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ACVECC Top 100(?) Papers > Cardiovascular > Flashcards

Cardiovascular Flashcards

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1
Q

Tag & Day (2008): What ECG changes are classically associated with hyperkalemia in dogs and cats?

A

Tall peaked T waves, prolonged PR interval, loss of P waves, widened QRS complex, and bradyarrhythmias.

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2
Q

Tag & Day (2008): At what serum potassium concentration do ECG changes typically begin to appear?

A

Changes typically appear at 6.0–6.5 mmol/L; more severe abnormalities are seen at higher levels (>7.5 mmol/L).

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3
Q

Tag & Day (2008): Why is bradycardia often paradoxical in hyperkalemia despite sympathetic activation?

A

Hyperkalemia impairs conduction velocity and causes SA/AV node suppression, overriding compensatory sympathetic effects.

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4
Q

Tag & Day (2008): What is the pathophysiologic basis for T wave changes in hyperkalemia?

A

Increased extracellular potassium shortens and sharpens the repolarization phase, producing tall, narrow T waves.

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5
Q

Tag & Day (2008): What advanced ECG changes are associated with severe hyperkalemia?

A

Widened QRS, loss of P waves, junctional or ventricular escape rhythms, and eventual sine wave patterns.

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6
Q

Tag & Day (2008): What is the significance of the QRS-T angle in hyperkalemia?

A

A widening QRS-T angle suggests ventricular conduction delay and is associated with more severe hyperkalemia.

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7
Q

Tag & Day (2008): Do all animals with hyperkalemia show ECG changes?

A

No; not all animals with elevated potassium will exhibit ECG changes—some tolerate hyperkalemia better, especially cats.

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8
Q

Tag & Day (2008): What was a key conclusion of the paper regarding ECG use?

A

ECG is a useful but not sensitive screening tool for hyperkalemia—reliance on potassium measurement is essential.

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9
Q

Tag & Day (2008): How did cats differ from dogs in ECG response to hyperkalemia?

A

Cats were less likely to show typical ECG changes, even at higher potassium levels, compared to dogs.

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10
Q

Tag & Day (2008): Why must ECG findings be interpreted in clinical context?

A

Because other conditions (e.g., hypoxia, acidemia, hypocalcemia) can modify ECG appearance or mimic hyperkalemia effects.

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11
Q

According to Langhorn & Willesen (2016), what are cardiac troponins and why are they important?

A

Cardiac troponins (especially cTnI and cTnT) are cardiac myocyte-specific structural proteins released into circulation following injury. They are highly sensitive and specific markers of myocardial damage.

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12
Q

According to Langhorn & Willesen (2016), which troponin isoform is most commonly measured in veterinary medicine?

A

cTnI is most commonly measured due to its high cardiac specificity and availability of assays.

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13
Q

According to Langhorn & Willesen (2016), what conditions commonly cause elevated cTnI in dogs and cats?

A

Common causes include myocarditis, trauma, sepsis/SIRS, GDV, heatstroke, CHF, pulmonary hypertension, neoplasia, and toxins.

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14
Q

According to Langhorn & Willesen (2016), what non-cardiac conditions may falsely elevate cTnI?

A

Hypoxia, systemic inflammation, renal dysfunction, and general critical illness can elevate cTnI without direct cardiac injury.

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15
Q

According to Langhorn & Willesen (2016), how does cTnI relate to prognosis in critically ill animals?

A

Elevated cTnI is associated with increased disease severity and worse prognosis, making it a negative prognostic indicator.

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16
Q

According to Langhorn & Willesen (2016), can cTnI distinguish cardiac from non-cardiac causes of respiratory distress?

A

Not reliably—cTnI can be elevated in both due to myocardial strain; echocardiography and other diagnostics are often needed.

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17
Q

According to Langhorn & Willesen (2016), how quickly does cTnI rise after myocardial injury?

