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Emergency Medicine > Chest Pain and ACS > Flashcards

Chest Pain and ACS Flashcards

1
Q

Myocardial necrosis + elevated cardiac enzymes

A

AMI

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2
Q

Twp types of AMI

A

STEMI

NSTEMI

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3
Q

phrase for either acute myocardial infarction or acute ischemia (unstable angina)

A

acute coronary syndrome

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4
Q

chest pain for inadequate myocardial perfusion → angina that is occurring more frequently and non-exertional → no STE or elevated biomarkers

A

Unstable Angina

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5
Q

sign often seen in ACS

A

Levine Sign

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6
Q

risk factors for CAD

A

SADCHF

smoking, age, DM, cholesterol, HTN, family hx

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7
Q

“ABC’s”…

A

immediate needs → airway, breathing, circulation

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8
Q

retrosternal, left chest, epigastric pain

A

acute coronary syndrome

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9
Q

character of pain associated with ACS

A

crushing, tightness, squeezing, pressure

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10
Q

Other symptoms associated with ACS

A

dyspnea
diaphoresis
nausea

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11
Q

physical exam findings associatedwith AMI

A

hypotension
diaphoresis
S3 Gallop

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12
Q 
retrosternal, Left anterior chest pain 
crush, squeeze, tight, pressure like
worse with exertion & better with rest 
diaphoresis, SOB, nausea 
lasts 2 - 30 minutes
A

classic chest pain

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13
Q

stabbing and well localized
pain that lasts 12 - 24 hours and is constant
positional or worsens with movement

A

Non-classic chest pain

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14
Q

Patient with AMI and this particular symptom have 2-4x higher risk of sudden cardiac death

A

dyspnea at rest

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15
Q

absence of chest pain despite ischemia → common in diabetics and elderly → atypical or less impressive symptoms

A

silent ischemia “silent MI”

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16
Q

Why do diabetics have worse prognosis in relation to MI?

A

2 - 4x greater risk of CAD → diabetes related atherosclerosis affects many systems

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17
Q

Other things beside ACS that can cause STE on EKG

A

pericarditis, myocarditis, BER, LVH, ventricular aneurysm

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18
Q

Cardiac Biomarker with high sensitivity and specificity

A

Troponin

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19
Q

Troponin is specific for ___ but not the ____

A

myocardial necrosis

mechanism

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20
Q

what do you want to look at when measuring troponin?

A

trend

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21
Q

When is troponin detectable?

When is it most reliable?

A

within 2 - 3 hours

at 6 hours

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22
Q

when do troponin levels peak?

A

48 hours

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23
Q

How long do Troponin levels remain elevated?

A

up to 10 days

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24
Q

small protein in skeletal and cardiac muscle

A

myoglobin

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25
Q

how long does it take myoglobin to rise?

A

3 hours

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26
Q

when will myoglobin peak?

A

4-9 hours

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27
Q

when will myoglobin return to baseline?

A

24 hors

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28
Q

When will Creatinin Kinase MC be elevated?

A

4 - 8 hours

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29
Q

When will Creatine Kinase MB peak?

A

12 -24 hours

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30
Q

when will creatine kinase MC return to normal?

A

36 - 72 hours

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31
Q

this scoring system is used to estimate 14 - 30 days mortality of patients

A

TIMI (Thrombosis in Myocardial Infarction) Score

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32
Q

chest pain from inadequate myocardial perfusion → no classic ST changes or elevated biomarkers

A

unstable angina

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33
Q

this occurs at rest, is prolonged lasting usually > 20 minutes

A

rest angina

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34
Q

new chest pain that limits physical acitivty (walking 1-2 blocks or 1 flight of stairs)

A

New-onset angina

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35
Q

Chest pain that has been previously diagnosed, has longer duration and is more frequent

A

increasing angina

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36
Q

How long does angina last and how long does it take to resolve?

A

< 10 -20 minutes

resolves within 2 - 5 minutes of rest/nitro

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37
Q

EKG findings in the setting of MI symptoms

A

STEMI

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38
Q

No EKG changes + elevated biomarkers

A

NSTEMI

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39
Q

How is unstable angina diagnosed?

