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LAM 1 > Equine Cardiology > Flashcards

Equine Cardiology Flashcards

1
Q

What heart sounds can be heard in a normal equine heart?

A

Two to four can be heart in a normal equine heart

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2
Q

What is a gallop rhyth?

A

Three seperate beats heard

Typically this is pathological but can be normal in the horse

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3
Q

What are the two most important tests for evaluating an equine heart?

A

Ascultation and ultrasound

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4
Q

Why is radiology unhelpful?

A

The normal equine heart is usually too big to get an accurate picture of

Smaller foals you may be able to get a good picture of

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5
Q

Why is ECG less useful in the horse than in other animals?

A

The purkinje fiber arrangement is not linear in the horse making vector analysis less accurate

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6
Q

How does the depolarization work in a horse?

A

Depolarize more in a wringing motion so the heart twists from the apex to the base as opposed to a linear motion

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7
Q

Which lead position is the most helpful in equine patients and why?

A

Lead 1 since you are able to maximize focus on the ventricular septum

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8
Q

Where are the leads placed typically in the horse?

A

Left arm at the thorax at the 5th ICS at the level of the elboy and right arm at the jugular furrow

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9
Q

T/F: ECG is an effective test to assess chamber enlargement.

A

False- horse hearts depolarize weirdly so vector analysis isn’t accurate

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10
Q

How do P-waves typically appear in a horse?

A

Biphasic

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11
Q

How do QRS complexes typically appear in a horse?

A

negative deflection due to intraventricular septum depolarization

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12
Q

How do T-waves typically appear in a horse?

A

Large and spiked due to repolarization of a lot of myocardium at once

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13
Q

What areas are you able to feel a jugular pulse in a normal horse?

A

No higher than the junction of the middle and distal third of the neck and with the the head in neutral carriage position

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14
Q

If you are able to feel pulses in places other than normal, what are they most likely due to?

A

Valvular insufficiency causing blood to regurgitate back into the cranial vena cava and jugular veins

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15
Q

What is the most common physiologic arrhythmia in the horse?

A

2nd degree Mobitz type 1 AV block

aka Wenkenbach

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16
Q

Why can horses have a normal Wenkenbach arrhythmia?

A

Persistent high vagal tone so any changes in it cause issues in communication between AV and SA node

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17
Q

How does 2nd degree Mobitz type 1 AV block appear on an ECG?

A

Progressive prolongation of the PR interval until there is a drop in regular beat pattern

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18
Q

Why do horses typically not present with sinus arrhythmias?

A

Because sinus arrhythmias are caused by decreased vagal tone and horses live at a really high vagal tone normally

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19
Q

What is the most common pathological arrhythmia in the horse?

A

Atrial fibrillation

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20
Q

Why is a-fib common in horses?

A

Due to increased cardiac size and high vagal tone

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21
Q

Why does a-fib occur?

A

The atria are not synchronized exactly and will not be at the same phase of polarization

Typically this isn’t an issue in a normal horse but can be detrimental to an athlete

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22
Q

What are the two kinds of a-fib that can manifest in the horse?

A

Paroxysmal and sustained

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23
Q

What is paroxysmal a-fib?

A

Single episode of a-fib causing poor performance during periods of high heart rate

Very easy to miss

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24
Q

What is sustained a-fib?

A

Go into a-fib and stay in it

Much easier to diagnose and not necessarily associated with high heart rate

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25
Q

T/F: Most a-fib cases are associated with underlying cardiac pathology.

A

False- usually have nothing else wrong

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26
Q

T/F: Presence of a systemic abnormality predisposes animals to a-fib.

A

True- especially electrolyte abnormalities

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27
Q

What are the clinical signs of a-fib?

A

Exercise intolerance and poor performance

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28
Q

What are some systemic underlying causes of a-fib?

A
  • EIPH
  • Myopathies
  • Colic
  • Collapse
  • CHF
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29
Q

What will a-fib sound like on auscultation?

