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Rosens > 64. ACS > Flashcards

64. ACS Flashcards

1
Q

ACS - what does this refer to?

A

constellation of clinical diseases occuring as a result of myocardial ischemia or infarction:
unstable angina - AMI

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2
Q

What is the leading cause of death among adults in industrialized countries?

A

CAD

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3
Q

Of those who present and have an MI, how many die within 30d?

A

30%

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4
Q

What factors play into prognosis of mortality post MI?

A

extent of infarct
time to intervention
whether pt underwent revascularization
residual LV function

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5
Q

How many MI’s are missed in the ED?

A

2% of pt with ACS

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6
Q

What is stable angina?

A

not ACS - transient, episodic CP from ischemia typically reproducible with physical or psychological stress

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7
Q

Canadian Cardiovascular Society Stable angina: class I defn

A

no angina with ordinary PA

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8
Q

Canadian Cardiovascular Society Stable angina: class II defn

A

minimal limitation of normal activity as angina occurs with exertion or emotional stress

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9
Q

Canadian Cardiovascular Society Stable angina: class III defn

A

severe limit of orginary PA as angina occurs even with exertion under normal physical conditions

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10
Q

Canadian Cardiovascular Society Stable angina: class IV defn

A

cannot do physical activity without discomfort as anginal sx occur at rest or very minimal PA

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11
Q

What is unstable angina?

A

new onset, occurrin at rest or minimal exertion
worsened from previous stable pain

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12
Q

What is rest angina?

A

at rest, lasting longer than 20 mins and occurs within 1 week of presentation

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13
Q

Increasing or progressive angina defn

A

previously known becomes for freq, longer duration, incr of one class (CCS) within last 2 months of at least class III

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14
Q

What are the pathophysiologic events underpinning unstable angina?

A

plaque rupture with thrombus and vasospasm

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15
Q

What is variant/Prinzmetal angina?

A

coronary artery vasospasm at rest with minimal fixed coronary artery lesions
may be relievedd by exercise or NTG
ECG looks like stemi

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16
Q

Myocardial infarction key defn

A

trop values above 99% ULN and at least one:
sx of MI
ECG changes: new stsegment or t wave change, development ofpathologic q wave
imaging eidence of loss of viable myocardium or regional wall motion abnormality consistent with ischemia
Angio or autopsy evidence of cornary thrombus

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17
Q

Type I MI defn

A

spont MI = ischemic from primary coronary event like a plaque erosion, rupture, fissuring or dissection with accompanying thrombus and vasospasm

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18
Q

Type II MI defn

A

demand supply mismatch

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19
Q

Type III MI defn

A

sudden unexpected cardiac death - including cardiac arrest, often with new MI signs - STsegment elevion, new LBBB

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20
Q

Type IV MI defn

A

assoc with coronary instrumentation - PCI

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21
Q

Type V MI

A

coronary artery bypass grafting
elevation of trop above 99% indicates periprocedural myocardial necorsis
If this incr is >5x ULN and: new pathologic q wave or LBBB, angiiographic documented new graft or native coronary artery oclusion or imaging evidencen ew loss viable myocardium

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22
Q

How is myocardial oxygen consumption defined?

A

HR
afterload
contractility
wall tension

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23
Q

What is characteristic finding of CAD?

A

thickening and obstruction coronary vessel artrial lumen by atherosclerotic plaque

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24
Q

Which atherosclerotic plaques are more likely to rupture?

A

fibro-lipid plaque - lipid rich core separated from arterial lumen by fibromuscular cap

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25
Q

How does thrombus formation occur in ACS?

A

endothelial damage and AS plaque disruption
platelet rich thrombus then occludes vesel lumen

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26
Q

What are considered most critical factors in infarction?

A

acute events of plaque rupture
plt activation
thrombus formation

rather than severity of underlying disease

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27
Q

ACS importnat factor: Vasospasm: what occurs in infarction?

A

central and CNS input incr, causing vasomo hyperactivity and spasm
symp stim may incr epi and serotonin and incr plt aggregation and neutrophil mediated vasoconstriction

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28
Q

Myocardial ischemia/infarction: what issues occur at the cellular level?

