Medical Nursing And Anaesthesia Flashcards
Cutaneous Anthrax
95% human disease
Spores from soil, meat, tanning, hide
Horses and pigs
Painless lesion and dark crust
Septicaemic anthrax
Ingested from soil - horses and cattle
Ingested from protein supplements - pigs
Inhale spores - humans
Bacteria germinate, multiply uncontrollably and release toxins, using up the body’s O2 supply
Incubation 1-14days
Humans/horses 24hrs till death
Cattle 1-2hrs till death
Pigs death is rare
Symptoms of septicaemic anthrax
Haemorrhage Toxaemia Enlarged spleen and LN inflammation Capillary thrombosis Blood vessel fluid loss Pulmonary oedema Septicaemia Circulatory collapse Extreme hypoxia Death
Pre death - dark blood from all orifices and increased ❤ and resp rate
Post death- dried dark blood round orifices and incomplete rigor mortis
What is Mycobacterium?
Gram +ve
Aerobic
Rods
M. Bovine
M. Tuberculosis
M. Avium- not psitticines
Spreads from all orifices
6mnths in faeces
1-4yrs in soil
How does Tb work
Inhalation or ingestion Local macrophages Lymph nodes Granuloma in lungs, liver and spleen - subclinical, military tb that is shedding Granuloma bursts then spreads Latent tb spread by coughing
Bovine Tb
XDRTb
Stock culls - restock after 1 monthbt surviving cows can sell pasteurised milk
Antibiotics not worth it for cattle
Vaccinations not available as current test looks for antibodies
Definition of a food allergy
Immunological adverse reaction Pruritis Genetic predisposition- defects of mucosal barrier or gut associated lymphoid tissue IgE type 1 hypersensitivity Viruses can cause sensitisation
Symptoms of food allergy?
V+ D+ Abdo pain Weight loss Haematemesis Altered appetite Histological changes - villus atrophy, eosinophils infiltrate, lymphocyte infiltrate, intraepithelial infiltrate Often mistaken for IBD Intradermal skin tests not helpful
3 diets for food adversions
Restricted antigen diet- one novel protein
Hydrolysed - proteins broken down so do not elicit an antigen response however can expose antigen epitope - type 4 reaction possible. Expensive
Elemental diet - hydrolysed feather protein. All peptides <1kD
Symptoms of IBD
Unknown cause V+D+ Haematemesis Abdo pain Weight loss Small int - melana, watery, large vol Large int - haematochezia, mucus, tenesmus, freq Borborygmi Flatus Polyphagia / anorexia Hypoproteinaemia causing ascites in abdo
Diagnosis and treatment of IBD
Histological diagnosis - endoscopy and biopsy
Immunosuppression - preds or cyclosporine (not if anorexic)
Highly digestible restricted fat diet
Patient prep for endoscopy
History Physical exam Faecal exam Routine lab tests Radiographs and ultrasound 12 hr fasting Take biopsies when doing the endoscopy
Colonoscopy prep
24-36hr starvation
Enema 1litre arm water for up to 30kg
Lavage - Iso-osmotic solutions, 2-4 doses 25ml/kg, NG tube, last dose 12hrs pre colonoscopy
GA for endoscopy
No nitrous oxide as 3rd space effect will cause overdistension of the stomach
Cuffed et tube to prevent aspiration if regurge occurs
Mouth gag
L lateral recumbancy so gastroantrum and ileum on top
Standard GA monitoring, be aware of cardiorespiratory compromise with over inflation
Food intolerance
Predictable- eaten something they shouldn’t
Unpredictable- non-immunological reaction occurring in a susceptible individual as idiosyncratic reactions
- differences in intestinal flora, enzyme activity and permeability
- could be an underlying genetic predisposition
Leptospirosis
20 strains, vaccines are strain specific
Cycling between domestic and wild animals
Worse in stressed or immunocompromised animals
Spread by stagnant water and urine
BARRIER NURSE
50% mortality in unvaccinated dogs
Causes kidney probs and cold like symptoms
Serology and pcr to diagnose
Antibiotics if detected early
L4 in U.K. Against canicola and icterohaeorrhagiae
Absolute contraindications of endoscopy
Unfit for anaesthesia due to unstable cardiac arrhythmia, cardiac failure, non reversible hypoxaemia, bleeding disorder)
Bowel perforation
Relative contraindications from endoscopy
Poor cardiopulmonary reserve
Uraemia
Hypoproteinaemia
Inadequate prep and investigation
Complications of endoscopy
Acute bradycardia - small dogs, vago-vagal reflex, atropine
Bacteraemia - give antibiotics if GI bleeding
Haemorrhage - severe h+ is rare, usually malignancy
Perforation - rare usually due to disease or vigorous insufflation
Infection transmission - not cleaned properly. Do top before tail
⬇️ venous return from gastric over distension - increase antropyloric contractility, compression of the caudal vena cava, decreased venous return and bp, decreased tidal vol and diaphragmatic compression
Components of an endoscope
Light source made of incoherent glass fibres
Insufflation
Suction
Flexible endoscope
Pros and cons of fibre optic endoscope
Pros
- portable
- cheap
- range of sizes
Cons
- faceted image
- smaller the size the lower the resolution
- fragile as coherent glass fibres
- hard to rotate
- need a CCD camera attachment for video
Pros and cons of video endoscope
Pros
- excellent quality
- hygienic as don’t need to look through eye piece
- assistant can also see the image
Cons
- expensive
- not easily portable
- small diameters not available
What are the 3 types of bacillus?
Licheniform - abortion in cattle
Cereus - food poisoning in humans / mastitis in cattle
Anthracis- horses cattle and humans - lethal
Spores
Aerobic
Catalase +ve
Characteristics of a benign tumour
Slow growth rate Well defined boundary Minimal impact on adjacent tissues Minimal impact on host No metastasis Paraneoplastic effects can occur due to release of physiologically active components
Characteristics of a malignant tumour
Fast growth rate
Undefined boundaries and may spread to adjacent tissues
Metastasis
Often life threatening due to destructive nature and metastasis into vital organs
Growth and invasion into adjacent tissues or destruction of bone
Paraneoplastic effects due to release of physiologically active components
When are tumours least susceptible to treatment
When first detectable as already began to slow down growth
Where do tumours metastasise to?
Blood -> liver and lungs
Lymphatics -> local then regional lymph nodes
Transcoelomic -> across pleural of peritoneal space
Iatrogenic -> seeding during FNA or trucut
What are the paraneoplastic effects?
Haematological complications
Hyperhistaminaemia
By-stander immune mediated reactions
Hypercalcaemia
Haematological complications due to paraneoplastic effects
Oestrogen producing cells are affected Bone marrow affected Non regenerative anaemia - lethargy, weakness, dyspnoea Thrombocytopenia - bleeding Leukopenia - infection risk
Hyperhistaminaemia due to paraneoplastic effects
Mast cells produce:
Histamine to stomach - anaphylactic shock
Proteases which prevent healing - delayed wound healing post sx
Heparin which prevents clotting - localised bleeding
Vasoactive amines - excess acid production and ulcers leading to peritonitis
Oedematous swelling with erythema and pruritis
By-stander immune mediated reactions due to paraneoplastic effects
IMHA - secondary
- fragmentation causing shistocytes, neuropathic so, myasthenia gravis
Skin disease - cats with pancreatic cancer lose hair and go shiny
Hypercalcaemia due to paraneoplastic effects
Tumours release parathyroid hormone related peptide (PTHrp) which increases calcium conc
-lymphosarcoma, anal sac adenocarcinoma, multiple myeloma
Diagnosis of cancer
History Exam Lab tests Diagnostics FNA Biopsy Can only make accurate diagnosis by histological exam of the cells collected from the tumour
Cancer stage classification
T - tumour size and invasiveness
N- spread to lymph nodes?
M - metastasis
Surgery to treat cancer
Most effective treatment option
Debulking a mass that can’t be removed completely increases cell turnover and improves the response to chemo
Radiotherapy as cancer treatment
Limited availability and expensive
Gamma or beta rays emitted close to tumour - brachytherapy
Radiation from external bea, directed at the tissue from a fixed distance - teletherapy
May need repeating
Side effects - neural necrosis, osteonecrosis, skin reddening, dermatitis, localised hair loss, dermal fibrosis
Chemotherapy as cancer treatment
Cytotoxic drugs kill a fixed % of cells
Use highest possible dose that is safe to use
Not effective in advanced disease
Combination chemo
Dangerous drugs to people - risk assessments
Types of chemo drugs
Anti-metabolites
Alkylating agents
Anti-tumour antibiotics - damage nucleic acids
Vinca alkaloids - damage microtubules
Tyrosine kinase inhibitors - stop cell signals
Platinum compounds
Enzymes
How is chemotherapy given?
Repeated intervals to allow normal tissue to recover
3 week cycles
Doses done by surface area rather than body weight so large animals aren’t overdosed
Phases of chemo treatment
Induction- decrease tumour burden to undetectable levels
Maintenance - maintain remission after induction but debatable if necessary
Rescue - if does not respond or relapses give more aggressive therapy. Second remission is harder to achieve and animal eventually becomes resistant to the drugs
When to use chemotherapy
The tumour has to be systemic and have a high growth rate - lymphoma
Sarcoma, carcinoma and melanoma are resistant as too slow growing
Drug combo to treat lymphoma
Cyclophosamide
Oncovin
Prednisolone
+/- doxorubicin
Risks of cytotoxic drugs to patients
GI toxicity
Myelosuppression
Phlebitis
Cyclophosphamide - sterile haemorrhagic cystitis
Doxorubicin - cardiotoxicity, maximum cumulative dose is 240mg/m2
Cisplatin - nephrotoxicity
Treatment of GI toxicity from cytotoxic drugs
IVFT
Antiemetics
Gastroprotectants
Chlorhexidine mouthwash
What is myelosuppresion?
Bone marrow suppression
Can lead to neutropenia and life threatening sepsis
Routine haematology needs to be done before each chemo treatment
Phlebitis due to chemo
Many dugs are irritant or vesicant
Check IV catheter first
Place IV catheter first stick so no holes for drugs to move out of veins and go subcut
What to do if perivascular leakage of cytotoxic drugs
Stop giving drugs Aspirate drug and flush with saline to dilute Draw back blood and remove IV IV hydrocortisone Cold compress Antidote for some drugs but is expensive
Lymphoma
Most common in dogs
Multicentric lymphoma
Can’t treat with sx as systemic
Chemo
What is the Monroe Kelly Hypothesis?
