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Arrhythmias Flashcards

1
Q

What is an arrhythmia?

A

Any deviation from the heart’s sinus rhythm

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2
Q

List the main types of supra-ventricular arrhythmias?

A
  1. Supraventricular tachycardia:

Atrial fibrillation

Atrial flutter

Ectopic atrial tachycardia

  1. Bradycardia

Sinus bradycardia

Sinus pauses

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3
Q

List the main types of ventricular arrhythmias

A
  1. PVC (premature ventricular complexes)
  2. Ventricular tachycardia
  3. Ventricular fibrillation
  4. Asystole
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4
Q

List the main types of Atrio ventricular node arrhythmias.

A
  1. AVNRT ( AVN Re-entry tachycardia)
  2. AVRT (AV reciprocating tachycardia)
  3. AV block (1st, 2nd and 3rd block)
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5
Q

What are the main causes of arrhythmias?

A
  1. Abnormal anatomy:

Left ventricular hypertrophy

accessory pathways

congenital HD

  1. Autonomic nervous system (ANS)

sympathetic stimulation: stress, exercise, hyperthyroidism

increased Vagal tone causing bradycardia

  1. Metabolic:

Hypoxia: Chronic Pulmonary disease, PE

Ischaemic myocardium: acute MI, angina

Electrolyte imbalance: K+, Ca 2+ , Mg 2+

  1. Inflammation: viral myocarditis
  2. Drugs:direct electrophysiologic effects or via ANS e.g. beta blockers
  3. Genetic: mutations of genes encoding cardiac ion channels e.g. the congenital long QT syndrome
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6
Q

What is an ectopic beat?

A

Beat or rhythms that originate in places other than the SA node

caused by altered automaticity (ischaemia)
or triggered activity (digoxin toxicity, Long QT syndrome)

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7
Q

What is the pathophysiology of a re-entry arrhythmia?

A

requires more than one conduction pathway, with different speed of conduction (depolarization) and recovery of excitability (refractoriness)

caused by accessory pathway tachycardia (wolf parkinson white syndrome)

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8
Q

where is the origin of a supraventricular arrhythmias?

A

above the ventricle

ie SA, atria, AV, HIS

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9
Q

where is the origin of a ventricular arrhythmia?

A

Ventricle

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10
Q

Discuss how a tachycardia forms.

A
  1. Ectopic focus may cause single beats or a sustained run of beats, that if faster than sinus rhythm it will take over the intrinsic rhythm
  2. Re-entry: triggered by an ectopic beat, resulting in a self perpetuating circuit.
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11
Q

Give causes of those which increase Phase 4 slope in myocyte graph causing increase in ectopics (heart rate)?

A

Hyperthermia

Hypoxia

Hypercapnia

Cardiac dilation

Hypokalaemia, prolongs repolarization

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12
Q

Give causes which decrease phase 4 slope in myocyte causing decrease in heart rate (bradycardia, heart block).

A

Hypothermia

hyperkalaemia

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13
Q

What is afterdepolarisation?

ii. what does this cause?

A

When a small depolarisation will occur in Phase 3 (terminal phase) of cardiac myocyte graph

ii. May cause triggered activity if it reaches threshold and lead to a sustained train of depolarisation
e. g.caused by digoxin toxicity

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14
Q

What are the general signs and symptoms of arrhythmias?

A
  1. Palpitations
  2. Chest pain
  3. Dysopnea
  4. Syncope (LOC)
  5. Presyncope (faintness)
  6. Hypotension
  7. Dizziness

can sometimes be asymptomatic

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15
Q

How would you diagnose an arrhythmia?

A
  1. 12 lead ECG (in tachycardia , during SR)
  2. CXR
  3. Echocardiogram - assess for structural heart disease

4.Stress ECG
Look for myocardial ischaemia, exercise related arrhythmias

5.24 hour ECG Holter monitoring
Event recorder: (capture the arrhythmia)

  1. Electrophysiological (EP) study
    Induce clinical arrhythmia to study mechanism and map arrhythmia
    can treat it by delivering radiofrequency ablation to extra pathway
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16
Q

Discuss the characteristics of Normal sinus arrhythmia.

A

Variation in heart rate due to reflex changes in vagal tone during the resp cycle

Inspiration reduces vagal tone and increases heart rate

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17
Q

What is the definition of sinus bradycardia?

A

Defined as heart rate <60bpm

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18
Q

What are the causes of Sinus bradycardia?

