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Cardiology > Large Animal Cardiology > Flashcards

Large Animal Cardiology Flashcards

1
Q

What are the contributing factors to cattle developing Bovine High Mountain Disease or pulmonary hypertension

A

-Genetics
-Pneumonia
-Migrating parasite larva
-high altitude
-poisoinous plants (Locoweeds- oxytropis and astragalus)
-nutrition
-Age
-illness
-body condition
-breed
-gender
-anything that leads to pulmonary hypertesion

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2
Q

What is the pathophysiology of BHMD

A

1) Altitude induced pulmonary hypoxia
2) Pulmonary shunting and vasoconstriction
3) Pulmonary artery hypertrophy
4) Pulmonary hypertension
5) Right ventricular hypertrophy
6) Right Ventricular failure
7) Death

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3
Q

Understand that at the present time the best means to identify those animals at risk for
BHMD:

A

Carry out a PAP measurement and cull those with high scores, i.e. >50mmHg

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4
Q

What is the economical affect that BHMD has on the cattle industry in high elevations:

A

This disease can often cause losses of greater than 5% of the calf crop resulting
in hundreds of thousands of dollars loss per year for the cattlemen in high
elevation. It is most likely the major concern and most costly loss for high
altitude ranchers

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5
Q

What is the use of PAP testing by high altitude ranchers

A

Trying to develop a genetically resistant herd to the effects of high altitude. By
utilizing the PAP test a rancher can use low testing PAP bulls to help minimize
BHMD losses in claves. To really attempt to control losses they may choose to
test all replacement females. This would then allow them to have an entire herd
that is genetically resistant to the effects of altitude

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6
Q

known as Hardware Disease by the rancher, and why it carries both of
these names. The often foreign body results in a bacterial infection of the entire
thoracic cavity

A

Traumatic Reticuloperitonitis/Pleuritis, Fibrinous Pericarditis

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7
Q

How might a rancher prevent Hardware disease

A

Hardware Disease is most often caused by a foreign object being ingested by the
animal, most commonly cattle but it has been seen in other animals. This object
is often metal and do to its weight falls to the lower portion of the stomach, most
commonly the reticulum were it penetrates the stomach wall and often the chest
cavity. Infection from the stomach contents then overwhelms the animal resulting
in death. This can often be prevented by using a magnet that is given orally.

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8
Q

What is the flow of blood through the body and the direction of
flow starting at the right ventricle:

A

Right ventricle, pulmonary artery, lungs, left pulmonary vein, left atrium, left
ventricle, arteries of body, organs, veins of body, cranial/caudal Vena Cava,
right atrium, right ventricle. Understand how this flow may be associated with
the clinical signs of BHMD as well as endocarditis

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9
Q

Where is endocarditis most common in bovines

A

most commonly found on the right side of the heart on the pulmonary
valve or the tricuspid

attle tend to develop periodical episodes of a bacteremia (bacteria in
their blood). This is often caused by concurrent illness or feeds much too high in
concentrates, grain. The bacteria then enter the blood stream, and now knowing
the flow of blood, you can see that the bacteria enter the right ventricle first and
begin to localize on the right tricuspid or pulmonary values. In humans and other
species the most common bacterial invasion of the body is from the lungs,
therefore entering the blood stream on the left side of the system invading the left
ventricle and its structures

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10
Q

These negatively charged cations from Streptomyces cinnamonensis help in
feed efficiency by; increasing rumen propionate and decreasing acetate and
enhancing rumen nitrogen metabolism into protein. They also help in being
coccidiostatic. Besides these benefits Ionophores can be cardio-toxic by causing
an influx of Na+ into the cell which induces an influx of Ca++ into the cell which
often results in mitochondrial damage and cells death.

A

Inophores (Monesin)

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11
Q

Increases rumen propionate and decreases acetate and enhances rumen nitrogen metabolism into protein

A

Inophores (Monesin)

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12
Q

What are the effects of rattlesnake bites

A

Local edema and inflammation around the bite wound. Rapid swelling of the face
and airway if bitten in the nose resulting in respiratory failure.
Thrombocytopenia and coagulopathies. Local severe infection and cellulitis
resulting in tissue necrosis and sloughing.

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13
Q

How do you approach a rattle snake bite in cattle

A

mergency supportive care including
oxygen therapy. Maintaining a functioning respiratory system by utilizing syringe
cases to keep nasal airway passages open or performing a tracheostomy.
Antibiotic therapy in hopes of preventing infection for the bite. Anti-
inflammatories, Laser therapy and Anti-venom may all be utilized.