A

Within 2–6 hours, peaking at 12–24 hours, and can remain elevated for several days depending on the extent of injury.

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18
Q

According to Winter et al. (2017), what signalment was most commonly associated with aortic thrombosis in dogs?

A

Large-breed, male dogs were overrepresented, with Labrador Retrievers being the most common breed.

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19
Q

According to Winter et al. (2017), what were the most common comorbidities associated with aortic thrombosis in dogs?

A

Neoplasia, protein-losing nephropathy, protein-losing enteropathy, hyperadrenocorticism, and immune-mediated diseases.

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20
Q

According to Winter et al. (2017), what clinical signs were most commonly reported in dogs with aortic thrombosis?

A

Hind limb weakness, paresis or paralysis, absent femoral pulses, pain, and cold limbs.

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21
Q

According to Winter et al. (2017), how often was the aortic thrombus located at the aortic trifurcation?

A

The majority of cases (≈85%) had thrombi at the aortic trifurcation (terminal aorta/iliac arteries).

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22
Q

According to Winter et al. (2017), what diagnostic methods were most commonly used to identify aortic thrombosis?

A

Abdominal ultrasound and computed tomography angiography were the primary diagnostic tools.

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23
Q

According to Winter et al. (2017), what was the median survival time for dogs diagnosed with aortic thrombosis?

A

Median survival time was 4 days overall, with long-term survival associated with surgical or aggressive medical management in a minority.

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24
Q

According to Winter et al. (2017), what prognostic factors were associated with improved survival?

A

Ambulatory status at presentation and response to therapy were associated with better outcomes.