A
  1. Physiological: Athletes lower hearbeat
  2. Cardiac: Ischaemia, iatrogenic, aortic valve disease,myocarditis, Post MI and cardiomyopathy
  3. Drug induced: Beta blockers, amiodarone, verapamil and digoxin
  4. Non-cardiac: Vasovagal (verycommon) endocrine (hyperthyroidism),Metabolic (hypoxia, hyperkalaemia)
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19
Q

How do you manage sinus bradycardia?

A
  1. Address the cause
  2. Give atropine if adverse effects and acute
  3. If atropine not sufficient then transcutaneous pacing or haemodynamic compromised (Hypotension, CHF)
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20
Q

What is sinus tachycardia?

A

When heart rate is greater than 100 bpm

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21
Q

What are the main causes of sinus tachycardia?

A
  1. Physiological: exercise, anxiety, hypotension, pain
  2. Bleed
  3. dehydration
  4. Drugs (caffeine, nicotine and salbutamol)
  5. Anaemia, sepsis , Co2 retention
  6. Hyperthyroidism, PE
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22
Q

How do you manage Sinus tachycardia?

A

Treat underlying cause

Beta blockers

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23
Q

What are the main symptoms of atrial ectopic beats?

A
  1. Palpitations

2. asymptomatic

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24
Q

How do you manage Atrial ectopic beats?

A
  1. Beta blockers may help

2. Avoid causes (caffeine, cigarettes)

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25
Q

What is the difference between AVRT and AVNRT?

A

AVRT - circuit using the AVN and AP’way (macro-reentry

AVRNT - circuit within the AVN (micro-reentry)

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26
Q

What is antidromic AVRT?

A

Retrograde (anticlockwise )conduction through AVN

properties:

  1. Wide QRS complex with delta wave
  2. P wave rarely seen
  3. if P-wave visible retrograde and occurs just before QRS
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27
Q

What is orthodromic AVRT?

A

Antegrade (clockwise) conduction through AVN

Properties:

  1. Normal QRS duration
  2. No delta wave
  3. Retrograde P wave after QRS
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28
Q

How do you manage supraventricular tachycardias?

A

Acute management:
Increase vagal tone: valsalva manoeuvre or carotid massage.
- Slow conduction in the AVN

carotid massage only used for young patients and with a low risk of stroke

IV Adenosine - not if asthmatic
IV Verapamil

Chronic management:
Avoid stimulants
Electrophysiologic study and Radiofrequency ablation (first line in young, symptomatic patients)
Beta blockers
Antiarrhythmic  drugs
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29
Q

What is an RFCA?

A

Radiofrequency catheter ablation

prevents tachycardias by attacking automatic focus or part of re entry circuit

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30
Q

What is heart block?

A

Disrupted passage of electrical impulse through the AV node

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31
Q

What is 1st degree heart block?

ii. How do you diagnose it?
iii. How do you manage it?

A

Conduction between atria and ventricles are delayed

ii. PR interval is prolonged (>0.2 s) and unchanging; no missed beats
iii. No treatment - should have long term follow up as more advance block may occur

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32
Q

What is 2nd degree heart block

ii. what are the two types?

A

Intermittent block at the AVN (dropped beats)

ii. Mobitz I and Mobitz II

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33
Q

What occurs in 2nd degree heart block Mobitz I?

A

PR interval is longer and longer until a QRS is missed, the pattern then resets- wenckebach phenomen

causes missed beat

usually vagal in origin

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34
Q

What occurs in 2nd degree heart block mobitz II?

A

Is when there is a fixed number of non conducted P waves for the number of QRS complexes.

PR interval is constant but there will be P waves without QRS.

Usually 2:1 or 3:1.

ECG: progressive lengthening of PR and then missed beat.

May deteriorate into complete heart block or asystole.

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35
Q

How do you manage Mobitz II?

A

Ventricular pacemaker

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36
Q

What is 3rd degree Heart block?

A

complete heart block - no impulses from atria and ventricles

P waves and QRS waves appear independent of each other

patient may become very bradycardic - may be Haemodynamicaly uncompromised

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37
Q

How do you manage 3rd degree heartblock?

A

Ventricular pacing

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38
Q

What are the causes of Heart block?

A
  1. IHD (especially inferior MI
  2. acute myocarditis
  3. Sick sinus syndrome
  4. Drugs: Digoxin toxicity B blockers and CBBs
  5. Age
  6. Calcification aortic valve disease
  7. Post- aortic valve surgery
  8. Genetic: Lenegre’s disease and myotonic dystrophy
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39
Q

What are the two main types of pacemakers?

