Effect of Regional and Systemic Changes in Vasomotor Tone on Finger Pressure Amplification
Abstract Pulse wave amplification, which leads to increased peripheral systolic pressures, is observed during vasoconstriction after head-up tilt and during exercise. This may influence finger pressure measurements with the Finapres. To distinguish between changes in regional vascular tone and changes in systemic hemodynamics as a cause of pulse wave amplification, we measured finger pressure, intra-arterial brachial artery pressure, heart rate, and left ventricular ejection time during high-dose intravenous and low-dose intra-arterial infusions of phenylephrine and sodium nitroprusside in eight subjects. Forearm blood flow was measured by means of venous occlusion plethysmography. Intravenous phenylephrine at the highest dose caused an increase in mean brachial artery pressure of 24±3 mm Hg, a decrease in heart rate of 10±11 beats per minute, and an increase in ejection time of 23±9 milliseconds (all P<.01), whereas pulse wave amplification was reduced. Finapres underestimated the rise in systolic brachial artery pressure of 41±9 mm Hg by 11±12 mm Hg (P<.01). Forearm blood flow did not change. Intravenous nitroprusside caused a decrease in mean brachial artery pressure of 23±9 mm Hg, an increase in heart rate of 18±11 beats per minute, and a decrease in ejection time of 36±31 milliseconds (all P<.01), whereas pulse wave amplification increased. Finapres underestimated the fall in systolic brachial artery pressure of 30±13 mm Hg by 9±10 mm Hg (P<.05). Forearm blood flow did not change. During regional infusion of phenylephrine and nitroprusside forearm flow halved and doubled, respectively. Blood pressure levels and pulse wave amplification were not affected. One subject performed dynamic exercise, which caused an increase in blood pressure and heart rate and a decrease in ejection time. As previously observed during bicycle exercise and contrary to the results with phenylephrine, the rise in systolic brachial artery pressure was overestimated with Finapres because of increased pulse wave amplification. We conclude that changes in regional vascular tone are not the main determinant of pulse wave amplification between the brachial and finger arteries. Changes in systemic hemodynamics, in particular changes in heart rate or ejection time, rather than changes in blood pressure level appear to be most important.
Continuous noninvasive finger pressure measurements with the Finapres as an alternative for invasive BAP or radial artery blood pressure measurements are increasingly being used to monitor blood pressure during physiological studies1 2 3 or administration of vasoactive drugs.4 5 6 7 Since pressure waves change in shape on their way to the periphery, finger pressure levels are not always identical to more centrally measured pressures, such as BAP.8 9 10 11 12 Also, the response of finger pressure to physiological or pharmacological interventions may differ from that of BAP.8 9 10 11 12 13
The peripheral pulse wave is influenced by pressure gradients and pulse wave reflections. Flow in narrow arteries leading to the finger induces a pressure gradient, causing finger pressure to fall below BAP. Such pressure differences have been observed in elderly people and in patients with atherosclerotic vascular disease.12 13 Pulse wave reflections result in an increase in pulse pressure, mainly because of an increase in systolic pressure.14 This PWA, defined as the difference between systolic finger pressure and BAP, is influenced by changes in vascular tone14 15 16 17 ; PWA has been shown to increase during vasoconstriction and decrease during vasodilatation.14 17 18 PWA is also affected by systemic factors, such as HR, LVET, and blood pressure.14
The overestimation of systolic BAP by finger pressure during head-up tilt10 12 and bicycle exercise8 has been ascribed to regional vasoconstriction. However, finger pressure measurements underestimated the rise in systolic BAP during vasoconstriction induced by graded intravenous infusion of phenylephrine.11 We conducted the present study to distinguish between changes in regional vascular tone and changes in systemic hemodynamics as a cause of PWA between the brachial and finger arteries.
Eight subjects (two women, six men) aged 32 to 67 years in whom brachial artery cannulation was performed for diagnostic reasons gave their consent to participate in the study. This study was approved by the institutional review committee. Two subjects had hypertension and used antihypertensive drugs at the time of the study. One of them used a calcium channel blocker and an angiotensin-converting enzyme inhibitor; the other used a calcium channel blocker, an angiotensin-converting enzyme inhibitor, a diuretic, and a β-adrenoceptor blocker.
Finger pressures were measured bilaterally in the middle finger with Finapres (original TNO model 5 and commercial Ohmeda 2300e) noninvasive blood pressure monitor. Finapres measures blood pressure by means of the volume-clamp method first described by Peñáz, and the “Physiocal” criteria developed by Wesseling and coworkers.18 19 BAP was measured in the brachial artery of the nondominant arm. After local anesthesia with a lidocaine solution, a 20-gauge polytetrafluoroethylene catheter (Quik-Cath, Travenol) was inserted into the artery. The catheter was connected to a disposable pressure transducer (DT-XX, Viggo-Spectramed) via 10-cm-long rigid tubing. The transducer was connected to an HP 78203D blood pressure monitor (Hewlett-Packard). Dynamic characteristics of the catheter-manometer system, as checked by the flushing method and by application of external pressure steps,20 showed a natural frequency of approximately 33 Hz and a damping coefficient of 0.46. The pressure transducer and finger cuffs were all kept at heart level to prevent hydrostatic pressure differences.
