Cardiology\ Coronary Artery Disease Flashcards

1
Q

Describe the initial pathogenesis of atherosclerosis

A
  • Endothelial injury leads to
    • increased leukocyte adhesion to the endothelium
    • increased endothelial permeability, and
    • endothelial release of hemostatic and vasoactive substances
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2
Q

How is angina pectoris diagnosed?

A

Clinical history of a retrosternal pressure-like or squeezing sensation, frequently with radiation to the arms, neck, and jaw

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3
Q

Chest pain relief with nitroglycerin is diagnostic for angina. True or false?

A

False. Nitroglycerin can also decrease pain due to esophageal spasm.

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4
Q

What characterizes chronic stable angina?

A

Reproducibility with a consistent amount of exertion and long-standing symptoms

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5
Q

How is exercise-induced angina diagnosed?

A

Stress test results demonstrate ST depression during exercise.

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6
Q

Which stress-test findings may imply a poorer prognosis in cases of chronic stable angina?

A
  • ST depression greater than 2 mm
  • ischemia at low stress levels
  • hypotension resulting from exertion
  • the presence of ischemic changes in more than five ECG leads
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7
Q

What three general management strategies should be considered in chronic stable angina?

A
  1. Modification of risk factors
  2. Symptomatic relief of angina via medication or interventional modalities
  3. Treatment of other contributing diseases
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8
Q

What other diseases may exacerbate chronic stable angina?

A
  • Fever
  • anemia
  • congestive heart failure
  • infection
  • thyrotoxicosis
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9
Q

What medications may provide symptomatic relief of angina?

A
  • Nitrates
  • calcium channel blockers
  • beta-blockers
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10
Q

Describe the mechanism by which nitrates provide symptomatic relief.

A

Vasodilation of the following:

  • Coronary vessels → increase myocardial oxygen supply
  • Peripheral veins → decrease venous return to the heart → preload reduction → decrease in myocardial oxygen demand
  • Peripheral arteries → decrease in peripheral vascular resistance → afterload reduction → decrease in myocardial oxygen demand
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11
Q

Do nitrates have a predominant effect on veins or arteries?

A

Veins (and therefore preload)

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12
Q

Describe the mechanism by which beta-blockers and calcium channel blockers provide symptomatic relief

A

Decrease myocardial oxygen demand by decreasingheart rate (HR), blood pressure (BP), and contractility

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13
Q

If angina continues despite maximal medical management, what strategies may be employed?

A
  • Cardiac catheterization to evaluate coronary anatomy
  • revascularisation can e considered via coronary angioplasty, stenting or CABG
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14
Q

Describe Prinzmetal variant angina

A

Angina at rest characterized by transient coronary artery spasm and ST elevation

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15
Q

What conditions fall under the heading of acute coronary syndromes (ACS)?

A
  • Unstable angina (UA)
  • non-ST-elevation myocardial infarction (MI) (NSTEMI)
  • ST-elevation MI (STEMI)
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16
Q

What physical exam findings are typical of ACS?

A
  • Tachycardia
  • transient S3 or S4
  • hypertension
  • mitral regurgitation secondary to ischemia of the papillary muscle
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17
Q

Describe UA

A
  • New onset angina (<2 months) with only minimal exertion
  • crescendo angina in the setting of existing stable angina
  • angina at rest of greater than 20 minutes
  • angina occurring greater than 24 hrs post-MI
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18
Q

What ECG findings may be seen in UA?

A

ST depression or symmetric T-wave inversions

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19
Q

In what percentage of patients does UA progress to MI?

A

Approximately 5%

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20
Q

In cases of UA, what are the major steps for providing symptomatic relief and preserving myocardial function?

A
  • Provide analgesia
  • improve coronary blood flow
  • prevent coronary thrombosis
  • decrease myocardial oxygen demand
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21
Q

What drug options should be considered to address analgesia?

A

Morphine to decrease pain and anxiety

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22
Q

Why is it important to control pain in a patient with UA?

A

Analgesia can decrease the sympathetic response (lower HR and BP), which decreases myocardial oxygen demand.

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23
Q

When should antiplatelet therapy be started?