A

based on history → nondiagnostic biomarkers and EKG

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40
Q

ST Depression on EKG indicates

A

ischemia

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41
Q

ST Elevation on EKG suggests

A

transmural injury

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42
Q

Leads V1, V2, V3

A

anteroseptal

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43
Q

Leads V1 - V4

A

anterior

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44
Q

Leads V1 - V, I and aVL

A

anterolateral

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45
Q

Leads I and aVL

A

lateral

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46
Q

Leads II, III, aVF

A

inferior

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47
Q

Leads II, III, aVF, V5 , V6

A

inferolateral

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48
Q

depressions and tall R wave in V1 and V2

A

posterior

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49
Q

New LBBB =

A

STEMI equivalent

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50
Q

what are you looking for on EKG?

A

1 mm STE in 2 + contiguous leads
reciprocal changes
Q waves

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51
Q

Wide QRS in V5 - V6

Deep S in V1 - V2

A

LBBB

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52
Q

rsR’ in V1 - V2

Deep S in V5 - V6

A

RBBB

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53
Q

Things that can interfere with diagnosing a STEMI

A 
pre-exisitng LBBB
peri/myocarditis 
paced rhythms 
hypokalemia 
digoxin effect 
LVH
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54
Q

Inverted T waves in V2 and V3

A

Wellens’ Sign

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55
Q

T or F: STEMI needs elevated biomarkers to “make the call”

A

False → STEMI doesn’t need elevated markers to diagnose

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56
Q

Diagnosis for 2 negative troponins + 2 hours apart + TIMI < 2

A

exclused MI as diagnosis

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57
Q

T or F: elevation of tropin correlates with prognosis

A

true → more elevated troponin elevation is always worse than less troponin elevation with respect to prognosis

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58
Q

Treatment for Chest pain

A

Aspirin
nitroglycerin
oxygen (if hypoxic)
Morphine

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59
Q

Treatment goal for STEMI if your hospital has catheter lab

A

< 90 minutes

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60
Q

mechanical reperfusion for MI

A

PCI +/- stent

61
Q

pharmacologic reperfusion for MI

A

fibrinolytic
antiplatelet
antithrombin

62
Q

Treatment goal for STEMI if your facility lacks cath lab

A

< 120 minutes

63
Q

If you can’t meet the 90 and 120 minute timeframes for MI, what do you do?

A

fibrinolysis within 30 minutes

64
Q

Three agents most STEMI patients receive in the ED

A

antiplatelet
antithrombin
nitrate

65
Q

Antiplatelet agents commonly used

A

ASA
clopidogrel
prasugrel
ticagrelor

66
Q

antithrombin agents commonly used

A

unfractionated heparin
enoxaparin
fondaparinux

67
Q

contraindications to nitrates in STEMI patient

A

hypotension
inferior STEMI
viagra

68
Q

Treatment for unstable angina/NSTEMI

A

antiplatelet (ASA, clopidogrel, prasugrel, ticagrelor)
antithrombin (UFH, enoxaparin, fondaparinux)
nitrates (nitroglycerin SL or IV)

69
Q

When would NSTEMI get PCI?

A

within 24 - 48 hours

70
Q

Preferred reperfusion therapy if less than 90 - 120 minute timeframe

A

Percutaneous Coronary Intervention (PCI)

71
Q

Indicated for STEMI if time to treatment is < 6 - 12 hours from symptom onset and patient has STE on EKG

A

TPA [fibrinolytic]

72
Q

When does TPA work best?

A

early
large infarction
anterior infarction

73
Q 
prior intracranial hemorrhage 
AVM 
intracranial neoplasm 
ischemic stroke in last 3 months 
active bleed 
suspected aortic disease or pericarditis
A

absolute CI for fibrinolytics

74
Q

STEMI patient who gets fibrinolytic needs what for at least 48 hours?

A

full dose anticoagulant (UFH, enoxaparin, fondaparinux)

75
Q

WHAT DO YOU WANT TO GIVE YOUR STEMI PATIENTS ??

