Cardiology Flashcards
Equipment for cardiac ultrasound
Cut out table
Chair/stool
Correct probe for patient
Ultrasound machine
Person to restrain
Environment needed for ultrasound
Quiet
Dark
Air conditioning (ideally)
Padded table
ECG pads
Preparation for cardiac ultrasound
Clipping
Spirit
Gel
Machine frequencies for cardiac ultrasound
Cats/small dogs 7.5MHz
Medium dogs 5MHz
Large dogs 2.5-3.5MHz
What does reducing gain do
Darken image
What are the right side views
Right parasternal long axis
Right parasternal short axis
What is the right parasternal long axis (4 chamber) view used to asses
Ventricle movement
Chamber diment
Valve morphology and motion
Left ventricle wall thickness and diameter/volume
How do you reach right parasternal long axis (5 chamber) view from (4 chamber)
Rotate probe anticlockwise 20° ift wrist to angle cranially
How do you get to right parasternal short axis view from parasternal long axis (4 chamber) view
Turn probe 90° thumb to bum
Tilt probe and slide up chest wall as necessary
What should the La:Ao be
<= 1.5 in dogs
<= 1.4 in cats
What shape is the aortic valve
Mercedes Benz sign
What does the ‘fish mouth’ view show
Left atrioventricular valve
What do you assess on cardiac ultrasound
Subjectively
- ventricular movement
- chamber dimensions
- valve morphology and motion
Quantitative
- left atrium diameter
- aorta diameter
- pulmonary artery diameter
- m-mode - EPSS, LV
What setting is best for measuring chamber size
M mode in dogs
In cats 2DE due to asymmetric hypertrophy
Key points on measuring in M mode
5% of dogs outside normal ranges
Some breeds have normals if not go off size
Ensure cursor between papillary muscles transacting LV in half for measuring
Clinical signs of left CHF pulmonary
oedema
Dyspnoea
Exercise intolerance
Cough
Not lying on chest
Fainting
Clinical signs of right CHF pulmonary
Ascites and pleural effusion
Exercise intolerance
Abdominal distension
Increased RR
Dyspnoea
When should you take a DV radiograph
Before either lateral
Where do you collimate for a cardiac radiograph
Thoracic inlet to caudal edge of scapula
Points for interpretation of radiographs
Assess technical quality
Don’t just look at heart and lungs
Assess respiratory system
Assess cardiac silhouette
What is the difference between deep and shallow chested dogs cardiac silhouettes
Deep chested much more upright and less contact with sternum
Shallow chested much more sternal contact
What is the vertebral heart score
Size of heart width + length compared to number of vertebral bodies
Normal total is between 8.5 and 10.5 vertebral bodies
How does pericardial effusion appear on radiography
Grossly enlarged cardiac silhouette
Distinct outline
Globular appearance
What classes as generalized heart enlargement
Heart takes up more that 2/3rds of the thorax
How does microcardia normally present
Hypovolemia
What are veins compared to arteries
Veins are central
Veins are ventral
How does HCM look of radiography
Heart shaped heart as two large atrial
How big is the normal feline heart
Width of 2 intercostal spaces
Normal DV heart width is 0.66 width of thorax at 5th rib
How does an old cats heart look on radiography
More horizontal
Prominent aortic arch
What is CHD
Congenital heart disease
Malformations of heart/vessels still present at birth
What are the different types of murmurs
Pathological - congenital/acquired
Physiological - anaemia
Innocent
Diagnostics for CHD
History/clinical exam give clues
ECG/radiography give clues
Echocardiography to diagnose
What should you do in practice with juvenile murmurs
Grade 3+ likely congenital abnormality
< Grade 2 reassess at 3/6 months
Atrial septal defect
Quiet to moderate systolic murmur
PMI at base
Right eccentric hypertrophy when severe
Can be incidental
Ventricular septal defect
Variable grade
PMI base of left and apex of right
Systolic murmur
Left ventricular eccentric hypertrophy
Small lesion is loud murmur
Aortic stenosis
Variable intensity, loud if severe
PMI left base to right
Systolic murmur
Left ventricular concentric hypertrophy
If severe poor pulses
Pulmonic stenosis
Variable loud if severe
Base left more than right
Systolic murmur
Right ventricular hypertrophy
Mitral valve dysplasia
Variable systolic murmur
PMI right apex
Right side volume load leading to eccentric hypertrophy
Patent ductus arteriosus
Usually loud continuous murmur
PMI at base and apex
Left side volume load with eccentric hypertrophy
Tetralogy of Fallot
Variable systolic murmur
PMI at base
Right ventricular hypertrophy
Shows cyanosis
What is aortic stenosis
Narrowing of the aorta
Common in boxers, newfoundland and golden retriever
Common type is sub-aortic stenosis
Signs - lethargy, exertional weakness, syncope, sudden death
What is patent ductus arteriosus
Blood shunting from aorta to pulmonary artery causing continuous murmur in axilla
Functional closure should occur in hours and permanent in days-weeks
Hyperkinetic pulses
Left sided congestive heart failure within 12 months
Surgical treatment
What are the 5 types of pulmonic stenosis
