ECG Processing Assignment -

Katherine Hughes
19334107
Abstract

In this report, Record 207 of the ‘MIT-BIH arrythmia database’ is chosen to be analysed and
processed due to its complexity as it includes both ventricular arrhythmias and conduction
abnormalities. Signal processing of the ECG waveform is used as it provides a means to non-
invasively interrogate the functionality of the heart. Beat-to-beat heart rate variability (HRV), caused
by the fluctuating balance of sympathetic and parasympathetic tone is examined. Qualitative
methods including the Poincaré plot are also used to evaluate HRV and a possible diagnosis.

Background

1. Introduction

An electrocardiogram (ECG) provides a direct measurement of rate, rhythm, time-dependent

electrical vector of the heart and thus allows the collective electrical activity of the heart to be
measured. It also provides necessary information about the origin and conduction of the cardiac
action potential within the heart. [1]

As different parts of the heart activate sequentially, it can attribute time-dependent changes in
electrical vector to different regions of the heart. The P wave reflects the atrial depolarization, the
QRS complex corresponds to ventricular depolarization and the T wave reflects ventricular
repolarization. This can be seen clearly in Figure 1.

Figure 1: Visualisation of ECG

When the heart observes a typical conduction process i.e., at a normal rate, the rhythm is called a
normal sinus rhythm. The careful examination of intervals, durations, and segments in ECG tracing
can reveal a great deal about conducted action potential and can contribute to the overall diagnosis
of a patient. Examples of the physiological and pathophysiological significance of these parameters
are defined below and can be seen in Figure 2.

As mentioned previously, the P-wave represents atrial depolarisation (AD). Therefore, the P-wave
duration indicates how long AD takes. AD initiates the contraction of the atrial musculature. As this
happens, the pressure within the atrial chambers increases, forcing increased blood flow across the
open atrioventricular (AV) valves. This leads to a rapid flow of blood into the ventricles. [2] The PR
interval thus indicates how long it takes for the action potential to conduct from the SA node to the
AV node, through to the bundle of His. The bundle of His divides into left and right pathways, called
bundle branches, to activate the ventricles. The QRS duration corresponds to the length of time it
takes for the wave of depolarization to spread throughout the ventricles. The QT interval indicates
how long the ventricles remain depolarized and is an estimate of the length of the overall
“ventricular” action potential. The QT segment gets shorter as the heart rate increases.

Figure 2: Typical conduction cycle at normal sinus rhythm

2. Sympathetic & Parasympathetic

The central nervous system consists of the brain, spinal cord, and all the nerves within the body. The
autonomic nervous system (ANS) is the part of this system that regulates involuntary body functions.
Within the ANS are the sympathetic and parasympathetic nervous systems, which control the same
parts of the body and general functions but have opposing effects due to various stimuli.

The sympathetic nervous system, known as the fight or flight response is initiated when we face a
perceived threat, emotional or physical. The associated automatic and involuntary responses
associated include increased heart rate, respiratory rate and blood pressure. It also includes
heightened awareness and increased perspiration. Sympathetic nervous system contributes to
accelerating heart rate, constricting blood vessels, and raising blood pressure. [3]
The parasympathetic nervous system, referred to as the rest and digest response, aims to decelerate
certain responses and return the body to a state of calm. The primary function of the
parasympathetic nervous system is to maintain long-term health and a healthy balance across the
body’s functions. [3] Parasympathetic responses include an increase of intestinal and glandular
activity, decreased heart rate, constriction of bronchial tubes in lungs, and relaxed sphincter
muscles.

In order to live with optimal health and proper function for as long as possible, it is necessary to
obtain a harmonious balance between both the sympathetic and parasympathetic nervous systems
as they are vital to our health and survival.

3. Arrythmias

Any change in cardiac rhythm from normal sinus rhythm is defined as an arrhythmia – some
arrhythmias are pathological and even life-threatening – others are normal and usually benign,
including sinus tachycardia and sinus arrhythmia. Tachycardia is described as a resting heart rate >
100 BPM. Conversely, bradycardia is defined as a resting heart rate < 60 BPM. It is important to note
that fit individuals will often have heart rates < 60 BPM and be optimally healthy.

