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Year 2 > Case 13 > Flashcards

Case 13 Flashcards

1
Q

Ionic current responsible for phase 4 of myocyte action potential

A

Ik1 - Inwardly rectifying potassium channels

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2
Q

Ionic current responsible for phase 0 of myocyte action potential

A

INa - Influx of sodium into cell

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3
Q

Ionic current responsible for phase 1 of myocyte action potential

A

Ito - Transient outward movement of potassium ions

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4
Q

Ionic current responsible for phase 2 of myocyte action potential

A

ICa,L - longlasting, inward movement of calcium

Ikr and Iks - rapid and slow outward movement of K+

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5
Q

Ionic currents increased by B-adrenergic stimulation

A

Iks, Ik1 and ICa,L

Calcium to a lesser extent than potassium

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6
Q

Effect of B-adrenergic stimulation on myocyte action potential

A

Shortens phase 2

Greater activation of potassium channels than calcium. So phase 2 ends sooner

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7
Q

Ryanodine receptor (RyR2)

A

Release of calcium in sarcoplasmic reticulum into sarcoplasm

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8
Q

Calsequestrin

A

Binds Ca2+ in SR lumen

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9
Q

FKBP

A

Inhibits RyR2

Dissociates from RyR2 on B-adrenergic stimulation - no longer inhibiting it.

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10
Q

SERCA2a

A

Ca2+ ATPase
In SR
Transports 2x Ca2+ per ATP

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11
Q

PMCA

A

Ca2+ ATPase
In sarcolemma (plasma membrane)
Transports 1x Ca2+ per ATP

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12
Q

Phospholamban

A

Regulator of SERCA2a

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13
Q

Calmodulin

A

Regulator of PMCA

Causes removal of Ca2+ when activated

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14
Q

Effect of sympathetic stimulation on phospholamban

A

Phospholamban is phosphorylated by PKA

Becomes less inhibitory of SERCA2a

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15
Q

TnT

A

Troponin which binds tropomyosin

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16
Q

TnC

A

Troponin which binds calcium

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17
Q

Effect of Ca2+ binding to TnC

A

Myosin and actin are able to interact

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18
Q

When TnI is phosphorylated by PKA

A

Sensitivity of myofilaments to Ca2+ is decreased

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19
Q

HCN channels

A

Hyperpolarisation-activated Cyclic Nucleotide-gated

Cause there to be an unstable resting potential (funny current)

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20
Q

Ionic current responsible for phase 4 of pacemaker action potential

A

If

Inward movement of Na+ via HCN channels

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21
Q

Ionic current responsible for phase 0 of pacemaker action potential

A

ICa,L

Inward movement of Ca2+

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22
Q

Ionic current responsible for phase 3 of pacemaker action potential

A

Ikr and Iks

Outward movement of K+

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23
Q

What is happening in the SAN to bring about tachycardia?

A

Increased binding of cAMP to HCN4 channels.
Increased Na+ entry into SAN cells.
Increased steepness of pacemaker potential.

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24
Q

What is happening in SAN to bring about bradycardia?

A

Decreased binding of cAMP to HCN4 - flattening of pacemaker potential.

Increased KACh (outward K+ current) - hyperpolarisation, takes longer for membrane potential to reach threshold.

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25
Q

I ncx (Ionic Current NCX)

A

Inward current via 3Na+(out)/Ca2+(in) exchange

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26
Q

I Ca,T (Ionic current Ca,T)

A

Inward T-type Ca2+ currents

Activated at negative potentials

Inactivated rapidly

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27
Q

I Kr (Ionic current Kr)

A

hERG channels

Associated with LQT2

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28
Q

I Ks (Ionic current Ks) channels are associated with…

A

LQT1

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29
Q

Dromotropic agents affect..

