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Cardiovascular Pathology > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

ischemia

A

refers to a lack of oxygen due to inadequate perfusion, which results from an imbalance between oxygen supply and demand

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2
Q

Narrowing of the coronary artery lumen can cause

A
  1. hypertension -> hypertrophy
  2. increased work load -> heart failure
  3. formation of a thrombus -> MI
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3
Q

risk factors for ischemic heart disease

A

smoking, hypertension, obesity, diabetes, hypercholesterolemia; some reversal of disease process with elimination of risk factors

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4
Q

Other associated problems with ischemic heart disease

A

thromboemboli, particularly from valvular vegetations; coronary artery spasm (cocaine); coronary arteritis; increased work load or decreased oxygen delivery of any cause; anomalous origin of the left coronary artery; chest trauma

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5
Q

Ischemia results from

A

oxygen supply/oxygen demand mis-match

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6
Q

Mechanism of ischemic injury

A

inadequate 02 delivery; occlusive disease; myocardial injury

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7
Q

most common cause of decreased perfusion

A

progressive stenosis with or without associated formation of thrombus

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8
Q

Other causes of decreased perfusion

A

thromboembolus, vasospasm, vasculitis, hyperperfusion secondary to hypovolemia

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9
Q

Causes of decreased oxygenation

A

anemia, carbon monoxide, congenital heart disease, asphyxia, lung disease

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10
Q

Important underlying principles of atherosclerosis

A

no specific correlation between the extent of stenosis and type or severity of ischemic heart disease; rapidity of decreased perfusion, tendency of thrombus formation

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11
Q

Critical event in atherosclerosis

A

abrupt mismatch of perfusion to demand

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12
Q

Decreased ability to meet an increase in demand once stenosis reaches

A

75%

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13
Q

coronary artery thrombus usually occurs

A

in the first 2 cm of the coronary vessel of LAD or left circumflex; occurs in the proximal and distal 1/3 of the right coronary artery

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14
Q

coronary artery thrombus formation usually results from

A

rupture of fissure of plaque with platelet aggregation, release of TXA2

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15
Q

Vasospasms are associated with

A

adrenergic stimulation, local factors (NO, endothelin, platelet factors including thromboxane)

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16
Q

Vasospasms have a clear association with

A

stress, excitement; more MI’s occur between 6AM and noon

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17
Q

Vasospasms may be mediated by

A

hypertension, increased platelet activity

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18
Q

conductance vessels and major sites of atherosclerosis

A

epicardial coronary vessels

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19
Q

Intramyocardial coronary vessels

A

resistance vessels (major determinant of autoregulation and flow)

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20
Q

Area at greatest risk for ischemia

A

subendocardium

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21
Q

What happens to myocytes with a decrease in O2

A

cells switch to anaerobic glycolysis within minutes; glucose is broken down into lactate; pH is reduced; impaired cell membrane function results in leakage of potassium and uptake of sodium

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22
Q

When does reversible injury become irreversible injury in the heart?

A

after 40 minutes of hypoxia

23
Q

Irreversible injury results in

A

necrosis and permanent loss of functional myocardium; may be diffuse as in acute MI or may involve slow loss of cells or groups of cells over time

24
Q

Morphological characteristics of reversible injury

A

“stunned myocytes”; mitochondrial swelling, relaxation of myofibrils, distortion of cristae

25
Q

Morphological characteristics of irreversible injury

A

chronic loss of individual myocytes, particularly in the subendocardial region; coagulative necrosis; apoptosis; area eventually becomes fibrotic

26
Q

Gross appearance of an MI

A

early: pallor +/- hyperemic border
3 to 7 days: hyperemic border with central, yellow-brown softening; possible hemorrhage
after 1 week: replacement with red-brown, depressed, scarred areas; scar appears grey and fiber-like

27
Q

Microscopic appearance of an MI

A

evolution of many stages beginning with necrosis of myocytes, inflammation, infiltration with inflammatory cells, clean up of necrotic debris, replacement of myocardium with scar tissue

28
Q

Reperfusion injury

A

additional myocyte injury with free radical formation, influx of Ca2+, hemorrhage; characterized by the presence of contraction bands in damaged myocytes

29
Q

Critical mismatch in an MI

A

when intramyocardial vessels are maximally dilated, coronary flow becomes the main determinant of the flow of oxygen; an increase in demand or temporary decrease in flow results in symptomatic ischemia

30
Q

chest pain in an MI

A

crushing pain over sternum radiating to left arm or back; usually not sharp of fluctuating; severe pain is accompanied by sweating, nausea, and vomiting

31
Q

diaphoresis

A

shortness of breath, sweating, nausea - usually signs of severe cardiac pain or insufficiency

32
Q

Troponin I and Troponin T

A

cardio specific and sensitive; increase along with CMB and stay elevated up to 7 days

33
Q

Creatinine kinase (MB isozyme)

A

MB isoenzyme is highly specific and sensitive marker; peaks at 12-24 hours; number of hours needed to peak correlates with infarct size

34
Q

Lactic dehydrogenase

A

peaks later and remains elevated (rises after 24 hours; peaks in 3-6 days, may not return to normal for 2 weeks)

35
Q

Causes of an MI

A
  1. pre-existing coronary disease + thrombus formation
  2. coronary spasm
  3. sudden loss of vascular volume
  4. hemopericardium/cardiac tamponade
36
Q

Most MIs are precipitated by what?

A

by a ruptured atherosclerotic plaque and subsequent thrombus formation

37
Q

where do thrombi usually form

A

within first few cm of vessel distribution (near ostia for right and left main coronaries, just distal to bifurcation for LAD, RC, and circumflex)

38
Q

Why are the characteristic features of inflammation in an MI delayed by 24-48 horus?

A

inflammation is initiated at borders and the process must migrate into the (usually large) necrotic area

39
Q

First visual signs of inflammation with an MI (within first 24 hours)

A

edema and separation of fibers at the margins

40
Q

hallmarks of coagulative necrosis

A

loss of nuclei and hypereosinophilic fibers

41
Q

describe the progression of the histopathologic features in an MI

A

coagulative necrosis (loss of nuclei and hypereosinophilic fibers) -> neutrofils migrate -> 2-4 days until cellular infiltrate become prominent -> subacute phase with macrophages and lymphocytes -> fibrosis occurs over next several weeks -> replacement of myocardium with fibrous scar

42
Q

Tissue weakest and most vulnerable to rupture after

A

4-5 days

43
Q

Early complications of an MI

A

dysfunctional heart muscle; arrhythmias; extensions of the infarct

44
Q

Late complications of an MI

A

aneurysm/dilatation; ventricular rupture (septal or free wall); mural thrombus; pericardial effusion/pericarditis; papillary muscle infarction with mitral insufficiency

45
Q

EKG changes with ischemia

A

inversion of the T wave; more severe, displacement of the ST segment; transient ST-segment depression reflexts subendocardial ischemia; transient ST-segment elevation suggests transmural ischemia; ischemia may induce ventricular arrhythmias

46
Q

What might a stress test elicit on an EKG

A

may elicit ST segment changes even in the absence of symptomatic angina; a positive result indicates CAD in 98%

47
Q

EKG changes in Prinzmetal’s angina

A

ST segment may be strikingly elevated

48
Q

EKG changes with an MI

A

Q waves or loss of R waves; subendocardial may only show ST segment changes; total occlusion results in ST-segment elevation and most individuals develop Q-waves; a minority that present without ST-segment elevation may develop Q-waves

49
Q

perfusion studies are indicated in

A
  1. patients with chronic stable or unstable angina who are severely symptomatic despite medical therapy
  2. patients with troublesome symptoms that present diagnostic difficulties
  3. patients with signs of severe ischemia regardless or presence of symptoms
50
Q

Treatment for angina

A

lifestyle changes; treat risk factors; treatment of underlying conditions; nitrates; beta blockers; calcium channel blockers; aspirin; platelet adhesion blockers

51
Q

Goal of myocardial infarction treatment

A

prevent fatal arrhythmias and re-establish blood flow to myocardium

52
Q

diagnose infarction with

A

12-lead EKG

53
Q

Management/Treatment of an MI

A

increase oxygenation; establish airway and IV access; aspirin; anti-arrhythmics; re-establish blood flow

54
Q

Ways to re-establish blood flow in an MI

A

angiography; PCI; fibrinolysis (most effective within 30 min)

Cardiovascular Pathology (8 decks)

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