Electrocardiogram 3: cardiac rhythm and conduction ...

Copyright EMAP Publishing 2021

This article is not for distribution

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Clinical Practice

Review

Cardiology

Keywords Electrocardiogram/Cardiac

conduction defects/Cardiac arrythmia

This article has been

double-blind peer reviewed

In this article...

¡ñ T

 ypes of rhythm and conduction defects that can be seen on an electrocardiogram

¡ñ How to assess rhythm disorders clinically

¡ñ 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.

T

his 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:

¡ñ Take a history of the complaint/

symptom with which the patient

presents;

Nursing Times [online] August 2021 / Vol 117 Issue 8

27

¡ñ

¡ñ

¡ñ

¡ñ

¡ñ

¡ñ

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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Clinical Practice

Review

tap out the rhythm of the beat they felt

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 aberrations in heart rhythm or conduction

defects. Be aware that there may be causes

of a cardiogenic or neurogenic nature (for

example, seizures) to consider in the differential diagnosis.

Other symptoms are increased breathlessness, sweating or chest pain; these

signs may be more common with tachycardias (see below). With the advent of fitness technology, such as smart watches,

some patients may present with or

without a history of symptoms after identifying abnormal activity on their ECG

mobile app.

Recognising cardiac arrhythmias

When considering whether cardiac

rhythms are normal, it is important to

understand the electrical conducting

system of the heart and how the ECG

works, which were covered in parts 1 and 2

of this series. In summary, the sinoatrial

node (SAN) is the natural pacemaker of the

heart, generating a signal without an

external stimulus. If this stops working,

other slower potential pacemakers in the

heart, such as the atrioventricular node

(AVN) or bundle of His, can take over

(Jarvis and Saman, 2018). In these circumstances, overall heart rate will be slower.

The key components of the cardiac conducting system are discussed below and

listed with their usual intrinsic rates in

Table 1.

Ectopic beats

Ectopic beats are common and characterised by single electrical impulses that originate away from the SAN as extra beats.

They are generally benign and of no

Fig 1. Ventricular ectopic beats

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

¡°It is important to keep an

open mind to the potential

causes and take a proper

clinical history¡±

clinical significance. In the presence of an

atrial ectopic (premature atrial contraction), an extra wave is seen within the

P-wave (atrial depolarisation) so it looks

different to normal on the ECG. Ventricular ectopic beats (premature ventricular

contractions) look more dramatic, with a:

¡ñ Large wave on the rhythm trace

typically not preceded by a P-wave;

¡ñ Wide overall QRS complex (ventricular

depolarisation) of more than 120

milliseconds (ms) and inverted T-wave

(ventricular repolarisation) (Fig 1).

If there are isolated ectopic beats, there

is likely to be little clinical significance or

action needed (Omar et al, 2011). However

sometimes there is a ventricular ectopic

beat after every normal QRS complex; this

is referred to as ventricular bigeminy and

suggests some ventricular irritability.

If the patient is symptomatic with frequent ectopic beats, make sure you ask

them about potential medications that can

interfere with heart rate (for example, salbutamol, digoxin, over-the-counter cold

and allergy drugs, or antiarrhythmic

drugs), as well as high caffeine and alcohol

consumption. Further investigations may

be needed, such as checking electrolytes

(potassium, magnesium and calcium) and

thyroid function and, sometimes, a

24-hour or 48-hour Holter monitor or ECG

may be required.

Table 1. Usual intrinsic rates of the cardiac conducting system

components

Component

Intrinsic rate, bpm

Sinoatrial node

60-70

Atrioventricular node

40-50

Atrial cells

55-60

Bundle of His to the Purkinje fibres

0-40

bpm = beats per minute.

Nursing Times [online] August 2021 / Vol 117 Issue 8

28

Sinus bradycardia

Sinus bradycardia is a slow heart rate of

¡Ü60 beats per minute (bpm), due to the

slowing down of the SAN. This may be

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

an increase in the vagal tone of the heart

caused by the vagus nerve (actually a group

of nerves that control parasympathetic

activity in the heart). Bradycardia can also

be caused by vomiting, straining (through

vagal effects), beta-blocker drugs and

raised intracranial pressure from head

injury/pathology. It can also happen in the

context of an inferior myocardial infarction in which the SAN is in the region supplied by an occluded coronary artery ¡ª

usually, the right coronary artery affecting

the sinoatrial artery.

