NON-INVASIVE MEASUREMENT OF BLOOD FLOW PARAMETERS

Abstract: The present invention relates to the non-invasive measurement of internal parameters of blood organs such as the heart central venous pressure. An electronic cuff apparatus (1) connected to a non-invasive cuff device (2) measures both the systolic (S) and diastolic (D) blood pressures and a non-invasive measuring device (13) measures the pulse rate (P). The electronic values of these variables are sent to a central controller (4) along a bus (3). A keyboard (7) connected to the controller (4) inputs data of the subject so as to retrieve values of M and C from a ROM (6). Using the variables of (P), (S) and (D) in the equation CVP = (M.S<2>/P(S - D)) - C, a microprocessor CPU (8) calculates values of CVP which can be displayed on a screen (9).

Description: NON-INVASIVE MEASUREMENT OF BLOOD FLOW PARAMETERS The present invention relates to the non-invasive measurement of internal parameters of blood organs, for example venous pressure and flow in various blood carrying organs of a subject. The invention relates more particularly to the non-invasive measurement of the heart central venous pressure. The central venous pressure (CVP) of a subject is a useful physical quantity to know in the medical field. For example, during the management of a critically ill subject or a subject under general anaesthetic, regular and accurate measurements of the pressure and volume of that subject's circulation are required. To measure the central venous pressure using known methods requires physical invasion of the subject. These invasive methods require not only surgical skill by medical staff carrying out the measurements but also sophisticated and expensive medical equipment. In third world countries, for example, such skill and equipment are generally in short supply. Known non-invasive methods relate only to the measurement of blood pressure and pulse rate. No such methods are known for measuring the central venous pressure. Indeed, no such non-invasive methods exist for measurement of the venous pressure or flow in the blood organs of a subject. It is an object of the present invention to overcome the disadvantages inherent in the known measurements of the central venous pressure, and to provide an apparatus by which values for venous pressure and flow can be obtained for a number of blood carrying organs of a subject. According to one aspect of the present invention, there is provided a non-invasive method for evaluating blood related internal parameters of blood organs of a subject, the method comprising:- a) monitoring the rate of beating P of the heart of the subject; b) monitoring the systolic blood pressure S; c) monitoring the changes (S - D) in the pressure of the subject ' s blood during beating of the heart; d) utilising a value X for evaluating -said internal parameters; wherein the value X is represented by the equation:- X = S 2 /P(S - D) According to another aspect of the present invention there is provided apparatus for non-invasively evaluating the blood related internal parameters of blood organs of a subject, the apparatus comprising:- means for obtaining measurements corresponding to the pulse rate P of the subject; means for obtaining measurements corresponding to the systolic blood pressure S of the subject; means for obtaining measurements corresponding to the changes (S - D) in the pressure of the subject's blood during beating of the heart; evaluating means utilising a value X for calculating said internal parameters; wherein the value X is represented by the equation:- X * = S 2 /P(S - D) . In a preferred embodiment, the method and apparatus of the invention can provide the central venous pressure CVP from measurements of systolic blood pressure S, diastolic blood pressure D and the pulse rate P together with already known values of M and C. This has the advantage that all of these variables can be measured non-invasively so that central venous pressure values can be determined using non-invasive measurements. Thus, in order to determine the central venous pressure, conventional blood pressure and pulse measuring equipment can be used which do not require a high degree of medical skill. An example of the present invention is described in detail below with reference to the accompanying drawings, in which:- Figure l shows a graph of central venous pressure in cmH 2 0 against values of a parameter X; Figure 2 shows a graph of central venous pressure in cmHg against values of the parameter X; Figure 3 shows a graph of the central venous pressure plotted against the pulse rate for a given blood pressure using the formula of the present invention; Figure 4 shows a schematic view of an apparatus embodying an aspect of the present invention. Figure 5 shows a graph of the fluid load factor plotted against the pulse pressure Figure 6 shows a graph of the central venous pressure plotted against the systolic blood pressure Figure 7 shows a graph of the central pulmonary venous pressure plotted against the value X . The following abbreviations are employed within the description:- SV = stroke volume of the heart ventricles CO = cardiac output, i.e. the volume of blood pumped by the heart ventricle per minute P = the pulse rate of the heart, i.e. the number of pulses of the heart per minute ABP = the arterial blood pressure VBP = the venous blood pressure CVP = the central venous pressure Y = the central venous pressure PR = the total mean peripheral resistance of the circulation PR, = the mean peripheral resistance for the venous side PR 2 = the mean peripheral resistance for the arterial side. S = systolic blood pressure D = diastolic blood pressure R = the pulse pressure S - D H = the output factor A = the measured packed cell volume E = the measured erythrocyte sedimentation rate in mm/hr = the measured depression of freezing point of plasma in °C ESR = erythrocyte sedimentation rate in mm/hr T = the measured total plasma protein concentration in g/1 F = a correction factor for osmolarity of plasma Z = a correction factor for total plasma proteins B = a correction factor for the ESR G = a correction factor for taking account of changes in viscosity The monitoring or management of the critically ill or a subject under a general anaesthetic can be achieved by looking at different medical quantities. The present invention allows simpler monitoring of various quantities for a subject without the use of an invasive technique. The following describes the basis for evaluating various of those quantities. The evaluation of the quantity known as the central venous pressure without the use of an invasive technique is described first. The volume of blood pumped out by each of the two ventricles of the heart per stroke is known as the stroke volume SV. The value of SV is effectively the difference between the diastolic and systolic end volumes, corresponding respectively to situations of maximum expansion and compression of the ventricles. The stroke volume is typically about 70 ml when the subject is at rest. Starling's Law defines the cardiac output CO, i.e. the volume of blood pumped out by each ventricle of the heart per minute, for a heart having a pulse rate P as CO = SV x P (1) Now it is known that for a fluid the following expression applies:- flow = pressure/resistance For a heart, it is assumed that flow can be considered s the cardiac output, the pressure in the system can be considered as the difference between the arterial blood pressure (ABP) and the venous blood pressure (VBP) , and the resistance can be considered as the total mean peripheral resistance (PR) offered by the arterioles and veins. Hence CO = (ABP - VBP)/PR cl/min (2) Thus, blood pressure which is given by the difference between the arterial and venous blood pressures is directly proportional to CO.PR. As the atria and the veins draining into them are in direct communication at all times except during atrial systole of the cardiac cycle, the central ' venous pressure CVP, as classically measured, can be equated with the pressure of the right atrium so it is assumed that under steady state conditions CVP is equal to VBP above. Now it is noted that the total mean peripheral resistance and blood pressure in equation (2) are