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Equine BCM Lecture > Equine Heart Dzs > Flashcards

Equine Heart Dzs Flashcards

1
Q

What electrolyte channels open during phase 0 of a cardiac action potential?

A

(Sodium voltage gated channels)

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2
Q

What electrolyte channels opened and closed during phase 1 of a cardiac action potential?

A

(Sodium close, potassium open)

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3
Q

Calcium channels are open/closed (choose) and potassium channels are open/closed (choose) during phase 3 of a cardiac action potential?

A

(Calcium channels are closed, and potassium channels are open)

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4
Q

Where does electrical activity in the heart start?

A

(Sinoatrial node)

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5
Q

Depolarization of which part of the heart is represented by the P wave in an ECG wave?

A

(Atrial depolarization)

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6
Q

Depolarization of the ventricles is indicated by what portion of an ECG wave?

A

(QRS complex)

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7
Q

Repolarization of the ventricles is indicated by what portion of an ECG wave?

A

(T wave)

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8
Q

Describe the placements of the ECG leads in a lead I base-apex ECG, be specific.

A

(White is placed at the point of the shoulder on the right side of the animal, black is placed in the axilla on the left side of the animal (at the apex of the heart), and red can be placed anywhere on the left side of the animal)

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9
Q

What should you evaluate when looking at an ECG of an animal?

A

(Heart rate, RR interval, P and QRS relationship (P before every QRS? Normal PR interval?), and complex morphology)

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10
Q

(T/F) It is normal for the P wave to be biphasic in a horse as long as it shows consistency.

A

(T, bc the atrium is large and it can take awhile for the entire atrium to depolarize)

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11
Q

A horse is considered to be in sinus tachycardia when their heart rate is above what value?

A

(50 bpm)

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12
Q

How can you determine if a bradyarrhythmia is caused by high parasympathetic tone?

A

(Exercise the horse to increase sympathetic tone, if its gone then it was physiologic, if it is still present it is pathologic)

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13
Q

Describe a sinus arrhythmia.

A

(Variable RR interval, each QRS is normal and preceded by a P wave, and the pauses are less than or equal to two normal P-P intervals)

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14
Q

What is the most common non-pathologic cardiac arrhythmia in horses?

A

(2nd degree AV block)

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15
Q

What is the difference between a 2nd degree AV block and an advanced 2nd degree AV block?

A

(2nd degree AV block is an occasional P wave not followed by a QRS wave, advanced 2nd degree AV block is two or more P waves not followed by a QRS complex; important to note that ALL QRS complexes are preceded by a P wave in these abnormal ECGs)

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16
Q

Describe a 3rd degree AV block.

A

(P waves present but have no association with QRS complexes, QRS complexes are wider with an irregular R-R interval)

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17
Q

What is the difference between 2nd degree AV blocks and premature atrial complexes?

A

1) the heart rate, will be slow with 2nd degree AV blocks and fast with premature atrial complexes

2) the pathology, 2nd degree AV blocks are normal SA node depolarizations that just don’t trigger the AV node and ventricles whereas premature atrial complexes are when sites of the atrium besides the SA node depolarize spontaneously, which can then trigger or not trigger the ventricles as well)

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18
Q

What is the most common pathologic arrhythmia in horses?

A

(Afib)

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19
Q

(T/F) All of the appropriate waves (P, QRS, and T) will be present on an ECG of a horse with atrial fibrillation, the P waves will just be at a much higher rate and will not be associated with QRS complexes.

A

(F, there will be a lack of P waves, this is the hallmark of Afib)

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20
Q

What structural heart disease is thought to be associated with atrial fibrillation in horses?

A

(Progressive atrial enlargement → as the larger the atria become, the less organize the electrical activity is thought to be; only issue is some horses without structural heart dz have afib so true etiology is unknown atm)

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21
Q

What electrolyte deficiency is thought to be associated with atrial fibrillation in horses?

A

(Hypokalemia)

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22
Q

What endocrine disorder is thought to be associated with atrial fibrillation in horses?

A

(Hyperthyroidism)

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23
Q

What things will affect the prognosis of conversion to NSR and maintenance of NSR in horses with afib?

A

(The duration of which they have had afib and heart size)

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24
Q

Why do horses with afib have suboptimal cardiac output?

