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CCN > Coronary Artery Disease > Flashcards

Coronary Artery Disease Flashcards

1
Q

How does CAD occur?

A

Results from atherosclerotic process, a disease of endothelial dysfunction that is chronic, systemic, and inflammatory.

Cholesterol deposits onto intima / endothelial layer and plague protrudes into coronary artery.

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2
Q

Which layer of the blood vessel does plaque attach to?

A

Intima / Endothelial

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3
Q

What is Acute Coronary Syndrome?

A

Acute episode of chest pain unrelieved by rest or reversal of precipitating factor or nitroglycerin.

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4
Q

What is the patho of ACS?

A

1) Plaque ruptures in coronary artery
2) Damaged area releases plaque contents and attracts platelets
3) Platelets adhere to area and become activated (platelet aggregation)
4) Fibrin deposits stabilize the thrombus
5) Abrupt decrease in coronary artery blood flow
6) Imbalance between myocardial O2 demand and supply leads to injury, ischemia, necrosis

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5
Q

What is angina?

A

Temporary chest pain associated with CA blockage or arterial spasm

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6
Q

What are the two types of ischemia?

A

1) Demand ischemia –> Increased O2 demand of cardiac muscle
2) Supply ischemia –> Structural or functional issues in CA leading to decreased blood flow and perfusion

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7
Q

What is stable angina?

A

Caused by known precipitating factors, controlled by rest, reversal of cause

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8
Q

What is pinzmetal angina?

A

Spasm of CA causing supply problem decreasing blood flow. Can lead to angina or arrythmia (most commonly V-fib), CAD may or may not be present

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9
Q

What is unstable angina?

A

Caused by plaque instability, rupture, and thrombus formation.
Causes INCOMPLETE CA occlusion. Can be a change from stable angina or occur suddenly, unable to be relieved

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10
Q

What are the goals of treatment for angina?

A

1) Increase myocardial O2 supply
2) Decrease myocardial O2 demand
3) Prevent MI
4) Intervene if unstable

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11
Q

What interventions can increase myocardial O2 supply?

A

O2, nitrates, Ca channel blockers to vasodilate

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12
Q

What interventions can decrease myocardial O2 demand?

A

Beta blockers, ACE inhibitors, analgesia

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13
Q

What interventions can prevent MI?

A

Platelet inhibitors, anticoagulants, antihypertensives, cholesterol lowering agents

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14
Q

What interventions if unstable angina?

A

PCI, IABP, CABG

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15
Q

What are the zones of injury for myocardial infarction?

A

1) Zone of ischemia
2) Zone of injury
3) Zone of necrosis

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16
Q

What is the zone of ischemia in MI?

A

Outer layer of infarcted myocardium, cells deprived of O2.

NSTEMI

T wave inversion due to impaired repolarization, ST depression

Goal to increase O2 supply

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17
Q

What is the zone of injury in MI?

A

Area surrounding the infarcted area, cells are injured and may die

STEMI

ST elevation with T wave inversion due to incomplete cell repolarization

Goal to stop progression to necrosis

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18
Q

What is the zone of necrosis in MI?

A

Dead tissue does not respond electrically or mechanically

Infarcted tissue eventually replaced with scar tissue

Pathological Q waves seen after 24 hrs from non-responsive cells

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19
Q

What is the effect of MI on CO?

A

Increase HR to compensate for low BP, preload stays high d/t decrease in FOC there is compensatory vasoconstriction which increases afterload

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20
Q

What is STEMI?

A

Irreversible cell death through all 3 layers of the heart.

ST elevation, pathological q waves, new LBB seen
Tissue death begins 30-45 mins up to 6 hrs

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21
Q

What is NSTEMI?

A

Irreversible cell death does not reach full thickness of myocardium (PARTIAL OCCLUSION)

ST depression, prominent T wave inversion, troponins elevated

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22
Q

Occlusion of RCA affects what area?

A

R atria, R ventricle, AV and SA node, inferior area of heart

Occlusions result in bradycardias, heart blocks, RV failure

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23
Q

Occlusion of L main coronary artery affects what area?

A

Anterior, lateral wall of LV. Can result in LV failed

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24
Q

Occlusion of the LAD affects what area?

A

Anterior LV, septum, bundle branches

Occlusions result in LV failure and conduction issues

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25
Q

Occlusion of the circumflex artery affects what area?

