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Pathophysiology Cardiac > Module #2 - Electrical Activity of the Heart > Flashcards

Module #2 - Electrical Activity of the Heart Flashcards

1
Q

What is syncytium?

A

Cardiac muscle fiber arrangement that allows rapid spread of electrical activity

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2
Q

What is automaticity?

A

Ability to spontaneously depolarize to action potential threshold

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3
Q

What is rhythmicity?

A

Regular generation of action potential by heart

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4
Q

What is NSR (normal sinus rhythm)?

A

Healthy heart –> heart beat originates from SA node @ ~ 70 bpm (resting)

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5
Q

What is bradycardia?

A

slowed HR

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6
Q

What is tachycardia?

A

elevated HR

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7
Q

Where does the spontaneous electrical activity of the heart originate?

A

SA node

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8
Q

Why does the electrical activity occur in the SA node?

A

Constant leakage of Na+ during diastole

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9
Q

What happens after the SA node reaches a certain threshold (d/t Na+ influx)?

A

Depolarization occurs –> spreads throughout atria –> systole (atrial contraction)

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10
Q

How fast does electrical depolarization need to occur?

A

Rapidly to allow for repolarization

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11
Q

How long is the electrical conduction time for atrial and ventricular depolarization?

A

0.2 seconds (will vary as HR changes)

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12
Q

Where is the SA node located?

A

R atria @ junction of SVC

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13
Q

What is the normal adult rate of action potentials in the SA node?

A

75 action potentials/minute

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14
Q

What is the rate of the SA node increased by?

A

Increased temp –> tachycardia w/ fever

Drugs –> effect nodal tissue

Inspiration

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15
Q

How does inspiration change the SA node rate?

A

Breifly decreases vagus tone to heart –> increase HR

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16
Q

What is respiratory sinus arrhythmia?

A

Normal occurrence –> result of inspiration/vagus reflex

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17
Q

What is the rate of the SA node decreased by?

A

Increased parasympathetic (vagus) influence

Decreased sympathetic influence

Meds –> digitalis (effects all nodal tissue)

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18
Q

After depolarization of the SA node, where does the depolarization spread?

A

Rapidly throughout atria

** ~ 0.1 s to spread complete atrial depolarization

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19
Q

What are the nodal pathways that travel throughout the atria?

A

Anterior

Middle

Posterior

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20
Q

What is the name of the anterior pathway and where does it transmit directly?

A

Bachmann bundle

Directly to left atria

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21
Q

Where does the posterior atrial pathway conduct?

A

SA node –> AV node

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22
Q

How long is the depolarization delayed at the AV node?

A

0.05 - 0.1 second

**slower conductivity of the node tissue

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23
Q

Which nervous system will shorten depolarization delay at the AV node?

A

Sympathetic nervous system

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24
Q

Which nervous system will prolong the depolarization delay at the AV node?

A

Parasympathetic (vagus) nervous system

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25
Q

Why is the depolarization delayed at the AV node?

A

Allows mechanical contraction of atria (atrial kick)

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26
Q

Where is the AV node located?

A

Right posterior portion of the intertribal septum

**just superior to tricuspid valve and anterior to osmium of coronary sinus

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27
Q

What is the normal adult rate of action potentials per minute @ the AV node?

A

50 action potentials per minute

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28
Q

What is the Bundle of His?

A

Continuation of AV node

Origin of right/left bundle branches

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29
Q

Where is the bundle of His located?

A

Posterior border of inter ventricular septum

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30
Q

How do the electrical Ap waves transmit through the Bundle of His?

A

Transmit quickly through bundle branches

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31
Q

Where does the Right Bundle Branch (RBB) go and is it branched?

A

Travels to right ventricular apex

Minimal branches

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32
Q

How is the Left Bundle Branch (LBB) branched?

A

2+ branches:

Left Anterior Bundle Branch (LABB)

Left Posterior Bundle Branch (LPBB)

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33
Q

What are the Purkinje fibers?

A

Terminal branches of the R/L Bundle Branches

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34
Q

Where doe the Purkinje fibers travel?

A

To ventricle apices

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35
Q

What do the Purkinje fibers do?

A

Rapidly transmit depolarization throughout ventricles

**spread from apex back to fibrous ring

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36
Q

How long does it take to spread complete ventricular depolarization?

A

~ 0.1 seconds

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37
Q

What is the intrinsic rate of action potentials per second of Purkinje fibers?

A

20 - 40 action potentials per second

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38
Q

Describe what is happening when you see a P wave on an ECG

A

SA node is depolarized and sends AP throughout atria

Action potential travels throughout atria via internal atrial pathways

~ 1/10 second to spread complete atrial depolarization

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39
Q

Describe what is happening when the AP arrives @ AV node

A

Slow conduction causes 1/10 second delay

**conductivity of AV nodal fibres influenced by ANS and drugs

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40
Q

What is the PR or PQ interval (not PR or PQ segment)?

A

Duration from start of atrial activation to start of ventricular activation

**Measured from beginning of P wave to beginning of Q or R wave (beginning of QRS complex)

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41
Q

What is the QRS complex

A

Ventricular depolarization

**may not always see a Q or S wave

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42
Q

What does the Q wave represent in the QRS complex?

A

Septal depolarization

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43
Q

What does the R wave represent in the QRS complex?

A

Ventricular depolarization

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44
Q

What does the S wave represent in the QRS complex?

A

Depolarization of the Purkinje fibrs

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45
Q

What is the ST segment (not St interval)?

A

Brief period of no electrical activity

**ventricles reach full depolarization

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46
Q

What does the T wave represent?

A

Ventricular depolarization

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47
Q

What does the U wave represent?

A

Repolarization of the papillary muscles or Purkinje fibers

Remnants of ventricular depolarization

Pathology (electrolyte disruption)

**not always seen

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48
Q

What is the QRS duration?

A

Ventricular depolarization

Atrial repolarization

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49
Q

What is the QT interval?

A

Ventricular depolarization

VEntricular repolarization

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50
Q

What is the ST interval (NOT ST segment)?

A

Ventricular depolarization

= QT interval - QRS duration

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51
Q

What is the difference between segments and intervals?

A

Segments = between waves

Intervals = include one or both waves

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52
Q

What is the normal P - R interval length?

A

0.12 - 0.20 seconds

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53
Q

When would you see lengthening of the P - R interval?

A

1° AV Block

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54
Q

What does an enlarged QRS represent?

A

Increase in duration

**Normal = 0.08 - 0.12 seconds

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55
Q

When would you see an enlarged QRS?

A

V-fib

Hyperkalemia

Bundle Branch Block

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56
Q

When would you see an enlarged QT interval?

A

Potential MI

Other pathologies

**Normal duration = 0.35 - 0.42 seconds

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57
Q

What are the causes of an elevated S - T segment?

A

Potential acute MI

Ischemia

Other pathologies

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58
Q

What are the causes of a depressed S - T segment?

A

Potential ischemia (myocardium receiving insufficient O2)

Acute posterior MI

Other Pathologies

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59
Q

What are the causes of a flat or inverted T-wave?

A

Potential ischemia ischemia

Hypokalemia

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60
Q

What are the causes of an elevated or tall T- wave?

A

Potential Hyperkalemia

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61
Q

What are the causes of a prominent U-wave?

A

Hypokalemia

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62
Q

What are examples of abnormal rhythms?

A

Heart Blocks

Ectopic Foci

Tachycardia

Ventricular Tachycardia

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63
Q

What is a heart block?

A

Complete/partial interruption of conduction between atria/ventricles

64
Q

What is considered a complete heart block?

A

3rd degree heart block

65
Q

What is considered an incomplete heart block?

A

1st and 2nd degree heart blcoks

66
Q

What happens to the pacemaker during a 3rd degree heart block?

A

Ventricles become pacemaker

35 - 45 bpm (atria beating @ rapid rate)

67
Q

What will the ECG pattern of a 3rd degree heart block look like?

A

The P waves occur at a faster rate that isn’t coordinated with the QRS waves.

68
Q

What happens during 1st degree heart block?

A

All atrial impulses reach ventricles but takes “long time”

69
Q

What does the ECG pattern of a 1st degree heart block look like?

A

This results in a longer, flatter line between the P and the R waves

70
Q

What happens during 2nd degree heart block?

A

Some but not all atrial impulses reach the ventricles –> won’t have ventricular depolarization for every atrial depolarization

71
Q

What will the ECG pattern of a 2nd degree heart block look like?

A

Pattern of QRS waves doesn’t follow each P wave as it normally would

72
Q

What is an example of an ectopic foci?

A

PVC = preventricular contraction

73
Q

What happens during PVC?

A

Myocardium in ventricle spontaneously depolarizes

74
Q

What will the ECG pattern of PVC look like?

A

Unexpected QRS between normal sinus rhythm

75
Q

What is atrial tachycardia?

A

Form of supra ventricular tachycardia (SVT)

Rapid heart rate originating in atria

76
Q

Which is more deadly, ventricular tachycardia/fibrillation or atrial ventricular tachycardia/fibrillation?

A

Ventricular tachycardia/fibrillation

77
Q

What happens to the heart during atrial tachycardia (besides pumping faster)?

A

Loses ability to pump efficiently

**Stasis of blood increases risk of clots

78
Q

What is atrial flutter?

A

Atria contract 200 - 350 action potential (HR) per minute

** AV node/ventricles can’t keep up and “max out” around 200 bpm

79
Q

What will pts w/ atrial flutter feel?

A

Characteristic sensations of regular palpitations

80
Q

What is atrial fibrillation (A-fib)?

A

Chaotic, uncoordinated depolarization

Atria “contract” > 300 - 350 action potentials (HR) per minute

**most common arrhythmia encountered in clinical practice

81
Q

What is ventricular tachycardia (V - tach)?

A

Rapid HR originating in ventricles

> 100 bpm and > 3 irregular beats (PVCs) in a row)

82
Q

What can V - tach lead to?

A

Ventricular fibrillation

83
Q

What is the treatment of Ventricular tachycardia?

A

Varies:

Can be acute emergency or may not require immediate intervention

84
Q

What is ventricular fibrillation (VF or V - fib)?

A

Rapid, chaotic, uncoordinated ventricular contractions

Functionally heart can’t act as a pump

85
Q

Is ventricular fibrillation an emergency?

A

YES!

Need BLS/ACLS interventions

Anything longer than few minutes = fatal

MC cause of death in MI = V-Fib

86
Q

What are the 2 types of cardiac action potentials (AP’s)?

A

Slow Response Action Potential

Fast Response Action Potential

87
Q

Where do slow response action potentials occur w/ in the heart?

A

Nodal Tissue –> SA node/AV node

88
Q

Where do fast response action potentials occur w/ in the heart?

A

Purkinje Fibers

Myocardial Cells of Atria/Ventricles

89
Q

What do the cardiac action potentials do?

A

Determine HR

Determine Contractility

Determine Conduction

90
Q

What are the intrinsic and extrinsic factors that influence cardiac action potentials?

A

Autonomic Nervous System –> sympathetic, parasympathetic

Drugs –> Anti-arrhythmic meds

Extra Cellular Fluid Ion Concentrations –> Na+, K+, Ca2+

91
Q

What are the distinguishing characteristics of slow response action potentials?

A

Leaky Membrane Potential

Drifting Resting Membrane Potential

Lack of Plateau

**all make SA node the pacemaker –> automaticity

92
Q

What are the 3 phases of slow response action potentials?

A

Phase 4

Phase 0

Phase 3

** No Phase 1 or 2

93
Q

What is Phase 4 of slow response action potential?

A

Slow depolarization

94
Q

Which phase is responsible for automaticity during slow response action potential?

A

Phase 4

95
Q

What happens during “leaky” membrane potential?

A

↑ Na+ into cell that depolarizes the membrane via “slow Na+ channels”

96
Q

What happens during Phase 4 of slow response action potential once membrane potential reaches -50 mV?

A

signals ↑ Ca2+ into cell via “transient calcium channels”

97
Q

When is an action potential triggered during Phase 4 of slow response action potential?

A

When Net total influx of Na+ and Ca2+ reach threshold (-40 to -30 mV)

98
Q

What is Phase 0 of slow response action potential?

A

Upstroke

99
Q

What happens during Phase 0 of slow response action potential?

A

↑↑ Ca2+ into cell via “slow long lasting calcium channels” –> depolarization of the membrane during action potential

100
Q

What is Phase 3 of slow response action potentials?

A

Repolarization

101
Q

What happens during Phase 3 of slow response action potentials?

A

↑↑ K+ out of cell = repolarization of the membrane back down to the resting membrane potential

102
Q

What is required for fast response action potentials?

A

Action potential from adjacent cell

103
Q

What are the phases of fast response action potential?

A

Phase 0

Phase 1

Phase 2

Phase 3

Phase 4

104
Q

What is phase 0 of fast response action potential?

A

Upstroke

105
Q

What happens during phase 0 of fast response action potential?

A

Action potential from adjacent cardiac cell depolarizes membrane to threshold voltage (approximately -70 mV)

Rapid ↑↑ Na+ into cell via fast Na+ channels that depolarizes the membrane

106
Q

What is phase 1 of fast response action potential?

A

Initial repolarization

107
Q

What happens during phase 1 of fast response action potential?

A

Initial ↑ K+ out of cell via transient K+ channels begins to repolarize the membrane

108
Q

What is phase 2 of fast response action potential?

A

Plateau

109
Q

What happens during phase 2 of fast response action potential?

A

↑ Ca2+ into cell via “slow long lasting calcium channels” that causes a plateau in the depolarization

** prolongs mechanical contraction, allows for adequate ejection for ventricles

110
Q

What is phase 3 of fast response action potential?

A

Repolarization

111
Q

What happens during phase 3 of fast response action potential?

A

↑↑ K+ out of cell combined with inactivation of “slow long lasting calcium channels” repolarizes the membrane back down to the resting membrane potential

112
Q

What is phase 4 of fast response action potential?

A

Resting membrane potential

113
Q

What happens during phase 4 of fast response action potential?

A

Inward/outward currents of K+ maintain resting membrane potential

↑ Ca2+ and Na+ channels closed (?)

114
Q

Where does the parasympathetic nervous system innervate the heart?

A

SA/AV nodes

Atria

115
Q

Where does the sympathetic nervous system innervate the heart?

A

Atria

Ventricles

Nodes

116
Q

What is the parasympathetic action on the heart?

A

↓ HR

↓ Conduction velocity

↓ Contractility of atria (small effect)

117
Q

How does the parasympathetic nervous system achieve its effects?

A

Promote/prolong K+ efflux out; Inhibit Na+ and Ca2+ influx into pacemaker cells

118
Q

What is the primary effect of parasympathetic stimulation on the atria?

A

hyperpolarizes cell membrane and decreases slope/increases duration of phase 4

119
Q

What is the parasympathetic effect on phase 3?

A

Hyperpolarize d/t ↑ K+ efflux out

120
Q

What is the sympathetic action on the heart?

A

↑ HR

↑ Contractility

↑ Relaxation rate

** less relaxation time

121
Q

How does the sympathetic nervous system achieve its effects?

A

Promote/prolong Ca2+ influx into pacemaker and cardiac muscles cells in both atria and ventricles

122
Q

What is the sympathetic effect on cardiac muscle cells and what does that mean?

A

↑ amplitude of Phase 2 –> ↑ contractility/↓ relaxation time

123
Q

What is the sympathetic effect on pacemaker cells and what does that mean?

A

↑ slope/↓ duration of Phase 4 –> ↑ rate/conduction velocity

124
Q

What are the 5 main classes in the Vaughan Williams classification of anti-arrhythmic agents?

A

Class I agents = Na+ channel blockers

Class II agents = Beta blockers

Class III agents = K+ channel blockers

Class IV agents = Ca2+ channel blockers

Class V agents = unknown mechanism

125
Q

What do class I agents do?

A

Inhibit Na+ channels –> ↓ HR

126
Q

How do class I agents ↓ HR?

A

Slows rate of depolarization of myocardial cells of atria/ventricles –> Phase 0

Slows rate of “leaky membrane” depolarization of nodal cells –> Phase 4

127
Q

What are the Class Ia agents?

A

Quinidine

Procainamide

Disopyramie

128
Q

What are the Class Ib agents?

A

Lidocaine

Mexiletine

Tocainide

Phenytoin

129
Q

What are the Class Ic agents?

A

Encainide

Flecainide

Moricizine

Propafenone

130
Q

What are the Class II agents (beta blockers) do?

A

↓ HR

↓ Contractility

131
Q

How do Class II agents (beta blockers) work?

A

Inhibit sympathetic activity on nodal cells/myocardial cells

132
Q

Name the Class II agents

A

Esmolol

Proranolol

Metoprolol

133
Q

What do the class III agents do?

A

↓ HR

134
Q

How do the class II agents ↓ HR?

A

Prolong K+ efflux –> prolong repolarization period

135
Q

Name the class III agents

A

Amiodarone

Azimilide

Bretylium

Clofilium

Dofetilide

Tedisamil

Ibutilide

Sematilide

Sotalol

136
Q

What do class IV agents do?

A

↓ HR

↓ contractility of heart

137
Q

How do class IV agents ↓ HR and ↓ contractility of heart?

A

Slow rate of depolarization of nodal cells (phase 0)

Inhibit plateau (phase 2)

138
Q

What are the 2 examples of class IV agents?

A

Verapamil

Diltiazem

139
Q

What is the only drug he has listed for class V agents?

A

Digoxin (digitalis)

140
Q

What does digoxin (digitalis) do?

A

↓ HR

141
Q

How does digoxin (digitalis) ↓HR ?

A

Stimulates CNS to ↑ parasympathetic activity on AV node

142
Q

What does [Na+] change in the ECF do to the heart?

A

Produces electrical changes of cardiac cells

**not as severe as alterations in ECF K+

143
Q

What does [K+] change in the ECF do to the heart

A

Alters repolarization

144
Q

What happens to the heart under hyperkalemic conditions?

A

Bradycardia

**severe hyperkalemia –> heart stopping

145
Q

What happens to phase 0 (fast response) under hyperkalemic conditions?

A

Resting membrane potential “lessens” (more positive) as ECF K+ ↑

146
Q

Why does the HR slow in response to hyperkalemic conditions?

A

D/t slower conduction velocity of the myocardial cell –> prolonged P wave, PR interval, QRS

**as cell membrane “lessens” (goes from -80 –> -70 –> -60) the conduction velocity slows

147
Q

What happens to Phase 2 and 3 (fast response) under hyperkalemic conditions?

A

↑ efflux of K+ out of myocardium during depolarization phases –> peaked T wave, shorten QT interval, ST set changes

Shortened repolarization

148
Q

What is the characteristic INITIAL ECG changes under hyperkalemic conditions?

A

Initial ↑ P-R interval

Shortening of QT interval

Tall/symmetric/peaked T waves

149
Q

What is the characteristic PROGRESSION ECG changes under hyperkalemic conditions?

A

Widening of QRS interval

Disappearance of P wave

Nodal/escape ventricular arrhythmias

150
Q

What are the characteristic TERMINAL ECG changes under hyperkalemic conditions?

A

QRS complex degenerates into sine wave pattern

Ventricular fibrillation/asystole “flatline”

151
Q

What happens to the heart under hypokalemic conditions?

A

Tachycardias

Arrhythmias

**can be fatal but coexisting morbidities just as fatal

152
Q

Why does hypokalemia cause tachycardias and arrhythmias?

A

Unlike other cells in the body cardiac cells become HYPERexcitable

153
Q

What happens to phase 2 and 3 (fast response) under hypokalemic conditions?

A

↑ ECF will prolong/slow depolarization –> delayed membrane potential –> reentrant arrythmias

154
Q

What is the INITIAL ECG change you would see under hypokalemic conditions?

A

Sagging of ST segment

T waves become progressively smaller

U wave becomes progressively larger

**don’t confuse this w/ QT prolongation

155
Q

What can hypokalemia do to contractions?

A

May produce premature ventricular/atrial contraction/tachyarrhythmias; 2nd or 3rd degree atrioventricular block

All can lead to potential ventricular fibrillation

156
Q

What happens to the heart under hypercalcemic conditions?

A

Cardiac rigor –> heart unable to relax

Plateau of APs is prolonged

Ca2+ w/in cardiac muscle-cross-bridge cycling would not be able to “release”

**super rare

Pathophysiology Cardiac (4 decks)

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