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Equine Final Year > LA Dysrhythmia > Flashcards

LA Dysrhythmia Flashcards

1
Q

What udnerlies endocardial diseased? (2)

How does it manifest?

A

•Endocardial disease

–Valvular regurgitation

–Jet lesions

–MANIFEST AS CARDIAC MURMURS

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2
Q

What underlies myocardial disease (2)? How does it manifest?

A

–Disruption to action potential propagation

–Abnormalities in contraction

–MANIFEST AS CARDIAC DYSRHYTHMIAS

•Collapse/sudden death

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3
Q

How does myocardial disease manifest? (4)

A

•No clinical signs

–Low level horses

–Or those that don’t need to use cardiac reserve

•Poor performance

–AF – race, eventers hunters

–VPD’s

•Collapse – rider safety

–Multiple VPD’s and VT

•V rarely death

–VT to VF

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4
Q

What is required for the myocardium function?

A

Heart muscle

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5
Q

What lies within the myocardium? (2)

A
  • Muscle fibres – special type
  • Extensive purkinjee fibre network
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6
Q

How do you diagnose cardiac dysrhytmias?

A

–ECG

  • Resting
  • Exercise
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7
Q

How can you evaluate underlying cardiac dysrhythmias? (2)

A

–ECG abnormal – often have underlying disease e.g. valve disease and then enlarged chambers

–Blood tests – myocarditis; but not as good as in dogs. Look for cardiac tryponin – when they move the cardiac tryponin sit within sarcolemer and form cross bridges to stop them over contracting or relaxing. Have to have trashed you heart muscle for this to be raised – why it is not as good in horses as we don’t tend to see muscle broken down

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8
Q

Which electrolytes may be abnormal with myocardial dysfunction? (3)

A
  • Potassium
  • Calcium – less common in the horse (but is seen in the sweaty endurance horses)
  • Magnesium – membrane stabiliser and helps to keep everything functioning
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9
Q

What conditions might lead to myocardial dysfunction? (4)

A
  • Electrolyte abnormalities
  • Increased myocardial muscle mass

–Less common – more seen in the trained heart. Eccentric (rather than concentric) hypertrophy

•Increased chamber size

–Cardiomyopathy

•Myocarditis

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10
Q

What clinical pathology can we look at to evaluate large animal myocardium? (2)

A

•Proteins

–Large molecules – released when cell membrane disrupted

–Cardiac troponin I

•Enzymes

–Small molecules – released by cell membrane dysfunction (ie less severe)

–Creatine kinase (Myocardial isoenzyme)

»MM isoe – skeletal

»BM isoe– cardiac

»BB isoe–brain

[Hydroxybutyrate dehydrogenase]

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11
Q

How common is myocarditis?

A

Rare as hens teeth………

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12
Q

What are the underlying causes of myocarditis? (5)

A

–Bacteria

–Borrelia burgdorferi – (Lyme disease)

–Viral

•FMD (farm- chronic poor performance), EIA (influenza), EVA, EIA, AHS (African horse sickness – not in UK yet)

–Parasitic

•Large strongyles, Toxoplasma, Sarcocystis (found in the muscle of many animals)

–(Thromboembolic – due to large strongyles)

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13
Q

What are the bacterial causes of myocarditis? (5)

A
  • Staph aureus
  • Strept equi
  • Clostridium chauvoei
  • Mycobacterium spp
  • Secondary to sepsis, pericarditis, endocarditis
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14
Q

How can you evaluate the myocardium? (3)

A

•Echocardiography

–Assessment of myocardial appearance

•Long and short axis

–Fractional shortening – at rest and following exercise

–NOT TDI!

•Tissue doppler imaging

–Strain and strain rate

  • Still a research tool
  • LA generally get global dx
  • Dobutamine-atropine stress echocardiography (IV)

–Can evaluate the heart at increasing heart rates

–Mimics what would happen at exercise

–Horse doesn’t necessarily like this

•Myocardial biopsies

–Can now be done standing

–Ultrasound guided

–Biopsy instrument into heart via JV

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15
Q

What cardiomyopathy is present?

A
  • Only DCM reported/ important – LA
  • Subacute or chronic
  • Dilated ventricle

–absence of VHD, congenital malformations, PD

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16
Q

What are the 2 congenital causes of myocardiitis?

A

–Red gene – HF (2-4yrs)

–Curly hair coat – Polled Herefords

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17
Q

What are the toxic causes of myocarditis? (3)

A

–Ionophores – Monensin, Lasolacid, Salinomycin (outbreaks of severe myocarditis leading to significant dysrhythmia)

–Gossypol

–Cassia occidentalis, Phalaris spp

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18
Q

What is this?