Bradycardia can be caused by diseases

such as sick sinus syndrome, when there is

an irreversible dysfunction of the SAN that

affects its ability to generate electrical

impulses to the heart. This can cause a

pause in electrical signals from the sinus

(lasting seconds to minutes), or electrical

impulses for which signals from the sinus

are slow or blocked. The dysfunction can

result in an alternating slow and fast heart

rate called bradycardia-tachycardia syndrome, or there may be atrioventricular

block (described later in this piece). When

there are symptoms due to sinus node

problems, the patient may need to have a

pacemaker inserted (National Institute for

Health and Care Excellence, 2014a).

Sinus tachycardia

In sinus tachycardia, the SAN is firing at a

rate of ¡Ý100bpm, but the rest of the conducting system is normal. There are many

benign causes, such as sinus tachycardia

in response to pain or exercise, as an adaptation in pregnancy, a response to caffeine

or a side-effect of medications such as salbutamol or digoxin.

Sinus tachycardia can also occur with

fever, infection, dehydration, electrolyte

(typically calcium, magnesium or potassium) abnormalities, and overactive thyroid. However, it can signify more-dangerous conditions, such as pulmonary



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Clinical Practice

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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

Nursing Times [online] August 2021 / Vol 117 Issue 8

30

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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Clinical Practice

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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.

Fig 4. Types of atrioventricular block on an ECG

4a. First-degree atrioventricular block

4b. Mobitz type I block

4c. Mobitz type II block

Conduction abnormalities

4d. Third-degree atriventricular block

Conduction defects can be caused by problems at the level of the AVN or through the

bundle of His and bundle branches.

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

Table 3. Characteristics of atrioventricular conduction defects

Heart block

Causes

ECG features

First-degree

atrioventricular

block

¡ñ Normal variant

¡ñ Regular rhythm

¡ñ Increased vagal tone

¡ñ One P-wave precedes every QRS

¡ñ Athletes

¡ñ PR interval: ¡Ý 0.20 seconds but constant

¡ñ Ischaemic heart disease

¡ñ QRS width ¡Ü0.12 seconds

¡ñ Low potassium

¡ñ Digoxin

¡ñ Beta-blockers and calcium channel blockers

Second-degree

atrioventricular

block

¡ñ Drug therapy (digoxin, beta-blockers, calcium

¡ñ

¡ñ

¡ñ

¡ñ

¡ñ

Third-degree

atrioventricular

block

channel blockers, amiodarone)

Coronary artery disease

New myocardial infarction

Rheumatic fever

Electrolyte abnormalities, eg low potassium

Myocarditis

¡ñ Idiopathic/unknown

¡ñ Congenital

¡ñ Ischaemic heart disease

¡ñ Aortic valve calcification

¡ñ Cardiac surgery and trauma

Mobitz type I

¡ñ Heart rate: 60-90 beats per minute

¡ñ Regular atrial rhythm, irregular ventricular rhythm

¡ñ Some P-waves not followed by a QRS complex

¡ñ PR interval becomes progressively longer until one P-wave is

not followed by a QRS complex when the cycle starts again

¡ñ QRS: ¡Ü0.12 seconds

Mobitz type II

¡ñ Atrial rate faster than ventricular rate depending on degree

of block, eg 2:1 block, 3:1 block

¡ñ Some P-waves are not followed by a QRS

¡ñ PR interval for conducted beats constant across the strip

¡ñ QRS: ¡Ü0.12 seconds for conducted beats

¡ñ Heart rate: 40-60 beats per minute

¡ñ No relationship between the P and the QRS waves, so no PR

interval

¡ñ QRS: ¡Ü0.12 seconds if controlled by the junction;

>0.12 seconds if paced by the ventricle

¡ñ Digoxin toxicity

¡ñ Diseases affecting bundle

Nursing Times [online] August 2021 / Vol 117 Issue 8

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