ACS Flashcards

1
Q

What does acute coronary syndrome (ACS) refer to?

A

A constellation of clinical diseases occurring as a result of acute myocardial ischemia or infarction

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2
Q

What is the most extreme clinical manifestation of acute coronary syndrome?

A

Sudden cardiac death (SCD) involving pulseless ventricular tachycardia or ventricular fibrillation

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3
Q

Why is the time between onset of symptoms and initiation of therapy critical in ACS?

A

It impacts the effectiveness of treatment and outcomes

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4
Q

What advancements in the mid-20th century significantly changed the approach to acute coronary care?

A
  • External defibrillators
  • Cardiac pacemakers
  • New pharmacologic agents
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5
Q

What did Kouwenhoven inaugurate in 1960 that is important for SCD management?

A

The era of cardiopulmonary resuscitation (CPR)

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6
Q

What is the recommended goal door-to-balloon time for percutaneous coronary intervention (PCI) in STEMI?

A

90 minutes

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7
Q

What should be administered if PCI is not feasible for STEMI patients?

A

Fibrinolytic therapy within 30 minutes

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8
Q

What are some limitations of the 12-lead ECG in suspected ACS?

A
  • Initial nondiagnostic findings
  • Evolving fluctuations with ongoing symptoms
  • Anatomic myocardial blind spots
  • Confounding patterns like left bundle branch block (LBBB)
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9
Q

What ECG patterns may indicate ischemia or impending infarction but do not meet traditional STEMI criteria?

A
  • Wellens syndrome
  • Significant aVR elevation
  • de Winter syndrome
  • Sgarbossa criteria
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10
Q

What clinical decision tools may assist in the risk stratification of patients with suspected ACS?

A
  • EDACS
  • HEART score
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11
Q

What does serial troponin testing combined with an accelerated diagnostic protocol help identify?

A

Patients at low risk for ACS

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12
Q

What may further reduce the time needed for evaluation in suspected ACS cases?

A

High-sensitivity troponin (hs-T) testing

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13
Q

What is the focus of current efforts in STEMI systems of care?

A
  • Establishment of regional cardiac centers
  • Expansion of interventional capabilities to smaller hospitals
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14
Q

What is the main focus of the evaluation methods for ACS patients without obvious STEMI?

A

To mature and improve the efficiency and safety of the rule-out myocardial infarction strategy.

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15
Q

Where is the R/O MI process appropriately performed?

A
  • Emergency Department (ED)
  • Observation settings
  • Acute care hospital units
  • Critical care hospital units
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16
Q

What recent development has improved the detection of significant ACS events?

A

High-sensitivity troponin testing.

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17
Q

What is the goal of ongoing improvements in chest pain evaluation strategies?

A

To further reduce the already low missed myocardial infarction rate in the ED.

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18
Q

What potential issue arises from attempts to lower the missed MI rate?

A

Increased unnecessary testing with associated risks and health system costs.

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19
Q

What must patients, physicians, and society recognize regarding ACS presentations?

A

Atypical, unusual, or unanticipated presentations will occur and may not be diagnosed initially.

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20
Q

What is the overall age-adjusted prevalence of heart disease?

A

10.6%

This prevalence reflects the general occurrence of heart disease across different age groups.

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21
Q

What is the age-adjusted prevalence of coronary heart disease for men?

A

7.2%

This statistic indicates the prevalence of coronary heart disease specifically among men.

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22
Q

What is the age-adjusted prevalence of coronary heart disease for women?

A

4.2%

This statistic indicates the prevalence of coronary heart disease specifically among women.

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23
Q

How many deaths from ischemic heart disease occur annually in the United States?

A

Over 1 million

This number reflects the serious impact of ischemic heart disease on public health.

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24
Q

Approximately how many deaths from ischemic heart disease occur in persons 65 years of age or younger?

A

160,000

This statistic highlights the significant number of deaths in younger populations.

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25
Q

What percentage of deaths from cardiovascular disease occur in women?

A

More than half

This indicates a significant gender disparity in cardiovascular mortality.

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26
Q

What significant reduction has occurred in the U.S. and Canada over the past 5 decades?

A

Age-adjusted mortality from CAD

This decline reflects improvements in healthcare and disease management.

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27
Q

What has accompanied the decline in mortality from CAD?

