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EKG 3 > 12 Lead Interpretation > Flashcards

12 Lead Interpretation Flashcards

1
Q

myocardial ischemia and infarction

A
  • Myocardial cells require oxygen & nutrients which are supplied by coronary arteries
  • Imbalance in supply vs. demand → ACS
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2
Q

Acute coronary syndrome sxs

A

-a constellation of symptoms related to obstruction of coronary arteries

  • CP → most common symptom:
  • Typical vs. Atypical (3/3 criteria vs. 2/3 criteria)
  • 1) presence of substernal CP
  • 2) discomfort that was provoked by exertion or emotional stress
  • 3) relieved by rest and/or nitroglycerin
  • SOB
  • N/V
  • diaphoresis
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3
Q

stable angina

A
  • Exertional
  • <20 minutes
  • Same pattern
  • Relieved with rest/medication
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4
Q

unstable angina

A
  • Occurs at rest
  • > 20 minutes
  • Different Pattern: Lasts longer, Feels different
  • Doesn’t respond to rest or medication
  • New onset angina that limits activity
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5
Q

which arteries serve lateral, inferior, anterior and septal portions of the heart

A

lateral: circumflex
inferior: R coronary a
anterior: L anterior descending a
septal: L anterior descending a

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6
Q

3 things to note for STEMI

A
  • ST segment
  • J point
  • Baseline
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7
Q

J point

A
  • J point - junction between the termination of the QRS complex and the beginning of the ST segment
  • The height of elevation is the vertical measurement from J point to baseline
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8
Q

MI criteria

A
  • New ST Elevation at the J point
  • Two anatomically contiguous leads
  • ≥1 mm in all leads other than V2-V3
  • V2-V3 needs to be ≥2 mm
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9
Q

contiguous leads associated with STEMI

A
  • coincide with the walls of the heart
  • coronary arteries feed the walls of the heart
  • therefore, if a coronary artery is blocked then we should see changes in the contiguous leads associated with that artery
  • II, III, aVF = inferior wall
  • V1, V2, V3, V4 = antior/septal wall
  • V5, V6, I, aVL = lateral wall
  • deep ST depression in V2 = posterior wall
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10
Q

posterior MI

A
  • Suspect this with any inferior or lateral MI

- Look at V1 – V3: Horizontal ST depression, Upright T waves, Tall R waves

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11
Q

Leads V7-V9

A
  • Leads V7-9 on the posterior chest wall:
  • V7 – L posterior axillary line
  • V8 – Tip of the L scapula
  • V9 – L paraspinal region NOTE: all are in the same horizontal plane as V6
  • If suspected posterior MI, Posterior infarction is confirmed by the presence ofST elevation and Q waves in the posterior leads (V7-9).
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12
Q

right-sided MI

A
  • Suspect this with any inferior MI (Esp in setting of a low cardiac output, Hypotension)
  • ST segment elevation in V1
  • ST elevation in lead III > lead II
  • Main goals of tx: maintain preload to the R ventricle, Q, BP, coronary artery filling pressures & prevent shock. BecauseNTGis a vasodilator, it is contraindicated as standard tx, or must be given w/ extreme care. KNOW
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13
Q

Does ST elevation always indicate MI?

A

NO!!

  • ST segment elevation does not always indicate MI
  • You must collect data to support your hypothesis: History, Physical Exam, ST segment elevation/depression/T wave changes, Reciprocal Changes on EKG
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14
Q

Reciprocal changes

A

Real Life: You look at EKG. You see ST segment elevation and suspect STEMI. You look at the rest of the EKG and see if there is ST depression anywhere.

Fancy Definition: Areas of ST depression seen on EKG in the anatomical areas bordering the area of ischemia.

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15
Q

Sites and reciprocal sites

A 
Septal - NONE
Anterior - NONE
Anteroseptal - NONE
Lateral - II, III, aVF
Anterolateral - II, III, aVF
Inferior - I, aVL
Posterior - V1, V2, V3, V4
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16
Q

Non-ST elevation MI criteria

A
  • New ST Depression at the J point
  • Horizontal or down-sloping ≥0.5 mm in two anatomically contiguous leads
  • And/orT inversion ≥1 mm in two contiguous leads
17
Q

Pathologic Q waves

A
  • Can be sign of old myocardial infarction
  • Criteria = Wide and Deeply Negative
  • > 0.04 seconds (one little box) wide
  • > 25% of the depth of the QRS complex
  • > 2mm in depth
  • The reason why Q waves do or do not develop following coronary occlusion is related to the duration of occlusion, the extent to which collateral vessels maintain myocardial viability during occlusion, and ultimately, to the size of the infarction. Loss of electromotive forces due to myocardial necrosis in MI leads to R wave loss. Delayed conduction through an ischemic area or conduction around it results in recording potentials from the opposite ventricular wall with Q wave formation in the appropriate leads.
18
Q

Symptoms of MI

A
  • Chest pain = classic symptom!
  • Left-sided chest tightness, heaviness, pressure, “an elephant sitting on the chest”
  • Can extend to the jaw, right chest, neck, back, down the arm, toothache
  • DM patients may not have any discomfort with MI due to neuropathy
  • Females more likely to have atypical symptoms
19
Q

Acute Coronary Syndrome

A
  • Based on ECG and cardiac enzymes, ACS is classified into:
  • STEMI: ST elevation, elevated cardiac enzymes
  • NSTEMI: ST depression, T-wave inversion, elevated cardiac enzymes
  • Unstable Angina: Non specific EKG changes, normal cardiac enzymes
20
Q

Cardiac enzymes

A
  • Troponin - good sensitivity & specificity
  • Other conditions can cause elevation in troponin such as renal failure or CHF
  • Increasing troponin trend → diagnosing MI
  • Order Troponin together with ECG when doing serial testing to rule out ACS
  • High sensitivity CRP
  • CK-MB (creatine kinase – MB isoenzyme) (more useful in certain situations such as post reperfusion MI or if troponin test is not available)
21
Q

STEMI managment

A
  • STEMI patients usually go straight to the cath lab from the ED
  • Goal: Door to balloon < 90 minutes.

Initial management for STEMI:

  • Cardiac monitor
  • Supplemental O2
  • Nitrates*
  • Beta blocker
  • Morphine
  • Clopidogrel
  • Aspirin
  • Good IV access
  • Call cardiology!
22
Q

Risk stratification: TIMI score

A

NSTEMI or unstable angina are risk stratified:

  • Age>=65
  • > = 3 CAD risk factors: HTN, hyperlipidemia, DM2, smoker, family h/o early MI
  • Documented CAD with >=50% stenosis
  • ST segment deviation
  • ≥ 2 anginal episodes in past 24 hours
  • Aspirin use in the past week (marker for more severe case)
  • Elevation of cardiac enzymes

Stratify risk based on number of variables
-Risk: 0-2: Low 3-4: Intermediate 5-7: High risk

23
Q

Managment of UA/NSTEMI

A

NSTEMI or EKG changes suggest ischemia with high risk:

  • Telemetry
  • Aspirin
  • Beta blocker
  • Nitrates
  • Heparin (UFH or LMWH)
  • ACE-I/ARB
  • Statin
  • Consider clopidogrel

EKG normal or non-specific changes with intermediate or low risk:

  • Telemetry
  • Serial troponins and EKGs
  • Consider pre-discharge stress test
24
Q

MI mimics

A
  • Everything with ST elevation is not an MI
  • Benign Early Repolarization
  • Pericarditis
  • Brugada syndrome
  • Others
25
Q

Benign early repolarization

A
  • Widespread ST segment elevation V2-V5
  • Notched J-point - “fish-hook” pattern
  • Tall T-waves in the precordial leads
  • Concave ST elevation
  • No reciprocal changes
26
Q

Pericarditis

A
  • Inflammation of the pericardium
  • Causes: Viral infection, Trauma, Drug induced, Post MI - Dressler’s syndrome
  • Signs: Pericardial friction rub, Possible pericardial effusion
27
Q

EKG changes in pericarditis

A
  • Widespread Concave ST Elevation withPR segment depression
  • Reciprocal ST depression with PR elevation in leads aVR and V1
28
Q

Brugada syndrome

A
  • Inherited channelopathy
  • Leads to ventricular arrhythmia and sudden death
  • V1 and V2
  • ST Elevation + Partial RBBB
29
Q

Brugada syndrome treatment and charting

A
  • Definitive Treatment = ICD
  • Diagnose this and save a life
  • Chart on every syncope patient: No Brugada, No WPW/pre-excitation, No HOCM, No long QT, No S1Q3T3

EKG 3 (2 decks)

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