Electrocardiography

Electrocardiography is a method for recording action potentials of the heart. The source of electric

activity of the heart is situated in the sinus node (sinoatrial or SA node) which consists of specialized

muscle cells. The sinoatrial node in humans, located in the right atrium at the superior vena cava, is in

the shape of a crescent and is about 15 mm long and 5 mm wide. The SA nodal cells are self-

excitatory, pacemaker cells. They generate an action potential at the rate of about 70 per minute. From

the sinus node, activation propagates throughout the atria, but cannot propagate directly across the

boundary between atria and ventricles, since a nonconducting barrier of fibrous tissue is present.

The atrioventricular node (AV node) is located at the boundary between the atria and ventricles; it has

an intrinsic frequency of about 50 pulses/min. However, if the AV node is triggered with a higher

pulse frequency, it follows this higher frequency. In a normal heart, the AV node provides the only

conducting path from the atria to the ventricles.

Propagation from the AV node to the ventricles is provided by a specialized conduction system.

Proximally, this system is composed of a common bundle, called the bundle of His. More distally, it

separates into two bundle branches propagating along each side of the septum, constituting the right

and left bundle branches. Even more distally the bundles ramify into Purkinje fibers, that diverge to

the inner sides of the ventricular walls.

From the inner side of the ventricular wall, the many activation sites, which propagates through the

ventricular mass toward the outer wall. After each ventricular muscle region has depolarized,

repolarization occurs.

Figure 1: Conduction system of heart

The main electrophysiological particularity of a myocardial muscle fibre is the long duration of its

action potential 200 - 300 ms.Each myocardial fibre undergoes 4 electrical changes during the cardiac

cycle:polarisation, depolarisation, transpolarisation, repolarisation.

Associated with the electric activation of cardiac muscle cell is its mechanical contraction, which

occurs a little later.

The small wave labeled P occurs during atrial depolarisation. The complex labeled QRS is the result

of ventricular depolarisation. Atrial repolarisation is masked by this ventricular depolarisation and

ventricular repolarisation gives rise to the T wave.

Figure 2: Formation of ECG signal

Under normal conditions, the S-A node controls the beat of the heart, thus the S-A node is the normal

pacemaker of the heart. The main function of the A-V node is a delay in the transmission. This delay

plays an important role in the synchronous contraction of the atrial and ventricular muscle. If the

connection between the S-A node and A-V node is interrupted, the A-V node becomes the

secondary heart pacemaker.

Electrocardiographic Leads

In medical practice an ECG record is not scanned right from the heart muscle but from the body

surface. For this purpose an international agreement was reached for distinguishing the leads:

1. Limb leads according to Einthoven (bipolar), indication I, II, III

2. Augmented Goldberg's leads (unipolar), indication aVR, aVL, aVF

3. Chest leads according to Wilson (unipolar), indication V1 - V6,

V = Wilson's terminal , a = augmented

Description of individual kinds of leads:

Einthoven's limb leads or standard limb leads: cardiac action potential is scanned bipolarly:

I. ....... between left hand (L) and right hand (R)

II. ....... between left leg (F) and right hand (R)

III. ...... between left leg (F) and left hand (L)

Goldberg's augmented leads are formed with the help of special electric processing of potentials

conveyed from the leads I, II, III. Using passive electrical circuits (voltage dividers), electrical

"centres" between the pairs of the limbs R-L, R-F, F-L are created. Then the action potentials are

scanned unipolarly between these newly created "centres" of limb electrodes R, L, F and the remaining

limb electrode. This processing of action potential is possible only after previous amplifying by input

amplifiers of the ECG device. Assuming that the recently created "centres" of leads have zero and

constant potential.

