Electrocardiogram 3: cardiac rhythm and conduction abnormalities - emap

Copyright EMAP Publishing 2021 This article is not for distribution except for journal club use

Clinical Practice

Review Cardiology

Keywords Electrocardiogram/Cardiac conduction defects/Cardiac arrythmia

This article has been double-blind peer reviewed

In this article...

Types of rhythm and conduction defects that can be seen on an electrocardiogram How to assess rhythm disorders clinically Knowledge of the unique rythmns of different disorders

Electrocardiogram 3: cardiac rhythm and conduction abnormalities

Key points

Cardiac rhythm and conduction defects, such as atrial fibrillation, are common

They can be an acute problem presenting for the first time or part of the course of a chronic disease

When considering whether cardiac rhythms are normal, nurses need to understand the electrical conducting system of the heart

A clinical history should include medicines and current symptoms when assessing rhythm disorders

It is important to understand the unique patterns in rate and waveform on the electrocardiogram that are associated with different disorders

Author Selina Jarvis is honorary research nurse, Guy's and St Thomas' NHS Foundation Trust.

Abstract This is the last in a three-part series on using an electrocardiogram to assess the heart's electrical activity. In this article, the focus is on cardiac rhythm and conduction abnormalities of the heart, which all have unique presenting characteristics. These characteristics include ectopic beats, tachycardias and atrioventricular block.

Citation Jarvis S (2021) Electrocardiogram 3: cardiac rhythm and conduction abnormalities. Nursing Times [online]; 117: 8, 27-32.

This is the final article in a threepart series on use of an electrocardiogram (ECG), a non-invasive and quick investigation that assesses the electrical activity of the heart. Part 1 looked at the purpose of the test, cardiac electrophysiology and the practicalities of doing an ECG, while part 2 looked at interpretation, with a particular focus on cardiac ischaemia. In this article, the focus is on abnormalities in rhythm and electrical conduction that can be identified on an ECG.

Cardiac arrhythmias and conduction defects are common. They can be an acute problem presenting for the first time, or part of a chronic disease course complicated by acute decompensation at periods of illness. Some arrhythmias may cause little to no symptoms and are fairly benign, while others are of greater concern and may lead to serious symptoms; at worst, they may predate a cardiac arrest if not recognised and treated promptly.

Clinical assessment of arrhythmia The following steps are key when assessing a patient presenting with an abnormal heart rhythm or conduction defect: Take a history of the complaint/

symptom with which the patient presents;

Consider whether there are any features of cardiac compromise (specifically, shock, syncope or fainting, myocardial ischaemia, heart failure);

Consider any relevant past medical history;

Take note of medications that may be associated with the condition;

Ask about family history of arrhythmias, cardiac disease or sudden cardiac death;

Consider relevant investigations, such as electrolyte abnormalities. Excess, or deficiencies in, potassium, magnesium or calcium can affect the balance of electrical charges inside and outside of cardiac cells, alter electrical signalling and cause arrhythmias;

Compare with previous ECG results if available.

Clinical symptoms There are various potential symptoms associated with an arrhythmia. One common symptom is palpitations but this can mean different things to different people. Some report it as an increased awareness of a heartbeat or fluttering in the chest, while others may report feeling an extra or missing beat or complain of an irregular heart rate. You can ask patients to

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Copyright EMAP Publishing 2021 This article is not for distribution except for journal club use

tap out the rhythm of the beat they felt Fig 1. Ventricular ectopic beats

onto a table with their hands or show you

their device if they have recorded an event.

Symptoms may also include dizziness

or syncope. Syncope may be due to a

simple faint, often when standing for a

long period of time or when standing up

from a sitting/recumbent position (postural) or at rest, and can be related to aber-

Source: Reproduced with the kind permission of Resuscitation Council UK.

rations in heart rhythm or conduction

defects. Be aware that there may be causes "It is important to keep an

of a cardiogenic or neurogenic nature (for example, seizures) to consider in the differential diagnosis.

open mind to the potential causes and take a proper

Sinus bradycardia Sinus bradycardia is a slow heart rate of 60 beats per minute (bpm), due to the slowing down of the SAN. This may be