Intracranial cavity is 80% brain, 10% CSF, 10% blood
If any increase, pressure increase causing seizures, papilloedema and depressed state
Blood brain barrier disrupted by trauma, inflammation and hypertension
Brain gets 15% cardiac output
Intracranial pressure
Influenced by cerebral perfusion pressure, PaO2, PaCO2 and cerebral metabolic activity
Cushing reflex - decreased heart rate and increased Bp
Cerebral perfusion pressure - pressure gradient between MAP and ICP
Cerebral blood flow autoregulated MAP 50-150mmHg
Coughing, v+, occluded jugular vein increase venous outflow pressure
PaCO2 and PaO2
4% increase of cerebral blood flow for 1mmHg increase of PaCO2
Intracerebral steal - vasodilation of undamaged vessels shunts blood away from damaged area as the damaged areas can’t autoregulate
Inverse steal - vasoconstriction of undamaged blood vessels shunts blood to damaged areas
Hypoxia can cause vasodilation
Anaesthetic considerations for neurodisease
Elevate head at 35 degree angle Mannitol - osmotic diuresis but can cause dehydration. Increases Blood flow so pressure decreases IPPV ETCO2 should be 30mmHg - capnography 100 O2 gas Preoxygenate and O2 on recovery Seizure watch - plans on kennel Anticonvulsants Bp
When doing a CIF tap what do you need to look out for
Watch the airway to make sure when neck is bent ET tube is not kinked and airway is not occluded
Drug considerations for neurodisease patients
Dexmedetomidine, sevo and ket have cerebral protectant effects
ACP - vasodilator so can increase ICP by increasing venous outflow
Barbiturates and hypothermia can decrease cerebral pressure
Potassium bromide can cause electrolyte imbalances
GA considerations for hyperthyroidism
Multi organ dysfunction
PuPd
Muscle weakness
Hypertrophic cardiomyelopathy - avoid stress
ECG
IVFT
Thermoregulation
Opioid with ACP
Avoid ket as increases cardiac contractility and predisposes to arrhythmias
Avoid Dexmedetomidine as causes bradycardia
Monitor ca2+, laryngeal paralysis and hypocalcaemia common post op
GA considerations for hypothyroidism
Dogs Megaoesophagus Decreased GI motility Obese and lethargic Bradycardia and hypotension Slow biotransformation of drugs Hypothermia risk Monitor cardiovascular system
GA considerations for hyperadrenocortism - Cushing’s
Pituitary tumour Overweight and lethargic Poor thermoregulation Bruising Risk of pulmonary thromboembolism - hypercoagulability - extreme clotting PuPd - Na retention and K excretion Risk of wound infection May or may not be on medical tx
GA considerations for Hypoadrenocortcism - Addisions
Hyperkalaemia Bradycardia Dehydration Weight loss Lethargy Stabilise before GA
GA considerations for Neuromuscular disorders
Aspiration and regurgitation pre disposition
Check gag reflex
Resp muscles may be affected - IPPV
Check capnography
Paradoxical breathing, low sao2, hypercapnia
Sternal recumbancy and elevated head on recovery
Myasthenia gravis so exaggerated response to NMBAs
GA considerations for oesophageal foreign bodies
Stabilise Dehydration a concern - IVFT Possible regurg Avoid morphine as causes v+ Cuff ET tube to prevent aspiration if regurg Pre GA radiographs to check for rupture Elevate head Suction for intubation Don't give but/bup incase of pneumothorax Analgesia
GA considerations for GI foreign bodies
Stabilise Avoid morphine Cuff ET tube Dehydration, hypovolaemia and acid base disturbances - IVFT Slow release of fluid from abdo, too fast will decrease blood pressure, but too much fluid puts pressure on diaphragm Monitor resp system Avoid nitrous oxide as fills dead space Heat loss
GA considerations for GDV
Emergency
Shocked patient
IVFT in large vol to support cardiovascular system
Decompress stomach to relieve pressure on diaphragm
Sx
Arrhythmia - pre op from pain and hypovolaemia
- post op from release of inflammatory components and potassium
Watch for h+ as usually clotting abnormalities
BG checks
Bp usually okay but perfusion poor
Intensive post op care
GA considerations for equine colic
Endotoxaemia
Fluid and electrolyte abnormalities
Distended viscera - ventilation compromise
NSAIDS, xylazine, opioids
Hartmanns
Decompress stomach
Ippv - decreases cardiac output so not good if low Bp
GA considerations for hepatic dysfunction
Portosystemic shunt, biliary obstruction, trauma
Liver produces a large amount of heat so when slow metabolism, prone to hypothermia
Albumin binds to GA drugs so decreased albumin means more free fraction so lower doses needed
Decreased clotting factor so h+ risk
Decreased hepatic clearance of drugs - use short acting ones
BG checks - predisposed to hypoglycaemia
Pre GA blood tests - plasma proteins, glucose, bile acid, liver enzymes, clotting, urea
Medical management of encephalopathy
Monitor inbalances and blood loss - water and na retention, k excretion
CVP
BP
Thermoregulation
Avoid hypoxia and hypercapnia
Ga drugs cause hypotension, hepatotoxicity and enzyme induction
GA considerations for insulinoma
BG checks Hypoglycaemic - avoid hyperglycaemia pre op as stimulates insulin release - avoid dexmedetomidine NMBA Avoid nsaids Prednisolone post op Post op pancreatitis risk
GA considerations for diabetes mellitus
Stabilise 1/2 dose insulin as starved 1st sx of day BG checks Needs to eat post op so find out fav food Give second half of insulin after eaten Quick recovery so short acting drugs Avoid medetomidine - hyperglycaemia IVFT incl glucose
Explain the spontaneous breathing mechanisms
During inspiration Pa > Palv
Air moves in and alveoli create a -ve inspiratory pressure as e alveolar volume increases
Diaphragm contracts and thorax expands
During expiration Palv > Pa
Thorax recoils and diaphragm relaxes creating positive pressure in the alveoli and air moves out
Minute volume calculation
Vt x resp rate
Vt = 10-15mL/kg
What is compliance?
Change in volume for any given pressure
The ability to stretch
Pressure for a small cat will cause lungs to expand too much whereas the same pressure in an obese dog will cause barely any movement in the lungs
How is ventilation controlled?
Higher brain centres - cerebral cortex Respiratory centres - medulla and pons Peripheral and central chemoreceptors Stretch receptors in lungs Irritant receptors Receptors in muscles and joints
Quantitative indications of using artificial ventilation
Failure to breathe - drugs ( opioids, NMBAs)
Control damage - cervical lesion or tetanus
Qualitative indications for artificial respiration
Low O2, high CO2 Drug induced resp depression Mechanical impairments - open thorax V/q mismatch Lung disease - asthma causing bronchospasm
Preventative indications for artificial ventilation
Prevent respiratory exhaustion
Icu cases
Poor ability to breathe - aspiration pneumonia
How does high frequency jet ventilation work?
Oscillating of lungs
400-500/minute
O2 passively diffuses in lungs
How does IPPV work?
Inverse mechanism
Create +ve pressure on inhalation
Manual IPPV
Rebreathing bag / ambu bag
Demand valve
Short inspiration
Assess thoracic movements
Pros and cons of manual IPPV
Pros Easy, economic Less harmful Easier to adapt to patients Not dependant on conditions
Cons
Depends on operator - hard to be consistent
Irregularity of breaths
Poor control of ventilatory parameters
Pros and cons of ventilators?
Pros Automatic Regular breaths Ventilatory parameters controlled Allows different types of ventilation Additional features - PEEP to prevent lung collapse at the end of expiration
Cons
Requires equipment and power supply
Complicated to operate
Injury risk
Types of controlled ventilation
Continuous mandatory
Intermittent mandatory - if patient stops breathing then it takes over
Synchronised intermittent mandatory - will try to mimic normal breathing pattern of patient
Additional features of ventilators
PEEP - positive end expiration pressure
PSV - pressure support ventilation
CPAP - continuous positive airway pressure
Pressure controlled vs volume controlled IPPV
Pressure controlled is used when risk of volume trauma e.g. Open thorax
Lots of pressure immediately causing lungs to expand quickly at first and then progressively
Risks of IPPV
Decreased cardiac output decreased venous return causing a direct effect on the heart
Poor perfusion of organs - use higher resp rate but careful with Vt as increase pressure of venous system
Increased sympathetic, RAa system and ADH
Acute trauma to the parenchyma - barotrauma
Shear stress effect - volutrauma ventilator induced lung injury (VILI). If ventilated for long period of time causes alveolar inflammation
Oxygen effects - ideally 100% for less than 6hrs to avoid radical issues
Acid base disturbances
High pressure won’t cause injury but high volume will
What are the variables and settings on a ventilator?
Breathing frequency Tidal vol / minute vol I:E ratio Inspiratory time or expiratory time Inspiratory flow rate - amount of vol/unit of time Peek inspiratory pressure Positive end expiratory pressure
How to calculate minute ventilation?
Breathing rate x tidal volume
Breathing rate =60/(inspiratory time + expiratory time)
Tidal volume = inspiratory time x inspiratory flow rate
Breathing phases controlled by triggering
Time triggered - set expiratory time
Pressure triggered - negative pressure generated by patient causes expiration
Volume triggered - set expiratory volume
Flow triggered - detection of a decrease in expiratory flow
Breathing phases controlled by cycling
Time cycled - set inspiratory time
Pressure cycled - changeover when predetermined pressure reached
Volume cycled - changeover when predetermined volume reached
Flow cycled - changeover when flow decreased to predetermined value
Breathing phases controlled by limiting
Safety, set maximum value of either pressure, volume, flow
Can stop inspiration prematurely if max pressure is reached
Features of a bag squeezer ventilator
Bellow connected to bag port
Ascending bellow - detection of air leak if does not go fully up
PEEP
Time cycled or pressure limited
Equine - pressure cycled or pressure limited
Features of a mechanical thumb ventilator
Newton valve
Action depends of flow from ventilator
Associated with ventilator
Tidal vol depends on fresh gas flow and time of occlusion of thumb
Blocks flow - changing the flow rate will have an impact on vol and pressure in the airways
Features of an intermittent blower ventilator
Proportional flow valve - electronically timed and activated
Or has a pneumatically timed oscillator
Divides the driving gas up into tidal volumes of a set size and rate
Features of a minute volume ventilator
Collect continuous flow of gas into a pressurised reservoir
Delivery to patient under positive pressure
Fresh gas flow is the intended minute volume
Expensive in terms of fresh gas flow
What must be done when setting up a ventilator?
