Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Cardiovascular II > Ischemic heart disease > Flashcards

Ischemic heart disease Flashcards

(98 cards)

Start Studying
1
Q

Clinical syndromes of ischemic heart disease

A

MI
Angina pectoris
Chronic IHD with HF
Sudden cardiac death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Determinants of myocardial oxygen supply

A

Coronary perfusion pressure
Coronary vascular resistance –> external compression and intrinsic regulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Determinants of myocardial oxygen demand

A

Wall stress
HR
Contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Coronary artery flow is directly proportional to what?

A

Perfusion pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Coronary artery flow is inversely proportional to what?

A

Coronary vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Value used to approximate coronary perfusion pressure

A

Aortic diastolic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Regulators of intrinsic control of coronary arterial tone

A

Accumulation of local metabolites
Endothelium-derived substances
Neural innervation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Change in vascular smooth muscle to increase coronary blood flow

A

Adenosine binds to receptors to reduce Ca entry into cells, resulting in relaxation and vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

NT receptors on coronary vessels

A

Alpha adrenergic
Beta-2 adrenergic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Result of stimulation of alpha adrenergic receptors on coronary vessels

A

Vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Result of stimulation of beta-2 adrenergic receptors on coronary vessels

A

Vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Way that beta blockers decrease HR?

A

Reduce ATP utilization and oxygen consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Affect of catecholamines on the heart

A

Increase force of contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Drug class with a negative inotropic effect

A

Beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hemodynamic significance of coronary A narrowing depends on these 2 things

A

Degree of stenosis
Amount of compensatory vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Causes of vessel endothelial cell dysfunction

A

Inappropriate vasoconstriction of coronary A
Loss of normal antithrombotic properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Angina type precipitated by exercise and relieved with rest or administration of vasodilators. Not usually associated with plaque disruption.

A

Stable/typical angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Uncommon episode of myocardial ischemia caused by coronary A spasm. Occurs at rest and responds promptly to vasodilators.

A

Prinzmetal variant angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Triggers of Prinzmetal angina

A

Smoking
Cocaine
Alcohol
Triptans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Pattern of increasingly frequent, prolonged, or severe angina. Caused by disruption of an atherosclerotic plaque

A

Unstable/crescendo angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Clinical syndrome of angina pectoris in the absence of significant atherosclerotic coronary stenoses on coronary angiography. Abnormal stress test and abnormal myocardial perfusion imaging.

A

Microvascular angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ECG findings during angina episode

A

ST depression
T wave flattening or inversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Contrasts used in nuclear stress test

A

Technetium-99m-labeled compound
Thalium-201

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Inotropic agent used in pharmacologic stress test

