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Cardio Exam 2 > ACS 1 - Quiz 3 > Flashcards

ACS 1 - Quiz 3 Flashcards

1
Q

continuum of ACS

A
  • unstable angina
  • NSTEMI
  • STEMI
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2
Q

STEMI stands for

A
  • ST Elevation Myocardial Infarction
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3
Q

NSTEMI stands for

A
  • Non-ST Elevation Myocardial Infarction
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4
Q

troponin levels of unstable angina

A
  • troponin is negative

- not actually myocyte death or necrosis

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5
Q

more than 90% of ACS results from

A
  • disruption of an atherosclerotic plaque

- with subsequent platelet aggregation and thrombus formation

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6
Q

major trigger for coronary thrombosis

A
  • atherosclerotic plaque rupture
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7
Q

atherosclerotic plaque rupture due to

A
  • chemical factors that destabilize the lesion

- physical stresses on the lesion

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8
Q

triggers for ACS

A
  • strenuous physical activity
  • emotional stress
  • SNS activation
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9
Q

coronary thrombosis exacerbated by

A
  • endothelial dysfunction
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10
Q

endothelial dysfunction leads to

A
  • vasoconstriction and diminished anti-thrombotic function
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11
Q

normal hemostasis

A

blood vessel injured –> disrupted endothelial surface

–> exposure of the thrombogenic connective tissue to circulating blood

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12
Q

primary hemostasis

A
  • first line of defense versus bleeding
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13
Q

primary hemostasis mediated by

A
  • circulating platelets

- form platelet plug

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14
Q

secondary hemostasis

A
  • sub endothelial tissue triggers coagulation cascade

- fibrin clot by thrombin activation

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15
Q

endogenous anti-thrombotic examples

A
  • antithrombin III
  • protein C and S
  • Tissue Factor Pathway Inhibitor
  • tissue plasminogen activator
  • Prostacyclin
  • nitric oxide
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16
Q

what are anti-thrombotics

A
  • safeguards to prevent spontaneous thrombosis and arterial occlusion
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17
Q

role of antithrombin

A
  • binds irreversibly to thrombin and other clotting factors
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18
Q

antithrombin increased effectiveness with

A
  • heparin
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19
Q

role of protein C and S

A
  • degrades factors Va and VIIIa
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20
Q

tissue factor pathway inhibitor

A
  • plasma serine protease inhibitor
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21
Q

tissue factor pathway inhibitor activated by

A
  • factor Xa
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22
Q

role of tissue factor pathway inhibitor

A
  • inhibits coagulation via extrinsic pathway
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23
Q

tPA secreted by

A
  • endothelial cells
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24
Q

tPA cleaves

A
  • plasminogen to form plasmin
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25
Q

tPA role

A
  • degrades fibrin clots
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26
Q

prostacyclin secreted by

A
  • endothelial cells
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27
Q

prostacyclin role

A
  • increases platelet levels of cAMP
  • inhibits platelet activation/aggregation
  • vasodilator
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28
Q

nitric oxide secreted by

A
  • endothelial cells
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29
Q

nitric oxide role

A
  • inhibits platelet activation

- potent vasodilator

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30
Q

which are partially occlusive thrombi

A
  • unstable angina

- NSTEMI

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31
Q

which are completely obstructive thrombi

A
  • STEMI
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32
Q

acute MI discrete focus of

A
  • coagulative necrosis in the heart
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33
Q

acute MI development related to

A
  • duration of ischemia

- metabolic rate of ischemic tissue

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34
Q

how many minutes of ischemia can cause infarct

A
  • 20-30 minutes
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35
Q

acute MI frequently result from

A
  • acute plaque rupture with coronary artery thrombosis
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36
Q

acute MI dissolution of thrombus frequent within

A
  • 12-24 hours
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37
Q

infarcts involve which ventricle

A
  • LV more commonly and extensively than RV
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38
Q

MI occurs when

A
  • ischemia is bad enough to cause myocyte necrosis
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39
Q

two types of infarct

A
  • transmural infarct

- subendocardial infarct

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40
Q

transmural infarct spans

A
  • entire thickness of myocardium
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41
Q

transmural infarct due to

A
  • prolonged, total occlusion of an epicardial coronary artery
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42
Q

subendocardial infarct involves

A
  • only innermost layers of the myocardium
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43
Q

which infarct is most susceptible to ischemia

A
  • subendocardial infarct
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44
Q

why is subendocardial infarct most susceptible to ischemia

A
  • poor collateral flow
  • adjacent to high-pressure ventricle
  • furthest from epicardial coronary arteries
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45
Q

amount of tissue that ultimately succumbs to infarction depends upon

A
  • degree of reperfusion and inflammatory response
  • oxygen demand of affected area
  • mass of myocardium perfused by the coronary artery
  • adequacy of collateral coronary flow
  • magnitude and duration of ischemia

DOMAM

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46
Q

collateral flow is supplies by

A
  • other coronaries
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47
Q

early MI changes - metabolism

A
  • rapid shift from aerobic to anaerobic metabolism
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48
Q

early MI changes - what accumulates

A
  • lactic acid accumulates
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49
Q

early MI changes - reduction in

A
  • ATP
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50
Q

early MI changes - ion changes

A
  • rising intracellular Na+

- abnormal electrolyte/ion shifts

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51
Q

rising of intracellular Na+ leads to

A
  • cellular edema
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52
Q

abnormal electrolyte/ion shifts leads to

A
  • arrhythmia risk
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53
Q

early MI changes - irreversible cell injury ensues in how many minutes

A
  • 20 minutes
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54
Q

macroscopic features of infarction <4 hours

A
  • no abnormality
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55
Q

macroscopic features of infarction 4-12 hours

A
  • occasional dark mottling
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56
Q

macroscopic features of infarction 12-24 hours

A
  • dark mottling
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57
Q

macroscopic features of infarction 1-3 days

A
  • mottling with developing yellow tan necrotic center
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58
Q

macroscopic features of infarction 3-14 days

A
  • maximally yellow-tan and soft

- depressed red-tan border

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59
Q

macroscopic features of infarction 2-8 weeks

A
  • gray-white scar

- progressive from border to core of infarct

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60
Q

macroscopic features of infarction > 2 months

A
  • mature scar
61
Q

microscopic features of infarction <4 hours

A
  • none
62
Q

microscopic features of infarction 4-12 hours

A
  • early coagulative necrosis
  • edema
  • hemorrhage
63
Q

microscopic features of infarction 12-24 hours

A
  • early PMNs
64
Q

microscopic features of infarction 1-3 days

A
  • marked interstitial PMNs
65
Q

microscopic features of infarction 3-14 days

A
  • macrophages and granulation tissue at border
66
Q

microscopic features of infarction 2-8 weeks

A
  • loss of cellularity

- increasing collagen

67
Q

microscopic features of infarction > 2 months

A
  • dense collagenous scar
68
Q

functional changes following MI

A
  • systolic and diastolic dysfunction
  • stunned myocardium
  • ischemic preconditioning
  • ventricular remodeling
69
Q

systolic dysfunctional changes

A
  • hypokinesis
  • akinesis
  • dyskinesis
70
Q

hypokinesis

A
  • local region with reduced contraction
71
Q

akinesis

A
  • local region with no contraction
72
Q

dyskinesis

A
  • local region that bulges outward with contraction
73
Q

diastolic dysfunction results in

A
  • reduced compliance

- elevated ventricular filling pressures

74
Q

stunned myocardium

A
  • prolonged, but reversible period of contractile dysfunction
75
Q

stunned myocardium how long does it take to recover?

