DISORDERS OF HEART RATE, RHYTHM AND CONDUCTION

Cardiac Lectures Dr. Ahmed Moyed Hussein

DISORDERS OF HEART RATE, RHYTHM AND CONDUCTION

The heart beat is normally initiated by an electrical discharge from the sinoatrial (sinus) node. The atria and ventricles then depolarize sequentially as electrical depolarization passes through specialized conducting tissues.

Fig: conductive system of the heart

The sinus node acts as a pacemaker and its intrinsic rate is regulated by the autonomic nervous system; vagal activity decreases the heart rate, and sympathetic activity increases it via cardiac sympathetic nerves and circulating catecholamines. If the sinus rate becomes unduly slow, another, more distal part of the conducting system may assume the role of pacemaker. This is known as an escape rhythm and may arise in the atrioventricular (AV) node or His bundle (junctional rhythm) or the ventricles (idioventricular rhythm).
A cardiac arrhythmia is a disturbance of the electrical rhythm of the heart. Arrhythmias are often a manifestation of structural heart disease but may also occur because of abnormal conduction or depolarization in an otherwise healthy heart. A heart rate of more than 100/min is called a tachycardia, and a heart rate of less than 60/min is called a bradycardia.
There are three main mechanisms of tachycardia:
• Increased automaticity: The tachycardia is produced by repeated spontaneous depolarisation of an ectopic focus, often in response to catecholamines.
• Re-entry: The tachycardia is initiated by an ectopic beat and sustained by a re-entry circuit, most tachyarrhythmias are due to re-entry.

Fig: The mechanism of re-entry. Re-entry can occur when there are two alternative pathways with different conducting properties (e.g. the AV node and an accessory pathway, or an area of normal and an area of ischaemic tissue). Here, pathway A conducts slowly and recovers quickly, while pathway B conducts rapidly and recovers slowly.
(1) In sinus rhythm, each impulse passes down both pathways before entering a common distal pathway.
(2) As the pathways recover at different rates, a premature impulse may find pathway A open and B closed.
(3) Pathway B may recover while the premature impulse is travelling selectively down pathway A. The impulse can then travel retrogradely up pathway B, setting up a closed loop or re-entry circuit.
(4) This may initiate a tachycardia that continues until the circuit is interrupted by a change in conduction rates or electrical depolarisation.

• Triggered activity: This can cause ventricular arrhythmias in patients with coronary artery disease. It is a form of secondary depolarization arising from an incompletely repolarised cell membrane.


Bradycardia may be due to:
• Reduced automaticity, e.g. sinus bradycardia.
• Blocked or abnormally slow conduction, e.g. AV block.
An arrhythmia may be ‘supraventricular’ (sinus, atrial or junctional) or ventricular in origin. Supraventricular rhythms usually produce narrow QRS complexes because the ventricles are depolarised in their normal sequence via the AV node and bundle of His. In contrast, ventricular rhythms produce broad, bizarre QRS complexes because the ventricles are activated in an abnormal sequence.

Symptoms of cardiac arrhythmias:

Bradycardias cause symptoms that reflect low cardiac output: fatigue, lightheadedness and syncope. Tachycardias cause rapid palpitation, dizziness, chest discomfort or breathlessness. Extreme tachycardias can cause syncope because the heart is unable to contract or relax properly at extreme rates. Extreme bradycardias or tachycardias can precipitate sudden death or cardiac arrest.

Palpitation: Palpitation is a very common and sometimes frightening symptom. Patients use the term to describe many sensations, including an unusually erratic, fast, slow or forceful heart beat, or even chest pain or breathlessness.
Initial evaluation should concentrate on determining its likely mechanism, and whether or not there is significant underlying heart disease. The diagnosis should be confirmed by an ECG recording during an episode using an ambulatory ECG monitor or a patient-activated ECG recorder.
Recurrent but short-lived bouts of an irregular heart beat are usually due to atrial or ventricular extrasystoles (ectopic beats). Some patients will describe the experience as a ‘flip’ or a ‘jolt’ in the chest, while others report dropped or missed beats.

Syncope and presyncope:

The term ‘syncope’ refers to sudden loss of consciousness due to reduced cerebral perfusion. ‘Presyncope’ refers to lightheadedness in which the individual thinks he or she may black out. Syncope affects around 20% of the population at some time and accounts for more than 5% of hospital admissions.
There are three principal mechanisms that underlie recurrent presyncope or syncope:
• cardiac syncope due to mechanical cardiac dysfunction or arrhythmia
• neurocardiogenic syncope, in which an abnormal autonomic reflex causes bradycardia and/or hypotension
• postural hypotension, in which physiological peripheral vasoconstriction on standing is impaired, lead to hypotension.
Loss of consciousness can also be caused by non-cardiac pathology, such as epilepsy, cerebrovascular ischaemia or hypoglycaemia.