A

Conduction speed in AVN

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30
Q

High conductance connexins

A

Cx40 and Cx43

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31
Q

Low conductance connexins

A

Cx30 and Cx45

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32
Q

Connexins expressed by AVN

A

Cx30 and Cx45

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33
Q

Activated tropomyosin…

A

Blocks actin from binding to myosin

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34
Q

Troponin:Ca2+ complex…

A

Pulls tropomyosin away from actin’s myosin binding site

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35
Q

In smooth muscle, calcium binds to…

A

Calmodulin

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36
Q

Calcium:Calmodulin complex in smooth muscle cells activates…

A

MLCK

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37
Q

Smooth muscle cross bridge activity is turned on by Ca2+-mediated changes in…

A

Thick filaments

Myosin

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38
Q

Skeletal muscle cross bridge activity is turned on by Ca2+-mediated changes in…

A

Thin filaments

Actin

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39
Q

Normal AVN delay

A

0.12-0.2s

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40
Q

On an ECG, AVN delay is represented by…

A

PR interval

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41
Q

Conduction velocity in Bundle of His

A

1m/s

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42
Q

Conduction velocity in Purkinje Fibres

A

5m/s

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43
Q

Why is conduction velocity higher in Purkinje Fibres than in Bundle of His?

A

Larger diameter

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44
Q

Mechanism for AVN reentry tachycardia

A

Activation enters AVN via slow pathway.

Retrogradely activates atria via fast pathway.

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45
Q

AVRTs can be…

A

Orthodromic or Antidromic

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46
Q

AVRT result from….

A

An accessory pathway

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47
Q

ECG features of an orthodromic AVRT

A

200-300bpm
P waves buried in QRS
T wave inversion
ST depression

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48
Q

ECG features of an antidromic AVRT

A

200-300bpm

Wide QRS

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49
Q

Bundle of Kent

A

Accessory pathway seen in Wolff-Parkinson White syndrome

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50
Q

Wolff-Parkinson-White Syndrome

A

AVRT resulting from a specific accessory pathway - the Bundle of Kent

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51
Q

ECG features seen in Wolff-Parkinson-White Syndrome

A

PR interval <120ms
Delta wave
QRS prolongation
ST segment and T wave changes

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52
Q

Delta Wave

A

Slurring, slow rise of initial portion of QRS

Seen in WPW Syndrome

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53
Q

Peri-infarct zone consists of…

A

Dense scar tissue dispersed between living, normal cells

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54
Q

How does scar tissue cause reentry tachycardia?

A

Flow of impulse perpendicular to line of muscle cells is much slower than usual.
When excitation reaches the end of the muscle cells, it is able to stimulate them perpendicularly in the opposite direction (since it is not in ERP)

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55
Q

Triggered Activity

A

Impulse initiation in cardiac fibres that is dependent on after depolarisations

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56
Q

After-depolarsations

A

Oscillations in membrane potential that follow the upstroke of an action potential.

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57
Q

Causes of repolarisation abnormalities (3)

A

Drugs
Genetic predisposition
Electrolyte imbalance

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58
Q

Why do cardiac cells have automaticity?

A

They can generate spontaneous action potentials due to diastolic depolarisation.

i.e. net inward current during phase 4 of action potential

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59
Q

Broad complex tachycardia

A

QRS complex >120ms

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60
Q

Narrow complex tachycardia

A

QRS complex <120ms

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61
Q

Causes of broad complex tachycardia

A

VT
SVT + BBB
Accessory pathway related

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62
Q

Causes of narrow complex tachycardia

A 
Atrial fibrillation
Atrial flutter 
Multifocal Atrial tachycardia 
AVNRT/AVRT (short PR)
Sinus tachy/Atrial tachy (long PR)
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63
Q

Tachycardia

A

> 100bpm

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64
Q

Sinus rhythm

A

P wave before every QRS complex
Normal PR interval (120-200ms)
Regular rhythm

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65
Q

Normal PR interval

A

120-200ms

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66
Q

Sinus Arrhythmia

A

Normal phenomenon in the young

Heart rate increases when a deep breath is taken in and out

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67
Q

Symptoms of arrhythmias

A 
Palpitations
Dyspnoea 
Presyncope (dizziness)
Chest pain
Sudden cardiac death
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68
Q

Since palpitations are a common symptom, you should also ask about (the palpitations)…

A

Duration
Onset
Associated symptoms

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69
Q

Why do arrhythmias cause dyspnoea?

