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ACVIM General Exam > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the pacemaker of the heart?

A

Sinoatrial Node

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2
Q

What kind of channel is opened to allow the action potential to occur in the SA node?

A

L-type calcium channels

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3
Q

What is the purpose of the AV nodal delay?

A

Allows time for atria to empty their blood into the ventricles prior to ventricular contraction

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4
Q

What is the underlying reason for slowed conduction through the AV node?

A
  1. Decreased numbers of gap junctions → increased resistance to conduction
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5
Q

What happens in phase 0 of the cardiac action potential?

A
  1. Fast Na channels OPEN

2. Depolarize to + 20 mV

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6
Q

What happens in phase 1 of the cardiac action potential?

A
  1. Fast Na channels CLOSE
  2. K ions leave cell through OPEN K channels
  3. Early repolarization phase
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7
Q

What happens in phase 2 of the cardiac action potential?

A

PLATEAU

  1. Ca channels OPEN and fast K channels CLOSE
  2. Brief initial depolarization occurs then AP plateaus
    - Increased Ca permeability
    - Decreased K permeability
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8
Q

What happens in phase 3 of the cardiac action potential?

A

RAPID REPOLARIZATION

  1. Ca channels CLOSE, Slow K channels OPEN
  2. K exits cells
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9
Q

What happens in phase 4 of the cardiac action potential?

A

Back at resting membrane potential

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10
Q

What is the equation for ejection fraction?

A
  1. EF = (SV/EDV) X 100

SV = Stroke volume = ~70ml
EDV = End Diastolic Volume = ~50ml
EF is normally >60%

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11
Q

Cardiac output is primarily determined by _____.

A

Venous return

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12
Q

What are causes of sinus bradycardia?

A
  1. Hypothermia
  2. Hyperkalemia
  3. High vagal tone
  4. Drug (Digoxin, opioids, β-blockers, Ca channel antagonists)
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13
Q

What are 3 types of rhythms without p waves?

A
  1. Atrial fibrillation
  2. Atrial standstill
  3. Sinus arrest
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14
Q

What is the definition of sinus arrest?

A
  1. No sinus complex for greater than 2 R-R intervals
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15
Q

What are the criteria for atrial standstill?

A
  1. No P waves
  2. Regular rhythm
  3. Slow
  4. Superventricular
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16
Q

If a patient with atrial standstill is given an atropine response test, the HR (will/will not) increase

A

Will not!

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17
Q

What are some underlying causes for atrial standstill?

A
  1. Atrial fibrosis → prevents proper conduction → ventricular escape beats → bradycardia
    - Uncommon, English springer spaniels predisposed
  2. Hyperkalemia → alters atrial transmembrane resting potential → atria become inexcusable at very high plasma K levels
    - e.g. blocked cats, Addisons disease in dogs, etc
  3. ECG artifact → waves are too small to see
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18
Q

What breed is predisposed to have atrial fibrosis?

A
  1. English Springer Spaniel
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19
Q

What are the criteria for atrial fibrillation?

A
  1. Tachycardia
  2. No P waves
  3. Irregular R-R interval
  4. Complexes are superventricular
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20
Q

What is the source of atrial depolarization in atrial fibrillation?

A
  1. NOT the SA node
  2. Often due to large atria (DCM, horses)
  3. AV node randomly selects portions of these multiple impulses and lets them through → why its an irregular rhythm
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21
Q

What are the characteristics for 1st degree AV block?

A
  1. P-Q interval too long
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22
Q

What are causes of 1st degree AV block?

A
  1. Drugs: β-blockers, Ca-channel blockers, Digoxin
  2. Increased vagal tone: GI, respiratory, or Neurologic disease
  3. Primary cardiac
  4. Normal variation
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23
Q

What treatment is recommended for 1st degree AV block?

A
  1. Treatment is not indicated → they are still hemodynamically stable
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24
Q

What are the characteristics of 2nd degree AV block?

A
  1. Intermittent failure of AV nodal conduction
    Mobitz Type 1: Irregular P-Q Interval
    Mobits Type 2: Fixed P-Q interval
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25
Q

What is the underlying cause of mobitz type 1 2nd degree AV block? Type 2?

A
  1. Secondary to increased vagal tone

2. Secondary to AV nodal pathology (fibrosis of the AV node)

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26
Q

How is mobitz type 1 2nd degree AV block treated? Type 2?

