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Acute cardiac life support > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

1
Q

In 2010, how many Americans experienced a new MI?

A

785,000

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2
Q

In 2010, how many Americans had a recurrent MI

A

470,000

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3
Q

How many silent MIs occur each year

A

195,000

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4
Q

What is the avg age of a persons first MI

A

64.5 for men, 70.3 for women

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5
Q

Abnormal thickening and hardening of vessel walls

A

Arteriosclerosis

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6
Q

Arteriosclerosis caused by build-up of fat-like deposits in the inner lining of large and middle sized aa.

A

Atherosclerosis

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7
Q

What is the usual cause of an Acute Coronary Syndrome (ACS)

A

Rupture of an atherosclerotic plaque

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8
Q

Initial event leading to atherosclerosis

A

Endothelial injury

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9
Q

What is the initial response of the vessel wall to an expanding plaque

A

Blood vessels expand outwardly to maintain size of lumen

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10
Q

At what point does a vessel stop growing outwardly when a plaque is forming

A

Plaque fills about 40% of the inside of the vessel

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11
Q

What % stenosis is required to cause symptoms in coronary aa.

A

70%

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12
Q

Features of a stable plaque

A

Thick fibrous cap that contains a large amount of collagen and smooth muscle but contains a relatively small lipid pool.

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13
Q

Feature of unstable plaques

A

Thin fibrous cap, thick fatty core

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14
Q

Events likely to trigger a plaque rupture

A 
Extreme physical activity
Severe emotional trauma
Sexual activity
Exposure to illicit drugs
Exposure to cold
Acute infection
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15
Q

General area in BVs likely for plaque rupture to occur

A

Vessel bifurcations due to speed of blood flow and turbulence created at these areas

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16
Q

3 vulnerable sites for plaque rupture w/in the coronary aa

A

Proximal part of the LAD
Near origin of the marginal branch on the RCA
Near the origin of the 1st obtuse marginal branch on the circumflex coronary a.

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17
Q

GpIIB/IIIA receptors link platelets via what molecule

A

Fibrinogen

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18
Q

Fibrinolytics stimulate the conversion of what to what

A

Plasminogen to plasmin (plasmin then dissolves the clot)

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19
Q

Most common cause of MI

A

Acute plaque rupture

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20
Q

Partial blockage of a coronary a. may cause what

A

Silent MI, unstable angina, NSTEMI or even sudden death

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21
Q

Complete coronary a. block causes what

A

STEMI

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22
Q

If you have a complete blockage but no ischemia, what’s the deal?

A

Development of collateral circulation

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23
Q

Other, less common causes of MIs

A

Coronary spasms (eg. cocaine), abnormalities of vessels, hypercoag, trauma to coronary aa. (CAs), CA emboli (rare)

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24
Q

How does cocaine cause an MI

A

Increases demand (incr. HR and contractility)
Decrease supply (vasoconstriction)
Stimulating platelet activation
Accelerating atherosclerosis

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25
Q

What other spasmodic dxs is Prinzmetals angia associated with

A

Migraines and Raynaud

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26
Q

What does typical angina do to the ST segment

A

Depression

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27
Q

What does Prinzmetals angina due to the ST segment

A

Elevation

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28
Q

What can you use to treat prinzmetals angina

A

Sublingual nitroglycerin (NTG)

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29
Q

What should you order before initiating treatment in any pt w/ possible ACS

A

12 lead EKG

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30
Q

What causes the pain/discomfort in pts w/ angina

A

Lactic acid and CO2 buildup in ischemic tissues

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31
Q

What are some things that do NOT describe ischemic chest discomfort

A

Sharp, worsened by inspiration, affected by muscle movement, pain is positional

Although indicate something other than ischemic heart probs

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32
Q

Common precipitating events for stable angina

A

Emotions, exercise, cold weather

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33
Q

% of MIs preceded by longstanding angina

A

18%

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34
Q

How long does unstable angina last

A

> 20 minutes

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35
Q

Innermost half of the myocardium is called what

A

Subendocardial

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36
Q

Outermost half of the myocardium is called what

A

Subepicardial area

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37
Q

What area of the heart is most vulnerable to ischemia

A

Endocardial and subendocardial areas

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38
Q

Criteria for acute MI

A

Rise of biomarkers (prefer troponin) w/ at least 1 of the following
Symptoms of ischemia
ECG changes indicating ischemia (ST-segment change or new LBBB)
Pathological Qs on EKG
Imaging evidence of loss of viable myocardium or new regional wall motion abnormality

39
Q

Criteria for prior MI

A

New pathologic Qs w/ or w/out symptoms
Imaging evidence of loss of viable myocardium that is thin and fails to contract
Pathologic findings of a healed or healing MI

40
Q

Who delays longer when seeking medical help for ischemic type chest discomfort, men or women?

A

Women

41
Q

SAMPLE history

A 
Signs and symptoms
Allergies
Medications/past Medical hx
Last oral intake
Events leading to incidence
42
Q

OPQRST (pain presentation)

A 
Onset
Provocation/Palliation/Position
Quality
Region/Radiation/Referral
Severity
Timing
43
Q

What day of the week is an MI most likely to happen? What season?

A

Monday

Winter

44
Q

If a pt has an MI before age 40, be suspicious of what?