A

(They lack atrial contribution to ventricular filling, leads to the development of exercise intolerance and increased heart rate (>220 bpm) to compensate for decreased cardiac output)

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25
Q

What other arrhythmia can result from the decreased cardiac output and decreased cardiac muscle oxygenation associated with afib in racehorses?

A

(Premature ventricular complexes)

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26
Q

What medical therapy can be used to convert horses in afib to NSR?

A

(Quinidine sulfate → sodium channel blocker that also affects potassium channels, prolongs the refractory period and slows action potential conduction)

27
Q

The progressively increased shocks applied for transvenous electrocardioversion must be delivered precisely on which wave of the ECG complex?

A

(The R wave)

28
Q

What are premature ventricular complexes and what are they associated with (aka what causes them but they don’t want to say cause because they haven’t proven it)?

A

(VPCs are premature, abnormal QRS complexes that are not preceded by a P wave, they are associated with colic, electrolyte abnormalities, myocarditis, and exercise)

29
Q

Ventricular tachycardia is considered how many or more PVCs in a row?

A

(3 or more PVCs in a row)

30
Q

Is uniform or multiform ventricular ectopy worse?

A

(Multiform; uniform is when all QRS complexes look the same (still abnormal but they are all at least similarly abnormal, this means they are sourced from the same location), multiform is when there are different types of QRS complexes, this means there are multiple portions of the ventricles sending out electrical impulses and if two were to go at the same time, bye bye life)

31
Q

Pair the following class of antiarrhythmic drug to 1) the type of blocker it is and 2) the phase it works on:

Class I

Potassium channel blockers
Beta blockers
Calcium channel blockers
Sodium channel blockers

Phase 0
Phase 1/3
Phase 2
Phase 4

A

(Phase 0, sodium channel blockers → lidocaine, quinidine)

32
Q

Pair the following class of antiarrhythmic drug to 1) the type of blocker it is and 2) the phase it works on:

Class II

Potassium channel blockers
Beta blockers
Calcium channel blockers
Sodium channel blockers

Phase 0
Phase 1/3
Phase 2
Phase 4

A

(Phase 4, beta blockers → sotalol)

33
Q

Pair the following class of antiarrhythmic drug to 1) the type of blocker it is and 2) the phase it works on:

Class III

Potassium channel blockers
Beta blockers
Calcium channel blockers
Sodium channel blockers

Phase 0
Phase 1/3
Phase 2
Phase 4

A

(Phase 1/3, potassium channel blockers → sotalol)

34
Q

Pair the following class of antiarrhythmic drug to 1) the type of blocker it is and 2) the phase it works on:

Class IV

Potassium channel blockers
Beta blockers
Calcium channel blockers
Sodium channel blockers

Phase 0
Phase 1/3
Phase 2
Phase 4

A

(Phase 2, calcium channel blockers → magnesium sulphate is a physiologic calcium channel blocker)

35
Q

What is the treatment of choice for torsades de pointes and digitalis toxicity?

A

(Magnesium sulphate)

36
Q

What is the difference between innocent, functional, and pathologic murmurs?

A

(Innocent and functional occur in the absence of structural cardiac disease, pathologic is associated with structural cardiac dz; innocent associated with an unknown origin, functional occurs with dehydration, colic, fever → resolves when you resolve the inciting cause)

37
Q

Decrescendo murmurs are classic for which heart pathology?

A

(Aortic regurgitation)

38
Q

You hear a murmur between S1 and S2 on the left side of a horse, what is most likely to be the problem?

A

(Mitral valve regurgitation → most common left sided systolic murmur in horses)

39
Q

You hear a murmur between S1 and S2 on the right side of a horse, what is most likely to be the problem?

A

(Tricuspid valve regurgitation → most common right sided systolic murmur in horses)

40
Q

You hear a murmur between S2 and S1 on the left side of a horse, what is most likely to be the problem?

A

(Aortic valve regurgitation → most common left sided diastolic murmur in horses)

41
Q

What are the causes of mitral regurgitation?

A

(Valvular dysplasia, degenerative thickening of the leaves, ruptured chordae tendineae, and endocarditis)

42
Q

Regurgitation at which valve is the most common cause of congestive heart failure in horses?

A

(Mitral, but mild MR is associated with a normal athletic performance and life expectancy so monitoring is extremely important bc it can progress to CHF, cardiac u/s annually)

43
Q

What are the causes of aortic regurgitation in horses?