A
  1. Treat underlying cause of increased vagal tone

2. If bradycardic/clinical → pacemaker

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27
Q

What diagnostic test can be done to differentiate type 1 from type 2 2nd degree AV block? What are the results for each type?

A
  1. Atropine response test
  2. Type 1 → AV block disappears
    Type 2 → AV block persists
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28
Q

What are the characteristics of 3rd degree AV block?

A
  1. No P waves conducted → sinus complexes (p waves not associated with AV node)
  2. AV node completely fibrosed
  3. Ventricular escape rhythm present
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29
Q

What are causes of 3rd degree AV block?

A

AV nodal pathology

  1. Fibrosis
  2. Infiltrative disease
  3. VSD
  4. Endocarditis
  5. Masses
  6. Infectious Diseases
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30
Q

What would be the result of an atropine response test in 3rd degree AV block?

A
  1. Increase P wave rate

2. No change in ventricular escape rate

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31
Q

What is the treatment for 3rd degree AV block?

A
  1. Pacemaker
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32
Q

What are the characteristics of a wandering pacemaker?

A
  1. P waves vary in morphology → normal P-R interval and QRS complexes
  2. Origin of depolarization moving around right atrium
  3. Normal in a dog with high vagal tone → often seen in respiratory sinus arrhythma
  4. No treatment indicated
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33
Q

What is indicated by a narrow QRS complex?

A
  1. Supraventricular origin
  2. Indicate rapid conduction through ventricular myocardium
    - When conduction spreads via bundle branches and purkinje system
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34
Q

What is indicated by a wide and bizarre QRS complex?

A
  1. Ventricular origin
  2. Suggest ventricles have taken more time to become polarized
  3. Spread of conduction has NOT taken place via bundle branche
    - Instead by passive cell-to-cell conduction (much slower)
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35
Q

What are differentials for wide, bizarre QRS complexes?

A
  1. Ventricular ectopic complexes (premature or escapes)

2. Bundle branch blocks

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36
Q

When should ventricular pre-mature complexes be treated?

A
  1. Hemodynamic compromise
  2. Rapid couplets and triplets
  3. Ventricular tachycardia
  4. R-on-T phenomenon
  5. Multiform VPCs
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37
Q

What are the characteristics of Ventricular Escape Complexes?

A
  1. NOT associated with p waves
  2. LATE - happens because of a pause - compensatory mechanism
  3. DO NOT TREAT
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38
Q

What are underlying causes for Bundle Branch Blocks?

A
  1. Result from damaging bundle branches from stretching
    - Hypertrophy
    - Infiltrative disease
    - Infarction
    - Idiopathic degeneration
    - Surgical manipulation
    - Congenital heart disease, acquired heart disease
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39
Q

What is indicated by a bundle branch block?

A
  1. Aberrant conduction system through myocardium → slower depolarization
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40
Q

A left bundle branch block will be (positive/negative) and a right bundle branch block will be (positive/negative)

A
  1. Positive

2. Negative

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41
Q

What are the characteristics of ventricular fibrillation?

A
  1. Rapid, irregular
  2. No organization
  3. No normal wave or complex can be seen
  4. Often follows ventricular tachycardia
  5. Fatal rhythm - causes cardiac arrest
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42
Q

How is ventricular fibrillation treated?

A
  1. Defibrillation

2. Precordial thump

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43
Q

What can be seen on an ECG with right atrial enlargement? What are some differentials?

A
  1. P-pulmonale
  2. Tall P waves
  3. ECG is not very sensitive for atrial enlargement → will be fairly advanced disease when you see ECG changes
  4. DDX: Lab with tricuspid valve dysplasia, chronic pulmonary disease
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44
Q

What can be seen on an ECG with left atrial enlargement?

A
  1. P-mitrale
  2. Wide P waves
  3. May become notched (“M shaped”)
  4. ECG is not very sensitive for atrial enlargement
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45
Q

What can be seen on an ECG with right ventricular enlargement?

A
  1. Large S waves in leads I, II, III, and aVF
  2. Right axis shift (complexes will be negative)
  3. Has to be significant enlargement in order to see
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46
Q

What can be seen on an ECG with left ventricular enlargement?

A
  1. Tall or wide QRS complex
  2. Left ventricular hypertrophy or dilation
  3. PDA (if very tall QRS)
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47
Q

What is the MOA of pimobendan?

