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

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 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

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Figure 3:Recovery of dept in anesthesia after administering a hypnotical drug.

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?

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

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Figure 4:ECG judged from the plethysmogram

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

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 plateau changes are generally known and their changes even more distinct. Probable difficulties are diagnosed more precisely.

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Figure 6:

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.

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Figure 7: system in the capnogram

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.

Due to greater variety and more frequent changes the enlarged T-peaks reveal 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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Figure 9: The enlarged ECG reveals more information.

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 by changes in blood “gasses”. The metabolism of the heart itself determines 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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Figure 10: Hose test registration Mercury line, Arterial line, ECG, plethysmogram

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).

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 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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Figure 12: towards the end of a general anesthetic.Capnogram. ECG. T-peaks

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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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