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Cardiology > Lectures 18-19: Stable CAD > Flashcards

Lectures 18-19: Stable CAD Flashcards

1
Q

Course of ischemic heart disease

A

Asymptomatic ischemia -> angina pectoris -> unstable angina -> myocardial infarction

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2
Q

Coronary flow occurs during…Minimum pressure?

A

Diastole; 60-65 mm Hg

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3
Q

What are two conditions that could lower diastolic pressure?

A

Hypotension or aortic regurgitation

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4
Q

Generally we don’t change pressure, but rather…

A

Resistance

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5
Q

What mediates vascular tone? (three classes)

A

Metabolic factors: adenosine*, acetate, hydrogen ions, CO2; Neural factors: NE –> alpha and beta receptors; Endothelium factors

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6
Q

Endothelial vasodilators and vasoconstriction. What dominates?

A

ACh, 5-HT, shear stress –> NO; thrombin, AII, Epi; healthy state = vasodilation, disease state = vasoconstriction

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7
Q

What can cause increased wall stress? How is this related to CAD?

A

Pressure/volume overload –> myocyte hypertrophy to normalize wall stress –> increased O2 demand of cardiac tissues

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8
Q

Besides enlarged myoctyes, what else can increase myocardial oxygen demand? (2)

A

Increased HR and contractility

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9
Q

Relationship between atherosclerotic plaques and CAD?

A

Reduce diameter of coronary arteries –> increased resistance

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10
Q

What is more important for increased resistance due to plaques…length of lesion or reduced diameter?

A

Reduced diameter (r^4)

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11
Q

What is the function of the coronary microvasculature? What happens in disease?

A

Modulates vasomotor tone; in disease, endothelium is impaired and vasodilation in response to needs does not occur

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12
Q

At rest, what level of stenosis is required for ischemia? How about exertion? What angina’s are associated with this? Why are these numbers so high?

A

~90% (unstable angina); ~70% (stable angina); flow is augmented by microvasculature

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13
Q

What are four ways that endothelial cell dysfunction can occur?

A

Release of endothelium-dependent vasodilators (prostacyclin/NO) may be impaired in response to normal stimuli (shear stress); Vasodilatory effects of local metabolites also blunted (i.e. adenosine); Vasoconstricting effects of catecholamines predominates; Loss of antithrombotic effect of endothelial cells in response to stimuli (ADP, serotonin, thromboxane) –> small thrombi

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14
Q

Two classes of non-atherosclerotic causes of ischemia and examples

A

Reduced O2 supply (aortic regurge, bleeding); Increased O2 demand (tachyarrhythmias, hypertensive crisis, severe aortic stenosis)

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15
Q

Impacts of ischemia (3)

A

Myocyte necrosis; stunned myocardium; hibernating myocardium

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16
Q

What is stunned myocardium

A

Transient systolic dysfunction after ischemic insult

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17
Q

What is hibernating myocardium

A

Chronic ventricular dysfunction due to multivessel CAD w/ reduced blood supply; revascularization treats this

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18
Q

Define stable angina

A

Retrosternal chest discomfort precipitated by exertion

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19
Q

Define unstable angina

A

New-onset severe angina or increased severity/frequency of stable symptoms

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20
Q

Define variant angina

A

Episodes of coronary spasm reduces O2 supply, occurs at rest

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21
Q

Define syndrome X. Treatment?

A

Chest pain but normal coronary arteries, due to microvasculature dysfunction; medically: cannot be treated surgically

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22
Q

Define silent ischemia. Treatment?

A

Ischemia w/out clinical symptoms; not sure if we should treat, currently addressed with ISCHEMIA trial

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23
Q

Stable angina: sensation

A

Pressure, tightness, heaviness, burning

24
Q

Stable angina: duration

A

Few minutes

25
Q

Stable angina: location

A

Diffuse, not focal

26
Q

Stable angina: associated sxs

A

SOB, fatigue, nausea

27
Q

Stable angina: precipitants

A

Exertion and emotional stress

28
Q

Stable angina: frequency

A

Distinguishes from unstable

29
Q

Systems on differential dx

A

Cardiac (spasm, pericarditis), GI, MSK

30
Q

Stable angina: ECG

A

Typically normal, not of high value

31
Q

What is one way to dx chronic stable angina?

A

Stress testing: make them exercise and then detect ischemia (ECG, echo, nuclear perfusion imaging)

32
Q

Describe coronary angiography

A

Invasive procedure requiring contrast media for direct visualization of stenotic lesions; gold standard in dx of CAD

33
Q

Describe nitrates: use, mechanism

A

Treatment of stable CAD; cause venodilation –> reduce LV volume –> reduce wall stress –> decrease mycoardial O2 demand

34
Q

Side effects of nitrates

A

Lightheadedness, headache

35
Q

T/F: Nitrates improve long-term survival

A

False

36
Q

Describe beta-blockers use for stable CAD

A

Reduce mycardial O2 demand by decreasing HR and contractility

37
Q

Side effects of beta-blockers (3)

A

Bronchospasm, bradycardia, impotence

38
Q

T/F: Beta-blockers improve long-term survival

A

True

39
Q

If a patient has had a prior MI, what do you give them?

A

Beta-blocker! Can extend life

40
Q

DON’T give beta-blockers to these three groups

A

Patients in shock, patients with airway disease, diabetics (may mask reflexive tachycadia from hypoglycemia)

41
Q

Ca2+ Channel Blockers…groups and effects

A

Dihydropyridines: vasodilating&raquo_space; cardiac depression; nondihydropyridines: cadiac depressant&raquo_space; vasodilating

42
Q

Once again, vasodilating improves CAD how?

A

Decreases myocardial O2 demand by reducing wall stress

43
Q

Should you combine Ca2+ blockers and beta-blockers?

A

NOPE: accentuate negative chronotropy/inotropy –> major bradycardia

44
Q

What is ranolazine?

A

New drug to treat angina w/ unclear molecular mechanism

45
Q

What does aspirin do?

A

Reduce risk of thrombotic complications by inhibition of platelet aggregation

46
Q

What is another antiplatelet therapy?

A

Thienopyridine (Clopidogrel): inhibits platelet receptor

47
Q

Why do we give a lipid lowering therapy? Quantity or quality of life? When do you give?

A

Lowers risk of death in patients at risk with established CAD (quantity); administer statin to patients with >7.5% risk of MI in 10 years

48
Q

Why would ACE inhibitors be helpful for CAD?

A

Reduce cardiac events

49
Q

Medical therapy for stable CAD (summary)

A

Quality: nitrate, beta-blocker, CCB, ranolazine; Quantity: aspirin, statin, beta-blocker, ACE-I

50
Q

Two revascularization options

A

Stenting and coronary artery bypass grafting

51
Q

What is a drug-eluting stent?

A

Stents coated with antiproliferative agent to inhibit restenosis but delays endothelializaion –> increased risk for thrombosis

52
Q

Two types of grafts

A

Venous and arterial (very high patency)

53
Q

What is the preferred strategy for complex patients (multivessel disease, left-main, diabetic)

A

Coronary artery bypass grafting

54
Q

Advantages/disadvantages of PCI

A

Advantages: low procedural risk, minimal recuperation; Disadvantages: need dual antiplatelet therapy, higher rates of revascularization

55
Q

Advantages/disadvantages of CABG

A

Advantages: complete revascularization, no need for long term DAPT, proven mortality benefit; Disadvantages: higher procedural risks, longer recuperation

Cardiology (22 decks)

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