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Clin Med II > L4: Ischemic Heart Disease > Flashcards

L4: Ischemic Heart Disease Flashcards

1
Q

What is the term for pathologic processes affecting the coronary arteries (atherosclerosis)

A

Coronary Artery Disease (CAD)

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2
Q

What is the term for diagnoses including angina pectoris, MI, silent MI, and mortality resulting from CAD?

A

Coronary Heart Disease (CHD)

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3
Q

What is the term for the pathologic process affecting the entire arterial circulation, resulting in stroke, TIA, angina, MI, claudication, and critical limb ischemia?

A

Cardiovascular Disease (CVD)

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4
Q

What is the term for irreversible death of the heart muscle due to prolonged lack of O2?

A

Myocardial Infarction (MI)

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5
Q

Where are the main arteries of the hard located? When does most perfusion occur?

A 
Epicardial region (opposed to endocardium)
Most perfusion occurs during diastole
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6
Q

Atheroscleortic plaques form: (2)

A
  • Sites of increased blood turbulence

- Branching points in the epicardial arteries

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7
Q

What is ischemic heart disease?

A

Condition in which there is an inadequate supply of blood and oxygen to a portion of the myocardium

O2 demand > O2 supply

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8
Q

What is the leading cause of death in the US? Is it more common in males or females?

A

Coronary Heart Disease (CHD)

M > F

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9
Q

__________ is the initial coronary event in 15% of patients with CHD.

A

Sudden Cardiac Death (SCD)

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10
Q

When does atherosclerosis begin?

A

Childhood

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11
Q

What is the role of nitric oxide in terms of our blood vessels?

A
  • Endothelial cells produce NO
  • NO inhibits plaque formation and has anti-inflammatory properties
  • NO keeps our blood flowing smoothly, eliminates plaque, and vasodilates
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12
Q

What causes endothelial dysfunction?

A

LDL and oxidized LDL = leads to atherosclerosis

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13
Q

What has an “atheroprotective” role in our vessels? Why?

A

HDL: anti-inflammatory and anti-oxidant properties

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14
Q

What are the modifiable risk factors for IHD (7)?

A
  • Diet
  • Inactivity
  • Obesity
  • Cigarette smoking
  • HTN
  • DM
  • Dyslipidemia (high LDL, low HDL, high triglycerides)
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15
Q

At what age are men most at risk for developing IHD? Women?

A

M > 45 years old

W > 55 years old

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16
Q

Almost 2/3rds of women who die suddenly from CHD have:

A

NO previous symptoms!

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17
Q

Atypical symptoms associated with IHD are more common in:

A
  • Women
  • Elderly
  • Patients with diabetes
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18
Q

Why do women often have increased mortality with IHD?

A

Often present without chest pain!

Delayed dx + delayed tx = increased mortality

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19
Q

In what situations are women more likely to die from IHD?

A

Greater likelihood of being induced by rest, sleep, and mental stress (rather than activity)

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20
Q

Transient ischemia may result in:

A

Angina pectoris

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21
Q

Prolonged ischemia may result in:

A

Myocardial infarction

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22
Q

Which condition may cause sx that urge patients to seek medical care, may be confused with other disorders, and may be completely “silent”?

A

Myocardial ischemia

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23
Q

What conditions fall under the umbrella of acute coronary syndrome?

A
  • Unstable angina
  • MI
    • Non-ST elevation MI (NSTEMI)
    • ST elevation MI (STEMI)
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24
Q

Define stable angina (angina pectoris).

A

Exertional or stress-related chest or arm discomfort that resolves with rest and/or the use of sublingual nitroglycerin

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25
Q

How long does stable angina typically last? What is the intensity pattern?

A
  • Usually no greater than 5-10 minutes

- Crescendo-decrescendo pattern

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26
Q

How would patients typically describe their “pain” while experiencing stable angina?

A
  • Typically not called pain*
  • Heaviness or pressure (“elephant on my chest”)
  • Tightness, squeezing, smothering, choking
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27
Q

What is Levine’s sign and what might this indicate?

A
  • Clenched fist over sternum

- May be indicative of stable angina

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28
Q

Where might patients complain of radiating pain when experiencing angina pectoris?

A

Shoulders, arm, neck, jaw, teeth, epigastrium, mid-back

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29
Q

What physical exam findings might you find in a patient with stable angina?

A

Tachycardia
Hypertension
Abnormal heart sounds

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30
Q

What are 4 atypical presentations/symptoms of stable angina? Who commonly presents with atypical sx?

A
  • Dyspnea
  • Nausea
  • Fatigue
  • Faintness

Elderly and DM patients. Dyspnea common in women.

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31
Q

What are some symptoms that are NOT likely to be ischemia or angina?

A
  • Sharp, fleeting stabs of chest pain
  • Prolonged, dull ache in the left precordial area
  • Any discomfort localized with one finger
  • Pain lasting for seconds or constant pain lasting for days
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32
Q

What 3 diagnostic studies would we order for angina?

A
  • EKG 12-lead (aka electrocardiogram)
  • Chest XR
  • Cardiac biomarkers
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33
Q

What might an EKG show in a patient with angina?

A

May have ST segment depression during episodes or discomfort (resolution of changes when pain resolves)

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34
Q

What 2 diagnostic studies would we consider ordering in patients presenting with atypical angina sx?

A

Cardiac stress testing (Exercise EKG or nuclear stress test with imaging) or coronary angiography

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35
Q

What is the Bruce protocol?

A

Exercise stress test: speed and incline are increased every THREE MINUTES until patient’s HR is at 85% maximum predicted for their age

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36
Q

What are we watching for while a patient is undergoing exercise EKG? (4)

A
  • EKG changes
  • Decreased myocardial perfusion seen on nuclear image
  • Drop in systolic BP > 10 mmHg
  • or any other symptoms
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37
Q

What does a nuclear stress test show us?

A

Perfusion defect will be seen in areas of hypoperfusion (compare resting to exercise/stress)

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38
Q

What does a stress echocardiogram show us?

A

Dx of ischemia related to development of WALL MOTION ABNORMALITY with exercise/stress

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39
Q

How do you calculate someone’s max heart rate?

A

220 - age

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40
Q

What is the gold standard for diagnosing CAD?

A

Coronary angiography (aka cardiac catheterization)

41
Q

What are the indications for a coronary angiography?

A
  • Known or suspected CAD
  • Atypical chest pain (stress test showing high risk for CAD)
  • Before valve surgery in pts with chest pain or EKG changes
42
Q

True or false: Coronary angiography demonstrates the presence of a “vulnerable plaque”

A

False!

43
Q

What are 4 medications (be very general) that can help treat stable angina?

A
  • Meds that decrease O2 demand
  • Meds that increase O2 supply
  • Antiplatelet medication
  • Statins
44
Q

What kind of diet would you recommend to a patient with CAD?

A

Plant-based diet

45
Q

Name 3 classes of medications that decrease O2 demand.

A
  • Nitrates
  • Beta-blockers
  • Ca2+ channel blockers
46
Q

What is the first line treatment for acute angina?

A

Short acting nitrates

47
Q

How do nitrates work on the heart?

A

PRELOAD reduction

48
Q

How do beta blockers work on the heart?

A

Decrease HR, NP and contractility = AFTERLOAD reduction

49
Q

What is the first line tx for chronic angina? What other medication can be used (though not first line)

A

Beta blockers (can also use long acting nitrates)

50
Q

What is the only antianginal medication proven to prevent re-infarction and improve survival post MI?

A

Beta blockers (hence use for tx of chronic angina)

51
Q

How do CCBs work on the heart?

A

Decrease BP and contractility = AFTERLOAD reduction

52
Q

When is the use of CCBs indicated?

A

For patients who do not respond to nitrates or beta blockers

53
Q

What are 2 classes of medications that increase oxygen supply?

A

Nitrates and CCBs

54
Q

How do nitrates and CCBS work on the heart (to help increase oxygen supply)?

A

Dilate coronary arteries

55
Q

How do treat with nitrates?

A

At onset of pain: 0.3-0.6 mg sublingually or by buccal spray&raquo_space; Repeat every 5 minutes for up to 3 doses&raquo_space; If still no relief, call 911 (or begin IV nitro if already hospitalized)

56
Q

What are 3 antiplatelet medications we can use to help treat stable angina?

A
  • Aspirin (75-325mg daily)
  • Clopidogrel (Plavix)
  • Combo of ASA and clopidogrel
57
Q

Patients with a hx of an MI have a risk of death from CHD that is ______ than those without known CVD

A

20 times higher :-(

58
Q

What role do statins play in tx of CHD?

