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291 Cards in this Set

  • Front
  • Back
What are the 3 most important features of the cardiac glycosides?
- positive inotropy
- negative chronotropy
(often used to slow down ventricular response to atrial fib)
- autonomic nervous system effects (decrease sympathetic stimulation)
Which pumps exist in the myocyte cell membrane?
- Na/K ATPase: pumps Na out and K in
- Na/Ca exchanger: concentration dependent: removes calcium from cell in exchange for sodium
Where do cardiac glycosides act and what does this result in?
block Na/K ATPase --> cell transiently hypernatramic
- this reduces activity of Na/Ca exchanger and more calcium stays in the cell --> positive inotropy
(within limits calcium concentration is proportional to number of crossbridges and thereby the force of contraction)
what are the cardiac glycoside's effects on the autonomic nervous system?
parasympathomimetic activity:
- decrease discharge at sinoatrial node
- decrease rate of conductino through the AV junction

sympathetic
- reduce the release of sympathetic neurotransmitter
- reduce the release of renin from the juxtaglomerular apparatus
what is the half life of digoxin? why is this important?
half life is over 30 hours: normally it takes 5 plasma half lives to attain steady state - with digoxin it will therefore take a week
what do you calculate digoxin dose on?
bas dose on body surface area - very low therapeutic index
what conditions (7) can result in digoxin toxicity?
- hypoproteinaemia, cardiac cachexia, obesity and ascities --> accidental overdosigng
- hypothyroidism: increases half life
- hypokalaemia (less K more digoxin can bind!)
- renal dysfunction --> decreased excretion
with which drug should you reduce digoxin dose?
any that are highly protein bound: calcium channel blockers
how often should you dose cats with digoxin?
every 2nd day as long half life (longer than in dogs)
how long after using digoxin should youa ssay plasma levels?
after one week
what is the mechanism of action of dobutamine?
B1 agonist --> increase in cAMP --> protein kinase A --> increased intracellular calcium
what are the indications of dobutamine?
- severe acute heart failure with poor left ventricular dysfunction: administered as IV infusion due to its very short half life

- used in horses to maintain MAP in anaesthesia
what are the mechanisms of pimobendan?
- PDEIII inhibitor and calcium sensitiser
* calcium sensitisation without increase in myocardial oxygen consumption: inotropic effect
* vasodilatory effect viw PDEIII and V inhibitions
(modulation of proinflammatory cytokines experimentally)
when should you administer pimobendan in relation to food?
an hour before: oral bioavailability decreases if food present
list the 4 classes of vasodilators
- Pimobendan
- ACE inhibitors
- calcium channel antagonist
- nitric oxide donors
what does angiotensin II do in the body (6)?
- aldosterone release
- cardiac fibrosis and hypertrophy
- casoconstriction
- baroreceptors less responsive to change in BP
- sensitises adrenceptors in vasculature to Nad
- promotes release of ADH and endothelin (vasoconstrictor)
What is bradykinin and what breaks it down?
bradykinin is a vasodilator. it is broken down by ACE
- ACE inhibitors therefore allow bradykinin to stick around
which ACE inhibitor is converted from prodrug to active drug by serum esterase?
enalapril - good for liver disease
what do you have to bear in mind with patient on ACE inhibitors and K sparing diuretics?
hyperkalaemia!
which ACE inhibitor may be better in dogs with renal disease?
benazepril
how does glyceryl trinitrate act and what is it used for?
used for acute management of pulmonary oedema and heart failure
- induces intracellular production of nitric oxide in vascular smooth muscle cell
--> cGMP increase and thereby smooth muscle relaxation
how does sodium nitroprusside act and what is it used for?
what do you need to bear in mind in storing it?
used for severe fulminant pulmonary oedema
- causes nitric oxide formation in vascular smooth muscle - given IV: LIGHT SENSITIVE!
where do class I antiarrhythmics act?
block Na channel
where do class II antiarrhythmics act
= B blockers
where do class II antiarrhythmics act?
K channels
wher eto class IV antiarrhythmics act?
= Ca channel blockers
Name 2 class Ia antiarrhythmics
- quinidine
- procainamide
name 2 class Ib antiarrhythmics?
- lidocaine
- mexilitene
name 3 class II antiarrhythmics?
- atenolol
- esmolol
- metoprolol
name 2 class II antiarrhythmics
- sotalol
- amiodarone
why do class I antiarrhythmics (Na channel blockers) not have an effect on nodal tissue?
only affect myocyte as pacemaker cells rely in Ca influx rather than sodium influx for firing of an action potential
what is quinidine used for (3)?
- atrial fibrillation in horse
- ventricular tachycardia in horse
- dogs with supraventricular tachycardia
what does quinidine do at low doses?
vagolytic: increases SAnode discharge and conduction
is quinidine protein bound?
yes, extensively so
what are some of the side effects/toxicities of quinidine?
- hypotension through a-adrenoceptor block
- GI upste
- heart block
- can precipitate digoxin toxicity (both protein bound)
what on the ECG indicates quinidine toxicity?
QT interval prolongatino of 25%
how do you treat digoxin toxicity?
- sodium bicarbonate: increases protein binding and lowers potassium
why is lidocaine only given IV?
because it goes under extensive first pass hepatic metabolism
how does lidocaine affect action potentials?
it accelerates repolarisation --> decreased conduction velocity