A

single chamber - right atria or right ventricle only

dual chamber - (paces the RA and RV)
Maintains A-V synchrony (preserves atrial kick)
Used for AVN disease

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40
Q

What are ventricular ectopics?

A

Ventricular ectopic are extra electrical impulses that arise from the ventricles.

The may occur healthy individuals but are also the most common post MI arrhythmia and indicate myocardial instability.

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41
Q

What are the main causes of ventricular ectopics?

A
  1. Structural causes: LVH, heart failure, myocarditis
  2. Metabolic: Ischaemic heart disease, electrolytes
  3. May be marker for inherited cardiac conditions
  4. If worse on exercise, need to investigate further
  5. Beta-blockers, Ablation of focus
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42
Q

What is ventricular tachycardia?

A

Type of broad complex tachycardia where ECG shows rate >100 bpm and QRS complexes >120ms

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43
Q

What are the causes of Ventricular tachycardia?

A

Coronary artery disease
A previous myocardial infarction

Rare causes:
- Cardiomyopathy
Inherited/ Familial arrhythmia syndromes
Long QT, Brugada syndrome

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44
Q

How do you diagnose VT?

A

ECG:

  1. The T waves are large with deflections opposite the QRS complexes.
  2. The ventricular rhythm is usually regular.
  3. P waves are usually not visible.
  4. The PR interval is not measurable.
  5. A-V dissociation may be present.
  6. V-A conduction may or may not be present.
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45
Q

How do you differentiate VT from SVT?

A

Difficult on ECG surface however several factors can help point to VT:

  1. +ve or -VE QRS concordance in all chest leads (i.e all +VE in R wave and all negative in QS)
  2. QRS >160ms
  3. Fusion or capture beats
  4. marked left deviation
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46
Q

What is the difference between monomorphic and polymorphic VT?

A

Monomorphic VT - where the shape of each heart beat on the ECG looks the same either being generated from increased automaticity of a single point in either the left or the right ventricle, or due to a reentry circuit within the ventricle - main cause is scarring of heart muscle from previous MI

Polymorphic VT (Torsade de pointes) - VT where has varying axis and may look like VF. Long QT is a predisposing factor. Long QT caused by congential (Long QT syndrome) or ischaemia.

47
Q

What is ventricular fibrillation?

A

Chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump

48
Q

What are the signs and symptoms of ventricular fibrillation?

A

o LOC.
o Absent pulse
o Cardiac arrest.

49
Q

How do you diagnose Ventricular fibrillation?

A

o Irregular, random baseline.

o No clear discernable waveforms

50
Q

How do you manage ventricular fibrillation?

A

Defibrillation (DC shock)

Cardiopulmonary resuscitation

51
Q

How do you manage VT?

A

Acute treatment:

Haemodynamically unstable VT: Synchronised DC shock

correct hypokalaemia and hypomagnesaemia

follow with amiodarone

Haemodynamically stable VT:

correct hypokalaemia and hypomagnesaemia

amiodarone via central line

after correction of VT - establish the cause

long term treatment:

  1. Correct ischemia if possible (revascularisation)
  2. Optimise CHF therapies.
  3. Anti-arrhythmic drugs to date have been shown to be ineffective and are associated with worse outcomes.
  4. Implantable cardiovertor defbrillators (ICD) if life threatening.
  5. VT catheter ablation.
52
Q

What arrhythmias count as broad complex tachycardias?

A
  1. VT
  2. VF
  3. atrial flutter with bundle branch block

4, Pre -excited tachycardias

  1. ventricular ectopics
53
Q

what is should you do with A wide QRS tachycardia with history of CAD/HF ?

A

manage as a VT unless stated otherwise

54
Q

Most ventricular arrhythmias occur in the setting of what?

55
Q

what can dual chamber devices detect?

A

bradyarrhythmias, as well as VT and VF

56
Q

Where do narrow complex tachycardias originate from?

A

supraventricular

57
Q

Define what a Narrow complex tachycardia is?

A

ECG shows rate >100 bpm and QRS complex duration <120 ms.

narrow QRS complexes occur when the ventricles are depolarised via the normal conduction pathways

58
Q

Give examples of narrow complex tachycardias?

A

Sinus tachycardia.

Supraventricular tachycardia.

Atrial fibrillation / atrial flutter.

Wolf Parkinson white syndrome.

59
Q

How do you manage narrow complex tachycardia?

