system
Connect to common gas outlet
Test system for leaks
Check unidirectional valves on circle
Specific tests to check integrity of
co-axial lack and co-axial Bain
main types of bone in birds
Pneumatic
Medullary
Blood collection - lizards
Ventral tail vein
Care with species that perform autotomy
Jugular vein
Can be considered for leopard geckos
Blood collection - snakes
Ventral tail vein
Recommended site
Care not to insert needle into hemipenes or cloacal musk glands
Cardiocentesis
CARE risks of laceration to ventricle and risk of pericardial haemorrhage
Blood collection - birds
Venepuncture sites
Right jugular vein
Can obtain large volumes
Gentle pressure to achieve haemostasis
Basilic (ulnar/brachial vein)
Extend wing and visualise vein
Vein runs over the elbow area
Care as haematoma formation is common
Medial metatarsal vein
Vein is very short in psittacines
Anaesthetic Machine Components
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
Oxygen failure warning device
If fitted (Ritchie whistle or electronic)
Vaporiser-
Expensive and need servicing
See maintenance lecture
Common gas outlet-
Anaesthetic mixture attaches to breathing system
Non-return valve
Oxygen flush -
Bypass vaporiser
35l/min
CARE with breathing system valves – expiratory = open
Intermittent positive pressure ventilation (IPPV)
uses a mechanical respirator to deliver a controlled pressure of a gas to assist in ventilation or expansion of the lungs, thereby providing an increased tidal volume for patients with a variety of pulmonary conditions.
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.
Breathing system check steps
Visual check
Leak test; If pop-off valve, close and inflate with thumb over end until no balloon creases
Bain – occlude end with syringe with oxygen at 2l/min – flow should drop
With no IAA – BREATH into circle to check valves (or use 2 bag method)
Soda Lime
used to absorb carbon dioxide
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.
Pre-Anaesthetic Fasting for common species
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 (gas distension) – controversial
Ruminants withdraw 6 hours and reduce concentrates 12-24 hours
Small exotics/furries – shorter times depending on species
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 (cats, why not dogs?) and WAIT
Try largest but have a range available
Cut to length – minimise dead space
Not possible with armoured tubes
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
More popular
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
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
V-gels
veterinary specific (rabbits and cats)
2 species where ETT placement can be challenging
Designed to anatomical standards
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
Aims of premedication
Sedation and anxiolysis facilitating handling of the animal
Reduction of the stress for the animal
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
Alpha2 Adrenoceptor Agonists (Alpha-2s)
Potent sedative and analgesic drugs
Xylazine was the first 2 agonist to be used in veterinary practice
Superseded by medetomidine & dexmedetomidine (cats & dogs), both lasting about 45 minutes
Xylazine (30minutes), detomidine (45 minutes)and romifidine (60 minutes, less ataxia) used in horses
Xylazine and detomidine used in cattle
The superior selectivity of dexmedetomidine makes it the theoretical 2 agonist of choice for use in small animals
can be injectable or oral gel
Sedation is profound & dose related
Alpha 2 agonists provide good analgesia through an agonist effect at spinal cord 2 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
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 2 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
Endogenous insulin secretion is reduced leading to a transient hyperglycaemia
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
#reversable- atipamezole
reversal of Alpha2 Adrenoceptor Agonists (Alpha-2s)
Alpha 2 sedation and analgesia is rapidly antagonised by the administration of atipamezole, a specific alpha2 adrenergic receptor antagonist
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
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 1 adrenoreceptors and can cause peripheral vasodilation and a fall in arterial blood pressure
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
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
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
Acepromazine gel (horses) & tablets
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….
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
Propofol
Injectable Induction Agent
Quick recovery with no hangover
Apnoea if given too quickly
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
Rapid onset of action -rapid uptake by CNS
Short period of unconsciousness (5-8 mins)
Large volume of distribution (lipophilic)
Rapid smooth emergence due to redistribution & efficient metabolism (hepatic and extra hepatic) metabolites inactive
Respiratory depression (apnoea) - IPPV - Speed of injection?
Cardiovascular depression
Rapid and smooth recovery
Suitable for top ups or TIVA
Muscle relaxation usually ok
Anticonvulsant ??
Not irritant, pain reported
Analgesia ?? probably not
↓ ICP (patients with raised and normal ICP)
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)
Alphaxalone
Injectable Induction Agent
Predictable
Single use vials
Apnoea
Rough recoveries
Dissociative agent & benzodiazepine
Injectable Induction Agent
IM or IV
Long recovery?
Can be rough recovery
Controlled drug
Thiobarbiturates -Thiopentone Sodium
Ultra short acting
However difficult (impossible) to source
Use currently in horses to ‘top up’
Prolonged recovery in sighthounds - metabolism and body fat
Massive skin sloughing if injected extra-vascularly
Injectable Steroid Anaesthetics
Steroid Anaesthetics – ‘Saffan’ – no longer available in UK in this form
Alphaxalone(6mg/ml)/alphadolone(3mg/ml)
Alphaxalone more potent
Solubilised by Cremaphor EL
Didn’t give it to dogs
Used in ruminants & pigs
Formulation without Cremaphor (instead a 2-hydroxypropyl-beta-cyclodextrin (HPBCD))
Alfaxan (Alfaxalone)
Is suitable for cats and dogs (& other spp)
Alfaxalone is a clear colourless neuroactive steroid
Causes anaesthesia by activating the GABA (inhibitory) receptor
Alfaxalone 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
Ketamine
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
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
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 ↑ ICP, ocular surgery, fever, hyperthyroidism
Schedule 2 CD
types of colic
Smooth muscle spasm-
Inflammation
Colitis / Ulceration-
Distension
Impaction
Gas accumulation-
Obstruction
Impaction
Tension on the mesentery-
Displacement
Tissue congestion/infarction/necrosis-
Torsion/volvulus
Strangulation
Clinical Signs of Colic
Mild signs – Restless, Pawing, Flank watching
Gas build up / inflammation of GIT / Smooth muscle spasms
Moderate signs - Lying down flat out, groaning-
Impaction or other simple obstruction
Very fractious, violent rolling-
Acute, severe strangulation
Dull, unresponsive-
End-stage – Severe illness due to colic
Inappetence
Reduced faecal output
Vocalising/grunting
Agitation
Pawing at the ground
Lip curling
Flank Watching
Lying down
For long periods
Repeatedly
Stretching to urinate
Rolling / Thrashing
Sweating excessively
Straining
“False” colic
Any non-gastrointestinal source of abdominal pain
Liver disease / hepatomegaly
Urinary disease-
Renal pain
Bladder Dz (urolithiasis)
Peritonitis
Intra-abdominal abscess
Intra-abdominal neoplasia
Reproductive disorders
Other
Non-abdominal, pain mistaken for colic
Oesophageal obstruction
Rhabdomyolosis (tying-up)
Laminitis
Pleuroneumonia
Assessment of Gastrointestinal Tract of a horse
Auscultation - GIT borborygmi of the ascending colon (caecum & LC)
Auscultation of GIT has some degree of specificity but low degree of sensitivity.
Hypermotility: Increased smooth muscle activity - ‘spasm’ colic
Local hypomotility: Localised stasis of GIT
General absence: GIT ileus – common finding in most colics
Very useful for monitoring cases – e.g. progressive loss of motility
Nasogastric Intubation for colic
Nasogastric reflux
Fluid/ingesta reflux from the stomach
>2 Litres of fluid is abnormal
Usually indicative of small intestinal obstruction (physical or functional)
Can occur due to LC displacement (pressure on duodenum)
Presence of gastric reflux has significant diagnostic value
Majority of cases with reflux need referring to hospital
Relieving reflux is also very therapeutic
>8L will stretch stomach and be a significant source of pain
palpable structures in a transrectal exam of a horse
ventral band of cecum
great vessels
caudal pole of left kidney
caudodorsal aspect of spleen
nephrosplenic space and ligament
fecal balls in small colon
inguanal rings in stallion
bladder when distended
Abnormalities: - Impaction
- Distension (Gas accumulation)
- Displacement
- Masses
Abdominocentesis
Assess for presence of changes in peritoneal fluid
Serosanguineous colour change/ Increased protein concentration- Serosal compromise – leakage of blood components
Increased Lactate concentration- Anaerobic tissue metabolism
Presence of ingesta- Rupture of GIT tract
High WBC count- Peritonitis
analgesia for colic in the horse
Analgesia
Imperative to provide some form of analgesia to a colic case
NSAIDs
