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Adv Exp Med Biol. 1999;471:453-67.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's
ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS.
Gábor Vereczkey, MD.
Cardiologist, Anaesthetist and Intensive Care Specialist
Cardiovascular Surgery Clinic,
Haynal Imre University of Health Sciences,
35. Szabolcs utca, Budapest, H-1135 Hungary
PMID: 10659179 [PubMed - indexed for MEDLINE]
KEY WORDS:
Oxygen Saturation Algorithm (OSA),
Arterial Oxygen Availability,
px, cx, Qx,
Non-invasive Hemodynamic Monitor System (NHMS),
Beat to beat analysis,
Pre-ejection Period, D/S
ABSTRACT:
Introduction: In an ICU it is crucial to have a reliable, trend-able method to evaluate total body
tissue oxygenation [1,2].
Methods: RADIOMETER’s ABL-625 Analyser with Siggaard Andersen’s Oxygen Saturation
Algorithm (OSA) is used to determine the arterial pH, pCO2, pO2, ctO2, p50, px, cx and Qx values,
glucose and lactate levels. There is no need for CV or PA catheterization. ASKIT’s NHMS is used
for continuous, long term measurement of postoperative SV, CO, SVR, PEP, VET, D/S and ACI.
The measured data saved in xxx.wks format are ready for further analysis in Excel.
Discussion: Following open heart surgery, there is a critical 24 hour period when careful
monitoring is required to maintain a satisfactory oxygen supply for the myocardium and all other
tissues of the body. To properely control this situation it is important to be continuously aware of
all the minutely haemodynamic changes and the globally available oxygen for the tissues [3] (that
is determined by the oxygen extraction tension (px), an all in one indicator of pO2, ctO2 and p50
of the ODC [4]. It is time consuming to calculate with all these parameters and requires accurate
mathematic approach [5]. The ABL-625 automatically displays the px, that with the extractable
oxygen (cx) value will determine the compensation factor of Qx, indicating what haemodynamic
changes are required to achieve satisfactory tissue oxygenation. Based on this Qx value, inodilator
therapy is used to improve flow and MAP to optimize afterload for the heart and perfuison for
coronary, cerebral, renal, mesenteric and other vascular beds. With the continuosly displayed PEP,
VET, SV, CO, MAP and SVR the perfusion pump speed can be optimized. If increased dose of
inodilators will not improve CO and px, but reduces the PEP, it is not worth further increasing the
dose as it will only provoke arrhythmias and myocardium oxygen supply deficiency.
Conclusions: The aim of this concerted respiratory and inodilator therapy is to achieve a px in the
reference range and a Qx close to 1.0, with low lactate levels.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
1.
INTRODUCTION
In an Intensive Care Unit it is crucial to have a reliable, trend-able method to evaluate total body
tissue oxygenation [1,2]. Though in physiology studies it is relatively simple to determine arterial
and mixed venous blood gas values and measure cardiac output with aortic flow-metric methods,
it raises ethical and principal problems in human clinical practice.
1.1.
Oxygen Consumption
1.1.1. The Principle of Oxygen Consumption:
As a principle, O2 consumption is an important indicator of a patient’s general condition. To gain
information about VO2, the difference between arterial (ctO2(a)) and mixed venous oxygen
content (ctO2(v)) will give the extracted volume of O2 from one litre of blood. If this ctO2(a-v) is
multiplied by the actual cardiac output, the result is the total body oxygen consumption in a
minute. VO2 = ctO2(a-v) * CO
1.1.2. The Simple But Clear Picture:
In elementary school biology studies everything was simple and clear regarding oxygen
consumption. In human arterial blood there is 20 ml/dl (200 ml/L) oxygen, while in venous blood
there is only 15 ml/dl (150 ml/L). If one contraction of the heart will push 70 ml of blood into the
aorta, 70 heartbeats a minute will pump 70 x 70 ml = 4900 ml blood into the circulation. This
approximately 5 L of blood will contain 5 x 200 ml = 1000 ml O2 in the arterial side, and 5 x 150
ml = 750 ml O2 in the venous side. The difference is the well-known 250 ml that is utilised in a
minute by the body.