Chest leads are scanned unipolarly against the Wilson's terminal, which is again created electrically,

by the connection of all three limb electrodes R, L, F into one point over identical resistors. This point,

the Wilson's terminal, will always have zero and constant potential. Like the Goldberg's extended

leads, and the Wilson's terminal are only capable of realisation in the case when the signal on the input

amplifier is amplified. The choice of a concrete and particular lead when using the ECG record is

conditioned by the diagnostic purpose of the physician.

Figure 3: Electrodes settings

ECG registration electrodes

ECG record of the heart action potentials is mainly registered from the skin using the metal electrodes.

These electrodes are made of sintered silver and provided with an electrolytically applied layer of

silver chloride. These components create (together with the ECG gel) a system which is called an

electrode of kind II in electrochemistry. The main advantage of such an electrode is that it is almost

unpolarizable. Unpolarizability is an important feature of electrodes used in registration of

biopotentials and also for measuring purposes in electrochemistry.

Basic description of physiological ECG curve

Figure4: ECG curve

1. Rhythm

• regular x irregular

• sinus x nonsinus

2. Frequency (calculation: 60/(0,04x|RR|) at the

recording speed of 25mm/s, or using

an ECG ruler)

3. Transmission intervals PQ up to 0,2s (5 mm at the recording

speed of 25mm/s)

QRS do 0,12 (3 mm at the recording

speed of 25mm/s)

4. Electric heart axis direction (-30° to 105°)

V1-V6

I

II III aVR + +

+ -

- - +

-

Evaluation of ECG record

Normal sinus rhythm

Normal sinus rhythm is the rhythm of a healthy normal heart, where the sinus node triggers the cardiac

activation. This is easily diagnosed by noting that the three deflections, P-QRS-T, follow in this order

and are differentiable. The sinus rhythm is normal if its frequency is between 60 and 100/min.

Figure5: Normal sinus rhythm

Sinus bradycardia

A sinus rhythm of less than 60/min is called sinus bradycardia. This may be a consequence of

increased vagal or parasympathetic tone.

Sinus tachycardia

A sinus rhythm of higher than 100/min is called sinus tachycardia. It occurs most often as a

physiological response to physical exercise or psychical stress, but may also result from congestive

heart failure

Figure6: Sinus tachycardia

Sinus arrhythmia

If the sinus rhythm is irregular such that the longest PP- or RR-interval exceeds the shortest interval by

0.16 s, the situation is called sinus arrhythmia. This arrhythmia is so common in young people that it is

not considered a heart disease. One origin for the sinus arrhythmia may be the vagus nerve, causes an

increase in heart rate during inspiration and a decrease during expiration.

All complexes normal, evenly spaced. Rate > 100/min

All complexes normal, evenly spaced. Rate 60 - 100/min

Figure7: Sinus arrhythmia

Wandering pacemaker

The origin of the atrial contraction may also vary or wander. Consequently, the P-waves will vary in

polarity, and the PQ-interval will also vary.

Figure8: Wandering pacemaker

Atrial fibrillation

The activation in the atria may also be fully irregular and chaotic, producing irregular fluctuations in

the baseline. A consequence is that the ventricular rate is rapid and irregular, though the QRS contour

is usually normal. Atrial fibrillation occurs as a consequence of rheumatic disease, atherosclerotic

disease, hyperthyroidism, and pericarditis. (It may also occur in healthy subjects as a result of strong

sympathetic activation.)

Figure9: Atrial fibrillation

Ventricular arrhythmias

Activation does not originate from the AV node. The inner walls of the ventricles are activated almost

simultaneously and the activation front proceeds mainly radially toward the outer walls. As a result,

Baseline irregular, ventricular response irregular

Variation in P-wave contour, P-R and P-P interval and therefore in R-R

intervals

All complexes normal, rhythm is irregular Longest R-R interval

exceeds shortest > 0.16 s

the QRS-complex is of relatively short duration. (The criterion for normal ventricular activation is a

QRS-interval shorter than 0.1 s. ).

Ventricular tachycardia

Activation of the ventricular muscle at a high rate (over 120/min), ventricular tachycardia is often a

consequence of ischemia and myocardial infarction.