A

Short axis of LV (mushroom)

RV wrapped round at top

M mode – drop line down centre of LV – see what heart is doing along a time

IV septum not doing much – normal

Free wall – contributing to heart pumping

Increase HR – septum will do more

19
Q

What do we need to interpret from an ECG?

A

Rate and rhythm

20
Q

Where do you place ECG on horse?

A

Yellow – R apex

Red – ½ up jugular groove

Green and black anywhere you want

DO NOT HAVE LADS ON DIFFERENT SIDES OF HORSE - pull off

21
Q

What is Telemetric/Holter systems and what is it useful for?

A
  • Affordable (£3000) and easy to use – the newest systems can be viewed on a computer whilst the trace is being recorded onto a memory card that can be reviewed at a later date
  • Useful for 24-hour continuous monitoring or for recording ECG’s whilst exercising
  • Small and easily attached to a girth

Place – modified lead system. Order of traffic lights – R, Y, G, B

22
Q

Discuss this ECG (at rest)

A

Base apex lead system
Positive P wave
Negative QRS – not too wide
Positive or negative T – ventricle repolarising
Upside down to what you expect in a dog

23
Q

Discuss this exercise ECG

A

Lots of things you cant see
Galloping – HR 180
Look at R- R intervals – is there a premature beat and does QRS look wide – har to tell!
The QRS here are changing size – the horses heart is moving too and from ECG electrodes – normal horses

24
Q

What is the most common horse physiological dysrhythmia?

A

–2nd degree AV block

•Not sinus dysrhythmia like in the dog – not a normal physiological (unless exercise occasionally). Dogs rate is controlled at SA node. In horses the rate is controlled in the AVN. Atria continue to fire – just don’t conduct through AVN

25
Q

What is going on here?

A

2nd degree AVB – normal
Normal QRS with P and T
Horse then decides after a consistent rate to have a P and no QRS
Physiological – get a PQ interval getting longer and then horses block s
Type 1
Sometimes if in right place you will hear a faint S4 otherwise you hear nothing for 2 r-r intervals

26
Q

What are the most common pathological dysrhytmias? (4)

A

–Atrial fibrillation

–Ventricular tachycardia

–3rd degree AV block (this ECG) more common in donkeys but still rare

–SV and V premature depolarising

27
Q

What causes atrial fibrillation?

A
  • MOST IMPORTANT CARDIAC DYSRHYTHMIA IN THE HORSE
  • Lack of coordinated atrial electrical activity
  • Can be triggered by electrolyte/acid-base imbalances, anaesthetic and drug administration (that causes bradycardia), exercise
  • Rather than taking SAN – AVN. It goes round and round the same housing estate with escaping. Circuits setting off in the atria – wobble like jelly. Chances of it forming these circuits rather than the direct SAN - AVN – high vagal tone, low HR and big atria
28
Q

What is the pathophysiology of atrial fibrillation?

A

•Horses particularly susceptible (esp large ones – TB’s, SB’s, Draught horses, trained). Athletic heart increasing the atria size. Also seen in cattle – reduction in milk yield and being a bit slow. Horses tend to only have CS at exercise (and only if they need their cardiac reserve)

–Large atrial mass (more likely when enlarged with disease – MR/TR)

–High vagal tone and low heart rate

•No effect upon cardiac output at rest, only when exercised as atrial contraction only contributes 25% of CO

29
Q

What are the clinical signs of atrial fibrillation? (7)

A
  • None- most of the time
  • Exercise intolerance/poor performance – eventers, race, hunt
  • Epistaxis

–dramatic

–Long R – R intervals – Increased pulmonary pressure and then develop EIPH

  • Weakness/syncope
  • Myopathy
  • Colic

–Electrolyte derangements

  • CHF
  • Cattle - primary GI disease (also foot rot and pneumonia). See anorexia and dec milk production

–RDA

30
Q

What are the 2 forms of AF?

