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Patho II Exam 1 > Acute Coronary Syndrome > Flashcards

Acute Coronary Syndrome Flashcards

1
Q

types of angina

A

–Printzmetal’s Variant Angina
–Chronic Stable Angina
–Unstable Angina

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2
Q

Printzmetal’s Variant Angina

A

–vasospasm
–supply ischemia
–not due to atherosclerosis

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3
Q

Unstable Angina

A

–thrombus
–supply ischemia
–due to atherosclerosis

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4
Q

causes of variant/vasospastic angina (Prinzmetal angina)

A

–coronary artery spasm
–endothelial dysfunction

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5
Q

characteristics of variant/vasospastic angina

A

–CAD may or may not be present
–onset: rest, minimal exertion, night
–elevated ST segment

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6
Q

characteristics of unstable plaque causing ACS

A

–large lipid core
–active inflammation
–smooth muscle cell proliferation into intima
–thin fibrous cap

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7
Q

specifics of unstable angina

A

–chest pain occurring for the first time
–chest pain more severe than usual with chronic angina
–new regions of the heart are undergoing myocardial ischemia
–emergency situation

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8
Q

why is there no infarction with unstable angina?

A

–occlusion is partial
–thrombus dissolves

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9
Q

EKG changes with unstable angina

A

might see ischemic changes, typically transient

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10
Q

are cardiac enzymes elevated with unstable angina?

A

no

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11
Q

theory of plaque rupture

A

–increased SNS activity
–plaque rupture
–thrombus formation

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12
Q

components of increased SNS activity leading to plaque rupture

A

–increased BP, HR, and force of contraction
–increased force of coronary artery blood flow
–increased force exerted against injured endothelium

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13
Q

components of plaque rupture leading to thrombus formation

A

–platelets adhere to ruptured plaque
–release substances that (1) attract more platelets and (2) contribute to vasospasm

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14
Q

contributing factors to increased SNS activity leading to plaque rupture

A

–psychological stress
–exercise
–circadian rhythms

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15
Q

signs of MI in men

A

–discomfort or tingling in arms, back, shoulder, or jaw
–chest pain
–SOB

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16
Q

signs of MI in women

A

–sudden dizziness
–heartburn-like feeling
–cold sweat
–unusual tiredness
–nausea or vomiting

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17
Q

general s/s of MI

A

–diaphoresis
–dyspnea
–extreme anxiety
–Levine’s sign (fist to chest)
–pallor
–retrosternal crushing chest pain that radiates to shoulder, arm, jaw, or back
–weak pulses

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18
Q

what is an acute MI?

A

ruptured plaque + thrombus

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19
Q

why do infarctions occur?

A

–blood flow disruption is prolonged
OR
–blood flow disruption is total

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20
Q

EKG changes with MI?

A

yes

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21
Q

cardiac enzyme elevation with MI?

A

yes

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22
Q

acute MI

A

acute coronary syndrome with prolonged ischemia without recovery

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23
Q

importance of ATP with ischemia/infarction

A

–decreased O2 = decreased ATP
–decreased ATP = decreased contractility

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24
Q

when does irreversible injury to cardiac muscle occur?

A

within 30 min to 4 hours

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25
Q

when does tissue necrosis begin?

A

by 4 hours

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26
Q

when is necrotic tissue cleared away?

A

by 1-2 weeks

27
Q

when does tough fibrous scar tissue replace necrotic tissue?

A

by 6 weeks

28
Q

three zones of tissue damage

A

–ischemia
–injury
–infarction

29
Q

infarction

A

–necrosis
–MI, dead cells
–beyond hope of recovery but can stop from increasing

30
Q

injury

A

–some recovery possible
–can still perfuse it and restore it to become viable
–not dead yet

31
Q

ischemia

A

full recovery possible

32
Q

how to prevent extension of infract?

A

–increase oxygen
–decrease the demand on the heart

33
Q

what influences the extent of damage in a MI?

A

–location or level of occlusion in the coronary artery
–length of time that the coronary artery has been occluded
–heart’s availability of collateral circulation

34
Q

ST segment in STEMI v. NSTEMI

A

STEMI = elevated
NSTEMI = depression or normal

35
Q

QRS in STEMI v. NSTEMI

A

STEMI = usually pathologic (wide), develops over hours
NSTEMI = normal

36
Q

T wave in STEMI v. NSTEMI

A

STEMI = peaked, then inverted
NSTEMI = inverted

37
Q

Trop in STEMI v. NSTEMI

A

STEMI = elevated
NSTEMI = elevated

38
Q

size of infarct in STEMI v. NSTEMI

A

STEMI = larger
NSTEMI = smaller

39
Q

outcomes of STEMI v. NSTEMI

A

STEMI = poor
NSTEMI = better

40
Q

left anterior descending artery

A

–supplies the left ventricle
–most commonly involved in MIs

41
Q

three main arteries that supply the heart with blood

A

–right coronary artery
–left circumflex artery
–left anterior descending artery

42
Q

diagnostics for acute MIs

A

–serum cholesterol, LDL, HDL, triglycerides
–ECG
–serum electrolytes
–serum glucose
–CRP
–serum homocysteine
–cardiac enzymes
–CXR
–CT scan
–cardiac angiogram and cardiac cath
–ECHO

43
Q

initial treatment of acute MIs

A

–oxygen
–morphine
–ASA
–nitro
–beta blocker
–thrombolytic agent

44
Q

when are thrombolytic agents used?

A

within 4-6 hours of beginning of MI

45
Q

reason for giving oxygen with MIs

A

increase O2 delivery to ischemic myocardium

46
Q

reason for giving ASA with MIs

A

suppresses platelet aggregation
–decreases mortality
–chew first dose

47
Q

reason for giving morphine with MIs

A

decreases pain
reduces preload and afterload
–helps preserve ischemic tissue

48
Q

reason for giving beta blocker

A

reduce HR and contractility
–reduces pain, infarct size, and mortality

49
Q

reason for giving nitro

A

reduces preload and afterload
limits infarct size
–does not reduce mortality

50
Q

example of fibrinolytic therapy

A

Alteplase (tPA)

51
Q

MOA of alteplase (tPA)

A

dissolves clot by converting plasminogen into plasmin

52
Q

advantages to alteplase (tPA)

A

most effective

53
Q

disadvantages to alteplase (tPA)

A

works best within 30-70 minutes

54
Q

main adverse effect of alteplase (tPA)

A

bleeding

55
Q

what is tPA always given with?

A

heparin and antiplatelet therapy

56
Q

side effects of nitro

A

–hypotension
–headache
–flushing

57
Q

what shouldn’t be given with nitro?

A

sildenafil (Viagra) –> severe hypotension

58
Q

interventions for reperfusion

A

stent/balloon angioplasty

59
Q

myocardial stunning

A

contributes to injury through rapid restoration of blood flow to the myocardium

60
Q

what is reperfusion injury caused by?

A

oxidized free radicals generated by WBCs and the cellular response to restored blood flow

61
Q

who suffers silent, asymptomatic MIs?

A

–diabetics
–older than age 65

62
Q

major causes of MI death

A

–hesitation
–delayed request for emergency care

63
Q

drug therapy post-MI

A

–ASA
–beta blocker
–ACE inhibitor
–statin

Patho II Exam 1 (5 decks)

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