Ischemic Heart Disease (Exam IV) Flashcards

1
Q

What chemical mediators are released from ischemia that activate cardiac nociceptors?

A

Adenosine and Bradykinin

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2
Q

What is the path for cardiac pain signals to reach the spinal cord?

A

Cardiac nociceptors → Afferent Neurons → T1 - T5 SNS ganglia and somatic nerve fibers.
- produce thalamic and cortical stimulation that results in chest pain of angina pectoris.

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3
Q

What is the CNS response to cardiac ischemia?

A
  • ↓ AV conduction and thus ↓HR
  • ↓ Contractility
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4
Q

Differentiate stable vs unstable angina.

A
  • Stable - No change in chest pain severity or frequency in 2-mo period.
  • Unstable - Increasing frequency and severity of chest pain.
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5
Q

Are cardiac biomarkers (troponin) present with unstable angina?

A

NO. If they were, that would be an MI.

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6
Q

What EKG abnormality is associated with old MI’s and/or current ischemia?

A

T-wave inversion

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7
Q

What is nuclear stress testing utilized for?

A

Coronary Perfusion assessment

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8
Q

What determines the significance of CAD during a nuclear stress test?

A

Size of the perfusion abnormality

Arrows point to arrows of lesser perfusion.

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9
Q

What test can differentiate a new vs and old perfusion abnormality?

A

Nuclear Stress Testing

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10
Q

What nuclear stress test tracers are used with exercise?

A

Thallium

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11
Q

What nuclear stress test drugs are used without exercise?

A

Atropine
Dobutamine
Pacing

To dilate (adenosine, dipyridamole)

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12
Q

When are adenosine and dipyridamole used with nuclear stress testing? Why?

A

Use to produce cardiac stress. These drugs dilate normal coronary arteries but evoke minimal or no change in diameter of artherosclerotic coronary arteries

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13
Q

What test would be useful for imaging wall motion abnormalities or valvular function?

A

Echocardiography

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14
Q

What is Prinzmetal Angina?

A

Coronary Spasm

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15
Q

What is the mechanism of action for aspirin?

A

COX-1 Inhibition → TXA2 inhibition → Plt aggregation inhibition.

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16
Q

How can aspirin be reversed?

A

Trick question. It can’t be, platelets are damaged until they die and are replaced.

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17
Q

What is the mechanism of action of abciximab, eptifibatide, and tirofiban?

A

Platelet glycoprotein IIb/IIIa receptor antagonists

Inhibit platelet activation, adhesion, and aggregation.

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18
Q

What drugs (discussed in lecture) are P2Y12 inhibitors?

Bonus points! Name the glycoprotein IIb/IIIa receptor antagonist?

A

-Clopidogrel, Prasugrel, ticagrelor

-Abciximab, eptifibatide, tirofiban

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19
Q

What common drug class will antagonize P2Y12 inhibitors?

A

PPIs

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20
Q

How does Prasugrel compare to Clopidogrel?

A

More predictable pharmacokinetics but greater bleeding risk.

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21
Q

How do P2Y12 inhibitors work?

A

Inhibit ADP receptor P2Y12 and thus inhibit platelet aggregation.

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22
Q

What drug classes are synergistic with nitrates?

A
  • β-blockers
  • CCBs
23
Q

When are nitrates contraindicated?

A
  • Aortic Stenosis
  • Hypertrophic Cardiomyopathy
24
Q

What drug class is the only one proven to prolong life in CAD patients?

A

β-blockers

25
Q

What properties do β-blockers have?

A
  • Anti-ischemia
  • Anti-HTN
  • Anti-dysrhythmic
26
Q

Which β blockers are cardioselective?

A
  • Atenolol
  • Metoprolol
  • Acebutolol
  • Bisoprolol
27
Q

Which β blockers are non-selective?

A
  • Propanolol
  • Nadolol
28
Q

What risk is associated with non-selective β blockers in asthma patients?

A

↑ risk of bronchospasm in reactive airway disease patients.

29
Q

What drug class is uniquely effective is decreasing the severity/frequency of coronary vasospasm?

A

CCBs

30
Q

Angiotensin II will increase what four things?

A
  • Myocardial hypertrophy
  • Interstitial myocardial fibrosis
  • Coronary vasoconstriction
  • Inflammatory responses
31
Q

Is troponin or CK-MB more specific for myocardial injury?

A

Troponin

32
Q

How soon with troponin start to increase after myocardial injury?

A

3 hours

33
Q

What diagnostic studies might indicate a myocardial infarction?

A
  • EKG: abnormality (ex. LBBB)
  • US: Regional wall motion abnormalities
34
Q

What are indications for PCI treatment of an MI?

A
  • Contraindicated tPa therapy
  • Severe HF and/or pulm edema
  • S/S for 2-3 hours
  • Mature clot

(Failure of medical therapy, >50% L main or >70% epicardio coronary arteries, impaired EF < 40%)

35
Q

What risks are associated with PCI (percutaneous coronary intervention) ?

A
  • Endothelial destruction
  • Bleeding
  • Thrombosis
36
Q

What is Dual Antiplatelet Therapy (DAPT) ?

A
  • ASA w/ P2Y12
37
Q

How long would one want to wait for elective surgery post angioplasty with no stenting?

A

2 - 4 weeks
* 2 weeks

38
Q

How long would one want to wait for elective surgery post angioplasty with bare-metal stent placement?

A

At least 30 days (12 weeks preferable)
* 6 weeks

39
Q

How long would one want to wait for elective surgery post angioplasty with drug-eluting stent placement?

A

At least 6 months (12 months if post ACS)
* 1 year

40
Q

How long would one want to wait for elective surgery post-CABG?

A

At least 6 weeks (12 weeks preferable)

41
Q

Is glycopyrrolate or atropine preferred for treatment of bradycardia?

A

Glycopyrrolate

42
Q

Are β blockers or ACE-inhibitors continued peri-operatively?

A

β-blockers

43
Q

Are β blockers or ACE-inhibitors discontinued 24 hours prior to surgery?

A

ACE inhibitors

44
Q

What components are worth 1 point on the Revised Cardiac Risk Index (RCRI) ?

A
45
Q

What % risk of major cardiac events would be conferred by a RCRI score of 0 ?

A

0.4%

46
Q

What % risk of major cardiac events would be conferred by a RCRI score of 1 ?

A

1.0%

47
Q

What % risk of major cardiac events would be conferred by a RCRI score of 2 ?

A

2.4%

48
Q

What % risk of major cardiac events would be conferred by a RCRI score of ≥3 ?

A

5.4%

49
Q

What does 1 MET equal?

A

3.5mLO₂/kg/min

50
Q

What drug is the preferred treatment for tachycardia?

A

Esmolol

51
Q

What anticholinergic is the better option for treatment of bradycardia in CAD patients?

A

Glycopyrrolate > Atropine

52
Q

What coronary artery would you expect to be effected from abnormalities noted on II, III, and aVF?

A

RCA

53
Q

What coronary artery would you expect to be effected from abnormalities noted on I and aVL?

A

Circumflex artery

54
Q

What coronary artery would you expect to be effected from abnormalities noted on V3 - V5?

A

LAD