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ECEIM consensus statements > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Give 6 negative prognostic factors in structural heart disease.

A

○ Progressive chamber remodelling- dilated and altered chamber shape
○ Chamber dysfunction
○ Great vessel enlargement
○ PHT
○ CHF
Potentially dangerous arrhythmias

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2
Q

Give the 8 instances where echocardiography is recommended

A
  1. A previously diagnosed ‘functional’ murmur that is louder on serial examination
    1. A grade >3 left sided murmur compatible with MR or AR
    2. A grade >4 right sided murmur compatible with TR
    3. A suspected VSD or other congenital heart lesion
    4. Continuous or combined systolic/diastolic murmur
    5. Clinically important arrhythmias, even in the absence of a murmur
    6. Suspected myocardial injury
  2. Suspicion of CHF
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3
Q

What 2 factors should be incorporated into an exercising ecg?

A

Work intensity should be at or slightly exceeding the horse’s customary activities
Should include some method of stimulating unexpected sympathetic stimulation

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4
Q

What 4 specific measurements should be incorporated into an exercise test?

A
  1. Effects of exercise on auscultation (HR, rhythm, murmurs)
  2. Peak HR during exercise
  3. HR and rhythm during different phases of exercise and recovery
  4. Optional: Echo before and after exercise (stress echocardiography)
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5
Q

Describe a typical MR murmur

A

Mid-late systolic or holo/pansystolic left sided

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6
Q

Give 6 Underlying lesions that may be responsible for MR

A

Mitral valve dysplasia
Degenerative or inflammatory valve thickening.
Prolapse= MVP
Thickened or ruptured chordae tendinae= RCT
Flail leaflet
Secondary to valve annulus or ventricular dilatation in severe AR, non-restrictive VSD or, rarely, cardiomyopathy.

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7
Q

What secondary changes occur in severe MR?

A

PHT and enlargement of the LA and LV

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8
Q

In the absence of PA catheterisation, what measures can be used to estimate PHT?

A

TR velocity and PA diameter

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9
Q

Why is assessment of LV function difficult in MR?

A

increased preload and reduced afterload.

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10
Q

What changes occur to LV function in acute/severe MR disease?

A

LV hyperdynamic: increased FS, dynamic compression of the RV and exuberant septal motion

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11
Q

What changes occur to LV function in chronic MR disease?

A

progressive remodelling and LV dysfunction. -> reduced FS to within or below normal range

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12
Q

What kind of MR jet is often under-estimated?

A

An MR jet that is eccentric, wall hugging or flat

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13
Q

What are the major negative prognostic indicators for MR?

A

○ Moderate-severe regurgitation
○ Endocarditis
○ RCT
○ Flail leaflet
○ Severe valvular thickening
○ Concurrent PA dilation
○ Increased TR velocity
○ Significant MR with AF or tachycardia

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14
Q

What is the most common cause of AR?

A

degenerative valve thickening and/or AV prolapse

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15
Q

Give 7 less common causes of AR

A

Congenital malformations
Leaflet tearing
Endocarditis
Valvulitis
Fenestrations
Aortic root disease
In association with VSD.

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16
Q

describe the AR murmur

A

left sided holodiastolic

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17
Q

What is the most common structural change of the AV associated with AV, as visible on 2D echocardiography?

A

thickening as a fibrous band-like lesion appearing as an echoic line parallel to the free edge if the left coronary leaflet

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18
Q

Which AV leaflet is most commonly affected in AR?

A

left coronary leaflet

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19
Q

What does premature closing of the MV on M-mode indicate?

A

markedly increased LV end diastolic pressure= severe AR.

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20
Q

Why may the MV not fully open in AR?

A

Eccentric jets directed towards the MV can prevent full MV opening.

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21
Q

Why may the MV flutter in AR?

A

Diastolic fluttering of the mitral or aortic valves, aortic root or IVS if the jet is directed towards these structures.

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22
Q

What does LA enlargement indicate in AR?

