1 RLE Skills NCM 112

First Semester 2020-2021

ECG Course Study Guide

University of the Cordilleras

College of Nursing
Hanna Lee H Antonio- UC Faculty

Electrocardiogram (ECG)

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ECG ASSESSMENT: AN INTRODUCTION FOR HEALTHCARE PROVIDERS

Introduction

What is an ECG? Electrocardiogram, also called an electrocardiograph or ECG, is a graphic

representation of two electrical events called depolarisation and repolarisation. Depolarisation is
the spread of the electrical impulse across the heart, and repolarisation is the recovery stage
following this. Current is detected by electrodes or conductors which are placed on the skin, and
is represented on the ECG graph paper as positive and negative deflections called waves and
complexes. When no current is being detected, you can see a flat line, called a baseline.

We now need to look in more detail at the ECG graph paper itself. On the screen, you can see a
magnified image of the paper. But on an ECG printout, one small square measures one millimetre
in width and one millimetre in height. Larger squares comprise five x five small squares, and are
identified by dark outlines.

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In a graph we have a vertical and a horizontal axis. On the vertical axis, we measure amplitude,
which is the amount of electrical force being generated. This means that the greater the force is,
the taller or deeper the deflections. On the vertical axis, 10 millimetres, or 10 small squares in
height are equivalent to one millivolt of electrical current.

On the horizontal axis, we measure time in seconds, which means the longer it takes for the
electrical forces to move across the heart tissue, the wider the wave forms will appear. One small
square or one millimetre on the horizontal axis is equivalent to 0.04 of a second, and this
corresponds to a standard paper speed of 25 millimetres a second.

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On the screen, you can now see an example of the 12-lead ECG, with the standard voltage and
time settings written along the bottom.

The ECG shows 12 leads, or viewpoints, of the heart. There are six limb leads, which are called I, II,
III, aVR, aVL, and aVF, and six chest leads, called C1 to C6.

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Although the leads are looking at the same electrical events, they are viewing these events from
different angles, so the wave forms in each lead will look slightly different. Having multiple
viewpoints is useful because it provides more detailed information about what may be happening
in different areas of the heart. You might compare this to watching a football match, where in
order to get to good overall picture of the action, you would need to have cameras positioned in
different locations around the pitch.

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Some of the 12 leads have similar views, so can be grouped together into specific areas or
territories. For example, leads I, aVL, C5, and C6 all view the left side of the heart, which is called
the lateral territory. Leads II, III, and aVF view the bottom of the heart, known as the inferior
territory. Finally, leads C1 to C4 all broadly view the front or anterior territory of the heart.

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Along the bottom of the ECG, you will usually see a continuous strip of lead II. This makes it easier
to assess the heart rhythm, without the distraction of the intermittently changing leads above.

INTRODUCTION TO THE HEART’S ELECTRICAL CONDUCTION SYSTEM

The heart lies in the space between the lungs, which is called the mediastinum. It is approximately
the size of a person's fist and consists of four muscular chambers, two atria and two ventricles.

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The role of the heart is to pump blood around the body, enabling oxygen, nutrients and waste
products to be transported to and from the different cells and organs. Blood travels through the
heart in the following way-- oxygen depleted blood returning from the body cells enters the right
atrium, and at the same time, blood which has been oxygenated in the lungs returns to the left
atrium.

The increase in volume of blood in the atria then starts to flow into both ventricles. This is facilitated
by contraction of the atrial walls. Once the ventricles are full of blood, they in turn contract and
eject their contents. Blood from the right ventricle travels to the lungs to pick up oxygen, and
blood which has already been oxygenated in the left ventricle travels to the rest of the body's
cells and organs.

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In order for blood to be pumped around the body as efficiently as possible, the atria and
ventricles need to contract in sequence. And it is the role of the heart's electrical conduction
system to control this. The conduction system is comprised of specialised cells embedded within
the heart's muscular walls.

These cells are able to generate and conduct electrical impulses, which in turn stimulate the heart
muscle to contract. The conduction system works as follows. Firstly, the sinus node generates an
electrical impulse which sweeps across both atria in a wave-like fashion. This spread of the impulse
is called a wave of depolarisation. The atria respond by contracting and this ejects blood into the
ventricles.

Meanwhile, the impulse reaches the atrioventricular node, which lies between the atria and the
ventricles, before travelling on through the bundle of His and right and left bundle branches. The
ventricles, which have now had sufficient time to fill with blood, contract in response to the
impulse.

