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Does the number of hypopnoeas influence therapy in patients with obstructive sleep apnoea?
RESPIRATORY
MEDICINE
(1998)
9.2, 1028-1031
Does the number of hypopnoeas influence therapy in patients with obstructive sleep apnoea? M.
CARRERA,
F. BARBS
AND A. G. N. AGUSTI
Serveide Pneumologia, Hospital Uniuersifari Son Durefa, Palma de MalIorca, Spain The definition of hypopnoea varies widely between sleep laboratories. This study sought to evaluate the impact upon therapeutic decision of the most commonly used one, which defines hypopnoea as a reduction in airflow of 50% (or more) accompanied by a decreased blood oxygen saturation of 4% (or more) (Agency for Health Care Policy and Research). We studied 109 consecutive patients (99 male) with an apnoea-hypopnoea index (AHI) greater than 5. The same investigator evaluated each patient twice. First, the hypopnoea index (HI) was unavailable to him by study design, and judgment was based upon the number of apnoeas and the clinical situation of the patient. Thereafter, he evaluated all patients again, in random order, this time taking into account the AH1 and the clinical condition of the patient. Therapeutic decision was compared at the end of the study. Mean age was 54 f 11 years ( f SD) and body mass index 33 f 6 kg m ~ 2. Most patients had normal spirometry and day-time arterial blood gases. Mean apnoea index (Al) was 35 & 24 h ~ ‘. Therapeutic decision based on the AI lead to conservative treatment (diet and sleep hygiene) in 32 cases and to active treatment in 77 patients [76 continuous positive airway pressure (CPAP) and one surgery]. The AH1 was 40 f 24 h - ‘. The consideration of the number of hypopnoeas lead to a therapeutic change only in four patients (3.7%) k2=0.36, P>O.3). These four patients had an AI of 15, 7, 3, and 9 h ’ and an AH1 of 22, 10, 46, and 17 h- ‘, respectively. Combined with their clinical data, this increase was considered a requirement for active treatment (CPAP). The most commonly used definition of hypopnoea has a small impact upon therapeutic decision in patients with obstructive sleep apnoea syndrome (OSAS). We suggest the need to develop new definitions of hypopnoea that incorporate other variables (neurophysiological, cardiovascular) of potential clinical relevance. Our results also show that the outcome of any new definition has to be assessed rigorously in terms of its clinical impact. RESPIR. MED.
(1998)
92,
1028-1031
Introduction The diagnosis of obstructive sleep apnoea syndrome (OSAS) requires overnight monitoring of neurophysiological and cardiopulmonary variables (polysomnography) to quantify, among other things, the number of apnoeas and hypopnoeas during sleep (1,2). Apnoea is unanimously defined as cessation in airflow of 10 s duration or longer (3,4). By contrast, there is no consensus on the definition of hypopnoea. A recent study (5) showed that, among 45 sleep laboratories in U.S.A. the reduction in airflow required to meet criteria for hypopnoea oscillates between any and 500/o, and the degree of arterial oxygen desaturation between any and 4%. This heterogeneity of definitions renders the comparison of results among different laboratories difficult. However, to arrive at an unanimously agreed definition of hypopnoea would be important only if Received 28 October 1997 and accepted in revised form 6 April 1998. Supported in part by ABEMAR. Correspondence should be addressed to: A. G. N. Agusti, Servei de Pneumologia, Hospital Universitari Son Dureta, C/Andrea Doria, 55. 07014 Palma de Mallorca, Spain. 0954.6111/98/081028+04
$12.0010
it has a clear impact on clinical practice. We undertook the current study to evaluate the impact upon the therapeutic decision of the definition of hypopnoea most commonly used in different laboratories (5), which is a reduction in airflow of 50% (or more), accompanied by decrease of blood oxygen saturation of 4% (or more) (Agency for Health Care Policy and Research) (3).
