Reliability of the Radial Arterial Pressure During Anesthesia

Reliability of the Radial Arterial Pressure During Anesthesia* Is Wrist Compression a Possible Diagnostic Test? Alfredo L Pauca, M.D.; Stephen L. Wallenhaupt, M.D., F.C.C.P.; and Neal D. Kon , M.D., F.C .C.P. Study objective: To evaluate wrist compression as a test to identify low radial from low systemic pressure and to see if the gradient found after cardipulmonary bypass is also present whenever hand vascular resistance may decrease. Design: This was a prospective study. Setting: Operating room area of a university medical center. Participants: (I) Forty patients undergoing coronary bypass grafting studied at discontinuation of cardiopulmonary bypass. (2) Twenty-six patients received isoflurane anesthesia before major noncardiac operations. (3) Hydraulic model: a fluid container with a tube 66-cm long, 6- to 1.8-mm internal diameter, connected at its base. lnteroentions: Before induction of anesthesia, the radial artery was cannulated and, in the first group, the aorta or femoral arteries as well. The radial pressure was compared consecutively with and without wrist compression. In the model, the pressure was recorded simultaneously at three sites along the tube while different flows ran through its distal end. Measurements and results: Overall, wrist compression increased radial (p
ence produced by wrist compression against the average of the (compared) radial pressures and considering increases ;;::4 mm Hg as real, showed that, in the rarst group, systolic arterial pressure (SAP) increased 13 ± 1.4 mm Hg in 22 of 40 patients; diastolic arterial pressure (DAP) increased 7.8 ± 1.1 mm Hg in 4; and mean arterial pressure (MAP) increased 7. 7 ± 1.6 mm Hg in 9 patients. In the second group, SAP increased 16.0 ± I. 7 mm Hg in 24 of 26 patients, DAP increased 6.0 ± 1.4 mm Hg in 5, and MAP increased 7.0 ± 0. 7 mm Hg in 18 of26 patients. In the model, base pressure at 94 mm Hg, the pressures were 1.2 to 28.1 mm Hg lower for flows ranging from 10 to 122 ml/min at the 54-cm distance (wrist equivalent). Conclusion: The systemic-radial artery pressure gradient seen at the end of cardiopulmonary bypass seems to be a phenomenon common to patients with decreased hand vascular resistance. Wrist compression decreases or abolishes the gradient in most cases. It does not produce false positives, so an increase indicates a greater aortic than radial pressure. The difference is likely to be only temporary. (Chest 1994; 105:69-75)

I

whole hand blood flow in the resting state);~ in undisturbed volunteers and patients should produce a similar central radial pressure diflerence. Why should increased HBF reduce radial MAP? If the MAP is measured simultaneously in the aorta and in a nearby major branch (ie, carotid, axillary) , the pressures are similar. If it is measured at some distance from the aorta, however, in a relatively small branch (ie. radial, dorsalis pedis), its value will depend on the regional vascular resistance. Normally the radial MAP is only a few millimeters of mercury lower than that in the aorta9 because the normal state of the hand vascular bed is one of vasoconstriction . ~ A severalfold increase in HBF produced by sedation and anesthesia'1·7 implies a decrease in HVR similar to that encountered in an arteriovenous fistula . 111 The general expression, simplified by omitting central venous pressure (CVP) from the left side of the following equation : MAP= systemic vascular resistance (SVR) x cardiac output (CO), when applied to the wrist (and whole hand blood flow measured), becomes

t is assumed that arterial BP measured directly in the radial artery accurately reflects the systemic arterial pressure (SAP) . At the conclusion of c-.mliopulmonary bypass (CPB). however. there is an aortoradial BP difference in some patients.1· 1 It has been suggested that this difference is largely due to a decrease in hand vascular resistance (HVR) and a consequent increase in hand blood flow (HBF) .~ This hypothesis was based on the observation that. in patients undergoing light opioid anesthesia, and prior to CPB, wrist compression did not increase me
Reprint requests: Ms. Lari11wre. Ed Asstl!\11esthesia, Bmcman Gra'L School ofMetlicille. Medical Cellff'l' Bled. \Vi11stoi!-Sale111, NC 2i/.5,