- but recovery from block rapid
what is the oral form of lidocaine?
mexiletine
do B blockers act on nodal tissue?
no but do slow HR and speed of conduction
Propranolol: mechanism of action? treatment? side effect and why?
acts on both B1 and B2 --> block. Also increases outward K current and reduces Na current
- B2 found in bronchi and vasculature: so can result in bronchospasm and vasoconstriction

used to treat HCM and arrhythmias either alone or in conjunction with other drugs
Which B blockers are B1 selective? What are they used for?
Atenolol and Esmolol
- used for SVT
why do you start and stop treatment with B blockers gradually?
because you can otherwise get B receptor downregulation
How does sotalol work?
it is a K channel blocker but also has B blocker effects
(removal of K takes a.p. back to normal resting) --> prolongation of action potential and decreases automaticity
- slows AV conduction
- does not require metabolism
name 3 calcium channel blockers
- verapamil
- diltiazem
- amlodipine
what is the downside with diltiazem? what is it used for?
it requires TID dosing due to very short half life

used for HCM in cat: improves filling of heart and has vasodilatory effects
--> immediate in terms of selectivity for cardiac and vascular smooth muscle
what is the treatment of choice for feline hypertension?
amlodipine: SID (slowly absorbed and prolonged duration of effect
name 4 drugs that are used to manage bradyarrhythmias
- atropine
- propantheline bromide
- glycopyrronium
- terbutaline
what is the mechanism of action of atropine and what is it used for?
- muscarinic antagonist: has parasympatholytic effect

used for sinus block, sinus arrest, AV block and sick sinus syndrome
what are 5 side effects of atropine use?
- CNS sitimulation (part. horse)
- constipation
- tachycardia
- urinary retention
- prolonged use --> refractoriness
what is the mechanism of propantheline bromide? what is an advantage of it cf atropine?
it is a muscarinic antagonist but is less lipid soluble than atropine and does not cross BBB
how does terbutaline work with regards to managing bradyarrhythmia?
is a B2 agonist but may have beneficial dromotropic effects: enhance speed of conduction
(are some B2 receptors in nodal tissue)
what are aminophylline, atemiphyline and theopylline?
methylxanthines
how do methylxanthines act?
- smooth muscle relaxation
- mild inotropic effect
- CNS stimulant
- improve conduction
- cause bronchodilation

--> non specific PDE inhibitors, antagonise adenosine and enhance catecholamine secretion
what is clopidogrel?
it is an adenosine diphosphate antagonist: has anti-ploatelet effect in cats when administered SID PO
what is ADP needed for?
platelet aggregation
what are low molecular weight heparin and what do they do?
they inhibit CF Xa - so have minimal effects on bleeding times (PT and APTT)
what is dalteparin?
a low molecular weight heparin
what % of glomerular filtrate is reabsorbed normally?
99%
what ion tanasporter is important throughout the length of the tubule?
Na/K ATPase: moves NA from the cell into extracellular fluid
what are the 5 mechanisms of transport of Na into the cell?
1) along electrochemical gradient
2) coupled to organic solute or phosphate
3) entry in exchange for positive ion (e.g. H or K)
4) entry with K and 2Cl (specific in LOH)
5) entry with Cl
what happens in the proximal convoluted tubule?
- water and Na are both reabsorbed
- Na reabsorption acompanies a Cl-
what happens in the descending loop of henle?
- waterr moves out of the tubule into the medulla due to the hypertonicity- Na may move back into the tubule because of the osmotic gradient created by the hypertonic medulla
what happens in the ascending loop of henle?
- sodium actively removed with one K and 2Cl into medulla --> hypertonicity

this part is impermeable to water
what takes place in the distal convoluted tubule?
urine is hypotonic here - Na is still removed (back to plasma) in this region with Cl ion. K and H are lost in filtrate here

but Na can be reabsorbed in exchange for K: ALDOSTERONE INFLUENCES - also alters # of Na pumps on basolateral membrane of tubular cells
what occurs in the collecting tubule?
ADH can control the amount of water reabsorption by altering permability here

H and K are excreted
what part of the renal tubule does aldosterone act on?
the distal convoluted tubule
what are chlorothiazide, hydrochlorothiazide, bendroflumethazide, and trichlormethiazide?
thiazide diuretics
how do thiazide diuretics work?
act on early distal convoluted tubule (excreted in PCT and need to be in tubule to exert effect)
- INHIBIT Na/Cl cotransport system by binding to it: preventing Na and Cl reabsorption thereby keeping water in lumen with the ions.

