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J Appl Physiol 89: 1569-1576, 2000;
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Vol. 89, Issue 4, 1569-1576, October 2000

Electrical admittance for filling of the heart during lower body negative pressure in humans

Yan Cai1, Søren Holm2, Morten Jenstrup1, Morten Strømstad3, Annika Eigtved2, Jørgen Warberg4, Liselotte Højgaard2, Lars Friberg2, and Niels H. Secher1,3

1 Department of Anesthesia, 2 Nuclear Medicine PET and Cyclotron Unit, and 3 Copenhagen Muscle Research Center, Rigshospitalet, DK-2100 Copenhagen; and 4 Department of Medical Physiology C, Panum Institute, University of Copenhagen, DK-2200 Copenhagen, Denmark


    ABSTRACT
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

To evaluate whether electrical admittance of intracellular water is applicable for monitoring filling of the heart, we determined the difference in intracellular water in the thorax (ThoraxICW), measured as the reciprocal value of the electrical impedance for the thorax at 1.5 and 100 kHz during lower body negative pressure (LBNP) in humans. Changes in ThoraxICW were compared with positron emission tomography-determined C15O-labeled erythrocytes over the heart. During -40 mmHg LBNP, the blood volume of the heart decreased by 21 ± 3% as the erythrocyte volume was reduced by 20 ± 2% and the plasma volume declined by 26 ± 2% (P < 0.01; n = 8). Over the heart region, LBNP was also associated with a decrease in the technetium-labeled erythrocyte activity by 26 ± 4% and, conversely, an increase over the lower leg by 92 ± 5% (P < 0.01; n = 6). For 15 subjects, LBNP increased thoracic impedance by 3.3 ± 0.3 Omega  (1.5 kHz) and 3.0 ± 0.4 Omega  (100 kHz), whereas leg impedance decreased by 9.0 ± 3.3 Omega  (1.5 kHz) and 6.1 ± 3 Omega  (100 kHz; P < 0.01). ThoraxICW was reduced by 7.1 ± 1.9 S · 10-4 (P < 0.01) and intracellular water in the leg tended to increase (from 37.8 ± 4.6 to 40.9 ± 5.0 S · 10-4; P = 0.08). The correlation between ThoraxICW and heart erythrocyte volume was 0.84 (P < 0.05). The results suggest that thoracic electrical admittance of intracellular water can be applied to evaluate changes in blood volume of the heart during LBNP in humans.

cardiac output; electrical impedance; heart rate; positron emission tomography; technetium-labeled erythrocytes


    INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

IN SITUATIONS IN WHICH bleeding, upright positioning, or anesthesia contribute to reductions in venous return, one approach to evaluate filling of the heart is to monitor thoracic impedance (TI; Refs. 5, 6, 11, 12, 17). TI relates inversely to the fluid content of the thoracic region, and, with the use of two frequencies, TI distinguishes between the extracellular water (ECW) and total body water (TBW; Refs. 2, 25, 29). Thus the difference in the reciprocal value of the impedance (the admittance) between a high- and a low-frequency current may reflect changes in the intracellular water volume (ICW; Refs. 2, 9, 26).

During acute changes, we assume, the distribution of erythrocytes accounts for most of the deviation in regional ICW, and electrical admittance reflects the distribution of erythrocytes in the body. To test the hypothesis that thoracic electrical admittance reflects filling of the heart, young subjects were exposed to lower body negative pressure (LBNP). Application of LBNP is associated with redistribution of blood from the thorax to the vascular beds in the abdomen and lower extremities to an extent that presyncopal symptoms may develop (13).

The blood volume of the heart was determined quantitatively by positron emission tomography (PET) based on inhalation of C15O (21, 22, 27). In a separate study, 99mTc-labeled erythrocytes were applied to determine the blood distribution between the thorax and the lower leg during LBNP (12). Plasma atrial natriuretic peptide (ANP) was measured to indicate the filling of the right atrium (11), and cardiac output (CO) was assessed together with central venous O2 saturation (SvO2; Refs. 4, 8).


    METHODS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Nine men participated in the PET study and six others in the 99mTc study. Their mean age was 28 (range 23-32) years, height 184 () cm, and weight 78 (71-92) kg with no significant differences between the participants in the two studies. The Ethics Committee of Copenhagen approved the project (J.nr.01-045/98), and informed consent was obtained.

The subjects reported to the laboratory in the morning after an overnight fast. After instrumentation, they were positioned in the LBNP chamber, which was sealed at the level of the iliac crest. To reduce movement of the subject, a bicycle saddle was provided, and the feet were supported. Thirty minutes of rest were followed by 20 min of supine control, 10 min of exposure to each of four LBNP pressures (-10, -20, -30, and -40 mmHg), and 20 min of recovery at atmospheric pressure. Negative pressure was graded by venting the output of a commercial vacuum cleaner, and data were collected at the end of each stage.

A cannula (1.0 mm ID, 19.5 gauge) was placed in the brachial artery of the nondominant arm for the measurement of mean arterial blood pressure (MAP). Another cannula (1.4 mm ID, 14 gauge) was introduced into the superior caval vein via the left basilic vein for central venous pressure (CVP) and SvO2. A three-lead electrocardiogram was used to record heart rate (HR), and pressures were measured by use of Bentley transducers (Uden, the Netherlands) positioned at the level of the right atrium in the midaxillary line and fastened to the subject. The transducers were connected to a Dialogue 2000 monitor (IBC-Danica, Copenhagen, Denmark).

TI and lower leg impedance (LI) were measured with a monitor that uses 200 µA at 1.5 and 100 kHz (C-guard, Danmeter, Odense, Denmark). The skin was cleaned with alcohol swabs. Pairs of electrodes (Q-10-25, Medicotest, Denmark) were used for the determination of TI. The electrodes were placed on the right sternocleidomastoid muscle and the upper left ribs in the midaxillary line with an internal distance of 5 cm. This electrode placement was also used when the correlation to changes in the central blood volume was evaluated (6, 12, 18, 19). For determination of LI, a pair of electrodes was placed on the caput tibiae and another pair on the lateral malleolus of the right leg. Changes in LI have been calibrated against the volume of the lower leg as calculated by its circumference (1). For all electrode placements, the outer two electrodes provided the electrical field, and the inner pair was sensing. Changes in ICW in the thorax (ThoraxICW) and in the leg (LegICW) were estimated as the difference between the reciprocal value of impedance at 100 and 1.5 kHz (1/Impedance at 100 kHz - 1/Impedance at 1.5 kHz) (2, 9, 26).

Stroke volume (SV) and CO were determined by impedance cardiography (Instrumentation for Medicine, Greenwich, CT; Ref. 20) and total peripheral resistance (TPR) was the ratio of MAP to CO. To avoid interaction between measurements, the cardiograph was disconnected when the other impedance values were recorded.

To determine the thoracic blood volume, we used a PET scanner (Advance, General Electric Medical Systems, Milwaukee, WI; Ref. 3) and C15O with a half-life of 118 s. PET estimates the regional concentration of the radioisotope quantitatively (28). The subject was placed in a supine position, and the axial imaging field (15 cm) was selected to cover both the heart and the lungs within 35 imaging planes. Using an external 68Ga radiation source for 20 min, we used a transmission scan for attenuation correction of the subsequent emission scans. After 2-min inhalation of C15O and a wait of 1 min to approach distribution equilibrium, a 5-min emission scan was carried out at each LBNP pressure. In the first four subjects, we observed a 1- to 3-cm caudal movement of the heart and lungs during LBNP. To evaluate to what extent such movement affected the determination of the blood volume in the region of interest (ROI), we applied a 2-min attenuation scan before each emission scan in five subjects. Within ROI, the blood volume is <A><AC>C</AC><AC>&cjs1171;</AC></A>PET/CB · V, where <A><AC>C</AC><AC>&cjs1171;</AC></A>PET is the average tracer concentration (kBq/ml), CB is the assumed "100%" blood concentration in left heart blood pool with C15O (kBq/ml), and V is the total volume of the ROI. Thus EV = BV · Hct, where EV is the erythrocyte volume, BV is blood volume, and Hct is hematocrit (22) in the brachial artery.

