From

Ecg
to

tmeg

by Frans Heinen
(and Pieter Groot)
INDEX

FOREWORD .....……………………………………………………… Page 2

GENERAL INTRODUCTION…...………………………………. Page 2

ECG ……………………………………………………………………… Page 4 and 5

PLETYSMOGRAM …………………………………………………. Page 6

CAPNOGRAM ………………………………………………………. Page 7 and 8

REGISTRATION ………………………………………………….… Page 9 and

10

SUMMARY/PREDICTIONS.................…………………….. Page 11, 12 and

13

INFLUENCE ON LUNGS AND HART..………………………. Page 14 and 15

AFTERWORD.……………………………………………………….. Page 16

ADD-ONS I, II, III, IV, V

and VI

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The NVAM (Dutch union of anaesthesists assistants) celebrates its 25 th
anniversary.
On this occasion the following article reflects and is also a continuation of an
article in the very first publication of the NTVA(Dutch magazine of
anaesthesists assistants)
A second reason for this article is that I am nearing my retirement so my job
as a anaesthesists assistant is nearly done. It feels good to end my career
with an article about our profession and at the same time pass on some
knowledge and work experience even if they are somewhat controversial.

From ECG to TMEG

General introduction
The anaesthesist assistant guides and supports the patient throughout both
short and longer surgical procedures. We use several types of anaesthetic
procedures during the operations one of them is general anaesthesic.
Watching the monitors for long stretches of time and following the
registrations of it is part of our task. During the general anaesthesia it is
common to guard the : electrocardiogram, plethysmogram, capnogram and
ventilation pressure etc. on the monitor.
This gives us a huge amount of information and a variety of data. Some
changes in registration (bodily functions) cannot be interpreted and that is
what I would like to talk about in this article.

This concerns;

• changes on the top and bottom line of the curve, but also in the
different peaks and even in the iso- electric line.

• a wave movement throughout the total picture, outside as well as

within these points.

• the individual differences of these wave movements.

• the influence of the situation of the moment, surgical-technical as well

as anaesthetically (stability, form and changes in anaesthesia).

• The changes in amplitude, this is outside the extra wave movements,

who will also return in other curves.(plethismogram, arterial -and cvp-
curve and capnogram)

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 Figure 1; registration of different curves.
(A change in one curve is noticeable in the others as well)

You will notice the changes at the same time in all registered curves.
Take a closer look at the changes and you will notice a change earlier in a
different curve.
By interpreting these early changes one could react more adequately by
administering analgesics, muscle relaxants or other medications.

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ECG
The present ECG being registered is callibrated at: 1 mV is approximately 1 cm
vertical.
To observe amplitude changes in
the ECG more easily and make it
easier to interpret it is best to
work with a bigger amplitude
(curve). Later I will register 2
ECG’s parallel from one diversion
registered with the same
recorder, 1 normal and 1
extremely enlarged so as only the
R- peaks can be registered, the
bottom line is no longer visable.
Note these ECG’s are being shown
in a slow writing speed,25mm/min.
This writing speed gives us more
information about the vertical
changes in the ECG. Electronically
these differences vary from
+10mV until -90mV.

During ECG registration we record

amplitude changes in the R- peaks
with each patient.

These amplitude changes are

easier to detect during a quite
phase. During (temporally) non
-ventilation we do notice changes
in the R- peaks, but without a
regular pattern. During ventilation
groups of R- peaks do
develop.With each next ventilation
this pattern returns, however with
a small change. After 3 or 4
ventilations the first changes of
groups of R- peaks return, thus
creating a repetitive pattern. After
±1½ minute, possibly the time it
takes to circulate the total blood
volume, we can see a repetition of
the previous pattern. In the P-
peaks we also notice a return of
the same P-peak every 4th or 5th
ventilation. This also shows a
pattern. All amplitude changes in
R-,P-,T- peaks are different and
don’t change at the same time in
respect to each other in the cycle.

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Figure 2; Note similarities in shape on
plethysmogram as well as ECG. (also
add-on IV)

Question that arises is whether this caused by:

1. changes in breathing (technical-mechanical

changes)
2. changes in diffusion(physiological changes)

We can well say the amplitude changes in the R-

peaks are not caused by technical-mechanical
changes, by recording at the same time 2 ECG’s
from the same diversions( derivation 2 according to
Einthoven)with the same patient. Being one
diversion from the thorax, (heart area) and the
other diversion peripheral(hands, feet c.q. fingers
and toes) Thus excluding mechanical expansion of
the thorax in the peripheral ECG.

Possible changes, by changing position of the heart

versus the place of the diversions ,can be excluded
because the amplitude- changes also occurring in
other curves.

Both ECG’s keep showing amplitude changes

caused by ventilation.

In conclusion: Amplitude changes during

spontaneous breathing or mechanical ventilation
originate during diffusion between lungs and blood.
The pulmonary function, diffusion/perfusion, will
show up on the ECG. The ECG in COPD patients
show specific changes in the R-peaks .

Diffusion of blood gasses correspond again with

pressure changes which are being registered by
amplitude changes in the curves.

There is an enormous diversity in changes of R-

peaks to be seen. They differ in each patient and
are absolutely individual.

The amplitude-change, wave movement:

• depends on the instant
• depends on a stable situation, surgically as
well as anaesthetically
• depends primarily on metabolic changes
• changes under the influence of: pain, muscle
relaxants, changes of position and the depth
of anaesthesia
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 • is being influenced by changes in the pressure of ventilation, frequency in
ventilation IE-ratio (Inspiration/Expiration)
• changes after administering drugs(hypnotics, muscle relaxants, analgesics
ect.)
• is being influenced by other causes such as the patients age , psyche ,
COPD ,ect.

There are no two people with the same changes in amplitude

Figure 3:Recovery of dept in

anesthesia after administering a

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 Plethysmogram
In the registration of the plethysmogram it appears that the start of the
plehtysmogram regularly follows the T-peak of the ECG. This registration changes
during the course of the anesthesia.

Strongly enlarged peaks in the plethysmogram show the exact model / configuration
as do the enlarged T-peaks on the ECG.

Amplitude and
configuration are two
different things:

-Each configuration-
change in the T-peak is
followed by a same
configuration-change in
peak of the
plethysmogram.

-All T-peaks change(as

do the R-peaks)in their
amplitude according to a
set system.
These amplitude
changes in the
plethysmogram and T-
peaks do differ but do so
at the same moment. On
different types of
equipment (either
integrated or detached )we see the same changes.
Question arising: Is this normal, a deviation in equipment, or (considering the ECG) a
physiological fact?

Figure 4:ECG judged from the plethysmogram In case of the plethysmogram

being equal to the T-peaks, we
might have to look at the plethysmogram to judge the ECG.

Figure 5: Configuration of T-peaks is equal to configuration of the

plethysmogram.
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Capnogram
The capnogram shows us primarily an expiratory curve in volume%. The curve of the
capnogram is absolutely personally bound. The possible electrical influence is
excluded by using different brands of equipment and registering on separate
monitors and recorders.

Each person has his/her own capnogram

The capnogram shows many different varieties especially on the plateau. To be able
to interpret the capnogram in an even better way we can use here the slow
registration speed of 25mm/min. and/or enlarge the amplitude until only the plateau
is being registered. The plateau in the capnogram shows the diffusion-perfusion part
of the ventilation cq.
exchanges of gasses .This is
the most important part.

By enlarging the capnogram

(±4x) we notice an enormous
variation in height of the CO2
level and the changes of the
plateau in the capnogram.
During slow registration of 25
mm/min it shows the change
in frequency of height even
better. Each change starts
slowly but is of great
importance in capnogram as
well as in for example ECG
and plethysmogram.

These changes are subject to

surgical-,technical-,
anaesthetical-or patient bound
changes . For example;
deflating the Tourniquet after
external vascular occlusion applied to a limb, loss of efficacy of muscle relaxant, or
change in position of the patient. The contractions of the heart muscle (cardiac
oscillations) show up on the plateau of the capnogram as well. A separate group
within the changes of the capnogram are the COPD patients. Within this group the
Figure 6: plateau changes are generally
known and their changes even
more distinct. Probable
difficulties are diagnosed more
precisely.

