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Module 15 > Equine Dysrhythmias: Detection, Diagnosis, Management > Flashcards

Equine Dysrhythmias: Detection, Diagnosis, Management Flashcards

1
Q

What are the heart sounds

A

S1: lub

S2: dup

S3: de

S4: lu

S4-S1-S2-S3

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2
Q

what is the cause of S4

A

atrial contraction

active ventricular filling with increase in atrial pressure

semilunar valve closed

this phase (S4) is followed by closure of mitral and tricuspid valve S1

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3
Q

what causes S1

A

AV valve closure occurs after rapid ventricular filling

ventricular contraction with increase in ventricular pressure is then followed by raised arterial pressure and reduced ventricular volume

semilunar valve closes directly after this contraction (S2)

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4
Q

what causes S2

A

semilunar valves close after ventricular contraction

deceleration of blood in the great vessels, and retrogradal flow against the valves creates the second heart sound

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5
Q

what causes S3

A

ventricular filling sound

there is passive filling of the ventricles as atrial pressure exceeds ventricular pressure, and deceleration of this blood results in S3

ventricle volume increases in this phase

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6
Q

what are the most common non pathological dysrhythmias (5)

A
  1. second degree AV block
  2. sinus block
  3. sinus arrhythmia
  4. atrial premature contractions
  5. ventricular premature contractions
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7
Q

which dysrhythmias should disappear with exercise or adrenaline

A
  1. second degree AV block
  2. sinus block
  3. sinus arrhythmia
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8
Q

what are bradyarrhythmias that are pathological

A
  1. third degree AV block
  2. sinus bradycardia
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9
Q

what are pathological dysrhythmias that occur with normal heart rate (3)

A
  1. atrial fibrillation
  2. atrial premature contractions
  3. ventricular premature contractions
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10
Q

what are tachyarhythmias

A
  1. AF, APCs or VPCs
  2. ventricular tachycardia
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11
Q

what should you observe on an ECG

A
  1. R-R interval: is it regular?
  2. paper speed to calculate HR
  3. look at P waves and QRS complexes, are they matched? is there a P wave for every QRS? is there a QRS complex for every P wave?
  4. are the P waves and T waves similar morphology?
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12
Q

what sounds occur during the P wave

A

S4

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13
Q

what sounds occur during the R wave

A

S1

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14
Q

what sounds occur during the T wave

A

S2

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15
Q

what is second degree atrioventricular block (mobitz type 2)

A

AV node blocks the impulses from progressing through the purkinje fibres and depolarizing the ventricles

it is normal for fit horses with high vagal tone

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16
Q

what rhythm is this

A

second degree AV block – mobitz type 2

AV node blocks the impulses from progressing through the purkinje fibres and depolarizing the ventricles

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17
Q

what rhythm is this

A

sinoatrial block

heard in horses with slow resting HR

complete pause where the isn’t SA node depolarization

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18
Q

what causes advanced second degree AVB or 3rd degree AVB

A
  1. electrolyte imbalances
  2. digitalis toxicity
  3. AV nodal disease (inflammatory, degenerative)
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19
Q

how is adavanced second degree AVB/3rd degree AVB treated

A

correct underlying cause

pacemaker

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20
Q

what is shown here

20 yo pony, showing collapse after competition over 3 month period

after atropine shown an AV block and abnormal QRS-T complex

A

sick sinus sydrome

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21
Q

what is shown here

A

3rd degree atrioventricular block

not a normal contraction between atrium and ventricles

massive reduction in CO and will be susceptible to low BP and collapse

22
Q

what are ventricular premature contractions/depolarizations

A

are extra, abnormal heartbeats that begin in the ventricles, or lower pumping chambers, and disrupt regular heart rhythm

23
Q

what rhythm is shown here

A

normal rate, abnormal rhythm

ventricular premature contractions/depolarizations (ectopic beats)

normal QRS with inverted morphology arising from a ventricular focus

24
Q

how do you investigate isolated ectopic beats

A
  1. serum electrolytes: Ca, Mg, Na, K, Cl
  2. markers of cardiac inflammation (cTnl)
  3. acute phase protein markers, white cell differential count
  4. 24h ECG monitoring to determine frequency
25
Q

how do you treat isolated ectopic beats

A
  1. correct electrolyte disturbances & investigate underlying cause
  2. ? corticosteroids if evidence of inflammatory focus
  3. pheytoin for treatment of VPCs
  4. rest
26
Q

what are tachydysrhythmias

A
  1. atrial fibrillation
  2. APCs/VPCs
  3. ventricular tachycardia
27
Q

what is atrial fibrillation

A

irregularly irregular pulse, which may be low, normal or high in rate

no detectable S4 in prolonged pauses

28
Q

what is typically present with atrial fibrillation

A

variable systolic murmur frequently present

variable jugular pulse wave-form

29
Q

what is the etiology of atrial fibrillation

A
  1. large atria
  2. high vagal tone
30
Q

how does a large atria cause atrial fibrillation

A

circadian movement of impulses

wave of depolarization meets atrial myocytes that have already repolarized allowing continuation of contraction

activity blocked at the AV node, resulting in atrial fibrillation without ventricular response

loss of coordination between AV and SA node

31
Q

how does high vagal tone cause atrial fibrillation

A

different duration of refractory period in different cells

32
Q

what are the cardiovascular effects of atrial fibrillation (4)