A

Stabilize plaques&raquo_space; Reduces clinical events, slows progression of coronary atherosclerosis, induces regression of coronary atheroscleorisi

59
Q

How would you prescribe statins in a patient with CHD?

A

High intensity dosage independent of baseline LDL-C (monitor this over time though)

60
Q

What 2 revascularization procedures can we perform to treat someone with stable angina?

A

Percutaneous Coronary Intervention (PCI) and Coronary Artery Bypass Grafting (CABG)

61
Q

When is a PCI indicated?

A

Hx of angina despite medical tx; evidence of ischemia on stress testing
*Can be performed with or without stent placement

62
Q

When is a CABG indicated?

A

When patient has left main coronary stenosis, or triple vessel disease

63
Q

What vessels are typically harvested for a CABG?

A

Great saphenous vein or internal mammary arteries

64
Q

What are 4 pathophysiological processes that can lead to Acute Coronary Syndrome?

A
  1. Plaque rupture or erosion with a superimposed occlusive thrombus *Most common!
  2. Dynamic obstruction (spasm)
  3. Progressive mechanical obstruction (plaque forming over a stent)
  4. UA secondary to increased myocardial oxygen demand and/or decreased supply
65
Q

What is Prinzmetal’s Angina?

A

Ischemic symptoms secondary to vasospasm; causes chest pain

66
Q

What would you see on an EKG during Prinzmetal’s Angina?

A

Transient ST-segment elevation

67
Q

Which population is more likely to experience Prinzmetal’s Angina?

A

Younger patients with fewer risk factors (20’s, 30’s, 40’s)

68
Q

What diagnostic test would be helpful in diagnosing in Prinzmetal’s Angina?

A

Coronary angiography (stress test generally unhelpful)

69
Q

What is the treatment for Prinzmetal’s angina?

A

Nitrates and CCB’s

70
Q

What is the presentation for patients with ACS? (6) Who may have an atypical presentation?

A
  • Ischemic pain
  • SOB
  • Weakness
  • Nausea
  • Anxiety
  • Sense of doom

-Atypical presentation in women, diabetics and elderly pts (sudden breathlessness)

71
Q

What is the typical presentation of Unstable Angina?

A

Ischemic discomfort AND 3 of the following:

  • Occurs AT REST (often lasts >10 minutes)
  • Severe and of NEW ONSET (within last 4-6 weeks)
  • Occurs with a CRESCENDO pattern (more severe, prolonged, and frequent than previously)
72
Q

What is the typical presentation for a Non ST Elevation MI (NSTEMI)?

A

Similar symptoms to UA with continued worsening

73
Q

How can you differentiate between a UA and NSTEMI based on clinical features (tests)?

A

UA: NO elevation of CK-MB or Troponin, Usually normal EKG (may have ST depression or T wave inversion)

NSTEMI: DEFINITE ELEVATION of CK-MB and/or Troponin (there has been MI!), EKG: typically no ST elevation, may have ST depression or T wave inversion

74
Q

How do you manage UA/NSTEMI?

A
  • Bedrest
  • Cardiac monitoring
  • IV access
  • Labs
  • Possible oxygen
  • Medication
  • Risk stratification, angiography, and revascularization with PCI or CABG if indicated
75
Q

When would you supply oxygen during management of a UA/STEMI?

A

Utilized only if arterial O2 < 90%, hypoxia, or acute respiratory distress

76
Q

What medications would you prescribe during management of a UA/STEMI? (7)

A
  • Sublingual nitroglycerin x 3 at 5 minute intervals
  • Morphine (avoided unless pain unacceptable and then with caution)
  • Beta blockers (metoprolol or atenolol started within 24 hours)
  • CCB as second line (if sx not relieved by nitrates or beta blokers)
  • High intensity statin therapy (atorvastatin 80mg/day)
  • Antiplatelet therapy in all NSTEMI pts if no contraindications (clopidogrel)
  • Anticoagulation (ASA, heparin)
77
Q

What are the risk factors for patients with UA/NSTEMI progressing to a STEMI? (Thrombosis In MI for Risk Stratification)

A

1 point each:

  • 65 years or older
  • > /= 3 risk factors for CHD
  • Prior coronary stenosis of >/= 50%
  • ST segment deviation on admission EKG
  • > /= 2 anginal episodes in prior 24 hours
  • Increased serum cardiac biomarkers
  • Aspirin use in prior 7 days
78
Q

What is the difference between an NSTEMI and STEMI?

