Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular II > Ischemic heart disease > Flashcards

Ischemic heart disease Flashcards

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
Q

Coronary vasodilators used in pharmacologic stress test

A

Adenosine
Dipyridamole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Hemodynamically significant atherosclerotic lesion results in increased blood flow to non-ischemic areas, which can than move to ischemic areas

A

Coronary steal syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Possible causes of coronary embolism that can cause MI

A

Endocarditis
Artificial heart valves
Paradoxical embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Timing of onset of ATP depletion in MI

A

Seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Timing of loss of contractility in MI

A

<2 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Timing of reduction of ATP to 50% of normal in MI

A

10 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Timing of reduction of ATP to 10% of normal in MI

A

40 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Timing of irreversible cell injury in MI

A

20-40 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Timing of microvascular injury in MI

A

> 1 hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Earliest detectable feature of myocyte necrosis that forms the basis of blood tests for irreversible myocyte damage

A

Disruption of integrity of sarcolemmal membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

First area of irreversible injury of ischemic myocytes in MI

A

Subendocardial zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Complications of MI that can occur within the first 24 hrs

A

Ventricular arrhythmias
HF
Cardiogenic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

When will early coagulation necrosis and edema be seen after MI?

A

4-12 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

When will contraction band necrosis and early neutrophilic infiltrates be seen after MI?

A

12-24 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

When will coagulation necrosis with loss of nuclei and striations, and brick neutrophilic infiltrate be seen after MI?

A

1-3 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Complication that can occur 1-3 days after MI

A

Post-infarction fibrinous pericarditis

41
Q

When will the gross heart have hyperemic border and central softening in the infarct area after MI?

42
Q

When will the gross heart be maximally soft and microscopically show granulation tissue at margins of infarct area after MI?

43
Q

When will there be well established granulation tissue after MI?

A

10-14 days

44
Q

When will area of infarct after MI appear as a gray white scar?

45
Q

Complication that can occur 3-5 days after MI

A

Interventricular septal rupture

46
Q

Complication that can occur 5-14 days after MI

A

Free wall rupture

47
Q

Complication that can occur 2-7 days after MI

A

Papillary muscle rupture

48
Q

Complication that can occur 3-7 days after MI

A

LV false aneurysm

49
Q

Complications that can occur 2 wks to several months after MI

A

Dressler syndrome
CHF
True ventricular aneurysm

50
Q

Gross histochemical stain that imparts a brick-red color to intact, non-infarcted myocardium where lactate dehydrogenase activity is preserved

A

Triphenyltetrazolium chloride (TTC)

51
Q

Morphology of reperfused infarct

A

Hemorrhagic
Contraction bands in irreversible injured myocytes

52
Q

What mediates damage in reperfusion injury?

A

Oxidative stress
Calcium overload
Inflammatory cells

53
Q

Intensely eosinophilic IC stripes composed of closely packed sarcomeres. Seen in reperfused MI.

A

Contraction bands

54
Q

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

A

Stunned myocardium

55
Q

Mechanism of delayed recovery in stunned myocardium

A

Ca overload and accumulation of oxygen-derived free radicals

56
Q

Refers to a tissue that manifests chronic ventricular contractile dysfunction due to a persistently reduced blood supply, usually because of multivessel CAD

A

Hibernating myocardium

57
Q

Imaging study to distinguish hibernating myocardium from infarcted

A

FDG-PET –> fluorodeoxyglucose positron emission tomography

58
Q

Cardiac troponins time to increase after infarct

A

3-12 hrs after infarction

59
Q

Time taken for cardiac troponin I to return to normal after infarct

60
Q

Time taken for cardiac troponin T to return to normal after infarct

61
Q

Time taken for CK-MB to show increase after infarct

62
Q

Time taken for CK-MB to return to normal levels after infarct

63
Q

Blood test used to assess for reinfarction

64
Q

Classic ECG pattern in MI

A

Inverted T waves
Elevated ST segments
New Q waves

65
Q

ECG finding that correlates with area of coagulation necrosis in MI

A

New Q waves

66
Q

ECG finding that correlates with injury to myocardial cells surrounding the areas of necrosis in MI

A

Elevated ST segments

67
Q

ECG finding that correlates with areas of ischemia at the periphery of the infarction

A

Inverted T waves

68
Q

ECG leads affected in anterior wall infarct or anteroseptal infarct

69
Q

ECG leads affected in anterolateral infarct

70
Q

ECG leads affected in lateral wall infarct

71
Q

ECG leads affected in inferior wall MI

72
Q

ECG leads affected in posterior wall MI

73
Q

Most common reason for death within 1 hr of MI

A

Fatal arrhythmia

74
Q

Complications of MI

A

Contractile dysfunction
Arrhythmias
Myocardial rupture
Ventricular aneurysm
Pericarditis
Infarct expansion
Mural thrombus
Papillary muscle dysfunction
Chronic IHD

75
Q

Complication of infarcts involving the inferoseptal myocardium

A

Heart block

76
Q

Most common site of ventricular free wall rupture

A

Anterolateral wall at mid-ventricular level

77
Q

Result of ventricular free wall rupture

A

Cardiac tamponade

78
Q

Result of rupture of ventricular septum

A

Acute VSD
L to R shunting
New holosystolic murmur

79
Q

Result of papillary muscle rupture

A

Acute onset of severe mitral regurgitation

80
Q

Localized hematoma communicating with the ventricular cavity, a contained free wall rupture

A

False aneurysm

81
Q

Late complication of large transmural infarcts that experience early expansion. Bound by scarred myocardium and paradoxically bulges during systole.

A

Ventricular true aneurysm

82
Q

Complications of ventricular true aneurysm

A

Mural thrombus
Arrhythmias
HF

83
Q

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.

A

Fibrinous/fibrinohemorrhagic pericarditis

84
Q

Triad of Dressler syndrome

A

Fever
Pericarditis
Pericardial effusion post MI

85
Q

Pathogenesis of Dressler syndrome

A

Autoantibodies directed against antigens within damaged pericardial tissue –> type II hypersensitivity

86
Q

Disproportionate stretching, thinning, and dilation of the infarct region due to weakening of necrotic muscle after MI. Associated with mural thrombus.

A

Infarct expansion

87
Q

Area at increased risk of infarct expansion after MI

A

Anteroseptal infarcts

88
Q

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.

A

Chronic IHD

89
Q

Common cause of restenosis of coronary vessel following PCI

A

Neointima formation

90
Q

Vascular smooth muscle cells migrate into stent to form a layer resembling tunica intima. Promoted by macrophages and inflammatory cells.

A

Neointima formation

91
Q

Non-coronary artery causes of sudden cardiac death

A

Cardiomyopathy
MVP
Cocaine
Myocarditis
WPW syndrome
Hereditary ion channelopathies

92
Q

Hereditary ion channelopathies

A

Long QT syndrome
Brugada syndrome

93
Q

Causes of sudden cardiac death in children

A

Pulmonary infection
AV stenosis
Cardiomyopathies –> usually hypertrophic
WPW syndrome

94
Q

Reason for sudden cardiac death in long QT syndrome

A

Increased susceptibility to malignant ventricular arrhythmias

95
Q

Genes affected by loss of function mutations leading to long QT syndrome

A

KCNQ1 –> K channel
KCNH2 –> K channel

96
Q

Genes affected by gain of function mutations leading to long QT syndrome

A

SCN5A –> Na channel
CAV3 –> Na current, caveolin

97
Q

3 acute coronary syndromes

A

Unstable angina
NSTEMI
STEMI

Cardiovascular II (29 decks)

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