Measurement of Foot Artery Blood Pressure by
Micromanometry in Normal Subjects and in Patients with Arterial Occlusive Disease ALFRED BOLLINGER, M.D., JEAN PIERRE BARRAS, M.D., AND FELIX MAHLER, M.D. SUMMARY Blood pressure was measured continuously in the posterior tibial or dorsalis pedis arteries using an isovolumetric system (steel cannulas of 0.18 mm, external diameter). The systolic values in the ankle arteries of 13 normal subjects at rest (154.3 ± 22.3 mm Hg) exceeded the systolic arm pressure (128.9 ± 20.1 mm Hg, P < 0.001), while diastolic values (69.9 ± 8.7 mm Hg) were not significantly different from the arm pressure. In 13 patients with arterial occlusive disease (AOD) the dicrotic notch, normally situated close to the footpoint of the downslope, was either displaced upward or abolished. Both mean systolic and diastolic values (94.9 ± 35.9 mm Hg and 62.5 ± 18.5 mm Hg, respectively) and also mean pressure amplitude were reduced compared to the corresponding arm
values (158.5 ± 28.2 mm Hg and 87.7 ± 6.0 mm Hg, respectively, all P < 0.001). Comparison between the systolic pressure values measured by micromanometry and by an indirect technique using Doppler ultrasound showed a good correlation (r = 0.87). During postocclusive reactive hyperemia, the initial pressure values were markedly diminished in normal subjects and reached control values within 40 sec. In patients with AOD, however, this reduction in pressure was more pronounced and prolonged. Flow measurements using plethysmography showed flow diversion from the foot to the calf as long as pressure values ranged below 40 mm Hg. This almost painless method appears useful for experimental and diagnostic studies in low pressure areas of the peripheral circulation.
INDIRECT SYSTOLIC BLOOD PRESSURE measurements in the low pressure area distal to arterial stenoses or occlusions have been introduced in routine clinical diagnosis. The methods currently used include mercury strain gauges,' Doppler ultrasound,' Xenon'33-clearance,"° spectroscopic procedures," and photoelectric devices.'2 All these techniques depend on determination of the onset of blood flow at a given cuff pressure as an indicator for the intravascular pressure. To the present, direct measurements required traumatic approaches such as surgical exposure of the dorsalis pedis artery.'3 A recently developed isovolumetric manometer connected to a steel microcannula allows percutaneous determination of blood pressure in small blood vessels by an almost painless procedure.'4 In the present study, pressure recordings were obtained not only in the foot arteries of normal subjects but also in poststenotic dorsalis pedis and posterior tibial arteries, previously not accessible to direct puncture. Since this method permits the continuous recording of pressure curves, systolic and diastolic values were studied at rest and during reactive hyperemia after three minutes of arterial occlusion. In order to evaluate the accuracy of an indirect technique using Doppler ultrasound, the direct measurements were used for comparison. In some experiments, the phenomenon of hemometakinesia was examined correlating ankle blood pressure during the course of reactive hyperemia to calf and foot blood flow measured during the same conditions.
female patients with a mean age of 58.2 years, range 35-81 years). The main complaint was intermittent claudication. Patients with rest pain or gangrene were not included. In each patient a thorough clinical and laboratory examination was performed including electronic oscillography," poststenotic systolic blood pressure measurements with Doppler ultrasound8' 9 and arteriography. The findings of ankle pulse palpation and of arteriography are listed in table 1. In seven patients, both dorsalis pedis and posterior tibial pulses were absent and in the remaining six patients barely palpable. Even in the cases with absent ankle pulses, flow signals could be detected by Doppler ultrasound. One of these patients presented marked edema of the lower leg. In an additional patient, medial calcinosis of the calf and foot arteries was diagnosed (diffuse "pipe-stem"-calcifications on the roentgenogram). There were no arterial occlusions in this case. The control group consisted of 13 healthy male volunteers with a mean age of 38.8 years (range 24-60 years). Their pedal pulses were easily palpable. Blood Pressure Measurements The direct determinations of blood pressure were performed by an isovolumetric manometer connected to a steel microneedle with an external diameter of 180,um and an internal diameter of 76 jtm. The system contains a manometer membrane and a mechanism of volume compensation which is operated by a feed-back circuit. Technical details have been described previously.'4 '6 Pressure curves of identical configuration and values within ± 1 mm Hg were obtained when measured simultaneously in a brachial artery with the micromanometric method and a conventional transducer.'6 Mean systolic ankle blood pressure evaluated by the indirect strain-gauge technique was 8.2 ± 9.1 mm Hg (N = 13) lower than mean intra-arterial systolic blood pressure.16 The patients were examined after resting in the supine position for 15-30 minutes. Location of the dorsalis pedis and posterior tibial arteries was made when a Doppler ultrasound flow velocity probe (Parks Electronics, model 806) in-
Methods Normal Patients and Subjects Thirteen patients with arteriosclerosis obliterans of the lower limbs were included in the study (ten male and three From the Peripheral Vascular Division, Department of Medicine, University of Zurich and Institute of Physiology, University of Basel, Switzerland. Address for reprints: Alfred Bollinger, M.D., Peripheral Vascular Division, Department of Medicine, University of Zurich, Kantonsspital, Ramistrasse 100, CH8006, Zurich, Switzerland. Received August 28, 1975; revision accepted for publication October 21, 1975.
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MICROMANOMETRY IN ARTERIAL DISEASE/Bollinger, Barras, Mahler dicated pulsations were faint or absent. At the point where maximal arterial flow signals were detected, the microneedle was inserted through the intact skin after sterilizing the area. No anesthesia was necessary. The needle was slowly advanced in the direction of the vessel until an arterial pressure signal was obtained as visualized on the oscilloscope. As soon as stable conditions were reached, blood pressure was registered on UV-photographic paper (Siemens Oscillofil 16) or on a forced-ink pen recorder (Gould-Brush, model 480). In the normal subjects with palpable foot arteries the puncture by a trained observer required not more than five minutes. The time needed in patients with faint or absent pulsations varied from one to 20 minutes. In four cases with severe ischemic disease not included in this series pressure measurements were not possible. In three healthy subjects and in 12 patients, immediately after registration of resting pressure, indirect measurements of systolic ankle pressure were performed by a trained observer. A standard pressure cuff around the ankle was inflated and the onset of blood flow velocity in the posterior tibial or the dorsalis pedis artery determined using a Doppler ultrasound flow detector (Parks Electronics, model 806). A mean of three to five determinations was used for the comparison with the average of the directly measured systolic pressure. In three normal subjects and in six patients a previously applied pressure cuff placed above the knee was then suddenly inflated by a reservoir to 300 mm Hg. The arterial
occlusion was maintained for three minutes. After the sudden release of cuff pressure, the changes in poststenotic blood pressure were continuously recorded until the resting values were attained or surpassed. For these registrations a paper speed of 1 mm/sec was used. At the end of the examination, the microneedle was withdrawn. Compression of the artery was not necessary, macroscopic bleeding did not occur. Arm pressure was measured by cuffs using the Korotkoff method. In ten of the 13 subjects the intra-arterial pressure of the cubital artery was determined by micromanometry as described for the foot arteries. Blood Flow Measurements In three normal subjects and in four patients calf and foot blood flow were measured by venous occlusion plethysmography in a second experiment at intervals of 30 sec before and during reactive hyperemia, while the cannulae still remained in the artery for intermittent pressure measurement. Mercury-in-silastic-strain gauges were used to assess the limb volume changes (U.G. Gutmann, Eurasburg, Western Germany). One venous occlusion cuff was placed above the knee, a second above the ankle. The strain gauges were adapted to the calf at the site of maximal circumference and to the foot. The venous occlusion cuffs were suddenly inflated from a pressure reservoir to 40 mm Hg and the plethysmographic curves were registered on a twochannel recorder (Servogor Metrawatt). In the intervals
TABLE 1. Clinical and Anaiographic Findings of the Patients Examined Patient/age/sex
Pedal pulses
Angiography
Main complaint
1/G.M. /81/F
Absent
Occlusion of right superficial femoral artery and posterior tibial artery Segmental occlusion of right common iliac artery Segmental stenosis of right common iliac artery (3 mm of internal diameter) Occlusion of right femoro-popliteal segment Stenosis of right superficial femoral artery Stenoses of abdominal aorta and both iliac arteries, occlusion of right superficial femoral artery Stenosis of left superficial femoral artery Occlusion of right common femoral artery Stenosis of left common iliac and left superficial femoral arteries Stenosis of right superficial femoral artery Occlusion of right superficial femoral artery Stenosis of left anterior tibial and fibular artery, occlusion of anterior tibial artery (proximal part) Stenosis of right common iliac artery, occlusion of right superficial femoral artery Calcification of calf and foot arteries (medial calcinosis). Peripheral arteries patent.