A

Reduced cardiac output

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70
Q

Why do arrhythmias cause chest pain?

A

O2 demand exceeds supply.

Demand may be high due to tachycardia

Supply may be low due to low cardiac output

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71
Q

Why do arrhythmias cause presyncope?

A

Inadequate cerebral perfusion

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72
Q

Prevalence of sudden cardiac death

A

1/1000 per year

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73
Q

Arrhythmias causing sudden cardiac death

A

Ventricular fibrillation
Polymorphic ventricular tachycardia
Monomorphic ventricular tachycardia

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74
Q

Proportion of sudden cardiac deaths with structurally abnormal heart

A

2/3

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75
Q

Proportion of sudden cardiac deaths resulting from coronary artery disease

A

80%

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76
Q

On an ECG, Ventricular ectopic beats…

A

Broad QRS

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77
Q

On an ECG, Atrial ectopic beats…

A

Narrow QRS
Inverted P waves
Compensatory pause afterwards

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78
Q

Paroxysmal AF

A

Episodes last <48hrs

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79
Q

Persistent AF

A

Episodes last 48hrs-1 week

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80
Q

Permanent AF

A

Symptoms occurring at all times

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81
Q

Structural heart disease causing AF

A

Valvular, Ischaemic, Hypertensive and congenital heart disease
Athletes heart
Cardiomyopathies

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82
Q

Causes of AF with no structural heart disease

A

Metabolic e.g. hyperthyroidism

Biochemical e.g. Hyperkalaemia

Drugs e.g. caffeine, alcohol

Severe infections

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83
Q

MOA of flecainide

A

VW Class Ic - Na+ channel blocker

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84
Q

MOA of Propafenone

A

VW Class Ic - Na+ channel blocker

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85
Q

MOA of amiodarone

A

VW Class III - K+ channel blocker

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86
Q

MOA of dronedarone

A

VW Class III - K+ channel blocker

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87
Q

First degree heart block

A

Prolonged PR interval (<200ms)

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88
Q

Second degree heart block

A

Occasionally a P wave does not elicit a QRS complex

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89
Q

Mobitz Type I Heart Block

A

PR interval gets longer until eventually, P wave fails to elicit a QRS complex

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90
Q

Mobitz Type II Heart Block

A

PR interval stays the same.

Occasionally, a P wave does not elicit a QRS complex

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91
Q

2:1 Heart Block

A

Every 2nd P wave does not elicit QRS

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92
Q

3:1 Heart Block

A

Every 3rd P wave does not elicit a QRS

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93
Q

Complete Heart block

A

Complete AV dissociation

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94
Q

Causes of Heart Block

A 
Age-related
Acute ischaemia 
Hyperkalaemia 
Hypothermia 
Hypothyroidism 
Drugs (AVN blockers)
Congenital 
Raised ICP
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95
Q

Management of heart block

A

Permanent Pacemaker

96
Q

Brugada syndrome

A

ECG shows ST elevation

Leading cause of sudden cardiac death in young males

97
Q

As a cardioaccelerator, Noradrenaline acts principally on…

A

Sinoatrial Node

98
Q

As a cardioinhibitor, Acetylcholine acts principally on…

A

Atrioventricular Node

99
Q

Indication for VW Class I

A

SVT, AVNRT, WPW

100
Q

VW Class I

A

Na+ channel blockers

101
Q

VW Class IA

A

Moderate Na+ channel blockers

Increase ERP

102
Q

VW Class IB

A

Weak Na+ channel blockers

Decrease ERP

103
Q

VW Class IC

A

Strong Na+ channel blockers

No effect on ERP

104
Q

VW Class IA Example

A

Procainamide

105
Q

VW Class IB Example

A

Lidocaine

106
Q

VW Class IC Example

A

Flecainide

107
Q

ADRs of Lidocaine in treatment of arrhythmias

A

Dizziness
Paraesthesia
Drowsiness
Bradycardia

108
Q

ADRs of Flecainide

A 
Oedema 
Dyspnoea 
Dizziness
Fever
Visual Disturbance
109
Q

Contraindications of Lidocaine

A

AV block

Myocardial depression

110
Q

Contraindications of flecainide

A

Heart failure
History of MI
heart block

111
Q

Indication for lidocaine (Class IB)

A

Ventricular tachycardias

112
Q

Indication for flecainide (Class IC)

A

For life threatening SVT and VT

113
Q

Indication for VW Class IA

A

AF
A.Flutter
SVT
VT

114
Q

VW Class II

A

Beta 1 Adrenoceptor Antagonists

115
Q

MOA of Bisoprolol

A

Beta 1 Adrenoceptor Antagonist

116
Q

Indication for bisoprolol

A

SVT

117
Q

ADRs of bisoprolol

A 
Hypotension 
Cardiac failure
Bronchospasm
Bradycardia
Cold Extremities 
Loss of libido
Sleep disturbance
118
Q

Contraindications of Bisoprolol

A 
COPD/Asthmatic
In cardiogenic shock
Bradycardia
Cardiac failure 
AV block
119
Q

Why should beta-blockers be used cautiously in patients with diabetes?

A

The drug will mask the warning sign (tachycardia) for insulin-induced hypoglycaemia

120
Q

VW Class III

A

K+ channel blockers

121
Q

VW Class III Example

A

Amiodarone

122
Q

Indications for VW Class III

A

VT, AF, WPW, Atrial Flutter

Tachyarrhythmias caused by reentry

123
Q

ADRs of Amiodarone

A 
Torsade de Pointes (esp. in those with LQT)
Bradycardia
AV Block 
Grey skin abnormalities 
Phototoxicity 
Liver failure 
Pulmonary fibrosis 
Sleep disorders 
Tremor 
Thyroid abnormalities
124
Q

Indications for Amiodarone

A

VT, AF, WPW, Atrial Flutter

Tachyarrhythmias caused by reentry

125
Q

Contraindications of Amiodarone

A

Heart block
SAN dysfunction
Iodine sensitive
Existing thyroid dysfunction

126
Q

VW Class IV

A

Ca2+ channel blockers

127
Q

VW Class IV Examples

A

Verapamil

Diltiazem

128
Q

Indications for VW Class IV

A

Paroxysmal SVT
AF (reduces ventricular rate)
Hypertension

129
Q

ADRs of verapamil

A 
Dyspnoea
Constipation
Arrhythmia
Tachycardia
Hypotension
Headache
Ankle oedema
130
Q

Contraindications of Verapamil

A 
Hypotension
Bradycardia
AV Block (2nd and 3rd)
Cardiogenic shock
Heart failure 
WPW
131
Q

VW Class V

A

Adenosine

132
Q

Indication for Adenosine

A

AVNRT

WPW

133
Q

MOA of Adenosine

A 
Binds to A1 receptor
Inhibits Adenylyl Cyclase
Decreased cAMP
Hyperpolarisation due to K+ traffic
Inhibits Ca2+ entry
134
Q

ADRs of adenosine

A

Flushing
headache
Rapid arterial hypotension
AV Block

135
Q

Contraindications of Adenosine

A

AV Block (2nd or 3rd)

136
Q

Why is rate control usually trialled first?