Bigeminy is a type of heart arrhythmia in which the heart beats once normally and once abnormally
in quick succession, followed by a pause. It can occur because of a heartbeat irregularity involving
either the atrium or ventricles. When it involves a heartbeat irregularity in the atrium, it is due to
premature atrial contractions (PACs). Conversely, bigeminy involving the ventricles is due to
premature ventricular contractions (PVCs). [4] Some cases of bigeminy are benign and transient and
do not require treatment. However, a person who experiences severe or frequent episodes of
bigeminy should see their doctor for a diagnosis.

Heart block is a type of arrhythmia described as the slowing down or interruption of the electrical
signal from the atria to the ventricles. First-degree atrioventricular (AV) block is a condition of
abnormally slow conduction through the AV node. This condition is generally asymptomatic and
discovered only on routine ECG analysis. Usually, this type of AV block is benign. However, if it is
associated with an acute myocardial infarction, it may lead to further AV defects.

Ventricular flutter and ventricular fibrillation (VF) are lethal arrhythmias characterized by chaotic,
disorganized electrical activity that results in failure of sequential cardiac contraction and inability to
maintain cardiac output. Ventricular flutter, which is characterized by a sine wave appearance on the
electrocardiogram (ECG), is a tachyarrhythmia closely related to ventricular fibrillation. Its
implications, causes, and consequences are very similar to ventricular fibrillation. The two
arrhythmias are therefore often classified together. Other disorders associated with ventricular
fibrillation are usually the cause of the condition. The immediate cause for most cases of ventricular
fibrillation is ischemic heart disease, or coronary artery disease, with the ischemia altering electrical
events to the point of causing complete lack of an organized rhythm. [5] A variety of ventricular
tachyarrhythmias can also lead to ventricular fibrillation.
Heart disease is one of the main causes of death in the world. And about 80% of sudden cardiac
death occurs due to ventricular tachyarrhythmia. Ventricular tachycardia (VT or V-tach) happens
when the lower chamber of the heart (ventricles) beat too fast to pump efficiently, meaning the
body doesn't receive enough oxygenated blood. Ventricular tachycardia episodes may be brief and
last only a couple of seconds without causing harm. Although, episodes lasting more than a few
seconds, known as sustained V-tach, can be life-threatening. Sometimes ventricular tachycardia can
even cause sudden cardiac arrest, especially if left untreated.

Dataset

The dataset used in this study, obtained from Physio-Bank, is entitled “MIT-BIH Arrhythmia
Database” and is available on-line. [6] The source of the ECGs included in the MIT-BIH Arrhythmia
Database is a set of over 4000 long-term Holter recordings that were obtained by the Beth Israel
Hospital Arrhythmia Laboratory between 1975 and 1979. Approximately 60% of these recordings
were obtained from inpatients. The database contains 23 records (numbered from 100 to 124
inclusive with some numbers missing) chosen at random from this set, and 25 records (numbered
from 200 to 234 inclusive, again with some numbers missing) selected from the same set to include
a variety of rare but clinically important phenomena that would not be well-represented by a small
random sample of Holter recordings. Each of the 48 records is slightly over 30 minutes long.

The first group is intended to serve as a representative sample of the variety of waveforms and
artifact that an arrhythmia detector might encounter in routine clinical use. A table of random
numbers was used to select tapes, and then to select half-hour segments of them.

Records in the second group were chosen to include complex arrhythmias and conduction
abnormalities. The subjects were 25 men aged 32 to 89 years, and 22 women aged 23 to 89 years.
The record that was chosen to be examined for this report is from the second group. [7]
Clinical Significance

The records which were chosen to be in the second group are of high clinical significance. The
datasets include complex ventricular, junctional, and supraventricular arrhythmias and conduction
abnormalities. Several of these records were selected due to features of the rhythm, QRS
morphology variation, or signal quality expected to present significant difficulty to arrhythmia
detectors; these records have thus gained substantial notoriety among database users. [7]

Record 207 is an extremely difficult record. The predominant rhythm is normal sinus with first
degree AV block and left bundle branch block (LBBB). There are periods when the conduction block
alternates to a right bundle branch block (RBBB) pattern. The PVCs are multiform. Idioventricular
rhythm appears following the longest episode of ventricular flutter. The record ends during the
episode of supraventricular tachycardia arrythmia (SVTA). Record 207 was chosen specifically to be
examined for this report as it presents various heart rate and conduction abnormalities and
stretches the limitations of the electrocardiogram’s diagnostic utility. [8]

Results/Discussion

Task 1.

