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HPIM Cardio > Ch268 Electrocardiography > Flashcards

Ch268 Electrocardiography Flashcards

1
Q

Graphic recording of electric potentials generated by the heart; noninvasive, inexpensive and highly versatile test

A

Electrocardiogram (ECG or EKG)

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2
Q

What do ECG leads display?

A

Instantaneous differences in potential between the electrodes

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3
Q

The initiating event for cardiac contraction

A

Depolarization

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4
Q

3 components that produce the electric currents through the heart

A
  1. Cardiac pacemaker cells
  2. Specialized conduction tissue
  3. Heart muscle
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5
Q

A collection of pacemaker cells where depolarization stimulus for normal hearbeat originates

A

Sinoatrial (SA) node or sinus node

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6
Q

T or F: Depolarization wavefronts spread through the ventricular wall from the epicardium to the endocardium triggering the ventricular contraction.

A

False

Endocardium to epicardium

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7
Q

ECG waveform representing atrial depolarization

A

P wave

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8
Q

ECG waveform representing ventricular depolarization

A

QRS complex

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9
Q

ECG waveform representing ventricular repolarization

A

ST-T-U complex

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10
Q

Junction between the end of QRS complex and beginning of ST segment

A

J point

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11
Q

What conditions can J point become apparent?

A

Acute pericarditis

Atrial infarction

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12
Q

Phase in the cardiac action potential corresponding to the onset of QRS

A

Phase 0 (rapid upstroke)

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13
Q

Phase in cardiac action potential corresponding to the isoelectric ST segment

A

Phase 2 (plateau)

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14
Q

Phase in cardiac action potential corresponding to the inscription of the T wave

A

Phase 3 (active repolarization)

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15
Q

Effects of hyperkalemia and flecainide on cardiac action potential

A
  1. Decrease slope of Phase 0
  2. Increase QRS duration
  3. Impairs Na influx
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16
Q

Effects of amiodarone and hypocalcemia on cardiac action potential

A
  1. Prolong Phase 2

2. Increase QT interval

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17
Q

Effect of digitalis or hypercalcemia on cardiac action potential

A

Shortens ventricular repolarization (Phase 2)

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18
Q

Four major ECG intervals

A
  1. RR
  2. PR
  3. QRS
  4. QT
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19
Q

Compute the heart rate using the RR interval

A

Divide the number of large squares between consecutive R waves into 300 OR

Divide the number of small squares into 1500

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20
Q

PR interval measures the time between atrial and ventricular depolarization including the physiologic delay imposed by stimulation cells in AV junction area, has the normal value of:

A

120-200ms

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21
Q

QRS interval reflects the duration of ventricular depolarization with normal value of

A

100-110ms or less

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22
Q

T or F: QT interval is directly proportional to the heart rate

A

False

QT interval varies inversely with heart rate

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23
Q

Can be calculated as QT/square root of RR

A

Corrected QT interval (QTc)

Normal value: =0.44s

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24
Q

What wave corresponds to a negative initial QRS deflection

A

Q wave

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25
Q

First positive deflection in QRS complex

A

R wave

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26
Q

The negative deflection after an R wave in QRS complex

A

S wave

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27
Q

An entirely negative QRS complex

A

QS wave

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28
Q

Leads that record potentials transmitted onto the frontal plane

A

Limb leads (6)

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29
Q

Leads that record potentials transmitted onto the horizontal plane

A

Chest (precordial) leads (6)

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30
Q

Diagram representing the spatial orientation and polarity of the six FRONTAL plane leads

A

Hexaxial diagram

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31
Q

Anatomical positions of leads V7, V8, V9

A

V7 midaxillary line
V8 posterior axillary line
V9 posterior scapular line

All in line with V4 (5th intercostal space)

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32
Q

Left axis deviation on hexaxial diagram

A

-90 to -30 degrees

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33
Q

Right axis deviation on hexaxial diagram

A

+100 to +180 degrees

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34
Q

Normal axis on hexaxial diagram

A

-30 to +100 degrees

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35
Q

Implications of left axis deviation

A
  1. Normal variant
  2. Left ventricular hypertrophy
  3. Block in anterior fascicle of left bundle system (left anterior fascicular block/hemiblock)
  4. Inferior MI
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36
Q

