SA- cardiac dz Flashcards by Bethany Dixon

what are the main4 effects of CHF

inc HR/arrhythmia
oedema and effusions
remodelling and fibrosis
vasoconstriction

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what 2 things try to counter RAAS

ANP
BNP
they are released due to chamber stretch and try to vasodil and diuresis
this can be used to dx

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what factors cause vasoconstriction in CHF

ANG II
endothelin
NA at a2-R
ADH

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due to bradykinin being decreased from the action of ACE, what other vasodilating factors are blocked

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what is the action of ANG II

decreased bradykinin
inc aldosterone
remodelling/fibrosis
ADH release
endothelin release
stem release of NA
constriction of off arteriole = inc GFR

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what is the purpose of ACE inhib

to counter the effects of ANGII

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what is the purpose of ANGII-r blockers (mainly human atm)

used to avoid ACE-Inhib SE in humans, but means bradykinin doesn’t increase. ALSO ANGII made by chymases too not just ACE

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ACE inhibit don’t always block enough aldosterone, so how do you do that?

sprinolactone - k sparing too

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what is the ‘la place’ relationship? (related to hypertrophy)

wall stress = radius x pressure / 2x wall thickness

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what ar the 2 forms of hypertrophy

eccentric (wider lumen)

- concentric (thicker wall)

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what is a path result of vol overload

mitral regurg

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how does physiological compensatory hypertrophy become pathological

if dilation is more than hypertrophy can compensate for –> myocardial cells ‘slip’ and heart fails

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do myocytes get fatter or longer in eccentric and concentric hypertrophy

concentric = fatter, p overload
eccentric = longer,, vol overload

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what is the 1st problem of CHF that needs addressing wrt tx

the Na and water retention

LHS - pull oedema; HS = ascite, pleural effusion and hepatomegaly

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how do you dress the na and water retention ?

diuretics

- 1st choice = furosemide

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what is the aim of diuretic tx

lowest poss dose
start bid/tid –> sid
train O to take resting RR and then can lower dose until RR increases

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what are the SE of furosemide that need to be monitored?

pre-renal azotaemia= U;Cr
hypokalaemia
short-term use only of RAAS+

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what might the effect of GI oedema be re drugs/furosemide

can’t be absorbed

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name a more potent 2nd choice diuretic

loop-diuretic torasemide

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describe the principles of a sequential nephron blockade

using diuretics acting on diff parts on the renal tubules

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what is indicated in pleural effusion

thoracocentessi

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what must you ascertain before beginning treatment of RHS CHF ?

whether due to pericardial effusion first

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what type of drugs are all the ACE inhib

pro-drugs

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ACE-I are almost always indicated in cases of CHF, however when should they not be given and why

in cases of severe hypotension, where furosemide is given in high doses OR if there is aortic stenosis

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what are the SE of ACE-I

hypotension renal impairment hyperkalaemia anorexia, d+. v+

how can pulmonary oedema be treated initially

with vasodilation - use furosemide IV - topical nitroglycerine (percutol) or as a patch

why would arteriodilators be useful>

to reduce systemic p, wo reducing perfusion. unloads failing heart

name some arteriodil drugs

pimobendan amlodipine hydrazine ACE-I

how does pimobendan work (vetmedin)

Ca++ sensitiser - so contractility increases wo any more Ca++ also inhibits PDE therefore = vasodil and +ve inotrope

why is it good that pimobendan doest inc intracellular Ca++

as it induces arrhythmias (makes it better than other PDE-I)

high sympathetic drive is the reason for tachycardia - how can this be reduced

- indirectly! b-blocker r blockade (digoxin)

why would b-blockers be VERY CI in the CHF patients

if not controlled - as sympathetic drive is crucial to maintaining the heart ! wo it, it will arrest - so get other bits sorted before you add bblockers

what is the effects of digoxin (B-blocker)

inc vagal tone - @ low end of dose rate - direct stem of vagal centre in CNS - sensitises baro-R - inc cardiac pacemaker response to ACh neg chronotrope, pos inotrope

digoxin is toxic and with a narrow therapeutic index - what signs do you need to look for>

- XS borborygmi - depression - anorexia - V+D - arrhythmias

what factors of a dog will predisp it to digoxin toxicity>

- thin - no skeltal m to bind - obese (doesn't go into the fat) - dose to Body SA - hypothyroid - impaired Renal fat - dobermann - hypoxia/acidosis/hypokalaemia - any other Ca++ channel blockers

how do you treat digoxin toxicity?

stop! ventricular arryth can be helped with lidocaine act charcoal 'digibind'

what it the gold std tx for CHF, MVD or DCM?