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14
Q

Vitamin E and Selenium deficiency in camelids causes

A

diaphragmatic paralysis and
respiratory death

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15
Q

Lab finding of bovines with Vitamin E and Selenium deficiency

A

CK often being greater than 50,000 and have been seen as high as 500,000

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16
Q

What is the therapy for bovines with Vitamin E / Selenium deficiency

A

herapy often is
vitamin E injection and oral supplementation. If selenium deficiency is suspected
further herd evaluation should be done and consider selenium supplementation or
treatment.
Practice Questions:

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17
Q

At the present time the best means to identify those animals at risk for Bovine High
Mountain Disease (BHMD) is?
a. Genetically DNA match them and cull those that are possible carriers.
b. Take all animals to high elevations about 8000 feet and leave them for 1 month, keep
only those that are alive and well after that elevated altitude stress.
c. Carry out a Pulmonary Arterial Pressure (PAP Measurement) and cull those with
high PAP scores, i.e. above 50mmHg.
d. Carry out a PAP Measurement and cull out those animals with low scores, i.e. below
40 mmHg

A

C

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18
Q

T/F: BHMD has little impact on the cattle industry in high elevations

A

False

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19
Q

A ranch family wants to try to develop a herd that they can utilized in high elevation and
produce bulls that they can market for high altitude use. They know of the PAP test but
desire to know how it can best be used or can it be used for this type of situation. How is
the PAP test best utilized in this situation?
a. PAP measure/test all animals and identify those animals with pulmonary hypertension
and eliminate them, especially all replacement heifers and bulls used in their breeding
program.
b. Explain to them that a PAP measurement is a means to genetically select those animals
not experiencing pulmonary hypertension (low PAP measurements) with hopes of
developing a genetically resistant herd to the effects of altitude.
c. Explain to them that the PAP test/measurement can be used as a marketing tool and a
means of supply genetically resistant bulls to the buyers for high altitude use.
d. All of the above.

A

D

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20
Q

Hardware Disease” as it is known by the rancher can best be described in medical
terminology as:
a. Traumatic Reticuloperitonitis/Pleuritis, Fibrinous Pericarditis
b. Lung Abscesses and infection
c. Rumenitis/Abomasitis

A

A

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21
Q

Hardware Disease is most often caused by_________, and often is prevented by using
a_______.

A

metal foreign object; magnet

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22
Q

You explain endocarditis most commonly affects
the ________ side of the heart in ruminants specifically the ________ valve. Often in
ruminant’s endocarditis can be and is most commonly associated with an __________
infection from the_______ associated with chronic acidosis secondary to a high
concentrate diet. Often ruminants with endocarditis will also have multiple bacterial
_______ abscesses. You recommend further work–up that may include,_______ and
______ _______ knowing neither may be 100% diagnostic. Treatment options at this
point may be long term ________ therapy with a guarded prognosis

A

right side of the heart in ruminants specifically the tricuspid valve. Often in ruminants endocarditis can be and is most commonly associated with a bacterial infection from the rumen associated with chronic acidosis secondary to a high concentrate diet. Often ruminants with endocarditis will also have multiple bacterial liver abscesses. You recommend further workup that might include echocardiogram and blood culture knowing neither may be 100% diagnostic. Treatment options at this point may be long term antibiotic therapy with a guarded prognosis

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23
Q

What is associated with ruminant endocarditis

A

associated with chronic acidosis secondary to a high concentrate diet

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24
Q

What else can help you diagnose Endocarditis in ruminants

A

You recommend further workup that might include echocardiogram and blood culture knowing neither may be 100% diagnostic.

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25
Q

You are asked to look at a 3 month old Limousine heifer that has not done well her entire
life. She is now 60 pounds lighter than the other heifers her age. On her physical exam
you find her to have a T-99.0, P-186, R-60. On lung auscultation there are louder sounds
in the lungs that you would expect for a calf this age. Her lung sounds are twice to volume
of her trachea sounds. On the left side of her thorax over the pulmonary valve there appears
to be an III/VI pansystoloic murmur. On the right side over the tricuspid value there is a
VI/VI pansystoloic murmur with a palatable thrill. You ask the rancher if you can do a PAP
test and the results you find are, PAP 140mmHg with a 160/104 systolic/diastolic. Your
best diagnosis and prognosis at this time for this progressively poor doing heifer with these
clinical findings?

A

Ventricular Septal Defect (VSD), since there are clinical signs at this time prognosis
would be poor

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26
Q

Which one of the following statements is correct regarding “high mountain disease?
a. Alveolar hypoxia is the primary stimulus for pulmonary arteriolar
vasoconstriction encountered in high mountain disease.
b. Pulmonary hypertension of high altitude is not reversible.
c. Death in high mountain disease results from acute pulmonary edema secondary to
right ventricular failure.
d. Only Angus breed cattle are susceptible to high mountain disease.
e. Edema of the brisket (“brisket disease”) is pathognomonic for high mountain
disease.

