Weeks 13/14 Quiz on Myocardial Ischemia and Acute Coronary Syndrome

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95 Terms

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what is an essential first-line tool used to diagnose ischemia and infarction?

EKG

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acute coronary syndrome (ACS)

A blanket term used to represent any symptoms related to

- unstable angina

- non-ST elevation myocardial infarction

- acute ST elevation myocardial infarction

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what is the diagnosis of acute coronary syndrome based on?

EKG and troponin levels

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troponin

protein released as a result of myocardial injury

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when does troponin show up in the blood in acute coronary syndrome?

may take up to 3 hours

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when do EKG changes occur in acute coronary syndrome?

may show within minutes

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diagnosis of unstable angina

- absence of ST elevation

- negative troponin

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diagnosis of non-ST elevation MI

- absence of ST elevation

- positive troponin

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diagnosis of ST elevation MI

- ST elevation

- positive troponin

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in ACS, what will changes on the EKG depend on?

- amount of time

- amount of myocardium that is affected

- location of the myocardium affected

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normal ST/T

represents ventricular repolarization

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where are the first signs of ischemia and infarction found on EKG?

ST/T

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ST segment

should be isoelectric

<p>should be isoelectric</p>
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T wave

- upright in all leads except aVR and V1

- height <5 mm precordial leads, <10 mm in limb leads

- asymmetric, slow rise to top then quick drop

<p>- upright in all leads except aVR and V1</p><p>- height &lt;5 mm precordial leads, &lt;10 mm in limb leads</p><p>- asymmetric, slow rise to top then quick drop</p>
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repolarization abnormalities in myocardial ischemia/infarction

- ST segment depression/elevation

- inverted or flat T waves

- hyperacute T waves

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depolarization abnormalities in myocardial ischemia/infarction

- occurs later

- abnormal Q waves

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EKG changes in ACS

- ST depression or elevation

- hyperacute (tall) T waves

- inverted T waves

- abnormal Q waves

- normal EKG

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fourth universal definition of MI (2018)

- new horizontal or down-sloping ST depression ≥0.5 mm in two anatomically contiguous leads or

- T-wave inversion >1 mm in two anatomically contiguous leads with prominent R wave or R/S ratio >1

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step 1 of evaluating ST elevation

- compare voltage of ST segment to TP segment (what should be the isoelectric baseline)

- note the number of blocks that separate the voltage height/depth (>0.5 mm)

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step 2 of evaluating ST elevation

note the morphology (horizontal, down-sloping, upsloping, etc.)

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T wave inversions

- T waves that flip from normal upright position

- indicative of ischemia if at least 1 mm deep

<p>- T waves that flip from normal upright position</p><p>- indicative of ischemia if at least 1 mm deep</p>
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ST/T wave concordance

T waves are normally upright in all leads with tall R waves and inverted where the S wave is dominant

<p>T waves are normally upright in all leads with tall R waves and inverted where the S wave is dominant</p>
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nonspecific ST/T waves

- T wave inversions/flattening

- differ from task force criteria

- can be signs of ischemia but may also be due to medications, hypertrophy, electrolyte abnormalities, etc.

- serial EKGs can help to find dynamic changes

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a normal EKG does not eliminate the possibility of an acute cardiac event

true

1 multiple choice option

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inferior leads

II, III, aVF

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inferior leads represent

right coronary artery (RCA)

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anterioseptal leads

V1, V2

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anterioseptal leads represent

left anterior descending (LAD)

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strictly anterior leads

V3, V4

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strictly anterior leads represent

left anterior descending (LAD)

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anteriolateral leads

V5, V6

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anteriolateral leads represent

left anterior descending (LAD)

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high lateral leads

I, aVL

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high lateral leads represent

left circumflex (LCX)

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about how many initial EKGs were normal in patients with an acute MI?