Methods We included in the study all the patients with an apnoeahypopnoea index (AHI) greater than 5 h - ’ attending by the Sleep Unit of our institution from July 1993 until December 1994. As part of their routine clinical evaluation all of them completed a questionnaire focused on sleeprelated symptoms. Also, we measured day-time arterial blood gases (IL BG3, Izasa, Spain) and forced spirometry (Warren E. Collins, MA, U.S.A.), and we obtained an EKG and a chest X-ray. An ENT evaluation was carried out only when clinically indicated. Occupational history was recorded. Nocturnal polysomnography (Ultrasom Nicolett, WI, U.S.A.) was obtained in all subjects during the first night in the sleep laboratory. It included recording 0
1998
W. B. SAUNDERS COMPANY
LID
HYPOPNOEAS
of oro-nasal flow by thermocouples (Pro-Tech Services, Inc. Woodinville, WA, U.S.A.) mounted on nasal prongs, thoraco-abdominal movements by stripes of stretching, submental electromyogram, electroculogram, electroencephalogram (C,A,, C,A,), electrocardiogram (DII derivation modified) and oxygen saturation (Criticare Systems Inc, WI, U.S.A.). Sleep stages scoring was done according to Rechtschaffen and Kales (6). Apnoea was defined as a cessation in airflow of 10 s or longer (3,4). Hypopnoea was defined as a reduction in airflow of 50% or more, accompanied by a decreased blood oxygen saturation of 4% or more with respect to baseline (3). Following the recommendations of the Spanish Society of Pulmonology and Thoracic Surgery (SEPAR) (4): (1) conservative treatment (diet and sleep hygiene) was advised whenever the AH1 was lower than 10; (2) an AH1 greater than 20 h ’ was considered as a criterion for active treatment. usually with continuous positive airway pressure (CPAP); and (3) when the AH1 was between 10 and 20 h ‘, therapeutic decision was individualized and based upon clinical data (mainly day-time symptoms, cardiovascular risk factors and occupation) and arterial blood gas data. The same investigator (F.B.) evaluated each chart (including clinical, functional and polygraphic data) on two separate occasions. First, with the hypopnoea index (HI) unavailable to him by study design; judgement was based upon the number of apnoeas and the clinical situation of the patients. Thereafter he evaluated all charts again, in random order (without knowing the previous decision), this time taking into account the AH1 and the clinical condition of the patient. At the end of the study, therapeutic decision was compared. This type of design is similar to that used by Douglas et u/. (7) to assess the clinical value of polysomnography in patients referred to a sleep unit. Results are shown as mean f standard deviation (SD) and range. The normal distribution of the data was confirmed using the Kolmogorov-Smirnov test. Differences between sample proportions were analysed by the Xl-test. The relationship between the apnoea index (AI) and the AH1 was assessed using the Spearman correlation test. A P value lower than 0.05 was considered significant.
TABLE
1. Anthropometric,
1029
AND THERAPY IN OSAS
gasometric
and spirometric
Mean f SD Age (years) Body mass index (kg m ~ ‘) PaO, (mmHg) PaCO, (mmHg) FEV, (% ref) FEVJFVC (X,)
54* 33 f 77% 41 f 85 f 94&
11 6 13 16 21 16
data
Range 2482 21-53 39-100 3ll80 299136 40-122
FEV,, Forced expiratory volume in I s. FVC, Forced vital capacity. Reference values were those of Rota et al. (8). TABLE
2. Polysomnographic
data
Apnoea index (h - ‘) Apnoea-hypopnoea index (h ~ ‘) Total sleep time (min) Sleep efficiency (0%) REM stage (%I) 1 +2 stage (‘l/u) 3+4 stage (‘%) Minimum arterial 0, saturation at night (%) Mean arterial 0, saturation at night (‘Z,) Time under 90% 0, saturation at night (min)
Mean f SD
Range
35&24 40 f 24 404 f I 89 f 12 16+ 12 693 18 16114
O-98 5-98 203-509 499100 O-72 13-100 O-84
7oi
13
41-99
9oi
8
57-99
123 f 130
o-497
50, ^
40
I
p : -0.1
.
P= 0.3
.
.
Results We studied 109 consecutive patients (99 male) with a mean age of 54 f 11 years. Each patient had at least one (mean 3; range l-7) of the following clinical features: a history of loud snoring, unsatisfying nocturnal sleep, disturbed sleep, changes of mood in the last months, morning headache, excessive day-time somnolence, cardiovascular disease and/ or polycythaemia. Table 1 presents their anthropometric. blood gas and spirometric data. Overall, patients were mildly obese and showed normal spirometry and day-time arterial blood gases, although wide inter-individual variation existed (Table 1). Table 2 shows the polysomnographic data. By definition, all patients had an AH1 greater than 5 h ~ ‘_ Mean AI was 35 h ~ ’ ( & 24) and mean AH1 was 40 h - ’ ( f 24) (Table 2). There was no significant
Number
of apnoeas
(h-l)
FIG. 1. Lack of relationship between the number of apnoeas h ’ and the number of hypopnoeas h - ’ in all the patients studied.
relationship between the AI and the AH1 @: - 0.1; P=O.3) (Fig. 1). Therapeutic decision based upon the AI alone led to conservative treatment (diet and sleep hygiene) in 32 cases and to active treatment in 77 patients (76 CPAP and one
1030
M. CARRERA
ET AL
surgery). When the same patients were evaluated using the AHI, conservative treatment was indicated in 28 cases and active treatment in 81 individuals @=0.36, P>O.3). Only in four out of the 109 patients studied (3.7%) therapeutic decision changed by considering the AHI. All four patients had an AI lower than 20 h - ’ (15, 7, 3 and 9 h - ’ . Their AH1 was 22, 10, 46 and 17 h-i, respectively. Combined with their clinical data, this change was considered a requirement for active treatment (CPAP). These four patients represent 11% of patients with an AI<20 h- ‘.
Discussion This investigation sought to assess the impact upon therapeutic decision of the most commonly used definition of hypopnoea (reduction of airflow of 50% or more accompanied by decreased blood oxygen saturation of 4% or more) (5). This is the definition recommended by the Agency for Health Care Policy and Research (3). Our results show that it has a minor clinical impact because, by considering the presence of hypopnoeas, a change in therapeutic decision occurred only in 3.7% of the patients. A recent study, has shown that there is enormous variability of the definition of hypopnoea among different laboratories (5). There is no consensus on the degree of airflow reduction required to categorize an event as hypopnoea, or on how to measure it, or if hypopnoea has to be defined as a function of the reduction in airflow or thoracoabdominal movements, or even on what neurological events (sleep fragmentation, change of frequency in electroencephalograph) (9) should be associated with airflow reduction in order to consider it as clinically significant. Consequently, many laboratories use their own definition of hypopnoea, making comparison of the results difficult and, more importantly, without having a clear knowledge of the real outcome of each definition. Our results apply to a particular definition of hypopnoea. Although this is the definition most commonly used in different laboratories (5), our results can not be extrapolated directly to all definitions currently in use. Within this conceptual frame though, our study underscores the small clinical impact of this definition and suggests that, if hypopnoeas really have to be incorporated into clinical judgement, other definitions should be evaluated. Our current records do not allow us to explore other alternatives in the population investigated herein. Previous studies (10) have shown that hypopnoeas can: (1) induce transitory awakenings (arousals) that fragment sleep and causes day-time sleepiness (10,ll); (2) associate intrathoracic pressure changes due to partial occlusion of the upper airway that lead to cardiocirculatory and haemodynamics disturbances (12); and (3) stimulate the sympathetic nervous system (13,14). The definition of hypopnoea evaluated in the present study does not include any of these potential consequences of hypopnoea. Given its small impact on clinical practice, we suggest that any future definition would probably need to include some of these neurological and/or cardiovascular parameters (9). Several methodological limitations should be considered. On the one hand, the possibility that we had mistaken
hypopnoeas for apnoeas. We believe that this is unlikely because, we used standard methodology (see Methods), and the number of hypopnoeas we observed was similar to that reported previously (1.516). On the other, we can not completely exclude some intra-observer variability in the therapeutic decision chosen. However, we think that this is probably minor because the short duration of the study (18 months) allowed us not to change the therapeutic protocol used. Further, this was easy to follow but rigid enough as to minimize this potential effect. In summary, our study shows that the most commonly used definition of hypopnoea (Agency for Health Care and Research) (3) has a small impact on therapeutic decision in patients with an AH1 greater than 5 h - ‘. We suggest the need to develop new definitions of hypopnoea that incorporate other variables (neurophysiological, cardiovascular) of potential relevance (9). From our results, it is also clear that the impact of any new definition has to be assessed rigorously in terms of its clinical outcome.