1.1.3. Traditional Blood Gas Interpretation in Real Intensive Care Patients:
Following university studies it is rather confusing in clinical practice when interpretation of blood
gases is an important question in cases of intensive care patients. To assess the condition of a
patient from arterial and mixed venous pO2, pCO2, pH, sO2, HCO3-, BE, in spite of all the
additional available parameters like avDO2, avpO2, AapO2, seems difficult and not clear at all.
1.2.
The Problem of Traditional Blood Gas Analysers
Traditional blood gas analysers measure pH, pCO2, and pO2 only. All other parameters are
calculated, and therefor can be misleading. After measuring arterial pO2 with a classic blood gas
analyser sO2 is calculated from an ideal oxygen dissociation curve that is built in the program of
the analyser.
1.2.1. The “Ideal” Oxygen Dissociation Curve
Most blood gas analysers use a “built in” “ideal” oxygen dissociation curve to calculate the likely
sO2 from the measured pO2. Some devices though use conductivity as a principle to determine
haematocrit and then calculate haemoglobin values from this, but only a few determine some of
the dys-haemoglobins to correct the “ideal” oxygen saturation.
None of these methods give information about the position of the ODC that is crucial in all forms
of respiratory and metabolic alkalosis and acidosis.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
1.2.2. Milliliters of Oxygen Meet Grams of Hemoglobin
There is a traditionally accepted figure of 1.39 ml O2, that 1 g hemoglobin can bind. The generally
used units are either mmHg or kPa for measuring gas pressures inside the body, while ambient
pressure is usually indicated in mbars or in atm. Life is often made complicated for no other
reason than tradition.
1.2.3. Partial Pressures of Gases
The generally used units are either mmHg or kPa for measuring gas pressures inside the body,
while ambient pressure is usually indicated in mbars or in atm. Life is often made complicated for
no other reason than tradition.
1.2.4. RADIOMETER’s ABL-625 Blood Gas Analyzer
The ABL-625 with Siggaard Andersen’s built in Oxygen Saturation Algorithm (OSA) is used to
determine the arterial pH, pCO2, pO2, and tHb (including FO2Hb, FHHb, FCOHb, FMetHb, FSHb,
FFHb), ctO2, p50, px, cx and Qx values, electrolite, glucose and lactate levels. There is no need for
central venous or pulmonary artery catheterisation to determine whether oxygen availability to the
tissues are acceptable or not.
1.3.
Cardiac Output Measurement:
Obviously this “Clear Picture” still requires invasive techniques and rather complicated cardiac
output measurements to determine oxygen consumption. This later approach is mainly due to the
thought that the more invasive techniques are used the more reliable information we gain.
1.3.1. Cardiac Output Measurement in Physiology Studies:
In physiology studies CO is usually determined with an invasive cardiac output measurement
device, like dye dilution, thermodilution, aortic-flow-metry. They require either pulmonary artery
catheterisation or chest opening to apply two rings around the aorta.
1.3.2. Cardiac Output Measurement in the Intensive Care Unit:
Similarly, in current intensive care practice it is usual to use pulmonary artery catheters. The aim
of these devices are to determine mixed venous blood gas parameters, like pO2(a), sO2(v), pCO2,
pH.
An arterial line is inserted to monitor blood pressure that is displayed as a curve with minutely
updated numeric figures of systolic, diastolic and mean arterial pressures and trends of these
figures are available.
A central venous line is inserted via the jugular, subclavian or femoral veins to administer
infusions and iv. medication. This line is often used to draw central venous blood samples to
determine central venous blood gas values like sO2(cv), pO2(cv), pCO2(cv) that are obviously not
equal to mixed venous values taken from the pulmonary artery.
To monitor cardiac output it has been almost obligatory in the past 2 decades to introduce a
pulmonary artery catheter. The aim of this Swan-Ganz catheter is to determine cardiac output by
thermo-dilution technique, to measure pulmonary pressures and with the inflation of a balloon in a
pulmonary end artery to estimate pulmonary capillary wedge pressure to gain information about
left atrial and ventricular filling pressures.
Other invasive techniques have also been used like dye-dilution, continuous cardiac output
monitoring using heaters in the catheter itself.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
1.3.3. Non-Invasive Monitoring
Automatic blood pressure monitors are available to determine systolic, diastolic and mean arterial
blood pressures in cases where invasive arterial monitoring is not required anymore. Trends of
these 1 to 60 minutely readings are also available.
