Ischemic Heart Disease Flashcards

1
Q

Define ischemic heart disease.

A

Imbalance between myocardial oxygen demand and supply

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2
Q

During what phase of the cardiac cycle is there the lease resistance to coronary artery blood flow?

A

Diastole

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3
Q

What is the most common site for coronary artery thrombosis?

A

LAD

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4
Q

What regions does the LAD perfuse?

A

Anterior LV, anterior 2/3 IVS, apex

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5
Q

What is the second most common site of coronary artery thrombosis?

A

RCA

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6
Q

What regions does the RCA perfuse?

A

Posterior LV, posterior 1/3 IVS, RV, posteriormedial papillary muscle, SA/AV nodes

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7
Q

What is the most common manifestation of IHD?

A

Angina pectoris

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8
Q

What are the causes of stable angina?

A

Atherosclerotic CAD (most common), AV stenosis or HTN w/ concentric LVH, hypertrophic cardiomyopathy, cocaine induced coronary artery vasoconstriction

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9
Q

What is the pathogenesis of stable angina pectoris?

A

Subendocardial ischemia; decreased coronary artery blood flow or concentric hypertrophy

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10
Q

What are the clinical findings in stable angina?

A

Exertion induced substernal chest pain, often accompanied by SOB, diaphoresis

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11
Q

What is the treatment for an acute episode of stable angina?

A

Nitroglycerin (0.3-0.6 mg SL q5min)

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12
Q

What is the mechanism of action for nitroglycerin?

A

Decreases oxygen demand (dec. preload due to venoldilation)

Increased oxygen supply (inc. coronary perfusion and decrease vasospasm)

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13
Q

In a patient with stable angina, what would be seen on ECG?

A

ST-segment depressions (>1mm)

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14
Q

Prinzmetal (variable) angina is characterized by intermittent coronary artery vasospasm at rest or w/o superimposed CAD. What would a stress test show?

A

ST-segment elevations

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15
Q

Define unstable angina.

A

Increased frequency and duration of angina episodes produced by less exertion or at rest; high frequency of progression of MI if untreated

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16
Q

What diagnostic tests are helpful in diagnosis IHD?

A

Resting ECG, stress test, coronary angiography

17
Q

What drugs are used to treat IHD; how do they work; when would you use them?

A

Nitrates
Beta-blockers (decreas oxygen demand by decreasing HR and contractility) initial tx for all patients with stable angina)
Ca channel blockers (decrease preload, wall stress, contractility, HR, coronary vasospasm and increase coronary perfusion; variant angina)
Aspirin for all, clopidogrel if pt allergic to aspirin
Heparin+aspirin (unstable angina)
Ranolazine (decresaes late inward Na current; stable angina for pts refractory to other drugs)
Statins (inhibit HMG-CoA which decreases LDL and increases HDL, also anti-inflammatory; pts w/ dyslipidemia)

18
Q

What are the side effects of nitrates?

A

Headaches, hypotension, reflex tachycardia

19
Q

What are the side effects of beta blockers?

A

Excessive bradycardia, decreased LV contractile function (worsening of HF), bronchoconstriction, fatigue, impotence

20
Q

What are the side effects of Ca channel blockers?

A

Headache/flushing, decreased LV contraction, marked bradycardia, edema, constipation

21
Q

What are the adverse effects of Ranolazine?

A

Dizziness, headache, constipation, nausea

22
Q

What drug is used to prevent thrombosis in revascularization procedures?

A

Abciximab

23
Q

When is CABG indicated?

A

Left main coronary artery disease or symptomatic 3 vessel disease

24
Q

What graft is the best for CABG?

A

Internal mammary artery>saphenous vein

25
Q

What is the pathogenesis of a MI?

A

Plaque rupture, thrombosis, infarct

26
Q

What role does TxA2 play in formation of an MI?

A

Aids in platelet aggregation and acts as vasoconstrictor

27
Q

What are the types of of MI?

A

STEMI and NSTEMI

28
Q

What are the two therapeutic methods of reperfusion in MI?

A

PCI, fibrinolytic therapy

29
Q

Why is early reperfusion important in MI?

A

Increases early and long term survival

30
Q

When do contraction bands appear?

A

Reperfusion of irreversibly damaged cells that leads to the entry of Ca in to cytosol causing hypercontraction

31
Q

When does coagulation necrosis appear following an MI?

A

24 hours

32
Q

When do macrophages break down the necrotic tissue and what danger exists during this period?

A

3-7 days; danger of rupture

33
Q

What are the clinical findings of MI?

A

Sudden onset of severe retrosternal pain, usually longer than 30 min, not relieved by nitroglycerin, usually radiates, associated with sweating/anxiety/hypotension

34
Q

What is the most common cause of death in STEMI?

A

V-fib

35
Q

What are the complications of STEMI?

A

Cardiogenic shock, arrhythmias (ventricular most common), CHF, rupture, mural thrombus, pericarditis, ventricular aneurysm

36
Q

Detail the temporal sequence of CK-MB.

A

Appears in 4-8 hours, peaks at 24 hours, disappears in 3 days

37
Q

Detail the temporal sequence of cardiac troponins.

A

Appear 3-12 hours, peak at 24 hours, disappear in 10 days

38
Q

What serum biomarker can be used to diagnose reinfarction?

A

CK-MB

39
Q

What serum biomarker is the gold standard for diagnosis of MI?

A

Cardiac troponins