Other symptoms are increased breath- clinical history"

lessness, sweating or chest pain; these

physiological, often occurring in fit individuals like athletes, and may be related to

signs may be more common with tachy- clinical significance. In the presence of an an increase in the vagal tone of the heart

cardias (see below). With the advent of fit- atrial ectopic (premature atrial contrac- caused by the vagus nerve (actually a group

ness technology, such as smart watches, tion), an extra wave is seen within the of nerves that control parasympathetic

some patients may present with or P-wave (atrial depolarisation) so it looks activity in the heart). Bradycardia can also

without a history of symptoms after iden- different to normal on the ECG. Ventric- be caused by vomiting, straining (through

tifying abnormal activity on their ECG ular ectopic beats (premature ventricular vagal effects), beta-blocker drugs and

mobile app.

contractions) look more dramatic, with a: raised intracranial pressure from head

Large wave on the rhythm trace

injury/pathology. It can also happen in the

Recognising cardiac arrhythmias

typically not preceded by a P-wave;

context of an inferior myocardial infarc-

When considering whether cardiac Wide overall QRS complex (ventricular tion in which the SAN is in the region sup-

rhythms are normal, it is important to depolarisation) of more than 120

plied by an occluded coronary artery --

understand the electrical conducting milliseconds (ms) and inverted T-wave usually, the right coronary artery affecting

system of the heart and how the ECG (ventricular repolarisation) (Fig 1).

the sinoatrial artery.

works, which were covered in parts 1 and 2 If there are isolated ectopic beats, there Bradycardia can be caused by diseases

of this series. In summary, the sinoatrial is likely to be little clinical significance or such as sick sinus syndrome, when there is

node (SAN) is the natural pacemaker of the action needed (Omar et al, 2011). However an irreversible dysfunction of the SAN that

heart, generating a signal without an sometimes there is a ventricular ectopic affects its ability to generate electrical

external stimulus. If this stops working, beat after every normal QRS complex; this impulses to the heart. This can cause a

other slower potential pacemakers in the is referred to as ventricular bigeminy and pause in electrical signals from the sinus

heart, such as the atrioventricular node suggests some ventricular irritability.

(lasting seconds to minutes), or electrical

(AVN) or bundle of His, can take over If the patient is symptomatic with fre- impulses for which signals from the sinus

(Jarvis and Saman, 2018). In these circum- quent ectopic beats, make sure you ask are slow or blocked. The dysfunction can

stances, overall heart rate will be slower. them about potential medications that can result in an alternating slow and fast heart

The key components of the cardiac con- interfere with heart rate (for example, sal- rate called bradycardia-tachycardia syn-

ducting system are discussed below and butamol, digoxin, over-the-counter cold drome, or there may be atrioventricular

listed with their usual intrinsic rates in and allergy drugs, or antiarrhythmic block (described later in this piece). When

Table 1.

drugs), as well as high caffeine and alcohol there are symptoms due to sinus node

consumption. Further investigations may problems, the patient may need to have a

Ectopic beats

be needed, such as checking electrolytes pacemaker inserted (National Institute for

Ectopic beats are common and character- (potassium, magnesium and calcium) and Health and Care Excellence, 2014a).

ised by single electrical impulses that orig- thyroid function and, sometimes, a

inate away from the SAN as extra beats. 24-hour or 48-hour Holter monitor or ECG Sinus tachycardia

They are generally benign and of no may be required.

In sinus tachycardia, the SAN is firing at a

rate of 100bpm, but the rest of the con-

Table 1. Usual intrinsic rates of the cardiac conducting system components

ducting system is normal. There are many benign causes, such as sinus tachycardia in response to pain or exercise, as an adap-

Component

Intrinsic rate, bpm

tation in pregnancy, a response to caffeine or a side-effect of medications such as sal-

Sinoatrial node

60-70

butamol or digoxin.

Atrioventricular node Atrial cells

40-50 55-60

Sinus tachycardia can also occur with fever, infection, dehydration, electrolyte (typically calcium, magnesium or potas-

Bundle of His to the Purkinje fibres

bpm = beats per minute.

0-40

sium) abnormalities, and overactive thyroid. However, it can signify more-dangerous conditions, such as pulmonary

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For more articles on cardiovascular care, go to cardiovascular

embolism, and it is important to keep an open mind to the potential causes and take a proper clinical history.