Acknowledgement The authors thank N. J. Douglas useful comments and criticisms.
(Edinburgh,
U.K.) for his
References 1. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993; 328: 123G-1235. 2. Block AJ, Boysen PG, Wynne JW, Hunt LA. Sleep apnea, hypopnea and oxygen desaturation in normal subjects. N Engl J Med 1979; 300: 513-517. 3. Agency for Health Care Policy and Research. Polysomnogrphy and Sleep Disorders Centers: Health Technology Assessment Reports. 1991, Number 4. US Dept of Health and Human Services, Public Health Service publication No. 92-0027, 1992. 4. Marin JM, ArLn X, Barbe F et al. Normativa sobre diagnaostico y tratamiento de apnea obstructiva de1 suetno (SAOS). Recomenaciones Sociedad Espafiola de Neumologia y Cirugia Toracica (SEPAR), No. 14. Ediciones Doyma S.A. Barcelona 1993: 13-14. 5. Moser NJ, Phillips BA, Berry DT, Harbison L. What is hypopnea anyway? Chest 1994; 105: 426428. 6. Rechtschaffen A, Kales A. Manual of standarized terminology, techniques and scoring system for the sleep stages of human subjects. Washington, D.C. U.S. Government Printing Office, 1968: 204. 7. Douglas NJ, Thomas S, Jan MA. Clinical value of polysomnography. Lancet 1992; 339: 347-350. 8. Rota J, Sanchis J, Agust-Vidal A et al. Spirometric reference values from a Mediterranean population. Bull Eur Physiopathiol Respir 1986; 22: 217-224. 9. Collard P, Dury M, Delguste P et al. Movement arousals and sleep-related disordered breathing in adults. Am J Respir Crit Care Med 1996; 154: 454459.
HYPOPNOEAS
10. Gould GA, Whyte F, Rhind GB et al. Sleep hypopnea syndrome. Am Rev Respir Dis 1988; 137: 895898. 11. Shepard JW. Excessive daytime sleepiness, upper airway resistance, and nocturnal arousals. Chest 1993; 104: 665-666. 12. Morgan BJ, Denahan T, Ebert TJ. Neurocirculatory consequences of negative intrathoracic pressure vs asphyxia during voluntary apnea. J Appl Physiol 1993; 74: 2967-2992. 13. Baylor P, Mouton A. Increased norepinephire variability in patients with sleep apnea syndrome. Am J Med 1995; 99: 61 l-661.
AND THERAPY IN OSAS
1031
14. Davies RJO, Belt PJ, Roberts SJ, Ali NJ, Stradling JR. Arterial blood pressure responses to graded transient arousal from sleep in normal humans. J Appl Physiol 1993; 74: 1123-l 130. 15. Bokinsky G, Miller M, Ault K, Husband P, Mitchell J. Spontaneous platelet activation and aggregation during obstructive sleep apnea and its response to therapy with nasal continuous positive airway pressure. Chest 1995; 10s: 625-630. 16. Boudewyns A, Sforza E, Zamagni M, Krieger J. Respiratory effort during sleep apneas after interruption of long-term CPAP treatment in patients with obstructive sleep apnea. Chest 1996; 110: 120-127.
MEDICINE
(1998)
9.2, 1028-1031
Does the number of hypopnoeas influence therapy in patients with obstructive sleep apnoea? M.
CARRERA,
F. BARBS
AND A. G. N. AGUSTI
Serveide Pneumologia, Hospital Uniuersifari Son Durefa, Palma de MalIorca, Spain The definition of hypopnoea varies widely between sleep laboratories. This study sought to evaluate the impact upon therapeutic decision of the most commonly used one, which defines hypopnoea as a reduction in airflow of 50% (or more) accompanied by a decreased blood oxygen saturation of 4% (or more) (Agency for Health Care Policy and Research). We studied 109 consecutive patients (99 male) with an apnoea-hypopnoea index (AHI) greater than 5. The same investigator evaluated each patient twice. First, the hypopnoea index (HI) was unavailable to him by study design, and judgment was based upon the number of apnoeas and the clinical situation of the patient. Thereafter, he evaluated all patients again, in random order, this time taking into account the AH1 and the clinical condition of the patient. Therapeutic decision was compared at the end of the study. Mean age was 54 f 11 years ( f SD) and body mass index 33 f 6 kg m ~ 2. Most patients had normal spirometry and day-time arterial blood gases. Mean apnoea index (Al) was 35 & 24 h ~ ‘. Therapeutic decision based on the AI lead to conservative treatment (diet and sleep hygiene) in 32 cases and to active treatment in 77 patients [76 continuous positive airway pressure (CPAP) and one surgery]. The AH1 was 40 f 24 h - ‘. The consideration of the number of hypopnoeas lead to a therapeutic change only in four patients (3.7%) k2=0.36, P>O.3). These four patients had an AI of 15, 7, 3, and 9 h ’ and an AH1 of 22, 10, 46, and 17 h- ‘, respectively. Combined with their clinical data, this increase was considered a requirement for active treatment (CPAP). The most commonly used definition of hypopnoea has a small impact upon therapeutic decision in patients with obstructive sleep apnoea syndrome (OSAS). We suggest the need to develop new definitions of hypopnoea that incorporate other variables (neurophysiological, cardiovascular) of potential clinical relevance. Our results also show that the outcome of any new definition has to be assessed rigorously in terms of its clinical impact. RESPIR. MED.
(1998)
92,
1028-1031
Introduction The diagnosis of obstructive sleep apnoea syndrome (OSAS) requires overnight monitoring of neurophysiological and cardiopulmonary variables (polysomnography) to quantify, among other things, the number of apnoeas and hypopnoeas during sleep (1,2). Apnoea is unanimously defined as cessation in airflow of 10 s duration or longer (3,4). By contrast, there is no consensus on the definition of hypopnoea. A recent study (5) showed that, among 45 sleep laboratories in U.S.A. the reduction in airflow required to meet criteria for hypopnoea oscillates between any and 500/o, and the degree of arterial oxygen desaturation between any and 4%. This heterogeneity of definitions renders the comparison of results among different laboratories difficult. However, to arrive at an unanimously agreed definition of hypopnoea would be important only if Received 28 October 1997 and accepted in revised form 6 April 1998. Supported in part by ABEMAR. Correspondence should be addressed to: A. G. N. Agusti, Servei de Pneumologia, Hospital Universitari Son Dureta, C/Andrea Doria, 55. 07014 Palma de Mallorca, Spain. 0954.6111/98/081028+04
$12.0010
it has a clear impact on clinical practice. We undertook the current study to evaluate the impact upon the therapeutic decision of the definition of hypopnoea most commonly used in different laboratories (5), which is a reduction in airflow of 50% (or more), accompanied by decrease of blood oxygen saturation of 4% (or more) (Agency for Health Care Policy and Research) (3).