A

Irregularly irregular

Tennis shoes in a dryer

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30
Q

What will pulses feel like with a-fib?

A

Variable strength with longer or shorter period due to erratic ventricular contraction and polarization

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31
Q

What do you look for on standard work ups to help diagnose any underlying causes of a-fib?

A

UA- fractional excretion

Blood- cardiac troponin-1 to assess for cardiac disease

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32
Q

What test is done to confirm a-fib?

A

ECG

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33
Q

What should be done to assess functionality of the heart in horses with a-fib?

A

Echocardiography to assess fractional shortening and diameter of chambers

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34
Q

What does treatment of a-fib depend on?

A

Heart rate and ultrasound foundings

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35
Q

What is the best case senario for treatment of a-fib?

A

Resolution spontaneously when not exercising

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36
Q

How do you treat an animal with a-fib with normal PE, HR

A

Quinidine PO

Can get complications if given IV

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37
Q

How do you treat an animal with a-fib with normal PE, HR>60bpm, and normal echo?

A

Digoxin first then quinidine

Digoxin first so that you bring the HR down to 60 then give quinidine

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38
Q

Why do you want to give digoxin prior to quinidine in higher HR with a-fib patients?

A

Quinidine is arrhythmogenic especially at higher heart rates

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39
Q

What qualifies as a complicated case of a-fib in a horse?

A

A-fib with underlying cardiac disease

Abnormal PE and abnormal echo

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40
Q

What is used to treat complicated cases of a-fib?

A

Digoxin and quinidine

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41
Q

What are the issues with quinidine in complicated a-fib cases?

A

Pro: maximizes cardiact output
Con: reduced efficacy due to underlying disease

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42
Q

T/F: Treatment often is not effective in complicated cases of a-fib.

A

True- not much you can do

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43
Q

What are some alternative therapies for treating a-fib?

A

Electrocardioversion or transvenous electrocardioversion- has to be under GA

No difference in long therm prognosis with electrical or chemical cardioversion

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44
Q

What is the most common issue with using digoxin and quinidine in the same animal?

A

Both highly protein bound so there is displacement when administering them at the same time which can lead to toxic levels free in circulation

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45
Q

What NSAID can also lead to protein binding issues in horses on digoxin/quinidine therapy?

A

Phenylbutazone

46
Q

What are some signs of quinidine toxicity?

A

GIT, neurologic behavior signs, cardiac signs, some idiosyncratic reactions

47
Q

What cardiac signs can be seen with quinidine toxicity?

A

Widening of QRS (~25%)

Can be prevented with dosage adjustment and regular ecg monitoring

48
Q

What is an idiosyncratic reaction associated with quinidine in the horse?

A

Rapid supraventricular tachycardia

Prevent by giving a test dosage of quinidine prior to starting on therapeutic regimen

49
Q

What is the test dosage typically given for quinidine?

A

5mg via nasogastric tube, recheck ecg 1 hours later then increase by 10g and check again

50
Q

How to do treat rapid supraventricular tachycardia associated with idiosyncratic quinidine reaction in the horse?

A

Digoxin and sodium bicarb

51
Q

What is the prognosis of a-fib in horses in general?

A

95% conversion rate

52
Q

What is the prognosis of a-fib in horses with an HR

A

With a murmur of 1-3/6 and

53
Q

What is the prognosis if there is a long duration of a-fib or concurrent cardiac disease?

A

80% conversion rate with 60% recurrence

Long term prognosis doesn’t change

54
Q

What are ventricular premature contractions typically associated with in horses?

A

Metabolic disease

55
Q

What are some potential causes for VPCs in horses?

A
  • Electrolyte abnormalities
  • Endotoxemia
  • Myocardial Inflammation (strangles or influenza)
  • Hypoxia
56
Q

How do you treat VPCs in horses?

A
  • Treat underlying disease

- Lidocaine (bolus or CRI drip)

57
Q

What are the grades of physiologic murmurs in the equine heart?

A

Grade 3-4 left heart base systolic ejection murmor

58
Q

What are physiologic murmurs created y?

