ACVIM SAIM (2023) > Cardiovascular > Flashcards

Cardiovascular Flashcards

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1
Q

What are the most common indications for pacemaker implantation in dogs?

What are some less common uses for pacing therapy in dogs?

A
  • High grade second degree AV block (3:1 conduction or less)
  • Third degree AV block
  • SSS
  • Atrial standstill
    NB: cats with AVB have faster V escape rhythm 90-120bpm so don’t typically require pacemaker.

Less common:
- Vasovagal syncope
- Chronic supraV tachyarrhythmias refractory to medical management (AFib, re-entrant A arrhythmias, ATach) - combo radiofreq ablation then pacing
- Refractory V tachyarrhythmias (e.g. long QT) - combo pacemaker + intracardiac defibrillators (case reports in dogs)

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2
Q

What is the incidence of sudden death in dogs with high grade AV block without pacemaker?

A

Up to 40% within 6 months of diagnosis

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3
Q

MMVD: What clinical signs have been identified as negative prognostic indicators?

A
  • cough,
  • exercise intolerance,
  • decreased appetite,
  • breathlessness/difficulty breathing
  • syncope
  • Mumur > III/VI
  • absence/loss of respiratory sinus arrhythmia
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4
Q

MMVD: What other changes (apart from clinical signs) have been associated with higher risk of CHF?

A
  • increase NT-proBNP
  • enlarged heart size
  • LA enlargement
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5
Q

How is PV/PA measured?

A
  • Right parasternal long view
  • trace line perpendicular to the medial PV passing through the center
  • Use M mode to measure inner edge to inner edge at the end of the T wave
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6
Q

What is tissue Doppler imaging-derived E/Emsept a predictor of?

A

Load independent CHF in dogs with MMVD

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7
Q

What is tissue doppler imaging (TDI)?

A

Form of doppler that measures the velocity of the heart muscles through different phases of the cardiac cycle.

TDI measures the excursion of the myocardium, rather than the blood flow. TDI is less load dependent than the transmitral flow pattern.

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8
Q

What does the E/Emsept measure?

A

Ratio of the transmitral peak early diastolic velocity to the tissue doppler-derived peak early diastolic velocity at the interventricular septal basal segment

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9
Q

La:Ao greater than what value is associated with worse outcomes in dogs with MMVD?

A

> 1.7

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10
Q

La:Ao greater than what value is associated with worse outcomes in dogs with MMVD?

A

> 1.7

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11
Q

What proportion of dogs with MMVD stage B2 have pulmonary hypertension?

A

Approx 1/3

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12
Q

What % of puppies have an innocent murmur?
What are the characteristics of this?
What may explain the presence of an innocent murmur?

A

15%
Systolic, musical, maximum 2/6 intensity, PMI left cardiac base
Anaemia was noted in these and may contribute to initial murmur that resolves with age and improvement in HCT.

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13
Q

what changes are expected to be seen on echo after PDA closure?

A
  1. reduced preload
    - reduction in LVIDd
    - reduced La:Ao
  2. Transient reduction in LV systolic function
    - reduced FA
    - LV dyssynchrony
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14
Q

At what cut off, what is the sensitivity and specificity of NTproBNP for discriminating between CHF and non-cardiac resp distress in dogs?

A

> 2447 pmol/L
sens 81%
spec 73%

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15
Q
  1. Describe the pathogenesis of patent ductus arteriosus (PDA).
  2. What is proportion of dogs & cats with congenital heart defects have PDA?
A
  1. ductus arteriosus is a vessel that develops from the embryonic
    left sixth aortic arch. Typically, ductal flow decreases dramatically
    within the first 12 hours of life in the neonatal dog, ceasing altogether
    within 7 days, but in some individuals the ductus can remain patent.8
    Direction of blood flow through the PDA is determined by the relative
    resistances of the pulmonary and systemic vascular beds. Flow therefore
    typically proceeds from left-to-right, that is, from the aorta to the
    pulmonary artery.
  2. Dogs: 11-30%, cats: 3%
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16
Q
  1. How does a reverse (right to left) PDA develop?
  2. What proportion of dogs and cats patients develop this?
  3. What are the treatment implications for reverse PDA?
A

Greet JVIM 2021
1. In animals with severe pulmonary hypertension, pulmonary vascular resistance can exceed systemic vascular resistance, leading to right-to-left shunting across the PDA, and mixing of deoxygenated blood in the descending aorta.
Increased
endothelial shear stress due to augmented pulmonary blood flow can
result in reactive vasoconstriction, progressive medial hypertrophy,
intimal proliferation of the pulmonary vasculature, and shunt reversal
(Eisenmenger’s physiology)

  1. 1-6% dogs with PDA. Cats»_space; common, 15-17%.

*NB: spectrum of disease - blood flow through the PDA can be continuously right-to-left or bidirectional, influenced by severity of PHT & SVR.

  1. PDA ligation is contraindicated
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17
Q

What does the E/A wave represent and what is a normal ratio?

In what pathological conditions will the E/A wave be unmeasurable?

A

E = peak velocity of blood flow across mitral valve in EARLY diastole (think E = early)
A = peak velocity of blood flow across mitral valve in LATE diastole (think A = after)
Also usually assess E wave deceleration.

Normal cats/dogs – E/A should be >1 (think E = Everest so should be higher). E/A ratio can decrease with age (can sit around 1 in older dogs).

When you cannot measure E/A ratio:
- Very fast HR e.g. cats. If cannot evaluate E/A ratio, likely some diastolic dysfunction. Measure isovolumic relaxation time (IVRT) instead as not affected by HR. Increased LA pressure shortens IVRT.
- AFib –> loss of A wave

With myocardial stiffening and delayed relaxation (e.g. HCM cats) –> decreased in E velocities.

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18
Q

Name conditions associated with:
a) HCM phenotype (cats)
b) DCM phenotype (cats)
c) DCM (dogs)

A

ACVIM Feline CM consensus 2020
a) Transient myocardial thickening (TMT), neoplastic infiltration, acromegaly, hyperT
b) Dietary taurine deficiency, tachycardia-mediated
c) Breed-specific gene mutations, taurine deficiency (American Cockers), toxins (doxorubicin), infectious (parvovirus infx @ 2-4wks old)

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19
Q

Which cat breeds are at-risk for HCM development?
Which associative gene mutations?

A

ACVIM Feline CM consensus 2020
Maine Coon, Ragdoll, British Shorthair, Persian, Bengal, Sphynx, Norwegian Forest cat, Birman.

Maine Coons homozygous for MYBPC3-A31P mutation
Ragdolls homozygous for MyBPC3-R820W mutation

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20
Q

Dog breeds predisposed to DCM?

A

Boxers (some have dietary carnitine deficiency)
Doberman Pinschers (not taurine-deficient)
Dalmations
Cocker Spaniels
NB: American Cockers - taurine deficient DCM (defects in taurine metabolism)

Golden Retrievers
Great Danes (not taurine-deficient)
Irish Wolfhounds Newfoundlands

Portuguese Water Dogs (juvenile form - onset several wks old)

Standard Schnauzers

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21
Q

Gene mutations associated with DCM in dogs?

A

German short-haired pointers - DMD
Dobers - PDK4, locus on chromosome 5
Boxers - STRN
Irish Wolfhounds - polymorphisms on chromosomes 1, 10, 15, 17, 21, 37

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22
Q

Normal LA pressure in dogs?

A

<10mmHg

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23
Q

What are the actions of Angiotensin 2? What receptor does it act on?

A

Acts on angiotensin receptor type 1 –> causes potent vasoconstriction, Na & H2O retention, aldosterone release, myocardial remodeling.

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24
Q

What was the major findings of the FAT CAT trial?

A

Hogan 2015 (J Vet Cardio)
Clopidogrel was shown to be superior to aspirin with :
- A lower FATE recurrence rate of 49% (vs 75%) & 1-year recurrence rate of 36% (vs 64%).
- Longer median time to FATE event (443 days) cf aspirin (192 days).

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25
What was the major findings of the FAT CAT trial?
Hogan 2015 (J Vet Cardio) Clopidogrel was shown to be superior to aspirin with : - A lower FATE recurrence rate of 49% (vs 75%) & 1-year recurrence rate of 36% (vs 64%). - Longer median time to FATE event (443 days) cf aspirin (192 days).
26
What major and minor criteria are included in the modified Duke criteria to diagnose infective endocarditis in dogs? What constitutes a definitive vs possible diagnosis?
Definitive dx = 2 major OR 1 major + 2 minor. Possible = 1 major + 1 minor OR 3 minor. MAJOR: - Echocardiographic valve lesion with typical characteristics of endocarditis: -- Oscillates independently of valve motion -- Associated with atrial aspect of mitral valve or ventricular aspect of aortic valve - Positive blood cultures: -- ≥2 positive blood cultures -- ≥3 with common skin contaminant - Evidence of new valve insufficiency MINOR: - PUO - SAS (esp Boxers) - Evidence of embolic signs - - Evidence of systemic IMD - Med-large breeds (>15kg) - Positive blood cultures not meeting major criteria - Bartonella spp serology ≥1:1024
27
What is urodilatin? Where is it produced & its roles?
Renal form of pro-ANP. Synthesized in distal tubules, local function in Na & volume regulation.
28
Medical management options for sick sinus syndrome?
Sympathomimetics (e.g. terbutaline) or anticholingergics (propantheline) - some dogs may respond if they have a partial response to an atropine response test.
29
What oral treatment may be administered in large/giant breeds with lone AFib that develop clinical signs (e.g. erratic HR during exercise)?
Chronic amiodarone (usually low dose)
30
What is a potential detrimental effect of excessive high vagal tone on atrial myocytes?
High vagal tone shortens the refractory period of the myocytes (non-uniform across the atria) > promotes reentrant arrhythmias esp **AFib**
31
What endocrinopathy is a risk factor for AFib? Does this improve with treatment?
Pariaut VCNA review Primary hypoT. May convert into sinus rhythm after levothyroxine supp.
32
ARVCM - Gene mutation, mode of inheritance & predisposed breeds - Describe the 3 forms of disease? - What ECG abnormalities are characteristic?
1. Striatin mutation - autosomal dominant with incomplete penetrance. Homozygotes younger & worse dz. Boxers. 2. 1 - Asymptomatic with occ VPCs. 2- Tachyarrhythmias, ex intolerance, syncope. 3 - myocardial systolic dysfunction, ventricular dilation +/- CHF, +/- sudden death 3. Ventricular ectopy (>100 VPCs/24hrs); LBBB morphology (positive in lead II)
33
ARVCM - Indications for treatment - Top 3 anti-arrhythmic therapies - Name 2 adjunct therapies that may be beneficial
No official guidelines but at least 2 criteria: ≥100 VPCs in 24hrs, presence of couplets/triplets/runs, R-on-T phenomenon on 24hr-Holter. Sotalol, mexiletine +/- amiodarone Fish oils, L-carnitine
34
What treatment should be considered prior to balloon pulmonary valvuloplasty in dogs with pulmonic stenosis, and what are the benefits?
Beta blockers 2-4 weeks pre-procedure. Decreases FOC of RV, slows HR, reduces myocardial O2 consumption. Improves GA stability, slows HR during procedure > more accurate balloon placement. Higher doses likely required for dogs with severe dynamic obstruction.
35
What is TAPSE (Tricuspid annular plane systolic excursion)? What disease conditions in dogs & cats does it have prognostic significance?