Non-invasive cardiac output measurement techniques like measuring temperature drop along the
extremities were used to estimate peripheral vascular resistance and from blood pressure readings
cardiac output could be determined.
Other non-invasive techniques using the Doppler principle seemed to be reliable, but rather
cumbersome to use them continuously.
The introduction of oesophageal Doppler heads seemed to have solved the problem of long term
continuous monitoring, but the position of the head can change depending on patient position.
Contour analysis based on pulse wave form processing gives information on the local flow and
pressure conditions of the actual extremity only.
Metabolic computers measuring O2 consumption and CO2 production from inspired and exhaled
gases made a breakthrough in both cardiac output and oxygen consumption measurements.
Impedance technology as a principle proved impressive, but pioneer impedance cardiographs were
rather unreliable due to insufficiencies in measurement principles and software analysis.
2.
METHODS
The combined use of RADIOMETER’s ABL 625 Blood Gas Analyser, that applies the new blood
gas parameters from Siggaard Andersen and ASKIT’s NHMS leads to a reliable, trendable and
reproducable semi-invasive haemodynamic monitoring technique. Only an indwelling arterial
catheter is required to take blood samples, and all the rest is non-invasive.
2.1. RADIOMETER’s ABL-625
This complex haemoxymeter, blood gas, electrolyte, glucose and lactate analyser [11], together
with Siggaard Andersen’s built in Oxygen Saturation Algorithm (OSA) is used to determine the
arterial pH, pCO2, pO2 (classic blood gas parameters), tHb, cteHb, FO2Hb, FHHb, FCOHb,
FMetHb, FSHb, FFHb, ctO2, p50 (Haemoxymeter parameters) and px, cx and Qx values (Siggaard
Andersen’s newly introduced Oxygen Saturation Algorithm parameters) and K+, Na+, Cl-, Ca++
(electrolites), glucose and lactate levels. Due to the newly introduced parameters of p x, cx and Qx
from Ole and Mad Siggaard Andersen, that are printed immediately in the blood gas results report,
there is no need for central venous or pulmonary artery catheterisation to determine whether
oxygen availability to the tissues are acceptable.
The simple but ingenious solution to solve the problems of traditional blood gas analysers came
from Siggaard Andersen when more than 10 000 Scandinavian blood gas samples were examined
to find correlation between sO2 and pO2 versus ctO2 and pO2. pO2 and saturation had no
correlation with ctO2.
2.1.1. Oxygen Content versus Oxygen Saturation:
With the help of a hemoximeter that measures tHb, O2Hb, HHb, COHb, MetHb, SHb and can be
corrected for FHb can easily tell the fraction of oxygenated hemoglobin, that is a real saturation
parameter versus sO2 were COHb, MetHb, SHb and FHb are not calculated with.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
2.1.2. O2 Molecules Meet Hemoglobin Molecules:
As one hemoglobin molecule binds one oxygen molecule, and if both oxygen and hemoglobin are
measured in mmol/L, saturation and fraction of oxygenated hemoglobin can be plotted on the
same “y” axis.
2.1.3. Partial Pressures of Gases
If pressures both inside and outside the body are indicated in kPa, calculations are made much
more simple, as the ambient pressure by definition is 100 kPa at sea level, which means that
fractions of inspired oxygen given in % will also tell us the inspired O2 pressure in kPa.
2.1.4. The “y” Axis:
Plotting ctO2 and ctHb instead of sO2 on the “y” axis changed the principal approach to blood gas
analysis. Now both pO2 and ctO2 together with ctHb is measured and p50 and the position of the
ODC curve is determined versus the measurement of pO2 only and calculation of sO2 from an
ideal ODC curve in other blood gas machines. It means that the actual position of the ODC is
determined for each and every blood sample. Haemoglobin (ctHb), effective haemoglobin (cteHb)
and oxygen content (ctO2) is indicated on the “y” axis against pO2(a) on the “x” axis.
2.1.5. Interpretation of the Clear Picture:
Now the blood gas status of a patient can be easily interpreted. The difference between ctO2(a) and
ctO2(v) will tell the consumed oxygen per liter of blood. If cardiac output is measured, VO2 can be
determined.
2.2.
The OSA and the “Deep Picture”
Siggaard Andersen’s Oxygen Saturation Algorithm (OSA) program introduced three new
parameters, px, cx and Qx into blood gas analysis, but also introduced the term of oxygen
availability versus oxygen delivery (DO2). This new concept of blood gas analysis is called the
“Deep Picture”.
2.2.1. Mesauring ctO2, (ctHb = FO2Hb + FHHb + FCOHb + FMetHb + FSHb + FFHb)
It is not just the question of plotting different parameters, but measuring versus calculating that
makes the principal difference.
If oxygen saturation is calculated from arterial pO2 the result can be acceptable only in ideal
situations which is definitely not the case in the intensive care unit.
2.2.2. cteHb: Effective Haemoglobin Concentration
Effective haemoglobine concentration is the amount of haemoglobin that can participate in O2
association and dissociation. cteHb = ctHb – (FCOHb + FMetHb + FSHb + FFHb)
2.2.3. p50 and the position of the ODC
If all hemoglobin and dyshemoglobin components are determined with a photometer and plotted
on the “y” axis versus the pO2 readings on the “x” axis, and these measurements are also
performed at half saturation, p50 and the position of the actual patient’s actual ODC curve is
determined.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
2.2.4. The real arterio-venous oxygen content difference (ctO2(a-v))
If ctO2 and ctHb (including FO2Hb + FHHb + FCOHb + FMetHb + FSHb +FFHb ) are measured
in both arterial and mixed venous blood, the difference of the ctO2(a) and ctO2(v) will give the
real ctO2(a-v) versus the calculated value from tHb measurements and saturation calculations.
2.2.5. Arterial Oxygen Availability
This term makes clear the difference between the “Traditional Blood Gas Analysis” and the “Deep
Picture Concept”. The available arterial oxygen is the amount of oxygen that is really available for
the tissues, in other words this is the amount of oxygen that can dissociate from haemoglobin. This
is defined by cteHb and the position of the ODC.
2.2.6. px:
Arterial Oxygen Extraction Tension
By principle px is the calculated pO2 in arterial blood after the extraction of 2.3 mmol O2 from 1 L
arterial blood. These calculations are based on the determined position of the ODC, that makes px
comparable to pO2(v) (mixed venous pO2) in normal oxygen consumption.
2.2.7. cx:
Extractable Arterial Oxygen Content
By principle cx is the calculated amount of oxygen that can be extracted from arterial blood at
normal px value (5.1 kPa), that is comparable to normal pO2(v).
2.2.8. Qx:
Cardiac Output Compensation Factor
The combined ratio between the actual px and the normal px of 5.1 kPa and the actual cx and the
normal cx of 2.3 mmol/L will give Qx. This value will inform us about the extent how we will have
to improve cardiac output to achieve acceptable tissue oxygenation among the given respiratory
and metabolic conditions.
2.2.9. Lactate
Following diminished peripheral perfusion of tissues due to increase in systemic vascular
resistance, anaerobic processes take place, that result in lactate production. Following open heart
surgery in extra-corporal circulation and hypothermia these lactate readings can be extremely
high.
2.2.10. How to interpret the “Deep Picture” using the new parameters: px, cx, Qx ?
One can question why these cx and px values are comparable to the real ctO2(a-v) and pO2(v).
They are definitely not equivalent to these real parameters. But if Qx is also involved one can
improve cardiac output, to the extent as determined by Qx, to achieve the goal of normal balance
between oxygen supply and demand. To make it simple, if Qx is 1.0 it also means that px and cx
are equivalent to pO2(v) and ctO2(a-v).
If one static parameter alone is to be chosen, that describes oxygen availability to the tissues at a
given moment, it is px. If px is in the normal range, we can be happy that the patient’s global tissue
oxygenation is acceptable. On the other hand, if dynamic information is requested to follow up
improvement or deterioration in the patient’s condition one has to monitor and trend some other
parameters as well. If px is in the normal range (that is individually defined for the actual patient
by the OSA program and printed in the blood gas report) the modified VO2 measurements are
VO2 = cx * CO. If px is not in the normal range, then cardiac output has to be corrected according
to the Qx value. For the safety of the patient lactate measurements are always there to check if
anaerobic processes are present. In other words the “Deep Picture” gives information about
oxygen availability to the tissues without the use of mixed venous blood sample data.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
2.3.