A
  • Reverberation of the great vessels

- Changes in viscosity like anemia or dehydration

59
Q

How do you definitely differentiate physiological from pathological murmurs?

A

Ultrasound

60
Q

What percentage of horses will have physiologic murmurs?

A

66%

Associated with rapid ejection of blood in early systole

61
Q

T/F: Congenital cardiac murmurs are common in the horse and are typically extremely pathological.

A

False- they are very uncommon and typically only apparent when exercising the animal

62
Q

What are the two most common congenital murmurs in the horse?

A

VSD ( most common) and PDA

63
Q

What are the characteristics of VSDs?

A

Typically incidental but can impact performance

usually 3-4/6 coarse band shaped pan-systolic murmur

64
Q

What are the characteristics of PDAs?

A

3-4/6 continuous machinery murmur over left heart base

65
Q

What are the clinical signs of mitral valve insufficiency?

A

Variable depending on severity of dysfunction and purpose of the horse

Mild: Exercise intolerance
Severe: Sudden death, cordae tendinae rupture, acute decompensation and failure

66
Q

T/F: Mitral insufficiency is the most likely valve dysfunction to lead to cardiac failure.

A

True

67
Q

What is the typical pathophysiology of mitral insufficiency?

A

Degenerative or inflammatory lesion

68
Q

What are typical findings of mitral insufficiency?

A

Grade 3 holosystolic or pan systolic band-shaped left 5th ICS murmur

69
Q

What are complications associated with mitral insufficiency?

A
  1. Sudden death
  2. Cordae tendinae rupture
  3. Pulmonary artery rupture (death)
70
Q

What is the prognosis of mitral insufficiency?

A

Prognosis worse for younger horses and athletes

71
Q

How do you monitor mitral insufficiency?

A

Re-echo every 3 to 9 months to check progression

72
Q

What kind of horses typically present with aortic insufficiency?

A

Older horses

If seen in younger is a cause for concern

73
Q

What are the clinical signs of aortic insufficiency?

A

Often incidental associated with degeneration of the aortic valve (nodules, fibrous bands, plaques)

2-4/6 pan- holo- or early diastolic decrescendo left PMI 4th ICS Murmur loudest on the left but can be heard on right

74
Q

What are some complications of aortic insufficiency?

A

Heart failure and aortic rupture

75
Q

T/F: Vegetative and inflammatory valve diseases carry a better prognosis than degenerative ones.

A

False- carry a worse prognosis

76
Q

T/F: Left sided overload has a poor prognosis especially if it is progressive.

A

True

77
Q

Tricupid insufficiency, all the things

A

Thoroughbreds are increased risk
Typically only see exercise intolerance

Diagnosis: Right sided holo/pan-systolic murmur that radiates concentrically from PMI over tricuspid valve

78
Q

What is the typical signalment of a vegetative endocarditis horse?

A

Most often

79
Q

What is the pathogenesis of vegetative endocarditis?

A

o Endothelial damage
o History of trauma to the endocardium or valve (Polyethylene catheter placed across the valvular surface )
o fibrinous clot formation of vegetation
o Bacteria able to adhere to endothelial damage – need bacteria from circulation
(Subclinical abscesses in the heart or Catheters)
o Local clotting activated

80
Q

What are the clinical signs of vegetative endocarditis?

A

Fever of unknown origin, tachycardia, murmur

Fever typically presenting complaint

81
Q

How do you diagnose vegetative endocarditis?

A

o CBC + Chem: Hyperproteinemia – Hyperglobulinemia with hyperfibrinogenemia, Leukocytosis – mature neutrophilia, Non-regenerative anemia
o Blood Culture
o Echocardiography (ECG)- Detect arrhythmias secondary to myocardial pathology (Most commonly APCs and atrial fibrilation)
o Electrocardiogram

82
Q

What are the common organism isolates of vegetative endocarditis?

A

Strep, Actinobacillus equili, E. coli

83
Q

Are blood cultures always useful for diagnosing vegetative endocarditis?

