Innovation in cardiology. A new diagnostic standard establishing criteria of
quantitative & qualitative evaluation of main parameters of the cardiac &
cardiovascular system according to ECG and Rheo based on cardiac cycle
phase analysis (for concurrent single-channel recording of cardiac signals
from ascending aorta)
M.Rudenko, O.Voronova, V.Zernov, K.Mamberger, D.Makedonsky,
S.Rudenko, S.Kolmakov, K.Weber
?Cardiocode– Finland?, Kuopio, Finland
Introduction. Over more than 50 years the theory of functioning of the cardiac & cardiovascular system remained unchanged. As a rule, all conventional diagnostics
methods are based on statistics data on changes in shapes of cardiac signals only, so that
it is impossible to determine the relevant cause-effect relations with respect to their
formation [1,2]. But a theory of elevated fluidity of liquid offered twenty five years ago
makes it possible to develop an innovative method of the phase analysis of the cardiac
cycle . The successful application of the said method in researches for the last 5
years has enabled a practical implementation of an indirect measuring concept with
respect to volumetric hemodynamic parameters . By evaluating hemodynamic
parameters upon examination of more than 3000 patients the Authors have identified
the actual cause-effect relations in formation of the respective ECG & Rheo so that new
capabilities are being offered in cardiology. This article should be treated as a logic
result reflecting a long-term experience accumulated in large-scale investigations
covering the complete cardiac & cardiovascular system operation.
Research objective. To provide a considerable increase in the quality and the reliability of diagnostics in cardiology.
Method. An application of hemodynamics theory based on the model of the liquid flow maintained in a living body which is characterized by low energy consumption
makes it possible to identify the cause-effect relations of the formation of the ECG and
the Rheo recorded from the ascending aorta . That is a prerequisite to determine the
phase mechanism of the heart operation which comprises ten phases, and further to
obtain data on interactions between the quantitative volumes of blood and, as a response
to it, the contraction function of the muscles of the heart and the blood vessels in every
cardiac cycle phase.
It has been found that the main characteristics in hemodynamics are as follows:
SV - stroke volume of blood, ml;
MV - minute stroke volume of blood, l;
PV – volume of blood entering the ventricle in early diastole phase characterizing 1
the suction function of the ventricle, ml;
- volume of blood entering the ventricle in atrial systole phase characterizing PV2
the contraction function of the atrium, ml;
PV - volume of blood ejected by the ventricle in fast emptying phase, ml; 3
PV- volume of blood ejected by the ventricle in slow emptying phase, ml; 4
PV – volume of blood (a share of SV) pumped by ascending aorta as peristaltic 5
The volumes of blood listed above are pumped by the heart within every cardiac cycle. Every parameter mentioned above can be treated as a final result of the operation of the heart in its cardiac cycle, and a complete set of the above parameters is capable of producing an integrated picture of the actual operation of the heart.
The formation of the required volumes of blood in every phase of the cardiac cycle depends on the performance of the segments of the heart being involved into the operation. Their functions can be evaluated with use of the phase analysis of the cardiac cycle. The main functional parameters to be evaluated on the qualitative basis are as follows:
- Function of aortic valve;
- Specific anatomic features of aortic valve;
- Elasticity of aorta;
- Availability / non-availability of ascending aorta dilatation;
- Availability / non-availability of narrowing of aorta mouth;
- Contractile function of myocardium;
- Contractile function of interventricular septum;
- Conditions or status of venous flow;
- Availability / non-availability of pre-insult (pre-blood-stroke) conditions;
- Availability / non-availability of stenosis of large blood vessels;
- Conditions or status of lungs function.
The favorable combination of the qualitative and quantitative phase analysis of the cardiac cycle allows determining the cause-effect relations of the performance of the heart within a wide range of the heart operation conditions from its norm up to extreme pathological cases. For this purpose, boundaries or transient conditions of the norm and pathology have been clearly defined, too. All this makes possible to detect the slightest deviations from the normal performance of the cardiovascular system. So, of great importance is the possibility to evaluate the performance of the heart of sportsmen.
