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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

32
Q

Classic sx of angina - “anginal equivalents”

A

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

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

34
Q

MC anginal equivalent sx

A

dyspnea

35
Q

Nontradiational acs pain factors

A

atypical feat of pain, presence of equivalent sx

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)

37
Q

Less common RF for CAD but important to consider

A

antiphospholipid syndrome
HIV
RA
SLE

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

39
Q

When does LV free wall rupture occur?

A

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

esp anterior wall stemi

40
Q

What finding is suggestive of LV free wall rupture?

A

pericardial effusion

41
Q

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

A

3-5d post large MI

42
Q

Findings of new iv septum rupture?

A

holosystolic murmur
flash pulmonary edema
HD collapse

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

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

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

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

47
Q

Earliest electro graphic finding in STEMI

A

Hyper QT wave

48
Q

What is the I point?

A

Junction between the QRS complex and the ST segment

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

50
Q

What is ST segment depression generally represent?

A

Sub endocardial ischaemia

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

52
Q

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

A

V1.
Possible and V2 to be normal

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

Page 19 starting at Takotsubo

A

Rosens (40 decks)

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