affected by changes in the diameter of the blood vessels. The diameter of the blood vessels is influenced by the baroreceptors which are stimulated by a rise or fall in blood pressure and the impulses of which are directed to the vasomotor centre of the brain. Vasomotor activity is also influenced by changes in the levels of carbon dioxide in circulating blood, oxygen lack, activity of the respiratory centre, activity of the sensory nerves of the body, general activity of the cerebral cortex, redistribution of blood to meet the requirements of certain body organs, the levels of circulating metabolites, and humoral factors. Thus, exercise and disease bring about a change in the blood volume by one or more of the above mentioned factors. As stated above, under steady state conditions (where flow into and out of the heart is stable) , it can be assumed that VBP «= CVP. Since the blood flow rate from the arterial side of the circulation is passed into the venous side and since energy can not be destroyed, but is transformed from one form to another, on the basis of flow mechanics, it will be apparent that for the venous side having a peripheral resistance PR, CVP proportional to ABP.PR, (3) A physiological law states that ABP = P.SV.PR so that for the arterial side where PR 2 is the mean peripheral resistance on the arterial side PR2 = ABP/P.SV (4) If it is assumed that the circuit of blood flow is without leakage, CVP is proportional to PR, multiplied by a value k, which is a function of ABP and which incorporates the constant from equation (3) , and ABP is proportional to PR 2 multiplied by a value k 2 that is a function of P.SV. In the steady state, mean venous flow = mean arterial flow so it can be assumed that PR, x k, = PR- x k 2 . Substituting for PR, and PR 2 using equations (3) and (4) above leads to the expression k, X CVP/ABP = k 2 X ABP/(P.SV) (5) Within the arterial circulation, the value S - D is the pulse pressure R which for its duration represents blood flow. Hence, it is possible to express SV as SV =- k-(S-D) (6) The actual pressure within the circulation can be expressed as ABP = k 4 x S (7) Substituting equations (6) and (7) in equation (5) leads to the expression k, x CVP/ (k 4 x S) = k 2 k 4 S/k 3 P (S - D) and CVP = k 2 k 4 -S/k,k 3 P(S - D) Defining a constant M as the value attributable to the values k,, k 2 , k 3 , k 4 gives the expression CVP = M.S 2 /P(S - D) (8) A value X has been found to have a great significance and can be defined as X = S"/P(S - D) (9) Substituting the value of X in equation (8) gives CVP = M.X (10) Hence by measuring values of CVP using classical invasive techniques together with measurement of the values of S, D and P making up the value of X, it is possible to obtain a graph to directly derive the value of M, subject to the premise that there is no flow without pulse. Figure 1 illustrates the results of experiments using classical invasive techniques to determine CVP, and the values of S, D and P. The latter are used to evaluate X and a plot is made of X against values of CVP which are in centimetres of water. Figure 2 illustrates experimental results with CVP in centimetres of mercury. As can be seen, it is found that a straight line graph results defined by the known equation y = x + c so that equation (10) should be corrected by the addition of a constant C to give the more accurate equation Y = M.X - C = M(S 2 /P(S - D)) - C (11) SO (S - D)P = M.S 2 /(Y + C) (12) where Y is equivalent to CVP and M is equivalent to m and C is equivalent to c. The value M is hence the slope of the graph in figures 1 and 2. It will be apparent therefore, that the value of M in equation (10) or (11) can be obtained empirically using real values of S, D, P and CVP obtained by invasive techniques for a normal subject. It has been found from the experimental results shown in figure 1 that M = 10 for values expressed in cmH 2 0, and from figure 2, M = 0.735 for values expressed in cmHg. The line shown in figures 1 and 2 can be shifted along the Y axis for different values of normal so that the following applies:- C = 5.29 for all readings with normal for Y set at 0 cmH 2 0 C = 3.29 for all readings with normal for Y set at 2 cmH 2 0 C = 1.29 for all readings with normal for Y set at 4 cmH 2 0 C = 1.2 for all readings pertaining to a preterm for Y set at 0 cmH 2 0 C = 1.36 for all readings pertaining to a neonate for Y set at 0 cmH 2 0 C = 1.84 for all readings pertaining to an infant for Y set at 0 cmH 20 C = 5.76 for all readings pertaining to a child for Y set at 0 cmH 2 o C = 0.389 for all readings with normal for Y set at 0 cmHg C = 0.242 for all readings with normal for Y set at 0.15 cmHg C = 0.095 for all readings with normal for Y set at 0.29 cmHg The above figures are subject to change depending on parameters of the subject, for example geographical location, age, race and sex of the population from which the measurements are derived. CVP of the general population is typically in the range 0 to 4 cmH 2 0 although others, such as in the US, claim the value to be 4 to 8 cmH 2 0. To check the validity of equation (11) , artificial values were used to examine whether trends from the results were consistent with medical practice. Figure 3 shows a graph of the central venous pressure plotted against the pulse rate for a given blood pressure. In this graph, the following underlying trends are found:- 1. For any arterial blood pressure, the central venous pressure falls with rise of pulse rate, and conversely, rises as pulse rate falls which is consistent with normal medical practice. 2. The pulse pressure R is approximately inversely proportional to the central venous pressure. The evaluation of the quantity known as the cardiac output CO without the use of an invasive technique is now described in combination with evaluation of a useful quantity defined as the output factor H. From equations (1) and (6) , it is possible to express cardiac output as CO = k 3 (S - D)P so C0/k 3 = (S - D)P The quantity H can be defined as C0/k 3 . Therefore, H = (S - D)P (13) which is a clinical relationship consistent with experience. In practice, it is found that H is approximately half of the cardiac output when measured by methods employing the Fick principle, i.e. CO = 2H which leads to the expression CO = 2(S - D)P (14) The cardiac output CO should be equal to the cardiac output when measured by the ultrasound/aorta technique. The disparity arises because the latter method assumes that the diameter of the aorta remain unchanged during pulsatile flow and that blood is a Newtonian fluid which it is not. Substituting (S-D)P from equation (12) into equations (13) and (14) gives H = M.S 2 /(Y - C) (15) CO = 2M.S 2 /(Y + C) (16) It is apparent therefore that values of CVP can be obtained by monitoring CO and S only as an alternative to the values to be monitored for equation (11) . The above quantities CVP, H and CO have been evaluated without any corrections. In practice, various correction factors can be included in all the above relationships. A first correction factor intends to take account of the varying viscosity of blood. It is noted that about 45% of the blood volume is made up of red cells, with a small fraction of this contributed by white cells. A measure of this is given by the packed cell volume PCV (haematocrit) , which varies with the number and size of red cells in the blood and with plasma volume. The viscosity of the blood increases with increasing packed cell volume. The packed cell volume is more readily measured in medical practice than the viscosity of blood so a correction factor on the basis of packed cell volume is included to account for variations in the blood viscosity. Given any pair of readings of CVP for a subject having blood packed cell volumes PCV, and PCV 2 with viscosity V, and V 2 respectively, then PCV,/PCV 2 = (a constant) .V,/V 2 The above constant can be calculated from a graph of known values of PCV and V and is found to be equal to 0.96. For a patient under normal conditions, PCV has a typical value of 45 and viscosity V of 2.8 centipoise. If PCV A and V A respectively represent packed cell volume and viscosity associated with abnormal conditions due to accident or illness, then PCV A /45 = 0.96 x V A /2.8. It should be noted that the value of PCV varies according to location, race, sex, age • etc. Since viscosity is indirectly proportional to flow, a correction factor G for taking account of changes in viscosity from normal can be defined by G = 2.8/V A . Substituting in the above equation gives G.