BUT most sodium reabsorbed by this time so are only moderate diuretics due to site of action
what other electrolytes do thiazide diuretics have an effect on?
- reduce loss of Ca
- increase loss of K since more sodium presented in collecting tubule (tries to take Na back in by exchanging it with K) and more urine flow due to increased volume
what are thiazide diuretics used for (4)?
- mild cardiac failure: manage oedema
- combination with other diuretics (frusemide)
- oedema secondary to hypoproteinaemia
- diabetes insipidus
how is it thought that thiazide diuretics can help in DI?
not really understood... but think:

- loss of Na and water in DCT --> hypovolaemia. more sodium and water reabsorbed in PCT so less urine in loop of Henle: less urine presented to collecting tubule
what are the main side effects of thiazides?
- hypokalaemia
- decrease effect in insulin (slightly diabetagenic)
- may potentiate anaesthetics and cardiac glycosides
how long until you see an effect with thiazide diuretics?
1 hour
how do loop diuretics work?
inhibit cotransport of Na/K/2Cl from the lumen into the tubule cell --> reduced hypertonicity of medulla responsible for reabsoprtion of water = DRAMATIC increase inw ater loss by kidney
which ion is also lost with use of loop diuretics?
K - due to decreased reabosprtion in ascending loop and increased sodium presentation in collecting tubule and distal convaluted tubule
- Ca loss is also increased (so good for paraneoplastic disease)
where do loop diuretics need to be in order to have an effect?
in the tubule!
how is furosemide metabolised?
via glucuronidation
what % oral bioavailability does furosemide have?
60%
how long until you get onset of action with loop diuretics?
1 hour (or 30 minutes if IV)
what is furosemide used for (3)
- oedema (heart failure)
- vasodilation: IV - helps reduce preload and increase renal perfusion
- promotes calcium loss so good for hypercalcaemia
what are the 2 main side effects of furosemide?
- hypovolaemia and hypokalaemia
- OTOTOXICITY: CARE WITH AMINOGLYCOSIDES
Name an aldosterone antagonist
Spironolactone
= loss of sodium and water with retention of potassium
what is spironolactone metabolised to?
canrenonate (inactive) and canrenone which is active metabolite (canrenoate can be converted to canrenone!) - prolonger duration of effect: canrenone half life is 16 hours
why does it take a long time for spironolactone to have effect?
because it alters the number of Na ATPase channels on basolateral membrane (one facing blood): this takes time
what should you watch for if treating animal with spironolactone and ACE inhibitors?
hyperkalaemia!
What are amiloride and triamterene and how do they exert their effect?
potassium sparing diuretics
- prevent reabsorption of sodium through the luminal Na channels: do not work on NaK ATPases!
--> reduce loss of K and increase loss of Na
how do amiloride and triamterene compare with regards to metabolism and duration of action?
amiloride: excreted unchanged in urine and has long half life (24 hours)
* ALSO LESS PROTEIN BOUND

triamterene: mertabolised in liver, some unchanged in urine - lasts 12 hours
what % oral bioavailability does furosemide have?
60%
how long until you get onset of action with loop diuretics?
1 hour (or 30 minutes if IV)
what is furosemide used for (3)
- oedema (heart failure)
- vasodilation: IV - helps reduce preload and increase renal perfusion
- promotes calcium loss so good for hypercalcaemia
what are the 2 main side effects of furosemide?
- hypovolaemia and hypokalaemia
- OTOTOXICITY: CARE WITH AMINOGLYCOSIDES
Name an aldosterone antagonist
Spironolactone
= loss of sodium and water with retention of potassium
what is spironolactone metabolised to?
canrenonate (inactive) and canrenone which is active metabolite (canrenoate can be converted to canrenone!) - prolonger duration of effect: canrenone half life is 16 hours
why does it take a long time for spironolactone to have effect?
because it alters the number of Na ATPase channels on basolateral membrane (one facing blood): this takes time
what should you watch for if treating animal with spironolactone and ACE inhibitors?
hyperkalaemia!
What are amiloride and triamterene and how do they exert their effect?
potassium sparing diuretics
- prevent reabsorption of sodium through the luminal Na channels: do not work on NaK ATPases!
--> reduce loss of K and increase loss of Na
how do amiloride and triamterene compare with regards to metabolism and duration of action?
amiloride: excreted unchanged in urine and has long half life (24 hours)
* ALSO LESS PROTEIN BOUND

triamterene: mertabolised in liver, some unchanged in urine - lasts 12 hours
what are K sparing diuretics used for and with?
with furosemide: compliment K loosing effect

