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Year 4 > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

what are the 4 cardiac arrest rhythms?

A

ventricular tachycardia
ventricular fibrillation
asystole
pulseless electrical activity

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2
Q

general treatment of tachycardia in an unstable patient?

A

consider up to 3 synchronised shocks

consider amiodarone infusion

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3
Q

general treatment of narrow complex tachycardia in a stable patient?

A 
AF = rate control with beta blocker or CCB (diltiazem)
flutter = control rate with beta blocker
SVT = vagal manoeuvres and adenosine
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4
Q

general treatment of broad complex tachycardia in a stable patient?

A

VT (or if unclear) = amiodarone infuison

known SVT with BBB = treat as normal SVT

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5
Q

what is the pathology in atrial flutter?

A

re-entrant rhythm
where the electrical signal re-circulates in the atria in a self-perpetuating loop due to extra electrical pathway
signal goes around and around the atria without interruption stimulating rapid atrial contraction
the signal makes its way into the ventricles every second lap due to the long refractory period from AV node causing an increased ventricular rate

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6
Q

atrial rate in atrial flutter?

A

around 300 bpm

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7
Q

ventricular rate in atrial flutter?

A

around 150

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8
Q

classic ECG appearence in atrial flutter?

A

sawtooth appearence with P wave after P wave

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9
Q

what conditions are associated with atrial flutter?

A

hypertension
ischaemic heart disease
cardiomyopathy
thyrotoxicosis

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10
Q

how is atrial flutter managed?

A

rate/rhythm control - beta blockers or cardioversion
radiofrequency ablation of re-entrant rhythm
anticoagulation if needed (based on CHA2DS2VASc score)

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11
Q

what causes SVT?

A

electrical signal re-entering the atria from the ventricles
normally the signal can only go from atria to ventricles but in SVT it finds a way from ventricles back up into atria
once signal is back in atria it travels back through the AV node and causes another ventricular contraction
this causes a self perpetuating electrical loop resulting in a narrow complex tachycardia

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12
Q

ECG features of SVT?

A

narrow QRS complex (<0.12)

looks like a QRS complex followed immediately by a T wave, QRS, T wave and so on

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13
Q

what is paroxysmal SVT?

A

situation where SVT reoccurs and remits in the same patient over time

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14
Q

what are the 3 main types of SVT?

A

AVNRT
AVRT
atrial tachycardia

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15
Q

what is the difference between AVNRT and AVRT?

A 
AVNRT = where the re-entry point is via the AV nose
AVRT = re-entry point is an accessory pathway
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16
Q

type of AVRT?

A

wolf parkinson white

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17
Q

what happens in atrial tachycardia?

A

signal originates in atria somewhere other than SA node

not caused by signal re-entering from ventricles but instead from abnormally generated electrical activity in atria

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18
Q

acute management of stable patients with SVT?

A 
continuous ECG monitoring 
valsalva 
carotid sinus massage
adenosine (verapamil is an alternative)
DC cardioversion (if above treatment fails)
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19
Q

how does adenosine work?

A

slows cardiac conduction primarily through the AV node

interrupts AV node/accessory pathway during SVT and resets it back to sinus rhythm

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20
Q

how is adenosine given?

A

needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway
given through a large proximal cannula (eg grey)
initially 6mg then 12mg then a further 12mg if no improvement between doses

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21
Q

what should you warn patient about before giving adenosine?

A

will cause brief period of asystole or bradycardia which can be very scary and may cause feeling of impending doom

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22
Q

when should adenosine be avoided?

A 
asthma
COPD
heart failure
heart block
severe hypotension
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23
Q

long term management of patients with paroxysmal SVT?

A

measures can be taken to prevent episodes including

  • medications (beta blockers, CCBs or amiodarone)
  • radiofrequency ablation
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24
Q

what is wolf parkinson white syndrome (WPW)?

A

type of AVRT caused by an extra electrical pathway connecting atria to ventricles
extra pathway that is present is often called the bundle of kent

25
Q

definitive treatment of WPW?

A

radiofrequency ablation of the accessory pathway

26
Q

ECG changes in WPW?

A 
short PR
wide QRS
delta wave (slurred upstroke on QRS)
27
Q

what is the risk if a patient has both WPW and AF/a.flutter?

A

risk that the chaotic atrial electrical activity can pass through the accessory pathway into the ventricles causing a polymorphic
wide complex tachycardia

28
Q

why are anti-arrhythmics such as beta blockers, CCBs and adenosine contraindicated in WPW with AF or flutter?

A

they reduce conduction through the AV node and therefore promote conduction through the accessory pathway

29
Q

how is radiofrequency ablation done?

A

catheter inserted in femoral vein and wire red through venous system under Xray guidance to the heart
once the location of abnormal activity is found, ablation (heat) is applied to burn the abnormal area
leaves scar tissue which doesnt conduct electricity

30
Q

what is torsades de pointes?

A

type of polymorphic VT

31
Q

how is QT interval affected in torsades de pointes?

A

torsades de pointes occurs in patients with a prolonged QT

32
Q

how does prolonged QT predispose to torsades de pointes?

A

prolonged QT means there is prolonged repolarisation of the heart
waiting a longer time for repolarisation can result in random spontaneous depolarisation in some areas of heart myocytes
these abnormal spontaneous depolarisations prior to repolarisations are known as afterdepolarisations and spread throughout the ventricle leading to ventricular contraction prior to proper repolarisation occuring

33
Q

can torsades de pointes spontaneously resolve?

A

yes

usually revert back into sinus rhythm or can progress into VT

34
Q

causes of prolonged QT?

A 
long QT syndrome (inherited)
medications
electrolyte disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)
35
Q

what medications can cause prolonged QT?

A 
antipsychotics
citalopram
flecainide
sotalol
amiodarone
macrolide antibiotics
36
Q

acute management of torsades de pointes?

A 
correct the cause (electrolyte disturbance or meds etc)
magnesium infusion (even if serum magnesium is normal)
defibrillation if VT occurs
37
Q

long term management of prolonged QT?

A 
avoid meds that prolong QT
correct electrolytes
beta blockers (not sotalol)
pacemaker or implantable defib
38
Q

what are ventricular ectopics?

A

premature ventricular beats caused by random electrical discharges from outside the atria

39
Q

who are ventricular ectopics most common in?

A

common in all ages and in healthy people but more common in people with pre-existing heart conditions (eg ischaemic heart disease or heart failure)

40
Q

how are ventricular ectopics diagnosed?

A

ECG showing individual random abnormal broad QRS complexes on a background of normal ECG

41
Q

what is bigeminy?

A

where the ventricular ectopics are occurring so frequently that they happen after every sinus beat

42
Q

ECG features of bigeminy?

A

looks like normal sinus beat followed by an ectopic then a normal beat then ectopic and so on

43
Q

how are ventricular ectopic managed?

A

check bloods for anaemia, electrolyte disturbance and thyroid abnormalities
no treatment needed in healthy people
seek cardio help in people with background heart conditions

44
Q

what is first degree heart block?

A

delayed conduction through the AV node

despite this though, every atrial impulse leads to a ventricular contraction meaning every P wave results in a QRS

45
Q

ECG features of 1st degree heart block?

A

prolonged PR interval (>0.2 seconds)

46
Q

what is 2nd degree heart block?

A

where some of the atrial impulses do not make it through the AV node to the ventricles
therefore not all P waves are followed by QRS

47
Q

types of 2nd degree heart block?

A

mobitz type 1

mobitz type 2

48
Q

what is mobitz type 1?

A

where atrial impulses becomes gradually weaker until it doesnt pass through the AV node
after failing to stimulate a ventricular contraction the atrial impulse returns to being strong
cycle then repeats

49
Q

ECG features of mobitz type 1?

A

PR interval gets progressively longer then a QRS is most

50
Q

what is mobitz type 2?

A

where there is intermittent failure/interruption of AV conduction resulting in missing QRS complexes
there is usually a set ratio of P waves to QRS complexes for example £ P waves to 1 QRS complex would be referred to as 3:1 block

51
Q

ECG features of mobitz type 2?

A

PR interval is normal

QRS dropped every so often

52
Q

risk in mobitz type 2?

A

risk of asystole

53
Q

what is 3rd degree heart block?

A

complete heart block

no observable relationship between P waves and QRS

54
Q

risk in 3rd degree heart block?

A

significant risk of asystole

55
Q

how is stable bradycardia/AV block managed?

A

observe

56
Q

how is unstable bradycardia/AV block or with risk of asystole managed?

A 
1st line = atropine 500mcg
2nd line (if no improvement with atropine) = atropine 500mcg (up to 6 doses), other inotropes such as noradrenaline or transcutaneous cardiac pacing using defibrillator
57
Q

management of bradycardia/AV block in patients at high risk of asystole (mobitz type 2,, complete block or previous asystole)?

A

temporary transvenous cardiac pacing using an electrode on the end of a wire that is inserted into a vein and fed to right atrium or ventricle to stimulate them directly
permanent implantable pacemaker when available

58
Q

what is atropine?

A

anti-muscarinic
works by inhibiting the parasympathetic nervous system
leads to side effects of pupil dilation, urinary retention, dry eyes and constipation

Year 4 (83 decks)

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