A
  1. Positive Inotrope → sensitizes and increases the binding of tropomyosin to calcium (via cAMP)
  2. Phosphodiesterase 3 inhibitor → vasodilation via increased cAMP levels causes decreased preload and afterload
  3. Increases IC Ca
  4. Activates protein kinase A → enhanced diastolic function
    - Also phosphorylates troponin I to increase the rate of myosin cross-bridge detachment
  5. Increased cAMP in smooth muscle causes vasodilation
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48
Q

What are the side effects of pimobendan?

A
  1. May worsen mitral valve regurgitation or increase risk of chord tendinae rupture in early CVD dogs
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49
Q

What was the EPIC (2016) study?

A
  1. Examined the effect of pimobendan in dogs with preclinical myxomatous mitral valve disease and cardiomegaly
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50
Q

What was the finding in the EPIC (2016) study? What were the recommendations?

A
  1. Prolongation of the preclinical period by ~15 months

2. Pimobendan is recommended in preclinical myxomatous mitral valve disease and cardiomegaly cases

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51
Q

What characteristics were used as inclusion criteria for the EPIC (2016) study?

A
  1. Left atrial to aortic ratio >= 1.6
  2. Normalized left ventricular internal diameter in diastole >= 1.7
  3. Vertebral heart sum > 10.5
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52
Q

What was the PROTECT (2012) study?

A
  1. Examined the efficacy of pimobendan in prevention of congestive heart failure or sudden death in Dobermans with preclinical DCM
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53
Q

What were the findings in the PROTECT (2012) study?

A
  1. Proportion of dogs reaching the primary endpoint was not different between groups
  2. The MEDIAN TIME to primary endpoint (CHF or sudden death) was significantly LONGER in the pimobendan group vs placebo (~9 months)
  3. The MEDIAN SURVIVAL TIME was significantly longer in the pimobendan group vs placebo (~5 months)
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54
Q

What is the MOA of dobutamine?

A

Synthetic Catecholamine
1. β1 > β2/α1 → Increase heart rate, contraction, and contractility; renin release (β1 effects) and Dilate blood vessels/bronchioles (β2 effects) and constrict arterioles (α1 effects)

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55
Q

What are the side effects of dobutamine?

A
  1. Mild vasoconstriction
  2. High doses: Tachycardia, arrhythmias
  3. Less tachycardia and vasoconstriction compared to dopamine
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56
Q

What is the MOA of digoxin?

A

Digitalis glycoside

  1. Positive inotrope → Blocks Na/K ATPase in cardiomyocyte → increased Na/Ca exchange → increased intracellular Ca
  2. Antiarrhythmic → lengthens phase 4 and 0 of action potential (in AV node)
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57
Q

What is the only positive inotrope that will slow heart rate?

A

Digoxin

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58
Q

What are the adverse effects of digoxin?

A
  1. Narrow therapeutic window: increased toxicity with hypokalemia
  2. GI (vomiting, diarrhea, anorexia) → most common
  3. Arrhythmogenic
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59
Q

What is the MOA of ACE inhibitors?

A

Enalapril, Benazapril

  1. Inhibits conversion of angiotensin I to angiotensin II
  2. Decreased angiotensin II and aldosterone which would normally:
    - Vasoconstriction
    - Myocardial fibrosis
    - Na and water retention
    - Increased SNS tone
    - Renal efferent arteriole constriction
  3. Decreased degradation of bradykinin
    - Bradykinin → natural vasodilator, stimulates synthesis of PG12/NO
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60
Q

What are the side effects of ACEi?

A
  1. Hypotension
  2. Anorexia
  3. Decreased GFR/RBF → azotemia, acute kidney injury
  4. NSAIDs diminish effects; interfere with bradykinin (inhibit formation of Pos)
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61
Q

What is the MOA of nitroprusside/nitroglycerine?

A

Nitrates

  1. Prodrug generates NO
    - NO 2nd messenger of cGMP → interacts with myosin light chain kinase in vascular smooth muscle → vasodilation
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62
Q

What are the side effects of nitroprusside/nitroglycerine?

A
  1. Hypotension
  2. Nitroprusside → cyanide toxicity
  3. Nitroglycerine → develop tolerance (runs out of NO precursors in 24 hours)
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63
Q

What is the MOA of amlodipine?