Close APL valve
What should the inspiration:expiration ratio be when using a ventilator
1:2
Short inspiration of 1 second
What needs to be monitored when ventilating
Spirometry
Capnography
Blood gas analysis
How do you stop IPPV?
Need to make sure spontaneous breathing is possible
Antagonise NMBA
Decrease respiratory depressant drugs like opioids
Allow co2 to increase, decrease ventilation from ventilator
Lacey Racial and ulnar fractures Cardiovascularly stable Long sx Significant post op pain expected
Pre-med - alpha 2 and methadone Induce propofol or alfaxalone Radial ulnar musculocutaneous nerve blocks or brachial plexus nerve blocks NSAIDs Methadone post op
Bertha
Ovariohysterectomy
Premed - alpha 2 or ACP and methadone
Propofol or alfaxlone induction
ISO
NSAID with premed as not expecting lots of blood loss - if worried about perfusion give post op
Benson
Castration
Cardiovascular dx- mitral valve dx will increase regurg or blood loss when slowing heart rate
ACP and bup Propofol or alfaxalone Sevo for quick recovery NSAID post op Intratesticular nerve block
Gracie
Bilateral sacro iliac luxation
Alpha 2 and methadone Epidural of bupivicaine and morphine lasts for 6 hours - beware of skin infections and clotting abnormalities Morphine can cause urine retention Propofol or alfaxalone ISO Methadone post op or fentanyl cri
One year old colt
Standing castration
Alpha 2 ( xylazine, rimifadine, dexmed) and opioid (but/bup) Intratesticular nerve block - lidocaine NSAID
Why use capnography?
Level of gas in blood
Tells you if there’s an obstruction or leak
How adequate the ventilation is
Cardiac output - decrease CO, decrease ECO2
Rebreathing
V/q mismatch
Alveolar dead space - mismatch between blood and alveolar co2
Equipment failure
Low V/Q
Low ventilation but there is perfusion
Atelectasis
Mucous plugging
High v/q
High ventilation but poor perfusion
Pulmonary embolism
Hypovolaemia, low cardiac output - cardiac arrest
What should ETCO2 be and what is it?
30-43 mmHg due to V/Q mismatch
It is the highest level of excreted CO2 which is closest to CO2 in the blood
Draw a capnograph trace and explain what each component means
Expiratory upstroke - gas from alveoli breathed out
Alveolar plateau - slanted. CO2 continuously excreted into alveoli so as they get smaller the CO2 conc increases
Inspiratory limb- inspiration
Alpha angle - increases as slope of plateau increases. Function of the degree of v/q mismatching
Beta angle - should be 90 degrees
What does it mean when the beta angle on a capnograph is not 90 degrees?
Phase IV
Obese patients
Poor thoracic compliance
Fast alveoli empty quickly at beginning so have high conc of CO2 at the end
What is the difference between ETCO2 and PaCO2?
5mmHg
Greater than this and means alveolar dead space
When will ETCO2 increase?
Heart rate, Bp, temp increases Ga too light Inadequate ventilation Increased cardiac output increases transfer of CO2 from periphery to lungs Increase body temp or metabolic rate
When will ETCO2 decrease?
Heart rate or Bp decreases as will reduce O2 production
Excessive ventilation
Decreased cardiac output or metabolic rate
Pulmonary embolism
Leak in machine or circuit
Draw a capnography trace for inspiratory obstruction
Check notes
Draw a capnograph for leaking ET tube
Check notes
Draw a capnograph for heart oscillations
Check notes
Draw a capnograph for surgeon leaning on chest
Check notes
Draw a capnograph for dilution of expired gases by fresh gas flow
Check notes
Draw a capnograph to show fighting IPPV and a leak in the sampling
Check notes
Draw capnograph to show cardiac arrest then cpr
Check notes
Limitations of pulse oximetry
Can give false high reading if carbon monoxide or paracetamol toxicity
Doesn’t tell you how many rbc there are just how effective they are
Vasoconstriction, movement and dark mm give false readings
ECG
Does not give cardiac output or pulse quality
Heart rate variability is the interval between the R-R waves. Indicator of nocioception - becomes less variable.
When are there alterations of the ECG during GA
Pain Artefact Diathermy Hypoxaemia Hypercapnia Hypotension Hypo/hyperthermia Electrolyte abnormalities
What does sinus bradycardia look like
Appropriate PQRST wave with each beat
What does AV block 2nd degree look like?
P waves with a few normal PQRST complexes.
Treat with atropine
What does AV block 3rd degree look like?
P waves with an abnormal QRS complex every so often as myocardium is firing without a signal
What does ventricular extra systole look like?
No P wave
Ventricular premature contractions caused by stimulation of the myocardium
No mitral valve closure
Lidocaine cri as sodium channel blocker
What does bigeminy look like
One normal complex then one ventricular extra systole
What does ventricular fibrillation look like
No normal complexes
What does atelectasis mean
No alveolar space
Usually from opening of the thorax
Increased risk of hypoxaemia
Why is thoracic surgery painful?
Skin incision
Nerve damage
Retraction is extremely painful
Inflammation
Preanaethesia prep for thoracic surgery
Blood type and availablity as bleeding probable
Fluids and drugs to combat hypotension
O2 and IPPV equipment for hypovemtilation
Check all equipment
Stabilise patient - chest drain if needed
Pre oxygenation especially if cardiac output isn’t optimal
Anaesthetic protocol for thoracic surgery - cardiovascular
Minimise cardiovascular depression
No alpha 2 agonists
Multimodal approach
Cardiovascular drugs
Anaesthetic protocol for thoracic surgery - respiratory
Minimise respiratory depression Premed opioid and ACP Rapid intubation Propofol / alfaxalone / ketamine Etomidate Use volatile agents for rapid recovery
Mechanical or manual ventilation in thoracic surgery?
Mechanical less demanding
Manual if atelectasis at end of sx as can assess how much pressure there is in lungs
Do you need NMBAs when starting IPPV?
Not compulsory but if NMBA still active use antagonists to reverse on recovery as will have severe resp depression
Risks of ventilation during thoracic surgery
Cardiovascular depression due to compromised venous return
Baro/volutrauma
Reexpansion of pulmonary oedema
When to stop ventilation
End of sx
Pulmonary reexpansion - useful in lavage atelectasis when lung is collapsed and rinsed
- do not do if lung has been collapsed for more than 12 hours as risk of oedema and the amount of pressure, volume and stress on lungs can be detrimental. Can aid with some O2 but don’t push it
Basic life support for thoracic surgery
Fluid therapy
Blood transfusion?
Management of hypothermia - classic ways
- warm fluids for lavage
Analgesic management for thoracic surgery
Opioids but may be contraindicated NSAIDs if no contraindication - hypovolaemia Ketamine - bolus or cri - antihyperalgesic - supports CV system Lidocaine - cri - anaesthetic sparing effect so better stability - antiinflammatory effects Intercostal block - bupivacaine Epidural - morphine
Recovery of thoracic surgery
Pulse ox with FIO2
Be ready to induce again
O2 - try to decrease aid asap
Fluid therapy - keep an eye on chest drain so losses accounted for
TlC - bladder, heat loss, pain assessments
Analgesia for orthopaedic or spinal patients
Multimodal is best NSAIDs Opioids Local nerve blocks Epidural
Local blocks enable a lighter plane of anaesthesia as sensation is abolished
Anaesthetic considerations for trauma patients
Gas exchange affected - pulmonary contusions
Arrhythmias - heart contusion
Pneumothorax
Increased intracranial pressure
Shock
Blood loss
Bladder rupture - hyperkalaemia - cardiac arrest
Cerebral, spinal cord and peripheral nerve rupture
What happens if there is a splenic rupture?
Don’t touch
Allow a few days to heal
GA considerations for paediatric patients needing orthopaedic surgery
Prone to hypoglycaemia so don’t starve as long as adults
Blood loss - small amounts can be critical
Immature renal and hepatic clearance of drugs
Incomplete blood brain barrier
Increased risk of hypothermia
High metabolic rate so high O2 consumption
Surgical fluid rate
5ml/kg/hr
Complications of orthopaedic surgery
Haemorrhage
Pneumothorax - thoracic spinal column sx
Air or pulmonary embolism - all sx
Impaired ventilation - high cervical spine sx or use of NMBA
Recovery of orthopaedic patients
Slow non excited recovery - sedate if necessary
Orthopaedic mattress
Residual motor block - 24hrs until full recovery
Challenge in horses for smooth recovery - incidence of refractive is high
What is base excess?
Amount of acid required to titrate 1 litre of blood to a pH of 7.4 at 37 degrees and a PaCO2 of 40mmHg
Result can be positive - alkalosis
Negative - acidosis
What is the anion gap?