Differential diagnosis of syncope:

Cardiac syncope is usually sudden but can be associated with premonitory lightheadedness, pal pitation or chest discomfort. The blackout is usually brief and recovery rapid.

Investigations for cardiac arrhythmias:

Electrocardiogram (ECG):
The electrocardiogram (ECG) is used to assess cardiac rhythm and conduction.

Ambulatory ECG:

Continuous (ambulatory) ECG recordings can be obtained using a portable digital recorder. These devices usually provide limb lead ECG recordings only, and can record for between 1 and 7 days. Ambulatory ECG recording is principally used in the investigation of patients with suspected arrhythmia, such as those with intermittent palpitation, dizziness or syncope. For these patients, a 12-lead ECG provides only a snapshot of the cardiac rhythm and is unlikely to detect an intermittent arrhythmia, so a longer period of recording is useful.
For patients with more infrequent symptoms, small, patient-activated ECG recorders (implantable loop recorder) are resemble a leadless pacemaker and are implanted subcutaneously. They have a lifespan of 1–3 years and are used to investigate patients with infrequent but potentially serious symptoms, such as syncope.

Electrophysiology study:

Patients with known or suspected arrhythmia are investigated by percutaneous placement of electrode catheters into the heart via the femoral and neck veins. Electrophysiology study (EPS) is most commonly performed to evaluate patients for catheter ablation, normally done during the same procedure. It is occasionally used for risk stratification of patients suspected of being at risk of ventricular arrhythmias.

Management of arrhythmia:

Anti-arrhythmic drug therapy
Classification:
Anti-arrhythmic drugs may be classified according to their mode or site of action into (The Vaughan-Williams classification):

Fig: classification of antiarrhythmic drugs according to their site of action.

Class I drugs:
Class I drugs act principally by suppressing excitability and slowing conduction in atrial or ventricular muscle. They block sodium channels, of which there are several types in cardiac tissue. These drugs should generally be avoided in patients with heart failure because they depress myocardial function.
Class Ia drugs: These prolong cardiac action potential duration and increase the tissue refractory period. They are used to prevent both atrial and ventricular arrhythmias.
Disopyramide. An effective drug but causes anticholinergic side-effects, such as urinary retention, and can precipitate glaucoma. It can depress myocardial function and should be avoided in cardiac failure.
Quinidine. Now rarely used, as it increases mortality and causes gastrointestinal upset.
Class Ib drugs:
These shorten the action potential and tissue refractory period. They act on channels found predominantly in ventricular myocardium and so are used to treat or prevent ventricular tachycardia and ventricular fibrillation.
Lidocaine. Must be given intravenously and has a very short plasma half-life, main side effects are: myocardial depression, confusion and convulsion.
Mexiletine. Can be given intravenously or orally, but has many side-effects.
Class Ic drugs: They are used mainly for prophylaxis of atrial fibrillation but are effective in prophylaxis and treatment of supraventricular or ventricular arrhythmias. They are useful for WPW syndrome because they block conduction in accessory pathways.
Flecainid: Effective for prevention of atrial fibrillation, and an intravenous infusion may be used for pharmacological cardioversion of atrial fibrillation. It should be prescribed along with an AV node-blocking drug, such as a β-blocker, to prevent pro-arrhythmia.
Propafenone.
Class II drugs:
This group comprises the β-adrenoceptor antagonists (β-blockers). These agents reduce the rate of SA node depolarisation and cause relative block in the AV node, making them useful for rate control in atrial flutter and atrial fibrillation. They reduce myocardial excitability and the risk of arrhythmic death in patients with coronary artery disease and heart failure.


Class III drugs:
Class III drugs act by prolonging the plateau phase of the action potential, thus lengthening the refractory period. These drugs are very effective at preventing atrial and ventricular tachyarrhythmias. They cause QT interval prolongation and can predispose to torsades de pointes and ventricular tachycardia, especially in patients with other predisposing risk factors.
Amiodarone: It is probably the most effective drug currently available for controlling paroxysmal atrial fibrillation. It is also used to prevent episodes of recurrent ventricular tachycardia, particularly in patients with poor left ventricular function or those with implantable defibrillators. Amiodarone has a very long tissue half-life (25–110 days). An intravenous or oral loading regime is often used to achieve therapeutic tissue concentrations rapidly. The drug’s effects may last for weeks or months after treatment has been stopped. Side-effects are common (up to one-third of patients) including: photosensitivity, skin discoloration, corneal deposits, thyroid dysfunction, alveolitis, nausea and vomiting, hepatotoxicity, peripheral neuropathy, torsades de pointes, potentiate digoxin and warfarin effect.