A

Ca-Channel Blocker (dihydropyridin specific)

  1. Blocks inward Ca movement in voltage gated channels → vasodilation
  2. Prolong phase 2
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64
Q

What are the side effects of amlodipine?

A
  1. Hypotension

2. Activate RAAS

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65
Q

What is the MOA of sildenafil?

A

PDE-V inhibitor

  1. Inhibits breakdown of cGMP
    - cGMP → interacts with myosin light chain kinase in vascular smooth muscle → vasodilation
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66
Q

What are the side effects with sildenafil?

A
  1. Hypotension (rarely)

- Contraindicated with nitrates

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67
Q

What is the MOA of Aspirin?

A

Nonselective COX inhibitor

  1. Decreased thromboxane 2 → irreversible inhibitor of platelet aggregation
  2. Decreases vasoconstriction
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68
Q

What are side effects of aspirin?

A
  1. GI Ulceration
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69
Q

What is the MOA of clopidogrel

A

Thienophyridine Anti-platelet Agent

  1. Blocks platelet ADP receptors
    - Decreased fibrinogen and vWF binding
  2. Decreased vasoconstriction
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70
Q

What are the side effects of clopidogrel?

A
  1. Rare

2. Decreased appetite, vomiting, diarrhea

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71
Q

What was found in the FAT CAT study (2015)

A

Clopidogrel administration significantly reduces the likelihood of recurrent ATE compared to aspirin in cats

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72
Q

What is the MOA of heparin?

A

Naturally occurring glycosaminoglycan

-Binds and catalyzes action of anti-thrombin II → inhibitor of factor Xa

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73
Q

What are side effects of heparin?

A
  1. Bleeding (less risk with low molecular weight formulation)
    - Monitor aPTT
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74
Q

What is the MOA of rivaroxaban, apixaban, and edoxaban?

A

Factor Xa inhibitors

1. Selectively and reversibly block activity of clotting factor Xa

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75
Q

What is the MOA of class 1A antiarrhythmics?

A

Procainamide, Quinidine

  1. Block fast Na channels in myocardium
    - Decreases rate of phase 0 depolarization
    - Decreases rate of phase 4 repolarization
  2. Increases effective refractory period
  3. Decreases automaticity/AV conduction
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76
Q

What are the side effects of class 1A antiarrhythmics?

A
  1. Hypotension

2. Tachycardia

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77
Q

What is the MOA of Class 1B antiarrhythmics?

A

Lidocain, Mexiletine, Tocainide

  1. Block fast Na channels in myocardium
    - Decreases rate of phase 0 depolarization
    - Decreases rate of phase 4 repolarization
  2. Decreases effective refractory period
  3. Slight increased AV conduction = BAD for SVT
78
Q

What are the side effects of class 1B antiarrhythmics?

A
  1. Lidocaine: CNS toxicity
    - Cats → hemolysis, methemoglobin, sudden death
  2. Mexiletine: Anorexia, vomiting
79
Q

What is the MOA of class II antiarrhythmics?

A

Atenolol, Propranolol, Esmolol

  1. Beta blockade (sympathetic)
    - Decrease HR
    - Decrease contractility
    - Decrease SA/AV node conduction
    - Decrease SNS tone (cardio + Reno-protective)
80
Q

What are the side effects of class II antiarrhythmics?

A
  1. Negative inotrope
  2. Bradyarrhythmias
  3. Hypotension
  4. Bronchospasm
  5. Must be up titrated and never stopped abruptly
81
Q

What is the MOA of sotalol, amiodarone?

A

Class II/III Antiarrhythmics

  1. K channel blocker
    - Prolong AP duration by decreasing slop of phase 3 depolarization
  2. Non-selective beta blockade
    - Prolongs AP and effective refractory period at AV node, atrial, and ventricular myocardium
82
Q

What are the side effects of class II/III antiarrhythmics?

A
  1. Negative inotrope
  2. Bradyarrhythmias (1st degree AV block)
  3. Hypotension
  4. Bronchospasm (B2)
83
Q

What is the MOA of class IV antiarrhythmics?

A

Diltiazem

  1. Non-dihydropyrimidine = heart specific
  2. Blocks inward Ca movement into voltage gated Ca channels of SA/AV node
    - Decreased heart rate and AV conduction
84
Q

What the side effects of class IV antiarrhythmics?