To limit the exposure to radioactivity, the distribution of erythrocytes to the lower legs was evaluated in another group of volunteers by use of a TCK-11 kit (6) and LBNP. The LBNP protocol was identical to that used for the PET study. Ten milliliters of blood were drawn from a forearm vein in a heparinized syringe and labeled with 37 MBq 99mTc pertechnetate to an initial binding efficiency of 98%. The 99mTc sample was then reinjected intravenously 30 min before the study. For the detection of 99mTc activity, a gamma camera with a rectangular, low-energy, high-resolution, parallel-hole collimator was used to image activity from the thorax. The ROI was selected to reflect the heart region. A relative measure of the erythrocyte activity was calculated from the mean count (total counts of ROI divided by the area). A collimated NaI single-probe detector integrating 10-s intervals was applied. The lower legs were evaluated with the active element 15 cm below the lateral margin of the patella (6). All measurements were corrected for decay using the half-life of technetium (T1/2 = 6.02 h), i.e., At = A0e-lambda t, where lambda  = ln2/T1/2, At is the activity to time t, and A0e is the activity to time 0; T1/2 is the half life of Tc.

For determination of ANP, 4 ml of arterial blood were taken in ice-cold polypropylene tubes containing heparin (20 IU/ml blood) and aprotinin (200 kIU/ml). Blood was kept on ice and, within 10 min of sampling was centrifuged at 4°C for 15 min at 3,000 rpm. The plasma was stored at -20°C. ANP was extracted from plasma by means of C18 cartridges (Sep-Pak, Waters) and determined by RIA (11). Blood samples for Hct and SvO2 were placed immediately on ice and were analyzed within minutes using an ABL 510 apparatus (Radiometer, Copenhagen, Denmark).

Data are presented as means ± SE, and statistical significance was set at a P value of 0.05. LBNP-related changes were assessed by the Friedman test, and the Wilcoxon or Mann-Whitney tests were used for comparisons. Correlations were performed with the Spearman test.


    RESULTS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Eleven subjects remained normotensive during LBNP. In four subjects, presyncopal symptoms (nausea, paleness, and a feeling of heat) developed, associated with decreases in MAP and HR. In one subject, presyncopal symptoms developed at -20 mmHg, and in the three others they appeared at -30 mmHg. The presyncopal symptoms disappeared immediately after return to atmospheric pressure.

Cardiovascular variables and ANP. All variables remained stable during supine rest. In normotensive subjects, MAP was 90 ± 3 mmHg and did not change significantly during LBNP (Fig. 1). HR (57 ± 3 beats/min) increased at LBNP -20 mmHg and reached 79 ± 4 beats/min at LBNP -40 mmHg. CVP (6 ± 1 mmHg) fell at LBNP -10 mmHg to stabilize at 0 ± 1 mmHg. SV (120 ± 6 ml) decreased at LBNP -20 mmHg and fell to 72 ± 5 ml, and CO was reduced from 7.1 ± 1.2 to 5.1 ± 0.8 l/min. SvO2 (75.7 ± 1.2%) decreased at LBNP -20 mmHg and dropped to 67.9 ± 1.5%. TPR (13.6 ± 1.6 mmHg min/l) increased at LBNP -30 mmHg and reached 18.2 ± 1.6 mmHg min/l.


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  		Fig. 1.   Heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), changes in thoracic impedance (Delta TI) at 1.5 kHz (circles) and 100 kHz (squares), changes in intracellular water over the thorax (Delta ThoraxICW), stroke volume (SV), cardiac output (CO), central venous O2 saturation (SvO2), changes in leg impedance (Delta LI) at 1.5 kHz (circles) and 100 kHz (squares), and changes in intracellular water in the leg (Delta LegICW) in 11 subjects from rest (10-20 min) to lower body negative pressure (LBNP) at -10, -20, -30, and -40 mmHg (30-60 min) and recovery (70-80 min). Values are means ± SE. * Different from baseline, P < 0.05. Solid symbols, different from preceding value, P < 0.05.

In the four subjects who developed presyncopal symptoms during LBNP, HR first increased from 59 ± 4 to 82 ± 4 beats/min and then dropped to 63 ± 2 beats/min at the time the presyncopal symptoms appeared. MAP dropped from 93 ± 3 to 69 ± 1 mmHg and CVP dropped from 7 ± 1 to 1 ± 1 mmHg. SV fell from 150 ± 6 to 83 ± 6 ml, CO from 8.6 ± 0.5 to 5.7 ± 0.4 l/min, and SvO2 from 84 ± 3% to 73 ± 3%. TPR increased from 10.8 ± 1.4 to 11.3 ± 1.3 mmHg min/l and then dropped to 10.8 ± 1.1 mmHg min/l as the presyncopal symptoms appeared. There were no significant differences in the decline in CVP, SV, CO, and SvO2 between the presyncopal and nonpresyncopal subjects. In all subjects, cardiovascular variables returned to control levels within 20 min of recovery.

ANP was reduced by 15 ± 3% at LBNP -40 mmHg, i.e., from a resting value of 23.9 ± 3.0 to 19.6 ± 2.5 pmol/l (n = 15; P < 0.01). Plasma ANP returned to the resting level 10 min after LBNP was terminated.

PET. At the end of the recovery period, the transmission image was similar to the one obtained at rest before application of LBNP (Fig. 2), indicating that movement of the thorax was <4 mm, which was consistent with observation of external landmarks. During LBNP, the heart and the lungs moved 1-3 cm caudally (Fig. 3); still, as judged by the transmission image, both regions remained within the imaging field. In contrast, the top of the liver moved out of the image and thereby contributed to overestimation of the reduction in "thoracic" blood volume.


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  		Fig. 2.   Positron emission tomography (PET) images acquired in 1 subject, including the transmission scan recorded before LBNP with the region of interest placed on the whole thorax, heart, and lung region, respectively (top); blood volume (BV) images obtained by C15O inhalation at LBNP from -10 to -40 mmHg with the region of interest placed on the left heart blood pool (4 middle rows); and the transmission scan recorded at the end of the study (bottom).



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  		Fig. 3.   PET attenuation scans over thorax at rest and at LBNP -40 mmHg for 1 subject. Scans show heart and lung regions; they moved caudally at LBNP -40 mmHg, with right arm lying at the body side.

During LBNP, movement of the organs and the concomitant enlargement of the lung space caused a mismatch between the original transmission and the emission data. In the five subjects who had separate transmission scans for each condition, there was an average underestimate of the volume of heart by 1.5%, 2.4%, 7.2%, and 8.4% at the four levels of LBNP. These values were calculated in comparison with the initial transmission scan and the LBNP pressure-specific 2-min scans. The average values listed above were then applied to the first four subjects.

The PET-determined heart blood volume began to decrease at LBNP -20 mmHg, falling from 783 ± 30 to 617 ± 26 ml (21 ± 3%; P < 0.01) at LBNP -40 mmHg, and there was a similar reduction for the lung blood volume (22 ± 4%; from 350 ± 30 to 267 ± 36 ml; P = 0.92; Fig. 4). Hct rose from 42.8 ± 0.8% to 44.4 ± 0.9%, indicating that the erythrocyte and plasma volume of the heart decreased from 335 ± 11 to 271 ± 9 ml (20 ± 2%) and from 448 ± 39 to 338 ± 39 ml (26 ± 2%), respectively (P < 0.01). The reduction in the thoracic blood volume, including the heart, lungs, thoracic muscles, and also the top of the liver, was larger (by 26 ± 3%; from 1,772 ± 96 to 1,299 ± 73 ml) than the blood volume reduction in the heart.


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  		Fig. 4.   BV of the heart and thorax, erythrocyte volume (EV) of the heart, hematocrit (Hct), BV of the lungs, and plasma volume (PV) of the heart in 8 subjects determined by PET during LBNP. Values are means ± SE. * Different from baseline, P < 0.05. Solid symbols, different from preceding value, P < 0.05.