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25
In Boswood et al. (2018), what was the primary goal of the EPIC study?
To determine whether pimobendan delays the onset of congestive heart failure (CHF) or cardiac-related death in dogs with preclinical (Stage B2) MMVD and cardiomegaly.
26
According to Boswood et al. (2018), what type of study was the EPIC trial?
Prospective, multicenter, randomized, placebo-controlled, double-blinded clinical trial.
27
What were the inclusion criteria in Boswood et al. (2018)?
Dogs had to have a typical MMVD murmur, LA:Ao ≥1.6, LVEDDN ≥1.7, and VHS >10.5.
28
What was the composite primary endpoint in Boswood et al. (2018)?
First occurrence of left-sided CHF, cardiac-related death, or euthanasia.
29
What were the median times to endpoint in Boswood et al. (2018)?
Pimobendan: 1228 days; Placebo: 766 days. Pimobendan delayed progression by ~15 months.
30
What hazard ratio was reported in Boswood et al. (2018) for reaching the primary endpoint?
HR 0.64 (95% CI 0.49–0.81), p < 0.001.
31
Did Boswood et al. (2018) report a survival benefit with pimobendan?
Yes. Pimobendan significantly prolonged the preclinical phase and delayed onset of CHF.
32
What adverse event profile was observed in Boswood et al. (2018)?
Adverse events were not significantly different between the pimobendan and placebo groups.
33
Based on Boswood et al. (2018), how did the EPIC study influence clinical practice?
Established pimobendan as the standard of care for dogs with Stage B2 MMVD and cardiomegaly.
34
ACVIM Concensus on MMVD (2019): What are the ACVIM stages of MMVD?
A: At risk; B1: Asymptomatic, no remodeling; B2: Asymptomatic with remodeling; C: CHF (current or prior); D: Refractory CHF.
35
ACVIM Concensus on MMVD (2019): What are the B2 diagnostic criteria for MMVD requiring initiation of pimobendan?
Murmur ≥ 3/6, LA:Ao ≥ 1.6, LVIDDN ≥ 1.7, VHS > 10.5. Ideally, all criteria should be met.
36
ACVIM Concensus on MMVD (2019): What is the recommended treatment for Stage B2 MMVD?
Pimobendan (0.25–0.3 mg/kg PO q12h) based on EPIC trial results. No diuretics or ACEi unless indicated for other reasons.
37
ACVIM Concensus on MMVD (2019): What histopathological changes define MMVD valves?
Myxomatous degeneration: expansion of the spongiosa, fragmentation/loss of collagen in the fibrosa, accumulation of glycosaminoglycans.
38
ACVIM Concensus on MMVD (2019): What neurohormonal systems are activated in MMVD pathophysiology?
RAAS, sympathetic nervous system, ADH axis — all contribute to volume retention and remodeling.
39
ACVIM Concensus on MMVD (2019): What causes pulmonary hypertension (PH) in MMVD?
Chronic LA pressure elevation leads to reactive post-capillary PH → ↑ RV afterload → eventual RV dysfunction.
40
ACVIM Concensus on MMVD (2019): When is furosemide recommended in MMVD?
Stage C (CHF present) or D (refractory CHF). Dose typically 1–2 mg/kg q12h PO, titrated to effect.
41
ACVIM Concensus on MMVD (2019): What medications are added in Stage C MMVD?
Pimobendan, furosemide, ACEi (e.g., enalapril/benazepril), +/- spironolactone.
42
ACVIM Concensus on MMVD (2019): What are indications to use spironolactone in MMVD?
Evidence of CHF or as part of Stage C treatment to counter aldosterone escape.
43
ACVIM Concensus on MMVD (2019): What are clinical signs of Stage C MMVD?
Cough, tachypnea, dyspnea, pulmonary edema, syncope, exercise intolerance.
44
ACVIM Concensus on MMVD (2019): What are treatment strategies for Stage D MMVD?
High-dose furosemide, combo diuretics (e.g., hydrochlorothiazide), dietary sodium restriction, adjunct therapies (e.g., sildenafil if PH).
45
ACVIM Concensus on MMVD (2019): What is the role of thoracic radiographs in MMVD diagnosis?
Evaluate for pulmonary edema and VHS; VHS > 10.5 supports left atrial/ventricular enlargement.
46
ACVIM Concensus on MMVD (2019): What is LVIDDN and how is it calculated?
Left ventricular internal diameter in diastole normalized to body weight (LVIDd/BW^0.294).
47
ACVIM Concensus on MMVD (2019): What does LA:Ao ratio indicate?
Left atrial size relative to aorta. Normal <1.6; enlargement supports diagnosis and guides staging.
48
ACVIM Concensus on MMVD (2019): What blood pressure targets are recommended in MMVD?