Measures (in mm) the maximum longitudinal distance the lateral tricuspid annulus travels toward the RV apex in systole. Acquired from the left apical 4-chamber view optimized for the RV in M-mode. TAPSE decreased in most dogs with severe PH. Decreased TAPSE associated with shorter survival in cats with HCM & Boxers with V arrhythmias.
36
What does the RV myocardial performance index (aka Tei index) measure?
Marker of global (systolic and diastolic) RV function. Tei index = isovolumic time (aka isovolumic contraction + relaxation time) / RV ejection time. Increased Tei > RV dysfunction (systolic dysfunction prolongs isovolumic contraction time; diastolic dysfunction prolongs isovolumic relaxation time)
37
What does RV strain & strain rate measure?
RV strain = tissue deformation (% change in tissue length cf original length) Strain rate (SR) = strain per sec Positive values = myocardial lengthening/thickening; negative values > myocardial shortening or thinning. Uses speckle tracing echo for measurements.
38
What specific adverse effect was identified in Maine Coons with cardiomyopathy receiving spironolactone, and what % were affected?
Severe facial dermatitis; 33%
39
When may pimobendan be considered for cats with HCM?
Severe (end-stage) HCM with evidence of decreased LV systolic function. Involves myocyte death & replacement fibrosis.
40
What echo parameters may be associated high-risk HCM (at risk of CHF or ATE)?
LA dilation (LA: Ao >1.8, LA >16mm) Reduced LA FS <12% LV FS
41
What cut-off values of the following are associated with increased risk of cardiac mortality in HCM cats? - Plasma NT-proBNP - cTnI What cut-off NT pro-BNP concentration is likely associated with high risk disease?
NT-proBNP >250pmol/L cTnI >0.7ng/mL NT-proBNP >100pmol/L (recc FU echo)
42
What is the potential benefit of L-arginine in treatment of pulmonary hypertension?
Main substrate (nitrogen donor) for nitric oxide (NO) production - NO mediates pulmonary vasodilation.
43
Class I anti-arrhythmics: - MOA - Phase of cardiac AP affected - Example drugs - Indications (& contraindications)
Na channel blockers, decrease Na influx so decrease slope of phase 0 during depolarisation. IA: intermediate (rarely used). **Quinidine, procainamide, disopyramide**. Can prolong duration of AP - QRS & Q-T. IB: fast (commonly used). **Lignocaine, mexiletine, phenytoin, tocainamide.** Increases threshold for VFib. Minimal effects on atrial, SA or AV node. Minimal effects on inotropy & conductivity (QRS & Q-T unchanged). IC: slow. **Flecainaide, encainide, propafenone**.*Depress FOC, CO & BP.*
44
Class II anti-arrhythmics: - MOA - Which is selective vs non-selective - Indications/contraindications
Beta blockers Selective (B1 only) - **bismolol, esmolol, atenolol, metoprolol** Nonselective (B1+B2) - **propanolol** B1+B2+A1 - **carvedilol** (also antioxidant - free radical scavenger) Indications - many (HOCM, SVT, VT, PS, SAS, DCM, phaeo) Contra - decompensated HF (CHF, low output), hypotension, basically acute dz; also hyperK
45
What are potential concerning CVS effects with using amlodipine as monotherapy for treatment of systemic hypertension with renal disease? What treatment strategy may attenuate this risk?
Amlodipine causes afferent arteriolar vasodilation. But may cause local RAAS activation --> efferent arteriolar constriction --> expose glomeruli to higher pressures & progressive damage. Using an ACE-I with amlodipine may help prevent this occurrence.
46
What are predisposing factors for digoxin toxicity?
1. Azotemia 2. HypoK - predisposes to myocardial toxicity by leaving more available binding sites on membrane Na+-K+-ATPase for digoxin 3. HyperCa & hyperNa - potentiate both inotropic & toxic effects of drug 4. HyperT potentiates myocardial effects of drug. HypoT prolongs drug T ½ (in people) 5. Hypoxia - sensitizes myocardium to toxic effects of drug 6. Drug interactions - concurrent admin of quinidine (displaces drug from muscle binding sites & increases serum [ ]), verapamil, amiodarone, spironolactone etc... many
