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CARDIAC OUTPUT AND ARTERIAL BLOOD-GAS TENSION DURING LAPAROSCOPY
Brit. J. Anaesth. (1972), 44,1155
CARDIAC OUTPUT AND ARTERIAL BLOOD-GAS TENSION DURING LAPAROSCOPY G. R. KELMAN, G. H. SwAPPyl. SMITH, R. J. BENZIE AND NANETTE L. M. GORDON SUMMARY
At the present time laparoscopy is a frequentlyperformed gynaecological procedure. Although the potential hazards of this "minor operation" are disputed, most anaesthetists consider that the insufflation of several litres of carbon dioxide into the peritoneal cavity of an anaesthetized patient imposes some degree of stress on the homeostatic ability of the cardiorespiratory system; and reports of acute cardiovascular collapse during laparoscopy are not infrequent, e.g. Arthure (1970). We recently reported (Smith et al., 1971) the effects of peritoneal carbon dioxide insufflation on intra-abdominal pressure (IAP), central venous pressure (CVP), intrathoracic pressure (ITP), airway pressure, femoral venous pressure, end-tidal Pco,, G. R. KELMAN, MJX, PH.D., M.RX.P., D.I.C,
Department
of Physiology, University of Aberdeen; G. H. SWAPP, MJtx.O.G., D.CJL, Department of Obstetrics and Gynaecology, I. SMITH,* F.F^JLC.S., D.OBST.R.C.O.G., Department of Anaesthetics, R. J. BENZIE.T MJtc.o.G., M.RX.G.P.,
Department of Obstetrics and Gynaecology,
NANETTE
L. M. GORDON, F.F.A.RX.S., Department of Anaesthetics,
Aberdeen Royal Infirmary, Scotland. Present addresses: * Department of Anaesthesia, Toronto General Hospital, Toronto, Ontario, Canada. t Department of Obstetrics and Gynaecology, University of Toronto, Toronto, Ontario, Canada.
heart rate and mean arterial blood pressure in 13 anaesthetized and artificially ventilated patients prior to laparoscopy. We suggested that moderate increases of IAP (up to 25 cm H2O) may be accompanied by increases of effective cardiac filling pressure (CVPITP), and therefore (by Starling's law) of increases of cardiac output. In the present paper we report the effects of this procedure on intravascular pressures, cardiac output and arterial blood-gas tensions in 39 anaesthetized, artificially ventilated patients, studied in either the horizontal or the 25° head-down position. METHODS
Patients. A total of 39 patients (mean age 33 years, range 18-53 years) was investigated, 21 in the horizontal and 18 in the 25° head-down position. All were undergoing laparoscopy for gynaecological reasons in Aberdeen Royal Infirmary, and all had agreed to the investigation after its nature had been explained to them at a preoperative visit. All patients were in good health, apart from the gynaecological condition necessitating laparoscopy; their only minor clinical abnormality being a slight degree of anaemia (Hb= 13.2 ±1.3 g/100 ml, mean ± SD). Cardiac out-
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We have measured, in 21 horizontal and 18 25° head-down anaesthetized, artificially ventilated patients, the effea of progressive increases of intra-abdominal pressure (IAP) before, during and after laparoscopy, on: CVP, intrathoracic pressure (ITP), femoral venous pressure (FVP), cardiac output (Q), heart rate, mean arterial blood pressure (MAP), peak airway pressure, FF/QO, and arterial blood-gas tensions. FVP paralleled the increase of IAP. In both horizontal and tilted patients increases of IAP to around 20 cm H , 0 were accompanied by increases of CVP (horizontal: 4.6 cm H 3 O; tilted: 10.2 cm H,O), by smaller increases of ITP (horizontal: 1.8 cm 11,0; tilted: 32 cm H,O), and by increases of Q (from 3.9 l./min per 70 kg to 5.0 l./min per 70 kg in horizontal position; and from 4.8 L/min per 70 kg to 5.3 L/min per 70 kg in tilted patients). Greater increases of IAP to around 40 cm HjO were accompanied by falls of CVP and Cj (to 4.4 l./min per 70 kg in both positions), accompanied by parallel changes of MAP and by moderate tachycardia. There was no arterial hypoxaemia, Pao* rising from 132.0 mm Hg to 135.4 mm Hg in the horizontal patients, and from 151.3 mm Hg to 155.2 mm Hg in the tilted patients; increases of Paoo3 were slight (from 28.6 mm Hg to 32.4 mm Hg in the horizontal patients, and from 25.3 to 30.9 mm Hg in the tilted patients).
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manometry. In the latter case mean pressure was assumed to be diastolic pressure plus one-third the pulse pressure. End-tidal Pco, (PE'OOJ) was measured with a fast response infra-red carbon dioxide analyser (HartAnaesthesia. Following premedication with papaveretum 15 mgnn and Braun, URAS IU). Heart rate was measured by a Devices instanmg and hyoscine 0.3 mg, given intramuscularly 1 hour previously, anaesthesia was induced with thio- taneous rate meter attached to an e.c.g. recorder. The pentone 250-350 mg. Tracheal intubation was per- e.c.g. wave-forms were recorded on magnetic tape formed under suxamethonium-induced muscular and later played back and scrutinized for the presence relaxation, and the patients were then artificially of arrhythmias. Except in the case of one patient ventilated with 70% nitrous oxide and 30% oxygen who developed nodal rhythm soon after the start of by a Howells ventilator. Muscular relaxation was the carbon dioxide insufflation, none were seen. maintained with alcuronium, given initially in a Cardiac output was measured by the indicator dose of 0.2 mg/kg body weight, and supplemented dilution technique using indocyanine green dye when necessary by one-quarter to one-third this and a Waters photoelectric cuvette and control unit. dose. Ventilatory minute volume was set initially to The concentration of dye in arterial blood as a give an end-tidal Pco3 of 25 ± 2 mm Hg; it was function of time was obtained by withdrawing blood, then maintained constant, so that alveolar (and at 0.5 ml/sec, from a radial arterial cannula through therefore arterial) Pco3 tended to rise as carbon the densitometer with a Gilford constant-rate withdioxide was absorbed from the peritoneal surfaces. drawal pump. Arterial blood-gas tensions (Pci,, Pea, and pH) were measured on samples of arterial blood with the Measurements. Intra-abdominal pressure (IAP) was measured appropriate Radiometer blood-gas electrodes. In view of uncertainty about the relationship of with a calibrated aneroid manometer, attached to the Verres needle through which carbon dioxide the right atrium to such anatomical landmarks as was introduced into the abdominal cavity. Pressure the mid-axillary line, no attempt was made to obtain measurements were made under conditions of no absolute values of CVP. Instead, all results were expressed as increase (ACVP) above the values obgas flow. Central venous pressure (CVP) was measured taining before the start of the carbon dioxide inwith a Devices electromanometer connected to a sufflation. For similar reasons the changes of FVP percutaneously introduced central venous catheter. and FTP which accompanied this procedure were This was used also for injection of indocyanine expressed as AFVP and AITP, respectively. green dye to determine cardiac output. Our criterion for correct placement of the catheter was the Experimental procedure. presence of dearly seen respiratory and cardiac One or two litre aliquots of carbon dioxide were pressure swings on the CVP tracing; no attempt introduced into the peritoneal cavity through a was made to determine the catheter's position Verres needle until the intra-abdominal pressure radiologically. exceeded, in most cases, 40 cm HjO. Appropriate Intrathoracic pressure (ITP) was estimated by a measurements were made after the introduction of Devices electromanometer and an 8 x 1 cm oeso- each aliquot of gas. The laparoscope was then inphageal balloon, positioned according to the tech- serted, endoscopy performed and the laparoscope removed. The abdomen was then progressively nique of Milic-Emili and associates (1964). Femoral venous pressure (FVP) was measured deflated, measurements being made after each with a Devices electromanometer connected to a reduction of IAP. percutaneously-introduced femoral venous cannula. Patients who were insufflated while horizontal FVP was not measured in patients who were preg- were placed into the 25° head-down position before nant, who were taking oral contraceptives, or who introduction of the laparoscope. This change of had a history of phlebothrombosis or other venous position disturbed the hydrostatic relationships abnormality. between the patient and the various pressure transMean arterial blood pressure (MAP) was ducers; in these patients, therefore, intravascular 'measured with a Devices electromanometer con- pressure measurements were made only during nected to a radial artery cannula, or by sphygmo- abdominal inflation. puts and arterial blood gas tensions were measured in eight of the horizontal, and in five of the tilted patients.
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CARDIAC OUTPUT AND ARTERIAL BLOOD-GAS TENSIONS
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RESULTS
A
r*r
IAP fcm H2O)
•ri Time •
FIG. 2. Effect of progressive increases of intra-abdominal pressure (IAP) on central venous pressure (CVP), intrathoracic pressure (ITP), cardiac output (Q) (5 patients), and arterial Poi and Pcoa in 18 patients in 25° head-down position before and after laparoscopy.
40
A IAP (cm H2O)
30 20 10
Time
FIG. 1. Effect of progressive increases of intra-abdominal pressure (IAP) on central venous pressure (CVP), intrathoracic pressure (ITP), cardiac output (0) (8 patients) and arterial Poj and Pcoi in 21 horizontal patients before and after laparoscopy.
gressive increase of cardiac filling pressure (CVPITP), the increase being greater in the tilted patients. At higher IAPs, however, CVP fell, causing a decrease of cardiac filling pressure. And in several patients an increase of IAP above 40 cm H , 0 was accompanied by a fall of CVP to below its level at the start of carbon dioxide insufflation; for example, in one tilted patient ACVP reached a mairimiim o f +9.5 cm IL.0 at an IAP of 2L8 cm IL.0 but fell to —3.0 cm r i , 0 when IAP was raised to 40.8 cm H,O. The IAP at which ACVP was mavim^l varied considerably from patient to patient; negative values of ACVP were, however, not seen at IAPs below 40 cm IL.O. FVP rose roughly in parallel with the increases of IAP (table I). When the laparoscope was removed, IAP had decreased by some 20 cm H , 0 (figs. 1 and 2). This was due to gas leakage during insertion and/or carbon dioxide uptake from the peritoneum. CVP was, however, at that time higher than before the start of the endoscopy. This biphasic dependence of
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The increase of IAP caused by a given volume of carbon dioxide varied with the laxity of the abdominal wall. Since, however, in this technique the physiological stress to the patient probably depends more on the increase of IAP than on the degree of abdominal distension per se, results have been grouped for IAPs within the ranges 0-10 cm HjO, 10-20 cm 11,0, etc. The average amount of gas needed to produce an IAP of 40 cm H^O was roughly 8 L; the time required to reach this pressure varied from patient to patient but was of the order of 15 min. (In the non-experimental situation with a standard flow rate of 1 l./min this time would be less.) Progressive increases of IAP to about 25 cm H , 0 were accompanied, in both horizontal and tilted patients, by progressive increases of CVP and by lesser increases of ITP (figs. 1 and 2, table I). (When means are based on less than four measurements standard errors have been omitted.) Moderate increases of IAP were thus accompanied by a pro-
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BRITISH JOURNAL OF ANAESTHESIA TABLE L Effect of progressive increases of intra-cbdominal pressure (JAF)on: central venous pressure (CVP), tnnxnhoracic pressure (ITP), femoral venous pressure (FVP), cardiac output (£>), heart rate (HR), mean arterial pressure (MAP% end-expired COj concentration (FE'OOJ, and peak airway pressvrt (AWP) in 21 horiiontal and 18 25° head-doom patients prior to laparoscopy. IAP (cm HiO) ACVP (cm HK» AITP (cm HiO) AFVP (cm HiO) 0 (l./min per 70 kg) HR (beats/min) MAP (mm Hg) FE-OO, (%)
Peak AWP (cm HiO)
40-50 2.6 ±0.9 2.2 ±0.5 45.0 ± ? 4.4 ±0.6 96.2 ±3.2 98.4 ±8.5 3.6 ± ? 22.7 ±1.6
30-40 8.8 ± ? 3.8 ±0.5 30.7 ±3.8 4.8 ± ? 71.7 ±9.9 98.0±1.5 3.8 ±0.2 19.0 ± ?
40-50 4.7 ±1.3 3.6 ± ? 39.3 ±5.0 4.4 ±0.7 76.5 ±6.6 91.1 ±7.7 3.7 ±0.2 20.5 ±1.0
0 — — 4.8 ±0.5 68.8 ±3.1 92.8 ±3.0 3.3 ±0.1 17.3 ±0.8
10-20 20-30 0-10 6.5 ±0.8 10.2 ±1.3 2.9 ±0.5 2.3 ±0.2 3.2 ±0.3 1.5 ±0.1 3.4 ±1.4 11.5±2.1 15.7 ±2.0 5.3 ±1.0 4.9 ±0.8 5.3 ±0.5 74.1 ±3.5 71.1 ±3.4 71.1 ±5.7 99.0 ±3.2 101.5 ±3.9 100.3 ±6.0 3.6 ±0.1 3.8 ±0.1 3.5 ±0.1 18.8±1.1 21.6 ±1.2 20.5 ±1.7
ACVP
A FVP (cm
A IAP (cmH,O)
FIG. 3. Effect of progressive increases of intra-abdominal pressure (IAP) on femoral venous pressure (FVP) and central venous pressure (CVP) in one patient undergoing laparoscopy in 25° head-down position.
CVP on IAP is well seen in figure 3, which refers to one head-down patient in whom measurements of IAP, CVP and FVP were made at frequent intervals before, during, and after laparoscopy. There was considerable inter-patient variation among cardiac outputs (normalized to a body weight of 70 kg) measured before the start of carbon dioxide insufflation. Standard errors have, therefore, been omitted from the mean outputs shown in figures 1 and 2, although the patterns seen in these figures are, in general, statistically significant when
expressed as changes from the control, preinsufnation values. In the horizontal patients (fig. 1) the increase of cardiac filling pressure at moderate IAPs was closely paralleled by an increase of cardiac output, which rose from a mean preinflation value of 3.9 l./min per 70 kg body weight to a maximum of 5.0 l./min per 70 kg when IAP lay between 20 and 30 cm H,O. As IAP was increased further, cardiac output fell to 4.4 l./min per 70 kg at IAPs above 40 cm H 3 O. This decrease of cardiac output at high IAPs was seen also in the tilted patients (fig. 2) in whom the outputs tended to be somewhat higher than those obtained in the horizontal patients (4.8 l./min per 70 kg before the start of the inflation rising to 5.3 l./min per 70 kg at IAPs between 10 and 20 cm HjO, and then falling to 4.4 L/min per 70 kg at IAPs above 40 cm H,O). In both horizontal and head-down patients, cardiac output when the laparoscope was removed was considerably above its value at the start of the endoscopy, when IAP was maximal In the horizontal patients cardiac output increased from a mean value of 4.4 l./min per 70 kg to 5.8 L/min per 70 kg, and by a similar amount in the tilted patients. As the abdomen was then progressively deflated cardiac output fell pari-passu with the decrease of CVP. These changes of cardiac output were accompanied throughout the procedure by moderate degrees of tachycardia (particularly in the horizontal patients), and by changes of mean arterial blood
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IAP (cm H»O) ACVP (cm HiO) AITP (cm HiO) AFVP (cm HiO) 0 (l/min per 70 kg) HR (beats/min) MAP (mm Hg) FE'oo, (%) Peak AWP (cm HjO)
Horizontal patients 30-40 0-10 0 20-30 10-20 1.9 ±0.7 4.6 ±1.6 3.5 ±0.5 1.6±0J — 2.2 ±0.4 1.8 ±0.4 1.9 ±0.4 1.2±0.3 — 5.8 ±0.7 12.3 ±2.0 20.7 ±4.2 33.5 ±2.3 — 4.4 ±0.5 5.0 ±0.8 4.5 ±0.5 4.6 ±0.5 3.9 ±0.4 79.3 ±2.4 89.2 ±2.3 89.6 ±2.6 89.7 ±4.1 93.5 ±5.2 93.6 ±2.0 102.9 ±2.9 103.6 ± 2 3 102.1 ±4.1 102.1 ± 5.8 3.8 ±0.3 3.9 ±0.4 3.7 ±0.1 3.6 ±0.1 3.4 ±0.0 15.9 ±0.3 16.7 ±0.5 19.3 ±1.1 20.7 ±0.8 21.0 ±1.0 Head-down patients
CARDIAC OUTPUT AND ARTERIAL BLOOD-GAS TENSIONS
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pressure paralleling the changes of cardiac output of cardiac output consequent on inferior vena caval (table I). In the horizontal patients, mean heart rate obstruction, analogous to that which accompanies increased from a control value of 79.3 beats/min the supine hypotension syndrome of pregnancy to 962 beats/min at IAPs above 40 cm R,O; the (Holmes, 1960). However, the present study shows corresponding figures for the head-down patients that, at IAPs up to 40 cm HjO, cardiac output is were 68.8 and 76.5 beats/min, respectively. Mean increased above the values usually found during this arterial blood pressure rose by some 10 mm Hg at type of anaesthesia in the absence of surgical IAPs up to 20-30 cm H,O; it then declined as IAP stimulation (Prys-Roberts et aL, 1967), and that it was increased further. In a few patients increase of is only at very high IAPs, and then only in some IAP above 40 cm H3O was accompanied by some patients, that cardiac output is reduced. degree of arterial hypotension. Three physiological mechanisms must be conArterial blood-gas tensions were measured at three sidered when seeking to explain these changes of points during the operative procedure—before the cardiac output: (a) changes of arterial Pea,, (b) start of the carbon dioxide insufflation, when IAP changes in effective cardiac filling pressure conwas at its height, i.e. immediately before the inser- sequent on changes of CVP, and (c) reflex changes tion of the laparoscope, and at the end of the endo- in sympathoadrenal activity. scopy before IAP was restored to normal (figs. 1 and Our patients were all artificially ventilated at con2). In the case of Pa, there was considerable patient- stant minute volume. Arterial Pco, therefore tended to-patient scatter (the standard deviation of control, to rise as carbon dioxide was absorbed from the preinsufflation measurements being, in the horizon- peritoneal surfaces. The measured increases of tal patients, ±33.9 mm Hg about a mean of 132.0 Paooj were, however, only of the order of 8 mm Hg; mm Hg, and in head-down patients ± 14.6 mm Hg and from the slope of the regression line relating about a mean of 151.3 mm Hg), but the pattern of cardiac output to Paooa during nitrous oxide anaeschange in individual patients was consistent: in- thesia (Prys-Roberts et al., 1967) this increase of crease of IAP was accompanied, in both horizontal Pcoj would be expected to cause an increase of and tilted patients, by a slight increase of Pao,. In cardiac output of only some 0.3 L/min. Yet cardiac the case of the horizontal patients (fig. 1), mean output increased by almost 2 l./min in the horizonPao, increased from a control, preinsufflation value tal patients, and by about 1 l./min in the tilted of 132.0 mm Hg to 135.4 mm Hg, and to 135.0 mm patients. Hg immediately before the abdomen was deflated Carbon dioxide retention cannot, therefore, be the when IAP was above 40 cm H,O; the corresponding major factor responsible for the changes of cardiac figures for the head-down patients (fig. 2) were output which we have observed; it may, however, 151.3 mm Hg, 155.2 mm Hg and 152.1 mm Hg, act synergistically with other mechanisms. respectively. The changes of cardiac output in this study These increases of Paoj were accompanied by pro- tended to parallel the changes of effective cardiac gressive increases of Paooa (figs. 1 and 2>—28.6, filling pressure (CVP-ITP) which accompanied 32.4 and 37.0 mm Hg in the horizontal patients, abdominal inflation (figs. 1 and 2). For example, as and 25.3, 30.9 and 32.6 mm Hg in the head-down IAP was increased to 20-30 cm H,O, there was a patients—and by increases of PE'OOJ (table I). There progressive increase of both cardiac output and was no change in patients' non-respiratory acid-base effective cardiac filling pressure, while the decrease state. Abdominal inflation was accompanied by of filling pressure which occurred when IAP was moderate increases of peak AWP (table I) in both raised further was accompanied by a fall of cardiac horizontal patients (15.9 cm H , 0 increasing to 22.7 output—a response which was reversed at the end cm H , 0 at IAPs above 40 cm H,O), and tilted of the endoscopy, when IAP was again in the region patients (17.3 cm H , 0 increasing to 20.5 cm H 2 O of 25 cm H,O. This is, of course, what would be expected if the changes in cardiac output during at high IAPs). laparoscopy depended mainly on changes in cardiac filling pressure, i.e. if they occurred chiefly as a DISCUSSION result of the Frank-Starling mechanism; and is the Reports of acute cardiovascular collapse occurring explanation suggested by Hodgson, McClelland and during laparoscopy are not infrequent. At the start Newton (1970) for the 25% increase in cardiac outof this investigation it seemed that the most likely put which they found in one artificially ventilated explanation for such episodes was an acute decrease patient undergoing laparoscopy.
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The increase of cardiac output which accompanies laparoscopy is thus probably the result of at least two factors acting in concord: (1) an increase of cardiac filling pressure, due partly to mechanical factors and partly to sympathetically-induced constriction of capacitance vessels, and (2) an increase of cardiac efferent sympathetic activity. The relative roles of these two factors cannot be clearly separated at the present time. In contrast to other workers, e.g. Baratz and Karis (1969) who found, in artificially ventilated patients receiving 1% halothane vaporized in 74% nitrous oxide, 25% oxygen, a fall of Paoa during laparoscopy from 92 to 81 mm Hg, we found no evidence of arterial hypoxaemia as a result of the abdominal insufflation of considerable quantities of carbon dioxide. In view of the diaphragmatic elevation and presumed reduction of FRC which must occur during this procedure even with artificial ventilation (Alexander, Noe and Brown, 1969), this was a somewhat surprising finding for which we have no explanation. Indeed, when the simultaneously-occurring changes of arterial Pco3 are taken into account, laparoscopy was accompanied by a reduction of the alveolar-to-arterial (A-a)Po, difference, rather than by an increase which would be expected if the procedure had been accompanied by alveolar collapse in die lung bases. This finding may be related to the theoretical prediction of Kelrnan, Prys-Roberts and Nunn (1967) that increases of cardiac output should, in the presence of a constant percentage pulmonary venous admixture, be accompanied by simultaneous decreases of the (A-a)Po2 difference. Although we found no hypoxaemia during laparoscopy, it must be remembered that our patients were breathing oxygen-enriched gas mixtures; and it is possible that some patients may become hypoxaemic when breathing air after laparoscopy, when residual carbon dioxide uptake from the peritoneum continues for a time. We have not investigated this problem in detail, but found, in 6 patients, mean venous PCo2 of 42.0 and 46.3 mm Hg, 15 and 25 min respectively after laparoscopy. These findings suggest that carbon dioxide uptake after laparoscopy is not a serious problem; but clearly further study is required on this topic. There is at the present time considerable dispute about the best anaesthetic technique for laparoscopy: some workers, e.g. Scott (Scott and Julian, 1972), advocate spontaneous respiration; others, e.g. Desmond and Gordon (1970), prefer artificial ventilation. This is not the place for a detailed discussion
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The biphasic changes of CVP found in the present study may be explained in terms of the following paradigm. Increase of IAP has two opposing effects on the cardiovascular system: it forces blood out of the abdominal organs and inferior vena cava into the central venous reservoir; at the same time it dams blood back in the legs, and thus tends to decrease the central blood volume. We suggest that at low IAPs the first process is the important one. However, as IAP is progressively raised, there comes a point at which the abdominal capacitance vessels are emptied; increase of IAP beyond this point causes progressive storage of blood in the legs and thus depletes the central venous reservoir, causing a fall in CVP and of cardiac output. Such a biphasic response is well seen in figure 3, and a similar picture is seen in the mean pressures shown in figures 1 and 2. The fact that FVP closely parallels IAP suggests that there are no effective anastomoses through which blood can by-pass the inferior vena cava when this is occluded by an increase of abdominal pressure. (The question arises whether the efficacy of such anastomoses depends on the patient's parity and on whether or not she is pregnant at the time of laparoscopy. Analysis of our present results does not permit a definite answer to this question, which is currently under investigation in a larger series of patients.) In figure 3, CVP does not return to its preoperation value when IAP is decreased to zero after laparoscopy. In conjunction with the normal or somewhat increased cardiac outputs found at that time, this suggests continuing constriction of capacitance vessels as a result of increased sympathoadrenal activity. The relatively high outputs found immediately before removal of the laparoscope (figs. 1 and 2), compared with values found at comparable IAPs during abdominal inflation also suggests increased sympathoadrenal activity; as does the tachycardia. (Bainbridge's reflex—an increase of heart rate in response to an increase of cardiac filling pressure—is generally thought to be of minimal importance in man although a rigorous investigation of this topic appears not to have been made.) This increase of sympathoadrenal activity is presumably a reflex response to the surgical stimulus of laparoscopy performed under fairly light anaesthesia. Anaesthetists who use epidural anaesthesia for laparoscopy say that this procedure is commonly accompanied by severe shoulder pain, presumably the result of stimulation of the diaphragmatic peritoneum.
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CARDIAC OUTPUT AND ARTERIAL BLOOD-GAS TENSIONS
laparoscopy is better understood, patients undergoing this operation should be carefully monitored. In view of the fall of CVP and cardiac output which may occur at high intra-abdominal pressures, IAP should be limited to, say, 30 cm rL.0, a pressure which gives good surgical exposure. Also, since these patients may have central hypovolaemia as a result of venous pooling in the legs, the use of IPPV with excessive inflation pressures should be avoided. ACKNOWLEDGEMENTS
We thank the staff of the Pulmonary Function Laboratory, Aberdeen Royal Infirmary, for performing the blood-gas analyses. This investigation was aided in part by a grant from the Scottish Hospitals Endowments Research Trust (to G.R.K.). REFERENCES
Alexander, G. D., Noe, F. E., and Brown, E. M. (1969). Anesthesia for pelvic laparoscopy. Anesth. Analg. Curr. Res., 48, 14. Arthure, H. (1970). Laparoscopy hazard. Brit. med. J., 4, 492. Baratz, R. A., and Karis, J. H. (1969). Blood gas studies during laparoscopy under general anesthesia. Anesthesiology, 30, 463. Desmond, J., and Gordon, R. A. (1970). Ventilation in patients anaesthetized for laparoscopy. Canad. Anaesth. Soc. J., 17, 378. Hodgson, C , McClelland, R. M. A., and Newton, J. R. (1970). Some effects of the peritoneal insufflation of carbon dioxide at laparoscopy. Anaesthesia, 25, 382. Holmes, F. (1960). The supine hypotension syndrome; its importance to the anaesthetist. Anaesthesia, 15, 298. Kelman, G. R., Nunn, J. F., Prys-Roberts, C , and Greenbaum, R. (1967). The influence of cardiac output on arterial oxygenation: a theoretical study. Brit. J. Anaesth., 39, 450. Milic-Emili, J., Mead, J., Turner, J. M., and Glauser, E. M. (1964). Improved technique for estimating pleural pressure from esophageal balloons. J. appl. Physiol, 19, 207. Price, H. L. (1967). Circulation during Anesthesia and Operation, p. 86. Springfield: Thomas. Prys-Roberts, C , Kelman, G. R., Greenbaum, R., and Robinson, R. H. (1967). Circulatory influences of artificial ventilation during nitrous oxide anaesthesia in man. I I : Results; the relative influence of mean intrathoracic pressure and arterial carbon dioxide tension. Brit. J. Anaesth.. 39, 533. Scott, D. B., and Julian, D. G. (1972). Observations on cardiac arrhythmias during laparoscopy. Brit. med. J., 1, 411. Smith, I., Benzie, R. J., Gordon, Nanette L. M., Kelman, G. R., and Swapp G. H. (1971). Cardiovascular effects of peritoneal insufflation of carbon dioxide for laparoscopy. Brit. med. J., 3, 410.