Maintain SBP between 100–160 mmHg; treat systemic hypertension if present.
49
ACVIM Concensus on MMVD (2019): What are complications of progressive MMVD?
Left-sided CHF, atrial fibrillation, PH, chordae tendineae rupture, LA tear, syncope.
50
ACVIM Concensus on MMVD (2019): How often should patients in Stage B2 be re-evaluated?
Every 4–6 months or sooner if clinical signs develop. Repeat thoracic rads, echo, BP.
51
ACVIM Concensus on MMVD (2019): What is the prognostic benefit of pimobendan in Stage B2 MMVD?
Delays time to onset of CHF by ~15 months in EPIC trial; improved survival.
52
ACVIM Concensus on MMVD (2019): What diagnostic imaging is essential for MMVD staging?
Thoracic radiographs and echocardiography.
53
ACVIM Concensus on MMVD (2019): What is the expected progression timeline from Stage B2 to Stage C?
Median ~1228 days in placebo dogs vs ~1400+ days in pimobendan-treated dogs (EPIC trial).
54
ACVIM Concensus on MMVD (2019): Is there a role for beta-blockers in MMVD?
No routine role; may be used in select cases with arrhythmias.
55
ACVIM Concensus on MMVD (2019): Should cough alone prompt MMVD treatment?
No — cough without other signs of CHF should not trigger diuretic or cardiac drug administration.
56
ACVIM Concensus on MMVD (2019): What echocardiographic changes define structural heart disease in Stage B2 MMVD?
Left atrial enlargement (LA:Ao ≥ 1.6), left ventricular dilation (LVIDDN ≥ 1.7), and mitral regurgitation.
57
ACVIM Concensus on MMVD (2019): How does MMVD affect afterload and preload?
Increases preload due to volume overload from MR; afterload is also elevated in later stages due to systemic RAAS activation.
58
ACVIM Concensus on MMVD (2019): What is the effect of mitral regurgitation on stroke volume?
Stroke volume becomes divided between forward flow and regurgitant volume, reducing effective forward output.
59
ACVIM Concensus on MMVD (2019): Why is left atrial enlargement important in MMVD?
It reflects chronic volume overload and predicts risk of CHF, atrial arrhythmias, and pulmonary hypertension.
60
ACVIM Concensus on MMVD (2019): What is the role of BNP or NT-proBNP in MMVD?
May be elevated with cardiac stretch; useful for diagnosis of CHF or differentiating cardiac vs. respiratory causes of dyspnea.
61
ACVIM Concensus on MMVD (2019): What is the pathophysiologic mechanism of CHF in MMVD?
Chronic MR → ↑ LA pressure → pulmonary venous congestion → pulmonary edema → CHF.
62
ACVIM Concensus on MMVD (2019): How does MMVD affect the pressure-volume loop?
Loss of isovolumetric contraction phase; loop becomes “flattened” due to continuous regurgitation into LA during systole.
63
ACVIM Concensus on MMVD (2019): What is chordae tendineae rupture and how does it present?
Acute worsening of MR with sudden onset CHF, often with loud murmur and rapid decompensation.
64
ACVIM Concensus on MMVD (2019): What echocardiographic parameter best correlates with MR severity?
LA:Ao ratio and regurgitant jet area, though quantitative measures are challenging.
65
ACVIM Concensus on MMVD (2019): Why should ACE inhibitors not be started in Stage B1?
No evidence of benefit in absence of remodeling; unnecessary RAAS inhibition may have side effects.
66
ACVIM Concensus on MMVD (2019): Why does spironolactone reduce mortality in MMVD?
Aldosterone contributes to myocardial fibrosis, sodium retention, and vascular remodeling; blockade reduces fibrosis and CHF progression.
67
ACVIM Concensus on MMVD (2019): What is the clinical significance of atrial fibrillation in dogs with MMVD?
Poor prognostic indicator; impairs diastolic filling, may precipitate CHF.
68
ACVIM Concensus on MMVD (2019): What dietary strategies are recommended for MMVD?
Moderate sodium restriction in Stage C and D, balanced diet, ensure adequate caloric intake to prevent cachexia.
69
ACVIM Concensus on MMVD (2019): What role does sildenafil play in MMVD?
Used in cases of concurrent pulmonary hypertension to reduce RV afterload.
70
ACVIM Concensus on MMVD (2019): Why is regular monitoring important in MMVD?
Disease is progressive; structural and functional changes can develop before clinical signs emerge.
71
ACVIM Concensus on MMVD (2019): What are contraindications for pimobendan?