Figure 3 – R-R intervals (produced in MATLAB)

Analysing Figure 3 above, it is clear there is a P-wave present, indicating that there is no atrial
fibrillation or AV nodal rhythm. The presence of a deep S wave in leads V1 or V2 is often interpreted
as evidence suggesting left ventricular hypertrophy. Since the maximal electric force in left
ventricular hypertrophy usually moves to the left and posteriorly, the presence of a deep S wave in
leads V1 or V2 often correlates well with this condition. [9]
Also, it is evident that there is wide QRS complexes with a duration > 120ms. This is a sign of right
bundle branch block as it represents the activation of the right ventricle being delayed. Additionally,
there is wide, slurred S-wave and an RSR' wave with an ‘M-shaped’ QRS complex, fulfilling the
diagnostic criteria of RBBB. Right bundle branch block can result from several conditions, such as:
heart disease due to high blood pressure in the lungs (pulmonary hypertension), chronic obstructive
lung disease (COPD) and blood clot in the lungs (pulmonary embolism). [10]

As stated earlier, PVCs are irregular heartbeats in the ventricles. Under normal conditions, a group of
cells called the “sinoatrial node” innervates the heart and controls the heartbeat. Some cases of PVC
occur when a group of fibres called the Purkinje fibres supply nerves to the heart instead of the
sinoatrial node. People with PVC report feeling a fluttering or a flip-flop feeling in their chest
Ventricular couplets are defined as two PVCs in a row. There is often a compensatory pause after the
second premature beat. The two premature beats may have an identical morphology (unifocal
couplet), or their morphology may differ (multifocal couplet). [11] A ventricular couplet is seen
around 33 seconds into the record, subsequently leading to ventricular tachycardia and ventricular
flutter.

As mentioned previously, ventricular tachycardia is an arrhythmia caused by irregular electrical

signals in the ventricles. There are several different forms of VT — the most common is
monomorphic VT, which originates from a single focus within the ventricles. The ECG features of
monomorphic VT are regular, broad complex tachycardia with uniform, identical QRS complexes (as
seen in Figure 4)

Ventricular tachycardia has a wide QRS duration, usually > 0.12 seconds. In this record, the short VT
episode has an irregular rhythm and a rate greater than 200 BPM, indicating that ventricular
fibrillation is to follow, which it does.

Figure 4 - Monomorphic VT
As mentioned previously, ventricular flutter (VF) is an arrhythmia, more specifically a tachycardia
affecting the ventricles with a rate usually over 250-350 beats/min, and one of the most
indiscernible. Electrical signals in the ventricles are fired in a very fast and uncontrolled manner.
Areas of ventricular muscle contract but there is no coordinated pattern of contraction so the heart
ceases to eject blood. Both ventricular flutter (VF) and ventricular fibrillation (VF/V-Fib) generally
result in loss of consciousness and are usually fatal within minutes unless intervention such as
resuscitation is successful. They are often classified together and are characterized on the ECG by a
continuous sinusoidal waveform without clear definition of the P-waves, QRS complexes or T waves.
The monomorphic sine wave is easily distinguishable (shown in Figure 5)

Figure 5 – Ventricular Flutter/Fibrillation (VF)

Task 2.

Figure 6 – Heart rate variability (produced in MATLAB)

In a person with a VT, a set of ventricular contractions are generated from a point within the
ventricles. And the heart rate rises from 100 beats per minute to 250 beats per minute (BPM) and
the outflow of the heart is severely disrupted. VT may also cause sudden arrest if not treated
immediately. VT is dangerous for two reasons: Firstly, this arrhythmia is usually caused when there is
already significant damage to the ventricles. Otherwise, VT usually causes the fatal state of
ventricular fibrillation because the ventricle muscle quickly stimulates.
From Figure 6, generated in Task 2 using MATLAB, it is clear that the heart rate is highly variable in
the first 7 seconds and for the entire second half of the recording (around 30 seconds in). During
ventricular tachycardia, the heart rate is usually anywhere between 120 and 300 BPM. However, it is
possible that the heart rate could be as high as 400 BPM, as seen in the figure, due to the ventricular
flutters/fibrillation. It has been shown that the heart rate can beat as fast as 400-500 BPM during VT.
This is significantly higher compared to the average 60-100 BPM.

The right bundle branch blockage may be accountable for the substantial decrease in the heart rate
after the first 7 seconds. The blockage of the electric signalling from the upper to the lower
chambers of the heart can slow the heart rate, leading to fainting, abnormal heart rhythms and
other serious complications. It is therefore a contributing factor to the VT subsequently seen.

Task 3.
The Poincaré plot represents the rhythm in the scatterplot. In a fit, healthy person, the Poincaré plot
displays a "torpedo" shape, as seen in Figure 7. This torpedo shape corresponds to a sinus rhythm. It
can be clearly seen that the torpedo is longer than wide, that the points within the diagram mostly
do not scatter and that they arrange centrally alongside a diagonal. [12] The length and width of a
Poincaré plot corresponds to standard time domain statistics, which is very useful.

Figure 7: Poincaré plot, sinus rhythm

Figure 8 – Zoomed version of Figure 9 Figure 9 – As it appears on MATLAB

Heart rate variability (HRV) is concerned with the analysis of the intervals between heartbeats. An
emerging quantitative-visual technique is the Poincaré plot, which takes a sequence of intervals and
plots each interval against the following interval. The geometry of this plot is categorized into
functional classes that indicate the degree of heart failure in a subject and has been shown to
distinguish between healthy and unhealthy subjects. Therefore, it is a valuable HRV analysis
technique due to its ability to display nonlinear aspects of the interval sequence. [13]

A successive RR interval plot was developed to analyse the arrhythmia in Record 207 and can be
seen in Figure 8 and Figure 9 above. The plot consists of a set of points with the x-value of (N)th RR
interval and the y-value of (N+1)th RR interval. The problem with analysing this dataset occurs when
attempting to quantitatively characterize the plot in order to acquire useful summary descriptors
that are independent of existing HRV measures. Researchers have investigated a number of
techniques: converting the two-dimensional plot into various one-dimensional views; the fitting of
an ellipse to the plot shape; and measuring the correlation coefficient of the plot. [13] Attempting to
fit an ellipse to this data would be impractical and not useful. The same goes for fitting a line of best
fit or measuring the correlation coefficient. These methods are insensitive to the nonlinear
characteristics of the intervals and evaluate the Poincaré plot as primarily a nonlinear technique.

Apart from time domain summary statistics, such as means and standard deviations, the Poincaré
plot is also capable of displaying the detailed beat-to-beat dynamics of the heart’s behaviour. From
analysing Figure 8, it is evident that there are small islands of points surrounding the main cloud,
possibly generated by ectopic rhythms that are separate from the sinus rhythm. In further studies,
these points should be removed from the RR interval record before calculating standard statistics
otherwise the quantities of interest will suffer serious distortion. The removal process is a tedious
beat-to-beat analysis that can only be partially automated and is, therefore, prone to human error.
After removal of ectopic intervals, the Poincaré plot can be examined for the presence of islands to
determine how successful the ectopy detection process was, and also to check if the removal
interpolation process has introduced serious distortion to the data. [13]

It is important to note that if the Poincaré plot shows a distinguishable pattern, this may suggest
different pathologies. An example of this is seen in Figure 10. This pattern is referred to as ‘Island
Pattern A’ and represents the presence of atrial flutter (with AV block) or atrial tachycardia (with AV
block). Overall, the Poincaré plot is helpful for proving atrial fibrillation and atrial flutter, breaks and
ectopic beats (VES, SVES). [12]

Figure 10 – Island Pattern A

Techniques do exist that characterize the dispersion of the points. An interesting study by Hnatkova
et al. has employed a unique density-based approach that has met with considerable success for risk
stratification after myocardial infarction. Cohen et al. have applied the central tendency measure to
second-order difference plots, and this technique could be applied to Poincaré plots also. [13]

Task 4.

