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spring cardiac theory > Chapter 8: CAD > Flashcards

Chapter 8: CAD Flashcards

1
Q

What is ISCHEMIA?

A

Deficient oxygen supply to the myocardium resulting in transient or reversible injury to the myocardium

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2
Q

What CAUSES ischemia?

A

Partial occlusion of a coronary artery due to atherosclerotic plaque

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3
Q

How does ischemia appear on ECHO?

A

there is normal wall motion at rest but abnormal wall motion with stress/exercise

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4
Q

What is an INFARCTION?

A

Irreversible injury to the myocardium due to prolonged ischemia

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5
Q

What CAUSES infarction?

A

Acute thrombotic total occlusion at the atherosclerotic plaque (plaque ruptures and clots so heart muscle dies)

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6
Q

How does infarction appear on ECHO when ACUTE (happening rn)?

A

demonstrates abnormal wall motion at rest (hypokinetic, akinetic, or dyskinetic) and unaffected segments are hyperkinetic bc they’re trying to compensate for failing segments

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7
Q

Define AKINETIC

A

absence of inward endocardial motion or wall thickening in systole - not thickening at all, moving very little

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8
Q

Define DYSKINETIC

A

outward motion or “bulging” of the segment in systole instead of moving inward

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9
Q

Define ANEURYSMAL

A

the wall segment is dyskinetic and bulging out in systole and diastole

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10
Q

Define HYPOKINETIC

A

wall thickening looks reduced during systole but is not absent

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11
Q

What is RIGHT DOMINANCE?

A

when RCA gives rise to the posterior descending artery in 80% of people

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12
Q

What is LEFT DOMINANCE?

A

when circumflex gives rise to the posterior descending artery in 20% of people

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13
Q

What type of MI demonstrates HYPOKINESIS? & How does it appear?

A
  • transient rest ischemia or NSTEMI
  • less wall thinning/brightness
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14
Q

What type of MI demonstrates AKINESIS? & How does it appear?

A
  • STEMI transmural
  • wall thinning/brightness
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15
Q

What 3 things are used to rule in infarct in the ER?

( only 2 of the 3 needed)

A
  1. typical clinical presentation
  2. diagnostic ECG changes
  3. elevation in cardiac enzymes ( troponin, creatine, kinase)
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16
Q

When is echo for EVALUATION OF INTERVENTIONAL THERAPY done?

A

when patient went to cath lab to get intervention done

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17
Q

What are the 2 types of intervention?

A
  1. PCI (angioplasty/stent)
  2. CABG
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18
Q

Why is an echo for EVALUATION OF INTERVENTIONAL THERAPY done?

A

to assess its effectiveness

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19
Q

When should an echo for EVALUATION OF INTERVENTIONAL THERAPY be performed and why?

A
  • several days post reperfusion therapy
  • bc when blood is restored, “stunned” myocardium needs several days to respond
20
Q

When is an echo for EVALUATION OF RESIDUAL IMPACT done?

A

4-6 weeks post MI

21
Q

What are we looking at during an echo for EVALUATION OF RESIDUAL IMPACT?

A

we are looking at the status/extent of infarcted segments. so the degree of wall motion and scarring

22
Q

What type of echo can we evaluate for hibernating myocardium?

A

echo for eval of residual impact

23
Q

What is HIBERNATING MYOCARDIUM?

A

border myocardium that is chronically ischemic but not infarcted

24
Q

How do we identify HIBERNATING MYOCARDIUM?

A

dobutamine stress testing: wall motion improves with a small dose and declines with higher doses

25
Q

What complications of MI can we see on echo?

A
  1. MR
  2. ventricular rupture
  3. pericardial effusion
  4. RV Infarction associated with inferior LV infarct
  5. LV aneurysm
  6. LV thrombus
  7. Acute or End Stage Ischemic Cardiomyopathy
26
Q

What can MR lead too?

A
  1. papillary muscle dysfunction
  2. rarely a partia or complete rupture of PM
  3. a new systolic murmur post MI
27
Q

How does a rarely a partial/complete rupture of PM appear on ECHO?

A

flail leaflet with attached mass

28
Q

What two types of ventricular rupture are there?

A
  1. ventricular septal defect
  2. ventricular free wall rupture
29
Q

Ventricular septal defect is due to what?

A

necrosis then rupture of a focal area of the IVS

30
Q

Rupture of focal area of ventricular free wall is due to what?

A

due to blood into pericardial sac

31
Q

How can ruptures be temporarily contained?

A

by a pseudoaneurysm that is preventing free flow of blood into pericardial sac

32
Q

How do you identify a pseudoaneurysm?

A
  1. wall is composed of pericardium
  2. narrow neck
  3. abrupt
  4. typically thrombus filled
  5. harsh transition from myocardium to nothing
33
Q

When is PERICARDIAL EFFUSION seen?

A
  • 2-4 days after MI
  • in transmural, large or anterior MI
34
Q

What is PERICARDITIS?

A

small to mod amount of fluid in pericardial sac accompanied by chest pain and ECG changes and is response to injury

35
Q

What is DRESSLER’S SYNDROME?

A

delayed form of pericarditis (weeks to months) & is an autoimmune response to the altered myo/pericardium

36
Q

What occurs during DRESSLER’S SYNDROME?

A
  • antibodies attack the area and cause inflammation and fluid accumulation
  • patient has chest pain and fever
37
Q

Why does Right Ventricular infarction associate with Inferior LV infarct?

A

Proximal occlusion of RCA impacts inferior LV and RV bc it feeds both

38
Q

A LV Aneurysm is due to what?

A

extensive damage of thinning dyskinetic walls creating distinct outpouching of an area of the ventricle

39
Q

How does a LV Aneurysm appear?

A
  1. Wall is a thin layer of myocardium
  2. Neck is wide
  3. smooth transition from normal to thin myocardium
40
Q

What type of aneurysms are the most common?

A

apical aneurysms

41
Q

How does an LV THROMBUS form?

A

Akinetic walls → stasis of blood → clot protruding or laminated against wall

42
Q

What increases the likelihood of a LV THROMBUS?

A
  1. Poor LV function
  2. Aneurysm
  3. Akinetic area
  4. Spontaneous contrast
43
Q

How can we differentiate a LV THROMBUS?

A

looking for an area of different echogenicity, distinct from the endo

44
Q

What happens when a THROMBUS embolizes?

A
  1. LV stroke
  2. pulmonary embolus of RV
45
Q

What is Acute or End Stage Ischemic Cardiomyopathy?

A

severe LV dysfunction and dilation due to an acute multi vessel or proximal event or many ischemic events over time

46
Q

What is a Non-ischemic cardiomyopathy?

A

poorly functioning ventricle that is not due to CAD or valvular disease but to other infection, virus or toxin

spring cardiac theory (11 decks)

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