A

ca, o2, cellular elements to damaged myocardium cause further reperfusion injury, prolonged ventricular dysfunction or reperfusion dysrhytmias
neutrphils are key in reperfusion injuries as they occlude cap lumens, decr blood flow, accel inflamm response nad produce chemoattractants, proteolytic enzyme, ROS

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29
Q

Which populations may not have your classic ACS signs and symptoms?

A

women
OA
diabetes

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30
Q

Angina true defn

A

tightening

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31
Q

If pain does radiate down arm in ACS, where is typical?

A

ulnar

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32
Q

Classic sx of angina - “anginal equivalents”

A

dyspnea, nausea, vomiting, diaphoresis, weakness, dizziness, excessive fatigue, or anxiety.

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33
Q

Name 10 ddx of chest pain

A

AMI
stable angina
pericarditis
pneumonia
ptx
pleurisy
boerhaave
pud
esophageal spasm
cholecystitis/biliary colic
herpes
unstable angina
prinzmetal angina
myocardial/pulmonary contusion
pe
phtn
ao dissection
gerd
gastritis/esophagitis
MW tear
pancreatitis
msk pain

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34
Q

MC anginal equivalent sx

A

dyspnea

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35
Q

Nontradiational acs pain factors

A

atypical feat of pain, presence of equivalent sx

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36
Q

Traditional RF for CAD

A

age, tobacco smoking, hypertension, diabetes mellitus, hyper- lipidemia, and family history of AMI at an early age (usually <50 years).

Additional risk factors to consider include markedly elevated body mass index, artificial or early menopause, and cocaine (or other sympathomimetic agent)

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37
Q

Less common RF for CAD but important to consider

A

antiphospholipid syndrome
HIV
RA
SLE

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38
Q

List 5 early complications of AMI

A

dysrhythmias - brady, AV block; tachy - VF, VT
LV free wall rupture
papillary m rupture with acute MR
iv septal rupture
stroke - embolic

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39
Q

When does LV free wall rupture occur?

A

1/3 of cases first 24h, others 3-5d

esp anterior wall stemi

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40
Q

What finding is suggestive of LV free wall rupture?

A

pericardial effusion

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41
Q

When does IV septum or pap muscle rupture tend to occur?

A

3-5d post large MI

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42
Q

Findings of new iv septum rupture?

A

holosystolic murmur
flash pulmonary edema
HD collapse

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43
Q

infarct vs Dressler pericarditis defn

A

AMI, can occur early or in a delayed fashion; the former is termed infarct-related pericarditis, and the latter is known as post-MI or Dressler syndrome - 1 week to several months

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44
Q

ECG findings consistent with stemi: females of any age

A

new ST elevation of greater than 1 mm in at least two contiguous leads except for leads V2 and V3, where diagnostic cut-offs are as follows: elevation 1.5 mm or greater in females of any age

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45
Q

ECG findings consistent with stemi: male <40y

A

new ST elevation of greater than 1 mm in at least two contiguous leads except for leads V2 and V3, where diagnostic cut-offs are as follows: elevation 2.5 mm or greater in males less than

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46
Q

ECG findings consistent with stemi: male >40y

A

new ST elevation of greater than 1 mm in at least two contiguous leads except for leads V2 and V3, where diagnostic cut-offs are as follows: 2 mm or greater in males greater than 40 years of age

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47
Q

Earliest electro graphic finding in STEMI

A

Hyper QT wave

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48
Q

What is the I point?

A

Junction between the QRS complex and the ST segment

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49
Q

What is differentiation of the SC segment elevation and ECG in BER?

A

Concavity of the ST elevation, more prominent as the corresponding S wave or negative deflection of the QRS complex becomes deeper

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50
Q

What is ST segment depression generally represent?

A

Sub endocardial ischaemia

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51
Q

Differential diagnosis of ST segment depression

A

Am I
Repolarization abnormality of LVH
Bundle branch block
Ventricular paste rhythm
Digoxin effect
Hyperkalemia
Hypokalemia
PE
ICH
Myocarditis
Related ST segment depression
Post cardioversion
Tacky dysrhythmia.
Pneumothorax

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52
Q

When is it normal to have tea wave and version i.e. what leads?