Power spectral density estimation is a commonly used analytic technique for quantifying cardiac
autonomic regulation. Power spectral analysis (PSA) of HRV is a non-invasive technique, based on
ECG sampling of RR interval variation, providing a dynamic assessment of sympathetic and
parasympathetic tone and reflects the relationship between them. Most non-trivial analyses of heart
rate variability (HRV) depend on PSD estimation. The instantaneous heart rate time series used as
the bases of these analyses are sampled at intrinsically irregular intervals (if the RR intervals were
uniform, there would be no HRV to analyse). Standard methods for PSD estimation include Fourier
transform and autoregressive methods and operate on time series with uniform intervals between
samples. To apply these techniques to heart rate time series therefore requires that the series
be resampled at uniform intervals, which was unfortunately not possible in this study. [14]

Standard methods of estimating the power spectral density (PSD) of irregularly sampled signals such
as instantaneous heart rate (HR) require resampling at uniform intervals and replacement of
unusable samples. The Lomb periodogram is a means of obtaining PSD estimates directly from
irregularly sampled time series, avoiding these requirements. [14]

Figure 11 – Periodogram (produced in MATLAB)

The Periodogram in Figure 11 is a graph showing the power spectrum density (PSD) of a signal - the
corresponding power of the frequency components of the signal. The graph consists of power
((m/s^2)/Hz) in y-axis and frequency (Hz) in x-axis. Abnormalities in ECGs are presented through
different frequency components in their respective PSD. Its physiological interpretation can be
understood as the parasympathetic (cardio-inhibitory) branch of the autonomic nervous system
functions at a faster rate than the sympathetic (cardio-stimulatory) system. The higher-frequency
peak corresponds to the parasympathetic component while the slightly more complex lower peak
corresponds to the dominantly sympathetic component. [1]

Analysing Figure 11 is quite difficult as there are numerous peaks. Also, the y-axis is incorrect as the
values are nearly all non-negative. The peak identified at 0.35 Hz on the x-axis could be considered
as high frequency and therefore represents parasympathetic nerve activity. It is otherwise difficult to
interpret the graph. Usually there would be two to three main peaks which would be categorised as
follows:

Very Low Frequency (VLF) <0.04 Hz

Low Frequency (LF), 0.04–0.15 Hz

High Frequency (HF) 0.15–0.4 Hz

where HF peaks reflect cardiac parasympathetic nerve activity while the LF peaks reflect the
sympathetic component. [15]

Under conditions leading to sinus node dysfunction, such as congestive heart failure, power spectral
analysis of HRV may not accurately predict the underlying sympathetic or sympathetic control. It is
influenced by many factors such as age, sex, position, breathing, smoking, hour of the day and
medications. [16] This could be a contributing factor as to why the PSA has not fully worked.

Conclusion

In the minute duration that was chosen to be analysed, it was evident that the patient experienced
continuing ventricular flutters as well as RBBB and VT. When examining the entire record (30
minutes of recording), due to the PQ interval being quite inconsistent, it is fair to interpret that the
predominant rhythm is sinus rhythm with AV block. AV block is defined by ECG changes that include
a PR interval of > 0.20 without disruption of atrial to ventricular conduction.
It is important to note that there was an incident of bigeminy at the beginning of the record that was
not easily visible in Figure 3. It was accounted for in the plot waveforms seen below in Figure 12. As
previously mentioned, bigeminy is a type of heart arrhythmia in which the heart beats once normally
and once abnormally in quick succession, followed by a pause. It does not always cause symptoms
and is usually not treated unless a person experiences severe or frequent episodes. In this case, the
patient may be prescribed beta-blockers.

These drugs are designed to slow the heart rate and reduce the irritability of the heart’s electrical
system, which can help reduce arrhythmia symptoms. A consequence of this is the PR intervals are
prolonged (> 0.2 s) due to a delay in conduction between the atria and ventricles. It is possible that
the use of beta-blockers could be a contributing cause to the acquired AV block discussed but an
evaluation of the patient’s medication would be necessary.

Figure 12 – Plot waveforms of Record 207

We do know that the patient has been prescribed Quinidine, a class 1a anti-arrhythmic which
reduces the velocity of cardiac conduction. This medication is used to treat or prevent many types of
irregular heart arrhythmias such as atrial fibrillation. Quinidine can greatly improve the ability to
perform normal activities by decreasing the number of irregular heartbeats. The Health Products
Regulatory Authority (HPRA) notes that Quinine, an isomer of quinidine, should be used with caution
in patients with atrial fibrillation or other serious heart disease as it may cause
hypoprothrombinaemia. Quinine has dose-dependent QT-prolonging effects and caution is
recommended in patients with conditions which predispose to QT-prolongation and in patients with
atrioventricular block, such as Record 207.

