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Drug Action I > Block 3 - ACS > Flashcards

Block 3 - ACS Flashcards

1
Q

What is CAD?

A

Reduced oxygen and nutrients supplied to myocardium as a result of reduced blood flow

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2
Q

What is CHD?

A

Buildup of plaque in coronary arteries

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3
Q

What is coronary circulation?

A

Blood flow to and from myocardium through coronary arteries and cardiac veins

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4
Q

What is angina pectoris?

A

Chest pain and discomfort due to heart not being able to receive enough perfusion of blood

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5
Q

What is myocardial ischemia?

A

Restriction of blood supply to heart muscle tissues, causing a shortage of oxygen and nutrients

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6
Q

What is MI?

A

an area of tissue death, or necrosis, related to obstructed blood flow to the myocardium

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7
Q

What causes MI?

A

atherosclerosis leading to a thromboembolism

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8
Q

What is auto regulation?

A

The brain maintains constant blood flow despite changes in perfusion pressure

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9
Q

What does the process of oxygenation consist of?

A

Ventilation, diffusion, and perfusion are essential for gas exchange to occur

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10
Q

Who are more at risk of CHD deaths?

A

Women, AA

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11
Q

What are Life’s simple 7 points?

A
  1. BP
  2. Physical activity
  3. Cholesterol
  4. Diet
  5. Weight
  6. Smoking status
  7. Blood glucose level
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12
Q

What are the medications used of CAD?

A
  1. AntiHTN
  2. Statins
  3. Insulin
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13
Q

Lifestyle modifications ____ risk factors for CAD

A

Lower

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14
Q

What is the function of coronary arteries?

A

Blood vessels that deliver necessary supplies of oxygen and nutrients required by myocardial cells to function and survive

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15
Q

Most blood flow to the myocardium is delivered during _____

A

Ventricular diastole

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16
Q

What does the left coronary artery supply blood to?

A
  1. Left atrium
  2. Left ventricle
  3. intervetricular septum
  4. AV bundles
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17
Q

What does the right coronary artery supply blood to? Why is it important?

A
  1. Right atrium
  2. Right ventricle
  3. interventriculat septum
  4. SA and AV nodes

Helps with cardiac conduction

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18
Q

What is the purpose of coronary collateral circulation?

A

Preserves function by enabling an alternative route for delivery of blood to the myocardium

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19
Q

When O2 exchange is insufficient, coronary arteries ___ to ___ blood flow

A

Dilate; increase

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20
Q

What can lead to narrowing of coronary arteries?

A

Atherosclerotic plaque → decrease BF → asymptomatic until blood is obstructed

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21
Q

Why is O2 balance important in cardiac tissue?

A
  1. Key to the production of sufficient arterial pressure to perfuse systemic and coronary circulation
  2. Coronary artery flow is reduced during systole
  3. Blood is delivered through the coronary arteries during diastole
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22
Q

What is coronary perfusion pressure?

A

The pressure of blood through coronary circulation from a pressure gradient between aortic and right atrial pressure

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23
Q

What factors are determined by MC O2 demand and consumption?

A
  1. HR
  2. Systolic pressure
  3. Left ventricular contractility
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24
Q

Injury of heart muscle can decrease blood flow leading to _____

A

hypoxia of myocardial cells

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25
Q

What happens to the heart if the blood supply is compromised for 10-15 minutes?

A

Myocardial cell injury is reversible and can recover to normal function

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26
Q

What happens to the heart if the blood supply is compromised for over 20 minutes?

A
  1. Death of myocardial fibers
  2. Irreversible injury is dependent of coronary collateral circulation
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27
Q

What factors accelerate myocardial injury?

A
  1. Increased MC O2 requirement (hypotension, vasospasm, tachycardia)
  2. Low O2 delivery (Hypotension, anemia)
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28
Q

Describe irreversible injury progression?

A

Subendocardium (inner) → subepicardium (outer)

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29
Q

A person may experience brief periods of ___ QD w/o ____

A

Ischemia; myocardial necrosis

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30
Q

What is stroke volume?

