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Advanced Principles C > Ischemic Heart Disease I > Flashcards

Ischemic Heart Disease I Flashcards

1
Q

Risk factors for cardiovascular disease?

A
  • Male
  • Age
  • High cholesterol
  • HTN
  • Smoking
  • DM
  • Obesity
  • Inactivity
  • Genetics
  • Stress
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2
Q

Main cause of ischemic heart disease?

A

Imbalance of myocardial oxygen supply and demand due to occluded coronary artery.

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3
Q

Name the metabolites released from an occluded artery.

A
  • Adenosine
  • Bradykinin
  • Lactic Acid
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4
Q

Description of Angina

A
  • Substernal pain
  • May radiate to neck or arm
  • Lasts minutes
  • Relieved by rest or NTG
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5
Q

Differentiate between chronic (stable) angina and unstable angina

A
  • Chronic: Does not change in intensity or duration over 2+ months.
  • Unstable: Rest pain or increased severity/frequency
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6
Q

Name ways to diagnosis CAD. What is the gold standard?

A
  • Subjective Symptoms
  • EKG
  • Nuclear imaging,
  • Echocardiography
  • Coronary angiography (gold standard)
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7
Q

What EKG pattern correlates with Subendocardial ischemia coinciding with chest pain?

A
  • ST segment depression
  • Transient T-wave inversion
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8
Q

What are the various types of ST segment depression?

Which one has a higher correlation to angina?

A
  • Upsloping
  • Downsloping
  • Horizontal (more likely to be angina related)
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9
Q

Negative Exercise EKG test makes chance of ________ vessel disease unlikely.

A

Three Vessel Disease

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10
Q

What test assess coronary perfusion and provides a greater sensitivity for ischemia than exercise testing?

A

Nuclear Stress Imaging

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11
Q

Tracers in nuclear imaging?

A
  • Thallium
  • Technetium
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12
Q

What does significant tracer uptake in nuclear stress imaging mean?

A
  • Normal circulation
  • Increase circulation with exercise
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13
Q

What does decrease tracer uptake in nuclear stress imaging mean?

A

Perfusion abnormality

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14
Q

What does absent uptake in nuclear stress imaging mean?

A

Old MI

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15
Q

When is pharmacologic stress testing (Nuclear Imaging w/o Exercise) used?

A
  • Musculoskeletal issues
  • Patient is deconditioned
  • PVD
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16
Q

What drugs/methods will produce tachycardia to create cardiac stress in Nuclear Imaging?

A
  • Atropine
  • Dobutamine
  • Pacing
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17
Q

What drugs are given in Nuclear Imagining to dilate coronary arteries?

A
  • Adenosine
  • Dipyridamole (Persantine)

Coronary dilation will be indicated by increased tracer.

No dilation of atheroscolerotic arteries indicated by decreased tracer.

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18
Q

Purpose of echocardiography?

A
  • Detects wall motion abnormalities (site of ischemia)
  • Assess valve function
  • Assess EF
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19
Q

Indications for coronary angiography?

A
  • Diagnosing ischemia
  • Assessing survivors of sudden cardiac death
  • Evaluating revascularization
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20
Q

What prognosis can be made from a coronary angiography?

A
  • Extent of atherosclerosis
  • Left Ventricular Function (EF)
  • Stability of plaque
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21
Q

Describe a “vulnerable plaque” seen in a coronary angiography.

A
  • Large Lipid Core
  • Thin fibrous capsule/cover
  • More likely to rupture and occlude
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22
Q

5 main drug classes used to treat for ischemic heart disease?

A
  • Anti-platelets
  • ACE inhibitors.
  • β-blockers
  • CCB
  • Nitrates
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23
Q

MOA of Aspirin

A

Inhibits COX-1 → Inhibits thromboxane A2 → Inhibits platelet aggregation.

  • Aspirin Dose: 75-325 mg/day
  • Decrease the risk of a cardiac event
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24
Q

MOA of Clopidogrel (Plavix)

A
  • Inhibits ADP receptor (P2Y12) to reduce platelet aggregation
  • Active metabolite variable in action (20% variability)

Clopidogrel is used in patients intolerant of ASA

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25
Q

Clopidogrel’s effectiveness is decreased with this drug.

A
  • PPI
  • PPI inhibit the enzyme that metabolizes clopidogrel from prodrug to active
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26
Q

MOA of Prasugrel (Effient)

A
  • Inhibits ADP receptor (P2Y12) to reduce platelet aggregation
  • Requires P450 enzyme to convert from prodrug to active metabolite
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27
Q

Key differences between Prasugrel and Clopidogrel?

A
  • Prasugrel is more rapidly absorbed
  • Prasugrel has faster onset of action
  • Prasugrel has less variability, more predictable
  • Prasugrel is more potent (higher risk of bleeding)
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28
Q

Nitrates’ primary effect?

A
  • Dilate coronary arteries
  • Decrease peripheral vascular resistance
  • Reduce afterload
  • Lower myocardial oxygen demand
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29
Q

Nitrates effect is synergistic with what drugs?

