Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

VSCI300 MOD > SA- cardiac dz > Flashcards

SA- cardiac dz Flashcards

1
Q

what are the main4 effects of CHF

A
  1. inc HR/arrhythmia
  2. oedema and effusions
  3. remodelling and fibrosis
  4. vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what 2 things try to counter RAAS

A
  • ANP
  • BNP
    they are released due to chamber stretch and try to vasodil and diuresis
    this can be used to dx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what factors cause vasoconstriction in CHF

A

ANG II
endothelin
NA at a2-R
ADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

PG

NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the action of ANG II

A
  • decreased bradykinin
  • inc aldosterone
  • remodelling/fibrosis
  • ADH release
  • endothelin release
  • stem release of NA
  • constriction of off arteriole = inc GFR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the purpose of ACE inhib

A

to counter the effects of ANGII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

sprinolactone - k sparing too

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

wall stress = radius x pressure / 2x wall thickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what ar the 2 forms of hypertrophy

A
  • eccentric (wider lumen)

- concentric (thicker wall)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is a path result of vol overload

A

mitral regurg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how does physiological compensatory hypertrophy become pathological

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

do myocytes get fatter or longer in eccentric and concentric hypertrophy

A 
concentric = fatter, p overload
eccentric = longer,, vol overload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

the Na and water retention

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how do you dress the na and water retention ?

A

diuretics

- 1st choice = furosemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the aim of diuretic tx

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

can’t be absorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

name a more potent 2nd choice diuretic

A

loop-diuretic torasemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

describe the principles of a sequential nephron blockade

A

using diuretics acting on diff parts on the renal tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is indicated in pleural effusion

A

thoracocentessi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what must you ascertain before beginning treatment of RHS CHF ?

A

whether due to pericardial effusion first

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what type of drugs are all the ACE inhib

A

pro-drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the SE of ACE-I

A

hypotension
renal impairment
hyperkalaemia
anorexia, d+. v+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how can pulmonary oedema be treated initially

A

with vasodilation

  • use furosemide IV
  • topical nitroglycerine (percutol) or as a patch
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

why would arteriodilators be useful>

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

name some arteriodil drugs

A

pimobendan
amlodipine
hydrazine
ACE-I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

how does pimobendan work (vetmedin)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

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

A
  • indirectly!
    b-blocker r blockade
    (digoxin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the effects of digoxin (B-blocker)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

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

A
  • XS borborygmi
  • depression
  • anorexia
  • V+D
  • arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

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

A
  • 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
36
Q

how do you treat digoxin toxicity?

A

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

37
Q

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

A
  • furosemide
  • ACE-I (benazepril)
  • pimobendan
  • spironolactone
38
Q

how fast does conduct thru the AVN?

A

=

0.1m/s

39
Q

how fast does it travel the perking fibres

A

4m/s

40
Q

is high vagal tone normal in dogs,

is it normal in cats

A

Y - hence why sinus arrhythmia occurs at normal/slower HR

N (cats) - look for causes e.g. asthma, rest compromise

41
Q

why is it okay for atrial depol position to vary

A

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

42
Q

when is sinus arrest okay

A

sleeping

brachycephalic breeds - extreme sinus arrhythmia

43
Q

what is sick sinus syndrome

A

arrhythmias due to SAN not working 100% normally

44
Q

how do VPCs appear on ecg

A

wide, bizarre QRS, with T wave in pop direction

45
Q

what is the r-on-t phenomenon

A

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

46
Q

why is ventricular tacky so imps to tx -

A

to prev ventricular fibrillation!

47
Q

what systemic dz states could cause VPC

A
  • GDV
  • splenic lesions
  • sepsis
  • pancreatitis
  • pyo
48
Q

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

A

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

49
Q

describe the different types of AV block

A

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

50
Q

what path deputation in the heart leads to atrial fibrill

A

atrial stretch

51
Q

how does a supra ventricular premature complex appear on ecg?

A

premature atrial but ectopic wave. can include junctional complexes.

52
Q

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

A

ocular pressure

carotid sinus massage

53
Q

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

A

3mV

OR it is suggestive of L vent hypertrophy

54
Q

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

A

0.06s - OR suggests V hypertrophy

55
Q

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

A

P mitrale = LA enlargement

56
Q

what does a tall P wave (p pulmonate) suggest

A

RA enlargement

57
Q

where do you place the ECG leads on a horse

A 
RA = Jug furrow
LA = left apex
RH = earth/thoracic inlet
58
Q

what is Left bundle branch block and how does it appear

A

cell-to-cell only transmission of depol in LV.

normal P:QRS; tall/wide (>0.08s) QRS, T waves opp direction,

59
Q

what is the difference in right bundle brach block and left

A

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

60
Q

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

A

HCM in cats

61
Q

what is the significance of the QT interval

A

tot time for Ventricular depol AND repol.

62
Q

is the T wave usually important?

A

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

63
Q

what does the ST interval show

A

the period bw depol and repol

64
Q

what is a long-axis view

A

base-apex

65
Q

what is a RPS long axis view

A

Right parasternal

the ‘home view’

66
Q

conventionally what structures are on the RHS

A

basilar structures

67
Q

what is fractional shortening?

A

calculating the systolic function
= difference in lumen diameter at diastoles and systole / diastole x 100

  • should be >25%
68
Q

when is the fractional shortening estimate of systolid fct not reliable

A

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

69
Q

what is the normal ejection fraction

A

> 50%

70
Q

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

A

assess how round LV is –> DCM

>1.7

71
Q

what is2D/B-mode ECG

A

normal / brightness mode

72
Q

what is M-mode ECG

A

an add-on which means can see time-mode.

can see the lumenal contractions more quantitatively

73
Q

name the diff doppler ECGs

A

spectral, colour flow and tissue doppler

74
Q

which form of doppler estimates velocity

A

spectral - but MUST be parellel to flow or will underestimate

75
Q

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

A

PW - spatially specific, just a small sample, cant penetrate deeply

CW - samples from many RBC, peak velocity recorded and deeper range

76
Q

if the spectral doppler is ‘filled’ what does it suggest

A

turbulent flow

77
Q

what colours on colour doppler mean towrds and away from transducer

A

BART

blue = away; red = towards

78
Q

why would you do a ‘sb-costal’ doppler scan

A

for oartic outflow assessment

79
Q

what is the normal aortic velocity

A

1.7m/s

80
Q

what is the modified bernouilli eq?

A

Pressure gradient = 4v^2

81
Q

what are the expected pressure gradients for aortic and pulmonary stenosis

A 
0-40mmHg = mild
>80mmHg = severe
82
Q

what does the E and A wave indicate on an ECG

A

E - early v filling

A - atrial contraction

83
Q

DCM

A

dilated heart chambers, pos w stenosis

84
Q

Myxomatous degenerative valvular dz and MV regurg

A

leaflets, ruptured choda tendinae, colour doppler = regurg

85
Q

HCM (cats)

A

vVV concentric walls and thin lumen (partic LV)

86
Q

Pericardial effusions

A

sitting in a sac of fluid - obvious

VSCI300 MOD (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions