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Cardiology > CVT Cardiology > Flashcards

CVT Cardiology Flashcards

1
Q

Which deficiency can be seen in cats with DCM?

A

Taurine deficiency (not as common now)

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2
Q

Which breeds in dogs have been noted to have taurine deficiency related DCM?

A

American cocker spaniel, Newfoundland, Goldens

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3
Q

Which supplement showed an increased survival in humans with DCM?

A

L-carnitine (role in long chain FA metabolism and energy production - Lots in heart)
No controlled studies in dogs

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4
Q

What supplement should be offered to all dogs with DCM (esp Boxers)?

A

L-carnitine (role in long chain FA metabolism and energy production - Lots in heart)
No controlled studies in dogs

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5
Q

Has an imbalance btwn oxidant and antioxidants been noted in dogs with DCM and CVD?

A

Yes! JVIM 2005

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6
Q

What is an antioxidant and has a role in energy production that could be consider for supplementation in dogs with cardiac disease?

A

Coenzyme Q10

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7
Q

What is an important component of diet in animals with cardiac disease?

A

Na restriction (based on level of their disease) - Should be <50 mg/100kcal

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8
Q

What is neurocardiogenic (Vasodepressor) Syncope?

A

“reflex-mediated syncope o Incompletely understood adrenergic-stimulated baroreceptor reflex mechanism = inappropriate stimulation of baroreceptor reflex
o Sympathetic surge = “empty ventricle syndrome” = vagal stimulation to brainstem from ventricular mechanoreceptors = sympathetic withdrawal = vasodilation and bradycardia
o Usually follows fight, flight, fright, startle

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9
Q

What is considered the #1 cause of syncope across all ages and breeds?

A

AV Block

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10
Q

What is considered the #1 cause of syncope in older Schnauzers, WHWT, Cockers?

A

SSS

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11
Q

What is considered a common cause of syncope in MR dogs?

A

Neurocardiogenic (Warning sign of high preload, rarely fatal)

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12
Q

What are the 2 main diseases that can predispose to situational relfex-mediated syncope?

A

Advanced MVDD and pulmonary hypertension

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13
Q

What is the #1 cause of syncope in cats?

A

AV block (neurocardiogenic and SSS rare)

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14
Q

What is essential in the diagnosis of syncope?

A

Documenting the heart rate with Holter during event

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15
Q

Name 4 metabolic causes of syncope.

A
  1. Hypoglycemia
  2. Endocrine (Addison’s)
  3. Hypoxia
  4. Anemia
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16
Q

What is the definition of systemic hypertension?

A

Systolic BP > 160 mmHg

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17
Q

What is the sensitivity and specificity of blood pressure readings when BP > 160 mmHg?

A

o Oscillometric and Doppler methods have only 53-71% sensitivity and 85-88% sensitivity in detecting BP > 160mmHg

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18
Q

Name the top 3 diseases in cats that result in hypertension.

A

§ #1 CKD: 20-65% (probably more like 20-30%)
§ Hyperthyroid: 10-86% (probably more like 10-30%)
§ Diabetes: prevalence of SHT poorly documented

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19
Q

What is important to remember about Sight hounds and blood pressure?

A

Sighthounds have BP 15 mmHg higher than other dogs

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20
Q

Name the target organs that are damaged with hypertension.

A
  1. Kidneys: Esp > 160 mmHg risk of glomerular and tubulointerstitial changes
  2. Ocular: Esp > 180 mmHg retinal/intraocular hemorrhage, vascular toruosity, retinal detachement
  3. Brain: Esp > 180 mmHg seizures, mentation change, vestibular dz
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21
Q

How long did it take for systemic hypertension to result in cardaic hypertrophy in dogs?

A

About 12 wks

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22
Q

What happens with the blood pressure cuff is too small?

A

cannot occlude artery so measured pressure HIGHER than actual pressure

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23
Q

What happens with the blood pressure cuff is too large?

A

occludes artery too soon so measured pressure LOWER than actual pressure

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24
Q

What is the ideal cuff size?

A

40% circumference of limb

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25
Q

Why do most animals (and humans) need multiple medications to control BP?

A

o May occur b/c need to directly vasodilate (amlodipine) AND limit ability of compensatory mechanisms to adjust to medication-induced changes (ACE-I)

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26
Q

What is the major concern of using Ca2+ channel blockers alone?

A

preferential dilation of renal afferent arterioles = increased intraglomerular pressure and can cause glomerular damage; ACE-I can protect glomerulus

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27
Q

What is the step wise apporach for chosing hypertension control in dogs?

A

□ ACE-I: decrease in BP 10%, limit proteinuria; can start SID and go up to BID if needed
□ Amlodipine: start SID, go to BID if needed; long half-life in dogs = evaluate after 1 week
□ Refractory HT: search again for underlying causes; consider hydralazine, prazosin, spironolactone, diuretics (proceed carefully and add each one step-wise with close BP monitoring; no good data on multi-drug plans in animals

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28
Q

Name 3 indications for pacing in dogs.

A

SSS, AB block, atrial standstill

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29
Q

What are the most common type of pacing?

A

transvenous, single-lead, single-chamber ventricular pacing (VVI)

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30
Q

What does VVI stand for in pacing?

A

ventricle is paced, ventricle is sensed, and the pacemaker inhibits itself in response to detection of native electrical activity

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31
Q

What are 4 parameters that can be adjusted in a pacemarker?

A

o Pulse Width: Duration of the pacemaker discharge in miliseconds
o Amplitude: Intensity of the pacemaker discharge in volts
o Sensitivity: Ability of the system to detect native electrical activity in the atria or ventricle

Refractory Period: Duration of time following a sensed or paced event that all activity is ignored by the pacemaker

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32
Q

What is a potential risk if your sensing and timing of discharge are off?

A

Ventricular fibrillation

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33
Q

What percentage of dogs had complications during pacemarker implanation?

A

About 55%

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34
Q

What is the most common complication with pacemarker implantation?

A

10% Overall dislodgement rate = Loss of sensing or pacing

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35
Q

What percentage of dogs got an infection of their pacemarker?

A

About 5 %

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36
Q

What percetnage of dogs are still alive at 3 years after placement of a pacemarker?

A

About 50%

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37
Q

What is rate responsive ventricular pacing?

A

§ Uses an activity sensor that attempts to match the paced heart rate with the patient’s activity (accelerometer, minute-ventilation sensor, thermometer, gravitation sensor or QT-interval sensor)

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38
Q

What is dual lead, dual chamber pacing?

A

(most commonly used in people) § Uses a second pacing lead within the right auricular appendage. This senses and paces the atrium, then stimulating a timed ventricular depolarization afterward via the right ventricle.
§ Retains AV synchrony.

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39
Q

What is pacemarker syndrome?

A

When atrial contribution to cardiac output and contraction of atria against closed AV valve - Leading to weakness, dyspnea, heart failure

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40
Q

What type of pacing is more physiologic and why?

A

Dual chamber pacing - It preserves syncrhony btwn atria and ventricles

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41
Q

What is SVT?

A

Rapid rhythms originating in the atria or using the atria or AV junction above the bundle of His as a component of the tachycardia circuit.

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42
Q

What is the purpose of a vagal maneuvers?

A

increase vagal toneàslowed sinus node discharge, prolonged AV conduction and refractoriness.
§ If an SVT abruptly terminates in response, possibilities are AV nodal re-entrant tachycardia, orthodromic AV reciprocating tachycardia, or sinus nodal re-entrant tachycardia. Lack of response doesn’t rule these out.

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43
Q

If blood pressure is compromised by SVT and patient does not repond to vagal maneuver, what can be tried?

A

Diltiazem (Slows AV node conduction and prolongs AV refractory period)
Esmolol (Short acting selective B1 blocker)
Procainamide (prolonges refractory period of ventricules)

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44
Q

Name 4 drugs that can work on the SA node.

A
  1. Beta Blockers
  2. Calcium channel blockers
  3. Digitalis
  4. Class III (K+ channel blocker)
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45
Q

Name6 drugs that can work on the AV node.

A
  1. Digoxin
  2. Beta Blockers
  3. Calcium Channel Blocker
  4. Class III (K+ channel blocker)
  5. Class IC (Na+ channel blocker)
  6. Adenosine
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46
Q

What can occur with persistent tachyarrhythmia?

A

Structural and electrical remodeling

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47
Q

What are 3 indications that you should treat ventricle arrhythmias?

A
  1. Clinical signs (hypotension = weakness, lethargy, exercise intolerance, syncope)
  2. tachycardiomyopathy
  3. Harbor the risk of death
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48
Q

In general which is worse, polymorphic VPCs or monmorphic?

A

Polymorphoric (except in Boxer with ARVC)

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49
Q

What is the frequency that R on T can result in V fib/sudden death in dogs?

A

Unknown!

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50
Q

What if German Shepherd VT?

A

young dogs (death 15-52 weeks); sudden death in 15% of affected dogs; rapid polymorphic VT; usually survive if make it to 2 years; mechanism thought to be triggered activity from early and delayed after depolarizations (don’t know how sustained VT or Vfib occur); death associated with changes in autonomic tone (sleep, early morning excitement)

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51
Q

What are 2 electrolyte abnormalities that should be considered if Vt not responding to lidocaine?

A

Hypokalemia and hypomagnesemia

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52
Q

If lidocaine fails for Vtach what other options are there?

A

Procainamide
Amiodaraone
PO sotalol, meiletine

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53
Q

What is the most common cause of arrhythmia in cats?

A

Associated with primary cardiac disease (generally do NOT present for CS related to arrhythmia (incidental)

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54
Q

What are the most common arrhythmias in cats?

A

BBB or LAFB (48.2%)
VPC (34%)
SVT (24%)
Av Block (12%)

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55
Q

What are the most common causes of 1st degree AV block in cats?

A

Digoxin toxicity, high vagal tone, structural heart diseases, no clinical significance

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56
Q

What are the most common causes of 2nd degree AV block in cats?

A

Cardiomyopathy, conduction, or alpha 2 agonists

Need pacemarked it clinical

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57
Q

What are the most common causes of 3rd degree AV block in cats?

A 
Older cat (> 11 yrs) 0 Cardiomyopathy, infiltraive dz, other structural heart dz, hyper T4, idiopathic (conduction system degeneration)
Need to treat with pacemaker if escape rate
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58
Q

What should you try first for VT in cats?

A

Beta blocker (IV - Propranolon or esmolol; PO - atenolol)

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59
Q

What does ST segment elevation suggest?

A

Myocardial hypoxia

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60
Q

What is cardioversion?

A

external transthoracic delivery of a DC current shock for restoration of sinus rhythm in patients with ventricular or SV tachyarrhythmias

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61
Q

When is a shock delivered to avoid inducing V fib?

A

Shock synchronized to R wave of QRS complex

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62
Q

What is cardioversion the most effective at treating?

A

Impulse re-entry (Afib, Aflutter, AV node re-entry, AV reciprocating tachycardias w/ accessory conduction, and Vtach)

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63
Q

How does cardioversion work?

A

shock simultaneously depolarizes all excitable myocardium and prolongs refractoriness = interrupts re-entrant circuits and establishes electrical homogeneity, terminating re-entry

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64
Q

When should cardioversion be considered?

A

Any tachycardia producing hypotension or CHF which does not respond to medical management

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65
Q

What is PDA and what does it stand for?

A

Patent ductus arteriosus

persistence of fetal ductus arteriosis = communication between descending aorta and MPA

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66
Q

What is the most common signalment of PDA?

A

Female (3:1) - Not in all breeds

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67
Q

What is the most common arrhythmia associated with PDA?

A

A-fib

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68
Q

What is the treatment for PDA?

A

Ductus closure ASAP! Surgical ligation or vascular occulsion

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69
Q

What is the standard vascular occluder for PDAs?

A

Amplatz canine ductal occluder

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70
Q

Which is better for PDA treatment, sx or catheter-based occlusion?

A

No difference in mortality

More major complicatons with sx and more minor complications with catheter based

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71
Q

What is a ventricular septal defect?

A

Hole in IVS allowing communication btwn RV/LV (present at birth)

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72
Q

Which spp are VSD more common in?

A

Cats

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73
Q

Which breeds get VSD?

A

WHWT, Lakeland terriers, English bulldogs, English springer spaniels (inherited)

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74
Q

What does a VSD result in?

A

Left to right shunt = Left sided volume overload

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75
Q

If a VSD results in excessive pulmonary overcirculation what can occur?

A

Development of pulmonary hypertension = Eisenmenger’s physiology
RV pressure overload = Promotes bidirectional or Right to left shunting (opposite from original direction)

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76
Q

Name 4 conditions that can results in right to left shunting.

A

§ Eisenmenger’s physiology (pulmonary hypertension reversing a left to right shunt)
§ Tetralogy of Fallot: VSD complicated by RVOTO and RV hypetrophy; right-to-left shunting predominates = hypoexemia, polycythemia
§ Double-chamber right ventricle: fibromuscular reaction and proliferation in RV = midventricular obstruction just distal to VSD (may close the VSD) = high pressures in proximal chamber = concentric hypertrophy of proximal chamber
§ Concurrent VSD and severe PS

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77
Q

How would Eisenmenger’s physiology appear on CXR?

A

o Eisenmenger’s physiology: MPA enlarged but remainder of pulmonary arteries small

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78
Q

What is the typical murmur for VSD?

A

“Blowing” Systolic murmur at right sternal border

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79
Q

What are CS that can results with right to left shunting?

A

Exercise intolerance, hypoxemia, polycythemia

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80
Q

What are 2 options to treat polycythemia?

A

Phlebotomy (to 62-65%)

Hydroxyura (bone marrow suppression)

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81
Q

Name 3 breeds that get pulmonic stenosis.

A

terriers, English bulldogs, Samoyeds, Chihuahuas, miniature Schnauzers, Labs, mastiffs, Chows, Newfoundlands, Basset hounds, Cockers; inherited in Beagles

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82
Q

What are the 3 types of pulmonic stenosis?

A

Subvalvular, valvular, supravalvular

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83
Q

What is a potential risk in certain breeds with pulmonic stenosis? Which breeds are affects?

A

· Anomalous left coronary artery (Bulldogs, Boxers):
o Single large coronary artery originates from right aortic sinus = divides into left/right
o Left coronary artery encircles MPA below valve = subvalvar obstruction

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84
Q

What is the most common murmur with pulmonic stenosis?

A

o Systolic murmur with PMI at left heart base; harsh ejection-quality crescendo-decrescendo

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85
Q

With moderate to severe pulmonic stenosis what would you see on CXR?

A

o Moderate to severe: RV enlargement, post-stenotic MPA dilation (DV > lateral)

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86
Q

Based on color doppler, velocity across pulmonary stenosis what are the grades?

A

§ PG = 4v2
§ Mild: up to 40-50mmHg
§ Moderate: 40-80 (or 100)mmHg
§ Severe: >80 (or 100) mmHg

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87
Q

What is potential medical treatment for pulmonic stenosis?

A

Treat CHF if present

Atenolol

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88
Q

What is the preferred treatment for pulmonic stenosis?

A

Balloon valvuloplasty

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89
Q

When should balloon valvuloplasty be considered for pulmonic stenosis?

A

o Should be performed ASAP = waiting only causes more RV hypertrophy
o Complication: “suicide right ventricle” = dynamic infundibular stenosis can become more severe following ballooning = increase in RV pressure as hypertrophied infundibulum creates subvalvar obstruction that can be worse than valvular obstruction)
o Bulldogs/Boxers with anomalous left coronary artery: ballooning can cause rupture of MPA and sudden death; can try less aggressive dilation, or surgical conduit around stenosis

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90
Q

What are potential major complications with balloon valvuloplasty?

A

o Major complications (rare): cardiac perforation, rupture of MPA, suicide RV, fatal arrhythmias

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91
Q

What are potential minor complications with balloon valvuloplasty?

A

Minor complications (more common): damaged TV, RBBB, temporary arrhythmias, hemorrhage from vascular access sites

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92
Q

Why can pressure gradients be higher following balloon valvuloplasty?

A

o PG may be higher after procedure vs. during (pulmonary valve leaflets can swell and cause increased obstruction; also, awake dogs have higher SV than anesthetized)

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93
Q

What is the long term prognosis for pulmonic stenosis if balloon valvuloplasty is performed?

A

Excellent (normal lifespans)

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94
Q

What is subaortic stenosis?

A

Fibrous lesion that partially or completely encircles subvalvular outflow tract

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95
Q

Which breeds get subaortic stenosis?

A

Newfoundlands (heritable; polygenic or autosomal dominant); GSD, Boxer, Golden, Rottweiler

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96
Q

What is important to consider about the pathogenesis of subaortic stenosis?

A

o Not present at birth; develops early in life (begins within 3 weeks) d/t morphologic abnormalities in LVOT that increase shear stress and induce proliferation of cells in LVOT; may progress for first 12mo

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97
Q

What are common complications with subarotic stenosis?

A

§ Severe: sudden death, arrhythmias (within 2-3 years)

§ Mild-moderate: infective endocarditis, CHF

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98
Q

What is the classic murmur for subarotic stenosis?

A

Left basilar systolic murmur

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99
Q

What can you feel in the pulses of animal with subaortic stenosis?

A

o Arterial pulses tardum and parvum (weak and late-rising)

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100
Q

Besides LV hypertrophy what can be seen on ECG for patient with subarotic stenosis?

A

ST segment depression suggests myocardial ischemia = Based on increased pressure gradient resulting in narrowed coronary vessles = myocardial ischemia

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101
Q

What can be seen on CXR in animals with subaortic stenosis?

A

post-stenotic dilation of ascending aorta

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102
Q

What is the primary diagnostic criterion for SAS on echo?

A

Peak Ao velocity is primary diagnostic criterion for SAS

§ Most think that >2.25m/s is definitely mild SAS; between 1.9-2.25m/s is grey zone

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103
Q

Which breed has a relative aortic stenosis and what is this?

A

Healthy Boxers: >50% have soft basilar ejection murmurs; those with murmurs have higher aortic velocities than dogs without murmurs = may be breed-related variance in outflow tract anatomic

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104
Q

What are the treatment options for SAS based on degree?

A

o Mild/moderate: not treated; generally have few complications and live normal lifespans
o Severe: often die suddenly from ventricular arrhythmias, but no good treatment option

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105
Q

Is there a benefit of balloon valvuloplasty in dogs with SAS?

A

NO! Not compared to atenolol alone
§ Presumed benefit of atenolol: decrease myocardial O2 demand (negative inotrope and chronotrope); improve myocardial perfusion during diastole; blunts SNS-instigated reflex-mediated syncope; may reduce arrhythmias?

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106
Q

What are the gradients for SAS grades?

A

§ Mild: 80mmHg
§ Pressure gradient is flow-dependent = depends on CSA and stroke volume (SNS activation will worsen apparent stenosis)

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107
Q

What is tricupsid valve dysplasia?

A

congenital malformation of right AV valve apparatus caused by abnormal tissue undermining of the RV during embryogenesis o Variety of abnormalities
§ Thickened, shortened, or elongated leaflets
§ Shortened or absent chordae tendinate
§ Abnormal papillary muscles

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108
Q

What is Ebstein’s anomaly?

A

Seen in animals that get tricspid dysplasia! congenital defect where origins of tricuspid leaflets are apically displaced into RV; may be associated with leaflet dysplasia; rare in vetmed

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109
Q

Which breeds get tricuspid valve dysplasia?

A

Labs (inheirted), Boxers, Goldens, Irish setters, Great Danes, GSD

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110
Q

What ECG abnormality is seen on 2/3 dogs with tricuspid valve dysplasia?

A 
o Splintered QRS in 2/3 of dogs (mechanism unknown; may be ventricular fibrosis, RBB conduction disturbances, accessory pathway conduction)
Atrial arrhythmias (APCs, AT, A flutter, Afib)
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111
Q

What is seen on CXR with tricuspid valve dysplasia?

A

o Right heart enlargement

o HUGE RA but normal MPA

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112
Q

What is treatment for tricupsid valve dysplasia?

A

o Instituted once R-CHF develops
o Furosemide, ACE-I, abdominocentesis, low Na+ diet, +/- pimobendan?
o Atrial fibrillation: digoxin, diltiazem
Balloon Valvuloplasty - reported twice was horrible!

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113
Q

What is the prognosis for dogs with tricuspid valve dysplasia?

A

depends on severity o Mild: may have normal lifespans

o Severe: R-CHF within a few years, though may survive >6yrs with treatment

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114
Q

What may be considered the #1 congenital cardiac abnormality in cats?

A

Mitral valve dysplasia

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115
Q

Which dogs breed get mitral valve dysplasia?

A

Great Danes, GSD, bull terriers, Goldens, Newfoundlands, Dalmatians, mastiffs

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116
Q

How is heart failure different from shock?

A

inability of the heart to maintain CO sufficient to meet tissue perfusion needs given adequate venous pressures (as distinguished from shock that has impaired venous return)

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117
Q

What happens during heart failure?

A

o Decreased CO and BP à trigger compensatory systems to maintain basal BP and target organ blood flow
§ SNS stimulation of heart
§ Vasoconstriction and redistribution of blood flow (SNS, RAAS, vasopressin, vascular endothelial systems)
§ Na+/water retention (RAAS, vasopressin, inhibition of natriuretic hormones)
o Chronic stimulation of control mechanisms à chronic states of vasoconstriction, Na+ retention, mediators of inflammation and tissue growth; heart remodeling (activation of fetal-gene programs, myocyte apoptosis, interstitial and replacement fibrosis)

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118
Q

What are the most common causes of heart failure in dogs?

A

MVD, DCM, pericardial disease, or HWD/PHT

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119
Q

What is the most common acquired heart disease in dogs?

A

Chronic valvular dz, Overall incidence > 40%

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120
Q

In which breed is chronic valvular disease considered to be genetic?

A

CKCS

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121
Q

Chronic valvular disease has generally been considered a non-inflammatory myxomatous vlave degeneration but newer evidence suggests what?

A

Role of serotonin, C-reactive protein, inflammatory cytokines, serotonin-transforming growth factor

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122
Q

What is the pathophysiology of chronic valvular disease?

A

valvular thickening → valvular regurgitation → dilation and hypertrophy of atria/ventricles → compensatory mechanisms (SNS, RAAS) to prevent CHF o CHF occurs when volume overload overwhelming, chordal rupture, or LV myocardial failure
o L-CHF can lead to PHT → R-CHF

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123
Q

Which sex is more effected by chronic valvular disease?

A

Males> females

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124
Q

What is known about treatment of asymptomatic dogs with chronic valvular disease with ACE-I?

A

Controversial (SVEP vs VETPROOF trials) - Generally only for moderate to severe cardiomegaly

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125
Q

What are the 3 mainstays for at home management of CHF?

A

Furosemide
ACE-I
Pimobendan

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126
Q

When do you consider that a CHF patient may have diuretic resistance?

A

When furosemide >2.2 mg/kg q12hrs

127
Q

What should be used if a ruptured chordae tendinae has occurred?

A

Nitroprusside (titer systolic BP to 90 mmHg)

128
Q

Name 3 main reasons for pulmonary hypertension?

A

Primary, secondary (chronic resp dz or long standing L-CHF)

129
Q

What is infective endocarditis?

A

Microbial invasion into endothelium of heart valve = proliferative or erosive lesion

130
Q

Which bacteria results in fibroblast proliferation during infective endocarditis?

A

Bartonella

131
Q

What percentage of dogs with infective endocarditis have Bartonella?

A

About 28% and about 45% of dogs that have negative blood cultures

132
Q

Which valve is more affected with bacterial endocarditis?

A

Aortic valve

133
Q

What is the difference btwn endocaritis and endocardiosis?

A

Osis = Maintain normal glistening surface

It is = disrupts surface (rough, broken) - NOT glistening

134
Q

Name several predisposing factors for infective endocarditis?

A

Bacteremia = Disko, prostatits, pneumonia, UTI, pyoderma, dental dz, catheters
Structural heart dz = SAS
Immunosupression
Steroids?? (controversial)

135
Q

What is the classic signalment for infective endocarditis?

A

Medium to large breed, male

136
Q

Which breed is predisposed to infective endocarditis?

A

GSD

137
Q

Which heart valves are more affected with infective endocarditis?

A

Mitral and aortic (left sided valves)

138
Q

Which is the #1 presenting CS in dogs with infective endocarditis?

A

Lameness

139
Q

If a patient has a diastolic murmur or new murmur what should you consider?

A

Infective endocarditis (89-96%)

140
Q

How many cases with infective endocarditis will have a negative blood culture?

A

60-70% of cases

141
Q

What are the most common isolates for infective endocarditis?

A

Staph, Strep, E. coli

142
Q

What is the sensitivity and specificity of blood cultures for infective endocarditis?

A

Sensitivity: 20%
Specificity: 93%

143
Q

What is the sensitivity and specificity of panbacterial PCR (16 rRNA) for infective endocarditis?

A

Sensitvity: 33%
Specificity: 94%

144
Q

What criteria are used for a diagnosis of infective endocarditis?

A

Modified Duke Criteria = need 2 major or 1 major + 3 minor or 5 minor
Possible: 1 major + 1 minor, or 3 minor
Reject: resolution within 4 days

145
Q

What are the major criteria for infective endocarditis?

A

ECHO - vegatative lesion, erosive lesion, abscess
New valvular insufficiency (esp if AI with no SAS)
2 + blood cultures

146
Q

What are the minor criteria for infective endocarditis?

A 
Fever
New murmur (esp diastolic)
ECHO - Valve thickening, AI
Medium to large dog (>15 kg)
SAS
Sequela = Thromboembolic dz, polyarthritis, glomerulonephritis
1 + blood culture
Bartonella serology (> 1:1024)
147
Q

What are potenial sequlea of infective endocarditis?

A
  1. CHF
  2. Immune-complex dz (IgM, IgG, C3) - Polyarthritis (75%), glomerulonephritis (36%)
  3. Thromboembolism - 70% at necrospy (kidneys, spleen, myocardium, brain)
148
Q

What is the treatment for infective endocarditis?

A

Long term (12 wk) bacteriocidal antibiotics

149
Q

When should prophylaxic antibiotics be given to dogs?

A

In dogs with SAS to prevent infective endocarditis prior to a procedure

150
Q

What is the prognosis for infective endocarditis?

A

Grave = weeks to months

151
Q

What disease is defines as myocardial disease that has systolic and diastolic dysfunction with chamber dilation?

A

Dilated cardiomyopathy

152
Q

What are potential sequela of DCM?

A

CHF

Sudden death

153
Q

What are 4 sporadic causes of DCM?

A
  1. Viral myocarditis
  2. Tachycardia-induced
  3. Taurine deficency
  4. Carnitine Deficiency
154
Q

What is the classic signalment for DCM?

A

Large and giant breed dogs; males

155
Q

What breeds predilection for DCM occurs in the US?

A

Dobermans, Irish Wolfhound, Great Dane, Boxer, American Cocker

156
Q

Which dog breed does not fit the classic signalment for DCM?

A

Cocker spaniel = consider taurine def

157
Q

Which dog breed has a juvenile form of DCM?

A

Portuguese water dog

158
Q

In Dobermans with is the association of VPCs and the development of DCM?

A

> 100 VPC in 24 hrs = Will develop DCM

159
Q

What presentage of dogs have atrial fibrillation at presentation for DCM?

A

About 75-97%

160
Q

What is the prognosis for DCM?

A

Guarded to poor

161
Q

What are 4 negative prognostic indicators for DCM?

A
  1. Younger age
  2. Breed
  3. R-CHF
  4. Afib
162
Q

For what drug is there a benefit in asymptomatic dogs with DCM?

A

ACE-I for DCM

163
Q

What is digoxin?

A

Weak + inotrope, neurohromal modulation (normalize baroreceptor activity - decreased SNS activation)
Treatment for DCM

164
Q

If you have a DCM dog and they have Afib and are not responding to digoxin alone, what can you add?

A

Diltazem, then atenolol (3rd line)

165
Q

What is arrhythmogenic right ventricular cardiomyopathy

A

Primary myocardial dz with 3 forms

  1. Asymptomatic with VPCs
  2. Symptomatic with VPCs
  3. Ventricular dilation, systolic dysfunction, VPCs/SVPCs
166
Q

Which breed gets ARVC?

A

Boxers

167
Q

What is the classic ECG finding in boxer with ARVC?

A

VPC, LBBB morphology (right sided)

168
Q

How is ARVC diagnosed?

A

Holter!! To establish pre-tx freq and complexity of arrhythmia
High suspicion if >100 VPC in 24 hrs and lots of complexity (couplets, triplets, bigeminy, Vtach)

169
Q

Why can the holter examination be normal in boxer with ARVC?

A

Up to 83% day to day variation in VPC freq in boxer

170
Q

What is the correlation bwtn # or complexity of VPCs in ARVC?

A

NO correlation bwtn # or complexity of VPCs and development of CS in affected dogs

171
Q

When should you consider treatment for an asympatomatic boxer with ARVC?

A

When > 1000 VPCs in 24 hrs
Runs of V Tach
or R on T

172
Q

What are treatment options for ARVC?

A

Sotalol
Mexiletine + sotalol/atenolol
Rapid Holter about 2-3 wks after tx started (need 80% reduction in VPCs and reduction in complexity)

173
Q

Which breed gets a slowly progressive primary myocardial disease leading to ventricular tachyarrhythmias, sudden death, CHF?

A

Dobermans

174
Q

What percentage of dobermans with DCM will die of sudden death?

A

About 30-50%, due to rapid Vtach that leads to V fib

More common in AM or after exercise

175
Q

What are the mainstays for DCM treatment?

A

ACEi, spironolactone, B-blockers

176
Q

What are the mainstays for DCM treatment?

A 
ACEi, spironolactone, B-blockers
For dobermans with DCM what are the recommended anti-arrhythmic treatments?	"Mexiletine
then carvedilol (if no CHF) and then amiodarone"
177
Q

When should you consider pimobendan in DCM?

A

For sure when dog is in CHF but maybe need to consider when FS

178
Q

What does syncope predict in dobermans with DCM?

A

Unlikely to progress to end-stage CHF but rather die of sudden death

179
Q

What is myocarditis?

A

insidious inflammatory disorder of myocardium characterized by leukocyte infiltration and nonischemic myocyte degeneration and necrosis

180
Q

Name common infectious causes of myocarditis?

A

Viral: parvovirus, distemper, herpesvirus, coronavirus, others
Bacterial (various)
Rickettsial: Richettsia, Ehrlichia, Bartonella
Spirochetal: Borrelia, Leptospira
Fungal (various)
Algal: Prototheca
Protozoal: Trypanosoma, Toxoplasma, Neospora, Trichineslla

181
Q

What are CS that may suggest myocardial abnormalities?

A

sudden onset ventricular arrhythmia, syncope, weakness, CHF, sudden death

182
Q

What do high levels of cardia Troponin I suggest?

A

Acute myocarditis (with mycytoysis and necrosis)

183
Q

What serologic testing should be performed when myocarditis is suspected?

A

Toxoplasmosis, borrelliosis, rickettsial dz, Barontella, Chagas dz

184
Q

What is thought to predispose cats to acute endomyocarditis?

A

URIs

185
Q

What should be consider in cats (paritcullary from Northern California) if transient fever, depression, lethargy, lymphadenopathy, myocarditis, and diaphragmitis?

A

Transmissible Myocarditis and Diaphragmitis (no caustive agent)

186
Q

What are the 4 most common secondary causes of mycoarditis in dogs?

A

Distemper, toxoplasmosis, lepto, leishmaniasis

187
Q

Which viral infection resulted in puppies with sudden death and CHF and potential DCM?

A

Parvovirus (no cases since 1980s)

188
Q

What is the causative agent of Chagas’s disease?

A 
§ Trypanosoma cruzi (hemoflagellate protozoon parasite)
# 1 mycoadritis in humans and dogs in latin america
189
Q

If you have a dog that has AV block and mycocarditis what should be considered?

A

Lyme (Borrelia burgdorferi)

190
Q

What causative agent result in multifocal myocarditis and valvular endocarditis?

A

Bartonella (B. vinsonii ssp berkhoffi)

191
Q

In which breed is atrial myocarditis described?

A

English springer spaniel - Unknown etiology

Atrial standstill, complete AV block

192
Q

Name the 7 most common secondary causes of myocarditis?

A 
Parvovirus
Distempter Virus
Bartonella
Borrelia
Leptospira
Trypanosoma
Toxoplasma
193
Q

What are 2 causes of secondary myocardial disease in cats?

A

Hyperthyroidism

Hypertension

194
Q

Which spp have a significant number of functional heart murmurs = no obvious anatomic or physiologic causes?

A

Cats!

195
Q

What are the mainstays of HCM treatment?

A
  1. B-blockers (reduce myocardial O2 consumption, slow HR)
  2. ACEi
  3. Ca channel bockers (slower HR, reduce dynamic OTO)
196
Q

What should be consider in cats with HCM and DLVOTO?

A

Atenolol to control DLVOTO but not severe bradycardia

197
Q

What can be considered in low-output CHF?

A

Dobutamine: + Inotrope improve CO regardless of underlying pathology (but will increased myocardial O2 consumption)

198
Q

What are the main treatment goals for HCM?

A

prevent Na+/H2O retention (lasix), modulate neurohormonal activation ACEI), delay myocardial changes (spironolactone), prevent ATE

199
Q

What is a poor prognostic indicator for ATE cats?

A

Hypothermia

200
Q

What disease in cats results in progressive atrophy of RV myocardium with fibrous and/or fatty replacement?

A

Right ventricular cardiomyopathy in cats

201
Q

What are the most common cat breeds to get right ventricular cardiomyopathy?

A

DSH and Birmans

202
Q

What is the prognosis for right ventircular cardiomyopathy in cats?

A

Poor prognosis once in CHF - progressive!

Some cats remain asymptomatic

203
Q

What is the classic signalment for ATE?

A

Middle aged males, mixed breeds (Abyssinian, Birman, Ragdoll

204
Q

IN what percentage of cats is ATE the first sign of heart disease?

A

76% of cases

205
Q

What is the number 1 neoplasia that can result in ATE?

A

Pulmonary carcinoma - Embolization of tumor cells from lungs

206
Q

What are considered to be the survival characteristics in cats with ATE?

A 
1 Limb affected
Some moto function
Higher rectal temps
High HR
Lower serum Phosphorus
207
Q

What was the best predictor of survival in cats with ATE?

A

Rectal temp (50% survival at 98.9 F)

208
Q

What are the mainstays in treatment of ATE?

A

Unfractionated heprain, low dose aspirin, analgesia, supportive care, CHF tx if needed

209
Q

Why is warfarin not recommended for ATE?

A

No benefit over aspirin in survival and higher risk of hemorrhage and lots of monitoring needed

210
Q

What are considered risk fators for ATE on echo?

A

Large artial size
““Smoke”” in atria
Consider antiplatelet or anticoagulant (no consensus yet)

211
Q

What is percardial effusion?

A

excessive fluid accumulation (normal: ~0.25mL/kg) fluid accumulation between outer fibrous parietal pericardium and inner serous visceral pericardium (epicardium)

212
Q

What is the pathophysiology of cardiac tamponade?

A

Pericardium noncompliant, so increased fluid volume leaded to increased intrapericaridal pressure = Excessed cardiac filling pressure = tamponade = limits heart filling = increased venous pressures with decreased CO (can reduce coronary perfusion, can lead to shock)
Even small volume can be horrible if acutely!

213
Q

What is pulsus paradoxus?

A

§ Cardiac tamponade exaggerates variation in arterial BP occurring during respiratory cycle
§ Inspiration normally causes decrease in left heart output (right heart pressing on left) = exaggerated in pericardial effusion causing up to 10mmHg fall in arterial pressure during inspiration

214
Q

What are the most common causes of pericardial effusion in dogs?

A

Neoplastic or idiopathic

215
Q

What are the most common causes of pericardial effusion in cats?

A

CHF or FIP (less likley LSA, systemic infections, renal failure)

216
Q

What are the most common neoplastic causes of pericardial effusions?

A

HAS (#1) - Right auricular (GSD, Goldnes, large breeds)
Heart Base Tumor (chemodectoma) = #2 - Boxer, Bosten terriers, Bulldogs
Pericardial mesothelioma

217
Q

What is the classic signalment for idiopathic pericardial effusion?

A

Medium to large breed dog (6-7yrs)

218
Q

What are potential causes for transudate effusion(modified) pericardial effusion?

A

CHF, peritoneopericardial diaphragmatic hernia, hypoalbuminemia, pericardial cysts, toxemias (uremia), increased vascular permeability

219
Q

What bacteria should be consider in patients with exudative pericardial effusion?

A

§ Infection from plant awn migration, bite wounds, other (aerobic and anaerobic bacteria, actinomyces, coccidiomycosis, TB, systemic protozoal
§ Sterile exudate: leptospirosis, distemper, uremia, idiopathic PE; cats with FIP and toxoplasmosis

220
Q

What is the classic sign on ECG of pericardial effusion?

A

Electrial alternans

221
Q

Discuss the use of pH of pericardial effusion to differentiate underlying disease?

A

High pH = noninflammatory (neoplastic) and low pH = Inflammatory (idiopathic/infectious)
No correlation in dogs :(

222
Q

On which side is it ideal to perform a pericardiocentesis?

A

Right side (cardiac notch to reduce lung injury)

223
Q

What MUST be monitored when performing a pericardiocenetsis?

A

ECG!

224
Q

What is the prognosis for idiopathic pericardial effusion?

A

Good prognosis (drainage to pleural space with pericardiotomy or ectomy)

225
Q

Why is feline heartworm disease under diagnosed?

A

cats frequently amicrofilaremic, serologic tests lack Sn/Sp for cats, worm burdens are small, aberrant sites more common than dogs, clinical signs nonspecific, and easily mistaken for asthma

226
Q

What percentage of indoor cats have HW?

A

About 25%, even though they are 100% indoors

227
Q

Why do feline HWI result in asthma like syndrome?

A

pulmonary response to in situ heartworms includes type II cell hyperplasia and activation of pulmonary intravascular MPs

228
Q

What percentage of cats are microfilaremic with HWI?

A

About 20-35%

229
Q

Why is the antigen SNAP test not good for feline HWI?

A

virtually 100% specific, but very insensitivy (cannot detect low worm burdens); detect antigens from reproductive tracts of mature female worms = not immagutre worm (

230
Q

How can the HW antibody test be used in cats?

A

Good to rule OUT infection (>99% negative predictive value)

Negative = no infection or early (

231
Q

Why do we not really need to HW test cats before starting on prevenative?

A

Cats are rarely microfilaremic and prevenative not rapidlu microfilaricidal

232
Q

What treatment is recommended in cats with HWI?

A

Montly preventative, short term steroids if resp signs

233
Q

A pulmonary artery > 1.6 times diameter of 9th rib on rads is suggstive of what disease in cats?

A

Heartworm

234
Q

What is a causative agent of heartworm disease?

A

Dirofilaria immitis

235
Q

What is the intermediate host of HW?

A

Mosquito

236
Q

What life stage is ingested by mosquito from infected animal with HW?

A

L1 (microfilaria)

237
Q

What life stage is transmitted to host following mosquito bite with HWD?

A

L3 = Infective

238
Q

When are HW considered to be in the lungs?

A

About 100 days post infection (L5)

239
Q

What is the patency of infection for HW?

A

About 6 months

240
Q

What are several reasons that you could have a false negative HW SNAP test?

A

immature infections, low worm burden, all-male infections, circulating Ag-Ab complexing

241
Q

What are the classes of HWI in dogs?

A

§ Class 1: mild (no clinical signs or occasional cough, no CXR signs)
§ Class 2: moderate (occasional cough, exercise intolerance mild CXR signs)
§ Class 3: severe (cough, dyspnea, R-CHF, exercise intolerance; severe CXR signs)
§ Class 4: very severe (caval syndrome)

242
Q

What is caval syndrome in HWI?

A

acute syndrome associated with large worm burden, severe PHT, RV dysfunction with tricuspid regurgitation; see hepatic congestion and IV hemolysis with hemoglobinuria

243
Q

What is the treatment for caval syndrome with HWI?

A

HW extraction

244
Q

What is the adulticide treatment for canine HWI?

A

Melarsomine, Split dose (1 injection then 1 month later 2 injections 24 hrs apart) § Split-dose has higher success than 2-dose (90% vs. 76% conversion to seronegativity), decreases lung injury, and allows for delay if significant adverse reaction; only drawback is cost, longer period of exercise restriction, and total increased dose of arsenical (may be bad if CKD)

245
Q

Why is monthly preventative used in treating HWI?

A

prevent further infection, destroy developing L4s that are not susceptible to adulticide, and eliminate microfilaria

246
Q

What organism when treated with tetracyclines caused HW female worm infertility?

A

Wolbachia (obligate intracellular gram-negative bacteria (Rickettsial))

247
Q

What is reach back with HW preventatives?

A

Efficacy against older infections than just larval

248
Q

Which preventative should be given as a microfilaricidal?

A

Milbemycin

249
Q

If a hyperthyroid cat presents with DCM, what should they be evaluated for?

A

Taurine deficiency

250
Q

What are the 2 most common causes of feline congential heart defects?

A

Mitral dysplasia and ventricular septal defects

251
Q

Why are feline RBCs more susceptible to oxiadtive injury?

A

Greater quantity of sulfhydryl groups on Hbg and reduced ability to convert methemoglobin to oxyhemoglobin

252
Q

What type of toxicity can occur with sodium nitroprusside?

A

Cyanide and thiocyante

253
Q

What is the benefit of nitroprisside administration?

A

Systemic and pulmonary dilation = Controlled reduction in preload and afterload

254
Q

When is nitroprusside useful?

A

Severe hypertension

Catastrophic heart failure

255
Q

Which mutation is common in maine coons and ragdolls with HCM?

A

MYBPC3 mutation

256
Q

What is the hallmark sign of HCM?

A

Concentric LVH (diffuse, asymmetric, segmental) > 6mm in diastole

257
Q

When on ECHO should you be assessing for HCM?

A

During diastole (Concentric wall >6mm)

258
Q

HCM results in _______ dysfunction.

A

Diastolic dysfunction

259
Q

What is HOCM?

A

HCM with LVOT obstruction with Systolic anterior motion of mitral valve

260
Q

What is a classic finding on ECG for HCM?

A

Left anterior fascicular block = Negative QRS in leads II and III and Positive QRS in Lead I

261
Q

What are the hallmark path findings in HCM?

A

Myofiber disarry and replacement fibrosis

262
Q

What are the 4 main risks with HCM?

A

CHF (edema +/- effusion
ATE (risk increased with LAA size and smoke)
Arrhythmias
Sudden death

263
Q

What are the mainstays in treatment for HCM?

A

Atenolol
Diltiazem
Antithrombotic (aspirin, Plavix, heparin)

264
Q

What is the MOA of atenolol?

A

Beta Blocker, relative B1 specific

265
Q

What is the MOA of diltiazem?

A 
Ca channel blocker, blocks L-type Ca channels only
Varying selectivity (nodal>myocardium> vasculature)
266
Q

What 3 animals get ARVC?

A

Boxers, bulldogs, and cats

267
Q

What mutation is thought to occur with ARVC?

A

RYR2 (Ryanodine) receptor mutation - Affects Ca2+ release by SR

268
Q

What are the 3 forms of ARVC?

A

Concealed, overt, systolic dysfunction

269
Q

What are the classic findings on ECG for ARVC?

A

R sided VPC (Left BBB morphology) = UP in lead II

270
Q

What can be seen on histopath for ARVC?

A

Fatty or fibrofatty replacement of RV +/- LV (epicardial to endocardial)

271
Q

What is the treatment for ARVC?

A

Sotalol
Mexilitine and atenolol
Consider L-carnitine

272
Q

What is aortic hypoplasia in boxers?

A

Relative aortic stenosis = arotic is relatively small, but no signs of SAS
Benign!

273
Q

What disease has an early onset in Cavaliers?

A

MVD

274
Q

Name 2 breeds that have polygenic threshold trait for MVD?

A

CKCS and Dachshunds

275
Q

Is a cordiae tendoniae rupture compatible with long term survival?

A

Yes, MST 394 days

276
Q

What is normal fractional shortening?

A

25-45%

277
Q

What is normal LA:Ao ratio?

A

Less than 1.5

278
Q

For MVD with is Stage A and what is recommended?

A

No disease = No tx

279
Q

For MVD with is Stage B1 and what is recommended?

A

Insignificant MR (no LAE) = No TX

280
Q

For MVD with is Stage B2 and what is recommended?

A

Significant MR (LAE) = No consensus reached

281
Q

For MVD with is Stage C and what is recommended?

A

CHF
Acute: Lasix, pimo, sedation, nitroprusside
Chronic: Lasix, pimo, ACEi, diet
Avoid beta blockers

282
Q

For MVD with is Stage D and what is recommended?

A

Refractory CHF
Diuresis
Aggressive afterload reduction

283
Q

Furosemide needs to be where in order to work?

A

On the luminal side

284
Q

Does pimobendan increased myocardial O2 demand?

A

NO

285
Q

How is enalaril excreted?

A

Renal excretion

286
Q

How is benazepril excreted?

A

Renal and biliary excretion

287
Q

Which drug may prevent myocardial and perivascular fibrosis and has resulted in a 69% reduction in mortality in treated CHF dogs?

A

Spironolactone

288
Q

Which breeds can get a juvenile form of DCM?

A

Dobermans and PWD

289
Q

What are two metabloic causes of DCM?

A

Taurine (Cockers)

Carnitine (Boxers)

290
Q

What is a toxic cause of DCM?

A

Adriamycin

291
Q

Why is taurine essential in cats?

A

Cats have less CSAD (cystine sulfinic acid decarboxylate) in order to form it

292
Q

Where is the majority of L-carnitine stored in the body?

A

Almost 100% in cardiac and skeletal mm

293
Q

What drug has been shown to improve survival in DCM dogs?

A

Pimobendan (130 days compared to 329 days)

294
Q

What can be found in >75% of DCM affected dobermans?

A

Ventricular ectopy

295
Q

What are the hallmarks of atrial fibrillation?

A

Irregular rhythm, no p waves, narrow QRS

296
Q

What percentage of dogs will develop cardiac changes with adriamycin?

A

About 20% - Used dexrazozone (Zinecard)

297
Q

What percentage of pulmonic stenosis was valvular?

A

About 90%

298
Q

Why is it important to perform a coronary angiogram prior to balloon valvuloplasty in bulldogs?

A

Bulldogs can have R2A coronary anomaly that if ballooned would be fatal

299
Q

What is the cause of SAS?

A

fibrocartilaginous ring

300
Q

What is important to remember about the development of SAS?

A

Congenital BUT develops postnatally

301
Q

In which breed is SAS polygenic?

A

Newfies

302
Q

What is the tx for SAS?

A

Only transient improvement with valvuloplasty

Atenolol and prophylatic abx

303
Q

What does HARD stand for?

A

Heartworm associated respiratory disease in cats

304
Q

What are common CS in cats with HWD?

A

Coughing, vomiting, sudden death 7%

305
Q

Which biomarker has high sensitivity and specificity for myocaridal damage?

A

Troponin (isoform TnI)

306
Q

What biomarker is increased in cats with HCM and CHF?

A

cTnI

307
Q

In dogs, when have cTnI been increased?

A 
Clinical and subclincial cardiac dz
Pulmonary hypertension
Pericaridal effusion due to HAS
Mycarditis with Babesia/Ehrlichia
Myocardial ischemic injury associated with GDV
Blunt thoracic and myocardial trauma
High dose of doxorubicin chemo
Oleander intoxication and snake bite
Increased age in dogs
Dogs with renal disease
308
Q

When is BNP detected?

A

Released from ventricle in response to increaed wall tension and stretch
Released as prohormone = cleaved into active hormone BNP and inactive NT-proBNP

309
Q

In dogs, when has BNP been found to be elevated?

A

Asymptomatic mod/sev MVD and CHF
Diagnosing heart failure in dogs with cough or dyspnea
Increased in severity of heart failure and may be used as tool to predict clincial outcome

310
Q

In cats, when has BNP been found to be elevated?

A

Not effective in mild/mod HCM but good in sev HCM
Differentiate cardiac vs noncardiac causes of dyspnea in cats
Higher levels if in severe CRF

311
Q

Which 2 dog breeds get SVT?

A

Labs and Boxers

312
Q

What are 3 options to treat SVT?

A
  1. Vagal maneuver
  2. Fluid Bolus
  3. Diltiazem
313
Q

What type of bundle branch block is always associated with pathology?

A

Left Bundle Branch Block

Cardiology (3 decks)

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