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CVS Pathology > Arrythmias > Flashcards

Arrythmias Flashcards

1
Q

Presentation of arrhythmias

A 
Asymptomatic 
Palpitations
SOB
Chest pain 
Fatigue
Embolism
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2
Q

Investigations of arrhythmias

A

ECG
Blood tests esp TFTs
ECHO

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3
Q

Therapeutic options for arrythmias

A

Digoxin / BB / Ca-antagonist + warfarin (aspirin if low risk)
vs
class Ic/III drugs +/- DC cardioversion
Electrical approaches (occasionally)
- pace and ablation of AV node
- substrate modification e.g. pulmonary vein ostial ablation, maze procedures
Anticoagulation

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4
Q

Definition of an arrhythmia

A

Any deviation from the normal rhythm of the heart

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5
Q

Types of arrhythmias

A

Supraventricular arrhythmia
Ventricular arrhythmia
Heart block

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6
Q

What are the supraventricular arrhythmias?

A

AF

SVT (junctional)

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7
Q

What does AF stand for?

A

Atrial fibrillation

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8
Q

What does SVT stand for?

A

Supra ventricular tachycardia

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9
Q

What are the ventricular arrhythmias?

A

Ventricular tachycardia

Ventricular fibrillation

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10
Q

What do you look at in an ECG?

A 
Rhythm 
Rate
QRS duration 
P wave visible before each QRS complex
P-R interval (< 5 small squares)
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11
Q

Anything above 5 small squares in a P-R interval would be classified as what?

A

1st degree block

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12
Q

What is a 1st degree AV block caused by?

A

Conduction delay through the AV node but all electrical signals reach the ventricles

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13
Q

Does 1st degree AV block tend to cause problems?

A

No

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14
Q

Normal P-R interval

A

0.12 - 0.2 s

3 - 5 small squares

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15
Q

What would be seen on the ECG in 1st degree heart block?

A

Prolonged P-R interval (>5 small squares)

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16
Q

Types of 2nd degree heart block

A

Mobitz type 1 or Wenckeback 2nd degree AV block

Morbitz Type II 2nd degree heart block

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17
Q

What is seen on an ECG in Mobitz Type 1 degree AV block?

A

Progressive PR prolongation until the sixth P wave fails to conduct through the ventricle - dropped QRS complex (P wave ratio 1:1 for 2, 3 or 4 cycles then 1:0)
P-P interval remains constant
Rate normal or slow
P wave rate normal but faster than QRS rate

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18
Q

What is seen on an ECG in Mobitz Type II 2nd degree heart block?

A

For example 2nd and 8th P waves are not conducted through the ventricle
P-P interval remains constant
Rate normal or slow
P wave ratio 2:1, 3:1
P wave rate normal but faster than QRS
P-R interval normal or prolonged but constant

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19
Q

What is 3rd degree heart block?

A

Complete heart block

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20
Q

What is seen on an ECG in 3rd degree heart block?

A 
P wave rate regular
P wave bears no relation to QRS complexes or ventricular activity (unrelated P wave)
Slow rate
QRS prolonged 
Varied P-R interval 
Complete AV block
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21
Q

When does 3rd degree heart block occur?

A

When atrial contractions are ‘normal’ but no electrical conduction is conveyed to the ventricles. The ventricles generate their own signal through an ‘escape mechanism’ from a focus somewhere in the ventricle.
The ventricular escape beats are usually slow

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22
Q

What would be seen on an ECG in Atrial flutter?

A 
Regular rhythm 
Rate approx. 110bpm 
QRS usually normal
P wave replaced with multiple F (flutter) waves, usually at a ratio of 2:1 (2F - 1QRS) but sometimes 3:1
P wave rate 300bpm
P-R interval not measurable
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23
Q

Is the AV node involved in Atrial flutter?

A

No

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24
Q

What does AF stand for?

A

Atrial fibrillation

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25
Q

What happens in atrial flutter?

A

Abnormal tissue generating rapid heart rate is in the atria but AV node not involved

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26
Q

What happens in AF?

A

Many sites within the atria generating their own impulses, leading to irregular conduction of impulses of the ventricles to generate the heartbeat.
Irregular rhythm can be felt on palpation of the pulse

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27
Q

Presentation of AF

A 
Asymptomatic 
Palpitations
Fatigue
Fainting / presyncope
Chest pain 
Poor exercise tolerance
CHF
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28
Q

What does AF look like on an ECG?

A 
Rhythm irregularly irregular
Rate 100 - 160 bpm but slower if on meds
QRS normal 
P wave not distinguishable 
P-R interval not measurable
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29
Q

What is SVT?

A

Supraventricular tachycardia

  1. AV nodal re-entrant tachycardia
  2. AV re-entrant tachycardia
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30
Q

Presentation of SVT

A

Palpitations
Dizziness
Dyspnoea

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31
Q

Treatment of SVT

A

1st line
- vagal maneuvers e.g. Valsalva manourvre or carotid sinus massage
If fail - adenosine
Electrical cardioversion

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32
Q

What happens in SVT?

A

A narrow complex tachycardia or atrial tachycardia which originates in the atria but is not under direct control from the SA node

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33
Q

What age groups can SVT occur in?

A

All age groups

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34
Q

What is seen on an ECG in SVT?

A 
Regular rhythm 
Rate 140 - 220 bpm 
QRS duration usually normal 
P wave often buried in preceding T wave 
P-R interval depends on site of supraventricular pacemaker
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35
Q

Where are the signals in SVT coming from?

A

NOT BY SINUS NODE

Coming from a collection of tissue around and involving the AV node

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36
Q

What does WPW Syndrome stand for?

A

Wolff-Parkinson White Syndrome

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37
Q

What is WPW Syndrome?

A

A condition that causes the heart to beat abnormally fast for periods of time, due to an extra electrical connection in the heart. This allows signals travel round in a loop causing episodes where the heart beats really fast
Have episodes of SVT

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38
Q

When does WPW syndrome develop?

A

Congenital but symptoms may not arise until later in life

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39
Q

Presentation of WPW syndrome

A 
Palpitations
Syncope
SOB
Chest pain  
Sweating 
Anxious
Finding physical activity exhausting
Fainting
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40
Q

Treatment of WPW syndrome

A

No treatment usually required

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41
Q

Treatment of ventricular fibrillation

A

Cardiac arrest protocol - immediate defibrillation

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42
Q

What happens in ventricular fibrillation

A

Disorganised electrical signals cause the ventricles to quiver instead of contract in a rhythmic fashion.

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43
Q

When may Ventricular fibrillation occur?

A

During or After MI

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44
Q

ECG in ventricular fibrillation

A

Rhythm irregular
Rate 300+, disorganised
QRS duration not recognisable
P wave not seen

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45
Q

Presentation of ventricular tachycardia

A

Palpitations
Chest pain
Dyspnoea
Dizziness/syncope

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46
Q

What usually causes ventricular tachycardia?

A

Structural heart disease

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47
Q

Treatment of ventricular tachycardia

A

Cardiac arrest protocol
DC cardioversion
Drugs

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48
Q

Prevention of ventricular tachycardia

A

Prevent underlying cause
AA drugs
ICU

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49
Q

ECG of ventricular tachycardia

A

Regular rhythm
Rate 180-190 bpm
QRS duration prolonged
P wave not seen

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50
Q

What happens in ventricular tachycardia?

A

Abnormal tissues in the ventricles generating a rapid and irregular heart rhythm
Poor CO is usually associated with this rhythm causing the pt to go into cardiac arrest

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51
Q

What would you see in Torsades de Pointes due to CHB/AF

A

Short long short RR intervals and prolonged repolarisation

Long QT syndrome

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52
Q

Indications for ICD therapy

A

Secondary prevention

  • cardiac arrest due to VF/VT not due to transient or reversible causes e.g. early phase of acute MI
  • Sustained VT causing syncope or significant compromise
  • Sustained VT with poor LV function
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53
Q

Definition of sinus bradycardia

A

A heart rate less than 60bpm

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54
Q

Examples of causes of bradycardia

A

Cardiac causes
Increased vagal tone from drug abuse
Hypoglycaemia
Brain injury with increased ICP

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55
Q

ECG of sinus bradycardia

A 
Regular rhythm 
Rare < 60 bpm 
QRS duration normal 
P wave visible before each QRS complex
P-R interval normal
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56
Q

What is sinus bradycardia often caused by?

A

Patients on beta blockers

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57
Q

What is sinus tachycardia?

A

An excessive heart rate > 100bpm which originates from the SA node

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58
Q

Example causes of sinus tachycardia

A

Fright
Illness
Exercise
Shock

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59
Q

ECG of sinus tachycardia

A 
Regular rhythm 
Rate > 100bpm 
QRS normal duration 
P wave visible before each QRS
P-R interval normal
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60
Q

When does sinus arrest occur?

A

Occurs when there is a sudden absence of electrical activity initiated by the SA node
Results in a pause in electrical activity seen on tracing. Hence there would be a drop in BP
The longer the pause, the further the BP will drop

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61
Q

What length of pause in sinus arrest is deemed a medical emergency?

A

6 Seconds

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62
Q

ECG after the pause in sinus arrest

A

Constant R - R intervals

Rhythm tracing irregular

63
Q

What is sick sinus syndrome post MI?

A

Asymptomatic SA node depression post MI

64
Q

What are ectopic beats?

A

Beats that occur before the next beat arising from the sinus node

65
Q

Where can ectopic beats arise from?

A

Either atria or ventricles of heart

66
Q

What do ectopic beats look like on ECG if they arise from the atria?

A

Very similar to normal beats

67
Q

What do ectopic beats look like on ECG if they arise from ventricles?

A

Look different to normal beats - wider and different shape as travel through His Purkinje system which takes longer

68
Q

Goals for medications for patients with AF

A

Maintain sinus rhythm
Avoid risks of complications e.g. stroke
Minimise symptoms

69
Q

What should patients with AF be given and why?

A

Warfarin if high risk
Clopidogrel
BOTH to minimise risk of thromboembolic events
Anti arrhythmic drugs

70
Q

Unstable patients requiring immediate DC cardioversion in AF

A

Decompensated HF
Hypotension
Uncontrolled angina/ischaemia

71
Q

Indications for a temporary pacemaker

A

Intermittent or sustained symptomatic bradycardia, particularly syncope
Prophylactic when patient at high risk for development for severe bradycardia e.g. 2nd or 3rd degree AV block, post anterior MI, even when asymptomatic

72
Q

Indications for permanent pacemaker

A

Symptomatic or profound 2/3rd degree AV block, particularly when the cause is unlikely to disappear
Probably Mobitz type II 2nd / 3rd degree AV block even if asymptomatic
AV block associated with Neuromuscular diseases
After or in preparation for AV node ablation
Alternating RBBB/LBBB
Syncope when bifasicular/trifasciular block and no other explanation
Sinus node disease associated with symptoms
Carotid sinus hypersensitivity/malignant vasovagal syncope

73
Q

What pump in the cells controls the resting membrane potential?

A

Sodium-potassium ATPase Pump

74
Q

What is an AP?

A

A Change in the distribution of ions causes cardiac cells to become excited - the movement of ions across the cardiac cells membrane results in the propagation of an electrical impulse which leads to the contraction of the myocardial muscle

75
Q

What is the classification of drugs used to treat arrhythmias?

A

Vaughan-Williams classification

76
Q

What are the Vaughan Williams classifications of drugs?

A 
Class I (a, b, c)
Class II
Class III
Class IV
Other
77
Q

What are the Class I drugs?

A

Membrane stabilising agents

Fast sodium channel blockers

78
Q

Examples of Class Ia drugs and what they do

A

Quinide, procainamide, Disopyramide
Block Na channels
Increase the AP duration

79
Q

What are class Ia drugs used for?

A 
AF
Premature atrial contractions
Premature ventricular contractions 
VT
WFWS
80
Q

Class Ib drugs and what they do

A

Tocainide, phenytoin, lidocaine
Block Sodium channels
Accelerate repolarisation
Decrease AP duration

81
Q

What are class IIb drugs used for?

A

Ventricular dysrhythmias only (premature ventricular contractions, VT, VF)

82
Q

What are the class Ic drugs and what are they used for?

A

Encainide, flecainide, propafenone
Block sodium channels (more pronounced effect)
Little effect on AP during or repolarisation

83
Q

What are class Ic drugs used for?

A

Severe ventricular dysrhythmias

May be used in AF/flutter

84
Q

What are the class II drugs? Give examples

A

Beta blockers

  • Atenolol
  • bisoprolol
  • propranolol
85
Q

What do beta blockers do?

A

Block sympathetic system stimulation, thus reducing transmission of impulses in the hearts conduction system
Depress phase 4 depolarisation

86
Q

What is bisoprolol first line for?

A

AF

87
Q

What are the class III drugs?

A

Amoidarone
Bretylium
Sotalol

88
Q

What do the class III drugs do?

A

Increase AP duration

Prolong repolarisation in phase 3

89
Q

What are class III drugs used for?

A

Dysrhythmias that are difficult to treat
Life threatening VT or fibrillation
AF resistant to other drugs
Sustained VT

90
Q

What are the Class IV drugs?

A

Verapamil
Diltiazem
CCBs

91
Q

What are the class IV drugs used for?

A

Paroxysmal SVT

Rate control for AF and flutter

92
Q

Examples of other anti dysrhytmics

A

Digoxin

Adenosine

93
Q

What is digoxin? How does it work?

A

Cardiac glycoside
Inhibits sodium potassium ATPase pump
Positive inotrope - improves strength of cardiac contraction
Allows more calcium available for contraction

94
Q

What is digoxin used for?

A

HF
AF
Rate control in elderly

95
Q

What needs to be monitored when using digoxin?

A

Potassium
Drug levels
Toxicity

96
Q

Signs of digoxin toxicity

A

Vision changes; yellow glow around objects
ECG; changes in T waves. Reverse tick appearance of ST segment in lateral leeds
N + V
Brady or tachycardia
Arrhythmias; VT or VF

97
Q

Treatment of digoxin toxicity

A 
Stop digoxin (long half life)
Digibind
98
Q

How does digibind work?

A

Digoxin immune antibody
Binds with digoxin, forming complex molecules
Excreted in urine

99
Q

What is adenosine used for?

A

Converts paroxysmal SVT to sinus rhythm

100
Q

What does adenosine do?

A

Slows conduction through the AV node

101
Q

S/E of adenosine

A

Causes asystole for a few seconds

102
Q

Side effects of all anti-dysrhythmics

A

ALL cause arrythmias

103
Q

What is amiodarone used for?

A

VT

Occasionally SVT

104
Q

Interactions of amoidarone

A

Digoxin

105
Q

S/Es of amoidarone

A 
Striking
- Thyroid (hypo or hyper)
- pulmonary fibrosis
- slate; grey pigmentation 
- corneal deposits
- LFT abnormalities
Amoidarone toxicity
106
Q

Indications for anticoagulation

A

AF
DVT/PE
After surgery
Immobilisation

107
Q

Examples of anticoagulants

A

Warfarin
Dabigatran
Rivaroxaban
Apixaban

108
Q

Pathology of arterial thrombosis and what is it associated with?

A 
Adherence of platelets to arterial walls
White in colour (full of cells/platelets)
Assosiated with 
- MI
-Stroke 
- Ischaemia
109
Q

Pathology of venous thrombosis and what is it associated with?

A 
Develops in areas of stagnated blood flow (e.g. DVT, LA)
Red in colour
Assosiated with 
- CHF
- cancer
- Surgery
110
Q

What is warfarin structurally related to?

A

Vitamin K

111
Q

What does warfarin do?

A

Inhibits production of active clotting factors

112
Q

Direct effect of warfarin depends on….

A

Concentration of warfarin in the liver
Rate of accumulation of warfarin (clearance is slow 36 hours)
Long t1/2 of clotting factors - slow onset of actions

113
Q

How is warfarin therapy monitored?

A

INR

114
Q

What does INR stand for?

A

International normalised ratio

115
Q

What is INR?

A

Actual thromboplastin time / Standard thromboplastin time

116
Q

What is a normal INR value?

A

1

117
Q

What is a therapeutic INR valve?

A

2.5 - 4.0 depending on clinical indication

118
Q

S/Es of warfarin

A

Bleeding

Teratogenic (chondrodysplasia)

119
Q

What trimesters should warfarin be avoided in and why?

A

1st and 3rd

Chondrodysplasia

120
Q

How is warfarin metabolised and therefore what drugs does it interact with?

A

Cytochrome P450 pathway

Macrolide antibiotics, antifungals, anti epileptic drugs

121
Q

What assess the bleeding risk with warfarin?

A

CHADS2 score

122
Q

What is looked at in the CHADS2 score?

A 
Congestive heart failure
HTN
Age > 75 y/o
DM
Stroke / TIA 
(Score 1 for each or 2 for stroke)
123
Q

Features of torsades de pointes

A

Long QT syndrome

Polymorphic VT

124
Q

Causes of long QT syndrome

A 
Genetic
Electrolyte abnormalities
- Hypocalcaemia
- Hypomagnesaemia
- Hypokalaemia 
Drugs
- anti arrythmics
- antibiotics (erythromycin, clarithromycin, ciprofloxacin)
- Psychotropic drugs (SSRIs, TCAs, Neuroleptic agents)
CNS lesions
- SAH 
- Ischaemic stroke
Malnutrition 
Hypothermia
125
Q

Who is adenosine contraindicated in and therefore what is used instead as treatment for SVT?

A

Asthmatics - use verapamil instead

126
Q

Prevention of episodes of SVT

A

Beta blockers

Radio-frequency ablation

127
Q

ECG features of hypokalaemia

A 
U waves
Small or absent T waves
Prolonged PR interval 
ST depression 
Long QT
128
Q

Appearance of atrial flutter on ECG

A

Sawtooth appearance

129
Q

What makes up bifasicular block?

A

Combination of RBBB + left anterior hemiblock or posterior hemiblock e.g. RBBB with left axis deviation

130
Q

What makes up trifasciular block?

A

Features of bifasciular block as above + 1st degree heart block

131
Q

Treatment of an asthmatic with AF

A

Anticoagulation

Rate limiting CCB (instead of BB) - dilitiazem

132
Q

Rate control vs rhythm control as treatment in AF

A 
Rate control as 1st line to people with AF
Rhythm control as 1st line if
- AF with reversible cause
- Coexistent heart failure
- First onset AF
133
Q

When is immediate DC cardioversion used in AF?

A

When there is life threatening haemodynamic instability caused by new onset AF

134
Q

What does hypothermia show on the ECG?

A

J waves / Osborn wave

Prolongation of all ECG intervals

135
Q

Causes of LBBB

A

MI

Aortic stenosis

136
Q

ECG finding of digoxin toxicity

A

Reverse tick sign

137
Q

What is T wave inversion on an ECG a sign of?

A

Ischaemia

138
Q

What is a holter monitor and what is it frequently used in?

A

Records a continuous ECG for 24, 48 or 72 hours

Used for investigation of AF

139
Q

Normal corrected QT interval

A

< 430 ms in males

< 450 ms in females

140
Q

What is long QT syndrome?

A

Rare inherited or acquired disorder where delayed repolarisation of the ventricles increases the propensity to ventricular tachyarrythmias - may lead to syncope, cardiac arrest or sudden death

141
Q

Treatment of symptomatic bradycardia

A

IV atropine

142
Q

Treatment of WPW syndrome

A

Accessory pathway ablation

143
Q

What agents are used to control rate in patients with AF?

A

BBs
CCBs
Digoxin

144
Q

What agents are used to maintain sinus rhythm in patients with a history of AF?

A

Sotalol
Amoidarone
Flecainide

145
Q

Factors favouring rate control in AF

A

> 65 y/o

History of IHD

146
Q

Factors favouring rhythm control in AF

A 
< 65 y/o 
Symptomatic 
1st presentation 
Lone AF or AF secondary to corrected precipitant (e.g. alcohol)
CHF
147
Q

Treatment of tosardes de pointes

A

IV magnesium

148
Q

Common ECG variants of athletes

A

High vagal tone

  • sinus bradycardia
  • 1st degree AV block
  • Wenckebach phenomenon (2nd degree AV block Mobitz type I)
  • Junctional escape rhythm
149
Q

What are the two most important causes of VT?

A
  1. Hypokalaemia

2. Hypomagnesia

150
Q

What is Mobitz type II an indication for?

A

Pacemaker

151
Q

What is used to treat symptomatic bradycardia if atropine fails?

A

External pacing

152
Q

What is used to pharmacologically cardiovert AF?

A

Amiodarone + Flecainide

153
Q

When would pharmacological vs electrical cardioversion be used in AF?

A

Haemodynamically unstable - electrical (and if stable but symptoms > 48 hours)
Haemodynamically stable - pharmacological

154
Q

Anticoagulation rules with cardioversion of AF

A

Patients must be either anticoagulated or have had symptoms < 48 hours to reduce the risk of stroke
Cardioversion must be delayed for at least 3 WEEKS of anticoagulation - during this rate control (BB) should be used

CVS Pathology (19 decks)

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