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EKG > Basics and history > Flashcards

Basics and history Flashcards

1
Q

Who used two dissimilar metals to create an electrical charge? (Hint: frogs legs dancing)

A

Luigi Galvani (1790)

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2
Q

Who experimented on deceased individuals with electricity?

A

Charles Kite (1788)

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3
Q

Who advocated the use of zinc and silver as the most effective metals to carry an electric current? (Hint: developed the “voltaic pile” which was the precursor to a battery)

A

Alessandro Volta (1800)

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4
Q

Who used the electrical theories of Galvani in public spectacles?

A

Giovanni Aldini (1792)

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5
Q

Who proved the electrical currents of the heart by attaching leads to frog heart and amputated leg?

A

Koelliker & Mueller (1856)

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6
Q

Who developed the string galvanometer that was used for the tracings of an EKG from the leads?

A

Willem Einthoven (1901)

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7
Q

Clinical uses of an EKG (6)

A
  1. Detection of arrhythmias and heart abnormalities
  2. Indication of myocardial damage
  3. Detection of electrolyte disturbances
  4. Screening tool for diagnosis of ischemic disease
  5. Can indicate anatomic and physiologic state of the heart (i.e. hypertrophy, stenosis, etc. )
  6. Can diagnose some non-cardiac pathology
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8
Q

Is the systemic circulation a high pressure or low pressure circulation?

A

high pressure (~120/80 mmHg)

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9
Q

Is the systemic circulation a low resistance or high resistance circulation?

A

high resistance

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10
Q

Is the pulmonary circulation a high pressure or low pressure circulation?

A

low pressure (~25/10 mmHg)

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11
Q

Is the pulmonary circulation a low resistance or high resistance circulation?

A

low resistance

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12
Q

What is considered to be a normal blood pressure?

A

120/80 mmHg (Systolic/Diastolic)

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13
Q

What type of cardiac cells are considered to be the heart’s electrical power source of the heart?

A

Pacemaker cells

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14
Q

What type of cardiac cells are considered to be the hard wiring of the heart?

A

Electrical conducting cells

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15
Q

What is the role of myocardial cells?

A

Provides the contractile machinery of the heart

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16
Q

What is the normal conduction pathway of the heart?

A

SA node –> AV node –> Bundle of his –> Bundle branches –> Purkinjie Fibers

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17
Q

What is the inherent rate of the SA node?

A

60-100bpm

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18
Q

What is the predominant pacemaker of the heart?

A

SA node

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19
Q

Contraction of the heart is initiated by the influx of what ion?

A

Ca++

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20
Q

During repolarization, there is an efflux of what ion?

A

K+

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21
Q

During rapid depolarization, there is an influx of what ion?

A

Na+

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22
Q

Which wave on the EKG represents atrial depolarization?

A

P wave

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23
Q

What event is occurring during the PR interval?

A

Beginning of atrial depolarization to the beginning of ventricular depolarization

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24
Q

What event is occurring during the PR segment?

A

The end of atrial depolarization to the beginning of ventricular depolarization

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25
Q

Which wave on the EKG represents ventricular depolarization?

A

QRS complex

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26
Q

What event is occurring during the QT interval?

A

Beginning of ventricular depolarization to the end of ventricular repolarization

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27
Q

What event is occurring during the ST segment?

A

The initial “plateau” phase of ventricular depolarization

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28
Q

Which wave on the EKG represents ventricular repolarization?

A

T wave

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29
Q

An action potential propagating toward a (+) lead produces a (-) or (+) signal?

A

(+)

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30
Q

A repolarization spreading toward a (+) lead produces a (-) or (+) signal?

A

(-)

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31
Q

Magnitude and polarity of the signal from an EKG depends on what two things?

A
  1. What the heart is doing electrically- (depolarizing/repolarizing)
  2. The position and orientation of the recording electrode
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32
Q

Who introduced the “augmented” (aV) leads?

A

Goldberger

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33
Q

What are the angles of the three standard limb leads (Leads I, II, III)?

A

I: 0 (R arm - and L arm +)
II: 60 (R arm - and legs +)
III: 120 (L arm - and legs +)

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34
Q

What are the angles of the three augmented leads (Leads aVL, aVF, and aVR)?