The most common form of analgesics used to treat colic
Slow onset and long duration of activity
Flunixin meglumine (Finadyne Solution)
1.1 mg/kg iv
Potent visceral analgesic
Can masks deterioration in CVS status
Ketaprofen (Ketofen)
1.1 - 2.2mg/kg iv
Phenylbutazone (Equipalazone Injection)
4.4mg/kg iv
Alpha-2 agonists-
Potent analgesics with rapid onset and short duration of action
Allow rapid re-assessment of case progression
Xylazine (Rompun, Virbaxyl)
Dose rate: 0.2-1.1mg/ml
Analgesia for 15-20min
Detomidine (Domosedan)
Dose rate: 0.01-0.02mg/kg
Analgesia for 1-2 hours
Romifidine (Sedivet)
Dose rate: 0.04-0.08mg/kg
Analgesia for 1-3 hours
Opiods-
Not first line analgesic
Usually reserved for higher degree of pain
Butorphanol (Torbugesic)
0.05-0.075mg/kg iv
Potent analgesic; 1 hour duration
Spasmolytics (Anticholinergics)
N-Butylscopolamine (Buscopan Injectable )
Smooth muscle relaxant
Rapid onset and short duration of activity
Good for;
Treating hypermotile/spasm type colic
‘Gas’ colic
Relaxing rectum prior to rectal examination
General Rules
For first-line treatment, or where diagnosis is uncertain, use short acting analgesic agents
Assessing progression, rapid recurrence of pain or deteriorating CV status is vital in the decision to refer
Beware the potent anti-inflammatory effects of flunixin, which can significantly ‘mask’ the early signs of endotoxaemia.
Only administer NSAIDs after the diagnosis or CV status have been established
fluid therapy for colic
Enteric fluids-
Indicated in the vast majority of colic cases
Most cases will have a degree of dehydration
Contraindicated if NG reflux is present, or suspect small intestinal lesion
Excellent way to rehydrate the colonic content (impactions)
Bolus(es) of isotonic fluids (tap water + NaCl + KCl)
5-8L can be given q2hrs
Purgatives
Liquid Paraffin; Magnesium Sulphate (Epsom Salts)
indicators of prognisis in olic in horses
Essentially, any indicators that the case won’t resolve with simple conservative therapy (analgesics & enteric fluids)
Non-response to analgesia
Significant CV compromise
Rapid deterioration despite therapy
Complex abnormalities on rectal exam
Presence of NG reflux
Recurrent/chronic cases with unclear Dx
82.9% survival rate for 1st opinion cases
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
Pharmacodynamics
Effect of drug on the body
Drugs are chemicals and as such interact chemically with biological/cellular molecules – most often proteins
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)
Meyer-Overton hypothesis
the theory of anaesthetic action which proposes that the potency of an anaesthetic agent is related to its lipid solubility. Potency is described by the minimum alveolar concentration (MAC) of an agent and lipid solubility by the oil:gas solubility coefficient.
Endogenous agonist
a compound naturally produced by the body which binds to and activates that receptor. For example, the primary endogenous agonist for serotonin receptors is serotonin, and the primary endogenous agonist for dopamine receptors is dopamine.
Efficacy:
the maximum therapeutic response that a drug can produce (example: morphine vs buprenorphine)
Agonism
Drug Target Interaction
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
Agonist: molecule/drug that binds and activates the receptor
Affinity: the tendency of a drug to bind to the receptor
Efficacy: the tendency of a drug to activate the receptor once bound
Affinity
the tendency of a drug to bind to the receptor
Efficacy:
the tendency of a drug to activate the receptor once bound
Antagonism
Drug Target Interaction
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
Competitive Antagonism
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)
Non-competitive Antagonism
Non-competitive antagonists either bind to a different receptor site
OR
Block the chain of events “post” binding - acting “downstream” of the receptor.
shift the efficacy of the agonist down
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 – why?
BUT……Some irreversible enzyme inhibitors are used in practice – e.g. aspirin, omeprazole
Inverse agonism
Inverse agonist: drug that reduces the activation of a receptor with constitutive activity (example: GABAA receptor)
Can be regarded as drugs with negative efficacy.
