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1 Permanent address: Unità Operativa Pneumologia, Ospedale S. Donato ASL8, Via P. Nenni 20, 52100 Arezzo, Italy. Key words: cerebral blood flow velocity, continuous positive airway pressure, end-tidal CO2 pressure, sleep disordered breathing, transcranial Doppler. Abbreviations: CBF, cerebral blood flow; CBFV, mean blood flow velocity in the middle cerebral artery; CI, confidence interval; CPAP, continuous positive airway pressure; CPAP0-pre, before CPAP; CPAP5, CPAP10 and CPAP15, CPAP at 5, 10 and 15 cmH2O respectively; CPAP0-post, after disconnection from CPAP; HR, heart rate; MAP, mean arterial pressure; PETCO2, end-tidal carbon dioxide tension; PI, Gosling pulsatility index; RR, respiratory rate; SDB, sleep disordered breathing; SpO2, transcutaneous haemoglobin oxygen saturation; TCD, transcranial Doppler. Correspondence: Dr. M. W. Elliott (e-mail mark.elliott@lineone.net).  Sleep disordered breathing is common in patients with cerebrovascular disease, and could exacerbate the cerebral damage in acute stroke. Data about the effects of continuous positive airway pressure (CPAP) upon cerebral perfusion are conflicting. We investigated whether increasing levels of CPAP may affect cerebral haemodynamics, assessed by transcranial Doppler (TCD) in normal humans. A group of 25 healthy young volunteers were evaluated before (CPAP0-pre), during (CPAP5, CPAP10 and CPAP15, denoting CPAP at 5, 10 and 15 cmH2O respectively) and after (CPAP0-post) application of incremental levels of CPAP delivered through a mouthpiece. The mean cerebral blood flow velocity (CBFV) and the pulsatility index (PI; an indirect measure of cerebrovascular resistance) in the middle cerebral artery were measured with TCD. Respiratory rate, heart rate, end-tidal carbon dioxide pressure (PETCO2), transcutaneous haemoglobin oxygen saturation (SpO2), mean arterial blood pressure and anxiety score were also recorded. Compared with CPAP0-pre, CBFV was significantly decreased as higher levels of CPAP were applied (P<0.0001). CPAP15 increased PI (P<0.05), PETCO2 was reduced by CPAP10 and CPAP15 (P<0.0001), and anxiety score and SpO2 increased at all levels of CPAP (P<0.05). Heart rate, respiratory rate and mean arterial pressure did not change. The decrease in CBFV was correlated with the fall in PETCO2 (CPAP15) and the increase in PI (CPAP10, CPAP15) (P<0.05). In conclusion, even low levels of CPAP delivered through a mouthpiece in awake, young volunteers led to a decrease in CBFV, measured by TCD. This fall in CBFV was associated with hypocapnia and with an increase in both cerebrovascular resistance and anxiety due to breathing against positive pressure. As the negative consequences of a fall in CBFV may outweigh the therapeutic effects of CPAP in the post-stroke setting, further studies of the cerebrovascular effects of CPAP with different interfaces in elderly patients with and without stroke are needed before intervention trials can be performed safely.
INTRODUCTION A clear association between snoring, sleep apnoea and increased risk of stroke has been shown in several studies [1–6]. Additionally, the prevalence of sleep disordered breathing (SDB) in patients with acute cerebrovascular disease is reported to be between 44% and 76% [7–11]. SDB in these patients may have a deleterious effect on critically ischaemic brain tissue through the repeated haemodynamic oscillations that are known to accompany both occlusion of the upper airway and the post-apnoeic phase [12–14]. However, there are conflicting data in the literature concerning the effects of upper airway obstruction on cerebral blood flow (CBF), even in non-stroke patients [6,15–18]. There are many treatments for obstructive sleep apnoea syndrome, but apart from weight loss the most useful and widely accepted therapy is nocturnal nasal continuous positive airway pressure (CPAP) [19]. As with positive end-expiratory pressure applied via an endotracheal tube during invasive mechanical ventilation [20,21], the increase in intrathoracic pressure during CPAP administered non-invasively at 10 cmH2O or above may have detrimental haemodynamic effects (i.e. reduced cardiac output due to decreased transmural cardiac pressures and venous return) [22]. Under normal conditions, cerebral autoregulation limits changes in CBF secondary to variations in cerebral perfusion pressure [23]. However, following acute stroke, loss of local cerebral autoregulation can occur, making CBF ‘pressure-dependent’ [24]. Therefore, while CPAP may abolish SDB, it may also compromise cerebral perfusion pressure because of a possible reduction in mean arterial pressure (MAP) and an increase in intracranial pressure due to impaired intracranial venous flow (cerebral perfusion pressure=MAP – intracranial pressure) [25–27]. There are conflicting data about the effects of CPAP on cerebral haemodynamics in human volunteers [28–30]. Therefore we performed the present study to assess the influence of incremental levels of CPAP on CBF velocity (CBFV) measured with transcranial Doppler (TCD) in normal young human subjects. METHODS The study group comprised 25 volunteers (14 male and 11 female) aged from 17 to 37 years [mean (S.D.) 27.9 (4.9) years], with a body mass index of 24.5 (3.6) kg/m2 (range 20.1–36 kg/m2). All subjects gave their informed consent to participate in the study. Volunteers with a history of pulmonary, cardiac or cerebral disease or who were receiving any medication were excluded. Poor insonation of the middle cerebral artery with TCD was also an exclusion criterion. The study was carried out in accordance with the Declaration of Helsinki (1989) of the World Medical Association, and was approved by the St James's University Hospital Local Ethics Committee. Each subject was investigated while awake and supine, breathing through a mouthpiece with the nose plugged. The study protocol involved evaluation of the subjects for 3 min at each of the following stages: (a) spontaneous breathing at baseline before institution of CPAP (CPAP0-pre); (b) breathing during increasing levels of CPAP (Sullivan ResMed® UK Ltd) administered through a mouthpiece at 5, 10 and 15 cmH2O (CPAP5, CPAP10 and CPAP15 respectively), taking care to avoid air leaks; and (c) spontaneous breathing after disconnection from CPAP (CPAP0-post). A period of 3 min was chosen as the length of each stage to allow acclimatization to the different pressure. This period is long enough to achieve a steady state, since cerebral vascular responses to changes in both arterial carbon dioxide pressure and intrathoracic pressure occur quickly [28,31]. Haring et al. [28] showed that cerebral and systemic haemodynamic changes occurred after 2.5 min and were not different from those recorded after 10 min of CPAP. At the end of each 3 min period, the following parameters were assessed: mean blood flow velocity in the middle cerebral artery (CBFV), Gosling pulsatility index (PI), respiratory rate (RR), end-tidal carbon dioxide tension (PETCO2), transcutaneous haemoglobin oxygen saturation (SpO2), heart rate (HR), MAP and anxiety score. CBFV and PI [32,33] were measured using a 2 MHz-pulsed TCD device (SciMed PCDop 842AQ; SciMed, Bristol, U.K.). PI was calculated from the recorded velocity tracings as an approximate index of cerebrovascular resistance according to the formula PI=(peak systolic velocity – end-diastolic velocity)/CBFV [33]. The probe, fixed with an elastic head band, was placed over the temporal bone, just above the zygomatic arch, in order to obtain a continuous measurement of CBFV. In all subjects, the left M1 segment of the middle cerebral artery was insonated at a depth of approx. 50 mm, keeping the insonation angle constant throughout the investigation [34]. The best signal was sought for each measurement. All TCD data were taken by the same investigator (R.S.) in order to avoid the reported between-investigator variability of 6% [35]. RR and PETCO2 were recorded continuously with an IR analyser (Morgan Capnograph; PK Morgan Ltd, Rainham, Kent, U.K.), sampling from the mouthpiece. In order to avoid the potential error of dilution in PETCO2 measurement due to the CPAP bias flow, a thin catheter was inserted into the mouthpiece as close as possible to its distal extremity and as far as possible from the CPAP expiratory port; furthermore, particular attention was paid to obtaining a reliable capnographic trace throughout the entire test. Changes in PETCO2 correlate well with changes in arterial carbon dioxide pressure in subjects with normal lungs [36]. MAP, SpO2 and HR were also measured non-invasively (Dinamap; Critikon, Bracknell, Berks., U.K.). To assess whether subjects found breathing with CPAP stressful, anxiety was assessed using a simple scale: ‘not at all anxious’ (1), ‘slightly anxious’ (2), ‘moderately anxious’ (3) and ‘highly anxious’ (4). All data are reported as mean (S.D.), as data were demonstrated to approximate to a normal distribution (skewness value <1). The effects of incremental levels of CPAP on the various parameters measured were assessed using the repeated-measures ANOVA test. CPAP0-pre values were compared with CPAP5, CPAP10, CPAP15 and CPAP0-post values by means of a paired two-tailed Student's t test if the ANOVA test was significant. Changes (D) were expressed as a percentage of CPAP0-pre data: D (%)=[100×(CPAP5, CPAP10, CPAP15 or CPAP0-post/CPAP0-pre) – 100]. In order to assess if any CPAP-induced responses of the measured parameters were associated with the changes in others, correlations between D values were tested with linear regression by applying the least-squares method. A value of P<0.05 was assumed to be statistically significant. Analyses were elaborated using version 10.0 of the SPSS statistical software package (SPSS Inc., Chicago, IL, U.S.A.). RESULTS Significant changes were seen in CBFV, PI, PETCO2, anxiety score and SpO2 with increasing CPAP when the repeated-measures ANOVA test was used. However, HR, RR and MAP did not change significantly with CPAP (Table 1).
Table 1 Results for each parameter before, during and after CPAP All values are mean (S.D.). Significance: *P<0.05 for change from baseline value (CPAP0-pre) as measured by paired Student's t test; listed P values indicate significance as measured by repeated-measures ANOVA.
Compared with CPAP0-pre values, CBFV was significantly reduced at all levels of CPAP. The decrease in CBFV at higher levels of CPAP was significantly greater than at CPAP5. PI increased significantly only at CPAP15, with no changes at lower levels. Compared with CPAP0-pre values, PETCO2 dropped significantly at higher levels of CPAP, but the decrease in PETCO2 at CPAP5 was not statistically significant. Both the anxiety caused by breathing against positive pressure and SpO2 increased significantly with higher levels of CPAP. After discontinuation of CPAP, all recorded parameters returned to CPAP0-pre values, with the exception of MAP, for which the CPAP0-post value was slightly but significantly reduced. Linear regression showed that the decrease in CBFV was significantly associated with the fall in PETCO2 at CPAP15 (Figure 1), as well as with the increase in PI at CPAP10 [P=0.02; r=0.474; 95% confidence interval (CI) -0.397 to -0.043] and CPAP15 [P=0.01; r=0.494; 95% CI -0.313 to -0.043]. This suggests that cerebral perfusion might be impaired by a hypocapnia-induced increase in cerebrovascular resistance. No significant correlations were found between the change in CBFV and changes in RR, HR, anxiety score, SpO2 and MAP. The PETCO2 response to CPAP was correlated with the increase in anxiety score at CPAP5 [P=0.04; r=0.418; 95% CI -0.015 to -0.0005], which in turn was probably associated with hyperventilation secondary to the stress of breathing under CPAP. No side effects were reported by any study participants. To investigate further the role of hypocapnia in the fall in CBFV, we repeated the study protocol in 20 subjects with the addition of 5% CO2 to the circuit at a flow able to maintain a constant PETCO2 while breathing during CPAP. We found that, during normocapnia, CBFV still decreased at lower levels of CPAP [CPAP5, 51.8 (11.6) cm/s; CPAP10, 51.7 (9.1) cm/s; CPAP0-pre, 55.5 (9.2) cm/s; P<0.001], but by a significantly lesser amount than during breathing of room air (CPAP5, 44.7 (9.7) cm/s; CPAP10, 44.3 (9.6) cm/s; CPAP0-pre, 55.5 (9.2) cm/s; P<0.00001]. At CPAP15, no decrease in CBFV occurred if PETCO2 was kept constant [CPAP15, 54.8 (11.0) cm/s; CPAP0-pre, 55.5 (9.2) cm/s; P>0.05]. This strongly suggests that the cerebrovascular effect of CPAP is mediated predominately through hypocapnia. DISCUSSION We observed that CPAP was associated with a significant decrease in CBFV, as measured by TCD, in normal volunteers studied during wakefulness. The higher the level of CPAP, the greater was the effect