Smith.Ch.30.DiseasesoftheCardiovascularSystem Flashcards

1
Q

Cardiac output values in resting horse range from

A

32 to 40L/min

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2
Q

What are methods to determine cardiac output?

A

Fick method
Doppler echocardiography
dye dilution/ thermodilution/ litium dilution

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3
Q

Where is the most common location of ventricular septal defect in large animals?

A

perimembranous

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4
Q

VSDs are more common in which equine breeds?

A

Welsh mountain ponies
Arabian
Standardbred
Quarterhorse

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5
Q

Why do ventricular septal defects occur?

A

failure of fusion of part of the endocardial cushion and the muscular ventricular septum or failure of fusion of the truncal and conal septa

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6
Q

Describe Eisenmenger complex

A

defect in which right-sided heart resistance to blood flow causes the shunt associated with VSD to become right to left (rare)
**cyanosis is a distinguishing feature

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7
Q

What size is a VSD (VSD to aortic root ratio) that is unlike to be hemodynamically significant?

A

less than 0.3

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8
Q

With moderate to large VSDs, horses are at greater risk for developing congestive heart failure sooner. Why?

A

-simultaneous heart dz or Left sided heart failure d/t chronic volume overload can increase pulmonary vascular resistance
-right ventricle– chronic pressure overload

**comb of pressure and volume overload= greater risk for developing CHF

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9
Q

Which horses with VSDs are at risk for development of CHF early in life and have a shortened life expectancy?

A

Large defects: >3.5 cm or VSD/aortic ratio of 0.64
peak shunt velocities: <3.5m/s

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10
Q

define patent ductus arteriosus

A

persistent patency of the vessel that connects pulmonary arterial system to the aorta
(pulmonary artery to aorta)

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11
Q

Why does the ductus arteriosus close?

A

In response to:
-lowered pulmonary vascular resistance
-increased systemic vascular resistance
-increased blood volume
-increased left ventricular pressure when breathing begins
-placental circulation removed

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12
Q

Clinical signs of a PDA are dependent on:

A

-length and diameter of the ductus arteriosus
direction of the shunted blood
presence of other cardiac defects

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13
Q

Describe PDA murmur

A

continuous machinery murmurs

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14
Q

Direction of PDA shunt usually occurs?

A

left to right
–produces left ventricular volume overload
-pulmonary hypertension & congestion
+/- right sided ventricular hypertrophy

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15
Q

When does switch of PDA shunt occur, to right to left?

A

When pulmonary resistance equal or exceeds the systemic vascular resistance

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16
Q

When is PDA closure expected in foals?

A

by 96 hours of age

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17
Q

In a foal with PDA, what is risk for future riding?

A

b/c of marked dilation of the pulmonary artery– rupture of pulmonary artery is possible

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18
Q

Define tetrology of fallot vs pentalogy of fallot

A
  1. biventricular origin (overriding) of aorta)
  2. Ventricular septal defect
  3. obstruction of pulmonary arterial flow (pulmonary stenosis)
  4. secondary right ventricular hypertrophy (d/t obstruction of pulmonary arterial flow)
  5. atrial septal defect or persistent ductus arteriosus
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19
Q

Pathogenesis of tetralogy/pentology of fallot

A

abnormal development of the conal septum in the embryonic heart– leads to narrowing of the right ventricular infundibulum (pulmonic stenosis), an inability of the conal septum to participate in closure of the interventricular foramen (VSD) and overriding of the aorta

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20
Q

What is the more common congenital cardiac defects that cause cyanosis in large animals?

A

tetralogy of fallot

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21
Q

C/s of cyanosis is observed when unoxygenated hemoglobin is reduced to:

A

<5 g/dL (unoxygenated hemoglobin)

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22
Q

Cyanosis resulting from heart failure or respiratory disease improves with what treatment?

A

oxygen administration

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23
Q

What is the most common atrial septal defect?

A

ostium secundum defect– patent foramen ovale PFO) is most frequent

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24
Q

Pathogenesis of persistent foramen ovale

A

failure of septum primum (valve of foramen ovale)- to become adherent to the crista dividens after birth, when changes in left and right atrial pressures produce functional closure of the formen ovale

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25
Q

In calves, what is the most common defect associated with PDA?

