and Alwyn Scott2
School of Computer Science, University of Manchester, Manchester, UK
Cardiology High Dependency Unit, Papworth Hospital NHS Foundation Trust, Cambridge, UK
The word arrhythmia derives from the Greek to mean loss or absence of rhythm. Essentially an arrhythmia is an irregular heartbeat and includes tachyarrhythmias and bradyarrhythmias. Abnormal electrical impulse conduction causes arrhythmias. There are several mechanisms of arrhythmia genesis, including; triggered activity, abnormal/enhanced automaticity, reentry and conduction delays. These mechanisms are discussed in more detail below with the exception of conduction delays, which are discussed in detail in Chap. 5. As many arrhythmias are caused by or sustained by ectopic foci it is necessary to gain an understanding of ectopy.
The term premature beat more accurately describes ectopic beats. Premature beats can originate from the atrial, junctional or ventricular regions of the heart. The most salient feature of a premature beat is a beat that occurs earlier than expected in the cardiac cycle and has a different morphology to the normal underlying rhythm (Fig. 6.1). The morphological changes are the key way of identifying the origin of a premature beat. The main differences between the different types of premature beat are summarised in Table 6.1.
A ventricular premature beat
The primary features of premature beats
Atrial premature beat (APB)
Junctional premature beat (JPB)
Ventricular premature beat (VPB)
A beat occurring earlier than expected with a P wave morphology differing from patients normal P wave
A beat occurring earlier than expected with no visible P wave. Alternatively the P wave may appear inverted and may occur before or after the QRS complex.
A beat occurring earlier than expected with a wide bizarre QRS complex. The T wave is usually in the opposite direction to the terminal portion of the QRS complex.
Premature Beat Origin
There are three primary mechanisms that are considered to be the cause of premature beats, they consist of:
Changes in the cellular threshold level increasing diastolic depolarization leading to premature beat formation
Damage to the myocardium can result in oscillation of the transmembrane potential. Leakage of positive ions into the cell creates after depolarizations leading to premature beats. Arrhythmias seen in Digoxin toxicity and long QT syndromes are thought to be caused by triggered activity
Reentry circuits/circus movement
Discussed in more detail later in the chapter
Compensatory and Non-compensatory Pauses
Compensatory pauses are temporary interruptions of sinus rhythm by a ‘gap’ or ‘pause’ with a duration that is a multiple of the normal cardiac cycle. To measure a compensatory pause, take three consecutive PQRST complexes from an otherwise regular rhythm. Measure the distance between the start of the first P wave of the first beat to the start of the P wave of the third beat. Next measure the same distance starting with the start of the P wave from the normal beat before the premature beat and ending with the start of the P wave of the normal beat following the premature beat. If this distance is the same as the previous one, the pause is a complete compensatory pause. If the start of the P wave on the third beat occurs earlier, the pause is termed an incomplete or non-compensatory pause. Ventricular premature beats are often followed by a complete compensatory pause. This is because atrial depolarization usually occurs as normal. An exception to this are interpolated premature beats, which are ventricular premature beats that occur exactly between two normal sinus beats and don’t have any compensatory pause. Atrial premature beats however usually produce incomplete compensatory pauses.
The majority of ventricular premature beats are benign and require no treatment. Patients can be advised to limit alcohol, tobacco and caffeine intake, occasionally beta blockers may be used. There are however some patterns of ventricular premature beat that can lead to more serious arrhythmias, such as VT and VF. These patterns include two or more ventricular premature beats occurring together (Table 6.2).
Pathological patterns of ventricular premature beat
2 ventricular premature beats occurring together
3 ventricular premature beats occurring together
4 ventricular premature beats occurring together
Most ventricular premature beats are unifocal, occurring from the same place and sharing the same morphology. Sometimes ventricular premature beats can be multifocal and originate from different areas in the ventricle. The presence of multifocal VPBs can indicate serious heart disease. Multifocal VPBs can be identified in the same way as ventricular premature beats with the exception that they differ in morphology from one another (Fig. 6.2).