= 43.2/PCV A . Defining the abnormal packed cell volume PCV A as A, then in the event of accidents or diseases where the packed cell volume is affected, G can be used to modify the above equations (11), (13) and (14) to give Y = M(S 2 /(S - D)P(43.2/A)) - C (17) H = P(S - D) (43.2/A) (18) CO = 2P(S - D) (43.2/A) (19) A second correction factor arises because the plasma proteins exert an osmotic pressure and affect the viscosity of the blood. Thus, it affects blood pressure and thereby blood flow. It is noted that the viscosity of blood offers resistance to flow. The viscosity of blood is affected by certain factors including the plasma proteins which exert an osmotic pressure and the erythrocyte sedimentation rate, which is a measure of the viscosity of plasma. This resistance is constant in a healthy subject but is increased in many diseases involving inflammation and tissue destruction. The degree of viscosity of the blood can be expressed by the erythrocyte sedimentation rate ESR, which is also more readily measured in medical practice than blood viscosity. A correction factor B to take account of changes in the ESR is included in the above relationships as they relate to flow. For a subject having normal plasma proteins of 8 g per 100 ml, an osmotic pressure of 25 mmHg, a PCV of 45 and a viscosity of 2.8 centipoise, the ESR is of the order of 10 mm per hour, and varies according to the geographical location, age, sex and race of the subject. Thus, for an abnormal ESR value E, the correction factor to take this into account is given by B = 10/E. Hence, in diseases where the ESR is abnormal, the sum total of correction to blood flow attributable to change of plasma viscosity is the product of B and G, so equations (17) , (18) and (19) are modified to become Y = M(S 2 /(S - D)P(10/E) (43.2/A)) - C H = P(S - D) (10/E) (43.2/A) CO = 2P(S - D) (10/E) (43.2/A) Another correction factor arises from the fact that under normal circumstances, the plasma osmolarity is equal to the osmolarity of the glomerular filtrate. However, plasma osmolarity changes in metabolic disorders, renal disorders, fluid or blood loss, maladjusted intake of nutrients, or a maladjusted fluid and/or blood therapy. The osmolarity of plasma is the sum of the molarities of its constituents which give rise to the plasma osmotic pressure, and these are sodium, potassium, chloride, bicarbonate, phosphate, protein, glucose, urea, uric acid and creatinine. However, over 99% of the osmolarity of plasma is due to sodium, chloride and bicarbonate ions alone. One of several methods by which the plasma osmolarity is readily measured in clinical practice is the depression of freezing point. A depression of 1.86 °C is equivalent to 22.4 atm of osmotic pressure. Plasma has an osmotic pressure of 300 mosmoIs/litre, which has a depression of freezing point of - 0.56 °C. If a value W represents the depression temperature associated with abnormal conditions, a correction factor F can be defined as F = 0.56/W This correction factor varies according to the geographical location, age, sex and race of the subject. The depression of vapour pressure of plasma can also be used. The osmotic pressure between blood and extracellular fluid depends upon protein molecules and is called the oncotic pressure, which is a property that is important at the capillary end of the circulation where tissue fluid is formed and resorbed. For a total plasma protein concentration of 8 g per 100 ml, the oncotic pressure is of the order of 25 mmHg, which is normal. If a value T represents the oncotic pressure associated with abnormal conditions, a correction factor Z can be defined as Z = 8/τ Changes in oncotic pressure are expected in the following:- heart disease with stagnant anoxia; anoxia in general which cause damage to capillary walls; renal disease; nutritional disorders; and a maladjusted fluid and or blood therapy. Hence correctional factors are taken into account for diseases and or accidents which involve the heart and general circulation, the kidneys, the brain, the liver, the lungs, the individual constituents of blood and the individual constituents of plasma. It is noted that an increase in plasma osmolarity causes an increase in plasma volume and an increase of plasma oncotic pressure causes an increase in plasma volume. Since an increase of flow is indirectly proportional to pressure, these correction factors further amend equations (17) , (18) and (19) to become Y - M(S 2 /(S - D)P(10/E) (43.2/A) (W/0.56) (T/8) ) - C ... (20) H = P(S - D) (10/E) (43.2/A) (W/0.56) (T/8) ... (21) CO ** = 2P(S - D) (10/E) (43.2/A) (W/0.56) (T/8) ... (22) An apparatus for evaluating the central venous pressure, output factor, and cardiac output is shown in figure 4. A subject to be monitored is defined by subject data corresponding to geographical location, age, race and sex of the subject. An inflatable cuff device 2 of a known electronic blood pressure apparatus 1 is attached to the subject to measure both the systolic and diastolic blood pressures. The electronic values corresponding to the systolic (S) and diastolic (D) blood pressures are sent to a central controller 4 along a bus 3. A pulse rate measuring device 13 of any convenient conventional type measures the rate of beating of the pulse and the electronic value corresponding to the heart rate P is sent to the controller 4 along a bus 5. The controller 4 comprises a microprocessor CPU 8 and a read only memory ROM 6. A keyboard 7 is also connected to the controller 4 to input details of the subject data and values for correction data. The ROM 6 contains values of M and C for the equation (10) according to the subject data. When the subject data is entered, values of M and C are retrieved from the ROM 6. The CPU 8 instructs the blood pressure apparatus 1 and pulse rate measuring device 13 to transfer current data concerning the values of S, D and P to the CPU for processing. These values are inserted into equation (10) together with the retrieved values of M and C and the value of CVP is displayed on a screen 9 together with the current values of S, D, and P. An ongoing hard copy version can also be provided by a printer (not shown) . When correction data is input, the equation employed to evaluate CVP is altered to that of equations (15) or (18) according to the data. The CPU may also be set up to evaluate values of the output factor H and cardiac output CO according to equations (16) or (19) and (17) or (20) respectively. These values can also be displayed on the screen 9. It will be apparent that the format of the displayed data can be single data or graphical. It will furthermore be apparent that other correction data may be applied to the basic equation and other medically valuable data can be obtained on the basis of the equation used to evaluate CVP. It will be appreciated that many modifications of the apparatus described in the above embodiment are possible without departing from the scope of the claims. Using experimental results of values of pulse pressure, pulse rate, and the quantity H, it has been found that for a given pulse pressure R, the unit change Q of the quantity H per pulse is constant. The results are plotted as the graph shown in Figure 5 which shows an underlying trend. For a given pulse pressure R the unit change of quantity Q is R cl per pulse. Defining Q as the fluid load factor or deficient factor, the graph gives Q = 10.R, but from above R — S - D. Therefore Q = 10. (S - D) (23) The above formula itself has no clinical significance. However, using a table of experimental results giving pulse pressure R, values of blood pressure BP, values of central venous pressure, and the (derived) values of the blood fluid load or deficit factor Q all for a given cardiac output CO, it is possible to plot a graph of values of the CVP in cmH 2 0 against the syβtolic blood pressure S cmHg. Such a plot is shown in figure 6 and showed an underlying trend. 