A

A

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27
Q

You are called out to look at a couple of calves that have been born without any
complications and have done well for about a week. After a week of life they seem to get
weak and lie around and be unwilling to nurse and often perish overnight. Your physical
exam is somewhat unremarkable. One calf that died the previous night you preformed a
necropsy on and found nothing remarkable. You recommended blood work on one of the
smaller still surviving calves and found they had a remarkable rise in CK @ 250,000 as
well as a Vitamin e level of 25 ( normal >150). You best explain to the rancher that this
is suggestive of, and your recommendations at this time might include

A

White Muscle disease, Vitamin and possible selenium deficiency. You
recommend further diagnostics including whole blood selenium levels on this calf
as well as a few others in the heard and begin Vitamin E injectable therapy in
those calves born already and in those cows still having to calve as well as
consider nutritional supplementation after further diagnostics are evaluated

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28
Q

What are the visual findings of cows with cardiac disease in ruminants

A

-Weight loss
-Brisket disease
-distension
-bottle jaw
-tachycardia
-exercise intolerance
-diarrhea
-decline in milk production
-arrhythmias
-heart murmurs
-cyanosis
-jugular distension
-rectal prolapse
-bloat

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29
Q

Is diarrhea a clinical sign of heart disease in ruminants?

A

yes

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30
Q

What is the most common congenital defect you see in cattle/ruminants *

A

Ventricular Septal Defects

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31
Q

What is the PAP of cattle with ventricular septal defects

A

PAP 114

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32
Q

What is really the only use of electrocardiograms in cattle **

A

Most useful for arrhythmias
-Atrial fibrillation**
-AV conduction disturbance
-Ventricular arrhythmias

*not useful for chamber enlargement

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33
Q

ECG in cattle is not diagnostic for

A

chamber enlargement

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34
Q

What is the most common arrhythmia in cattle *

A

Atrial fibrillation

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35
Q

What ECG lead do you use in cattle *

A

Base-Apex Lead
Negative lead: right jugular furrow
Positive lead: left thorax in the 5th intercostal space (level of elbow)

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36
Q

Where are the ECG leads in cattle

A

Base-Apex Lead
Negative lead: right jugular furrow
Positive lead: left thorax in the 5th intercostal space (level of elbow)

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37
Q

How can you get arrhythmias in cattle

A

GI disease equal electrolyte imbalances
toxemia
neoplasia

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38
Q

How can GI disease lead to arrhythmias in cattle

A

1) Electrolyte imbalances
2) Toxemia
3) Neoplasia

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39
Q

What should you think when you see a cattle with atrial fibrillation

A

GI issues: electrolyte imbalances

*Vagas nerve vs sympathetic (pain)

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40
Q

Is quinidine or digoxin indicated for the treatment of cattle arrhythmias

A

NO- treat the underlying condition

-Oral and IV electrolytes
-Correct the metabolic acidosis/alkalosis
-Glucose

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41
Q

How do you treat arrhythmias in cattle

A

Treat Underlying (likely GI) cause
-Oral and IV electrolytes
-Correct the metabolic acidosis/alkalosis
-Glucose

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42
Q

When is atrial fibrillation serious in cattle and you need to move rapidly

A

when potassium is so high that they are bradycardic

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43
Q

What is most common cause of cor pulmonale in humans

A

hypoxic pulmonary hypertension

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44
Q

pulmonary hypertension occurs with

A

alveolar hypoxia in conditions such as emphysema, sleep apnea, alveolar hypoxia of altitude, high altitude pulmonary hypertension

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45
Q

What is the pathophysiology of BHMD **

A

1) Alveolar hypoxia
2) Pulmonary vasoconstriction
3) Pulmonary Remodeling
4) Pulmonary Hypertension
5) Right Ventricular Hypertrophy
6) Right Ventricular Dilation
7) Right heart congestive failure

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46
Q

What is the normal Pulmonary Artery pressure (PAP)

A

around 36-40mmHg

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47
Q

How does increased pulmonary artery pressure occur

A

there is hypertrophy of the pulmonary artery smooth muscle

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48
Q

What livestock species are hyper reactive to hypoxia

A

Bovine
Porcine

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49
Q

What species are hyporeactive to hypoxia

A

Ovine
Caprine
Canine
Llama
Alpaca
Yak- really good

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50
Q

Pulmonary artery smooth muscle responsiveness is _______________

A

genetically determined

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51
Q

pitting edema

A

cardiac disease is a main cause of this
where the tissue is imprintable when pressure is applied

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52
Q

What would you see on necropsy of a cow with BHMD

A

1) Brisket edema/ pitting
2) SQ edema
3) Fluid and adhesions
4) Possible aneurism (pulmonary hypertension)
5) Congested liver (right sided CHF) - Nutmeg Liver
6) Enlarged Right Ventricle and Atrium
7) Cerebral Hypoxia

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53
Q

What is the rule of 10 in bovine

A

there is likely 10x more fluid in the chest that you see

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54
Q

How do you treat Brisket Edema

A

1) Diuretics
2) Antibiotics
3) Warming environment
4) Limited water and salt intake
5) Thoracocentessis *
6) Supportive care
7) Move to lower elevation or hyperbaric chamber
8) other: ?