Implications of right axis deviation

A
  1. Normal variant (children and young adults)
  2. Due to reversal of left and right arm electrodes
  3. Right ventricular overload (acute or chronic)
  4. Infarction of lateral wall of left ventricle
  5. Dextrocardia
  6. Left pneumothorax
  7. Left posterior fascicular block
37
Q

T or F: The normal U wave is small, rounded deflection (=1mm) that has same polarity as the T wave

38
Q

Drugs that abnormally increases U wave amplitude

A
  1. Dofetilide
  2. Amiodarone
  3. Sotalol
  4. Quinidine

Condition: Hypokalemia

39
Q

Very prominent U waves are a marker of increased susceptibility to this type of ventricular tachycardia

A

Torsades de pointes

40
Q

Increased P wave amplitude (peaked P waves) also referred as P-pulmonale has normal value of

A

> /= 2.5mm

41
Q

Pattern that produces a biphasic P wave in V1 with broad negative component or a broad often notched P wave in one or more limb leads

A

P-mitrale

Typically from left atrial overload

42
Q

Condition produced due to sustained, severe pressure load characterized by relatively tall R wave in lead V1 (R >/= S wave), usually with right axis deviation

A

Right VENTRICULAR hypertrophy

43
Q

Pattern attributed to repolarization abnormalities in acutely or chronically overloaded muscle described as ST depression and T-wave inversion in the right-to-midprecordial leads

A

Formerly called right ventricular “strain”

44
Q

T or F: Acute cor pulmonale due to pulmonary embolism can present with normal ECG

45
Q

The most common arrhythmia

A

Sinus tachycardia

46
Q

ECG finding in this condition is associated with small R waves in right-to-midprecordial leads (slow R-wave progression) due in part to downward displacement of diaphragm and heart in obstructive lung disease

A

Chronic cor pulmonale

47
Q

Sokolow-Lyon criteria to assess left ventricular hypertrophy

A

SV1 + (RV5 or RV6) >35mm

48
Q

T or F: Prominent precordial voltages may occur as a normal variant in the elderly.

A

False

Athletic or young individuals

49
Q

Sensitivity of conventional voltage criteria for LVH is decreased in these type of population

A

Obese persons and smokers

50
Q

QRS interval in COMPLETE bundle branch blocks

A

> /= 120 ms

51
Q

QRS interval in INCOMPLETE bundle branch blocks

A

100-120 ms

52
Q

RBBB are more common in subjects without structural heart disease but may also occur with heart disease such as

A

Congenital (ASD)

Acquired (e.g. valvular, ischemic)

53
Q

Often a marker of one of four underlying conditions associated with increased risk of CV morbidity and mortality rates

54
Q

4 conditions associated with increased risk of CV morbidity and mortality

A
  1. Coronary heart disease
  2. Hypertensive heart disease
  3. Aortic valve disease
  4. Cardiomyopathy
55
Q

T or F: Bundle branch blocks can be rate-related such that is can occur when the heart rate exceeds some critical value

56
Q

T or F: Bundle branch blocks can be intermittent

57
Q

Primary repolarization abnormalities (ST-T wave changes) can occur in these conditions

A
  1. Ischemia
  2. Electrolyte imbalance
  3. Digitalis
58
Q

Most common cause of marked left axis deviation in adults

A

Left ANTERIOR fascicular block (QRS axis more negative than -45 degrees)

59
Q

T or F: Left POSTERIOR fascicular block (QRS axis more rightward than +110-120 degrees) is extremely rare and requires exclusion of other factors causing right axis deviation

60
Q

Which has higher risk of progression to high-degree AV block:
A. Chronic bifascicular block in asymptomatic individual
B. New bifascicular block with acute MI

A

B. New fascicular block with acute MI

61
Q

Alternation of right and left bundle branch block is a sign of what disease?