Normally 15-25mmol/l
Increases - lactic acidosis ( shock, GDV, severe tissue perfusion)
- ketoacidosis (uncontrolled diabetes)
Decreased - hypoproteinaemia (portosystemic shunt, kidney dx, GI dx)
Can appear normal if GI carbonate loss
PaO2
Should be x5 higher than inspired O2 - room air is 21% so PaO2 is 105mmHg
There needs to be a big drop in PaO2 before you see a drop in SaO2 so SaO2 is a late indicator of hypoxia - should worry if drops below 95%
Respiratory alkalosis
Compensating to the left as system is trying to replace CO2
Usually hypocapnoeic but oxygenating well
Blood pH is higher than norm - alkalaemia
Metabolic acidosis
Drop in base excess
Hco3 will increase as H increases because compensation has shifted right to get rid of CO2
Hypercapnia
Metabolic acidosis and respiratory alkalosis
Base excess low Hypocapnic pH normal Anion gap low HCO3 low Mixed acid base disturbance Give bicarbonate but don't mix with hartmanns
Observation of animals in respiratory distress
Hands off approach
Body position to maximise tidal vol - neck extended and elbows abducted in sternal
Inspiratory dyspnoea - upper airway obstruction
Expiratory dyspnoea - lower airway obstruction
Slow laboured pattern - parenchyma disease
Rapid shallow pattern - pleural space disease
Paradoxical breathing - severe resp disease
Auscultation of animals in respiratory distress
Normal lung sounds barely audible Crackles - fluid Wheezes - airways narrowing No lung sounds - pleural space disease Stertorous or strider - upper airways
Upper airway disorder causes in cats
Foreign body
Nasopharyngeal polyps
Laryngeal tumours
Lower airway disorders in cats
Feline lower respiratory tract disease
Parenchymal lung disease causes in cats
Pulmonary oedema
Haemorrhage
Infection
Pleural space disease causes in cats
Pneumothorax
Pleural effusion
How to stabilise a cat in resp distress
Hands off - oxygen cage for a while
Calm quiet environment where they feel safe
Keep an eye on them
If any emergency procedures need to be undertaken do so gently and with minimal stress
What do you need to set up for thoracocentesis
19g butterfly needle 3 way tap Syringe Skin prep Sterile gloves Ultrasound machine Tubes for sampling
Clip hair over 7-8th intercostal space
In an emergency how would you give drugs to a distressed cat
I/M
Name a bronchodilator
Terbutaline is a B-2 agonist
0.05mg/kg I/M in cats
What corticosteroid can you give to a cat in resp distress
Dexamethasone
0.25-0.5mg/kg Im or IV
Deals with acute inflammation
Which problem can thoracocentesis not help
Diaphragmatic hernia
What can cause pneumothorax
Chronic bronchitis and asthma
How do you intubate a cat with laryngeal paralysis
Using a dog urinary catheter through an ET tube
What are hypothermia and hypotension signs of in cats
Sepsis or infection
Why is anaemia a problem in cats
Cats able to adjust their lifestyle to compensate so by the time symptoms show it’s quite profound
Rbc lifespan in cats is 70 days
Feline haemoglobin has a low affinity for o2 so can tolerate anaemia well
Clinical signs of anaemia in cats
Pale mms - check nose and pads if unpigmented
Lethargy and exercise intolerance
Tachycardia
Tachypnoea
Signs associated with the underlying cause
Pica - lick concrete or eat soil
Lymphadenopathy and splenomegaly
Why perform a haematological examination when investigating anaemia
Confirms presence and type of anaemia
Features that suggest regenerative anaemia in cats
Increased mean cell vol
Presence of significant anisocytosis and polychromasia
Increased reticulocyte count
What reticulocytes occur in cats
Aggregate form that is the only type seen in dogs - tells you what’s happening in the bone marrow and last 24hrs
Punctate form- can last a very long time. Don’t count these when doing a reticulocyte count
Which reticulocyte is rarely seen in non anaemia cats
Aggregate form
When can regenerative anaemia become non regenerative anaemia
When chronic blood loss causes iron deficiency which impairs rbc formation - rarely seen
FeLV
Chronic disease
Infectious and inflammatory diseases
Two main causes of regenerative anaemia
Blood loss
Haemolysis
Causes of haemolytic anaemia
FeLV Parasites Primary or secondary immune mediated haemolytic anaemia Heinz body anaemia Severe hypophosphataemia Incompatible blood transfusions Neonatal isoerythrolysis Inherited defects
How does mycoplasma haemofelis cause feline infectious anaemia
Attaches to rbc so body recognises it as foreign and destroys it
Symptoms of feline infectious anaemia
Pallor Lethargy Weight loss Anorexia Pyrexia Dehydration
Diagnosis of feline infectious anaemia
Polymerase chain reaction
Treatment of feline infectious anaemia
Doxycycline antibiotic pill with food or water to prevent oesophageal stricture
What do you know about Heinz body anaemia
Irreversibly denatured oxidised haemoglobin
Small portion normal in cats as sensitive to oxidative damage
Paracetamol toxicity
Onions
Lymphoma
Diabetic ketoacidosis
Rbc conraining Heinz body is destroyed
Neonatal isoerythrolysis
Gives birth to young that are a different blood type
Mothers agglutinating antibodies are passed through colostrum
These cause haemolysis of the youngs rbcs
Common in Persian, British shorthair or Birman cats as type B
Non regenerative anaemia causes
Bone marrow disorders
Suppression of bone marrow due to systemic disease
Most anaemia cats have non regenerative anaemia
Bone marrow disorders
Myeloproliferative disease - abnormal proliferation of rbc
Melodysplastic disease - abnormal production rbc in bone marrow
Marrow failure - failure of stem cell production
Toxins - chemotherapeutic agents, chloramphenicol
How do you treat anaemia
Diagnose the underlying cause
Treat the cause
Supportive treatment such as blood transfusions, EPO and androgenic hormones
When to give a blood transfusion in a cat suffering from anaemia
PCV less then 10- above and cat has coping mechanism
Moderate acute anaemia rather than profound chronic anaemia as clinically more severe
Tachycardia
Lethargy
Pale mm
Slow crt
How can you stimulate the bone marrow
Anabolic steroids stimulate erythroid precursors via EPO activation
Prednisolone therapy
What is erythropoietin
Hormone release by kidneys that increases the rate of production of rbcs in response to falling levels of oxygen in the tissues
What is a bleeding disorder
Abnormal condition allowing blood to escape from injured vessels or interfering with haemastasis
What is primary haemastasis
Reflex constriction of blood vessels
Platelet plug
What is secondary haemastasis
Stabilisation of platelet plug by fibrin which is a result of activation of the clotting cascade
Which clotting factor helps platelet adhesion
Von wilebrands factor
Primary haemostatic disorders
Qualitative and quantitative platelet disorders
Vessel wall defects so can’t vasoconstrict
Which coagulation factors are in the intrinsic pathway
XII, IX, XI, VIII
Ca2
Which coagulation factors are in the extrinsic pathways
VII, III,
Ca2
Which coagulation factors are in the common pathway
V, X
Ca2
Where are coagulation factors synthesised
Liver
Which coagulation factors require the liver to use vitamin k
II, VII, IV, X
What is tertiary haemastasis
Limiting reactions to ensure clotting is localised to injured area
Prostacyclin, proteins C and S
Antithrombin binds to heparin to inactivate many factors
Clinical signs of primary haemostatic disorders
Petechiae and ecchymotic haemorrhages Multiple sights of bleeding Prolonged bleeding Venepuncture bleeding Surface bleeding from mm
Clinical signs of secondary haemostatic disorders
Haematomas
Localised sight of bleeding
Delayed bleeding or rebleeding from cuts
Single large bleed that’s deep or from a cavity
Screening tests for primary haemostatic disorders
Platelet count
Buccal mucosal bleeding time
Lab tests for secondary haemostatic disorders
Activated clotting time
Activated partial thromboplastin time
Prothrombin time
What does the buccal mucosal bleeding time test look for
Platelet function or number
What does activated clotting time test for
Evaluates intrinsic and extrinsic pathways
Will be prolonged in haemophilia, deficiencies in factors of the intrinsic and common pathways,
Disseminated intravascular coagulation
Rodenticide toxicity
Liver dysfunction
Normal < 165sec
What does activated partial thromboplastin time and prothrombin time test for
Sodium citrate tubes tested in lab
APTT looks at intrinsic and common pathways
PT looks at extrinsic and common pathways - very sensitive to vit k deficiencies and rodenticide toxicities as factor VII has shortest half life
What is chronic kidney disease
Gradual loss of functional nephrons and deterioration in renal function
Older dogs and cats
Cause often hard to determine
Causes of chronic kidney disease
Chronic interstitial nephritis Glomerulonephropathies Infection Nephrotoxins and drugs e.g. Ethylene glycol Neoplasia Inherited or congenital disease
Clinical signs of CKD
PUPD
Dehydration
Anorexia
Halitosis
Hypertension
Hypokalaemia due to decreased intake and increased urinary loss
Anaemia due to uraemic toxins, reduced rbc lifespan and erythropoietin deficiency
Proteinuria
Hyperphosphataemia as not excreted in urine
Renal secondary hyperparathyroidism
Uti
How do you test for CKD
SG will be low Sediment Dipstick Culture and sensitivity Urinanalysis will show azotaemia Biochem and haem Blood pressure Ultrasound
Staging of CKD
Called IRIS
Based on serum creatinine levels when rehydrated
Additional substaging based on proteinuria and hypertension
Recognises that CKD is progressive
Aims of treatment for CKD
Treat underlying dx
Correct and maintain fluid balance
Manage clinical signs
Delay the progression
Why do you need to correct and maintain fluid balance of patients with CKD
Dehydration spdecreases renal perfusion and renal function
Acute decompensation - IV fluids x2 maintenance and correct over 24hrs. Measure urea and creatinine when rehydrated to assess degree of azotaemia
Chronic underlying dehydration - ongoing fluid support at home, moist food with additional water, broths, multiple water bowls. Subcut fluids. Prevent acute decompensation
How do you manage the clinical signs of CKD with diet
Diet
Restricted phosphate and protein diet as improves survival time
High fat to maintain weight
Omega 3 PUFAs
Increased potassium and vit B, E
Fermentable fibre
Decrease sodium to decrease risk of hypertension
Treatment of vomiting and nausea
Gastroprotectants
Sucralfate
Antiemetics
Management of inappetance or anorexia
Control nausea
Smelly foods
Mirtazapine
Enteral feeding if severe
Treatment of constipation
Oral lactulose
Fluid therapy
Correction of hypokalaemia
Potassium supplementation oral potassium gluconate if eating
Potassium chloride IV
Management of hyperphosphataemia
Diet
Oral phosphate binding drugs with food
Management of systemic hypertension
Amlodipine decreases Bp
Angiotensin converting enzyme inhibitor decreases pressure in glomerulus so decreases proteinuria
Telmisartin
Restricted sodium diet
Management of proteinuria
Telmisartin
Benazepril
Anaesthetic considerations for rhinoscopy and bronchoscopy
Painful - deep plane anaesthesia
Anti tussives to prevent coughing reflex
May involve extubation - flow by oxygen and TIVA or use a laryngeal mask
Cats usually have reflex bronchoconstriction - anticholinergic, salbutamol or terbutaline sub cut an hour before scope to prevent acute asthma crisis
Monitor in recovery
GA considerations for BOAS
Pre oxygenate before intubation
Don’t leave unattended once pre med given as upper airway obstruction due to muscles relaxing
Intubation difficult due to laryngeal collapse, narrow trachea
Risk of aspiration so elevate head on recovery and keep in sternal in sx. Cuff tube
Risk of tube kinking in sx so use reinforced tube
Soft tissue swelling can cause breathing difficulty in recovery - extubate late, hang by upper canines on cage door
May need to do tracheostomy
Calm down with sedative but can lose control of airway so careful
GA considerations for laryngeal surgery
Emergency tracheostomy or calm down with sedative
May need to extubate so oxygen flow by and use TIVA
tube cuff may be in the surgical field
Blood from surgery in upper airway so extubate with mildly inflated cuff
GA considerations of dental procedures
Reinforced tubes to prevent kinking
Mouth gag - end of syringe as can cause blindness in cats
Cuffed tube
Pack throat
Heat pad and towels and foil to keep patient warm
Locoregional nerve blocks for pain relief as can be quite painful
GA considerations of ocular procedures
Et tube can kink
Torsion of tube can cause laryngeal laceration in cats
Accessibility to patient is limited - can’t see palpebral reflex or eye position
Catheter in back leg
Eye may need to be central - stay sutures, sub tenons injection with local anaesthetic, NMBA
High intraocular pressure should be avoided - keep ETCO2 low and ventilate, avoid jug vein obstruction
Quiet recovery to prevent thrashing - empty bladder, pain relief, sedate if necessary, buster collar - get used to it prior to sx
Locoregional techniques for the eye
Enucleatio - sub tenons
Ocular procedures in standing horses - auriculo palpebral nerve only blocks motor so no sensation loss
- retrobulbar block for enucleation
- four point block of supra orbital nerve, lacrimal nerve, infratrochlear nerve and zygomatic nerve gives loss of sensation
- local infiltration of eyelids
What to prepare for BOAS sx
May need setting camera and endoscope
Laryngoscopes with 2 blades - one to pull down tongue and one to pull up soft palate
Long Q tips
Good light source
Sternal positioning with head up and ET tube ventrally
Components of the BOAS
Stenotic nares Aberrant turbinates Overlong soft palate Naso-pharyngeal hyperplasia and macroglossia Saccule inside the larynx protrude Tonsillitis enlargement Hypoplastic trachea - thin and small Bronchial collapse Same amount of soft tissue in smaller space so more resistance to air flow
What other signs are present in BOAS patients and how are they managed
Gastrointestinal signs Improve after airway sx Can be as bad as resp signs Cardiac sphincter remains open causing regurg, v+ and acid reflux Metoclopramide CRI pre and post op Sucralfate, omeprazole, ranitidine
Surgical considerations of aural and nasopharyngeal polyps
Young cats Originate from middle ear epithelium Sneezing, URT obstruction, stertor Diagnose with oral exam, rhinoscopy and CT resection with bulla osteotomy Good results post sx and with steroids
What is the anion gap?