A
  • β-blockers
  • CCB
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30
Q

Nitrates are contraindicated in patients with these cardiac conditions

A
  • Hypertrophic cardiomyopathy
  • Aortic Stenosis
  • Afterload needs to be maintained in these conditions, nitrates will reduce the afterload
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31
Q

Why do we need an 8-12 hour window of “nitrate-free” zone?

A
  • To prevent nitrate tolerance
  • Give time to restore receptor’s sensitivity to nitrates (usually bedtime to morning)
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32
Q

Principle drug for stable angina

A

β-blockers

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33
Q

Purpose of beta-blockers in ischemia?

A
  • Decrease myocardial oxygen demand
  • Prolong diastole (↑coronary perfusion)
  • Decrease re-infarction
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34
Q

Name β1-blockers drugs

A
  • Atenolol (commonly used)
  • Metoprolol (commonly used)
  • Bisoprolol
  • Acebutolol
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35
Q

Conditions where β-blockers are contraindicated

A
  • Severe bradycardia
  • Sick sinus syndrome (SSS)
  • Severe reactive airways
  • 2nd/3rd degree heart block
  • Uncontrolled CHF
36
Q

How does β-blockers mask the signs of hypoglycemia?

A

β-blockers mask Sx of hypoglycemia by blocking the SNS responses, such as tachycardia, tremors, and sweating, which are typical warning signs of low blood sugar.

37
Q

Three properties of β-blockers

A
  • Anti-anginal
  • Anti-hypertensive
  • Anti-dysrhythmic
38
Q

What does the Surgical Care Improvement Project (SCIP) say about patients receiving β-blockers?

A
  • Surgery patients on β-blocker prior to admission must receive dose w/i 24 hr prior to case
  • No indication for acute initiation of β-blocker therapy …must initiate 1-4 weeks prior to non-cardiac surgery
39
Q

Name the specific channels CCB inhibit.

A

L-type calcium channels located in smooth muscles, cardiac myocytes, and SA/AV nodes

40
Q

Common CCB used

A
  • Amlodipine (Norvasc)
  • Nicardipine (Cardene)
41
Q

CCB are most useful in treating this type of angina.

A

Prinzmetal’s ( Variant) Angina

42
Q

Role of calcium channel blockers?

A
  • Decrease vascular tone
  • Dilate coronary arteries
  • Improve supply/demand
43
Q

CCB are potent vasodilators which can lead to these effects.

A
  • Hypotension
  • Peripheral Edema
  • HA
44
Q

What does ANG II promote?

A
  • Inflammatory response
  • Atheroma formation
  • Coronary vasoconstriction
  • Myocardial hypertrophy
45
Q

ACE inhibitors are indicated for patients with CAD and _______, _______, and/or ________.

A
  • HTN
  • LV dysfunction
  • DM
46
Q

Consideration of ACE-inhibitors with anesthesia.

A
  • ACE inhibitors SIGNIFICANTLY increases hypotensive effects of anesthesia.
  • HOLD 24 HOURS before surgery
47
Q

Patho of acute coronary syndrome

A

Focal disruption of a plaque → coagulation cascade → thrombus formation → Imbalance of O2 supply/demand → ACS

48
Q

STEMI mortality rate with early perfusion vs without

A
  • Early perfusion: 6.5%
  • Without: 15-20%
49
Q

What is the prognosis of a STEMI dependent on?

A
  • LV Function
  • Residual ischemia
  • Ventricular dysrhythmias
50
Q

What is the first biomarker to peak with an MI?

When does this biomarker peak?

A
  • Myoglobin
  • Peaks at 4-12 hours
51
Q

If a patient came in 3 days after his chest pain? What biomarkers will be elevated if this patient had an infarction?

A
  • LDH
  • Troponin
52
Q

Order the cardiac biomarkers that peak first to last

A
  • Myoglobin
  • Total CK
  • CK-MB
  • Troponin
  • LDH
53
Q

Treatment for STEMI

A
  • MONA
  • Anti-platelet
  • β-blockers
  • Reperfusion (thrombolytics, angioplasty, stent, CABG)
54
Q

EKG Diagnosis of a NSTEMI

A
  • ST-depression and/or deep T-wave inversion WITH pain
  • Elevated biomarkers
55
Q

Treatment for NSTEMI

A
  • O2
  • β-blocker
  • Antiplatelet vs Heparin
  • Consider early interventions
56
Q

These type of drugs should be avoided in NSTEMI, can increase mortality.

A
  • No thrombolytics for NSTEMI patients
  • Thrombolytics are only for complete occlusions
57
Q

When does V-fib occur after an MI.
Treatment.

A
  • 1st four hours
  • Defib w/ 200-300 Joules
58
Q

Asymptomatic VT can be treated with what drugs?

A
  • Lidocaine
  • Amiodarone
  • Treat symptomatic VT with cardioversion
59
Q

Treatment for A-flutter/A-fib if patient is unstable.

What can be given for rate control.

A
  • Cardioversion for unstable patients
  • β-blockers for rate control
60
Q

MI to what region of the heart will result in Sinus Brady?