A

ventricular dysfunction, volume retention or concurrent MR

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23
Q

Give 3 as yet unvalidated measurements of AR severity

A

regurgitant signal duration, pressure half time, velocity time integral of AR compared to forward flow.

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24
Q

Above which pulse pressure is AR progression more likely?

A

60mmHg

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25
Q

When is echocardiography of a suspected TR indicated?

A

grade 4/6 or louder
Poor performance
Concurrent thrombophlebitis
With fever of unknown origin
PPE

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26
Q

Give 3 findings that would indicate a TR was benign/ training related

A

Valve is structurally normal
RA and RV are normal in size
Regurgitant jet is thin and directed towards the aorta

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27
Q

Above which TR velocity should you suspect PHT?

A

3.5m/s

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28
Q

Give 3 findings on echo that would indicate a TR was clinically significant.

A

Structural or motion abnormalities in the TV
RA and RV enlargement
Jet is wider at origin and occupies a larger area in the RA (often central or towards the RA wall).

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29
Q

In which breeds is VSD predisposed?

A
  • Welsh sec A, Standardbreds and Arabians over-represented
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30
Q

Describe the typical VSD

A

peri membranous, located ventral to the tricuspid leaflet and below the junction of the right and non-coronary cusps of the aortic valve.

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31
Q

Give 3 types of VSD

A

perimembranous, subarterial, muscular

32
Q

describe a subarterial vsd

A

beneath the semilunar valves

33
Q

describe a muscular VSD

A

apical

34
Q

Up to what VSD diameter is the VSD unlikely to be haemodynamically important?

A

2.5cm

35
Q

Flows above what peak velocity is indicative if a better prognosis in VSDs?

A

4.5m/s

36
Q

what does a peak flow velocity of <4.5m/s across a VSD indicate?

A

greater shunt volume.

37
Q

what may reduce the functional size of a VSD?

A

TV adhesions, fibrous tissue proliferation

38
Q

Give 6 prognostic criteria for VSDs

A

Size of VSD
Size of cardiac chambers
Maximal shunt velocity
Presence of significant AR or MR
PHT
CHF

39
Q

What arrhythmia is commonly associated with an aorto-pulmonary fistula?

A

VT

40
Q

What breed is predisposed to aorto-cardiac fistulae?

A

Freisians

41
Q

describe the clinical presentation of an aorto-cardiac fistula

A

bounding arterial pulses, tachycardia, and a grade 1–3/6 holosystolic and early-to-mid diastolic murmur loudest dorsal to the aortic valve

may be in acute CHF, or just poor performance

42
Q

Describe the criteria for a high grade 2nd degree AVB

A

> 2 consecutively blocked P wave

43
Q

Should horses with a high grade AVB be ridden?

A

Horses with high-grade second degree AVB that disappears with exercise should only be ridden or driven by an informed adult, and the HR and rhythm should be frequently monitored.

Horses with high-grade second degree AVB during exercise or after atropine administration should be rested and re-evaluated; they are considered less safe to ride or drive than their age-matched peers

44
Q

describe the appearance of an APC on an ECG

A

ectopic, premature atrial activation (P’), usually with changes to P wave morphology

Can be conducted with a variable P’-R interval or blocked at the AVN

The conducted QRS is generally normal but can be abnormal with secondary ST segment and T wave changes.

45
Q

Are horses with APCs safe to ride?

A
  • Horses with occasional PACs that are over driven during exercise and those with occasional PACs during exercise are considered as safe to ride or drive as their age-matched peers
46
Q

What is the definition of VT?

A

3+ repetitive or linked VPCs.

47
Q

Do VPCs have a compensatory pause?

A

generally yes

48
Q

What is ‘bruit de cannon’?

A

Rapid, generally irregular rhythm with variable intensity or ‘booming’ heart sounds associated with VT

49
Q

Describe a PVC on an ECG

A

premature QRS without P, wide and bizarre, and followed by a large T wave of opposite polarity.

