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SEE/BOARD STUDY > APEX Monitoring III: CARDIAC RHYTHMS > Flashcards

APEX Monitoring III: CARDIAC RHYTHMS Flashcards

1
Q

Which pathway depolarizes the LA?

A

Bachman bundle

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2
Q

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

A

Bachmann bundle
Wenckebach tract
Thorel tract

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3
Q

Kent’s bundle is a

A

Pathologic accessory pathway that is responsible for Wolf Parkinson-White syndrome.

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4
Q

Cardiac Conduction system contains:

A 
SA node
Internodal tracts
AV node
Bundle of HIS
Bundle Branches
Purkinje fibers
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5
Q

3 internodal tracts

A

Anterior Internodal tract
MIddle Internodal tract
Posterior internodal tract

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6
Q

The anterior internodal tract is the

A

Bachmann bundle

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7
Q

The middle internodal tract

A

Wenckeback tract

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8
Q

The posterior internodal tract

A

Thorel tract

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9
Q

Conduction velocity quantified

A

how fast an electrochemical impulse propagates along a neural pathway.

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10
Q

Conduction velocities of the cardiac conduction pathway : SA and AV nodes

A

0.02 - 0.1 m/sec (slow conduction )

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11
Q

Conduction velocities of the cardiac conduction pathway : HIS bundle, bundle branches and purkinje fibers

A

1-4 m/sec (fast conduction)

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12
Q

Conduction velocities of the cardiac conduction pathway : MYOCARDIAL MUSCLE CELLS

A

0.3 - 1 m/sec (intermediate)

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13
Q

Conduction velocity is a funciton of

A

Resting membrane potential
Amplitude of the action potentila
Rate or change in membrane potential during phase O

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14
Q

Conduction velocity is affected by

A 
ANS tone
Hyperkalemia induced closure of fast Na+ channesl 
Ischemia
Acidosis
Antiarrhythmic drugs
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15
Q

There is a band of connective tissue that electrically isolates the atria from the

A

ventricles.

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16
Q

What is the only electrical pathway between the cardiac chambers?

A

AV node

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17
Q

AV node is the

A

Gatekeeper of electrical transmission between the atria and the ventricles.

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18
Q

Accessory Pathway : James Fiber

A

Connect Atrium to AV node

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19
Q

Accessory Pathway : Atria HIsian Fiber

A

Connect Atrium to HIs bundle

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20
Q

Accessory Pathway : Kent’s Bundle

A

Connect Atrium to Ventricle

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21
Q

Accessory Pathway : Mahaim Bundle

A

AV node to ventricle

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22
Q

What are the 5 phases of the ventricular action potential

A

0 , 1, 2, 3, 4

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23
Q

Phase O is

A

Rapid depolarization (QRS)

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24
Q

Phase 1 is the

A

Initial repolarization (QRS)

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25
Q

Phase 2 is the

A

plateau phase (QT interval)

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26
Q

Phase 3 is the

A

Final repolarization (T Wave)

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27
Q

Phase 4 is the

A

Resting phase (T -> QRS)

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28
Q

Depolarization Na+ movement

A

In

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29
Q

Initial repolarization ion movement

A

Cl- –> in

K+ –> out

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30
Q

Plateau movement ion movement

A

Ca2+ in

K-> Out

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31
Q

Final repolarization ion movement

A

K + out

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32
Q

Resting phase ion movement

A

Na+ Out

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33
Q

What is the ABSOLUTE REFRACTORY period?

A

No stimulus (no matter how strong) can depolarize the myocyte.

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34
Q

What is the RELATIVE REFRACTORY period?

A

Larger than normal stimulus required to depolarize the myocyte.

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35
Q

EKG event: P Wave : Electrical event in ATRIA and ventricle

A

Atria: depolarization begins

Ventricles; NONE

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36
Q

EKG event: PR INTERVAL: Electrical event in ATRIA and ventricle

A

Atria: Depolarization complete
Ventricles: NONE

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37
Q

EKG event:QRS : Electrical event in ATRIA and ventricles

A

ATRIA: Repolarization
Ventricles: Depolarization begins

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38
Q

EKG event: ST segment : Electrical event in ATRIA and ventricle

A

ATRIA:NONE
VENTRICLES: DEPOLARIZATION complete

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39
Q

EKG event: T Wave : Electrical event in ATRIA and ventricles

A

ATRIA: NONE
VENTRICLES: Repolarization begins

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40
Q

EKG event: after T Wave : Electrical event in ATRIA and ventricl

A

Atria: NONE

REPOLARIZATION complete

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41
Q

EKG signs of Pericarditis

A

PR interval depression

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42
Q

EKG signs of HYPOKALEMIA

A

U wave

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43
Q

EKG signs of Intracranial hemorrhage

A

Peaked T wave

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44
Q

EKG signs of WPW syndrome

A

Delta wave

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45
Q

Duration of P wave in sec____

A

0.08-0.12

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46
Q

Amplitude of P wave in mm

A

< 2.5

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47
Q

Prolonged with 1st degree HB

A

P wave

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48
Q

PR intervanl normal

A

0.12 -0.20 sec

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49
Q

Q wave when to consider MI

A

Amplitude is greater than 1/3 R wave
Duration is greater than 0.04 seconds
Depth is greater than 1 mm

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50
Q

Normal QRS is

A

<0.10

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51
Q

Normal QRS amplitude progressively

A

increase from V1-V6, normal R wave progression.

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52
Q

If QRS complex if increased consider

A

LVH
BBB
Ectopic beat
WPW

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53
Q

QTc interval normal value in men

A

< 0.45

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54
Q

QTc interval normal value in women

A

< 0.47

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55
Q

ST segment when to consider MI

A

ST elevation or depression greater than 1 mm

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56
Q

ST elevation also caused by (other than the obvious MI)

A

Hyperkalemia

Endocarditis

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57
Q

T wave amplitude should be in precordial leads

A

Less than 10mm

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58
Q

T wave amplitude should be in limb leads

A

Less than 6 mm

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59
Q

Usually T wave points in the

A

Same direction as QRS

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60
Q

When T wave point in opposite direction of QRS

A

if repolarization is prolonged by MI, BBB

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61
Q

Peaked T waves are caused by

A

MI
LVH
Intracranial bleed

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62
Q

U wave if greater than

A

1.5mm, consider HYPOKALEMIA

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63
Q

Where is the J point ?

A

The point where the QRS complex and the ST segment begins.

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64
Q

By measuring the J point, relative to the PR segment we can

A

quantify the amount of ST elevation and depression

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65
Q

High potassium on T, QT, QRS

Early to late signs

A 
Narrow peaked T
Short QT
Wide QRS
Low P amplitude
Wide PR
Nodal BLOCK 
Sine wave fusion of QRS and T --> VF or asystole.
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66
Q

Too low potassium on QT

A

Long QT interval

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67
Q

Hypercalcemia on QT

A

Short QT

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68
Q

Hypocalcemia on QT

A

Long QT

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69
Q

Very low mag on QT

A

Long QT

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70
Q

The waveform on the EKG is a measure of the

A

Mean electrical vector

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71
Q

2 vectors to understand

A

Vector of depolarization

Vector of repolarization

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72
Q

Each lead consist of

A

One negative electrode

One positive electrode

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73
Q

Vector of depolarization

A

QRS complex

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74
Q

Direction the heart

A

Depolarizes from 1, base =>apex and 2. Endocardium–> Epicardium

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75
Q

Polarity the myocytes go from

A

internally (-) to internally (+) THIS PRODUCES A POSITIVE ELECTRICAL CURRENT

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76
Q

When does a positive deflection occur?

A

when the vector of depolarization TOWARDS the positive electrode.

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77
Q

When does a negative deflection occur?

A

when the vector of depolarization AWAY from the positive electrode.

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78
Q

When does a BIPHASIC deflection occurs?

A

when the vector of depolarization PERPENDICULAR to the positive electrode.

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79
Q

Vector of REPOLARIZATION

A

T wave

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80
Q

Direction the heart repolarizes form

A
  1. apex –> Base and 2. Epicardium –> Endocardium
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81
Q

Think of repolarization as the

A

Opposite of depolarization

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82
Q

Polarity the myocytes from internally (+) to internally (-) this produces a

A

Negative electrical current

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83
Q

A positive deflection occurs when the wave travels

A

AWAY from the positive electrode

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84
Q

The vector of repolarization travels in the

A

Opposite direction as the vector of depolarization

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85
Q

The vector of repolarization produces a

A

negative current

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86
Q

12 leads are

A

12 cameras

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87
Q

How many bipolar leads

A

3

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88
Q

How many limb leads

A

3

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89
Q

How many precordial leads

A

6

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90
Q

What are the bipolar leads

A

I, II, III

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91
Q

What are the limb leads

A

aVR
aVL
aVF

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92
Q

What are the precordial leads

A 
V1
V2
V3
V4
V5
V6
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93
Q

Septum leads are

A

V1, V2

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94
Q

Anterior leads are

A

V3, V4

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95
Q

Lateral leads are

A

I, aVL, V5, V6

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96
Q

Inferior leads are

A

II, III, aVF

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97
Q

The mean electrical vector tends to point to

A

Towards areas of hypertrophy (more tissue to depolarize)

Away from areas of Myocardial infarction (The vector must travel around these areas)

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98
Q

The mean electrical vector normal value is between

A

-30 degrees and +90 degrees

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99
Q

Axis represents the

A

direction of the mean electrical vector in the frontal area.

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100
Q

Examine those 2 leads to determine axis

A

I and aVF

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101
Q

Normal axis: I and AVF

A

Both positive

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102
Q

Left axis deviation

A

Lead I positive

Lead avF negative

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103
Q

Right axis deviation

A

Lead I negative

Lead avF positive

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104
Q

Extreme Right axis deviation

A

Lead I and avF negative

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105
Q

Leads reaching toward each other then we have (l pointing down and avF pointing up)

A

Right axis deviation

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106
Q

Leads Leaving each other (L pointing up and avF pointing down_ then we have

A

LEFT AXIS deviation

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107
Q

Left axis is more

A

more negative than -30 degrees

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108
Q

Right axis is more

A

More positive than 90 degrees.

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109
Q

Axis deviation with COPD

A

Right

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110
Q

Axis deviation with chronic HTN

A

Left

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111
Q

Axis deviation with Acute bronchospasm

A

Right

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112
Q

Axis deviation with Cor pulmonale

A

Right

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113
Q

Axis deviation with Pulmonary HTN

A

Right

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114
Q

Axis devation with PE

A

right

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115
Q

Axis deviation with LBBB

A

Left

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116
Q

Axis deviation with Aortic stenosis

A

Left

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117
Q

Axis deviation with aortic insuffieciency

A

Left

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118
Q

Axis deviation with mitral regurgitation

A

Left

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119
Q

Adenosine is an

A

Endogenous nucleoside slows the conduction through the AV node.

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120
Q

ACtion of adenosine

A

Stimulate the cardiac adenosine-1 receptor , adenosine activates K currents, which hyperpolarizes the cell membrane and reduces action potential.

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121
Q

2 things Adenosine good for

A

SVT

WPW

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122
Q

Adenosine effective in treating Afib?

A

No

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123
Q

Adenosine effective in treating Aflutter?

A

No

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124
Q

Adenosine effective in treating Torsdades de pointes

A

No

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125
Q

Lidocaine class

A

IB

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126
Q

Amiodarone Class

A

III

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127
Q

Beta Blocker antiarrythmic class

A

Class II

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128
Q

CCB antiarrythmic class

A

Class IV.

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129
Q

Class I drugs inhibit

A

fast sodium channels

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130
Q

Class II drugs decrease the

A

rate of depolarization

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131
Q

Class III drugs inhibit

A

Posstaium ion channels

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132
Q

Class IV drugs inhibit

A

Slow calcium channels.

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133
Q

Sinus arrhythmia occurs when the

A

SA note pacing rate with respiration. its usually benign

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134
Q

What is the Bainbridge reflex?

A

When an increased in venous return stretches the RA and SA node causing the HR to increase. It should make sense that it would cause sinus arrythmia.

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135
Q

Inhalation effect on on intrathoracic pressure?

A

Decrease intrathoracic pressure –> Increase VR and increase HR.

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136
Q

Exhalation effect on on intrathoracic pressure?

A

Increase intrathoracic pressure –> Decrease VR and decrease HR.

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137
Q

SInus bradycardia defined as

A

HR < 60

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138
Q

What is the most common source of bradycardia?

A

Increased vagal tone.

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139
Q

What is the first line of Tx for bradycardia?

A

Atropine.

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140
Q

What can cause paradoxical bradycardia with atropine? Mediated by?

A

Underdosing it < 0.5mg IV. Presynaptic muscarinic receptors.

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141
Q

Severely symptomatic patients with bradycardia should receive

A

Immediate transcutaneous pacing.

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142
Q

Beta Blocker or CCB overdose treatment.

A

GLUCAGON

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143
Q

How does glucagon work ?

A

Stimulating glucagon on the myocardium. INCREASING cAMP leading to increase HR, contractility, and AV conduction.

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144
Q

What is the initial dose of glucagon?

A

50-70mcg/kg q3-5 min, can be FOLLOWED By infusion at 2-10 mg/hr

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145
Q

What causes tachycardia?

A

Increase intrinsic firing rate of the SA node or sympathetic stimulation.

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146
Q

Some etiologies of tachycardia

A

Hypovolemia, hypoxemia, infection. MH, Thyrotoxicosis

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147
Q

What is the effect of tachycardia on oxygen balance?

A

Increase myocardial oxygen demand WHILE decreasing oxygen supply.

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148
Q

Tachycardia can precipitate what ?

A

MI and CHF in patients with POOR CARDIAC RESERVE>

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149
Q

Tachycardia and patients with CAD

A

Precipitate MI and/or infarction

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150
Q

Best initial treatment of tachycardia

A

Treating the underlying cause

151
Q

Best 2nd treatment of tachycardia

A

rate control with Bblockers or CCBs.

152
Q

AFib is an

A

irregular rhythm with the absence of a P wave

153
Q

With Afib, Chaotic electrical activity in the

A

Atrium is conducted to the ventricle at a varied and irregular

154
Q

Afib and effect on CO

A

LOSS OF ATRIAL kick

155
Q

Afib and perioperative mortality

A

Increase risk

156
Q

Main problem with afib is

A

Risk of atrial thrombus formation (risk of stroke)

157
Q

Afib with RVR

A

reduces diastolic filing time and is ASSOCIATED WITH severe reduction in CO

158
Q

Afib with RVR associated with severe reduction of CO as manifested by

A

syncope
chest pain
SOB

159
Q

2 Treatments of Afib with RVR

A

Beta blockers, CCB, Digoxin

AND anticoagulation

160
Q

Acute onset of Afib treated with

A

Cardioversion (start at 100Joules)

161
Q

AFIB onset and its implications

A

If onset is older than 48 hours (or if onset is undertermined) a TEE must be performed to rule out atrial thrombus.

162
Q

Arrhythmia that is an indication to cancel surgery

A

new onset afib; aflutter

163
Q

What is the most COMMON POSTOP tachydysrhythmia? when does it usually occurs and who is at risk?

A

Atrial fibrillation ; 2-4 days’’ older patients post CT surgery.

164
Q

Aflutter compared to afib is

A

Organized supraventricular rhythm

165
Q

Aflutter is recognizable with what kind of pattern.

A

Saw tooth pattern

166
Q

In aflutter what is the atrial rate

167
Q

During a flutter , each atrial depolarization produces an

A

Atrial contraction , but not all atrial depolarizations are conducted past the AV node.

168
Q

Usually defined with AFLUTTER

A

Defined ration of atrial to ventricular contractions.

169
Q

In atrial flutter, what prevents all impulses from being transmitted to the ventricles?

A

Effective refractory period.

170
Q

If atrial flutter onset is older than 48 hours or unknown?

A

TEE must be performed to r/o atrial thrombus.

171
Q

Risk with RVR

A

can lead to hemodynamic instability

172
Q

Treatment of aflutter

A

Rate control or cardioversion

173
Q

Hemodynamically unstable atrial flutter should be treated with cardioversion start at

174
Q

PVC originated from Foci b

A

Below the AV node, such as the QRS complex is wide

175
Q

PVCs that arise from a single location are

A

unifocal (the morphology is the same on the EKG)

176
Q

PVCs that arise from multiple location are

A

Multifocal (different QRS morphologies on the EKG)

177
Q

Electrolytes disturbances associated with PVCs

A

Hypomagnesemia

Hypokalemia

178
Q

Heart issues associated with PVCs

A

MI or infarction
SNS stimulation (acidosis, Hypercabia, hypoxia)
Valvular disease
Cardiomyopathy

179
Q

Associated with PVCs other factors

A

Caffeine
Cocaine
Alcohol

180
Q

A PVC that lands on the

A

2nd half of the T wave meaning during the relative refractory period can precipitate the R on T phenomenon

181
Q

PVCS should be treated when?

A

Frequent > 6 /min polymorphic or occurs in runs of 3 or more

182
Q

Treatment of PVCs

A

reverse underlying cause

Repositioning central line that may be irritating the RA

183
Q

Medication treatment of PVCs

A

Treated with LIDOCAINE 1-1.5 mg/kg. if not resolved follow by infusion 1-4 mg/min

184
Q

What is BRUGADA Syndrome?

A

Sodium ion channelpathy in the heart.

185
Q

What can BRUGADA syndrome cause?

A

Sudden nocturnal death due to Vtach or fibrillation

186
Q

Brugada most common in males from

A

SOUTHEAST asia

187
Q

BRUGADA syndrome Diagnosis EKG findings include a

A

RBBB and ST segment elevation in V1-V3

188
Q

Pt with BRUGADA syndrome may require

A

ICD or pad placement during surgery.

189
Q

First degree HB : THE PRI is

A

> 0.20 second

190
Q

Affected regions in first degree

A

AV node or HIS bundle

191
Q

Etiology of HB

A

Age related degenrative changes, CAD, digoxin and amiodarone.

192
Q

Treatment of HB

A

Monitor (usually asymptomatic)

193
Q

Longer, longer, longer, drop then you have a

A

Wenckebach (2nd degree type I HB)

194
Q

PR interval In 2nd degree HB type I

A

The PR interval becomes progressively long with each cycle, but the last P wave does not conduct to the ventricles, then the cycle repeats.

195
Q

Why does the PR gets longer with a 2nd degree HB type I

A

Each successive depolarization increases the duration of the refractory period in the AV node. The last P in the cycle dropped, because it arrives at the AV node while it’s in the ABSOLUTE refractory period. This beat is not conducted but the pause that follows provides enough time for the AV node to reset. Then the cycle repeats.

196
Q

Affected region in 2nd degree HB type I

197
Q

Etiology in 2nd degree HB type I

A

structural conduction defect, MI, BBlockers, CCBs, digoxin, sympatholytics agents.

198
Q

Treatment of 2nd degree HB type I

A

Asymptomatic: just monitor
Symptomatic: then GIVE ATROPINE

199
Q

2nd degree HB Block (Mobitz type II) if some Ps dont get through then you have a

200
Q

2nd degree HB Block (Mobitz type II) Some Ps conduct to the ventricles, while

A

Others don’t (there is usually a set ratio 2:1 or 3:1. After the dropped QRS the next P arrives right on time.

201
Q

Affected region on 2nd degree HB Block Mobitz type II.

A

HIs bundle or bundle branche

202
Q

Etiology in 2nd degree HB Block Mobitz type II

A

structural conduction defect or infarction .

203
Q

Treatment of 2nd degree HB Block Mobitz type II

A

Often symptomatic
Pacemaker
atropine often not effective.

204
Q

Key point of 2nd degree HB Block Mobitz type II

A

HIGH RISK OF PROGRESSING TO COMPLETE HB>

205
Q

If Ps and Qs dont agree then you have

A

3rd degree.

206
Q

AV dissociation with atria and ventricles have their onw rates

A

Third degree HB

207
Q

With 3rd degree HB block in the AV node has a

A

narrow QRS (rate 45-55bpm)

208
Q

With 3rd degree HB block Below the AV node has a

A

wide QRS (rate 30-40)

209
Q

Etiology of 3rd degree HB

A

Fibrotic degeneration of the atrial conduction system. Lenegre’s disease.

210
Q

Treatment of 3rd degree HB

A

PM

ISOPROTERENOL (chemical PM)

211
Q

3rd Degree HB symptoms

A

Often symptomatic: syncope, dyspnea, weakness, vertigo.

212
Q

Key points about 3rd degree HB symptoms

A

Can lead to CHF due to decreased HR and CO

213
Q

Stokes-Adams attack is associated with

A

3rd degree HB

214
Q

What is STOKES-ADAMs ATTaCK?

A

Decreased CO –> Decrease cerebral perfusion –> Syncope

215
Q

How are antiarrhythmic drugs are classified according to their ability to

A

Block specific ion channels and currents of the cardiac action potential

216
Q

Mechanism of action of CLASS IA

A

Moderate depression of phase O

Prolongs phase 3 repolarization (K+ channel block –> Prolonged QT )

217
Q

Class I anti-arhythmic action on what 2 phases

A

Phase 0 and Phase 3

218
Q

Mechanism of action of CLASS IB

A

Weak depression of phase O

Shortened phase 3

219
Q

Examples of Class IA

A

Quinidine
Procainamide
Disopyramide

220
Q

Examples of Class IB

A

Lidocaine, Phenytoin

221
Q

Mechanism of action of CLASS IC

A

STRONG depression of phase O

Little effect on phase 3 repolarization

222
Q

Examples of Class IC

A

Flecainide, Propafenone

223
Q

Class 2 are the

A

Beta Blockers

224
Q

Mechanism of action of Beta Blockers

A

Slows phase 4 depolarization in SA node

225
Q

Class III are the

A

K+ Channels

226
Q

Mechanism of action of K+ Channel Blockers (Class III)

A

Prolongs Phase 3 repolarization (prolonged QT)

Increase ERP

227
Q

Class IV are the

A

Ca2+ Channel blockers

228
Q

Mechanism of action of Ca2+ CCB

A

Decrease conduction through the AV node

229
Q

How is adenosine metabolized

230
Q

Half time of adenosine

231
Q

Adenosine useful for

A

SVT

WPW with a narrow QRS

232
Q

Adenosine and reactive airway

A

Bronchospasm in asthmatic patients.

233
Q

How to dose adenosine? Peripheral IV

A

First dose: 6mg

Second dose : 12 mg if required

234
Q

How to dose adenosine? Central line

A

First dose: 3 mg

Second dose: 6mg

235
Q

WPW is associated with : what kind of re-entry

A

Atrial -ventricular reentry

236
Q

When does WPW occurs?

A

When an accessory pathway joins the atrium to the ventricle: called Kent’s Bundle

237
Q

Most common cause of tachyarrythmias are

A

Reentry pathways

238
Q

Explain the impulse conduction through the normal pathway?

A

SA node –> AV node –> HIS bundle –> Bundle branches—> purkinje fibers

239
Q

Can impulse move backwards?

A

No because all the tissues behind the impulse remain in the absolute refractory period

240
Q

What is the ratio of SA node depolarization and cardiac contraction?

241
Q

Single pathway conduction system: how does it occur?

A

As the cardiac impulse propagates, it may encounter an area that can create an electrical circuit. It will travel along both pathways. Left and right at the same speed. Meet in the middle and cancel each other out.NO opportunity for reentry.

242
Q

What is reentry?

A

single cardiac impulse can move backwards and excite the same part of the myocardium over andover.

243
Q

Ratio of SA node discharge and cardiac contraction can exceed 1:1 ratio, there is a risk that

A

an impuse that circles around the reentry pathway will precipitate a reentry tachyarrhythmia.

244
Q

How to break a circuit for reentry? 2 ways

A

Slowing down conduction velocity through the circuit

Increasing the refractory period of the cells at the location of the unidirectional block

245
Q

3 possible causes of reentry?

A

Conduction occurs over a long distance
Conduction velocity is too slow
Refractory period is shorter.

246
Q

Example of conduction over a long distance

A

Left atrial dilation due to mitral stenosis

247
Q

Example of conduction velocity is too slow

A

Ischemia

Hyperkalemia

248
Q

Refractory period is shorter example

A

Epinephrine

Electric shock from alternating current.

249
Q

Patient with WPW develops afib during surgery , 2 medications to give

A

Procainamide

Amiodarone

250
Q

What is the most common pre-excitation syndrome?

251
Q

Defining feature of WPW

A

Consists of an accessory conduction pathway that bypasses the AV node (Kent’s bundle)

252
Q

The accessory pathway forms a direct line of communication between the atrium and the ventricel

A

Kent’s bundle

253
Q

During the normal conduction pathway, the cardiac impulse is delayed where?

A

At the AV node, meaning the AV node has a long refractory period.

254
Q

What happens during the accessory pathway?

A

There is not delay , impulse move quickly from the atrium to the ventricle. There is no gatekeeper function .

255
Q

How is WPW Diagnosed?

A

routine EKG , or hx of tachydysrhythmias.

256
Q

Characteristicts of WPW on EKG

A

**Delta wave
**Short PR < 0.12 second
***wide QRS complex
possible t wave inversion

257
Q

Why is there a delta wave?

A

Because of ventricular preexcitation.

258
Q

WPW syndrome is classified in

A

Type A and type B.

259
Q

WPW type A

A

right bundle branch block with right ventricular hypertrophy

260
Q

WPW Type B

A

resembles left bundle branch block with left ventricle hypertrophy.

261
Q

Most common tachydysrhythmia associated with WPW?

A

AV nodal reentry tachycardia

262
Q

AV nodal reentry tachycardia classified as

A

Orthodromic or antidromic

263
Q

Orthodromic vs antidromic: more common

A

Orthodromic (`90% cases) Antidromic (10% of cases)

264
Q

Reentry conduction pathway with orthodromic

A

Atrium –> AV node –> Ventricle–> Accessory pathway —> Atrium

265
Q

Reentry conduction pathway with antidromic

A

Atrium –> Accessory pathway —> Ventricle–> AV node –> ATrium

266
Q

QRS morphology with orthodromic

267
Q

QRS morphology with antidromic

268
Q

QRS in orthodromic: what happens with ventricular depolarization?

A

Normal via the HIS- Purkinje system

269
Q

QRS in antidromic: what happens with ventricular depolarization?

A

Ventricular depolarization is slower since HIS system is bypassed.

270
Q

Goal of Treatment of orthodromic

A

Block conduction at the AV node pathway (Increase the AV node refractory period)

271
Q

Block conduction at the AV node pathway for orthodromic treatment include

A 
Vagal maneuvers
Amiodarone
Adenosine
BBlockers
Veraparmil
Cardioversion
272
Q

Goal of Treatment of antidromic:

A

Block conduction at the accessory pathway (Increase accessory pathway refractory period)

273
Q

Block conduction at the accessory pathway with those treatment for antidromic

A

Procainamide
Amiodarone
Cardioversion .

274
Q

Do not do this with antidromic pathway?

A

Do not give agents that increase the refractory period of the AV node, because doing so will favor conduction through the accessory pathway.

275
Q

Orthodromic vs antidromic which one is more dangerous?

A

Antidromic

276
Q

Why is antidromic more dangerous?

A

Because the gatekeeper function of the AV node is bypassed and the HR can increase well beyond the heart’s pumping ability (dramatically reduces filling time)

277
Q

If you give an AV nodal blocking drug to a patient with antidromic AVNRT what will happen?

A

You will force the conduction along the accessory pathway. This can induce Vfib. THEREFORE avoid drugs that BLOCK CONDUCTION through the AV node.

278
Q

Drugs to AVOID with antidromic AVNRT include

A 
Adenosine
Digoxin
CCBs (Diltiazem and verapamil)
BBlockers
Lidocaine.
279
Q

Safe opitions for both orthodromic and ANTIDROMIC AVNRT?

A

Amiodarone

Cardioversion

280
Q

Afib and WPW : Because there is no delay in the accessory pathway,

A

A rapid atrial rate can be conducted to the ventricles in a 1:1 ration .

281
Q

During atrial fibrillaiton , the atria can depolarize up to

A

300x per minutes.

282
Q

Combination of AF and WPW can precipitate 3 thins

A

CHF
Vfib
Death .

283
Q

Why is Procainamide the tx of choice for WPW?

A

It increases the REFRACTORY PERIOD in the accessory pathway.

284
Q

IF the patient is hemodynamically unstable,best option is

A

Cardioversion

285
Q

What is the definitive treatment for accessory pathway?

A

Radiofrequency ablation

286
Q

Risk with radiofrequency ablation of pathways involving the Left atrium?

A

Imposes a risk of thermal injury to the left atrium and the esophagus.

287
Q

What is required when there is ablation of a pathway involving the left atrium?

A

Esophageal temperature is required.

If the temperature rises during periods of ablation, YOU MUST INFORM THE CARDIOLOGIST IMMEDIATELY.

288
Q

Increases the likelihood of torsades de pointes in the patient with Long QT syndrome 3 things

A

Furosemide
Hyperventilation
Methadone

289
Q

Patients with long QT syndrome at risk for

A

Torsades de pointes.

290
Q

Patients with long QT syndrome should not receive

291
Q

The only narcotic known to increase the QT interval

292
Q

Furosemide and QT interval

A

Can cause hypokalemia and hypomagnesemia which can further prolong the QT interval

293
Q

Hyperventilation and QT

A

Hyperventilation shifts K+into cells, decreases serum K and prolong the QT interval

294
Q

Twisting of the spikes

A

Torsades de pointes.

295
Q

Underlying cause of torsade de pintes?

A

Delay in ventricular repolarization (phase 3 of the action potential). se

296
Q

Torsades de pointes is ______But can deteriorate to

A

Self limiting; ventricular fibrillation.

297
Q

Torsades de pointes QT

A

Torsades associated with long QT

298
Q

Causes of torsade de pointes mnemonic

A 
Phenothiazines
Other meds
Intracranial bleed
No known cause
Type I antiarrythmics
Electrolytes disturbance
Syndromes
299
Q

Antiemetic drugs causes Long QT

A

Haloperinol
Droperinol
Ondansetron

300
Q

Antiarrhythmic causing prolonged QT

A

Amiodarone (especially with hypokalemia)

Quinidine

301
Q

Genetic syndromes associated with Prolonged QT

A

Romano-ward syndrome

Timothy syndrome

302
Q

QT interval and HR

A

Inversely related with HR.

303
Q

Prolonged QT parameter in men

A

> 0.45 seconds

304
Q

Prolonged QT parameter in women

A

> 0.47 seconds

305
Q

Other text consider QT _______ prolong

A

> 40 seconds

306
Q

PVC or poorly timed pacer discharge during the

A

relative refractory periods (during the second half of the T wave) can cause torsades pointes. (R on T phenomenon)

307
Q

Prevention and treatment: Patients with Long QT syndrome may require

A

Beta blocker prophylaxis and /or ICD placement

Avoid SNS stimulation

308
Q

Acute treatment for torsades de pointes include

A

Reversing the UNDERLYING cause and/or shorten the QT interval.

309
Q

Acute treatment of torsades de pointes with meds

A

Magnesium sulfate

Cardiac pacing to increase th HR will reduce the action potential duration and the QT interval.

310
Q

Pacemaker Position I is

A

Chamber PACED

311
Q

Pacemaker positionII is

A

Chamber SENSED

312
Q

Pacemaker position III is

A

Response to sensed event

313
Q

Pacemaker position IV is

A

Programmability

314
Q

PM mnemonic for position

315
Q

When is a pacemaker required?

A

Heart unable to produce a normal rate and rhythm.

316
Q

3 major indications for pacemaker

A

Long QT syndrome
Dilated cardiomyopathy
Hypertrophic obstructive cardiomyopathy

317
Q

Major indications for pacemaker nodal issue

A

Symptomatic diseases of impulse formation (SA node disease or AV node disease

318
Q

What does a pacemaker consistst of

A

Pulse generator and pacing leads that deliver electrical current to the heart.

319
Q

Epicardial leads function

A

stimulate the surface of the heart.

320
Q

Transvenous lead function

A

stimulated the cardiac chambers (RA and or RV)

321
Q

Position I can be one of 4

A

O=none
A=Atrium
V= Ventricle
D= Dual

322
Q

Position II can be one of 4

A

O=none
A=Atrium
V= Ventricle
D= Dual

323
Q

Position III can be one of 4

A

T= Sensed activity tells the pacemaker to fire
I = Sensed activity tells the pacemaker NOT to fire
D-= if native activity is sensed , then pacing is inhibited
If native activity is not sense, then the pacemaker fire.

324
Q

Position III can be one of 4

A

None
triggered
Inhibited
Dual(D+T)

325
Q

Position IV can be one of 2

A 
O= none
R= rate modulation
326
Q

None or rate modulcaiton indicates the

A

programmability of the pacemaker. ability to adjust HR in response to physiologic need. Sensors can measure respiration, acid base status,vibration,etc.

327
Q

Position V indicates that

A

The PM can pace multiples sites.

328
Q

This mode improves AV synchrony

329
Q

This of this as a bckup mode: only fires when the native heart rate fails belowa predetermined rate

A

Single-Chamber demand pacing

330
Q

This of this as a bckup mode: only fires when the native heart rate fails belowa predetermined rate

A

Single-Chamber demand pacing : AAI, VVI

331
Q

This mode makes sure that the atrium contracts first followed by the ventricle

A

Dual-chamber AV sequential Demand Pacing (DDD)

332
Q

There is no sense or inhibition with this mode

A

Asynchronous pacing

333
Q

There is no sense or inhibition with this mode

A

Asynchronous pacing AOO, VOO, DOO

334
Q

IF the atrium is paced, what happens to the electrical signal>

A

Travels through the AV node and the QRS maintain its normal , narrow appearance.

335
Q

IF the ventricle is paced, what happens to the electrical signal>

A

is delivered beyond the AV node and the QRS takes on a WIDE APPEARANCE>

336
Q

The pacemaker can fail to capture because of

A

hypocarbia (which can cause HYPOKALEMIA) made the myocardium more resistant to depolarizaiton.

337
Q

Types of scapel that decreases the chance of EMI

A

Ultrasonic Harmonic Scapel.

338
Q

Electrocautery that reduces the risk of EMI

A

Changing from coagulation to cutting

339
Q

Hypothermia and HR

A

Bradycardia

340
Q

MAGNET role : placing a magnet over the device does what?

A

Converts the PACEMAKER to an asynchronous mode.

341
Q

The best answer for magnet is to

A

consult with the manufacture to determine how a magnet affects the pacemaker.

342
Q

Magnet over an ICD

A

Suspends the ICD and prevents shock delivery

343
Q

PM and ICD magnet

A

Suspeds the ICD and prevents shock delivery

Has no effect on the PM function (PM will be subject to EMI)

344
Q

How to minimize the risk of PM failure

A
  1. Pulse generator failure
  2. Lead failure
  3. Failure to capture.
345
Q

Risk of EMI is the greatest with the use of

A

Electrocautery and radiofrequency ablation.

346
Q

Monopolar vs bipolar cautery?

A

Monopolar causes more EMI than bipolar

347
Q

If surgeon insists of monopolar cautery

A

Insist on short bursts (0.5 seconds)

348
Q

The risk of EMI is highest when

A

the electrocautery tip is used within a 15 cm radius of the pulse generator

349
Q

Conditions that may cause PM to fire but there may be a failure to capture?

A

Hyper and hypokalemia
Hypocapnia
Hypothermia
MI

350
Q

MRI contraindicated

351
Q

Lithotripsy and PM

A

LIthotripsy is not contraindicated, beam should be directed away from the pulse generator.

352
Q

ECT and PM

A

ECT not contraindicated.

353
Q

Not a reason to avoid this med with PM

A

Succinylcholine

354
Q

The single most important informationto know preoperatively when the pacemaker fails?

A

Preoperatively find out what the patient’s underlying rhythm is .
Consider isoproterenol, Epinephrine and/or atropine.

355
Q

K+ and conditions that can affect PM

A

Hyper and hypokalemia

356
Q

4 others conditions that can affect PM

A 
Hypocapnia (Intracellular K shift)
Hypothermia
MI
Fibrotic tissue buildup around the pacing leads
Antiarrhythmic medications.
357
Q

Hyper/hypocalcemia with QT

A

Hyper makes it shorter , hypo makes it longer.

358
Q

When QT at risk for torsades

A

When longer than >0.5 seconds

359
Q

What is the lead that is always positive

360
Q

What is the lead that is always negative

361
Q

Left AXIS Deviation is

362
Q

Right AXIS deviation is

A

> 90 degrees

363
Q

What is the MOST COMMON CAUSE of ACUTE MI

A

Sinus tachycardia (because it simultaneously increases myocardial oxygen demands while decreasing O2 supply.

364
Q

3 meds for a flutter

A

Amiodarone
Diltiazem
Verapamil

365
Q

PVCs causes by

A

Digoxin toxicity

Hypokalemia

366
Q

Best drug for the treatment of symptomatic PVCs

A

Lidocaine.

367
Q

Safest to administer to a patient with prolonged QT syndrome?

A

Metoprolol

368
Q

Genetic disorder linked to MH

A

King DENBOROUGH

369
Q

2 potential causes of 1st degree HB

A

Amiodarone

Advanced age

370
Q

Reference point for measuring changes in the ST segment is

A

PR segment

371
Q

Adenosine best in the treatment of

372
Q

Allows you to quantify the amount of ST elevation and depression

373
Q

Causes the greatest risk of EMI

A

Coagulation setting of a MONOPOLAR CAUTERY.

SEE/BOARD STUDY (20 decks)

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