Normally 15-25mmol/l
Increases - lactic acidosis ( shock, GDV, severe tissue perfusion)
- ketoacidosis (uncontrolled diabetes)
Decreased - hypoproteinaemia (portosystemic shunt, kidney dx, GI dx)
Can appear normal if GI carbonate loss
PaO2
Should be x5 higher than inspired O2 - room air is 21% so PaO2 is 105mmHg
There needs to be a big drop in PaO2 before you see a drop in SaO2 so SaO2 is a late indicator of hypoxia - should worry if drops below 95%
Respiratory alkalosis
Compensating to the left as system is trying to replace CO2
Usually hypocapnoeic but oxygenating well
Blood pH is higher than norm - alkalaemia
Metabolic acidosis
Drop in base excess
Hco3 will increase as H increases because compensation has shifted right to get rid of CO2
Hypercapnia
Metabolic acidosis and respiratory alkalosis
Base excess low Hypocapnic pH normal Anion gap low HCO3 low Mixed acid base disturbance Give bicarbonate but don't mix with hartmanns
Observation of animals in respiratory distress
Hands off approach
Body position to maximise tidal vol - neck extended and elbows abducted in sternal
Inspiratory dyspnoea - upper airway obstruction
Expiratory dyspnoea - lower airway obstruction
Slow laboured pattern - parenchyma disease
Rapid shallow pattern - pleural space disease
Paradoxical breathing - severe resp disease
Auscultation of animals in respiratory distress
Normal lung sounds barely audible Crackles - fluid Wheezes - airways narrowing No lung sounds - pleural space disease Stertorous or strider - upper airways
Upper airway disorder causes in cats
Foreign body
Nasopharyngeal polyps
Laryngeal tumours
Lower airway disorders in cats
Feline lower respiratory tract disease
Parenchymal lung disease causes in cats
Pulmonary oedema
Haemorrhage
Infection
Pleural space disease causes in cats
Pneumothorax
Pleural effusion
How to stabilise a cat in resp distress
Hands off - oxygen cage for a while
Calm quiet environment where they feel safe
Keep an eye on them
If any emergency procedures need to be undertaken do so gently and with minimal stress
What do you need to set up for thoracocentesis
19g butterfly needle 3 way tap Syringe Skin prep Sterile gloves Ultrasound machine Tubes for sampling
Clip hair over 7-8th intercostal space
In an emergency how would you give drugs to a distressed cat
I/M
Name a bronchodilator
Terbutaline is a B-2 agonist
0.05mg/kg I/M in cats
What corticosteroid can you give to a cat in resp distress
Dexamethasone
0.25-0.5mg/kg Im or IV
Deals with acute inflammation
Which problem can thoracocentesis not help
Diaphragmatic hernia
What can cause pneumothorax
Chronic bronchitis and asthma
How do you intubate a cat with laryngeal paralysis
Using a dog urinary catheter through an ET tube
What are hypothermia and hypotension signs of in cats
Sepsis or infection
Why is anaemia a problem in cats
Cats able to adjust their lifestyle to compensate so by the time symptoms show it’s quite profound
Rbc lifespan in cats is 70 days
Feline haemoglobin has a low affinity for o2 so can tolerate anaemia well
Clinical signs of anaemia in cats
Pale mms - check nose and pads if unpigmented
Lethargy and exercise intolerance
Tachycardia
Tachypnoea
Signs associated with the underlying cause
Pica - lick concrete or eat soil
Lymphadenopathy and splenomegaly
Why perform a haematological examination when investigating anaemia
Confirms presence and type of anaemia
Features that suggest regenerative anaemia in cats
Increased mean cell vol
Presence of significant anisocytosis and polychromasia
Increased reticulocyte count
What reticulocytes occur in cats
Aggregate form that is the only type seen in dogs - tells you what’s happening in the bone marrow and last 24hrs
Punctate form- can last a very long time. Don’t count these when doing a reticulocyte count
Which reticulocyte is rarely seen in non anaemia cats
Aggregate form
When can regenerative anaemia become non regenerative anaemia
When chronic blood loss causes iron deficiency which impairs rbc formation - rarely seen
FeLV
Chronic disease
Infectious and inflammatory diseases
Two main causes of regenerative anaemia
Blood loss
Haemolysis
Causes of haemolytic anaemia
FeLV Parasites Primary or secondary immune mediated haemolytic anaemia Heinz body anaemia Severe hypophosphataemia Incompatible blood transfusions Neonatal isoerythrolysis Inherited defects
How does mycoplasma haemofelis cause feline infectious anaemia
Attaches to rbc so body recognises it as foreign and destroys it
Symptoms of feline infectious anaemia
Pallor Lethargy Weight loss Anorexia Pyrexia Dehydration
Diagnosis of feline infectious anaemia
Polymerase chain reaction
Treatment of feline infectious anaemia
Doxycycline antibiotic pill with food or water to prevent oesophageal stricture
What do you know about Heinz body anaemia
Irreversibly denatured oxidised haemoglobin
Small portion normal in cats as sensitive to oxidative damage
Paracetamol toxicity
Onions
Lymphoma
Diabetic ketoacidosis
Rbc conraining Heinz body is destroyed
Neonatal isoerythrolysis
Gives birth to young that are a different blood type
Mothers agglutinating antibodies are passed through colostrum
These cause haemolysis of the youngs rbcs
Common in Persian, British shorthair or Birman cats as type B
Non regenerative anaemia causes
Bone marrow disorders
Suppression of bone marrow due to systemic disease
Most anaemia cats have non regenerative anaemia
Bone marrow disorders
Myeloproliferative disease - abnormal proliferation of rbc
Melodysplastic disease - abnormal production rbc in bone marrow
Marrow failure - failure of stem cell production
Toxins - chemotherapeutic agents, chloramphenicol
How do you treat anaemia
Diagnose the underlying cause
Treat the cause
Supportive treatment such as blood transfusions, EPO and androgenic hormones
When to give a blood transfusion in a cat suffering from anaemia
PCV less then 10- above and cat has coping mechanism
Moderate acute anaemia rather than profound chronic anaemia as clinically more severe
Tachycardia
Lethargy
Pale mm
Slow crt
How can you stimulate the bone marrow
Anabolic steroids stimulate erythroid precursors via EPO activation
Prednisolone therapy
What is erythropoietin
Hormone release by kidneys that increases the rate of production of rbcs in response to falling levels of oxygen in the tissues
What is a bleeding disorder
Abnormal condition allowing blood to escape from injured vessels or interfering with haemastasis
What is primary haemastasis
Reflex constriction of blood vessels
Platelet plug
What is secondary haemastasis
Stabilisation of platelet plug by fibrin which is a result of activation of the clotting cascade
Which clotting factor helps platelet adhesion
Von wilebrands factor
Primary haemostatic disorders
Qualitative and quantitative platelet disorders
Vessel wall defects so can’t vasoconstrict
Which coagulation factors are in the intrinsic pathway
XII, IX, XI, VIII
Ca2
Which coagulation factors are in the extrinsic pathways
VII, III,
Ca2
Which coagulation factors are in the common pathway
V, X
Ca2
Where are coagulation factors synthesised
Liver
Which coagulation factors require the liver to use vitamin k
II, VII, IV, X
What is tertiary haemastasis
Limiting reactions to ensure clotting is localised to injured area
Prostacyclin, proteins C and S
Antithrombin binds to heparin to inactivate many factors
Clinical signs of primary haemostatic disorders
Petechiae and ecchymotic haemorrhages Multiple sights of bleeding Prolonged bleeding Venepuncture bleeding Surface bleeding from mm
Clinical signs of secondary haemostatic disorders
Haematomas
Localised sight of bleeding
Delayed bleeding or rebleeding from cuts
Single large bleed that’s deep or from a cavity
Screening tests for primary haemostatic disorders
Platelet count
Buccal mucosal bleeding time
Lab tests for secondary haemostatic disorders
Activated clotting time
Activated partial thromboplastin time
Prothrombin time
What does the buccal mucosal bleeding time test look for
Platelet function or number
What does activated clotting time test for
Evaluates intrinsic and extrinsic pathways
Will be prolonged in haemophilia, deficiencies in factors of the intrinsic and common pathways,
Disseminated intravascular coagulation
Rodenticide toxicity
Liver dysfunction
Normal < 165sec
What does activated partial thromboplastin time and prothrombin time test for