A

persistent foramen ovale

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26
Q

atrial septal defect murmur

A

holosystolic crescendo-decrescendo murmur at the left heart base

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27
Q

triscupid valve atresia c/s

A

cyanosis
crescendo-decrescendo or bandshape holosystolic murmur or pansystolic murmur audible over the rigth and left heart base
tachycardia
tachypnea
weak peripheral pulses
polycythemia (common)

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28
Q

Define persistent truncus arteriosus

A

one arterial vessel leaves the heart above a VSD

**coronary and pulmonary arteries and aorta arise from this vessel

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29
Q

Pseudotruncus arteriosus definition

A

presence of a remnant of an atretic pulmonary trunk
**congenital cardiac disease

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30
Q

What are the most common aortic anomalies seen in foals and calves?

A

dextropositioning or transposition of the aorta
**other anomalies: persistence of the right aortic arch and double aortic arch (may cause esophageal compression)

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31
Q

What is Eisenmenger complex?

A

Switch in blood flow from right to left side of the heart, to the left to right (results in decreased oxygenation of blood)

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32
Q

Ectopia cordis cervicalis is a relatively common defect in which species?

A

cattle

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33
Q

What defects are associated with ectopia cordis cervicalis?

A

defects of the heart, great vessels, neck (torticollis), ribs and sternebrae

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34
Q

Chronic active infection such as what, can predispose animals to the development of bacterial endocarditis or nonvegetative valvulitis?

A

foot abscesses
rumenitis
reticular abscess
other septic process lead to sustained or recurrent bacteria

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35
Q

What are the most common bacterial isolates from equine and bovine endocarditis cases are:

A

streptococci
Pasturella or Acitnobacillus spp
Truepuerella pyogenes (formerly Arcabobacterium pyognes)

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36
Q

Lesions of aortic and pulmonic valves can produce what kind of murmurs?

A

systolic
diastolic (most common in lg animals)
or Both

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37
Q

Aortic regurgitation in horses is most commonly associated with

A

degenerative valve disease

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38
Q

pulmonary regurgitation in cattle is most commonly associated with

A

bacterial endocarditis

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39
Q

Describe aortic valve lesion murmurs

A

holodiastolic
descrescendo
musical murmurs
**can be descrescendo, soft & blowing

water hammer or bounding arterial pulse (assoc w/ sig L ventricular overload

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40
Q

Signs of congestive heart failure in cattle/horses

A

tachycardia
coughing
respiratory distress
jugular venous distention
subcutaneous edema
ascites
mammary vein distention (cattle)

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41
Q

describe murmur of ruptured chordae tendinae?

A

radiating musical murmur– distinctive honking quality
*may have band shaped pansystolic murmur

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42
Q

acute onset of respiratory distress with coughing and expectorating foamy pulmonary edema fluid is a relatively consistent feature of what cardiac abnormality?

A

ruptured chordae tendinae

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43
Q

Describe murmur of mitral valve prolapse

A

crescendo midsystolic to late systolic or holosystolic murmur with PMI over the mitral valve area

(similar with tricuspid valve prolapse)

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44
Q

Triscupid valve lesions in horses vs cattle are most commonly due to:

A

cattle: bacterial endocarditis, neoplasia of the right atrium

horse: bacterial endocarditis from septic jugular vein thrombosis

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45
Q

Echo evidence of mitral valve regurgitation

A

-INC left atrial and left ventircular dimensions
-rounding of left ventricular apex
- pattern of left sided volume overload
+/- INC fractional shortening
-bulging of interatrial septum toward the right
-larger than nomral pulmonary artery (>aortic root)– severe pulmonary hypertension

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46
Q

Tricuspid regurgitation echocardiac evidence

A

right atrial and right ventricular enlargement with paradoxical septal motion
–> visualizing lesions of endocarditis or neoplasia

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47
Q

aortic regurgitation echocardiographic evidence

A

left ventricular dilation
increased aortic root diameter
decreased aortic root diameter during diastole evidence of inc severity of aortic regurgitation
INC left ventricular fractional shortening
diastolic fluttering of the septal mitral valve leaflet
high frequency vibrations of the interventricular septum or aortic valve in diastole

–>visualization of valve prolapse, fenestration, healing endocarditis lesions or tears

