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Echo 2 > Module 13 : Ischemic Heart Disease > Flashcards

Module 13 : Ischemic Heart Disease Flashcards

1
Q

what are the 2 main causes of ischemic heart disease

A
  • atherosclerotic (most common)

- non atherosclerotic (least common)

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2
Q

what are the 2 atherosclerotic causes of ischemic heart disease

A
  • angina pectoris

- acute coronary system

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3
Q

what are the 2 types of angina pectoris

A
  • stable

- unstable

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4
Q

what are the 2 different acute coronary syndromes

A
  • STEMI ( ST - elevation MI)

- NSTEMI (non ST elevation MI)

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5
Q

what are all the causes of non atherosclerotic ischemic heart disease

A
  • emboli into coronary artery
  • trauma
  • dissection of aorta
  • arteritis / vasculitis
  • radiation therapy
  • coronary spasm
  • cocaine / amphetamines
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6
Q

what is ischemia

A
  • decreased blood supply to the myocardium or increased demand of blood
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7
Q

what are the 2 most common causes of ischemia

A 
- coronary arterial disease 
   \+ plaque in the vessel which impedes blood flow 
- increased metabolic demand 
  \+ hypertrophic cardiomyopathy 
  \+ aortic stenosis
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8
Q

what is infarction

A
  • death or necrosis of tissue which results from prolonged ischemia or total occlusion of blood flow to the tissue
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9
Q

what happens to everything downstream to the obstruction what will change that

A
  • dies

- unless there is collateral circulation from another vessel

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10
Q

is ischemia non reversible

A
  • reversible
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11
Q

is infarct reversible

A
  • non reversible
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12
Q

when does cell death start

A
  • within 1 hour and is complete by 4 hours
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13
Q

what are 2 symptoms of ischemia

A
  • SOB/Fatigue
  • angina pectoris
    + due to reduced O2 to a section of myocardium
    + heaviness burning or aching pain
    + women atypical symptoms
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14
Q

what are the symptoms of myocardial infarct

A
  • SOB/Fatigue
  • angina pectoris
  • sweating
  • nausea
  • vomiting
  • anxiety
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15
Q

what are the characteristics of stable angina

A
  • predictable regular chest pain
  • stable atheromatous plaque
  • relieved with rest or nitroglycerine
  • manageable with medication
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16
Q

what are the characteristics of unstable angina

A
  • more intense or painful
  • not predictable
  • result of plaque rupture
  • may require immediate by pass or PCI
  • medications help minimally to stable
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17
Q

what are 2 other types of angina

A
  • variant angina = prinsmetal angina
    + 1-6am not related to exercise
  • microvascular angina
    + possibly due to microvascular dysfunction
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18
Q

what is the atherosclerotic plaque

A
  • plaque progress from fatty streak on intima to a fractured cap of a plaque to superficial erosion of the endocardial layer
  • usually occurs just distal to an arterial branching
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19
Q

what is PCI

A
  • percutaneous coronary intervention
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20
Q

steps of a PCI

A
  • catheter inserted into stenosed artery
  • balloon inflated to displace the plaque
  • steroid eluding stent
  • steroid allows endothelium to from back through it
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21
Q

what is a Coronary Artery Bypass Graft CABG

A
  • open heart surgery
  • pre surgical angiogram and echo must be performed
  • patient must stop taking blood thinners first to prevent bleeding
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22
Q

what 2 things does a CABG

A
  • dissecting the chest

- heart-lung bypass

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23
Q

what vessels are used and how are they attached in CABG

A
  • greater saphenous vein or internal mammary artery harvested
  • plug one end proximal and one end distal to blockage
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24
Q

when is a CABG performed

A
  • blockage in unreachable percutaneously with catheter
  • too many blockages to stent > 3 or 4
  • when vessels become unstable or ruptures during PCI procedure
  • presents late with MI
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25
Q

what are some cons to doing CABG

A
  • higher mortality and morbidity
  • longer recovery time
  • more severe risks
  • cannot be done on frail patients
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26
Q

how much does the survival rate drop by with every minute without a pulse

A
  • 10%
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27
Q

what are the 2 treatments of ischemic heart disease

A
  • risk factor modification

- chest pain relief

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28
Q

what are some of the things to modify risk factors

A
  • smoking cessation
  • lower lipid diet
  • exercise
  • stress management
  • alcohol reduction
  • weight reduction
  • salt reduction
  • BP reduction
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29
Q