A

Lateral, posterior LV

Occlusions result in L free wall damage, aneurysm

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26
Q

What CA supplies the anterior area of the heart?

A

LAD

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27
Q

What CA supplies to septal area of the heart?

A

LAD

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28
Q

What CA supplies the lateral area of the heart?

A

Circumflex

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29
Q

What CA supplies the inferior area of the heart?

A

RCA

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30
Q

What CA supplies the posterior area of the heart?

A

RCA, circumflex

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31
Q

What CA supplies the R ventricle?

A

RCA

32
Q

What CA supplies L ventricle?

A

LAD, circumflex

33
Q

What is the diagnostic criteria for acute MI?

A

Must have 2 of the following:

1) Hx of ischemic chest discomfort
2) Serial 12 lead ECG changes
3) Rise and fall in cardiac enzymes

34
Q

What are ECG changes seen in acute MI?

A

NSTEMI –> ST depression, T wave inversion

STEMI –> Persistent ST elevation, pathological Q waves, new LBBB

35
Q

What causes ischemic chest pain?

A

Pain is sensed by the vagus nerve and expressed differently per individual

36
Q

What are some typical descriptors of ischemic chest pain?

A

Pressure / pain > 10 mins, retrosternal pain radiating to arms, jaw, neck, diaphoresis, dyspnea, nausea, syncope

37
Q

What are some atypical descriptors of ischemic chest pain?

A

Epigastric pain, indigestion, heartburn, increasing dyspnea in the absence of chest pain, discomfort in shoulder, neck, back, jaw, ear

38
Q

Why do we need to treat pain in ACS?

A

Increase SNS response causes increase in HR which further decreases CA perfusion leading to extension of injury

39
Q

What are the cardiac enzyme biomarkers for MI?

A

1) Cardiac troponin 1

2) CK/MB

40
Q

How does troponin 1 change with MI?

A

Rise 4-6 hrs post MI, peak at 10-24 hrs, fall 10-15 days post

Is cardiac specific, measured on admission and 3-6 hrs later. If high value, predictive of future risk of cardiac events

41
Q

How does CK / MB change with MI?

A

Rise 4-8 hrs, peak 15-24 hrs, fall 2-3 days.

Less specific than trops, require more muscle death to be detectable. Beneficial to diagnose extension or reinfarction

42
Q

What are diagnostic tests for MI?

A

Chest x ray, echocardiography, LV function

43
Q

What are the two types of echocardiography?

A

1) Trans esophageal echo (TEE) –> Visualizes valves, structural view
2) Trans thoracic echo (TTE) –> Visualizing walls, blood flow through ventricles

44
Q

How is L ventricular function graded?

A 
Grade 1 (E/F > 60%) 
Grade 2 (E/F > 40%)
Grade 3 (E/F 20-40%)
Grade 4 (E/F < 20%)
45
Q

How is ejection fraction calculated?

A

EF% = SV / EDV (end diastolic volume)

46
Q

What are treatments for STEMI?

A

Goal to open to occluded artery, prevent further myocardial injury or death.

PCI –> Gold standard, should be done within 90 mins provided ischemic pain < 12 hrs

Fibrinolytic therapy

CABG –> Used for severe heart failure or cardiogenic shock

IABP

Targeted temperature management / cooling

47
Q

What should be given during / post PCI?

A

Antiplatelet therapy such as aspirin, tecagralor

Anticoagulants such as heparin

48
Q

What should be done if pt can’t get PCI fast enough?

A

Fibrinolytic therapy

49
Q

What is Targeted Temperature Management?

A

Done for pts with STEMI presenting with v fib or pulseless v tach, targeted temp 32 - 36 for 24 hrs for neuroprotection.

Decrease metabolic demand, rest the heart, decrease risk of brain ischemia. CO2 targets set to prevent cerebral vasodilation increasing ICP

Analgesics, sedatives, intubation

50
Q

What are treatments for NSTEMI?

A

Goal to prevent total occlusion, recurrent infarction, plaque thromboembolization

Initially managed with anti-anginal, dual antiplatelets, anticoagulants

Risk of future cardiac events determined and invasive treatment may be done

51
Q

Is fibrinolytic therapy indicated for NSTEMI?

A

No. Risk of ICH

52
Q

What are the two reperfusion treatments?

A

1) PCI

2) Fibrinolytic therapy

53
Q

How does PCI work?