- also used in management of severe cardiac failure
what are the 3 main important features of osmotic diuretics?
- freely filtered b glomerulus
- reabsorption is limited
- pharmacologically inert
what is the mode of action of mannitol?
j- as Na and water removed in PCT, mannitol becomes progressively concentrateds: this reduces the reabsorption of water in the PCT
--> NA removal then declines

PG release is enhanced: and this further reduces the hypertonicity of the medulla (blood flow removes Na and K and stome accumulating) --> less water reabsorbed in descending LOH
what is mannitol used for (3)
- management of ARF to restore urine production
- reduce CSF pressure
- reduce intraocular pressure in glaucoma
how is mannitol administered?
IV: WATCH can pull fluid into circulation --> transient increase which can lead to decompensation in some animals e.g. those with cardiac disease!
what does carbonic anhydrase do and where?
(HCO3 originally attached to Na)
convert
HCO3 + H <--> H2O and CO2

this occurs in lumen and cell of PCT
- water and CO2 are absorbed in cell and carbonic anhydrase allows reformation of HCO3 and H. H is left in urine and HCO2 goes back into plasma
what happens when carbonic anhydrase is inhibited?
bicarb stays in lumen with Na and K --> rise in urine volume and increase in urinary pH: more alkaline

--> metabolic acidosis due to reduced HCO3 which in turn reduces actions of diuretic
what is acetazolamide?
= carbonic anhydrase inhibitor - used to treat glaucoma since carbonic anhydrase on the ciliary epithelia is involved in the formation of aqueous humour
what are the side effects of acetazolamide?
- possibly teratogenic
- calculi formation due to altered urinary pH
- GI upset
- hypokalaemia
name 2 other examples of carbonic anhydrase inhibitors?
diclofenamide
dorzolamide
what haematological disorder can result in cardiomegaly?
anaemia
which dogs are prone to chronic respiratory disease?
those that are obese
how can you test the pressure of the right atrium?
via hepatojugular reflux: press liver and cranial abdomen. this will result in increase venous return to R atrium - get jugular distension if pressure of R atrium already increased
in what conditions may you see jugular pulsation (4)?
tricuspid regurgitation
some arrhythmias
pericardial effusion
pulmonic stenosis
when do bounding pulses occur? give 3 examples
due to high output state such as in
- anaemia
- pregnancy
- pyrexia
when do water hammer pulses occur? give 2 conditions
when there is a low diastolic pressure such as in PDA or anaemia
what is pulsus alterans due to?
calcium abnormalitie in heart disease
what is pulsus paradoxus?
pulse is weak when breath in and stronger when breath out - e.g. with pericardial effusion
what does S3 reflect?
early ventricular filling
what does S4 reflect?
late ventricular filling
what exactly is a gallop rhythm? what is it associated with?
a gallop rhythm is when S3 or S4 can be heard - it is associated with increased ventricular filling or still ventricular walls
where do murmurs due to aortic stenosis extend?
to right hemithorax and thoracic inlet
in which conditions may you hear a diastolic murmur (2)?
aortic regurgitation and mitral stenosis
which conditions results in continuous murmurs?
PDA and aortic stenosis/regurgitation
what abnormalities may be detected on auscultation on the RHS of the chest?
VSD
tricuspid stenosis
subaortic stenosis
when can a change in the grade of a murmur occur?
with dynamic obstruction of L ventricular outflow tract in cats
what is the normal VHS in a dog?
8.5-10.5
what is the normal VHS in a cat?
under 8
what conditions can result in generalised cardiomegaly as seen on radiography?
- pericardial effusion
- peritoneo-pericardial diaphragmatic hernia
- DCM
what may L atrial enlargement look like on DV view?
may look separated by round ST density and seen as a bulge at 2-3 oclock position
what conditions can result in L ventricular enlargement without LA enlargement?
- aortic stenosis
- HCM
Where is the RA located on DV?
at 9-11 o'clock
Where do you see rounding on radiograph if RV enlarged (on DV)
6-9 o'clock
in which conditions may you see dilation of aorta/pumonary artery?
aortic/pulmonary stenosis or with PDA
where are bulges of
1) post stenotic aortic dilation
2) post stenotic pulmonary dilation
seen on DV?
1) 12-1 o'clock (prominent arch on lateral)
2) 1-2 o'clock (bulges over trachea on lateral
where does pulmonary oedema start in dogs?
in hilar area (interstitial at first)
- looks patchy in cats
why may you want to include cranial abdomen on radiography when investigating cardiac disease?
to get an idea of hepatomegaly or ascites may be involved
name 3 cardiac disease markers
proANP
troponin
BNP
what has cardiac catheterisation been superceded by? what was it used for?
superceded by doppler