Infundibular
Sub-valvular
Valvular
Supra-valvular (rare)
Anomalous coronary artery
Signs of pulmonic stenosis
Many asymptomatic
Right sided heart failure, syncope, exercise intolerance, sudden death
2oclock bulge on x-ray
Prominent right apical beat
Radiation cranially/ventrally
Prominent jugular pulses
High frequency systolic ejection murmur
What is a VSD
Many different locations in dogs normally high in membraneous septum
Leads to volume overload of pulmonary trunk and circulation and LV and LA
CS - exercise intolerance and LCHF
Primary causes of heart disease
Chronic degenerative valve disease (mitral)
Heart muscle disease (cardiomyopathy)
Valve/endocardial infection
Pericardial disease
Rate/rhythm abnormalities
What equals cardiac output
HR + SV
Pathophysiology of heart failure
Cause leads to cardiac output falling leading to fall in blood pressure
What mechanisms restore BP
Sympathetic NS activation
RAAS
Cardiac enlargement
Chronic degenerative valvular disease
Regurgitation means fall in forward flow and therefore fall in cardiac output
Dilated cardiomyopathy cause of heart failure
Systolic failure leads to fall in stroke volume and therefore reduce cardiac output
What is HCM/RCM
Ventricle cannot fill so cardiac output falls
How does the sympathetic nervous system increase cardiac output
Brain tells heart to pump quicker/constrict vessels to increase pressure
Compensatory mechanisms for heart failure
Increased heart rate
Vasoconstriction
Increased contractility
Retention of salt and water
Cardiac enlargement
Treatment of heart failure
Many animals present with oedema
Manipulate mechanisms with to reduce fluid build up with diuretics, antagonist RAAS and vasodilate with pimobendan
Don’t overdo treatment
Types of left sided heart failure
Mitral valve
DCM
HCM
RCM
Right sided heart failure
Primary - tricuspid valve and pericardial effusion
Typical presentation of heart failure
Cough/dyspnoea
exercise intolerance
Collapse
Heart disease
Non-specific malaise/weight loss
What does digoxin do
Improves contractility
Causes arrythmias, slows heart rate, increases vagal tone, decreases sympathetic tone, alters baroreceptor sensitivity
Narrow therapeutic range not used first line
What does pimobendan do
Increases cardiac contractility, gold standard
Calcium sensitizing positive inotrope
PDEIII inhibitor - vasodilator
Antithrombotic
HCM/RCM treatment
Heart fills poorly so
Treatment - positive lusitropes (help heart relax)
Calcium channel blockers - diltiazem/verapamil
Beta blockers - propranolol, atenolol
Licensed product for HCM
Diltiazem
what is cyanosis
blueish discolouration of the skin and mucous membranes
occurs if 2g/dl or more of deoxyhaemoglobin is present
central vs perhipheral cyanosis
central - desaturation of arterial blood or presence of Hb derivative
peripheral - desaturation of blood due to regional reduction in flow
what is the normal o2 saturation of arterial blood
95-97%
at what o2 saturation does an animal become cyanotic
below 80%
what priority does cyanosis have
emergency as severely hypoxic
overrides all emergencies except arterial bleed
normally present mouth breathing and cyanotic as ‘hungry’ for air
what is the pericardial sac made up of
inner visceral layer and outer parietal layer
function of the pericardium
prevents distension within the chest cavity
reduces friction
equalises gravitational forces
prevents overdilation
regulation between stroke volumes
what ligaments hold the heart in position
to sterum via sterno-pericardial ligament and diaphragm via phrenico-pericardial ligament
what can go wrong with the pericardium
fill with fluid - blood, exudate, transudate
neoplasia
congenital disorders - pericardial peritoneal diaphragmatic hernias, pericardial cysts
constrictive
what does pathology within the pericardial space cause
cardiac tamponade leading to low cardiac output/shock short term and right sided congestive heart failure long term
why is the right side of the heart more effected in pericardial disease
there is a greater area of contact between the pericardium and the right ventricle than the left and the thinner walls put it at higher risk
CS of pericardial disease
acute - sudden onset exercise intolerance, collapse, shock, rapid death possible
chronic - history of ascites, progressive exercise intolerance, lethargy, GI signs, collapse
CS
jugular distension, +hepatojugular reflex, ascites, tachycardia, muffled heart sounds, weak femoral pulses, paleMM, tachypnoea/dyspnoea, GIT signs
diagnosis of pericardial disease
clinical signs
echocardiography - can see effusion, mass, herniation and cysts
ECG - tachycardia with small complexes and electrical alternans (base moves up and down)
radiography - globoid silhouette with sharp outline
treatment for pericardial disease
emergency care
oxygen
iv fluids
pericardiocentesis
pericardial strip
pericardiocentesis procedure
left lateral recumbency - sterile prep with local
ultrasound guided
place catheter between 4th and 6th intercostal space at level of costochondral junction
risk related to level of effusion
