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

www.cardiocode.de

 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 [3]. 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 [4]. 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 [3]. 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;

PV1 – volume of blood entering the ventricle in early diastole phase characterizing the suction function of the ventricle, ml;

PV2 - volume of blood entering the ventricle in atrial systole phase characterizing the contraction function of the atrium, ml;

PV3 - volume of blood ejected by the ventricle in fast emptying phase, ml;

PV- volume of blood ejected by the ventricle in slow emptying phase, ml;

PV5 – volume of blood (a share of SV) pumped by ascending aorta as peristaltic pump, ml.

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;

- Elasticityofaorta;

- 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.

 Results.

        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:

?s/d = F(V)

where Ps/d – values of systolic and diastolic pressures in ventricular systole phases;

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

 

 

Deviationinoperationinaphase

Compensation response to adeviation in operation in the preceding or the succeeding phase

1

QRS phase cannot reduce the volume of the ventricles to trim them in accordance with the actual volume of blood received by them

The amplitude of SL phase is increased to enhance the tension of heart muscles in order to build up the normal systolic pressure

2

A pressure in the ventricle is below its normal level so that it requires a compensation by an increase in the suction function of the aorta to provide the normal blood circulation through the blood vessels.

The high amplitude of ?wave increasing the suction function of aorta.

3

The low amplitude of R wave characterizing a decrease in the contraction of the interventricular septum.

An increased amplitude of ?wave responsible for an increase in the amplitude of the ventricle contraction to trim the ventricles in accordance with the volume of blood actually received by them

4

The low amplitude of R wave in combination with the low amplitude of S wave determining a decrease in the contraction of the muscles of the interventricular septum and the ventricle walls producing a pressure fall up to a pressure below the required level in the ventricles.

An increased amplitude of ?wave responsible for an increase in the suction function of aorta. An increased amplitude of SL wave might be available, too, which is responsible for building-up the required pressure in the ventricles as a compensation mechanism correcting then an improper operation of QRS complex.

5

A deficient stroke volume due to general weakness in the contraction of the ventricles producing an improper difference in pressures between the aorta and the atrium.

U wave generation supporting the blood circulation through the blood vessels.

6

The curve shows a dip of Q wave indicating a loss of function of the atrioventicular valve.

It occurs in a combination with some other compensation mechanisms one of which is represented by U wave.

7

An oxygen deficit in tissues or a deficient flow rate of blood in the blood vessels in phase T?P?detected

?wave is generated closer to ? wave.

8

An increase in the time required for the injection of blood volumes from the atria into the ventricles to produce the required pressure level in the ventricles.

An extension of phase P?Q is available.

9

According to the RHEO curve, an increase in the pressure up to point L in phase SL is found.

The normal mechanism of the regulation of the minimum pressure in the aorta. The 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, the pressure is increasing in phase RS.

Blood leakage through the atrioventicular valve is available.

11

Doubled contraction frequency (vibration) of the muscles of the interventricular septum is available. R wave bifurcation is found.

Interventricular septum muscles contractility is weakened.

12

Doubled contraction frequency (vibration) of the muscles of the ventricles is available. S wave bifurcation is found.

Ventricle wall muscles contractility is weakened.

13

Disturbance in transportation of liquid through cell membranes of the muscles of the interventricular septum or the ventricle walls. Swelling of muscle cells.

A change in the amplitude of R wave in orthostatic testing for the interventricular septum muscle cells occurs, and, correspondingly, a change in the amplitude of S wave for ventricle walls is available.

 

 Table 2. Cardiac & cardiovascular system pathology cases - applicable diagnostics criteria

 

 

Diagnostics factor

Diagnosticscriteria

1

A weak pressure building-up in the aorta in phase Lj – fast emptying.

According to the RHEO curve, a pressure in phase Lj is under 0,5 of the normal pressure value.

2

Hindered venousflow.

According to the RHEO curve, a pressure in the aorta after dicrotic trough remains constant or is being built-up.

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 phase Lj.

A delay in building-up or failure to 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 is being registered.

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 ventricle walls.

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) conditions.

Short-time arteric pressure surges 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. Theyarecalledby us hemopulses.

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 - «locking-up”.

 


Conclusions.

     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 ?, 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.

 References

1. New Definition of Myocardial Infarction 
    JACC. – Vol. 36 N3. 2000. September 2000. – ?. 959-969. 
2. K.Caro, .T.Pedley, R.Shroter, W.Sid. The mechanics of the circulation. - M.: Mir, 1981. - 624 pages.
3. Theoretical Principles of Heart Cycle Phase Analysis. – Moscow,
    Helsinki: ICM Publishing House, 2007, 336 pages.