1. If the heart were a pump with a fixed output, then for a given pulse pressure R (the pressure difference between two points in the arterial limb of the circulation) , central venous pressure CVP is directly proportional to the blood pressure BP, and the central venous pressure CVP rises with rise in blood pressure BP. 2. When the central venous pressure CVP is above zero, there is a positive fluid tension which is termed the fluid load. When the central venous pressure CVP is below zero, there is a negative fluid tension which is termed the fluid deficit. Thus, in the absence of a circulation without peripheral resistance and capacitance vessels, fluid is added or taken away from the system. This is the basis of all treatment pertaining to the heart and the general circulation. In vivo, the veins hold most of the blood in the body, and it is this capacity which is very important in maintaining the stroke volume of the ventricles. The fluid load factor Q therefore reflects the capacity (total volume) of the capacitance vessels. However, the heart is not a pump with a fixed output. There is auto-regulation in the function of the heart, the peripheral resistances, and capacitance vessels as known from the aforementioned basic physiological properties of the heart and circulation. Also, blood is a non-Newtonian fluid. Altogether, the heart and haemodynamic state of the circulation vary in health and disease in the same individual. Accordingly, such factors must be allowed for. Auto-regulation of the peripheral resistance PR is given from equation (8) CVP = .S P(S - D) = Therefore, M ** = Y(S - D)P/S 2 , where M is a constant for the peripheral resistance PR (Steady State) . In vivo in a clinical sense, the fluid load factor Q should be qualified by peripheral resistance so that equation (23) should be corrected by M. Therefore, Q.M = 10(S - D) Substituting for M Q.Y(S - D)P/S 2 = 10(S - D) Q = 10(S - D)S 2 /Y(S - D)P Q = 10S 2 /Y.P (24) Q is used to evaluate the fluid load (or deficit) of any two readings as follows: Flow F = Pressure / Resistance Volume = Flow . Cross sectional ' area . Resistance Volume — Pressure . cross sectional area From Hagen - Poiselle's law, (PI.Pressure.Radius 4 / Length) = (Flow.Viscosity.8/Pressure) In a subject whose circulation undergoes a change Q, to Q 2 , the pressure factor in the capacitance vessels is the central venous pressure CVP (Y) and the flow multiplied by viscosity factor is accounted for by the cardiac output CO. Therefore, the volume change = (Y,.CO,.8) - (Y 2 .C0 2 .8) which as a fraction of Q represents net fluid change, the fluid load or deficit Fd. Therefore Fd = Y, . CO, . 8/Q, - Y 2 . C0 2 . 8 /Q 2 Since Y is measured in cmH 2 0 a correction factor must be applied to give Fd = 8((Y,.C0,/Q,) - (Y 2 .C0 2 /Q 2 ))0.0735 Substituting for Q from equation (24) gives Fd = 8((Y, 2 .CO,.P,/10.S,-) - (Y 2 2 .CO 2 .P 2 /10.S- 2 ) )0.0735 The above value for the fluid load or deficit correlates in clinical practice with volumes required to correct the fluid load or deficit for values of the central venous pressure CVP of any pair of readings. Thus, if the central venous pressure CVP drops in practice because of loss of fluid (e.g. blood) , the value Fd gives a value for the amount of fluid that needs to be added back to the blood circuit (or taken out for heart failure) . It has been found that the general principle of obtaining the value X can be applied quite generally to blood carrying organs of a subject, that is to say an equivalent value X (and their related parameters) can be obtained and applied for these different organs. A study has been made using the non invasive measurement of the central venous pressure principle to evaluate the central pulmonary venous pressure CVP p (which is the pressure in the left atrium. Applying the value of X from equation (9) to give an equivalent X p for the central pulmonary venous pressure gives X p = S p 2 /P(S p - D p ) where S p equals the pulmonary systolic blood pressure and D p equals the pulmonary diastolic pressure. Figure 7 shows a graph of CVP p against X p . For example, a normal situation has pulmonary systolic blood pressure (PSBP) as 2.5 cmHg, pulmonary diastolic pressure as 0.8 cmHg, left atrial pressure as 0.5 cmHg, and a pulse rate of 68/min. Using other experimental values, the slope of the graph M p is found empirically to be 9.242. The slope of the graph for the systemic circulation M as it relates to the central venous pressure is 10. Thus, the ratio of the central pulmonary venous pressure to that of the systemic pressure is expressed by 9.242 / 10 = 0.9242 From equation (20) , with Y equal to CVP Y p = 0.9242.S 2 .8.E.A.0.56/P(S - D)10.W.T.43.2 (25) However, the pulmonary blood pressure is also indirectly proportional to the oxygen saturation (or tension) of circulating blood. Thus, there is a rise of pulmonary blood pressure with fall of oxygen saturation (or tension) . Therefore, for an oxygen saturation of U%, a correction factor V for this is. V = U / 101. 29 Making this correction to equation (25) gives Y p = 0.9242.S .8.E.A.0.56.101.29)/P(S - D)10.W.T.43.2.U .. (26) This measurement of the central pulmonary venous pressure CPV p seems to cast doubt on the usefulness of pulmonary wedge pressure PWP in clinical practice. This may be because the pulmonary wedge pressure measurement is invasive. It relies upon a balloon taking up the radius of a small branch of the pulmonary artery with a disregard for the relationship between the wall tension, the internal pressure, and radius of the balloon and hence that of a small branch of the pulmonary artery. Furthermore, the measurement may not be dynamic enough to sense changes in the radius of a small branch of the pulmonary artery which accompany changes of oxygen saturation (or tension) of circulating blood. It is apparent that in the presence of hypoxia, pulmonary cardiac output is initially lower than that of the systemic cardiac output. The paradoxical effect of low oxygen tension upon the pulmonary and systemic vasculature is well documented, and as the challenge of hypoxia is prolonged, the compensatory rise of systemic cardiac output is accommodated by reserves of pulmonary capacitance vessels, which when it becomes depleted, the full clinical effects of low oxygen tension consequent upon the systemic circulation become manifest. Further, cardiac and pulmonary circulatory alterations from that of the foetus to that of the neonate, child, and, finally, to that of the adult basically involve a change from ventricles acting in parallel to those acting in series and consequent upon the closure of a series of shunts, maturity of the major organs, and general growth. The following factors reflect the changes seen in the general circulation of the preterm, neonate, infant, and child when compared individually and collectively to that of the adult general circulation. l.The ductus venosus shunts oxygenated blood from the umbilical vein at a tension of 80 mmHg to the inferior vena cava which already contains blood at a tension of 30 mmHg, thereby, to by-pass an immature liver. Much of the blood arriving by the umbilical vein effectively reaches the left atrium at a tension of 65 mmHg by being shunted to by-pass the right atrium, having been directed into the foramen ovale by the via sinistra of the crista dividens of the inferior vena cava. 2. A third shunt system empties blood from the right ventricle directly into the aorta, thereby to by-pass the immature lungs. 3. At birth the shunts close off, thereby causing a change in the balance which had existed between the systemic and pulmonary vascular resistance; that is the systemic vascular resistance increases, while that of the pulmonary vascular resistance is reduced. The ductus arteriosus and venosus cease to function within three days of birth. The foramen ovale ceases to function within three weeks of birth. 4. As the major organs of the body begin to function and mature, so their blood flow requirements increase. 5. The difference in the value of pressure and volume measurements which exists between that of the preterm, neonate, infant, child and the adult is consequent upon growth of the muscle bulk of the heart, enlargement of the chambers of the heart, and general metabolism. Direct measurements of these changes are made, but for clinical purposes it is sufficient to use changes in the measurement of the surface area of a subject as a general index to represent these changes. 