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Even the capnogram has its own system

In a stable condition the plateau slowly changes its shape, until after 3 or 4
ventilations the first curve returns. Just as on the ECG we see the forming of groups
of capnograms in which changes slowly evolve. Besides a system in the capnogram
and ECG of the same patient all other registrations (plethysmogram ect.)participate;
they interconnect in a precise way but don’t have to run synchronous.

Figure 7: system in the capnogram

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Registration
The current ECG being registered is verified at : 1 mV approximately 1cm vertical,
registration speed around 25 mm/sec. To detect and interpret amplitude changes in
the ECG in a simpler way it is best to work with an enlarged amplitude (curve). Such
an ECG is very informative. A writer(recorder) is being used for registration. The ECG
recorder speed is 25 mm/min=2½cm/min. This slow speed is actually indispensable
to be able to detect amplitude changes in the curves from the ECG, pletysmogram,
arterial curve, CVD, as well as changes in the capnogram. By regularly registering in
between at a normal speed, it is easier to interpret the trend . All changes appear
also at the trend speed of 25mm/min. More facts surface at a slow registration
speed which could not be followed at a higher speed.(for example a vertical change
of 1mm/5min); to judge at value is impossible at this speed.

Recording an ECG at the same time, central as well as peripheral , gives a signal
almost simultaneously, note! not at the same time! The peripheral ECG is a fraction
behind.

Example: A patient having vein problems who is known with a occlusion in the aorta,
we record before the operation a central as well as a peripheral ECG at the same
time. At this moment there is a difference in measurement of amplitude changes.
After the bypass operation we also notice in the peripheral ECG a larger amplitude
change but changes the time between both ECG’s as well.

The state/condition of the vascular system influences the amplitude of the

ECG

The real reason of calibration of the ECG at 1mV± 1 cm is unknown. This

calibration is probably adopted out of need of a default calibration which shows a
neat curve who can be equally interpreted at any place.

The changes of peaks in the enlarged ECG are out of proportion

The T-peaks start playing a more prominent role. Especially the T-peak becomes
more enlarged then the R-peak, which does not participate in enlargement. The
shape of each T-peak is different and changes like the R-peaks in groups with each
ventilation; which reappear
later in the same
configuration of the next
group.

When registering only the T-

peaks in a strong enlarged
ECG, we see amplitude
changes as well. These
amplitude changes are not
equal to the R-peaks and
here we notice more
changes with larger wave
movements which result in a
much greater variety. (Add-
on I and II)

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Figure 8: Amplitude changes in the T-peak are
more profound in enlarged ECG.

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Due to greater variety and more frequent changes the enlarged T-peaks
reveal more information.

Figure 9: The enlarged ECG reveals more information.

This system again depends on several influences such as surgical-technical,

anaesthesiological or patient related matters.

Following previous observations some questions arise:

• Which is the right amplitude to review and register the ECG?

• Is the default calibration and assessment still the right one?

• Is there a need to link the mechanical function of the heart and the electrical
signal of the heart?

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Summary/predictions
Can we conclude perhaps, with previous information, the readings of ECG,
capnogram, plethysmogram basically being the same? To date we cannot interpret
their true value. Previous chapters show us the existing interrelationships but the
correct technique to draw conclusions from one given fact has not been found yet.
Looking at this from an electrical point of view, a high voltage does not mean much
in case of none existing or very low currant. Physiologically we also speak of an
electrical current. Why accept the electrical voltage (ECG/EEG) and not accept the
electrical current? The amount of electrons(the current of electrons)can be
calculated. Wherever there is a current one finds a resistor. From these given facts
we are able to measure current and resistance in the bloodstream. What is the use of
all this? To understand the functioning of the human body from a basic point of view.
The human body is equipped with a co-ordinate system , which controls everything
and from which we can reason its behavior/function in a logical way. With this in
mind it should be possible to withdraw simply more information from one given fact.
To be able to do so all we need is to take a fresh look at all the old given facts and
approach them afresh without current conservative theories.

Test

Put a water filled flexible hose from app. 12 meters long on the ground and
seal both ends. Connect an ECG , plethysmogram and arterial pressure
electrode at the end of the hose and connect the leads with a
monitor/recorder. Apply a strong/short impulse at the beginning of the
hose. The monitor(recorder) shows a
peak wave in all curves.