A

•Paroxysmal – lasts less than 24-48 hrs and spontaneously convert

–Sometimes associated with K+ depletion (Furosemide- used in ROW prior to racing) and administration of bicarbonate. May be able to control with diet

–Can get with exercise or competition – hard to diagnose as everytime you see them they are normal

•Sustained

31
Q

What is seen on physical exam of AF? (3)

A

•Irregularly irregular rhythm

–Becomes less irregular with chronicity

•HR and pulse quality varies in intensity

–Booming S1 on auscultation

–Normally have an audible S3

–NO S4- active atrial contraction

•Helps distinguish from other dysrhythmias

–Usually normal or decreased HR; occ increased and will be increased if associated HF

•Abnormally high heart rates at exercise – to counteract the CO (idioventicular responses)

–Can be associated with VPD’s at exercise

–Should perform exercising ECG’s on these animals; to understand if safe for riding

32
Q

How can we diagnose AF? (3)

A
  • Auscultation and physical examination
  • Resting ECG

–No p wave

–Normal qrs complex and t waves

–f (fibrillation) waves – wobbling baseling

•Further diagnostics PRIOR to attempting treatment (don’t need to treat them all):

–Assessment of electrolytes and acid-base abnormalities

–Echocardiography to assess for underlying cause/chamber enlargement

–Exercising ECG

33
Q

Discuss this ECG

A

Atrial fib

Normal QRST

Instead of P with QRS

Have F waves along baseline

Variable R - R

34
Q

What are the treatment options for AF? (3)

A
  1. Nothing
  2. Quinidine sulphate (Quinidine gluconate
  3. DC Cardioversion (equiv of paddles on ER)
35
Q

How does Quinidine work?

Why do we need to take care?

A

–Negative inotrope

–Many untoward side effects

  • Fatal dysrhythmias
  • Colitis – drug very irritant to mucosa and ulcers
  • Laminitis (not too common) /nasal oedema (nearly all get this)/ataxia

–Use with caution – WARN owner and get signed consent

  • Need repeated physical examinations
  • Auscultation
  • Continuous ECG monitoring (at time and for 24hrs after)

–First signs of toxicity – wide QRS

-Check acid-base and electrolytes prior to treatment

36
Q

How does DC cardioversion work?

A

–2 Wires into heart of anaesthetised horse via jugular vein – one just in RA, other through ride side and into PA. Shock the heart – want to restart this route

–Positioned using ultrasound and radiography

–Increased current to try and stop heart and convert to sinus rhythm

37
Q

When do you shock for DV cardioverision?

A

Shock on QRS

(DO NOT SHOCK ON T = VENTRICULAR FIBRILLATION)

38
Q

What is the prognosis of AF?

For: Paroxysmal, sustained no cardiac dx, sustain underlying dx, sustained HF?

A
  • Paroxsymal – excellent to good – unless keeps recurring
  • Sustained, no underlying cardiac disease (e.g. valvular). Cardioconver 80%

–< 3months – good either technique

–>3 months – better with DC conversion

–Risk of re-fibrillation – risk factors there

•Sustained, underlying cardiac disease (mitral and tricuspid regurgitation)

–Average with DC conversion

–More likely to re-fibrillate than category above

•Sustained, heart failure – DO NOT CARDIOCONVERT

–Poor to grave

39
Q

Other than AF what other dysrhythmias do horses get? (4)

A
  • APD’s
  • VPD’s
  • VT
  • Third degree AV block

Note:

•RHYTHMS NOT COMPATIBLE WITH LIFE

–Asystole

–VF – unusual in horses

40
Q

12 year old TB National Hunt horse

  • Destined to run in the Gold Cup this season
  • Pulled up this am lethargic and performing poorly on the gallops. OK yesterday
  • Has a IV/VI holosystolic band-shaped murmur PMI LICS 5 that radiates widely (cranioventrally) and an irregular rhythm

What has thh horse got?

A

•MITRAL REGURGITATION and irregular rhythm

Not regular

No P for every QRS

Atrial fib

W and B – funky T wave = ventricular ectopic (may or may not be a problem – depend on exercise ECG)

Needs cardiovert

41
Q
  • Yearling TB gelding presented with signs of colic
  • Castrated 5 days ago
  • HR 100 BPM
  • No obvious GI abnormalities
  • Appears normovolaemic

What is going on?

A

False colic

No P for every QRS

W + B

Largely the same

Monomoprhic TC

Treated with MG – didn’t do mch

Given lidocaine and decreased (given by infusion)

Developed VT and then died

Had huge fibrosis through septum

42
Q
  • 12 year old International Showjumper
  • Murmur and dysrhythmia noted prior to sedation
  • No effects upon performance
A

Artefacts - skin twitch from clips

Underlying AF

43
Q

What is seen on this exercise ECG?

A

W + B RT complexes

Ventricular premature depolarisation

Risk turning VT then VF

Then dropped dead in a field

Equine Final Year (102 decks)

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