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(PA School) Cardiology > EKG ACS > Flashcards

EKG ACS Flashcards

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1
Q

Describe the left main coronary artery (widowmaker)

A

Circumflex – primarily LA and LV
Left lateral leads – I, aVL, V5, V6
Anterior interventricular – anterior myocardium and anterior 2/3 of septum and apex
Anterior leads – V2-4

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2
Q

Describe the right coronary artery

A

Proximal RA and RV
Inferior leads II, III, aVF
Posterior IV branch – posterior 1/3 septum
Posterior leads (reciprocal of anterior leads)

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3
Q

ACS pathophys
1) What is the classic symptom of cardiac ischemia?
2) What causes a mismatch of supply and demand?
3) ~____% stenosis is sufficient to result in exertional angina

A

1) Cardiac chest pain (pressure) = Angina
2) Progressive stenosis of coronary arteries from ASCVD
3) ~ 70%

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4
Q

Describe the characteristics of ACS plaques

A

1) Cap: initially thin = dangerous
2) Lipid core: large is dangerous
3) Inflammatory cells within the plaque: results in instability – dangerous

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5
Q

What limits predicting patient’s risk with ACS?

A

Neither stress test or standard cardiac catheterizations can distinguish a stable from unstable plaque

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6
Q

____________ stabilize the plaque, result in some regression, and are to some degree anti-inflammatory …. All helpful in preventing ACS

A

STATINS

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7
Q

What are the 3 components of ACS Dx?

A

1) History and PE
2) EKG changes
3) Cardiac enzymes

(No one component by itself is sufficient to diagnose)

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8
Q

Characteristic EKG changes with ACS begin with onset and evolve over time; serial EKGs @ ________ minute intervals

A

15-30

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9
Q

ACS EKG changes:
1) What do you see first?
2) What else changes?
3) What else should be noted?

A

1) Hyper acute T-waves early, then T wave inversion
2) ST segment changes
3) Appearance of Q waves

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10
Q

ECG criteria for ACS: What is the best baseline?

A

T-G

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11
Q

ECG criteria for ACS: Everything is 1 mm (except V2 &V3); explain what this means

A

ST elevation or depression – 1 mm measured 2 small boxes after J-point
Q-Waves – more than 1mm wide x 1mm deep
Classic – more than1mm and/or depth 25% or more of R-Wave height

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12
Q

ECG criteria for ACS: Everything is 1 mm in at least _________ contiguous leads; explain

A

1) Left lateral = I, aVL, V5-6
2) Anterior (posterior) = V2,3,4
3) Inferior = II,III, aVF

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13
Q

List the ECG criteria for ACS

A

1) Everything is 1 mm (except V2 &V3)
-ST elevation or depression; 1 mm measured 2 small boxes after J-point
-Q-Waves – more than 1mm wide x 1mm deep
-Classic – more than1mm and/or depth 25% or more of R-Wave height
2) Should be in 2 contiguous leads:
-Left lateral = I, aVL, V5-6
-Anterior (posterior) = V2,3,4
-Inferior = II,III, aVF

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14
Q

T wave changes reflect myocardial ischemia (early ACS); are these changes permanent? Explain

A

1) Potentially reversible
2) Myocardial cell death – T waves persist for months or years

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15
Q

Describe T wave changes in ACS

A

1) T wave changes reflect myocardial ischemia (early ACS)
-Potentially reversible
-Myocardial cell death means T waves persist for months or years
2) Onset of MI = hyperacute T waves = tall or peaking T waves… Nearly same as QRS in same lead
3) Few minutes to hours after onset MI, T waves invert

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16
Q

What are the exceptions to T wave inversion in ACS?

A

1) Pseudonormalization – patients with T wave inversion, ischemia can cause them to revert to normal – compared to previous EKG
2) Normal to see T wave inversion in leads V1-3 in children and young adults, and in AA athletes
3) Isolated inverted T wave in lead III is a normal variant
4) T wave inversion expected in lead aVR

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17
Q

Define pseudonormalization

A

Patients with T wave inversion (due to prior MI), ischemia can cause them to revert to normal (compared to previous EKG)

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18
Q

It’s normal to see T wave inversion in leads V1-3 in who?

A

Children and young adults, and in AA athletes

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19
Q

1) Isolated inverted T wave in lead ______ is a normal variant
2) T wave inversion expected in lead ______

A

1) lead III (3)
2) lead aVR

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20
Q

What happens first in ST segment elevation

A

1) T wave changes = Hyperacute
-T wave inversion – may persist for months or years

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21
Q

Describe the second change that occurs acutely in evolving STEMI

A

1) ST elevation (STE); STE usually = myocardial injury
-STE usually return to baseline in a few hours
-Persistent STE often indicates ventricular aneurysm

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22
Q

Define early repolarization

A

J-point elevation along with small notch or slur in the downslope of R wave

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23
Q

J point elevation:
1) What is it very common in?
2) What is the J point?
3) Who is it often seen in? In what leads?

A

1) Normal hearts
2) The site where the ST segment takes off from the QRS complex
3) Young healthy patients, especially leads V-1,2,3

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24
Q

Notch or slur in the downslope of R wave + J point elevation = what?

A

Early repolarization

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25
When is STE bowed upward (like a frowny face) and merge is imperceptible with the T wave?
MI
26
J point elevation, STE bowed down (smiley face) and T wave maintains is ___________________
independent wave form
27
Criteria favor Dx of ______________- vs. JPE/early repolarization
STEMI
28
What are the guidelines to diagnose a STEMI?
1) Plus, ST elevation must be present in at least 2 contiguous leads 2) Compare to old ECG to see if J-point elevation present or STE is new 3) J-point elevation will not change on serial ECGs – STE evolves as MI evolves
29
Describe Brugada syndrome (a genetic condition caused by dysfunctional cardiac Na+ channels)
1) Sudden cardiac death can occur spontaneously 2) RBBB and ST elevation in V1-3 with peculiar peaked down sloping shape, esp in V1-2 3) Management is ICD to counter VF
30
What is responsible for nearly ½ of sudden deaths in young healthy patients without structural heart disease like HoCM?
Brugada syndrome
31
1) Appearance of new Q waves indicate irreversible myocardial cell death and is diagnostic of MI; when do these occur? 2) How long do they last?
1) Usually appear within several hours of onset of STEMI but may take several days to evolve -ST segment usually has returned to baseline by the time Q waves have appeared 2) Q waves usually persist for life
32
Why do new Q waves appear?
1) Region of myocardium dies – becomes electrically silent 2) Electrical vectors of the heart directed AWAY from site of infarction 3) Electrode overlying the infarct will record a deep negative deflection = Q wave
33
Describe reciprocal changes
1) Leads distant to the site of infarction will see an apparent increase in electrical forces moving toward them = tall R wave 2) Applies to T wave & ST segment changes as well as Q waves
34
Reciprocal changes: 1) Give an example 2) When these changes are present, what Dx is more likely?
1) STE in lead II with reciprocal ST depression in V3 2) STEMI
35
Normal Q waves: 1) Small septal Q waves normal in what leads? 2) Isolated Q waves also normally seen in what lead?
1) Left lateral leads – I, aVL, V5-6 2) Lead III = normal variant if not also seen in other inferior leads (II, aVF)
36
Describe Pathologic Q waves
1) Q wave > 0.04 sec duration (1 small box) 2) Depth of Q wave must be at least 25% the height of the R wave in the same QRS complex 3) Noted in 2+ contiguous leads
37
If you note significant Q waves on EKG in a patient “incidentally” on 12 lead EKG in whom you do not suspect MI …. Look closely for_______________ preceding the negative wave …. This is a S wave!
small R wave
38
Summary: EKG changes of an evolving STEMI
1) Acutely, the T wave peaks and then inverts – indicates myocardial ischemia and progression If true MI, then T wave may remain inverted for months to years 2) Acutely, STE and merges with T wave – reflects myocardial injury If true MI, then STE usually returns to baseline within a few hours 3) New Q waves appear within hours to days – reflect MI Usually persist for life
39
What is the one thing that would return to baseline after a few hours if an acute MI?
STE
40
What does the RCA perfuse?