how is chest pain relief accomplished

A 
- nitrates = nitroglycerine 
  \+ causes vasodilation effects 
       - lowers arterial resistance and effect veins
  \+ administration 
      - pills under tongue 
      - spray under the tongue 
   \+ aspirin
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30
Q

what are the 3 medical treatments for ischemic heart disease

A
  • anticoagulation
  • beta blockers
  • calcium channel blockers
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31
Q

how does anticoagulation treat ischemic heart disease

A 
- for prevention of risk of thrombi = but increased risk of bleeding 
  \+ anti platelet drugs = makes more slippery 
  \+ anticoagulants = breaks the fibrinogen strands to prevent formation of clots
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32
Q

how do beta blockers treat ischemic heart disease

A
  • lower HR, BP and afterload

- improve survival by lowering O2 demand

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33
Q

how do calcium channel blockers treat ischemic heart disease

A
  • lower muscle contraction including tunica media of the coronaries
  • increasing lumen diameter lowering afterload
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34
Q

what are the 5 tests to diagnose IHD

A
  • ECG (ST depression or elevation)
  • stress test (exercise or pharmacological)
  • echo (wall motion abn)
  • MIBI (nuclear) stress test
  • cardiac CT or MRI - perfusion defects
  • coronary angiogram
35
Q

which test is the gold standard for diagnosing IHD

A
  • coronary angiogram
36
Q

what does the acute phase of MI require

A
  • blood work with enzymes
    + CKMB
    + Troponin C
37
Q

what is the treatment for MI

A 
MONA
M = morphine
O = oxygen 
N = nitrates (not for low BP, inferior MI, or viagra)
A = aspirin 
 - plus heparin 
 - thrombosis 
 - reperfusion
38
Q

what differential diagnose should we exclude

A
  • aortic dissection
  • tension pneumothorax
  • pericardial disease
  • pleural effusion
39
Q

what is a thrombolytic

A
  • cuts the long chains of plasminogen

- prevents plasminogen from forming fibrinogen strands found in blood clot

40
Q

what is TPA

A
  • tissue plasminogen activator
  • most effective MI clot busting
    + streptokinase
    + urokinase
41
Q

what are the 2 types of MI

A
  • STEMI

- NSTEMI

42
Q

what is a STEMI

A
  • usually transmural infarct
    + through the whole thickness of the myocardium
  • ST segment ELEVATED over affected area
  • seen in ANTERIOR MI LEADS
43
Q

what is NSTEMI

A
  • infarct that causes a zone of ischemia with small zone of cell death
  • usually subendocardial MI only
  • ST segment DEPRESSION
44
Q

what does a normal ECG look like

A
  • ST segment is at same level as TP segment = isoelectric
45
Q

what does ST segment depression indicate

A
  • ischemia
46
Q

what does ST segment elevation indicate

A
  • infarction
47
Q

what happens to the Q wave in patients with ST segment elevation who get reperfusion therapy

A
  • end up with necrosis shown by Q wave
48
Q

what happens to the Q wave in patients with NSTEMI infarcts

A
  • less necrosis
  • non q wave MI
  • ECG normal
49
Q

what are the other ECG changes that occur with MI

A
  • arrhythmias
  • conduction defects
    + AV block, LBBB
  • Q waves - old MI
  • peaked T waves - acute MI
  • symmetric flat or reversed T waves= chronic ischemia
50
Q

what are the three main coronary arteries

A
  • LAD = anterior IV sulcus
  • Circumflex CFX = runs laterally along AV sulcus toward the posterior aspect of heart
  • RCA = heads rightward laterally toward the back of the heart
51
Q

what is the role of echo in wall motion analysis

A
  • assess walls kinesis from all veins
  • assess wall thickening
  • measure all chamber sizes, EF, Estimate diastolic function, RVSP
  • assess regurge/stenosis
52
Q

what two things must happen for wall motion to be considered normal

A
  • wall motion normal

- wall thickening normal

53
Q

what is a con of WMA (wall motion anomaly)