measures intracardiac pressure, blood gas and angiography
what separates atria from ventricles?
annulus fibrosis
what does the L bundle branch divide into?
anterior and posterior fascicles
what are the 6 points you should look for when interpreting an ECG?
- HR
- rhythm: regular vs irregular
- if P for every QRS and QRS for every P
- if P and WRS consistently and reasonably related (PQ interval)
- if all complexes look the same
- P waves and WRS in normal limits in lead II
what is the normal P amplitude in a dog vs a cat?
dog: < 0.4mV
cat: < 0.2mV
what is the normal R amplitude in a dog vs cat?
dog: 2.5-3 mV
cat: 0.9mV
how high should the T amplitude be in relation to R?
it should be 1/4 of R
what does a wide P wave indicate?
left atrial enlargement
what does a tall P wave indicate?
R atrial enlargement
what does a wide WRS indicated?
LV enlargement or LBB block
what does a Tall R indicate?
LV enlargement
what does a small R suggest?
- pericardial effusion
- obesity
- hypothyroidism
what does an alternate R wave height suggest=
pericardial effusion
what does a deep S wave indicate?
RV enlargement - usually hypertrophy
what does a wide S indicate
RBB block
when do you see long QT intervals?
hypocalcaemia
hypokalaemia
hypothermia
when do you see ST elevation/depressions?
hypoxia
infarct
what does ST coving suggest?
LV enlargement (when R slides into T)
what is sinus arrest/sinus block usually due to?
high vagal tone
what other conditions may you see sinus arrest/block in?
brachycephalic with respiratory disease, hypothyroidism, B blockers, hypothermia, calcium blocks

if prolonged --> syncope. escape beats attempt to rescue arrested heart
what may be seen on ECG with sinus block?
no evidence of atrial activity for a period in excess of 2 proceeding R-R: exact multiple of proceeding R to R
how do you treat sinur arrest/block
- propantheline
- terbutaline
- pacemaker
wchich breed is sinus sick syndrome usually seen in?
Schnauzer - get brady tachy syndrom
what is sinus sick syndrome? how does it usually present?
sinus arrest without escapes with no response to atropine - may get SVT

usually presents with syncope
what can be seen on ECG with atrial standstill? how is it treated (if not caused by hyperkalaemia)?
no P waves, slow rate with possibility of bizarre and wide WRS

- atropine, propanthein, terbutaline, pacemaker
what is 1st degree AV block due to and what is seen on ECG?

how is it treated?
increased vagal tone, can also be due to hyperkalaemia

PQ interval is prolonged

NO need to treat
what is seen with 2nd degree block on ECG?
P waves not conducted
what is seen with Mobitz type I 2nd degree AV block?
PR may be variable and increase prior to block
what is Wanchebacks phenomenon and how is it reversed?
= when PR interval increases prior to 2nd degree block: atropine revers it
what is Mobitz type II 2nd degree block?
PR constant = disease of conduction system and therefore at risk of developing 3rd degree block
what is seen on ECG with 3rd degree block?
constant and regular P wave rate not associated with QRS: ventricles beat at escape rate which is lower than P wave rate
what may be seen clinically in 3rd degree block?
sounds like metronomce on auscultation, atrial and ventricular pulse may be visible on jugular, present with syncope
what infectious disease can result in 3rd degree block?
lyme disease
what is bundle branch block due to? what can be seen on ECG with both variants?
abnormal depolarisation

WRS look bizarre and ventricular in origin but will have an associated P wave
what can you see on ECG of RBBB?
wide QRS with deep S wave
what can you see on ECG with LBBB?
wide QRS with tall R wave
how do you treat BBB?
no treatment needed
what are SVP complexes usually due to? what is seen on ECG?
atrial stretch/infiltration

