1. Module 3 ECG Rhythm Recognition

2. What to Look for on a rhythm strip
Are all the P waves alike?
Are all the QRS complexes alike?
Are all the P waves and QRS complexes related or occurring independently?
Is there a P wave in front of every QRS complex?
Is the PR interval constant or does it vary?
Is the PR interval too short (<0.12 s) or too long (>0.2 s)?
Is the QRS complex widened (>0.12 s)?

3. Normal Sinus Rhythm NSR is a rate of between 60-100bpm.
Each beat normally has one P wave, one corresponding QRS complex and T wave.
The R-R intervals should be regular and constant.
The P-R interval is within normal range.

4. Sinus Bradycardia R-R intervals constant and regular.
All waveforms are present, and there is 1 P-wave to each QRS complex.
The rate is <60bpm but not usually <40bpm.
Patients usually asymptomatic and no treatment is required.
Often caused by beta-blockers/calcium channel blockers.
May also be seen in athletes and occur during sleep.
Other causes of sinus bradycardia may include Ischeamic Heart Disease; hypothyroidism, hypothermia, sick sinus syndrome or raised intracranial pressure (e.g. following head injury).

5. Sinus Tachycardia R-R intervals constant and regular.
One P-wave per QRS complex.
All waveforms present.
Rate is >100bpm, but not usually >130bpm at rest.
Occurs normally in exercise/stress. Patient is usually asymptomatic.
Other causes may be hypovolaemia/underlying medical problems.
Underlying medical causes may include Ischeamic Heart Disease, anaemia, caffeine, hyperthyroidism, pulmonary embolus, bronchodilators such as Salbutamol / Atrovent.

6. Muscle Tremor
P P P P
All waveforms are present, but are difficult to define due to the wavering appearance on the isoelectric line.
Common causes of muscle tremor are patient shivering or anxiety.
It may be difficult to accurately assess an ECG where muscle tremor is present.

7. Electrical Interference
It may be difficult to make any assessment of an ECG where there is electrical interference; none of the waveforms are clearly defined.
Common causes of this phenomenon are any electrical appliances in close proximity to the ECG machine: i.e TV, electrical beds, infusion pumps etc.
Usually once all appliances are unplugged, a satisfactory quality ECG can be carried out.

8. Atrial extrasystoles (AE)
AE’s are a common form of supraventricular extrasystole.
Cause is atrial beat arising outside the sinus node.
Patients are generally asymptomatic and there is no treatment indicated.
A trial extrasystole falling on a critical time of atrial repolarisation may trigger atrial fibrillation (AF) in some vulnerable patients.

9. Atrial Fibrillation (AF)x
Atrial Fibrillation (AF) x x x x x
The atrial depolarisation is disorganised resulting in a chaotic ventricular rhythm.
The ventricular response rate may be normal/fast/slow.
This is a common arrhythmia, especially in the elderly; around 5-10% of whom experience AF.
Treatment is usually with oral drug therapy, although may be successfully electrically cardioverted in patients with persisting AF of recent onset.
The chaotic nature of Atrial Fibrillation leads to the loss of atrial contraction which may reduce cardiac output.
Atrial Fibrillation is associated with a very high risk of systemic embolism especially when it is prolonged, in the presence of other cardiac disease and in the elderly. Those at high risk require anticoagulation.
Causes of Atrial Fibrillation; Hypertension; IHD; hyperthyroidism; sick sinus syndrome; alcohol; rheumatic mitral valve disease; cardiomyopathy; atrial-septal defect; pericarditis, myocarditis, pulmonary embolism, pneumonia, cardiac surgery, idiopathic
DC cardioversion may be of use in those patients who have recent onset AF; although adequate anticoagulation should be achieved first.

10. Atrial Flutter x x x
A malfunction in the pattern of atrial depolarisation. A flutter usually gives atrial waves in the range of bpm.
The AV node usually blocks 1/2 of these impulses and gives a ventricular response rate of 150bpm.
Atrial flutter is usually regular in rhythm and displays a ‘saw-toothed’ appearance (especially V1) as above.
Very responsive to DC electrical cardioversion.
Carotid Sinus Massage (CSM) may slow the ventricular response but dose not influence the flutter wave. The causes are similar to Atrial Fibrillation.
It is responsive to DC cardioversion.

11. Supraventricular Tachycardia (SVT)x
SVT is a general term for tachycardias that originate above the ventricles.
Rate may be in the range of bpm
Commonly starts in early adult life and is normally inconvenient but benign.
Vagal manouevres should be used initially. Adenosine and/or cardioversion used in hospital.
The term 'supra-ventricular' simply means that the electrical impulse originates above the ventricles - i.e. in the atria.
SVT is often used as a 'blanket' term for any fast arrhythmia of atrial origin; and treatment is dictated by the underlying rhythm.

12. Paroxysmal Supraventricular Tachycardias
May be SVT, AF, Atrial flutter.
The term paroxysmal indicates that the arrhythmia is intermittent and self-terminating.
Atrial flutter carries a similar risk of thromboembolism as atrial fibrillation and may require anticoagulation.