CO =cardiac output; CPB =cardiopulmonary bypass; CVP central venous pressW"e; DAP diastolic arterial pres: sW"e; HBF =hand bloOd flow; HR =heart rate; HVR =hand vascular resistance; ID = intemal diameter; MAP = mean arterial pressW"e; PP =pulse pressW"e; SAP =systolic arterial pressW"e; SVR =systemic vasCular resistance

=

=

CHEST I 105 I 1 I JANUARY.

1994

69

MAP= HVRxHBF. When HVR decreases, HBF should increase proportionately to preserve MAP. However, this might not be physically possible because of the limited diameter of the artery, upstream arterial occlusion, or excessive forearm blood flow. 1 Although wrist compression has been used3 to study the radial artery hypotension associated with CPB, that report included only 23 patients, and those findings have not been confirmed by other investigators. There is the remote possibility that this maneuver might artificially produce a radial MAP higher than that measured in the aorta or femoral artery. The objectives of this study were (a) to re-evaluate the effect of wrist compression as a tool to separate low radial artery pressure from authentic low systemic blood pressure in patients whose aortic or femoral pressures could be simultaneously monitored and (b) to find out whether this maneuver would also increase the radial MAP in patients during anesthetic states other than at the conclusion of CPB. METHODS

Clinical Measurements With institutional approval and after obtaining written consent, we recorded the radial artery pressure with and without wrist eompression in 40 patients, 38 men and 2 women (group 1), undergoing coronary artery bypass grafting. Patients with unequal bilateral arm cuff pressures determined oscillometrically were excluded, as well as those who exceeded the normal" aorta/femoral radial MAP difference of 3 mm Hg or less measured before CPB. Fentanyl was the primary anesthetic and pancuronium, the muscle relaxant. Radial artery pressures were measured through 5-cm 20gauge Teflon catheters, 91-cm high-pressure tubing, and a model T36AD-R transducer (Spectromed, Inc, Oxnard, CaliO. Frequency response and damping coefficient of the system were obtained by the flush method'' at the end of the oomparison. Systemic pressure was measured in the femoral artery in 27 patients (in 9 of these, the aortic and femoral pressures also were compared) or the aorta in 13 patients. All catheters were placed facing upstream; the tip of that in the ascending aorta was positioned close to the aortic wall. All transducers were calibrated statically with a mercury manometer and maintained at the same level. Cardiac output and central venous pressure (CVP) were secured through a thermodilution pulmonary artery catheter. Wrist compression was provided by a 38-mm wide pediatric BP cuff placed on the wrist overlying the radial catheter, distal to the tip. and inflated to 150 to 220 mm Hg. This method rather than manual compression3 was used for the sake of uniformity. In no instance did this compression blunt the sharpness of the pressure tracing. indicating that the occluding pressure neither kinked nor occluded the lip of the catheter. After discontinuation of CPB, while the patients were hemodynamically stable, the radial pressure was recorded for a period of 10 s without wrist compression, followed by a similar period with wrist compression, and a final one without <.'<>mpression. Ventilation was stopped during the recordings. Systemic pressure and pulse rate were recorded simultaneously, and CO was measured before and after the pressure recording. In order to ensure that the <.'Onsecutively recorded radial pressures were measured under similar, if not identical conditions, a changing CVP, heart rate (HR), or systemic pressure during the recording period invalidated the comparison, and a second recording was made. Data were printed on a thermolinear recorder (Siemens Medical Systems, Inc, Iselin, NJ) and electronically averaged every