P wave associated with premature complex but can be hidden in preceding T wave
what is considered SVT and what is the HR usually?
when over 4 premature SV complexes in a run: HR usually over 300bpm
how do you treat SVT?
B blockers
cardiac glycosides
calcium chennel antagonists
what conditions can result in atrial fibrillation
atrial stretch: DCM, endocardiosis
how is atrial fib treated? qhat is the aim of treatment?
digoxin
B block if HR over 160
calcium channel blockers

aim to decrease ventricular rate
which drugs used to treat tachyarrhythmias are not used in cats?
cardiac glycosides
what are VPC due to?
stretch, hypoxia, infiltration of ventricular wall, GDV, splenic mass, pancreatitis, pyometra
what is considered ventricular tachycardia?
more then 4 VPC occurring together
name 5 breeds predisposed to aortic stenosis?
boxers
gsd
rotties
goldens
newfoundland
which are the 2 most common congenital heart diseases of cats?
VSD followed by AV valve dysplasia
how is aortic stenosis graded?
by measuring velocity of outflow on echo
what may you see on ECG with aortic stenosis?
increase R amplitude and QRS duration
can get ST depression if myocardial hypoxia occurs
ventricular arrhythmias
how do you treat aortic stenosis?
prophylactic ABS for bacterial endocarditis
exercise restriction
B blockers
Calcium channel blockers
when does closure of ductus arteriosus normally occur?
hours to days after whelping
what are 2 physiological responses in a PDA reverse shunt?
- polycythaemia
- pulmonary hypertension
can get L sided failure as increased blood to L ventricle and volume overload --> eccentric hypertrophy of LV and HL weakness
name 7 breeds that are predisposed to PDA. What sex is it more commonly seen in
females

CKCS, GSD, collies, shetlands, poms, poodles, springer spaniel
what can be seen on ECG in PDA?
wide P wave, tall R, atrial and ventricular PC, atrial fib
when is surgery not an option for PDA cases?
when there is a left to right shunt
which breeds are predisposed to pulmonary stenosis (7)
boxers, beagles, bull amstiff, bull dogs, cockers, mini schnauzers, terriers
how may pulmonary stenosis present?
with syncope, ascites - weak pulse
what may be seen on ECG with pulmonary stenosis?
deep S wave in lead I, II and II and tall P wave as R heart big
which 5 breeds are predisposed to tricuspide valve dysplasia?
labs, goldens, GSD; irish setters, great danes
what are the clinical signs with tricuspid valve dysplasia
jugular distension/pulsation, ascities, pleural effusion
what may be seen on ECG with tricuspid valve dysplasia?
deep S and tall P in lead II, SV arrhythmia

- labs tend to get SVT
which 3 breeds are predisposed to mitral valve dysplasia
goldens, english bull terrier, great dane
what can be heard on auscultation of an animal with mitral valve dysplasia?
pansystolic murmur
what is seen on ECG with mitral valve dyasplasia
tall R, wide WRS, wide P wave in lead II with or without SV arrhythmias
how are mitral valve dysplasias usually treated?
diuretics, Ace inhibitors, positive inotropes
what tends to happen in VSD?
get left to right shunt --> lungs overperfused and increased blood to LV --> LV hypertrophy and L-CHF

but if defect really large will get R to L shunt --> hypoxia and polycythaemia
which 3 breeds are predisposed to VSDs?
keeshond, english bulldog, english springer spaniel
what may be heard on auscultation of VSD?
concurrent murmur of pulmonic stenosis over L heart base
what surgical treatment is available for VSD?
pulmonary artery banding: palliative

mainly treat to decrease signs of CHF
which breed is predisposed to tetralogy of fallot and how is it treated
Keeshond: ALWAYS GET R TO L SHUNT!

phlebotomy, hydroxyurea and B blockers used to treat
what is angiostrongulus vasorum? how big is it?
French heartworm, aka lungworm

- 2.5cm long
describe the pathogenesis/cycle of angiostrongulus vasorum
parasite found in pulmonary artery and right ventricle: eggs are laid in pulmonary parenchyma. these hate to L1 which are coughed up and swallowed and passed in faeces

snails/slugs act as intermediate hosts: these eat larvae in dog poo - dogs get infected by eating snail/slug --> parasite in intestine and go to right heart via lymphatic system or portal veing where they develop to adults
what is the prepatent period of A. vasorum?
50-60 days
where is A vasorum found?
in southern england and wales
where is crenosoma vulpis found and which dogs does it typically affect?
found all over the UK. usually affects older dogs (has similar cycle to A vasorum)
what are the clinical signs of A vasorum?
cough, haematuria, weak/lame, anaemia, pulmonary crepitation, R sided heart failure, collpase/dyspnoea, respiratory distress, DIC if severe, parasitic embolism may occur
what may be seen on haematology in A vasorum case (3)?
- eosinophilia
- thrombocytopaenia
- anaemia
how long does it take post infection to develop lung parenchymal changes detected by radiography?
7-9 weeks. get patchy alveolar and interstitial pattern with pulmonary congestion and possible R heart enlargement
how is A. vasorum diagnosed?
by finding L1 in faeces
how do you treat A. vasorum? what is the prognosis?
levamisol, IVM, mebendazole, fenbendazole, oxygen and dex if thromboembolism/DIC