A
  1. Negative inotrope
  2. Vasodilation/Hypotension (rare)
  3. Bradyarrthythmias
  4. Vomiting
85
Q

What are the different stages of canine chronic valvular disease?

A

A: Predisposed
B1: Appears healthy, heart murmur, likely no cardiac remodeling (no clinical signs)
B2: Appears healthy, heart murmur, evidence of cardiac remodeling (no clinical signs)
C: Current or previous CHF
D: CHF refractory to treatment

86
Q

In the resting state, _____ blocks myosin binding sites on actin

A

Tropomyosin

87
Q

Which section of the vasculature controls peripheral resistance?

A

Arterioles

88
Q

The major role of the sympathetic nervous system is in control of (vasoconstriction/vasodilation)

A

Vasoconstriction

89
Q

Baroreceptors sense (increased/decreased) pressure

A

Increased

90
Q

What happens when baroreceptors sense a high BP?

A

They inhibit the sympathetic vasoconstrictor center in the medulla and excite the parasympathetic center
- Systemic vasodilation, decreased HR, and contractility → leads to decreased BP

91
Q

What are chemoreceptors sensitive to?

A
  1. Lack of oxygen (very sensitive)
  2. Increased CO2
  3. Increased hydrogen ion concentration
92
Q

The _____ of a blood vessel plays the greatest role of all factors in determining rate of blood flow

A

Diameter

93
Q

What is indicated by the S1 heart sound?

A
  1. Closure of the mitral and tricuspid valves → onset of systole
94
Q

What is indicated by the S2 heart sound?

A
  1. Closure of aortic and pulmonic valves → end of systole
95
Q

What is indicated by split S2 heart sound?

A

Most common cause is the late closure of pulmonic valve (right heart disease) → most common causes of this being R-L PDA and pulmonary hypertension

96
Q

What is indicated by S3 heart sound?

A
  1. Rapid filling of ventricles from atria
    - Not normally heard
    - Indicated decreased ventricular compliance
    - In dogs think DCM
97
Q

What is indicated by S4 heart sound?

A
  1. Atrial kick, follows atrial contraction
    - Not normally heard
    - Should not be present in A fib or flutter
    - Indicates decreased ventricular compliance
    - In cats think HCM
    - Pressure overloads
98
Q

What is indicated by a systolic click?

A
  1. Heard between S1 and S2

2. Associated with degenerative valve disease → MV prolapse

99
Q

What is the inheritance pattern for arrhythmogenic right ventricular cardiomyopathy?

A

Autosomal dominant

100
Q

What is the most common presenting complaint with ARVC?

A

Syncope

101
Q

How is ARVC treated?

A
  1. Sotalol (class II/III antiarrhythmogenic)
  2. Mexiletine (class 1B antiarrhythmogenic) + atenolol (Class II antiarrhythmogenic)
    * Must document a reduction in ventricular arrhythmias by 75% and ventricular tachycardia by 90%*
102
Q

What kind of arrhythmia is seen in the cat with hyperkalemia?

A

Atrial standstill

* Hyperkalemia does not necessarily cause bradycardia in the cat

103
Q

What are the most common congenital defects in dogs?

A
  1. SAS
  2. PDA
  3. PS
104
Q

What are the most common congenital defects in cats?

A
  1. MV dysplasia

2. VSD

105
Q

Which breeds are at risk for VSD

A
  1. Westies
  2. Lakelenad terriers
  3. Bulldogs
  4. English springer spaniel
106
Q

What is the pathophysiology of L → R shunting in VSDs?

A

Left heart overload → left side overload in diastole → over time LV can exhibit compensatory hypertrophy

107
Q

In general, an isolated VSD in a dog or cat does NOT cause CHF unless the diameter is _____ % of the aortic diameter

A

> 60- 70%

108
Q

What radiographic changes can be seen with VSD?

A
  1. Mild LA and LV enlargemetn
  2. Over circulation of the lungs → enlarged pulmonary veins and arteries → potential MPA dilation
  3. Usually right heart enlargement
109
Q

What is the treatment for VSD?

A
  1. Majority of dogs that survive to their first vaccine are unlikely to develop CHF or other complications
  2. Small VSD → no treatment
  3. Moderate to Severe → can start on enalapril
  4. Sildenafil if significant pulmonary hypertension
  5. Surgery
    - Pulmonary artery banding
    - Closure of VSD
110
Q

What is the sequelae of ASD?

