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Cardiology > Arrhythmias > Flashcards

Arrhythmias Flashcards

Atrial fibrillation Atrial Flutter WPW Brugada Heart block SVT Ventricular tachycardia Ventricular fibrillation Prolonged QT

1
Q

what is atrial fibrillation?

A

chaotic irregular atrial rhythm

AVN responds intermittently so there is irregular ventricular rate

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2
Q

What does AF increase the risk of?

A

embolic strokes

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3
Q

What are the causes of AF?

A
  • HF/ischaemia
  • HTN
  • MI
  • PE
  • mitral valve disease
  • Pneumonia
  • Hyperthyroidism
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4
Q

What are the sx of AF

A

Palpitations, SOB, chest pain, faintness, asymptomatic

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5
Q

What is the one main sign of AF

A

irregularly irregular pulse

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6
Q

What can be found on ECG in AF

A

absent p waves

irregular QRS complexes

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7
Q

What are the 3 main types of AF?

A
  1. paroxysmal - 2 or more episodes that self-terminate (<7 days)
  2. persistent - episodes that don’t self-terminate (>7 days)
  3. permanent - continuous AF that can’t be cardioverted (chronic)
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8
Q

Give the management of acute AF

A
  1. O2, U+E, emergency cardioversion
  2. Rx associated illness e.g. MI
  3. Control ventricular rate: diltiazem, verapamil, metoprolol
  4. start full anticoagulation w LMWH
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9
Q

What are the two main options for treatment of AF

A
  1. RATE control - BB or CCB (diltiazem)+ digoxin if needed

2. Rhythm control - cardio version, get the pt into and maintain normal sinus rhythm

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10
Q

When can a patient not be cardioverted and why?

A

if they have had sx for more than 48hrs or aren’t on anticoagulants as the moment a pt switches from AF to sinus rhythm is the highest risk of embolism

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11
Q

What is the management of AF w onset under 48hrs

A

Heparinise
Those w RF s for ischaemic stroke - lifelong anticoagulation
Cardioversion

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12
Q

What are the types of cardio version? when are they used?

A
  1. electrical cardioversion ‘DC’

2. pharmacological - amiodarone if structural HD (most elderly ppl), flecainide if not

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13
Q

What is the management of AF >48rs

A

Anticoagulation for at least 3 weeks prior to cardio version
Electrical cv recommended
Anticoagulate for 4 weeks

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14
Q

What is atrial flutter

A

form of SVT where there is succession of rapid atrial depolarisation waves

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15
Q

How does atrial flutter appear on ECG?

A

Sawtooth pattern

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16
Q

What is the treatment of atrial flutter?

A

similar to AF but is more sensitive to electrical CV and requires lower energy levels
Cure is radio frequency ablation of tricuspid valve isthmus

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17
Q

What is 1st degree HB

A

PR interval is >0.2s

always generates a QRS

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18
Q

What are the sx and rx of 1st degree HB

A

usually asymptomatic, no Rx needed

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19
Q

What are the different types of 2nd degree heart block?§

A

1st (wenkebach) - progressive prolongation of PR interval until QRS is dropped
2nd PR interval constant but P wave often not followed by QRS complex

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20
Q

What is 3rd degree hb?

A

complete HB, no association between p waves and QRS c

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21
Q

What is the management of 2nd and 3rd degree heart blocks?

A

type 1 - none unless symptomatic, atropine IV or temp pacemaker
type 2 - permanent pacemaker
3rd degree - permanent pacemaker unless cause is reversible

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22
Q

What is Wolff Parkinson white?

A

congenital accessory conducting pathway (bundle of Kent) between atria and ventricles causing atrioventricular re-entry tachycardia (paroxysmal SVT)

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23
Q

Why is WPW dangerous?

A

episodes of AF or an abnormal heart rhythm can degenerate to VF as the accessory pathway doesn’t have the rate slowing properties of the AV node

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24
Q

What are the symptoms in WPW

A

palpitations, SOB, lightheadedness and syncope

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25
Q

What findings can be found on ECG in WPW?

A 
In normal sinus rhythm:
short PR interval
Wide QRS
Delta waves - slurred upstroke of QRS
Right axis deviation (if L sided accessory pathway)
During a re-entry tachycardia: 
no p waves 
tachycardia
Often indistinguishable from other forms of SVT
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26
Q

What is the treatment for:
I) stable WPW
ii) unstable WPW

A 
Stable:
Procainamide if wide QRS
Adenosine or CCB if narrow QRS
Unstable:
Electrical CV 
Long term definitive therapy: radio frequency catheter ablation
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27
Q

What is the inheritance pattern of Brugada syndrome?

A

autosomal dominant

mutation of SCN5A gene - encodes myocardial sodium ion channel protein

28
Q

In what group of people is Brugada syndrome more common?

A

asian

29
Q

Why is brugada syndrome dangerous?

A

can cause fainting or sudden cardiac death due to serious abnormal heart rhythms e.g. VF or polymorphic ventricular tachycardia

30
Q

What ECG changes can be seen in Brugada syndrome

A

Convex ST segment elevation >2mm in >1 of V1-3 followed by negative T wave
Partial RBBB appearance

31
Q

what is the treatment of Brugada syndrome?

