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Pharmacy 302 > ECG and Arrhythmias > Flashcards

ECG and Arrhythmias Flashcards

1
Q

What is the approximate normal heart rate in beats per minute (BPM)?

A

~70bpm

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2
Q

What heart rate in BPM is classified as Bradycardia? What heart rate in BPM is classified as Tachycardia?

A

<60bpm
>100bpm

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3
Q

Which part of the heart is the APEX? What is the native pacemaker of the heart?

A

Bottom tip
SA node

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4
Q

What is the typical BPM range of the SA node?

A

60-100bpm

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5
Q

What is another name for latent pacemakers? What term describes pacemakers other than the SA node?

A

Ectopic pacemakers
Latent pacemakers

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6
Q

What is the typical BPM range of the AV node? What is the typical BPM range of the Bundle of His? What is the typical BPM range of the Purkinje fibers?

A

50-60bpm
50-60bpm
30-40bpm

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7
Q

Through which heart structure does the cardiac impulse spread rapidly? Where is the cardiac impulse delayed in the heart’s conduction pathway?

A

Atria
AV node

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8
Q

How long is the delay at the AV node? Via which fibers does the cardiac impulse spread rapidly to the ventricles?

A

0.1s
Purkinje fibres

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9
Q

To which surfaces of the ventricles do Purkinje fibers transmit the cardiac impulse? Does the cardiac impulse spread more or less rapidly epicardially?

A

Endocardial surfaces
Less rapidly

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10
Q

How many milliseconds does it take for the cardiac impulse to go from the SA node to the AV node? How many milliseconds does it take for the cardiac impulse to travel through the Bundle of His? How many milliseconds does it take for the cardiac impulse to travel through the Purkinje fibres?

A

30ms
130ms
30-40ms

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11
Q

Which system controls heart rate?

A

Autonomic NS

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12
Q

Which branch of the autonomic nervous system has vagal activity? What are the 2 branches of the autonomic nervous system that control heart rate?

A

Parasympathetic
Parasympathetic and sympathetic

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13
Q

What happens during phase 4 depolarisation?

A

K+ efflux
Ca2+ influx
If influx
Deactivation of K+ channels

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14
Q

How many leads does a typical ECG have?

A

12

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15
Q

How many chest leads does a 12 lead ECG have? How many limb leads does a 12 lead ECG have?

A

6
6

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16
Q

What is the normal range of the QRS complex?

A

120-200ms

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17
Q

What can an elevated ST segment on an ECG indicate?

A

MI

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18
Q

On an ECG, which of these equations describes diastole? On an ECG, which interval represents systole?

A

RR-QT
QT interval

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19
Q

How can heart rate be calculated from an ECG?

A

(n-1/△ t)* 60
n = number of r waves
△t = time between them

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20
Q

What is a common type of ECG trace used for quick heart rhythm assessment?

A

Rhythm strip

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21
Q

Name the three types of leads used in ECGs?

A

Chest, augmented, bipolar limb

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22
Q

How is cardiac arrhythmia generally defined in relation to normal sinus rhythm?

A

Any change

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23
Q

What are the causes of arrhythmias?

A
  1. Increased sinus node automaticity
  2. Decreased sinus node automaticity
  3. Escape rhythms
  4. Enhanced automaticity of latent pacemakers (ectopic beats/rhythms)
  5. Triggered activity (after depolarisations): hypokaleamia, drug toxicity
  6. Conduction abnormalities/block
  7. Unidirectional block and re-entry
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24
Q

What is a typical BPM range for sinus tachycardia? What drives sinus tachycardia?

A

100-180
Sinus node

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25
Q

What changes in autonomic tone can cause sinus tachycardia?

A

Decreased vagal and increased sympathetic

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26
Q

When sinus tachycardia is observed, what is the recommended approach?

A

Treat the cause

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27
Q

What heart rate defines sinus bradycardia? When can sinus bradycardia be considered normal?

A

<60bpm
During sleep or a fit athlete

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28
Q

What cardiac event can lead to sinus bradycardia due to interrupted blood supply to the SA node? What electrolyte imbalance can induce sinus bradycardia?

A

Following MI
Hyperkalaemia

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29
Q

What thyroid condition can induce sinus bradycardia? Can the body tolerate sinus bradycardia?

A

Hypothyroidism
As low as 45bpm

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30
Q

What is the general approach to treating sinus bradycardia?

A

Treat underlying condition
Stop medication

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31
Q

What ECG characteristic defines sinus arrest? Which ECG complex is missing in sinus arrest?

A

Missing beats
PQRST complex

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32
Q

What is the difference between a sinus pause and a sinus arrest in terms of missing beats?

A

Pause is 1-2, arrest is 3+

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33
Q

What is the primary characteristic of sick sinus syndrome? How does heart rate respond to exercise in individuals with sick sinus syndrome?

A

Slow resting heart rate
Does not increase

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34
Q

What causes can lead to sick sinus syndrome?

A

Drug induced
Intense vagal activity
Degeneration of the pacemaker

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35
Q

Is sinus arrhythmia considered a normal phenomenon?

A

Yes

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36
Q

How can sick sinus syndrome be treated?

A

Artificial pacemaker

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37
Q

What happens to heart rate during inspiration in sinus arrhythmia? In what age groups is sinus arrhythmia typically more pronounced?

A

Accelerates
Children and young adults

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38
Q

What happens to heart rate during expiration in sinus arrhythmia? What fluctuations cause sinus arrhythmia?

A

Slows down
Vagal activity

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39
Q

How much can normal heart beats vary due to fluctuations in vagal activity?

A

o.5-3%

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40
Q

What type of altered balance can lead to inactivation of INa or ICa? What type of injury can lead to inactivation of INa or ICa?

A

Ionic currents
Injured tissue

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41
Q

How excitable is depolarized tissue? How does the conduction spread in depolarized tissue?

A

Less excitable
Slowly

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42
Q

What can a completely inexcitable tissue cause?

A

Complete conduction block

43
Q

What abnormality can bypass the AV node?

A

Aberrant conduction pathway

44
Q

What does bypassing the AV node normally impose? What can a second conduction pathway predispose? Which syndrome involves a bypass of the AV node?

A

Conduction delay
Supraventricular arrythmias
Wolff-Parkinson-White

45
Q

Which interval is shortened in Wolff-Parkinson-White syndrome? Which complex is widened in Wolff-Parkinson-White syndrome?

A

PR interval
QRS complex

46
Q

What is affected by first degree AV block?

A

AV node conduction

47
Q

What two processes are required for re-entry?

A

Unidirectional block and slowed conduction

48
Q

What is the ratio of P waves to QRS complexes in first degree AV block? What is the PR interval like in first degree AV block? What is the normal range for the PR interval?

A

1:1
Unusually long
120-200ms

49
Q

Is first degree AV block usually a serious condition requiring treatment? When might first-degree AV block be observed in young people? What autonomic tone can cause first-degree AV block?

A

Benign
During sleep
High vagal

50
Q

What happens to the PR interval until the AV node fails in second degree AV block? In 2nd degree AV block is atrial rhythm regular? In 2nd degree AV block, what happens to ventricular depolarisation every Nth cycle? What symptoms can be associated with second-degree AV block?

A

Lengthens
Yes
Is missing
Dizziness, syncope

51
Q

In bundle branch blocks, where does the ventricular conduction system fail? How does depolarization occur in bundle branch blocks?

A

His-Purkinje fibre system
Slow depolarisation

52
Q

What does bundle branch block do to the QRS complex? What effect does bundle branch block have on contraction?

A

Wide QRS complex
Slow contraction loss

53
Q

What lung disease can cause right BBB? Right BBB occurs in conditions such as blood clots to the what?

A

Chronic lung disease
Lung

54
Q

What ECG characteristic is associated with atrial flutter? What does it mean if atrial flutter II is transient?

A

Saw-tooth appearance
Comes and goes

55
Q

What symptom is least likely to occur when atrial flutter is less than 100 BPM? What are symptoms of faster rates of atrial flutter?

A

Asymptomatic
Palpitations, dyspnea, weakness

56
Q

What is a potential risk associated with atrial flutter?

A

Atrial thromboembolism

57
Q

What are treatments for atrial flutter?

A

Electrical cardioversion
Pacemaker
Pharmacological therapy
Catheter ablation

58
Q

What atrial rate characterizes atrial fibrillation? Why is the ventricular rhythm irregular in atrial fibrillation? What is observed about P waves in an ECG of a patient with atrial fibrillation?

A

350-600 discharges per minute
Only some impulses reach ventricles
Discrete P waves not discernable

59
Q

What causes atrial fibrillation? What is a typical ventricular rate in untreated atrial fibrillation?

A

Wandering re-entrant circuits
140-160 BPM

60
Q

What are causes of atrial fibrillation?

A

Enlarged atria
Heart failure
Hypertension
CAD
Thyrotoxicosis
Alcohol

61
Q

Why is a rapid ventricular rate dangerous in atrial fibrillation? What is a dangerous consequence of blood stasis in atrial fibrillation?

A

It reduces cardiac output
Thrombus/emboli

62
Q

What are two classifications of ventricular tachycardia? What underlying conditions are associated with ventricular tachycardia?

A

Sustained or non-sustained
Structural heart disease, MI, heart failure

63
Q

What are treatments for atrial fibrillation?

A

Antiarrhythmic drugs
Electrical cardioversion
Catheter ablation
Maze procedure

64
Q

What is the appearance of QRS complexes in ventricular tachycardia? What is the typical rate in ventricular tachycardia? What causes polymorphic ventricular tachycardia? What causes monomorphic ventricular tachycardia?

A

Wide
100-200bpm
Delayed repolarisation long QT
Re-entrant circuit in ventricle

65
Q

What symptoms can occur in ventricular tachycardia? Why is ventricular tachycardia dangerous?

A

Syncope, pulmonary oedema, cardiac arrest
Can deteriorate into VF

66
Q

What are treatments for ventricular tachycardia?

A

Electrical cardioversion
IV antiarrhythmic drugs

67
Q

What term describes a type of VT with identical QRS complexes?

A

Monomorphic VT

68
Q

What is the major consequence of ventricular fibrillation? What is the likely outcome if ventricular fibrillation is not quickly reversed? What occurs to the ventricles during ventricular fibrillation?

A

Loss of cardiac output
Death
Quiver but do not contract

69
Q

What are causes of ventricular fibrillation?

A

Heart disease (major cause of mortality in MI)
Low K+
Electric shock
Some drugs

70
Q

What device might survivors of ventricular fibrillation receive?

A

ICD (implantable cardioverter defibrillator)

71
Q

What are treatments for ventricular fibrillation?

A

Prompt electrical defibrillation
IV antiarrhythmic drug to prevent recurrence

72
Q

How does the lead of an ICD differ from that of a pacemaker?

A

Larger, to allow a larger shock

73
Q

What is the primary characteristic of congenital long-QT syndromes? What causes long QT syndromes? What type of channel is often affected in Long-QT syndromes?

A

Prolonged ventricular repolarisation
Different mutations
K+

74
Q

What symptoms are associated with Long-QT syndromes? What dangerous arrhythmia can Long-QT syndrome lead to?

A

Can be asymptomatic
Ventricular arrhythmias

75
Q

What does SADS stand for?

A

Sudden arrhythmic death syndrome

76
Q

For Long-QT syndrome type 1 (LQT1), what is the associated gene, protein, and mechanism?

A

Gene: KCNQ1
Protein: KvLQT1 (α subunit of Iks K+ channel)
Mechanism: Decreased K+ current

77
Q

What inheritance pattern is associated with LQT1? What inheritance pattern is associated with LQT2?

A

AD and AR
AD

78
Q

For Long-QT syndrome type 2 (LQT2), what is the associated gene, protein, and mechanism?

A

Gene: KCNH2
Protein: HERG (α subunit of IKr)
Mechanism: Decreased K+ current

79
Q

For Long-QT syndrome type 3 (LQT3), what is the associated gene, protein, and mechanism? What inheritance pattern is associated with LQT3?

A

Gene: SCN5A
Protein: NAV 1.5
Mechanism: Increased Na+ current
AD

80
Q

For Long-QT syndrome type 4 (LQT4), what is the associated gene, protein, and mechanism? What inheritance pattern is associated with LQT4?

A

Gene: ANK2
Protein: Ankyrin-B (structural protein)
Mechanism: Not clear
AD

81
Q

For Long-QT syndrome type 5 (LQT5), what is the associated gene, protein, and mechanism? What inheritance pattern is associated with LQT5?

A

Gene: KCNE1
Protein: minK (β subunit of IKS)
Mechanism: Decreased K+ Current
AD and AR

82
Q

For Long-QT syndrome type 6 (LQT6), what is the associated gene, protein, and mechanism? What inheritance pattern is associated with LQT6?

A

Gene: KCNE2
Protein: MiRP1 (β subunit of IKR)
Mechanism: Decreased K+ Current
AD

83
Q

For Long-QT syndrome type 7 (LQT7), what is the associated gene, protein, and mechanism? What inheritance pattern is associated with LQT7?

A

Gene: KCNJ2
Protein: IK1 (inward rectifier channel)
Mechanism: Decreased K+ Current
AD

84
Q

What happens during Phase 0 of the cardiac action potential (ventricular myocyte)? What causes the short repolarization in Phase 1 of the cardiac action potential? What characterises Phase 2 of the cardiac action potential? What happens during Phase 3 of the cardiac action potential?

A

Rapid depolarisation (Na+ influx)
K+ efflux
Delay in repolarisation (Ca2+ entry)
Rapid repolarisation (K+ efflux)

85
Q

What is the duration of the cardiac action potential?

86
Q

What is the main event in Phase 4 of the cardiac action potential?

A

Automaticity (slow depolarisation)

87
Q

What current is responsible for the pacemaker potential in the SA node? What must the pacemaker potential reach to trigger an action potential?

A

If slow Na+ current
Threshold

88
Q

What period occurs directly before the relative refractory period? What is another name for the relative refractory period? What period occurs directly after the relative refractory period?

A

Absolute refractory period
Vulnerable period
Supranormal period

89
Q

What are the major modes of action for anti-arrhythmic drugs?

A

Decrease slope of phase 4 (slow rate)
Increase threshold potential (slow phase 0)
Increase refractory period (lengthen action potential)

90
Q

How does prolonging the refractory period help to prevent arrhythmias? How does impairing conduction help prevent arrhythmias?

A

Impulse dies out
Impulse dies out before re-entry

91
Q

What is the overall aim of anti-arrhythmic drugs? What is the most widely used classification system for anti-arrhythmic drugs?

A

Prevent re-entrant circuits (loops)
Vaughan-Williams classification

92
Q

What are the four classes of anti-arrhythmic drugs in the Vaughan-Williams classification?

A

Class I: sodium channel blockade
Class II: catecholamine blockade
Class III: lengthening of refractoriness
Class IV: calcium channel blockade

93
Q

What effect do Class 1 antiarrhythmics have on conduction? What effect do Class 1 antiarrhythmics have on sodium channels? In what type of tissue do Class 1 antiarrhythmics slow conduction the most? What other type of channel can Class 1 antiarrhythmics block? What ECG change can Class 1 antiarrhythmics cause?

A

Slow conduction
Restrict rapid inflow of Na+
Damaged tissue
K+ channels
PR prolonged

94
Q

What effect do class 1b antiarrhythmics like lidocaine have on premature beats? What effect do class 1c antiarrhythmics have on excitability? What type of rhythms are class 1c antiarrhythmics used to suppress?

A

Supresses premature beats
General reduction in excitability
Re-entrant rhythms

95
Q

What causes ventricular dysrhythmias following MI?

A

Increased symp activation

96
Q

How do beta-blockers affect the AV node refractory period? What is the effect of beta-blockers on delayed afterdepolarizations?

A

Increase
Reduce delayed afterdepolarisations

97
Q

When are Class II antiarrhythmics useful? What other action do class II antiarrhythmics possess?

A

Tachyarrhythmias driven by overactive sympathetic system
Membrane stabilising action

98
Q

What effect does amiodarone have on cardiac action potential duration? What effect does amiodarone have on ectopic activity? In what type of tachycardias is amiodarone useful?

A

Prolongs cardiac action potential
Suppresses
Re-entrant tachycardias

99
Q

What channels does amiodarone block? What change can amiodarone cause on an ECG? Where is amiodarone extensively bound? What is the elimination half life of amiodarone?

A

K+ channels
Prolongs QT, widens QRS
Tissue
10-100 days

100
Q

How is amiodarone typically administered initially? What are some adverse effects of amiodarone?

A
  • As a loading dose
    Photosensitive rash
    Thyroid abnormalities
    Pulmonary fibrosis
    Corneal deposits
101
Q

Besides being a Class III antiarrhythmic, what other action does Sotalol possess? What effect does Sotalol have on the slow outward K+ current?

A

Non-selective B-adrenoceptor blocker
Delays slow outward K+ current

102
Q

How does sotalol compare to amiodarone in effectiveness and adverse effects?

A

Less effective but has less adverse effects

103
Q

What dangerous type of ventricular tachycardia can Class III drugs produce? What type of drugs should be avoided while taking class III drugs?

A

Polymorphic ventricular tachycardia (torsades de pointes)
Drugs that lengthen QT interval

Pharmacy 302 (28 decks)

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