The results of our investigations show that, when considering a separate cardiac cycle, the function of every subsequent phase is corrected by the value of a deviation from the function norm in the previous phase. Such interaction is responsible for establishing a compensation mechanism in the phase operation of the heart and the blood vessels. Therefore, the phases responsible for filling the heart with blood effect those phases that produce the initial minimum and the maximum arteric pressures,
respectively, and vice versa. So, if pathology is available, then it is important to identify
that phase which is responsible for origination of deviations in next phases. On the face
of it, it seems to be an intractable problem. But a solution might be offered in this case
by an experienced doctor who is trained in using the cardiac cycle phase analysis
procedures in the proper way.
In general, the dependence of the functions of the systole phases on current results
of the operation of the diastolic phases can be described as follows:
Р= F(V) s/d
where P – values of systolic and diastolic pressures in ventricular systole phases; s/d
V – volume of blood entered the ventricles in diastolic phase.
So, this compensation mechanism is a tool in the qualitative analysis of the cardiac
signals recorded as the relevant ECG and Rheo curves. Upon analysis of the measured
hemodynamic values, first, a phase shall be identified where deviations from the normal
values occur. Then, possible causes of the deviations shall be evaluated. If all values are
within their respective norms, the entire complex of the phase structure shall be
analyzed for the purpose of the qualitative evaluation of the stability in the operation in
every phase in question.
Table 1. Compensation mechanism in cardiac cycle structure
Deviation in operation in a phase Compensation response to a deviation in
operation in the preceding or the
1 QRS phase cannot reduce the The amplitude of SL phase is increased to
volume of the ventricles to trim enhance the tension of heart muscles in
them in accordance with the order to build up the normal systolic
actual volume of blood received pressure
2 A pressure in the ventricle is The high amplitude of Т wave increasing
below its normal level so that it the suction function of aorta.
requires a compensation by an
increase in the suction function
of the aorta to provide the
normal blood circulation through
the blood vessels.
3 The low amplitude of R wave An increased amplitude of Т wave
characterizing a decrease in the responsible for an increase in the amplitude
contraction of the of the ventricle contraction to trim the
interventricular septum. ventricles in accordance with the volume of
blood actually received by them
4 The low amplitude of R wave in An increased amplitude of Т wave
combination with the low responsible for an increase in the suction
amplitude of S wave determining function of aorta. An increased amplitude
a decrease in the contraction of of SL wave might be available, too, which
the muscles of the is responsible for building-up the required
interventricular septum and the pressure in the ventricles as a
ventricle walls producing a compensation mechanism correcting then
pressure fall up to a pressure an improper operation of QRS complex.
below the required level in the
5 A deficient stroke volume due to U wave generation supporting the blood
general weakness in the circulation through the blood vessels.
contraction of the ventricles
producing an improper
difference in pressures between
the aorta and the atrium.
6 The curve shows a dip of Q It occurs in a combination with some other
wave indicating a loss of compensation mechanisms one of which is
function of the atrioventicular represented by U wave.
7 An oxygen deficit in tissues or a Р wave is generated closer to Т wave.
deficient flow rate of blood in
the blood vessels in phase TP кн
8 An increase in the time required An extension of phase PQ is available. к
for the injection of blood
volumes from the atria into the
ventricles to produce the
required pressure level in the
9 According to the RHEO curve, The normal mechanism of the regulation of
an increase in the pressure up to the minimum pressure in the aorta. The
point L in phase SL is found. pressure can be built up to provide a
compensation for an increase in resistance
of the blood vessels so that the normal
blood flow after T wave is being produced. 10 According to the RHEO curve, Blood leakage through the atrioventicular
the pressure is increasing in valve is available.
11 Doubled contraction frequency Interventricular septum muscles
(vibration) of the muscles of the contractility is weakened.
interventricular septum is
available. R wave bifurcation is
12 Doubled contraction frequency Ventricle wall muscles contractility is
(vibration) of the muscles of the weakened.
ventricles is available. S wave
bifurcation is found.
13 Disturbance in transportation of A change in the amplitude of R wave in
liquid through cell membranes of orthostatic testing for the interventricular
the muscles of the septum muscle cells occurs, and,
interventricular septum or the correspondingly, a change in the amplitude
ventricle walls. Swelling of of S wave for ventricle walls is available.