Assessing tachycardias A normal heart rate is 60-100bpm; tachycardia refers to a fast heart rate of >100bpm. It has different causes and the reason for the fast heart rate can originate from the atria or the ventricles. Tachycardia may be transient, lasting for seconds or minutes, but can also last for several days.

It is possible to differentiate between tachycardias that originate in the atria or ventricles by looking at the width of the QRS complex, which is normally 120ms. In tachycardia originating in the atria (supraventricular), the QRS is typically narrow (100bpm and a QRS complex of >120ms. For the most part, a broad complex tachycardia is likely to be due to a ventricular tachycardia and it is safest to consider this first, given the urgency for treatment.

In some cases, the problem may originate in the atria, such as with AF when a defect of electrical impulses down the bundle branches results in an ECG

suggestive of a broad complex tachycardia. In this case of AF with a bundle branch block, there would be an absence of P-waves and the rhythm would be irregular, along with the broad QRS complex. Looking at the QRS complex may also be helpful in ventricular tachycardia because the heart rate is regular and the QRS looks monomorphic (uniform) throughout the ECG trace.

It is crucial to recognise ventricular tachycardia on an ECG or cardiac monitor because it needs urgent medical attention; guidance on this can be found in the Resuscitation Council UK's guidelines by Soar et al (2021).

Depending on whether there are adverse features and signs of haemodynamic compromise, such as shock, syncope, or chest pain, electrical cardioversion may need to be considered to bring the heart back into sinus rhythm.

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Fig 4. Types of atrioventricular block on an ECG

4a. First-degree atrioventricular block 4b. Mobitz type I block 4c. Mobitz type II block 4d. Third-degree atriventricular block

Source: Reproduced with the kind permission of Resuscitation Council UK.

Pharmacological agents are another option for rate control and treatments include beta-blockers, calcium channel blockers or chemical cardioversion with amiodarone.

In polymorphic ventricular tachycardia (Fig 3a), the shape of the QRS complexes look very different to monomorphic complexes (Fig 3b). In a condition called torsades de pointes, the broad complex QRS complexes are polymorphic and look to be twisting around the electrical baseline with prolongation of the QT interval (Fig 3a). Torsades de pointes is a dangerous heart rhythm that can lead to dizziness and syncope; in addition, although in some cases it may spontaneously revert to sinus rhythm, it can also lead to a cardiac arrest with ventricular fibrillation. After checking electrolyte levels and giving magnesium intravenously, if needed, electrical cardioversion may be required.

Causes of ventricular tachycardia and torsades de pointes are outlined in Table 2.

Conduction abnormalities Conduction defects can be caused by problems at the level of the AVN or through the bundle of His and bundle branches.

Table 3. Characteristics of atrioventricular conduction defects

Heart block

Causes

ECG features

First-degree atrioventricular block

Second-degree atrioventricular block

Normal variant Increased vagal tone Athletes Ischaemic heart disease Low potassium Digoxin Beta-blockers and calcium channel blockers

Drug therapy (digoxin, beta-blockers, calcium channel blockers, amiodarone)

Coronary artery disease New myocardial infarction Rheumatic fever Electrolyte abnormalities, eg low potassium Myocarditis

Third-degree atrioventricular block

Idiopathic/unknown Congenital Ischaemic heart disease Aortic valve calcification Cardiac surgery and trauma Digoxin toxicity Diseases affecting bundle

Regular rhythm One P-wave precedes every QRS PR interval: 0.20 seconds but constant QRS width 0.12 seconds

Mobitz type I Heart rate: 60-90 beats per minute Regular atrial rhythm, irregular ventricular rhythm Some P-waves not followed by a QRS complex PR interval becomes progressively longer until one P-wave is

not followed by a QRS complex when the cycle starts again QRS: 0.12 seconds Mobitz type II Atrial rate faster than ventricular rate depending on degree

of block, eg 2:1 block, 3:1 block Some P-waves are not followed by a QRS PR interval for conducted beats constant across the strip QRS: 0.12 seconds for conducted beats Heart rate: 40-60 beats per minute No relationship between the P and the QRS waves, so no PR

interval QRS: 0.12 seconds if controlled by the junction;

>0.12 seconds if paced by the ventricle

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