ASKIT’s NHMS
2.3.1. The Principle of Non-invasive Haemodynamic Monitor System
ASKIT’s Non-Invasive Hemodynamic Monitor System use ECG, ICG, PCG, ABPM and a unique
software that calculates beat to beat values and displays all three curves and the blood pressure
readings that can easily be called back continuously, together with the first derivative of the ICG,
the dz/dt curve. Though by principle this device is a non-invasive haemodynamic monitor it is also
capable of accepting and displaying continuous blood pressure readings from invasive blood
pressure monitors. (13, 14, 15)
2.3.2. The Electro-Mechanical Components of Systole
Thanks to the exact timing of the electro-mechanical components with the help of the combined
analysis of ECG, ICG and PCG, the pre-ejection period (from the beginning of the Q-wave to the
second component of the first heart sound), the ventricular ejection time (from the second
component of the first heart sound to the first component of the second heart sound) and the
complete electro-mechanical systole can be continuously recorded and displayed.
2.3.3. The first derivative curve (dz/dt) of the impedance cardiogram
The dz/dt curve represents flow of blood in the chest, from the inlet of the inferior and superior
cava veins to the diaphragmatic outlet of the aorta. The shape of this derivative curve is
comparable to aortic and carotid artery flow patterns. From the height and the steepness of the
individual cycles of the dz/dt curve stroke volume is determined on a beat to beat basis. Cardiac
output is determined by stroke volume and heart rate. Furthermore the shape of the dz/dt curve
contains all the information regarding flow and contractility, like the information in an ECG curve
is much more than the measurable heights and distances in it.
2.3.4. “Long Term Monitoring” with ASKIT’s NHMS
Following open heart surgery, patients are monitored continuously by ASKIT’s NHMS “long term
monitoring” program. This Non-Invasive Hemodynamic Monitoring System (NHMS), based on
combined impedance cardiographic (ICG), electrocardiographic (ECG), phonocardiographic
(PCG) and automatic blood pressure monitoring (ABPM), is used for continuous, “long term
monitoring” and measurement of postoperative stroke volume (SV), cardiac output (CO), systolic, diastolic- and mean arterial pressures (PS, PD, MABP), systemic vascular resistance (SVR), preejection period (PEP), ventricular ejection time (VET), electro-mechanical systolic time (QS2) and
all their indexes, rate pressure product (RPP), diastolic and systolic peak dz/dt ratio (D/S), ECG R
peak and dz/dtmax index (RZ) and acceleration index (ACI).
2.3.5 Displayed Curves of ECG, ICG, PCG
ECG, ICG, PCG are continuously displayed on the screen.
2.3.6. Numeric Display of Z0, CO, SVR and PEP:
Four, alarm limited, continuously updated numeric parameters are displayed on the screen. In our
practice Z0, CO, SVR and PEP is displayed as large on screen digits and continuously updated
according to the last 9 cardiac cycles. (Any 4 parameters can be displayed, but it must be defined
before the start of “Long Term Monitoring”).
2.3.7. Trends of any 4 parameters can be viewed at a time either in numeric or in graphic form.
Change of trend selection can be made even during the “long term monitoring” process.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
2.3.8. The xxx.wks file
The measured data are all available in trends and if saved in xxx.wks format they are ready for
further analysis in Excel or Works Spreadsheet.
3.
RESULTS
From ASKIT’s NHMS the saved xxx.wks files of a male patient following coronary bypass
surgery were imported to MS.Works 3.0 and these were further imported to Powerpoint in
MS.Office 97 to create diagrams for the examination of his 16 hour trends of different parameters.
Non-Invasive blood pressure measurements were automatically set to 15 minutes. All related
parameters were also updated according to these readings. The monitored parameters are grouped
according to their function and values that are comparable in one chart.
(Please see all Charts with Explanations at the end of this article.)
4.