6. Physiologically, the following cardiovascular responses are noted for the preterm, neonate, infant, and the child. i. there is bradycardia in response to low oxygen tension; ii. there is tachycardia in response to acidosis or low pH of circulating blood (low oxygen tensions causes anaerobic metabolism) ; iii. there is half the concentration of carbonic anhydrase at birth, therefore the release of carbon dioxide in the lungs is handicapped, which contribute to the low pH as is found in the neonate; iv. there is a high haemoglobin and haematocrit value at birth. Hence, in the preterm, neonate, infant, child, the following correction factors are required. 1. A correction factor V for oxygen saturation of U% is given by V = U/101.29 as in equation (26) 2. A correction factor B h for the pH of blood is given by B^ = PH b /7.44 3. A correction factor N for a surface area SA is given by: N = SA/1.8 The figures 101.29, 7.44 and 1.8 are normal values for the average adult.Therefore, when the correction factors as outlined above are made to equations (20) , (21) and (22) , the central venous pressure, the output factor and the cardiac output respectively for a preterm, neonate, infant and child is given by Y k , H k and CO k as follows: Y k = (M.S 2 )/((S - D)P(10/E) (43.2/A) (W/0.56) (T/8) . (U/101.29) (PH b /7.44) (N/l.8)) - C (27) H k = P(S - D) (10/E) (43.2/A) (W/0.56) (T/8) . (U/101.29) (PH b /7.44) (N/l.8) (28) CO k = 2P(S - D) (10/E) (43.2/A) (W/0.56) (T/8) . (U/101.29) (PH b /7.44) (N/l.8) (29) The measurement of the left atrial pressure Y p (central pulmonary venous pressure) has been derived from the non invasive measurement of the central venous pressure. In the child, infant, neonate and the preterm, this pressure is given as follows making correction to equation (26) for the factors in respect of the pH and surface area Y pk = (0.9242.S 2 .8.E. .0.56.101.29. 7.44.1.8)/ (P(S - D) .10.W.T.43.2.U.PH b .SA) (30) A more meaningful indication of the workload of the heart is given by the power W (in watts) being generated by each ventricle to maintain the general circulation. Power is the product of pressure differential and flow (with the pressure measured in pascals (kPas) and flow measured in cubic meters per second (m 3 sec-1)) . The power generated by the left ventricle W L can be evaluated by taking the pressure differential which is the left atrial pressure Y p subtracted from the left ventricular mean ejection pressure (systolic blood pressure) S - Y p /0.75 where 0.75 is a conversion factor for cmHg converted to kPas. The output of the heart CO from equation (16) converted to the same units is CO = 2(M.S 2 )/(60. (Y + C).100) Therefore, W L = ((S - Y p )/0.75) ((2M.S 2 )/60(Y + C)100)) (31) For the child, infant, neonate and the preterm, it is possible to substitute values of Y k for Y p and Y k for Y. The cardiac output of the pulmonary circulation CO is equal to that of the systemic circulation "CO" in a healthy subject at rest. This non invasive measurement of the central venous pressure CVP is used to derive the right ventricular systolic pressure S R as follows. From equation (16) CO p = 2.M R .S R 7(Y + C) where M R is a constant with the same function given to M in equation (16). From equation (14) CO = 2.(S - D)P. It follows that CO = CP p for a healthy subject, so that 2.M R .S R 2 /(Y + C) = 2.(S - D)P (32) Substituting experimental results of a normal subject at rest into this equation, these being a right ventricular pressure of 2.5 cmHg, a cardiac output of 544 cl/min and a central venous pressure of 0.004 cmH 2 0 gives M R = 272 * 5.295 / 2.5 2 = 230.394 Applying the correction factors to CO gives 230.394.S R /(Y + C) = P(S - D) (10/E) (43.2/A) (W/0.56)(T/8) Therefore, S R = Square root (P(S - D) (10/E) (43.2/A) . (W/0.56) (T/8) (Y + C)/230.394 (33) Similarly, the right ventricular pressure S Rk in a child infant, neonate and the preterm is given by; S Rk = Square root (P(S - D) (10/E) (43.2/A) (W/0.56) (T/8) . (U/101.29) (PH/7.44) (N/l.8) (Y + C)/230.39_4 (34) The power generated by the left ventricle has already been shown. In a similar manner, the right ventricle with its mean ventricular ejection pressure (right ventricular systolic blood pressure S R ) , the power W R can be derived as follows. The pressure differential is the right atrial pressure Y in cmH 2 o subtracted from the right ventricular ejection pressure S R which is (S./0.75) - (Y/10.2) with conversion factors to kPas. Using the cardiac output C0 P from equation (32) for flow (converted to kPas) gives W R = ( (S R /0.75) - (Y/10.2 ) ) (2 .M R . S R 2 /60 (Y + C) 100) (35) For the child, infant, neonate and the preterm, the values of S Rk is substituted for S R and Y k for Y. On the basis of the non invasive measurement of the central venous pressure CVP, it is possible to derive an index for changes in the intracerebral pressure ICP. 1. The contents of the cranium are brain tissue, water, cerebral blood volume CBV and cerebrospinal fluid CSF. Once the fontanelles fuse at age eighteen months, the brain is regarded as several organs within a compact structure with separate functional needs and separate patterns of regional blood flow. 2. Intracranial pressure ICP depends in part on an accurate balance between arterial inflow and venous-drainage. 3. The normal cerebral blood flow rate CBF is 55 ml/100 g of brain tissue/min and is regulated by: a. the arterial blood pressure. CBF is 15% of left ventricular output with the patient in a supine position. Generally, CBF does not alter with blood pressure values between 90 and 180 mmHg. b. Venous pressure c. Arterial blood carbon dioxide tension PaC0 2 , the normal value of which is 40 mmHg. CBF is increased 100% with PaC0 2 of 60 to 80 mmHg whilst CBF falls by some 30% with PaC0 2 of less than 26 mmHg. d. Temperature e. Drugs f. Neurogenic factors 4.The normal value of ICP is 100 - 150 mmH-O. ICP is generally recorded by measuring the pressure of cerebrospinal fluid CSF. The source of CSF is by secretion of the choroid arterial plexuses of the 3rd, 4th and lateral ventricles of the brain. 0.5 l/min of CSF is secreted, and, this is independent of brain ventricular pressure. The CSF is drained into the venous sinuses of the brain via arachnoid villi, and into the lymph stream via the pacchionia bodies. The absorption of CSF is directly proportional to the CSF pressure. The source of CSF pressure is the secretory pressure of the choroid plexuses. CSF itself does not usually contribute to a raised intracranial pressure ICP unless its flow is blocked or its absorption prevented. 5. ICP is closely related to venous rather than arterial pressure. 6. The cerebral veins act as a buffer to postural and other physiological changes in CSF pressure. Cerebral venous sinuses have semi-rigid walls and do not respond directly to CSF pressure. Their internal pressure is related to the pressure in the internal jugular vein. The venous drainage system from the cerebral veins to the right atrium of the heart has no valves and, as a result, it readily transmits pressure changes. 7. The following will result in a raised ICP: obstructing the jugular veins (Queckenstedt's test); space occupying lesions; sleep; uraemia; alcoholism; cerebral oedema resulting from inflammation; neoplasm; trauma and anoxia; rise of PaCo 2 ; congestive cardiac failure; and mediastinal tumours. 8. The following will result in a fall of ICP: dehydration; wasting diseases; leakage of CSF; blood loss; and drugs. Cerebral blood flow rate CBF is shared equally by the two hemispheres of the brain. Since ICP is common to both hemispheres, the flow rate to each hemisphere is given by C0/2, which is the output factor H. Let ICP be denoted by I b , let the cerebral mean arterial systolic blood pressure be S b , let cerebral mean arterial diastolic blood pressure be D b , and let the CBF rate be He cl/min. Flow rate is given by the quantity H as in equation (15) . Normal CBF is 55 ml/100 mg brain/min. Therefore He = He / 55 per kilo of brain tissue. Similarly, for K kilos of brain He = 55.K cl/min flow (36) Using Du Bois's formula to make corrections for the surface areas, K = (He / 55Jw 0 - 425 .!. 