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Cardiology > Ischemic Heart Disease and Acute Coronary Syndromes > Flashcards

Ischemic Heart Disease and Acute Coronary Syndromes Flashcards

1
Q

Arises from the right aortic sinus and runs in the coronary sulcus or AV groove

A

Right Coronary Artery

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2
Q

The right coronary artery supplied what?

A

Right atrium
Most of right ventricle
Part of the LV (diaphragmatic surface)
Part of the AV septum
SA node (70% of people)
AV node (80% of people)

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3
Q

Arises from the left aortic sinus of the ascending aorta

A

Left Coronary System

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4
Q

The left main coronary artery passes between what structures?

A

the LA and the pulmonary artery

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5
Q

The left coronary system divides into what two arteries?

A

left anterior descending artery (LAD) and the circumflex
coronary artery (CCA)

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6
Q

The left coronary system supplies what?

A

Left atrium
Most of the left ventricle
Part of the right ventricle (CCA)
Most of ventricular septum (LAD)

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7
Q

Ischemia has what 3 principal biochemical components?

A

Hypoxia (including anoxia)
Insufficiency of metabolic substrates
Accumulation of metabolic waste

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8
Q

What is the leading cause of death in industrialized nations?

A

Ischemic Heart Disease

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9
Q

A condition of imbalance between myocardial oxygen supply and
demand

A

Ischemic Heart Disease

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10
Q

What remains the most common manifestation of ischemic heart disease?

A

Angina pectoris

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11
Q

List some risk factors for angina pectoris

A

Advancing age
Tobacco smoking
Diabetes mellitus
Elevated total and LDL cholesterol
Low HDL cholesterol
hypertension
Abdominal obesity
Ethnic characteristics
Family history of premature
coronary heart disease
Obesity (not limited to abdominal obesity)
Physical inactivity
Psychosocial factors
Elevated serum homocysteine
Elevated serum lipoprotein(a)
Elevated serum triglycerides
Inflammatory markers (CRP)
Prothrombic factors (fibrinogen)
Small LDL particles

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12
Q

Chronic pattern of transient angina pectoris, precipitated by physical
activity or emotional upset, relieved by rest within a few minutes

Episodes often associated with temporary depression of the ST segment, but permanent myocardial damage does not result

A

Stable Angina

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13
Q

Focal coronary spasm in absence of overt atherosclerotic lesions

Intense spasm reduces coronary O2supply and results in angina

Chest pain occurs at rest

A

Variant Angina

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14
Q

Another term for Variant Angina is

A

“Prinzmetal angina”

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15
Q

Ischemia occurring in absence of perceptible discomfort or pain

May be only manifestation of CAD, first symptom may be death! May not even have chest pain at all

Particularly common among diabetic patients, elderly, patients with
peripheral neuropathy

A

Silent Ischemia

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16
Q

Typical angina symptoms with NO evidence of significant atherosclerotic coronary stenoses on angiogram

Inadequate vasodilator reserve of coronary resistance vessels
(microvasculature)

Better prognosis than overt atherosclerotic disease

A

Syndrome X

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17
Q

What is a + Levine sign?

A

clutching their chest

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18
Q

What classification of angina is described below?

No pain with ordinary activity

A

Class I

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19
Q

What classification of angina is described below?

slight limitation of activity (managed pain)

Pain at >2 blocks, Pain at 1 flight of stairs

A

Class II

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20
Q

What classification of angina is described below?

marked limitation

Pain at <2 blocks, Pain during 1 flight

A

Class III

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21
Q

What classification of angina is described below?

Pain with any activity or at rest

A

Class IV

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22
Q

What are some other causes of Angina Pectoris that are not CAD?

A

Fever
Tachyarrhythmias
Catecholamines
Emotional stress
Hyperthyroidism
Any process that increases myocardial demand

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23
Q

What is the most frequently used modality to detect ischemia?

A

The EKG

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24
Q

When should stress testing be stopped?