A

RIGHT ventricular volume overload

111
Q

What is the second most common canine congenital heart abnormality?

A

PDA

112
Q

What kind of murmur is heard with a PDA?

A

Continuous murmur

113
Q

PDAs cause (left/right) heart overload

A

Left

114
Q

What is the most common arrhythmia identified with PDAs?

A

A-fib

115
Q

What is the most common complication of coil occlusion in PDAs?

A

Coil embolization of other vessels

116
Q

What are the components of Tetralogy of Fallot?

A
  1. RVOT obstruction (pulmonic stenosis)
  2. Secondary right ventricular hypertrophy
  3. Subaortic VSD
  4. Overriding/Rightward positioned aorta
117
Q

What is the pathophysiology of tetralogy of Fallot?

A

Outflow obstruction and elevated RV. pressure → R→L shunt → Left atrium and LV are small and underdeveloped

118
Q

What are the clinical findings associated with tetralogy of Fallot?

A
  1. Most cases, the murmur is due to pulmonic stenosis (left systolic)
  2. Rads may not show MPA enlargement because all of the blood is shunting to the left (different from normal PS)
  3. Polycythemia
119
Q

What is the treatment for tetralogy of Fallot?

A
  1. Close VSD
  2. Systemic-pulmonary shunt
  3. Phlebotomy + hydroxyurea
120
Q

Ventral septal defect murmurs are (directly/inversely) related to the size of the defect

A

Inversely

121
Q

What are the two types of pulmonic stenosis?

A
  1. Valve leaflet fusion

2. Valvular dysplasia

122
Q

Which breeds may have an aberrant left coronary artery originating from the right aortic sinus? Why is this an important considering in pulmonic stenosis cases?

A
  1. English bulldogs and Boxers

2. DO NOT BALLOON

123
Q

What clinical signs are assoc. with pulmonic stenosis?

A
  1. Exercise intolerance/shortness of breath
  2. Syncope (sudden death is rare)
  3. Left basal murmur +/- systolic click
124
Q

What changes can be seen on radiographs and echocardiogram with pulmonic stenosis?

A
  1. Prominent RV and poststenotic dilation of the MPA
  2. Dynamic infundibular stenosis → the walls of the ventricle come together in systole and add to their own outflow obstruction
125
Q

What is the most common congenital heart defect in dogs?

A
  1. SAS
126
Q

What is the only structural disease that predisposes dogs to endocarditis?

A
  1. SAS
127
Q

What is unique about the progression of SAS compared to other congenital defects?

A
  1. It can progress up to 12 months of age → need to recheck in 1 year to see if the lesion has progressed
128
Q

What changes on radiographs or echo can be seen with SAS?

A
  1. Enlarged LV → LV concentric hypertrophy

2. May have aortic insufficiency

129
Q

What is an important complication associated with SAS?

A

Endocarditis (can often be bartonella)

130
Q

How is SAS treated?

A
  1. Mild to moderate → usually dont treat
  2. β blockers for more severe cases to reduce myocardial O2 demand
  3. ABX prior to elective surgical or dental procedures!!
131
Q

What is the underlying defect in tricuspid valve dysplasia?

A
  1. Abnormal tissue undermining the RV during embryogenesis
    - Thickened, shortened, or elongated leaflets
    - Usually causes tricuspid regurgitation but can have some component of tricuspid stenosis
132
Q

What is the pattern of inheritance for tricuspid valve dysplasia? Which breed?

A
  1. Autosomal dominant

2. Labs

133
Q

What is a common finding on ECG for tricuspid valve dysplasia?

A
  1. Splintered QRS (2/3 of dogs with TVD will have this)
134
Q

What changes can be seen on radiographs and echo with TVD?

A
  1. RA enlargement +/- caudal vena cava enlargement if in CHF

2. Large papillary muscles

135
Q

What is the treatment for tricuspid valve dysplasia?

A
  1. ACEi + diuretics → once ascites is present
  2. Pimobendan (but not labeled for this disease)
  3. Digoxin for a-fib
  4. TV replacement
136
Q

What is the most common congenital defect in cats?

A
  1. Mitral valve dysplasia
137
Q

What are the components of mitral valve dysplasia?

A
  1. Annular enlargement
  2. Short, thick leafs
  3. Short and stout or long and thin chordae tendinae
  4. Upward malposition of atrophic or hypertrophic papillary muscles
  5. Insertion of one papillary muscle directly into one or both sides
138
Q

What are the consequences of mitral valve dysplasia?