A

V1.
Possible and V2 to be normal

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53
Q

Definition of Wellen syndrome

A

The scheme, tea wave inversion: deep, symmetrical, T-wave, inversions, i.e. type one or by phasic T wave changes type two and the anterior precordial leads suggestive of myocardial, ischaemia and typically manifest in a pain-free state

54
Q

Where is the occlusion in Wellen syndrome?

A

LAD

55
Q

Differential diagnosis of T-wave inversion

A

ECS
Ventricular hypertrophy
Bundle branch block
Myocarditis
Pericarditis
PE
Pneumothorax
Wolff-Parkinson-White
Cerebral vascular accident
Hypokalemia
G.I. disorder
Hyperventilation
Persistent juvenile pattern.
Normal variant

56
Q

What time does it take for pathologic Q wave to develop?

A

8 to 12 hours

57
Q

Septal info leads

A

V1 and V2

58
Q

Anterior versus lateral wall leads

A

Anterior equals B1 – before, lateral equals one, AVL, V5, V6

59
Q

Right ventricular wall AMI will see what lead ST segment elevation?

A

V4R

60
Q

What lead would you expect to see elevated in a posterior wall AMI versus depression?

A

Elevation in V-8, V9 and depression in V1 to be three

61
Q

What artery serves the anterior wall of the heart?

A

LAD

62
Q

ST segment elevation and leaded AVR is concerning for what occlusion?

A

Left main coronary artery and elevation greater than 0.5 MV is approximately 83% specific for left main disease

63
Q

What is a de Winter tea wave?

A

Prominent tea wave with joint depression, producing ST segment depression seen in precordial leads, coupled with ST segment elevation in AVR

64
Q

What does a de Winter tea wave indicate in terms of vessel concerning?

A

Proximal LAD

65
Q

Leads two, three and AVF indicate inferior wall apart. What artery supplies this?

A

RCA

66
Q

If patients with inferior wall hearts are not supplied by the RCA, what is the other artery that supplies them?

A

Left circumflex

67
Q

What findings on an ECG are sensitive for a right coronary artery inclusion

A

Elevation inferior leads that is greater in lead three ST segment then lead to along with ST segment depression in AVL, one or both

68
Q

What do EKG findings of ST segment elevation and lead V1 and the presence of an ST segment elevation inferior leads suggest?

A

Inferior am I with concomitant right ventricular infarction

69
Q

What percentage of inferior or inferior lateral infractions also have posterior infarcts?

A

15 to 20%

70
Q

What are indications that you may have a posterior infarction?

A

Reciprocal ST segment change in the right precordial leads, 1 to 3, horizontal, ST segment, depression, upright, tea, wave, tall, wide, our wave and our wave amplitude to S wave amplitude ratio greater than one

Post your leads eight and nine

71
Q

What percentage of inferior heart attacks have associated infarction of the right ventricle?

A

33%

72
Q

What do you expect to see in an inferior heart attack along with a right ventricular infarction?

A

ST segment elevation in Leeds, two, three, ABF and ST selling elevation in V1

With ST segment and elevation in lead three greater than leads to and AVF when coexists

73
Q

Name six characteristics of BER that you will see on an ECG

A

ET segment elevation.
Upward concavity of the initial portion of the ST segment.
Notching of the terminal portion of the QRS complex at the JP point
Symmetric concordant T wave of large amplitude
Diffuse ST segment elevation.
Relative temporal stability over the short term

74
Q

What ECG changes will you see with a left ventricular aneurysm?

A

ST segment elevation of any morphology typically in Leeds B1 to V6 and leads one and AVL.
Q waves may be present.
Typically the amplitude of a wave to the QRS complex exceeds 0.36 in any single lead equals more likely whereas less than 0.36 in all leads, likely ventricular aneurism

75
Q

Sgarbossa criteria

A

ST segment elevation at least 1 mm that is concordant with the QRS complex.
ST segment depression at least 1 mm in lead V1, V2 or V3
ST segment elevation of at least 5 mm that is discordant with the QRS complex or in the modified version, excessive discordance by ST to S ratio of greater than 0.25 is considered diagnostic of AMI

76
Q

What is Takutsubo?