Multifocal/multiform ventricular premature beats
Bigeminy and Trigeminy
A regular repeating pattern of premature beats. Bigeminy can be identified by a repeating pattern of normal beat followed by premature beat. Trigeminy is identified by a repeating pattern of premature beat following every two intrinsic beats. Ventricular bigeminy/trigeminy is another pattern of ventricular premature beat that can predispose individuals to dangerous arrhythmias, such as VT/VF. An example of ventricular bigeminy/trigemniny and atrial bigeminy can be seen in Figs. 6.3 and 6.4.
(Top) Ventricular bigeminy, (bottom) ventricular trigeminy
Or SVT is a tachycardia that originates from above the ventricles (Fig. 6.5). Therefore SVT is a blanket term for many different forms of tachycardia (Table 6.3). The term SVT is often used when the specific rhythm can not be identified. SVTs usually manifest with rapid narrow QRS complexes, with the caveat of aberrancy, which is discussed later in the chapter.
Types of SVT
Multifocal atrial tachycardia
AV node reentry tachycardia (AVNRT)
AV reciprocating tachycardia (AVRT)
ST depression and T wave inversion (signs of ischemia) are often associated with SVT. The rate is usually between 100 and 250 BPM. As the electrical impulse travels through the AV node, drugs such as Adenosine can be used to initiate a transient AV block. This can reveal the underlying rhythm making a diagnosis possible. Alternatively the rhythm may be terminated completely if it caused by a reentry pathway that utilizes the AV node. Another option often used to terminate or reveal an underlying rhythm is the use of vagal maneuvers. Some of these maneuvers can even be taught to patients to help them deal with future episodes of SVT.
The human autonomic nervous system encompasses the sympathetic and parasympathetic divisions. The autonomic nervous system regulates organs and glands at a subconscious level. Stimulating vagal efferent discharge has the effect of inducing transient AV nodal block. This in turn has the effect of terminating tachycardias that subsist on AV conduction, such as AVNRT and AVRT. Other SVTs may be more easily diagnosed by stimulation of the vagus nerve. The vagus nerve can be stimulated by using vagal manoeuvres. Table 6.4 lists some of these vagal manoeuvres.
Forced expiration against a closed glottis. This can be done by closing the patients mouth and getting them to pinch their nose. The patient then exhales as if blowing up a balloon. Alternatively a 10 ml syringe may be used. Ask the patient to blow into the tip of the syringe and try to move the plunger.
Forced inspiration against a closed glottis. Essentially the opposite of the valsalva manoeuvre.
Often used with children. An ice cold bag is applied to the face. This reduces the risk of aspiration associated with submerging the face in ice cold water.
Carotid sinus massage
Rotational pressure is applied to the right carotid artery for between 5 and 10 s. Patients should be monitored (including ECG and BP) during procedure. Doctors will often listen for a carotid bruit with a stethoscope as this is a good indicator of carotid arterial stenosis.
Carotid sinus massage is contraindicated in patients with:
History of TIA or stroke in last 3 months
Occlusion of carotid artery
History of VT or VF
Previous adverse reaction to sinus massage
Contraindicated due to the risk of retinal detachment.
Not technically a manoeuvre but can be used to stimulate the vagal nerve. Encourage the patent to cough hard.
The single most commonly encountered arrhythmia increases the annual risk of stroke by around 4–5 %. The incidence of Atrial fibrillation (AF) increases with age. AF is also often seen in patients following cardiac surgery.
AF is characterised on the ECG by an irregularly irregular rhythm (Fig. 6.6) best seen in the rhythm strip of an ECG. There is no pattern to the irregularity and a chaotic baseline consisting of fibrillatory waves, termed ‘f’ waves is usually observed. The other salient feature of AF is the complete absence of P waves, best seen in leads II and V1. AF is caused by the presence of multiple ectopic foci in the atria, usually located near the pulmonary veins. These foci act as triggers increasing the atrial rate. The AV node however prevents the majority of impulses being conducted to the ventricles. If this was not the case the outcome would be catastrophic. AF with a ventricular rate <100 BPM is termed ‘controlled AF’, whereas >100 BPM is referred to as ‘uncontrolled’ or ‘fast’ AF. Fibrillation of the atria reduces cardiac output by more than 20 % via loss of ‘atrial kick’. The atrial kick is the contribution made by the atria prior to ventricular systole. It has the effect of boosting the efficiency of ventricular ejection.