The flow in the arm with the brachial artery cannula was measured with an electrocardiograph-triggered venous-occlusion plethysmograph (Periflow SU 4, Janssen Scientific Instruments). A mercury-in-Silastic strain gauge was positioned around the mid-forearm. The venous occlusion pressure of 60 mm Hg was intermittently applied for a period of six heart beats, with a recovery period of six heart beats.
After instrumentation and a 30-minute stabilization period, four experiments were performed in random order. Each experiment consisted of one 6-minute control period and three 6-minute periods during which incremental doses of vasoactive drugs were administered either via the brachial artery to achieve regional effects or via a catheter (Venflon 2, BOC Ohmeda AB) in a forearm vein of the contralateral arm to achieve systemic effects. Forearm blood flow was measured during the third minute of each 6-minute period. Finger artery pressure and BAP were compared during the 6th minute of the control period and of each infusion period. Since infusions via the brachial artery catheter impair the dynamic performance of a catheter-manometer system, these infusions were interrupted during the 6th minute of the control period and each infusion period.
Phenylephrine and sodium nitroprusside were dissolved in 0.9% NaCl. The intravenous doses of phenylephrine were 0.4, 0.8, and 1.6 μg · kg−1 · min−111 and of sodium nitroprusside were 0.5, 1.0, and 2.0 μg · kg−1 · min−1. The intra-arterial infusion rates were 50 times lower than the intravenous infusion rates of both compounds. One subject did not receive the intermediate dose of nitroprusside, and four subjects did not receive the highest intravenous dose of nitroprusside because BAP became too low at the lower doses. In one subject the protocol was extended. After a control period the subject performed exercise for 3 minutes by intermittently lifting a 7.5-kg weight with the right arm. Finger artery pressure and BAP were measured in the left arm.
Data Recording and Analysis
BAP, finger pressures, and a marker signal were recorded on a strip-chart recorder (Gould TA 2000) and were converted (analog-to-digital, codas software, Dataq Instruments Inc) at a sampling rate of 100 Hz and resolution of 0.25 mm Hg and stored in an on-line computer (Olivetti M380). BAP and finger pressure were subsequently calibrated against the same reference (Ametek pressure transducer). Integrated plethysmographic signals were recorded on the strip-chart recorder only. Four-second averages of systolic, mean, and diastolic BAP and finger pressure, HR, and LVET were computed off-line with FAST system programs (TNO-BMI). LVET was estimated from the time interval between the systolic upstroke and the pressure dip of the dicrotic notch in the BAP registrations. The second derivative of the BAP wave was used when a notch was absent or insufficiently clear.
All data are presented as mean±SD. Differences between finger and arterial blood pressures before and during infusions were compared using paired Student’s t tests and the Bonferroni method to correct for multiple comparisons.
Ipsilateral and contralateral finger pressures did not differ during the experiments. During the control periods systolic finger pressures overestimated systolic BAP by 8.4±7.5 mm Hg (P<.05, Fig 1⇓), whereas mean and diastolic finger pressures did not differ significantly from BAP (Fig 1⇓).
Intravenous infusion of phenylephrine caused an increase in blood pressure and LVET and a decrease in HR (Table 1⇓). Finger pressure measurements in both hands underestimated the rise of systolic BAP (Table 2⇓, Figs 1⇑ and 2⇓) but not the rise of mean and diastolic BAP (Table 2⇓, Fig 1⇑). Intravenous infusion of nitroprusside resulted in a decrease in blood pressure and LVET and an increase in HR (Table 1⇓). Finger pressure measurements underestimated the decrease in systolic BAP but not the decrease in mean and diastolic BAP (Table 2⇓, Figs 1⇑ and 2⇓). Results obtained in the two subjects taking antihypertensive drugs did not differ from the results in the six other subjects.
Intra-arterial infusion of phenylephrine or nitroprusside did not influence BAP (Fig 3⇓) or HR (data not shown), and differences between BAP and ipsilateral or contralateral finger measurements also did not change (Fig 3⇓, Table 3⇓). Similar results were obtained when calculations were based on pressures obtained during the first 10 seconds instead of the entire 60-second period after interruption of intra-arterial infusions (data not shown).
Forearm Blood Flow
Forearm blood flow did not change significantly in response to intravenous infusions of phenylephrine and nitroprusside. In all subjects intra-arterial infusion of phenylephrine caused a decrease of forearm blood flow from 3.2±1.6 to 2.3±1.6 mL · min−1 · 100 mL−1 (P<.05), whereas intra-arterial infusion of sodium nitroprusside caused an increase of forearm blood flow from 3.3±1.0 to 7.0±1.5 mL · min−1 · 100 mL−1 (P<.01). BAP did not change during intra-arterial infusions, and forearm resistance therefore increased during intra-arterial phenylephrine and decreased during intra-arterial nitroprusside infusion.