A

aVL: -30 (other limbs - L arm +)
aVF: 90 (other limbs - legs +)
aVR: -150 (other limbs - R arm +)

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35
Q

What are the inferior leads?

A

aVF, II and III

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36
Q

What are the left lateral leads?

A

I, aVL, V5 and V6

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37
Q

What is the right-ventricular leads?

A

aVR and V1

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38
Q

What are the anterior leads?

A

V2

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39
Q

One small square is equal to how many sec?

A

0.04sec

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40
Q

One large square is equal to how many sec and how many mV?

A

0.2 sec and 1/2mV

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41
Q

One small square is equal to how many mm?

A

1mm

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42
Q

What are the septal leads?

A

V3 and V4

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43
Q

List the rates (bpm) from one big square to the next.

A 
300,
150
100
75
60
50
30
Or...you can count the number of large squares and divide by 300
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44
Q

What rate is considered a normal sinus rhythm?

A

60-100 bpm (3-5 large squares)

45
Q

What rate is considered a sinus tachycardia?

A

> 100 bpm (less than 3 large squares)

46
Q

What are some of the causes of tachycardia? (10)

A 
Pain
Fear/anxiety
Exercise
Hyperthyroid
Anemia
Hypovolemia
MH
Pheochromocytoma
Sepsis
Drug abuse/caffeine
47
Q

How would you treat tachycardia? (4)

A

Resolve underlying cause
Vagal maneuvers (carotid massage, valsalva, gagging)
AV blocking agents (adenosine, verapamil)
Beta blockers

48
Q

What rate is considered a sinus bradycardia?

A

40-59 bpm (more than 5 large squares)

49
Q

What are some of the causes of bradycardia? (6)

A 
Hypothyroid
Vagal maneuvers
Athleticism
Sleep
Severe HTN
Beta blockers
50
Q

How would you treat chronic bradycardia? (2)

A

pacemaker

thyroid therapy

51
Q

How would you treat acute bradycardia? (3)

A

Cease stimulation
Atropine
Glycopyrrolate

52
Q

What are the causes of a sinus arrhythmia? (2)

A

Spontaneous breathing

Heart disease

53
Q

What is the intrinsic rate of the atrium?

A

60-80 bpm

54
Q

What is the intrinsic rate of the AV junction?

A

40-60 bpm

55
Q

What is the intrinsic rate of the ventricle?

A

20-40 bpm

56
Q

The heart’s “fail-safe” pacing mechanism, utilizing automaticity foci in the atria, the ventricles and the AV junction.

A

Overdrive suppression

57
Q

When the SA node stops firing and you see a “dropped beat”

A

Sinus arrest.

58
Q

If a sinus arrest occurs, and nothing happens, what can this lead to?

A

Asystole

59
Q

Type of arrhythmia where there are aberrant or inverted P waves and the rates are regular

A

Junctional escape

60
Q

Abnormal rhythms that arise from elsewhere other than the SA node and are essentially sustained escape beats.

A

Ectopic rhythms

61
Q

Absolutely regular rhythm, rate 150-250 bpm and P waves buried in the QRS complex.

A

PSVT

62
Q

Treaments for PSVT. (3)

A

Adenosine
Esmolol
Vagal maneuvers

63
Q

Absolutely regular rhythm, rate 250-350 bpm, characteristic saw-tooth pattern.

A

Atrial flutter

64
Q

What is the most common type of atrial flutter?

A

2:1

65
Q

Can a carotid massage treat atrial flutter?

A

No, it can be used for diagnosis but doesn’t treat it.

66
Q

Chaotic atrial activity with undulating baseline with no true P waves, and an irregularly irregular AV conduction.

A

Atrial fibrillation

67
Q

What are the symptoms of atrial fibrillation? (2)

A

syncope

low bp

68
Q

What are the underlying pathology of atrial fibrillation?

A 
mitral valve disease
CAD
hyperthyroidism
PE
pericarditis
69
Q

How can you treat A-fib?

A

Cardioversion

anti-coagulants

70
Q

Irregular rhythm occurring from random firing of various atrial foci with easily identifiable various P waves.

A

Multi-focal atrial tachycardia (MAT)

71
Q

Warm up and cool down phases.