Sodium citrate tubes tested in lab
APTT looks at intrinsic and common pathways
PT looks at extrinsic and common pathways - very sensitive to vit k deficiencies and rodenticide toxicities as factor VII has shortest half life
What is chronic kidney disease
Gradual loss of functional nephrons and deterioration in renal function
Older dogs and cats
Cause often hard to determine
Causes of chronic kidney disease
Chronic interstitial nephritis Glomerulonephropathies Infection Nephrotoxins and drugs e.g. Ethylene glycol Neoplasia Inherited or congenital disease
Clinical signs of CKD
PUPD
Dehydration
Anorexia
Halitosis
Hypertension
Hypokalaemia due to decreased intake and increased urinary loss
Anaemia due to uraemic toxins, reduced rbc lifespan and erythropoietin deficiency
Proteinuria
Hyperphosphataemia as not excreted in urine
Renal secondary hyperparathyroidism
Uti
How do you test for CKD
SG will be low Sediment Dipstick Culture and sensitivity Urinanalysis will show azotaemia Biochem and haem Blood pressure Ultrasound
Staging of CKD
Called IRIS
Based on serum creatinine levels when rehydrated
Additional substaging based on proteinuria and hypertension
Recognises that CKD is progressive
Aims of treatment for CKD
Treat underlying dx
Correct and maintain fluid balance
Manage clinical signs
Delay the progression
Why do you need to correct and maintain fluid balance of patients with CKD
Dehydration spdecreases renal perfusion and renal function
Acute decompensation - IV fluids x2 maintenance and correct over 24hrs. Measure urea and creatinine when rehydrated to assess degree of azotaemia
Chronic underlying dehydration - ongoing fluid support at home, moist food with additional water, broths, multiple water bowls. Subcut fluids. Prevent acute decompensation
How do you manage the clinical signs of CKD with diet
Diet
Restricted phosphate and protein diet as improves survival time
High fat to maintain weight
Omega 3 PUFAs
Increased potassium and vit B, E
Fermentable fibre
Decrease sodium to decrease risk of hypertension
Treatment of vomiting and nausea
Gastroprotectants
Sucralfate
Antiemetics
Management of inappetance or anorexia
Control nausea
Smelly foods
Mirtazapine
Enteral feeding if severe
Treatment of constipation
Oral lactulose
Fluid therapy
Correction of hypokalaemia
Potassium supplementation oral potassium gluconate if eating
Potassium chloride IV
Management of hyperphosphataemia
Diet
Oral phosphate binding drugs with food
Management of systemic hypertension
Amlodipine decreases Bp
Angiotensin converting enzyme inhibitor decreases pressure in glomerulus so decreases proteinuria
Telmisartin
Restricted sodium diet
Management of proteinuria
Telmisartin
Benazepril
Anaesthetic considerations for rhinoscopy and bronchoscopy
Painful - deep plane anaesthesia
Anti tussives to prevent coughing reflex
May involve extubation - flow by oxygen and TIVA or use a laryngeal mask
Cats usually have reflex bronchoconstriction - anticholinergic, salbutamol or terbutaline sub cut an hour before scope to prevent acute asthma crisis
Monitor in recovery
GA considerations for BOAS
Pre oxygenate before intubation
Don’t leave unattended once pre med given as upper airway obstruction due to muscles relaxing
Intubation difficult due to laryngeal collapse, narrow trachea
Risk of aspiration so elevate head on recovery and keep in sternal in sx. Cuff tube
Risk of tube kinking in sx so use reinforced tube
Soft tissue swelling can cause breathing difficulty in recovery - extubate late, hang by upper canines on cage door
May need to do tracheostomy
Calm down with sedative but can lose control of airway so careful
GA considerations for laryngeal surgery
Emergency tracheostomy or calm down with sedative
May need to extubate so oxygen flow by and use TIVA
tube cuff may be in the surgical field
Blood from surgery in upper airway so extubate with mildly inflated cuff
GA considerations of dental procedures
Reinforced tubes to prevent kinking
Mouth gag - end of syringe as can cause blindness in cats
Cuffed tube
Pack throat
Heat pad and towels and foil to keep patient warm
Locoregional nerve blocks for pain relief as can be quite painful
What is normal resp rate
< 35bpm
Features of pleural space disease
Restrictive breathing pattern
Increased rate but reduced depth
Features of lung parenchyma disease
Inspiratory and expiratory dyspnoea
Lung tissue affected
Why is monitoring patients in resp distress important
Need to receive enough oxygen to treat hypoxia and distress
Can’t have too much oxygen or will develop oxygen toxicity
Need lowest oxygen level patient can tolerate
Long term should be less than 60%
What physical exam should be performed on patients in resp distress
Resp rate and effort Anxiety levels HR and pulse quality Mm Arterial blood gas for PaO2 Pulse ox
What should Pa02 be
On room air 100mmHg
On 100% oxygen 500mmHg
Depends on oxygen and barometric pressure
When has a patient got hypoxaemia
PaO2 <80mmHg
SaO2 <95%
Diagnosis and stabilisation of pleural effusion or pneumothorax
X rays Ultrasound Physical exam Thoracocentesis Samples for cytology, culture, biochem
Signs of left sided heart failure
Pulmonary oedema Tachypnoea Dyspnoea Cough Pulmonary crackles
Signs of right sided heart failure
Distended peripheral veins
Pulsation of jugular veins
Ascites
Pleural effusion in cats
What do cats with heart failure present with in general
Tachycardia Weak pulses Pale mm Slow CRT Cats can present with hypothermia and bradycardia
Why is the emergency stabilisation of a dog with congestive heart failure
Minimise stress Oxygen Furosemide 2mg/kg IV Record an ECG If in myocardial failure then pimobendan 0.15mg/kg IV
What should you monitor when a dog has congestive heart failure
Resp rate needs to be below 40
Blood pressure needs to be over 80 systolic
If the patient improves then HR, RR reduces, pulses and CRT improves and patient will look brighter
What further investigations should you do if a patient has CHF
Haematology
Biochem
Echocardiography
Thoracic radiographs
When a patient with CHF has been stabilised, what are the next steps
Get eating asap
Life long treatment of furosemide, pimobendan, ACE inhibitor, spironolactone
Home asap
What should normal systolic blood pressure be
120-140mmHg
What are the signs of pericardial effusion
Right sided heart failure Distended jug veins Pulsating hug veins Ascites Tachycardia Weak pulses
What is the diagnosis and treatment of pericardial effusion
Physical exam and echocardiography Pericardiocentesis IVFT No furosemide Hospital for 24-48hrs Can recur - if no marked improvement then neoplasia possible
What are the signs of hypertrophic cardiomyopathy
Cats
Tachypnoea, dyspnoea, open mouthed breathing
Heart murmur or gallop
Tachy or bradycardia
Hypothermia
Aortic thromboembolism - sudden onset paresis, cold legs, painful and stiff muscles, pale and blue foot pads and nail beds
What is the emergency stabilisation for cats with hypertrophic cardiomyopathy
No stress Furosemide Oxygen Thoracocentesis if pleural effusion Treat hypothermia Pain meds
Once stable what is the treatment for hypertrophic cardiomyopathy
Furosemide
ACE inhibitor
If aortic thromboembolism- aspirin, clopidogrel, low molecular weight heparin
What is a bradyarrhythmia
3rd degree atrioventricular block Complete and sustained interruption of conduction from the atria to the ventricles in the atrioventricular node No P wave P and QRS not associated Wide and bizarre complexes Need a pacemaker
What is a tachyarrhythmia
Supraventricular tachycardia - regular tachycardia originating from one place in atria. Narrow QRS but regular
Atrial fibrillation - tachycardia from multiple places in atria. Chaotic rhythm. Irregular R-R distances. No P waves
Ventricular tachycardia - tachycardia from ventricles. Regular with wide and bizarre QRS
What diseases are associated with Right sided Heart Failure
Pericardial effusion
Congenital cardiac disease
What diseases are associated with left sided heart failure
Degenerative valvular disease
Dilated cardiomyopathy
Lost the potential adverse side effects that could occur during anaesthesia of:
12 yr JRT dental and potential extractions
16yr old DSH full extraction
What are the potential adverse effects of NMBA. What will you see clinically and what you should do.