A

Fewer ADRs

Safer for patients

137
Q

CHADS2VASC

A

Congestive Heart Failure/LV dysfunction (1)

Hypertension (1)

Age > 75 (2)

Diabetes Mellitus (1)

Stroke/Thromboembolism (2)

Vascular Disease (1)

Age 64-75 (1)

Sex (female) (1)

138
Q

Administration of Warfarin

A

Oral

139
Q

MOA of Warfarin

A

Vitamin K Carboxylase inhibitor

140
Q

Clotting factor synthesis inhibited by Warfarin

A

VII, IX, X

141
Q

Monitoring for warfarin

A

Regular measurement of Prothrombin Time to determine INR

142
Q

Normal INR

A

<1.1

143
Q

Target INR for those taking anticoagulants

A

2-3

144
Q

Antedote for Warfarin

A

Vitamin K

145
Q

Administration of Heparin

A

IV

146
Q

MOA of heparin

A

Activates anti-thrombin III which inactivates thrombin and Factor Xa

147
Q

MOA of Fondaparinux

A

LMWH

Inhibits Factor Xa only

148
Q

Monitoring of Heparin

A

Regular measurement of prothrombin time against activated partial thromboplastin time (aPTT)

149
Q

Antedote for Heparin

A

Protamine Sulphate

150
Q

MOA of Dabigatran

A

Thrombin Inhibitor

151
Q

MOA of Rivaroxaban

A

Factor X inhibitor

152
Q

MOA of Apixaban

A

Factor X inhibitor

153
Q

Synergism of warfarin and heparin causes…

A

Penile Necrosis

154
Q

Fundoscopy for hypertensive crisis shows…

A

Cotton wool spots
Flame haemorrhages
Papilloedema

155
Q

Urinalysis in hypertension shows..

A

Increased albumin:creatinine ratio

ACR

156
Q

Important blood tests in investigating hypertension

A 
Plasma glucose
Electrolyes 
Creatinine
Estimated GFR
Serum total cholesterol
HDL cholesterol
157
Q

Prohypertensive proteins

A

Angiotensinogen

Renal epithelial Na+ channels

158
Q

Adrenoceptors found on the surface of blood vessels

A

Alpha 1 and 2

159
Q

Function of Renin

A

Converts Angiotensinogen to Angiotensin I

160
Q

Function of ACE

A

Converts Angiotensin I to Angiotensin II

161
Q

Who is offered treatment for hypertension?

A 
Stage 1, >80yo with one or more of the following:
Target organ damage 
Diabetes 
CVD
Renal disease 
10yr risk of CVD >20%

All patients with stage 2 hypertension

162
Q

Initial treatment for patients under 55, not of African/Caribbean origin
With Hypertension

A
  1. ACE inhibitors

If not tolerated:

  1. ARB
163
Q

Initial treatment for patients over 55, or of African/Caribbean origin with Hypertension

A
  1. CCBs

If CCB causes oedema or there is evidence of heart failure:

  1. Thiazide-like diuretic
164
Q

If step 1 is ineffective, step 2 anti-hypertensive treatment is…

A

CCB/Thiazide-like diuretic + ACE/ARB

ARB>ACE for African/Caribbean origin

165
Q

If step 2 is ineffective, step 3 anti-hypertensive treatment is…

A

ACE/ARB + CCB + Thiazide-like diuretic

166
Q

If step 3 is ineffective, step 4 anti-hypertensive treatment is…

A

Addition of low dose spironolactone if K+<4.5mmol/L
OR
Increase dose of thiazide-like diuretic if K+>4.5mmol/L

167
Q

MOA of Ramipril

A

ACE inhibitor

168
Q

Method of BP reduction by ramipril

A

Blocks Na+ reuptake in kidneys (and therefore water reuptake)

Limits LV remodelling

Reduces vasomotor tone (since there is less angiotensin II)

169
Q

Contraindications of ACE inhibitors

A

Hypersensitivity to ACE inhibitors

Renovascular disease

170
Q

ADRs of ACE inhibitors

A 
Hypotension
Renal impairment 
Persistent dry cough
angioedema 
Rash
171
Q

Method of BP reduction by Losartan

A

Blocks Na+ reuptake in kidneys (and therefore water reuptake)