DISCUSSION
Following open heart surgery, there is a critical 24-48 hour period when thorough monitoring is
required to maintain a satisfactory oxygen supply for both the heart and all other tissues of the
body. To properly control this situation it is important to be continuously aware of all the minutely
haemodynamic changes (including SV, HR, CO, SVR, PEP, VET, ACI) and the globally available
oxygen for the tissues [3,4,5,6] (that is determined not only by the classic pO2(a), and sO2(a)
figures, but the cteHb, ctO2(a) and the position of the ODC [12] as defined by the p50. Calculating
with all these parameters in mind is time consuming and requires accurate mathematical approach
[7,8,9,10]. RADIOMETER’s ABL-625 together with the above parameter’s automatically
displays Siggaard Andersen’s oxygen extraction tension or px value (an all in one indicator of pO2,
ctO2 and p50 of the ODC [4]), that with the 9extractable oxygen or cx value will determine the
compensation factor of Qx, that indicates what haemodynamic changes are required to achieve
satisfactory tissue oxygenation at the given respiratory condition. Based on this Qx value,
inodilator therapy (dopamine, dobutamine, dopexamine, adrenaline, noradrenaline or PDEinhibitors) are used to improve flow and MAP to optimise afterload for the heart and perfusion for
coronary, cerebral, renal, mesenteric and other vascular beds. With the continuously displayed
PEP, VET, SV, CO, MAP and SVR the infusion speed of the syringe pumps containing inodilator
agents can be optimized. If further increase in a given inodilator agent or a combination of them
will not improve CO and px, but reduces the PEP, it is not worth further increasing the speed of
the pump as the 1, 1, 2 and  receptor stimulation of these agents will only provoke
arrhythmia and myocardium oxygen supply deficiency. Instead of risking the patients myocardium
and general condition with trial and error, the treating doctor can decide immediately at the
bedside to stop further increasing the dose of inotrpic and vasodilator agents.
4.1. Conclusions
The aim of this concerted respiratory and inodilator therapy, continuously monitored by the ABL625 and the NHMS, is to achieve a px in the reference range and a Qx close to 1.0 with low lactate
levels. If these goals are met and the patient’s clinical condition is satisfactory, we can be satisfied
with the postoperative treatment of our patient.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
Chart 1.
Basic Impedance & Blood Pressure & Heart Rate
3.1. Chart 1.
Basic Impedance & Blood Pressure & Heart Rate
This diagram shows the trends of Z0, MABP, PS, PD, HR and SV.
3.1.1. Z0
(Basic Impedance)
Basic impedance has not changed significantly which means that the patient’s overall fluid
balance was normal.
3.1.2. MABP (Mean Arterial Blood Pressure)
There is a peak in mean arterial blood pressure due to an increase in systemic vascular resistance
that is predominantly caused by reduced body temperature following the relatively short reperfusion period following ECC. As this patient was given combined midazolam and fentanyl
anaesthesia this early rise in blood pressure also falls in the range of recovering from midazolam.
Following the first peak there is a gradual rise within the next 8 hours with a second peak just
before the end of monitoring. This later falls into the range of full recovery from anaesthesia
including the elimination of fentanyl and extubation.
3.1.3. PS
(Systolic Blood Pressure)
Generally the same applies as for MABP.
3.1.4. PD
(Diastolic Blood Pressure)
Generally the same applies as for MABP.
3.1.5. HR
(Heart Rate)
There is a continuous gradual increase in heart rate from 75/min to 90/min with a sharp increase at
the end of monitoring, that falls within the period of extubation.
3.1.6. SV
(Stroke Volume)
Stroke volume shows a gradual decrease from 60 ml to 53 ml.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
Chart 2.
Contractility & Pre-ejection Period
3.2. Chart 2.
Contractility & Pre-ejection Period
This diagram shows the trends of HR, SV, LVSERI and PEP
3.2.1. LVSERI
(Left Ventricular Systolic Ejection Rate Index)
This is a contractility parameter that is derived from a per se three dimensional parameter, so it
describes the improvement of contractility during the course of this early postoperative recovery.
Though SV is reduced from 60 ml to 53 ml, the contractility of the myocardium is gradually
improving.
3.2.2. PEP
(Pre-Ejection Period)
The electric component of the electro-mechanical systole shortens to a small extent from 120 msec
to 105 msec. It is worth looking at the period of increased heart rate and blood pressure readings
during the 15th hour when due to full recovery from anaesthesia and the last minutes with the
endotracheal tube, the adrenaline outflow reduced PEP to around 80 ms.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
Chart 3.