47
What are the adverse effects of excessive dietary Na restriction in patients with clinical HF?
Increase neurohormonal (esp RAAS) activation Worsen dilutional hypoNa (seen with CHF) Worsen inappetance/anorexia (low palatability)
48
What is the treatment of choice for pulmonic stenosis in dogs & benefits? In which cases is this treatment not appropriate and why?
Balloon valvuloplasty. 50+% successful reduction of pressure gradient in 75-80% of dogs post-balloon. Dogs undergoing balloon tx had 53% reduction in mortality vs those that did not. Cases not amenable to ballooning = hypoplasia of the pulmonary annulus, anomalous development of the coronary arteries, subvalvular PS --> high risk of avulsion of the coronary artery or rupture of the pulmonary annulus. Conservative ballooning with smaller balloons have been trialled with variable results.
49
What is the recommended treatment for subaortic stenosis in dogs? What are negative prognostic factors?
NOT ballooning (unlike PS) - not proven to confer better survival benefit over medical management with beta blockers (atenolol). Also exercise restriction, +/- prophylactic abx prior to procedures (endocarditis risk) Px poor! 50% dogs - sudden death within 1st 3 years. Neg px factors: predisposed to infective endocarditis, L-CHF (likely to develop >3yrs). Also dvpt of A or V rrhythmias, worsening MR
50
What is Eisenmenger's syndrome and a classic clinical manifestation? What is a potential medical treatment that may benefit & its mechanism?
Occurs when a L to R shunting cardiac defect (e.g. VSD, large/non-restrictive VSD, ASD, PDA) causes pulmonary overperfusion (R heart vol overload) --> leading to pulmonary hypertension --> R heart pressure increases & equilibrates with (L) systemic arterial pressure --> eventual reversed (R to L) shunting --> deoxygenated blood flow from RV to aorta. Differential cyanosis (worse with exercise) Sildanefil - PDE-5 inhibitor --> reduces pulmonary resistance via NO-dependent pulmonary vasodilation.
51
What are the 4 structural abnormalities that occur with Tetralogy of Fallot?
1. VSD (usually large, non-resistive) 2. Dextropositioned/overriding aorta 3. Pulmonic stenosis 4. RV hypertrophy
52
What are the major vs minor criteria used to diagnose of infective endocarditis in dogs? What criteria should be fulfilled to meet a definite vs possible diagnosis of IE?
Major criteria: - Positive echo (vegetative or erosive lesion or abscess) - New valvular insufficiency (r/o SAS) - Positive blood cultures (at least 2/3, or all 3 if skin contaminant) Minor criteria: - Pyrexia - IMD, TE dz - Positive Bartonella serology -Medium to large dog (>15kg) - SAS - Positive blood culture not meeting major criteria Definite: 2 major criteria, or 1 major + 2 minor Possible: 1 major + 1 minor, or 3 minor
53
Name 5 negative prognostic factors for infective endocarditis in dogs?
- Aortic valve involvement (MST 3d in one study) + evidence of volume overload - Bartonella infections (aortic IE most common) - G- infections - Septic embolization or metastatic infection - Concurrent treatment with corticosteroids even with concurrent abx Also - Late diagnosis and treatment commencement - Valvular vegetations - Cardiac/renal renal complications not responding to tx - Thrombocytopaenia - Elevated ALP - Hypoalbuminaemia (70% mortality with this finding) - Tx with bacteriostatic abx, premature termination of abx
54
Which dogs are at high risk of clinical DCM based on Holter criteria?
50 VPCs/24hrs or with couplets or triplets
55
1. What breeds get taurine responsive DCM? 2. What is a predisposing factor identified in Dalmatians diagnosed with DCM that can be rectified? 3. Which 2 breeds often develop AFib prior to onset of clinical DCM/structural evidence of?