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of this matter; but we believe that our results show that, in patients with a normal cardiovascular system, artificial ventilation provides a considerable safety margin It prevents cardiac arrhythmias and arterial hypercapnia and hypoxaemia; and the reduction of cardiac output and arterial hypotension which may occur at very high intra-abdominal pressures do not occur until IAP exceeds at least 40 cm H,O. This is greater than the pressure—of the order of 30 cm H2O—required for satisfactory surgical exposure. The volume of carbon dioxide required to raise IAP to about 30 cm H , 0 varies considerably from patient to patient. At this pressure the space between the peritoneum of die anterior abdominal wall and the intra-abdominal organs in the lower abdomen is such that the risk of injury to these organs during introduction of the 11 mm trocar for the laparoscope is minimal. In addition, this pressure compresses the gut against the posterior abdominal wall, ensuring a clear view of the pelvic viscera and minimizing risk of injury to intestine, ureter, etc., when diathermy is used (Annual Report of Medical and Dental Defence Union of Scotland, 1971). There remains the fact that our results do not suggest a cause for the acute cardiovascular collapse which has been reported during laparoscopy, even at quite moderate IAPs. Pressures of up to 40 cm HjO appear to be well tolerated; and in artificially ventilated patients, inspiring an oxygen-enriched gas mixture (30%), arterial hypoxaemia does not seem to occur. We have seen one case of cardiac arrest (successfully resuscitated) since starting the present investigation; this near-disaster was probably the result of carbon dioxide embolism, and will be discussed in greater detail elsewhere. The remaining factor to be considered is the possibility of severe bradycardia and/or cardiac asystole from a reflex increase of cardiac vagal tone consequent on peritoneal manipulation. While there is no evidence at present to suggest that this phenomenon is important during laparoscopy, the reflex is well established (see e.g. Price, 1967), and we suggest it should not be dismissed out of hand. Our results suggest that the homeostatic ability of an anaesthetized and artificially ventilated patient's cardiovascular system is such that it can withstand an increase of IAP up to at least 40 cm HjO. We do not, however, wish our results to engender a false sense of security; and we would recommend that, until the applied physiology of
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1162 DEBIT CARDIAQUE ET PRESSIONS DES GAZ SANGUINS ARTERIELS DURANT LA LAPAROSCOPIE SOMMAIRE
HERZMINUTENVOLUMEN UND ARTERIELLE BLUTGASDRUCKE WAHREND DER LAPAROSKOPIE ZUSAMMENFA S SUNG
Bei narkotisierten, kiinstlich beatmeten Patienten, von denen 21 waagerecht und 18 mit einer Kopfsenkung von 25° gelagert waren, wurde die Wirkung von progredient ansteigendem intraabdominellen Druck (LAP) vor, wfihrend und nachder Laparoskopie auf: ZVD, intratborakalen Druck (TTP), Femoralvenendruck (FVP), Herzminutenvohimen (Q), Herzfrequenz, mittel. art. Blutdruck (MAP), Luftwegespitzendruck, FE'OO, und auf die Blutgasdrucke gemessen. Der FVP lief dem Anstieg des IAP parallel. Sowohl bei den waagerecht gelagerten Patienten als auch bei den gekippten gingen die Anstiege des IAP auf ca. 20 cm HiO einher mit
GASTO CARDIACO Y TENSIONES GASEOSAS EN LA SANGRE ARTERIAL DURANTE LA LAPAROSCOPIA RESUMEN
Hemos medido en 21 pacientes horizontales y 18 pacientes con inchnaci6n hacia abajo de 25° de la cabeza anestesiados y ventilados artificiahnente el efecto de incrementos progresivos de la presi6n intraabdominal (IAP) antes, durante y despues de la laparoscopia sobre: CVP, presion intratoracica (ITP), presi6n venosa femoral (FVP), gasto cardlaco (0), frecuenda canHaca, presi6n arterial media (MAP), presi6n pico de la via aerea, FE'OO, y tensiones gaseosas en la sangre arteriaL FVP varii paralelamente con el incremento de IAP. Tanto en pacientes horizontales como en pacientes inclinados, los uicrenientos de IAP de aproximadamente 20 cm H,O fueron acompariados por incrementos de CVP (horizontal: 4,6 cm HiO; indinado: 10^ cm H,O), por incrementos menores de ITP (horizontal 1,8 cm HjO; indinado 3J. cm H,O), y por incrementos de Q (desde 3,9 l./min por 70 kg hasta 5,0 l./min para 70 kg en poskidn horizontal; y desde 4,8 L/min para 70 kg hasta 53 L/min para 70 kg en padentes inclinados). Incrementos mayores de IAP de alrededor de 40 cm HjO fueron acompanados por cafdas de CVP y Q (hasta 4,4 L/min para 70 kg en ambas posiciones), junto con cambios paralelos de MAP y taquicardia moderada. No hubo hipoxemia arterial, aumentando la Pao, desde 132,0 mm Hg hasta 135,4 mm Hg en los pacientes horizootales y desde 1513 mm Hg hasta 155,2 mm Hg en los pacientes inclinados; los incrementos de Paooj fueron ligeros (desde 28,6 mm Hg hasta 32,4 mm Hg en padentes horizontales y desdrt 25,3 hasta 30,9 mm Hg en tos padentes inclidados).
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Chez dcs patients anesthesias, artifidellement yentiles dont 21 en position horizon talc et 18 en position inclinee a 25*, tfite basse, nous avons mesuri l'effet de 1'augmentation progressive de la pression intraabdominale (JAP) avant, pendant etapres laparoscopie sur: CVP, pression intrathoracique (FTP), pression veineuse femorale (FVP), dibit cardiaque (Q), frequence cardiaque, pression arrfrielle moyenne (MAP), pression mgTirrmli» des voies d'air, FE'OO, et pressions des gaz sangiiins arteriels. L'augmentatkm de FVP etait parallele 4 ceJle de IAP. Aussi bien chez les malades en position horizontale qu'inclinee, on observa que les augmentations de IAP a environ 20 cm H,O itaient accompagnees d'augmentations de CVP (horizontal: 4,6 cm H,O; inclirrf: 10,2 cm H,O), d'augmentations moins prononcees de ITP (horizontal: 1,8 cm HjO; inclined 3,2 cm HiO), et d'augmentations de 0 (de 3,9 1/min par 70 kg i 5,0 1/min par 70 kg en position horizontale; et de 4,8 1/min par 70 kg a 53 1/min par 70 kg en position inclinee). Des plus fortes augmentations de IAP a environ 40 cm HtO s'accompagnaient de chutes de CVP et Q (a 4,4 1/min par 70 kg dans les deux positions), avec modifications paralleles de MAP et tachycardia moderee. II n'y avait pas dTiypoxeinie arte'rielle, la Paca augmentant de 132 mm Hg a 135,4 mm Hg chez les patients horizontaux, et de 151,3 mm Hg a 155^2 mm Hg chez les malades en position inclinee; les augmentations de la Paoo, etaient legeres (de 28,6 mm Hg a 32,4 mm Hg et de 253 a 30,9 mm Hg resp. en position horizontale et inclinee).
Ansuegen des CVD (waagerecht 4.6 cm HiO, gekippt 10.2 a n HiO), mit geringeren Anstiegen des ITP (waagerecht: 1.8 cm H,O, gekippt: 3.2 cm HjO) und mit Anstiegen von Q (waagerecht: von 3.9 L/min/70 kg auf 5.0 L/min/70 kg, gekippt: von 4.8 L/min/70 kg auf 5.3 L/min/70 kg). Hohere Anstiege von IAP auf ca 40 cm H J O waren von einem ZVD- und Q-Abfall begleitet (auf 4.4 l./min/70 kg in beiden Positiooen), und von parallel verlaufenden VerSnderungen von MAP und einer maOiggradigen Tachycardie. Es entstand keine arterielle Hypoxamie, bei einem Pao,-Anstieg von 132.0 mm Hg auf 135.4 mm Hg bei waagerecht gelagerten und von 151.3 mm Hg auf 155.2 mm Hg bei gekippten Patienten. Anstiege von Paooi waren gering (von 28.6 mm Hg auf 32.4 mm Hg bei waagerecht gelagerten und von 25.3 auf 30.9 mm Hg bei gekippten Patienten).