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48
Q

Besides echocardiographic evidence of bacterial endocarditis, what are other C/s and diagnostics that indicate endocarditis

A

anemia
neutrophilia (a left shift may be present)
increases serum globulin concen
INC SAA
hyperfibrinogenemia
liver enzymes INC
urinalysis (+/- pyuria or hematuria)
positive blood culture w/ febrile episodes
other lab abnormalities of sepsis

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49
Q

Most horses with mitral valve regurgitation do not develop fulminant pulmonary edema, instead they develop

A

chronic pulmonary hypertension leading to subtle respiratory signs associated with interstitial pulmonary edema and subsequent development of right-sided CHF

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50
Q

In regards to valvular heart disease in horses, what is the most common valves involved?

A

Aortic is most commonly effected with degenerative valve changes
**followed by mitral valve, tricuspid valve and pulmonic valve

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51
Q

Jet lesions occur due to

A

asosciated with high -velocity turbulent regurgitant blood flow
**usually found in the receiving chamber

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52
Q

What lesions can cause moderate to severe valvular regurgitation and are more likely to progress rapidly and warrant a guarded to poor prognosis?

A

ruptured chordae tedinae
flail valve leaflets
marked valvular thickening

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53
Q

Treatment of endocarditis can ultimately result in?

A

scarring of the valve leaflet, that leads to progression fo regurgitation and death of animal

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54
Q

When treating cattle for bacterial endocarditis, the antibiotic of choise is?

A

antibiotic with gram positive coverage

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55
Q

Indication of clopidogrel in treatment of bacterial endocarditis? (in horses)

A

to prevent platelet adhesion and increased size of the valvular mass

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56
Q

Use of what medicatiosn can be used in cattle to prevent platelet adhesion and increased size of the valvular mass?

A

aspirin (100 mg/kg/day)
low-dose sodium heparin (subcu 30 to 40 units/kg twice daily)

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57
Q

Horses benefit (as do other spp) from the use of vasodilators in treatment of heart failure, what drug has been shown to be beneficial in horses with treatment of moderate MR or AR?

A

angiotensin converting enzyme (ACE inhibitors)
**benazepril: 0.5 mg/kg PO once daily

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58
Q

How do effective parasite control measures prevent predisposing causes of valvular heart disease?

A

trauma to heart valves
microembolism
infarction

**in horses

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59
Q

Define cor pulmonale

A

refer to the effect of the lung dysfunction on the heart and therefore a secondary form of heart idsease

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60
Q

Pathogenesis of cor pulmonale

A

pulmonary hypertension that leads to right ventricular hypertrophy–> dilation or failure

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61
Q

What is the primary cause of the cor pulmonale in cattle?

A

High mountain disease (brisket disease, high-altitude disease)

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62
Q

Pathogenesis of High mountain disease?

A

hypoxic vasoconstriction from high-altitude dwelling

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63
Q

What disease or factors contribute to the development of High Mountain disease?

A

pneumonia
lungworm
ingestion of locoweed (Oxytropis and Astragalus spp)
chronic pulmonary disease

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64
Q

What are the primary presenting clinical signs of brisket disease?

A

subcutaneous edema of the brisket, ventral thorax, submandibular area and occasionally limbs
lethargy
weakness
bulging eyes
diarrhea
collapse
death may occur
tachycardia (with a gallop rhythm, +/- splitting of S2 heart sound

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65
Q

Why would there be splitting of the S2 heart sound in brisket disease?

A

because pulmonary hypertension may accentuate the separation of the aortic and pulmonic valve closures, producing an audible splitting of the S2
**most notable on inspiration

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66
Q

Horses with clinical signs of cor pulmonale?

A

RAO–> leading to cor pulmonale
labored breathing
coughing
exercise intolerance
wheezes ausculted bilaterally

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67
Q

Differentials for clinical signs of right sided heart failure

A

bacterial endocarditis or TR
cardiomyopathy
cardiac lymphosarcoma/ other thoracic neoplasms
traumatic reticulopericarditis
left sided heart fialure
pleuritis or pleural effusion
congenital pulmonic valve stenosis (rare)

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68
Q

The response to hypoxia in brisket disease is dependent on:

A

amount of smooth mm in the pulmonary arteries

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69
Q

Brisket disease path:
Chronic pulmonary artery hypertension causes

A

pressure overload in the right ventricle
– responds with increased workload with hypertrophy, dilation or failure (dep on speed of which the condition develops)

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70
Q

Chronic right sided heart failure can lead to what?