A
  1. Mitral insufficiency → LEFT sided CHF
  2. Impaired left ventricular diastolic filling across a stenotic mitral valve
  3. Obstruction to left ventricular ejection via inappropriate systolic displacement of the MV into the LVOT
139
Q

What is the treatment for mitral valve dysplasia?

A
  1. β blockers (atenolol)
    - alleviates the dynamic LVOT and minimizes LV concentric hypertrophy
    - Carvedilol → β blocker with minimal α blocker effects → decrease myocardial oxygen demand, improve LV ejection fraction in cardiomyopathy
140
Q

What finding is a good marker that pulmonary hypertension is present?

A

Tricuspid regurgitation

141
Q

Which breeds are predisposed to chronic valvular disease?

A
  1. Cavaliers

2. Dachshunds

142
Q

Why does atrial fibrillation occur in chronic valvular disease?

A

LA enlargement → prolongation of conduction pathways allows impulses to re-enter muscle that is already recovering from refractoriness → a-fib

143
Q

Which valves are almost exclusively affected by endocarditis?

A
  1. Mitral and aortic valves
144
Q

Which valve does bartonella affect in endocarditis?

A

Aortic valve → especially in SAS

145
Q

Dogs with myxomatous valvular degeneration (are/are not) at an increased risk for endocarditis

A

Are not

146
Q

What are risk factors for endocarditis?

A
  1. Underlying heart disease → SAS
  2. Previous endocarditis
  3. Pacemaker implantation
  4. Recurrent bacteremia
147
Q

What is the pathophysiology for endocarditis?

A
  1. Mechanical lesion on valve leaflet promotes bacterial colonization within the endothelium
  2. Extracellular matrix proteins (thromboplastin = TF + PL) triggers coagulation
  3. Coagulum forms on damaged endothelium → fibrinogen, fibrin, and platelet proteins avidly bind bacteria
148
Q

What are sequelae of endocarditis?

A
  1. Constant immune complex production

- Deposited in joints, glomeruli, skin +/- thromboembolism

149
Q

What are the most common causative organisms for endocarditis?

A
  1. Streptococcus, Staphylococcus, E. coli → most common (>50% of infections)
  2. Bartonella
150
Q

What clinical signs are common with endocarditis?

A
  1. Heart murmur → diastolic murmur most suspicious
  2. Arrhythmias common
  3. Fever
  4. Most/moderate non regenerative anemia → ~50% of cases
  5. Neutrophilic leukocytosis with monocytosis
  6. Azotemia
151
Q

What are the major criteria for endocarditis diagnosis? Minor?

A

MAJOR

  1. Positive blood culture for typical organism
  2. Vegetative lesion or new valvular regurgitation on echo

MINOR

  1. Predisposing condition
  2. Fever
  3. Embolic disease
  4. Immune mediated disease
  5. Echo showing suspicious findigns
  6. Blood culture with atypical organism

*Need 2 major criteria OR 1 major + 2 minor OR 5 minor for diagnosis

152
Q

What is the treatment for endocarditis?

A
  1. Antibiotics for 6-8 weeks
    - Aminoglycosides or fluoroquinolone + beta lactase while waiting on cultures
    - Azithromycin for bartonella
153
Q

Which dog breeds have the highest incidence of dilated cardiomyopathy?

A
  1. Dobermans

2. Boxers

154
Q

What is the most common cause of dilated cardiomyopathy?

A
  1. Idiopathic
155
Q

What is the primary affected chamber in dilated cardiomyopathy?

A

systolic and diastolic dysfunction with chamber dilation primarily involving the left ventricle with variable right ventricular changes

156
Q

What is the most common cause of dilated cardiomyopathy in cats?

A

Taurin depletion

*Serum levels ARE an accurate assessment of taurine levels → should be tested in any dogs on a weird diet

157
Q

What can be caused by a carnitine deficiency?

A
  1. Dilated cardiomyopathy (reported in a family of Boxers)

2. Serum levels are NOT representative of myocardial deficiency → often need an endomyocardial biopsy

158
Q

What physical exam findings are found with dilated cardiomyopathy?

A
  1. Murmur
  2. S3 heart sound
  3. EKG → signs of LA (p-mitrale - widened p wave) and LV (tall R wave) enlargement; a-fib; VPCs
159
Q

What are poor prognostic factors for dilated cardiomyopathy?