Intermittent claudication after 50 m Intermittent claudication after 100-200 m Intermittent claudication after strenuous exercise only
2/T.M. /41/M Weakly palpable
3/F.H. /35/M
Palpable
4/M.H. /70/M
Absent
5/D.B. /47/M Weakly palpable
6/C.M. /57/M
Absent
7/D.R. /69/M
Weakly palpable
8/B.G. /41/M
Absent
9/E.A. /49/M
Absent
10/F.F. /56/M Weakly palpable
11/F.B. /75/F
Absent
12/H.H. /66/M Weakly palpable 13/S.E. /69/F
14/B.R. /75/M
Absent Palpable
507
Intermittent claudication after 500 m Intermittent claudication after 450 m Intermittent claudication after 200 m
Intermittent claudication after 700 m Intermittent claudication after 300 m Intermittent claudication after 50 m Intermittent claudication after 500 m
Intermittent claudication after 50 m No intermittent claudication because of concomitant
coxarthrosis Intermittent claudication after 200 m
No intermittent claudication
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between the blood flow measurements direct blood pressure was monitored continuously with deflated occluding cuffs. Results
Blood Pressure Measurement at Rest
Blood pressures of the ankle arteries were obtained in 13 healthy subjects without impairment of peripheral arterial circulation (table 2). The systolic values (154.3 ± 22.3 mm Hg) of the dorsalis pedis or the posterior tibial artery exceeded in each of the 13 subjects the values determined from the arm (average 128.9 ± 20.1 mm Hg, P < 0.001), while the diastolic ankle pressures (average 69.9 ± 8.7 mm Hg) were not significantly different from the arm values (71.3 ± 7.8 mm Hg). Thus, pressure amplitude in the normal subjects was larger in the ankle artery (84.4 ± 15.6 mm Hg) than in the brachial artery (57.6 ± 16.4 mm Hg, P < 0.001). TABLE 2. Direct and Indirect Blood Pressure in the Ankle Arteries of Patients and Normal Subjects Blood pressure (mm Hg) Ankle Ankle direct indir. D D S S
Arm
No.
S
Artery
Arterial Occlusive Disease 81 F 41 M 35 M 70 M 47 M 57 M 69 M 41 M 49 M 56 M 75 F 66 M 69 F M 58.2 SD P*
1 2 3 4 5 6 7 8 9 10 11 12 13
185 85 130 85 185 85 80 190 90 145 80 115 100 175 140 95 125 85 145 90 200 85 85 145 180 95 158.5 87.7 28.2 6.0
57 42 95 56 166 98 100 69 99 70 66 55 118 68 39 34 62 87 108 73 34 49 137 68 113 83 94.9 62.5 35.9 18.5 0.001 0.001
66
95 107 97 72 85
d.p.
p.t. p.t. p.t. p.t.
215 138 109
d.p. d.p. d.p. d.p. d.p. d.p. d.p. d.p.
>300
p.t.
122 143 136
d.p.
86
89
Mediasclerosis (Patent Arteries) 75 M 180 Normal Subjects 15 32 M 110 16 24 M 120 17 26 M 120 18 34 M 122 19 34 M 130 20 48 M 107 21 34 M 141 22 50 M 120 23 36 M 125 24 35 M 121 25 60 M 165 26 57 F 175 27 34 M 120 M 38.8 128.9 SD 20.1 P* 14
Pt
80
60 80 80 65 65 67 75 72 65 63 79 84 72 71.3 7.8
205
136 150 151 157 151 130 182 134 146 141 181 206 141 154.3 22.3 0.001 0.01 0.001 0.001
72
58 63 64 71 65 68 78 68 66 68 87 86 67 69.9 8.7 NS
-
-
p.t. p.t. p.t. p.t. p.t. p.t. p.t. p.t. p.t. p.t. p.t. p.t.
NS
Nos. 15-17: Indirect measurement (Korotkoff): arm. Nos. 18-27: Direct measurement: arm and ankle.
*Significance level for comparison between arm and ankle pressure. tSignificance level for comparison between the patients and normal subjects. Abbreviations: M = mean; d.p. = dorsalis pedis artery; p.t. = posterior tibial artery;
SD = standard deviation; NS = not significant.
VOL. 53, No. 3, MARCH 1976
Figure 1 shows an original recording of a pressure curve from a normal subject and one patient in whom mediasclerosis of the lower leg arteries was diagnosed by the roentgenogram, but the ankle pulses were vigorously palpable and the pulse tracings registered from the big toe by electronic oscillography were normal. The difference between arm and ankle pressure and the pressure amplitude (205/72 mm Hg, fig. 1) are remarkable in this case with rigid lower leg arteries. Poststenotic blood pressure was measured in 13 patients with arterial occlusive disease (table 2). In every instance, the systolic and, with one exception, also diastolic values were lower than the corresponding arm artery pressures. The mean systolic (158.5 ± 28.2 mm Hg) and diastolic values (87.7 ± 6.0 mm Hg) at the arm were significantly higher than in the poststenotic ankle arteries (94.9 ± 35.9 mm Hg systolic and 62.5 ± 18.5 mm Hg diastolic, P < 0.001). Furthermore, the pressure amplitude of the ankle arteries (32.5 ± 20.1 mm Hg) was significantly reduced compared with the arm values (70.8 ± 28.3 mm Hg, P < 0.002). There were considerable inter-individual differences in these measures, reflecting the differences in severity of arterial occlusive disease among the patients. The lowest value measured in the dorsalis pedis artery was 39/34 mm Hg. The arteriogram of this patient showed a complete occlusion of the common femoral artery including the proximal part of the profunda femoris artery. The other extreme was represented by a patient with a stenosis of the left common iliac artery causing intermittent claudication only after strenuous exercise. His blood pressure in the posterior tibial artery amounted to 166/98 mm Hg (arm pressure 185/85 mm Hg). Figure 2 shows the original tracings of three patients with different degrees of arterial insufficiency. In most of the patients, no dicrotism was present. A dicrotic wave was found only in cases with very well compensated occlusions or stenoses. The dicrotic wave, however, was not located near the diastolic base line as in the normal subjects, but at about half pressure amplitude level. In order to evaluate the accuracy of indirect ankle blood pressure determinations, directly and indirectly measured systolic ankle blood pressures were compared. Figure 3 shows the correlation between direct and indirect measurements. The agreement is good (r = 0.87) and the differences between the two methods within the same artery did not exceed 15 mm Hg in general. In two instances, however, the systolic ankle blood pressure was markedly overestimated by the Doppler ultrasound technique (cases 11 and 14, table 2). The first of these patients had severe edema of the lower leg and the second patient had "pipe-stem" calcifications of the anterior and posterior tibial arteries due to medial calcinosis. At values above 100 mm Hg the pressures obtained by the indirect method were underestimated compared to those determined by micromanometry, while at lower pressures overestimation predominated. Blood Pressure during Reactive Hyperemia In three normal subjects, blood pressure in the ankle arteries fell slowly after application of the suprasystolic pressure and finally reached values that were near zero. Within the first heart cycle after the release of the cuff, positive pressures with a reduced pressure amplitude were
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MICROMANOMETRY IN ARTERIAL DISEASE/Bollinger, Barras, Mahler
509
mm Hg
150
100 T,
50 lsec FIGURE 1. Original blood pressure tracings obtained by direct micromanometry in the posterior tibial artery. Left panel shows the recording in a normal subject (No. 17, arm blood pressure 120/80 mm Hg). Right panel in a patient with calcified mediasclerosis of the calf arteries without arterial occlusion (patient 14, arm blood pressure 180/80 mm Hg).