A

implantable cardioverter defibrillator

32
Q

What can cause 3rd degree heart block?

A 
Coronary ischaemia - most common:
- Inferior wall MI - damage resolves 
- Anterior wall mI - extensive permanent damage
Hyperkalaemia
Congenital - lupus
33
Q

How does atropine work?

A

reduces vagal stimulation through the AV node

34
Q

What is supraventricular tachycardia?

A

sudden onset of narrow complex tachycardia

35
Q

How is SVT different to ST?

A 
SVT:
begins abruptly
HR: 160-240
Terminated by vagal manoeuvre 
ST:
Begins more slowly
Rate <160
Not terminated by vagal manoeuvre
36
Q

What is the management of paroxysmal SVT?

A

Acute: vagal manoeuvres e.g. valsalva, carotid sinus massage (differentiates between tachy of ventricular origin)
IV adenosine: 6mg ->12mg
Electrical CV

37
Q

How are episodes of PSVT prevented?

A

beta blockers

radio frequency ablation

38
Q

What is an alternative for adenosine?

A

verapamil

39
Q

When is carotid sinus massage CI and why?

A

in elderly due to risk of stroke in those w atherosclerotic plaques in carotid arteries

40
Q

how do vagal manoeuvres work?

A

increase the resistance of the AV node to transmit impulses through the activation of the parasympathetic nervous system conducted to the heart by th vagus nerve

41
Q

How does adenosine work?

A

increases atrioventricular (AV) node refractoriness

42
Q

What SVTs does adenosine not work and why?

A

atrial flutter and AF as they don’t involve the AV node

43
Q

In who should adenosine not be given to and why?

A

Those who will not tolerate its transient bradycardic effects e.g. hypotension, coronary ischaemia, decompensated HF
asthma or COPD due to bronchospasm

44
Q

What can cause ectopic beats?

A

post MI or normal healthy adults

45
Q

When are those with ectopic beats at risk of VF?

A

if no gap before T wave

46
Q

What is the treatment of ectopics?

A

iv amiodarone or just observe

47
Q

Why is VT dangerous?

A

can turn into VF

48
Q

What can be seen on ECG in VT?

A

Broad QRS
No p waves
T waves difficult to identify
Regular QRS w rate ~200bpm

49
Q

what can cause VT

A 
Commonly: 
Coronary heart disease
heart failure 
cardiomyopathy 
valvular disease
Less commonly:
Brugada
long QT
prinzmetals angina 
sarcoidosis
50
Q

What are the two main types of VT

A

monomorphic - commonly due to MI

Polymorphic - e.g. torsades de pointer caused by prolonged QT interval

51
Q

What is the treatment of VT

A

If haemodynamically unstable (adverse signs SBP<90, chest pain, HF): immediate cardioversion
If stable:
amiodarone (central line ideally) IV w dextrose or lidocaine or procainamide
if drugs fail, electrical CV

52
Q

What drug should not be used in VT and why?

A

verapamil as can precipitate cardiac arrest

53
Q

When should lidocaine be used with caution in vt?

A

in those w severe LV impairment

54
Q

How can further VTs be prevented?

A

surgical isoplation of arrhythmogenic area or implantable cardioverter defibrillator (indicated if severe lv function)

55
Q

What is the treatment of VF?

A

asynchronised DC shock

56
Q

What is a capture beat?

A

when the SA node captures ventricles in midst of AV dissociation to produce a normal QRS complex

57
Q

What is a fusion beat

A

supra ventricular + ventricular pulse coincide to produce hybrid complex

58
Q

What are the congenital causes of prolonged QT

A

Jervell-Lange-Nielsen syndrome (inc deafness)

Romano-Ward syndrome

59
Q

What drugs cause long QT syndrome

A 
Class 1a anti-arrhythmic drugs e.g. amiodarone, sotalol
TCAs, SSRIs
Methadone
Chloroquine 
Erythromycin
Haloperidol
Ondansetron
60
Q

What are other causes of long QT syndrome

A 
Electrolyte imbalances:
- hypocalcaemia
- hypokalaemia
- hypomagnesaemia 
Acute MI
Myocarditis 
Hypothermia
SAH
61
Q

What is the management of long QT syndrome?

A

avoid precipitants
beta blocker
implantable cardioverter defibrillator

62
Q

When does bradycardia require treatment?

A
  1. signs of haemodynamic compromise:
    - shock - hypotension, pallor, cold extremities, clammy, confusion, impaired consciousness
    - syncope
    - Myocardial ischaemia
    - HF
  2. Risk of asystole
63
Q

what is the treatment for bradycardia peri-arrest

A

atropine 500mcg IV (max 300mg)
transcutaneous pacing
isoprenaline/adrenaline titrated IV

64
Q

What are risk factors for asystole in Bradycardia

A
  • complete HB w broad complex QRS
  • Recent asystole
  • Mobitz type II AV block
  • Ventricular pause >3 seconds
65
Q

What is the treatment of torsades de pointes?

A

IV magnesium sulphate

66
Q

What is the normal QTC n men and women ?

A

<430 in males

<450 in females

67
Q

In long QT syndrome, when are implantable cardiodefibrillators required as treatment?

A

QTc >500 or prev cardiac arrest

Cardiology (13 decks)

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