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55
Q

You check for pulmonary artery pressure for BHMD but what else can contribute to the development? *

A

Anything that gives you hypoxia
-Fibrinous Bronchopneumonia

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56
Q

T/F: Fibrinous Bronchopneumonia can cause a cow to develop BHMD

A

True- it results in hypoxia

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57
Q

What plants might cause brisket disease through hypoxia

A

Locoweeds -Oxytropis spp and Astragalus)

*Swainsonine

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58
Q

Locoweeds -Oxytropis spp and Astragalus) can cause

A

Brisket Disease by destroying the arterioles and creating hypoxia leading to BHMD

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59
Q

How do you diagnose BHMD

A

Best by pulmonary artery pressure
-History/atitude
-ECG
-Echocardiography

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60
Q

What is the normal pulmonary artery pressure in cattle

A

mean: 36mmHg

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61
Q

You should cull all animals with a PAP ____________ *

A

above 50mmHg

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62
Q

At this time, what is the best means of identifying cattle at risk of pulmonary hypertension and help ID those at risk for genetic carriers

A

PAP testing

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63
Q

How do you do PAP testing in cattle

A

Needle into jugular into RA and RV into pulmonary artery to measure the pressure

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64
Q

If you want to develop a genetic herd of cattle that are resistant to high altitudes you want to select ones with a PAP

A

of under 50mmHg (cull the others)

*ideally 41mmHg

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65
Q

What are the age effects of PAP testing in cattle

A

<10 months: unpredictable, used for screening only

> 18 months: stable and reliable

Most accurate: >12 months and elevations >6500 feet

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66
Q

When is PAP testing the most accurate

A

Most accurate: >12 months of age and elevations >6500 feet

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67
Q

How does body condition of cattle affect PAP

A

excessive body condition increases PAP

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68
Q

How does altitude affect PAP testing

A

Altitudes <5000 feet are only for screening

there is 1-1.5 mmHg increase per 1000 feet elevation rise

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69
Q

Why might you see hardware disease cases around parturition

A

they are pushing

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70
Q

What is the pathogenesis of traumatic pericarditis

A

1) Pericardial effusion- transudate or exudate
2) Decreased venous return
3) Decreased atrial and ventricular filling
4) Decreased cardiac output

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71
Q

What are the clinical signs of pericarditis in cattle

A

2-5 days post partum: decreased milk production, anorexia, odontopresis (Bruxism), respiratory grunt
positive wither test
CV: muffled heart sounds, tachycardia, splashing sounds, friction rub, poor U/S images

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72
Q

If there is history of calving in the last month, what should you be suspicious for? **

A

Hardware disease

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73
Q

What are your diagnostics for pericarditis in cattle

A

-ECG (Base Apex Leads)
-Ech
-Metal detector
-Radiography
-Laparotomy

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74
Q

What are the CV clinical signs of cattle with pericarditis

A

CV: muffled heart sounds, tachycardia, splashing sounds, friction rub, poor U/S images

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75
Q

What is the normal ECG for cattle with pericarditis

A

tamponade- not depolarizing well
muffled because the fluid is blocking the conduction

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76
Q

How do you treat Hardware disease in pericarditis

A

Pericardiocentesis- be careful for endotoxic shock
Transudative: NSAIDS
Exudative: Antibiotics, Pericardotomy, Digitalis + diuretics

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77
Q

What should you be careful about when doing a pericardiocentesis in cattle

A

Endotoxic shock and death

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78
Q

Upon cattle pericardiocentesis, you see an exudate. What should you do for treatment

A

Exudative: Antibiotics, Digitalis + diuretics

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79
Q

Upon cattle pericardiocentesis, you see an transucate . What should you do for treatment

A

Transudative: NSAIDS

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80
Q

Is a pericardotomy in cattle indicated

A

no- poor prognosis and very painful and expensive

you cant fix it anymore because of constrictive fibrous pericarditis

*Need local anesthesia, 5th rib resection, and antibiotics

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81
Q

What is them most common neoplasia of cattle

A

Lymphosarcoma
-Can invade the myocardium

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82
Q

What valve do cattle typically get endocarditis on

A

Tricuspid valve

83
Q

What is the pathogenesis of endocarditis in cattle

A

Hemodynamics- jet/venturi effect
Endothelial damage
Bacteremia
Agglutins
Bacterial adherence

84
Q

Dogs and cats typically get endocarditis on their mitral valve, why do ruminants typically get it on their tricuspid valve *

A

Rumen leaks bacteriemia causing Liver abscesses and the bacteria goes straight to the tricuspid valve

85
Q

What is the main bacteria that causes endocarditis in cattle

A

Trueperella, others (Ecoli)

86
Q

What are the consequences of endocarditis in ruminants

A

-Thrombotic Endocarditis
-Weight loss
-Intermittent pyrexia
-Heart murmur
-Congestive heart failure
-Metastatic disease
-Hematology: anemia, leukocytosis, hyperproteinemia (hyperglobulinemia), monocytosis, azotemia

