Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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
|