Anesth Analg 2001;92:415-417
© 2001 International Anesthesia Research Society
NEUROSURGICAL ANESTHESIA
The Effect of Continuous Positive Airway Pressure on Cerebral Blood Flow Velocity in Awake Volunteers
Robert A. Bowie, FRCA,
Paddy J. O’Connor, FRCA,
Jonathan G. Hardman, FRCA, and
Ravi P. Mahajan, FFARCSI
University Department of Anaesthesia and Intensive Care, City Hospital, Nottingham, UK
Address correspondence and reprint requests to Dr. Ravi P. Mahajan, Department of Anaesthesia, Nottingham City Hospital, Hucknall Road, Nottingham NG5 1PB. Address e-mail to ravi.mahajan{at}nottingham.ac.uk
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Abstract
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We measured the effect of 5 and 10 cm H2O continuous positive airways pressure (CPAP) on middle cerebral artery blood flow velocity (FV) in 15 awake, healthy volunteers by using transcranial Doppler ultrasonography. Mean, systolic, and diastolic FV plus pulsatility index were recorded. No significant change in any measured variable was observed with the application of 5 or 10 cm H2O CPAP. These results are in contrast to those of a previous study, which found a significant increase in mean FV and a decrease in pulsatility index during the application of 12 cm H2O CPAP.
Implications: Our study implies that the application of continuous positive airway pressure (CPAP) does not affect transcranial Doppler monitoring of the middle cerebral artery blood flow velocity and that the effect of CPAP on cerebral hemodynamics is less than had been previously suggested.
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Introduction
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The use of transcranial Doppler monitoring (TCD) to provide a continuous measurement of blood flow velocity (FV) in the basal cerebral arteries is an accepted and increasingly common practice (1). Under the assumption that the diameter of the insonated vessel remains constant during the study period, changes in FV can be taken to reflect changes in cerebral blood flow (CBF) (2–4).
Continuous positive airway pressure (CPAP) has benefits in patients with respiratory dysfunction. These benefits include improved arterial oxygenation and reduced work of breathing. A previous study in nine spontaneously breathing human volunteers found that 12 cm H2O CPAP caused a significant increase in middle cerebral artery (MCA) FV and a significant decrease in pulsatility index (PI) (5). These results suggest that application of CPAP may confound interpretation of MCA FV data. However, if the increase in MCA FV is caused by vasodilatation of the cerebral vascular bed distal to the MCA, as a decrease in PI would indicate, then the volume of the intracranial vascular compartment should also increase. This may subsequently increase intracranial pressure, with possible deleterious consequences, and could preclude a population of patients from the possible benefits of CPAP. Work examining the effect of 5 to 15 cm H2O positive end-expiratory pressure (PEEP) on anesthetized and ventilated patients found a significant decrease in MCA FV and an increase in PI, the opposite of the effect observed with CPAP (6). However, these results are confounded by the fact that increasing PEEP caused a decrease in mean arterial pressure (MAP). In a similar study of anesthetized and ventilated patients, 10 cm H2O PEEP caused no change in MAP and had no significant effect on TCD values (7).
In view of these conflicting results and the significance of the possible cerebral hemodynamic effects of CPAP, we felt it was important to reexamine the effects of CPAP on MCA FV in spontaneously breathing human volunteers.
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Methods
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Local ethics committee approval was obtained before obtaining written informed consent from all volunteers studied. Power analysis indicated that 15 subjects would give the study a power of 0.95 to observe the increase in MCA FV seen by Haring et al. (5) (i.e., mean [SD] 45 [9] vs 59 [11] cm/s). The inclusion criteria were the following: age 18–40 yr, body mass index 22–28 kg/m2, no history of vascular problems, no history of headaches, no previous head injury, and no vasoactive medication. All volunteers were studied in the supine position. The left MCA was identified via the temporal window. The depth, FV wave form, and relationship to anatomical features of the insonated artery were consistent with the MCA, as has been previously described (8). A 2-MHz pulsed TCD probe with specific software (SciMed PCDop 842AQ; SciMed, Bristol, UK) was used to record data onto a digital audiotape for subsequent analysis. Probe fixation in a head brace maintained the arterial insonation angle. MAP, heart rate, and peripheral oxygen saturation were recorded in a noninvasive manner throughout (Datex Cardiocap 2; Datex-Ohmeda, Helsinki, Finland). CPAP was administered via a tightly fitting mouthpiece attached to a high-flow air circuit. A nose clip was worn. ETCO2 was continually measured (Datex Capnomac; Datex-Ohmeda) by sidestream sampling from the mouthpiece. Mean FV (FVm), systolic FV (FVs), diastolic FV (FVd), and PI were recorded at baseline (no CPAP) and then at 5 and 10 cm H2O of CPAP. In addition, the power of the reflected Doppler signal was also measured continuously. The order of the two CPAP levels was selected randomly. Measurements were taken after each level of CPAP had been applied for 5 min, and during this period ETCO2 was maintained within 0.75 mm Hg of baseline. Because the data at baseline and at 5 and 10 cm H2O CPAP are mutually determinant, changes from baseline were assessed with repeated measures two-tailed analysis of variance.
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Results
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Eleven men and four women (age 25–40 yr) participated in the study. No statistically significant changes from baseline were found in FVm, FVs, FVd, PI, or MAP at either 5 or 10 cm H2O CPAP ( Table 1). Figure 1 illustrates individual changes in FVm at differing levels of CPAP. Reflected TCD power values changed by <5% throughout the study.
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Table 1. Diastolic Flow Velocity (FVd), Systolic Flow Velocity (FVs), Mean Flow Velocity (FVm), Pulsatility Index (PI), and Mean Arterial Pressure (MAP) at Varying Levels of Continuous Positive Airway Pressure (CPAP)
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Figure 1. Individual middle cerebral artery mean flow velocities (FVm) at varying levels of continuous positive airway pressure (CPAP).