A

Amount of blood pumped from the ventricle during one contraction

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31
Q

What is preload?

A

Amount of volume in the right or left ventricle at the end of diastole

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32
Q

What is after load?

A

Pressure that the heart has to contract against to eject blood from the ventricle during systole

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33
Q

How does ischemia disrupt conduction of the heart?

A
  1. Disrupts the electrical charge transmission of cardiac muscle fibers
  2. Affecting ability to contract and limits perfusion
34
Q

What are the main structures of the cardiac conduction system?

A
  1. SA and AV nodes
  2. Bundle of HIS
  3. L and R bundle branches
  4. Purkinje fibers
35
Q

What occurs during the PR interval?

A

SA node depolarization and contraction

36
Q

What occurs during the PR segment?

A

Delay in activity at AV node

37
Q

What occurs in QRS complexes?

A

Ventricular depolarization and contraction

38
Q

What occurs in the QT interval?

A

Heart rests and depolarizes beginning next contraction

39
Q

Progression from ischemia could lead to?

A

Infarction

40
Q

What are the steps of the ischemic cascade?

A
  1. Occlusion of the coronary artery leading to perfusion abnormalities → ischemia
  2. Chest pain and MI
41
Q

Cardiac relaxation is caused by?

A

Ca2+ is pumped out of cardiomyocytes or into the SR

Process requires ATP

42
Q

When O2 is not available, ___ metabolism switches to ____ metabolism

A

aerobic; anaerobic

43
Q

What occurs during anaerobic metabolism?

A
  1. Imbalance of ATP production and consumption
  2. Impairs cardiomyocyte relaxation → diastolic dysfunction
  3. Accumulation of Ca2+ and lactic acid → systolic dysfunction → angina symptoms
44
Q

What factors does ECG abnormalities depend on?

A
  1. Time of ischemia
  2. Actue or chronic process
  3. Extent of ischemia
  4. Underlying conditions
45
Q

What occurs during acute ischemia?

A
  1. Deviation of ST segment from isoelectric line
  2. Reduces TMP → decrease amplitude of action potential plateau phase
46
Q

What is the normal function of ST segment?

A

plateau phase of the ventricular action potential

47
Q

What does a deviated ST segment indicate?

A

Voltage gradient between the normal and ischemic cells causes an injury current between the normal and ischemic zones in the myocardium

48
Q

What is subendocardial injury? What does it cause?

A

Involves only the inner layer of the ventricle → ST-segemnt depression

49
Q

What is transferal injury? What does it cause?

A

Affects the outer ventricular layer → ST-segment elevation with the presence of ST-segment depression in other leads

50
Q

What happens if ischemia chronic?

A

Irreversible injury → death

51
Q

What is stable angina?

A

Chronic form of ischemic heart disease (CHD)

Occurs with increased myocardial oxygen demand and reduced blood flow → chest discomfort

52
Q

Obstructive CAD narrows the diameter of the artery more than ___ leading to ___

A

60%; flow limitations

53
Q

What are the symptoms of stable angina>

A
  1. Squeezing
  2. Tightness
  3. Crushing
  4. Suffocating
  5. Pressure
54
Q

Postprandial angina results for ____

A

Redistribution of coronary blood flow

55
Q

What is silent ischemia? How often does it occur?

A

Defective angina warning system for peripheral and central neural processing of pain → no angina pectoris

56
Q

What is cardiac syndrome X?

A
  1. Patients who present with angina pectoris but have no obvious associated cardiac or systemic disease
  2. No visible atherosclerosis of ischemia
57
Q

What is coronary microvascular dysfunction?

A

Damage to the walls and inner linings of small coronary arteries that can lead to narrowing, spasms, and decreased blood flow

Nonobstructive coronary heart disease

58
Q

What are the types of ACS?

