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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
Anemia will lead to what?
decreased supply
26
Atherosclerotic plaques will lead to what?
decreased supply
27
Precipitating factors (P)
What caused the pain?
28
Palliative measures (P)
What caused the pain to dissipate?
29
Quality (Q)
Description of pain
30
Region (R)
Where is the pain?
31
Severity (S) | Pain scale 0-10
``` 0= no pain 10= worst pain of life ```
32
Temporal Pattern (T)
How long did the pain last? (20 mins)
33
Myoglobin
Normal values:
34
Cardiac Troponin | ***Most specific biomarker for cardiac cell death***
Normal values:
35
Creatine Kinase (CK)
Normal values:28-220 ng/mL TIme to Rise: 4-8 hours Time to Peak: 20 hours Time to Normalization: 2-3 days
36
CK-MB
Normal values:
37
Lactate Dehydrogenase (LDH)
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
identifies presence of myocardial ischemia | Changes on ECG are dependent on the severity of ischemia
Electrocardiogram (ECG or EKG)
39
T-wave Inversion
T-wave segment is pointing upside down instead of right side up
40
ST-segment Depression
ST segment of ECG is dipping lower than normal
41
ST-segment Elevation
ST-segment of ECG is rising way above normal and is the most concerning
42
Cardiac stress test/Exercise-tolerance test
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
Angiography (aka cardiac catherterization)
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
70-80% of lumen covered | thick and fibrous cap
Stable IHD
45
50-60% of lumen covered | thin and unstable cap
Acute Coronary Syndrome
46
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
Stable Ischemic Heart Disease (Chronic ischemia)
47
Exercise or activity induced?
Precipitating factors
48
rest, SL NGT
Palliative measure
49
Squeezing pressure
Quality
50
Substernal
Region
51
Left/right arms, jaw, neck, abdomen, back
Radiation
52
5-7/10
Severity
53
Temporal
54
Negative
Cardiac Markers
55
ECG
Normal T-wave inversion or ST-segment depression
56
Increase in oxygen demand with no acute change in oxygen supply
DEMAND ISSUE (SA)
57
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
Acute Coronary Syndrome (acute ischemia)
58
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
Disruption of endothelial lining
59
plaque rupture exposes circulating platelets to adhesion proteins (von Willebrand factor and collagen) platelets bind to adhesive proteins
Platelet Adhesion
60
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
Platelet activation/secretion
61
platelets undergo a conformational change and lose distinct discoid shape glycoprotein IIb/IIIa receptor becomes exposed and active
Platelet shape change
62
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
Platelet aggregation
63
No change in oxygen demand with an abrupt decrease in oxygen supply
Supply Issue
64
new onset angina (
Unstable angina
65
myocardial ischemia persists long enough that cardiac cells die and myocardium becomes necrotic - cardiac markers: positive (+)
Myocardial infarction (MI)
66
ST-segment elevation results from severe infarction
STEMI | highest risk of death
67
Any other EKG changes that occur without ST-segment elevation
NSTEMI
68
what ethnic groups are more affected by IHD?
American Indians or Alaska Natives Asians or Pacific Islanders Non-Hispanic blacks Non-Hispanic whites
69
Rest w/no exertional component
UA NSTEMI STEMI (Precipitating Factors)
70
Rest or NTG does not help
UA NSTEMI STEMI (Palliative measures)
71
Crushing tightness feeling
UA NSTEMI STEMI (Quality)
72
Substernal
UA NSTEMI STEMI (Region)
73
left/right arms, jaw, neck, abdomen, back
UA NSTEMI STEMI (Radiation)
74
> 20 minutes
UA NSTEMI STEMI (Temporal)
75
Negative cardiac markers
UA
76
Positive Cardiac markers
NSTEMI | STEMI
77
Normal ST-segment depression T-wave inversion
UA NSTEMI (EKG changes)
78
ST-segment elevation
STEMI | EKG changes
79
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"
Wavefront Ischemia
80
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
Hibernating/Stunned Myocardium
81
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
Silent Myocardial Ischemia
82
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
Disease Progression and Prognosis
83
``` 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) ```
Complications

Cardio Exam 3 (6 decks)

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