A

Assess for hemodynamic instability

Unstable:
1st line: DC cardioversion, up to 3 times.

2nd line: Amiodarone, 300mg IV over 10-20 minutes.
If unsuccessful, repeat shock and get help.
 Then give amiodarone 900mg over 24 hours.

Stable: regular
Assess ECG for regularity. If regular follow this pathway:
1st line: Vagal manoeuvres - carotid massage, valsalva’s.
2nd line: - Adenosine
1st dose: 6mg IV bolus.
2nd dose :12mg IV bolus.
3rd dose: 12mg IV bolus.

If sinus rhythm not achieved, call for help.

Contraindications: asthma, 2nd or 3rd degree heart block, accessory pathways.

Side effects: flushing, chest tightness, nausea, lightheadedness within about 60 seconds.

stable: irregular
Treat as AF.

60
Q

How do you diagnose wolff-parkinson white syndrome?

A

ECG:
short PR interval

widened QRS due to slurred upstroke (R) - delta wave in V1 lead

61
Q

What is atrial fibrillation?

A

Disorganised electrical activity of the atria resulting in an irregular heartbeat

It can be paroxysmal, chronic or permanent. Paroxysmal atrial fibrillation is usually associated with normal hearts, whereas chronic atrial fibrillation is usually associated with heart disease.

62
Q

What is the pathophysiology of AF?

A

the multiple wavelets of reentry do not allow the atria to organise.

The ectopic focus or foci are said to be located around or within the muscle sleeves of the ostia in the pulmonary veins.

Rapid atrial pacing will induce AF.

63
Q

What is paroxysmal AF?

A

Lasts less than 48 hours

Paroxysmal

64
Q

What is persistent AF?

A

Last more than 48 hours can still be cardioverted to NSR

unlikey to spontaneously revert to NSR

65
Q

What is permanent AF?

A

Inability of pharmacologic or non-pharmacologic methods to restore NSR

66
Q

What are the causes of AF?

A

alcohol abuse - holiday heart syndrome causes paroxysmal AF. Most common cause

Hypertension

Congestive heart failure (CHF)

Sick sinus syndrome

coronary heart disease

obesity

thyroid disease - Weight loss and diarrhoea and increase in basal metabolism

familial

cardiac valve disease

COPD/pneumonia

septicaemia

pericarditis

mitral stenosis - mid diastolic murmur heard best at apex held in expiration

67
Q

What is lone (idiopathic AF)

A

Absence of any heart disease and no evidence of ventricular dysfunction

A diagnosis of exclusion

68
Q

What are the symptoms of AF?

A

Can be asymptomatic

Palpitations

dizziness

syncope

chest pain

Dyspnea

sweatiness

fatigue

69
Q

How do you diagnose AF?

A

Atrial rate >300 bom

Rhythm: irregular

Ventricular rate: variable
depends on:

AV node conduction properties

sympathetic and parasympathetic tone

presence of drugs which act on AV node

Absence of P wave

absence of ‘f’ wave

Bloods: FBC, U&E, TFT, alcohol level +/- troponin

70
Q

What is pseudo regularisation?

A

AF with fast ventricular response

71
Q

What does AF do to cardiac output?

A

decreases value - Lost ‘atrial kick’ and decreased filling times (reduced diastole)

72
Q

How do you manage AF?

A

1.Haemodynamically unstable or acute emergency?

ABCDE

Emergency cardioversion

Haemodynamically stable
Either rhythm or rate control

Rhythm control: Maintain SR

1.Restoration of normal sinus rhythm (NSR)

DCCV (most common way to treat AF)
or
anti arrhythmic drugs (flecainide, sotalol and amiodarone)

can also use radiofrequency ablation

  1. Maintenance of NSR

Anti-arrhythmic drugs

Catheter ablation of atrial focus/ pulmonary
veins

Surgery (Maze procedure)

Rate control: Accept AF but control ventricular rate

drugs below can either be used alone or in combo
Digoxin
Betablockers
Verapamil, diltiazem

if not work then “ablate and pace” ”, or completely ablate the AV node via radio frequency ablation and have the patient’s heart rate controlled by a pacing system - will need to have chronic anticoagulation

73
Q

What are the main indications of anti coagulation in AF?

A
  1. Thyrotoxicosis
  2. Hypertrophic cardiomyopathy

3.Valvular AF (warfarin only)
mitral valve disease: MS and MR

4.Non valvular AF with 2 or more risk factors
Age >75
Hypertension
Heart failure
Previous stroke/ thromboembolism
CAD / DM
Diabetes

consider if 1 factor

74
Q

What is atrial flutter?