Contractility & Electro-Mechanical Components
3.3. Chart 3.
Contractility & Electro-Mechanical Components
This diagram shows the trends of HR, SV, LVSERI, PEP, VET and QS2.
SV, PEP, VET and QS2 gradually decrease while LVSERI and HR gradually increase, that are
consistent with the improvement of myocardial function, due to both revascularisation and
recovery from anaesthesia.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
Chart 4.
Contractility & Myocardial Oxygenation
3.4. Chart 4.
Contractility & Myocardial Oxygenation
This diagram shows the trends of P/V, A2/A1, D/S and ACI
3.4.1. P/V (PEP/VET)
A minimal increase from 0.45 to 0.5 can be observed that is due to a reduction of VET to a larger
extent than PEP. This also means that the risk of arrhythmia is relatively low, in spite of the fact
that PEP in itself also diminished.
3.4.2. A2/A1 (Regurgitation or Dyskinesis Index)
This index if bigger than 0.85 suggests that there is either regurgitation (due to either aortic or or
mitral valve incompetence) or dyskinesis of the heart. It is worth looking at the period of the 3 rd,
4th , 5th and 8th, 9th, 10th, 11th hours when there were dyskinetic periods due to an increase in SVR,
MABP, PS, PD and the start of full recovery from anaesthesia when adrenaline levels started to
rise. These periods are parallel with the increase in D/S value that suggests myocardial oxygen
supply insufficiency.
3.4.3. D/S (Diastolic Peak / Systolic Peak of the dz/dt Curve)
If there is an increase in the height of the diastolic component of the dz/dt curve it means that the
end diastolic filling pressure is high. It leads to dyskinesis that is an earlier sign of myocardial
oxygen supply insufficiency than ST-segment changes in an ECG, than the patient complains
about angina or than any kinetic changes in echocardiography.
3.4.4. ACI (Acceleration Index)
Acceleration is a three dimensional parameter in impedance cardiography that together with
LVSERI informs about myocardial function. Figures of ACI decrease when there is an increase in
A2/A1 or D/S.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
Chart 5.
Contractility & Systemic Vascular Resistance
3.5. Chart 5.
Contractility & Systemic Vascular Resistance
This diagram shows the trends of HR, SV, PEP, VET, QS2, RR and SVR
3.5.1. SVR
(Systemic Vascular Resistance)
There is a sharp increase in SVR due to a body temperature drop following the relatively short reperfusion period after the ECC on 28 ºC.
3.5.2. RR
(R-R distance in the ECG)
With the increase in heart rate there is a parallel decrease in RR.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
Chart 6.
3.6
Contractility & Rate Pressure Product & Systemic Vascular Resistance
Chart 6.
Contractility & Rate Pressure Product & Systemic Vascular Resistance
3.6.1. SVRI
(Systemic Vascular Resistance Index (easier to compare with RPP))
There is a peak of 4000 dyn.sec.cm-5 that is parallel with the first peak in RPP increase. It is
important that at the second peak of RPP there is no increase in SVR and SVRI.
3.6.2. RPP
(Rate Pressure Product (HR x PS))
There is a parallel peak of RPP with SVR and SVRI increase, caused by a dominant increase in
systolic blood pressure (PS), while there is no increase in SVR and SVRI at the second RPP peak.
This later RPP increase is dominantly caused by an increase in HR.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
Chart 7.
Cardiac Output & Oxygen Consumption & Lactate
3.7. Chart 7.
Cardiac Output & Oxygen Consumption & Lactate
In this chart a gradual increase in cardiac output (CO) and cardiac index (CI) is seen with a low
VO2 at the beginning of the early postoperative period. This low VO2 increases with opening of
the peripheral vasculature and remains high due to an oxygen deficit caused by an increase in
peripheral vascular resistance in the early postoperative period. By the time of extubation VO2
almost came back to normal, but adrenaline outflow caused a second increase in oxygen
consumption. Lactate levels were high during the first hours, and they go back to normal after the
oxygen deficit was settled.
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
ACKNOWLEDGEMENTS
I would like to say a big thank you to those who provided me with excellent material and critical
comments to complete this paper.