what does it mean if your pericardiocentesis sample clots
it is fresh blood and could be related to damage you have caused
if it doesnt clot it has been sat around and clotting factors have been exhausted
complications of pericardiocentesis
cardiac puncture
arrhythmias
dissemination of infection/neoplasia
atrial fibrillation
myocardial stunning
neoplasia will reoccur
acquired disorders causing pericardial disease in dogs
pericardial effusion
cardiac neoplasia - haemangiosarcoma, heart base tumours, mesotheliomas, lymphosarcoma
idiopathic
left atrial rupture
coagulopathies
acquired disorders causing pericardial disease in cats
congestive heart failure
FIP
haemangiosarcoma of the heart
geriatric dogs, often GSD
normally around right atrium/right auricular appendage
metastasis common - CT before surgical resection
tumours of the heart base
chemodectomas/ectopic thyroid carcinomas
common in geriatric/brachycephalic
around aortic arch
rarely metastasise but cant treat
mesotheliomas
from serous membranes into pericardium, pleura, peritoneum and tunica vaginalis
present in rchf
treat with pericardectomy
idiopathic pericardial disease
idiopathic haemorrhage
large breed - st bernards etc
cardiac tamponade and rchf
treated by pericardiocentesis to remove fluid, pericardectomy if reoccuring 3+ times
left atrial rupture
secondary to cvd with jet lesions from severe mitral regurge
acute tamponade/forward failure (not enough blood pumped leading to BP drop and shock
do not pericardiocentese
occasionally able to repair
ckcs common
PPDH
peritoneal pericardial diaphragmatic hernia
congential
weimaraners/persians predisposed, umbilical hernias/abnormal sterum associated
often incidental finding
gi signs and cardiac tamponade can be seen
surgical correction possible
constrictive pericardial disease
complication of long term pericardial effusion
cs - rchf, exercsie intolerance and collapse
diagnosis - diminished ecg complexes in all leads, easier with history
treatment - pericardectomy
treatment aims of congestive heart failure
aims - control salt and water retention, reduce cardiac workload - decrease afterload and physical activity/stress
improve pump function
standard chf therapy
triple/quad therapy
diuretics - control salt and water
pimobendan
ace inhibitors
aldosterone antagonists
+/- anti-dysrhythmic mediation
Stages if heart disease
a - high risk but no disorders
b1 - asymptomatic, no remodelling but structural disease. wieght control and monitoring
b2 - asymptomatic with cardiac remodelling - la enlargement. consider pimobendan. regular checks
c - clinical signs - double/triple/quad therapy
diuretics for heart disease
control oedema formation
loop - furosemide - first line, very potent , 3x daily but individually tailored, vasodilator if given IV. take care in cats as can lead to restrictive/hypertrophic diseases. Torasemide - sid but more expensive.
Potassium sparing - spirolactone - aldosterone antagonist to spare potassium
vasodilators for chf
ace inhibitors
venous dilators - decrease preload, reduce fluid build up (glyceryl trinitrate)
atrial dilators - reduce afterload by increasing output and reducing valve leakage (hyralazinel)
drugs to decrease salt and water retention
imadipril
enalapril
benazepril
ramipril
care for azotaemia and hypotension, monitor renal parameters
what is cardalis
combination of ace inhibitor - benazepril - and aldosterone antagonist - spirolactone
given once a day, small tablet and good for cats
when is pinobendan used
stage b2 and c chf
what is stage d chf
obvious clinical signs
progressively worsening
obvious clinical signs at rest
death
emergency CHF therapy
presentation - coughing, dyspnoeic, cyanotic, coughing up fluid, raised chest
furosemide - 2mg/kg initially then 1mg/kg hourly
oxygen supplementation
pimobendan IV
rest - avoid stress
sedation if necessary
anti-dysrhythmics as necessary
once stable - pimobendan and start spirolactone
extra management for chf
low salt diet
exercise regime - consistency and dont push them
aspirate fluid if enough to cause any dyspnoea
feline thromboembolic disease
treat/prevent
has classic presentation
echocardiography for any without history of heart disease
reoccurrence common 1/3rd will reclot
very painful, often screaming
clopidogrel function
inhibits platelet aggregation
fairly safe - some mild neutropaenia reported
bitter tasting
give in hcm to break down clots before they form
monitoring of chf
respiratory rate
coexisting diseases - can contribute to failure/therapies used
complications of treatment for chf
renal insufficiency
electrolyte imbalances
potassium loss with furosemide
potassium retention with acei
biomarkers for chf
can measure natriuretic peptides - bnp/anp - are expensive
markers of myocardial disease - troponins - not well validated
what do you assess for in chf
efficacy of therapeutic regime
frequency of assessment determined by - failure severity, patient stability, economic guidelines
assess for side effects/toxicity - weight, blood profiles
causes of intractable cough