A
  • takes days to weeks to recover
76
Q

ischemic preconditioning

A
  • renders tissue more resistant to future episodes of ischemia
77
Q

ventricular remodeling changes geometry of which myocardium

A
  • infarcted and noninfarcted myocardium
78
Q

ventricular remolding results in

A
  • ventricular dilatation
  • infarct expansion
  • myocyte slide-to-slide slippage
79
Q

ventricular remolding advantages

A
  • mechanically disadvantageous
80
Q

ventricular remolding wall stress

A
  • increased wall stress
81
Q

MI complications

A
  • arrhythmias
  • LV failure, cardiogenic shock
  • extension of infarct
  • myocardium free wall rupture
  • septal perforation
  • papillary muscle rupture
  • aneurysm
  • mural thrombosis
82
Q

result of LV failure

A
  • high grade stenosis of all coronary vessels
83
Q

myocardial free wall rupture occurs when

A
  • first 3 weeks
84
Q

myocardial free wall rupture most common

A
  • days 3-7

- when wall is weakest

85
Q

myocardial free wall rupture complication of

A
  • large infarcts
86
Q

myocardial free wall rupture occurs at

A
  • junction of infarct and normal muscle
87
Q

septal perforation results in

A
  • left to right shunt
88
Q

papillary muscle rupture results in

A
  • mitral regurgitation

- massive MV incompetence

89
Q

aneurysm result

A
  • wall bulges outward during systole
90
Q

aneurysm - as infarct matures

A
  • fibrous scar progressively stretches
91
Q

aneurysm - increased risk for

A
  • myocardial rupture

BASICALLY AS THE WALL IS STRETCHING IT IS FAR MORE LIKELY TO RUPTURE

92
Q

aneurysm - predisposes to

A
  • mural thrombosis
93
Q

aneurysm - effect on workload

A
  • increases workload
94
Q

mural thrombosis - seen in

A
  • fatal acute myocardial infarct

- after apical infarcts

95
Q

mural thrombosis predisposes to

A
  • systemic embolization
96
Q

MI symptoms - nausea, vomiting, weakness is what kind of effect

A
  • parasympathetic
97
Q

MI symptoms - diaphoresis, cool/clammy skin is what kind of effect?

A
  • sympathetic
98
Q

MI symptoms - fever is what kind of effect

A
  • inflammatory
99
Q

evidence of systemic hypoperfusion

A
  • hypotension
  • tachycardia
  • impaired cognition
  • cool extremities
  • end-organ injury
100
Q

evidence of heart failure

A
  • elevated jugular venous pulsation
  • pulmonary crackles
  • gallops - S3,S4
  • new murmurs
101
Q

ischemia compromises which part of the cardiac cycle

A
  • diastolic, filling function
102
Q

EKG abnormalities for clinical detection of ischemia

A
  • new ST segment elevation > 1mm
  • new ST segment depression
  • new T wave inversion
103
Q

what are labile T wave inversions

A
  • change after rest and nitroglycerin
104
Q

ST segment represents

A
  • period between depolarization and repolarization of left ventricle
105
Q

ST segment should be about how long

A
  • about the same size as PR segment
106
Q

subendocardial injury results in what ST effect

A
  • ST depression
107
Q

transmural injury results in what ST effect

A
  • ST elevation
108
Q

high risk features of MI

A
  • increased age
  • low BP
  • elevated HR
  • heart failure
  • anterior location
109
Q

definition of acute MI values

A
  • rise/fall of troponin

- one value above 99th percentile

110
Q

definition of acute MI - symptoms

A
  • symptoms of acute ischemia
111
Q

definition of acute MI - ECG

A
  • new ST-T changes
  • LBBB
  • pathological Q waves
112
Q

definition of acute MI - imaging

A
  • loss of viable myocardium

- regional wall motion abnormality

113
Q

definition of acute MI - angiography of autopsy

A
  • intracoronary thrombus
114
Q

which troponins do we use?