A

Diminished mortality from acute myocardial infarction (AMI)

This indicates progress in treating heart attacks and related conditions.

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28
Q

What factors have contributed to the decline in AMI mortality?

A
  • Reduction in cigarette smoking
  • Improved management of hypertension
  • Improved management of hyperlipidemia
  • Improved management of diabetes mellitus
  • Advances in medical treatment

These factors reflect both lifestyle changes and medical advancements.

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29
Q

What is the second most common reason for patient attendance in the emergency department (ED)?

A

Chest pain

This highlights the prevalence of chest pain as a symptom prompting urgent medical care.

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30
Q

How many annual visits to EDs in the United States are accounted for by chest pain?

A

Approximately 7.49 million

This statistic underscores the frequency of chest pain as a medical concern.

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31
Q

What is the primary cause for men presenting to the ED?

A

Chest pain

This indicates a gender difference in reasons for ED visits.

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32
Q

What is the third most common reason for women presenting to the ED?

A

Chest pain

This shows that while common, chest pain is not always the leading reason for women.

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33
Q

How has the admission rate for acute coronary syndrome (ACS) changed over the past 15 years?

A

Not significantly changed

This suggests that while treatment has improved, the incidence rate remains stable.

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34
Q

Approximately how many persons experience an acute myocardial infarction (AMI) each year in the United States?

A

900,000

This figure reflects the high incidence of heart attacks in the population.

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35
Q

What percentage of AMI patients die within 30 days of the event?

A

30%

This statistic highlights the immediate risks following a heart attack.

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36
Q

When do approximately half of the deaths from AMI occur?

A

Soon after symptom onset and before arrival in the ED

This emphasizes the critical nature of rapid intervention in heart attack cases.

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37
Q

What usually causes deaths within 2 hours of an AMI event?

A

ACS-related dysrhythmia

This indicates the importance of monitoring heart rhythm post-event.

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38
Q

What percentage of patients with an MI are rehospitalized within 1 year of their index event?

A

Approximately 50%

This highlights the ongoing health challenges faced by MI patients.

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39
Q

What factors largely determine the prognosis of AMI?

A
  • Extent of the infarct
  • Time to intervention
  • Whether the patient underwent revascularization
  • Residual left ventricular function

These factors illustrate the complexity of heart attack recovery.

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40
Q

What is the true rate of ‘missed ACS’ in the ED?

A

Approximately 2%

This statistic points to the challenges in accurately diagnosing ACS in emergency settings.

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41
Q

What is stable angina pectoris?

A

Transient, episodic chest discomfort resulting from myocardial ischemia

Not considered a form of ACS; typically predictable and reproducible

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42
Q

What can provoke an attack of stable angina?

A

Physical or psychological stress such as:
* Physical exertion
* Emotional stress
* Anemia
* Dysrhythmias
* Environmental exposures

Resolves spontaneously with rest or nitroglycerin (NTG)

43
Q

What is the CCS classification for Class I angina?

A

No angina with ordinary physical activity

CCS stands for Canadian Cardiovascular Society

44
Q

What characterizes Class II angina in the CCS classification?

A

Minimal limitation of normal activity; angina occurs with exertion or emotional stress

Indicates some level of physical activity is affected

45
Q

What defines Class III angina in the CCS classification?

A

Severe limitation of ordinary physical activity; angina occurs with exertion under normal physical conditions

Significant impact on daily activities

46
Q

What is Class IV angina according to the CCS classification?

A

Inability to perform any physical activity without discomfort; anginal symptoms occur at rest or with minimal physical exertion

Most severe classification

47
Q

How is unstable angina best defined?

A

Angina that is new onset, occurring at rest, or worsening from a previously stable pattern

Includes increased frequency, duration, or resistance to medications

48
Q

What is rest angina?

A

Angina occurring at rest, lasting longer than 20 minutes, within 1 week of presentation

Considered a serious symptom

49
Q

What characterizes new-onset angina?

A

Angina of at least CCS classification class II severity, with onset within the previous 2 months

Important for diagnosis of unstable angina

50
Q

What is increasing or progressive angina?

A

A previously known anginal pattern that becomes more frequent, longer in duration, or increased by one class within the previous 2 months of at least class III severity

Indicative of worsening condition

51
Q

What is another name for unstable angina?