Figure10: Ventricular tachycardia

Ventricular fibrillation

When ventricular depolarization occurs chaotically, without QRS-complexes, usually involving an

insufficiency in pumping blood. The ventricular fibrillation may be stopped with an external

defibrillator pulse.

Figure11: Ventricular fibrillation

Each myocardial fibre (cell) behaves as electrical dipole during phases of depolarisation and

repolarisation, forming a current�dipole vector. The total current�vector at any instant is the sum of

the vectors for all the cells in the heart.

Determination of electric axis of the heart in the frontal plane

Each myocardial fibre (cell) behaves as electrical dipole during phases of depolarisation and

repolarisation, forming a current-dipole vector. The total current-vector at any instant is the sum of

the vectors for all the cells in the heart.

The cardiac vector is associated with the electric field vector produced by the instantaneous charge

distribution during the cardiac cycle.

Projection of the trajectory of the terminal point of the heart vector forms the vectocardiogram. The

vectorcardiogram is composed of P, QRS and T loops. In clinical practice the most frequently used is

the frontal vectocardiogram.

Rapid, wide, irregular ventricular complexes

Wide ventricular complexes. Rate> 120/min

Figure12: Vectorcardiogram (Silbernagl a Despopoulos 1993)

The normal range of the electric axis lies between +30° and -110° in the frontal plane and between

+30° and -30° in the transverse plane.

Deviation of the electric axis to the right is an indication of increased electric activity in the right

ventricle due to increased right ventricular mass. This is usually a consequence of chronic obstructive

lung disease, pulmonary emboli, certain types of congenital heart disease, or other disorders causing

severe pulmonary hypertension and cor pulmonale.

Deviation of the electric axis to the left is an indication of increased electric activity in the left

ventricle due to increased left ventricular mass. This is usually a consequence of hypertension, aortic

stenosis, ischemic heart disease, or some intraventricular conduction defect.

Cardiac stress test

Cardiac stress test (or Cardiac diagnostic test) is a test used in medicine and cardiology to measure the

heart's ability to respond to external stress in a controlled clinical environment. The stress response is

induced by exercise or drug stimulation. Cardiac stress tests compare the coronary circulation while

the patient is at rest with the same patient's circulation observed during maximum physical exertion,

showing any abnormal blood flow to the heart's muscle tissue (the myocardium). The results can be

interpreted as a reflection on the general physical condition of the test patient. This test can be used to

diagnose ischemic heart disease, and for patient prognosis after a heart attack (myocardial infarction).

Once the stress test is completed, the patient generally is advised to not suddenly stop activity, but to

slowly decrease the intensity of the exercise over the course of several minutes.

Stress cardiac imaging is not recommended for asymptomatic, low-risk patients as part of their routine

care. Some estimates show that such screening accounts for 45% of cardiac stress imaging, and

evidence does not show that this results in better outcomes for patients. Unless high-risk markers are

present, such as diabetes in patients aged over 40, peripheral arterial disease; or a risk of coronary

heart disease greater than 2 percent yearly, most health societies do not recommend the test as a

routine procedure.

Absolute contraindications to cardiac stress test include:

• Acute myocardial infarction within 48 hours

• Unstable angina not yet stabilized with medical therapy

• Uncontrolled cardiac arrhythmia, which may have significant hemodynamic responses (e.g.

ventricular tachycardia)

• Severe symptomatic aortic stenosis, aortic dissection, pulmonary embolism, and pericarditis

• Multivessel coronary artery diseases that have a high risk of producing an acute myocardial

infarction

TASK: Measure ECG in rest and Cardiac stress test

Set electrodes onto a patient. Labels of the limb electrodes are followed: R (RA) – right arm, red;

L (LA) – left arm, yellow, F (LL) – left leg, green; N (RL) – right leg, black. Limb leads are generally

set on palm side of forearm and laterally to calf. Within cardiac stress test the placement is modified.