A

Target heart rate reached (85% of maximal predicted HR)
Signs of myocardial ischemia
Angina develops
Patient too fatigued to continue

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25
Q

What is the target heart rate in a stress test?

A

85% of maximal predicted HR

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26
Q

When to order a stress test?

A

No acute evidence for MI

Patient stabilized - No recurrent chest pain on medical treatment

Stress study to provoke ischemia

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27
Q

If the stress study is positive, what imaging is indicated?

A

coronary angiography

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28
Q

What is a positive test on a stress test?

A

Typical chest pain reproduced

> 1mm horizontal or downsloping ST segment depression

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29
Q

What are the contraindications for a stress test?

A

Acute myocardial infarction (within 2 days)
Unstable angina (not previously stabilized by medical treatment)
Severe, symptomatic aortic stenosis
Ventricular tachyarrhythmia
Uncontrolled/symptomatic heart failure
Acute PE or pulmonary infarction
Acute myocarditis or pericarditis
Acute aortic dissection

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30
Q

This imaging uses injected, radioactive labeled tracers and gamma camera detectors (taking pictures)

A

Myocardial Perfusion scanning

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31
Q

Pharmacological stress tests use what medications to mimic the effects of exercise?

A

IV dipyridamole (Persantine)
adenosine (Lexiscan)
IV dobutamine

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32
Q

What are the contraindications for a myocardial perfusion scan?

A

Severe AS
HOCM
Uncontrolled HTN
Uncontrolled AF
Severe ventricular arrhythmias

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33
Q

What is the gold standard for evaluating the anatomy of the coronary artery tree and can definitively diagnosis CAD?

A

Coronary Angiography

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34
Q

What are the treatment goals for angina pectoris?

A

Decrease frequency of attacks
Prevent acute coronary syndromes
Prolong survival

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35
Q

List some lifestyle modifications to encourage in patients with angina pectoris

A

Smoking cessation – very important
Weight loss
Exercise
Serum glucose control
Cholesterol reduction
Blood pressure control

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36
Q

What is the mainstay of treatment for angina pectoris?

A

Beta Blockers

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37
Q

All patients with CAD should take what adjunct therapy indefinitely?

A

ASA (81-325mg/day)

38
Q

Procedure for angina pectoris:

Deploy a stent to where the blockage is located

A

Percutaneous coronary intervention (PCI)

39
Q

Procedure for angina pectoris:

Graft portion of patient’s native blood vessels to bypass obstructed coronary arteries

Typically recommended when you have multiple vessels that need
revascularization

A

Coronary artery bypass graft

40
Q

Umbrella term for situations where the blood supplied to the heart muscle is suddenly blocked

A

Acute coronary syndromes

41
Q

What are the three acute coronary syndromes?

A

Unstable angina
Non-ST elevated myocardial infarction (NSTEMI)
ST elevated myocardial infarction (STEMI)

42
Q

Closely related in pathogenesis, but different in severity in
presentation

account for 40-50% of all admissions to cardiac care
units

Temporary imbalance in the myocardial oxygen supply and demand

A

UA/NSTEMI

43
Q

More than what percentage of UA/NSTEMI cases result from disruption of atherosclerotic plaque with subsequent platelet aggregation and intracoronary thrombus formation?

A

90%

44
Q

Usually secondary to reduced myocardial perfusion resulting from coronary artery atherothrombosis

Nonocclusive thrombus (not 100% blocked)

No rise in cardiac enzymes – can be precursor to an acute MI

A

Unstable Angina

45
Q

Presents as an acceleration of ischemic symptoms

Sudden increase in the tempo and duration of ischemic episodes (brought on by lesser degree of exertion -crescendo pattern of chest pain)

Angina occurs at rest, without provocation, or with minimal exertion

A

Unstable Angina

46
Q

What is the difference between unstable angina and an MI?