A

Left apical ballooning ballooning syndrome with STE without obstructive CAD evidence

77
Q

What type of MI, despite no STE needs urgent Revasc?

A

Acute posterior mi

78
Q

Where do posterior leads go?

A

V8 and 9 at same level of v4 to 6 but under Scapula

79
Q

What leads are used for RV MI? Which are most sensitive?

A

V1R to 6
V4R -

80
Q

When should additional ecg leads be used?

A

St segment changed in more than one less
Equivocal changed in inferior or lateral leads
All inferior stemi
Hypotension in ACS

81
Q

What is the recommended timing for a serial ecg?

A

Q20 mins

82
Q

What is the definition of an elevated troponin?

A

Above 99% in healthy population

83
Q

High trop but no ACS - list 5 other cardiology causes

A

HF
LVH
Myocarditis
Pericarditis
Non penetrating cardiac trauma

84
Q

What non cardiac causes can raise troponin?

A

Physical exertion
Renal insufficiency
Multiple trauma
PE
Sepsis
Multi organ failure

85
Q

What does bnp help with in ACS?

A

Long and short term mortality predictor

86
Q

When should one exercise stress test someone?

A

Resolution sx
Low to mod suspicion ACS

87
Q

False positive ddx of stress test

A

Aortic stenosis or insufficiency
HCM
Htn
Av fistula
Anemia
Hemoglobinopathies
Low CO states
Copd
Dig toxicity
Hyperventilation
MVP
bbb

88
Q

Findings on pocus consistent with MI

A

Regional systolic wall abnormalities
Complications - ac MR, pericardial effusion, ventricular septal and free wall rupture, intracardiac thrombus

89
Q

What medication is ordered for a stress test and what does it do?

A

Dipyridamole and adenosine to induce myocardial perfusion and reveal ischemia in susceptible patients

90
Q

Myocardial scintegrsphy - what is this?

A

Tec-99 used to show slow redistribution to ischemic myocardium. High sn

91
Q

What does the heart score tell you?

A

Risk of MACE within 30d

92
Q

HEART score components ;list them

A

Score 0-2
History
ECG
Age
Rf
Trop

93
Q

HEART score - history 0-2 points

A

0 - not sounding ACS
- 1 mixed omelet traditional and not
2 traditional

94
Q

HEART SCORE - ecg

A

0 N
1 - no st Depn but has repop abnormal- bbb, lvh, dig effect, implanted RV pm, past mi +- unchanged repol abnormalities
2 - ste or depn typically new

95
Q

HEART SCORE - age

A

0 - less than 45
1- 45-64
2- 65

96
Q

HEART SCORE - RF

A

0 - none
1- 1-2
2- 3 or more RF or documented cardiac or systemic AS vascular disease

Ie DM, smoker, htn, high cholesterol, obesity, family hx of CAD

Systemic disease: pad, mi, pci, stroke

97
Q

HEART SCORE - trop

A

0 - < discrimination level
1- elevated 1-3x normal
Trip > 3x normal

98
Q

Heart score - at what level to consider adm vs not even if repeat trop negative?

A

<4 okay
>|= 4

99
Q

5 key aspects of ACS physiology that guide management

A
  1. Endothelial damage through plaque disruption and irregular luminal lesions with shear injury
  2. Platelet aggregation
  3. Thrombus formation causing partial or total lumen occlusion
  4. Ca vasospasm
  5. Reperfusion injury caused by oxygen free radicals, ca and neutrophils
100
Q

Time to benefit of STEMI and reperfusion therapy - how does this. Change over time?

A

Max within 1 hour
Less within 2 (40-60% of max benefit)
Then dwindled to 15-40% up to 6 hours

101
Q

Under pci within ? Mins

A

90

102
Q

If no access pci for stemi, receive fibrinolytic therapy within ? Mins of arrival

A

30

103
Q

4 D’s to address delays in mi to cath

A

Door
Data ecg
Decision
Drug

104
Q

Meds in ED for ACS

A

Aspirin first off
Once confirmed ACS then clopidogrel or ticagrelor
Antithrombin agent - heparin, enoxaparin

Stemi: fibrinolytic - streptokinase/tpa/tenecteplase

CP, opioids: NTG

105
Q

What 4 meds may be considered for ACS once in patient?