Table 2. Cardiac & cardiovascular system pathology cases - applicable diagnostics
Diagnostics factor Diagnostics criteria
1 A weak pressure building-up in the According to the RHEO curve, a
aorta in phase Lj – fast emptying. pressure in phase Lj is under 0,5 of
the normal pressure value. 2 Hindered venous flow. According to the RHEO curve, a
pressure in the aorta after dicrotic
trough remains constant or is being
3 Stenosis of aorta is available. According to the RHEO curve, after
its maximum, there some
disturbances as low-amplitude
changes are recorded. 4 A delay in opening of aortic valve in A delay in building-up or failure to
phase Lj. build-up the required aortic pressure
in phase Lj.
5 Aorta mouth narrowing A delay in building-up arteric
pressure as a “step” at the leading
edge of the RHEO when point j is
6 Aortic dilatation A decrease in the pressure on the
RHEO curve in phase Lj, when
expecting a pressure increase. 7 Passivity in contractility of the S wave is not available.
8 A decrease in aorta elasticity. According to the RHEO curve, the
apex is either flat or bifurcated. 9 Pre-insult (pre-blood-stroke) Short-time arteric pressure surges
conditions. which occur spontaneously on the
RHEO curve at different time points
of closing of the valves. As critical
should be treated high amplitudes of
pulses. They are called by us
10 A sign of sudden cardiac death. An abnormal single QRS complex
showing a very high amplitude that
is accompanied by a large stroke
volume and a high amplitude of the
contraction of the interventricular
septum followed by its spasm -
There are three nerval centres which are responsible for the complete control of
the heart. They are as follows: the low-pressure baroreceptors located in the aorta;
the SA node – the sinoatrial node in the right atrium and the AV node – the
atrioventricular node. An arteric pressure decrease up to its lower level is taken by
the low-pressure baroreceptors which are initiating in this case the operation of the
SA node. Thereafter the following processes shall be started: generation of wave Р,
injection of the required volume of blood from the atrium into the ventricle in
order to close the atrioventricular valve. This valve is being closed as soon as
pressure levels of 10 and 5 mm hg in the left atrium and right atrium, respectively,
have been reached. This point of time corresponds to point Q on the ECG curve.
The complete closing of the atrioventricular valve establishes the required
conditions for building-up of the proper level of the final arteric pressure. Upon
closing of this valve, the AV node is starting its operation: this node is responsible
for the generation of QRS complex. The purpose of the operation of this node is to
provide the contraction but not the tension of the muscles of the interventricular
septum and the ventricle walls sizing in such a way the required geometric volume
for receiving blood to be pumped therein. In tension phase SL, an appropriate
muscle pressure of the muscles is being built-up that is applied to the volume of
blood available in the ventricles. This determines the level of the maximum
systolic pressure in the aorta upon receipt of the stroke volume of blood by the
aorta. In phase SL, and sometimes in phase RS, too, there is a mechanism of the
regulation of the minimum diastolic pressure in the aorta in operation. The volume
of blood circulating within the entire cardiovascular system is a constant value. In
a pathology case, when some blood vessels show their pathological narrowing, a
minor quantity of blood is leaking into the heart valves increasing in such a way
the minimum aortic pressure in the aorta which results, in its turn, in an increase in
the maximum pressure in general, since the stroke volume of blood is added to the
said leakage. In essence, this mechanism works as follows: a certain volume of
blood is leaking into the aorta via the closed valve. This is indicated by a slight
increase in the arteric pressure on the RHEO in phase SL or up to point S in phase
RS. The said leakage seems to be quasi excessive volume in the phase of the early
diastole when the ventricles are filled with blood, due to narrowing of the blood
vessels and an increase in their flow resistance. This quasi excessive volume of
blood cannot stagnate in the blood vessels and is being displaced then due to the
above mentioned factors. It is the same minor volume of blood that enters the heart
and creates an effect of the excessive volume. Therefore, this leakage is
transported by the heart practically unhindered throughout all phases of the cardiac
cycle. The circulation of this volume can be stopped upon normalization of the
blood vessel resistance only provided that the proper distribution of the said
excessive volume within the entire capacity of the blood vessel system is obtained.
All this considered, it can be concluded that the main control mechanism in the
heart operation is the respective pressure level reached in every cardiac cycle phase.
The different pressure levels, in their turn, depend on the actual phase-related
volumes of blood.
Now these investigations in the field of the cardiac cycle phase mechanism are
being continued by us.
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