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Cardio Exam 3 > Ischemic Heart Disease (IHD) > Flashcards

Ischemic Heart Disease (IHD) Flashcards

1
Q

Location: Branch of Aorta

Supplies Blood to: Divides into left anterior descending and circumflex arteries

A

Left Coronary Artery (LCA)

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2
Q

Location: Anterior wall of left ventricle

Supplies Blood to: Anterior wall of left ventricle, anterior inter-ventricular septum and anterior papillary muscle

A

Anterior inter-ventricular artery (AIA)

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3
Q

Location: Lateral wall of left ventricle

Supplies Blood to: Posterior and lateral wall of left ventricle

A

Circumflex Artery (CA)

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4
Q

Location: Right ventricle

Supplies Blood to: Right ventricle, sino-atrial node, atrioventricular node, and posterior papillary muscle

A

Right Coronary Artery (RCA)

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5
Q

Most common cause of IHD

Plaques form due to accumulation of LDL resulting in thickening of coronary arteries and decreased lumen size

A

Atherosclerosis

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6
Q

Quivering of coronary vasculature–> prevents blood flow
can occur in both atherosclerotic and non-atherosclerotic coronary arteries
Ischemia-induced chest pain secondary to coronary vasospasm
Patients are generally younger and do not have many IHD risk factors

A

Coronary artery vasospasm (aka Prinzmetal’s Angina or variant angina)

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7
Q

Oxygen delivered to coronary tissues

A

Myocardial oxygen supply

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8
Q

Oxygen needed by coronary tissues to function

A

Myocardial oxygen demand

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9
Q

Describe a time that a person may experience an increase in myocardial oxygen demand.

A

walking, running, climbing stairs, etc.

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10
Q

How does the body compensate for the increase in demand?

A

Vasodilation

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11
Q

What is pressure that drives Oxygen supply?

A

Perfusion pressure

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12
Q

Ability of coronary vasculature to maintain constant blood flow despite changes in perfusion pressures

A

Autoregulation

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13
Q

Larger lesions result in greater blockage

A

Lesion size

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14
Q

Oxygen deprivation results in vasodilation of coronary arteries

A

Hypoxia

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15
Q

Responsible for vasodilation

A

Nitric Oxide

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16
Q

Dependent on hemoglobin

A

Oxygen carrying capacity

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17
Q

Normal extraction= 65-75%

A

Oxygen extraction capacity

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18
Q

Myocardium perfused during diastole

Pressures during systole too great to allow blood flow through coronary vessels

A

Diastolic filling time

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19
Q

Vessels generated in response to past ischemia

often seen in patients with long-standing stable plaques

A

Collateral blood flow

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20
Q

Volume of blood in the left ventricle at the end of diastole

A

Preload

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21
Q

Resistance against which heart must pump to eject blood

A

afterload

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22
Q

determinate of diastolic filling time

A

Heart Rate

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23
Q

A Nitric oxide deficiency will lead to what?

A

decreased supply

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24
Q

Running up a flight of stairs will lead to what?

A

increased demand

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25
Q

Anemia will lead to what?

A

decreased supply

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26
Q

Atherosclerotic plaques will lead to what?

A

decreased supply

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27
Q

Precipitating factors (P)

A

What caused the pain?

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28
Q

Palliative measures (P)

A

What caused the pain to dissipate?

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29
Q

Quality (Q)

A

Description of pain

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30
Q

Region (R)

A

Where is the pain?

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31
Q

Severity (S)

Pain scale 0-10

A 
0= no pain
10= worst pain of life
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32
Q

Temporal Pattern (T)

A

How long did the pain last? (20 mins)

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33
Q

Myoglobin

A

Normal values:

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34
Q

Cardiac Troponin

Most specific biomarker for cardiac cell death

A

Normal values:

35
Q

Creatine Kinase (CK)

A

Normal values:28-220 ng/mL
TIme to Rise: 4-8 hours
Time to Peak: 20 hours
Time to Normalization: 2-3 days

36
Q

CK-MB

A

Normal values:

37
Q

Lactate Dehydrogenase (LDH)

A

Normal Values: 313-618 ng/mL
Time to Rise: 24-48 hours
Time to Peak: 3-6 days
Time to Normalization: 8-14 days

38
Q

identifies presence of myocardial ischemia

Changes on ECG are dependent on the severity of ischemia

A

Electrocardiogram (ECG or EKG)

39
Q

T-wave Inversion

A

T-wave segment is pointing upside down instead of right side up

40
Q

ST-segment Depression

A

ST segment of ECG is dipping lower than normal

41
Q

ST-segment Elevation

A

ST-segment of ECG is rising way above normal and is the most concerning

42
Q

Cardiac stress test/Exercise-tolerance test

A

exposes patients to an increase in myocardial oxygen demand
patient is evaluated on cardiovascular response to increased oxygen demand
usually reserved for patients with stable diseases

43
Q

Angiography (aka cardiac catherterization)

A

GOLD STANDARD
a catheter is fed through the femoral, brachial or radial artery into the aorta until the tip reaches a coronary artery
IV contrast dye is injected through the catheter and flows through the coronary arteries
radiologic imaging of coronary circulation is taken throughout the procedure
useful for diagnosis of coronary anatomy and prognosis of disease

44
Q

70-80% of lumen covered

thick and fibrous cap

A

Stable IHD

45
Q

50-60% of lumen covered

thin and unstable cap

A

Acute Coronary Syndrome

46
Q

AKA stable angina (SA)
increase in oxygen demand in the setting of a fixed decrease in oxygen supply due to atherosclerotic disease
activity results in myocardium requiring more oxygen

A

Stable Ischemic Heart Disease (Chronic ischemia)

47
Q

Exercise or activity induced?