upon CBFV. The fall in CBFV was correlated with a decrease in PETCO2, which in turn was related to anxiety score. The main limitation of TCD is that it measures velocity rather than flow. However, the technique is able to estimate CBF if the diameter of the insonated artery remains constant [CBF (m3/s)=CBFV (m/s)×area (m2)]. It is widely accepted that changes in cerebral perfusion through the large arteries on the surface of the brain, such as the middle cerebral artery, are due mainly to changes in velocity, with only insignificant changes in vessel diameter [33,37–40]. The reduction in CBFV found in our study could be explained either by a decrease in CBF due to the constriction of small resistance vessels (if the diameter of the insonated artery was unchanged) or by vasodilatation of the middle cerebral artery at the site of TCD measurement. The fact that hypocapnia constricts cerebral arteries [39,41] suggests that the fall in CBFV found in the present study is more likely to have been due to a reduction in CBF. PI is considered to be an indirect index of vascular resistance, as it can be helpful in detecting intracranial cerebral artery occlusion [32,42]; therefore the increase in PI that we observed during CPAP was likely to be due to a hypocapnia-induced increase in cerebrovascular tone, with a consequent reduction in CBFV. Cerebral perfusion pressure may have also been reduced and could have led to the decrease in CBFV. CPAP is known to increase intrathoracic pressure, and therefore potentially could increase central venous and intracranial pressure and reduce cardiac output [25–27]. Despite the fact that MAP did not alter during the different levels of CPAP administered during the study, we cannot exclude the possibility that some minor changes in cardiac output may have occurred. However, small changes in both cardiac output and intracranial pressure would have little influence on CBF if autoregulation was intact [23]. Direct measurement of cardiac output and central venous pressure would have more accurately discriminated the effects of central haemodynamic changes from the consequences of anxiety-induced hyperventilation upon CBFV in these normal subjects. As our results seemed to suggest that hypocapnia was the major factor in the observed reduction in CBFV, we repeated the study with the addition of CO2 to the circuit to maintain a constant PETCO2 in 20 subjects. We found that, during normocapnia at higher levels of CPAP (CPAP15), no decrease in CBFV occurred, while at lower levels (CPAP5 and CPAP10) CBFV still decreased, but by a significantly lesser amount. This would be in keeping with our initial finding that the cerebrovascular effect of CPAP is mediated predominately through hypocapnia. Another possible limitation is that our study population was restricted only to young normal people. However, ethical concerns about possible deleterious effects of CPAP prevented us from studying either older people or patients with cerebrovascular diseases. The few studies examining the effects of CPAP upon cerebral perfusion are limited to healthy subjects, and their results are conflicting [28–30]. Haring et al. [28] evaluated CBFV and PI using TCD in nine healthy young volunteers during CPAP of 12 cmH2O, applied through a mouthpiece for 10 min. CBFV and MAP increased, while PI decreased significantly, after 2.5 min of CPAP. PETCO2 and HR did not change throughout the investigation. The authors suggested that the CPAP-induced increase in CBFV may have been due to cerebral vasodilatation evoked by cortical activation, as a degree of stress or anxiety (not quantified) was experienced by all participants. Droste et al. [29] investigated 23 patients with obstructive sleep apnoea syndrome and 16 healthy young adults during 10 min of spontaneous breathing, followed by 20 min with a nasal CPAP of 9 cmH2O and then 10 min of spontaneous breathing while wearing a nasal CPAP mask. PETCO2 was recorded in only 14 subjects (nine controls). Compared with spontaneous breathing, CBFV and PETCO2 were unchanged during CPAP; the authors reported a slight, but significant, increase in both systolic and diastolic blood pressure. They concluded that nasal CPAP of 9 cmH2O was a safe treatment because of the capacity of cerebral autoregulation to keep CBFV constant. Recently, Bowie et al. [30] did not observe any changes in CBFV or PI (measured with TCD), MAP or PETCO2 after 5 min of CPAP at 5 and 10 cmH2O delivered through a mouthpiece in 15 awake healthy volunteers; all participants reported the influence of CPAP on their breathing, but none found it distressing. There are a number of possible explanations for these differences. Firstly, there are differences in PETCO2; in some subjects it was unchanged (subjects were trained to normoventilate during CPAP) or it was not always measured. Carbon dioxide is well recognized to have a substantial effect upon the cerebral circulation [39,41,43] and it is not surprising that PETCO2 should change with CPAP. In our series, we registered a progressive decrease in PETCO2 without changes in RR, and therefore tidal volume must have increased. By increasing pulmonary functional residual capacity, CPAP shifts the lung pressure–volume curve to a more compliant area, with the result that tidal volume and alveolar ventilation increase [21]. However, this is unlikely to be important in normal subjects, in whom functional residual capacity is not reduced. The sensation of breathing against CPAP could cause hyperventilation due to anxiety, and our simple scale suggested increasing anxiety as CPAP increased. In addition to causing hyperventilation, anxiety may have a direct effect upon CBF. CBFV has been shown, using TCD, to change during mental tasks [44]. We did not train our subjects to breathe in a particular way, and this may be more relevant in patients with acute stroke who are not trained either. Secondly, differences in the subjects' position during investigations may have affected cerebral haemodynamics. Recent experimental data [45] showed that cerebral venous pressure did not increase with positive end-expiratory pressure when the head was elevated, but increased linearly with increasing positive end-expiratory pressure in the prone position. Our patients were studied supine, as were those in the study of Bowie et al. [30], but the position of the subjects was not reported in other studies. Thirdly, in only one of the studies reported [29] was CPAP delivered by means of a nasal mask, which is one of the most comfortable and common interfaces applied to treat SDB. The use of a mouthpiece might be more stressful, as it requires the nose to be plugged and the lips to be tightly sealed. Despite this clear limitation, we chose the mouthpiece because it allows more accurate monitoring of PETCO2 due to the smaller dead space, when compared with a nasal mask. Obviously, this interface could have an influence on the distress experienced by our subjects. Fourthly, two of the previous studies [28,29] submitted volunteers to only one level of CPAP. Like Bowie et al. [30], we tested the effects of different and increasing levels of CPAP upon CBFV, with the aim of obtaining greater validity from our results. In our subjects we applied CPAP of 15 cmH2O, which is unlikely to be used in controlling SDB. However, this high level of CPAP was useful in our study, as it emphasized the effects of CPAP by minimizing possible bias. Finally, in common with some other studies [26,30], we did not find any changes in MAP during CPAP. However, Haring et al. [28] and Droste et al. [29] found a significant increase in MAP, possibly because of sympathetic nervous system stimulation. We found a slight, but significant, drop in MAP after disconnection of CPAP compared with baseline. This could reflect the cessation of a stress-mediated increase in activity of the sympathetic nervous system, which is in keeping with the rapid reduction in anxiety score we found in the recovery phase. Our volunteers might have been understandably anxious before application of CPAP, thus explaining the lack of rise in MAP during CPAP but resulting in the fall after disconnection of CPAP. In conclusion, our present study has shown that even low levels of CPAP applied through a mouthpiece may reduce CBFV evaluated with TCD in awake healthy young humans. These CPAP-induced effects on cerebral haemodynamics are likely to be explained by increased cerebrovascular resistance caused by the hypocapnia consequent upon hyperventilation. This, in turn, is probably caused by the anxiety induced by the sensation of breathing against positive pressure. These effects of CPAP could assume greater importance in patients with acute stroke in whom cerebral autoregulation is impaired. Obviously, our data obtained in young healthy subjects while awake cannot be applied to elderly people with stroke during sleep, especially if they develop SDB. There is evidence from an in vitro study of basilar artery specimens to suggest that cerebral vasoconstrictor responses are reduced with age [46]; furthermore, cerebrovascular reactivity to CO2 is impaired in patients with obstructive sleep apnoea syndrome [47]. However, the results of the present study indicate that further evaluation needs to be undertaken before CPAP is used in acute stroke. If the patient does not sleep, becomes anxious because of the mask and hyperventilates, any potential beneficial effect of reducing SDB may be lost. 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Received 31 October 2002/3 February 2003; accepted 11 February 2003 Published as Immediate Publication 11 February 2003, DOI 10.1042/CS20020305
© 2003 The Biochemical Society |
Figure 1 Correlation between changes in PETCO2 [delta-PetCO2 (%)] and changes in CBFV [delta-CBFV (%)] at CPAP15 |
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