unstable lchf
enlarged la
bronchomalacia
co-existing chronic airway disease
ruptured chordae tendinae
present as acute emergency
severe dyspnoea, cyanotic
stressed
pulmonary hypertension causes
alveolar hypoxia with vasoconstriction/remodelling
pulmonary vascular obstructive disease
pulmonary overcirculation
high pulmonary venous pressure
idiopathic
pericardial effusion due to left atrial tear
acute bleed into pericardium
can present with acute tamponade and poor output
avoid pericardiocentesis as can move the clot
what is tussive syncope
syncope associated with coughing/wretching/gagging
disposed mechanisms
- increased intrathoracic pressure = reduced venous return
- decreased cerebral blood flow due to increased cerebral pressure
- tachyarrhythmias
usually small breed dogs with chronic bronchitis/small airway disease, CDVD, collapsing trachea, brachycephalic
complications of feline cardiomyoapthy
pleural effusion
refractory heart failure
thromboembolic disease
thromboembolic disease in cats
complication of hcm, rcm, fucm
sudden onset and looks like neurological/trauma
clot in atrium due to static blood, endothelial damage and hypercoaguable blood
present - cold, cyanotic, paralysed hind limbs with absent pulses, hypothermic with painful firm muscles, can be sudden death
treat with analgesia - aspirin, clopidogrel, nursing care
1/3 survive
CDVD
chronic degenerative valvular disease
laxity of valve lesions leading to prolapse
can get strike lesions on atrium
pathology of valve disease
degeneration of mv/+tv (60% mv only )
most pronounced at free margins leading to proliferation of the fibroblasts in the spongiosa layer. inflammation/degeneration of the fibrous layer
classes of valvular degeneration
1- small discrete nodules on edge of valve
2 - thickened irregular free edges
3 - grossly thickened/nodular with lesions extending to base of CT
4 - further severity of class 3
reason for regurgitation
pressure in the aorta doesnt drop below 80mmHg where as in the atrium it’s ~10mmHg meaning when the valve doesnt function blood flows back into the atrium
signalment for valvular disease
middle-old
small breeds CKCS/poodles/maltese
typical history of CHF
murmur of mitral insufficiency
PMI - left apex radiating dorsally
murmur grade related to severity
significant if - grade 3+, heart rate >120, loss of sinus arrythmia, precordial thrill, dysrhythmia +/- pulse deficits
history - exercise intolerance, cough, breathlessness, dyspnoea, weightloss
murmur on CE
radiographic abnormalities for MR
left cardiomegaly
straightening of distal trachea
increased cardiac silhouette
straightening of caudal heart border and loss of waist
left atrial tending - bulge in 2-3 o’clock
radiographic abnormalities of TR
dorsal tracheal deviation
increased sternal/diaphragmatic contact
reverse D shape in DV
can see generalised cardiomegaly
RCHF signs - ascites, pleural effusion
endocarditis
bacterial infection of endocardium - typically 1 or more valves
normally presents medically with and variable murmur
can have pyrexia, shifting lameness, lethargy, anorexia and weightloss
causes of heart murmurs
innocent - no cause
physiological - change in blood viscosity
pathological - acquired heart disease
what is systemic hypertension
persistently elevated systemic blood pressure
what are the cut off values for hypertension
systolic >160
diastolic >80
normal increase of 1-3mmHg per year over 8.
sighthounds naturally 10-20mmHg higher
how do you calculate blood pressure
BP = (stroke volume x heart rate) x peripheral vascular resistance
Initiating causes of hypertension
chronic fluid accumulation due to increased cardiac output
persistently increased heart rate
chronic vasoconstriction
perpetuating causes of hypertension
small arteries change - extravasation of plasma into the vessel walls
vascular smooth muscle hypertrophy - increased artery tone increasing blood pressure
kidney disease - abnormal salt level increase BP
aetiology of hypertension
artefacts - stress induced
primary - idiopathic - rare
secondary - with underlying disease
- renal - dogs with CRF often have hypertension
- HAC - increases renal salt/water retention
- Hyperthyroidism - increased myocardial sensitivity to cathecolamines
- Diabetes mellitus - hyperglycaemia, overproduction of renin = vasoconstriction
- drugs
- diet
clinical signs of hypertension
> 180mmHg or 30mmHg in 48h
Hypertensive retinopathy
Hypertensive encepalopathy
Proteinuria
Left ventricular hypertrophy
measurements of BP
Direct - arterial catheter
Indirect - compressive cuff
Doppler - wear loud headphones , need training
Oscillometric - automatic but time consuming
what size should the cuff be BP
40% the cuff site circumference
treatment for hypertension
treat underlying disease
restrict salt in diet
Diuretics - emergency
beta blockers - reduce heart rate/contactility
ACEI - block RAAS
Ca channel blockers - vasodilate
Angiotensin II receptor blocker
treatment goals for hypertension
reduce BP - <150/95
decrease proteinuria
alleviate CS
Pulmonary hypertension