70

9.4 s. The MAP was obtained by electronic integration. All data are expressed as mean± SEM. Changes produced by wrist compression in radial systolic arterial pressure (SAP), MAP, diastolic arterial pressure (DAP), and pulse pressure (PP), which is SAP-DAP, were evaluated by the Wilcoxon signed-rank test. Only the radial MAP was compared with that measured simultaneously in the femoral or aortic arteries by the paired sample t test (only one comparison was made from each patient; te, one free radial aorta/femoral pressure difference was compared with the next radial aorta/femoral difference with wrist oompression); SAP and DAP were not compared because the length and diameter of the cannulae used in the femoral artery and aorta were different from those used in the radial artery. Their frequency responses and damping coefficients are expected to be different. Correlations of the changes in radial SAP, MAP, DAP, and PP, between themselves as well as with CO, hematocrit level, age, core temperature, and SVR (calculated using the systemic MAP) were sought. The second group consisted of 26 patients, 23 men and 3 women, scheduled to undergo major surgery with the use of general anesthesia, who required direct arterial pressure monitoring. The radial artery pressure was recorded as in the previous group. They were studied while undergoing anesthesia, but without surgical stimulation. Anesthesia induction consisted of fentanyl 2 to 3 llg/ kg, thiopental 3 to 4 mglkg. and succinylcholine 1.5 mglkg. Maintenance was with 50 percent nitrous oxide in 50 percent oxygen, plus isoflurane, 0.5 to 2 percent inspired. The recordings were done 10 to 15 min after induction, before surgery had started. Central arterial BP was not monitored. The pressure measuring system was analogous to that used in the previous group, except that the length of the high-pressure tubing connecting the radial catheter to the transducer was reduced to 30 em. This was done to secure satisfactory frequency response and damping coefficients which would decrease the number of variables inherent in the comparison of blood pressures. The SAP, DAP, and MAP were compared for the effect of oompression. Pressure recordings were obtained during apnea. The incidence and magnitude of the pressure increases produced by wrist compression were evaluated by plotting such increases against the average of the two compared pressures.12. 13 This allowed us to separately assess increases of 4 mm Hg 14 or more in each group, as well as to calculate the percentage of patients who showed a clinically significant increase, te, of 5 mm Hg or more for DAP and MAP and of 10 mm Hg or more for the SAP.' 3

Laboratory Model The hydrostatic pressure of a column of water - 130 em high was measured at 3 points in a chain of tubes connected in a series: at the base of the column, through the side of a connector with a 5mm internal diameter (ID), and at the next 2- through 3-way stop(.'()cks with a 1.8-mm ID: a tube 30-cm long with a 5-mm ID, a tube 24cm long with a 2.3-mm ID; and a tube 12-cm long with a 1.8-mm ID. The three sections loosely approximate the length and diameter of the subclavian-axillary-brachial, radial, and palmar arterial segments. The pressure was recorded simultaneously at the junction of the tube with the container, at 30 em and at 54 em from the base. The pressures were recorded by three transducers, calibrated statically to a mercury standard and maintained at the same level, at 10-, 17-, 29-, 44-, 71-, 101-, and 122-mVmin flows running through the end of the chain. Considering that flows 3 to 5 times higher than those seen in this study only produce 0.04 mm Hg higher end-on than lateral pressure,• we only measured lateral pressure. The pressures were recorded on a fast response thermal recorder (Siemens Medical Systems), and run at 25 mm/s for 10 s. The sequence was repeated four times and the results averaged. The flows were chosen arbitrarily from those readily obtained when the fluid ran through catheters: 22 gauge - 3-cm long. 20 Radial Arterial Pressure During Anesthesia (Pauca, Wal/enhaupt, Kon)

Table 1-Dacriptive Statiatic. Unchanged Variables Age, yr Weight, kg Core temperature, ("C, rectal) CO,Umin SVR, dyneosocm -• Hematocrit, % Frequency response, Hz Damping coefficient

Values (First Group)

Values (Second Group)

