EKG Flashcards

1
Q

Analyze on every ECG

A
  1. Rate
  2. Rhythm
  3. Interval
  4. Axis
  5. Ischemia
  6. Pacemaker
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2
Q

one large box represents…

A
  • 0.2 sec of time
  • 5mm of amplitude
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3
Q

one small box represents…

A
  • 0.04 sec of time
  • 1 mm of amplitude
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4
Q

high lateral

A
  • I
  • aVL
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5
Q

lateral

A
  • V5
  • V6
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6
Q

septal

A
  • Vi
  • V2
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7
Q

anterior

A
  • V2
  • V3
  • V4
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8
Q

inferior

A
  • II
  • III
  • aVF
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9
Q

rate

A
  • Assume standard paper speed 25 mm/sec
  • Regular Rhythm

– Count the number of large boxes between P waves, R waves or pacer spikes

– Beats per minute = 300 / # of large boxes

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10
Q

sinus bradycardia

A

•<60 bpm

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11
Q

sinus tachycardia

A
  • >100 bpm
  • Sinus tachycardia

– Regular

– P wave before each QRS

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12
Q

irregular rate

A

•differences in bpm across the ECG

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13
Q

rhythm

A
  • Most difficult and complex part of ECG interpretation
  • Computer interpretation often wrong
  • Need to look at:

– P wave morphology

– QRS morphology

– P:QRS relationship

P:QRS = 1

– P wave precedes every QRS

– Sinus rhythm

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14
Q

if P wave FOLLOWS every QRS…

A

P:QRS = 1

– P wave follows every QRS

– Super ventricular tachycardia (SVT)

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15
Q

if P:QRS < 1 or NO P waves…

A

P:QRS < 1 or NO P WAVES

– Atrial fibrillation

– Irregular irregular

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16
Q

if P:QRS > 1 or NO P wave…

A

P:QRS < 1 or NO P WAVES

– Junctional rhythm

– From below the AV node

17
Q

P:QRS < 1 or NO P wave…

A

P:QRS < 1 or NO P WAVES

– Ventricular rhythm

– From the ventricle, wide complex

18
Q

P:QRS

A
19
Q
A
  • P wave 0.8 - .10 ms
  • PR interval 0.12 - 0.20 ms
  • QRS complex 0.06 - 0.10 ms
  • QTc <0.44 ms
20
Q

PR interval

A
  • Represents conduction time from the onset of atrial depolarization to onset of ventricular activation
  • Measure from beginning of P wave to first deflection of QRS complex
  • Normal PR duration 0.12 – 0.20 sec
  • Increased PR duration > 0.20 sec

1 big block!

21
Q

1st Degree AV Block

A
  • The distance from the beginning of the P wave until the beginning of the QRS complex is > 0.20 sec.
  • This is first degree AV block.
22
Q

QRS interval

A

•<120 ms

smaller than 3 small boxes!

23
Q

RBBB

A
  • prolonged QRS
  • Extra deflection in V1 reflects the rapid depolarization of the left ventricle followed by the slower depolarization of the right ventricle. The last electrical activity is thus to the right, or towards lead V1.
24
Q

LBBB

A
  • prolonged QRS interval
  • Normally the septum is activated from left to right.
  • In LBBB, the normal direction of septal depolarization is reversed (becomes right to left), as the impulse spreads first to the RV via the right bundle branch and then to the LV via the septum.
  • This sequence of activation extends the QRS duration to > 120 ms. The overall direction of depolarization (from right to left) produces tall R waves in the lateral leads (I, V5-6) and deep S waves in the right precordial leads (V1-3), and usually leads to left axis deviation.
  • difficult to call ischemia in LBBB
  • As the ventricles are activated sequentially (right, then left) rather than simultaneously, this produces a broad or notched (‘M’-shaped) R wave in the lateral leads.
25
Q

QT interval

A
  • Represents total duration of ventricular systole
  • Measure from beginning of QRS to end of T wave
  • Normal QT < 0.35 – 0.43 sec
  • Increased QT > 0.44 sec
26
Q

axis

A

•Represents major vector of ventricular activation

27
Q
A
28
Q

ST interval

A

•Abnormalities of the ST segment can suggest ischemia

– After depolarization & repolarization period

•Normal is to be “isoelectric”

– ST depression = ischemia

– ST elevation = active infarction

29
Q

ST interval criteria

A

•Infarction:

New ST segment elevation at J-point in two contiguous leads

– > 1 mm in all leads except V1&V2

– In V1&V2, >2mm in men > 40 yo, > 2.5 mm in men < 40 yo, > 1.5mm in women

•Ischemia:

New horizontal or downsloping ST changes > 0.5 mm in two contiguous leads

– And / or T wave inversion > 1 mm with prominent R wave

•The higher the ST segment elevation the clinically more severe the infarction.

30
Q

Other causes of ST changes

A
  • LBBB
  • RBBB
  • LVH
  • RVH
  • pericarditis
  • BER
31
Q

old infarctions

A
  • Old infarctions are represented as lack of R waves OR presence of Q waves
  • No all Q waves are pathologic Q waves can be related to:

– Anatomic and positional effects

– Myocardial injury or loss (duration, extent, size of MI)

– Ventricular enlargement

– Altered conduction (LBBB or pre-excitation pattens)

32
Q

2nd Degree AV Block

A
  • not all P waves lead to QRS
  • Type 1
  • Type 2
33
Q

2nd Degree AV block Type 1

A
  • Mobitz I (also known as Wenckebach)
  • Lesser degree of AVB Variable
  • PR interval Usually narrow
  • QRS Usually above the HIS complex in AV node
  • Usually no pacer needed
34
Q

2nd Degree AV block Type 2

A
  • Mobitz II
  • Higher degree of AVB
  • PR interval the same
  • Can have WIDE QRS complex
  • Usually below the AV node
  • Increased incidence of progressing to 3rd degree
  • May need pacer
35
Q

3rd Degree AV block

A
  • Regular p waves and QRS, but INDEPENDENT of each other
  • Acquired vs. congenital
  • Pacer often required
  • No electrical connection between atrial and ventricles
  • no P waves lead to QRS
36
Q

supraventricular tachycardia

A
  • Rate 160 bpm –> tachycardia
  • No p waves, regular –> SVT
  • Normal axis, narrow complex
  • Non-specific T wave flattening
37
Q

torsades

A
  • Multiple ventricular foci with the resultant QRS complexes varying in amplitude, axis and duration
  • Torsade de pointes (TdP)

– QT prolongation

– QRS complexes “twist” around the isoelectric line. (For TdP to be diagnosed, the patient has to have evidence of both VT and QT prolongation)