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Cardiology Boards > Cardiomyopathies > Flashcards

Cardiomyopathies Flashcards

1
Q

Mitral doppler findings RCM

A

Fast E wave, stops abruptly

Almost no A wave

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2
Q

PV doppler RCM

A

Very little systolic flow

Rapid inflow in early diastole, stops abruptly

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3
Q

Treatment of RCM

A

Cautious diuresis
Cautious BB
May need transplant

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4
Q

Amyloid features

A

Very thick walls
Speckled appearance
EKG normal or low voltage

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5
Q

Hypereosinophilia features

A

Fuzzy around myocardium, thrombus-like deposition in apices
If mobile elements -> anticoagulant
Hydroxyurea, steroids

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6
Q

ARVD features

A

Fatty replacement of RV free wall -> R heart failure
Arrhythmias
Repolarization abnormality, conduction delay
30% with FH
Often need ICD, no competitive athletics

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7
Q

LV non-compaction features

A

Non-compacted myocardium
Crypts and recesses
Increased risk for LV dilation, CHF, possible SCD

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8
Q

LV non-compaction and normal systolic function

A

treat as stage B HF

Use HCM / DCM criteria for SCD risk

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9
Q

LV non-compaction and reduced systolic function

A

treat as stage B or C HF
A/C if EF < 35%
Use HCM / DCM criteria for SCD risk

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10
Q

Ddx for thick walls

A 
LVH
HCM
Renal failure
Amyloid
Glycogen storage disease
Anderson-fabry's disease
Freiderich's ataxia
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11
Q

Athletic heart

A 
LVH
LVEDD > 55 mm
Responds to de-training
Super-normal exercise capacity
No MRI scar tissue or perfusion defects
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12
Q

EKG in apical HCM

A

Deep narrow T waves

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13
Q

HCM echo screening in children

A

No later than onset of puberty or at any consideration of competitive athletics
Every 12-18 months

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14
Q

HCM echo screening in adults

A

Every 5 years

Stop at 60 if normal

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15
Q

Genetic testing for screening in HCM

A

If HCM patient has known mutation, genetic testing preferred for screening
If no known mutation, imaging necessary

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16
Q

Pathophysiology of HCM

A

Diastolic dysfunction in 100% (increased LAP, dec CO)

Obstruction, SAM / MR in 70% (high LAP, subendocardial ischemia, MR, decreased CO)

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17
Q

Significant gradient at rest in HCM

A

> 30

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18
Q

Gradient to produce class III-IV symptoms in HCM

A

> 40-50

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19
Q

HCM LVOT gradient worsens with

A

More vigorous contraction
Decreased resistance
Decreased volume

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20
Q

Avoid in HCM

A

Positive inotropes
Pure vasodilators
High-dose diuretics

21
Q

Meds in HCM

A

Decrease contractility
Beta blockers
Verapamil, diltiazem
Disopyramide as adjunct

22
Q

Indications for myectomy / alcohol septal ablation in HCM

A

LVOT obstruction

Symptoms and impaired QoL despite meds

23
Q

Risk factors for SCD in HCM

A 
NSVT
Massive LVH
FH 1st deg relative < 45
Unexplained syncope last 6 months
Abnormal BP response to exercise
24
Q

ICD indications for HCM class I

A

Prior cardiac arrest or sustained VT

25
Q

ICD indications for HCM class IIa

A

FH-SCD, LV thickness > 30mm, recent unexplained syncope

NSVT or abnormal BP response to exercise + risk modifiers

26
Q

Risk modifiers for HCM and ICD

A 
Young
Wall thickness close to 30
Remote FH SCD
LVOT obstruction without planned intervention
Delayed enhancement 
Septal ablation
Known specific HCM mutations
Syncope < 5 years ago
27
Q

Sarcoid cMRI

A

Midmyocardial and epicardial LGE, particularly in basal septum and basal lateral wall

28
Q

Fabry’s disease

A

Preserved EF, chest pain, normal coronaries, LVH, renal dysfunction, FH (X-linked)

29
Q

CYP inhibitors which increase taco or calcineurin inhibitor levels

A

Azoles
Diltiazem
Verapamil

30
Q

pHTN 6MWT target for success

A

> 380 m

31
Q

HF predictors of poor hospital prognosis

A

low SBP, elevated BUN, elevated Cr

32
Q

Dose for anthracycline toxicity

A

3-5% with 400 mg/m
7-26% at 550 mg/m
18-48% at 700 mg/m

33
Q

Risk factors for antracycline toxicity

A

1) intravenous bolus administration,
2) higher single doses,
3) history of prior mediastinal irradiation,
4) use of other concomitant agents known to have cardiotoxic effects, such as cyclophosphamide, trastuzumab, and paclitaxel,
5) female sex,
6) underlying cardiovascular disease,
7) extremes of patient age (both very young and old age), and
8) increased length of time since anthracycline completion.

34
Q

Diagnosis of familial cardiomyopathy

A

3 generations involved, genetic testing not necessary

35
Q

Screening for familial cardiomyopathy

A

1st degree relatives

Echo every 3-5 years

36
Q

Hereditary hemochromatosis

A 
Iron overload (ferritin > 300, transferrin saturation >55%), 
T2 < 20 ms on CMR,
Evidence of heart disease (reduced EF,rrestrictivefilling, pulmonary hypertension)
37
Q

IV iron in HF

A

Class II or III HF, ferritin < 100 or ferritin 100-299 and iron sat <20%

38
Q

ARVC EKG

A

TWI in anterior precordial leads, high-frequency, low amplitude deflection at end of QRS complex (epsilon waves)

39
Q

ARVC echo

A

RV dilatation, RV dysfunction

40
Q

ARVC mutation

A

AD

plakoglobin

41
Q

Killip 1

A

No signs of hF

42
Q

Killip 2

A

Rales (crackles) in the lungs, an S3, and elevated jugular venous pressure

43
Q

Killip 3

A

Acute pulmonary edema

44
Q

Killip 4

A

Cardiogenic shock or hypotension (systolic blood pressure <90 mm Hg) and evidence of peripheral vasoconstriction.

45
Q

Chemotherapy induced cardiomyopathy

A

decrease in cardiac LVEF that was either global or more severe in the septum
HF symptoms
Decline in LVEF of ≤5-55% with accompanying signs or symptoms of CHF or a decline in LVEF of ≤10-55% without accompanying signs or symptoms.

46
Q

Cardiotoxic agents to monitor

A

anthracyclines, trastuzumab, sunitinib

47
Q

Tyrosine kinase inhibitors complications

A

Thrombotic events

48
Q

Vent to increase O2

A

FiO2, PEEP

49
Q

Vent to increase ventilation

A

RR, tidal volume

Cardiology Boards (11 decks)

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