Class IV drugs:

These block the ‘slow calcium channel’, which is important for impulse generation and conduction in atrial and nodal tissue, although it is also present in ventricular muscle. Their main indications are prevention of supraventricular tachycardia (by blocking the AV node) and rate control in patients with atrial fibrillation.
Verapamil: The most widely used drug in this class. Intravenous verapamil may cause profound bradycardia or hypotension, and should not be used in conjunction with β-blockers.
Diltiazem: Has similar properties.

Other anti-arrhythmic drugs

Atropine sulphate (0.6 mg IV, repeated if necessary to a maximum of 3 mg): Increases the sinus rate and SA and AV conduction, and is the treatment of choice for severe bradycardia or hypotension due to vagal overactivity.
Repeat dosing may be necessary because the drug disappears rapidly from the circulation after parenteral administration. Side-effects: dry mouth, thirst, blurred vision, atrial and ventricular extrasystole.

Adenosine: It produces transient AV block lasting a few seconds. It is used to terminate supraventricular tachycardias when the AV node is part of the re-entry circuit, or to help establish the diagnosis in difficult arrhythmias, such as atrial flutter with 2 : 1 AV block. Adenosine is given as an intravenous bolus, initially 3 mg over 2 seconds. If there is no response after 1–2 minutes, 6 mg should be given; if necessary, after another 1–2 minutes, the maximum dose of 12 mg may be given. Patients should be warned to expect short-lived and sometimes distressing flushing, breathlessness and chest pain. Adenosine can cause bronchospasm and should be avoided in asthmatics.

Digoxin: It slows conduction and prolongs the refractory period in the AV node, this effect helps to control the ventricular rate in atrial fibrillation and may interrupt supraventricular tachycardias involving the AV node. Digoxin is largely excreted by the kidneys, and the maintenance dose should be reduced in children, older people and those with renal impairment. It is widely distributed and has a long tissue half-life (36 hours), so that effects may persist for several days. Measurement of plasma digoxin concentration helps identify digoxin toxicity or under-treatment.

Therapeutic procedures:

External defibrillation and cardioversion:
The heart can be completely depolarised by passing a sufficiently large electrical current through it from an external source. This will interrupt any arrhythmia and produce a brief period of asystole that is usually followed by the resumption of sinus rhythm. Defibrillators deliver a direct current, high-energy, short-duration shock via two large electrodes or paddles coated with conducting jelly or a gel pad, positioned over the upper right sternal edge and the apex. Modern units deliver a biphasic shock, during which the shock polarity is reversed mid-shock This reduces the total shock energy required to depolarize the heart.
Electrical cardioversion:
This is the termination of an organised rhythm, such as atrial fibrillation or ventricular tachycardia, with a synchronized shock, usually under general anaesthesia. The shock is delivered immediately after detection of the R wave ( synchronized shock) because, if it is applied during ventricular repolarization (on the T wave), it may provoke ventricular fibrillation. High-energy shocks may cause chest wall pain post-procedure, so, if there is no urgency, it is appropriate to begin with a lower-amplitude shock (e.g. 50 joules), going on to larger shocks if necessary.
Defibrillation:
This is the delivery of an unsynchronized shock during a cardiac arrest caused by ventricular fibrillation. The precise timing of the discharge is not important in this situation. In ventricular fibrillation and other emergencies, the energy of the first and second shocks should be 150 joules and thereafter up to 200 joules; there is no need for an anaesthetic, as the patient is unconscious.

Catheter ablation:
Catheter ablation therapy is the treatment of choice for patients with supraventricular tachycardia or atrial flutter, and is a useful treatment for some patients with atrial fibrillation or ventricular arrhythmias.
A series of catheter electrodes are inserted into the heart via the venous system and are used to record the activation sequence of the heart in sinus rhythm, during tachycardia and after pacing manoeuvres. Once the arrhythmia focus or circuit is identified (e.g. an accessory pathway in WPW syndrome), a catheter is used to ablate the culprit tissue. For many arrhythmias, radiofrequency ablation is very attractive because it offers the prospect of a lifetime cure, thereby eliminating the need for long-term drug therapy.


Implantable cardiac defibrillators (ICD):
ICDs treat ventricular tachyarrhythmias using overdrive pacing, cardioversion or defibrillation. They are implanted in a similar manner to pacemakers. It is indicated in patients with previous attacks or at risk of ventricular arrhythmias.