A
  1. Younger age at onset of CHF
  2. Breed
  3. Concurrent dyspnea and ascites
160
Q

What is the treatment for doberman cardiomyopathy?

A
  1. Carvedilol → may help with VT and sudden death
  2. Amiodarone
  3. ACEi, spironolactone, and β blockers prior to CHF
161
Q

What is the pathophysiology underlying doberman cardiomyopathy?

A

Impaired myocardial energy production and loss of cellular ability to produce ATP

162
Q

Where do VPCs originate from in doberman cardiomyopathy?

A
  1. LEFT VENTRICLE

- This is opposite from Boxers

163
Q

What are causes of secondary myocarditis in dogs? Cats?

A
  1. Trypanosoma cruzi, Leishmania, Toxo, Lyme, Bartonella, Leptospirosis
  2. Toxoplasma
164
Q

2/3 of ARVC can be attributed to what?

A

Myocarditis

165
Q

What is the only definitive way to diagnose myocarditis?

A

Endomyocardial biopsy

166
Q

What is the treatment for myocarditis? What should be avoided?

A
  1. ACEi

2. Digoxin → can induce pro-inflammatory mediators, myocardial spasm, and arrhythmias

167
Q

What is the underlying genetic cause in HCM for main coones and rag dolls?

A
  1. There are two separate myosin-binding protein C
    - Maine Coons → A31P
    - Rag Doll → RM820W
168
Q

What is a unique side effect in cats on spironolactone?

A
  1. Develop chronic skin lesions
169
Q

What is the treatment for HCM in cats?

A
  1. β blockers
  2. Diltiazem
  3. ATE prophylaxis
170
Q

What are the effects on the following in cardiogenic shock?

  1. Cardiac output
  2. Arterial BP
  3. Venous BP
A
  1. Decreased
  2. Decreased
  3. Increased
171
Q

What can delay CHF for dobermans and large dogs with MVD but NOT small breed dogs?

A

Enalapril

172
Q

What breed can have a normal variant systemic hypertensions?

A

Sitehounds

173
Q

What is the breakpoint for renal damage and neurologic/ophthalmic damage in systemic hypertension?

A
  1. > 160

2. > 180

174
Q

What are the most common inciting causes of systemic hypertension in cats?

A
  1. Chronic renal disease
  2. Hyperthyroidism
  3. Diabetes mellitus
175
Q

What are the most common inciting causes of systemic hypertension in dogs?

A
  1. Chronic renal disease
  2. Cushing’s
  3. Diabetes mellitus
176
Q

What is the treatment for systemic hypertension?

A
  1. Treat underlying cause

2. Amlodipine

177
Q

What is the common denominator in all neurally mediated syncope?

A

Vagal input to the CV center of the brainstem → sympathetic withdrawal accompanied by vagal outflow → bradycardia and vasodilation

178
Q

What is the most common recognized cause of canine syncope across all breeds and ages? Cats?

A
  1. Advanced heart block

2. Heart rhythm disturbance

179
Q

What is the normal amount of pericardial fluid?

A

0.25 ml/kg

180
Q

What is a common underlying etiology for constrictive pericarditis?

A

Coccidiodes

181
Q

Name the disease

  1. High CVP
  2. Ascites
  3. NORMAL heart on rads
A

Constrictive pericarditis

182
Q

Which heartworm life stage enters the blood and is carried to the lungs 100 days after infection?

A

L5

183
Q

Which heartworm life stage is ingested by mosquitos?

A

L1

184
Q

Which heartworm life stage enters the dog tissues?

A

L3

185
Q

What is the best screening test for feline heartworm disease?

A

Feline Ab test

186
Q

What are the causes of hypoxemia? Which will NOT respond to 100% O2

A
  1. Hypoventilation
  2. Shunt → will not respond to 100% O2
  3. Diffusion impairment
  4. V/Q mismatch
187
Q

What determines the length of the PR interval?

A

Conductance through the AV node

188
Q

What will shorten the PR interval?

A

Sympathetic stimulation

189
Q

Which part of the heart does not have parasympathetic innervation?

A

Ventricles

190
Q

What increases cardiac oxygen consumption?

A
  1. Increased afterload
  2. Increased size of the heart
  3. Increased HR
  4. Increased contractility

ACVIM General Exam (15 decks)

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