Treatment for Sinus Brady.

A
  • Inferior Wall
  • Atropine or Pacing to treat sinus brady
61
Q

When does pericarditis occur after an MI?

A
  • 1-4 days post MI
  • 10-15% of patients
62
Q

Sx of Pericarditis

A
  • Pain is worse laying down
  • Pain from inspiration d/t pericardial friction rub
  • ST-segment changes through 12-lead EKG
63
Q

Treatment for Pericarditis

A
  • Self resolves with time
  • Treat pain and inflammation w/ ASA, indomethacin, steroids
64
Q

Describe Dressler’s Syndrome

A
  • Pericarditis that appears weeks to months after an acute MI
  • Immune mediated pericarditis
65
Q

How does MI cause mitral regurgitation?

A

Ischemic injury to papillary muscle will cause them to rupture

66
Q

Treatment for mitral valve regurgitation

A
  • LV afterload reduction (diuretics, nitrates)
  • IABP to improve coronary perfusion
  • MR = FAST, FULL, FOWARD
67
Q

If the mitral valve regurgitation is severe what can it lead to?

A
  • Pulmonary Edema
  • Cardiogenic Shock
68
Q

Cardiogenic shock is usually developed if more than ____-% of the myocardium is infarcted.

A

40%

69
Q

Treatment for Cardiogenic Shock

A
  • Reverse mechanical complications (pap ruptures, MR)
  • Improve BP (levo, vaso, dopamine, dobutamine)
  • Treat pulmonary edema (diuretics, vent)
  • Restore coronary flow (IABP/LVAD)
70
Q

How does a IABP work?

A
  • Inflates in diastole to improve coronary perfusion
  • Deflates before systole to reduce afterload and promotes forward flow
71
Q

When will IABP be contraindicated?

A
  • Aortic Insufficiency
  • Aortic Aneurysm
  • Severe PVD
  • Severe Coagulopathy
72
Q

Complications to IABP

A
  • Limb ischemia
  • Aortic dissection
  • Hemorrhage from insertion site
  • Helium emboli
  • Infection
73
Q

High Lateral Leads:
Inferior Leads:
Septal Leads:
Anterior Leads:
Lateral Leads:

A

High Lateral Leads: Lead I, aVL
Inferior Leads: Lead II, Lead III, aVF
Septal Leads: V1, V2
Anterior Leads: V3, V4
Lateral Leads: V5, V6

74
Q

The circumflex artery is typically associated with which lead?

A
  • Lateral Leads
  • Lead I, aVL, V5, and V6
75
Q

The right coronary artery is typically associated with which lead?

A
  • Inferior Leads
  • Lead II, Lead III, and aVF
76
Q

The LAD is typically associated with which lead?

A
  • Septal and Anterior Leads
  • V1 to V4
77
Q
A
  • Inverted T-waves seen in V1 to V4 suggesting a NSTEMI
  • Myocardial Ischemia to LAD

Please note that these interpretations of the 12-Lead EKG reflect my own analysis and have not been independently verified for accuracy

78
Q
A
  • Widespread ST-elevation throughout
  • Reciprocal ST-depression in aVR
  • Pericarditis

Please note that these interpretations of the 12-Lead EKG reflect my own analysis and have not been independently verified for accuracy

79
Q
A
  • ST-elevation in Lead II, Lead III, and aVF
  • Reciprocal ST depression in aVL
  • Inferior STEMI affecting right coronary artery

Please note that these interpretations of the 12-Lead EKG reflect my own analysis and have not been independently verified for accuracy

80
Q

Which type of PTCA will have a lower incidence of restenosis?

A

Drug-eluting stents (DES)

Although DES have a low rate of stenosis, the risk significantly increases if antiplatelet therapy is d/c in the first year.

81
Q

When will bare metal stents be appropriate?

A

More appropriate in patients needing urgent surgeries

82
Q

How long does re-endothelialization take for angioplasty, bare metal stents, and drug-eluting stents?

A
  • Angioplasty: 2-3 weeks
  • Bare metal stents: 12 weeks
  • Drug-eluting stents: 1 year
83
Q

DAPT recommendation length for angioplasty, bare metal stents, and drug-eluting stents?

A
  • Angioplasty: 2 weeks
  • Bare metal stents: 6 weeks
  • Drug-eluting stents: 3 months
84
Q

Adverse effects of Stent Placement

A
  • Thrombosis if DAPT is d/c (↑risk w/ DM, low EF)
  • Bleeding from operation (increased mortality in spinal cord, aneurysm, and prostatectomy surgery)
85
Q

DAPT Recommendations and Neuraxial Interventions

A
86
Q

Indications for Routine/Scheduled CABG

A
  • Medical therapy fails
  • Left main lesion > 50% stenosis
  • EF <40% with significant disease
  • Three or more vessels with disease
87
Q

Indications for EMERGENCY CABG

A
  • Failed angioplasty
  • MI-related septal rupture
  • MI-related mitral regurgitation
  • Perforated coronary arteries during stenting
  • Cardiogenic shock

Advanced Principles C (11 decks)

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