A

aspirin 325 mg ASAP (reduces mortality by 23%)

76
Q

When would you ever hold aspirin in a patient?

A

severe allergy or active PUD

give clipidogrel if true allergy

77
Q

this is indicated in patients with ACS → reduces the risk of AMI in unstable angina

A

Heparin + ASA

78
Q

how should you titrate your nitrate?

A

titrate to BP not pain reduction

79
Q

How can nitrate worsen infarct in certain instances?

A

inferior infarct that is volume dependent → hypotension exacerbation

80
Q

This agent is antiarrhythmic + anti-ischemic + antihypertensive

A

Beta Blocker

81
Q

How is BB helpful?

A

decreases O2 demand
decreases HR
decreases arterial pressure
decreases myocardial contractility

82
Q

when would you administer BB in STEMI or NSTEMI?

A

PO metoprolo within 24 hours

83
Q

Contraindications for BB in STEMI/NSTEMI

A 
CHF 
decrease CO 
> 70 
BP < 120 
HR > 110 or < 60 
block 
asthma
84
Q

this agent reduces left ventricular dysfunction/dilation → slows development of CHF

A

ACE inhibitor

85
Q

NSTEMI or unstable angina with EF < 40% - give?

A

ACE inhibitor

86
Q

When would you give ACE for STEMI or HF?

A

within first 24 hours

87
Q

what do you usually avoid giving a patient after MI?

88
Q

Coronary vasodilator that suppresses automaticity and protects myocytes → data conflicts on mortality benefit

89
Q

what will most patients (72-100%) in CCU have after AMI?

A

dysrhythmias → A-fib, AV blocks, PVC, V-tach, CHF, pericarditis, papillary muscle rupture, ventricular wall rupture

90
Q

treatment for A-fib in post MI

A

BB → atenolol or metorpolol

anticoagulate

91
Q

3rd degree complete heart block usually presents after which two AMI?

A

anterior

inferior

92
Q

recommended treatment for 3rd degree heart block

A

pacing (won’t reduce mortality though)

93
Q

this rhythm presents commonly shortly after AMI and is usually transient

A

ventricular tachycardia

94
Q

which rhythm do you want to avoid delayed treatment?

95
Q

HF congestion is commonly caused by

A

post MI LV diastolic function

96
Q

when will ventricular free wall rupture occur?

A

1 - 5 days post infarct

97
Q

signs of ventricular free wall rupture

A

hypotension
tachycardia
confusion
agitation

98
Q

Patient who had MI 2 - 8 days prior now has CP + dyspnea + NEW HOLOSYSTOLIC MURMUR (@ LLSB)

A

rupture of intraventricular septum

99
Q

Patient had inferior MI 3 - 5 days prior and now has dyspnea + new HF + pulmonary edema + new holosystolic murmur

A

papillary muscle rupture

100
Q

Patient had AMI 2 - 4 days prior and now has positional CP worse with inspiration and better sitting forward

A

pericarditis

101
Q

Symptomatic treatment for pericarditis

A

ASA or cochicine

102
Q

CP + Fever + pleuropericarditis on EKG → last post MI syndrome presenting 2 - 10 weeks after

A

Dressler Syndrome

103
Q

Treatment for Cocaine or Amphetamine Induced ACS

A

ASA
nitrates
Benzo

104
Q

what do you avoid with cocaine/amphetamine induced ACS?

A

BB for 24 hours

105
Q

when would you need emergent treatment for bradycardia?

A

hypoperfusion/hypotension

106
Q

what is the MC cause of bradycardia?

A

factors outside the cardiac system (ACS, drugs, hypoxia, etc)

107
Q

this drug enhances the automaticity of the heart and is vagolytic

108
Q

SA node fires at < 60 bpm and AV conduction remains intact

A

sinus bradycardia

109
Q

Prolonged PR (> 200 or 0.2 sec)

A

first degree block

110
Q

progressive prolongation of PRI then dropped beat → often due to blocked AV node

A

second degree type I (wenckebach)

111
Q

NO lengthening of PRI → non-conducted beats with P-wave that “march out” → wide QRS

A

second degree type II (Mobitz II)

112
Q

ventricular reate of 30 - 45 bpm + atria firing at 60 - 100

A

third degree (complete) block

113
Q

Treatment for tachycardia in stable patients?