A

Statin
Ccb
Beta blocker
Acei

106
Q

What o2 level to target in ACS?

A

> /94%

107
Q

What MI should you not give ntg in ?

A

Any if hypotension

But particularly inferior with Rv infarct as well

108
Q

What SBP hold ntg at for mi?

A

<90

109
Q

If ntg spray or patch not feasible, what level of infusion?

A

10 microgram per min titrated to pain sx

110
Q

Can you give metoprolol in hf?

A

No

111
Q

Aspirin mechanism ACS

A

Irreversible bind of cyclooxygenase and removed plt for 8-10d thus stopping production of thromboxane 2 which increases plt aggregation

112
Q

Aspirin mechanism ACS

A

Irreversible bind of cyclooxygenase and removed plt for 8-10d thus stopping production of thromboxane 2 which increases plt aggregation

113
Q

What type of meds are clopidogrel and ticagrelor

A

P2y12 receptor inhibit agent to stronger irreversible inhibit platelet aggregation for duration of plt life

ticagrelor does not require heparin activation

114
Q

Concerns of ticagrelor over plavix

A

More bleed risk

115
Q

How long should clopidogrel or ticagrelor be held if going for cabg?

A

24h min

116
Q

Indication for glycoprotein iib/iiia receptor inhibitor ; abciximab in ACS?

A

Only useful if known undergoing pci
Not usually given ed

117
Q

How does UFH work?

A

Antithrombin iii binding to inactivate ii/thrombin and activate factor X so cannot fibrinogen to fibrin

Also inactivate xai and is through antithrombin and interaction with plt

118
Q

UFH dose

A

Initial bolus 60u per kg to max 4000 u and infusion 12u/kg/hr to goal aPTT 1.5-2.5

119
Q

LMWH mechanism

A

Similar to UFH approx 1/3 mw of heparin - 1/3 bind to Antithrombin iii, remaining to factor xa

120
Q

Why use LMWH over UFH

A

Easier admin
Greater bioavailability
More consistent therapeutic response in pt
Longer serum half life

Some greater benefit overall for high risk non stemi who are treated immediate without pci - vs if stemi and immediate recommend UFH

121
Q

CI to heparin therapy in ACS

A

Ongoing hemorrhage
Predisposition to same

122
Q

Fondaparinux: what is this?

A

Selective factor xa I

123
Q

Fondaparinux pros and cons ACS

A

Pro: reduced risk hemorrhage, mi and death compared to heparins

Con; increased risk of cath associated thrombi during pci - needs UFH when invasive strategy chosen

124
Q

When to give fibrinolytic?

A

Stemi NOT for NSTEMI
NOT for older than 75 as risk hemorrhagic stroke

Onset of ischemia within 12 hours (best within 6 hours)
Anticipated primary pci will not occur in timely fashion

NOT if bp persistently higher than 200/120
Relative CI if active diabetic hemorrhagic retinopathy
Not if cpr > 10 mins or extensive chest trauma
Hx of stroke or tia
Recent surgery (relative) - within 2-4 weeks

Watch closely if cardiogenic shock or hf (pci preferred5

125
Q

What outcomes is pci better than fibrinolytic in?

A

More eligibility
Lower risk Ic bleed
Higher initial reperfusion
Earlier definition of coronary anatomy
Safe early hospital discharge

126
Q

Is rescue pci significantly better than conservative management?

A

Not apparently per lit

127
Q

If you can get pci within 90 min should you get fibrinolytic?

A

No!!!
Worse outcomes

128
Q

Why is fibrinolytic therapy not an option in cardiogenic shock ACS?

A

Poor perfusion didn’t allow thrombus to be exposed

129
Q

Most frequent cause of VT of Vfib OHCA

A

ACS

130
Q

Unfavorable OHCA presentations

A

Unwitnessed arrest
Initial nonshockable rythm
No bystander intervention
Prolonged arrest time > 30 min
Ongoing CPR at Ed arrival
Abnormal studies: ph <7.20, lactate > 7
Age > 85
ESRD
Noncardiogenic cause of arrest.

Rosens (48 decks)

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