prognosis good if subclinical or mildly affected
how big are dirofilaria immitis worms?
females 30cm and males 23 cm
what is the pathophysiology/cycle of D. immitis?
pulmonary artery and sometimes the right heart are infected
- mosquito transfers parasite (it mature 10-14 days in mosquito): once in dog it migrates and moults in 3 months
- final maturation in 3-4 months occurs in pulmonary arteries: microfilaria are found in circulation --> pulmonary hypertensionn and R-CHF (due to cor pulmonale)
what disease may be detected that is associated with D immitis?
immune complex glomerular disease
what are some of the clinical signs of D immitis?
cough, tachy/dyspnoea, syncope, haemoptysis, ascities, hepatomegaly, pyrexia, weight loss, caval syndrome
what may be heard on auscultation of D immitis case?
split heart sounds
what is caval syndrome?
weak, haemoglobinaemia/uria: LOTS OF WORMS IN RIGHT VENTRICLE --> poorl cardiac output and intravascular haemolysis: DIC complication
what can be seen on haematology in D immitis case?
anaemia
neutrophilia
lymphopaenia
eosinophilia
basophilia
what can be detected on radiography in D immitis case?
R heart enlargment, pulmonary arteries tortuous, interstitial/alveolar changes with or without granulomas in parenchyma
how does D immitis infection differ between dogs and cats and why is this significant?
do not get circulating microfilaria in cats: important as this is used as a means of diagnosing infection
what are the clinical signs of D. immitis in cats?
mimic asthma: lethargy, anorexia, vomiting, coughing, dyspnoea, syncope, death, chylothorax
what are the 3 main diagnostic techniques undertaken to diagnose D immitis?
ID microfilaria: wet blood smears, Knott test or filter test
(not good for cats as few circulating microfilaria

Microfilaria antibody test: ELISA and flouresent antibody tests - NON SPECIFIC AND INSENSITIVE
female adult heartowrm antigen test: ELISA - high specificity and sensitivity
what may interfere with interpretation of microfilaria identification in D immitis infections?
dirofilaria petalonema reconditum: harmless parasite that also produces microfilaria
which adulticides are used in D immitis treatment? what do you need to watch for when treating?
melarsomine, thiacetarsemide

watch for emboli! (treat with steroids and antibiotics)
which drugs attack microfilaria in D imitis?
avermectin and milbemycin oxime (used as prevention)
what is the most common pericardial disease in dogs?
idiopathic benign pericardial haemorrhage
what is the most common cause of pericardial disease in cats?
FIP
which breeds are predisposed to idiopathic pericardial effusion?
goldens, st bernards, GSD
which breeds are predisposed to RA haemangiosarcoma?
GSD, and goldens
what may be seen on radiography in pericardial efusion case?
CVC distended and may have pleural effusion
what is seen on ECG in pericardial effusion case?
electrical alterans and small WRS
what is electrical alterans due to?
heart swining back and forth
what drugs should be avoided in pericardial effusion and why?
diuretics as can result in severe hypotension
what recumbency do you have patient lying in on pericardiocentesis? what are your landmarks for pericardiocentesis?
L lateral recumbency

place local anasthetic in 5-65th intercostal space at costochondral junction and place pericardial catheter with stylet in here via small incision: pass catheter through skin and intercostal muscles into pleural space: use extension set with 3way tap and large syringe attached
how do you differentiate pericardial effusion from RV blood?
fluid will not clot
what is the prognosis for pericardial effusion?
reasonable if idiopathic, guarded if inflammatory
what drug can result in DCM?
doxorubisin
what deficiency in boxers can result in DCM?
carnitine deficiency
what deficiency in cockers can result in DCM?
carnitine and taurine deficiencies
which breeds are predisposed to DCM and what sex?
males

great danes, irish wolfhounds, newfoundlands, irish setters, labs, dobermans, boxers, old english sheepdogs, springers, cockers
what is the history of DCM in
1) boxer
2) dobermann
3) giant breeds
4) spaniels
1) collapse: ventricular arrhythmia
2) DObermann: cough and dyspnoea (L-CHF and ventricular arrhythmia)
3) ascites - biventricular failure and atrial fib
4) cough, exercise intolerance and dyspnoea
what may be found on clinical exam of DCM case?
diastolic gallop
arrhythmia
low grade murmur due to AV insufficiency
pallor
weak pulses
how is DCM treated
ACE inhibitors, diuretics, pimobendan/digoxin
what is the prognosis of DCM in dobermans? in cockers?
dob: 3-12 months

cocker: 3-4 years
how may occult DCM preswent?
with slow A fib or intermittent collapse
what was feline DCM due to previously and why?
taurine deficiency: cats fed dog food
what are cats with DCM predisposed to?
thromboembolism
which breeds are preidposed to idiopathic/primary feline HCM?
maine coon and american short hairs - males
when may dynamic obstruction or L or R outflow tract occur in feline HCM?
if septal hypertrophy occurs - get obstruction in systole
what is systolic anterior motion of mitral valve?
when mitral leaflet gets sucked into outflow tract in sysole
what are the clinical findings in feline HCM?
murmur, diastolic gallop , brady/tachyarrhythmia, muffled if pleural effusion, crackles if oedema, cyanotic HL if thromboembolism
what is classically seen on radiography in feline HCM?
valentine shaped heart on DV - both atria big: may see oedema and pleural effusion or elongated heart as well
what is seen on ECG in feline HCM?
can be normal!