A

Cocaine use

45
Q

Most common symptom of infarction

A

Chest discomfort

46
Q

Levine’s sign

A

Pt describes discomfort by placing a clenched fist against their sternum

47
Q

Angina equivalents

A 
Signs of myocardial ischemia other than discomfort
Dsypnea
Dizziness
Dysrrhythmias
Sweating
Fatigue
Generalized weakness
Isolated arm or jaw pain
Palpitations
Syncope
N/v
48
Q

Why are diabetic pts more likely to present with atypical MI symptoms

A

Autonomic dysfunction

49
Q

Most frequent symptom of MI reqardless of race

A

SOB

50
Q

Goals of reperfusion therapy

A

Fibrinolytics w/in 30 minutes of arrival or PCI w/in 90 minutes

51
Q

EKG changes associated w/ myocardial ISCHEMIA

A

ST-segment depression and T-wave inversion

52
Q

EKG changes associated with myocardial INJURY

A

ST-segment elevation

53
Q

EKG change in the hyperacute phase of MI

A

Tall T waves (often not seen because this phase has passed by the time pt receives help)

54
Q

EKG change in early acute phase of MI

A

ST-segment elevation (occurs within first hour or few hours)

55
Q

EKG change in late acute phase of MI

A

T-wave inversion

56
Q

EKG change in fully evolved phase of MI

A

Pathologic Q

57
Q

What is a pathologic Q

A

Q wave that is .04 seconds or more wide (i.e. one small box or more) or that is more than 1/3 the amplitude of the R wave

58
Q

What EKG change generally remains in the healed phase of MI

A

Abnormal Q wave (indicates dead tissue)

59
Q

Anterior wall MI

A

Indicative changes:V3, V4
Reciprocal changes:V7, V8, V9
Artery: Mid portion LAD

60
Q

Anteroseptal MI

A

Indicative changes: V1-4
Reciprocal changes:V7, V8, V9
Artery: LAD proximal occlusion

61
Q

Anterolateral MI

A

Indicative changes:I, aVL, V3-6
Reciprocal changes: II, III, aVF, V7-9
Artery: LAD

62
Q

Inferior MI

A

Indicative changes: II, III, aVF
Reciprocal changes: I, aVL
Artery: RCA

63
Q

Lateral MI

A

Indicative changes:I, aVL, V5, V6

Reciprocal changes: II, III, aVF

64
Q

Septum MI

A

Indicative changes: V1, V2

Reciprocal changes: V7-9

65
Q

Inferobasal (posterior) MI

A

Indicative changes: V7-9

Reciprocal changes:V1-3

66
Q

Right ventricle MI

A

Indicative changes: V1R -V6R

Reciprocal changes: 1, aVL

67
Q

When should you suspect a RVI

A

EKG suggest inferior infarct (II, III, aVF)

68
Q

Clinical triad of RVI

A

Hypotension, JVD, clear lung sounds

69
Q

NTG AEs

A

Headache, flushing, tachycardia, dizziness, orthostatic hypotension

70
Q

Potent narcotic analgesic and anxiolytic

A

Morphine

71
Q

Effects of morphine tx

A

Venodilation, decreased HR and systolic BP

This all reduces O2 demand

72
Q

Preferred analgesic for pts w/ STEMI who experience persistent chest discomfort unresponsive to nitrates

A

Morphine

73
Q

How do ACEIs help with fluid accumulation

A

Increase renal blood flow which helps get rid of sodium and fluid

74
Q

MONA; what is it used for and what is it

A

Mnemonic for meds used in ACS

Morphine
O2
NTG
ASA

75
Q

When should you give ASA and clopidogrel in pts experiencing ACS

A

As soon as possible

76
Q

What should you do with a pt who presents w/ STEMI and is on NSAIDS (except for ASA)

A

Discontinue the NSAIDs

77
Q

MOA for unfractionated heparin

A

Cofactor for activation of antithrombin, decreases thrombin, and decreases factor Xa

78
Q

LMWH MOA

A

Act more via inhibition of Xa

79
Q

Drug that directly inhibits Xa and is administered subQ

A

Fondaparinux

80
Q

Direct thrombin inhibitor give IV

A

Bivalirudin

81
Q

Contemporary percutaneous coronary intervention (PCI)

A

Gp IIb/IIIa inhibitors and a thienopyridine (clopidogrel)

82
Q

What is Rescue PCI

A

PCI performed after unsuccessful reperfusion attempts w/ fibrinolytics

83
Q

4 intervals of total ischemic time

A
  1. Onset of symptoms to arrival of EMS
  2. Arrival of EMS personnel to hospital arrival
  3. Hospital arrival to 12-lead EKG
  4. 12-lead EKG to drug/balloon
84
Q

When are fibrinolytics indicated in ACS

A

Only for UA/NSTEMI who also have true posterior MI

85
Q

Where are grafts used in CABG usually taken from

A

Internal mammary a., radial a. or saphenous vein

86
Q

When does ventricular rupture usually occur after an MI

A

10-14 days

87
Q

Most consistent finding for ventricular septal rupture

A

New loud systolic murmur heard best at LLSB, often accompanied by a palpable thrill

88
Q

What kind of MI can lead to papillary muscle dysfunction

A

Inferior wall infarct

89
Q

What often precedes cardiac tamponade in MI patients

A

Cardiac wall rupture

90
Q

Cardiac wall ruptures are most likely to occur where?

A

Lateral wall of LV

91
Q

Common mechanical sequelae of MIs

A 
Ventricular aneurysm
Ventricular septal rupture
Papillary muscle dysfunction
Cardiac wall rupture
LV failure/cardiogenic shock
RV failure (often due to LV failure)
92
Q

Embolic complications of MIs

A

Stroke, DVT, PE

93
Q

Inflammatory complications of MIs

A

Pericarditis

94
Q

What can you use to treat pain due to pericarditis

A

ASA (other NSAIDs are contraindicated in the first 7-10 days)

Acute cardiac life support (5 decks)

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