A

Precipitating factors

48
Q

rest, SL NGT

A

Palliative measure

49
Q

Squeezing pressure

50
Q

Substernal

51
Q

Left/right arms, jaw, neck, abdomen, back

52
Q

5-7/10

53
Q
54
Q

Negative

A

Cardiac Markers

55
Q

ECG

A

Normal
T-wave inversion
or
ST-segment depression

56
Q

Increase in oxygen demand with no acute change in oxygen supply

A

DEMAND ISSUE (SA)

57
Q

Abrupt decrease in oxygen supply due to thrombus formation within the coronary arteries
shear stress within the coronary arteries can result in plaque rupture if the cap is disrupted
- the contents of the plaque are thrombogenic causing platelet adhesion, activation, and aggregation
- the clot formed results in near or complete blockage of the artery lumen resulting in a lack of oxygen supply

A

Acute Coronary Syndrome (acute ischemia)

58
Q

inner surface of blood vessel lined with endothelial cells
endothelial lining disturbed due to blood flow and/or vascular trauma
exposure of thrombogenic substances to the circulating blood

A

Disruption of endothelial lining

59
Q

plaque rupture exposes circulating platelets to adhesion proteins (von Willebrand factor and collagen)
platelets bind to adhesive proteins

A

Platelet Adhesion

60
Q

thromboxane A2 and adenosine diphosphate (ADP) are secreted from the platelet

  • ADP binds to P2Y12 receptor causing activation of a secondary messenger system
  • thromboxane A2 and ADP stimulate neighboring platelets to secrete additional thromboxane A2 and ADP
A

Platelet activation/secretion

61
Q

platelets undergo a conformational change and lose distinct discoid shape
glycoprotein IIb/IIIa receptor becomes exposed and active

A

Platelet shape change

62
Q

circulating fibrinogen has two binding sites for the glycoprotein IIb/IIIa receptor
fibrinogen binds to glycoprotein IIb/IIIa receptor on two different platelets promoting thrombus growth

A

Platelet aggregation

63
Q

No change in oxygen demand with an abrupt decrease in oxygen supply

A

Supply Issue

64
Q

new onset angina (

A

Unstable angina

65
Q

myocardial ischemia persists long enough that cardiac cells die and myocardium becomes necrotic
- cardiac markers: positive (+)

A

Myocardial infarction (MI)

66
Q

ST-segment elevation results from severe infarction

A

STEMI

highest risk of death

67
Q

Any other EKG changes that occur without ST-segment elevation

68
Q

what ethnic groups are more affected by IHD?

A

American Indians or Alaska Natives
Asians or Pacific Islanders
Non-Hispanic blacks
Non-Hispanic whites

69
Q

Rest w/no exertional component

A

UA
NSTEMI
STEMI
(Precipitating Factors)

70
Q

Rest or NTG does not help

A

UA
NSTEMI
STEMI
(Palliative measures)

71
Q

Crushing tightness feeling

A

UA
NSTEMI
STEMI
(Quality)

72
Q

Substernal

A

UA
NSTEMI
STEMI
(Region)

73
Q

left/right arms, jaw, neck, abdomen, back

A

UA
NSTEMI
STEMI
(Radiation)

74
Q

> 20 minutes

A

UA
NSTEMI
STEMI
(Temporal)

75
Q

Negative cardiac markers

76
Q

Positive Cardiac markers

A

NSTEMI

STEMI

77
Q

Normal
ST-segment depression
T-wave inversion

A

UA
NSTEMI
(EKG changes)

78
Q

ST-segment elevation

A

STEMI

EKG changes

79
Q

Ischemia progresses from the endocardium to the epicardium
blood flow needs to be restored as soon as possible to prevent myocardial cell death
- myocardial tissue begins to die after 3 hours without coronary blood flow
“Time is Muscle”

A

Wavefront Ischemia

80
Q

Area of ischemic myocardial tissue surrounding an area of infarcted myocardial tissue
Hibernating/stunned myocardial tissue can be salvaged within 12-24 hours of ischemia
Amount of collateral circulation has direct impact on amount of salvageable myocardium

A

Hibernating/Stunned Myocardium

81
Q

Ischemia occurring without traditional symptoms
- aka “Atypical chest pain”
Occurs in elderly, women and diabetics
Often results in poor prognosis because not treated
- will feel sweaty, tired and may have nausea

A

Silent Myocardial Ischemia

82
Q

Disease severity dependent on multiple factors

  • extent of coronary artery occlusion
  • # of coronary arteries occluded
  • duration of time w/decreased or absent blood flow
  • amount of collateral blood flow
  • amount of natural fibrinolysis
A

Disease Progression and Prognosis

83
Q 
Conduction disturbances
- sinus bradycardia
- heart block (1st, 2nd, and 3rd degree)
Atrial arrhythmias
-atrial fibrillation/flutter
Ventricular arrhythmias
- ventricular tachycardia or fibrillation
Heart failure
Valvular dysfunction
Ventricular aneurysm
Cardiogenic shock
Recurrent ischemia/infarction
Venous thromboembolism
Stroke
Pericarditis
Post-MI syndrome (Dressler's Syndrome)
A

Complications

Cardio Exam 3 (6 decks)

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