A

Trifascicular disease

62
Q

Factors that slows down the ventricular conduction

A
  1. Hyperkalemia

2. Drugs (Class I antiarrhythmic agents, TCA, Phenothiazines)

63
Q

Diagnostic triad of Wolff-Parkinson-White

A
  1. Wide QRS complex
  2. Relatively short PR interval
  3. Slurring of the initial part of QRS (Delta wave)
64
Q

Prolongation of QRS duration due to preexcitation of the ventricles via a bypass tract is seen in this condition

A

Wolff-Parkinson-White (WPW)

65
Q

Cornerstone in diagnosis of acute and chronic ischemic heart disease

66
Q

Effect of severe, acute ischemia on resting membrane potential and action potential

A

Lowers resting membrane potential

Shortens duration of AP

67
Q

ST changes seen in:
A. Transmural ischemia
B. Ischemia in subendocardium

A

A. ST elevations, Hyperacute T waves

B. ST depression

68
Q

Posterior wall ischemia can be indirectly recognized due to this reciprocal changes

A

ST depression in leads V1 to V3

69
Q

REVERSIBLE TRANSMURAL ischemia due to coronary vasospasm in these conditions may cause transient ST SEGMENT ELEVATIONS WITHOUT development of Q WAVES

A
  1. Prinzmetal’s variant angina

2. Tako-tsubo “stress” cardiomyopathy syndrome

70
Q

Pattern in severe anterior wall ischemia causing prominent T wave inversions in precordial leads that is associated with high grade stenosis of left anterior descending coronary artery

A

Wellens T waves

71
Q

T or F: Transmural infarcts may occur without Q waves and subendocardial infarcts sometimes may be associated with Q waves.

72
Q

Differential diagnosis of ST segment elevations

A
  1. Ischemia / MI
  2. Acute pericarditis
  3. Normal variants
  4. LVH/LBBB
  5. Others: Acute pulmo embolism, Brugada patterns, Hypercalcemia, Hyperkalemia, Hypothermia, Myocarditis, Tumor invading left ventricle, Trauma to ventricles, Class 1C antiarrhythmic drugs
73
Q

ECG finding seen in hypothermia

A

J wave / Osborn wave

Distinctive convex elevation of J point

74
Q

Conditions that may cause ST segment depression mimicking subendocardial ischemia

A
  1. Digoxin
  2. Ventricular hypertrophy
  3. Hypokalemia
75
Q

May cause prominent T wave inversions

A
  1. Ventricular hypertrophy
  2. Cardiomyopathies
  3. Myocarditis
  4. Cerebrovascular injury (bleed)
76
Q

This condition causes cardiac arrest with a slow sinusoidal type of mechanism (“sine-wave” pattern) followed by asystole

A

Hyperkalemia

77
Q

This condition prolongs ventricular repolarization often with prominent U waves

A

Hypokalemia

78
Q

Class IA, TCA, phenothiazines and Class III antiarrhythmics produce these ECG changes

A

Prolongation of QT interval

They increase the duration of ventricular action potential

79
Q

ECG pattern that may occur with intracranial bleeds particularly subarachnoid hemorrhage

A

“CVA T-wave” pattern

Deep wide T-wave inversions

80
Q

ECG changes in hypocalcemia vs hypercalcemia

A

Hypo: Prolongs QT interval (ST portion)
Hyper: Shortens QT interval
(Also digitalis)

81
Q

Characteristic finding on ECG due to digitalis

A

“scooping” of the ST-T wave complex (digitalis effect)

82
Q

Defined as peak-to-trough QRS amplitudes of =5mm in the six limb leads and/or =10mm in the chest leads

A

Low QRS voltage

83
Q

Conditions that produce low QRS voltage

A
  1. Pericardial effusion
  2. Pleural effusion
  3. COPD
  4. Infiltrative cardiomyopathies
  5. Anasarca
84
Q

A beat-to-beat alternation in one or more components of the ECG signal

A

Electrical alternans

85
Q

ECG findings that are relatively specific sign of pericardial effusion with cardiac tamponade

A

Total electrical alternans (P-QRST-T) with sinus tachycardia

86
Q

Sign of electrical instability and may precede ventricular tachyarrhythmias

A

Pure repolarization (ST-T or U wave) alternans

87
Q

14 points that should be analyzed in every ECG

A
  1. Standardization (calibration) and technical features
  2. Rhythm
  3. Heart Rate
  4. PR interval/AV conduction
  5. QRS interval
  6. QT/QTc intervals
  7. Mean QRS electrical axis
  8. P waves
  9. QRS voltages
  10. Precordial R-wave progression
  11. Abnormal Q waves
  12. ST segments
  13. T waves
  14. U waves
88
Q

T or F: Computerized interpretation should not be accepted without careful clinician review.

HPIM Cardio (10 decks)

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