A

diastolic dysfunction of the left ventricle

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71
Q

Why does ingestion of locoweed (oxytropis and Astragulus spp) predispose cattle to right sided heart failure?

A

Swainsonine
** causes toxic mycoardial damage

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72
Q

Brisket disease is common in cattle, kept over what altittude?

A

over 6000 feet

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73
Q

In what seasons is high mountain disease most commonly seen?

A

fall and winter

** due to cold weather exacerbating pulmonary hypertension

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74
Q

Is cor pulmonale reversible in HMD?

A

Yes–if animal is brought to lower altitudes

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75
Q

When do cattle not have reversible cor pulmonale?

A

-other lugn disease
- mean PAP of 50 to 55 mm HG
**rare
- once heart failure develops

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76
Q

Selection of breeding stock to prevent HMD?

A

low or normal PAPs at altitudes above 5000 feet

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77
Q

Define myocarditis

A

inflammation of the myocardium caused by bacterial, viral or parasitic organism or thromboembolic disease

78
Q

What are common causes of bacterial myocarditis?

A

Stpahylococcus aureus
Streptococcus equi
Clostridium chauveoei
Mycobacterium spp

79
Q

What are known viral causes of myocarditis?

A

foot and mouth disease
equine infectious anemia
equine viral arteritis
equine influenza
African horse sickness

80
Q

What are known parasitic causes of myocarditis?

A

strongylosis
cysticercosis
sarcocystic infection in ruminentas

81
Q

Define cardiomyopathy

A

subacute or chronic disease of the ventricular myocardium that occurs without anatomic valvular disease, congenital malformations of the heart or vessels or pulmonary disease

82
Q

Hypertensive cardiomyopathy ahs been detected in horses associated with what diseases?

A

chronic renal disease
pain assoc with chronic laminitis
ponies with EMS

83
Q

Dilated cardiomyopathy is associated with:

A

-ventricular dilation
increased ventricular mass
decreases systolic function

84
Q

What known genetic predispositions exist for the development of inherited/genetic cardiomyopathy

A
  1. red holstein gene in Holstein Friesan cattle
  2. curly hair coat in polled herefords and in Japanese black calves
85
Q

What toxic components can cause cardiomyopathy?

A

monensin
lasalocid
salinomycin
gossypol
Cassia occidentalis
phalris spp
vit E and selenium deficiency
copper deficiency
excessive molybdenum
high sulfatestes (secondary copper deficiency)
Acer family (plant tox)
rattle snake envenomation

86
Q

It is difficult to distinguish C/s of myocarditis from what diseases?

A

colic
respiratory disease
lameness
septicemia

–C/s of myalgia, reluctance to move exercise intolerance

87
Q

Differentials for causes of dilated cardiomyopathy

A
  1. nutritional (Vit E, selenium, copper deficiency)
  2. toxic: monensin, gossypol, salinomycin, lasalocid, hypoglycin A, Cassia spp., or Phalaris)
  3. Infectious (viral, bacterial, or parasitic)
  4. Drug induced
88
Q

Differential diagnosis for dilated cardiomyopathy?

A

young– congenital heart defects, cor pulmonale, nutritional myodegeneration

Adults– bacterial endocarditis, cardiac neoplasia, thoracic abscess, pericarditis, pleuritis, diaphragmatic hernia

89
Q

In an attempt to compensate for the reduced cardiac output, how is circulating fluid volume increased in cardiomyopathy

A

activation of renin-angiotensin aldosterone system & iNC arterial resistance

90
Q

What leads to the development of pulmonary edea in heart failure?

A

reduced cardiac output–> stim renin-angiotensin-aldosterone system– INC arterial resistance

– INC ventricular preload (venous return)
– INC afterload (arterial resistance)
–> causes pulmonary edema & reduced cardiac contractility

91
Q

Microscopic abnormalities associated with cardiomyopathy

A
  1. INC fibrous tissue in interstitium in absence of inflammation (or foci of inflammation
  2. variation in cross-section of cardiomyocytes
  3. degeneration of adjacent myocardial fibers
  4. myocardial vacuolation and degeneration with necrosis and fibrosis
92
Q

Prompt administration of what drug can be beneficial to survivors of ionphore toxicosis?