What other analgesics can be used
What does capnometry mean
Measurement of CO2 concentrations in respired gases and a numerical display of the expired conc
What is capnography
Measurement of CO2 concentrations in respired gases and graphical display of CO2 waveform
What is a capnograph
Display of CO2 waveform
Why is measurement of respired gases helpful in anaesthesia
Adequacy of respiration Info on cardiac output Can inform on presence of rebreathing Can provide info on v/q matching Can provide info on alveolar dead space when combined with PaO2 Detect equipment errors
How does a capnograph measure CO2
Infrared light absorbed by molecules that have two or more different atoms
Amount of infrared light absorbed is proportional to the the absorbing substance - Beers law
Advantages and disadvantages of side stream capnography
Can be used in non intubated patients
Resilient
Easy to connect
Easy to disinfect
Slow response time
Water vapour can condense in line
Line can become kinked
Water vapour pressure changes CO2 concentrations - need a water trap
Advantages and disadvantages of main stream capnography
No sampling line so rapid response
No effect of water pressure as cuvette is heated
No scavenging needed
No obstruction
Sensors add drag to breathing system
Vulnerable to damage
Difficult to clean and disinfect
Only intubated patients
What causes low V/Q
Mucous plugging of bronchioles
Et tube in a main bronchus
Atelectasis
Causes of high V/Q
Pulmonary embolism
Hypovolaemia
Low cardiac output
Cardiac arrest
Normal PaCO2 and ETCO2
PaCO2 - 35-45
ETCO2 - 30-43
Why would inspiratory CO2 not be zero
Faulty expiratory valve on a circle
Exhausted soda lime
Inadequate inspiratory flow on a non rebreathing circuit
Insufficient expiratory time
When is treatment indicated for arrhythmias
Effect on overall CVS function
Associated with pulse deficit
Each ventricular extra systole looks different
Effect on cardiac output signalled by low ETCO2 or MABP
What anaesthetic drugs cause muscle relaxation
Alpha 2s Benzodiazepines Acepromazine Propofol Alfaxalone Thiopental Volatiles
What anaesthetic drugs do not provide muscle relaxation
Opioids - methanol, fentanyl
Dissociative - ketamine
Name a central acting muscle relaxant
Guaiphenesine - equine
Inhibits interneurons at spinal level
Mechanism of action of neuromuscular blocking agents
Post synaptic nicotinic Ach receptors on the neuromuscular junction
Two Ach need to bind to the two alpha sub units on the receptors
Clearance from synaptic cleft by acetylcholine esterase
Non depolarising blocks compete with Ach
Depolarising activates receptor and keeps it activated making it insensitive to natural Ach
What are the consequences of full neuromuscular block
Respiratory failure
Behavioural and physical signs of anaesthetic depth are gone
Indications for the use of NMBA
Ocular surgery - central eye position
Mechanical ventilation, mainly ICU ventilation case
Reposition of fracture or dislocated joint
Better surgical access to abdominal or thoracic cavity
Mydriasis in birds
Intubation
Pharmacology of atracurium
Non depolarising Binds to Ach receptor but is inactive Only one site of receptor needs to be bound Intermediate acting 30-40mins Ideal for renal/hepatic patient Minimal to no cardiovascular response Might cause histamine release
What is the pharmacology of vecuronium
Aminosteroid Non depolarising 20mins Excreted unchanged via bile so unsuitable for hepatic patient No cardiovascular side effects
Pharmacology of suxamethonium
Depolarising 2 Ach molecules joined together so mimics natural Ach and leads to depolarisation - contraction before relaxation Degraded by plasmacholinesterase Cardiovascular responses, arrhythmia, hypertension Increased ICP Increased intragastric pressure Increased intracranial pressure Malignant hyperthermia Non reversible
How do you monitor a NMB
Respiration unreliable - IPPV
Peripheral motor nerve stimulation - stimulate a peripheral nerve. Train of 4 electrical impulses applied over 2 sec period. Loss of T1 100% blocked. Block worn off when T4/T1 is back to 0.9. Only possible for non depolarising block.
How do you antagonise a neuromuscular block
Anticholinesterases inhibit Ach breakdown in cleft so can compete with NMBA. Only antagonise when block wears off.
Neostigmine - slow onset, longer acting
Edrophonium - fast onset, shorter acting
Cardiovascular consequences so use atropine with edrophonium and glycopyrrolate for neostigmine
Why do you only give one dose of NMBAs
Phase II block after more than one dose
What factors influence the duration of the neuromuscular blockade
Volatile agent Hypothermia Hepatic/ renal insufficiency Electrolyte acid base abnormalities Muscle diseases Aminoglycoside antibiotics Dose administered
What are the general anaesthetic principles of airway surgery
Schedule first Keep calm Careful monitoring Corticosteroids Hydration Thermoregulation Recovery is critical
What are the features of laryngeal paralysis
Elderly dogs Hyperthermia Dehydration Do not stress Give oxygen Sedation of ACP, opioid and corticosteroid helps breathing
What is the recovery plan for dogs with laryngeal recovery
Rapid calm recovery Extubate late Give oxygen Monitor carefully Avoid barking or excitement - analgesia
What are the anaesthetic considerations for BOAS
Avoid stress Use harness Avoid profound sedation as can suffocate Oxygen Gentle intubation Suction as saliva pre intubation and blood post surgery Corticosteroids Rapid smooth recovery
Anaesthetic considerations for bronchoscopy or tracheal foreign bodies
Pre existing respiratory compromise Anticholinergic Pre oxygenate In cats can't always pass bronchoscope through et tube Risk of environmental pollution Pneumothorax
How do you control intraocular eye pressure during ophthalmology surgery
Prevent pressure on jug veins Stop coughing, retching or vomiting No hypertension Prevent hypoxia or hypercapnia Don't put pressure on the globe Don't use ketamine or atropine
What drugs are used in ophthalmology that can cause issues during anaesthetic
Sympathomimetics - epinephrine causes hypertension and arrhthmias
Parasympatholytics - atropine and tropicamide can cause tachycardia and arrhythmias
Parasympathomimetics - Ach can cause bradycardia and hypotension
Mannitol - initial increase in circulating blood flow followed by diuresis so causes haemodynamic instability
CAI - causes metabolic acidosis
How is a central eye maintained during anaesthesia for ocular surgery
Ketamine Stay sutures Correct depth of anaesthesia Ophthalmic nerve block Muscle relaxant
What is the maintenance and recovery of GA from ocular surgery
Oesophageal stethoscope
Difficult to monitor
Calm recovery - analgesia and sedation
Monitor temp
Excitable 6yr lab
Eyelid tumour
Anaesthetic plan
Dexmedetomidine and bup
NSAID
Local block
Induction and maintenance requirements reduced
Bulldog
BOAS
surgery to correct entropion
Anaesthetic plan
Pethidine and nsaid
Pre oxygenate
Propofol
Iso or sevo
Cat
Ocular trauma
Anaesthetic plan
Control IOP ACP and pethidine sedation Hindlimb catheter Avoid ketamine for induction Avoid hypoxia or hypercapnia NSAID Stay sutures or NMBA - IPPV
Dog
Enucleation due to glaucoma
Anaesthetic plan
ACP and methadone
NSAID
Retrobulbar block
Blood loss
Dog Cataract sx Elderly Possible diabetetic Anaesthetic plan
Low dose ACP and bup IVFT Control IOP IPPV ECG Capnography Pulse ox Central eye - atracurium or vecurium Direct blood pressure Peripheral nerve stimulator NMBA antagonist Ensure spontaneous breathing before end anaesthetic Keep quiet NSAIDs
How can you make feline senior clinics a success
For healthy cats
Monitoring clinics
Maximise our involvement and skills
What needs to be considered when setting up a senior clinic
Who will run it
Where will it be held
Time management
How will you promote the clinic and recruit cats
How do you promote senior pet clinics
Newsletters Social media Word of mouth - vets and receptionists Post op checks Vaccination or flea checks Obesity clinics Dental clinics Client open evenings
What age is senior for a cat
7-8years
Common conditions of senior cats
Kidney disease Hyperthyroidism Dental disease IBD Hypertension Degenerative joint disease
Consultation structure for senior cat clinic
History Weigh Blood pressure Discuss findings Clinical exam Discuss findings Diagnostic tests if needed Summarise and arrange a revisit
What should feline senior diets contain
Reduced energy
Reduced fat
Reduced calcium and phosphorus
Increased fibre
What does orthpnoea mean
Only able to breathe standing or sitting up
What does hyperpnoea mean
Increased depth of breathing
How do you do a temporary tracheostomy
Sedate or induce patient
Jet ventilate with any tube you can get into the airway eg urinary catheter
Placed between the larynx and thoracic inlet
Wide bore IV catheter or tracheostomy tube
Blade cuts 50% of trachea in circumference
Clippers
Attach oxygen
Stay sutures on upper and lower tracheal ring that are labelled
What do you do if a BOAS patient is stressed
ACP or butorphanol sedation
May need intubation or emergency tracheostomy
Oxygen therapy
IV access
If temp is >40.9 then cool down to 39.9 by continuously pouring tap water over them and place fan
When auscultating the lungs, what can each quadrant tell you
Crackles caudally - pulmonary oedema
Crackles cranially - aspiration pneumonia
Dull lung sounds dorsal - pneumothorax
Dull lung sounds ventrally - pleural effusion
Which arteries do you measure arterial blood gas from
Dorsal metatarsal
Femoral
How do you calculate the partial pressure of inspired o2
Barometric pressure at sea level - 760mmHg
Inspired air has 47mmHg of water vapour
PO2 = 0.21 x (760-47) = 150mmHg
What can the PAO2/FIO2 ratio and A-A gradient tell us
If there is efficient gas exchange
If the ratio is less than 300 then there is lung disease or inflammatory process
The A-A gradient should be as low as possible
150xFIO2-(PaCO2/0.8) - PaO2
How should you approach a patient in cardiorespiratory distress
Oxygen Hands off approach Resp rate, pattern and effort Mm colour and CRT Pulse quality and HR SpO2 Sternal recumbency ETCO2 PaO2 Temp espesh in oxygen cage Ventilation if needed Nebulisation Postulated feeding
What are right sided cardiac emergencies
Tricuspid valve disease
Pulmonic stenosis
Pericardial effusion
What are whole heart emergencies
Dilated cardiomyopathy Congenital defects Hypertrophic cardiomyopathy Endocarditis Ventricular tachycardia Atrial fibrillation Ventricular fibrillation Sick sinus syndrome 3rd degree AV block
What is a left sided heart emergency
Mitral valve degenerative disease
What is preload of the heart
Volume of blood in left ventricle before contraction
What is afterload of the heart
Resistance in the left ventricle wall when blood is ejected
What happens when cardia output decreases
Blood pressure decreases
Renin-angiotensin system activated
How do you diagnose heart disease
Auscultation History Echo ECG Thoracic radiographs Bloods - haem, biochem, electrolytes, proBNP
What is dilated cardiomyopathy
Systolic dysfunction
Large dogs
Atrial fibrillation
Causes can be idiopathic, viral infection or taurine deficiency
Decrease in contractility so decrease in cardiac output
Renin-angiotensin system activated to increase preload and increase pressure in ventricles
Dilation of ventricles and enlargement of atrium
What is hypertrophic cardiomyopathy
Cats Diastolic dysfunction so decreased preload Tissue fibrosis of ventricles Atrial enlargement Diltazem to increase coronary blood flow Nitroglycerin to dilate coronary arteries Furosemide causes pulmonary oedema Aim to reduce systemic resistance
What is cardiac tamponade
Pericardial effusion Right side Compresses and effects CO Obstructive shock Electrical alternans Pericardiocentesis Cause usually neoplasia NO FUROSEMIDE
How do you do a pericardiocentesis
Clip and prep over apex of heart Long 21G needle Ultrasound guided Monitor ECG as many have VPCs Check fluid drained isn't clotting as then in heart Culture and cytology Mild sedation needed
What is endocarditis
Bacterial infection Mitral and aortic valves affected Blood culture IVFT Ventricular tachycardia, idioventricular ventricular arrhythmias Antibiotics and supportive care
What is degenerative heart disease
Mitral valve LCHF Tricuspid RCHF Small dogs Nodular and thick Regurgitation Give furosemide, ACE inhibitors and dilazem
When should you be worried with arrhythmias and how should they be treated
Ventricular tachycardia - HR>180, syncope
-lidocaine
Supra ventricular tachycardia- HR>180, syncope
- diltiazem
3rd degree AV block - syncope, bradycardia
- pacemaker
Atrial fibrillation- lethargy, syncope, HR>180
-pimobendan
Ventricular fibrillation - now.