Limits LV remodelling

Reduces vasomotor tone (since there is less angiotensin II bound to its receptor)

172
Q

MOA of Losartan

A

ARB

173
Q

ARBs should be used with caution in patients with…

A

Renal artery stenosis

Aortic/Mitral valve stenosis

174
Q

ADRs of ARBs

A

Hypotension - dizziness
Hyperkalaemia (occasionally)
Angioedema (rare)

175
Q

Method of BP reduction by CCBs

A

Negative chronotrope and inotrope

Prevents vascular smooth muscle cell contraction

176
Q

MOA of Nifedipine

A

CCB

177
Q

MOA of Isradipine

A

CCB

178
Q

Contraindications of CCBs

A

Cardiogenic shock
Aortic stenosis
Recent MI (within 1 month)
Acute/Unstable Angina

179
Q

ADRs of CCBs

A 
GI disturbance
Oedema 
Palpitations 
Headache
Lethargy 
Dizziness
180
Q

MOA of Furosamide

A

Blocks Na/K/Cl reabsorption in loop of Henle

Loop diuretic

181
Q

Contraindications of Furosamide

A

Hypokalaemia
Hyponatraemia
Renal failure
Comatose associated with liver cirrhosis

182
Q

ADRs of furosamide

A

GI disturbance
Increased serum cholesterol
Electrolyte disturbance
Hyperglycaemia

183
Q

MOA of Bendroflumethiazide

A

Blocks Na/Cl absorption in DCT

Thiazide diuretic

184
Q

Contraindications of bendroflumethiazide

A 
Hypokalaemia 
Hyponatraemia 
Hypocalcaemia 
Hyperuricaemia (high uric acid in blood)
Addison's Disease
185
Q

ADRs of bendroflumethiazide

A

GI disturbance
Electrolyte disturbance
Hyperglycaemia

186
Q

MOA of Spironolactone

A

Blocks aldosterone receptor in collecting duct. Blocking Na+ reabsorption but K+ sparing.

187
Q

Contraindications of spironolactone

A

Hyperkalaemia
Anuria
Addison’s Disease

188
Q

ADRs of Spironolactone

A 
GI disturbance
Gynaecomastia
Breast pain
Menstrual disturbance 
Drowsiness/Dizziness
Hyperkalaemia 
Hyponatraemia
189
Q

Advantages of ARBs over ACE inhibitors?

A

ARBs do not prevent production of angiotensin II altogether
So angiotensin II can still exert its effects in other areas of the body.

ARB does not cause cough.

190
Q

Method of BP reduction by bisoprolol

A

Inhibition of renin release

Negative chronotrope and inotrope

191
Q

Method of BP reduction by GTN spray

A

Releases NO causing vasodilation

192
Q

How does NO cause vasodilation?

A 
Activation of guanylyl cyclase.
Increased cGMP
Causing:
Increased K+ efflux
Decreased Ca2+ influx 
Increased MLC phosphatase
193
Q

Rhythm Strip

A

Prolonged reading from a single lead (usually lead II)

Useful for analysis of heart rate and rhythm

194
Q

aVR is predominantly…

A

Negative

195
Q

T wave inversion is normal in…

A

aVR and V1

Children

196
Q

Sinus Rhythm

A

Regular rhythm
P waves followed by QRS complexes
Normal PR interval (120-200ms)

197
Q

Enlargement of Right Atrium

ECG shows…

A

Tall pointed P waves

198
Q

Enlarged left atrium

ECG shows…

A

Bifid P waves

199
Q

P-mitrale

A

Bifid P waves due to enlarged Left Atrium

200
Q

Right ventricular hypertrophy

ECG shows…

A

Taller R waves in V1 (R:S >1)

Deeper S waves in V5 or V6 (R:S <1)

201
Q

Deep, broad Q waves indicate…

A

Permanent myocardial damage from MI

202
Q

Permanent myocardial damage from an inferior MI

ECG shows…

A

Deep, broad Q waves in II, III and aVF

203
Q

Right bundle branch block

ECG shows…

A

Prolonged QRS (>120ms)