AF is often detected through manual pulse palpation. When GPs record manual pulses during routine visits leading to the detection of AF, there is a reduction in the incidence of stroke. Unfortunately due the use of technology manual pulse palpation is not being carried out as frequently as it once was. Most machines used to take patients observations do however display the patients pulse. If the pulse is ‘jumping around’ on the machine in an irregular manner then manual palpation should be carried out. If the pulse appears to be irregular a 12-lead ECG should be carried out.
If the arrhythmia persists, initial electrical remodelling of the atria is subsequently followed by structural remodelling, which in turn helps to maintain the arrhythmia. Atrial remodelling refers to any persisting change in the structure or function of the atria. Atrial remodeling makes it more likely that ectopic or reentry activity will occur. Structural changes induced by AF occur at a cellular level and include many factors, such as: an increase in myocyte cell size, myolysis, changes to the shape of mitochondria, changes to structural proteins and fragmentation of the sarcoplasmic reticulum. Both electrical and structural remodelling maintain the arrhythmia, the longer a patient has AF, the more likely these changes are to occur.
Atrial fibrillation can be further classified as:
Paroxysmal Atrial Fibrillation
Terminates spontaneously, usually in less than 7 days
Persistent Atrial Fibrillation
Does not terminate spontaneously and lasts longer than 7 days
Permanent Atrial Fibrillation
Not terminated or reverted.
Patients presenting with AF who have been in fibrillation for longer than 48 h require anticoagulation prior to direct current cardioversion (DCCV). This is due to the possibility that intramural thrombus may accumulate in the atria, often around the left atrial appendage. When the normal motion of the atrium is recommenced, there is a risk that the thrombus may migrate causing a stroke. To mitigate against this anticoagulation is given for weeks before and after the cardioversion. If this is not possible due to hemodynamic compromise requiring immediate treatment, IV heparin can be administered prior to the cardioversion.
Patients with a prior history of AF suffering a new incidence of AF for less than 48 h can suffer from remodelling of the atria caused by the previous episodes of AF. In this case there may be an increased risk involved in DCCV. To be sure that there are no intramural thrombi present the patient may have a transoesophageal echocardiogram (TOE). This involves passing an ultrasound sensor into the oesophagus to better view the chambers of the heart.
Treatment for AF focuses on either rate control or rhythm control. Rate control aims to reduce symptoms associated with the high heart rates and to prevent cardiomyopathy secondary to the tachycardia. Rhythm control on the other hand aims to terminate the underlying rhythm. Generally paroxysmal AF is treated initially with rhythm control. Permanent AF alternatively is usually treated with rate control strategies. Persistent AF can be treated with either. In these patients rhythm control is often tried first if they are younger, symptomatic or have congestive heart failure. Rate control is attempted first in older patients (>65 years), unsuitable for cardioversion or treatment with antiarrhythmic drugs or with coronary artery disease. If either of the options attempted first fails the patient may be considered for the alternative strategy. Figures 6.7 and 6.8 show the treatment algorithms recommended by NICE in their management of atrial fibrillation guidelines for both rhythm and rate control (2014). The symptoms and causes of AF are listed in Tables 6.5 and 6.6.
Rate control strategies adapted from NICE, (2014) guidelines on the management of AF
Rhythm control strategies adapted from NICE, (2014) guidelines on the management of AF
Symptoms of AF
Loss of consciousness
Causes of AF
Sick Sinus Syndrome (SSS)
Rheumatic valve disease
Ischemic heart disease
Pulmonary Embolism (PE)
Atrial Septal Defect (ASD)
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