CARDIAC OUTPUT AND ARTERIAL BLOOD-GAS TENSION DURING LAPAROSCOPY G. R. KELMAN, G. H. SwAPPyl. SMITH, R. J. BENZIE AND NANETTE L. M. GORDON SUMMARY
At the present time laparoscopy is a frequentlyperformed gynaecological procedure. Although the potential hazards of this "minor operation" are disputed, most anaesthetists consider that the insufflation of several litres of carbon dioxide into the peritoneal cavity of an anaesthetized patient imposes some degree of stress on the homeostatic ability of the cardiorespiratory system; and reports of acute cardiovascular collapse during laparoscopy are not infrequent, e.g. Arthure (1970). We recently reported (Smith et al., 1971) the effects of peritoneal carbon dioxide insufflation on intra-abdominal pressure (IAP), central venous pressure (CVP), intrathoracic pressure (ITP), airway pressure, femoral venous pressure, end-tidal Pco,, G. R. KELMAN, MJX, PH.D., M.RX.P., D.I.C,
Department
of Physiology, University of Aberdeen; G. H. SWAPP, MJtx.O.G., D.CJL, Department of Obstetrics and Gynaecology, I. SMITH,* F.F^JLC.S., D.OBST.R.C.O.G., Department of Anaesthetics, R. J. BENZIE.T MJtc.o.G., M.RX.G.P.,
Department of Obstetrics and Gynaecology,
NANETTE
L. M. GORDON, F.F.A.RX.S., Department of Anaesthetics,
Aberdeen Royal Infirmary, Scotland. Present addresses: * Department of Anaesthesia, Toronto General Hospital, Toronto, Ontario, Canada. t Department of Obstetrics and Gynaecology, University of Toronto, Toronto, Ontario, Canada.
heart rate and mean arterial blood pressure in 13 anaesthetized and artificially ventilated patients prior to laparoscopy. We suggested that moderate increases of IAP (up to 25 cm H2O) may be accompanied by increases of effective cardiac filling pressure (CVPITP), and therefore (by Starling's law) of increases of cardiac output. In the present paper we report the effects of this procedure on intravascular pressures, cardiac output and arterial blood-gas tensions in 39 anaesthetized, artificially ventilated patients, studied in either the horizontal or the 25° head-down position. METHODS
Patients. A total of 39 patients (mean age 33 years, range 18-53 years) was investigated, 21 in the horizontal and 18 in the 25° head-down position. All were undergoing laparoscopy for gynaecological reasons in Aberdeen Royal Infirmary, and all had agreed to the investigation after its nature had been explained to them at a preoperative visit. All patients were in good health, apart from the gynaecological condition necessitating laparoscopy; their only minor clinical abnormality being a slight degree of anaemia (Hb= 13.2 ±1.3 g/100 ml, mean ± SD). Cardiac out-
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We have measured, in 21 horizontal and 18 25° head-down anaesthetized, artificially ventilated patients, the effea of progressive increases of intra-abdominal pressure (IAP) before, during and after laparoscopy, on: CVP, intrathoracic pressure (ITP), femoral venous pressure (FVP), cardiac output (Q), heart rate, mean arterial blood pressure (MAP), peak airway pressure, FF/QO, and arterial blood-gas tensions. FVP paralleled the increase of IAP. In both horizontal and tilted patients increases of IAP to around 20 cm H , 0 were accompanied by increases of CVP (horizontal: 4.6 cm H 3 O; tilted: 10.2 cm H,O), by smaller increases of ITP (horizontal: 1.8 cm 11,0; tilted: 32 cm H,O), and by increases of Q (from 3.9 l./min per 70 kg to 5.0 l./min per 70 kg in horizontal position; and from 4.8 L/min per 70 kg to 5.3 L/min per 70 kg in tilted patients). Greater increases of IAP to around 40 cm HjO were accompanied by falls of CVP and Cj (to 4.4 l./min per 70 kg in both positions), accompanied by parallel changes of MAP and by moderate tachycardia. There was no arterial hypoxaemia, Pao* rising from 132.0 mm Hg to 135.4 mm Hg in the horizontal patients, and from 151.3 mm Hg to 155.2 mm Hg in the tilted patients; increases of Paoo3 were slight (from 28.6 mm Hg to 32.4 mm Hg in the horizontal patients, and from 25.3 to 30.9 mm Hg in the tilted patients).
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manometry. In the latter case mean pressure was assumed to be diastolic pressure plus one-third the pulse pressure. End-tidal Pco, (PE'OOJ) was measured with a fast response infra-red carbon dioxide analyser (HartAnaesthesia. Following premedication with papaveretum 15 mgnn and Braun, URAS IU). Heart rate was measured by a Devices instanmg and hyoscine 0.3 mg, given intramuscularly 1 hour previously, anaesthesia was induced with thio- taneous rate meter attached to an e.c.g. recorder. The pentone 250-350 mg. Tracheal intubation was per- e.c.g. wave-forms were recorded on magnetic tape formed under suxamethonium-induced muscular and later played back and scrutinized for the presence relaxation, and the patients were then artificially of arrhythmias. Except in the case of one patient ventilated with 70% nitrous oxide and 30% oxygen who developed nodal rhythm soon after the start of by a Howells ventilator. Muscular relaxation was the carbon dioxide insufflation, none were seen. maintained with alcuronium, given initially in a Cardiac output was measured by the indicator dose of 0.2 mg/kg body weight, and supplemented dilution technique using indocyanine green dye when necessary by one-quarter to one-third this and a Waters photoelectric cuvette and control unit. dose. Ventilatory minute volume was set initially to The concentration of dye in arterial blood as a give an end-tidal Pco3 of 25 ± 2 mm Hg; it was function of time was obtained by withdrawing blood, then maintained constant, so that alveolar (and at 0.5 ml/sec, from a radial arterial cannula through therefore arterial) Pco3 tended to rise as carbon the densitometer with a Gilford constant-rate withdioxide was absorbed from the peritoneal surfaces. drawal pump. Arterial blood-gas tensions (Pci,, Pea, and pH) were measured on samples of arterial blood with the Measurements. Intra-abdominal pressure (IAP) was measured appropriate Radiometer blood-gas electrodes. In view of uncertainty about the relationship of with a calibrated aneroid manometer, attached to the Verres needle through which carbon dioxide the right atrium to such anatomical landmarks as was introduced into the abdominal cavity. Pressure the mid-axillary line, no attempt was made to obtain measurements were made under conditions of no absolute values of CVP. Instead, all results were expressed as increase (ACVP) above the values obgas flow. Central venous pressure (CVP) was measured taining before the start of the carbon dioxide inwith a Devices electromanometer connected to a sufflation. For similar reasons the changes of FVP percutaneously introduced central venous catheter. and FTP which accompanied this procedure were This was used also for injection of indocyanine expressed as AFVP and AITP, respectively. green dye to determine cardiac output. Our criterion for correct placement of the catheter was the Experimental procedure. presence of dearly seen respiratory and cardiac One or two litre aliquots of carbon dioxide were pressure swings on the CVP tracing; no attempt introduced into the peritoneal cavity through a was made to determine the catheter's position Verres needle until the intra-abdominal pressure radiologically. exceeded, in most cases, 40 cm HjO. Appropriate Intrathoracic pressure (ITP) was estimated by a measurements were made after the introduction of Devices electromanometer and an 8 x 1 cm oeso- each aliquot of gas. The laparoscope was then inphageal balloon, positioned according to the tech- serted, endoscopy performed and the laparoscope removed. The abdomen was then progressively nique of Milic-Emili and associates (1964). Femoral venous pressure (FVP) was measured deflated, measurements being made after each with a Devices electromanometer connected to a reduction of IAP. percutaneously-introduced femoral venous cannula. Patients who were insufflated while horizontal FVP was not measured in patients who were preg- were placed into the 25° head-down position before nant, who were taking oral contraceptives, or who introduction of the laparoscope. This change of had a history of phlebothrombosis or other venous position disturbed the hydrostatic relationships abnormality. between the patient and the various pressure transMean arterial blood pressure (MAP) was ducers; in these patients, therefore, intravascular 'measured with a Devices electromanometer con- pressure measurements were made only during nected to a radial artery cannula, or by sphygmo- abdominal inflation. puts and arterial blood gas tensions were measured in eight of the horizontal, and in five of the tilted patients.
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CARDIAC OUTPUT AND ARTERIAL BLOOD-GAS TENSIONS
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RESULTS
A
r*r
IAP fcm H2O)
•ri Time •
FIG. 2. Effect of progressive increases of intra-abdominal pressure (IAP) on central venous pressure (CVP), intrathoracic pressure (ITP), cardiac output (Q) (5 patients), and arterial Poi and Pcoa in 18 patients in 25° head-down position before and after laparoscopy.