A

Unstable angina will have NO biochemical evidence of myocardial necrosis (NO elevated cardiac enzymes)

47
Q

Usually secondary to reduced myocardial perfusion resulting from
coronary artery atherothrombosis

Nonocclusive thrombus (not 100% blocked)

Clinically similar presentation as UA

Difference: Evidence of myonecrosis

A

NSTEMI

48
Q

If cardiac markers are elevated without evolution of Q waves, what condition should you suspect?

A

NSTEMI

49
Q

What are are the biochemical marker of choice in the evaluation of myonecrosis and the diagnosis of NSTEMI?

A

Cardiac troponins

50
Q

In cases of UA/NSTEMI, an elevated what implies a worse prognosis?

A

troponin

51
Q

What elevated biochemical inflammatory markers are associated with a higher risk of mortality?

A

CRP
Serum amyloid
Fibrinogen

52
Q

In the treatment of UA/NSTEMI, what medication is the cornerstone of therapy?

A

Nitrates

53
Q

Although Nitrates help with UA/NSTEMI symptoms, what does it not affect?

A

does not decrease incidence of progression to MI or death

54
Q

ASA reduces risk of developing MI in UA/NSTEMI patients by what percentage?

A

50%

55
Q

In UA/NSTEMI patients, what is the ASA regimen?

A

81mg a day (should be preceded by a loading dose of 160-325mg on first day of presentation)

56
Q

What class of medications are documented to reduce frequency of both symptomatic and asymptomatic ischemic episodes in stable and unstable angina, and decrease reinfarction and mortality rates in post-infarction patients?

A

Beta Blockers

57
Q

In patients with UA/NSTEMI, what high-risk features benefit from early invasive intervention?

A

Older age
Long-duration of ischemia
Angina at rest
ST segment EKG changes
Positive cardiac enzymes

58
Q

What procedure in patients with UA is relatively superior to medical therapy for controlling symptoms and improving effort tolerance and ventricular fxn?

A

Surgical revascularization - Coronary artery bypass surgery

59
Q

What is the approach for long-term risk reduction in UA/NSTEMI – ABCDE?

A

A – antiplatelet therapy (ASA, clopidogrel)
B – beta blockers, BP control
C – cholesterol modifying agent, converting enzyme inhibitors (ACE-I),
cessation of smoking
D – dietary management
E – exercise and weight control

60
Q

Acute plaque rupture and thrombosis with complete occlusion

Much more life threatening – thrombus has occluded the vessel 100%

ST elevation = tombstone (Will see this in 100% blockage)

Chest pain + ST elevation in 2 contiguous leads

A

STEMI

61
Q

Proximal occlusion of this artery is potentially fatal – called the “widow maker”

A

Left anterior descending (LAD)

62
Q

1/3 patients with LV inferior wall develop what?

A

RV infarct

63
Q

The ONLY time we give fluids in HF

A

RV Infarct

64
Q

Cardiac markers of choice for patients with ACS

A

Troponins I and T

65
Q

Proteins found in cardiac muscle cells released when myocytes damaged

It will be the first marker to elevate post MI

A

Troponins

66
Q

Troponins will be elevated up to how many days post MI?

A

10

67
Q

This biomarker is released from injured myocytes early, and is a sensitive marker for detecting injury

Not specific – skeletal muscle trauma

Cleared renally

A

Myoglobin

68
Q

This biomarker generally rise within 4-8 hours after a heart attack and peak within 12-24 hours, then return normal within 3-4 days

Should see a rise and fall pattern - Lack of rise-fall pattern suspect skeletal muscle origin

A

Creatine Kinase (CK) isoforms

69
Q

What is the pre-hospital management of a STEMI?

A

Administer to all patients with suspected MI (ASA 162-325mg chewed within 5 minutes)

Continuous cardiac monitoring

Oxygen

Sublingual NTG

ABCs if necessary

70
Q

What is the dose of ASA in patients with a suspected MI?

A

ASA 162-325mg

71
Q

In the ED, all MI patients should receive what class of medication unless contraindicated?

A

Beta blocker

72
Q

What are the two definitive therapies of an MI?

A

Fibrinolytic (30 min)

PCI (90 min)

73
Q

For fibrinolytic therapy in MIs, what is the door to needle time?