60.0±3.1 76.0± 1.5 36.2±0.1

51.2±3.3 74.0±2.0

5.8±0.2 850.0±50 23.1±0 20.0±0.6 0.25±0.01

39.7±0.7 22.0±0.9 0.28±0.02

gauge - 5-and 3-cm long, 18 gauge - 5- and 3-cm long, and 16 gauge - 5-cm long at the end of the chain of tubes. The accuracy of the flows was ensured by measuring the fluid collected in a graduated container for 2 min (Fig 1). RESULTS

Clinical Obseroations General characteristics of both groups are found in Table 1. All patients in the first group had documented obstructive coronary artery disease. The patients of the second group were ASA I-III; all had been in good health until minor symptoms or a routine examination uncovered their present pathologic state. The frequency response and damping coefficient of the pres-

94mm Hg

12 em 30 e_m_"""',..... 24 em~ .,.__ •

)ill

CD FIGURE 1. Schematic representation of the pressure model (not to scale). The large capacity of the container maintained a constant head of pressure during the 10 s each flow was run. The arrows indicate the sites of the pressure measurements. All three pressures were measured simultaneously during each flow.

Table 2-Effect ofWritt Cornpreaion on &dial Artery Preaure (Firat Group)* Compression Status

MAP

SAP

DAP

pp

No compression, 66.0±1.7 89.0±2.4 52.0± 1.4 36.7± 1.2 mmHg Wrist compressed, 69.0±1.8 96.0±2.2 54.0± 1.5 43.0± 1.2 mmHg !:J., mmHgt 2.8±0.6 7.2±1.2 1.6±0.4 6.3±0.8 Average of aortal 72.0±1.4 97.0±2.3 55.0±1.4 42.0± 1.0 femoral , mm Hg *The CVP, HR, CO, and total SVR remained unchanged. t!:J.=difference between wrist compression vs no compression; all differences were significant (p<0.001).

sure measuring system used in the second group were slightly higher than those in the first group, but they were not significantly different (p>0.05). Tables 2 and 3 show the effect of wrist compression. Wrist compression produced statistically significant (p
SAP

DAP

pp

No compression, 71.0±2.1 102.0±3.2 57.0±2.5 45.0±1.5 mmHg Wrist compressed, 76.0±2.0 ll6.0±2.6 59.0±2.6 57.0±1.6 mmHg !:J., mm Hg* 5.0±1.0 14.0± 1.4 2.0±0.5 12.0± 1.2 *!:J. =difference; all differences were significant (p<0.001). CHEST I 105 I 1 I JANUARY, 1994

71

Table 4-Effect of Distal Flow on the Pre88Ure Meaaured at 1, 30, and 54 em From the BaBe of the Container 0

0 0 0

0

0

o 'b &o

80

0

0~--~--~----~------~----.---,

40

60

80

100

17

29

44

71

101

122

At1cm At30cm At54cm

94.0 93.5 93.0

94.0 93.0 92.0

94.0 92.5 90.0

94.0 92.0 87.0

94.0 91.0 81.0

94.0 89.5 73.0

94.0 89.0 66.0

by plotting the pressure differences (with vs without wrist compression) against the average of the two compared pressures. 12 This also permitted consideration of clinically significant differences in pressure, 13•14 ie, increases of 10 mm Hg or more for the SAP and of 5 mm Hg or more for the DAP and MAP. In the first group: (a) the maximum increase in SAP exceeded 30 mm Hg; it was 10 mm Hg or more in 17 (43 percent) patients; (b) the maximum increase in MAP exceeded 15 mm Hg, 5 mm Hg or more in 7 patients ( 18 percent); and (c) the increase in DAP reached 10 mrri Hg, 5 mm Hg or more in 4 patients (10 percent [Fig 2]). In the second group (Fig 3): (a) the maximum increase iii SAP reached 40 mm Hg, 10 mm Hg or more in 18 patients (69 percent); (b) the maximum increase in MAP reached 16 mm Hg, 5 mm Hg or more in 15 patients (58 percent); and (c) the increase in DAP reached 11 mm Hg, 5 mm Hg or more in 2 patients (8 percent).