40
A IAP (cm H2O)
30 20 10
Time
FIG. 1. Effect of progressive increases of intra-abdominal pressure (IAP) on central venous pressure (CVP), intrathoracic pressure (ITP), cardiac output (0) (8 patients) and arterial Poj and Pcoi in 21 horizontal patients before and after laparoscopy.
gressive increase of cardiac filling pressure (CVPITP), the increase being greater in the tilted patients. At higher IAPs, however, CVP fell, causing a decrease of cardiac filling pressure. And in several patients an increase of IAP above 40 cm H , 0 was accompanied by a fall of CVP to below its level at the start of carbon dioxide insufflation; for example, in one tilted patient ACVP reached a mairimiim o f +9.5 cm IL.0 at an IAP of 2L8 cm IL.0 but fell to —3.0 cm r i , 0 when IAP was raised to 40.8 cm H,O. The IAP at which ACVP was mavim^l varied considerably from patient to patient; negative values of ACVP were, however, not seen at IAPs below 40 cm IL.O. FVP rose roughly in parallel with the increases of IAP (table I). When the laparoscope was removed, IAP had decreased by some 20 cm H , 0 (figs. 1 and 2). This was due to gas leakage during insertion and/or carbon dioxide uptake from the peritoneum. CVP was, however, at that time higher than before the start of the endoscopy. This biphasic dependence of
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The increase of IAP caused by a given volume of carbon dioxide varied with the laxity of the abdominal wall. Since, however, in this technique the physiological stress to the patient probably depends more on the increase of IAP than on the degree of abdominal distension per se, results have been grouped for IAPs within the ranges 0-10 cm HjO, 10-20 cm 11,0, etc. The average amount of gas needed to produce an IAP of 40 cm H^O was roughly 8 L; the time required to reach this pressure varied from patient to patient but was of the order of 15 min. (In the non-experimental situation with a standard flow rate of 1 l./min this time would be less.) Progressive increases of IAP to about 25 cm H , 0 were accompanied, in both horizontal and tilted patients, by progressive increases of CVP and by lesser increases of ITP (figs. 1 and 2, table I). (When means are based on less than four measurements standard errors have been omitted.) Moderate increases of IAP were thus accompanied by a pro-
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BRITISH JOURNAL OF ANAESTHESIA TABLE L Effect of progressive increases of intra-cbdominal pressure (JAF)on: central venous pressure (CVP), tnnxnhoracic pressure (ITP), femoral venous pressure (FVP), cardiac output (£>), heart rate (HR), mean arterial pressure (MAP% end-expired COj concentration (FE'OOJ, and peak airway pressvrt (AWP) in 21 horiiontal and 18 25° head-doom patients prior to laparoscopy. IAP (cm HiO) ACVP (cm HK» AITP (cm HiO) AFVP (cm HiO) 0 (l./min per 70 kg) HR (beats/min) MAP (mm Hg) FE-OO, (%)
Peak AWP (cm HiO)
40-50 2.6 ±0.9 2.2 ±0.5 45.0 ± ? 4.4 ±0.6 96.2 ±3.2 98.4 ±8.5 3.6 ± ? 22.7 ±1.6
30-40 8.8 ± ? 3.8 ±0.5 30.7 ±3.8 4.8 ± ? 71.7 ±9.9 98.0±1.5 3.8 ±0.2 19.0 ± ?
40-50 4.7 ±1.3 3.6 ± ? 39.3 ±5.0 4.4 ±0.7 76.5 ±6.6 91.1 ±7.7 3.7 ±0.2 20.5 ±1.0
0 — — 4.8 ±0.5 68.8 ±3.1 92.8 ±3.0 3.3 ±0.1 17.3 ±0.8
10-20 20-30 0-10 6.5 ±0.8 10.2 ±1.3 2.9 ±0.5 2.3 ±0.2 3.2 ±0.3 1.5 ±0.1 3.4 ±1.4 11.5±2.1 15.7 ±2.0 5.3 ±1.0 4.9 ±0.8 5.3 ±0.5 74.1 ±3.5 71.1 ±3.4 71.1 ±5.7 99.0 ±3.2 101.5 ±3.9 100.3 ±6.0 3.6 ±0.1 3.8 ±0.1 3.5 ±0.1 18.8±1.1 21.6 ±1.2 20.5 ±1.7
ACVP
A FVP (cm
A IAP (cmH,O)
FIG. 3. Effect of progressive increases of intra-abdominal pressure (IAP) on femoral venous pressure (FVP) and central venous pressure (CVP) in one patient undergoing laparoscopy in 25° head-down position.
CVP on IAP is well seen in figure 3, which refers to one head-down patient in whom measurements of IAP, CVP and FVP were made at frequent intervals before, during, and after laparoscopy. There was considerable inter-patient variation among cardiac outputs (normalized to a body weight of 70 kg) measured before the start of carbon dioxide insufflation. Standard errors have, therefore, been omitted from the mean outputs shown in figures 1 and 2, although the patterns seen in these figures are, in general, statistically significant when
expressed as changes from the control, preinsufnation values. In the horizontal patients (fig. 1) the increase of cardiac filling pressure at moderate IAPs was closely paralleled by an increase of cardiac output, which rose from a mean preinflation value of 3.9 l./min per 70 kg body weight to a maximum of 5.0 l./min per 70 kg when IAP lay between 20 and 30 cm H,O. As IAP was increased further, cardiac output fell to 4.4 l./min per 70 kg at IAPs above 40 cm H 3 O. This decrease of cardiac output at high IAPs was seen also in the tilted patients (fig. 2) in whom the outputs tended to be somewhat higher than those obtained in the horizontal patients (4.8 l./min per 70 kg before the start of the inflation rising to 5.3 l./min per 70 kg at IAPs between 10 and 20 cm HjO, and then falling to 4.4 L/min per 70 kg at IAPs above 40 cm H,O). In both horizontal and head-down patients, cardiac output when the laparoscope was removed was considerably above its value at the start of the endoscopy, when IAP was maximal In the horizontal patients cardiac output increased from a mean value of 4.4 l./min per 70 kg to 5.8 L/min per 70 kg, and by a similar amount in the tilted patients. As the abdomen was then progressively deflated cardiac output fell pari-passu with the decrease of CVP. These changes of cardiac output were accompanied throughout the procedure by moderate degrees of tachycardia (particularly in the horizontal patients), and by changes of mean arterial blood
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IAP (cm H»O) ACVP (cm HiO) AITP (cm HiO) AFVP (cm HiO) 0 (l/min per 70 kg) HR (beats/min) MAP (mm Hg) FE'oo, (%) Peak AWP (cm HjO)
Horizontal patients 30-40 0-10 0 20-30 10-20 1.9 ±0.7 4.6 ±1.6 3.5 ±0.5 1.6±0J — 2.2 ±0.4 1.8 ±0.4 1.9 ±0.4 1.2±0.3 — 5.8 ±0.7 12.3 ±2.0 20.7 ±4.2 33.5 ±2.3 — 4.4 ±0.5 5.0 ±0.8 4.5 ±0.5 4.6 ±0.5 3.9 ±0.4 79.3 ±2.4 89.2 ±2.3 89.6 ±2.6 89.7 ±4.1 93.5 ±5.2 93.6 ±2.0 102.9 ±2.9 103.6 ± 2 3 102.1 ±4.1 102.1 ± 5.8 3.8 ±0.3 3.9 ±0.4 3.7 ±0.1 3.6 ±0.1 3.4 ±0.0 15.9 ±0.3 16.7 ±0.5 19.3 ±1.1 20.7 ±0.8 21.0 ±1.0 Head-down patients
CARDIAC OUTPUT AND ARTERIAL BLOOD-GAS TENSIONS
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pressure paralleling the changes of cardiac output of cardiac output consequent on inferior vena caval (table I). In the horizontal patients, mean heart rate obstruction, analogous to that which accompanies increased from a control value of 79.3 beats/min the supine hypotension syndrome of pregnancy to 962 beats/min at IAPs above 40 cm R,O; the (Holmes, 1960). However, the present study shows corresponding figures for the head-down patients that, at IAPs up to 40 cm HjO, cardiac output is were 68.8 and 76.5 beats/min, respectively. Mean increased above the values usually found during this arterial blood pressure rose by some 10 mm Hg at type of anaesthesia in the absence of surgical IAPs up to 20-30 cm H,O; it then declined as IAP stimulation (Prys-Roberts et aL, 1967), and that it was increased further. In a few patients increase of is only at very high IAPs, and then only in some IAP above 40 cm H3O was accompanied by some patients, that cardiac output is reduced. degree of arterial hypotension. Three physiological mechanisms must be conArterial blood-gas tensions were measured at three sidered when seeking to explain these changes of points during the operative procedure—before the cardiac output: (a) changes of arterial Pea,, (b) start of the carbon dioxide insufflation, when IAP changes in effective cardiac filling pressure conwas at its height, i.e. immediately before the inser- sequent on changes of CVP, and (c) reflex changes tion of the laparoscope, and at the end of the endo- in sympathoadrenal activity. scopy before IAP was restored to normal (figs. 1 and Our patients were all artificially ventilated at con2). In the case of Pa, there was considerable patient- stant minute volume. Arterial Pco, therefore tended to-patient scatter (the standard deviation of control, to rise as carbon dioxide was absorbed from the preinsufflation measurements being, in the horizon- peritoneal surfaces. The measured increases of tal patients, ±33.9 mm Hg about a mean of 132.0 Paooj were, however, only of the order of 8 mm Hg; mm Hg, and in head-down patients ± 14.6 mm Hg and from the slope of the regression line relating about a mean of 151.3 mm Hg), but the pattern of cardiac output to Paooa during nitrous oxide anaeschange in individual patients was consistent: in- thesia (Prys-Roberts et al., 1967) this increase of crease of IAP was accompanied, in both horizontal Pcoj would be expected to cause an increase of and tilted patients, by a slight increase of Pao,. In cardiac output of only some 0.3 L/min. Yet cardiac the case of the horizontal patients (fig. 1), mean output increased by almost 2 l./min in the horizonPao, increased from a control, preinsufflation value tal patients, and by about 1 l./min in the tilted of 132.0 mm Hg to 135.4 mm Hg, and to 135.0 mm patients. Hg immediately before the abdomen was deflated Carbon dioxide retention cannot, therefore, be the when IAP was above 40 cm H,O; the corresponding major factor responsible for the changes of cardiac figures for the head-down patients (fig. 2) were output which we have observed; it may, however, 151.3 mm Hg, 155.2 mm Hg and 152.1 mm Hg, act