Treatment in unstable patients?

A

stable → IV meds

unstable → electrical therapy

114
Q

first step in resolving tachycardia

A

vagal maneuvers

115
Q

treats tachycardia by blocking AV conduction

116
Q

If patient with tachycardia was unstable or fefractory to meds, what do you do?

A

syncronized cardioversion

117
Q

what should you give patient presenting with A-fib who needs cardioversion - urgent or stable instance?

A

urgent → heparin before or right after

stable → anticoag for 3 - 4 weeks then cardiversion

118
Q

first line in rate control for a-fib or flutter

119
Q

what do you give patients with recurrent paroxysmal atrial fib

A

flecainide or propafenone

120
Q

which arrhythmia is very responsive to electrical cardioversion ?

A

atrial flutter

121
Q

when discharging a patient with a fib or flutter what do you want to bridge their anticoag with?

A

enoxaparin

122
Q

Preferred med for rapid treatment of wide complex tachycardia or new a-fib

A

amiodarone

123
Q

preferred pharmacologic agent for V-tach if stable and have good LV function

A

procainamide

124
Q

disorganized depolarizations with no cardiac output → usually ischemic disease +/- AMI

A

ventricular fibrillation

125
Q

acute elevated BP > 180/120 + end organ damage (brain, aorta, kidneys, eye)

A

hypertensive emergency

126
Q

Profoundly elevated BP WITHOUT end organ damage

A

hypertensive urgency

127
Q

Oral therapy for severely elevated BP

A

labetalol, captopril, losartan, nifedipine, clonidine

128
Q

oral therapy for elevated BP

A

HCTZ, lisinopril, amlodipine

129
Q

goal of treating high blood pressure

A

minimize end-organ damage while avoiding hypoperfusion

130
Q

Umbrella term for DVT and PE

A

venous thromboembolism (VTE)

131
Q

when does thromboembolism occur?

A

when coagulation exceeds removal by fibrinolysis

132
Q

when will you see PE symptoms?

A

when 20% of vasculature is occluded

133
Q

dyspnea unexplained by auscultation + pleuritic chest pain + abnormal CXR and EKG + tachycardia + clear lungs + S3 or split S2

134
Q

EKG with sinus tachycardia + S1Q3T3 + RBBB

135
Q

calf pain elicited by passive foot dorsiflexion

A

Homan’s sign

136
Q

pale or white limb as the result of proximal DVT that causes complete obstruction + increased swelling + increased comparement pressure + extreme pain

A

phlegmasia alba dolens

137
Q

If the leg turns dusky or blue color?

A

phlegmasia cerulean dolens

138
Q

wedge shape lung oligemia on CXR for PE

A

Westermark sign

139
Q

peripheral dome shaped dense opacity on CXR

A

Hampton Hump

140
Q

Treatment for VTE

A

systemic anticoagulation (UFH, LMWH)

141
Q

isolated calf DVT

A

LMWH + warfarin

142
Q

only approved fibrinolytic for PE

A

Alteplace (TPA)

143
Q

two greatest risk factors for occlusive arterial disease

A

smoking and DM

144
Q

MC location for occlusive arterial disease

A

femoropopliteal

145
Q

MC cause of 2/3 of all peripheral emboli

146
Q

Six Ps of arterial occlusion

A

Pain, Pallor, Paralysis, Pulselessness, Paresthesia, Polar

147
Q

How is arterial occlusive pain relieved?

A

hanging feet over the edge of the bed

148
Q

How do you differentiate claudication from occlusion?

A

acute limb ischemia in claudication is NOT relieved by rest or gravity

149
Q

initial therapy for arterial occlusion

A

heparin + ASA

Emergency Medicine (6 decks)

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