- furosemide - ACE-I (benazepril) - pimobendan - spironolactone

how fast does conduct thru the AVN?

= | 0.1m/s

how fast does it travel the perking fibres

4m/s

is high vagal tone normal in dogs, | is it normal in cats

Y - hence why sinus arrhythmia occurs at normal/slower HR | N (cats) - look for causes e.g. asthma, rest compromise

why is it okay for atrial depol position to vary

because the SA N is large in the dog - so the exact area will change

when is sinus arrest okay

sleeping | brachycephalic breeds - extreme sinus arrhythmia

what is sick sinus syndrome

arrhythmias due to SAN not working 100% normally

how do VPCs appear on ecg

wide, bizarre QRS, with T wave in pop direction

what is the r-on-t phenomenon

when the T wave superimposes itself on the preceding R wave. can lead to V fibr

why is ventricular tacky so imps to tx -

to prev ventricular fibrillation!

what systemic dz states could cause VPC

- GDV - splenic lesions - sepsis - pancreatitis - pyo

what are ventricular escape complexes (NB - never suppress these!)

when the supraventricular rhythm is slow than word normally be the case. QRS are really wide (slow)

describe the different types of AV block

1st - PR interval is too long (>0.13s) 2nd - some P waves are not followed by QRS. can be normal in horse at rest 3rd - complete, no associ of P waves with QRS

what path deputation in the heart leads to atrial fibrill

atrial stretch

how does a supra ventricular premature complex appear on ecg?

premature atrial but ectopic wave. can include junctional complexes.

in an emergency, how can supreventrivcular tachycardias be treated (clue no drugs)

ocular pressure | carotid sinus massage

in large breed dog, what is the maximum mV that the R-wave should read on lead II?

3mV | OR it is suggestive of L vent hypertrophy

in large breed dog what is the maximum time it should take the QRS complex

0.06s - OR suggests V hypertrophy

if th P wave duration is more than 0.04s then what does it sugges

P mitrale = LA enlargement

what does a tall P wave (p pulmonate) suggest

RA enlargement

where do you place the ECG leads on a horse

``` RA = Jug furrow LA = left apex RH = earth/thoracic inlet ```

what is Left bundle branch block and how does it appear

cell-to-cell only transmission of depol in LV. | normal P:QRS; tall/wide (>0.08s) QRS, T waves opp direction,

what is the difference in right bundle brach block and left

the side indicated by -'ve QRS deep/wide S waves

what dz state is left anterior fascicular block common (cats)

HCM in cats

what is the significance of the QT interval

tot time for Ventricular depol AND repol.

is the T wave usually important?

no - varies, but should be stable per dog. spikes t wave indicate hypERkalamia

what does the ST interval show

the period bw depol and repol

what is a long-axis view

base-apex

what is a RPS long axis view

Right parasternal | the 'home view'

conventionally what structures are on the RHS

basilar structures

what is fractional shortening?

calculating the systolic function = difference in lumen diameter at diastoles and systole / diastole x 100 - should be >25%

when is the fractional shortening estimate of systolid fct not reliable

if mitral regurg wall motion abn RHS heart dz from P overload

what is the normal ejection fraction

>50%

what is the index of sphericity, and why is it useful

assess how round LV is --> DCM | >1.7

what is2D/B-mode ECG

normal / brightness mode

what is M-mode ECG

an add-on which means can see time-mode. | can see the lumenal contractions more quantitatively

name the diff doppler ECGs

spectral, colour flow and tissue doppler

which form of doppler estimates velocity

spectral - but MUST be parellel to flow or will underestimate

what are the diff bw pulse wave and continual wave spectral dopplers

PW - spatially specific, just a small sample, cant penetrate deeply CW - samples from many RBC, peak velocity recorded and deeper range

if the spectral doppler is 'filled' what does it suggest

turbulent flow

what colours on colour doppler mean towrds and away from transducer

BART | blue = away; red = towards

why would you do a 'sb-costal' doppler scan

for oartic outflow assessment

what is the normal aortic velocity

1.7m/s

what is the modified bernouilli eq?

Pressure gradient = 4v^2

what are the expected pressure gradients for aortic and pulmonary stenosis

``` 0-40mmHg = mild >80mmHg = severe ```

what does the E and A wave indicate on an ECG

E - early v filling | A - atrial contraction

DCM

dilated heart chambers, pos w stenosis

Myxomatous degenerative valvular dz and MV regurg

leaflets, ruptured choda tendinae, colour doppler = regurg

HCM (cats)

vVV concentric walls and thin lumen (partic LV)

Pericardial effusions

sitting in a sac of fluid - obvious