1. GRs (familial). American Cocker Spaniels (not English CSPs) - also supp L-carnitine. 2. Being fed a low protein diet (for treatment of urate urolithiasis). Taurine and L-carnitine were not low in these dogs based on studies. Switch to higher protein diet if possible. 3. Great Danes, Irish wolfhounds
56
At what cut-off taurine levels is supplementation recommended? How long does it typically take to observe echocardiographic improvements with taurine supplementation in DCM dogs?
Taurine 200-250nmol/L (low end RI) esp for GRs. Based on WHOLE BLOOD taurine [ ]. (No breed specific RIs yet) 3-6months, can be longer.
57
What are the 2 main clinical manifestations of canine parvoviral myocarditis based on age?
1. Per-acute form: puppies 3-8 wks old, acute dyspnoea due to LCHF and usually die within hours. 2. Juvenile dogs generally <1yo. Clinical presentation similar to DCM.
58
At what cut-off pressure for dynamic LVOTO associated with SAM is treatment recommended in cats? What treatment?
>80mmHg pressure gradient. Beta blocker (atenolol). Diltiazem also considered but less effective
59
What differences in ANP response occur between cardiac dz associated with pericardial effusion vs other cardiac dz?
In pericardial effusion, ANP does not increase as there is external compression on the heart (so no atrial stretch to stimulate release) --> prevents natriuresis & worsens effects of increased blood vol & venous P.
60
Define pulsus paradoxus & how it occurs with pericardial effusion?
- Normally during inspiration, intrathoracic P decreases --> blood flows preferentially into the pulmonary vv. + RA & RV (most compliant intrathoracic vessels & cardiac chambers). - Blood pooling in pulmonary vv. reduces preload of L heart --> reduces LV SV. Conversely, **RV SV increases** during inspiration due to increased R heart filling (occurs at the expense of LV filling as R side is more compliant) - Decreased LV SV leads to loss of pulse pressure
61
What endocrinopathy may chronic pericardial effusions mimic and why?
HypoA. Chronic effusions lead to decr Na+ & incr K+ from reduced effective circulating volume = 'pseudohypoA'
62
Describe ECG changes characteristic of electrical alternans?
Alteration in amplitude & contour of QRS complexes (+/- T waves) with every alternate beat. Results from swinging motion of the heart within the pericardium, more common with large vol effusions. Also see low amplitude QRS complexes (<1mV) due to effusion insulating the electrical signals from the heart from being transmitted to the body surface/ECG (increases to normal amplitude after therapeutic pericardiocentesis)
63
Name some infectious causes of pericarditis in dogs?
Fungal - Coccidioides immitis Leishmaniasis Leptospirosis Canine distemper virus
64
For which cardiac neoplasm may pericardiectomy confer a reasonably good prognosis in dogs?
Chemodectomas - MST 730d (only 42d with pericardiocentesis)
65
What is a common cause of constrictive pericarditis in dogs?
Coccidioides immitis infection
66
Hypertensive encephalopathy has a predilection for ..... in the CNS. Prediposed sites include ....... in the brain, and ...... in cats with ischemic myelopathy.
ACVIM consensus/Ettinger White matter Cerebrum (parietal & occipital lobes) > reactive seizures etc. C1-C5 (esp C2-C3) > cervical ventroflexion, weakness
67
Central venous pressure (CVP) monitoring allows assessment of patient's volume status. CVP .....cm H2O indicates hypovolemia (fluid loss) or vasodilation (decreased SVR). High CVP of ...... indicates ....... (3 causes).
< 0cmH2O >10cmH2O - IV volume overload (incr preload), R HF, increased SVR (afterload).
ACVIM SAIM (2023)
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