0

20

10

•When the flow was stopped, all3 transducers read 94 mm Hg.

0 0

-5

Flow, mVmin*

Pressure Data, mmHg

120

140

FlGt;RE 2. First group. Plot of the pressure differences against the average of the two compared pressures ([free wrist + wrist compressed]/2). Solid circles, DAP; squares, MAP; open circles, SAP. The bar tacks from left to right represent the mean ± 2 SD of the differences in DAP, MAP, and SAP. Differences of 3 mm Hg or less have been omitted for the sake of clarity. Differences of 10 mm Hg or more for SAP= 17, of 5 mm Hg or more for MAP= 7, and for DAP = 4 patients. Notice the lack of relationship between the pressure differences, and the magnitude of the measured pressures. The mean± 2 SD encompass 95 percent of the pressure differences.

patients with whom these were compared. The only significant correlations were between changes in SAP and changes in PP (r = 0.87; p <0.001), between changes in DAP and changes in MAP (r = 0.72; p <0.()()1), and between. changes in MAP and age (r = -0.47; p <0.001) in the first group. In the second group, the only significant correlation was (r = 0.81; p<0.001) a change in MAP and a change in DAP elicited with oompression. A graphic view of the effect of wrist compression on the pressure differences for each group was obtained

140

Laboratory Model With pressure at the junction of the tube with the container at 94 mm Hg and with flows ranging from 10 to 122 ml/min, the pressures at the 30-cm site ranged from 93.5 to 89.0 min Hg and those at the 54em site, 93.0 to 66.0 mm Hg. Thus, within these flows, the pressures at "the wrist-equivalent" site were 1.0 to 28.0 mm Hg lower than those at the base of the

0

.!35

J: ~

0

-20

~

E E 15

0


0

! 10

l

f

j

5 0 -50

20

40

00

00

100

120

1~

100

Averaoe radial pressure [(compressed +free wrist)/2) mmHg 72

100

FIGt;RE 3 . Second group. Plot of the pressure differences against the average of the two compared pressures ([free wrist +wrist compressed)/2). Solid circles, DAP; squares, MAP; open circles, SAP. The bar tacks from left to right represent the mean± 2 SD of the differences in DAP, MAP, and SAP. All comparisons have been included. There is no relationship between the pressure differences and the magnitude of the measured pressures. The mean ± 2 SD encompass 95 percent of the pressure differences. As in Figure 3 , it shows the greater magnituile of the SAP differences against those of the MAP and DAP, as well as their incidence: SAP is greater than MAP; MAP is greater than DAP. Comptession elicited positive or no changes in SAP and MAP.

Radial Arterial Pressure During Anesthesia (Psuca, Wsllenhsupt, Kon)

container (Table 4). When the end of the tube was occluded, stopping the flow, all3 transducers read 94 · mm Hg. DISCUSSION

