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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
tPA role
- degrades fibrin clots
26
prostacyclin secreted by
- endothelial cells
27
prostacyclin role
- increases platelet levels of cAMP - inhibits platelet activation/aggregation - vasodilator
28
nitric oxide secreted by
- endothelial cells
29
nitric oxide role
- inhibits platelet activation | - potent vasodilator
30
which are partially occlusive thrombi
- unstable angina | - NSTEMI
31
which are completely obstructive thrombi
- STEMI
32
acute MI discrete focus of
- coagulative necrosis in the heart
33
acute MI development related to
- duration of ischemia | - metabolic rate of ischemic tissue
34
how many minutes of ischemia can cause infarct
- 20-30 minutes
35
acute MI frequently result from
- acute plaque rupture with coronary artery thrombosis
36
acute MI dissolution of thrombus frequent within
- 12-24 hours
37
infarcts involve which ventricle
- LV more commonly and extensively than RV
38
MI occurs when
- ischemia is bad enough to cause myocyte necrosis
39
two types of infarct
- transmural infarct | - subendocardial infarct
40
transmural infarct spans
- entire thickness of myocardium
41
transmural infarct due to
- prolonged, total occlusion of an epicardial coronary artery
42
subendocardial infarct involves
- only innermost layers of the myocardium
43
which infarct is most susceptible to ischemia
- subendocardial infarct
44
why is subendocardial infarct most susceptible to ischemia
- poor collateral flow - adjacent to high-pressure ventricle - furthest from epicardial coronary arteries
45
amount of tissue that ultimately succumbs to infarction depends upon
- 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
46
collateral flow is supplies by
- other coronaries
47
early MI changes - metabolism
- rapid shift from aerobic to anaerobic metabolism
48
early MI changes - what accumulates
- lactic acid accumulates
49
early MI changes - reduction in
- ATP
50
early MI changes - ion changes
- rising intracellular Na+ | - abnormal electrolyte/ion shifts
51
rising of intracellular Na+ leads to
- cellular edema
52
abnormal electrolyte/ion shifts leads to
- arrhythmia risk
53
early MI changes - irreversible cell injury ensues in how many minutes
- 20 minutes
54
macroscopic features of infarction <4 hours
- no abnormality
55
macroscopic features of infarction 4-12 hours
- occasional dark mottling
56
macroscopic features of infarction 12-24 hours
- dark mottling
57
macroscopic features of infarction 1-3 days
- mottling with developing yellow tan necrotic center
58
macroscopic features of infarction 3-14 days
- maximally yellow-tan and soft | - depressed red-tan border
59
macroscopic features of infarction 2-8 weeks
- gray-white scar | - progressive from border to core of infarct
60
macroscopic features of infarction > 2 months
- mature scar
61
microscopic features of infarction <4 hours
- none
62
microscopic features of infarction 4-12 hours
- early coagulative necrosis - edema - hemorrhage
63
microscopic features of infarction 12-24 hours
- early PMNs
64
microscopic features of infarction 1-3 days
- marked interstitial PMNs
65
microscopic features of infarction 3-14 days
- macrophages and granulation tissue at border
66
microscopic features of infarction 2-8 weeks
- loss of cellularity | - increasing collagen
67
microscopic features of infarction > 2 months
- dense collagenous scar
68
functional changes following MI
- systolic and diastolic dysfunction - stunned myocardium - ischemic preconditioning - ventricular remodeling
69
systolic dysfunctional changes
- hypokinesis - akinesis - dyskinesis
70
hypokinesis
- local region with reduced contraction
71
akinesis
- local region with no contraction
72
dyskinesis
- local region that bulges outward with contraction
73
diastolic dysfunction results in
- reduced compliance | - elevated ventricular filling pressures
74
stunned myocardium
- prolonged, but reversible period of contractile dysfunction
75
stunned myocardium how long does it take to recover?
- takes days to weeks to recover
76
ischemic preconditioning
- renders tissue more resistant to future episodes of ischemia
77
ventricular remodeling changes geometry of which myocardium
- infarcted and noninfarcted myocardium
78
ventricular remolding results in
- ventricular dilatation - infarct expansion - myocyte slide-to-slide slippage
79
ventricular remolding advantages
- mechanically disadvantageous
80
ventricular remolding wall stress
- increased wall stress
81
MI complications
- arrhythmias - LV failure, cardiogenic shock - extension of infarct - myocardium free wall rupture - septal perforation - papillary muscle rupture - aneurysm - mural thrombosis
82
result of LV failure
- high grade stenosis of all coronary vessels
83
myocardial free wall rupture occurs when
- first 3 weeks
84
myocardial free wall rupture most common
- days 3-7 | - when wall is weakest
85
myocardial free wall rupture complication of
- large infarcts
86
myocardial free wall rupture occurs at
- junction of infarct and normal muscle
87
septal perforation results in
- left to right shunt
88
papillary muscle rupture results in
- mitral regurgitation | - massive MV incompetence
89
aneurysm result
- wall bulges outward during systole
90
aneurysm - as infarct matures
- fibrous scar progressively stretches
91
aneurysm - increased risk for
- myocardial rupture BASICALLY AS THE WALL IS STRETCHING IT IS FAR MORE LIKELY TO RUPTURE
92
aneurysm - predisposes to
- mural thrombosis
93
aneurysm - effect on workload
- increases workload
94
mural thrombosis - seen in
- fatal acute myocardial infarct | - after apical infarcts
95
mural thrombosis predisposes to
- systemic embolization
96
MI symptoms - nausea, vomiting, weakness is what kind of effect
- parasympathetic
97
MI symptoms - diaphoresis, cool/clammy skin is what kind of effect?