A

rapid and regular form of reentrant atrial tachycardia.

75
Q

What is the pathophysiology of atrial flutter?

A

With counterclockwise flutter, a macro-reentrant circuit exists.

This circuit is sustained by a critical isthmus.

Caused by rapid atrial pacing and/or the introduction of multiple premature beats near the low septum.

usually paroxysmal

The arrhythmia may also convert spontaneously to AF

May result in thrombo-emblism

76
Q

How do you diagnose Atrial flutter?

A

ECG:

atrial Rate >300 bpm

ventricular rate 150 bpm

QRS normal

Conduction: normal but physiological 2:1

rhythm: normally regular can be variable

P wave: saw tooth F waves

77
Q

How do you manage Atrial flutter?

A
  1. RF ablation (80-90% long term success)
  2. Pharmacologic therapy:

Slow the ventricular rate

Restore sinus rhythm

Maintain sinus rhythm once converted

  1. Cardioversion
  2. Warfarin for prevention of thromboembolism
78
Q

what are the main alterations in impulse formation?

A
  1. changes in automaticity

2. Triggered activity

79
Q

What are the main abnormalities in impulse conductions which cause arrhythmias?

A
  1. re entry
  2. Conduction block
  3. accessory tracts
80
Q

Compare the SA node pacemakers against the latent pacemakers.

A

SA node pacemaking is more dominant

SA node ( 70-80 b.pm)

AV node ( 50 - 60) (latent pacemaker)

Purkinje fibres ( 30-40) (latent pacemaker)

81
Q

What are the two main types of afterdepolarisations?

A

Early

delayed

82
Q

describe what happens in early afterdepolarisation.

A

occurs during the inciting action potential within:

phase 2 (terminal plateau) – AD mediated by Ca2+ channels (when Na+ channels are still inactivated)

phase 3 (repolarization) – AD mediated by Na+ channels (when partial recovery of Na+ channels from inactivation has occurred)

83
Q

What is early after depolarisation associated with?

A
  1. slow heart rate
  2. Associated with purkinje fibre issues
  3. Prolongation of of action potential and drugs (solatol) which prolongs the QT interval
  4. Associated with polymorphic VT
84
Q

Describe what happens in delayed afterdepolarisations.

A

occur after complete repolarization
are caused by

  1. large increases in Ca2+
  2. excessive Ca2+ results in:
    i. oscillatory release of Ca2+ from the sarcoplasmic reticulum (SR)
    ii. a transient inward current (Iti, involving Na+-influx) that occurs in phase 4
85
Q

What are delayed afterdepolarisations associated with?

A
  1. Fast heart rate
  2. are increased and decreased in incidence by prolongation and shortening of the duration of the action potential by drugs, respectively
  3. may be triggered by drugs that increase Ca2+ influx (e.g. catecholamines), or release, from the SR (e.g. digoxin)
86
Q

Discuss the following factors regarding Drug class IA:

  1. Give an example
  2. describe its action
  3. what does it target?
A
  1. Disopyramide
  2. Associate with and dissociate from Na+ channels at a moderate rate. Slow rate of rise of AP and prolong refractory period
  3. Voltage-activated Na+ channel
87
Q

Discuss the following factors regarding Drug class IB:

  1. Give an example
  2. describe its action
  3. what does it target?
A
  1. Lignocaine
  2. Associate with and dissociate from Na+ channels at a rapid rate. Prevent premature beats
  3. Voltage-activated Na+ channel
88
Q

Discuss the following factors regarding Drug class IC:

  1. Give an example
  2. describe its action
  3. what does it target?
A
  1. Flecainide
  2. Associate with and dissociate from Na+ channels at a slow rate. Depress conduction
  3. Voltage-activated Na+ channel
89
Q

Discuss the following factors regarding Drug class II:

  1. Give an example
  2. describe its action
  3. what does it target?
A
  1. Metoprolol
  2. Decrease rate of depolarization in SA and AV nodes
  3. Beta adrenoceptor - as antagonist
90
Q

Discuss the following factors regarding Drug class III:

  1. Give an example
  2. describe its action
  3. what does it target?
A
  1. Amiodarone
  2. Prolong AP duration increasing refractory period
  3. Voltage-activated K+ channels (plus others)
91
Q

Discuss the following factors regarding Drug class IV:

  1. Give an example
  2. describe its action
  3. what does it target?
A
  1. Verapamil
  2. Slow conduction in SA and AV nodes. Decrease force of cardiac contraction
  3. Voltage-activated Ca2+ channels
92
Q

What effect does Ischaemic myocardium have on the myocytes?

ii. what does this mean?