In the first group of patients, wrist compression reproduced previous findings; 3 ie, it significantly increased SAP, DAP, and MAP and reducecl the ma~i­ tude and incidence of systemic radial MAP difference. As expected, wrist compression did not produce higher radial than systemic MAP, since this variable is not affected by alterations of wave reflections, 14 which arterial compression will produce, nor by additional pressure from kinetic energy since flow velocity in the radial artery is insufficient to produce a measurable amplification of the MAP;9 aqd distal occlusion abolishes flow. This confirmatioq permitted us to assume that the increase in MAP in response to wrist compression in the second group of patients represents a systemic radial pressure gradient. Because the two groups differed in age, state of health, and anesthesia method, and the first was studied after a !ong surgical procedure and exposure to CPB, while the second was spared from surgical stimulation, their responses to wrist compression are not comparable by standard statistical methods. A plausible comparison can be established by weighing the incidence of clinically significant increases. 12. 15 The 10 mm Hg or more increases in SAP were present in 17 of 40 patients (43 percent) in the first group and in 18 of 26 patients (69 percent) in the second. Increases in DAP at the 5 mm Hg or greater level were similar, 10 percent and 8 percent, respectively. Increases in MAP occurred in 7 of 40 patients (18 percent) in the first group and in 15 of 26 patients (58 percent) in the second group. Because the radial SAP is normally la,rgely dependent on wave reflection, 14 the low natural resonance of the radial artery, 16 and these effects cannot be evaluated in a clinical setting, radial systolic pressure can only be considered a rough approximation to that measured in the aorta or femoral artery. The radial MAP, on the other hand, reliably reflects that present in the aorta in awake men 17 and in 92 percent of narcotic-anesthetized patients. 18 The increase in MAP produced by wrist compression was of similar magnitude in both groups, but it was three times as frequent in the nonsurgically stimulated patients undergoing isoflurane anesthesia than in the post-CPB patients. Thus, it is poss~ble that the systemic radial pressure gradient is not a peri-CPB event but one related tp states accompanied by decreased HVR.4·8 Because simultaneous measurement of aortic and femoral MAP in nine patients produced no measurable differences, confirming a previous report, 15 these pressures were considered equivalent and called systemic

pressure. Comparison of the systemic and radial MAP disclosed that compression decreased the maximal difference from 20 to 7 mm Hg and the incidence of 5 mm Hg or more difference from 30 to 16 percent; thus, this syndrome, in addition to a decrease in HVR, must have other causative factors. Although this study was not designed to find causative factors for the systemic radial MAP gradient associated with CPB, over the course of the study we gained the clinical impression that healthier patients were more likely to show lower radial than central pressures; however, the only correlation found was a weak one between the changes produced by wrist compression on the MAP and age (r = -0.47; p < 0.01). This correlation was absent in the patients not subjected to CPB. No other variable, including CO, HR, core and blood temperature, or hematocrit level showed a significant correlation. Because this study was designed to explore the wrist compression maneuver as a tool to differentiate local radial low blood pressure from systemic low pressure under clinical conditions, pressure data were collected using standard fluid-connected transducers.19.20 The components of the radial artery pressure waveform, other than the MAP, cannot be compared with the aortic, regardless of the kind of transducer used. Use of high-frequency response micromanometers ( > 100 Hz) would measure a waveform already deformed by the low brachial-radial resonance (3 and 6 Hz). 16 Thus, the central MAP was considered the true pressure. In this study, there are some real and some apparent weakpesses. The first real weakness was that the comparisons were not done simultaneously. Based on the stringent requirements that we imposed for the comparisons-steady HR, femoral or aortic, and CVP pressure tracings, absence of surgical stimulation, respiratory movements, or active bleeding, we assumed that the radial pressure remained stable during the 20 s that the recording took place. The second real weakness was that the periods of comparison were brief, and we did not repeat them over a period of time. However, the minimal number of variation-free pressure cycles averaged during each comparison was ten, which had to be compared with the next or the preceding batch. The goal was to compare the radial arterial pressure with and without the treatment while the aortic or femoral pressure remained unchanged for a minimum of 20 s. The third real weakness was that although it is difficult to explain the increase in MAP in response to wrist compression by other than restoration of HVR by this maneuver, only whole hand blood flow measurements can back up this theory and we could not do this measurement. Nevertheless, Pauca and Hopkins4 and Pauca,6 ·7 using volum·e displacement plethysmography, have shown that anestheCHEST I 105 I 1 I JANUARY,