Tall R wave in V1 (M)
Wide, slurred S wave in V6 (W)

MaRRoW

204
Q

Left bundle branch block

ECG shows…

A

Prolonged QRS (>120ms)

Dominant S wave in V1 (W)
Notched R wave in V6 (M)

WiLLiaM

205
Q

Cardiac ischaemia

ECG shows…

A

ST depression in associated leads

206
Q

Anterior Myocardial Infarction

ECG shows…

A

ST elevation in V1-V6

207
Q

Septal MI

ECG shows…

A

ST elevation in V1-V4

208
Q

Lateral MI

ECG shows…

A

ST elevation in I, aVL, V5 and V6

209
Q

Inferior MI

ECG shows…

A

St elevation in II, III and aVF

210
Q

Anterior MI is due to infarction in which coronary artery?

A

LAD

211
Q

Septal MI is due to infarction in which coronary artery?

A

LAD

212
Q

Lateral MI is due to infarction in which coronary artery?

A

Left circumflex

213
Q

Inferior MI is due to infarction in which coronary artery?

A 
RCA (80%)
Left Circumflex (20%)
214
Q

Hyperkalaemia

ECG shows…

A

Tall T waves

215
Q

Pathological inverted T waves:

A 
Raised ICP
BBB
Ventricular HTN
PE
Hypertrophic Cardiomyopathy
MI or ischaemia
216
Q

Normal PR interal

A

120-200ms

217
Q

Normal QRS complex

A

80-100ms

218
Q

Normal RR interval

A

0.6-1.2s

219
Q

ECG - 1 square =

A

0.04s/0.1mV

220
Q

Management of MI

A

Primary Percutaneous Intervention

221
Q

Heart rhythm abnormalities associated with MI

A

Atrial fibrillation
Complete heart block
VT
VF (Arrest)

222
Q

Long QT syndrome

ECG shows…

A

T wave flattening
Prominent U waves
Long QT interval due to fusion of T and U waves

223
Q

Rhythm abnormality associated with LQT syndrome

A

Torsade de Pointes (Polymorphic VT)

224
Q

Main causes of LQT syndrome (3)

A

Drugs
Myocardial Ischaemia
Electrolyte imbalance (esp. Hypokalaemia)

225
Q

Wolff Parkinson White Syndrome

ECG shows…

A

Delta waves
Short PR interval
Broad QRS complex

226
Q

Rhythm abnormalities associated with WPW

A

AF
Narrow complex tachycardia
VF

227
Q

Patient with AF has there AVN ablated and a pacemaker implanted.

What drug treatment must they continue?

A

Anticoagulants - since atria are still fibrillating so there is no change in stroke risk.

228
Q

Rhythm control treatments:

A

Class Ic
Class III
DC Cardioversion
PVI

229
Q

Rate control treatment:

A

Class II
Class IV
Pace and Ablate

230
Q

Primary prevention ICD

A

When cardiac arrest risk is proportional to scar burden.

Prior MI and EF <30%

231
Q

Secondary prevention ICD

A

Life threatening cardiac episode:
Cardiac arrest with no obvious reversible cause
Syncopal VT and structural Heart Disease
Non syncopal VT and EF<35%

232
Q

Management of Atrial Fibrillation

A

Beta blocker or CCB

Ineffective?
Beta blocker and CCB (or digoxin if sedentary)

Ineffective?
Rhythm control - VW Ic or III or DC cardioversion

233
Q

Management of Atrial flutter

A

Beta blocker OR Diltiazem (CCB) or Verapamil (CCB)

Ineffective?
Add digoxin

234
Q

Management of Ventricular Tachycardia

A

DC cardioversion

OR Amiodarone and DC cardioversion

235
Q

Management of Wolff-Parkinson White

A

Amiodarone
Flecainide (VW Ic)

Ablation of accessory pathway.

Year 2 (17 decks)

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