pulmonary circulation usually low pressure, low resistance, high capacitance
defined as systolic pulmonary artery pressure >35mmHg and diastolic >10mmHg
caused by alveolar hypoxia
Clinical signs of pulmonary hypertension
suspect when persistent respiratory difficulty, fatigue and exercise intolerance without cause
common signs;
exercise intolerance, cough, respiratory difficulty, syncope
right sided murmur
Diagnosis of pulmonary hypertension
Thoracic radiographs - cardiomegaly, enlarged pulmonary arteries, Right apical murmur, right sided heart failure sign
Echocardiography - RV hypertrophy (>1/2 LV thickness), RA enlargement, pulmonary artery dilation, flattened IVS
Treatment of Pulmonary hypertension
Treat underlying disease
Sildenafil -effective in some but limited capacity for dilation
Pimobendan - inodilator, antithrombotic
Oxygen
Enothelin antagonists
What causes pulmonary overcirculation
left to right congenital
leads to pulmonary arterial remodelling
raises perfusion pressure and damages pulmonary vessels
pathophysiology of chronic pulmonary venous hypertension
can cause structural changes in pulmonary capillaries and increase arteriole resistance
pulmonary vascular resistance leads to pulmonary oedema
VSD
left to right shunt between the cranial ventricles
should close after birth
Patent ductus arteriosus
communication between the pulmonary artery and the aorta leading to hypertrophy of the right ventricle
Pulmonic stenosis
common in dogs
thickened/distorted pulmonary valve due to distorted fusion of valvular cushions
Dysplasia of right atrioventricular valve
common in cats
focal/diffuse thickening of valve leaflets
parts of valve leaflets may be fused with ventricular wall
HCM
hypertrophic cardiomyopathy
enlarged heart with symmetrical concentric hypertrophy, more prominent in LV
Heart neoplasia
dog - cardiac haemangiosarcoma , often in RA, are only common neoplasm
Causes of enlarged abdomen
Fat
Fluid
Feotus
Flatus/flatulence
Faeces
Ftumour
Forganomegaly
What should you always do is presented with a dog with ascites
ultrasound it’s heart
Indications for thoracic surgery
Pulmonary - primary lung tumour, idiopathic pneumothorax, pulmonary FB, lung lobe torsion
Cardiac - vascular ring anomaly - PRAA, PDA, pericardiectomy, mitral valve repair
Miscellaneous - thymectomy, thoracic duct ligation, oesophagostomy, tracheal avulsion, exploratory
Thoracoscopy points
gives the animal unilateral pneumothorax - on lateral
triangulate ports for vision
How is best to ligate the bronchus in a lung lobectomy
triple layered staples for watertight seal
Lung lobe popping
can produce tension pneumothorax - pressure building with breathing
air blebs can also do the same
Pulmonary FB treatment
attempt endoscopic removal
lobectomy if too deep
have been known to migrate through abdomen and burst through flank
Lung lobe torsion
can be secondary to pleural effusion
more common in deep chested
Presentation of persistent right aortic arch (PRAA)
outpouching of the oesophagus
dont cope moving onto solid food so often PTS with breeder
How can a PDA be treated
placement of an amplatz stent - expensive
can ligate - dont cut, just double ligate as will bleed a lot
Pericardiocentesis
large bore cannula with 3 way stopcock
4/5/6th ICS on right below costochondral junction
How do you remove a thymoma
median sternotomy
Indications for pacemaker implantation
symptomatic bradycardia
advanced 2/3rd degree AV block
sick sinus syndrome
persistent atrial standstill (no P wave)
vasovagal syncope
DCM
dilated cardiomyopathy
common in dog
impaired myocardial contractility with dilation of LV +/- RV
Tachyarrythmias are common
end stage of many diseases, diagnosis of exclusion
Pathophysiology of HCM
eccentric hypertrophy of LV
systolic failure - forward - not enough blood to body as ventricle flabby and does not push with enough force
diastolic failure - backward - congestion, blood stuck in the heart
left atrial dilation with increase pressure
signalment for HCM
breed - doberman, newfoundland, st bernard, lab, great dane, cocker, boxer, gsd
age - middle aged but reported as young as 6m
size - >12kg
males more severe but genders equally represented
clinical DCM exam
tachycardia +/- arrythmias
variable pulses/deficits
LCHF+/- RCHF
soft MR/TR murmurs
with forward failure - pale MM, sluggish CRT and cool extremities
ECG if dysrhythmic with DCM
Normal
wide +/- tall complexes
Arrhythmogenic right ventricular cardiomyopathy
boxers.
myofibre atrophy, fibrosis, fatty infiltration - fibrotic heart
stage 1 - asymptomatic with ventricular arrythmias
stage 2 - symptomatic - normal heart size and lV function but dogs syncopal/weak
stage 3 - CHF, poor myocardial function, CHF and ventricular arrhythmias
CS - ventricular arrythmias, syncope, sudden death
Diagnosis - 25 holter
Treatment - treat LCHF, anti-arrhythmic, sotalol commonly used
Myocardial diseases in the cat
HCM - hypertropic
RCM - restrictive
DCM - dilated
ARVC - arrhythmogenic right ventricular
FUCM - feline unclassified
how do cats present
dyspnoeic - panting - cats dont pant!!