synergistically with other mechanisms. respectively. The changes of cardiac output in this study These increases of Paoj were accompanied by pro- tended to parallel the changes of effective cardiac gressive increases of Paooa (figs. 1 and 2>—28.6, filling pressure (CVP-ITP) which accompanied 32.4 and 37.0 mm Hg in the horizontal patients, abdominal inflation (figs. 1 and 2). For example, as and 25.3, 30.9 and 32.6 mm Hg in the head-down IAP was increased to 20-30 cm H,O, there was a patients—and by increases of PE'OOJ (table I). There progressive increase of both cardiac output and was no change in patients' non-respiratory acid-base effective cardiac filling pressure, while the decrease state. Abdominal inflation was accompanied by of filling pressure which occurred when IAP was moderate increases of peak AWP (table I) in both raised further was accompanied by a fall of cardiac horizontal patients (15.9 cm H , 0 increasing to 22.7 output—a response which was reversed at the end cm H , 0 at IAPs above 40 cm H,O), and tilted of the endoscopy, when IAP was again in the region patients (17.3 cm H , 0 increasing to 20.5 cm H 2 O of 25 cm H,O. This is, of course, what would be expected if the changes in cardiac output during at high IAPs). laparoscopy depended mainly on changes in cardiac filling pressure, i.e. if they occurred chiefly as a DISCUSSION result of the Frank-Starling mechanism; and is the Reports of acute cardiovascular collapse occurring explanation suggested by Hodgson, McClelland and during laparoscopy are not infrequent. At the start Newton (1970) for the 25% increase in cardiac outof this investigation it seemed that the most likely put which they found in one artificially ventilated explanation for such episodes was an acute decrease patient undergoing laparoscopy.
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The increase of cardiac output which accompanies laparoscopy is thus probably the result of at least two factors acting in concord: (1) an increase of cardiac filling pressure, due partly to mechanical factors and partly to sympathetically-induced constriction of capacitance vessels, and (2) an increase of cardiac efferent sympathetic activity. The relative roles of these two factors cannot be clearly separated at the present time. In contrast to other workers, e.g. Baratz and Karis (1969) who found, in artificially ventilated patients receiving 1% halothane vaporized in 74% nitrous oxide, 25% oxygen, a fall of Paoa during laparoscopy from 92 to 81 mm Hg, we found no evidence of arterial hypoxaemia as a result of the abdominal insufflation of considerable quantities of carbon dioxide. In view of the diaphragmatic elevation and presumed reduction of FRC which must occur during this procedure even with artificial ventilation (Alexander, Noe and Brown, 1969), this was a somewhat surprising finding for which we have no explanation. Indeed, when the simultaneously-occurring changes of arterial Pco3 are taken into account, laparoscopy was accompanied by a reduction of the alveolar-to-arterial (A-a)Po, difference, rather than by an increase which would be expected if the procedure had been accompanied by alveolar collapse in die lung bases. This finding may be related to the theoretical prediction of Kelrnan, Prys-Roberts and Nunn (1967) that increases of cardiac output should, in the presence of a constant percentage pulmonary venous admixture, be accompanied by simultaneous decreases of the (A-a)Po2 difference. Although we found no hypoxaemia during laparoscopy, it must be remembered that our patients were breathing oxygen-enriched gas mixtures; and it is possible that some patients may become hypoxaemic when breathing air after laparoscopy, when residual carbon dioxide uptake from the peritoneum continues for a time. We have not investigated this problem in detail, but found, in 6 patients, mean venous PCo2 of 42.0 and 46.3 mm Hg, 15 and 25 min respectively after laparoscopy. These findings suggest that carbon dioxide uptake after laparoscopy is not a serious problem; but clearly further study is required on this topic. There is at the present time considerable dispute about the best anaesthetic technique for laparoscopy: some workers, e.g. Scott (Scott and Julian, 1972), advocate spontaneous respiration; others, e.g. Desmond and Gordon (1970), prefer artificial ventilation. This is not the place for a detailed discussion
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The biphasic changes of CVP found in the present study may be explained in terms of the following paradigm. Increase of IAP has two opposing effects on the cardiovascular system: it forces blood out of the abdominal organs and inferior vena cava into the central venous reservoir; at the same time it dams blood back in the legs, and thus tends to decrease the central blood volume. We suggest that at low IAPs the first process is the important one. However, as IAP is progressively raised, there comes a point at which the abdominal capacitance vessels are emptied; increase of IAP beyond this point causes progressive storage of blood in the legs and thus depletes the central venous reservoir, causing a fall in CVP and of cardiac output. Such a biphasic response is well seen in figure 3, and a similar picture is seen in the mean pressures shown in figures 1 and 2. The fact that FVP closely parallels IAP suggests that there are no effective anastomoses through which blood can by-pass the inferior vena cava when this is occluded by an increase of abdominal pressure. (The question arises whether the efficacy of such anastomoses depends on the patient's parity and on whether or not she is pregnant at the time of laparoscopy. Analysis of our present results does not permit a definite answer to this question, which is currently under investigation in a larger series of patients.) In figure 3, CVP does not return to its preoperation value when IAP is decreased to zero after laparoscopy. In conjunction with the normal or somewhat increased cardiac outputs found at that time, this suggests continuing constriction of capacitance vessels as a result of increased sympathoadrenal activity. The relatively high outputs found immediately before removal of the laparoscope (figs. 1 and 2), compared with values found at comparable IAPs during abdominal inflation also suggests increased sympathoadrenal activity; as does the tachycardia. (Bainbridge's reflex—an increase of heart rate in response to an increase of cardiac filling pressure—is generally thought to be of minimal importance in man although a rigorous investigation of this topic appears not to have been made.) This increase of sympathoadrenal activity is presumably a reflex response to the surgical stimulus of laparoscopy performed under fairly light anaesthesia. Anaesthetists who use epidural anaesthesia for laparoscopy say that this procedure is commonly accompanied by severe shoulder pain, presumably the result of stimulation of the diaphragmatic peritoneum.
BRITISH JOURNAL OF ANAESTHESIA
CARDIAC OUTPUT AND ARTERIAL BLOOD-GAS TENSIONS
laparoscopy is better understood, patients undergoing this operation should be carefully monitored. In view of the fall of CVP and cardiac output which may occur at high intra-abdominal pressures, IAP should be limited to, say, 30 cm rL.0, a pressure which gives good surgical exposure. Also, since these patients may have central hypovolaemia as a result of venous pooling in the legs, the use of IPPV with excessive inflation pressures should be avoided. ACKNOWLEDGEMENTS
We thank the staff of the Pulmonary Function Laboratory, Aberdeen Royal Infirmary, for performing the blood-gas analyses. This investigation was aided in part by a grant from the Scottish Hospitals Endowments Research Trust (to G.R.K.). REFERENCES
Alexander, G. D., Noe, F. E., and Brown, E. M. (1969). Anesthesia for pelvic laparoscopy. Anesth. Analg. Curr. Res., 48, 14. Arthure, H. (1970). Laparoscopy hazard. Brit. med. J., 4, 492. Baratz, R. A., and Karis, J. H. (1969). Blood gas studies during laparoscopy under general anesthesia. Anesthesiology, 30, 463. Desmond, J., and Gordon, R. A. (1970). Ventilation in patients anaesthetized for laparoscopy. Canad. Anaesth. Soc. J., 17, 378. Hodgson, C , McClelland, R. M. A., and Newton, J. R. (1970). Some effects of the peritoneal insufflation of carbon dioxide at laparoscopy. Anaesthesia, 25, 382. Holmes, F. (1960). The supine hypotension syndrome; its importance to the anaesthetist. Anaesthesia, 15, 298. Kelman, G. R., Nunn, J. F., Prys-Roberts, C , and Greenbaum, R. (1967). The influence of cardiac output on arterial oxygenation: a theoretical study. Brit. J. Anaesth., 39, 450. Milic-Emili, J., Mead, J., Turner, J. M., and Glauser, E. M. (1964). Improved technique for estimating pleural pressure from esophageal balloons. J. appl. Physiol, 19, 207. Price, H. L. (1967). Circulation during Anesthesia and Operation, p. 86. Springfield: Thomas. Prys-Roberts, C , Kelman, G. R., Greenbaum, R., and Robinson, R. H. (1967). Circulatory influences of artificial ventilation during nitrous oxide anaesthesia in man. I I : Results; the relative influence of mean intrathoracic pressure and arterial carbon dioxide tension. Brit. J. Anaesth.. 39, 533. Scott, D. B., and Julian, D. G. (1972). Observations on cardiac arrhythmias during laparoscopy. Brit. med. J., 1, 411. Smith, I., Benzie, R. J., Gordon, Nanette L. M., Kelman, G. R., and Swapp G. H. (1971). Cardiovascular effects of peritoneal insufflation of carbon dioxide for laparoscopy. Brit. med. J., 3, 410.