recorded. The systolic pressure values measured at the beginning of reactive hyperemia in the normal subjects were reduced by 37% or more of resting values (table 3). The dicrotic wave was absent during this initial period. Pressure increased steadily, and within about 40 seconds the initial values of pressure and amplitude were reached again and dicrotism was restored. Figure 4, upper panel, shows original tracings from a normal subject before and during reactive hyperemia. The patients showed qualitatively the same reaction. The pressure reduction during reactive hyperemia, however, was
mm
quantitatively more pronounced and prolonged (table 3). After release of the arterial occlusion cuff, the poststenotic pressure rose only slowly. In some cases, blood pressure amplitude was initially abolished and developed progressively toward the initial values. Figure 4, lower panel, shows an example for the pressure reaction during reactive hyperemia in a patient with arterial occlusive disease. Comparison of Poststenotic Blood Pressure and Flow Alternated measurements of poststenotic pressure and of foot and calf blood flow were performed to analyze the
Hg
100
5;0O
-
Isec
mmHg 1001
................
_.I-
f
.1
...
---------- -
50
H~< ..... r-
e
-z
-Z- S;_
0L ______________
tsec
FIGURE 2. Original blood pressure tracings in the artery of three patients with arterial .occlusive disease of different severity. Top panel shows the recording in a patient with stenosis of the left common iliac and superficialfemoral artery (No. 9, arm blood pressure 125/85 mm Hg), middle panel
........dorsalis pedis
in a patient with occlusion of the superficialfemoral artery (No. 11, arm blood pressure 200/85 mm Hg); and lower panel in a patient with occlusion of the common femoral artery (No. 8, arm blood pressure; 140/95 mm Hg).
mmHg *
100 _ |4 ; ,- '''
1 --
..
50
T
,
, 1
-4
I sec
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5 10
!. ,
CIRCULATION
52/47 mm Hg in the former patient and to 17/14 mm Hg in the latter during the early phase of reactive hyperemia (fig. 5, lower panels).
*
healthy subjects
*
occlusive disease
V
edema or mediasclerosis
mmHg direct pressure micronoametry)
FIGURE 3. Correlation between simultaneous direct (micromanometry) and indirect (Doppler ultrasound) systolic ankle pressure values in 13 patients and three normal subjects. The line indicates the line of identity. The correlation coefficient was 0.87. The patient with edema suffered from severe arterial occlusive disease, while in the patient with calcified mediasclerosis (indirect pressure > 300 mm Hg) the peripheral arteries were patent.
pressure-flow relationship during reactive hyperemia. Measurements were obtained in three normal subjects and in four patients. The results are listed in table 3. In the patients no. 4, 5 and 7, no or very low foot flow values were measured as long as the ankle pressures were below 40 mm Hg, while increased flow was recorded simultaneously at the calves. Typical examples are represented in figure 5. The decrease in blood pressure during the reactive hyperemia phase was associated with an increase in calf blood flow. As expected reactive hyperemia flow values in patients did not reach the level attained by the normal subjects. Peak flow was reduced and the time course of reactive hyperemia delayed. Immediately after release of the arterial occlusion cuff, the foot blood flow did not show a uniform pattern. In patient 2 the foot peak flow was measured within the first 10 sec, whereas in patient 4 there was no measurable flow at that time. Blood pressure in the ankle arteries was reduced to
mmHg 150 _
..... ...
1wot 50
__
......... ......_J
art.occlusion
.- - ---- --t
_
.. .....
-
_
4 L 4..
0
Discussion In normal subjects, pressure curves of the dorsalis pedis artery have been recorded by means of direct puncture.'7' 18 Using micromanometry'4 it was possible to measure blood pressure even in foot arteries with absent or faint pulsations, as was shown in 13 patients (table 2, fig. 2) and reported in two preliminary examples.'6 The formal appearance of the pressure curves in these patients reflected the hemodynamic significance of the leg artery stenoses or occlusions. In cases with mild ischemia, the dicrotic notch, which is normally located at the base of the pressure curve of the foot arteries was less prominent and displaced upward on the descending limb of the pressure pulse. In the pressure curves of patients with severe ischemia, however, the dicrotic notch was not discernible and the pressure amplitude was markedly decreased or nearly abolished (lowest pressure values encountered at rest: 39/34 mm Hg), a finding which confirms the results of measurements after surgical exposure of the pedal arteries.'3 Measurements after a circulatory arrest of specific duration or after exercise are more sensitive than measurements at rest for the evaluation of the poststenotic circulatory dynamics, as is known from studies using indirect methods.", 2, 6, 1, In agreement with the results of Wallace and Stead'9 and of Rowell and coworkers,2' who directly recorded radial artery pressure after arterial occlusion, an initial decrease of pulsatile blood pressure was found during reactive hyperemia even in healthy volunteers (table 3, fig. 4, upper panel). The pressure reduction lasted no more than 40 sec after three minutes of circulatory arrest in normal subjects. In the patients with arterial occlusive disease, however, the pressure fell to lower absolute values than in normals and the initial postocclusive pulse excursions were small or even lacking (fig. 4, lower panel). The resting values
...... .........
S
1min
mmHg
VOL. 53, No. 3, MARCH 1976
s_
1min
art.occlusion
FIGURE 4. Ankle blood pressure before and during occlusion of the femoral artery above the knee for 3 min and during the reactive hyperemia after release of the cuff Upper panel shows the pressure reaction in a normal volunteer (No. 16, arm blood pressure 120/80 mm Hg) and lower panel recordings in a patient with occlusion of the superficial femoral artery (No. 13, arm blood pressure 180/95 mm Hg).
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MICROMANOMETRY IN ARTERIAL DISEASE/Bollinger, Barras, Mahler
511
TABLE 3. Blood Pressure and Flow Measurements During Reactive Hyperemia in Patients and Normal Subjects 0-15 sec
Resting
Q5 No.
P
C
Reactive hyperemia 45-60 sec
15-30 sec Q
F
P
C
Patients 2 102/62 3.5 1.3 52/47 4 98/67 1.9 0.7 17/14 5 83/60 2.0 1.2 25/22 7 107/65 4.0 0.9 26/22
F
14.0 4.3 11.2 n.m. 14.0 n.m. 12.7 n.m.