heart failure
EMERGENCE
what is anaemia
a decreased haematocrit, pcv or haemoglobin
what is pcv
percentage of packed red cells within blood volume
signs of anaemia
inadequate perfusion - pale MM, lethargy, exercise intolerance
compensatory mechanism - tachypnoea, tachycardia
other sign - poor pulse, haemic/flow heart murmur
signs related to underlying pathology - splenomegaly, lymphadenopathy, pain, pica, icterus, malaena
grade of anaemia
none - canine 41-58, feline 31-48
mild - canine 30-40, feline 25-30
moderate - canine 20-30, feline 15-25
severe canine <20, feline <15
RBC indices for anaemia
MCV - mean corpuscular volume, changes with large/small RBCs
MCHC - mean corpuscular haemoglobin concentration - amount of haemoglobin in RBCs, also affected by cell volume
Regeneration factors
reticulocytes = regeneration - MCV increases
Anisocytosis = variable RBC size
nucleated RBCs, basophilic stippling, howell-jolly bodies, heinz bodies
regenerative vs non-regenerative anaemia
regenerative - haemorrhage/haemolysis body actively trying to put out more rbcs
non regenerative - decreased bone marrow production, can be pre-regenerative or through chronic haemorrhage leading to non-regenerative
what is the most common cause of haemolysis
IMHA
reaction to normal self antigen
primary immune dysfunction with loss of tolerance
can be reaction to infectious antigen bound to cell surface
causes of non-regenerative anaemia
intra-marrow - infection, chronic damage, neoplasia, lack of raw materials
extra-marrow - ckd, excessive oestrogen, some types of FeLV
clinical signs of anaemia
pallor
icterus
tachypnoea
pyrexia if infectious
weak, thready, bounding or absent pulses, cold extremities
haematemesis, melaena
trauma
collapse, coma, death
treatment of anaemia
stabilisation
- oxygen
- temperature management
- fluid therapy
- analgesia
treat concurrent conditions
confirm and characterise anaemia
Tfast, radiography, abdominal ultrasound
haematology/biochemistry
blood products
treatment of haemolysis
immunosuppressive therapy
glucocorticoids
adjunct agents - azathioprine, mycophenolate mofetil, ciclosporin, leflunomide
Babesia
intracellular protozoa transmitted by ticks
CS - pallor, jaundice, pyrexia, haemoglobinuria, cardiovascular compromise, weakness, inappetance
treatment - imidocarb (unlicensed), azythromycin and doxycycline
NO corticosteroid
oxidative damage
caused by heavy metals and rape/kale/cabbages and some drugs
oxidation of haemoglobin to heinz bodies
Ehrlicha
tick transmission
CS - grumbling thrombocytopaenia, hyperglobulinaemia, depression, fever, weight loss, poor appetite, enlarged lymph nodes, epistaxis, petechiae, ecchymoses
Treatment - doxycycline
CME - chronic monocytic ehrlichia
profound thrombocytopaenia
non-regenerative anaemia
emaciation
swelling of hindlegs/scrotum
uveitis/neuro signs from thrombocytopaenia
glomerulonephritis from hyperglobulinaemia
Doxycycline to treat
in what breed is macrocytosis normal
poodles
in what breed is microcytosis normal
Akitas
what are codocytes
bullseye appearance erythrocytes with haemoglobinised area surrounded by pallor with haemoglobin band around the outside
seen in iron deficiency, liver disease, cholestasis and after splenectomy
what are schistocytes
irregular fragmented erythrocytes
markers of DIC
fragment with trauma
seen in IMHA, thrombosis, haemangiosarcoma, glomerulonephritis, CHF, valvular heart disease, doxorubicin toxicosis and myelofibrosis
what does rouleaux formation indicate
inflammation related to plasma being ‘sticky’ with increased globulin
how does the saline agglutination test work
mix 1 drop blood with 1 drop saline
agglutination will persist, rouleaux will disperse
regenerative anaemia signs
basophilic stippling - small dark blue aggregates in RBCs, associated with intensely regenerative anaemia but also with lead poisoning
nucleated erythrocytes - early release of RBCs
howell-jolly bodies - darkish blue remnants in RBCs
mycoplasma haemofelis (haemobartonella felis)
pleomorphic, can appear as chains, discs or rods, superficial or embedded into RBC membranes
Diagnosed on PCR
CS - regenerative anaemia, pyrexia and malaise
misleading blood results
MCV - swelling or shrinkage, misidentification with pairs/triplets in analyser
High MCHC - rbcs dont tend to cram in extra haemoglobin
RBCs can be miscounted/mistaken for platelets
anaemia classification
Normocytic normochromic - anaemia of illness/pre regenerative, rarely non-regenerative