A

Stent inserted into affected CA, antiplatelet and anticoags infusing.

54
Q

How does fibrinolytic therapy work?

A

Indicated only for STEMI, dissolves existing clot by breaking down fibrin, fibrinogen

**Must be done within 6 hrs of symptoms, after that the clot is well established

Recommended:
-ase ‘s

55
Q

What meds will pts need post PCI?

A

Post procedure pt will need dual antiplatelet therapy up to 1 year and ASA indefinetely

56
Q

What to monitor for during administration of fibrinolytic therapy?

A

Hypotension (allergix rx, bleeding, heart failure)
S&S hemorrhagic stroke
Signs of re-perfusion, re-occlusion
Ensure antiplatelets and anticoags also running

57
Q

How does morphine manage MI? What are SE?

A

Controls pain, decrease SNS response, decrease O2 demand.

Vasodilation decrease cardiac workload

Can decrease GI motility and cause nausea, emesis, hypotension

Can interfere with absorption of antiplatelets

58
Q

How is O2 used to treat MI?

A

Not recommended unless hypoxemic, dyspneic, or with heart failure

59
Q

How is nitroglycerin used to treat MI?

A

Improves ischemic chest pain, vasodilation of CA

Monitor pt comfort with titration, can cause compensatory tachy

Doesn’t decrease injury in STEMI, just helps with pain related to vasospasm

60
Q

How are anticoagulants used to treat MI?

A

Prevents clot from getting larger, does not dissolve clot

61
Q

How do platelet inhibitors help treat MI?

A

Prevents thrombus formation, used for initial and ongoing treatment

1) Antiplatelets (Aspirin) usually first line therapy, 160 - 325mg asap
2) PZY12 receptor inhibitors prevent fibrin formation (clopidogrel, ticagrelor)
3) GP 11B / 11A inhibitors prevent thrombin formation (Integrellin, aggrostat)

62
Q

What are PZY12 receptor inhibitors?

A

prevent fibrin formation (clopidogrel, ticagrelor)

63
Q

What are GP 11B / 11A inhibitors?

A

prevent thrombin formation (Integrellin, aggrostat)

64
Q

How are beta blockers used to treat MI?

A

Blocks beta 1 receptors in heart, decrease HR, FOC, workload, ischemia

Monitor for hypotension, bradycardias. Should be administered in 1st 24 hrs given no contraindications

65
Q

How are ACE inhibitors and ARBs used to treat MI?

A

Cause vasodilation, decrease afterload, workload, BP

Ace inhibitors: -prils
ARBS: -sartans

66
Q

How do statins work to treat MI?

A

Work in liver to decrease LDLs, triglycerides, HDL.

Lowers risk of CAD, all pts should be started on statins once stabilized from MI

67
Q

How do Ca channel blockers work to treat MI?

A

Control HR, treat ischemia, decrease HR for pts who cannot tolerate beta blockers

Decrease afterload, vasodilation, workload

Example is amlodipine

68
Q

What is the most common complication of CAD?

A

Dysrhythmias

69
Q

Why is LV failure a complication of CAD

A

Inability of LV to pump blood resulting in decreased CO, systemic vasoconstriction occurs which increases afterload.

Pt at risk for pulmonary edema

70
Q

How is LV failure treated?

A

Promote diuresis, inotropes, decrease LV afterload with ace inhibitors, vasodilators, beta blockers when tolerated

71
Q

Why is RV failure a complication of CAD

A

Often associated with inferior MI, inability of RV to pump blood forward result in blood backing up into systemic venous system

72
Q

How is RV failure treated?

A

Optimize preload, decrease RV afterload, inotropes

73
Q

What is LV aneurysm?

A

Often associated with anterior STEMI, weakening / thinning of heart walls in areas of necrosis results in blood pocket which may lead to wall rupture or cardiac tamponade

74
Q

What is ventricular - septal defect?

A

Rupture of ventricular - septal wall causing massive blood shift from L to R ventricle

High surgical mortality rate

75
Q

What is papillary muscle rupture?

A

Causes mitral valve regurgitation, shift from L ventricle to L atrium

Requires urgent surgery

76
Q

What is pericarditis and what are symptoms and treatments?

A

Inflammation of pericardium

SS: Pericardial friction rub, global ST elevation

Treated with ASA, colchicine, tylenol, narcotics

CCN (27 decks)

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