A

administration of Vit E

93
Q

Why are corticosteroids controversial in treatment of cardiomyopathy?

A

Possible viral recruidescence if the cause is viral

94
Q

What are therapeutic strategies used for treatment of dilated cardiomyopathy?

A
  1. positive inotropic agents (digoxin)
  2. diuretics
  3. vasodilators
  4. rest
    5 +/- removal of pleural or abdominal fluid
95
Q

When is the use of digoxin contraindicated in the treatment of dilated cardiomyopathy?

A

monensin toxicosis

96
Q

Ideally the peak and trough concentration of digoxin should be between:

A

1 to 2 ng/mL

97
Q

Before treatment of digoxin therapy what should be addressed int eh patient?

A

dehydration
acid-base balance
electrolyte abnormalities

98
Q

When should the dose of digoxin be reduced in patietns?

A

with elevated creatinine or blood ure anitrogen levels

99
Q

What diuretic is most commonly used in large animals?

A

furosemide: 1 mg/kg

100
Q

Which ACE inhibitor is most effective in horses?

A

benazepril
Other ace inhibitors: quinapril, ramipril, enalapril

101
Q

Define pericarditis

A

inflammation of the pericardium that results in accumulation of fluid or exudate between the visceral and parietal pericardium

102
Q

Causes of pericarditis in large animals

A

-penetration of ingested foreign objects or external wounds
-hematogenous spread (septicemia) of infection
-extension of infection from the lung or pleura
-viral infections (equine viral arteritis or equine influenza)
-neoplasia
-Mare reproductive loss syndrome (MRLS) (Actinobacillus spp)

103
Q

What are the most consistent clinical signs on auscultation with pericarditis?

A

tachycardia
muffling of heart sounds
absence of lung sounds in ventral thorax
dorsally lung ounds are louder thn normal

104
Q

Contrast auscultation of pericarditis vs pleuritis?

A

lung sounds are muffled ventrally (heart sounds are not0
radiation fo heart sounds over a wider aea than normal

105
Q

Cattle: When auscultated with splashing sounds sometimes referred to as “washing machine murmur or rub”, what does this mean clinically?

A
  • can be attributed to accumulation of gas and fluid in pericardium
    **indicative of presence of gas forming (anaerobic organisms)
    **grave prognosis
106
Q

Electrocardiogram abnormalities that are can be seen with pericarditis?

A
  1. decreased amplitude of the QRS complexes (<1.5 mV in the base apex lead)
  2. electrical alternans (altered congifuration fo the P, WRS or T complexes on a regular basis)
  3. ST segment elevation or slurring

+/- right -axis deviation int eh stanard limb leads

107
Q

What is the safest site to perofrm a pericardiocentesis?

A

left fifth (fourth in cattle) intercotal space 2.5 to 10 cm dorsal to teh olecranon, above the level of the lateral thoracic vein

108
Q

What bacteria is commonly associated with pericarditis and mare reproductive loss syndrome?

A

Actinobacillus organisms

109
Q

What are the consequences of pericardial effusion to the heart?

A
  • decreased distensibility (increased ventricular end-diastolic pressure) of the heart
    – impairs the hearts ability to fill in diastole
    –INC atrial pressure
  • reduce venous flow or venous return to the heart and diastolic perfusion of the myocardium

–> decreased ventricular contractility, stroke volume and cardiac output

110
Q

Difference between effusive and constrictive pericarditis

A

effusive: presence of pericardial fluid causes hemodynamic consequences
**removal of fluid beneficial

constrictive: reduction in ventricular compliance d/t fibrinous or fibrotic involvement of pericardium and epicardium
**removal of fluid not beneficial

111
Q

Exposure to what was the greatest risk factor for the development of fibrinous pericarditis during the mare reproductive and loss syndrome epidemic?

A

Eastern tent caterpillars

112
Q

Traumatic pericarditis is not uncommon in cattle, but occurs in less than what percentage of cattle with traumatic reticuloperitonitis?

A

less than10%

113
Q

Treatment of pericarditis in horses

A

– placement of a large bore indwelling chest tube into the pericardial sac under echocardiographic guidance and drainage and lavage of the pericardial sac
–> with local infusion of antibiotics

114
Q

Why can diuretics results in worsening heart failure with pericarditis?