A

Preinfarction angina

Also known as accelerating or crescendo angina, and intermediate coronary syndrome

52
Q

What are the intracoronary events of unstable angina?

A

Plaque rupture, thrombus formation, and vasospasm

Often characterized by chest pain and electrocardiographic abnormalities

53
Q

What does variant angina (Prinzmetal angina) result from?

A

Coronary artery vasospasm at rest with minimal fixed coronary artery lesions

May be relieved by exercise or nitroglycerin

54
Q

What is observed on an ECG during variant angina?

A

ST segment elevation

Clinically indistinguishable from plaque rupture-related STEMI

55
Q

What is acute myocardial infarction on a cellular level?

A

Myocardial cell death with necrosis of the myocardium.

56
Q

What are the clinical criteria developed by ACC and ESC to define myocardial injury and myocardial infarction?

A

The Fourth Universal Definition of Myocardial Infarction.

57
Q

What indicates myocardial injury?

A

Elevated cardiac troponin values with at least one value above the 99th percentile upper reference limit.

58
Q

When is myocardial injury considered acute?

A

If there is a rise or fall of the troponin values.

59
Q

What constitutes a myocardial infarction?

A

Acute myocardial injury with an abnormal serum troponin value above the 99th percentile and associated with at least one of the following:
* Symptoms of myocardial ischemia
* Electrocardiographic abnormalities
* Imaging evidence of loss of viable myocardium
* Angiographic or autopsy evidence of coronary thrombus.

60
Q

What are the five primary types of acute myocardial infarction?

A

Type 1, Type 2, Type 3, Type 4, Type 5.

61
Q

What characterizes Type 1 myocardial infarction?

A

Spontaneous MI related to ischemia from a primary coronary event.

E.g. plaque erosion rupture, erosion, fissuring,
or dissection with accompanying thrombus formation and vasospasm. Type 1 infarctions represent the true ACS event.

62
Q

What is Type 2 myocardial infarction caused by?

A

Increased oxygen demand or decreased supply.

As seen in coronary artery spasm, coronary embolism, severe anemia, compromising arrhythmias, or significant systemic hypotension related to a range of causes

63
Q

What does Type 3 myocardial infarction refer to?

A

Sudden unexpected cardiac death with symptoms suggestive of myocardial ischemia, accompanied by presumably new ST segment elevation or new left bundle branch block (LBBB) pattern.

Fresh coronary thrombus is noted
via angiography or autopsy; death occurs before appropriate blood
sampling to detect the abnormal cardiac biomarker

64
Q

What defines Type 4 myocardial infarction?

A

MI associated with coronary instrumentation, such as after percutaneous coronary intervention (PCI).

65
Q

What are the criteria for defining PCI-related myocardial infarction?

A

Elevations of cardiac biomarkers above the 99th percentile URL, with increases greater than three times the 99th percentile URL.

66
Q

What is Type 5 myocardial infarction associated with?

A

Coronary artery bypass grafting (CABG).

67
Q

What defines CABG-related myocardial infarction?

A

Elevations of cardiac biomarkers above the 99th percentile URL, with increases greater than five times the 99th percentile URL and any of the following:
* New pathologic Q waves or new LBBB
* Angiographically documented new graft or native coronary artery occlusion
* Imaging evidence of new loss of viable myocardium.

68
Q

Why is the classification of myocardial infarction important?

A

Diagnostic and management issues differ depending on the subtype of MI.

69
Q

What is the management approach for Type 1 myocardial infarction?

A

Attention to platelet and coagulation system inhibition and therapy aimed at correction of vasospasm.

70
Q

What is the management approach for Type 2 myocardial infarction?

A

identifying and treating the inciting pathophysiologic situation causing imbalance in oxygen delivery and
myocyte requirements

71
Q

What serum markers and ECG abnormalities classify AMI at presentation?

A

NSTEMI and STEMI.

72
Q

What characterizes NSTEMI?

A

Chest pain or anginal equivalent, abnormal ECG lacking ST segment elevation, and elevated serum troponin.

73
Q

What characterizes STEMI?

A

Chest pain or anginal equivalent, abnormal ECG with ST segment elevation, and elevated serum troponin.

74
Q

What are the implications of differentiating between STEMI and NSTEMI?

A

Important implications in management, outcome, and prognosis for patients with AMI.