Considering the outcome of the hose-test

and identifiable resemblances between
the different curves, shouldn’t we revise
the interpretation of the ECG and add new
values to it? It would look as follows: The
rising line in the T-peak would become the
output of the heart and the iso-electrical
line the re-polarization phase. The R-peak
would become the blockage in the AV-
ganglion. Iso-electric does not mean
horizontal. Physiologically and electrically
speaking a lot of things are happening.
The ECG becomes a three dimensional
fact, in voltage, current and resistance,
which fits in well with the metabolic
changes in the heart and body, by which
the discharge is continued throughout the
body via the bloodstream together with the electrical conduction. In the chapter ECG
we mentioned how amplitude changes in the ECG originate primarily by
physiological changes of the heart, caused Figure 10: Hose test registration
by changes in blood “gasses”. The Mercury line, Arterial line, ECG,
plethysmogram
metabolism of the heart itself determines

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the changes of amplitude in the ECG. An independent mechanism under direct
cerebral influence.

A contraction of the heart muscle results in an extra electrical wave on top

of the heart power(heart action)

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Changes in the ECG could be primarily cardiac origin, cerebral or pulmonal, or
originate from the system from which and for which the heart should be the
“pump”(motor). A mechanical wave originates, caused by the pump function of the
heart, contraction and output itself and the metabolic change. At the same time an
extra electrical wave cq. voltage/current is formed precisely by the mechanical
wave itself, think of the ” hose-test “; theoretically speaking that is just the way it is.
As If an extra impulse on top of the heart action. All must run in cadence; if not,
resistance is met.

The conduction itself, mechanical and electrical, works fortifying. This extra
voltage/current potency given fact has to fit in with the potency from the heart itself,
the so called electrocardiogram, assuming the ECG originates primarily from the
heart. The ECG is also to be recorded peripherally; no extra waves or potencies to be
measured here. In this case, would we rather talk about an ECG or TMEG?

TMEG.(Total Metabolic Electro Gram)

The continuation/conduction of the ECG has to fit in with the metabolic changes,
arterial towards venous. It has to fit in with the total body periphery, the body in
total(Does the heart beat or the body, or both?) Conduction is primarily being
continued throughout and with the bloodstream. The exchange of gasses in the cell
as well as in the entire body should fit into the system, call it the ECG, but even
better the TMEG. The metabolic change in the periphery(in total)has to accompany
the same way and with the same mechanical change(from the pump function of the
heart);that is a fact. The heart does not necessarily have to be positioned primarily
in-between the electrical leads to be recorded. We can take readings from the left
upper arm, abdomen or elsewhere. You can imagine measuring two frequencies of
the ECG on the human body , on condition that they are calibrated and/or run in
cadence. The influence both ways , physiology of the lungs, and function of the heart
is being set by the heart rate or part of the heart rate, also by part of the
electrocardiogram. This adjustment which is extremely refined shows on the ECG.

The given fact of a certain system existing in the amplitude changes, does raise
questions: e.g. is this the total gas exchange of the total blood volume and can we
even derive and calculate the cardiac output from it? The fact only one system exists
also answers questions, e.g. everything is minutely tuned/intertwined and they
interact; ventilation, function of the heart, pressure system and conduction. Think of
the simultaneous changes in ECG, plethysmogram and amplitude. Not in the same
manor, but at the same time.

In that case the ECG, including current abnormalities, could be primarily or partially a
cerebral anomaly, with a variety in causes: anatomical, somatically, psychical or
combined and/or different causes. In case of the ECG originating cerebrally, the heart
could possibly function as an amplifier with and due to its own metabolism. In this
case a mal function of the heart itself could play a great part. When a situation like
this one occurs, the heart has to react, to compensate the occurring problems in the
human body(could be metabolic, mechanical or psychical).The cardiac pump function
is an extremely refined system, in which disorders may occur. Thinking of vein
blockage and changing amplitude of the ECG( deceased patient with electrical
activities of the heart muscle with an ECG but without a functioning heart: peripheral
death).