0 - 725 .0.00718 kilo (37) From equations (13) and(15) M.S b 2 /(Ib + C) = (S b - D b )P = He (38) It is accepted that (S b - D b )P = 15 / 100 . H (39) Substituting for He in equation (37) K = (S b - D b ) (P/SSJw 0*425 .!. 0 ' 725 .0.00718 Then substituting for K in equation (36) First, substituting the value of (S b - D b )P from equation (39) gives He = (15/100)H. 0 - 425 .!. 0 - 725 .0.00718 (41) Therefore, according to equation (38) M. S fa 2 / (Ib + C) = (15/100) H.W°- 425 .h 0 - 725 . 0. 00718 (lb + C) = (M. S^IOO/ISJ J /H.W 0*425 .!. 0 - 725 . 0. 00718 (42) A correction factor for PaC0 2 mmHg is given by r/40, wherein r is the PaC0 2 of the patient. Applying the aforementioned other correction factors gives (Ib+C)= (M.S^IOO/ISJJ/H.W 0 - 425 ... 0 - 725 .0.00718. (r/40) (101/U) (43.2/A) (7.44/PH) (10/E) (T/8) (W/0.56) Therefore , lb ~ - (M. S b 2 ( 100/15) ) /H.W°- 4 5 . h 0 - 725 . 0. 00718 . (r/40) ( 101/U) (43 . 2/A) (7 . 44 /PH) ( 10/E) (T/ 8 ) (W/ 0 . 56 ) - C ( 43 ) Systemic arterial blood pressure S can be substituted for S b and the pressure lb is derived for a compact cranium. Also from this non-invasive measurement of the central venous pressure CVP, an index for changes in the glomerular filtration rate, GFR can be derived as follows. 1. There are two kidneys in the body and each weighs 120-170 gm. 2. The arteries supplying each organ passes directly from the abdominal aorta. Each vessel divides into five seg ental end arteries. 3. A renal tubule and its glomerulus is called a nephron. A glomerulus consists of a mass of capillary vessels surrounded by the blind end of an expanded renal tubule called the Bowman's capsule. The Bowman's capsule is concerned with the filtering of substances from the blood stream and then to pass the filtrate into a complex renal tubular apparatus. Each kidney has 1.5 million nephrons. 4. The kidneys maintain the body fluids at a constant composition by the maintenance of the blood pH, blood electrolytes, and the water balance. 5. The kidneys excrete metabolic waste products from the body in the form of urea, uric acid, creatinine, surplus acids, and surplus alkalis in urine. 6. Urine is formed by: glomerular filtration which is non selective, a selective renal tubular reabsorption, and by renal tubular secretion. 7. There are abnormal constituents of urine, the presence of which signals an underlying disorder. These include the following:- glucose for which there is a renal threshold of 10 mmol/1; ketones; plasma albumin; red cells; galactose; drugs; hormones; phenylketones; and poisons. 8. The normal renal blood flow is 22% of the cardiac output, i.e. 120 cl/min. The glomerular filtration rate is defined as the amount of fluid passing from the capillaries in the glomerulus into the lumen of renal tubules every minute. 9. The pressure in the glomerular capillaries is referred to as the effective filtration pressure EFP. The EFP drives out fluid and this force is opposed by the osmotic pull of plasma proteins, and hydrostatic pressure of 6 cmHg which exists in the Bowman's capsule. 10. Water filtered is 1/lOth of renal blood flow. 12 cl/min of water are filtered and a total of 1600 gm/day of crystalloids. 99% of fluid filtered is reabsorbed. THe specific gravity SG U of urine is 1.003 to 1.030. The SG of plasma is in the range of 1.025 to 1.029. The SG U of urine is increased in disease because of protein debris. In diabetes mellitus, when large quantities of glucose are reaching the urine, the SG U is high. In tubular damage and diabetes insipidus, the SG U is very low. 11. There are no symptoms of renal failure until the GFR has fallen from 12 cl/min to below 3 cl/min and at which stage it is claimed that half one kidney is still functioning. For a GFR below 0.5 cl/min, renal dialysis or transplant is required to save the subject's life. There are two main aspects of renal disease, failure to correct osmole excretion, and the failure to correct water excretion. 12. The regulation of sodium reabsorption is under the control of the hormone aldosterone. Angiotensin stimulates the release of aldosterone from the adrenal cortex. 13. The secreting mechanism of potassium is coupled to that of hydrogen ions. If K+ excretion is high, it prevents the excretion of H+, which results in a state of hyperkalaemie metabolic acidosis. When blood K+ levels are compensated for by excessive secretion of H+ by the kidney tubules into urine, it results in a state of hypokalaemic metabolic alkalosis. 14. The enzyme renin reduces renal blood flow RBF, the effects of which are long standing. 15. High arterial blood C0 2 content of blood and low 0 2 content reduce RBF. 16. RBF is maintained with a temperature drop from 37 °C to 28 °C. Generally, there is an increase of RBF with fall in temperature. 17. Blood creatinine levels are raised in renal diseases. 18. Other factors which affect RBF are, blood urea levels which are raised in disease, the blood haematocrit or haemoglobin fall associated with haemorrhage, plasma osmolarity, and blood pH or hydrogen ion concentration. Let RBF rate be denoted by CO. cl/min, and let the volume of water filtered be denoted by GW cl. Now we know that CO. is 22% of CO, therefore, from equation (16) C0 r = (22/100)2M.S 2 /(Y + C) (44) Therefore, the water filtered by the glomerulus GW is one tenth of the RBF and is given by GW = (1/10) (22/100)2M.S 2 /(Y + C) (45) However, 99% of water filtered is reabsorbed to leave 1% of this which is equal to the volume of urine V α produced in cl/min. Therefore, V u = (1/100) (1/10) (22/100)2M.S 2 /(Y + C) (46) For the above equation, the following correction factors are required in addition to those already mentioned for values of CO, Y and C. a. Urinary pH (pH u ) which is given by pH u /6.25 b. Urinary sugar (us) in mg/24hr which is given by (us + 4.8)/4.8 c. Blood creatinine (cr) in micro mol/1 which is give by 50/cr d. Urinary specific gravity (sg u ) which is given by 1.026/sg e. Body temperature (bt) in °C which is given by 37/bt f. Blood potassium (sk) in micro mol/1 which is given by 4.4/sk Therefor , V. * = (1/100) (1/10) (22/100)2M.S 2 /(Y + C) (pH u /6.25) . ((US + 4.8)/4.8) (50/cr) (1.026/sg u ) (37/bt) (4.4/sk>. (47) Accordingly, C0 r is subject to the same correction factors. Therefore, CO r = (22/100)2M.S 2 /(Y + C) (pH u /6.25) ((us + 4.8)/4.8). (50/cr) (1.026/sg u ) (37/bt) (4.4/sk) (48) Also from this non invasive measurement of the central venous pressure CVP, an index for plaeento-uterine function can be derived as follows. 1. The diagnosis of a pregnancy is made by the measure of the hormone human chorionic gonadotrophin HCG concentrations in maternal blood. HCG titre corresponds with the age of gestation. It is reduced in abnormal pregnancies, ectopic pregnancies, and spontaneous abortion. The duration of a pregnancy is 266 days following fertilization. 2. There is an increase of 30% of blood volume by term, in a healthy pregnant woman. There has been a progressive haemo-dilution of maternal blood which is shown by an increase in plasma protein to red cells ration, and a fall in maternal serum iron. 3. There is an increase of uterine blood flow rate of 1 1/min. 4. The human placenta is of the haemomonochorial type; at term there is only a single layer of foetal chorionic tissue (syncytiotrophoblast STB) which separates maternal blood from foetal capillary endothelium. 5. The STB and placenta together constitute an organ which produces:- hormones which are HCG; progesterones; oestrogens; and placental lactogens; enzymes for the active transport of substances; and for pinocytosis whereby macro molecules are engulfed. 6. Blood enters the maternal sinuses in the placenta in jets from the open ends of placental arterioles. Venous blood is drained into the uterine veins. Two umbilical arteries and an umbilical vein are carried from the foetus to the placenta in the foetal umbilical cord. 7. Changes in placental blood flow depend upon:- maternal cardiac c=output and its distribution; vasomotor tone of the uterine vessels; the state of uterine contraction; and pathological changes in the placenta. 