A

Reduce venous return and preload in animals with pericarditis
= compromise to cardiac output & worsening heart failure

115
Q

Removal of what trees can be beneficial in prevention of exposure to Eastern tent caterpillar?

A

black cherry trees

116
Q

What is the most common cardiac tumor in large animls?

A

lymphosarcoma

117
Q

Examples of neoplasias that may involve structures adjacent to the heart and may extend to the heart or heart base in horses,

A

mesotheliomas
melanomas
lipomas
fibrosarcoma
adenocarcinomas
other cacrinomas
squamous cell carcinomas

118
Q

Lymphosarcoma is the most common cause of cardiac tumors in cattle, which has a predilection site for?

A

right atrial myocardium

**RV not uncommon, rare: LA or LV

119
Q

Although more than 50% of cattle in some parts of the United State are infected with BLV, what percentage develop lymphosarcoma?

A

1 to 4 %

120
Q

Thymic lympohosarcoma, which is not associated with BLV infections, also involving the heart can occur in what age of cattle?

A

cattle younger than 30 months of age

121
Q

The prognosis for survival for cardiac neoplasia?

A

poor– death expected within 6 months

122
Q

Control/prevention of cardiac tumors can only be performed for which tumors?

A

BLV
–> isolation of BLV pos and BLV neg animals
–> use of individual or serialized supplies
–>feeding colostrum from serologically negative cows only
–> frequent testing (at least every 6 months) & isolation of serologically positive animals over 6 months of age)

123
Q

Define aneurysms

A

vascular dilations, develop from weakening of the medial elastic coat of blood vessels

124
Q

Medial weakness of blood vessels seen in aneurysms can be caused by:

A

progression of intimal atherosclertoic lesions that has enlarged from hemorrhage
calcification
ulceration
thrombus formation

125
Q

Causes of aneurysms in large animsl

A

**unknown
trauma (internal or external)
sepsis
parasite migration
degenerative vascular disease
atherosclerosis
aging changes (dilation, elongation and loss of elasticity of blood vessels)

126
Q

Congenital aneurysms of what structure of the heart have been reported in horses?

A

sinus of Valsalva

127
Q

Define thrombosis

A

formation of a clot that obstructs blood flow in the circulatory system

128
Q

causes of thrombosis

A

trauma
venous stasis
catheterization for adminsiterin gmedication or fluids
needle penetration
indwelling acehters
thrombogenic solutions
bacterial contamination

129
Q

Secondary thrombosis causes:

A

perivascular inflammation caused by cellulitis, lymphangitis or other source so fbacterial invasion round the blood vessel

130
Q

Examples of a hypercoagulable states:

A

dehydration
endotxemia
anemia
hypotension
stress
stasis

131
Q

Define mebolism

A

foreign material carried in the bloodstream

132
Q

In large animals, embolis most commonly occur with:

A

bacterial endocarditis
thromboplhebitis
omphalophlebitis
parasitic arteritis

133
Q

Calves with aorto or aortoiliac thrombosis clinical signs?

A

weakness
lameness
knuckling
paresis
paralysis of the hindlimbs
inability to rise
cold hindlimbs
lacking a femoral pulse

134
Q

Aortopulmonary rupture and fistulization occur in what breed?

A

Fresians

135
Q

What is the most common outcome of aneurysm of a major vessel?

A

thoughout to be rupture

136
Q

Unruptured aneurysms may have other complications such as

A

thrombosis or emoblization o fthe thrombus

137
Q

In Friesians, rupture of the aorta occurs into the pulmonary artery at what location?

A

at the level of th eligamentum arteriosum and into the surrounding perivascular stuctures

138
Q

Spontaneous thromboembolism is commonly associated with?

A

parasitism in horses
**aorta and cranial mesenteric arteries are the most common sites frequently involved

139
Q

What are risk factors for catehter associated thrombophlebitis

A

large intestinal disease
hypoproteinemia
endotoxemia
salmonellosis
fever
diarrhea
localled produced fluids

140
Q

Arteriosclerosis recognized in cattle is most frequently caused by:

A

excessive vitamin D3 supplementation
ingestion of calcinogenic plans: Soamum malaxocylon, estrum dirunum or Trisetum flavescens

141
Q

In horses arteriosclerotic lesions were caused by lesions induced by what organism?

