cardiac arrhythmia

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.
A detailed description of the sensation is essential and patients should be asked to describe their symptoms clearly, or to demonstrate the sensation of rhythm by tapping with their hand. A provisional diagnosis can usually be made on the basis of a thorough history. 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.
Palpitation is usually benign and, even if the patient’s symptoms are due to an arrhythmia, the outlook is good if there is no underlying structural heart disease. Most cases are due to an awareness of the normal heart beat, a sinus tachycardia or benign extrasystoles, in which case an explanation and reassurance may be all that is required. Palpitation associated with presyncope or syncope may reflect more serious structural or electrical disease and should be investigated without delay.

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 syncopy:


Cardiac syncope is usually sudden but can be associated with premonitory lightheadedness, palpitation 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.
The basis of an ECG recording is that the electrical depolarisation of myocardial tissue produces a small dipole current which can be detected by electrode pairs on the body surface. These signals are amplified and either printed or displayed on a monitor.

Fig: ECG wave

During sinus rhythm, the SA node triggers atrial depolarisation, producing a P wave. Depolarisation proceeds slowly through the AV node, which is too small to produce a depolarisation wave detectable from the body surface. The bundle of His, bundle branches and Purkinje system are then activated, initiating ventricular myocardial depolarisation, which produces the QRS complex.
The muscle mass of the ventricles is much larger than that of the atria, so the QRS complex is larger than the P wave. The interval between the onset of the P wave and the onset of the QRS complex is termed the ‘PR interval’ and largely reflects the duration of AV nodal conduction.
Repolarisation is slower and spreads from the epicardium to the endocardium. Atrial repolarisation does not cause a detectable signal but ventricular repolarisation produces the T wave. The QT interval represents the total duration of ventricular depolarisation and repolarisation.
The standard 12–lead ECG:
The 12-lead ECG is generated from ten physical electrodes that are attached to the skin. One electrode is attached to each limb and six electrodes are attached to the chest.
The twelve ‘leads’ of the ECG refer to recordings made from pairs or sets of these electrodes. They comprise three groups: three dipole limb leads (leads I, II and III), three augmented voltage limb leads (leads aVR, aVL and aVF) and six unipole chest leads (leads V1-V6).

Fig: normal ECG

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.