ECGs + Arrhythmias Flashcards

1
Q

When is ECG monitoring required?

A
  • Cardiac arrest
  • Syncope
  • Chest pain
  • Persistent arrhythmia
  • Shock or other severe illnesses
  • Other indications - severe electrolyte disturbances, poisoning, during and after interventions e.g. major surgery
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2
Q

When should you start and stop ECG monitoring in a cardiac arrest?

A

You should establish cardiac monitoring as soon as possible during cardiac arrest. In many patients who have been resuscitated from cardiac arrest there is a substantial risk of further arrhythmia and cardiac arrest.

It is important to maintain cardiac monitoring in people who have been resuscitated from cardiac arrest until you are confident that the risk of recurrence is very low.

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3
Q

A patient presents to A&E with syncope. Why is a 12-lead ECG indicated in this patient?

A

Some people experience syncope (transient loss of consciousness due to a reduction in blood supply to the brain) caused by an intermittent cardiac arrhythmia that, if not documented and treated, could lead to cardiac arrest or sudden death. However, the arrhythmia may not still be present at the time of initial assessment.

If a person presents with syncope you should undertake careful clinical assessment and record a 12-lead ECG.

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4
Q

A patient presents to A&E with syncope. You record a 12-lead ECG. In what circumstances is admission and cardiac monitoring NOT necessary?

A

ECG monitoring and hospital admission are not usually required for people who have experienced:

  • uncomplicated (vasovagal) fainting
  • situational syncope (e.g. cough syncope or micturition syncope) or
  • syncope due to orthostatic hypotension
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5
Q

A patient presents to A&E with syncope. You record a 12-lead ECG. In what circumstances is admission and cardiac monitoring necessary?

A

Start ECG monitoring and arrange further expert cardiovascular assessment in those patients who have had:

  • unexplained syncope, especially during exercise
  • syncope and have evidence of structural heart disease
  • syncope and have an abnormal ECG (especially a prolonged QT interval).
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6
Q

What type of ECG would you request for a patient admitted to A&E with chest pain?

A

People experiencing chest pain due to acute coronary syndromes will be at risk of developing a cardiac arrhythmia that may place them at risk of cardiac arrest and death.

Single-lead ECG monitoring is not a reliable technique for detecting evidence of myocardial ischaemia (ST-segment depression). Record serial 12-lead ECGs in people experiencing chest pain suggestive of an acute coronary syndrome.

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7
Q

When is ECG monitoring appropriate for a persistent arrhythmia?

A

A persistent arrhythmia + SYMPTOMS e.g. hypotension, heart failure

Monitor the ECG (along with other physiological measurements) to identify and respond to deterioration at the earliest possible time.

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8
Q

What are the 3 different types of ECG monitoring?

A
  • In emergency situations such as cardiac arrest, the cardiac rhythm must be assessed as soon as possible. Self-adhesive pads are used for monitoring rhythm and hands-free shock delivery.
  • If a patient requires monitoring, but is not so critically ill that defibrillator pads are likely to be needed, 3-lead monitoring is the standard form of ECG monitoring employed by many cardiac monitors and defibrillators in general clinical use.
  • The heart is a three-dimensional organ and the 12-lead ECG addresses this by examining the heart’s electrical signals from 12 different directions. In some clinical settings, such as a cardiac care unit, 12-lead monitoring is available to enable early detection of ECG abnormalities that may be seen in a limited number of leads.
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9
Q

If an arrhythmia has been detected by a 3-lead ECG monitor, what further investigation can give you more information about the arrhythmia?

A

record a 12-lead ECG during an arrhythmia that has been detected by simpler monitoring

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10
Q

Where are the pads/electrodes placed for a defibrillator and a 3-lead ECG monitor?

A
  • defibrillator - pads should be applied beneath the right clavicle and in the left mid-axillary line, overlying the V6 ECG electrode position. This is also known as the pectoral/apical position and facilitates rapid rhythm assessment and defibrillation. These pads should be applied whilst CPR is in progress with the aim of minimising interruptions in chest compressions.
  • 3 lead - the electrodes are placed over the bony parts of the shoulders and that the ‘leg’ electrode is often placed on the lower left chest wall over ribs or costal cartilages, to minimise artefact from underlying muscle
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11
Q

What does the p wave represent?

A

In normal sinus rhythm, depolarisation begins in pacemaker cells at the sino-atrial (SA) node.

A wave of depolarisation then spreads from the SA node through the atrial myocardium. This is seen on the ECG as the P wave.

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12
Q

What does the P-R interval represent?

A

When the electrical impulse in the atria reaches the AV node it is conducted slowly, represented on the ECG largely by the isoelectric portion of the PR interval.

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13
Q

What does the QRS complex represent?

A

The bundle of His carries the Purkinje fibres from the AV node and then divides into right and left bundle branches, spreading out through the right and left ventricles respectively.

Rapid conduction down these fibres ensures that the ventricles contract in a co-ordinated fashion. Depolarisation of the bundle of His, bundle branches and ventricular myocardium is seen on the ECG as the QRS complex.

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14
Q

What is the mechanical response of the heart to the electrical impulse represented by the p wave?

A

p wave - atrial depolarisation

mechanical response to this = atrial contraction

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15
Q

What is the mechanical response of the heart to the electrical impulse represented by the QRS complex?

A

QRS complex - ventricular depolarisation

mechanical response to this = ventricular contraction

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16
Q

What is meant by sinus rhythm?

A

Sinus rhythm

The atria and ventricles are contracting in sequence at the same rate (approximately 60 beats min-1 and myocardial activity is coordinated.

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17
Q

Describe the pathophysiology and management.

A

Ventricular fibrillation

The electrical activity is chaotic, there is no coordinated muscle activity in either the atria or ventricles and the pumping action of the heart is lost. Urgent defibrillation is indicated as soon as it is safe to do so and treated according to the ‘shockable’ algorithm.

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18
Q

Describe the pathophysiology and management.

A

Ventricular tachycardia

The ventricles are contracting at a much faster rate than the atria. There may or may not be a pulse rhythm - confirmation of cardiac arrest will dictate the action taken.

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19
Q

Describe the pathophysiology and management.

A

Asystole

Neither the atria or ventricles exhibit any electrical or mechanical activity.

  • If you cannot see any electrical activity check the patient: are there signs of life?
    • If not, then cardiac arrest is confirmed and CPR should be started.
    • If electrical activity is present and the patient shows signs of life, then continue with the next steps of rhythm recognition. Be aware that poor electrode contact or placement will affect the ECG trace.
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20
Q

How do you measure

1) PR interval
2) QRS duration
3) QT interval

A
  1. PR interval = beginning of p to beginning of q
  2. QRS duration = beginning of q to end of s
  3. QT interval = beginning of q to end of t
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21
Q

6-stage approach to interpreting ECG rhythm strips…

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 width of the QRS complex normal (narrow) or prolonged (broad)?
  5. Is atrial activity present?
  6. Is atrial activity linked to ventricular activity, if so, how?
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22
Q

How do you calculate ventricular rate from an ECG rhythm strip?

A

number of R-R intervals in 6s (30 big squares) x10

if rhythm strip not long enough,

number of R-R intervals in 3s (15 big squares) x20

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23
Q

What is normal heart rate?

A

The normal heart rate (ventricular rate) at rest is 60-100 beats min-1

Bradycardia is a heart rate slower than 60 min-1

Tachycardia is a heart rate faster than 100 min-1

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24
Q

How do you work out if the QRS rhythm is regular or irregular? What should you do if it is irregular?

A

measure out each R-R interval and compare it to others in the rhythm strip

If the QRS rhythm is irregular you will need to decide:

is this totally irregular, with no recognisable pattern of R-R interval?

is the basic rhythm regular, with intermittent irregularity?

is there a recurring cyclical variation in the R-R intervals?

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25
Q

What is the upper limit of normal for QRS duration?

A

The upper limit of normal for the QRS duration is 0.12 s (3 small squares on ECG paper at 25 mm s-1). If the QRS width is less than this, the rhythm almost certainly originates from above the bifurcation of the bundle of His and may be from the SA node, atria or AV node, but not from the ventricular myocardium.

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26
Q

If the QRS duration is longer than 3 small squares, where is the rhythm originating?

A

If the QRS duration is 0.12 s or more the rhythm may be coming from ventricular myocardium or may be a supraventricular rhythm, transmitted with aberrant conduction (i.e. bundle branch block).

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27
Q

What do normal p waves look like in the different leads?

A

During sinus rhythm in a healthy person P waves are usually positive deflections in lead II and shallow, biphasic deflections in V1. For example:

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28
Q

When is it difficult to see atrial activity on an ECG even though it is present?

A

During a sustained tachycardia with a rapid QRS rate, atrial activity may not be visible between the QRS complexes. It is important not to persuade yourself that you can see atrial activity unless you are sure that it is visible.

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29
Q

Which leads are the best to look at when suspecting atrial flutter?

A

During atrial flutter, atrial activity is seen as flutter waves - an absolutely regular repetitive deflection with a ‘saw-tooth’ appearance, often at a rate of 260-300 min-1. Typical atrial flutter is seen best in the inferior ECG leads (II, III, aVF).

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30
Q

What does it mean if there are variations in the PR interval?

A

If there is a consistent interval between each P wave and the following QRS complex, it is likely that conduction between atrium and ventricle is occurring with each beat and that ventricular depolarisation is triggered by atrial depolarisation. If there are variations in the PR interval and the QRS rate is slower than the atrial rate this is likely to indicate a degree of heart block.

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31
Q

Ventricular fibrillation or Polymorphic VT (Torsades de pointes VT)?

A

Ventricular fibrillation

The rhythm abnormality that is most likely to be mistaken for VF is polymorphic VT (torsades de pointes VT). Patients may be pulseless and lose consciousness during this rhythm; it may terminate spontaneously, or may degenerate into VF. If this rhythm is present and the patient is in clinical cardiac arrest the appropriate treatment is defibrillation, so mistaking the rhythm for VF will not result in inappropriate treatment.

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32
Q

Ventricular fibrillation or Polymorphic VT (Torsades de pointes)

A

Torsades de pointes

The rhythm abnormality that is most likely to be mistaken for VF is polymorphic VT (torsades de pointes VT). Patients may be pulseless and lose consciousness during this rhythm; it may terminate spontaneously, or may degenerate into VF. If this rhythm is present and the patient is in clinical cardiac arrest the appropriate treatment is defibrillation, so mistaking the rhythm for VF will not result in inappropriate treatment.

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33
Q

What are the different types of ventricular tachycardia?

A

In VT the QRS morphology may be:

  • monomorphic - a regular rhythm strip pattern
  • polymorphic - the morphology of the QRS complexes varies from complex to complex - one form of polymorphic VT is torsades de pointes VT, in which there is a sinusoidal pattern of variation in QRS amplitude.
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34
Q

Does VT always result in cardiac arrest?

A

VT may generate a detectable cardiac output (e.g. pulse) in some situations but in others may cause loss of cardiac output resulting in cardiac arrest. It may also degenerate into VF.

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35
Q

What is the difference between asystole and ventricular asystole?

A

If the patient is pulseless and there is no electrical activity on the ECG, this is asystole. The absence of any electrical activity indicates asystole in atria as well as ventricles. Occasionally ventricular asystole (sometimes called ventricular standstill) occurs in the presence of continued P wave activity in the atria. Atrial contraction alone will not maintain cardiac output, so cardiac arrest will be present, but patients with ventricular standstill and continued P wave activity may have a better chance of survival as cardiac pacing may restore ventricular contraction.

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36
Q

What should you do if you are not sure whether the defibrillator is showing very fine VF or asystole?

A

Sometimes during cardiac arrest it is not certain whether the ECG shows asystole or very fine VF. The best treatment in this situation is immediate high-quality CPR. If the patient was in fine VF then good CPR may increase the amplitude and frequency of VF, making it easier to identify and more likely to respond to defibrillation. If the patient is in asystole, CPR is the appropriate treatment and the presence of asystole is likely to be recognised by its persistence.

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37
Q

What rhythm would you expect with PEA?

A

PEA does not refer to a specific cardiac rhythm. It defines the clinical absence of cardiac output despite electrical activity that would normally be expected to produce a cardiac output.

It often has a poor prognosis, especially when caused by large acute myocardial infarction. Other treatable causes include:

  • massive pulmonary embolism
  • tension pneumothorax
  • cardiac tamponade
  • acute, severe blood loss
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38
Q

You have been called to see a patient experiencing palpitations. The ward nurse gives you some background information. James Canolay, a 68 year old male, has been experiencing light-headedness for the last hour. He has been unable to shake off a cold for the last few weeks and was admitted via his GP earlier this morning for investigations. The results of your observations are as follows:

A - Clear and talking
B - RR 30 min-1, chest clear, SpO2 92%
C - P140-1, ECG monitor in place. BP 100/60 mmHg, CRT 2 s, Temp 37.5°C, no cannula in situ
D - Alert, blood sugar normal
E - Nothing significant found

During the ABCDE assessment an ECG monitor has been attached. Diagnosis and management?

A

Atrial fibrillation

From the history it is clear that this is new onset atrial fibrillation with a less than 48 hour history.

Immediate management - cardioversion + heparinisation. Either:

  • Electrical - DC cardioversion
  • Pharmacological - Flecainide (no evidence of structural heart disease), Amiodarone (evidence of structural heart disease)

Long-term management - Patients who have risk factors for ischaemic stroke should be put on lifelong oral anticoagulation.

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39
Q

Sunita Kundu is a 71-year-old female who is in the day-case unit, having just had an arthroscopy for a painful, swollen knee. During routine observations her pulse was noticed to be irregular.

On assessment of the patient you discover the following:

A - Awake and talking
B - Breathing without apparent distress, RR 11 min-1
C - P 42 min-1, BP 112/68 mmHg, CRT < 2s
D - Complaining of some pain in the knee
E - Bandaged knee, drug chart indicates that she has just been given oral analgesia, but no other drugs

Your colleague hands you Mrs Kundu’s ECG rhythm strip and asks for your interpretation. Diagnosis and Management?

A

Second degree AV block of Mobitz 1 (Wenckebach)

Mobitz I is usually a benign rhythm, causing minimal haemodynamic disturbance and with low risk of progression to third degree heart block.

Asymptomatic patients do not require treatment.

Symptomatic patients usually respond to atropine.

Permanent pacing is rarely required.

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40
Q

Mr Sven Anderberg has been admitted to the Emergency Department after experiencing rapid palpitation and increasing chest pain for the last 3 h.

Mr Anderberg made an uncomplicated recovery from inferior wall myocardial infarction 6 years ago. There is no other significant past history. Initial assessment has demonstrated:

A - Not compromised, talking
B - Breathing spontaneously RR 15 min-1
C - HR > 200 min-1, BP 86/47 mmHg, CRT 4 s
D - Alert
E - Looks pale, sweating

As part of his initial assessment your team has recorded a rhythm strip. Diagnosis and management?

A

Sven Anderberg’s history and ECG findings are most likely to be due to ventricular tachycardia. A supraventricular tachycardia with bundle branch block could cause similar ECG appearances but it is safest to manage regular broad-complex tachycardia as VT unless it has been proven to be supraventricular in origin.

He has a pulse but is unstable so immediate cardioversion is indicated.

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41
Q

Walter Smith has just been admitted to the ED after suffering transient loss of consciousness.

Mr Smith has had a few similar events over the last few weeks but has not previously sought medical help. The paramedics who attended him reported that he had a slow pulse rate. On examination you find:

A - No abnormality, talking normally
B - No apparent respiratory distress, RR 12 min-1
C - HR 36 min-1, BP 178/69 mmHg, CRT 2 s
D - Alert, blood glucose 5 mmol L-1
E - No other abnormality

Diagnosis and Management?

A

Complete AV block (Third degree heart block) with Inferior STEMI

Patients with third degree heart block are at high risk of ventricular standstill and sudden cardiac death.

They require urgent admission for cardiac monitoring, backup temporary pacing and usually insertion of a permanent pacemaker.

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42
Q

A patient with asthma has been admitted with increasing breathlessness despite increased treatment for his asthma. Following initial assessment an ECG monitor has been attached.

Adrian Morel is a 55-year-old male who had a recent chest infection causing an exacerbation of his asthma. Following treatment with an antibiotic, steroids and increased bronchodilators his cough has settled and he feels less wheezy, but he is much more breathless on exertion than usual. Initial assessment has revealed:

A - Patent, able to speak normally
B - No obvious wheeze, RR 13 min-1. SpO2 96% on air
C - P regular, HR 142 min-1, BP 138/76 mmHg, CRT 2 s
D - Alert
E - No other abnormalities identified

Diagnosis and Management?

A

Atrial activity is seen as a saw-tooth pattern with a rate of about 300 min-1. The relationship between atrial waves and QRS complexes is 2:1 which gives a QRS rate of 150 min-1.

Mr Morel has a regular, narrow-complex tachycardia, with saw-tooth atrial activity and a 2:1 relationship between atrial and ventricular activity.

Supraventricular tachy when patient is stable:

While on continuous ECG monitoring:

Valsava – blow hard against resistance e.g. into plastic syringe to maintain vagal tone

Carotid sinus massage – press for five seconds on carotid sinus on one side to increase vagal tone

Adenosine – terminates conduction through AVN

(These techniques usually work to unmask the atrial flutter and definitive management with cardioversion is usually req)

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43
Q

Which are the lateral leads?

A

I, aVL, V6

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44
Q

Which are the inferior leads?

A

II, III, aVF

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45
Q

Which are the anterior leads?

A

V2, V3, V4

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46
Q

Is a normal QRS complex in lead aVR a positive or negative deflection?

A

The normal QRS complex in lead aVR is a mainly negative deflection. The T wave is also negative; this is a normal feature in this lead and is therefore not an inverted T wave.

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47
Q

Is a normal QRS complex in lead V1 a positive or negative deflection?

A

The normal QRS complex in lead V1 is a mainly negative deflection. The T wave is often also negative, but may be flat or upright in some people. These are all possible normal features in this lead; a negative T wave in lead V1 is usually normal and not inverted.

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48
Q

There is t wave inversion in lead III. Does this mean there are inferior ischaemic changes?

A

not necessarily

The normal QRS complex in lead III is often but not always predominantly a positive deflection. The T wave in lead III tends to follow the direction of the QRS complex, so when the QRS complex in this lead is negative, the T wave is often negative also. When the T wave in lead III is negative look at the direction of the QRS complex and look at the ECG complexes in the other inferior leads (II and aVF). If there are abnormalities in these other leads, a negative T wave in lead III is more likely to represent true T-wave inversion.

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49
Q

In which leads is t wave inversion a normal variant?

A

aVR, V1, III

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50
Q

A patient presents with chest pain. What does this ECG suggest?

A

On this ECG there is deep T-wave inversion in the anterolateral chest leads and in the lateral limb leads (I and aVL) in a patient with clinical features of myocardial infarction.

This is acute coronary syndrome. It could be an NSTEMI or unstable angina - positive troponin will tell you that an MI has occurred. T-wave inversion of this nature suggests a high-risk situation, requiring early assessment and treatment by a cardiologist, after the usual initial measures for all acute coronary syndromes.

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51
Q

A patient presents with chest pain. What does this ECG suggest?

A

This ECG shows obvious depression of the ST segments in the anterior and lateral leads.

This is acute coronary syndrome. It could be an NSTEMI or unstable angina - positive troponin will tell you that an MI has occurred. ST-depression of this nature suggests a high-risk situation, requiring early assessment and treatment by a cardiologist, after the usual initial measures for all acute coronary syndromes.

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52
Q

A patient presents with chest pain. What does this ECG suggest?

A

There is ST-segment elevation in the anterior chest leads and in the lateral leads, so this is an anterolateral ST-elevation MI.

Immediate management of ACS and immediate consideration of reperfusion therapy is required.

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53
Q

A patient presents with chest pain. What does this ECG suggest?

A

There is ST-segment elevation in leads II, III and aVF, the inferior leads.

In the presence of a clinical suspicion of an acute coronary syndrome this indicates acute inferior STEMI.

Immediate management of ACS and reperfusion therapy is indicated.

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54
Q

A patient presents with chest pain. What does this ECG suggest?

A

The main ECG abnormality in people with acute posterior-wall STEMI is usually ST-segment depression in the anterior leads, a reciprocal change reflecting ST-segment elevation at the back of the heart.

If you see ST depression in leads V1-V3 in this clinical setting, consider recording posterior leads to look for ST elevation, and look for other clues that this may be posterior-wall infarction.

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55
Q

Does a normal ECG exclude an acute MI?

A

no

56
Q

Which of these requires immediate reperfusion:

  • ST elevation
  • ST depression
  • T wave inversion
A

ST-elevation indicates a need for immediate reperfusion therapy

T-wave inversion and ST-segment depression may be present with non-ST-elevation MI but are not specific for this diagnosis. These features do not require immediate reperfusion.

57
Q

Does this patient need ECG monitoring?

An anxious man with a pulse of 110min-1 and a strong family history of heart disease.

A

no - tachycardia is a normal response to anxiety

58
Q

Do q waves always indicate previous MI?

A

The time at which Q waves appear in the evolution of acute myocardial infarction is very variable and they can be seen very early; in many people they persist and provide evidence of previous infarction on ECGs recorded at a later date.

59
Q

What is shown in this ECG?

A

anterior wall STEMI (ST elevation in anterior leads and q waves in the anterior leads)

treatment of ACS + immediate reperfusion

60
Q

How should you approach a patient in whom an arrhythmia is suspected?

A

When an arrhythmia is present or suspected, start by assessing the patient using the ABCDE approach. Use this to determine the presence or absence of adverse features and then go on to assess the nature of the arrhythmia.

61
Q

When approaching a patient with a suspected arrhythmia, after an A-E assessment, you should look for the presence of adverse features. What is meant by this?

A

Adverse features imply that a patient’s condition is unstable and at risk of deterioration.

Adverse features include: shock, syncope, myocardial ischaemia, heart failure

62
Q

What are the signs and symptoms of shock?

A

hypotension (systolic blood pressure <90 mmHg), pallor, sweating, cold extremities, confusion and impaired consciousness

63
Q

What is meant by syncope?

A

transient loss of consciousness because of global reduction in blood flow to the brain

64
Q

What are the signs and symptoms of heart failure?

A

pulmonary oedema and/or raised jugular venous pressure (with or without peripheral oedema and liver enlargement)

65
Q

What are the signs and symptoms of myocardial ischaemia?

A

typical ischaemic chest pain and/or evidence of myocardial ischaemia on a 12-lead ECG

66
Q

Continuous ECG montioring is essential

a) before
b) during
c) after

any intervention to detect any change in rhythm.

a b or c?

A

A B & C

67
Q

What are the general immediate management options for any arrhythmia?

A
  • No treatment needed
  • Pharmacological (drug treatment)
  • Simple clinical intervention (i.e. vagal manoeuvres)
  • Electrical (cardioversion for tachyarrhythmia)
68
Q

Why might electrical interventions be preferred over drug interventions for the treatment of arrhythmias in some patients?

A

Most drugs act more slowly and less reliably than electrical treatments, so electrical treatment is usually the preferred treatment for an unstable patient with adverse features.

69
Q

You are on duty in the cardiology ward when a nurse asks you to see a 65-year-old patient who is in a monitored bed. After a rapid SBAR handover which reveals that 36 hours ago he had PPCI for an anterior STEMI. You carry out an ABCDE assessment and find:

A - Clear, complaining of feeling unwell
B - Respiratory rate 26 min-1, SpO2 94% on air
C - Pale, heart rate 220 min-1, BP 70/42 mmHg,
CRT 3-4 s
D - Alert, blood glucose 5.6 mmol L-1
E - Nil of note

Diagnosis?

A

Regular broad-complex tachycardia.

The QRS rate is fast (220 min-1), the rhythm is regular and the QRS complex width is broad (greater than 0.12 s). Atrial activity is not visible, so it is not possible to identify a relationship with ventricular activity

Shock

We can tell that shock is present because he is pale and his systolic BP is less than 90 mmHg. This is the only adverse feature.

70
Q

You are on duty in the cardiology ward when a nurse asks you to see a 65-year-old patient who is in a monitored bed. After a rapid SBAR handover which reveals that 36 hours ago he had PPCI for an anterior STEMI. You carry out an ABCDE assessment and find:

A - Clear, complaining of feeling unwell
B - Respiratory rate 26 min-1, SpO2 94% on air
C - Pale, heart rate 220 min-1, BP 70/42 mmHg,
CRT 3-4 s
D - Alert, blood glucose 5.6 mmol L-1
E - Nil of note

What immediate treatment is appropriate for this patient?

A

Broad complex tachycardia

Adverse event = shock

According to algorithm:

1) synchronised DC cardioversion, up to 3 attempts, if the first shock does not terminate the arrhythmia
2) If cardioversion does not correct the rhythm give amiodarone 300 mg IV over 10-20 min and repeat the synchronised DC shock, followed by 900mg of amiodarone over 24 h

Alert senior and check electrolytes/other potential reversible causes.

71
Q

You are working in the Emergency Department and you are asked to see a 48-year-old woman. After a rapid SBAR handover from the nurse in charge which reveals that she has been having palpitations for about 12 hour and now has some chest pain. You carry out an ABCDE assessment and find:

A - Clear, complaining of chest pain
B - Respiratory rate 16 min-1, no added breath sounds on auscultation, SpO2 97% on air
C - Heart rate 180 min-1, BP 110/90 mmHg, CRT < 2s
D - Alert, blood glucose 5.5 mmol L-1
E - Nil of note

You decide that the patient has a tachycardia, but decide there are no adverse features. While awaiting a 12-lead ECG, you ask the nurse to run off a rhythm strip.

Interpret the ECG.

A

regular, narrow-complex tachycardia.

The rate is fast (120 min-1). The rhythm is regular. The QRS complex width is normal (less than 0.12 s). Atrial activity is not visible. Therefore, it is not possible to identify its relationship with ventricular activity

72
Q

You are working in the Emergency Department and you are asked to see a 48-year-old woman. After a rapid SBAR handover from the nurse in charge which reveals that she has been having palpitations for about 12 hour and now has some chest pain. You carry out an ABCDE assessment and find:

A - Clear, complaining of chest pain
B - Respiratory rate 16 min-1, no added breath sounds on auscultation, SpO2 97% on air
C - Heart rate 180 min-1, BP 110/90 mmHg, CRT < 2s
D - Alert, blood glucose 5.5 mmol L-1
E - Nil of note

You decide that the patient has a tachycardia, but decide there are no adverse features. While awaiting a 12-lead ECG, you ask the nurse to run off a rhythm strip.

Management?

A

regular, narrow-complex tachycardia

1) vagal manouvres - Carotid sinus massage or the Valsalva manoeuvre
2) adenosine - adenosine 6 mg IV as a very rapid bolus
3) Alert a senior and ensure any reversible causes e.g. electrolyte abnormalities are corrected

73
Q

In the absence of adverse features, regular narrow-complex tachyarrhythmia may be treated with vagal manouevres. What will happen if the rhythm is atrial flutter?

A

If the rhythm is atrial flutter with 2:1 conduction, slowing of the ventricular response will often occur and reveal flutter waves, if this is the case seek expert help.

74
Q

If the patient has a narrow complex tachyarrhythmia and adverse features, what simple intervention can be done while waiting for synchronised DC cardioversion?

A

If a patient has adverse features and is at risk of deterioration because of the tachyarrhythmia then vagal manoeuvres may be considered whilst preparations are being made for synchronised cardioversion. Synchronised cardioversion is discussed further in ‘Perform synchronised cardioversion’. If vagal manoeuvres terminate the arrhythmia, cardioversion will not be needed.

75
Q

In the absence of adverse features, regular narrow-complex tachyarrhythmia may be treated with vagal manouevres or adenosine. What important steps should be considered when giving adenosine?

A

If vagal manoeuvres have been attempted and the arrhythmia persists (and it is not atrial flutter) give adenosine 6 mg IV as a very rapid bolus.

Use a large cannula and a large (e.g. antecubital) vein. Remember to:

1) check for contraindications such as asthma
2) warn the patient that they will feel unwell and experience chest discomfort for a few seconds after the injection
3) record the ECG continuously (preferably multi-lead) during the injection.

76
Q

A patient is given adenosine for a narrow complex tachyarrhythmia. The ventricular rate slowed transiently, then speeded up again. What is the likely diagnosis?

A

SVT - look for atrial activity such as atrial flutter (or other atrial tachycardia) and treat accordingly.

77
Q

If a narrow complex tachyarrhythmia does not respond to adenosine, what are the next steps?

A

If there is no response to adenosine 6 mg, give a 12 mg bolus. If there is again no response give one further 12 mg bolus. Lack of response to adenosine will occur if the bolus is given too slowly or into a small peripheral vein.

78
Q

If a narrow complex tachycardia is treated with vagal manouvres and the slowing of the ventricular rate reveals flutter waves. What would be the next step in your management?

A

Diagnosis is likely to be atrial flutter. In the first instance this may be treated with drugs to control rate (for example, a ß-blocker).

79
Q

You are in the post-anaesthesia care unit when a colleague asks for assistance. A 78-year-old man who is recovering from a hernia repair has suddenly developed a tachycardia. After a rapid SBAR handover, where the only other finding of note is that he is a known hypertensive treated with a diuretic, you carry out an ABCDE assessment and find:

A - Clear, not complaining of anything
B - Respiratory rate 18 min-1, SpO2 96% on 30% oxygen
C - Heart rate 170 min-1, BP 100/60 mmHg, CRT < 2s
D - Alert, blood glucose 4.0 mmol L-1
E - Nil of note

While waiting for a 12-lead ECG, you ask one of the nurses to record a rhythm strip to help with a diagnosis.

A

fast atrial fibrillation

The rate is fast (200 min-1). The rhythm is irregular. The QRS complex width is normal (less than 0.12 s).

80
Q

You are in the post-anaesthesia care unit when a colleague asks for assistance. A 78-year-old man who is recovering from a hernia repair has suddenly developed a tachycardia. After a rapid SBAR handover, where the only other finding of note is that he is a known hypertensive treated with a diuretic, you carry out an ABCDE assessment and find:

A - Clear, not complaining of anything
B - Respiratory rate 18 min-1, SpO2 96% on 30% oxygen
C - Heart rate 170 min-1, BP 100/60 mmHg, CRT < 2s
D - Alert, blood glucose 4.0 mmol L-1
E - Nil of note

While waiting for a 12-lead ECG, you ask one of the nurses to record a rhythm strip to help with a diagnosis.

Management?

A

fast atrial fibrillation - seek advice of senior to determine whether rate or rhythm control is best for the individual pt

1) rate control orally - beta blocker

A beta blocker is the most appropriate treatment in this situation. Decide whether to use the oral or IV route, depending on the urgency of response needed and the patient’s current ability to swallow and absorb a drug given orally. There are no adverse signs so electrical cardioversion is not the first-line treatment.

Diltiazem may be used in patients where beta blockade is contraindicated or has been given previously and not tolerated.

There are no signs of heart failure to suggest that digoxin should be first-line treatment for rate control.

Remember to seek expert help to plan this man’s further assessment and treatment.

81
Q

A 65 year old gentleman presents with new-onset AF. It started 1 hour ago and he is being considered for rhythm control. Name some contraindications for the use of flecainide. What are the alternatives?

A

CI for flecainide - heart failure, known left ventricular impairment, ischaemic heart disease, or a prolonged QT interval

alternatives - Amiodarone (300 mg over 20-60 min followed by 900 mg over 24 h) may be used to attempt chemical cardioversion but is less often effective than drugs like flecainide and takes longer to work / /Electrical cardioversion remains an option in this setting and will restore sinus rhythm in more patients than chemical cardioversion.

82
Q

What are the options for treatment of AF?

A

1) rate control orally - beta blocker or diltiazem (in patients in whom beta blockade is contraindicated (e.g. by asthma) or not tolerated) or digoxin (patients with heart failure)
2) If the duration of atrial fibrillation is under 48 hours, and rhythm control is considered the appropriate strategy, cardioversion may be appropriate - flecainide, amioadarone (takes longer and less effective), electrical DC cardioversion

83
Q

You are in the post-anaesthesia care unit when a colleague asks for assistance. A 78-year-old man who is recovering from a hernia repair has suddenly developed a tachycardia. After a rapid SBAR handover, where the only other finding of note is that he is a known hypertensive treated with a diuretic, you carry out an ABCDE assessment and find:

A - Clear, not complaining of anything
B - Respiratory rate 18 min-1, SpO2 96% on 30% oxygen
C - Heart rate 170 min-1, BP 100/60 mmHg, CRT < 2s
D - Alert, blood glucose 4.0 mmol L-1
E - Nil of note

ECG shows AF. The patient is given IV metoprolol but 30 min later he complains of chest discomfort. The result of an assessment using the ABCDE approach is shown here.

Based on this assessment, which of the following is appropriate?

A

The patient has adverse features (chest discomfort and hypotension) and the onset of atrial fibrillation was less than 48 h ago. Anticoagulation, initially with low-molecular-weight heparin or unfractionated heparin, and then sedation and electrical synchronised cardioversion is the most appropriate treatment.

84
Q

If someone has been in AF for less than 48 hours and cardioversion is required urgently because they are unstable, should they be anticoagulated?

A

YES

EITHER regular low-molecular-weight heparin in therapeutic dose

OR an IV bolus of unfractionated heparin followed by a continuous infusion to maintain the activated partial thromboplastin time (APTT) at 1.5-2.0 times the control value

85
Q

Can any patient with AF be treated with cardioversion?

A

The longer a patient remains in atrial fibrillation (AF) the greater is the likelihood of atrial thrombus developing.

In general, patients who have been in AF for longer than 48 hours should not be treated by cardioversion

86
Q

If a patient who has had AF for more than 48 hours is to be treated with cardioversion, what should be done?

A

n general, patients who have been in AF for longer than 48 hours should not be treated by cardioversion (electrical or chemical) until they have been fully anticoagulated for at least 3 weeks, or unless transoesophageal echocardiography has detected no evidence of atrial thrombus.

87
Q

Once cardioversion for AF has been completed, does the patient need to remain on anticoagulation?

A

Continue heparin therapy and commence oral anticoagulation after successful cardioversion. Seek expert advice on the duration of anticoagulation, which should be a minimum of 4 weeks, but substantially longer treatment is required in many cases depending on CHADS-VASc and the risk of AF reoccurring.

88
Q

Does electrical cardioversion need to be carried out under sedation?

A

yes

general anaesthesia or conscious sedation given by a healthcare professional with the appropriate training and competence.

89
Q

Why is it important to ensure that the defibrillator is set to deliver a synchronised shock rather than an unsynchronised shock when performing cardioversion for AF?

A

The first step in preparing to administer electrical cardioversion is to ensure that the defibrillator is set to deliver a synchronised shock. An unsynchronised shock could coincide with a T wave and cause ventricular fibrillation (VF). By avoiding the relative refractory period, the risk of inducing VF is minimised.

90
Q

Which wave of the ECG is a synchronised shock meant to coincide wtih?

A

Whether electrical cardioversion is used to treat an atrial or a ventricular tachyarrhythmia, the shock must be synchronised to coincide with the R wave.

91
Q

What energy is a synchronised shock for AF or broad complex tachycardia delivered at?

A

For a broad-complex tachycardia or atrial fibrillation, start with a 120-150 J biphasic shock and increase in increments if this fails to a maximum of three attempts.

92
Q

What energy is a synchronised shock for atrial flutter and regular narrow complex tachycardia delivered at?

A

Atrial flutter and regular narrow-complex tachycardia will often be terminated by lower-energy shocks: start with 70-120 J biphasic.

93
Q

Which types of pads are used for electrical cardioversion in AF or atrial flutter?

A

For patients who are in atrial fibrillation or atrial flutter, use anteroposterior self-adhesive padpositions when it is practical to do so.

94
Q

How is a synchronised shock delivered?

A

Before delivering the shock, double check that it will be synchronised. As in this picture, most defibrillators display a mark above each QRS complex to indicate this. Make sure that team members are not touching the patient or the bed and that oxygen is removed. Press the shock button and keep it pressed until after the shock has occurred - there may be a slight delay before the shock is delivered. If further shocks are needed, reactivate the synchronisation switch before each shock if necessary.

95
Q

In a stable patient with a broad-complex tachycardia what would be the recommended first-line treatment?

A

amiodarone 300 mg intravenously over 20-60 min

n a stable patient, drug therapy is recommended before electrical therapy, and the only electrical therapy that might be considered would be synchronised cardioversion in a patient who had not responded to drug therapy or who developed adverse features later.

96
Q

In atrial fibrillation, CPR should be done in an unresponsive patient with a heart rate of 125min-1 and no palpable pulse.

True or False?

A

true

In a pulseless patient with AF this is PEA and requires immediate CPR.

97
Q

In a patient with atrial fibrillation, synchronised cardioversion should be used in a patient with a heart rate of 35min-1 and BP 175/68mmHg.

True or False?

A

Cardiac pacing is used to treat bradycardia, not tachycardia. Conversely synchronised cardioversion is used as first-line treatment for tachyarrhythmia in patients with adverse features.

98
Q

Are bradycardias always pathological?

A

no, a bradycardia may be:

  • a physiological state in very fit people or during sleep
  • an expected result of treatment (e.g. with a ß-blocker)
99
Q

What can cause a pathological bradycardia?

A

Pathological bradycardia may be caused by malfunction of the SA node or from partial or complete failure of atrioventricular conduction.

100
Q

Why is extreme bradycardia dangerous?

A

A heart rate that is extremely low can lead to dangerously low cardiac output and cardiac arrest

101
Q

Diagnosis and Management?

A

First-degree atrioventricular block

The PR interval is the time between the onset of the P wave and the start of the QRS complex (whether this begins with a Q wave or R wave). The normal PR interval is 0.12-0.20 s (or 3-5 small squares).

First-degree atrioventricular (AV) block is present when the PR interval is > 0.20 s and is a common finding. It represents a delay in conduction through the AV junction (the AV node and immediately adjacent myocardium).

First-degree AV block rarely causes any symptoms and as an isolated finding rarely requires treatment.

102
Q

Diagnosis and Management?

A

Mobitz Type I AV block (also called Wenckebach AV block)

The PR interval shows progressive prolongation after each successive P wave until a P wave occurs without a resulting QRS complex. Often the cycle is then repeated.

The need for treatment is dictated by the effect of the arrhythmia on the patient and the risk of developing more severe AV block or asystole.

103
Q

Diagnosis and Management?

A

Mobitz Type II AV block

There is a constant PR interval in the conducted beats but some of the P waves are not conducted (i.e. followed by QRS complexes), in this case producing 2:1 AV block. This may occur randomly, without any consistent pattern. People with Mobitz II AV block have an increased risk of progression to complete AV block and asystole.

2:1 AV block describes the situation in which only alternate P waves are followed by a QRS complex. 2:1 AV block may be due to Mobitz I or Mobitz II AV block and it may be difficult to distinguish which it is from the ECG appearance. If bundle branch block is present (broad QRS complexes) as well as 2:1 block, this is likely to be Mobitz II block.

104
Q

Diagnosis and Management?

A

3:1 AV block

This shows a 3:1 AV block, which is less common and is usually a form of Mobitz II AV block.

Immediate decisions about treatment of these rhythms will be determined by the effect of the resulting bradycardia on the patient. After identifying and providing any necessary immediate treatment, continue cardiac monitoring and arrange expert cardiological assessment.

105
Q

Diagnosis and Management?

A

Third-degree atrioventricular block

In third-degree (complete) AV block, there is no relationship between P waves and QRS complexes; atrial and ventricular depolarisation arises independently from separate ‘pacemakers’. The site of the ‘pacemaker’ stimulating the ventricles will determine the ventricular rate and QRS width.

A pacemaker site in the AV node or proximal bundle of His may have an intrinsic rate of 40-50 min-1 or sometimes higher and will have a narrow QRS complex unless additional bundle branch block is present.

A pacemaker site in the distal His-Purkinje fibres or ventricular myocardium will produce broad QRS complexes, often have a rate of 30-40 min-1 or less, and is more likely to stop abruptly, resulting in asystole.

106
Q

Diagnosis?

A

Agonal rhythm

Agonal rhythm occurs in dying patients.
It is characterised by the presence of slow, irregular, wide ventricular complexes, often of varying morphology. These are unlikely to produce a pulse.

Agonal rhythm is seen commonly during the later stages of unsuccessful resuscitation attempts. The complexes slow inexorably and often become progressively broader before all recognisable activity is lost.

107
Q

What is atropine?

A

Indication - Symptomatic bradycardia

Contraindication - Do not give to patients who have had a cardiac transplant

Dose - 500 mcg IV, repeated every 3-5 min to maximum of 3 mg

Actions

  • Blocks vagus nerve
  • Increases sinus rate
  • Increases atrioventricular conduction

Side effects

  • Blurred vision, dry mouth, urinary retention
  • Confusion
108
Q

Can non-invasive pacing be established by an ALS provider?

A

yes

In some cardiac arrest or peri-arrest settings, use of cardiac pacing can be life-saving.

Non-invasive pacing may be used to maintain cardiac output temporarily while expert help to deliver longer-term treatment is obtained.

Non-invasive pacing can be established rapidly and is well within the capabilities of an ALS provider.

109
Q

What are the different types of implanted devices that deliver pacing?

A
  • pacemakers implanted for the treatment of bradycardia (single or dual-chamber)
  • biventricular pacemakers (implanted for left ventricular failure)
  • ICDs (which have pacing capability)
110
Q

What is percussion pacing?

A

When bradycardia is so profound that it causes clinical cardiac arrest, percussion pacing may be used in preference to CPR because it may produce an adequate cardiac output with less trauma to the patient.

To perform percussion pacing:

With the side of a closed fist deliver repeated firm thumps to the praecordium just lateral to the lower left sternal edge.

Raise the hand about 20 cm above the chest for each thump.

If initial thumps do not produce a QRS complex try using slightly harder thumps and try moving the point of contact around the praecordium until a site is found that produces repeated ventricular stimulation.

If attempted percussion pacing does not achieve a cardiac output within a few seconds, start CPR.

111
Q

A 78-year-old man is sent into the Medical Admissions Unit by his GP after suffering sudden, transient loss of consciousness.

He feels mildly breathless on walking short distances.

Using the ABCDE approach, you find:

A : Clear
B : Spontaneous breathing, rate 18 min-1, fine inspiratory basal crackles bilaterally
C : Looks pale, P 45 min-1, BP 90/50 mmHg, CRT 3 s
D : Alert, glucose 4.5 mmol L-1
E : Nil of note

Based on his clinical course and initial rhythm, what action will you take?

A

Atropine 500mcg IV

The patient presented after an episode of syncope. He also has signs of heart failure. The rhythm is second-degree AV block (Mobitz II) and therefore he may be at risk of asystole. As a result of this you give atropine.

112
Q

A 78-year-old man is sent into the Medical Admissions Unit by his GP after suffering sudden, transient loss of consciousness.

He feels mildly breathless on walking short distances.

Using the ABCDE approach, you find:

A : Clear
B : Spontaneous breathing, rate 18 min-1, fine inspiratory basal crackles bilaterally
C : Looks pale, P 45 min-1, BP 90/50 mmHg, CRT 3 s
D : Alert, glucose 4.5 mmol L-1
E : Nil of note

You decide to administer atropine 500mcg IV. The patient has not responded to this and his ECG deteriorates from the rhythm below to third degree heart block. What are your next steps?

A

Repeat doses of atropine up to a total of 3 mg. Where IV atropine at maximal doses has not been effective, depending on the availability of prompt expert help, transvenous pacing should be arranged without delay.

Where expert help and emergency transvenous pacing are not available without delay, interim measures (transcutaneous pacing or other drugs) can be considered whilst transvenous pacing is arranged.

113
Q

Diagnosis?

A

Third-degree (complete) atrioventricular block.

The heart rate is below 30 min-1. The QRS rhythm is regular. The QRS complex width is broad (greater than 0.12 s). Atrial activity is visible, there are normal P waves. However, atrial activity (P waves) and ventricular activity (QRS complexes) are unrelated.

114
Q

How is transcutaneous pacing carried out?

A

Arrange sedation where necessary.

Ensure the skin is dry and free from excess hair.

Apply monitoring leads and electrode pads.

Select an appropriate pacing rate.

Turn on the pacemaker.

Gradually increase the current (if the device requires this) while observing the patient.

Observe the ECG for a pacing spike until each spike is followed by a QRS complex (electrical capture).

Confirm whether electrical capture is associated with mechanical response by feeling for a pulse.

115
Q

In a patient with a bradycardia and adverse features, who does not response to atropine, transcutaneous pacing should be considered as an interim measure.

True or False?

A

True

In a patient with a bradycardia and adverse features, if there is no response to atropine or if atropine is unlikely to be effective, transcutaneous pacing should be considered as an interim measure unless immediate transvenous pacing is available.

116
Q

Name 3 drugs that can cause bradycardia.

A

Drug-induced bradycardia may be caused by several drugs, including beta blockers, diltiazem, digoxin, amiodarone and lithium.

117
Q

Analgesia and sedation should be considered where necessary during transcutaneous pacing

True or False?

A

True

Conscious patients usually experience considerable discomfort during transcutaneous pacing. They will often require intravenous analgesia and/or sedation if prolonged transcutaneous pacing is necessary.

118
Q

What is the difference between synchronised and unsynchronised cardioversion?

A

Synchronised cardioversion

  • Low energy shock
  • When the sync option is engaged on a defibrillator and the shock button pushes, there is a delay in the shock so the machine reads and synchronises with the patients rhythm to deliver electricity synchronised with the highest point of the R wave
  • Avoids delivery of a low energy shock during cardiac repolarisation (T wave) as this can precipitate ventricular fibrillation
  • Indications: AF, atrial flutter, supraventricular tachycardias

Unsynchronised cardioversion (defibrillation)

  • High energy shock
  • Delivered as soon as the shock button is pushed on a defibrillator so the shock may fall randomly anywhere within the cardiac cycle
  • Indications: when there is no coordinated intrinsic electrical activity in the heart (pulseless VT/VF) or the defibrillator fails to synchronise in an unstable patient
119
Q

Where do blood clots form in AF?

A

Left atrial appendage

120
Q

With what CHA2DS2-VASc score should anticoagulation be considered?

A

Consider in men if CHA2DS2-VASc score 1, taking bleeding risk into account (do not offer if 0)

Offer anticoagulation if CHA2DS2-VASc score 2 or above, taking bleeding risk into account (do not offer if score is 1 in females)

121
Q

Which antiocagulation drug is first line in AF?

A

apixaban

122
Q

What rhythm could a broad complex tachycardia be?

A

any regular BCT should be assumed to be ventricular in origin

123
Q

How would you carry out a valsava manouvre?

A

low hard against resistance e.g. into plastic syringe to maintain vagal tone

124
Q

How would you carry out a carotid sinus massage?

A

press for five seconds on carotid sinus on one side to increase vagal tone

125
Q

What is LBBB?

A

Normally the septum is activated from left to right, producing small Q waves in the lateral leads

In LBBB, the normal direction of septal depolarisation is reversed (becomes right to left), as the impulse spreads first to the right ventricle via the right bundle branch and then to the left ventricle via the septum

126
Q

What causes the changes seen on an ECG in LBBB?

A

Right to left depolarisation extends the QRS duration to >120ms and eliminates the normal septal Q waves in the lateral leads

The overall direction of depolarisation from right to left produces tall R waves in the lateral leads (I, aVL, v5, v6) deep S waves in the right precordial leads (V1-V3), and usually leads to left axis deviation

As the ventricles are activates sequentially (right then left) rather than simultaneously, this produces a broad or notched (M-shaped) R wave in the lateral leads

127
Q

diagnosis?

A

Broad QRS complex

Left axis deviation

Late R wave progression

V1 is negative, V6 is positive

WiLliaM – W in V1 (W in right sided leads) and M in V6 (M in lateral leads)

128
Q

What causes the changes seen on an ECG in RBBB?

A
  • Activation of the right ventricle is delayed as depolarisation has to spread across the septum from the left ventricle.
  • The left ventricle is activated normally, meaning that the early part of the QRS complex is unchanged
  • The delayed right ventricular activation produces a secondary R wave in the right precordial leads (V1-V3) and a wide slurred S wave in the lateral leads
  • Delayed activation of the right ventricle also gives rise to secondary repolarisation abnormalities with ST depression and T wave inversion in the right precordial leads
  • In isolated RBBB, the cardiac axis is unchanged, as left ventricular activation proceeds normally via the left bundle branch
129
Q

What is bifascicular block?

A

RBBB + left axis deviation (left anterior fascicle blocked)/right axis deviation (left posterior fascicle blocked)

130
Q

What is trifascicular block?

A

RBBB + left axis deviation (left anterior fascicle blocked)/right axis deviation (left posterior fascicle blocked) + prolonged PR interval (poor conduction at AV node)

131
Q
A

RBBB

132
Q
A

bifascicular block

133
Q
A

trifascicular block

134
Q

What is Wolf-Parkinson-White?

A

Combination of the presence of a congenital accessory pathway and episodes of tachyarrhythmia. The accessory pathway is known as the bundle of Kent which usually allows anterograde and retrograde conduction.

The accessory pathway conducts the impulse faster then the AV node leading to pre-excitation and a short P-R interval

On reaching the ventricles, the pre-excitation impulse is not conducted via the conducting system leading to slow ventricular activation. This creates the delta wave and t wave abnormalities

135
Q

If the rate is 300 or 150, what should be considered?

A

Atrial flutter 1:1 conduction – 300

Atrial flutter 2:1 conduction – 150

Atrial fibrillation

136
Q

What is the difference between AF with BBB and AF with aberrancy?

A

Aberrancy –

When the heart is slow (<100bpm, doesn’t have to always be this slow), QRS is narrow and there is no BBB

When the heart is fast (approx 300bpm), QRS is broad and there is functional BBB

Pre-existing BBB -

When the heart is slow (<100bpm), QRS is broad and there is BBB

When the heart is fast (approx 300bpm), QRS in broad and there is BBB