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73

sia produced by thiopental, halothane, and nitrous oxide, as well as sedation with meperidine, increased total hand blood flow in all nonsurgically stimulated patients. The increasing effect of isoflurane on hand blood flow has been shown by Stevens et al 5 through the assessment of finger blood flow. The first apparent weakness was that discarding tracings where the CVP, HR, systemic pressure, etc, were not steady during the time of the recording might give the impression that we selected our results. On the contrary, in order to compare the variable radial arterial pressure with and without treatment (wrist compression), the other variables (CVP, HR, systemic pressure, etc) had to remain stable. The second apparent weakness was that we planned to exclude from the comparison patients whose aorta/femoralradial MAP difference exceeded the normal 9 3 mm Hg or more measured prior to CPB. This was a proviso to exclude patients with clinically undetected arterial abnormality in the arm under study. By chance we found none. The second group of patients was younger and had no clinical evidence of atherosclerosis. The third apparent weakness was that our hydraulic model has several flaws as representative of the brachial and radial artery circulation. This model only is an illustration of the effect of blood flow on pressure at a peripheral site. It shows that pressure decreases when the distal flow increases as a consequence of decreased resistance, while the central pressure (aorto/femoral equivalent) is unaffected. This model simulates only MAP and is restricted to 94 mm Hg. It is not applicable to changes in SAP or DAP because the flow generated is nonpulsatile and within nonelastic tubes. Even though the 30- and 54-cm measurement sites are similarly located in relation to the brachial and radial arterial sites, measurements at the 30-cm sit~ were done as the flow went through a stopcock of 1.8-mm ID while the next tube section was larger (2.3 mm). When we substituted the small diameter stopcock for a larger one (2.4 mm), the maximal pressure difference at the 54-cm site increased from 28 to 37 mm Hg and the maximal flow increased from 122 to 180 mVmin. This finding emphasizes the role of proximal resistance on flow and distal pressure, but we are not prepared to explore it further at present. Although the pressure measured at the 54-cm site might roughly represent that measured at the radial artery, in physiologically intact patients the interplay of local and systemic regulatory mechanisms that control vascular resistance;21 greatly reduces the qualitative similitude of our model. A difference between end-on and lateral pressure in our model is unlikely because this difference only reaches 0.04 mm Hg at 10 mVs,9 while the maximal flow we measured was 3 mVs (180 mVmin). The clinical significance of these findings is that 74

direct radial artery BP monitoring might underestimate the systemic MAP by 5 to 20 mm Hg in 50 percent or more of patients under isoflurane-based anesthesia when they are free from surgical stimulation. The underestimation probably does not endanger the care of most patients, since most clinicians do not tolerate unwanted low blood pressure. However, when fine-tuned controlled hypotension is intended and inhalation anesthetics are to be used for this purpose, wrist compression could be a helpful tool to estimate the systemic-radial pressure difference. Nevertheless, for reliable estimates of SVR, the MAP should probably be measured in the femoral artery or in a direct aortic branch, close to its origin. Our assessment of the wrist compression effect on MAP, in non-CPB patients, has been restricted to patients undergoing isoflurane-midazolan-nitrous oxide anesthesia to standardize anesthetic conditions. Observations not included in this study were positive responses during thoracic epidural anesthesia, intravenous sedation, and induction of anesthesia with thiopental or midazolam-fentanyl. Negative responses to wrist compression were seen in awake patients, older patients undergoing abdominal aortic aneurysmectomies under narcotic based anesthesia, and patients with low cardiac output. Abolition of the systemic-peripheral MAP differences by distal occlusion of the cannulated artery was first found in the brachial artery,;x1;x0 and it is likely to be reproducible proximal to most regions where the vascular resistance can undergo wide swings. We conclude that systemic radial artery pressure gradient does not seem to be a unique post-CPB event but a phenomenon common to patients with probably decreased HVR. Wrist compression would partially restore the normal vasoconstriction-dominated state of the hand, and since it does not produce falsepositives, any increase in MAP produced by its application indicates a greater aortic than radial pressure. It could be a harmless and simple diagnostic tool that can be applied manually if the arm is accessible or by a pediatric blood pressure cuff if it is not. ACKNOWLEDGMENT: The authors wish to thank Robert James, biostatistician. Wilson Somerville, medical editor, and VickY Cranfill, senior word processor, for their assistance in the preparation of this article. REFERENCES