A
  • absence of a RWMA does not exclude the possibility of ischemia
54
Q

what factors may cause abnormal septal wall motion

A
  • LBB
  • WPW
  • paced rhythms
55
Q

what might abnormal wall motion be caused from

A
  • subarachnoid hemorrhage
  • cardiac sarcoidosis
  • takosubo CMO
56
Q

what are the 5 types fo wall motion

A
  • hyperkinesis = enhanced wall motion
  • normal = > 40% wall thickening
  • hypokinesis = reduced wall thickening and motion < 40% > 5 %
  • akinesis = no wall thickening or little
  • dyskinesis = no wall thickening moving wall opposite way
57
Q

how is wall motion scoring done

A
  • each of the 16 segment is scored a number out of 4
  • score 1 = normal wall motion (>40% )
  • score 2 = hypokinetic (< 40% >5%)
  • score 3 = akinetic (< 5%)
  • score 4 = aneurysmal
58
Q

what is the wall motion scoring index WMSI equation

A
  • sum of all wall motion scores / number of segments visuaized
  • if 2 or more segments are not seen they are not counted in the sum
59
Q

what does a higher WMSI mean

A
  • lower the systolic function
60
Q

what is a sigmoid septum

A
  • basal septal focal hypertrophy
  • myocardial disarray related to reduced perfusion in that segment
  • more prominent in diabetes and elderly patients
61
Q

what is the prognosis of a signed septum

A
  • correlates with inreased risk for adverse cardiac events
62
Q

what are 7 post MI complications

A
  • secondary MI
  • thrombus formation
  • aneurysm
  • dresslers
  • acquired VSD due to myocardial necrosis
  • CHF, sys/diast
  • ventricular arrhythmia
63
Q

what is RV myocardial infarction RVMI associated with

A
  • inferior MI

- inferior wall is perfused by the RCA

64
Q

what is a complication of IHD/CAD

A
  • papillary muscle dysfunction
    + ischemia of pap muscle segment
    + improper contraction of the segment and pap muscle
    + affects MV function leading to eccentric mitral regurgitation
    + rupture more common with inferior MI
    + may also occur in right heart and TV
65
Q

what are 2 complications of echo in MI

A
  • LV thrombus

- VSD or wall rupture

66
Q

what is an LV thrombus

A
  • echo dense mass - in apec
  • protruding or mural
  • requires 2 views
  • high frequency probe zoom
  • risk of embolization
67
Q

what is a VSD or wall rupture

A
  • rupture of inter ventricular septum
  • loud harsh systolic murmur left sternal border
  • thrill
  • high velocity flow across septum
  • flow into pericardium for wall rupture
68
Q

How is thrombus formed

A
  • stagnant blood will clot
  • with a new MI larger areas of the heart will no longer contract especially at apex leading to low velocity stagnant flow
69
Q

what kind of MIs have more common chance of thrombus

A
  • anterior MI
70
Q

when do 50% of thrombus form post MI

A
  • within 48 hours
71
Q

when do 95% of thrombus form post MI

A
  • first 2 weeks
72
Q

describe embolization of thrombi

A
  • 10% of all thrombi

- 1-3. months post MI

73
Q

what are 4 increased risks that thrombi will embolism

A
  • protruding
  • large size
  • mobile
  • adjacent to hypermobile segment
74
Q

characteristics of laminar thrombus

A
  • suspect when apex thickness> septal thickness
  • adjacent to hypo/akinetic walls ( anterior/septal)
  • indicates older thrombus
  • use color doppler
75
Q

characteristics fo protruding thrombus

A
  • recently formed thrombus
  • less echogenic
  • more mobile
  • higher risk of embolization
  • protrudes into LV cavity
76
Q

what is LV contrast enhancement and when is it used

A
  • used to help visualize LV when poor

- micro bubbles opacify the LV cavity or myocardium

77
Q

what are 4 applications of contrast enhancement

A
  • detect intracardiac shunts
  • enhance doppler signals
  • LV opacification
  • myocardial perfusion
78
Q

what are the right heart application for micro bubble contrast

A
  • agitated saline
  • used to assess for intacardiac shunts
  • larger > 5 microns
  • do not pass through lungs
  • if bubbles seen on left means shunt
79
Q

what are the left heart applications of micro bubble contrast

A
  • smaller size < 5 microns
  • LV opacification
  • wall motion analysis
  • myocardial perfusion
80
Q

characteristics of pseudoaneruysms

A
  • narrow neck
  • wall rupture
  • filled with thrombi
81
Q

characteristics of true aneurysms

A
  • wide neck
  • all 3 layers of wall
  • may leak into pericardium
  • usually at apex
82
Q

processes of wall rupture as a result of MI

A
  • MI damages wall
  • wall thins and becomes necrotic
  • wall weakens
  • wall ruptures
  • shunt occurs
83
Q

what is dresslers syndrome

A
  • acute pericarditis post infarct
  • 24-96 hours after MI
  • pericardium may look bright over abs wall motion area
  • related to autoimmune response to necrosis
84
Q

what are 3 main features of dresslers syndrome

A
  • fever
  • pleuritic pain
  • pericardial effusion
  • tamponade rare

Echo 2 (18 decks)

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