87
Q

How do you diagnose endocarditis in cattle

A

Clinical signs
cardiac examination
blood culture

88
Q

Do cows with endocarditis have heart murmurs

A

Most have no murmurs
-tricuspid valve lesions often have no audible murmur

89
Q

What are the hematology changes seen in bovine endocarditis

A

Anemia
Leukocytosis
Hyperproteinemia (hyperglobulinemia)
Monocytosis
Azotemia

90
Q

How do you treat endocarditis in cattle

A

Antibiotics: Bacterial culture, prolonged treatment

Possible: Digoxin (IV only in ruminants, vasodilators- hydralzine (Eq), diuretics

91
Q

How many blood cultures do you need to diagnose endocarditis in cattle

A

5
Sample when pyrexic, before antibiotic therapy, collect steriliy,

*Culture aerobically and anaerobically

92
Q

If a rancher says their cow died of brisket disease, what are 4 things that might have caused this that you need to rule out

A

1) Congestive heart failure
2) Pericarditis
3) Endocarditis (tricuspid)
4) Pulmonary Hypertension

93
Q

What are differentials for murmurs in a systemically well horse

A

1) Mitral Valve Regurgitation- ruptured chrodae tendinea
2) Tricuspid valve regurgitation
3) Aortic regurgitation (insufficiency)
4) Ventricular septal defect
5) PDA
6) Aorti-cardiac fistula
7) Flow murmurs

94
Q

What are heart murmurs associated with systemic disease in horses

A

Vegetative endocarditis
Pericardits

95
Q

What is the most sensitive early indicator of cardiovascular toxicity in cattle

A

Arrhythmias- atrial Fibrillation with atrial fibrillation

96
Q

Why is the heart susceptible to toxins

A

high energy demands of myocardium make it very susceptible to toxins that decrease oxygen availability (hypoxia)

97
Q

What is the best example of nitrate poisoning

A

chocolate colored mucous membranes and blood

98
Q

alters Ca2+ and Na+ transport causing an increase in intracellular Ca2+ leads to excess Ca2+ accumulation and causes myonecrosis in cattle

A

Inophores- Monesin

99
Q

gosspol causes

A

hyperkalemia (phospholipid binder) and myonecrosis of heart

100
Q

an acute or chronic degenerative process involving the ventricular myocardium

A

cardiomyopathy

101
Q

What are sudden death problems occurring in feedlots related to

A

cardiac myopathies
-enlarged cardiac muscle rounded appearance

102
Q

An 8mo calf presents for acute respiratory distress, collapsed, lung auscultation is normal, flared nostrils, and lung films is normal, tachycardia, panting.
CK: 45,000
overal weakness could not stand,
respiratory breathing pattern: abdominal push
Tropinin: mildly high
What is diagnosis

A

Vitamin E/ Selenium deficiency

103
Q

Alpacas with Vitamin E/ Selenium deficiecy get

A

Diaphragmatic Paralysis- based on extreme elevated CK and clinical signs

104
Q

a fat soluble vitamin that serves as an antioxidant to protect and preserve cell membranes and proteins from oxidative damage

A

Vitamin E

105
Q

Vitamin E is synergistic with

A

Selenium

106
Q

Can you rule out Vitamin E/ Selenium deficiency if they are on green fresh forage?

A

No- it use to be the case but not anymore. it should be on your differentials

107
Q

What are clinical signs of Vitamin E/ Selenium deficiency in cattle/alpacas/ lambs

A

acute damage to muscle and nerve cells
signs: stiffness, stilted gait, muscle pain, weakness, recumbency
elevated muscle enzymes: CK* and AST

108
Q

Vitamin E associated diaphragm paralysis

A

neuropathy of phrenic nerve
rapid (days) onset of respiratory effort
-increased respiratory rate
-open mouth breathing
-nasal flaring
-inspiratory effort
-intercostal and abdominal breathing

No fever
no response to antibiotics

*Does improve with Injectable Vitamin E

109
Q

How do you treat Vitamin E deficiency in livestock

A

supplement vitamin E
-oral
-injectable

*can improve the phrenic nerve

110
Q

Is Vitamin E or selenium deficiency more common in Colorado

A

Vitamin E deficiency

111
Q

CK is diagnostic for Vitamin E/ Selenium deficiency in cattle. What else is

A

Arterial blood gas: hypercapnea (hypoventilation) and hypoxia

CBC: normal and stress leukogram

Serum chem: elevated CK* and elevated AST

112
Q

How do you prevent Vitamin E/ Selenium deficiency

A

Provide fresh pasture
increase vitamin E in supplements: salts over blocks, vitamin and mineral supplements

113
Q

Vitamin E/ Selenium deficiency is seen in

A

lambs, calfs, crias

114
Q

How do inophores cause myocardial damage

A

interferes with K+ ad Ca++ transport leading to severe mitochondrial damage

115
Q

What is the prognosis of ruminant inophore use

A

animals that survive the acute exposure or have a low dose chronic exposure may show signs of congestive heart failure as well as poor weight gain and growth