During exercise BAP increased from 127/79 to 175/110 mm Hg and HR from 90 to 107 beats per minute, whereas LVET decreased from 295 to 279 milliseconds in one subject. Systolic finger pressure measurements overestimated the rise in systolic BAP by 9.7 mm Hg (Fig 4⇓).
Peripheral PWA has been observed to increase during vasoconstriction and decrease during vasodilatation.14 15 17 18 It was therefore an unexpected observation that PWA between the brachial and finger arteries was reduced by systemic intravenous administration of phenylephrine.11 The present study confirmed this observation. It further showed a rise in PWA during intravenous infusion of sodium nitroprusside. The changes in PWA were mainly due to an effect on systolic pressure levels. Because of these effects, finger pressure measurements underestimated the increase in systolic BAP caused by intravenous phenylephrine and the decrease in systolic BAP caused by intravenous nitroprusside (Figs 1⇑ and 2⇑).
These unexpected changes in peripheral PWA cannot be attributed to changes in regional vascular tone. Regional infusion of phenylephrine and nitroprusside, in doses sufficient to halve or double forearm blood flow, respectively, but without an effect on systemic hemodynamics, had no effect on PWA (Fig 3⇑, Table 3⇑).
One could argue that the latter observation is an artifact. Both BAP and finger pressure might have been influenced to the same extent. If that were true, both BAP and ipsilateral finger pressures would differ from contralaterally measured finger pressures during regional infusions, but such differences were not observed (Fig 3⇑, Table 3⇑). The observed natural frequency of approximately 33 Hz and the damping coefficient of approximately 0.46 exclude the possibility that the difference between responses of systolic BAP and finger pressure measurements can be explained by the use of an overdamped catheter-manometer system.20
The intravenous infusions of nitroprusside and phenylephrine revealed that PWA increased concomitantly with a decrease in BP, an increase in HR, and a decrease in LVET (Fig 2⇑, Table 1⇑). Our infusion studies do not allow us to distinguish between the separate effects of changes in BP, HR, or LVET on PWA. Intravenous phenylephrine caused an increase in BAP, a baroreflex-mediated bradycardia, and prolonged LVETs. Intravenous nitroprusside had an opposite effect. In a previous study we observed that during exercise the increase in BP and HR and the decrease in LVET were associated with increased PWA.8 To distinguish between the effects of exercise and infusion of vasoactive drugs in the same subject, we studied PWA also during exercise in one of the subjects of the present study (Fig 4⇑). During both exercise and intravenous nitroprusside infusion, the decrease in LVET and increase in HR were associated with an increase in PWA (Figs 2⇑ and 4⇑). However, the increase in BAP during exercise was associated with an increase in PWA,8 and the increase in BAP during intravenous phenylephrine was associated with a decrease in PWA (Figs 2⇑ and 4⇑). Therefore, it seems that HR and LVET, and not blood pressure, are the main determinants of PWA between the brachial and finger arteries in this study. This finding is in agreement with previous observations showing that PWA between the aorta and brachial arteries is mainly determined by LVET.16 It should be noted that our results might have been influenced by the fact that LVET was estimated from the brachial artery registrations. LVETs obtained in this way closely resemble actual LVETs but are not always accurate.21
The longer the LVET, the more chance that a reflected pressure wave adds to the incoming pressure wave while the latter is still in the systolic phase. This will increase the systolic pressure of the proximal pressure wave and decrease PWA. Shorter LVETs cause the reflected pressure wave to add to the incoming pressure wave late during systole or during diastole and therefore do not affect the systolic pressure of the proximal wave. Apart from this explanation in the time domain, changes of PWA can also be explained in the frequency domain. The transfer function between BAP and finger arterial pressure shows a maximal amplification for pressure fluctuations around 7 Hz.22 An increase in HR, and thus in the frequency content of the incoming pressure wave, might thus be expected to result in an increased PWA.
In previous studies the increase in PWA between the brachial and finger arteries observed during bicycle exercise or head-up tilt was explained by regional vasoconstriction.8 10 12 In light of the present findings we think that the increase in HR and decrease in LVET associated with these conditions offer a better explanation. The changes in HR and LVET also explain the decrease in PWA, which has been observed during the blood pressure overshoot immediately after Valsalva’s maneuver,9 12 13 a situation characterized by vasoconstriction, increased blood pressure levels, and, most importantly, bradycardia.
In conclusion, systolic finger pressure measurements underestimated the response to systemic phenylephrine and nitroprusside infusions as measured in the brachial artery. This underestimation, which was caused by a respective decrease and increase in PWA, should be attributed to changes in systemic hemodynamics and not to changes in regional vasomotor tone. In view of the different patterns of PWA observed during systemic infusion of vasoactive drugs and during exercise, we conclude that HR and LVET rather than blood pressure level are the main determinants of PWA between the brachial and finger arteries.
Selected Abbreviations and Acronyms
|BAP||=||brachial artery pressure|
|LVET||=||left ventricular ejection time|
|PWA||=||pulse wave amplification|
- Received February 20, 1995.
- Revision received March 8, 1995.
- Accepted May 3, 1995.
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