A
  • troponin I and T
115
Q

CK-MB diagnosis of MI

A
  • upper limit of normal

- 2.5% of total CK (creatine kinase)

116
Q

importance of collecting samples for diagnosis of MI

A
  • always collect serial samples
117
Q

non-cardiac causes of troponin elevation

A
  • acute HF
  • PE
  • shock
  • aortic dissection
  • myocarditis
  • trauma
  • ICD discharge
118
Q

STEMI diagnosis

A
  • > 1 mm ST segment elevation in 2 contiguous leads
  • > 2 mm ST segment elevation in 2 contiguous precordial leads
  • new LBBB
119
Q

contiguous leads II, III, and AVF point to which anatomic location

A
  • inferior
120
Q

contiguous leads II, III, and AVF point to which coronary artery

A
  • RCA > Lcx
121
Q

V2-V4 point to which anatomic location

A
  • anterior
122
Q

V2-V4 point to which coronary artery

A
  • LAD
123
Q

V1-V4 point to which anatomic location

A
  • anteroseptal

note:
V1/V2 = septal
V3/V4 = anterior

124
Q

V1-V4 point to which coronary artery

A
  • LAD
125
Q

I, aVL, V5, V6 point to which anatomic location

A
  • lateral
126
Q

I, aVL, V5, V6 point to which coronary artery

A
  • Lcx > LAD
127
Q

LBBB points to which anatomic location

A
  • anterior
128
Q

LBBB points to which coronary artery

A

LAD

129
Q

V4R points to which anatomic location

A
  • right ventricle
130
Q

V4R points to which coronary artery

A
  • RCA
131
Q

V1,V2 ST depression points to which anatomic location

A
  • posterior
132
Q

V1,V2 ST depression points to which coronary artery

A
  • RCA > Lcx
133
Q

MI localization

in LAD

A
  • anterior LV
  • anterior 2/3 septum
  • apical LV
134
Q

MI Localization

in LCX

A
  • lateral LV

- posterolateral LV

135
Q

MI Localization

in RCA

A
  • posterior LV
  • posterior 1/3rd septum
  • posterior papillary muscle
  • “inferior” or “diaphragmatic”
136
Q

STEMI treated with

A
  • emergency cardiac catheterization
137
Q

pathologic Q waves are indicative of

A
  • prior transmural STEMI

- not seen in UA or NSTEMI

138
Q

diagnostic criteria for pathologic Q waves

A
  • > 1 mm wide
    25% of overall amplitude of QRS complex
  • present in > 2 contiguous leads
139
Q

variant (prinzmetal) angina

A
  • focal coronary artery spam in absence of overt atherosclerotic lesions
140
Q

variant (prinzmetal) angina presents with

A
  • chest pain

- transient ST elevation

141
Q

variant (prinzmetal) angina due to

A
  • smooth muscle hyperreactivity

- endothelial dysfunction

142
Q

variant (prinzmetal) angina diagnosis

A
  • intracoronary acetylcholine provokes spasm
143
Q

variant (prinzmetal) angina treatment

A
  • nitrates

- calcium channel blockers

144
Q

UA or NSTEMI symptoms

A
  • rest angina > 20 minutes
  • new onset angina that limits activity
  • increasing angina in unstable pattern
  • +/- T wave inversion or ST depression
145
Q

TIMI risk score for risk stratification in NSTEMI and Unstable Angina

A 
> 65 years of age
- known CAD (>50% coronary stenosis)
 >3 risk factors for CAD
- aspirin use within past 7 days
> 2 episodes of angina within past 24 hours
- ST changes > 0.5 mm
- elevated cardiac markers
146
Q

other causes of ACS

A
  • decreased myocardial oxygen supply

- increase in myocardial oxygen demand

147
Q

decreased myocardial oxygen supply due to

A
  • decreased perfusion pressure due to hypotension
  • anemia
  • coronary artery dissection or emboli
148
Q

increased in myocardial oxygen demand due to

A
  • rapid tachyarrhythmias
  • acute hypertension
  • aortic stenosis

Cardio Exam 2 (29 decks)

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