A

NSTEMI: Non-occlusive thrombus
STEMI: Occlusive thrombus and transmural infarcation

79
Q

When is an acute MI (STEMI) most likely to occur (time of day)?

A

Common within a few hours of awakening in the morning

80
Q

What are the identifiable precipitating factors for a STEMI seen in 50% of cases? (3)

A
  • Vigorous exercise
  • Extreme emotional stress
  • Medical or surgical illness
81
Q

What are 2 primary causes of a STEMI? Which is most common?

A
  1. Rupture of vulnerable plaque (most common) = results in COMPLETE OCCLUSION of a coronary artery
  2. Slowly developing stenosis of coronary artery (less common; collateral vessels usually develop to get BF to affected areas)
82
Q

What is the onset, peak, and duration of CK enzymes post MI?

A

Onset: 3-12 hours
Peak: 18-24 hours
Duration: 36-48 hours

83
Q

What is the onset, peak, and duration of Troponins enzymes post MI?

A

Onset: 3-12 hours
Peak: 18-24 hours
Duration: Up to 10 days

84
Q

What does an ST elevation indicate? What about a depression?

A

Elevation=cell death

Depression=ischemia

85
Q

A patient presents with no ST-segment elevation with (+) markers. They likely have:

A

NSTEMI

86
Q

A patient presents with +/- ST-segment elevations with (-) makers. They likely have:

A

UA

87
Q

A patient presents with ST-segment elevations and (+) markers. They likely have:

A

STEMI

88
Q

How do you manage a STEMI?

A
  • Bed rest
  • Cardiac monitoring
  • IV access
  • Labs (enzymes, electrolytes, CBC, Coags)
  • ACLS protocol when indicated*
  • Medication
  • Fibrinolysis*
  • Select reperfusion strategy*

*different than NSTEMI

89
Q

What medications would you prescribe during management of an NSTEMI? (7)

A
  • ASA 325mg chewed and swallowed*
  • Sublingual nitro
  • Beta blockers if no contraindications (metoprolol)
  • High intensity statin therapy if possible before PCI*
  • Anticoagulation therapy + antiplatelet therapy (in addition to ASA)
90
Q

Which reperfusion strategy is preferred in management of an NSTEMI?

A

Primary PCI strongly preferred (over CABG)
-Activate cardiac cath team or surgical team when indicated

*****Risk stratification!

91
Q

When would you provide fibrinolysis during management of an NSTEMI?

A
  • PCI not available within 120 minutes of first medical contact
  • Symptoms <12 hours
  • No contraindications
92
Q

What are the absolute contraindications to thrombolytic (fibrinolytic) therapy? (5)

A
  • Hx of intracranial hemorrhage
  • Hx of stroke in past year
  • Poorly controlled HTN (SBP > 180 and/or DBP > 110)
  • Suspected aortic dissection
  • Active internal bleeding
93
Q

What are some relative contraindications to thrombolytic therapy?

A
  • Current anticoagulant use (INR > 2)
  • Recent invasive procedure
  • Prolonged CPR
  • Known bleeding diathesis
  • Pregnancy
  • Active peptic ulcer disease
  • Hemorrhagic ophthalmic condition
  • Hx of severe HTN that is currently well controlled
  • Use of streptokinase in preceding 5 days-2 years
  • Concern for possible allergic rxn
94
Q

What are 7 potential post MI complications?

A
  • Recurrent ischemia
  • Pump failure (may lead to inpatient death)
  • Ventricular arrhythmias
  • Pericarditis/Dressler’s syndrome
  • Mural thrombus (thrombi attached to the vessel wall)
  • Cardiac rupture/LV aneurysm
  • Depression
95
Q

What is Dressler’s Syndrome?

A

Chest pain due to pericardial inflammation following MI, CABG, or traumatic injury to heart

96
Q

What are 4 post MI management techniques?

A
  • Risk stratification
  • Treat risk factors
  • Meds
  • Specialists if indicated
97
Q

What medications may be prescribed/continued post MI?

A
  • Beta blockers
  • Aspirin
  • If LV dysfunction, consider ACE-I or ARB
98
Q

Regular exercise and physical fitness can decrease risk of ______ post MI?

A

Recurrent events

99
Q

What are the goals of cardiac rehabilitation?

A
  • Increase exercise tolerance and functional capacity
  • Decrease cardiovascular mortality
  • Decrease emotional stress

Clin Med II (9 decks)

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