P
C
P
C
Qfp0F
74/54 4.8 3.2 104/72 3.3 2.3 20/17 30/26 9.3 0.9 36/29
54/49 12.8 1.7 54/46 3.4 2.2 68/56 6.8 1.8
75-90 sec
105-120 see
Q_ P
C
F
P
C
F
97/68 4.2 2.7 107/73 2.2 1.4 82/68 6.8 59/53 2.7 110/65 3.2
1.5 1.2 1.3
96/76
1.5 1.4
3.6 3.4 4.3
85/65
107/64
1.4
Normal subjects 15 126/62 1.3 0.8 72/47 19.0 3.4 113/62 3.2 1.0 123/61 1.0 1.0 16 136/56 1.8 0.7 85/53 26.2 4.0 128/66 5.0 0.5 138/65 2.2 0.9 17 134/67 1.8 0.7 65/50 33.0 4.8 121/65 3.4 2.4 135/65 1.8 0.8 Abbreviations: P = direct pressure measurement in mm Hg; Q = flow measured by venous occlusion plethysmography in ml/100 ml * min; C flow; F = foot blood flow; n.m. = not measurable.
were not reached 45 sec after release of the occlusion cuff. The duration of the pressure response increased with increasing severity of ischemia. Although in a group of patients (nos. 2, 4, 7) the resting pressure values were com-
=
calf blood
parable, their reaction to arterial occlusion showed considerable variability. This observation is consistent with the fact that the functional importance of arterial stenoses is better discriminated by measurements during provoked sub-
FIGURE 5. Diagrammatic representation of direct systolic (P5) and diastolic (Pd) ankle pressure and bloodflow in the calf(Qc) and in the foot (QF) during resting state and during reactive hyperemia. Upper left panel shows the course of an experiment in a normal subject (No. 15, arm blood pressure 110/60 mm Hg), lower left panel in a patient with moderate arterial occlusive disease (No. 2, arm blood pressure 130/85 mm Hg), and lower right panel in a patient with more severe arterial occlusive disease (No. 4, arm blood pressure 190/80 mm Hg). In the last patient reactive hyperemia during the initial phase was confined to the calf. Foot blood flow rose only after the peak flow at the calf was reached (phenomenon of hemometakinesia).
3' art.occlusion
reactive hyperemia
pW. I/meoi ~~~~~~~~~~ml/ m
a
mIltOOmi/min
Hg~~~~~~~~~~~~~~~~~~~~p
100
tO
'7~
~ ~ ~~~~~~~~~~~~P
Pd
-10
P
a~~~~~~~~~~~~~~~a
50.
50
5
5
.. -------
'QC
I:ii:::--
rest
1
3'art.occtlsion
reactive hyperemia
2
min
rest
3'art. occlusion
2 reactive hvperemia
3
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4
min
CIRCULATION
512
maximal vasodilatation than during resting conditions.7 9 Similar conclusions were drawn from a study in patients with aortoiliac disease evaluating femoral artery pressure during reactive hyperemia.2' The correlation between blood pressure of the ankle arteries measured by micromanometry and by an indirect
technique using Doppler ultrasound showed a good agreement of the systolic values with exception of two cases presenting with the marked edema or Moenckeberg's sclerosis of the lower leg arteries (fig. 3). The last two conditions do not permit an appropriate hemodynamic evaluation by indirect methods. Medial calcinosis may be severe enough to prevent compression by a standard blood pressure cuff (pseudohypertension).22 23 Direct measurements as used in this study are necessary to avoid falsely high readings. In three normal subjects and in four patients, calf and foot blood flow during reactive hyperemia were measured by venous occlusion plethysmography alternating with measurements of the ankle blood pressure. In agreement with earlier results8' 24-26 the postocclusive calf flow increase was reduced and delayed in the patients with arterial occlusive disease. In the cases with a pressure fall to 30 mm Hg or more, low or not measurable foot blood flow was observed, while hyperemic values were recorded simultaneously at the calf. This phenomenon has been described as hemometakinesia27 or blood flow diversion.28 Although fow measurements using venous occlusion plethysmography are open to criticism when venous occluding pressure is within the range of the arterial pressure and therefore possibly influencing the arterial inflow to the foot, the presence of such low pressure values offers a physiological explanation for the phenomenon of hemometakinesia. If local perfusion pressure is reduced initially during reactive hyperemia to the range of the capillary or venular pressure, the arterio-venous pressure gradient is abolished and blood flow ceases. In the postocclusive pressure range of about 30-40 mm Hg, hemometakinesia could also be explained by a critical closure of the resistance vessels.29 The measurement of poststenotic blood pressure by trans-
cutaneous micromanometry offers several advantages
as
compared to indirect methods. It permits continuous registration of blood pressure curves suitable for formal analysis. Systolic as well as diastolic values are obtained accurately even in very low pressure ranges, where indirect methods are questionable. The method described appears to be a promising investigative tool for use in pathophysiological problems in the low pressure areas distal to arterial occlusions and for evaluation of pharmacological agents. In addition, it also proved useful in clinical diagnosis, when local conditions such as edema or mediasclerosis render the indirect measurements unreliable. Acknowledgment The authors wish to thank Ms. M. Schlumpf, Mr. R. Chassot and Mr. M. Michel for their valuable technical assistance and Ms. B. Fest for secretarial
help.
VOL. 53, No. 3, MARCH 1976 References
1. Sumner DS, Strandness DE Jr.: The relationship between calf blood flow and ankle blood pressure in patients with intermittent claudication. Surgery 65: 763, 1969 2. Strandness DE: Exercise testing in the evaluation of patients undergoing direct arterial surgery. J Cardiovasc Surg 11: 192, 1970 3. Gundersen J: Segmental measurements of systolic blood pressure in the extremities including the thumb and the great toe. Acta Chir Scand (suppl) 426: 10, 1972 4. Carter SA, Lezack JD: Digital systolic pressures in the lower limb in arterial disease. Circulation 43: 905, 1971 5. Yao ST: Hemodynamic studies in peripheral arterial disease. Br J Surg 57: 761, 1970 6. Thulesius 0, Gjores JE: Use of Doppler shift detection for determining peripheral arterial blood pressure. Angiology 22: 594, 1971 7. Carter SA: Response of ankle systolic pressure to leg exercise in mild or questionable arterial disease. N Engl J Med 287: 578, 1972 8. Bollinger A, Mahler F, Gruentzig A: Peripheral hemodynamics in patients with coarctation, normotensive and hypertensive arteriosclerosis obliterans of the lower limbs. Angiology 22: 354, 1971 9. Bollinger A, Schlumpf M, Butti P, Gruentzig A: Measurement of systolic ankle blood pressure with Doppler ultrasound at rest and after exercise in patients with leg artery occlusions. Scand J Clin Lab Invest 31(suppl 128): 123, 1973 10. Lassen NA, Holstein P: Use of radioisotopes in assessment of distal blood flow and distal blood pressure in arterial insufficiency. Surg Clin N Am 54: 39, 1974 11. Downs AR, Gaskell P, Morrow I, Munson CL: Assessment of arterial obstruction in vessels supplying the fingers by measurement of local blood pressures and the skin temperature response test - correlation with angiographic evidence. Surgery 77: 530, 1975 12. Gyntelberg F, Nielsen PE, L6nsmann-Poulsen H: Skin blood pressure in hypertensive subjects measured by photoelectric technique. Scand J Clin Lab Invest 33: 45, 1974 13. Cappelen C, Hall KV: The effect of obstructive arterial disease on the peripheral arterial blood pressure, registrations from the dorsalis pedis artery of normal persons and patients before and after operation. Surgery 48: 888, 1960 14. Barras JP: Direct measurements of blood pressure by transcutaneous micropuncture of peripheral arteries, use of a new developed isovolumetric manometer. Scand J Clin Lab Invest 31(suppl 128): 153, 1973 15. Kappert A: Diagnosis of Peripheral Vascular Diseases. Bern, Stuttgart, Vienna, Huber, 1971 16. Nielsen PE, Barras JP, Holstein P: Systolic pressure amplification in the arteries of normal subjects. Scand J Clin Lab Invest 33: 371, 1974 17. Hamilton WF, Woodbury RA, Harper HT: Physiologic relationship between intrathoracic, intraspinal and arterial pressures. JAMA 107: 853, 1936 18. Kroeker