15-20%

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if the patient continues to have signs and symptoms consistent with ischemia/infarction, an EKG must be repeated

at least every 15-30 minutes

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as injury progresses, the EKG

will continue to change

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EKG findings associated with ischemia

- ST depression

- T wave inversion

- hyperacute T waves

- straightening of T waves

- isolated T wave inversion in aVL

- new upright T in V1 (NUTV1)

- Wellens' syndrome

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hyperacute T waves

- symmetrical, broad-based waves that are taller than normal

- often the earliest sign of acute ischemia

- serial EKGs should be performed

- can be first sign of impending STEMI

- may be so large that the QRS will fit inside

<p>- symmetrical, broad-based waves that are taller than normal</p><p>- often the earliest sign of acute ischemia</p><p>- serial EKGs should be performed</p><p>- can be first sign of impending STEMI</p><p>- may be so large that the QRS will fit inside</p>
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straight T waves

- often in association with hyperacute/tall T waves

- R-T sign or "checkmark" sign

- should be considered ischemia until proven otherwise

<p>- often in association with hyperacute/tall T waves</p><p>- R-T sign or "checkmark" sign</p><p>- should be considered ischemia until proven otherwise</p>
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T wave inversion in aVL

- isolated

- high specificity for LAD occlusion (86.9%)

- seen in only 9.8%

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new upright T wave in V1 (NUTV1)

- T wave should be inverted in V1

- association with coronary artery disease

- if new finding in patient with symptoms of angina, ischemia should be considered

- 84% had significant CAD

- most frequently associated with LCX and/or RCA stenosis >75%

- if old EKG is available, look for T wave that is taller in V1 than V6

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Wellens' syndrome

- first described in 1982

- deep symmetrical T waves in V2 and V3 (specific for critical stenosis of LAD)

- sent home all patients in first study, and 75% returned with large anterior MI

- second study: admitted all, all 180 underwent cath, all 180 had stenosis of LAD (50-100% with 89% average)

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Wellens' syndrome type A

biphasic T waves in leads V2 and V3 (25%)

<p>biphasic T waves in leads V2 and V3 (25%)</p>
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Wellens' syndrome type B

- deeply inverted T wave in V2 and V3

- may spread to other precordial leads (75%)

<p>- deeply inverted T wave in V2 and V3</p><p>- may spread to other precordial leads (75%)</p>
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Wellens' wave patterns

- type A or B plus

- isoelectric or minimally elevated ST segment (<1 mm)

- no precordial Q waves

- history of angina

- pattern present in pain-free state

- normal or slightly elevated cardiac biomarkers

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acute STEMI is usually due to

the rupture of a vulnerable atherosclerotic plaque

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patho of acute STEMI

- rupture of plaque

- clotting cascade initiated that then occludes the artery with thrombus

- within seconds, tissue becomes ischemic

- permanent cell death within 20 minutes

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what can an acute STEMI cause?

decrease in cardiac output arrhythmias

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symptoms of STEMI

- chest discomfort (persists for 30-60 mins)

- radiation to neck, left jaw, shoulder, left arm, etc.

- shortness of breath

- diaphoresis

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which populations are more likely to present in an atypical way when having a STEMI?

women and diabetics

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about how many females did not have chest pain while having a STEMI?

43%

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J point

end of the QRS which determines elevation or depression

<p>end of the QRS which determines elevation or depression</p>
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EKG findings of a STEMI depend on

- duration

- size

- location

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EKG evolution of a STEMI

- hyperacute T waves

- T wave straightening

- ST elevation

- Q-wave development

- T wave inversion

<p>- hyperacute T waves</p><p>- T wave straightening</p><p>- ST elevation</p><p>- Q-wave development</p><p>- T wave inversion</p>
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EKG evolution of a STEMI (1)

- normal EKG

- 45% of initial EKGs are nondiagnostic and another 20% can be completely normal

- if concern for ACS remains, repeat the EKG every 15-30 minutes

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EKG evolution of a STEMI (2)

- hyperacute T waves

- T waves that are unusually tall compared to the QRS complex

- often seen with ST straightening (checkmark sign)

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EKG evolution of a STEMI (3)

- ST elevation

- hallmark of acute myocardial injury

- ST will remain elevated until the affected tissue necroses or blood flow is restored