A
  1. Non–ST-segment elevation acute coronary syndrome (NSTE-ACS): Unstable angina (UA) and Non–ST-segment elevation myocardial infarction (NSTEMI)
  2. ST-segment elevation myocardial infarction (STEMI
59
Q

What types of ACS is acute MI? Therapy options?

A

NSTEMI or STEMI

Repercussion of coronary arteries (invasive PCI)

60
Q

When could acute MI be NSTE-ACS?

A

Acceleration in frequency and severity but no myocardial necrosis

61
Q

What are the risk factors of ACS?

A

CAD
Triggers

62
Q

How is CAD similar to ACS?

A

atherosclerotic plaque ruptures, causing thrombogenesis and blood flow obstruction

63
Q

What is the hallmark of ACS?

A

Sudden imbalance of myocardial oxygen consumption and myocardial demand

64
Q

What are characteristics of Non-ST-Segement Elevation ACS?

A

Encompasses unstable angina and NSTEMI

Absence of ST-segement elevation → continuum of disorders

65
Q

What are the characterizations of NSTEMI?

A

Absence of ST elevation but the presence of elevated biomarkers of necrosis

66
Q

What are the differences between unstable angina and NSTEMI?

A
  1. Degree of ischemia
  2. Whether damage is enough to release biomarkers of myocardial necrosis
67
Q

What is the patho of non-st segment elevation ACS?

A
  1. Atherosclerotic plaque rupture
  2. Coronary artery vasoconstriction (prinzmetal angina)
  3. Myocardial oxygen demand and supply imbalance
  4. Gradual narrowing of epicardial coronary arteries
  5. Coagulation cascade activation
68
Q

What is prinzmetal angina?

A

in transmural ischemia and left ventricle dysfunction

69
Q

What are clinical manifestation of NSTSEACS?

A
  1. Chest pain described as pressure and heaviness
  2. Angina equivalents without chest pain
  3. Nocturnal angina or pleuritic chest pain
70
Q

What are the clinical biomarkers of recognizing NSTSE-ACS?

A
  1. 12 lead ECG
  2. Serial cardiac troponin
  3. Inclusion of myoglobin and creatine kinase MB (CK-MB)
  4. BNP
  5. Fasting lipid profile
71
Q

What is STEMI

A

More precise MI (STE: ST-segment elevation, MI)

72
Q

Prevention of STEMI requires rapid:

A

Recognition, reprefusion treatment, management

73
Q

What are the characterizations of STEMI?

A
  1. Disruption of atherosclerotic plaque
  2. Platelet activation and thrombosis
  3. Disrupted blood flow
  4. Imbalance of myocardial oxygen supply and demand
74
Q

Severe and persistant MC necrosis occurs within ___hrs?

A

6

75
Q

What causes heightened inflammation with prothrombin components?

A

Imbalances of clot-dissolving enzymes (e.g., tissue plasminogen activator, TPA) and their inhibitors (e.g., plasminogen activator inhibitor-1) may increase a person’s risk for MI.

76
Q

What are the outcomes of non obstructive CAD?

A
  1. Insignificant stenosis
  2. Plaque rupture and subsequent occlusion
77
Q

What are the risk factors of STEMI?

A
  1. Nonobstructive CAD
  2. Multivessel CAD
  3. Short-term exposure to ambient fine particulate matter air pollution
78
Q

What are the causes of STEMI?

A
  1. Prinzmental angina
  2. Contusion
  3. Cocaine abuse
  4. Embolus
  5. A fib
79
Q

Clinical manifestations of STEMI?

A
  1. Chest pain
  2. Dyspnea
  3. Changes in vital signs
  4. Altered mental status
  5. DZ
  6. Weakness
  7. Palpitations
80
Q

What are the biomarkers for STEMI indications?

A
  1. Troponin
  2. Myoglobin
  3. creatinine kinase-MB (CK-MB)
  4. CRP
  5. BNP
  6. serum lipid levels
81
Q

What are complications of ACS?

A
  1. Inflammatory complications
  2. Embolic events
  3. Mechanical complications

Drug Action I (32 decks)

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