EJ, Wood EH: Comparison of simultaneously recorded central and peripheral arterial pressure pulses during rest, exercise and tilted position in man. Circ Res 3: 623, 1955 19. Wallace JM, Stead EA: Fall in pressure in radial artery during reactive hyperemia. Circ Res 7: 876, 1959 20. Rowell LB, Brengelmann GL, Blackmon JR, Bruce RA, Murray JA: Disparities between aortic and peripheral pulse pressures induced by upright exercise and vasomotor changes in man. Circulation 37: 954, 1968 21. Brener BL, Raines JK, Darling RC, Austen WG: Measurement of systolic femoral arterial pressure during reactive hyperemia, an estimate of aortoiliac disease. Circulation 49 and 50(suppl II): 11-259, 1974 22. Taguchi JT, Suwangool P: "Pipe-stem" brachial arteries, a cause of pseudohypertension. JAMA 228: 733, 1974 23. Reimamn H, Bollinger A: Pseudohypertonie bei Mediasklerose. Schweiz med Wschr 104: 1813, 1974 24. Shepherd JT: Physiology of the circulation in human limbs in health and disease. Philadelphia and London, Saunders, 1963 25. Fronek A, Johansen K, Dilley RB, Bernstein EF: Ultrasonographically monitored postocclusive reactive hyperemia in the diagnosis of peripheral arterial occlusive disease. Circulation 48: 149, 1973 26. Ehringer H: Die reaktive Hyperamie nach arterieller Sperre. Series Angiologica, Huber 13: 20, 1971 27. DeBakey ME, Burch GE, Ray T, Ochsner A: The "borrow-lending" haemodynamic principle (hemometakinesia) and its application in peripheral vascular disturbances. Ann Surg 126: 850, 1947 28. Winsor T, Hyman C, Payne JH: Exercise and limb circulation in health and disease. Arch Surg 78: 184, 1959 29. Allwood MJ: Redistribution of blood flow in limbs with obstruction of a main artery. Clin Sci 22: 279, 1962
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Measurement of foot artery blood pressure by micromanometry in normal subjects and in patients with arterial occlusive disease. A Bollinger, J P Barras and F Mahler Circulation. 1976;53:506-512 doi: 10.1161/01.CIR.53.3.506 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1976 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539
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Micromanometry in Normal Subjects and in Patients with Arterial Occlusive Disease ALFRED BOLLINGER, M.D., JEAN PIERRE BARRAS, M.D., AND FELIX MAHLER, M.D. SUMMARY Blood pressure was measured continuously in the posterior tibial or dorsalis pedis arteries using an isovolumetric system (steel cannulas of 0.18 mm, external diameter). The systolic values in the ankle arteries of 13 normal subjects at rest (154.3 ± 22.3 mm Hg) exceeded the systolic arm pressure (128.9 ± 20.1 mm Hg, P < 0.001), while diastolic values (69.9 ± 8.7 mm Hg) were not significantly different from the arm pressure. In 13 patients with arterial occlusive disease (AOD) the dicrotic notch, normally situated close to the footpoint of the downslope, was either displaced upward or abolished. Both mean systolic and diastolic values (94.9 ± 35.9 mm Hg and 62.5 ± 18.5 mm Hg, respectively) and also mean pressure amplitude were reduced compared to the corresponding arm
values (158.5 ± 28.2 mm Hg and 87.7 ± 6.0 mm Hg, respectively, all P < 0.001). Comparison between the systolic pressure values measured by micromanometry and by an indirect technique using Doppler ultrasound showed a good correlation (r = 0.87). During postocclusive reactive hyperemia, the initial pressure values were markedly diminished in normal subjects and reached control values within 40 sec. In patients with AOD, however, this reduction in pressure was more pronounced and prolonged. Flow measurements using plethysmography showed flow diversion from the foot to the calf as long as pressure values ranged below 40 mm Hg. This almost painless method appears useful for experimental and diagnostic studies in low pressure areas of the peripheral circulation.
INDIRECT SYSTOLIC BLOOD PRESSURE measurements in the low pressure area distal to arterial stenoses or occlusions have been introduced in routine clinical diagnosis. The methods currently used include mercury strain gauges,' Doppler ultrasound,' Xenon'33-clearance,"° spectroscopic procedures," and photoelectric devices.'2 All these techniques depend on determination of the onset of blood flow at a given cuff pressure as an indicator for the intravascular pressure. To the present, direct measurements required traumatic approaches such as surgical exposure of the dorsalis pedis artery.'3 A recently developed isovolumetric manometer connected to a steel microcannula allows percutaneous determination of blood pressure in small blood vessels by an almost painless procedure.'4 In the present study, pressure recordings were obtained not only in the foot arteries of normal subjects but also in poststenotic dorsalis pedis and posterior tibial arteries, previously not accessible to direct puncture. Since this method permits the continuous recording of pressure curves, systolic and diastolic values were studied at rest and during reactive hyperemia after three minutes of arterial occlusion. In order to evaluate the accuracy of an indirect technique using Doppler ultrasound, the direct measurements were used for comparison. In some experiments, the phenomenon of hemometakinesia was examined correlating ankle blood pressure during the course of reactive hyperemia to calf and foot blood flow measured during the same conditions.
female patients with a mean age of 58.2 years, range 35-81 years). The main complaint was intermittent claudication. Patients with rest pain or gangrene were not included. In each patient a thorough clinical and laboratory examination was performed including electronic oscillography," poststenotic systolic blood pressure measurements with Doppler ultrasound8' 9 and arteriography. The findings of ankle pulse palpation and of arteriography are listed in table 1. In seven patients, both dorsalis pedis and posterior tibial pulses were absent and in the remaining six patients barely palpable. Even in the cases with absent ankle pulses, flow signals could be detected by Doppler ultrasound. One of these patients presented marked edema of the lower leg. In an additional patient, medial calcinosis of the calf and foot arteries was diagnosed (diffuse "pipe-stem"-calcifications on the roentgenogram). There were no arterial occlusions in this case. The control group consisted of 13 healthy male volunteers with a mean age of 38.8 years (range 24-60 years). Their pedal pulses were easily palpable. Blood Pressure Measurements The direct determinations of blood pressure were performed by an isovolumetric manometer connected to a steel microneedle with an external diameter of 180,um and an internal diameter of 76 jtm. The system contains a manometer membrane and a mechanism of volume compensation which is operated by a feed-back circuit. Technical details have been described previously.'4 '6 Pressure curves of identical configuration and values within ± 1 mm Hg were obtained when measured simultaneously in a brachial artery with the micromanometric method and a conventional transducer.'6 Mean systolic ankle blood pressure evaluated by the indirect strain-gauge technique was 8.2 ± 9.1 mm Hg (N = 13) lower than mean intra-arterial systolic blood pressure.16 The patients were examined after resting in the supine position for 15-30 minutes. Location of the dorsalis pedis and posterior tibial arteries was made when a Doppler ultrasound flow velocity probe (Parks Electronics, model 806) in-
Methods Normal Patients and Subjects Thirteen patients with arteriosclerosis obliterans of the lower limbs were included in the study (ten male and three From the Peripheral Vascular Division, Department of Medicine, University of Zurich and Institute of Physiology, University of Basel, Switzerland. Address for reprints: Alfred Bollinger, M.D., Peripheral Vascular Division, Department of Medicine, University of Zurich, Kantonsspital, Ramistrasse 100, CH8006, Zurich, Switzerland. Received August 28, 1975; revision accepted for publication October 21, 1975.