macrocytic hypochromic - highly regenerative
microcytic hypochromic - iron deficiency - chronic blood loss, without anaemia - portosystemic shunt
what is relative polycythaemia
apparent increase in RBC due to decrease in circulatory fluid - often increases in TP/albumin
no increased RBC production
fear/excitement/pain can cause splenic contraction which can cause this
will resolve with time/rehydration
absolute polycythaemia
increase in RBC mass due to increased production
Primary polycythaemia - rare myeloproliferative disorders, abnormal response of RBC precursors, normal EPO
secondary polycythaemia - chronic renal tissue hypoxia, renal tumours or cysts likely, increased EPO
what care do you need to take with digoxin
can gave animals absolutely any rhythm abnormality
primary causes of dysrhythmias
structural heart disease
metabolic
electrolyte disorders
trauma
drugs/toxins
sepsis and neoplasia
when do you treat dysrhythmias
if treatment will improve survival or to alleviate clinical signs
disturbances if rate is too low or too high as cardiac output falls due to lack of contraction or lack of time for heart filling
Bradydysrhythmias
variations of sinus arrythmia - not clinically significant
Clinically significant
- high grade 2nd degree AV block - lots of P waves not conducted
- 3rd degree block
- sinus arrest - secondary to hyperkalaemia
- sick sinus syndrome - SAN not firing
- atrial standstill - long sinus pauses
CS - weakness, lethargy, syncope
Treatment - treat primary issue eg. electrolyte disturbances, place pacemaker
anti-dysrhythmic drug classes
class 1 - block sodium channels eg lidocaine
class 2 - beta blockers eg propranolol/atenolol
class 3 - potassium channel blockers eg sotalol/amiodarone
class 4 - calcium channel blockers eg diltiazem/verapamil
management of supraventricular tachydysrhythmia
diltiazem/sotalol PO or
verapamil IV
management of ventricular tachydysrhythmia
sotalol PO
lidocaine IV
when to perform blood transfusion
decision based on; tachycardia, poor pulses, weakness, tachypnoea, collapse
PCV <20% dogs, <10-15% cats
types of immunodeficency disorders
congenital - primary
acquired - FPT, chronic infection, inflammatory/neoplastic disease, drugs, malnutrition, toxins, stress
immune system neoplasia types
lymphoid cell neoplasia
common - lymphoma, lymphoid leukaemia, cutaneous histiocytoma
rarer - multiple myeloma, plasmacytoma, histiocytic sarcoma
Major immune diseases
haemolymphatic - IMHA, IMTP, immune mediated neutropenia
endocrine - hypothyroidism, hypoadrenocortism
cutaneous - canine dermatomyositis, discoid lupus erythematosus (DLE), pemphigus-pemphigoid complex
Musculoskeletal/neuromuscular - polyarthritis, myasthenia gravis, polymyositis/polyneuritis
CNS - MUO, granulomatous meningioencephalitis
GI - IBD/chronic enteropathy
Pancreatitis
Renal - glomerulonephropathies
Multi-systemic involvement - systemic lupus erythematosus (SLE), polyarthritis and meningitis, pancreatitis and dry eye.
types of shock
cardiogenic
hypovolaemic
distributive
cryptic
obstructive
signs of hypovolaemic shock
pale
slow crt
high HR
low rectal temp
weak pulses
increased RR
signs of distributive shock
red MM
short/fast CRT
high HR
pyrexia
bounding pulses
increased RR
signs of obstructive shock
pale
increased CRT
increased HR/RR
low temp
poor pulses
metabolic acidosis
signs of cardiogenic shock
primary cardiac disease
pale
slow CRT
heart rate - high/low/arrythmic
low temp
pulses- weak/deficits
RR high
feline blood groups
A (weak anti-type B)
B (strong anti-type A) - fatal
AB (no antibodies)
must blood match prior to transfusion
feline neonatal isoerythrolysis
type a or ab kittens to type b queen
leads to fading puppies
canine blood types
DEA - 1,3,4,5,6,7,8
can be +/-
match blood + to + and - to -
first transfusion ok. after dea 1+ to dea1- can cause acutre haemolysis/death
what does stored whole blood lack
Platelets, WBCs and clotting factors
plasma - FFP - use
used for coagulopathies
what is cyroprecipitate
plasma fraction from FFP
concentrated clotting factors
fibrinogen, factor VIII, von willebrands
pre-treatment for vWD deficiency
what is cyrosupernatant
remaining plasma fraction after cyro-precipitate formed
contains plasma proteins and vitK dependent clotting factors. used as frozen plasma
deciding what to transfuse
replace what is lacking, benefits must outweigh drawbacks
canine blood collection
donor - fit/healthy, 1-8yo, >25kg, good temperament, never travelled, vaccinated.
