093014 ischemic heart disease

Question 1

ischemic heart disease

Answer 1

imbalance btwn supply and demand for oxygen and nutrients and removal of metabolites

Question 2

IHD caused by atherosclerotic narrowing-coronary blood flow is reduced by how much

Answer 2

greater than 90%

Question 3

causes of decreased blood flow

Answer 3

fixed atherosclerotic narrowing
acute plaque change (can rupture, embolize)
thrombosis overlying ruptured plaque
vasospasm

Question 4

fixed obstruction

Answer 4

narrowing of greater than 70% causes symptomatic ischemia with exercise

greater than 90% stenosis causes ischemia at rest

often multiple arteries affected (most commonly-first several cm of LAD, left circumflex, entire length of right coronary artery

effects are modified by collaterals

Question 5

acute plaque change

Answer 5

unpredictable and abrupt conversion of stable plaque to an unstable atherothrombotic lesion that results in myocardial ischemia (rupture, fissures, ulcerations…or hemorrhage into atheroma)

results in acute coronary syndromes (acute MI, unstable angina, sudden cardiac death)

Question 6

what are the influences contributing to acute plaque change?

Answer 6

intrinsic and extrinsic factors

Question 7

what are intrinsic factors contributing to acute plaque change

Answer 7

large areas of foam cells or lipid
thin fibrous cap
most dangerous lesions are the moderately stenotic (50-75%), lipid rich atheromas-soft core
abundant inflammation
few smooth muscle cells

mechanical stress

Question 8

what extrinsic factors contribute to acute plaque change

Answer 8

adrenergic stimulation (upon awakening, emotional)

Question 9

coronary thrombosis

Answer 9

partial or total thrombosis superimposed on a partially stenotic plaque

critical to pathogenesis of acute coronary syndromes

if total occlusion–get acute transmural MI or can get sudden death

if incomplete occlusion/mural thrombus–you’re more likely to have unstable angina, acute subendocardial infarction, or sudden death and can have emboli

Question 10

unstable angina

Answer 10

usually as a result of rupture of plaque with thrombosis. incomplete occlusion of artery

Question 11

four basic syndromes of ischemic heart disease

Answer 11

angina pectoris
myocardial infarction
chronic ischemic heart disease
sudden cardiac death

Question 12

angina pectoris

Answer 12

paroxysmal and recurrent attacks of chest pain caused by transient myocardial ischemia-15 seconds to 15 minutes (no cellular necrosis)

three patterns: stable, prinzmetal, unstable

Question 13

stable angina

Answer 13

produced by physical activity or emotional excitmenet, attributed to chronic stenosis

Question 14

Prinzmetal angina

Answer 14

due to coronary artery spasm at rest

Question 15

unstable angina

Answer 15

occurs with progressively increasing frequency and progressively less effort, often at rest and of prolonged duration (induced by disruption of plaque with superimposed partial thrombosis. often a prodrome of acute MI)

Question 16

myocardial infarction

Answer 16

death of cardiac muscle due to ischemia

Question 17

risk factors for MI

Answer 17

increasing age and predisposition to atherosclerosis (HTN, smoking, diabetes, increased cholesterol and/or lipids)

Question 18

pathogenesis of MI in 90% is

Answer 18

acute plaque change resulting in thrombosis and occlusion of coronary artery

in 10% of cases, due to vasospasm, emboli or unexplained

Question 19

myocardial response to ischemia

Answer 19

60 seconds of ischemia–loss of contractility

loss of blood supply causes reversible damage in early stages

in 20-40 minutes–IRREVERSIBLE damage (coagulative necrosis)

early thrombolytic therapy (3-4 hours)–reperfusion and limit the size of infarct

arrthymias (induced by myocardial irrititability secondary to ischemia–ventricular fibrillation)-can lead to sudden death

Question 20

MI frequencies in three main coronary arteries

Answer 20

LAD-most common (40-50%)
RCA-second most common (30-40%)
LCA-least common (15-20%)

Question 21

MI gross morphology

Answer 21

under 12 hrs: not apparent (tetrazolium stain–pale areas post 2-3 hrs)

12-24 hrs: dark red blue mottling (b/c of stagnant blood)

1-14 days:
early–sharply defined yellow tan area
late–still yellow tan centrally but with hyperemic peripheral zone due to granulation tissue

greater than 2 weeks:
gray-white scar begins to form

Question 22

MI histology

Answer 22

4-12 hrs: wavy fibers

12 hrs-7 days: coagulative necrosis becomes well established and ongoing (initially pyknotic nuclei, hyper-eosinophilic myocytes. followed by neutrophils, loss of nuclei and striations. by day 7, macrophages at border)

7-14 days: granulation tissue well established. collagen begins to deposit

greater than 14 days: progressively more collagen deposition. eventually DENSE FIBROUS SCAR.

Question 23

reperfusion injury for acute MI usually occurs after

Answer 23

thrombolysis, baloon angioplasty, or bypass grafts

Question 24

reperfusion prevents necrosis if it occurs within how long?

Answer 24

20 minutes

Question 25

necrotic cells have contraction bands because

Answer 25

influx of calcium (calcium is released from SR)

Question 26

reperfusion injury may result from

Answer 26

oxygen free radicals released from leukocytes

microvascular injury causing hemorrhage and endothelial swelling that occludes capillaries-no flow

platelet and complement activation

Question 27

chest pain in an MI is NOT relieved by

Answer 27

nitroglycerin or rest

Question 28

what findings would you see with MI?

Answer 28

chest pain
rapid weak pulse
diaphoresis
dyspnea due to pulmonary edema

10-15% of pts-no symptoms

ECG

lab-cardiac enzymes, CRP

Question 29

complications of MI

Answer 29

contractile dysfunction

cardiogenic shock (damage to 40% or more of left ventricle)

arrhythmia early in course (sudden death)

myocardial rupture (3-7 days)–free wall, ventricular septum, papillary muscle

pericarditis (2-3 days)

mural thrombus and thromboembolism (due to pooled blood)

ventricular aneurysm (late)

papillary muscle dysfxn (secondary to scarring or fibrosis)

progressive heart failure (late)

Question 30

chronic ischemic heart disease

Answer 30

elderly pts with progressive heart failure due to ischemic myocardial damage (post infarction cardiac decompensation. or severe coronary artery disease without infarction but with myocardial dysfxn.)

Question 31

morphology of chronic ischemic heart disease

Answer 31

enlarged heavy heart with left ventricular hypertrophy and dilation. dilation is due to blood staying behind in heart due to heart failure.

coronary atherosclerosis, scars

Question 32

sudden cardiac death

Answer 32

unexpected death from cardiac causes. death due to lethal arrhythmia.

most often due to ischemic heart disease (80-90% of sudden cardiac death)

non-atherosclerotic causes are hypertrophy, cardiac conduction system abnormalities, mitral valve prolapse, congenital abnormalities, myocarditis, cardiomyopathy, pulmonary HTN

Question 33

morphology of sudden cardiac death

Answer 33

typically coronary atherosclerosis with acute plaque change. typically has had MI before or has pathology associated with non-atherosclerotic causes.