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.
Therapeutic index
toxic dose (or LD50) ÷ effective dose (or ED50)
Large TI is safer!
Drug receptor types
Ion channel cell surface transmembrane receptor
Ligand regulated enzyme
E.g. insulin receptor
G-protein coupled receptors
Protein synthesis regulating receptor
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
Self-Antagonism
When a drug becomes antagonistic to its own effects
Loss of target sensitivity is caused by
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
Who oversees UK veterinary medicine legislation?
The Veterinary Medicines Directorate (VMD), which is an executive agency, sponsored by the Department for Environment, Food & Rural Affairs
VMD is responsible for;
monitoring and taking action on reports of adverse events from veterinary medicines
testing for residues of veterinary medicines or illegal substances in animals and animal products
assessing applications for and authorising companies to sell veterinary medicines
controlling how veterinary medicines are made and distributed
advising government ministers on developing veterinary medicines policy and putting it into action
making, updating and enforcing UK legislation on veterinary medicines
POM-V
Prescription-only Medicine – Veterinarian
must be prescribed by a veterinary surgeon, who must first carry out a clinical assessment of the animal under his or her care.
POM-VPS
Prescription-only Medicine – Veterinarian, Pharmacist, Suitably Qualified Person
medicines may be prescribed in circumstances where a veterinary surgeon has carried out a clinical assessment and has the animals under his or her care. However, the Veterinary Medicines Regulations provide that POM-VPS may be prescribed in circumstances where the veterinary surgeon, pharmacist or SQP has made no clinical assessment of the animals and the animals are not under the prescriber’s care.
NFA-VPS
Non-Food Animal – Veterinarian, Pharmacist, Suitably Qualified Person
medicines may be supplied in circumstances where the veterinary surgeon or SQP is satisfied that the person who will use the product is competent to do so safely, and intends to use it for the purpose for which it is authorised.
AVM-GSL
Authorised Veterinary Medicine – General Sales List
the cascade
The cascade is a risk-based decision tree to aid prescribing on a case-by-case basis.
Initially a VS should prescribe a medicine authorised in the jurisdiction where they are practising, for use in the target species, for the condition being treated, and used at the manufacturer’s recommended dosage.
If no such product exists, follow the cascade.
Nb. There is separate guidance on the Cascade for veterinary surgeons practising in England/Wales/Scotland, and for those in Northern Ireland. Please refer to VMD website
The treatment in any particular case is restricted to animals on a single holding
Any medicine imported from another country must be authorised for use in a food-producing species in that country
The pharmacologically active substances contained in the medicine must be listed either
for use in NI – in table 1 of the Annex to Regulation (EU) No. 37/2010 (this table replaces Annexes I, II or III of Council Regulation (EEC) 2377/90);
for use in GB – in the GB MRL Register as part of the VMD’s Product Information Database.
The veterinary surgeon responsible for prescribing the medicine must specify an appropriate withdrawal period
The veterinary surgeon responsible for prescribing the medicine must keep specified records
What are controlled drugs(CDs)?
Controlled drugs (CDs) are listed in Schedules 1 to 5 of the Misuse of Drugs Regulations 2001
Veterinary medicines only contain CDs in Schedules 2, 3, 4 and 5
Schedule 1 drugs include drugs such as cannabis or LSD – highly addictive, no therapeutic value
Schedule 2 CDs have therapeutic value but are highly addictive
Licenced examples;
Methadone
Fentanyl
Pethidine
Ketamine
Schedule 3 includes buprenorphine, barbiturates and some benzodiazepines which are also subject to special prescription writing requirements. Some are also subject to special storage requirements
Schedule 4 and schedule 5 drugs have no additional special controls
Ketamine WAS Schedule 4
Since November 2015 reclassified as Schedule 2
Now subject to full schedule 2 legal requirements
Schedule 2s: Obtained from wholesalers providing a signed prescription has been issued by the requesting veterinary surgeon
Must keep requisition records for at least 2 years
Schedule 2 or 3 CDs ; written prescription must be signed by the person issuing it which may be hand-written, typed in a computerised form or computer generated.
This prescription is only valid for 28 days.