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of this matter; but we believe that our results show that, in patients with a normal cardiovascular system, artificial ventilation provides a considerable safety margin It prevents cardiac arrhythmias and arterial hypercapnia and hypoxaemia; and the reduction of cardiac output and arterial hypotension which may occur at very high intra-abdominal pressures do not occur until IAP exceeds at least 40 cm H,O. This is greater than the pressure—of the order of 30 cm H2O—required for satisfactory surgical exposure. The volume of carbon dioxide required to raise IAP to about 30 cm H , 0 varies considerably from patient to patient. At this pressure the space between the peritoneum of die anterior abdominal wall and the intra-abdominal organs in the lower abdomen is such that the risk of injury to these organs during introduction of the 11 mm trocar for the laparoscope is minimal. In addition, this pressure compresses the gut against the posterior abdominal wall, ensuring a clear view of the pelvic viscera and minimizing risk of injury to intestine, ureter, etc., when diathermy is used (Annual Report of Medical and Dental Defence Union of Scotland, 1971). There remains the fact that our results do not suggest a cause for the acute cardiovascular collapse which has been reported during laparoscopy, even at quite moderate IAPs. Pressures of up to 40 cm HjO appear to be well tolerated; and in artificially ventilated patients, inspiring an oxygen-enriched gas mixture (30%), arterial hypoxaemia does not seem to occur. We have seen one case of cardiac arrest (successfully resuscitated) since starting the present investigation; this near-disaster was probably the result of carbon dioxide embolism, and will be discussed in greater detail elsewhere. The remaining factor to be considered is the possibility of severe bradycardia and/or cardiac asystole from a reflex increase of cardiac vagal tone consequent on peritoneal manipulation. While there is no evidence at present to suggest that this phenomenon is important during laparoscopy, the reflex is well established (see e.g. Price, 1967), and we suggest it should not be dismissed out of hand. Our results suggest that the homeostatic ability of an anaesthetized and artificially ventilated patient's cardiovascular system is such that it can withstand an increase of IAP up to at least 40 cm HjO. We do not, however, wish our results to engender a false sense of security; and we would recommend that, until the applied physiology of
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1162 DEBIT CARDIAQUE ET PRESSIONS DES GAZ SANGUINS ARTERIELS DURANT LA LAPAROSCOPIE SOMMAIRE
HERZMINUTENVOLUMEN UND ARTERIELLE BLUTGASDRUCKE WAHREND DER LAPAROSKOPIE ZUSAMMENFA S SUNG
Bei narkotisierten, kiinstlich beatmeten Patienten, von denen 21 waagerecht und 18 mit einer Kopfsenkung von 25° gelagert waren, wurde die Wirkung von progredient ansteigendem intraabdominellen Druck (LAP) vor, wfihrend und nachder Laparoskopie auf: ZVD, intratborakalen Druck (TTP), Femoralvenendruck (FVP), Herzminutenvohimen (Q), Herzfrequenz, mittel. art. Blutdruck (MAP), Luftwegespitzendruck, FE'OO, und auf die Blutgasdrucke gemessen. Der FVP lief dem Anstieg des IAP parallel. Sowohl bei den waagerecht gelagerten Patienten als auch bei den gekippten gingen die Anstiege des IAP auf ca. 20 cm HiO einher mit
GASTO CARDIACO Y TENSIONES GASEOSAS EN LA SANGRE ARTERIAL DURANTE LA LAPAROSCOPIA RESUMEN
Hemos medido en 21 pacientes horizontales y 18 pacientes con inchnaci6n hacia abajo de 25° de la cabeza anestesiados y ventilados artificiahnente el efecto de incrementos progresivos de la presi6n intraabdominal (IAP) antes, durante y despues de la laparoscopia sobre: CVP, presion intratoracica (ITP), presi6n venosa femoral (FVP), gasto cardlaco (0), frecuenda canHaca, presi6n arterial media (MAP), presi6n pico de la via aerea, FE'OO, y tensiones gaseosas en la sangre arteriaL FVP varii paralelamente con el incremento de IAP. Tanto en pacientes horizontales como en pacientes inclinados, los uicrenientos de IAP de aproximadamente 20 cm H,O fueron acompariados por incrementos de CVP (horizontal: 4,6 cm HiO; indinado: 10^ cm H,O), por incrementos menores de ITP (horizontal 1,8 cm HjO; indinado 3J. cm H,O), y por incrementos de Q (desde 3,9 l./min por 70 kg hasta 5,0 l./min para 70 kg en poskidn horizontal; y desde 4,8 L/min para 70 kg hasta 53 L/min para 70 kg en padentes inclinados). Incrementos mayores de IAP de alrededor de 40 cm HjO fueron acompanados por cafdas de CVP y Q (hasta 4,4 L/min para 70 kg en ambas posiciones), junto con cambios paralelos de MAP y taquicardia moderada. No hubo hipoxemia arterial, aumentando la Pao, desde 132,0 mm Hg hasta 135,4 mm Hg en los pacientes horizootales y desde 1513 mm Hg hasta 155,2 mm Hg en los pacientes inclinados; los incrementos de Paooj fueron ligeros (desde 28,6 mm Hg hasta 32,4 mm Hg en padentes horizontales y desdrt 25,3 hasta 30,9 mm Hg en tos padentes inclidados).
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Chez dcs patients anesthesias, artifidellement yentiles dont 21 en position horizon talc et 18 en position inclinee a 25*, tfite basse, nous avons mesuri l'effet de 1'augmentation progressive de la pression intraabdominale (JAP) avant, pendant etapres laparoscopie sur: CVP, pression intrathoracique (FTP), pression veineuse femorale (FVP), dibit cardiaque (Q), frequence cardiaque, pression arrfrielle moyenne (MAP), pression mgTirrmli» des voies d'air, FE'OO, et pressions des gaz sangiiins arteriels. L'augmentatkm de FVP etait parallele 4 ceJle de IAP. Aussi bien chez les malades en position horizontale qu'inclinee, on observa que les augmentations de IAP a environ 20 cm H,O itaient accompagnees d'augmentations de CVP (horizontal: 4,6 cm H,O; inclirrf: 10,2 cm H,O), d'augmentations moins prononcees de ITP (horizontal: 1,8 cm HjO; inclined 3,2 cm HiO), et d'augmentations de 0 (de 3,9 1/min par 70 kg i 5,0 1/min par 70 kg en position horizontale; et de 4,8 1/min par 70 kg a 53 1/min par 70 kg en position inclinee). Des plus fortes augmentations de IAP a environ 40 cm HtO s'accompagnaient de chutes de CVP et Q (a 4,4 1/min par 70 kg dans les deux positions), avec modifications paralleles de MAP et tachycardia moderee. II n'y avait pas dTiypoxeinie arte'rielle, la Paca augmentant de 132 mm Hg a 135,4 mm Hg chez les patients horizontaux, et de 151,3 mm Hg a 155^2 mm Hg chez les malades en position inclinee; les augmentations de la Paoo, etaient legeres (de 28,6 mm Hg a 32,4 mm Hg et de 253 a 30,9 mm Hg resp. en position horizontale et inclinee).
Ansuegen des CVD (waagerecht 4.6 cm HiO, gekippt 10.2 a n HiO), mit geringeren Anstiegen des ITP (waagerecht: 1.8 cm H,O, gekippt: 3.2 cm HjO) und mit Anstiegen von Q (waagerecht: von 3.9 L/min/70 kg auf 5.0 L/min/70 kg, gekippt: von 4.8 L/min/70 kg auf 5.3 L/min/70 kg). Hohere Anstiege von IAP auf ca 40 cm H J O waren von einem ZVD- und Q-Abfall begleitet (auf 4.4 l./min/70 kg in beiden Positiooen), und von parallel verlaufenden VerSnderungen von MAP und einer maOiggradigen Tachycardie. Es entstand keine arterielle Hypoxamie, bei einem Pao,-Anstieg von 132.0 mm Hg auf 135.4 mm Hg bei waagerecht gelagerten und von 151.3 mm Hg auf 155.2 mm Hg bei gekippten Patienten. Anstiege von Paooi waren gering (von 28.6 mm Hg auf 32.4 mm Hg bei waagerecht gelagerten und von 25.3 auf 30.9 mm Hg bei gekippten Patienten).