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MICROMANOMETRY IN ARTERIAL DISEASE/Bollinger, Barras, Mahler dicated pulsations were faint or absent. At the point where maximal arterial flow signals were detected, the microneedle was inserted through the intact skin after sterilizing the area. No anesthesia was necessary. The needle was slowly advanced in the direction of the vessel until an arterial pressure signal was obtained as visualized on the oscilloscope. As soon as stable conditions were reached, blood pressure was registered on UV-photographic paper (Siemens Oscillofil 16) or on a forced-ink pen recorder (Gould-Brush, model 480). In the normal subjects with palpable foot arteries the puncture by a trained observer required not more than five minutes. The time needed in patients with faint or absent pulsations varied from one to 20 minutes. In four cases with severe ischemic disease not included in this series pressure measurements were not possible. In three healthy subjects and in 12 patients, immediately after registration of resting pressure, indirect measurements of systolic ankle pressure were performed by a trained observer. A standard pressure cuff around the ankle was inflated and the onset of blood flow velocity in the posterior tibial or the dorsalis pedis artery determined using a Doppler ultrasound flow detector (Parks Electronics, model 806). A mean of three to five determinations was used for the comparison with the average of the directly measured systolic pressure. In three normal subjects and in six patients a previously applied pressure cuff placed above the knee was then suddenly inflated by a reservoir to 300 mm Hg. The arterial
occlusion was maintained for three minutes. After the sudden release of cuff pressure, the changes in poststenotic blood pressure were continuously recorded until the resting values were attained or surpassed. For these registrations a paper speed of 1 mm/sec was used. At the end of the examination, the microneedle was withdrawn. Compression of the artery was not necessary, macroscopic bleeding did not occur. Arm pressure was measured by cuffs using the Korotkoff method. In ten of the 13 subjects the intra-arterial pressure of the cubital artery was determined by micromanometry as described for the foot arteries. Blood Flow Measurements In three normal subjects and in four patients calf and foot blood flow were measured by venous occlusion plethysmography in a second experiment at intervals of 30 sec before and during reactive hyperemia, while the cannulae still remained in the artery for intermittent pressure measurement. Mercury-in-silastic-strain gauges were used to assess the limb volume changes (U.G. Gutmann, Eurasburg, Western Germany). One venous occlusion cuff was placed above the knee, a second above the ankle. The strain gauges were adapted to the calf at the site of maximal circumference and to the foot. The venous occlusion cuffs were suddenly inflated from a pressure reservoir to 40 mm Hg and the plethysmographic curves were registered on a twochannel recorder (Servogor Metrawatt). In the intervals
TABLE 1. Clinical and Anaiographic Findings of the Patients Examined Patient/age/sex
Pedal pulses
Angiography
Main complaint
1/G.M. /81/F
Absent
Occlusion of right superficial femoral artery and posterior tibial artery Segmental occlusion of right common iliac artery Segmental stenosis of right common iliac artery (3 mm of internal diameter) Occlusion of right femoro-popliteal segment Stenosis of right superficial femoral artery Stenoses of abdominal aorta and both iliac arteries, occlusion of right superficial femoral artery Stenosis of left superficial femoral artery Occlusion of right common femoral artery Stenosis of left common iliac and left superficial femoral arteries Stenosis of right superficial femoral artery Occlusion of right superficial femoral artery Stenosis of left anterior tibial and fibular artery, occlusion of anterior tibial artery (proximal part) Stenosis of right common iliac artery, occlusion of right superficial femoral artery Calcification of calf and foot arteries (medial calcinosis). Peripheral arteries patent.
Intermittent claudication after 50 m Intermittent claudication after 100-200 m Intermittent claudication after strenuous exercise only
2/T.M. /41/M Weakly palpable
3/F.H. /35/M
Palpable
4/M.H. /70/M
Absent
5/D.B. /47/M Weakly palpable
6/C.M. /57/M
Absent
7/D.R. /69/M
Weakly palpable
8/B.G. /41/M
Absent
9/E.A. /49/M
Absent
10/F.F. /56/M Weakly palpable
11/F.B. /75/F
Absent
12/H.H. /66/M Weakly palpable 13/S.E. /69/F
14/B.R. /75/M
Absent Palpable
507
Intermittent claudication after 500 m Intermittent claudication after 450 m Intermittent claudication after 200 m
Intermittent claudication after 700 m Intermittent claudication after 300 m Intermittent claudication after 50 m Intermittent claudication after 500 m
Intermittent claudication after 50 m No intermittent claudication because of concomitant
coxarthrosis Intermittent claudication after 200 m
No intermittent claudication
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between the blood flow measurements direct blood pressure was monitored continuously with deflated occluding cuffs. Results
Blood Pressure Measurement at Rest
Blood pressures of the ankle arteries were obtained in 13 healthy subjects without impairment of peripheral arterial circulation (table 2). The systolic values (154.3 ± 22.3 mm Hg) of the dorsalis pedis or the posterior tibial artery exceeded in each of the 13 subjects the values determined from the arm (average 128.9 ± 20.1 mm Hg, P < 0.001), while the diastolic ankle pressures (average 69.9 ± 8.7 mm Hg) were not significantly different from the arm values (71.3 ± 7.8 mm Hg). Thus, pressure amplitude in the normal subjects was larger in the ankle artery (84.4 ± 15.6 mm Hg) than in the brachial artery (57.6 ± 16.4 mm Hg, P < 0.001). TABLE 2. Direct and Indirect Blood Pressure in the Ankle Arteries of Patients and Normal Subjects Blood pressure (mm Hg) Ankle Ankle direct indir. D D S S
Arm
No.
S
Artery
Arterial Occlusive Disease 81 F 41 M 35 M 70 M 47 M 57 M 69 M 41 M 49 M 56 M 75 F 66 M 69 F M 58.2 SD P*
1 2 3 4 5 6 7 8 9 10 11 12 13
185 85 130 85 185 85 80 190 90 145 80 115 100 175 140 95 125 85 145 90 200 85 85 145 180 95 158.5 87.7 28.2 6.0
57 42 95 56 166 98 100 69 99 70 66 55 118 68 39 34 62 87 108 73 34 49 137 68 113 83 94.9 62.5 35.9 18.5 0.001 0.001
66
95 107 97 72 85
d.p.
p.t. p.t. p.t. p.t.
215 138 109
d.p. d.p. d.p. d.p. d.p. d.p. d.p. d.p.
>300
p.t.
122 143 136
d.p.
86
89
Mediasclerosis (Patent Arteries) 75 M 180 Normal Subjects 15 32 M 110 16 24 M 120 17 26 M 120 18 34 M 122 19 34 M 130 20 48 M 107 21 34 M 141 22 50 M 120 23 36 M 125 24 35 M 121 25 60 M 165 26 57 F 175 27 34 M 120 M 38.8 128.9 SD 20.1 P* 14
Pt
80
60 80 80 65 65 67 75 72 65 63 79 84 72 71.3 7.8
205
136 150 151 157 151 130 182 134 146 141 181 206 141 154.3 22.3 0.001 0.01 0.001 0.001
72
58 63 64 71 65 68 78 68 66 68 87 86 67 69.9 8.7 NS
-
-
p.t. p.t. p.t. p.t. p.t. p.t. p.t. p.t. p.t. p.t. p.t. p.t.
NS
Nos. 15-17: Indirect measurement (Korotkoff): arm. Nos. 18-27: Direct measurement: arm and ankle.