75
Q

What organizations have separate clinical guidelines for the management of patients with non-ST segment elevation ACS and with STEMI?

A

ACC and American Heart Association (AHA).

76
Q

What is the underlying pathophysiology of ACS?

A

Myocardial ischemia due to inadequate perfusion to meet myocardial oxygen demand

Myocardial oxygen consumption is influenced by heart rate, afterload, contractility, and wall tension.

77
Q

What typically causes inadequate perfusion in ACS?

A

Coronary arterial vessel stenosis due to atherosclerotic CAD

78
Q

At what level of vessel stenosis do ischemic symptoms usually appear at rest?

A

Greater than 95% obstruction to flow

79
Q

What can trigger myocardial ischemia despite minimal vessel stenosis?

A

Increased physiologic stress and increased myocardial oxygen consumption

80
Q

What characterizes CAD?

A

Thickening and obstruction of the coronary vessel arterial lumen by atherosclerotic plaques

81
Q

What are fibrous plaques considered in CAD?

A

Stable but can produce anginal symptoms with exercise

82
Q

What are vulnerable or unstable fibro-lipid plaques prone to?

A

Rupture, leading to inflammatory events, thrombus formation, and myocardial necrosis

83
Q

What initiates the pathophysiologic process of ACS?

A

Rupture of vulnerable plaques

84
Q

What role do platelets play in ACS?

A

Major role in thrombotic response to plaque rupture and subsequent ACS

85
Q

How do platelet-rich thrombi compare to fibrin- and erythrocyte-rich thrombi?

A

More resistant to fibrinolysis

86
Q

What are the consequences of a thrombus occluding a vessel lumen?

A

Myocardial ischemia, hypoxia, acidosis, and potentially infarction

87
Q

What is noted in UA regarding vessel stenosis?

A

Acute stenosis of the vessel is usually present; complete obstruction in only 20% of cases

88
Q

What prevents cessation of blood flow in UA cases with acute stenosis?

A

Extensive collateral vessel circulation

89
Q

What is the difference between UA and AMI regarding thrombus characteristics?

A

In AMI, the thrombus is fixed and persistent, causing myonecrosis

90
Q

What do angiographic studies indicate about coronary plaque lesions preceding infarction?

A

Often less than 50% stenotic

91
Q

What critical factors contribute to infarction in ACS?

A

Acute events of plaque rupture, platelet activation, and thrombus formation

92
Q

What can induce vasospasm after significant coronary vessel occlusion?

A

Local mediators and vasoactive substances

93
Q

What role does sympathetic nervous system input play after coronary occlusion?

A

Increases vasomotor hyperreactivity and coronary vasospasm

94
Q

What percentage of MIs occur due to coronary artery spasm without significant CAD?

A

Approximately 10%

95
Q

What can happen after reopening of the initial obstructing lesion?

A

Embolization can obstruct the microvasculature, leading to hypoperfusion and ischemia

Such embolization leads to hypoperfusion
and ischemia of the distal myocardial tissue, even after reopening of the
more proximal, initial obstructing lesion

96
Q

What can the introduction of calcium, oxygen, and cellular elements into ischemic myocardium lead to?

A

Irreversible myocardial damage, reperfusion injury, myocardial stunning, or reperfusion dysrhythmias

97
Q

What role do neutrophils play in reperfusion injury?

A

Occluding capillary lumens and accelerating the inflammatory response

98
Q

What type of pain is more likely to indicate angina?

A

Dull, pressure

Angina is typically characterized by a dull, pressure-like pain rather than sharp or stabbing pain.

99
Q

What is the typical duration of anginal pain?

A

2–5 min, often 15–20 min

Anginal episodes usually last a few minutes, unlike other types of pain that can last seconds or hours.

100
Q

What onset pattern is more characteristic of angina?

A

Gradual

Anginal pain tends to develop gradually rather than occurring suddenly.

101
Q

Where is anginal pain typically located?

A

Substernal

Angina usually presents as substernal pain, as opposed to pain located in the lateral chest wall or back.

102
Q

Is anginal pain reproducible with exertion?

A

Yes

Anginal discomfort is often reproducible with physical exertion, unlike pain that may arise with inspiration.

103
Q

Are associated symptoms present in angina?

A

Present

Angina often comes with other symptoms, whereas non-anginal pain is typically absent of these.