- defibrillation
Sick sinus syndrome - multiple syncope, bradycardia
- pacemaker
What types of ECG monitors are there
Mulitparameter monitors - continuous monitoring
Paper trace recording machine - diagnostic value
Holter monitoring - monitoring over longer period, manually noting events. Pads on chest (1 left, 2 right) and body pack
Telemetry - monitoring patients from a distance
When obtaining an ECG what position should your patient be in
Right lateral
How do you prevent problems with an ECG
Make sure leads on correct legs
Check settings on machine
Make sure leads don’t cross over patients chest
Minimise movement
Stop panting or purring
Check contact of electrodes against skin and ensure they haven’t dried out
Remove interference
When are ECGs used
Diagnostic work up
Triage
Anaesthesia
Monitoring inpatients with known arrhythmias
Critical patients
Newly identified pulse deficits
CPR
metabolic or electrolyte abnormalities
During pericardiocentesis or jugular catheter placement
Hands off method of monitoring eg blood transfusions
What heart rate do you see with hyperkalaemia
Bradycardia
No P spikey T
What is the conduction system of the heart
Sinoatrial note - pacemaker. p wave
Atrioventricular node - slows impulse down
Atrioventricular ring - depolarisation of atrium
Bundle of His -‘spread depolarisation wave towards ventricles
Right and left bundle fibres - depolarise right and left ventricles
Prukinje fibres - depolarisation of myocardium
Then repolarisation
What are the cell types in the heart
Electrical cells - conduction system of the heart. Orderly distribution. Spontaneously generate electrical impulses to the next cell and receive them
Myocardial cells - make up the wall. Contractility and stretchability
Cells at rest are polarised.
ECG
P wave - SAN to AVN. Depolarisation in atria. Travelling to +vet electrode so positive spike. Width is time taken
P-R interval - complete depolarisation of atria. Return to baseline. AVN depolarised
QRS - contraction of ventricles
Q wave - depolarisation of septum. Travels away from positive electrode so negative spike
R wave - ventricles depolarised. Big wave as larger muscle mass
S wave - finishing depolarisation ventricles. Negative
T waves- repolarisation. Can be positive or negative
How do you interpret an ECG
Rate Rhythm - regular, regularly irregular, irregularly irregular Is there a p wave for every QRS Sinus or ventricular arrhythmias Intermittent or continuous
What is an ectopic beat
Out of place beat Did not originate from SAN Originate in atria or ventricles VPC - wide and bizarre QRS with no P wave APC, JPC- narrow with no P wave SVT
What are escape beats
Ectopic beats due to SAN failure with bradycardia
Rescue for the heart by generating an impulse before cardiac standstill
Wide and bizarre with no P wave
Av blocks
Affect PR interval
1st degree prolonged PR interval
2nd degree type 1 - PR gets longer and longer then snaps back
Type 2 - PR interval the same. Occasional p waves with no QRS
3rd degree - p waves sometimes followed by an escape beat or tall QRS-T. P waves occur faster. Actual heart rate is slow.
Hyperkalaemia arrhythmias
Tall T wave gets higher
Long PR interval and wide QRS duration
Eventually absent P wave and sinusoidal wave
Treat with insulin and glucose
May then need to redose with potassium after
Sick sinus syndrome
Abnormal SA node function Bradycardia, tachycardia and periods of arrest Can get failure of escape beats Need pacemaker WHWT common
Features of pacemakers
Treat bradycardia Last 5-10years Expensive Care with neck restraint No jugular samples Remove when animal is euthanised
Risks of pacemakers
Infection Lead dislodgement Failure GA related issues Lead fracture Venous thrombosis
Blood gas and acid base values
pH 7.35-7.45
PaO2 80-100mmHg
PaCO2 35-45mmHg
HCO3 21-24 bicarbonate buffer
BE +2 or -2mEq H ions needed to return the pH back to normal
Anion gap dogs 12-24mEq/L cats 13-27mEq/L
Acid base imbalances
Metabolic acidosis pH <7.35 acidaemia
-compensatory factors pH in normal limits but HCO3 very low and PaCO2 is also low
Metabolic alkalosis pH >7.45 alkalaemia
-compensatory factors pH within normal limits but HCO3 very high and PaCO2 also high
Increase in lactate can also cause metabolic acidosis
Respiratory alkalosis PaCO2 <35mmHg so body hyperventilates to get rid of CO2
Respiratory acidosis PaCO2 >45mmHg so body will hypoventilate to retain CO2 to bring the pH down
6yr bulldog He hypoplastic trachea and mitral valve insufficiency pH 7.063 PaCO2 106.7mmHg HCO3 28.4 BE 4.2
Metabolic acidosis
Respiratory acidosis
Primary respiratory acidosis with a partial compensatory metabolic alkalosis
7yr lab Hx pancreatic duct adenocarcinoma and peritonitis pH 7.202 PaCO2 19.8mmHg HCO3 7.4mEq/L BE -18.5
Acidaemia
Respiratory alkalosis
Metabolic acidosis from HCO3 and BE
Metabolic acidosis with a compensatory respiratory alkalosis
6yr Boston terrier pH 7.49 PaCO2 47mmHg HCO3 34.8mEq/L BE 10.2
Metabolic alkalosis from HCO3 and BE
Respiratory acidosis
Metabolic alkalosis with compensatory respiratory acidosis
Causes of metabolic acidosis
Diarrhoea Diabetic ketoacidosis Renal failure Addison's disease Lactic acidosis (sepsis)
Causes of respiratory alkalosis
Vomiting - loss of H ions
Hypoalbuminaemia - weak acid. Should not be less than 50
Upper GI obstruction (vomiting)
What is Kirby’s rule of 20
Critical parameters to be checked in critical care patients
Fluid balance - assess hydration and replace fluid loss like for like eg blood with blood
Albumin levels - keep above 20. Measure TS.
Glucose - hypotensive, septic, anorexic and puppy patients.
Electrolytes and acidbase - acidaemia seen in sepsis. Low magnesium can cause potassium to stay low. Everything has a knock on effect
Oxygenation and ventilation
Level of consciousness and mentation
Blood pressure
HR, rhythm, contractility and pulse quality
Temperature
Coagulation - risk of developing DIC and thrombocytopaenia
PCV - haematocrit x3 = PCV
Renal function - urine output 1-2ml/kg/hr
Immune status, AB choice and WBC count - neutropenic patients barrier nursed
GI motility - due to stress and opioids
Drug doses and metabolism - calculate daily. Consider drug accumulation
Nutrition - cats need arginine and taurine. Calculate RER daily. Feeding tube?
Pain management - pain score. Multimodal analgesia
Patient mobilisation and nursing care - minimal restraint. Recumbent patients. Physio. Prevent scalding
Wound care
TLC!!!!!!!
How can you correct hypoalbuminaemia
Plasma - hard to get hold of
Blood transfusion
Food - best way to increase
When is potassium low in patients
Renal disease
GI losses
Sepsis
What can high potassium cause
Bradycardia
Caused by Addison’s or urinary obstruction
What can low and high levels of sodium cause
CNS signs
What can low phosphate cause
RBC haemolysis
Usually due to anorexia
What can cause a loss of consciousness or mentation
Hypotension
Hypoglycaemia
Hyperammonaemia
3yr MN huntaway Ascending paralysis Cranial nerve deficits - no blink or gag Impaired respiration - aspiration pneumonia SpO2 90% RR 84 HR 124-158 Mm red CRT 1s Bp 100mmHg Corneal melting ulcers Suspect toxin ingestion - botulism Nursing considerations?
Recumbent - turn every 4 hours Oxygen therapy Feeding tube Eye drops every 15 mins Keep upright- propped up Inco sheets and barrier cream ECG IVFT Pain score Temp Monitor mentation Check Bp daily Check glucose, electrolytes and coags at admit Nebulisation and coupage Urinary catheter and monitor output Physio IV catheter and urinary catheter care
10yr female JRT Brain tumour removal sx Propofol coma 24 hours HR95 RR 18 Bp 135mmHg Paralysis / semicomatose - gag present 20% blood loss in sx SpO2 100% Blind Nursing considerations?
ECG and HR - decrease could mean raised ICP. Check pulses for change as risk of thromboembolism
Bp measured every 2-4hrs - monitor for increase as could be raised ICP
Blood loss during sx so hypertonic saline (oncotic pull)
IVFT and syringe water
Glasgow coma score and painscore
Analgesia - opioids at high dose to encourage sedation
Move slowly and ensure she’s aware
Urinary catheter - monitor output and care for it
Barrier cream
Turn every 4 hours
Keep head elevated
Bloods - monitor twice daily
Monitor RR for aspiration pneumonia and thromboembolism
PCV - blood transfusion?
NPO for 24hrs post coma - feeding tube
Quiet environment with minimal handling and padded bed. TLC
2yr MN DLH Status epilepticus HR 240 RR 60 Bp sys 60mmHg Ventilator for 3 days HE, PSS Nursing considerations?
IVFT to support Bp
Hypotension despite fluids so given vassopressors
Bloods x4 day
Bp monitor is response to fluids, ventilation and vasopressors
HR and ECG - monitor for decrease as could be raised ICP and monitor for changes relating to ventilation, fluids and drugs
Coags - monitor for bleeding as PSS prone to reduced clotting factors
Monitor U+
Drugs - accumulation
Feeding tube
Analgesia CRI
Turn every 4 hours
Faecal scald
Quiet environment with minimal stimuli. Gentql handling and padded bed
How should you nurse the ventilator patient
Eye care Mouth care Airway Humidification Physio and repositioning Lines, drains, tubes Urination/ defecation Drugs Treat underlying dx Communication Record keeping Acid base, blood gases and electrolytes
