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APEX-Equipment > EQUIPMENT-cardiac rhythm monitors > Flashcards

EQUIPMENT-cardiac rhythm monitors Flashcards

1
Q

What are the 3 internodal tracts that travel from the SA node to the AV node

A
  1. Anterior internodal tract (Bachmann bundle)
  2. Middle internodal tract (Wenckebach tract)
  3. Posterior internodal tract (Thorel tract)
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2
Q

Compare the conduction velocities of the cardiac conduction pathway from fastest to slowest

A 
SA node
AV node
His Bundle
Bundle branches
Purkinje fibers
Myocardial muscle cells
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3
Q

Conduction velocity is a function of what 3 factors

A
  1. Resting membrane potential
  2. Amplitude of the AP
  3. Rate of change in the membrane potential during phase 0
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4
Q

What 5 factors affect conduction velocity

A
  1. ANS tone
  2. Hyperkalemia induced closure of Na+ channels
  3. Ischemia
  4. Acidosis
  5. Antiarrhythmic drugs
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5
Q

Atrial depolarization occurs during which EKG events (2)

A 
P wave (begins)
Pr interval (ends)
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6
Q

Atrial repolarization occurs during which EKG event

A

QRS complex

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7
Q

Ventricular depolarization occurs during which EKG events

A 
QRS complex (begins)
ST segment (ends)
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8
Q

Ventricular repolarization occurs during which EKG events

A 
T wave (begins)
After T wave (ends)
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9
Q

P wave:
Duration=
Amplitude=

A 
Duration= 0.08 - 0.12 sec
Amplitude= <2.5 mm
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10
Q

PR interval

A

0.12 - 0.20 sec

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11
Q

Q wave:
Duration=
Amplitude=

A 
Duration= < 0.04 sec
Amplitude= <0.4 - 0.5 mm
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12
Q

QRS complex:
Duration=
Amplitude=

A 
Duration= <0.10 sec
Amplitude= progressive increase from V1 to V6
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13
Q

What does a biphasis P wave indicate

A
  1. Mitral stenosis

2. LA enlargement

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14
Q

What does a tall P wave suggest

A
  1. Cor pulmonale

2. RA enlargement

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15
Q

What does a prolonged PR interval indicate

A

1st degree HB

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16
Q

What does PR interval depression indicate

A
  1. Viral pericarditis

2. Atrial infarction

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17
Q

What 3 alterations in the Q wave can indicate MI

A
  1. Amplitude greater than 1/3 of R wave
  2. Duration > 0.04 sec
  3. Depth > 1 mm
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18
Q

What 4 abnormalities occurs with increased QRS complex duration

A
  1. LVH
  2. BBB
  3. Ectopy
  4. WPW
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19
Q

QTc interval:

Duration =

A

Men <0.45

Women < 0.47

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20
Q

What are 3 causes of elevated ST segment

A
  1. MI (> 1 mm)
  2. Hyperkalemia
  3. Endocarditis
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21
Q

Describe causes of negative T wave

A
  1. MI

2. BBB

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22
Q

What are 3 causes of peaked T wave

A
  1. MI
  2. LVH
  3. ICH
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23
Q

When is a U wave present

A

hypokalemia?

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24
Q

How is ST segment elevation or depression determined

A

By measuring the beginning (J point) relative to the PR segment
+/- 1 mm is significant

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25
Q

What 6 EKG changes occur with elevated K+

From early to late appearance

A
  1. Narrow, peaked T
  2. Short QT
  3. Wide QRS
  4. Low amplitude P
  5. Wide PR
  6. Nodal block
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26
Q

What 4 EKG changes occur with low K+

A
  1. U wave
  2. ST depression
  3. Flat T wave
  4. Long QT interval
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27
Q

What EKG changes occur when Ca++ is abnormal
High=
Low=

A 
High= short QT
Low= Long QT
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28
Q

What EKG changes occur when Mg++ is severely abnormal
High=
Low=

A 
High= heart block, cardiac arrest
Low= Long QT
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29
Q

What does a positive deflection indicate in EKG

A

Depolarization travels TOWARD positive electrode

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30
Q

What does a negative deflection indicate for EKGs

A

Depolarization travels AWAY from positive electrode

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31
Q

What does a biphasis deflection indicate for EKGs

A

Depolarization travels PERPENDICULAR to the positive electrode

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32
Q

What is the directionality of depolarization

A

Base to apex

Endocardium to epicardium

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33
Q

How does polarity of the myocyte change during depolarization

A

Myocyte goes from internally NEG to internally POS

This produces positive electrical current

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34
Q

What is the directionality of repolarization

A

Apex to base

Epicardium to endocardium

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35
Q

How does polarity of the myocyte change during repolarization

A

Myocyte foes from internally POS to internally NEG

Produces negative electrical current

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36
Q

Why is the T wave positively reflected during repolarization

A

Because repolarization travels in the opposite direction with a negative current (double negative)

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37
Q

What are the bipolar leads

A

Leads I, II, III

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38
Q

What are the limb leads

A

Leads aVR, aVL, aVF

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39
Q

What are the precordial leads

A

Leads V1 - V6

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40
Q

What do leads II, III, aVF monitor

Vessel and location

A

Inferior

RCA

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41
Q

What do leads I, aVL, V5, V6 monitor

Vessel and location

A

Lateral

CxA

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42
Q

What do leads V1 - V4 monitor

Vessel and location

A

Septum

LAD

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43
Q

What does the EKG axis represent

A

The direction of the mean electrical vector in the frontal plane

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44
Q

What is the easiest method to determine axis deviation

A

Examine lead I aVF

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45
Q

What does normal axis deflection look like

A

Lead I = +

Lead aVF= +

46
Q

What does left axis deviation look like

A

Lead I = +

Lead aVF= -

47
Q

What does right axis deviation look like

A

Lead I = -

Lead aVF=+

48
Q

What does extreme right axis deviation look like

A

Lead I = -

Lead aVF= -

49
Q

What are 5 common causes of right axis deviation

A
  1. COPD
  2. Cor pulmonale
  3. Acute bronchospasm
  4. PE
  5. Pulm HTN
50
Q

What are 5 common causes of left axis deviation

A
  1. Chronic HTN
  2. LBBB
  3. AS
  4. AI
  5. Mitral regurg
51
Q

What is normal axis deviation measurement
Left axis=
Right axis=

A 
Normal= -30 to +90 degrees
Left= more neg than -30
Right = more pos than +90
52
Q

Where does the mean electrical vector tend to point

A
  1. TOWARDS areas of hypertrophy
    - more tissue to depol
  2. AWAY from areas of infarction
    - vector moves around MI
53
Q

What reflex mediates sinus arrhythmia

A

Bainbridge reflex

SA node pacing varies with respirations (d/t changes in intrathoracic pressure)

54
Q

How is glucagon useful in some bradycardias

A

Useful for BB or CCB overdose

Glucagon receptors are stimulated on myocardium, increasing cAMP and HR

55
Q

What is the dose for glucagon for BB/CCB OD

A 
Initial = 50 - 70 mcg/kg
Infusion = 2-10 mg/hr
56
Q

1st line treatment for bradycardia

Treatment for symptomatic bradycard

A

1st line = atropine

Symptomatic = transcutaneous pacing

57
Q

1 physiologic causes of ST

A
  1. increased intrinsic firing of SA node

2. SNS stimulation

58
Q

How does ST affect myocardial O2 supply and demand

A 
Demand = increased
Supply = decreased
59
Q

Why is ST not tolerated in pts with poor cardiac reserve or CAD

A

Poor reserve = Precipitate MI or CHF

CAD = precipitate ischemia or infarction

60
Q

How does AFib affect CO

A
  1. Loss of atrial kick
  2. Reduced diastolic filling time with RVR
  3. Decreased CO
61
Q

What medications are used to treat afib

A
  1. BB
  2. CCB
  3. Digoxin
  4. Anticoags to prevent thrombus
62
Q

Initial cardioversion energy for acute onset a-fib

A

100 joules

63
Q

How does a-flutter differ from a-fib

A

A-flutter has an organized supraventricular rhythm

Atrial rate >250

64
Q

Describe a-flutter

A

Each atrial depolarization produces an atrial contraction

Not all atrial depolarization conduct past AV node

65
Q

Initial cardioversion energy for a-flutter

A

50 joules

66
Q

When does a junctional rhythm occur

A

When AV node functions as dominant pacemaker

Rate 40 - 60 bpm

67
Q

Why is junctional rhythm slower

A

Rate of phase 4 depolarization of the AV node is slow

68
Q

2 causes of Junctional rhythm

A
  1. SA node depression (volatile anesthetics)
  2. SA node block
  3. Prolonged conduction at the AV node
69
Q

What are premature ventricular contractions (PVCs)

A

Contractions that originate from foci below the AV node

-reason for wide QRS

70
Q

What are 7 conditions that can develop PVCs

A
  1. SNS stimulation
  2. MI
  3. Valvular dz
  4. Cardiomyopathy
  5. Prolonged QT interval
  6. Hypokalemia
  7. Hypomagnesemia
  8. Digitalis tox
  9. CVC
71
Q

How can PVCs lead to further dysrhythmias

A

If PVC lands on second half of T wave, can precipitate R on T phenomenon

72
Q

What medication can be given for symptomatic PVCs

A

Lidocaine 1.0 - 1.5 mg/kg

73
Q

Treatment for V fib

A

Immediate CPR

Defibrillation

74
Q

Treatment for asystole

A

CPR

NO shocks

75
Q

What is Brugada syndrome

A

Na+ ion channelopathy in heart

Can lead to V-Tach or V-Fib

76
Q

What are diagnostic EKG changes of Brugada syndrome

A

RBBB w/ ST-segment elevation in leads V1-V3

77
Q

Treatment and considerations for patients with Brugada syndrome

A

ICD placement

Pad placement during surgery

78
Q

Describe a 2nd-degree Mobitz type 1 block

A

PR interval progressively longer

P wave drops QRS

79
Q

Describe a 2nd-degree Mobitz type 2 block

A

Some Ps conduct to ventricle, other Ps drop QRS

NO PROLONGATION

80
Q

Treatment for 2nd-degree blocks
Type 1
Type 2

A

Type 1 = atropine

Type 2 = pacing (atropine NOT useful)

81
Q

Describe a 3rd-degree heart block

A

The atria and ventricle each have their own rates

AV dissociation

82
Q

Treatment for 2rd-degree heart block

A
  1. pacemaker

2. Isoproterenol

83
Q

What altered conduction regions produce the following block
2nd degree T1
2nd degree T2

A

2nd degree T1 = AV node

2nd degree T2 = His bundle or bundle branches

84
Q 
What is the mechanism of class 1 antiarrhythmic drugs
Ex:
A

Inhibition of fast Na+ channels

Ex: lidocaine, procainamide, phenytoin

85
Q 
What is the mechanism of class 2 antiarrhythmic drugs
Ex:
A

Decrease the rate of phase 4 depol

Ex: BB

86
Q 
What is the mechanism of class 3 antiarrhythmic drugs
Ex:
A

Inhibits K+ ion channels and prolongs phase 3 repol

Ex: amiodarone

87
Q 
What is the mechanism of class 4 antiarrhythmic drugs
Ex:
A

Inhibits slow Ca++ channels, slows conduction velocity through AV node
Ex: CCB, diltiazem, verapamil

88
Q

What is the mechanism of action and dose for adenosine

A

MOA = Slows conduction through AV node by stimulating adenosine-1 receptor, causing K+ efflux and hyperpolarizing the cell membrane

Dose = 3 mg - 12 mg IVP

89
Q

In which dysrhythmic conditions is adenosine useful

A

SVT

WPW w/ narrow QRS

90
Q

In which pts should adenosine be used with caution and why

A

Asthma pts

Can cause bronchospasms

91
Q

What are 3 causes of re-entry pathways

A
  1. Conduction occurs over a long distance
  2. Conduction velocity is too low
  3. Refractory period is shorter
92
Q

What are 2 ways to disrupt a reentry circuit

A
  1. Slow the conduction velocity through the circuit

2. Increase the refractory period of the cells at the location of the unidirectional block

93
Q

What is the most common cause of tachydysrhythmias

A

Re-entry pathway

94
Q

How can mitral stenosis cause a re-entry pathway

A

Conduction must occur over a longer distance

95
Q

how can ischemia cause a reentry pathway

A

Conduction velocity through the affected region is too slow

96
Q

How can epinephrine cause a reentry pathway

A

It shortens the duration of the refractory period

97
Q

What is the defining feature of WPW

A

An accessory conduction pathway (Kent’s bundle) that bypasses the AV node (connect atrium and ventricle)
There is a conduction delay

98
Q

What is a key diagnostic feature of WPW on EKG

A

delta wave

99
Q

What is the most common tachydysrhythmia associated with WPW

A

AV nodal reentry tachycardia

100
Q

What is the morphology and treatment (6) for orthodromic AVNRT

A

Morphology = narrow QRS
Treatment = increase refractory period at AV NODE
-vagal maneuver, amio, adenosine, BB, CCB, cardiovert

101
Q

What is the morphology and treatment (2) for antidromic AVNRT

A

Morphology = wide QRS complex

Treatment = increase refractory period of the ACCESSORY pathway
-procainamide, cardiovert

102
Q

What agents (5) should be avoid when treating antidromic AVNRT

A

Medications that increase the refractory period (opposite of orthodromic AVNRT)
-adenosine, digoxin, CCB, BB, lidocaine

103
Q 
What do each of the following positions categorize in pacemakers
Position 1
Position 2
Position 3
Position 4
Position 5
A 
Position 1 = chamber paced
Position 2 = chamber sensed
Position 3 = response to sensed activity
Position 4 = programmability options
Position 5 = PM can pace multiple sites
104
Q

How are the following pacing modes indicated in their settings
Asynchronous =
Single-chamber=
Dual-chamber=

A 
Asynchronous = AOO, VOO, DOO
Single-chamber= AAI, VVI
Dual-chamber= DDD
105
Q

What does failure to capture indicate

A

The PM delivers an electrical stimulus but fails to trigger myocardial depolarization

106
Q

What does magnet placement do to a PPM

A

Converts the PM to asynchronous mode

107
Q

What does a magnet placement do to an ICD

A

Suspends the ICD and prevents shock delivery

108
Q

What does a magnet placement do to a PM/ICD

A

Suspends ICD

No effect on PM function

109
Q

Which setting of electrocautery causes more EMI with a PM

A

coag > cutting

110
Q

What type of cautery causes more EMI in pts with PM

A

Monopolar > bipolar=US harmonic

111
Q

When is EMI risk highest in the presence of electrocautery

A

When tip is used w/in 15 cm radius of pulse generator

112
Q

Where should the cautery ground pad be placed in pts with PM/AICD

A

As far away from pulse generator and in location that prevents a direct line of current through PM

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