A

Makes them partially depolarised and makes action potential duration longer

ii.
the inactivated state of the Na+ channel is available to Na+ channel blockers for a greater period of time

the rate of channel recovery from block is decreased

93
Q

Which anti arrhythmic drugs effect the atria?

A

IC and III

94
Q

Which anti arrhythmic drugs effect the ventricles?

95
Q

Which anti arrhythmic drugs effect the AV node?

A

Adenosine, digoxin, classes II, IV

96
Q

Which anti arrhythmic drugs effect the Atria and ventricles

AV accessory pathways?

A

Amiodarone, sotalol, classes IA, IC

97
Q

What does Adenosine activate?

ii. what effect does this have?
iii. what does it treat

A

activates A1-adenosine receptors coupled to Gi/o

ii. Opens ACh-sensitive K+ channels (GIRK)

Hyperpolarizes the AV node briefly, suppressing impulse conduction

iii. Used to terminate paroxysmal supraventricular tachycardia (PSVT – atrial firing rate of 140-250 beats per minute) caused by re-entry involving the AV node, SA node, or atrial tissue

98
Q

How do you administer adenosine?

99
Q

What does digoxin activate?

ii. what effect does this do?
iii. what does it treat?

A

Stimulates vagal activity

ii.
Slows conduction and prolongs refractory period in AV node and bundle of His

iii.Used to treat atrial fibrillation (AF) – chaotic re-entrant impulse conduction through the atrium

100
Q

How is digoxin administered?

A

IV infusion or oral

101
Q

What is the role of Verapamil

ii. What effect does this do
iii. what does it treat?

A

blocks L-type voltage-activated Ca2+ channels

ii. Slows conduction and prolongs refractory period in AV node and bundle of His
iii. Used to treat atrial flutter (AF) and fibrillation (AF) – chaotic re-entrant impulse conduction through the atria that may be conducted via the AV node to the ventricles

102
Q

What are the side effects of verapamil?

A

In high dose may cause heart block

Should be used with great caution in combination with other drugs that have a negative ionotropic effect

Largely replaced by adenosine for acute treatment, still used for prophylaxis

103
Q

How is verapamil administered?

A

Oral ( type IV agent)

104
Q

What is the role of Lignocaine?

ii. What effect does this do?
iii. what does it treat?

A
  1. rapidly blocks voltage-activated Na+ channels
  2. Due to rapid unblocking primarily affects Na+ channels in areas of the myocardium that discharge action potentials at high rate (e.g. an ischaemic zone)
  3. Treatment of ventricular arrhythmias following MI
105
Q

How is lignocaine administered?

A

IV (type IB drug)

106
Q

What is the role of Disopyramide and procainamide?

ii. What effect does this do?
iii. what does it treat?

A

moderate rate of block and unblock of voltage-activated Na+ channels

  1. Block open channels and are thus use-dependent
  2. Disopyramide is used (orally) to prevent recurrent ventricular arrhythmias, procainamide (IV) to treat ventricular arrhythmias following myocardial infarction
107
Q

What is the role of Flecainide?

ii. What effect does this do?
iii. what does it treat?

A

slow rate of block and unblock of voltage-activated Na+ channels

ii. Strongly depresses conduction in the myocardium and reduces contractility
iii. prophylaxis of paroxysmal atrial fibrillation

108
Q

what are the side effects of flecainide

A

negative ionotropic action

may trigger serious ventricular arrhythmias

109
Q

What is the role of Propranolol and atenolol (Type II agents, β-blockers)

ii. what does it treat?

A

suppresses impulse conduction through the AV node

ii. SVTs

110
Q

What is the role of Amiodarone and sotolol (type III agents)?

ii. What effect does this do?
iii. what does it treat?

A

slow repolarization of the AP by block of voltage-activated K+ channels .

increases action potential duration and the effective refractory period

ii. Supresses re-entry
iii. SVT and VT

111
Q

What are the side effects of Amiodarone

A

pulmonary fibrosis

thyroid disorders

photosensitivity reactions

peripheral neuropathy

112
Q

what can AF cause?

A

systemic embolism

113
Q

A major sign of MI on an ECG is what?

A

Development of ST depression on excercise

My Cardiovascular (8 decks)

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