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The process starts again with another impulse being generated. As each cycle originates at the
sinus node, it is referred to as a sinus beat. And where this cycle occurs repeatedly, it is called sinus
rhythm. This represents the normal sequence of events leading to controlled electrical activation
and contraction of the heart. We will revisit the concept of sinus rhythm in week two of the course.

Why is sinus rhythm important for maintaining a normal blood pressure?

In order to understand the relationship between sinus rhythm and blood pressure, we first need to
focus on the concept of blood pressure.

Simply put, blood pressure is the outwards force which blood exerts on the walls of arteries. We
need to keep this pressure within certain limits, so that nutrients, oxygen and waste products can
be transported effectively around the body, between the various cells and organs.

Diagram depicting blood pressure in an artery

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Blood pressure is determined by two factors: the volume of blood being pumped out of the heart
within a given timeframe and the resistance to the flow of this blood within the blood vessels
(referred to as peripheral vascular resistance).

When we record a blood pressure, we get two values. The top value is called the systolic pressure
and this relates to the contraction of the ventricles and ejection of blood from the heart, causing
a pressure wave through the arterial system. We can detect this pressure wave when we feel a
person’s pulse. The bottom value within the blood pressure recording is called the diastolic
pressure, which is the background pressure within the arteries when the heart is resting between
beats.

The volume of blood pumped out of a ventricle (usually referring to the left ventricle) in one beat
is called the stroke volume and the volume ejected from the ventricle in one minute is called the
cardiac output.

Cardiac output can be represented by the following equation:

Cardiac output = stroke volume x heart rate (the number of stroke volumes in one minute).

Cardiac output is related to blood pressure as follows:

Blood pressure = cardiac output x peripheral vascular resistance

The above illustrates why the effective ejection of blood from the heart is crucial for maintaining
blood pressure. Sinus rhythm co-ordinates the order and timing of atrial and ventricular
contraction, ensuring that the atria have contracted and emptied their contents into the
ventricles before the ventricles then contract. This helps to optimise stroke volume and cardiac
output.
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How do arrhythmias affect people?

Arrhythmias can have a number of physiological effects which may lead to a range of symptoms.

In particular, there is a loss of the normal co-ordinated depolarisation and contraction of the atria
and the ventricles, which occurs with sinus rhythm and which we have explored in previous steps.
For example, in the case of atrial fibrillation, the chaotic electrical activity within the atria causes
uncoordinated and ineffective contraction of the atria and therefore reduced filling of the
ventricles. This is referred to as loss of the ‘atria kick’.

Diagram depicting Atrial fibrillation

The impaired ventricular filling reduces the amount of blood which can be ejected from the heart
during each ventricular contraction (stroke volume).

Cardiac output and blood pressure may also, therefore, be reduced due to the following
relationships:

Stroke volume ↓ x heart rate = cardiac output ↓

Cardiac output ↓ x peripheral vascular resistance = blood pressure

In addition, stroke volume may also be negatively affected by the abnormal changes in heart
rate which commonly occur with arrhythmias. Atrial fibrillation, for example, is associated with
tachycardia (a fast heart rate) and you might think, looking at the equations above, that this
would improve cardiac output and blood pressure. The problem is that the ventricles fill when the
heart is at rest, and at very fast rates the time available between beats for this filling to take place
is reduced. At the other end of the spectrum, some arrhythmias are associated with bradycardia
(a slow heart rate) which means there are less ventricular contractions per minute, leading to a
direct reduction in output:

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Stroke volume x heart rate↓ = cardiac output

Tachyarrhythmias also require the heart muscle to work harder to maintain the increased heart
rate. This increased workload requires more oxygen and if this demand cannot be met by the
supply of blood, the person may experience chest pain.

These negative effects on cardiac output, blood pressure and oxygen supply to the heart can
lead to a range of symptoms which vary in their severity, depending on the type of arrhythmia,
the underlying health of the person affected and how long they have had the arrhythmia.
Possible signs and symptoms include:

 Palpitations

 Tiredness

 Reduced tolerance to exercise

 Shortness of breath

 Chest pain

 Dizziness

 Loss of consciousness

 Cardiac arrest

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TROUBLESHOOTING AND INTRODUCTION TO ECG INTERPRETATION PARAMETERS FOR NORMAL

SINUS RHYTHM

Parameters for normal sinus rhythm:

In an earlier step, we have seen how the electrical activity of the heart is represented on an ECG.
The presence of a P wave, followed by a QRS complex and a T wave represents what we call a
normal sinus beat, indicating that the impulse has been generated at the sinus node and then
spread across the atria and the ventricles.

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There are a wide variety of different measurements which can be taken to examine the wave
forms and their relationships in greater detail; however, we're just going to briefly look at two of
these, which are of particular significance.