Repeat dispenses on the same prescription are not allowed with schedule 2 or 3 drugs
Recommended that you keep a copy of a CD requisition to assist in complying with the law on wholesale supply
RCVS considers that a veterinary nurse may draw up and administer a CD
Provided the veterinary surgeon
Prescribed the drug to a specific animal
Decided on the dose
Authorised that it be drawn up and is confident that the veterinary nurse is competent to draw up and administer the prescribed dose
A veterinary surgeon does not need to be present when the drugs are drawn up or administered
but the legal responsibility for the supply of the CDs remains with the veterinary surgeon
Recommended to have a standard operating procedure
Veterinary nurses may administer CDs out of hours when there is no vet on the premises
A veterinary nurse is not able to decide to give a CD or change the dose (i.e. make prescribing decisions) without the instructions of a veterinary surgeon
records of Schedule 2 CDs
Complete records of Schedule 2 CDs must be kept in a Controlled Drugs Register (CDR)
CDR = either a computerised system or a bound book separated into each class of drug with a separate page for each strength and form of that drug at the top of each page.
Loose leaf registers or card index systems are not allowed
CDR entries must be
In chronological order, made in ink or in a computerised form in which every entry can be audited, and made on the day of the transaction
The book must be kept at the premises to which it relates and be available for inspection at any time
It must be kept for a minimum of two years after the date of the last entry
The CDR must record for all CD purchased and supplied
The date supply received, name and address of supplier and quantity received
The CDR must record for all CDs administered or supplied
The date supplied, name and address of person supplied, details of the authority to possess (prescriber or licence holder’s details) and the quantity supplied
storage of Schedule 2 and Schedule 3 CDs
Schedule 2 and Schedule 3 CDs containing buprenorphine must be kept in a locked container which is constructed and maintained to prevent unauthorised access to the drugs and can only be opened by a veterinary surgeon or other authorised person
The room housing this container should be lockable and tidy to avoid drugs being misplaced
CD container keys should not be kept with keys to other parts of the building
The room should not normally be accessible to clients
Any returned CDs should not be re-used and should be destroyed according to regulations.
Pain pathways
Analgesics may act at different sites
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, delta, kappa, 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
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
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
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 ≈ 90 minutes
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)
Naloxone
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
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)
Butorphanol
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- suppress coughing
LIMITED ANALGESIA
list 9 Local anaesthetic agents
Lidocaine
Prilocaine (+lidocaine)
Bupivicaine
Mepivicaine
Ropivicaine
Etidocaine
Amethocaine
Proparacaine
Cocaine
Local anaesthetic agents
Lidocaine
Prilocaine (+lidocaine)
Bupivicaine
Mepivicaine
Ropivicaine
Etidocaine
Amethocaine
Proparacaine
Cocaine
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.
Non-Steroidal Anti-Inflammatory Drugs (NSAID)
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, poSome licensed for pre-operative use
Carprofen and meloxicam have revolutionized perioperative pain management in UK in last 3 decades
Carprofen
Firocoxib
Meloxicam
Deracoxib
Etodolac –
Ketoprofen
Cimicoxib
Mavacoxib
Robenacoxib
Grapiprant
Paracetamol ? and codeine (opioid)
Phenylbutazone
Tolfenamic acid
Tepoxalin*
Vedaprofen
Keterolac
Aspirin
Licensed NSAIDs for horses-
Phenylbutazone
Suxibuzone
Firocoxib
Meloxicam
Flunixin meglumine
Vedaprofen
Carprofen
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
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
Grapiprant (Galliprant™)
Piprant class NSAID
Non-cyclooxygenase inhibiting non-steroidal anti-inflammatory drug
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
Naloxone
antagonism of pure mu opioids
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
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
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
Sedation including standing sedation for equine/large animal
Premedication
PIVA/TIVA
Epidural
Rescue analgesia
One of the few classes of drugs with an antagonist- atipamazole
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
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)
penicillin mechanism of action and target
inhibits cell wall synthesis and gram positive bacteria
ampicillin mechanism of action and target
inhibits cell wall cynthesis
broad spectrum
bacitracin mechanism of action and target
inhibits cell wall synthesis
skin ointment for gram positive bacteria
cephalosporin mechanism of action and target
inhibits cell wall synthesis
broad spectrum