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Discussion
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The only previous study on the effect of CPAP on MCA FV showed a significant increase in FVm when 12 cm H2O CPAP was applied (5). One explanation for this was that the discomfort of CPAP caused cortical activation, increasing CBF via flow-metabolism coupling. However, unlike healthy volunteers, patients with respiratory distress are likely to experience a reduction in cortical activation as a result of the successful use of CPAP. There are important implications if respiratory or cardiovascular changes caused by CPAP are responsible for the increased CBF, rather than the discomfort of the circuit. All subjects in our study noticed the influence of CPAP on their breathing, but none found it distressing, although we used 5 and 10 cm H2O CPAP as compared with 12 cm H2O CPAP by Haring et al. (5). Measurements were taken five minutes after application of CPAP, because this was in the middle of the period of greatest change seen by Haring et al. (5). Continuous measurement of FVm during this time showed no increase. Our selection of the level of CPAP was based on the common practice in our institution.
In TCD studies of this type, the assumption is made that the insonated MCA undergoes no significant change in caliber. The weight of evidence would suggest that for the large, basal cerebral vessels, this is the case (2,3). Recent studies have shown that changes in arterial carbon dioxide levels may affect arterial caliber by up to 9% (9). End-tidal CO2 tension was maintained constant during this study, and there is evidence that if the power of the reflected TCD signal remains constant, as in this study, then it can be assumed that no change in vessel caliber has occurred (4). We did not measure arterial carbon dioxide tension in our subjects. However, it is possible that the arterial to end-tidal CO2 gradient may have changed with the application of CPAP.
Previous work has shown a decrease in MCA FVm and MAP when PEEP was applied to anesthetized patients (6). Both PEEP and CPAP increase intrathoracic pressure and pulmonary vascular resistance and therefore may increase jugular venous pressure and intracranial pressure. Inhaled anesthetics affect cerebral hemodynamics (10,11) and, in combination with a decreased cerebral perfusion pressure (caused by increased cerebral venous pressure and lowered MAP), may explain a decrease in FVm. Our volunteers were assumed to have intact cerebral reactivity, and none experienced a decrease in MAP. However, they may all have experienced an increase in cerebral venous pressure caused by increased intrathoracic pressure and resultant decrease in cerebral perfusion pressure. In the face of a decreased cerebral perfusion pressure, cerebral autoregulation responds with vasodilatation, which would be reflected by a decrease in PI. If this vasodilatation did occur, then the small decrease in PI we observed failed to reach statistical significance, although one needs to be cautious in interpreting changes in PI to reflect changes in vascular resistance.
Our work shows that the application of 5 and 10 cm H2O CPAP to healthy spontaneously breathing volunteers causes no significant changes in MCA FV as measured by Doppler ultrasonography. This has implications for the use of TCD for assessing changes in cerebral hemodynamics in patients receiving CPAP.
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References
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-
Bishop CCR, Powell S, Rutt D, Brouse NL. Transcranial Doppler measurement of middle cerebral artery blood flow velocity: a validation study. Stroke 1986; 17: 913–5.[Abstract/Free Full Text]
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Kirkham FJ, Padayachee TS, Parsons S, et al. Transcranial measurement of blood velocities in the basal cerebral arteries using pulsed Doppler ultrasound velocity as an index of flow. Ultrasound Med Biol 1986; 12: 15–21.[Web of Science][Medline]
-
Newell DW, Aaslid R, Lam A, et al. Comparison of flow and velocity during dynamic autoregulation testing in humans. Stroke 1994; 25: 793–7.[Abstract]
-
Busija DW, Heistad DD, Marcus ML. Continuous measurements of cerebral blood flow in anesthetized cats and dogs. Am J Physiol 1981; 241: H228–34.[Abstract/Free Full Text]
-
Haring HP, Hormann C, Schalow S, Benzer A. Continuous positive airway pressure breathing increases cerebral blood flow velocity in humans. Anesth Analg 1994; 79: 883–5.[Abstract/Free Full Text]
-
Werner C, Kochs E, Dietz R, Schulte am Esch J. The effect of positive end-expiratory pressure on the blood flow velocity in the basal cerebral arteries during general anesthesia. Anasth Intensivther Notfallmed 1990; 25: 331–4.[Medline]
-
Muhling J, Thiel A, Zahn P, et al. Effects of different kinds of ventilation and positioning measures on blood flow velocity in the middle cerebral artery. Anasthesiol Intensivmed Notfallmed Schmerzther 1996; 31: 474–80.[Medline]
-
Aaslid R. Transcranial Doppler examination techniques. In: Aaslid R, ed. Transcranial Doppler sonography. Wien: Springer-Verlag, 1986: 39–59.
-
Valdueza JM, Draganski B, Hoffmann O, et al. Analysis of CO2 vasomotor reactivity and vessel diameter changes by simultaneous venous and arterial Doppler recordings. Stroke 1999; 30: 81–6.[Abstract/Free Full Text]
-
Algosson L, Messeter K, Rosen I, Holmin T. Effects of nitrous oxide on cerebral haemodynamics and metabolism during isoflurane anesthesia in man. Acta Anaesthesiol Scand 1992; 36: 46–52.[Web of Science][Medline]
-
Bedforth NM, Girling KJ, Harrison JM, Mahajan RP. The effects of sevoflurane and nitrous oxide on middle cerebral artery blood flow velocity and transient hyperemic response. Anesth Analg 1999; 89: 170–4.[Abstract/Free Full Text]
Accepted for publication October 3, 2000.
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Abstract
Introduction