1) AV nodal branch 2) RCA perfuses most of the RV 3) Right marginal branch and continues as posterior IV septal branch
41
LCA divides into the ______________________ and left ________________
anterior IV branch (LAD); circumflex
42
What supplies the AV node in ~10% of pts?
LCA
43
Inferior infarct: 1) What is it? 2) What 3 leads is it seen in? What kind of changes? 3) What is an exception?
1) RCA occlusion 2) Leads II, III, aVF -Reciprocal changes in anterior and left lateral leads -Common to see T wave inversion in aVL during acute inferior MI; early sign of inferior MI 3) 50% of Q waves in 6 months from inferior MI will lose criteria for path Q waves
44
Lateral infarct: 1) What is it? 2) What 3 leads is it seen in? 3) Where may you see reciprocal changes?
1) Occlusion of Left circumflex br. of LCA 2) Leads I, aVL, V5-6 3) Reciprocal changes may be seen in inferior leads
45
Anterior infarct: 1) What is it? What leads is it seen in? 2) When is it an anterolateral MI? What leads is this seen in? 3) Where are reciprocal changes seen?
1) Most often occlusion of the Anterior IV br. of LCA (LAD) Leads V1-6 (V2,3,4) 2) If left main occluded; Leads V1-6, I, aVL 3) Reciprocal changes when seen are in inferior leads
46
What may signify an anterior MI…but not specific for anterior MI….may be seen in RVH, improper lead placement, obesity?
R wave in V3 is not larger than 3 mV
47
What often involves bulk of LV myocardium & has a devastating clinical affect?
Anterior stemi
48
Describe DeWinter's T-Waves
1) Patient with CP 2) Upsloping ST depression leading into tall symmetric hyperacute T waves in precordial leads = anterior IV branch (LAD) infarct = anterior infarct 3) Considered equivalent as ST segment elevation 4) Seen in ~ 2% of LAD MI
49
Where is DeWinter's T-waves seen?
V2-V5 and kinda in V6
50
Describe Wellens' waves
1) Deeply inverted or biphasic T waves in leads V2-4 predict proximal occlusion of the anterior IV branch of LCA (LAD) – cause for concern 2) Upright portion of T wave occurs first followed by inversion of terminal portion of T wave, +/- ST segment elevation
51
"Upright portion of T wave occurs first followed by inversion of terminal portion of T wave, +/- ST segment elevation" describes what?
Wellens' waves
52
Posterior infarct 1) Define this 2) Is it easily diagnosed? 3) What does diagnosis require?
1) Occlusion of RCA (same artery involved in most inferior infarcts), rarely occurs in isolation; posteroinferior or posterolateral infarct 2) Most often misdiagnosed, especially if occurs in isolation (10% of posterior MI) 3) Diagnosis requires finding reciprocal lead changes in the anterior leads, i.e., ST depression and Tall R waves in anterior leads – mirror images of anterior MI on EKG
53
NSTEMI: 1) What is it? What 2 things are absent? 2) Is it localized? Explain
1) Subendocardial infarction No ST elevation or Q wave formation 2) Localized just like STEMI except - EKG changes are T wave inversion and ST depression
54
NSTEMI: 1) Is it more or less common than STEMI? 2) Is it more or less lethal? Explain
1) More common than STEMI 2) Lower initial risk of mortality; higher risk of for further infarction and mortality than STEMI
55
Takotsubo cardiomyopathy “broken heart syndrome”: 1) What does it mimic? 2) What may be mildly elevated? What may develop?
1) Closely mimic acute STEMI with T wave inversion and ST elevation -Clean coronary arteries 2) Troponins levels may be mildly elevated May develop transient HF – “apical ballooning syndrome”
56
Takotsubo cardiomyopathy “broken heart syndrome”: 1) What are some potential causes? 2) Other causes of MI with normal arteries (MINOCA) incl what? 3) How does it resolve?
1) May be general vasomotor dysfunction as is associated with Reynaud's and migraine HA 2) small vessel CAD, myocarditis, coronary vasospasm, spontaneous coronary artery dissection 3) Usually spontaneously resolves over weeks/months, may reoccur
57
Describe Angina (stable or unstable)
EKG may demonstrate T wave inversion & ST depression Between attacks, EKG usually normal Troponins are within normal limits set by laboratory
58
Describe Prinzmetal angina
Angina + ST elevation Can occur at any time (dose not depend on progression of ASCVD or exertion) Coronary artery spasm in absence of significant ASCVD ST elevation reflects reversible transmural injury ST segments often will not have the rounded domed shaped appearance of true infarct & return quickly to baseline with NTG
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(PA School) Cardiology (53 decks)

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