The patient is also prescribed digoxin, a cardiac glycoside. This is a class of medications that inhibit
the Na+ K+ ATPase enzyme, increasing the force of heart contractions. It is the most commonly
prescribed cardiac glycoside and can be used to treat atrial fibrillation, atrial flutter, and congestive
heart failure.

One of the most widely studied drug interactions is the interaction between digoxin and quinidine.
Patients who receive the combination almost always will have a significant elevation in their digoxin
plasma concentrations. This poses a problem as digoxin excess and toxicity continues to be an
important clinical problem which may have potential associated arrhythmias and may be life-
threatening. Patients may also suffer digoxin induced toxicity, including anorexia, altered colour
vision, and mental changes.
The HPRA concludes that ‘quinine increases plasma concentrations of cardiac glycosides and
reduced dosage of concomitant cardiac glycosides such as digoxin to half the maintenance dose may
be necessary.’ [17] Although quinidine therapy is usually considered contraindicated in patients with
coronary disease (CD) who develop ventricular arrhythmias, this therapy may be lifesaving for these
patients developing arrhythmic storms attributable to polymorphic ventricular tachycardia.

To conclude, Heart rate variability (HRV) analysis attempts to assess cardiac autonomic regulation
through quantification of sinus rhythm variability. The sinus rhythm times series is derived from the
R-R interval sequence of the ECG. Relatively high frequency variations in sinus rhythm reflect
parasympathetic (vagal) modulation, and slower variations reflect a dominant sympathetic
modulation. Although Heart rate variability (HRV) has been widely applied in basic and clinical
research studies, its clinical application is very limited at present. These limitations are due to lack of
standardization of methodology and application to different non-comparable subsets of subjects, as
well as to the confounding effects of age, gender, drugs, health status, and chronobiologic
variations, among others. [18] Furthermore, in elderly subjects, a spuriously high value of certain
measures on computed HRV values may be due to the effects of erratic supraventricular rhythm due
to subtle atrial ectopy, wandering atrial pacemaker, or sinus node conduction abnormalities such as
congestive heart failure. [18] This is extremely significant to this study as the patient is 89 years old
and is speculated to possibly be suffering from CHD given the medications listed. (Quinidine and
Digoxin)
References
1. MEU33B10 Quantitative Physiology Lecture Notes

2. Ashley, Euan A, and Josef Niebauer. “Conquering the ECG.” Nih.gov, Remedica, 2019.
www.ncbi.nlm.nih.gov/books/NBK2214/.

3. “Sympathetic vs. Parasympathetic and Why They Matter.” Experience Family Chiropractic, 1 Feb.
2018, www.efchealth.com/sympathetic-vs-parasympathetic-matter/

4. “Bigeminy: Causes, Symptoms, and Treatments.” Www.medicalnewstoday.com, 20 Jan. 2022,

www.medicalnewstoday.com/articles/320072.

5. “Heart Ventricle Flutter - an Overview | ScienceDirect Topics.” Www.sciencedirect.com,

www.sciencedirect.com/topics/medicine-and-dentistry/heart-ventricle-flutter.

6. “PhysioBank ATM.” Archive.physionet.org, archive.physionet.org/cgi-bin/atm/ATM.

7. “MIT-BIH Arrhythmia Database Directory (Introduction).” Archive.physionet.org,

archive.physionet.org/physiobank/database/html/mitdbdir/intro.htm#symbols.

8. “MIT-BIH Arrhythmia Database Directory (Records).” Archive.physionet.org,

archive.physionet.org/physiobank/database/html/mitdbdir/records.htm#207.

9. SHUBIN, HERBERT, and DAVID C. LEVINSON. “The Deep S Wave in Leads V1, V2, and V3in Right
Ventricular Hypertrophy.” Circulation, vol. 18, no. 3, Sept. 1958, pp. 410–417,
10.1161/01.cir.18.3.410.

10. “Articles.” Cedars-Sinai, www.cedars-sinai.org/health-library/diseases-and-conditions/r/right-

bundle-branch-block.html.

11. “Premature Ventricular Complex (PVC). ECG Library Diagnosis. Life in the Fast Lane, Aug. 2018,
litfl.com/premature-ventricular-complex-pvc-ecg-library/.

12. “CDN-007 - AF Diagnostics - Custo Diagnostic News - Custo Med GmbH - Documentation.”
Customed.de, 2018, www.customed.de/docs/display/CDN/CDN-007+-+AF+Diagnostics.