R and L are fixed symmetrically onto subclavian socket (medially to deltoid muscle), L – axillary line

over ilium bone, N – over ilium bone or on back. Precordial electrodes are labeled V1-V6 or C1-C6.

V1 is placed between 4th and 5

th rib right to sternum, V2 symmetrically to V1(left to sternum), V4

between 5th and 6

th rib mid-clavicular line, V6 between 5

th and 6

th rib mid-axillary line, V3 is between

V2 and V4, and V5 between V4 and V6.

Figure13: ECG electrodes location

Run program Cardiax. Add new patient and fill in name, code (any number), date of birth, sex, height,

weight.

Figure14: Main Windows of Cardiax

Check parameters of measurements at menu Setup.

Figure15: Setup window

Figure16: Setup Windows for printing

Figure17: Setup Windows for the stress test

Set the stress test. Maximum workload set according to formula: 1.5 x [(2.5 x weight) – age] for a

woman; 1.5 x [(3 x weight) – age] for a man. Stress phase takes 4x2 minutes with beginning workload

60W. Set Increase of load to have equal increment during the test (4 rises of workload) between 60W

and maximum workload. (Ask for assistance if needed.)Max. heartrate is set automatically from your

age by formula 220 – age.

Figure18: Setup Windows fort he stress test

Confirm the changes by pressing Apply and OK.

Open the patient records list.

Run the ECG at menu Record – ECG record. Patient is resting. Set the filter on and press the recording

button (red spot). Wait approximately 20s and press stop button (green square). Print the record into

pdf file. Evaluate the rhythm (regular/irregular, sinusoidal …), heart rate (from R spikes distance),

calculate the heart axis in the frontal plane using Einthoven’s triangle.

Run the Cardiac stress test at menu Record – Stress test. Check the setup for the test.

Monitoring window contains:

• blood pressure

• time indicator for blood pressure measurement

• time of the test

• time of actual workload level in progress

• actual workload

Figure19: Monitoring window

During the whole test you manually measure blood pressure (BP). The time indicator for blood

pressure measurement appears at 1:20 of each level. During 40s you measure BP and write the value

into white box in format: SBP/DBP. DO NOT PRESS ENTER for confirming the value, the program

loads it automatically. The program starts the relaxing phase when some of the parameters reach the

preset value and if you do not want to continue in the stress phase. Start the test.

Start of stress phase

Relaxing phase

Increase of workload

Decrease of workload

Set constant workload (increment is stopped until pressing again)

ECG filter

Set amplitude of record (5, 10 or 20 mm/mV)

Set speed of record (25, 50, 100 or 200 mm/s)

Stop the test after 6 minutes of relaxing phase at menu Mode – Stop.

Evaluation

The final report contains 4 main parts: List of records, Graphs, ST Trend and ST Level.

Figure20: Final report

Each record print into pdf file. Find maximum workload, heart rate, blood pressure. Follow the

changes of BP and HR through the stress and the relaxing phase. Print the card Graphs into pdf file.

Compare 6 records – 4 stress and 2 relaxing. Press key F3 to mark the record and the icon Compare

selected ECG recordings. Evaluate the changes through time (generally in II. lead). Print the

comparison into pdf file. Show the average electrocardiograms of the chest and the limb leads through

the stress test.

Figure21: Comparisonof ECG recording through different time

Figure22: Average electrocardiograms

Resources:

Malmivuo J, Plonsey R. Bioelectromagnetism. http://www.bem.fi/

Silbernagl S a Despopoulos A. Atlas fyziologie člověka. Grada 1993.

Widimský J a Lefflerová K. Zátěžové EKG testy v kardiologii. Triton 2003.

Chaloupka V, Elbl L a kolektiv. Zátěžové metody v kardiologii. Grada 2003.

Hampton JR. EKG stručně, jasně, přehledně. Grada 1996.