116
Q

What is the treatment for fog fever

A

ionophores- decreases the production of 3-methyl-indole

117
Q

How do you differentiate Vitamin E deficiency from Vitamin D deficiency (Rickets)

A

With rickets it is hypovitaminosis D due to lack of UV activation of Vitamin D
*Hypophosphatemia <5mg/dl is seen with Rickets
Do a Serum Vit D analysis

118
Q

What would you see on arterial blood gas analysis of an alpaca with vitamin E def

A

hypercapnea (hypoventilation)
hypoxia

119
Q

What are causes of cardiomyopathy in cattle

A

1) Ionophore toxicity
2) Plant toxins- gossypol
3) Snake venom
4) Cantharidin
5) Selenium/ Vitamin E deficiency
6) Lymphosarcoma

120
Q

How do you treat ionophore toxicity

A

activated charcoal and saline
cathartic
IV fluids
Selenium/ Vitamin E

121
Q

What are the uses for inophores

A

-increase feed efficiency
-coccidostatic
-helps control bloating (bacterial selection and promotion)
-Increases rumen propionate decreases acetate
-Decreases production of 3-methyl-indole (tx for fog fever)
-restore ruminal pH, inhibiting Strep bovis the main bacteria causing ruminal lactici acidosis

122
Q

What are the downsides to inophores

A

can cause myocardial disease
causes influx of Na+ into cell followed by Ca+ resulting in mitochondrial death

123
Q

What are your differentials for cardiomyopathy in cattle

A

1) gosspol poisoning
2) vitamin E/ selenium deficiency
3) Poisoning by ionophores
4) sodium fluoro acetate, lethal rodenticide
5) plants containing cardiac glycosides
6) Staph aureus, Histophilus somni, and Mycobacterium spp can cause myocarditis with subsequent cardiomyopathy

124
Q

How do ionophores cause myofibrillar hypercontraction and degeneration

A

Rapdily bind cations and create movement across cell membranes resulting in abnormal cellular Na+ intake and loss of hydrogen ion; calcium enters the cell secondarily with a loss of membrane gradients

calcium is sequestered in mitcohondria leading to failure of oxidative phosphorylation, ATP depletion, loss of Na/K pumps, and mitochondrial swelling and disruption

*Increased cystolic calcium causes hypercontraction and rapid onset necrosis

125
Q

What are the target tissues of inophore toxicity

A

skeletal muscle and myocardium
-pale areas and streaks in the myocardium and sub-epicardial and myocardial hemorrhages

126
Q

a 5yo hostein cow calves 4 days ago and is now not eating or drinking. Her temp is elevated and she has an ECG that shows atrial fibrillation. Based on these findings what is the preferred course of treatment for this cow?

A

Oral and IV fluids and electrolytes and antibiotics

127
Q

What makes the S4 sound

A

atrial kick- the atria are squeezing

128
Q

What makes the S3 sound

A

diastolic filling

129
Q

What covers the pulmonic valve in the horse and makes it hard to hear

A

the triceps muscle- need to push hard to hear it

130
Q

What are the 7 criteria for describing a murmur

A

1) Grade (1-6)
2) Timing (Systolic, Diastolic, Continuous)
3) Duration (Early, Holo, Pan)
4) Quality (Blowing, Course, Musical, Honking)
5) Shape (Crescendo, Descrescendo, Cresendo- Decrescendo, Band shaped)
6) Location= PMI
7) Variability (exercise, stress/ pain, excitement, sedation (alpha-2), buscopan, phenylephrine)

131
Q

systolic murmurs are heard between the

A

lub dub

132
Q

diastolic murmurs are heard between the

A

dub lub

133
Q

What does an early/early-mid murmur mean

A

shorter time closer to the S1 or S2 sound

134
Q

What does holo mean

A

the whole way between Si and S2
S1 and S2 are audible

135
Q

What does a pan- murmur mean

A

it extended over S1 and S2

136
Q

What are the different murmur quality descriptors?

A

Blowing
Course
Musical
Honking

137
Q

A crescendo murmur means

A

it gets louder over time

138
Q

A decrescendo murmur means

A

it is getting softer over time

139
Q

a band shaped murmur means

A

it stays the same volume the whole time

140
Q

Why might there be variability in a murmur heard

A

(exercise, stress/ pain, excitement, sedation (alpha-2), buscopan, phenylephrine)

141
Q

All left sided systolic murmurs in the horse are __________________ until proven otherwise

A

mitral regurgitation

142
Q

In a horse with left sided systolic murmur, they will have

A

mitral regurgitation

143
Q

What murmur does a horse with mitral regurgitation have

A

left sided systolic murmur

144
Q

You hear a left sided systolic murmur in a horse, indicating mitral regurgitation. When do you recommend echocardiogram

A

-Pre-purchase
-Grade >3-6/6
-Pansystolic
-Other signs of heart disease/ failure (Exercise intolerance, increased resting heart rate/respiratory rate, atrial fibrillation)

145
Q

In a horse, is mitral valve prolapse good news when you hear a left sided systolic murmur