- mostly dead, slightly alive myocardium

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STEMI criteria

new ST elevation at the J point that is ≥1 mm in two anatomically continuous leads

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exceptions in STEMI criteria

- V2 and V3 ≥2 mm in men ≥40 years

- V2 and V3 ≥2.5 mm in men <40 years

- V2 and V3 ≥1.5 mm in women

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ST morphology

- ST elevation in any shape can indicate STEMI

- horizontal vs. convex

<p>- ST elevation in any shape can indicate STEMI</p><p>- horizontal vs. convex</p>
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which ST morphology is more worrisome?

convex ("tombstone")

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EKG evolution of a STEMI (4)

- abnormal Q waves

- pathologic Q waves are abnormally wide or large that result of the absence of voltage from dead tissue

- Q waves can remain forever, and the timing of the MI cannot be based on their presence

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when do abnormal Q waves usually develop?

within 6-14 hours, average 9 hours after onset

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abnormal Q waves

- Q wave >0.04 sec

- Q wave is present in lead that usually has an initial R wave (i.e., V2 or V3)

- Q wave amplitude >25% of the following R wave

<p>- Q wave &gt;0.04 sec</p><p>- Q wave is present in lead that usually has an initial R wave (i.e., V2 or V3)</p><p>- Q wave amplitude &gt;25% of the following R wave</p>
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EKG evolution of a STEMI (5)

- T wave inversion

- as ST segment elevation begins to fall, T waves become inverted

- this can remain for months

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reciprocity

- ST elevation can be seen in numerous other conditions

- reciprocity confirms the diagnosis of STEMI

- mirror image of injury: presence of ST depression in leads opposite of ST elevation (i.e., lateral leads vs. inferior leads)

<p>- ST elevation can be seen in numerous other conditions</p><p>- reciprocity confirms the diagnosis of STEMI</p><p>- mirror image of injury: presence of ST depression in leads opposite of ST elevation (i.e., lateral leads vs. inferior leads)</p>
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localization of STEMI

- MI frequently named by location

- can provide clues to the culprit vessel

<p>- MI frequently named by location</p><p>- can provide clues to the culprit vessel</p>
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anterior MI

- result of occlusion of LAD or diagonal/septal branches

- have the worst prognosis of any infarct

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characteristics of anterior MI

- ST elevation in 2 or more contiguous precordial leads (V1-V6)

- reciprocal depression in the inferior leads (particularly III and aVF)

<p>- ST elevation in 2 or more contiguous precordial leads (V1-V6)</p><p>- reciprocal depression in the inferior leads (particularly III and aVF)</p>
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characteristics of anterioseptal MI

- ST elevation in V1 and V2

- reciprocal ST depression in the inferior and/or lateral leads

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anterioapical MI

aka "strictly anterior"

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characteristics of anterioapical MI

- ST elevation in V3 and V4

- reciprocal ST depression in the inferior leads

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anteriolateral MI

aka "lateral" or "high lateral"

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characteristics of anteriolateral MI

- ST elevation in V5 and V6

- reciprocal depression in inferior leads and occasionally V1 and V2

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inferior MI

- most often an occlusion of the right coronary artery (RCA) but can be due to the left circumflex (18%)

- can injure the right ventricle causing hemodynamic and electrical complications

- can extend to the posterior myocardium

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characteristics of inferior MI

- ST elevation in II, III, and aVF

- reciprocal ST depression in I and aVL

<p>- ST elevation in II, III, and aVF</p><p>- reciprocal ST depression in I and aVL</p>
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right ventricular infarct

- up to 50% of inferior STEMIs will involve the right ventricle

- higher in hospital mortality and morbidity

- decrease in preload causing hypotension

- SA and AV node fed by RCA can be injured causing brady/tachyarrhythmias

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treatment of right ventricular infarct

- avoid nitrates and morphine (further decreases preload)

- support with IV fluids/inotropic medications

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characteristics of RV infarct

