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Echo 2 > Module 16 : Restrictive and Other Cardiomyopathies > Flashcards

Module 16 : Restrictive and Other Cardiomyopathies Flashcards

1
Q

what is another term for restrictive cardiomyopathy RCMO

A
  • infiltrative CMO
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2
Q

what does RCMO refer to

A
  • disease other than ischemici heart disease which cause increased resistance to LV filling due to increased myocardial stiffness
  • increased LVEDP
  • increase mLAP
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3
Q

what is the main cause of RCMO

A
  • abnormal infiltration, storage, or fibrosis within the myocardium
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4
Q

what are the 4 classes of RCMO

A
  • non infiltrative
  • infiltrative
  • storage disease
  • endomyocardial
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5
Q

what are the 2 main causes of non infiltrative RCMO

A
  • HCMO

- diabetic CMO

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6
Q

what are the 2 causes of infiltrative RCMOq

A
  • amyloidosis

- sarcoidosis

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7
Q

what is a main cause of storage disease RCMO

A
  • GSD
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8
Q

what are the 2 endomyocardial causes of rCMO

A
  • endomyocardial fobroelastosis

- carcinoid heart disease

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9
Q

what is the etiology of infiltrative RCMO

A
  • disease of heart muscle secondary to a disorder that produces histological changes to cardiac muscle by depositing a substance inside or in between muscle cells
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10
Q

what 2 things may infiltrative RCMO lead to

A
  • infiltration of myocardium

- restrictive filling pattern

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11
Q

what are the 3 clinical findings of RCMO

A
  • diastolic dysfunction (HFnEF) backwards failure
  • early stags normal systolic function
  • arrhythmias
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12
Q

what are the echo findings in RCMO

A
  • LV cavity size normal
  • wall thickness increased
  • bi atrial enlargments
  • small pericardial effusion
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13
Q

what are the 5 roles of echo in RCMO

A
  • asses chamber function and size
  • degree of DD
  • degree of MR or TR
  • determine RVSP
  • differentiate from constrictive pericarditis
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14
Q

what will the ECG look like with RCMO

A
  • atrial and ventricular arrhythmias
  • low voltage QRS
  • conduction defects
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15
Q

what are the 5 medical treatments of restrictive CMO

A
  • treat underlying aetiology
  • diuretics
  • ace inhibitors
  • anticoagulnats
  • anti arrhythmias
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16
Q

what are the 2 surgical treatments of RCMP

A
  • pace maker / defibrilaors

- cardiac transplant

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17
Q

what is the most common type of RCMO

A
  • amyloidosis
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18
Q

what is amyloidosis RCMO

A
  • deposits of amyloid protein in between myocytes

- inderdiagnosed

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19
Q

is diagnosis of amyloid CMO easy or hard

A
  • very difficult
20
Q

what 5 other organs may be affected by amyloid CMP

A
  • heart
  • liver
  • kidnyes
  • spleen
  • skin
21
Q

what are the 4 classifications of amyloid disease

A
  • primary idiopathic = more common in males
  • secondary
  • familial
  • senile
22
Q

what will amyloid CMO look like eon ECG

A
  • low voltage ECG
  • LVH plus low voltage ECG importnatn
  • pseudo infarction
  • afib
  • ventricular arrhytmias
  • conduction defects
23
Q

what are the 4 medical treatments of amyloid CMO

A
  • digitalis, digoxin
  • diuretics
  • vasodilators
  • anticoagulants
24
Q

what are the 4 surgical treatments of amyloid CMO

A
  • bone marrow stem cell transplant
  • pacemaker
  • implantable device
  • transplant
25
Q

what are the 7 echo features of amyloid CMO

A
  • granular speckled appearance
  • concentric LVH and RVH
  • WMA
  • asymmetric septal thickening
  • bi atrial enlargements
  • pericardial effusion
  • PHTN
26
Q

what does an increase in wall thickness mean in regards to DD

A
  • thick the wall = more severe diastolic dysfunction
27
Q

what are the early changes in systolic function with amyloidosis

A
  • LV systolic function normal and normal size
28
Q

what are the late changes seen in systolic function with amyloidosis

A

LV may dilates

- LVEF reduce

29
Q

what is sarcoidosis

A
  • multiple granulomatous disease which involves the heart
  • females more
  • rare
30
Q

what is theist common site for granulomas to infiltrate

A
  • lungs
31
Q

what are the clinical features of sarcoidosis

A
  • progressive heart failure
  • diffuse pulmonary fibrosis = PHTN
  • death
  • dysrhtymias
  • 3rd degree AV blocks
32
Q

what are the echo features of sarcoidosis

A
  • pericardial effusion
  • increase anterior RV thickness > 5mm
  • PTHN
  • RV dysfunction
  • MR/TR
  • DD
  • late = dilation of LV, wall thinning, reduced EF, WMA
33
Q

what is hemochromatosis and what are the 2 groups

A
  • iron storage disease affecting multiple organ systems resulting in organ damage and malfunction
  • primary, secondary
34
Q

what is primary hemochromatosis

A
  • inherited
35
Q

what is secondary hemochromatosis

A
  • iron overload due to repeated blood transactions with patients with chronic anemia, hemodialysis, alcoholic liver disease
36
Q

what is the clinical pentad of hemochromatosis

A
  • CHF
  • cirrhosis
  • impotence
  • diabetes
  • arthritis
37
Q

what will the ECG look like with hemochromatosis

A
  • AF
  • low voltage
  • SVTs
  • AV blocks
38
Q

what is another name for endomyocardial syndrome

A
  • hypereosinphilic

- perisitant elevated blood eosinophil counts

39
Q

what are the four causes of perisitant elevated blood eosinophil counts

A
  • idiopathic
  • malignant
  • reactive
  • infectious
40
Q

what does endomyocardial syndrome evolve from

A
  • infiltration of eosinophils to thrombosis

- restriction due to fibrotic tissues that lines myocardium decreased LV function and CHF then death

41
Q

what is GSD

A
  • excessive storage of glycogen in tissue
  • hereditary
  • heart becomes enlarged and globular in shape
  • thickened RV LV and IVS
42
Q

what are 4 other infiltrative CMOS

A
  • arrhytmogenic RV dysplaisia
  • carcinoid heart disease
  • fabrys disease
  • collagen disorders
43
Q

characteristics of arrhytmogenic RV dysplasia

A
  • genetiv
  • fibrofatty
  • RV systolic and diastolic dysfunction
  • RV dilation RV small aneurysms
  • RV trabeculation get bigger
  • normal LV
  • arrhytmias
44
Q

characteristics of LV non compaction

A
  • gentic
  • LV wall thickening with deep recess between trabeculae
  • hypokinesis
  • arrhytmias
  • heart failure
45
Q

development of LV non compaction

A
  • embryonic development
  • before coronary arteries blood supplied by trebeculation in blood
  • once coronaries developed the LV compass from epicardium to endocardium and base to apex
  • LV non compaction is seen usually in apex

Echo 2 (18 decks)

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