The subject who developed presyncopal symptoms in the PET study had the lowest blood volume in the heart (680 ml), and it dropped to 520 ml (23%) when the presyncopal symptoms appeared. In this subject, Hct increased from 47.8 to 49.0%, suggesting that the erythrocyte and plasma volume of the heart dropped from 325 to 254 ml (22%) and from 355 to 265 ml (26%), respectively.

During the recovery period, the erythrocyte volume in the thorax returned to resting values within 10 min. However, even after 20 min, the plasma and blood volume of the heart remained 75 ± 20 and 90 ± 21 ml lower than the resting value, respectively.

99mTc-labeled erythrocytes. Over the heart region, the gamma camera count rate decreased by 26 ± 4% at LBNP -40 mmHg and similarly by 25 ± 3% in those subjects who developed presyncopal symptoms. Hct rose from 41.5 ± 1.3 to 43.2 ± 1.0% at LBNP -40 mmHg and from 41.5 ± 1.7 to 43.2 ± 1.4% in subjects who had presyncopal symptoms. Thus there was a similar change in plasma volume for two groups of subjects. Conversely, over the lower leg, the 99mTc count rate increased by 92 ± 5% at LBNP -40 mmHg. The elevated count rate over the lower leg was lower for those who developed presyncopal symptoms (by 60 ± 10%; Fig. 5). Ten minutes after return to atmospheric pressure, the activity of 99mTc in the heart and the lower leg was 3.8 ± 1.1% and 1.1 ± 1.2% lower than the control value, respectively.


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  		Fig. 5.   Individual changes in the activity of 99mTc-labeled erythrocytes over heart and leg in 6 subjects during LBNP. Values are means ± SE.

Electrical impedance. After 30 min of supine rest, TI was 50.3 ± 2.3 Omega  at 1.5 kHz and 37.6 ± 1.8 Omega  at 100 kHz. There was an increase in TI at LBNP -20 mmHg, and, at LBNP -40 mmHg, TI was elevated by 3.1 ± 0.4 Omega  (1.5 kHz) and 2.8 ± 0.4 Omega  (100 kHz; P < 0.01; n = 11; Fig. 1). In those subjects who developed presyncopal symptoms, the increase in TI was similar (4.2 ± 0.8 Omega ; 1.5 kHz and 3.3 ± 0.6 Omega ; 100 kHz; n = 4). After 30 min of rest, ThoraxICW was 69.0 ± 5.4 S · 10-4, and it decreased at LBNP -20 mmHg to be reduced by 6.7 ± 1.9 S · 10-4 at LBNP -40 mmHg (P < 0.01). At the time the presyncopal symptoms developed, the reduction in ThoraxICW was similar (7.0 ± 0.6 S · 10-4).

After 30 min of rest, LI was 90.7 ± 6.8 Omega  at 1.5 kHz and 69.7 ± 6.2 Omega  at 100 kHz. LI decreased at LBNP -20 mmHg and was reduced by 8.7 ± 3.2 Omega  (1.5 kHz) and by 6.0 ± 3.0 Omega  (100 kHz) at LBNP -40 mmHg. The decrease was smaller in those subjects who developed presyncopal symptoms (3.6 ± 2 Omega ; 1.5 kHz and 2.0 ± 1.8 Omega ; 100 kHz). In normotensive subjects, LegICW tended to increase (from 37.8 ± 4.6 to 40.9 ± 5.0 S; P = 0.08), whereas the change was small in those subjects who developed presyncopal symptoms.

ThoraxICW returned to the control value within 10 min after LBNP. However, after 20 min of recovery, TI remained 1.1 ± 0.3 Omega  (1.5 kHz) and 0.8 ± 0.2 Omega  (100 kHz) above the resting value. Conversely, LI remained 3.5 ± 2.7 Omega  (1.5 kHz) and 2.0 ± 2.7 Omega  (100 kHz) lower than at rest.

Changes in TI and the heart blood volume were correlated (Table 1). TI at 100 kHz exhibited the highest median correlation with changes in the blood volume of the heart [0.85 (0.74 - 0.95)] and was significant for all subjects. Changes in ThoraxICW and in the erythrocyte volume in the heart were correlated in 14 of the 15 subjects [0.84 (0.62 - 0.96)], and TI at 1.5 kHz had the lowest median correlation with changes in the erythrocyte volume [0.78 (0.43 - 0.90)] and was significant in 12 of the 15 subjects.