LV outflow tract obstruction (e.g., HOCM), though rare in dogs; caution in arrhythmias without CHF.
72
ACVIM Concensus on MMVD (2019): What are key differences in murmur intensity between MMVD stages?
Murmur intensity does not always correlate with severity; however, a murmur ≥ grade 3/6 is required for Stage B2 classification.
73
What are the five primary classifications of feline cardiomyopathy per Luis Fuentes et al. 2020?
HCM, RCM, DCM, ARVC, and unclassified cardiomyopathies.
74
According to Luis Fuentes et al. 2020, what defines hypertrophic cardiomyopathy (HCM)?
Increased LV wall thickness (>6 mm) not explained by another cause, often asymmetric, with diastolic dysfunction.
75
What does Luis Fuentes et al. 2020 recommend for staging feline cardiomyopathies?
Four stages: A (at risk), B1 (asymptomatic without atrial enlargement), B2 (asymptomatic with atrial enlargement), C (CHF or ATE), and D (refractory CHF).
76
What diagnostic tools are emphasized by Luis Fuentes et al. 2020 in evaluating feline cardiomyopathy?
Echocardiography, thoracic radiographs, NT-proBNP, ECG (less useful), and clinical assessment.
77
What biomarker is supported for use in diagnosing occult cardiomyopathy in dyspneic cats (Luis Fuentes et al. 2020)?
NT-proBNP (point-of-care or lab-based testing).
78
According to Luis Fuentes et al. 2020, what echocardiographic feature suggests high risk for ATE or CHF?
Left atrial enlargement (LA:Ao > 1.5) and presence of spontaneous echocardiographic contrast (SEC).
79
How does the consensus define restrictive cardiomyopathy (RCM)?
Normal LV wall thickness with biatrial enlargement and impaired diastolic function.
80
What is the treatment approach for Stage B2 cats per Luis Fuentes et al. 2020?
Consider clopidogrel if at high risk for ATE (e.g., LA enlargement, SEC); no diuretics or pimobendan unless signs of CHF.
81
What drugs are recommended for cats in Stage C (CHF) in Luis Fuentes et al. 2020?
Furosemide, clopidogrel (if risk of ATE), pimobendan (if systolic dysfunction present), and supportive care.
82
What is the drug of choice for ATE prevention in cats per Luis Fuentes et al. 2020?
Clopidogrel; superior to aspirin. Dual therapy (clopidogrel + rivaroxaban) may be considered in very high-risk cases.
83
What treatment is not recommended in cats with normal systolic function per Luis Fuentes et al. 2020?
Pimobendan, unless there's systolic dysfunction (e.g., DCM or hypokinetic HCM).
84
How should cats in Stage D (refractory CHF) be managed according to the guidelines?
Higher-dose diuretics, thoracocentesis PRN, aldosterone antagonists, dietary sodium restriction, and palliation.
85
What is the most common cause of sudden death in cats with cardiomyopathy?
Aortic thromboembolism or malignant arrhythmias (ventricular tachycardia).
86
What is a key echocardiographic feature of arrhythmogenic right ventricular cardiomyopathy (ARVC)?
RV dilation and dysfunction, fibrofatty infiltration (histologic), with arrhythmias.
87
What is the recommended follow-up for asymptomatic cats with HCM Stage B1?
Echocardiography annually or sooner if clinical signs develop.
88
What does Luis Fuentes et al. 2020 recommend regarding taurine supplementation?
Only in confirmed cases of taurine deficiency or suspected DCM (rare in cats fed commercial diets).
89
What is the updated definition of pulmonary hypertension (PH) in the ACVIM 2020 guidelines by Reinero et al.?
PH is defined as an increase in pulmonary artery pressure, diagnosed when tricuspid regurgitation velocity (TRV) exceeds 3.4 m/s on echocardiography (implying systolic PAP > 50 mmHg), in conjunction with clinical and radiographic findings.
90
According to Reinero et al. 2020, what is the recommended classification scheme for PH in dogs?
PH is classified into 6 groups: (1) Pulmonary arterial hypertension (PAH), (2) Left heart disease, (3) Respiratory disease/hypoxia, (4) Pulmonary embolism/thrombosis, (5) Parasitic disease, and (6) Multifactorial/unclear mechanisms.
91
What echocardiographic variable is considered central to diagnosing PH per Reinero et al. (2020)?
Tricuspid regurgitation velocity (TRV) > 3.4 m/s is a key diagnostic criterion for PH.
92
In Reinero et al., how is PH severity categorized based on TRV?