13. Brennan, Michael, et al. “Do Existing Measures of Poincare Plot Geometry Reflect Nonlinear
Features of Heart Rate Variability?” Undefined, 2001, www.semanticscholar.org/paper/Do-existing-
measures-of-Poincare-plot-geometry-of-Brennan-
Palaniswami/06929de43a205a1f079b774cd2458c0d5ca0a181#paper-header

15. “Spectral Analysis of Heart Rate without Resampling.” Archive.physionet.org,

archive.physionet.org/physiotools/lomb/lomb.html.

16. ‘’The LF/HF ratio does not accurately measure cardiac sympatho-vagal balance’’, Frontiers of
Physiology. https://www.frontiersin.org/articles/10.3389/fphys.2013.00026/full
17. Cohen, Hagit, et al. “Power Spectral Analysis of Heart Rate Variability in Psychiatry.”
Psychotherapy and Psychosomatics, vol. 68, no. 2, 1999, pp. 59–66, www.jstor.org/stable/48510510.

18. Health Products Regulatory Authority Summary of Product Characteristics. 2021.

19. “Heart Rate Variability Analysis with the HRV Toolkit.” Archive.physionet.org,
archive.physionet.org/tutorials/hrv-toolkit/

Figures:
1. Conduction of Heart: https://meducation.net/resources/63559-Activation-of-atria-ventricles-
and-recovery-wave

2. ECG wave cycle: https://litfl.com/qt-interval-ecg-library/

3. Task 1 Produced in MATLAB (see appendix for code)

4. Ventricular Tachycardia: https://litfl.com/ventricular-tachycardia-monomorphic-ecg-library/

5. Ventricular Flutter: https://litfl.com/ventricular-flutter-ecg-library/

6. Task 2 Produced in MATLAB

7. Normal Sinus Rhythm: https://www.customed.de/docs/display/CDN/CDN-007+-+AF+Diagnostics

8. Task 3 Produced in MATLAB

9. Task 3 Produced in MATLAB

10. Island Pattern A: https://www.customed.de/docs/display/CDN/CDN-007+-+AF+Diagnostics

11. Task 4 Produced in MATLAB

12. Plot waveforms of Record 207 available at https://archive.physionet.org/cgi-bin/atm/ATM

Appendix

MIT-BIH Database, Record 207: Plotted Waveforms

MATLAB Code for Task 1-4

ECG_hrv = readmatrix("Record207.csv");

Hz = 360; %no. of samples/60

timestamp = 1/Hz;
k = length(ECG_hrv);
t = (0:k-1)*timestamp; %time

%%%%%%% Task 1 - R-R Intervals %%%%%%%

figure(1)
plot (t, ECG_hrv, 'Color', [0.6350 0.0780 0.1840], 'LineWidth', 0.5)
title ('R-R Intervals')
ylabel ('ECG (mV)')
xlabel ('Time (sec)')

height = 0.5; %height

distance = 1; %distance

[peak_amp, peak_time] = findpeaks(ECG_hrv, 'MinPeakHeight', height, 'MinPeakDistance',distance);

real_time = t(peak_time);

for i = 1:1:length(peak_time) - 1
peak_interval(i) = real_time(i + 1) - real_time(i);
BPM(i) = 60/peak_interval(i);
time_BPM (i) = real_time(i + 1);
end
%%%%%%%% Task 2 - Heart Rate Variability %%%%%%%%
figure (2)
plot (time_BPM, BPM, 'b-','LineWidth',1);
ylim([60 400]);
title ('Heart Rate Variability');
xlabel('Time (sec)');
ylabel('Heart Rate (bpm)');

for i = 2:1:length(peak_interval)
rr1(i-1) = peak_interval(i-1);
rr2(i-1) = peak_interval(i);
end

%%%%%%%% Task 3 - Poincare Plot %%%%%%%%

figure (3)
plot (rr2, rr1, 'k.')
title('Poincare Plot')
xlabel('RRI[i+1] (sec)')
ylabel('RRI[i] (sec)')

%%%%%%%% Task 4 - Power Spectral Analysis %%%%%%%%

figure(4)
periodogram(ECG_hrv, [], length(peak_amp), "onesided")
xlabel('Frequency (Hz)')
ylabel('Power (m/s^2)/Hz')