8. Damage to the placenta is repaired by fibrin deposition from the maternal circulation. THe dysmature or ageing placenta has a reduced area available for maternal and foetal exchange. 9. The transfer of 0 2 and C0 2 is by simple diffusion to follow a concentration gradient, and it is a passive process governed by physical laws; the difference between the dissociation curves of maternal and foetal blood enhances respiratory gas exchange; foetal haemoglobin F hgb has a higher affinity for 0 2 than does maternal, M hgb ; the haematocrit rises in the foetus while it falls below normal values in the mother; and by the "Double Bohr" effect, the transfer of acids from the foetus to the mother causes foetal Ph to rise with a consequent Bohr shift to the left to increase affinity of foetal blood to 0 2 , and the acid reaching maternal circulation causes maternal pH to fall with a consequent Bohr shift to the right that 0 2 is released to the foetus. 10. Other substances cross the placenta by:- a facilitated diffusion at a rate more rapid than physical laws would alow, i.e. glucose; by active transport processes to cross the placenta against a concentration gradient, i/e. amino acids and enzymes; by pinocytosis; and by leakage across defects in the placenta, i.e. escape of foetal proteins. 11. There is a progressive fall of maternal blood creatinine and urea concentrations which is associated with an increase in renal blood flow rate. 12. Pressure in the uterus rises to 4 cmHg during a uterine contraction at parturition and enough to impair placental blood flow. 13. Amniotic fluid embolism is the result of amniotic fluid reaching maternal circulation; Foetal material containing cells, vernix or meeonium precipitates a massive conversion of fibrinogen to fibrin. There is consequent blockage of maternal pulmonary circulation, while fibrinogen depletion of maternal blood causes uncontrollable haemorrhage due to the failure of coagulation. 14. Pre-eclampsia is characterized by hypertension, oedema, and albuminuria. There is widespread intravascular coagulation and the progressive diminution in placental efficiency due to deposition of fibrin on the maternal side of the placenta. The cardiac output of the non pregnant female is CO with a central venous pressure of Y. The cardiac output of the pregnant female is defined as CO^ with a central venous pressure of Y_... The cardiac output at rest of a healthy expectant mother is close to her pre-pregnant value and since there is an increase in blood volume in pregnancy, it follows, that (CO„, + rheological changes associated with pregnancy)- CO= 0 When there is a breakdown of the feoto-placental axis, there is a commensurate rise in maternal cardiac output, which is seen to rise to a maximum immediately following parturition when some of the 30% gain in blood volume during the pregnancy (placental blood volume) is emptied into the systemic circulation. Then, CO is greater than CO and immediately after parturition, CO pu = (CO.30%) + CO In addition to those correction factors inherent in calculating cardiac output CO, the following correction factors are required when accounting for CO . i) For a foetal length L in cms which is given by (L + 150) /50 ii) For maternal urinary pH, pH u which is given by 6.025/Ph u iii)For maternal urinary specific gravity SG U which is given by 1.025/SG U iv) For maternal urinary glucose concentration us in mg/24hr which is given by (us + 4.8) /4.8 v) For maternal serum iron concentration fe in micro mol/1 which is given by 22.5/fe Therefore, from equation (22) , CO^ =2P(S-D) (10/E) (43.2/A) (W/0.56) (T/8) ( (L + 150) /50) ((us + 4.8)/4.8) (pH u /6.025) (1.025/SG U ) (22.5/fe) and from equation (16) , the central venous pressure of the pregnant female CVP which is equal to Y is Y^ = (2M.S 2 /C pu ) - C and Y^ = (M.S 2 /P(S-D) (10/E) (43.2/A) (W/0.56) (T/8) ( (L + 150) /50) ((us+4.8)/4.8) (pH u /6.025) (1.025/SG (22.5/fe) )-C It will be apparent that the present invention can be applied broadly and is not limited to the blood organs described herein.

Claims: CLAIMS 1. A non-invasive method for evaluating blood related internal parameters of blood organs of a subject, the method comprising:- a) monitoring the rate of beating P of the heart of the subject; b) monitoring the systolic blood pressure S; c) monitoring the changes (S - D) in the pressure of the subject's blood during beating of the heart; d) utilising a value X for evaluating said internal parameters; wherein the value X is represented by the equation:- X = S 2 /P(S - D) 2. A method as claimed in claim 1 wherein step c) comprises measuring the diastolic pressure D. 3. A non-invasive method for evaluating blood related internal parameters of blood organs of a subject, the method comprising:- a) monitoring the cardiac output CO of the heart of the subject; b) monitoring the systolic blood pressure S; c) utilising a value X for evaluating said internal parameters; wherein the value X is represented by the equation:- X = 2S 2 /CO 4. A method as claimed in claim 3 wherein the central venous pressure of the heart CVP is evaluated according to the equation:- CVP = (2M.S 2 /CO) - C where M and C have predetermined values which vary according to the subject. 5. A method according to claim 1 or 2 wherein the central venous pressure of the heart CVP is evaluated according to the equation:- CVP = M.X where M has a predetermined value which varies according to the subject. 6. A method according to claim 5 wherein the central venous pressure of the heart CVP is evaluated according to the equation:- CVP = M.X - C where C has a predetermined value which varies according to the subject. 7. A method according to claim 1 or 2 wherein the central pulmonary venous pressure of the heart CVP p is evaluated according to the equation:- CVP n P = MP n .X 8. A method according to claim 6 wherein the central pulmonary venous pressure of the heart CVP p is evaluated according to the equation:- CVP p = M p .X where M has a predetermined value which varies according to the subject. 9. A method according to claim 6 wherein the cardiac output of the heart CO is evaluated according to the equation:- CO = 2M.S 2 /(CVP + C) 10. A method according to claim 6 wherein an output factor H of the heart is evaluated according to the equation:- H = M.S 2 /(CVP + C) 11. A method according to claim 6 wherein the fluid load or deficit factor of the heart Q is evaluated according to the equation:- Q = 10S 2 /CVP.P 12. A method according to claim 6 wherein the fluid load or deficit Fd of the blood circulation is evaluated according to the equation:- Fd = 8((CVP, 2 .CO,.P,/10.S, 2 ) - (CVP 2 2 .CO 2 .P 2 /10.S 2 2 ))0.0735 where CO is the cardiac output of the heart and subscripts indicate first and second values of the parameters. 13. A method according to claim 8 wherein the power of the left ventricle of the heart W L is evaluated according to the equation:- L = ((S - CVP p )/0.75) ((2M.S 2 )/60(CVP + C)100 14. A method according to claim 6 wherein the right ventricular systolic pressure of the heart S R is evaluated according to the equation:- S R = Square root (P(S - D) (CVP + CJ/230.3 15. A method according to claim 14 wherein the power of the right ventricle of the heart W R is evaluated according to the equation:- W R = ((S R /0.75) - (CVP/10.2)) (2.M R .S R /60(CVP + C)100) 16. A method according to claim 10 wherein the intracerebral pressure lb of the brain is evaluated according to the equation:- lb = (M.S 2 (lOO/15))/H.w 0 - 425 .h 0 - 725 .0.00718 - C 17. A method according to claim 6 wherein the volume of urine production V v is evaluated according to the equation:- V u = (1/100) (1/10) (22/100)2M.S 2 /(CVP + C) 18. A method according to claim 6 wherein the renal blood flow rate C0 p is evaluated according to the equation:- CO. = (22/100)2M.S 2 / (CVP + C) 19. A method according to claim 6 wherein the cardiac oouuttppuutt ooff «a pregnant female CO is evaluated according to the equation:- CO^ = 2P(S-D)((L + 150)/50) 20. A method according to claim 19 wherein the central venous pressure of the pregnant female CVP is evaluated according to the equation:- CVP^ = (2M.S 2 /C pu ) - C 21. A method according to claim 19 or 20 wherein said equation is corrected by one or more of (L + 150)/50, 6.025/Ph u , 1.025/SG U , (us + 4.8)/4.8, 22.5/fe, where L is the foetal length, PH U is the maternal urinary pH, SG U is the .aaternal urinary specific gravity, us is the maternal urinary glucose concentration, and fe is the maternal serum iron concentration. 