A

Strongylus vulgarus

142
Q

Ingestion of calcinogenic plants in horses, results in lesion in what locations?

A

aorta

143
Q

Examples of anticoagulant therapy that may be effective in preventing the thrombus formation

A

clopidogrel: 2 mg/kg PO twice daily
aspirin; 100 mg/kg PO once daily ruminants
sodium heparin: 20 to 40 units/kg SC twice daily

144
Q

Atrial fibrillation is characterized by

A

lack of coordinated atrial electrical activity
– caused by an abnormality of impulse conduction that results from multiple small rapid and random reentrant activation of the atria or by one or more discrete rotors

145
Q

What shortens the action potential duration in atrial myocardial cells, making atrial fibrilation more likely to occur in horses?

A

high resting vagal tone

146
Q

Causes of atrial fibrillation

A

atrial enlargement from atrial myocardial disease
atrioventricular valvular regurgitation
ventricular failure
myocarditis
endocarditis
autnomic nervous system imbalance
electrolyte or acid base distrubances
anesthetic drugs or tranquilzier adminitstration

147
Q

Define “lone Afib”

A

no undelrying cardiac disease can befound

148
Q

Cattle with atrial fibrillation usually have what undelrying disease?

A

gastrointesitnal disease

149
Q

Define paroxysmal atrial fribillation

A

usually lasts no more than 24 to 48 hours abefore spontaneous conversion to sinus thythm occurs

150
Q

What is a common cause of paroxysmal atrial fibrillation inhorses?

A

transient potassium depletion associated with administration of furosemide

151
Q

What supplements are associated with atrial fibrillation in horses?

A

bicarbonate “milk shakes”- paroxysmal AF
-iatrogenic hyperthyroidism– admin of Thyro L
-supplements containing kelp or ground up shell fish

152
Q

Describe atrial fibrillation arrhythmias

A

irregularly irregular
- absent 4th heart sound

153
Q

Differentiate 2nd degree AV block from atrial fibrillation

A

Second degree AV block– regularly irregular rhythm, audible fourth heart sound

Atrial fibrillation– regularly irregular, absent 4th heart sound

154
Q

Most cattle with atrial fibrillation of what underlying acid-base distrubance?

A

metabolic alkalosis

**experimentally metabolic alkalosis with hypokalemia have results in devleopmetn of Afib

155
Q

When is cardiac troponin (cTnI) elevated in horses with afib?

A

acute AF: w/in 4 to 6 hours after onset of Afib

156
Q

What if cTnI remains elevated in horses with afib?

A

Activ emyocardial disease shoul dbe suspected

157
Q

electrocardiogram abnormalities in Afib

A

irregular R-R interval
QT interval and appaearnce of T wave may vary
pwaves absent (replaced by fibrillation waves)

158
Q

Echocardiographic image that should be performed to indicate left atrial enlargement

A

2 chamber: measure in peak systole
**stbd, thgbd: 13.5cm or less

LA to AO ratio in 2D short axis view (provides mroe info on LA enlargement)

159
Q

Which breeds have the highest incidence of AF?

A

standardbred
thoroughbred
draft horses

160
Q

In horses with atrial fibrillation what is the most common valvular lesions?

A

mitral valve disease

161
Q

Quinidine in the treatment of atrial fibrillation:

A

negative inotrope at high dosages
-causes systemic hypotension
-increases ventricular reponse rate

162
Q

What are possible negative side effects of quinidine?

A

nasal edema
cutaneous reactions (urticaria or wheals)
laminitis
colic
marked diarrhea
ataxia

163
Q

Max number of consecutive doses of quinidine to administer?

A

4 doses

164
Q

When should therapy with quinidine be discontinued

A

QRS complex prolongation ( more than 25% of pretreatment value)
fast (>80 to 100 bpm) sustained supraventricular arrhythmia
ventricular rhythm
colic
marked diarrhea
ataxia
nasal edema
laminitis

165
Q

How often administer a dose of quinidine?

A

1 dose every 2 hours

166
Q

What medication can be administered in addition to quinidine to assist in cardioversion from afib to normal sinus rythm?