*Significance level for comparison between arm and ankle pressure. tSignificance level for comparison between the patients and normal subjects. Abbreviations: M = mean; d.p. = dorsalis pedis artery; p.t. = posterior tibial artery;
SD = standard deviation; NS = not significant.
VOL. 53, No. 3, MARCH 1976
Figure 1 shows an original recording of a pressure curve from a normal subject and one patient in whom mediasclerosis of the lower leg arteries was diagnosed by the roentgenogram, but the ankle pulses were vigorously palpable and the pulse tracings registered from the big toe by electronic oscillography were normal. The difference between arm and ankle pressure and the pressure amplitude (205/72 mm Hg, fig. 1) are remarkable in this case with rigid lower leg arteries. Poststenotic blood pressure was measured in 13 patients with arterial occlusive disease (table 2). In every instance, the systolic and, with one exception, also diastolic values were lower than the corresponding arm artery pressures. The mean systolic (158.5 ± 28.2 mm Hg) and diastolic values (87.7 ± 6.0 mm Hg) at the arm were significantly higher than in the poststenotic ankle arteries (94.9 ± 35.9 mm Hg systolic and 62.5 ± 18.5 mm Hg diastolic, P < 0.001). Furthermore, the pressure amplitude of the ankle arteries (32.5 ± 20.1 mm Hg) was significantly reduced compared with the arm values (70.8 ± 28.3 mm Hg, P < 0.002). There were considerable inter-individual differences in these measures, reflecting the differences in severity of arterial occlusive disease among the patients. The lowest value measured in the dorsalis pedis artery was 39/34 mm Hg. The arteriogram of this patient showed a complete occlusion of the common femoral artery including the proximal part of the profunda femoris artery. The other extreme was represented by a patient with a stenosis of the left common iliac artery causing intermittent claudication only after strenuous exercise. His blood pressure in the posterior tibial artery amounted to 166/98 mm Hg (arm pressure 185/85 mm Hg). Figure 2 shows the original tracings of three patients with different degrees of arterial insufficiency. In most of the patients, no dicrotism was present. A dicrotic wave was found only in cases with very well compensated occlusions or stenoses. The dicrotic wave, however, was not located near the diastolic base line as in the normal subjects, but at about half pressure amplitude level. In order to evaluate the accuracy of indirect ankle blood pressure determinations, directly and indirectly measured systolic ankle blood pressures were compared. Figure 3 shows the correlation between direct and indirect measurements. The agreement is good (r = 0.87) and the differences between the two methods within the same artery did not exceed 15 mm Hg in general. In two instances, however, the systolic ankle blood pressure was markedly overestimated by the Doppler ultrasound technique (cases 11 and 14, table 2). The first of these patients had severe edema of the lower leg and the second patient had "pipe-stem" calcifications of the anterior and posterior tibial arteries due to medial calcinosis. At values above 100 mm Hg the pressures obtained by the indirect method were underestimated compared to those determined by micromanometry, while at lower pressures overestimation predominated. Blood Pressure during Reactive Hyperemia In three normal subjects, blood pressure in the ankle arteries fell slowly after application of the suprasystolic pressure and finally reached values that were near zero. Within the first heart cycle after the release of the cuff, positive pressures with a reduced pressure amplitude were
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MICROMANOMETRY IN ARTERIAL DISEASE/Bollinger, Barras, Mahler
509
mm Hg
150
100 T,
50 lsec FIGURE 1. Original blood pressure tracings obtained by direct micromanometry in the posterior tibial artery. Left panel shows the recording in a normal subject (No. 17, arm blood pressure 120/80 mm Hg). Right panel in a patient with calcified mediasclerosis of the calf arteries without arterial occlusion (patient 14, arm blood pressure 180/80 mm Hg).
recorded. The systolic pressure values measured at the beginning of reactive hyperemia in the normal subjects were reduced by 37% or more of resting values (table 3). The dicrotic wave was absent during this initial period. Pressure increased steadily, and within about 40 seconds the initial values of pressure and amplitude were reached again and dicrotism was restored. Figure 4, upper panel, shows original tracings from a normal subject before and during reactive hyperemia. The patients showed qualitatively the same reaction. The pressure reduction during reactive hyperemia, however, was
mm
quantitatively more pronounced and prolonged (table 3). After release of the arterial occlusion cuff, the poststenotic pressure rose only slowly. In some cases, blood pressure amplitude was initially abolished and developed progressively toward the initial values. Figure 4, lower panel, shows an example for the pressure reaction during reactive hyperemia in a patient with arterial occlusive disease. Comparison of Poststenotic Blood Pressure and Flow Alternated measurements of poststenotic pressure and of foot and calf blood flow were performed to analyze the
Hg
100
5;0O
-
Isec
mmHg 1001
................
_.I-
f
.1
...
---------- -
50
H~< ..... r-
e
-z
-Z- S;_
0L ______________
tsec
FIGURE 2. Original blood pressure tracings in the artery of three patients with arterial .occlusive disease of different severity. Top panel shows the recording in a patient with stenosis of the left common iliac and superficialfemoral artery (No. 9, arm blood pressure 125/85 mm Hg), middle panel
........dorsalis pedis
in a patient with occlusion of the superficialfemoral artery (No. 11, arm blood pressure 200/85 mm Hg); and lower panel in a patient with occlusion of the common femoral artery (No. 8, arm blood pressure; 140/95 mm Hg).
mmHg *
100 _ |4 ; ,- '''
1 --
..
50
T
,
, 1
-4
I sec
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5 10
!. ,
CIRCULATION
52/47 mm Hg in the former patient and to 17/14 mm Hg in the latter during the early phase of reactive hyperemia (fig. 5, lower panels).
*
healthy subjects
*
occlusive disease
V
edema or mediasclerosis
mmHg direct pressure micronoametry)
FIGURE 3. Correlation between simultaneous direct (micromanometry) and indirect (Doppler ultrasound) systolic ankle pressure values in 13 patients and three normal subjects. The line indicates the line of identity. The correlation coefficient was 0.87. The patient with edema suffered from severe arterial occlusive disease, while in the patient with calcified mediasclerosis (indirect pressure > 300 mm Hg) the peripheral arteries were patent.
pressure-flow relationship during reactive hyperemia. Measurements were obtained in three normal subjects and in four patients. The results are listed in table 3. In the patients no. 4, 5 and 7, no or very low foot flow values were measured as long as the ankle pressures were below 40 mm Hg, while increased flow was recorded simultaneously at the calves. Typical examples are represented in figure 5. The decrease in blood pressure during the reactive hyperemia phase was associated with an increase in calf blood flow. As expected reactive hyperemia flow values in patients did not reach the level attained by the normal subjects. Peak flow was reduced and the time course of reactive hyperemia delayed. Immediately after release of the arterial occlusion cuff, the foot blood flow did not show a uniform pattern. In patient 2 the foot peak flow was measured within the first 10 sec, whereas in patient 4 there was no measurable flow at that time. Blood pressure in the ankle arteries was reduced to
mmHg 150 _
..... ...
1wot 50
__
......... ......_J
art.occlusion
.- - ---- --t
_
.. .....