- ST elevation in V1

- ST elevation in lead III>lead II

- ST elevation in V1>V2

- ST elevation in V1 and ST depression in V2 (highly specific)

- ST elevation in V3R and V6R

<p>- ST elevation in V1 </p><p>- ST elevation in lead III&gt;lead II </p><p>- ST elevation in V1&gt;V2 </p><p>- ST elevation in V1 and ST depression in V2 (highly specific) </p><p>- ST elevation in V3R and V6R </p>
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right-sided chest leads

- placed in mirror image on right side of the chest

- V1 becomes V1R and so on

<p>- placed in mirror image on right side of the chest</p><p>- V1 becomes V1R and so on</p>
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what is the most useful right-sided chest lead?

- V4R as it sits at the right mid-clavicular line at the 5th intercostal space

- greater than 1 mm of ST elevation in V4R is 88% sensitive and 78% specific for a RV STEMI

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posterior infarct

- up to 15-20% of STEMIs will involve posterior myocardium

- usually is an extension of inferior or lateral MI

- rarely, it can occur in isolation (3%)

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why can a posterior MI be easily missed?

it does not have ST elevation typically seen in STEMI

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diagnosis of posterior infarct

- ST depression in V1 and V2

- posterior leads can be placed to help visualize the posterior myocardium

- ≥0.5 mm of ST elevation is required in the posterior leads to make the diagnosis of posterior MI

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posterior leads

- placed under left scapula

- V7, V8, V9

- most often, wires from V4-V6 are removed and placed on the back

<p>- placed under left scapula</p><p>- V7, V8, V9</p><p>- most often, wires from V4-V6 are removed and placed on the back</p>
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characteristics of posterior MI

- horizontal ST segment depression and upright T waves in V1 and V2

- dominant R waves in V2 (R/S ratio >1)

- ST segment elevation in V7-V9

<p>- horizontal ST segment depression and upright T waves in V1 and V2</p><p>- dominant R waves in V2 (R/S ratio &gt;1)</p><p>- ST segment elevation in V7-V9</p>
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isolated ST depression in V1-V3

- usually less than 0.5 mm

- can be caused by LCX occlusion

- use of posterior leads can help uncover this condition as it should be treated as a STEMI

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characteristics of isolated LCX occlusion

- ST depression ≥0.5 mm in leads V1-V3

- ST elevation ≥0.5 mm in leads V7-V9

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ST elevation in aVR

elevation >1 mm could indicate

- left main stenosis

- proximal LAD occlusion or

- three vessel disease

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characteristics of conditions that cause ST elevation in aVR

- ST elevation in aVR ≥1 mm

- ST elevation in aVR > V1

- widespread ST elevation except in inferior leads

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DeWinter's T waves

- STEMI equivalent first described in 2008

- tall symmetric T waves in the precordial leads with upsloped ST depression

- considered an acute occlusion of the LAD and the patient should have emergent reperfusion (may occur in up to 2% of LAD occlusions)

<p>- STEMI equivalent first described in 2008</p><p>- tall symmetric T waves in the precordial leads with upsloped ST depression</p><p>- considered an acute occlusion of the LAD and the patient should have emergent reperfusion (may occur in up to 2% of LAD occlusions)</p>
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characteristics of DeWinter's T waves

- tall, symmetric waves in the precordial leads

- upsloped ST segment depression >1 mm at the J point in the precordial leads

- absence of ST elevation

- ST segment elevation (0.5-1 mm) in aVR

<p>- tall, symmetric waves in the precordial leads</p><p>- upsloped ST segment depression &gt;1 mm at the J point in the precordial leads</p><p>- absence of ST elevation</p><p>- ST segment elevation (0.5-1 mm) in aVR</p>
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what is the most validated tool to make the diagnosis of STEMI in the presence of LBBB?

Sgarbossa criteria

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Sgarbossa criteria

- first published in 1996

- STEMI and LBBB

- LBBB has appropriate discordance of ST segment

<p>- first published in 1996</p><p>- STEMI and LBBB</p><p>- LBBB has appropriate discordance of ST segment</p>