A

(Age related valvular degeneration or valvular prolapse)

44
Q

Why is tricuspid regurgitation a common finding in equine athletes?

A

(Bc as they exercise regularly, the right side of the heart becomes more robust and muscular which can cause tricuspid regurg)

45
Q

What are the goals for treatment of valvular regurg?

A

(Decrease cardiac work by decreasing afterload (by decreasing systemic vascular resistance), slow progression of cardiac chamber enlargement, and improve cardiac contractility)

46
Q

What type of drug is benazepril and what does it do for the heart?

A

(ACE inhibitor, decreased afterload, improves systolic function and cardiac output, and slows cardiac remodeling via an unknown mechanism)

47
Q

What type of drug is digoxin and what does it do for the heart?

A

(Cardiac glycoside, increases parasympathetic tone therefore reducing vasoconstriction and slowing the heart rate which helps to improve stroke volume (lower heart rate allows for greater diastolic filling which increases end-diastolic volume which increases stroke volume (stroke volume = end-diastolic volume minus end-systolic volume))

48
Q

What is the most common congenital cardiac anomaly in horses?

A

(Ventricular septal defects)

49
Q

What is the normal flow of blood through a PDA, what can cause it to reverse, and what results from the reversal?

A

(Normal flow → aorta to pulmonary artery; causes of reversal → if defect is large and/or chronic and if pulmonary hypertension is present; results of reversal → cyanosis +/- syncope)

50
Q

What are the characteristics of a restrictive ventricular septal defect that is associated with a good prognosis for athleticism?

A

(Size of less than 2.8 cm and a shunt speed of faster than 4 m/s (indicates normal pressure differential b/w right and left heart))

51
Q

How do horses with infective endocarditis commonly present,what might you find clinpath wise, and what might you find on an ECG?

A

(Fever, weight loss, inflammatory leukogram with hyperfibrinogenemia and hyperglobulinemia, and may have concurrent arrhythmias)

52
Q

What are the three types of pericarditis?

A

(Effusive, fibrinous, and constrictive)

53
Q

What clinical signs result from cardiac tamponade, which can occur in horses with constrictive pericarditis?

A

(Increased heart and resp rate, increased jugular pulses, weak arterial pulses, and ventral edema)

54
Q

What would you look for on a CBC in a horse with pericarditis to indicate infection versus idiopathic/neoplastic?

A

(Leukocytosis and increased acute phase proteins (SAA, fibrinogen) would indicate infection)

55
Q

What diagnostic imaging modality is best for cases of pericarditis?

A

(Ultrasound → look for fluid/fibrin in the pericardial space)

56
Q

What is the purpose of submitting blood for a cardiac troponin test?

A

(cTNI is a marker for myocardial damage, will help to guide therapy depending on severity of damage to the heart)

57
Q

What are the normal values for protein and TNCC for pericardial fluid?

A

(Protein < 2.5 g/dL, TNCC < 1500 x 10^6/L)

58
Q

Describe the difference between the pericardial fluid in an idiopathic versus bacterial pericarditis case.

A

(Idiopathic → increased protein and non-degenerate neutrophils; bacterial → degenerate neutrophils, may see bacteria)

59
Q

What are the most common toxic causes of myocarditis in horses?

A

(Cardiac glycoside plants specifically oleander, cantharidin formed by blister beetles, and ionophores such as monensin or lasalocid)

60
Q

What deficiency is associated with nutritional myodegeneration?

A

(Vitamin E and/or selenium deficiency, both help to protect cells against free radicals, chronic deficiencies lead to fibrosis of muscles that are constantly in work i.e. heart, prognosis is guarded but some can improve with tx)

61
Q

Why is an ECG and echocardiogram indicated in myocarditis cases?

A

(ECG to identify cardiac arrhythmias, echo to image the myocardium and calculate fractional shortening to get information about cardiac output)

62
Q

Fractional shortening that persists over a few weeks at what percent or lower in cases of myocarditis indicate a poorer prognosis?

A

(20%, normal is 30-45%)

63
Q

What are the clinical signs associated with aortic rupture?

A

(Besides per acute death? Colic, tachycardia, sweating, and a continuous murmur, all shortly followed by death)

Equine BCM Lecture (16 decks)

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