                              
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  		Table 1.   Variables correlated to blood, erythrocyte, and plasma volume in the heart region as determined by C15O and 99mTc for 15 subjects


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

As assessed by PET and by a gamma camera-based determination of the distribution of labeled erythrocytes, the difference in ThoraxICW between 1.5 and 100 kHz reflected changes in the amount of erythrocytes within the heart during LBNP in young, healthy subjects. A 10-min exposure to -40 mmHg LBNP reduced the volume of the heart by ~23%, corresponding to a 20% reduction in the erythrocyte volume and a 26% decline in the plasma volume, whereas the blood volume of the lower leg increased by 92%. These changes were reflected by TI and LI at both 1.5 and 100 kHz.

ThoraxICW and the reduced filling of the heart. Both C15O- and 99mTc-labeled erythrocytes demonstrated that the reduction in the count over the heart was by ~20% during LBNP -40 mmHg, and the erythrocyte count returned to the control value within 10 min after atmospheric pressure was reestablished. These changes were reflected in the deviation of ThoraxICW. There is no fluid shift between erythrocytes and blood plasma during LBNP (7). Therefore, the distribution of erythrocytes determined the deviation of ICW. The individual correlation for ThoraxICW and the erythrocyte volume was significant in 14 of the 15 subjects, and it was never below 0.6.

The calculation of ThoraxICW is based on the assumption that, at a high and a low frequency, TI reflects TBW and ECW, respectively (12, 29). The cell membrane insulates the intracellular space, but, at higher frequencies, this influence diminishes, and current flows through both the intra- and extracellular environments, i.e., TBW. Thus a difference in admittance of a high- and a low-frequency current would reflect changes in ICW. With the application of current at different frequencies, the precision in predicting ECW changes little with the use of 1-5 kHz and with the use of 50-1,000 kHz in predicting TBW (15). Thus 1.5 kHz was used as the low-frequency and 100 kHz as the high-frequency current. At 1.5 kHz, TI changed more than that at 100 kHz. At both frequencies, TI was higher than the resting value, even after 20 min of recovery, suggesting that the ECW remained reduced in the thoracic region. Conversely, leg edema remained after LBNP, and there was a lower plasma volume in the heart, as determined by PET. Accordingly, changes in TI at 1.5 kHz and in the plasma volume were correlated, as were TI at 100 kHz and the blood volume. The low correlation between TI at 1.5 kHz and blood and erythrocyte volume indicates that TI at 1.5 kHz, as expected, was imprecise in indicating changes in ICW.

There was no difference in the incremental change of TI or in the reduction of ThoraxICW for normotensive subjects and for subjects who developed presyncopal symptoms. The variation in tolerance to LBNP could be due to differences in plasma and blood volume among the subjects (10). The subject who developed presyncopal symptoms had the smallest plasma volume. Together with the data obtained by PET, a 1-Omega change in TI corresponded to a 6.8 (1.5 kHz) and 7.5% (100 kHz) deviation in volume, whereas for a 1-S · 10-4 change in ThoraxICW, the value was 3%.

Murray et al. (13) reported that, after 10-min exposure to -40 mmHg LBNP, the central blood volume (CBV) was reduced by 19%, as measured by CO (l/min), determined with a dye dilution, times the transit time (min). Such a determination of CBV represents the volume of the heart and lungs and also the blood volume in the arterial vessels to the distance (in time) of the tip of the arterial cannula. Thus CBV cannot differentiate between blood in the heart and that in the lungs. With PET and C15O, we demonstrated that there was no difference in the reduction of the blood volume in the heart and lungs during LBNP.