A

Dobutamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Coronary vasodilators used in pharmacologic stress test
Adenosine Dipyridamole
26
Hemodynamically significant atherosclerotic lesion results in increased blood flow to non-ischemic areas, which can than move to ischemic areas
Coronary steal syndrome
27
Possible causes of coronary embolism that can cause MI
Endocarditis Artificial heart valves Paradoxical embolism
28
Timing of onset of ATP depletion in MI
Seconds
29
Timing of loss of contractility in MI
<2 min
30
Timing of reduction of ATP to 50% of normal in MI
10 min
31
Timing of reduction of ATP to 10% of normal in MI
40 min
32
Timing of irreversible cell injury in MI
20-40 min
33
Timing of microvascular injury in MI
>1 hr
34
Earliest detectable feature of myocyte necrosis that forms the basis of blood tests for irreversible myocyte damage
Disruption of integrity of sarcolemmal membrane
35
First area of irreversible injury of ischemic myocytes in MI
Subendocardial zone
36
Complications of MI that can occur within the first 24 hrs
Ventricular arrhythmias HF Cardiogenic shock
37
When will early coagulation necrosis and edema be seen after MI?
4-12 hrs
38
When will contraction band necrosis and early neutrophilic infiltrates be seen after MI?
12-24 hrs
39
When will coagulation necrosis with loss of nuclei and striations, and brick neutrophilic infiltrate be seen after MI?
1-3 days
40
Complication that can occur 1-3 days after MI
Post-infarction fibrinous pericarditis
41
When will the gross heart have hyperemic border and central softening in the infarct area after MI?
3-7 days
42
When will the gross heart be maximally soft and microscopically show granulation tissue at margins of infarct area after MI?
7-10 days
43
When will there be well established granulation tissue after MI?
10-14 days
44
When will area of infarct after MI appear as a gray white scar?
2-8 wks
45
Complication that can occur 3-5 days after MI
Interventricular septal rupture
46
Complication that can occur 5-14 days after MI
Free wall rupture
47
Complication that can occur 2-7 days after MI
Papillary muscle rupture
48
Complication that can occur 3-7 days after MI
LV false aneurysm
49
Complications that can occur 2 wks to several months after MI
Dressler syndrome CHF True ventricular aneurysm
50
Gross histochemical stain that imparts a brick-red color to intact, non-infarcted myocardium where lactate dehydrogenase activity is preserved
Triphenyltetrazolium chloride (TTC)
51
Morphology of reperfused infarct
Hemorrhagic Contraction bands in irreversible injured myocytes
52
What mediates damage in reperfusion injury?
Oxidative stress Calcium overload Inflammatory cells
53
Intensely eosinophilic IC stripes composed of closely packed sarcomeres. Seen in reperfused MI.
Contraction bands
54
Refers to tissue that demonstrates prolonged systolic dysfunction after an episode of severe, acute, transient ischemia without necrosis --> even after return of normal blood flow
Stunned myocardium
55
Mechanism of delayed recovery in stunned myocardium
Ca overload and accumulation of oxygen-derived free radicals
56
Refers to a tissue that manifests chronic ventricular contractile dysfunction due to a persistently reduced blood supply, usually because of multivessel CAD
Hibernating myocardium
57
Imaging study to distinguish hibernating myocardium from infarcted
FDG-PET --> fluorodeoxyglucose positron emission tomography
58
Cardiac troponins time to increase after infarct
3-12 hrs after infarction
59
Time taken for cardiac troponin I to return to normal after infarct
5-10 days
60
Time taken for cardiac troponin T to return to normal after infarct
5-14 days
61
Time taken for CK-MB to show increase after infarct
6-12 hrs
62
Time taken for CK-MB to return to normal levels after infarct
48-72 hrs
63
Blood test used to assess for reinfarction
CK-MB
64
Classic ECG pattern in MI
Inverted T waves Elevated ST segments New Q waves
65
ECG finding that correlates with area of coagulation necrosis in MI
New Q waves
66
ECG finding that correlates with injury to myocardial cells surrounding the areas of necrosis in MI
Elevated ST segments
67
ECG finding that correlates with areas of ischemia at the periphery of the infarction
Inverted T waves
68
ECG leads affected in anterior wall infarct or anteroseptal infarct
V1-V2
69
ECG leads affected in anterolateral infarct
V4-V6 I aVL
70
ECG leads affected in lateral wall infarct
I aVL
71
ECG leads affected in inferior wall MI
II-III aVF
72
ECG leads affected in posterior wall MI
V7-V9
73
Most common reason for death within 1 hr of MI
Fatal arrhythmia
74
Complications of MI
Contractile dysfunction Arrhythmias Myocardial rupture Ventricular aneurysm Pericarditis Infarct expansion Mural thrombus Papillary muscle dysfunction Chronic IHD
75
Complication of infarcts involving the inferoseptal myocardium
Heart block
76
Most common site of ventricular free wall rupture
Anterolateral wall at mid-ventricular level
77
Result of ventricular free wall rupture
Cardiac tamponade
78
Result of rupture of ventricular septum
Acute VSD L to R shunting New holosystolic murmur
79
Result of papillary muscle rupture
Acute onset of severe mitral regurgitation
80
Localized hematoma communicating with the ventricular cavity, a contained free wall rupture
False aneurysm
81
Late complication of large transmural infarcts that experience early expansion. Bound by scarred myocardium and paradoxically bulges during systole.
Ventricular true aneurysm
82
Complications of ventricular true aneurysm
Mural thrombus Arrhythmias HF
83
Caused by increased vessel permeability in pericardium resulting in exudate of acute inflammation from underlying myocardial inflammation from MI. Precordial friction rub present on ausculation.
Fibrinous/fibrinohemorrhagic pericarditis
84
Triad of Dressler syndrome
Fever Pericarditis Pericardial effusion post MI
85
Pathogenesis of Dressler syndrome
Autoantibodies directed against antigens within damaged pericardial tissue --> type II hypersensitivity
86
Disproportionate stretching, thinning, and dilation of the infarct region due to weakening of necrotic muscle after MI. Associated with mural thrombus.
Infarct expansion
87
Area at increased risk of infarct expansion after MI
Anteroseptal infarcts
88
Insidious onset of progressive CHF characterized by LV dilation due to accumulated ischemic myocardial damage and replacement fibrosis, and functional loss of hypertrophied non-infarcted cardiac myocytes.
Chronic IHD
89
Common cause of restenosis of coronary vessel following PCI
Neointima formation
90
Vascular smooth muscle cells migrate into stent to form a layer resembling tunica intima. Promoted by macrophages and inflammatory cells.
Neointima formation
91
Non-coronary artery causes of sudden cardiac death
Cardiomyopathy MVP Cocaine Myocarditis WPW syndrome Hereditary ion channelopathies
92
Hereditary ion channelopathies
Long QT syndrome Brugada syndrome
93
Causes of sudden cardiac death in children
Pulmonary infection AV stenosis Cardiomyopathies --> usually hypertrophic WPW syndrome
94
Reason for sudden cardiac death in long QT syndrome
Increased susceptibility to malignant ventricular arrhythmias
95
Genes affected by loss of function mutations leading to long QT syndrome
KCNQ1 --> K channel KCNH2 --> K channel
96
Genes affected by gain of function mutations leading to long QT syndrome
SCN5A --> Na channel CAV3 --> Na current, caveolin
97
3 acute coronary syndromes
Unstable angina NSTEMI STEMI
98

Cardiovascular II (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions