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ALS/GIC > Rhythm recognition > Flashcards

Rhythm recognition Flashcards

1
Q

What risk factors may make an arrythmia more likely to result in cardiac arrest?

A
  • Persistent
  • Structural heart disease
  • Chest pain
  • Heart failure
  • Reduced GCS or shock
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2
Q

Following successful resuscitation of a cardiac arrest what is there a significant risk of and what therefore should be done ?

A
  • Sig. risk of further arrhythmia and cardiac arrest.
  • Thus maintain ECG monitoring post resuscitation until this risk is low.
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3
Q

In all patients with an arrhytmia even if they are already on cardiac monitoring what investigation should be carried out in order to more accurately characterise the arrhytmia ?

A

Establish ECG monitoring and also carry out a 12-lead ECG

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4
Q

In patients who experience syncope what could be causing this and is this always present when carrying out initial assessment ?

A

An intermittent cardiac arrhytmia - ECG may be normal (hence we often investigate with 24-72hr tapes)

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5
Q

Do episodes of syncope due to uncomplicated faints (vasovagal), situational syncope (cough, micturation) or orthostatic hypotension, require admission to hospital or cardiac monitoring ?

A

If clear that it is the cause then no hospital admission and ECG monitoring is not needed.

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6
Q

In patients with unexplained syncope, especially during exercise or syncope + evidence of structural heart disease or syncope + abnormal ECG (e.g. long QTc) what should be done ?

A

ECG monitoring + admit + cardio review.

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7
Q

Is ECG monitoring a reliable method to detect myocardial ischaemia/ACS?

A

No you need to record serial 12-lead ECG’s if assessing for ACS.

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8
Q

When an arrythmia is present should you treat the patient or the ECG?

A

Patient, assess them and then interpret the ECG

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9
Q

What is the correct positioning of electrodes to set up ECG monitoring ?

A
  • Red for right arm (usually right shoulder join)
  • YeLLow for left arm (usually left shoulder joint)
  • Green for leG (usually lower left chest wall)

This is modified limb lead positioning - leads I, II & III

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10
Q

What is the general limb lead best for ECG monitoring and why?

A

Lead II - as it usually good amplitude p-waves and QRS complexes.

Note if required you can switch to another lead if it provides a better ECG signal i.e. lead I or III.

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11
Q

In an emergency situation what is the easiest way to assess the cardiac rhythm ?

A

Applying the adhesive defibrillator pads

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12
Q

What can you only really use ECG monitors for ?

A

Rhythm recognition. Not anything more complex e.g. ACS detection etc.

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13
Q

When you detect an arrythmia on an ECG monitor what should you try and do ? (aside from mx of the arrhythmia)

A

Record a rhythm strip if possible.

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14
Q

If an arrhytmia persists on an ECG monitor what should you do ?

A

Record a 12-lead ECG

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15
Q

Why is it important to record a patients response to treatment (e.g. carotid sinus massage, adenosine) of arrhytmia ?

A

Response to tx helps determine the nature and origin of the arrhytmia.

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16
Q

Go over these videos

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17
Q

In NSR where does depolarisation of cardiac cells begin ?

A

In a group of specialised pacemaker cells called the SA node

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18
Q

Where is the SA node located ?

A

Close to the entry of the SVC into the right atrium

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19
Q

Following depolarisation in the SA node what happens ?

A

A wave of depolarisation the spreads through the atrial myocardium (atrial depolarisation)

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20
Q

What does atrial depolarisation represent on an ECG and what is happening here in the cardiac cycle ?

A
  • It is seen as the p-wave.
  • Atrial contraction is occuring.
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21
Q

Following atrial depolarisation (atrial contraction) where does the electrical impulse transmit to ?

A
  • First there is slow conduction through the AV node (allowing atrial contraction to finish)
  • Then rapid conduction through bundle of His which divdes into left and right bundle branches, spreading out through the left and right ventricle respectively. (rapid conduction down these fibres ensures the ventricles contract in a co-ordinated fashion)
  • The wave of depolarisation then ends in the purkinje fibres.
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22
Q

What is depolarisation of the ventricles seen as on an ECG and what does it represent in the cardiac cycle ?

A
  • Seen as the QRS complex
  • This represents ventricular contraction
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23
Q

What is AV nodal delay represented as on an ECG?

A

The PR segment.

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24
Q

What does the T-wave segment on an ECG represent ?

A

Ventricular repolarisation - the recovery of the resting membrane potential in the cells of the conducting system and ventricular myocardium

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25
Q

Why is atrial repolarisation not visible on an ECG?

A

Its masked by the QRS complex

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26
Q

What is the normal duration of a QRS complex and what does its duration tell you about the origin of an arrhytmia?

A

< 0.12s
If narrow (<0.12s) - orginates from above bifrucation of the bundle of His (SA node, atria or AV node)
If broad - originates from ventricular myocardium or may be supraventricular with BBB.

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27
Q

What happens to the normal electrical impulse pathway in bundle branch block?

A
  • One of the branches is diseased or damaged which prevents rapid conduction down the damaged bundle brach. This results in the depolarising impulse travelling faster down the other bundle branch to its ventricle and more slowly through the damaged one.
  • The result is a broad QRS complex (>0.12s)
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28
Q

What is the 6-stage system for analysing ECG rhythms?

A
  1. Is there any electrical activity?
  2. What is the ventricular (QRS) rate?
  3. Is the QRS rhythm regular or irregular?
  4. Is the QRS complex narrow or broad?
  5. Is atrial activity present?
  6. Is atrial activity related to ventricular activity and if so how?
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29
Q

If you cannot see electrical activity on an ECG what should you do ?

A
  • Check for a pulse!
  • Then if there is a pulse check that the gain is not too low and that the electrodes are all connected.
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30
Q

What does a completley straight line on an ECG usually suggest?

A

That an ECG lead is disconnected.

Note - during asystole the ECG usually shows slight undulation of the baseline and may show electrical interference due to respiratory movement or chest compressions.

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31
Q

Can atrial activity continue after ventricular systole ?

A

Yes! - recognition of ventricular standstill is important because cardiac pacing may achieve a cardiac output here.

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32
Q

What rhythm is shown here ?

A

Ventricular standstill - you can see ongoing sinus p-waves

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33
Q

What happens in ventricular fibrillation?

A
  • All co-orindation of electrical activity is lost.
  • There is no effective ventricular contraction and no detectable CO.
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34
Q

Do people in true ventricular fibrillation stay concious for long ?

A

NO - they will be concious for a few seconds.

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35
Q

If someone has what appears to be sustained ventricular fibrillation but remains concious what might it be ?

A

Artefact

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36
Q

What rhythm is shown?

A

Coarse VF

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36
Q

What are the 2 different types/classification of ventricular fibrillation (VF) ?

A

Coarse or fine VF.

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37
Q

What rhythm is shown?

A

Fine VF

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38
Q

Should you spend time distinguishing fine VF from asystole ?

A

No! - If it looks like VF shock the patient, if it looks like asystole then dont.

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39
Q

What is the standard paper speed of ECG’s?

A

25mm/second ==> bolder lines every 5mm which means one second is represented by 5 large squares

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40
Q

What is the best way of calculating a patients heart rate on ECG even if its irregular?

A

Count the number of R-waves in 6secs (30 large squares) then x10.

i.e. you have counted number of cardiac cycles in 60 secs.

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41
Q

Calculate the HR on this rhythm strip

A

Ans = 196bpm

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42
Q

If the R-R intervals are totally irregular and the QRS complexes are of a constant morphology what is the most likely arrhytmia ?

A

AF

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43
Q

What rhythm is shown here ?

A

AF

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44
Q

A regular underlying rhythm may be made to look irregular by extrasystoles (ectopic beats). What are the 3 main classifications of ectopic beats?

A
  • Premature ventricular complexes (PVC’s)
  • Premature atrial complexes (PAC’s)
  • Premature junctional complexes (PJC’s)
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45
Q

Go over PVC’s

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46
Q

Go over PAC’s

47
Q

Go over PJC’s

48
Q

Are PVC’s and PAC’s normal or abnormal?

A
  • Usually a normal electrophysiological phenomenom
  • May cause sensation of ‘skipping a beat’ if they occur regularly.
49
Q

If the QRS complex of an ectopic beat is narrow where does it suggest it originated from ?

A

Supraventricular origin (atrial or AV node)

50
Q

If the QRS complex of an ectopic beat is borad where does it suggest it originated from ?

A

Ventricular or supraventricular with bundle branch block

51
Q

What might some ventricular ectopic beats be accompanied by shortly after?

A

A p-wave, caused by retrograde depolarisation of the atria.

52
Q

What rhythm is shown here ?

A

PVC

53
Q

What rhythm is shown here ?

A

Junctional escape beat

54
Q

What is an escape beat and when do they occur?

A
  • If the normal cardiac pacemaker (SA node) failts or operates abnormally slowly, cardiac depolarisation may be initiated from a subsidiary pacemaker.
  • This subsidiary pacemaker may be from atrial myocardium, AV node, conducting fibres or ventricular myocardium.
  • The resulting rhythm will be slower than the NSR.
55
Q

What are the 2 main types of escape rhythms ?

A

Junctional or ventricular escape rhythms.

56
Q

Go over ventricular escape rhythms

57
Q

Go over junctional escape rhythms

58
Q

What is the difference in the QRS complex between junctional and ventricular escape rhythms?

A
  • Junctional escape rhythms - usually narrow QRS (can be broad if patient has BBB)
  • Ventricular escape rhythms - broad QRS
59
Q

What is another name for a ventricular escape rhythm?

A

Idioventricular escape rhythm

60
Q

What is an accelarate Idioventricular escape rhythm and when might you see it?

A
  • It is an Idioventricular escape rhythm with a normal HR (recall it should be slower 20-40bpm)
  • This might be seen post thromboylsis or PCI for MI ‘reperfusion arrhytmia’.
61
Q

Is an accelerated Idioventricular escape rhythm worrying ?

A

Not usually.

62
Q

It can be hard to identify p-wave activity, what leads are useful for assessing for p-wave activity ?

A

V1 & Lead II

63
Q

What are U-waves ?

A

A small deflection immediately following the T-wave

More info on LITFL:

https://litfl.com/u-wave-ecg-library/

64
Q

What are the characterisitc features of atrial flutter?

A
  • Narrow complex tachycardia
  • Regular atrial activity at ~300 bpm
  • Loss of the isoelectric baseline
  • “Saw-tooth” pattern of inverted flutter waves seen best in leads II, III, aVF
  • Upright flutter waves in V1 that may resemble P waves
  • Ventricular rate depends on AV conduction ratio

https://litfl.com/atrial-flutter-ecg-library/

65
Q

What are the characteristic features of atrial fibrillation?

A
  • Irregularly irregular rhythm
  • No P waves
  • Absence of an isoelectric baseline
  • Variable ventricular rate
  • QRS complexes usually < 120ms, unless pre-existing bundle branch block, accessory pathway, or rate-related aberrant conduction
  • Fibrillatory waves may mimic P waves leading to misdiagnosis, they are rapid deviations from baseline of varying amplitude and duration, usually best seen in V1.

https://litfl.com/atrial-fibrillation-ecg-library/

66
Q

During a tachyarrhytmia it may be difficult to identify p-waves to determine if the rhythm is atrial in origin or not, what can be given to help identify this ?

A

You can reveal atrial activity by slowing ventricular rate with transient increase in AV block using IV adenosine or vagal stimulation.
This will allow you to assess the p-waves.

67
Q

Sinus p-waves are upright in leads II & aVF, what direction are they if there is backward depolarisation of the atria in junctional or vetricular escape rhythms?

A

Inverted - because depolarisation is backward to normal

68
Q

It is important to determine the relationship between the p-waves and QRS complexes, where is this best done ?

A

The rhythm strip

69
Q

What are the different types of AV block and describe their appearance

A

1st degree AV block - prolonged PR interval > 0.2s
2nd degree AV block Mobitz type 1 - progressive PR prolongation until a dropped QRS complex
2nd degree AV block Mobitz type 2 - constant PR interval but p-wave is often not followed by QRS complex
3rd degree AV block (complete heart block) - no association with P-waves and QRS complexes.

Normal PR interval is 0.12-0.2s

70
Q

What are the 3 categories of cardiac arrest rhythms ?

A

1. Shockable - VF & pVT
2. Non-shockable - PEA & Asystole
3. Exreme bradycardia and rarley very fast SVT can cause such a fall in CO that they result in cardiac arrest

71
Q

If the patient is concious or has a pulse can the rhythm realistically be VF?

A

No.

72
Q

What 2 arrhytmias can mimic VF?

A

Polymorphic VT and pre-exited Atrial fibrillation/flutter.

73
Q

What are the 2 main types of pre-exitation pathways which occur in sinus rhythm ? i.e. not causing dangerous arrhytmia at that point

A

WPW and Lown-Ganong-Levine (LGL) Syndrome

https://litfl.com/pre-excitation-syndromes-ecg-library/

74
Q

What are the 2 tachyarrhytmias which can occur as a result of pre-exitation syndromes ?

A
  • Atrial fibrillation/flutter in pre-exitation
  • Atrioventricular re-entry tachycardia (AVRT)

https://litfl.com/atrial-fibrillation-in-pre-excitation/

75
Q

What can both polymorphic VT and AF in pre-exitation both lead too?

A

Both can lead to cardiac arrest ==> if misdiagnosed in a cardiac arrest the tx will be the same.

76
Q

What determines the management of a ventricular tachycardia (VT)?

A

Whether or not there is a pulse!

77
Q

What are the 2 different types of VT?

A

Monomorphic and polymorphic

78
Q

What can VT degenerate into ?

A

VF.

Recall that VT itself however can result in cardiac arrest regardless of if it degenerates into VF or not.

79
Q

What are the key features of monomorphic VT?

A
  • Regular, broad complex tachycardia
  • Uniform QRS complexes within each lead — each QRS is identical (except for fusion/capture beats)
  • Rate is 100-300bpm

https://litfl.com/ventricular-tachycardia-monomorphic-ecg-library/

80
Q

What rhythm is shown?

A

Monomorphic VT

81
Q

Describe what fusion and capture beats are which may be seen in monomorphic VT

A
  • Atrial activity may continue independantly of ventricular activity in VT, the presence of p waves dissociated from QRS complexes during broad complex tachycardia confirms VT.
  • Occasionally these atrial impulses may be conducted to the ventricles causing capture or fusion beats.
  • Capture beats — occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration
  • Fusion beats — occur when a wave of depolarisation travelling from AV node occurs simultaneously with a wave of depolarisation travelling up from the ventricular focus producing a hybrid QRS complex (of the normal QRS complex and complex of the monomorphic VT).
82
Q

SVT + bundle branch block can produce a broad complex tachycardia proving diagnostically tricky. Regardless what is the safest approach to broad complex tachycardias?

A

To assume all broad complex tachycardias are VT until proven otherwise.

83
Q

What are the characteristic features of polymorphic VT (PMVT) and what is the most important sub-type of PMVT?

A
  • Polymorphic ventricular tachycardia (PVT) is a form of ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complex varying in amplitude, axis, and duration. The most common cause of PVT is myocardial ischaemia/infarction.
  • Torsades de pointes (TdP) is a specific form of PVT occurring in the context of QT prolongation — it has a characteristic morphology in which the QRS complexes “twist” around the isoelectric line.
84
Q

What are patients with TdP usually deficient in ?

A

Usually hypomagnesaemic and hypokalaemic.

85
Q

What does the tx of TdP usually include ?

A

IV mg2+ &/or IV K+

86
Q

What drug is it important to remember should not be used in TdP?

A
  • QTc prolonging drugs, in-particular Amiodarone as this can cause cardiac arrest. (but recall its used for REGULAR broad complex tachycardias so could be an easy mistake to make).
87
Q

Define PEA

A

Electrical activity that you would normally expect to be associated with cardiac output (pulse).

88
Q

List potential causes of PEA

A

Severe fluid depletion or blood loss.
Cardiac tamponade
Massive PE
Tension pneumothorax.

89
Q

Can bradycardia be normal?

A

It may be physiological in very fit people or during sleep.

90
Q

Why can bradycardia occur during sleep?

A

There is increased vagal/parasympathetic tone during sleep which lowers HR.

91
Q

What rhythm is shown?

A

VT with capture and fusion beats.

92
Q

What rhythm is shown?

A

bradycardia

93
Q

What rhythm is shown?

A

atrial and ventricular pacing rhythm

94
Q

What rhythm is shown?

A

1st degree AV block

95
Q

What rhythm is shown?

A

2nd degree AV block mobitz type 1

96
Q

What rhythm is shown?

A

2nd degree AV block mobitz type 2 (2:1)

97
Q

What rhythm is shown?

A

2nd degree AV block mobitz type 2 (3:1)

98
Q

What rhythm is shown?

A

3rd degree AV block - complete heart block

99
Q

List potential causes of 1st degree AV block

A
  • Physiological - well trained athletes
  • Fibrosis of conducting system
  • IHD
  • Structural heart disease
  • Drugs
100
Q

Does 1st degree AV block or mobitx type 1 AV block require tx ?

A

No

101
Q

Does mobitz type II and 3rd degree AV block require tx?

A

Yes

102
Q

What rhythm is shown here and when is it usually seen?

A

Agonal rhythm usually seen in dying patients, progresses to asystole

103
Q

What may a broad-complex tachycardia be due to ?

A

Ventricular tachycardia
Or SVT + BBB

104
Q

Where does a Supra-ventricular tachycardia (SVT) originate from ?

A

From above the bifrucation of the bundle of His.

105
Q

In a SVT what will the QRS complexes be?

A

Narrow
OR broad if BBB present

106
Q

What are the 3 main SVT’s?

A
  • Regular narrow-complex tachycardia ‘SVT’
  • Atrial fibrillation
  • Atrial flutter
107
Q

What rhythm is shown?

A

Regular narrow complex tachycardia ‘SVT’

108
Q

What rhythm is shown?

A

Atrial flutter with high-degree AV block causing extreme bradycardia (20bpm)

109
Q

What does prolongation of QTc predispose to ?

A

Ventricular arrythmia particularly TdP & VF.

110
Q

Define what the QTc interval is

A

This is the start of the QRS complex to the end of the T-wave

111
Q

What lead is the QTc best calculated from?

A

**Lead II ** is best
(or Lead I & V5).

112
Q

What factor affects the QTc substantially?

A

Heart rate - QTc shortens as it increases

113
Q

What is considered a prolonged QTc in men and women

A

Men > 450ms
Women > 470ms

114
Q

A QTc greater than what significantly increases the risk of sudden cardiac death ?

A

> 500ms

ALS/GIC (14 decks)

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