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Medical > Cardiomyopathy, EKG > Flashcards

Cardiomyopathy, EKG Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the standard (old) classification system for cardiomyopathies?

A
  • Dilated Cardiomyopathy (DCM)
  • Hypertrophic Cardiomyopathy (HCM)
  • Restrictive Cardiomyopathy (RCM)
  • Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D)
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2
Q

What is the newer classification system of Cardiomyopathies?

A

Differentiates cases in which myocardial pathology occurs:

  • Primary cardiomyopathy - in isolation from extracardiac illness
  • Secondary Cardiomyopathy - occurs as a manifestation of a generalized, multisystem disorder
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3
Q

What are the subcategories of the newer cardiomyopathy classification system?

A
  • Genetic
  • Mixed
  • Acquired
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4
Q

What are two distinct but similar disorders characterized by RCM as a consequence of dense endocardial scarring with associated thrombus formation, commonly resulting in reduction in ventricular cavity size?

A
  • Endomyocardial fibrosis (Davies disease)
  • Loeffler endocarditis
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5
Q

What is the most common phenotypic expression of cardiomyopathy?

A
  • Dilated Cardiomyopathy (DCM)
    • wide variety of primary and secondry processes affecting the myocardium
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6
Q

What are the pathologic findings in DCM?

A
  • four-chamber cardiac enlargement (usually)
  • histologic evidence
    • myocyte hypertrophy
    • interstitial fibrosis
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7
Q

What percentage of DCM are interited?

What is crucial in identifyig these etiologies?

A
  • 20-35%
  • detailed family history
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8
Q

When does endomyocardial biopsy have the highest yield?

A
  • DCM
    • fulminant presentations with rapidly progressive HF or significant electrical instability
  • RCM
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9
Q

What precentage of DCM cases are classified as idiopathic/undiagnosed?

A

50%

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10
Q

What is the most common secondary cause of cardiomyopathy in the developing world?

A

Chronic overuse of alcohol

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11
Q

What are the pathophysiologic effects of acute cocaine intoxication leading to DCM?

A
  • abrupt catecholamine surges
  • severe hypertension
  • increases in LV afterload and wall stress
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12
Q

What are the pathophysiologic effects of chronic cocaine intoxication that can lead to DCM?

A
  • Chronic-cocaine related catecholamine stimulation
  • alterations in G protein-related signaling (similar to pheochromocytoma) –> LV dysfunction
  • Procoagulant effects + coronary vasospasm –> ischemic myocardial injury or infarction (even in the absence of coronary atherosclerosis)
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13
Q

What chemotherapeutic medications (class) are particularly associated with DCM?

A

Anthracyclines (doxorubicin, daunorubicin)

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14
Q

Who is at greatest risk for developing DCM from anthracyclines?

A
  • High-dose (cumulative dose > 550 mg/m2
  • extremes of age
  • adjuvant radiation or comcomitant treatment with nonanthracyclines
    • taxanes (paclitaxel and docetaxel)
    • human epidermal growth factor receptor-2 (HER-2) antagonist (trastuzumab)
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15
Q

What are the recommendations/guidelines for chemotherapy induced LV dysfunction?

A

ACE and BB in all patient’s with reduced EF to prevent development of symptomatic HF

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16
Q

What trial demonstrated attenuated declines in LV systolic dysfunction and enhanced clinical outcomes in patients with hematologic malignancies receiving anthracycline-based therapy?

What medications were administered in the trial?

A
  • OVERCOME (preventiOn of left Ventricular dysfunction with Enalapril and caRvedilol in patients submitted to intensive ChemOtherapy for the treatment of Malignant hEmopathies) trial
  • Carvedilol and Enalapril
17
Q

X-linked DCM leads to an absence or severe reduction of this?

A

dystrophin (protein found in skeletal muscle)

18
Q

Mutations in genes for dystrophyin production are associated with these disease processes?

A
  • X-linked DCM
  • Muscular dysrophies (commonly complicated by DCM)
    • Duchenne
    • Becker
19
Q
  • X-linked cardioskeletal myopathy associated with mitochondrial dysfunction and cyclic neutorpenia
  • typically present in male infants with HF
    • mutation in the gene tafazzin encoding an acyltransferase
A

Barth Syndrome

20
Q

Mutations in the gene tafazzin (enconding acyltransferases) can lead to these cardiomyopathies with associated arrhythmias and risk of sudden cardiac death?

A
  • Barth Syndrome
  • DCM
  • Endocardial fibroelastosis
  • LV noncompaction (LVNC)
21
Q

Define a normal P wave on EKG?

A
  • normal axis: 0-75 degress
  • upright in leads I and II
22
Q

Define a normal PR interval on EKG?

A

PR interval (120-200ms)

23
Q

Define a normal QRS on EKG?

A

QRS complex (normal axis: -30 to 105 degrees; duration < 120ms)

24
Q

Define a normal ST-segment on EKG?

A

ST segment (usually isoelectric with less than 1mm of elevation/depression in limb leads)

25
Q

Define normal T waves on EKG?

A

T wave (upright in I, II, V3-V6) and normal configuration and duration

26
Q

Define sinus arrhythmia on EKG?

A
  • normal P wave axis (0-75 degrees; upright in leads I and II)
  • P-P interval varies by > 10% or 0.16s
27
Q
A
  • Sinus arrhythmia
  • LVH
  • Acute pericarditis
28
Q
A
  • Sinus rhythm
  • AV junctional rhythm/tachycardia
  • PVC’s
  • 3rd degree AV block
  • Inferior MI
29
Q
A
  • Sinus arrhythmia
  • Anterior or anteroseptal, age recent or probably acute
30
Q

Define anterior or anteroseptal age recent or probably acute MI?

A
  • Pathological Q waves
    • must be greater than or equal to 30ms wide and 0.1mV deep in amplitude or QS complex) in anterior (V3-V4) or anteroseptal (V1-V3) leads; Q wave width may only be 20ms wide in V2-V3
  • Evidence of acute or evolving myocardial injury
    • ST elevation in two contiguous leads greater than or equal to 2 mm in men or 1.5mm in women in V2-V3 and/or 1 mm in other anterior or anteroseptal leads)
31
Q
A
32
Q

What is the ECG criteria for LAFB?

A
  • LAD (-45 to - 90 degrees)
  • Small q waves and big R waves ( = qR complexes) in I and aVL
  • Small r waves and big S waves in ( = rS complexes) in II, III, aVF
  • QRS duration normal or slightly prolonged (80-110ms)
  • Prolonged R wave peak time in aVL > 45 ms
  • Increased QRS voltage in limb leads
33
Q

What is the DDx for dynamic LVOT obstruction?

A
  • HCM
  • Amyloidosis
  • Hypertensive heart disease
  • Apical and mid-LV infarction
  • Reduced LV chamber size

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