1 Stern DH, Gerson Jl , Allen FB, Parker FB. Can we trust the direct radial artery pressure immediately following cardiopulmonary bypass? Anesthesiology 1985; 62:557-61 2 Mohr R, Lavee J, Goor DA. Inaccuracy of radial artery pressure measurement after cardiac operations. J Thorac Cardiovasc Surg 1987; 94:286-90 3 Pauca AL, Hudspeth AS, Wallenhaupt SL, Tucker WY, Kon ND, Mills SA, et al. Radial artery-to-aorta pressure difference after discontinuation of cardiopulmonary bypass. Anesthesiology 1989; 70:935-41 4 Pauca AL, Hopkins AM . Acute effects of halothane, nitrous Radial Arterial Pressure During Anesthesia (Psuca, Wsltenhsupt, Kon)

oxide and thiopentone on the upper limb blood flow. Br J Anaesth 1971; 43:326-34 5 Stevens WC, Cromwell TH, Halsey MJ, Eger EI II, Shakespeare TF, Bahlman SH. The cardiovascular effects of a new inhalational anesthetic, Forane, in human volunteers at constant arterial carbon dioxide tension. Anesthesiology 1971; 35:8-16 6 Pauca AL. Upper limb blood flow during hexamethoniuminduced hypotension. Br J Anaesth 1988; 60:151-56 7 Pauca AL. Effect of pethidine premedication and halothane anaesthesia on upper limb blood flow. Br J Anaesth 1992; 68:621-22 8 Fox RH, Edholm OG. Nervous control of the cutaneous circulation. Br Med Bull 1963; 19:110-14 9 Burton AC. Physiology and biophysics of the circulation. 2nd ed. Chicago: Year Book Medical Pub, 1972; 60-106 10 Pauca AL, Meredith JW. Possibility of A-V shunting upon cardiopulmonary bypass discontinuation. Anesthesiology 1987; 67:91-94 11 Gardner RM. Direct blood pressure measurement-dynamic response requirements. Anesthesiology 1981; 54:227-36 12 Bland JM, Altman DC. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet 1986; 1:307-10

13 Gibbs NM, Larach DR, Derr JA. The accuracy of Finapres™ noninvasive mean arterial pressure measurements in anesthetized patients. Anesthesiology 1991; 74:647-5214 O'Rourke MF. Arterial function in health and disease. New York: Churchill-Livingstone, 1982; 2-146 15 Rich GF, Lubanski RE, McLoughlin TM. Differences between aortic and radial artery pressure associated with cardiopulmonary bypass. Anesthesiology 1992; 77:63-66 16 Schwid HA, Taylor LA, Smith NT. Computer model analysis of the radial artery pressure waveform. J Clin Monit 1987; 3:220-28 17 Kroeker EJ, Wood EH. Comparison of the simultaneously recorded central and peripheral arterial pressure pulses during rest, exercise and tilted position in man. Circ Res 1955; 3:623-32 18 Pauca AL, Wallenhaupt SL, Kon ND, Tucker WY. Does the radial artery pressure accurately reflect aortic pressure? Chest 1992; 102:1193-98 19 Sykes MK, Vickers MD, Hull CJ. Principles of clinical measurement. London: Blackwell Scientific Publications, 1981; 162-69 20 Shinozaki T, Deane RS, Mazuzan JE. The dynamic responses of liquid-filled catheter systems for the direct measurement of blood pressure. Anesthesiology 1980; 53:498-504 21 Bevan JA, Halpern W, Mulvany MJ. The resistance vasculature. Tetowa, NJ: Humana Press, 1991

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