LegICW and venous pooling in the leg. LBNP induced venous pooling in the vascular beds of the legs, as verified by the distribution of 99mTc-labeled erythrocytes and by recording of LI. The increased count rate (60%) was lower in the presyncopal subjects than in the normotensive subjects (92%) as a smaller LBNP was reached. The larger decrease in LI at 1.5 kHz (9.0 Omega ) than in LI at 100 kHz (7.0 Omega ) reflected pooling of plasma and edema in the leg. LegICW tended to rise and remain elevated after 20 min of recovery. This was so despite the 99mTc-labeled erythrocytes reestablishing baseline values immediately after return to atmospheric pressure. This discrepancy is likely related to LBNP-induced intracellular edema in addition to changes in the distribution of erythrocytes in the body and an interstitial edema as indicated by LI at 1.5 kHz.

During LBNP, extravasation of fluid in the lower body (13) resulted in an elevated Hct. According to Tjin et al. (30), a 10% change in Hct increases resistivity by only 0.9%. Accordingly, it does not appear to be necessary to compensate for the small change in admittance that may have arisen from the noted 7% increase in Hct.

During 50° head-up tilt, 99mTc-labeled erythrocyte volume increases in the leg by 68%, and LI at 100 kHz decreases by 3 Omega  (12). The present results suggest that, in terms of the amount of fluid shifted to the leg, -40 mmHg LBNP is similar to head-up tilt to more than 50°. Musgrave et al. (14) report that -40 mmHg LBNP is similar to 70° head-up tilt when a calculation of blood in the leg is estimated by water immersion technique, whereas Patwardhan et al. (16) indicate that -48 mmHg LBNP corresponds to 50° head-up tilt in terms of change in calf circumference.

Methodological aspects. Progressive levels of LBNP caused the heart and the lungs to move 1-3 cm caudally. We applied an attenuation scan before each emission scan in five subjects. On the basis of these results, a correction was applied for the four subjects who had only a baseline attenuation scan. This scan was used to calculate an attenuation factor for each detector pair. The factor represented the fraction of photons from an external positron source that was attenuated by the tissue. The factor was used to "scale up" the regional tissue activity data in the subsequent emission scan along the line of projection between two coincident detectors. By doing so, we observed that the thoracic blood volume was reduced more (26%) than the volume calculated both for the heart and the lungs (21%). The difference between the reduction in organ and thoracic blood volume reflected that the top of the liver moved out of the image during LBNP.

We did not correct for the biological decay of the 99mTc tracer (6). After correction for physical decay, 99mTc activity was reduced by 3.8 and 1.1% over the thorax and the lower leg at the end of the recovery period. Thus there was a small overestimate of the reduction in 99mTc activity over the heart and, correspondingly, an underestimate of the lower leg blood volume during LBNP. The biological decay of 99mTc could explain some of the difference in the reduction in heart volume determined by 99mTc and C15O.

In conclusion, we found thoracic admittance to correlate with changes of the erythrocyte volume of the heart during LBNP in young, healthy men. This result supports an evaluation of the electrical properties of the thorax for monitoring the intravascular volume in situations in which the erythrocyte and plasma volumes do not vary in parallel, e.g., during sustained head-up tilt or in bleeding patients receiving an isotonic saline infusion.


    ACKNOWLEDGEMENTS

We gratefully acknowledge Mette Secher for assistance in data collection; Helle J. Larsen, Kate Pedersen, Brita Dondera, Bitten Vindberg, and Hanne Jørgensen for technical assistance; and Mikael Jensen and the staff in the cyclotron unit for providing the C15O. We also thank Birgitte Hanel and Tommi Bo Lindhardt for valuable discussion of the implication of the 99mTc tracer instability.


    FOOTNOTES

This study was supported by the Danish National Research Foundation (504-14), and the John and Birthe Meyer Foundation is gratefully acknowledged for the donation of the cyclotron and PET scanners.

Address for reprint requests and other correspondence: Y. Cai, Dept. of Anesthesia, Rigshospitalet 2041, Blegdamsvej 9, DK-2100 Copenhagen Ø, Denmark (E-mail: caiyan{at}yahoo.com).

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Received 15 October 1999; accepted in final form 5 May 2000.


    REFERENCES
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

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J APPL PHYSIOL 89(4):1569-1576
8750-7587/00 $5.00 Copyright © 2000 the American Physiological Society


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