ECGs + Arrhythmias Flashcards
When is ECG monitoring required?
- 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
When should you start and stop ECG monitoring in a cardiac arrest?
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.
A patient presents to A&E with syncope. Why is a 12-lead ECG indicated in this patient?
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.
A patient presents to A&E with syncope. You record a 12-lead ECG. In what circumstances is admission and cardiac monitoring NOT necessary?
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
A patient presents to A&E with syncope. You record a 12-lead ECG. In what circumstances is admission and cardiac monitoring necessary?
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).
What type of ECG would you request for a patient admitted to A&E with chest pain?
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.
When is ECG monitoring appropriate for a persistent arrhythmia?
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.
What are the 3 different types of ECG monitoring?
- 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.
If an arrhythmia has been detected by a 3-lead ECG monitor, what further investigation can give you more information about the arrhythmia?
record a 12-lead ECG during an arrhythmia that has been detected by simpler monitoring
Where are the pads/electrodes placed for a defibrillator and a 3-lead ECG monitor?
- 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
What does the p wave represent?
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.
What does the P-R interval represent?
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.
What does the QRS complex represent?
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.
What is the mechanical response of the heart to the electrical impulse represented by the p wave?
p wave - atrial depolarisation
mechanical response to this = atrial contraction
What is the mechanical response of the heart to the electrical impulse represented by the QRS complex?
QRS complex - ventricular depolarisation
mechanical response to this = ventricular contraction
What is meant by sinus rhythm?
Sinus rhythm
The atria and ventricles are contracting in sequence at the same rate (approximately 60 beats min-1 and myocardial activity is coordinated.
Describe the pathophysiology and management.
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.
Describe the pathophysiology and management.
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.
Describe the pathophysiology and management.
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.
How do you measure
1) PR interval
2) QRS duration
3) QT interval
- PR interval = beginning of p to beginning of q
- QRS duration = beginning of q to end of s
- QT interval = beginning of q to end of t
6-stage approach to interpreting ECG rhythm strips…
- Is there any electrical activity?
- What is the ventricular (QRS) rate?
- Is the QRS rhythm regular or irregular?
- Is the width of the QRS complex normal (narrow) or prolonged (broad)?
- Is atrial activity present?
- Is atrial activity linked to ventricular activity, if so, how?
How do you calculate ventricular rate from an ECG rhythm strip?
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
What is normal heart rate?
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
How do you work out if the QRS rhythm is regular or irregular? What should you do if it is irregular?
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?
What is the upper limit of normal for QRS duration?
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.
If the QRS duration is longer than 3 small squares, where is the rhythm originating?
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).
What do normal p waves look like in the different leads?
During sinus rhythm in a healthy person P waves are usually positive deflections in lead II and shallow, biphasic deflections in V1. For example:
When is it difficult to see atrial activity on an ECG even though it is present?
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.
Which leads are the best to look at when suspecting atrial flutter?
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).
What does it mean if there are variations in the PR interval?
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.
Ventricular fibrillation or Polymorphic VT (Torsades de pointes VT)?
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.
Ventricular fibrillation or Polymorphic VT (Torsades de pointes)
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.
What are the different types of ventricular tachycardia?
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.
Does VT always result in cardiac arrest?
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.
What is the difference between asystole and ventricular asystole?
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.
What should you do if you are not sure whether the defibrillator is showing very fine VF or asystole?
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.
What rhythm would you expect with PEA?
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
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?
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.
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?
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.
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?
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.
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?
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.
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?
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)
Which are the lateral leads?
I, aVL, V6
Which are the inferior leads?
II, III, aVF
Which are the anterior leads?
V2, V3, V4
Is a normal QRS complex in lead aVR a positive or negative deflection?
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.
Is a normal QRS complex in lead V1 a positive or negative deflection?
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.
There is t wave inversion in lead III. Does this mean there are inferior ischaemic changes?
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.
In which leads is t wave inversion a normal variant?
aVR, V1, III
A patient presents with chest pain. What does this ECG suggest?
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.
A patient presents with chest pain. What does this ECG suggest?
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.
A patient presents with chest pain. What does this ECG suggest?
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.
A patient presents with chest pain. What does this ECG suggest?
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.
A patient presents with chest pain. What does this ECG suggest?
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.