-
_
4 L 4..
0
Discussion In normal subjects, pressure curves of the dorsalis pedis artery have been recorded by means of direct puncture.'7' 18 Using micromanometry'4 it was possible to measure blood pressure even in foot arteries with absent or faint pulsations, as was shown in 13 patients (table 2, fig. 2) and reported in two preliminary examples.'6 The formal appearance of the pressure curves in these patients reflected the hemodynamic significance of the leg artery stenoses or occlusions. In cases with mild ischemia, the dicrotic notch, which is normally located at the base of the pressure curve of the foot arteries was less prominent and displaced upward on the descending limb of the pressure pulse. In the pressure curves of patients with severe ischemia, however, the dicrotic notch was not discernible and the pressure amplitude was markedly decreased or nearly abolished (lowest pressure values encountered at rest: 39/34 mm Hg), a finding which confirms the results of measurements after surgical exposure of the pedal arteries.'3 Measurements after a circulatory arrest of specific duration or after exercise are more sensitive than measurements at rest for the evaluation of the poststenotic circulatory dynamics, as is known from studies using indirect methods.", 2, 6, 1, In agreement with the results of Wallace and Stead'9 and of Rowell and coworkers,2' who directly recorded radial artery pressure after arterial occlusion, an initial decrease of pulsatile blood pressure was found during reactive hyperemia even in healthy volunteers (table 3, fig. 4, upper panel). The pressure reduction lasted no more than 40 sec after three minutes of circulatory arrest in normal subjects. In the patients with arterial occlusive disease, however, the pressure fell to lower absolute values than in normals and the initial postocclusive pulse excursions were small or even lacking (fig. 4, lower panel). The resting values
...... .........
S
1min
mmHg
VOL. 53, No. 3, MARCH 1976
s_
1min
art.occlusion
FIGURE 4. Ankle blood pressure before and during occlusion of the femoral artery above the knee for 3 min and during the reactive hyperemia after release of the cuff Upper panel shows the pressure reaction in a normal volunteer (No. 16, arm blood pressure 120/80 mm Hg) and lower panel recordings in a patient with occlusion of the superficial femoral artery (No. 13, arm blood pressure 180/95 mm Hg).
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511
TABLE 3. Blood Pressure and Flow Measurements During Reactive Hyperemia in Patients and Normal Subjects 0-15 sec
Resting
Q5 No.
P
C
Reactive hyperemia 45-60 sec
15-30 sec Q
F
P
C
Patients 2 102/62 3.5 1.3 52/47 4 98/67 1.9 0.7 17/14 5 83/60 2.0 1.2 25/22 7 107/65 4.0 0.9 26/22
F
14.0 4.3 11.2 n.m. 14.0 n.m. 12.7 n.m.
P
C
P
C
Qfp0F
74/54 4.8 3.2 104/72 3.3 2.3 20/17 30/26 9.3 0.9 36/29
54/49 12.8 1.7 54/46 3.4 2.2 68/56 6.8 1.8
75-90 sec
105-120 see
Q_ P
C
F
P
C
F
97/68 4.2 2.7 107/73 2.2 1.4 82/68 6.8 59/53 2.7 110/65 3.2
1.5 1.2 1.3
96/76
1.5 1.4
3.6 3.4 4.3
85/65
107/64
1.4
Normal subjects 15 126/62 1.3 0.8 72/47 19.0 3.4 113/62 3.2 1.0 123/61 1.0 1.0 16 136/56 1.8 0.7 85/53 26.2 4.0 128/66 5.0 0.5 138/65 2.2 0.9 17 134/67 1.8 0.7 65/50 33.0 4.8 121/65 3.4 2.4 135/65 1.8 0.8 Abbreviations: P = direct pressure measurement in mm Hg; Q = flow measured by venous occlusion plethysmography in ml/100 ml * min; C flow; F = foot blood flow; n.m. = not measurable.
were not reached 45 sec after release of the occlusion cuff. The duration of the pressure response increased with increasing severity of ischemia. Although in a group of patients (nos. 2, 4, 7) the resting pressure values were com-
=
calf blood
parable, their reaction to arterial occlusion showed considerable variability. This observation is consistent with the fact that the functional importance of arterial stenoses is better discriminated by measurements during provoked sub-
FIGURE 5. Diagrammatic representation of direct systolic (P5) and diastolic (Pd) ankle pressure and bloodflow in the calf(Qc) and in the foot (QF) during resting state and during reactive hyperemia. Upper left panel shows the course of an experiment in a normal subject (No. 15, arm blood pressure 110/60 mm Hg), lower left panel in a patient with moderate arterial occlusive disease (No. 2, arm blood pressure 130/85 mm Hg), and lower right panel in a patient with more severe arterial occlusive disease (No. 4, arm blood pressure 190/80 mm Hg). In the last patient reactive hyperemia during the initial phase was confined to the calf. Foot blood flow rose only after the peak flow at the calf was reached (phenomenon of hemometakinesia).
3' art.occlusion
reactive hyperemia
pW. I/meoi ~~~~~~~~~~ml/ m
a
mIltOOmi/min
Hg~~~~~~~~~~~~~~~~~~~~p
100
tO
'7~
~ ~ ~~~~~~~~~~~~P
Pd
-10
P
a~~~~~~~~~~~~~~~a
50.
50
5
5
.. -------
'QC
I:ii:::--
rest
1
3'art.occtlsion
reactive hyperemia
2
min
rest
3'art. occlusion
2 reactive hvperemia
3
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4
min
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512
maximal vasodilatation than during resting conditions.7 9 Similar conclusions were drawn from a study in patients with aortoiliac disease evaluating femoral artery pressure during reactive hyperemia.2' The correlation between blood pressure of the ankle arteries measured by micromanometry and by an indirect
technique using Doppler ultrasound showed a good agreement of the systolic values with exception of two cases presenting with the marked edema or Moenckeberg's sclerosis of the lower leg arteries (fig. 3). The last two conditions do not permit an appropriate hemodynamic evaluation by indirect methods. Medial calcinosis may be severe enough to prevent compression by a standard blood pressure cuff (pseudohypertension).22 23 Direct measurements as used in this study are necessary to avoid falsely high readings. In three normal subjects and in four patients, calf and foot blood flow during reactive hyperemia were measured by venous occlusion plethysmography alternating with measurements of the ankle blood pressure. In agreement with earlier results8' 24-26 the postocclusive calf flow increase was reduced and delayed in the patients with arterial occlusive disease. In the cases with a pressure fall to 30 mm Hg or more, low or not measurable foot blood flow was observed, while hyperemic values were recorded simultaneously at the calf. This phenomenon has been described as hemometakinesia27 or blood flow diversion.28 Although fow measurements using venous occlusion plethysmography are open to criticism when venous occluding pressure is within the range of the arterial pressure and therefore possibly influencing the arterial inflow to the foot, the presence of such low pressure values offers a physiological explanation for the phenomenon of hemometakinesia. If local perfusion pressure is reduced initially during reactive hyperemia to the range of the capillary or venular pressure, the arterio-venous pressure gradient is abolished and blood flow ceases. In the postocclusive pressure range of about 30-40 mm Hg, hemometakinesia could also be explained by a critical closure of the resistance vessels.29 The measurement of poststenotic blood pressure by trans-
cutaneous micromanometry offers several advantages
as
compared to indirect methods. It permits continuous registration of blood pressure curves suitable for formal analysis. Systolic as well as diastolic values are obtained accurately even in very low pressure ranges, where indirect methods are questionable. The method described appears to be a promising investigative tool for use in pathophysiological problems in the low pressure areas distal to arterial occlusions and for evaluation of pharmacological agents. In addition, it also proved useful in clinical diagnosis, when local conditions such as edema or mediasclerosis render the indirect measurements unreliable. Acknowledgment The authors wish to thank Ms. M. Schlumpf, Mr. R. Chassot and Mr. M. Michel for their valuable technical assistance and Ms. B. Fest for secretarial
help.
VOL. 53, No. 3, MARCH 1976 References
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Measurement of foot artery blood pressure by micromanometry in normal subjects and in patients with arterial occlusive disease. A Bollinger, J P Barras and F Mahler Circulation. 1976;53:506-512 doi: 10.1161/01.CIR.53.3.506 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1976 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539
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