- sympathetic
98
MI symptoms - fever is what kind of effect
- inflammatory
99
evidence of systemic hypoperfusion
- hypotension - tachycardia - impaired cognition - cool extremities - end-organ injury
100
evidence of heart failure
- elevated jugular venous pulsation - pulmonary crackles - gallops - S3,S4 - new murmurs
101
ischemia compromises which part of the cardiac cycle
- diastolic, filling function
102
EKG abnormalities for clinical detection of ischemia
- new ST segment elevation > 1mm - new ST segment depression - new T wave inversion
103
what are labile T wave inversions
- change after rest and nitroglycerin
104
ST segment represents
- period between depolarization and repolarization of left ventricle
105
ST segment should be about how long
- about the same size as PR segment
106
subendocardial injury results in what ST effect
- ST depression
107
transmural injury results in what ST effect
- ST elevation
108
high risk features of MI
- increased age - low BP - elevated HR - heart failure - anterior location
109
definition of acute MI values
- rise/fall of troponin | - one value above 99th percentile
110
definition of acute MI - symptoms
- symptoms of acute ischemia
111
definition of acute MI - ECG
- new ST-T changes - LBBB - pathological Q waves
112
definition of acute MI - imaging
- loss of viable myocardium | - regional wall motion abnormality
113
definition of acute MI - angiography of autopsy
- intracoronary thrombus
114
which troponins do we use?
- troponin I and T
115
CK-MB diagnosis of MI
- upper limit of normal | - 2.5% of total CK (creatine kinase)
116
importance of collecting samples for diagnosis of MI
- always collect serial samples
117
non-cardiac causes of troponin elevation
- acute HF - PE - shock - aortic dissection - myocarditis - trauma - ICD discharge
118
STEMI diagnosis
- >1 mm ST segment elevation in 2 contiguous leads - > 2 mm ST segment elevation in 2 contiguous precordial leads - new LBBB
119
contiguous leads II, III, and AVF point to which anatomic location
- inferior
120
contiguous leads II, III, and AVF point to which coronary artery
- RCA > Lcx
121
V2-V4 point to which anatomic location
- anterior
122
V2-V4 point to which coronary artery
- LAD
123
V1-V4 point to which anatomic location
- anteroseptal note: V1/V2 = septal V3/V4 = anterior
124
V1-V4 point to which coronary artery
- LAD
125
I, aVL, V5, V6 point to which anatomic location
- lateral
126
I, aVL, V5, V6 point to which coronary artery
- Lcx > LAD
127
LBBB points to which anatomic location
- anterior
128
LBBB points to which coronary artery
LAD
129
V4R points to which anatomic location
- right ventricle
130
V4R points to which coronary artery
- RCA
131
V1,V2 ST depression points to which anatomic location
- posterior
132
V1,V2 ST depression points to which coronary artery
- RCA > Lcx
133
MI localization in LAD
- anterior LV - anterior 2/3 septum - apical LV
134
MI Localization in LCX
- lateral LV | - posterolateral LV
135
MI Localization in RCA
- posterior LV - posterior 1/3rd septum - posterior papillary muscle - "inferior" or "diaphragmatic"
136
STEMI treated with
- emergency cardiac catheterization
137
pathologic Q waves are indicative of
- prior transmural STEMI | - not seen in UA or NSTEMI
138
diagnostic criteria for pathologic Q waves
- > 1 mm wide > 25% of overall amplitude of QRS complex - present in > 2 contiguous leads
139
variant (prinzmetal) angina
- focal coronary artery spam in absence of overt atherosclerotic lesions
140
variant (prinzmetal) angina presents with
- chest pain | - transient ST elevation
141
variant (prinzmetal) angina due to
- smooth muscle hyperreactivity | - endothelial dysfunction
142
variant (prinzmetal) angina diagnosis
- intracoronary acetylcholine provokes spasm
143
variant (prinzmetal) angina treatment
- nitrates | - calcium channel blockers
144
UA or NSTEMI symptoms
- rest angina > 20 minutes - new onset angina that limits activity - increasing angina in unstable pattern - +/- T wave inversion or ST depression
145
TIMI risk score for risk stratification in NSTEMI and Unstable Angina
``` > 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
other causes of ACS
- decreased myocardial oxygen supply | - increase in myocardial oxygen demand
147
decreased myocardial oxygen supply due to
- decreased perfusion pressure due to hypotension - anemia - coronary artery dissection or emboli
148
increased in myocardial oxygen demand due to
- rapid tachyarrhythmias - acute hypertension - aortic stenosis

Cardio Exam 2 (29 decks)

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