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BCC > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

What syndromes are associated with ischemic heart disease?

A

Homocystinuria and hyperuricemia

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2
Q

What is the formula for myocardial oxygen supply?

A

MvO2 = CBF * (CaO2 - CvO2) where CaO2 = 1.34 * Hb * SaO2 + 0.003 * PaO2

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3
Q

What is normal coronary blood flow? Myocardial oxygen consumption?

A

CBF = 0.7 - 1 mL/min/g of cardiac tissue; MvO2 = 0.1 mL/min/g of cardiac tissue

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4
Q

What is the autoregulation range of coronary blood flow?

A

40 - 140 mmHg (vasodilation at the low end and vasoconstriction at the high end)

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5
Q

What happens to the autoregulation range of coronary blood flow with stress?

A

The range gets smaller since the HR, SBP, and contractility goes up

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6
Q

How much oxygen does the myocardium extract at rest?

A

70-80% of oxygen

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7
Q

What is coronary flow reserve?

A

The heart’s ability to increase coronary blood flow above baseline; the ratio of maximum coronary blood flow to baseline coronary blood flow

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8
Q

What factors reduce coronary flow reserve?

A

Tachycardia + increased preload (increase in compressive resistance to diastolic perfusion) + anything that increases baseline CBF (i.e. increase O2 consumption, anemia, hypoxia)

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9
Q

How do you calculate total coronary resistance?

A

Add the resistances in series: R1 (large epicardial arteries with minimal resistance) + R2 (small arteries and arterioles) + R3 (extravascular compressive resistance that is mainly based on systolic contraction)

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10
Q

Why is the subendocardium primarily perfused in diastole?

A

Systolic contraction of the LV increases resistance in the coronary beds (increases R3)

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11
Q

When is the subepicardium perfused?

A

Throughout the cardiac cycle since in systole, the subepicardial pressure is equal to pleural pressures (unlike the subendocardium which is only perfused during diastole)

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12
Q

What happens with beta1 innervation? Beta2? Alpha1?

A

Beta1 = increased contractility and myocardial oxygen consumption leading to vasodilation; Beta2 = direct vasodilation; Alpha1 = direct vasoconstriction

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13
Q

What local mediators are present in the coronary vasculature to help with vasodilation?

A

Nitric oxide + endothelium-dependent hyperpolarizing factor (EDHF) + prostacyclin

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14
Q

How does nitric oxide help with vasodilation? What does oxidative stress do to it?

A

cGMP-mediated pathway which causes vasodilation; oxidative stress inactivates NO via a superoxide (doesn’t allow for vasodilation)

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15
Q

How does Endothelium-dependent hyperpolarizing factor (EDHF) cause vasodilation?

A

Responds to bradykinin and shear stress -> hyperpolarization of vascular smooth muscle -> vasodilation

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16
Q

How does prostacyclin help with vasodilation?

A

Gets produced from arachidonic acid by COX -> vasodilation

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17
Q

What does endothelin do in the coronary vasculature?

A

Slow-acting vasoconstrictor

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18
Q

What do platelets release to cause effects at the coronary vasculature?

A

Serotonin (vasoconstriction) + ADP (vasodilation due to NO production) + vWF + fibronectin + thrombospondin + PDGR (proliferation of smooth muscle after vessel damage)

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19
Q

What contributes to myocardial work?

A

External work (moving stroke volume against an arterial pressure) + Internal work (potential energy)

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20
Q

What is myocardial work efficiency?

A

External work / O2 consumption

21
Q

What happens when you have plaque rupture in the coronary vessels?

A

Thrombogenic subendothelial substrates leads to platelet adherence (GP1b binds vWF and GPIIb/IIIa binds vWF/fibrinogen/fibronectin) -> this leads to platelet activation (epi, collagen, and thrombin bind platelets leading to activation of phospholipase C and phospholipase A2 -> activates thromboxane A2 (platelet aggregation and vasoconstriction) + prostacyclin (vasodilation))

22
Q

What are angina equivalents and who are these symptoms more common in?

A

Mid-epigastric discomfort + dyspnea + exercise intolerance + fatigue; more often seen in women, older adults, and diabetics

23
Q

What are the cutoffs for ST-depression and elevations?

A

ST-depression: >/= 0.5mm; STEMI: >/= 1mm in multiple leads

24
Q

Does a normal ECG rule out ACS?

A

No

25
Q

When can you see an elevated troponin if it isn’t ACS?

A

Renal disease, sepsis, COVID-19, infection, PE, stroke

26
Q

What is a Bruce protocol?

A

The protocol for stress echoes

27
Q

What is myocardial flow reserve?

A

The ratio of maximum blood flow to resting blood flow; this is the equivalent to coronary flow reserve

28
Q

What does it mean if you have attenuation artifact on nuclear myocardial perfusion study?

A

Depicts a fixed perfusion defect but has normal wall motion movement on echo

29
Q

What does it mean if you have scar tissue noted on nuclear myocardial perfusion study?

A

Fixed defects in perfusion with abnormal wall motion on echo

30
Q

What does it mean if you have ischemia noted on nuclear myocardial perfusion study?

A

Reversible defects in perfusion with normal or abnormal wall motion

31
Q

What are contraindications to nuclear studies?

A

Contraindication to vasodilators + bronchospastic disease + use of dipyridamole-containing meds + use of methylxanthines + hypersensitivity to adenosine or regadenoson

32
Q

What are the indications for cardiac cath?

A

Stable ischemic heart disease with negative non-invasive studies but high suspicion for disease + unstable angina + STEMI

33
Q

What are the AHA/ACC classifications of lesions for cath?

A

Type A (<10mm, <45 degree, little/no calcification, not totally occluded), Type B (10-20mm, 45-90 degree, totally occlusion <3 mon, ostial lesion), Type C (>20mm, >90 degree, total occlusion > 3mon, degenerated vein graft)

34
Q

What is silent ischemia and how frequent is it seen?

A

Ischemia 2/2 autonomic neuropathy; seen in 1/3 of patients with chronic stable angina

35
Q

What is Type 1 ischemia?

A

Acute coronary syndrome

36
Q

What is Type 2 ischemia?

A

Demand ischemia (tachycardia is most common cause of this)

37
Q

How long should you be on dual antiplatelet therapy after DES or BMS?

A

DES: 6 months; BMS: 1 month; If it is 2/2 ACS, then it should be for 12 months

38
Q

Does LVH increase or decrease myocardial wall stress?

A

Decreases since there is increased wall thickness and more tissue to take the pressure

39
Q

What plasma protein levels decrease with STEMI? What plasma proteins are increased?

A

Anticoagulant factors (i.e. Protein C, Antithrombin, and alpha-2 macroglobulin); Procoagulant factors are increased (fibrinogen, factor VIII, vWF, alpha-1 antitrypsin)

40
Q

What determines right or left dominance in coronary anatomy?

A

If the PDA comes off the RCA, it is right dominant; if the PDA comes off the LCX, it is left dominant

41
Q

What major branches come off the LCX? LAD?

A

LAD = diagonals and septal perforators; LCX = obtuse marginal

42
Q

When is CABG preferred over PCI?

A

Left main disease or left main equivalent (>70% stenosis between proximal LAD and LCX) + triple vessel disease + proximal LAD stenosis

43
Q

What is stunned myocardium? How long does it take for function to return?

A

Viable myocardium with contractile dysfunction; usually seen after brief periods of ischemia with transient myocardial dysfunction; responds well to inotropes; restoration of function in hours to weeks

44
Q

What is hibernating myocardium?

A

Reversible, chronic contractile dysfunction in areas that receive enough blood flow for viability (but not full flow); function can be partially or fully restored after reperfusion (takes weeks to months)

45
Q

What is necrotic myocardium?

A

Fibrotic or scarred myocardium; tissue is no longer viable even after revascularization

46
Q

How do you test for myocardial viability?

A

Via viability testing; Dobutamine stress echo, SPECT, PET

47
Q

What is the preferred intervention in single-vessel disease? Two-vessel disease? Three-vessel disease?

A

Single vessel = DES; Two vessel = PCI with DES, if LAD involved, CABG; Three vessel = CABG

48
Q

What is the second most important graft after the LAD to use?

A

Radial artery

BCC (29 decks)

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