The first is called the PR interval, which is the distance from the beginning of the P wave to the

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beginning of the QRS complex. It therefore includes the whole of the P wave and the gap
between the P and the QRS. This interval tells us whether or not there is normal conduction
between the atria and the ventricles. And a normal PR interval is between three and five small
squares in width. The second measurement is the QRS duration, which should be no more than 2.5
small squares in width. A normal QRS duration tells us that the ventricles are depolarising normally.

A run of continuous sinus beats, as you see here, is called sinus rhythm.

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When assessing ECG for the presence of sinus rhythm, you should look for the following features:
Distinct P waves should be present.

Every P wave should be followed by a QRS complex and a T wave. The P waves, QRS complexes,
and T waves should look similar across the rhythm strip. And the PR interval should be constant and
within the normal range of three to five small squares.

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This indicates that the same electrical events are happening over and over again, and there is a
normal connection between the atria and the ventricles.

The heart rate is also usually regular. And this can be confirmed by looking for consistent intervals
between the peaks of neighbouring QRS complexes.
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RELATIONSHIP BETWEEN SINUS RHYTHM AND THE ECG WAVEFORMS

In week one of the course, we looked at the normal electrical conduction of the heart, known as
sinus rhythm, and how this is linked to coordinated contraction and movement of blood. We now
need to think about how the electrical activity is represented on an ECG as waves and
complexes. A normal sinus beat starts with the generation of an electrical impulse at the sinus
node and the spread of this impulse as what is called a wave of depolarisation across the atria.
This event is represented on the ECG as a smooth, rounded wave form called a p-wave.

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The second step in the process is the impulse moving through the atrioventricular node and the
bundle of his. This does not produce a deflection on the ECG, so it's represented by a gap
between the end of the p-wave and the beginning of the next wave form. Following this, the
impulse travels down both bundle branches and depolarises the ventricles. This is represented by
the QRS complex, which can vary in its shape, but is often of two or three deflections. After
depolarisation, repolarisation of the ventricles occurs. And this is represented by an asymmetric t-
wave.

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SUPRAVENTRICULAR ARRHYTHMIAS: AN INTRODUCTION

Supraventricular arrhythmias, an introduction.
Abnormal heart rhythms occur when the electrical impulse does not originate at the sinus node
and follow the normal path through the atria and ventricles. There are many causes of
arrhythmias, including coronary heart disease, hypoxia and congenital heart disease. Broadly
speaking, arrhythmias can be divided into two main types, supraventricular and ventricular,
depending on their origin.

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Supraventricular arrhythmias arise from a problem within the atria, the AV node, or the bundle of
His. Examples include atrial fibrillation, atrial flutter, and supraventricular tachycardia. All these
arrhythmias are characterised by the absence of normal P waves and are typically associated
with fast heart rates. However, because they affect atrial rather than ventricular depolarisation,
QRS complexes are usually normal. Atrial fibrillation is a common supraventricular arrhythmia in
which multiple areas within the atrial muscle tissue generate impulses randomly and at a very fast
rate. Some of these impulses will travel through the atrial ventricular node and depolarise the
ventricles in the normal fashion.

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On the ECG, P waves will be absent, although you may be able to see some small non-uniform
wave forms called fifibrillation waves. These represent the chaotic atrial activity. As the impulses
are generated randomly within the atria, the overall heart rate is also irregular. QRS complexes
appear normal.

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One of the risks of atrial fibrillation is that the uncoordinated depolarisation and contraction within
the atria can lead to pooling of blood and clot formation. If part of the clot then breaks off or
embolises, it can potentially travel through the bloodstream to the brain and cause a stroke.
Because of this, people with chronic atrial fibrillation may require long term anticoagulation
therapy.

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Exercises 1: Study the following ECG placement closely. At the end of the course, you will be able
to identify the correct ECG electrode placements.

Placement of the 12 ECG leads

Chest (Precordial) Electrodes and Placement

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» V1 - Fourth intercostal space on the right sternum

» V2 - Fourth intercostal space at the left sternum
» V3 - Midway between placement of V2 and V4
» V4 - Fifth intercostal space at the midclavicular line
» V5 - Anterior axillary line on the same horizontal level as V4
» V6 - Mid-axillary line on the same horizontal level as V4 and V5

Limb (Extremity) Electrodes and Placement

» RA (Right Arm) - Anywhere between the right shoulder and right elbow
» RL (Right Leg) - Anywhere below the right torso and above the right ankle
» LA (Left Arm) - Anywhere between the left shoulder and the left elbow
» LL (Left Leg) - Anywhere below the left torso and above the left ankle

Credit to St. George’s University London

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