jugular vein in lateral recumbency - 450ml
feline blood collection
donor - healthy 1-8yo, >4kg, preferably indoor
lateral/dorsal, jugular vein, 11-13ml/kg
volume of blood for transfusion
(target pcv - recipient pcv)/donor pcv x kg x N
N = 90 in dogs, N= 60 in cats
clinical signs of transfusion reaction
increase in temperature, change in respiratory/heart rate, change in MM colour, visible oedema, GI signs,
signs of acute haemolytic transfusion reaction
uncommon
fever, tachycardia, dyspnoea, muscle tremors, V+, weakness, collapse, haemoglobinaemia, haemoglobinuria, shock, death
stop transfusion immediately, IVFT, corticosteorids
delayed haemolytic reaction
extravascular haemolysis 3-21d post transfusion
incompatible first transfusion care occur
reduced lifespan of donated erythrocytes
hyperbilirubinaemia +/- uria
febrile non-haemolytic transfusion reaction
acute hypersensitivity
most common with whole blood
mild/transient fever
leukoreduction to minimise
acute hypersensitivity blood reaction
anaphylactic IgE antibodies activating mast cells, mild reactions can lead to hypotensive shock
stop transfusion
therapeutics for transfusion reactions
clinical exam - CRS, temperature, haemoglobinuria
supportive treatment - IVFT, corticosteroids, oxygen, antihistamines, adrenaline, diurectics
what is the difference between primary and secondary immunodeficiency
primary - genetic, rare, can affect neutrophils, lymphocytes, immunoglobulins. commonly repeated infections in young animals pure bred/multiple in a litter common
secondary - more common - immunosenesence, medical immunosuppression, specific infections (fiv/parvo), chronic disease
IMHA
young-middle age antibody mediated haemolysis often resulting in anaemia
primary - no known causative trigger, inherited predisposition (cocker, springer and poodles)
secondary - underlying condition trigger eg infection, neoplasia, drugs/toxins/vaccination
cats triggered by fip.felv. chronic bacterial infection, mycoplasma
IMHA diagnosis
confirm anaemia - low pcv <20%
check for regeneration
left shift neutrophilia common
check platelet levels (can have imtp too)
look for spherocytes
autoagglutination test - 4 drop saline + 1 drop blood - rouleaux = inflammation, agglutination = clumping
treatment of IMHA
underlying trigger/disease
immunosuppression - glucocorticoids
** must ensure no infections beforehand
risk of death through thromboembolic disease
IMTP
middle age female cocker, old english, gsd, poodles
primary - autoimmune production of antibodies against normal platelet antigens
secondary - antibodies targeting non self antigens adsorbed onto platelet surface
present with anaemia/bleeding - petechiae, eccymoses, haematomas, epistaxis, gingival bleeding, malaena
diagnosis of imtp
low platelet count
in primary biochem/coagulation profiles often normal
can have concurrent anaemia
treatment for imtp
acute - transfusion, not often needed. vincristine immunosuppressant activity
long term - prednisolone initially whilst azathioprine kicks in
risk of death - haemorrhage
monitor platelet levels monthly, immunosuppressive for min 4-6 months
10-15% mortality
signs of primary haemostasis dysfunction
petechiae/ecchymoses
bleeding from MM
multiple bleeding sites
haematomas (rare)
signs of secondary haemostasis dysfunction
peteachiae/eccymoses rare
deep/cavity bleeds more common, can bleed from MM
sometimes single bleeding sites
haematomas common
requirements to make a clot
platelets, endothelial cells, von-willebrands factor protein sticks platelets together
platelet agonists such as thrombin and collagen
physiologic factors - nitric oxide/prostacyclin
diascopy
does the lesion blanch under a glass slide
yes - vascular vasodilation
no - in skin haemorrhage - petechiae
thrombocytopathia
inherited/drug induced defects, platelet dysplasia
diagnosis - normal PLT prolonged BMBT
normal vWF. dx of exclusion
tx - withdraw drugs eg nsaids, blod transfusion if anaemia
what should you do before neutering a doberman
buccal mucosal bleeding time
enzymatic coagulation factors
XI, X, IX, VII, II
factor VII depletes first - v high PT, aPTT a little high
vitamin K deficiency
essential in functioning of coagulation factors II, VII, IX and X
occurs with rodenticide/slug pellets and some severe hepatic/cholestatic disease as fat soluble
wont see coag issues for a week
wbct
whole blood clotting time - tube should clot within 20 mins
one stage prothrombin time
OSPT
aka prothrombin time measures extrinsic and common pathways
prolonged with sufficient deficiency of any factor (<30% normal)
activated partial thromboplastin time
APTT
measure of intrinsic and common pathways
single factor <30% normal prolongs
congenital disorders of secondary haemostasis
haemophilia
factor VIII deficiency (haemeophilia A), factor IX deficiency (haemophilia B)
sex linked, males, spontaneous bleeding
APTT increases
acquired disorders of secondary haemostasis
vitamin K antagonism - depletion of II, VII, iX and X
hepatic disease - clotting and inhibitory factors produced in liver - factors go down, coags go up
what is the triad of contributers to thrombosis
endothelial injury
abnormal blood flow
hypercoagubility
DIC
excessive activation of haemostatic pathways - high thrombin and microvascular thrombi
coagulation factors/platelets used up - haemorrhage
triggers - endothelial damage (electrocution/heat stroke (sepsis). platelet activation - viral disease. release of tissue procoagulants - trauma, pancreatitis, bacterial infection etc - anything can cause it
dx - thrombocytopaenia (or dropping count), hypofibrinogenaemia (coagulation factors used up), schistocytes (rbc fragments)
tx - underlying cause or death is coming
neutrophil toxic change
rapid neutropoiesis
foamy cytoplasm - dispersed organellas
diffuse cytoplasmic basophilic - persistent cytoplasmic rna
dohle bodies - focal blue-grey cytoplasmic structures
asynchronus nuclear maturation
monocytosis
inflammation - can imply chronic or necrosis
steroid/stress
eosinophilia causes
hypersensitivity
parasitism
hypoadrenocorticism
paraneoplastic
idiopathic eosinophilic syndromes
rare - eosinophilia leukaemia
eosinopaenia causes
glucocorticoids, stress, inflammation