A

it will be mid-late systolic, bad shaped, course murmur and it is a better prognosis and good news to your client

146
Q

Yuu hear a systolic murmur of a horse over mitral valve alongside musical/hoking, high grade >3 and thrill. What likely happened

A

Ruptured Chordae Tendinea- poor prognosis

147
Q

What left sided systolic murmur is a poor prognosis in a horse

A

Chordae tendinae rupture

musical/hoking, high grade >3 and thrill. What likely happened

148
Q

When might you hear an ejection/ flow murmur in a horse
Grade <3

A

Alpha-2
Excitement
Hemodynamic compromise change (anemia)

*normal valves and disappear, good prognosis

149
Q

What is a flow/ejection murmur in a horse

A

it is a murmur that is heard due to alpha-2, excitement for hemodynamic changes like anemia. - variable

Normal valves and should disappear, good prognosis

150
Q

In the horse, all right sided only systolic murmurs in the horse is

A

tricuspid regurgitation until proven otherwise

151
Q

When do you recommend doing echo on a horse with tricuspid regurgitation

A

> Grade 3/6
Pansystolic
Musical
*In conjunction with heart disease

152
Q

All Left sided systolic murmurs in the horse is mitral regurgitation unless it is

A

Flow ejection (variable due to drugs, excitement, or hemodynamic)
Ruptured Chordae tendinae

153
Q

What horse breeds really get tricuspid regurgitation

A

Standardbreds overrepresented

154
Q

What is the most common congenital defect in the horse

A

Ventricular Septal Defect
*Grade 4-6 pansystolic, band shaped course murmur with PMI over tricuspid valve
with
Lower grade holosystolic-pansystolic crescendo-decrescendo over left pulmonic valve (relative pulmonic stenosis)

155
Q

You hear a horse with:
*Grade 4-6 pansystolic, band shaped course murmur with PMI over tricuspid valve
with
Lower grade holosystolic-pansystolic crescendo-decrescendo over left pulmonic valve
What is the diagnosis

A

Ventricular septal defect in a horse

156
Q

If you hear a systolic right sided murmur over tricuspid in a horse, why do you need to be sure to hear one over the left pulmonic valve too **

A

Systolic murmurs over both the tricuspid and left pulmonic valve means the horse likely has ventricular septal defect
*most common congenital abnormality in horse

157
Q

What murmur will you hear in a horse with aortic regurgitation (common in older horses >10yo)

A

holodiastolic decrescendo musical murmur with PMI: aortic

158
Q

What is occuring if you hear a horse with a diastolic murmur over the aorta

A

aortic regurgitation

159
Q

You have a horse with a grade 2 continuous band shaped blowing murmur with PMI over the left heart base that does not radiate over vary.
What likely is happening

A

Patent Ductus Arteriosus (PDA)

160
Q

T/F: PDA are normal in neonates <96 hours old

A

true

161
Q

What murmur do you hear in horses with grade 2 continuous band shaped blowing murmur with PMI over the left heart base that does not radiate over vary.

A

PDA

162
Q

Can you ride horses with aortocardiac fistula

A

No- risk for collapse, arrhythmias, SCD

163
Q

When should you do echo on a horse with aortocardiac fistula

A

Always warrants and echo

164
Q

What murmur do you hear in a horse with a right sided continuous machinery murmur

A

Aortocardiac fistula

165
Q

What murmur do you hear in a horse with an aortocardiac fistula

A

right sided continuous machinery murmur

166
Q

What is the only possible cause of a diastolic murmur in a horse

A

aortic regurgitation

167
Q

You hear a continuous murmur in an adult horse, what could likely be happening?
What if it were young horse?

A

PDA: foal
Aortocardiac Fistula: adult

168
Q

What valves are most common in horses with vegetative endocarditis

A

aortic and mitral

169
Q

What are the criteria for diagnosing vegetative endocarditis in horses

A

Need two minor and one major to diagnose it or you really just get the vibe

Major criteria: microbial growth on blood culture, echo abnormalities of valves, new or different murmur

Minor criteria: predisposing factors, fever, thromboembolic disease, clinpath evidence of bacterial infection, immunologic disease

170
Q

How do you treat vegetative endocarditis in horse

A

Antibiotics: -cidal, prolonged IV, ideally choice made based on positive blood culture

Antithrombotics: Aspiring, clopidogrel, enoxaparin

Prognosis is generally poor for this disease

171
Q

How might horses get vegetative endocarditis iatrogenically

A

jugular catheter site infection causes the infection of the

172
Q

Eastern tent caterpillars are associated with

A

pericarditis

173
Q

What causes Mare Reproductive loss syndrome

A

eastern tent caterpillars -> pericarditis

174
Q

How do you treat pericarditis in horse

A

Drain, if tamponade suspected
Lavage
Antimicrobials

175
Q

Why might a horse get myocarditis

A

1) Monensin toxicity
2) Strongylus vulgaris
3) Rattle snakes
4) Cantharidin (blister beetles)

