Acute Coronary Syndromes Flashcards

(94 cards)

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
What other spasmodic dxs is Prinzmetals angia associated with
Migraines and Raynaud
26
What does typical angina do to the ST segment
Depression
27
What does Prinzmetals angina due to the ST segment
Elevation
28
What can you use to treat prinzmetals angina
Sublingual nitroglycerin (NTG)
29
What should you order before initiating treatment in any pt w/ possible ACS
12 lead EKG
30
What causes the pain/discomfort in pts w/ angina
Lactic acid and CO2 buildup in ischemic tissues
31
What are some things that do NOT describe ischemic chest discomfort
Sharp, worsened by inspiration, affected by muscle movement, pain is positional Although indicate something other than ischemic heart probs
32
Common precipitating events for stable angina
Emotions, exercise, cold weather
33
% of MIs preceded by longstanding angina
18%
34
How long does unstable angina last
>20 minutes
35
Innermost half of the myocardium is called what
Subendocardial
36
Outermost half of the myocardium is called what
Subepicardial area
37
What area of the heart is most vulnerable to ischemia
Endocardial and subendocardial areas
38
Criteria for acute MI
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
Criteria for prior MI
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
Who delays longer when seeking medical help for ischemic type chest discomfort, men or women?
Women
41
SAMPLE history
``` Signs and symptoms Allergies Medications/past Medical hx Last oral intake Events leading to incidence ```
42
OPQRST (pain presentation)
``` Onset Provocation/Palliation/Position Quality Region/Radiation/Referral Severity Timing ```
43
What day of the week is an MI most likely to happen? What season?
Monday | Winter
44
If a pt has an MI before age 40, be suspicious of what?
Cocaine use
45
Most common symptom of infarction
Chest discomfort
46
Levine's sign
Pt describes discomfort by placing a clenched fist against their sternum
47
Angina equivalents
``` Signs of myocardial ischemia other than discomfort Dsypnea Dizziness Dysrrhythmias Sweating Fatigue Generalized weakness Isolated arm or jaw pain Palpitations Syncope N/v ```
48
Why are diabetic pts more likely to present with atypical MI symptoms
Autonomic dysfunction
49
Most frequent symptom of MI reqardless of race
SOB
50
Goals of reperfusion therapy
Fibrinolytics w/in 30 minutes of arrival or PCI w/in 90 minutes
51
EKG changes associated w/ myocardial ISCHEMIA
ST-segment depression and T-wave inversion
52
EKG changes associated with myocardial INJURY
ST-segment elevation
53
EKG change in the hyperacute phase of MI
Tall T waves (often not seen because this phase has passed by the time pt receives help)
54
EKG change in early acute phase of MI
ST-segment elevation (occurs within first hour or few hours)
55
EKG change in late acute phase of MI
T-wave inversion
56
EKG change in fully evolved phase of MI
Pathologic Q
57
What is a pathologic Q
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
What EKG change generally remains in the healed phase of MI
Abnormal Q wave (indicates dead tissue)
59
Anterior wall MI
Indicative changes:V3, V4 Reciprocal changes:V7, V8, V9 Artery: Mid portion LAD
60
Anteroseptal MI
Indicative changes: V1-4 Reciprocal changes:V7, V8, V9 Artery: LAD proximal occlusion
61
Anterolateral MI
Indicative changes:I, aVL, V3-6 Reciprocal changes: II, III, aVF, V7-9 Artery: LAD
62
Inferior MI
Indicative changes: II, III, aVF Reciprocal changes: I, aVL Artery: RCA
63
Lateral MI
Indicative changes:I, aVL, V5, V6 | Reciprocal changes: II, III, aVF
64
Septum MI
Indicative changes: V1, V2 | Reciprocal changes: V7-9
65
Inferobasal (posterior) MI
Indicative changes: V7-9 | Reciprocal changes:V1-3
66
Right ventricle MI
Indicative changes: V1R -V6R | Reciprocal changes: 1, aVL
67
When should you suspect a RVI
EKG suggest inferior infarct (II, III, aVF)
68
Clinical triad of RVI
Hypotension, JVD, clear lung sounds
69
NTG AEs
Headache, flushing, tachycardia, dizziness, orthostatic hypotension
70
Potent narcotic analgesic and anxiolytic
Morphine
71
Effects of morphine tx
Venodilation, decreased HR and systolic BP This all reduces O2 demand
72
Preferred analgesic for pts w/ STEMI who experience persistent chest discomfort unresponsive to nitrates
Morphine
73
How do ACEIs help with fluid accumulation
Increase renal blood flow which helps get rid of sodium and fluid
74
MONA; what is it used for and what is it
Mnemonic for meds used in ACS Morphine O2 NTG ASA
75
When should you give ASA and clopidogrel in pts experiencing ACS
As soon as possible
76
What should you do with a pt who presents w/ STEMI and is on NSAIDS (except for ASA)
Discontinue the NSAIDs
77
MOA for unfractionated heparin
Cofactor for activation of antithrombin, decreases thrombin, and decreases factor Xa
78
LMWH MOA
Act more via inhibition of Xa
79
Drug that directly inhibits Xa and is administered subQ
Fondaparinux
80
Direct thrombin inhibitor give IV
Bivalirudin
81
Contemporary percutaneous coronary intervention (PCI)
Gp IIb/IIIa inhibitors and a thienopyridine (clopidogrel)
82
What is Rescue PCI
PCI performed after unsuccessful reperfusion attempts w/ fibrinolytics
83
4 intervals of total ischemic time
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
When are fibrinolytics indicated in ACS
Only for UA/NSTEMI who also have true posterior MI
85
Where are grafts used in CABG usually taken from
Internal mammary a., radial a. or saphenous vein
86
When does ventricular rupture usually occur after an MI
10-14 days
87
Most consistent finding for ventricular septal rupture
New loud systolic murmur heard best at LLSB, often accompanied by a palpable thrill
88
What kind of MI can lead to papillary muscle dysfunction
Inferior wall infarct
89
What often precedes cardiac tamponade in MI patients
Cardiac wall rupture
90
Cardiac wall ruptures are most likely to occur where?
Lateral wall of LV
91
Common mechanical sequelae of MIs
``` Ventricular aneurysm Ventricular septal rupture Papillary muscle dysfunction Cardiac wall rupture LV failure/cardiogenic shock RV failure (often due to LV failure) ```
92
Embolic complications of MIs
Stroke, DVT, PE
93
Inflammatory complications of MIs
Pericarditis
94
What can you use to treat pain due to pericarditis
ASA (other NSAIDs are contraindicated in the first 7-10 days)