A

Paroxysmal Atrial tachycardia (PAT)

72
Q

Any obstruction or delay of the normal pathways of electrical conduction in the heart.

A

Conduction blockade

73
Q

What are the 3 types of conduction blockades?

A

Sinus node block
AV node block
Bundle branch block

74
Q

Characterized by a prolonged delay in conduction at the AV node and results in long PR interval >0.2sec

A

First degree AV block

75
Q

Type of block that is also known as the “Wenckebach block”

A

Second degree AV block (Mobitz type I)

76
Q

Progressive lengthening of PR interval with each beat and then a “dropped beat”

A

Second degree AV, Type I

77
Q

Conduction block in the bundle of his, where the conduction is all-or-none.

A

Second degree, Mobitz Type II

78
Q

Dropped beat without PR interval lengthening.

A

Second degree, Type II

79
Q

Also known as a “complete heart block” because the atria and ventricles are being driven by different pacemakers.

A

Third degree AV block

80
Q

AV dissociation between P and QRS.

Regular P wave rate of 60-100bpm with ventricular escape rhythms of 30-45bpm

A

Third degree AV block

81
Q

Conduction through the right bundle branch is blocked

A

RBBB

82
Q

“Rabbit ears” in leads V1 and V2 with deep S waves in the other precordial leads

A

RBBB

83
Q

Conduction through the left bundle branches are blocked.

A

LBBB

84
Q

“Rabbit ears” in leads V5 and V6 with deep S waves in V1 and V2

A

LBBB

85
Q

What is the most common type of bifasicular block?

A

RBBB with incomplete anterior LBBB

86
Q

In which incomplete block do you see a left axis deviation?

A

Anterior LBBB

87
Q

In which incomplete block do you see right axis deviation?

A

Posterior LBBB

88
Q

Tall positive R waves in lateral leads (I, aVL, V5, V6) and deep S waves in inferior leads (II, III, aVF) and left axis deviation.

A

Anterior LBBB

89
Q

Tall R waves inferiorly and deep S waves laterally with right axis deviation.

A

Posterior LBBB

90
Q

Only one of the three fascicles is conduction.

A

Bifascicular blocks

91
Q

What type of syndromes uses accessory pathways for the conduction of the heart?

A

Pre-excitation syndromes

92
Q

Are pre-excitation syndromes more common in males or females?

A

males

93
Q

Pre-excitation syndromes can be present in healthy or diseased hearts, but they are most commonly seen with what disorders? (3)

A

MVP
Hypertrophic cardiomyopathy
congenital disorders

94
Q

What is the accessory pathway used in WPW?

A

The Bundle of Kent

95
Q

Premature depolarization of the ventricles with the presence of delta waves.

A

WPW

96
Q

When can WPW be harmful?

A

When it occurs with A-Fib due to inefficient CO

97
Q

What is the accessory pathway used in LGL?

A

James fibers pathways

98
Q

No part of the ventricles are depolarized independently with shortened PR intervals.

A

LGL

99
Q

Global T wave peaking, PR interval prolongation and P wave disappearance, and QRS in sine wave formation

A

Hyperkalemia

100
Q

Which electrolyte disturbance has presence of U wave?

A

Hypokalemia

101
Q

Which electrolyte disturbance has QT prolongation?

A

Hypocalcemia

102
Q

Which electrolyte disturbance has QT shortening?

A

Hypercalcemia

103
Q

Sinus bradycardia, presence of J (osborn) waves and slow atrial fibrillation.

A

Hypothermia

104
Q

What plant is the drug Digoxin synthesized from?

A

Black nightshade

105
Q

What would you see if there were toxic levels of Digoxin? (3)

A

sinus exit block
AV nodal blockade
PAT

106
Q 
These pharmacological drugs can cause prolongation of which interval?
Sotalol
Quinidine
Procainamide
Disopryramide
Amiodarone
Tricyclic antidepressents
Phenothiazines
Erythromycins
A

QT prolongation

107
Q

Beck’s triad is seen in what condition?

A

pericarditis

108
Q

What is Beck’s triad?

A

Jugular vein distention
muffled heart sounds
hypotension

EKG (1 decks)

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