toerhweise wide and tall P waves, tall R waves, atrial or ventricular premature complexes, afib or LAFB
why may LAFB occur in feline HCM?
because of damage to bundle branch
what should you check before diagnosing a cat with feline HCM
kidneys, thyroid, retina, and blood pressure
how is feline HCM treated?
B block/calcium channel antagonist, diuretics, ACE inhibitors, aspirin longterm or possible clopidogrel to prevent emboli forming
what is the prognosis for feline HCM?
poor if emboli, guarded if CHF signs?
what result in secondary feline HCM?
hypertension, hyperthyroid, acromegaly
what may be seen with feline restrictive CM?
atria dilated but ventricle normal - manage as for HCM and may be early stage of HCM
what is seen with feline unclassified CM on echo? what is it thought to be?
thought to be end stage HCM
- ventricle dilated, walls hypertrophies, systolic function poor
why does platelet aggregation occur readily in cats normally?
because have high platelet mass/kg
what is seen in feline thromboembolism?
HL paresis, pain, SPASM OF GASTROCNEMIUS, cyanotic nail bed, absence of femoral pulse
how do you acutely manage feline thromboembolism?
buprenorphine/morphine
ACP: vasodilate and decrease anxiety
heparin
aspirin
IVFT
physio
treat underlying disease
what should you warn clients of prior to embarking on treatment of feline thromboembolism?
that it recurrs
when does pain caused by feline thromboembolism ease off? how long until HL function returns?

what percentage recover?
pain eases off i 3-4 days
HL function returns by 14 days

25-30% fully recover, but many recur
how can myocarditis be diagnosed?
high serum troponin: released on myocardial damage

heart size normal but still have arrhythmia
what may myocarditis be secondary to (6)?
toxoplasma
neospora
parvo
ehrlichia
borrelia
neoplasia
list 5 breeds that are prone to developing valvular endocardiosis, sex?
males
CKCS,
cockers
poodles
terriers
dachshunds
what may be heard on auscultation in sever valvular endocardiosis?
if really bad mitral endocardiosis may radiate to R side of heart - so will not know if tricuspid or mitral in origin
when may radiographic changes of valvular endocardiosis occur?
can occcur before clinical signs of CHF
what may be seen on ECG in collies/lerchers with endocardiosis?
atrial fibrillation
how is endocardiosis treated?
CHF (cough, ascites, exercise intolerance, dyspnoea):
furosemide
ACE inhibitors
pimobendan

if very advanced can administer other diuretics

digoxin if marked tachycardia or atrial fibrillation
what is bacterial endocarditis associated with?
PERIODONTAL DISEASE IN DOGS OR IN aortic valve stenosis
how is bacterial endocarditis diagnosed?
take 3 blood samples in 1 day for culture

can perform urinalysis

(L heart goes to joints and kidneys)
how long of an antimicrobial treatment does endocarditis require?
4-6 weeks: IV at first!
what gauge needle is used for thoracocentesis?
21 gauge
which drugs decrease preload (5)?
furosemide
hydrochlorthiazide
sprinolactone/amiloride
glyceril trinitrate
ace inhibitors (enala, benaze, rami, imiropril)
which drugs decrease afterload (3)?
hydralazine: arterial dilator (mitral insufficiency - may get hypotension and reflex tachycardia)
ace inhibitors
pimobendan: inodilator
which drugs (3) treat systolic failure
digoxin
dobutamine
pimobendan
when do you stop digoxin treatment?
if any signs of anorexia, V/D, arrhythmias
which patients should you decrease digoxin dose in?
those that are obses, have fluid retension, kidney failure or are dobermanns
what do you aim to do when treating diastolic failure?
improve relaxation, slow heart rate, decrease contractility
what drugs are used to improve cardiac relaxation?
diltiazem and verapamil: calcium antagonists

decreae myocardial oxygen consumption and improve relazation by decreasing subendocardial ischaemia - also negative chronotrope: improve filling
what drugs are used to slow HR?
propanolol, atenolol (B blockers)
which drugs decrease contractility?
B blockers and calcium channel antagonists