Dr. Ivar Gothgen, Head of Intensive Care Unit, University Hospital, Copenhagen, Denmark,
Ms. Inge Birkemose Møller, Radiometer International, Copenhagen, Denmark,
Mr. János Hegyi, WIP-Radiometer, Hungary,
Mr. Imre Jakobitz, General Manager, ASKIT, Hungary
Mr. János Lakatos, Chief Engineer, ASKIT, Hungary
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Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
BLOOD GAS OF PARAMETERS (in order of appearance in the text):
VO2
ctO2(a)
ctO2(v)
ctO2(a-v)
pO2
pCO2
pH
sO2
HCO3BE
avDO2
avpO2
pO2(a-v)
sO2(a-v)
pO2(A-a)
AapO2
pO2(a/A)
ctHb
ceHb
cO2Hb
cHHb
cCOHb
cMetHb
cSHb
cFHb)
FO2Hb
FHHb
FCOHb
FMetHb
FSHb
FFHb)
ctO2
p50
px
= (pO2(x))
cx
= (ctO2(x))
Qx
sO2(cv)
pO2(cv)
pCO2(cv)
sO2(cv)
pO2(cv)
pCO2(cv)
Oxygen consumption
Arterial oxygen content
Mixed venous oxygen content
Arterio-venous oxygen content difference
Partial pressure of oxygen
Partial pressure of carbon dioxide
Negative logarithm of hydrogen ion concentration
Oxygen saturation
Bicarbonate
Base excess
Arterio-venous oxygen difference (in hemodynamic calculations)
Arterio-venous oxygen tension difference
Arterio-venous oxygen tension difference
Arterio-venous oxygen saturation difference
Alveolo-arterial oxygen tension difference
Alveolo arterial oxygen tension difference
Ratio of arterial and alveolar oxygen tension
Concentration of total hemoglobin
Concentration of effective hemoglobin
Concentration of oxygenated hemoglobin
Concentration of reduced hemoglobin
Concentration of carboxy-hemoglobin
Concentration of met-hemoglobin
Concentration of sulf-hemoglobin
Concentration of fetal hemoglobin
Fraction of oxygenated hemoglobin
Fraction of reduced hemoglobin
Fraction of carboxy-hemoglobin
Fraction of met-hemoglobin
Fraction of sulf-hemoglobin
Fraction of fetal hemoglobin
Oxygen content
Oxygen tension at half saturation
Oxygen extraction tension in arterial blood
Extractable oxygen content from arterial blood
Cardiac output compensation factor
Central venous oxygen saturation
Central venous oxygen tension
Central venous carbon-dioxide tension
Mixed venous (pulmonary artery) oxygen saturation
Mixed venous (pulmonary artery) oxygen tension
Mixed venous (pulmonary artery) carbon-dioxide tension
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.
NON-INVASIVE HAEMODYNAMIC PARAMETERS (in order of appearance in the text):
NHMS
ICG
ECG
PCG
ABPM
SV
CO
CI
PS
PD
MABP
SVR
PEP
VET
QS2
RPP
D/S
RZ
ACI
Z0
LVSERI
P/V
A2/A1
Non-invasive Hemodynamic Monitoring System
impedance cardiograph
electrocardiograph
phonocardiograph
automatic blood pressure monitor
stroke volume
cardiac output
Cardiac Index
Systolic Arterial Blood Pressure
Diastolic Arterial Blood Pressure
Mean Arterial Blood Pressure
Systemic Vascular Resistance
Pre-Ejection Period
Ventricular Ejection Time
Electro-Mechanical Systole Time
Rate Pressure Product (HR * PS)
Ratio of Diastolic Peak dz/dt and Systolic Peak dz/dt
ECG R peak and dz/dtmax index
Acceleration Index
Basic Impedance
Left Ventricular Systolic Ejection Rate Index
Ratio of electric and mechanical systole (PEP/VET)
Regurgitation or Dyskinesis Index
Gábor Vereczkey, MD.
Assessment of tissue oxygenation in a cardiovascular ICU with Radiometer's ABL-625, Siggaard Andersen's OSA and ASKIT's NHMS
Adv Exp Med Biol. 1999;471:453-67.