176
Q

What parasite can cause myocarditis in horse

A

Strongylus vulgaris

177
Q

When horses get myocarditis from either monensin toxicity, strongylus vulgaris, rattle snakes, or cantharidin. What is the result

A

fibrosis and development of ventricular arrhythmias

178
Q

How do you diagnose myocarditis in horses

A

echo appearance
cTnl (cardiac troponin)
history

179
Q

What side of the heart do you tap for a horse with pericarditis

A

left side

180
Q

How do you treat congestive heart failure in horses

A

Furosemide
Antithrombotics
Digoxin
*Prognosis is generally poor, unless underlying cause can be addressed

181
Q

What are the clinical signs of equine congestive heart failure

A

tachycardia
pulmonary edema
plueural effusion
jugular distension/ pulsation
hepatic congestion
atrial fibrillation
ascites
ventral edema

182
Q

What ECG set up do you use in a horse

A

Base-Apex ECG- read off of lead II

183
Q

What does a horse ECG look like on lead II

A

P wave: can sometimes be two waves, wide

QRS: Negative R wave

T: positive T wave

184
Q

What are exercising ECGs used for in horses

A

-Assess fitness
-Determine if arrhythmias are overdriven with exercise
-Determine if arrhythmias are overdriven with exercise
-Determine if arrhythmias degrade with exercise
-Assess cardiac compensation for disease
-Safety assessment
*Must be as rigorous as the work required of horse will be

185
Q

Exercise ECGs in horses need to be

A

as rigorous as the work required of horse will be

186
Q

What is normal heart rate for a horse

A

28-48bpm (mini horses run higher into the 50s)

foals: 80-120

187
Q

What is a normal heart rate for a foal

A

80-120

(nx for adult is 28-48bpm)

188
Q

What arrhythmias are common in horses

A

Atrial fibrillation
Atrial premature contraction
ventricular premature contraction
2nd degree AV block

189
Q

What AV block is commonly seen in horses*

A

Second Degree AV block- mostly a benign result of high vagal tone
*should ablate with exercise or administration of atropine

190
Q

Second Degree AV block in horses is extremely common. What is significant about it

A

almost always a benign result of high vagal tone.
Should ablate with exercise or administration of atropine

Not always benging if it is high degree (>2 consecutive block beats)

191
Q

2nd degree AV block in horses is typically benign but when is it not

A

When there is high degree- presence of >2 consecutive blocked beats
Block does not resolve with exercise

192
Q

What are the recommendations to horses with second degree AV block

A

High Degree that disappears with exercise: only be ridden or driven by an informed adult

high degree that disappears with exercise or atropine should be rested and re-evaluated but considered less safe to ride or drive

*Horses with symptomatic bradyarrhythmias generally have a poor prognosis and are not safe to ride

193
Q

For a 2nd degree AV block to be advanced/ high grade there needs to be (in horse)

A

greater than 2 consecutive blocked beats

194
Q

How do you manage a horse with advanced 2nd degree AV block

A

pacemaker implantation

195
Q

What is the most important arrhythmia in horses leading to poor performance

A

Atrial fibrillation

196
Q

What are the hallmarks for atrial fibrillation in horse

A

f waves
No P waves
Irregular R-R intervals

197
Q

Atrial fibrillation in horses might be due to

A

1) Genetics (Standardbreds)
2) Age- older
3) Atrial Dilation (ex: mitral valve regurgitation)
4) Strenuous exercise
5) Concurrent cardiac disease
6) APCs

198
Q

How do you treat atrial fibrillation in a horse

A

Convert to sinus rhythm
1) Quinidine Conversion (Class 1a Na+ Channel Blocker) -expensive
2) Transvenous Electrical Conversion (TVEC)

199
Q

When should you consider converting a horse in atrial fibrillation

A

1) No structural cardiac disease
2) Horses has been in atrial fibrillation <4months
3) Maximum atheletic capacity
4) Rode by a child rider
5) If this is first occurence

200
Q

What should you do if the clients opt not to convert atrial fibrillation in horse

A

Horse can be used if
1) Used by informed consenting adult
2) HR <220bpm sustained during maximal exercise
3) No concurrent ventricular arrhythmias during exercise determined

201
Q

What do you see on ECG of a horse with atrial premature complexes

A

Irregular RR interval with normal QRS morphology
P waves occasionally evident

202
Q

What causes atrial premature complexes in horses

A

changes to autonomic tone
hypokalemia
drugs (catecholamines, anesthetics)
systemic disease-colic, fever, hemorrhage
structural cardiac disease

203
Q

What should you tell the client if their horse has atrial premature complexes

A

APCs can be overdriven with exercise or are occasional during exercise

*possibility for degrading into Afibrillaton is likely higher than those without APCS

204
Q

What do ventricular premature complexes look like in horses

A

Ectopic focis originating in the ventricles generating aberrant ventricular depolarization
Early beat, no p wave
Abnormal T wave repolarization
QRS does not match

Cardiology (8 decks)

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