A

Door to needle time of 30 minutes

74
Q

When should fibrinolytic therapy be used in MIs?

A

Use when PCI contraindicated or cannot be performed within 90 minutes from first medical contact

75
Q

What is the time frame that fibrinolytic therapy can be used in MIs?

A

<12 hours after onset 🡪 anything greater cannot perform this

76
Q

For fibrinolytic reperfusion therapy in MI’s, what are the absolute contraindications to this therapy?

A

Any prior intracranial hemorrhage

Known malignant intracranial neoplasm

Known structural cerebral vascular lesion (AVM)

Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours

Suspected aortic dissection

Active bleeding or bleeding diathesis

Significant closed head trauma or facial trauma within 3 months

77
Q

For fibrinolytic reperfusion therapy in MI’s, what are the relative contraindications to this therapy?

A

History of chronic, severe, poorly controlled HTN

Severe uncontrolled HTN on presentation (>180/>110)

History of prior ischemic stroke >3 months, dementia, or known intracranial pathology not covered in contraindications

Traumatic or prolonged (>10min) CPR or major surgery (<3 weeks)

Recent internal bleeding (2-4 weeks)

Noncompressible vascular punctures

Pregnancy

Active peptic ulcer

Current use of anticoagulants (the higher the INR, the higher the risk of bleeding)

Streptokinase/anistreplase: prior exposure (>5 days) or prior allergic reaction

78
Q

For fibrinolytic reperfusion therapy in MI’s, what is the complication to be aware of?

A

Bleeding 🡪 particularly intracranial hemorrhage

79
Q

Compare the results of fibrinolytic therapy v PCI

A

Optimal coronary flow achieved in >90% of patients - PCI

Fibrinolytic patency rate 65% (recurrent events common)

80
Q

PCI superior to fibrinolytic therapy in MIs when:

A

Performed without significant delay
By experienced clinicals
In experienced centers

81
Q

Primary PCI always preferred over fibrinolytic therapy in what certain cases?

A

Cardiogenic shock
Severe HF of pulmonary edema
Contraindications to fibrinolytic therapy

82
Q

What is the time frame that primary percutaneous coronary intervention therapy can be used in MIs?

A

<12 hours after onset – if afterward cannot performed

83
Q

What is the preferred reperfusion approach if it can be performed within 90 minutes of hospital presentation in patients with MI?

A

primary percutaneous coronary intervention

84
Q

Data suggests that all patients with STEMI, whether they undergo primary PCI or fibrinolytic therapy, benefit from early administration of what medication?

A

clopidogrel

85
Q

What is the dosing for clopidogrel in STEMI patients?

A

300mg loading dose

Followed by 75mg PO daily

86
Q

STEMI - treatment times to remember:

10 minutes 🡪

30 minutes 🡪

90 minutes 🡪

3 hours (symptom onset) 🡪

12 hours (symptom onset) 🡪

A

10 minutes 🡪 time for ED evaluation

30 minutes 🡪 door to needle

90 minutes 🡪 door to balloon

3 hours (symptom onset) 🡪 fibrinolytic vs. PCI therapy

12 hours (symptom onset) 🡪 time limit for revascularization therapies as supported by data

87
Q

Post MI, what class of medications need to be avoided indefinitely?

A

Avoid NSAIDs indefinitely

88
Q

What arrhythmia is largely responsible for pre-hospital sudden cardiac death in STEMI patients?

A

Ventricular Fibrillation

89
Q

Uncommon form of pericarditis that can be a STEMI complication

Immune process directed against damaged myocardium

Fever, malaise, sharp pleuritic pain, leukocytosis, elevated ESR,
pericardial effusion

A

Dressler syndrome

90
Q

What are the post-MI patients that are higher risk for reinfarction?

A

Advanced age (>65)
Prior MI
Anterior location of MI
Postinfarction angina
NSTEMI
Diabetes
HF
Mechanical complications

Cardiology (13 decks)

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