A

No, commonly come up negative even if present

84
Q

How do you treat vegetative endocarditis?

A

Antimicrobials for 4-6wks (Typically KOen and gentamicin IV)

Flunixin and asprin

85
Q

When should you recheck blood culture?

A

60 days after stopping treatment

Only if primary blood cultures came up positive

86
Q

What are some causes of heart failure in the horse?

A

o Mitral Insufficiency
o Vegetative endocarditis
o Pericarditis
o Toxicities

87
Q

T/F: Heart failure is unusual in horses

A

True

88
Q

What two drugs are cardiotoxic in the horse and what animals are they typically used in?

A
  • Monensin in cattle feed

- Lasalocid in poultry feed

89
Q

What is the typical signalment for pericarditis in the horse?

A

No particular signalment

Food animals typically a result of hardware disease

90
Q

What are the typical causes of pericarditis in a horse?

A

Typically infectious process with concurrent history of respiratory disease

  • Viral respiratory disease
  • Pleuropneumonia
  • Sepsis
91
Q

What are the two types of pericarditis found in the horse?

A

Effusive and constrictive (fibrinous)

92
Q

What kind of fluid is typically found in effusive pericarditis?

A

Transudate

Typically a result of viral respiratory disease

93
Q

What typically causes constrictive pericarditis?

A

Pleuropneumonia cases due to fibrin being laid down on the myocardium

94
Q

What typically causes heart failure in constrictive pericarditis cases?

A

Pre-load issues- cannot acquire enough volume to maintain CO

Typically signs of right heart failure appear first

95
Q

What conditions can cause a mix of constrictive and effusive pericarditis?

A

Pleuropneumonia and sepsis

96
Q

What are some clinical signs of acute pericarditis?

A 
o Ventral edema
o Distended jugular/veins
o Poor pulses
o Weakness
o Listlessness
o Syncope
o Fever

Typical signs of infection

97
Q

What are the CBC and Chem findings in a horse with pericarditis?

A

Anemia, leukocytosis, hyperfibrinogenemia, elevated creatinine, hyponatremia, hyperkalemia, increased CVP

98
Q

When should ECG be used especially in pericarditis cases?

A

When draining pericardial fluid

ECG will go nuts if you accidentally poke the myocardium

99
Q

How do you treat effusive pericarditis?

A

Pericardiocentesis

100
Q

How do you treat constrictive pericarditis?

A

Pericardiocentesis and pericardectomy

Typically done under GA

101
Q

What are two main causes of endo/myocardial lesions?

A

Hypoxia/ischemia and toxins

102
Q

How do you treat heart failure in a horse?

A

Furosemide, Digoxin, Enalaprin, Hydralazine

Just like everything else….

103
Q

What is the history of a horse with suspected ionophore toxicity?

A

Ingestion of cattle or poultry feed

104
Q

What are the clinical signs of ionophore toxicity?

A

o Colic: restlessness, anorexia, profuse sweating
o Reluctance to move, pyrexia, muscle trembling
o Hind limb weakness
o Arrhythmias most likely to develop within first few days to weeks of ingestion

105
Q

What is the typical cause of death with ionophore toxicity?

A

Fatal arrhythmia

106
Q

How long should horses be monitored after recovering from ionophore toxicity?

A

At least a year

107
Q

How do you treat ionophore toxicity in horses?

A

Maybe vit E and Selenium
Nasogastric intubation and activated charcoal administration if recently ingested
Stall rest and balanced electrolyte fluids

108
Q

T/F: Digoxin is contraindicated in monensin toxicosis.

A

True- can cause a massive Ca influx and cause more myocardial necrosis

109
Q

What is prognosis based on with monensin toxicity?

A

Fractional shortening on echo

30-40% good prognosis
10%-20% grave prognosis but will have residual myocardial issues

110
Q

T/F: Myocardial enzymes are not good prognostic indicators for survival or severity of myocardial damage.

A

True

LAM 1 (10 decks)

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