22. A method according to any one of claims 4 to 21 wherein said equation is corrected by a correction factor F. 23. A method according to claim 22 wherein said correction factor F comprises one or more of 10/E, 43.2/A, W/0.56, T/8, where E = the measured erythrocyte sedimentation rate, A = the measured packed cell volume, W = the measured depression of freezing point of plasma, and T = the measured total plasma protein concentration. 24. A method according to any one of claims 4 to 23 wherein said equation is corrected by a blood correction factor K to compensate for the early stages of foetal and child growth. 25. A method according to claim 24 wherein said correction factor K comprises one or more of U/101.29, PH b /7.44, SA/1.8, r/40, cr/50 where U = the oxygen saturation of the blood, PH b = the pH of the blood, SA = the surface area of the subject, r = the PaC0 2 of the subject, and cr = blood creatinine. 26. Apparatus for non-invasively evaluating the blood related internal parameters of blood organs of a subject, the apparatus comprising:- means for obtaining measurements corresponding to the pulse rate P of the subject; means for obtaining measurements corresponding to the systolic blood pressure S of the subject; means for obtaining measurements corresponding to the changes (S - D) in the pressure of the subject's blood during beating of the heart; evaluating means utilising a value X for calculating said internal parameters; wherein the value X is represented by the equation:- X = S 2 /P(S - D) . 27. Apparatus according to claim 26 the means for obtaining changes in the pressure of the subject's blood comprises means for obtaining measurements corresponding to the diastolic blood pressure D of the subject. 28. Apparatus for non-invasively evaluating the blood related internal parameters of blood organs of a subject, the apparatus comprising:- means for obtaining measurements corresponding to the cardiac output CO of the subject; means for obtaining measurements corresponding to the systolic blood pressure S of the subject; evaluating means utilising a value X for calculating said internal parameters; wherein the value X is represented by the equation:- X = 2S 2 /CO 29. Apparatus according to claim 28 wherein said evaluating means calculates the central venous pressure CVP of the heart according to the equation:- CVP = (2M.S 2 /CO) - C where M and C have predetermined values which vary according to the subject. 30. Apparatus according to claim 26 or 27 wherein the evaluating means calculates the central venous pressure of the heart CVP according to the equation:- CVP = M.X where M has a predetermined value which varies according to the subject. 31. Apparatus according to claim 30 wherein the evaluating means calculates the central venous pressure of the heart CVP according to the equation:- CVP = M.X - C where C has a predetermined value which varies according to the subject. 32. Apparatus according to claim 26 or 27 wherein the evaluating means calculates the central pulmonary venous pressure of the heart CVP according to the equation:- CVPp n = Mp n .X 33. Apparatus according to claim 31 wherein the evaluating means calculates the central pulmonary venous pressure of the heart CVP according to the equation:- CVP n p = Mp n .X where M has a predetermined value whic «h varies according to the subject. 34. Apparatus according to claim 31 wherein the evaluating calculates the cardiac output of the heart CO according to the equation:- CO = 2M.S 2 /(CVP + C) 35. Apparatus according to claim 31 wherein the evaluating means calculates an output factor H of the heart according to the equation:- H = M.S 2 /(CVP + C) 36. Apparatus according to claim 31 wherein the evaluating means calculates the luid load or deficit factor of the heart Q according to the equation:- Q = 10S 2 /CVP.P 37. Apparatus according to claim 31 wherein the evaluating means calculates the fluid load or deficit Fd of the blood circulation according to the equation:- Fd = δUCV ^.CO j .P^lO.S, 2 ) - (CVP 2 2 .CO 2 .P 2 /10.S 2 2 ))0.0735 where CO is the cardiac output ' of the heart and subscripts indicate first and second values of the parameters. 38. Apparatus according to claim 33 wherein the evaluating means calculates the power of the left ventricle of the heart W L according to the equation:- W L = ((S - CVP p )/0.75) ((2M.S 2 )/60(CVP + C)100 39. Apparatus according to claim 31 wherein the evaluating means calculates the right ventricular systolic pressure of the heart S R is evaluated according to the equation:- * S R = Square root (P(S - D) (CVP + C)/230.3 40. Apparatus according to claim 39 wherein the evaluating means calculates the power of the right ventricle of the heart W R according to the equation:- W R = ((S-/0.75) - (CVP/10.2)) (2.M R .S R 2 /60(CVP + C)100) 41. Apparatus according to claim 35 wherein the evaluating means calculates the intracerebral pressure lb of the brain is evaluated according to the equation:- lb = (M.S 2 (100/15))/H.W°- 425 .h 0 - 725 .0.00718 - C 42. Apparatus according to claim 31 wherein the evaluating means calculates the volume of urine production V u according to the equation:- V u = (1/100) (1/10) (22/100)2M.S 2 /(CVP + C) 43. Apparatus according to claim 31 wherein the evaluating means calculates the renal blood flow rate CO_ according to the equation:- CO. = (22/100) 2M. S 2 / (CVP + C) 44. Apparatus according to claim 31 wherein the evaluating means calculates the cardiac, output of a pregnant female CO according to the equation:- CO p ,. = 2P(S-D)((L + 150)/50) 45. Apparatus according to claim 31 wherein the evaluating means calculates the central venous pressure of the pregnant female CVP according to the equation:- CVP p ,. = (2M.S 2 /C pu ) - C 46. A method according to claim 44 or 45 wherein said equation is corrected by one or more of (L + ' 150)/50, 6_025/Ph u , 1.025/SG U , (us + 4.8)/4.8, 22.5/fe, where L is the foetal length, PH U is the maternal urinary pH, SG U is the maternal urinary specific gravity, us is the maternal urinary glucose concentration, and fe is the maternal serum iron concentration. 47. Apparatus according to any one of claims 26 to 46 wherein said evaluating means applies a correction factor F to said equation. 48. Apparatus according to claim 47 wherein said correction factor F comprises one or more of 10/E, 43.2/A, W/0.56, T/8, where E = the measured erythrocyte sedimentation rate, A * = the measured packed cell volume, W = the measured depression of freezing point of plasma, and T * * *** the measured total plasma protein concentration. 49. Apparatus according to any one of claims 26 to 48 wherein evaluating means applies a correction factor K to said equation to compensate for the early stages of foetal and child growth. 50. Apparatus according to claim 49 wherein said correction factor K comprises one or more of U/101.29, PH/7.44, SA/1.8 where U = the oxygen saturation of the blood, PH = the pH of the blood, SA = the surface area of the subject, according to the equation 51. Apparatus according to any one of claims claim 26 to 50 including input means for inputting a value of K and C for said subject. 52. Apparatus according to any on «e of claims 26 to 50 including input means for inputting data on a subject, and wherein the evaluating means include store means storing values of K and C which are retrieved on the basis of said input subject data. 53. Apparatus according to any one of claims 26 to 52 including display means for displaying the calculated parameter. 54. Apparatus according to any one of claims 26 to 53 including output means for outputting hard copy of a present or ongoing value of said calculated parameter.

Inventors: ABLETT GRAHAM KEITH, AKINYEMI SAMUEL NATHANIEL OLAL, ABLETT, GRAHAM, KEITH, AKINYEMI, SAMUEL, NATHANIEL, OLALEKAN
Applicants: AKINYEMI SAMUEL NATHANIEL OLAL, AKINYEMI, SAMUEL, NATHANIEL, OLALEKAN
Application year: 1992
Main classification: G06F15
IPC codes: G06F17, G06F19