A

digoxin (11 microg/kgPO twice daily)
**can be helpful in cases, if conversion has not occurred in 24 to 48 hours

167
Q

Caveat to combination therapy of digoxin and quinidine?

A

concurrent admin of digoxin and quinidine results in an increased plasma digoxin concentration

168
Q

Digoxin can be indicated prior to pretreatment of atrial fibrillation in what circumstance?

A

When high heart hearts (want < 60 bpm in horses, <100 bpm in cattle before quinidine treatment)

very low FS (<24%) indicative of underlying myocardial disease

169
Q

If furosemide cannot be removed from therapeutic tx regimen in a horse, what can be added to teh diet to prevent potassium depletion ?

A

KCL

170
Q

At exercise, horses with atrial fibrillation heart rate should not exceed?

A

220 bpm

171
Q

Define ventricular tachycardia

A

cardiac arrhythmia characterized by a rapid rhythm originating in teh ventricle
**originates below hte bundle of HIS in specilized conduction system surround the ventircular myocardium or both

172
Q

Clinical signs associated with ventricular tahycardia

A

exerciseintolerance
syncope episodes
depression
weakness
colic
resp distress
coughing
ventral edema
pulmonary edema

173
Q

In cattle ventricular tachycardia occurs most frequently secondary to

A

sepsis and toxemia

174
Q

Large pulse waves seen in teh jugular vein are called cannon “a” waves that occur when?

A

atrium and ventricle contract simultaenously

175
Q

When are signs of right sided CHF (ventral edema, venous distention) with ventricular tachycardia?

A

sustained uniform VT and increase in servity the longer duration and mroe rapid the rate of arrhthmias

176
Q

When are signs of left sided CHF (coughing, expectoration of foamy fluid, respiratory distress) seen in ventricular tachycardia

A

multiform VT

177
Q

What clinical signs help distinguish VT from sinus or supraventricular tachycardia?

A

presence of jugular pulses
bruit de cannon in an animal with rapid rhythm

178
Q

Diagnosis of VT is made how?

A

ECG: series of 4 or mor ventricular premature complexes
**VPC may be widened and bizarre or WRS duration and apparent normal

179
Q

Vtach: morphology of QRS complexes can be described as:

A

uniform (similar)
vary in morphology (multiform)

180
Q

What is commonly seen with ventricular tachycardia in association with the atrium?

A

atrioventricular dissociation
– atrial rate slower than the ventricular rate
– may see fusion and/or capture beats
– VT can be sustained or paroxysmal

181
Q

What should be considered in horses with acute onset of uniform VT and colic?

A

rupture of the aortic root at the right sinus of valsalva

182
Q

What is a mechanism described in exercise induced VT in horses?

A

sympathetic stimulation (increasing the amplitude of early afterdepolarizations)

183
Q

What is an important cause of sustained VT?

A

reetnry in the ventricle

184
Q

What is though tot be one of the leading causes of sudden cardiac death in horses when other causes of death cannot be found on postmortem examination?

A

Ventricular tachycardia leading to ventricular fibrillation

185
Q

Which gender is at increased risk for aortic root and sinus of Valsalva rupture?

A

males
– usu. middle-aged at time of rupture

186
Q

VT is more likely seen in large animals of any age with what diseases?

A

GI disease
horses– following severe hemorrhage

187
Q

Does slow, uniform VT require treatment?

A

often resolves or improves significantly with correction of underlying electrolyte or metabolic imbalances w/o requiring antiarrhythmic therapy

188
Q

Horses with sustained heart rate >120 bpm, uniform VT treatment

A

antiarrythmic therapy

189
Q

ECG findings associated with life threatening VT

A

multiform origin for the ventricula rpremature depolarizations
-torsades de pointes (wdie VT)
-presence of an R wave superimposedon preceding T wave (R on T)

190
Q

large animal with following C/S treatment recommendation?
-C/S of CHF & hemodynamic collapse
-Heart rate <120 bpm
-Multiform VT (+/- R on T)

A

treat as cardiovascular emergecy– death from ventricular fibrillation is likely w/o antiarrythmic therapy

191
Q

What drugs can be used to tx life-threatning VT:

A

lidocaine
quinidine gluconate
magnesium sulfate
IV procainamide, IV and oral propafenone (refractory VT), IV flecainide
sotalol