13. Wolff-Parkinson-White Syndrome (WPW)
Normal pathway
Accessory pathway
Paroxysmal tachycardia
Delta wave PR
anterograde / retrograde conduction
WPW is a syndrome with a characteristic electrocardiogram - shortened PR interval (<0.12secs) and a slurred upstroke on the QRS complex (delta wave) together with a tendency to supraventricular arrhythmias.
It is caused by an accessory conduction pathway which bypasses the AV node.
WPW: this is a condition in which an accessory pathway (Bundle of Kent) is the dominant conduction system.
Conduction via the accessory pathway can produce a very rapid ventricular response rate - which can be life-threatening. Any drug which inhibits the conduction via the AV node can be dangerous and some drugs can increase the rate of conduction through the accessory pathway. If the patient is compromised, the treatment of choice is cardioversion. Recurrent episodes may be treated with drugs which slow the conduction through the accessory pathway (i.e. anti-arrythmics, betablockers) but if ineffective, radio-freqency ablation may be an option.

14. Junctional Rhythm (Nodal)x
High Mid Low
When the electrical pathway originates further down in the conduction system, but is still coming from or near the AV node, a ‘nodal’ (junctional) rhythm occurs.
If the pacemaker is high - an inverted P-wave may occur before the QRS complext.
If the pacemaker is within the node - the P-wave is usually absent.
If the conducting pathway is lower down, then the P-wave may have an inverted appearance and occur after the QRS and even resemble a S wave.
Junctional rhythms: If the impulse originates close to the AV Junction, there will be an inverted (retrograde) P wave - signifying that the conduction is travelling 'backwards'. The atria are still depolarised before the ventricles.
Any impulse originating within the AV junction, will hide the P-wave. The atrial contraction is still present, but the electrical manifestation may be visible as a notch on the QRS, or may be hidden altogether. The atria and ventricles depolarise simultaneously.
A P-wave occurring after the QRS on the ECG signifies an impulse originating lower down in the Bundle of His. In this case, the ventricles are depolarised before the atria.
Causes of Junctional Rhythms: most are idiopathic. Other causes include; Sick Sinus Syndrome Ischaemic AV node (e.g inferior MI); acutely post cardiac surgery; inflammatory processes such as rheumatic fever; medications such as beta-blockers, calcium channel blockers, anti-arrythmic therapies may also cause junctional rhythms.

15. First-degree Heart Block
P P
The measurement from the start of the P-wave to the start of the R-wave is prolonged to >5 sm squares (0.20secs).
The P-waves and R-waves remain constant and regular.
The heart rate is usually within normal parameters.
Patient is not compromised and no treatment indicated.
Caused by delay within the AV node.
1st AVB: This rhythm may be seen in healthy individuals (especially athletes) who have no symptoms and do not require any treatment as there is no progression to worsening heart block: However, if seen as part of bifasicular block, it may indicate a severe conduction defect for which further treatment is indicated.

16. Second-degree Heart Block Mobitz type I (Wenckebach)?
P P P P
The P-R interval becomes progressively elongated with each heart beat; eventually conduction fails completely.
The cycle then repeats itself once again.
May be seen in individuals with high vagal tone especial during sleep.
Where it occurs in complication of inferior MI, it does not usually require a pacemaker and often may be reversed with myocardial reperfusion.
2nd degree AVB - Mobitz Type I (Wenckebach) results from alteration to conduction through the AV node and can occur in periods of high vagal activity (sleep).
In the case of INFERIOR MI, this rhythm only requires pacing if the patient is symptomatic, and fails to respond to atropine. It may be reversed with reperfusion therapy.

17. Second-degree Heart Block Mobitz type II?
Most P-waves conducted as normal - followed by QRS.
The P-R interval is normal and usually constant.
Occasionally, the atrial conduction is not followed by a QRS complex.
Thought to be caused by an abnormality in the bundle of His.
Considered more serious than type I block in that it can progress to complete heart block without warning.
2nd AVB - Mobitz Type II usually results from abnormal conduction below the AV node. It can proceed to Complete Heart Block without warning, and thus is more serious than Mobitz I. This rhythm will require pacing.

18. ? ? ? 2:1 Heart Block Every alternate P-wave is not conducted.
Cannot be classified as either Mobitz Type I or Mobitz Type II.
Use of a pacemaker may be considered.
2:1 Heart Block- Another form of 2nd AVB, in this case there are non-conducted P-waves every alternate beat. The conducted P-waves have a normal P-R interval. Once again, considered to be a higher risk form of heart block, pacemaker insertion depends upon symptoms / haemodynamic stability.

19. Third-degree Heart Block (complete heart block)x x
P P P P P P
The P-P and R-R intervals are each usually regular but have no relation to each other.
This dissociation is due to a block at the AV junction.
The block may be at the AV nodal level when the QRS is usually narrow. This may be congenital, but can occur commonly as a complication to an inferior infarction. Pacing is not always required. It may occur at the level of the bundle branches when any QRS complexes will be wide and the rate very slow.

20. Ventricular (Unifocal) Extrasystole
Occasional extrasystoles are common in healthy adults.
3 or more in a row may be described as VT, but shorter runs are usually called salvoes.
The morphology of each ectopic is unchanged if depolarisation originates from a single focus.

21. Coupled Ventricular Extrasystole
This is the term used when every alternate beat is an extrasystole.
Treated only in exceptional circumstances.
Coupled extrasystole may cause bigeminy: the condition in which alternate ectopic beats of the heart are transmitted to the pulse and felt as a double pulse beat followed by a pause.

22. Couplets x
A couplet is where there are 2 ventricular ectopics in a row.
Not usually treated except in circumstances that make the patient vulnerable to more serious arrhythmias

23. R on T Extrasystole x
When the ventricular extrasystole falls on the T-wave. This may trigger serious ventricular arrhythmias.

24. Ventricular (Multifocal) Extrasystole
Where the origin of the ectopic beat originates from differing foci within the ventricle.
This may signify a high degree of ventricular excitability.
Although extrasystoles may occasionally precipitate more malignant arrhythmias, any decision on treatment should be made only after considering the risk of anti-arrhythmic drugs.

25. Paced Beats x
Pacing wire
A ventricular paced beat will display a broadened QRS complex.
The slim, deflection immediately preceding the R-wave denotes the pacing spike (arrowed above).

26. Idioventricular Rhythmx
Often seen with reperfusion following acute MI, idioventricular rhythm can be regarded as ‘slow VT’.
The QRS is broad and bizarre, but uniform and regular.
The rate is less than 100bpm.
Usually no treatment is indicated.

27. Torsades de Pointes
From the French ‘twisting of points’. This describes a form of VT where the cardiac axis twists round the isoelectric line.
The rhythm may be intermittent and self-terminating. If it lasts more than a few seconds the patient will become symptomatic.
Common causes are electrical imbalance - i.e K+ and/or Mg++ depletion or prolonged Q-T interval frequently caused by drugs such as Sotalol/Amiodarone or tricyclic antidepressants.

28. Ventricular Tachycardia (VT)x
The origin of the heartbeat is in the ventricles, producing a QRS complex >0.12secs.
3 ventricular beats in succession may be called VT (or salvoes).
VT can range in rate from bpm and the patient may be conscious and asymptomatic, symptomatic, or unconscious. Treatment will depend principally on the patients’ clinical status.
VT has many causes including: acute MI, Ischeamic Heart Disease, hypertrophic cardiomyopathy, dilated cardiomyopathy, mitral valve prolapse, myocarditis, electrolyte imbalance, anti-arrhythmic drugs, idiopathic or congenital causes.
Symptoms vary between nil, to mild dizziness & palpitations to full loss of consciousness.
Treatment, according to patients’ clinical presentation, varies from medical cardioversion with anti-arrhythmic drugs to overdrive pacing to DC cardioversion where the patient is compromised.
Long term prophylaxis may require the insertion of a implantable cardiac defibrillator (ICD).

29. Ventricular Fibrillation (VF)x
Ventricular Fibrillation (VF) x x x x x x x x x
The ventricles are ‘quivering’, leading to a complete loss of cardiac output.
Bizarre complexes are characteristic, but are variable amplitude (course / fine VF).
The most common arrhythmia causing cardiac arrest, but becomes finer as minutes pass and soon becomes indistinguishable with asystole.
Patient will require immediate defibrillation (10% reduction in success rate as each minute passes).
Most common cause of death in early acute MI.
VF when untreated causes fatality very quickly. Most commonly seen in the acute phase of MI - (half of these occur in the first hour). Requires defibrillation as soon as possible, as for each minute lost, the rate of survival decreases by 10%.

30. Ventricular Standstill
No ventricular response to atrial depolarisation.
There is no cardiac output and the patient is in cardiac arrest.
Pacing is required. It is usually effective if atrial activity is present.

31. Pulseless Electrical Activity (PEA)
PEA describes a condition where QRS complexes continue but no cardiac output can be detected.
8 treatable causes: ‘4 Ts’ Tamponade ‘4 Hs’ Haemothorax Toxicity Hypovolaemia Tension pneumothorax Hypo/hyperkalaemia Thrombo-embolic Hypothermia
No cardiac output, although the rhythm displayed may be that of a non
life threatening nature.
Treatment is life support as per non-VT/VF protocol until a cause is established.
PEA - Prognosis is poor unless a treatable cause can be found and treated quickly. The electrical rhythm may display any rhythm which would normally be associated with a cardiac output; but the patient is in cardiac arrest.

32. Asystole Implies the absence of ventricular activity.
No QRS complexes are present.
Patient is in a state of full cardiac arrest.
In asystole - always check patient, check leads, check monitoring mode (? Paddles), increase the monitoring gain to rule out fine VF.
Asystole - The prognosis for resuscitation/recovery is poor unless a treatable cause can be found. It is important to check first that all leads and monitoring equipment are as they should be; then consider the possibility that this may be ‘fine VF’. When convinced that the rhythm is indeed Asystole, then a DC shock should be administered.