ECG and arrhythmia classification :
Narrow complex arrhythmias (arise above bifurcation of the bundle of His) – QRS duration <0.1s (2.5 small squares)
Broad complex arrhythmias (arise from ventricles or are conducted abnormally from a site above the ventricles so that a delay occurs (rarer). QRS duration is >0.1s (2.5 small squares).
Narrow complex arrhythmias
· Sinus arrhythmia
· Sinus tachycardia
· Sinus bradycardia
· Junctional tachycardia
· Atrial tachycardia, Atrial flutter
· Atrial fibrillation
· Atrial ectopics
Broad complex arrhythmias
· Ventricular ectopics
· Ventricular tachycardia
· Supraventricular tachycardia with BBB
· Ventricular fibrillation
NARROW COMPLEX ARRHYTHMIAS:
Sinus arrhythmia: Irregular spacing of normal complexes associated with respiration. The P-R interval is constant, but there are beat-to-beat changes in R-R interval. Normal, especially in young people.
- Because in inspiration, the negative pressure sucks more blood into the chest, which cardiac output. This is detected by baroreceptors which HR).
Sinus tachycardia: Rate over 100bpm. Normal P-QRS-T complexes are present.
· Heart failure
· Drugs – atropine, ether, ketamine, catecholamines
Management – correction of underlying disease.
· b-blockers if tachycardia causes myocardial ischemia in patient with IHD
Sinus bradycardia: Heart rate of <60bpm. May be normal in athletic people, or with increased vagal tone.
· Drugs - b-blockers, digoxin, anticholinesterase drugs, halothane
· Sick sinus syndrome (fibrosis of AV node)
· Raised intracranial pressure
Management: Often not necessary in a fit young person (unless rate is <45-50bpm) and/or there is haemodynamic compromise. You may consider:
· Correct underlying cause
Arrhythmias due to re-entry
· Where there is anatomical branching and re-joining of a conduction pathway.
· If one limb is slower than the other, the impulse may pass normally down one limb but be blocked in the other. Where the pathways rejoin, the impulse can then spread backwards up the abnormal pathway. If it arrives at a time when the first pathway is no longer refractory to activation, it can pass right around the circuit repeatedly, activating it and resulting in tachycardia
· Wolf-Parkinson-White syndrome (anatomical “accessory” pathway between the atria and ventricles) “Macro-reentry circuit” (Other macro re-entry circuits can exist in the atrial/ventricular myocardium and cause paroxysmal atrial flutter, AF, ventricular tachycardia).
· In Junctional tachycardia, there are “micro re-entry” circuits within the AV node itself
Junctional tachycardia: Micro re-entry circuits in or near the AV node (or, as in W-P-W, from an accessory conduction pathway between the atria and ventricles).
· Narrow complex tachycardia with rate of 150-200bpm
· SHORT P-R
· Slurred upstroke on the R wave (Delta wave in V4 in WPW)
· Inverted T waves in V2-5 are characteristic
Management: This arrhythmia may be associated with severe circulatory disturbance
· If they are haemodynamically compromised -cardioversion
· Carotid sinus massage (rarely converts to sinus rhythm, but slows the rate and will reveal the underlying rhythm if in doubt) (helps differentiate from atrial flutter/AF)
o The carotid sinus is a small dilatation of the proximal part of the internal carotid artery at the level of the superior border of the thyroid cartilage. It is vagally innervated and is involved in the control mechanism for causing a fall in HR and CO in response to rise in arterial pressure. Gentle pressure here may result in slowing of the heart and occasionally, termination of re-entry SVT. Never do on both sides or it can cause asystole and occlusion of the main arterial blood supply to the brain.
· Adenosine (slows AV conduction so is useful for terminating re-entry SVTs of the WPW type)
· Verapamil, b-blockers, amiodarone, flecainide may control the rate of convert to sinus rhythm
Atrial tachycardia and Atrial flutter: Due to an ectopic focus depolarising from anywhere within the atria. They contract faster than 150bmp and P waves can be seen superimposed on T waves of the preceding beats.
· AV node conducts at a maximum of 200bpm, so if the atrial rate is faster, AV block will occur (Typically see ventricular rate as 150bpm with atrial flutter)
· If the atrial rate is >250bpm, there is no flat baseline between P waves and you get “sawtooth” pattern
· Can occur with any type of block (2:1, 3:1, 4:1)
· Atrial tachycardia is typically a paroxysmal arrhythmia with intermittent tachycardia and palpitations (may be precipitated by many factors – stress, alcohol, caffeine)
o With 2:1 block = characteristic of digitalis toxicity
Management: Very sensitive to direct current cardioversion (almost 100% success rate), so should be used first line if there is haemodynamic compromise
· Carotid sinus massage and adenosine ® slow AV conduction and reveal underlying rhythm and block if there is doubt
· Other drug treatment as for AF
Atrial fibrillation: Very common. It is a chaotic and uncoordinated atrial depolarisation (absence of P waves), with an irregular baseline and completely irregular ventricular rate. The ventricular response rate will normally be rapid – about 120-200 bpm.
· Myocardial disease/pericardial disease
· Mitral valve disease
· Electrolyte disturbance (esp. Hypokalaemia or hypomagnesaemia)
· Thoracic surgery
Since contraction of the atria contributes 30% to ventricular filling, the onset of AF may result in significant ¯ in CO. Fast AF may precipitate cardiac failure, pulmonary oedema and myocardial ischaemia and systemic thromboembolism may occur if blood clots in the fibrillating atria form.