A

Immediately after UA is suspected

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24
Q

What drug should be used to provide antiplatelet action acutely?

A

Aspirin 162-325 mg

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25
What drug options should be used to provide long-term antiplatelet action?
Aspirin 81-325 mg and clopidogrel 75 mg, daily
26
What class of drugs should be used to reduce myocardial demand in all patients with UA/NSTEMI?
Beta-blockers
27
Is thrombolytic therapy used in the treatment of UA and NSTEMI?
No
28
Following stabilization of the UA/NSTEMI patient, what further studies should be undertaken in low-risk patients?
Noninvasive stress testing
29
Following stabilization of the UA/NSTEMI patient, what further studies should be undertaken in high-risk patients?
Cardiac catheterization followed by revascularization procedures, if indicated
30
How is UA differentiated from NSTEMI?
In NSTEMI, ischemia is significant enough to cause myocardial damage, leading to an elevation of troponin I and creatine kinase from cardiac muscle (CK-MB)
31
Which biomarker is the most sensitive and specific for myocardial injury?
Troponin I
32
How are NSTEMI and STEMI similar?
In both conditions, troponin I and CK-MB are elevated
33
How are NSTEMI and STEMI different?
* In STEMIs, ECGs show ST segment elevations or Q waves in at least two contiguous leads. * In NSTEMIs, ECGs show ST segment depression but lack ST segment elevations or Q waves.
34
ECG changes in which leads are indicative of Anterior wall ischemia?
V1-V6
35
ECG changes indicative of Anteroseptal ischemia?
V1-V3
36
ECG changes indicative of Lateral ischemia?
AVL, I, V4-V6
37
ECG changes indicative Inferior ischemia?
II, III, aVF
38
What group of patients are more likely to present with atypical symptoms of myocardial infarction?
* Women * diabetics * the elderly
39
What accounts for most of the deaths that take place within a few hours of a STEMI?
Ventricular tachyarrhythmia
40
ECG changes during a STEMI - immediate
41
ECG changes during a STEMI - Minutes
42
ECG changes during a STEMI - Hours
43
ECG changes during a STEMI 24-48 hrs
44
ECG changes during a STEMI Days tp weeks
45
What does echocardiography show during STEMI?
* LV hypokinesis or akinesis in the area supplied by the occluded vessel
46
What two pharmacologic agents should be started immediately after diagnosing a patient with either NSTEMI or STEMI?
1. Aspirin 2. Anti-thrombotic agents (unfractionated or LMW heparin)
47
Despite its increased effectiveness, when is LMW heparin contraindicated?
Renal insufficiency as it is cleared by kidneys
48
What steps should be taken after diagnosis of either NSTEMI or STEMI?
1. Aspirin 2. anit-thrombotic agents(unfractionated or LMW heparing - unless renal insufficiency) 3. Morphine if indicated 4. Oxygen if indicated 5. Nitroglycerin 6. Anxiolytics if indicated 7. Beta-blockers
49
How should the first dose of aspirin be taken?
* Chewed, to ensure rapid uptake
50
If the patient continues to show ST-elevation and has persistent angina, what therapy should be initiated?
* Reperfusion with primary angioplasty or * initiation of thrombolysis * tissue Plasminogen activator
51
Tissue plasminogen activator (tPA) can restore patency to an occluded coronary vessel in what percentage of patients?
Approximately 75%-80%
52
Primary angioplasty can restore patency to an occluded coronary vessel in what percentage of patients?
approx. 95%
53
Beyond what period of time from the onset of initial symptoms does thrombolysis lose effectiveness?
6 hours
54
What is the major limitation of primary angioplasty?
Lack of widespread availability
55
Following thrombolysis, for how long should heparin be continued?
24-48 hours
56
How long should aspirin be continued?
Indefinitely
57
What other drugs should be initiated on a long-term basis?
* Beta-blockers * ACEI * high-dose statins (eg, atorvastatin 80 mg once daily)
58
What diagnostic study should be performed several days after acute MI
Echocardiography
59
What vaccination should be given to patients with coronary artery disease?
* annual influenza * pneumococcal
60