A

usually no clinical signs at rest

  1. decreased ventricular filling at exercise (atrial contraction contributes to last 1/3 of ventricular filling)
  2. decreased force of ventricular contraction
  3. increased heart rate at exercise compared to horse without AF to compensate for decreased stroke volume
  4. owner may report horse to be lethargic or to have prolonged recovery after exercise. Depending on work of horse, AF may be noted incidentally on clincal exam
33
Q

what rhythm is shown here

A

atrial fibrillation

irregular RR intervals

long pauses before there is QRS complexes

fibrillation waves, no normal P waves

34
Q

what rhythm is shown

A

atrial fibrillation

variable pauses between heart beats (up to 6-7s pauses before QRS comes in)

fibrillation wave

irregular RR interval

35
Q

how do you determine whether or not an AF is a candidate for cardioversion (9)

A
  1. is there underlying heart disease
  2. duration of dysrhythmia (more likely to convert if <6 weeks in AF)
  3. type of work required? is maximal CO required?
  4. cost
  5. side-effects
  6. poor prognosis if pathological murmur (esp MR) with volume overload
  7. prev unsuccessful treatment
  8. heart rate > 55 bpm
  9. more likely to revert to AF if there is chamber enlargement
36
Q

what is used during cardioversion therapy

A

quinidine sulphate 22 mg/kg per os at 2h intervals

37
Q

how is atrial fibrillation treated

A

titrated quinidine sulphate

38
Q

what are the side effects of quinidine sulphate (3)

A

1. vagolytic agent: supraventricular tachycardia may result from loss of AV node blockade of atrial impulses

2. prolongs action potential: ventricular tachycardia is more serious side effect, which can be fatal if not addressed

3. alpha adrenoceptor antagonist: vasodilation, hypotension –> can cause collapse if already in congestive heart failure

39
Q

what are common signs of quinidine sulphate toxicity

A
  1. depression, colic, diarrhea
  2. muzzle swelling
40
Q

what are serious side effects of quinidine sulphate

A
  1. marked supraventricular tachycardia (100-120 bpm)
  2. severe colic
  3. weakness
  4. laminitis
  5. hypotension and collapse
  6. sudden death –> most likely due to severe ventricular tachycardia
41
Q

how is quinidine sulphate toxicity managed

A
  1. stop dosing
  2. mineral oil given via NG tube to decrease absorption
  3. sodium bicarbonate protein binding and reduce availability of QS
42
Q

how do you manage serious cardiac side effects from quinidine sulphate (5)

A
  1. lignocaine infusion to reduce ventricular response rate if >100 bpm
  2. digoxin IV to decrease tachycardia
  3. MgSO4 infusion if torsades de pointes develops
  4. shock fluids
  5. absolute rest
43
Q

what is torsades de pointes

A

prolonged QT and ventricular tachycardia

treated by magnesium sulphate bolus injections of 4 mg/kg every 2 minutes –> blocks calcium channels

44
Q

what rhythm is shown

A

torsades de pointes

45
Q

what is transvenous electrical cardioversion

A

catheters placed in RA and left PA

synchronous electrical shock delivered, timed to QRS complex

46
Q

when do ventricular ectopic beats become a problem

A

if the HR is above 100 bpm

if R-on-T phenomenon is present

47
Q

what is shown here

A

ventricular ectopic beats

48
Q

what rhythm is shown here

A

ventricular tachycardia

ventricular ectopic beats with HR over 100

49
Q

how is ventricular tachydysrhythmias treated

A

procainamide infusion at 1 mg/kg/min

avoid quinidine gluconate if concurrent hypotensive cardiac output failure

lignocaine infusion (20-50 mcg/kg/min IV)

consider MgSO4 infusion if VT refractory to treatment

50
Q

what can cause ventricular tachydysrhythmias (4)

A
  1. myocardial hypoxia
  2. electrolyte derangement
  3. myocardial inflammation
  4. secondary to endotoxemia
51
Q

how is equine myocarditis diagnosed

A
  1. clinical pathology
  2. echocardiography
  3. assay for cardiac troponin I myocardial polypeptide

may follow viral finection such as equine influenza

52
Q

how is equine myocarditis treated

A
  1. acute anti-dysrhythmic theray
  2. dexamethasone if non life-threatening ventricular tachycardia
  3. pasture rest

dependent on HR and clinical picture

Module 15 (27 decks)

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