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 All amplitude changes in R-,T-,P-peaks in the system aren’t equal and don’t change
at the same time either in respect to one and other. Concluding the changes in
amplitude are caused by the metabolism of the heart. In case of these changes being
equal we would find a set pattern.

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Figure 11: Effects in registration after discontinuing Tourniquet.
Release Tourniquet. Ventilation pressure curve. Enlarged capnogram(without basic
line)P-peaks.T-peaks. Enlarged ECG.Plethysmogram
Impact on lungs and heart
During the final stages of general anaesthetic ,at the moment of artificial ventilation
changing to spontaneous breathing, we always find great amplitude changes in the
ECG particularly in the T-peaks . During the beginning of the general anaesthesia
they are visible as well but in a different pattern. What does this look like? After the
total blood volume has finished one cycle in ±1½ minute the same
system(pattern)returns in e.g. the R-peaks. This is impossible in 3 or 4 ventilations ,
while the same capnogram pattern does return. In the remainder-lung volume there
still is a reasonably stable concentration of oxygen and CO2 with tiny differences per
heartbeat and ventilation. It is a physiological happening based on old-age when we
adjust the ventilation to get the best possible heart-function. The physiological
adjustment is disturbed with artificial ventilation/ breathing in respect to heart
frequency. There still is a noticeable change in heart rate but spontaneous breathing
is impossible.(disadvantage of artificial ventilation which is not without risks) The

Figure 12: towards the end of a general anesthetic.

Capnogram. ECG. T-peaks

fine tuning in the system of our functioning is temporarily changed by e.g. artificial
ventilation.

There are visible changes in the groups of R-peaks in patients with severe lung
deviations. In this lies the proof of amplitude changes in the ECG primarily caused by
physiological changes in the heart due to changes of “gasses ”in the blood. These
aren’t just age related but the general condition of the lungs is responsible.

COPD and smoking have an absolute impact on the heart muscle

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The enormous diversity of amplitude changes in the ECG, are individually connected.
These can be separated in multiple groups ( Take note! Comparable amplitude of the
ECG but not entirely). Take for instance the elderly patient , COPD patients,
smokers but also children , who were administered a fluothane based general
anaesthetic in the past.

After adjustments being made to the ventilation, to optimize the heart function, we
could consider changing the patients positioning, e.g. in case of a heart attack. This
could be left- or right Trendelenburg position, head raised, or feet high, ect. We
know for example that Trendelenburg position can be effective. How would this fit in
with the fine tuned ventilation opposed to the functioning of the heart , and vise
verse, and the metabolic functioning? Is it therapeutically responsible to ventilate a
patient, suffering heart failure and severe to no lung function, at once after
intubation with 100 % oxygen? What would be the consequences? For instance in
patients who upon arrival, pass away after intubation and being administered 100 %
oxygen? The body compensational mechanism is going at full speed, by acting
promptly and adequately one adds another problem which can be fatal for the
patient. Supporting ventilation and a slow build-up in ventilation, combined with
other therapies, will show you a better result.

It is possible that a cardiac dysfunction is actually a primary pulmonary problem,

considering the function and anatomy of the lungs and its influence on the ECG. The
enormous vascular system and lungs make it possible for the heart to function or
dysfunction. Each breath changes the ECG in amplitude. We still don’t combine all
information, we examine blood pressure, breathing, heart rate ect. separately, where
as this is all interconnected(one). You cannot look at, study, assess or treat the
given facts separately. Medical specialists don’t exist anymore.

Epilogue
For over 25 years I have worked as a anaesthetic assistant. During this period the
article has evolved. It feels good to end my career with this article. I would like to
thank Nel Teunisse, who was brave enough to start the typing although I have a
terrible handwriting . And also Pieter Groot for further development and adding final
touches to the article, as well as many other people who supported me in all this
time.

Frans Heinen.

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-20-
Registratie apparatuur niet meer toereikend Bijlage 2

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T-top verandering bij toediening 100ml Nacl 0,9% onder druk Bijlage 3

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 Overeenkomsten in R-toppen groepjes Bijlage 5

Veranderingen in de T-toppen bij ventilatiestop Bijlage 6

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