Mild (TRV 3.0–3.4 m/s), Moderate (TRV 3.5–4.3 m/s), Severe (>4.3 m/s). However, classification must be combined with clinical signs.
93
What are key limitations of echocardiography alone in diagnosing PH according to the guidelines?
TRV measurement can be falsely elevated or underestimated; right-sided heart disease or low flow states may affect values. Must be interpreted with clinical context.
94
What role do thoracic radiographs play in diagnosing PH per Reinero et al. 2020?
Radiographs may show pulmonary arterial enlargement, right heart enlargement, or interstitial patterns but are non-specific and supportive only.
95
What is the role of sildenafil in canine PH per Reinero et al. (2020)?
Sildenafil is recommended as a first-line treatment for moderate-to-severe PH, especially in Group 1, 3, and 5 PH. Use with caution in Group 2 (LHD-associated PH).
96
How is pulmonary arterial hypertension (Group 1 PH) treated according to the guidelines?
Phosphodiesterase-5 inhibitors like sildenafil are the primary treatment. Underlying causes (e.g., idiopathic PAH or congenital disease) should be addressed if present.
97
How should PH due to left heart disease (Group 2) be approached therapeutically?
Treat the underlying cardiac condition first. Vasodilator therapy (e.g., sildenafil) is used cautiously and only if right heart failure or severe PH is present.
98
How does Reinero et al. 2020 recommend monitoring PH therapy response?
Monitor clinical signs (respiratory rate, exercise tolerance), echocardiography (TRV trends), and NT-proBNP levels where applicable.
99
What is the importance of NT-proBNP in PH per Reinero et al.?
NT-proBNP is a potential marker for right heart strain, but not specific to PH. It may aid in diagnosis and monitoring but should not replace echocardiography.
100
According to Reinero et al. 2020, how does chronic hypoxia contribute to the development of pulmonary hypertension?
Chronic alveolar hypoxia causes pulmonary vasoconstriction and vascular remodeling, leading to increased pulmonary vascular resistance and elevated pulmonary artery pressure (Group 3 PH).
101
What are the histopathologic changes seen in pulmonary vasculature in chronic PH?
Medial hypertrophy, intimal proliferation and fibrosis, plexiform lesions, and thrombosis of pulmonary arteries.
102
How does pulmonary hypertension affect the right ventricle pathophysiologically?
Chronic pressure overload leads to RV concentric hypertrophy, dilation, decreased contractility, and eventual right-sided heart failure.
103
What is ventricular interdependence and why is it relevant in PH according to Reinero et al.?
Ventricular interdependence refers to the mechanical interaction between the ventricles; RV dilation in PH impairs LV filling, reducing cardiac output.
104
Why is Group 2 PH (due to left heart disease) pathophysiologically distinct from other groups?
It arises from backward transmission of elevated left atrial pressure, leading to post-capillary pulmonary hypertension with less vasoconstriction and remodeling initially.
105
What echocardiographic signs suggest right heart remodeling in PH?
Right atrial enlargement, RV hypertrophy/dilation, flattening or paradoxical motion of the interventricular septum, and dilated pulmonary artery.
106
Why is sildenafil contraindicated in some cases of Group 2 PH?
Sildenafil may worsen pulmonary edema by unmasking elevated pulmonary capillary wedge pressure in left heart disease.
107
What diagnostic role does pulmonary arterial acceleration time (AT) have in PH?
Decreased AT (<58 ms) on echocardiography suggests elevated pulmonary pressures; shorter times indicate more severe PH.
108
What are the physiologic mechanisms targeted by phosphodiesterase-5 inhibitors like sildenafil in PH?
PDE5 inhibitors prevent degradation of cGMP, enhancing nitric oxide-mediated vasodilation in the pulmonary vasculature, reducing pulmonary arterial pressure.
109
How does Group 4 PH differ mechanistically from Group 1 PH?
Group 4 results from thromboembolic or obstructive causes (e.g., ATE, HW disease), while Group 1 involves idiopathic or congenital vascular disease with intrinsic vascular remodeling.

ACVECC Top 100(?) Papers (11 decks)

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