50
Q

Give 5 characteristics of a complex or potentially “malignant” VA:

A

multiform or polymorphic QRS morphology
short coupling intervals (especially R-on-T timing)
sustained VT
rapid ventricular rate (exceeding 120 beats/min)
repetitive ectopic activity (couplets, VT).

51
Q

Describe an accelerated idioventricular rhythm

A

Monomorphic
start with a relatively long coupling interval
become established at relatively slow ventricular rates (50–80/min at rest)

52
Q

Following resolution of VT, how long should a horse be in NSR before re-evaluation?

A

4 weeks.

53
Q

describe paroxysmal AF

A

Acute onset AF: generally spontaneously convert to NSR within 24-48hours.

54
Q

decribe lone AF

A

AF in the absence of detectable underlying heart disease

55
Q

In which breed has AF been demonstrated to be heritable?

A

standardbreds

56
Q

Describe AF on an ECG

A

Irregularly irregular R-R interval with normal QRS morphology, the absence of P waves and the presence of “f” waves.

57
Q

What is the difference between AF and atrial flutter

A

Flutter waves resemble saw-toothed P waves with-out an isoelectric shelf and have a regular atrial rate of about 170–275/min, while fibrillation waves are less organized and faster (275–500/min on intracardiac electrograms)

58
Q

What is atrial flutter?

A

a slow macro-re-entry variation on AF.

59
Q

Describe atrial flutter on an ECG

A

Flutter waves resemble saw-toothed P waves with-out an isoelectric shelf and have a regular atrial rate of about 170–275/min

AV conduction in atrial flutter is usually variable, resulting in a ventricular rate response that can be irregular or regular during periods of increased sympathetic tone.

Patterns of 3 : 1, 2 : 1, or 1 : 1atrial-to-ventricular conduction can be observed.

60
Q

does a slighlty increased LAD in a horse with AF indicate structurally significant remodelling?

A

No: A slight increase in LA size can result from AF, even in the absence of MR.

61
Q

Why is LV function difficult to assess in AF?

A

ventricular dyssynchrony=tachycardia induced LV dysfunction

Also hampered by the preload and HR dependence of many echo indices.

62
Q

Aside from affect on performance, when is cardioversion of AF recommended?

A

Average max HR at normal activity level 220bpm
Concurrent VA observed (usually resolve after cardioversion).

63
Q

Give 3 management strategies for AF

A

No treatment
Pharmacologic cardioversion
TVEC

64
Q

When should horses not be cardioverted?

A

CHF
First 24-48hours of AF (may spontaneously convert

65
Q

what is the reported success rate of AF cardioversion?

A

65–90%

66
Q

Indications for Quinidine

A

Lone AF
AF with mild LA enlargement
Comorbidities in which GA or TVEC not option

67
Q

Contraindications for quinidine

A

Rapid ventricular response to AF
Complex ventricular ectopy (risk polymorphic VT with Quinidine)

68
Q

Indications for TVEC

A

one AF
AF with mild LA enlargement
horses either intolerant of or unresponsive to quinidine treatment or horses in which quinidine is contraindicated (see above)

69
Q

What are the risks associated with TVEC?

A

GA
Development of fatal arrhythmia
The immediate recurrence of AF (IRAF) within the first 24 hours after cardioversion, although infrequent, is more likely than with quinidine cardioversion.

70
Q

During which wave is the shock delivered in TVEC?

A

R

71
Q

when is AF recurrence rate lowest?

A

○ Rate is lowest (15%) in lone AF of recent onset (<1month)

72
Q

Give 5 anti-arrhythmic drugs that may reduce AF recurrence?

A

propafenone, sotalol, flecainide, amiodarone, phenytoin

73
Q

What medications should be avoided after cardioversion of AF?

A

furosemide, supplements containing sodium bicarbonate, and thyroid hormones after cardioversion.

74
Q

How long should horses with paroxysmal AF be rested?

A

1 week

75
Q

How long should horses with sustained AF be rested after cardioversion?

A

4-6 weeks, or until LA function normalised

76
Q
A

ECEIM consensus statements (6 decks)

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