Management: Treatment is aimed at restoration of sinus rhythm if possible and if not, maintaining the rate to <100bpm and prevention of embolic complications. Management depends on how long it has been present.
· Correct precipitating factors where possible
· DC cardioversion (for recent onset)
· Digoxin – to slow ventricular rate
· Amiodarone – to restore sinus rhythm
· Verapamil – control ventricular rate
· b-blockers – sometimes used to control ventricular rate
· Aim to control ventricular rate to <100bpm – allows time for adequate ventricle filling and maintains CO
· b-blockers of verapamil
When AF has been present for more than a few hours, anticoagulation is necessary before cardioversion to prevent the risk of embolisation. (Usually warfarin for 3 weeks prior to elective DCC)
Atrial ectopic beats: An abnormal P wave is followed by a normal QRS. The P wave is not always easily visible
· “Ectopic” indicates that depolarisation originated in an abnormal place – get an abnormally shaped P wave
· If the focus depolarises EARLY, the beat produced is an extrasystole (premature) and may be followed by a compensatory pause
· If the underlying SA node is slow, sometimes an atrial focus takes over – escape beat as it occurs after a SMALL DELAY
· Any heart disease
· Ischaemia, hypoxia
· Light anaesthesia
· Anaesthetic drugs
Management: Correction of underlying cause and treatment is not necessary unless runs of atrial tachycardia occur.
BROAD COMPLEX ARRHYTHMIAS
Ventricular ectopic beats: Depolarisation spreads from a focus in the ventricles by an abnormal (\slow) pathway, so the QRS is wide and abnormal. (T wave is also abnormal in shape).
· Usually benign if there is no structural heart disease
· May be associated with abnormalities – Hypokalaemia, light anaesthesia (with halothane), raised CO2, intracranial pressure
The onset of runs of VT should be taken seriously where:
· There is a bigeminal rhythm (one ectopic beat with every normal beat)
· If they occur in runs of 2 or more (or more than 5/minute)
· Where they are multifocal (arising from different foci – hence having different shapes)
· Where the R wave is superimposed on the T wave
· Small dose of b-blocker
· If underlying sinus rhythm is slow, increase the rate with IV atropine (as ventricular ectopics could be a form of escape beat)
· Lignocaine is the drug of choice
· Alternatives – amiodarone
Ventricular tachycardia: A focus in the ventricular muscle depolarises at high frequency. Excitation spreads through the ventricles by an abnormal pathway. There are no P waves, wide QRS which may be slightly irregular/vary in shape.
Can be triggered by:
· Fluid overload
· Electrolyte imbalance (low K, Mg)
· Myocardial ischaemia
· Adrenaline injection
· Synchronised direct current cardioversion if the patient is haemodynamically unstable
· If they relapse back into VT – lignocaine, amiodarone can sustain sinus rhythm
· NOT verapamil
Supraventricular tachycardia with bundle branch block: Where there is abnormal conduction from the atria to the ventricles, a SVT may be broad complex if there is a BBB. Sometimes it can be due to ischaemia.
BUT – all tachycardias should be treated as VT if there is any doubt.
· RBBB : V1 looks more at the right side of the heart, so if the right ventricle is the last to depolarise due to a block, you see the last deflection in V6 will be negative (going away from the left of the heart) and the last deflection in V1 will be positive (going towards the right of the heart)
· LBBB (much more common): V6 looks at the left heart, so if the left ventricle is the last depolarising due to a block, you see last deflection in V6 will be positive and the last deflection in V1 will be negative (going away from the right of the heart)
Ventricular fibrillation: This results in cardiac arrest. There is chaotic and disorganised contraction of ventricular muscle and no QRS complexes can be identified on the ECG.
Management: Immediate DCC
DISTURBANCES OF CONDUCTION
First degree block: PR interval is >0.2s (delayed). Usually benign, but can progress to 2nd degree block.
Second degree block – Mobitz type I (Wendebach): Progressive lengthening of the PR interval and then failure of conduction of an atrial beat. This is followed by a conducted beat with a short PR interval. The cycle then repeats
· Common with inferior MI, tends to be self-limiting and doesn’t tend to require treatment
Secondary degree block – Mobitz type II: When excitation intermittently fails to pass through to the ventricles. Most beats are conducted normally, but occasionally, there is atrial contraction without a subsequent ventricular contraction
· Often progresses to complete heart block
Second degree block – 2:1 type: Where there is alternate conducted and non-conducted beats resulting in 2 P waves for every QRS. A 3:1 or 4:1 block may also exist.
· May herald complete heart block
Third degree (complete) heart block: Complete failure of conduction from the atria to the ventricles, so the ventricles are excited by an escape mechanism (slow) from a focus in the ventricles. There is no relationship between the P waves and the QRS complexes and the QRS complexes are abnormally shaped.
· May be transient due to vagal stimulation (responds to IV atropine)
· Acute inferior MI (due to AV nodal ischaemia)
· Anterior MI – indicates more extensive damage, including the His-Purkinje system
Bundle branch block: If the impulse from the SA and AV nodes reaches the IV septum normally, the PR interval will be normal, but if there is a subsequent delay in depolarisation of the L/R bundle branches, there will be a delay in depolarisation of part of the ventricular muscle and the QRS complex will be wide and abnormal
· RBBB – often found in normal, may indicate right heart problems
· LBBB – often indicates heart disease