Methods We included in the study all the patients with an apnoeahypopnoea index (AHI) greater than 5 h - ’ attending by the Sleep Unit of our institution from July 1993 until December 1994. As part of their routine clinical evaluation all of them completed a questionnaire focused on sleeprelated symptoms. Also, we measured day-time arterial blood gases (IL BG3, Izasa, Spain) and forced spirometry (Warren E. Collins, MA, U.S.A.), and we obtained an EKG and a chest X-ray. An ENT evaluation was carried out only when clinically indicated. Occupational history was recorded. Nocturnal polysomnography (Ultrasom Nicolett, WI, U.S.A.) was obtained in all subjects during the first night in the sleep laboratory. It included recording 0
1998
W. B. SAUNDERS COMPANY
LID
HYPOPNOEAS
of oro-nasal flow by thermocouples (Pro-Tech Services, Inc. Woodinville, WA, U.S.A.) mounted on nasal prongs, thoraco-abdominal movements by stripes of stretching, submental electromyogram, electroculogram, electroencephalogram (C,A,, C,A,), electrocardiogram (DII derivation modified) and oxygen saturation (Criticare Systems Inc, WI, U.S.A.). Sleep stages scoring was done according to Rechtschaffen and Kales (6). Apnoea was defined as a cessation in airflow of 10 s or longer (3,4). Hypopnoea was defined as a reduction in airflow of 50% or more, accompanied by a decreased blood oxygen saturation of 4% or more with respect to baseline (3). Following the recommendations of the Spanish Society of Pulmonology and Thoracic Surgery (SEPAR) (4): (1) conservative treatment (diet and sleep hygiene) was advised whenever the AH1 was lower than 10; (2) an AH1 greater than 20 h ’ was considered as a criterion for active treatment. usually with continuous positive airway pressure (CPAP); and (3) when the AH1 was between 10 and 20 h ‘, therapeutic decision was individualized and based upon clinical data (mainly day-time symptoms, cardiovascular risk factors and occupation) and arterial blood gas data. The same investigator (F.B.) evaluated each chart (including clinical, functional and polygraphic data) on two separate occasions. First, with the hypopnoea index (HI) unavailable to him by study design; judgement was based upon the number of apnoeas and the clinical situation of the patients. Thereafter he evaluated all charts again, in random order (without knowing the previous decision), this time taking into account the AH1 and the clinical condition of the patient. At the end of the study, therapeutic decision was compared. This type of design is similar to that used by Douglas et u/. (7) to assess the clinical value of polysomnography in patients referred to a sleep unit. Results are shown as mean f standard deviation (SD) and range. The normal distribution of the data was confirmed using the Kolmogorov-Smirnov test. Differences between sample proportions were analysed by the Xl-test. The relationship between the apnoea index (AI) and the AH1 was assessed using the Spearman correlation test. A P value lower than 0.05 was considered significant.
TABLE
1. Anthropometric,
1029
AND THERAPY IN OSAS
gasometric
and spirometric
Mean f SD Age (years) Body mass index (kg m ~ ‘) PaO, (mmHg) PaCO, (mmHg) FEV, (% ref) FEVJFVC (X,)
54* 33 f 77% 41 f 85 f 94&
11 6 13 16 21 16
data
Range 2482 21-53 39-100 3ll80 299136 40-122
FEV,, Forced expiratory volume in I s. FVC, Forced vital capacity. Reference values were those of Rota et al. (8). TABLE
2. Polysomnographic
data
Apnoea index (h - ‘) Apnoea-hypopnoea index (h ~ ‘) Total sleep time (min) Sleep efficiency (0%) REM stage (%I) 1 +2 stage (‘l/u) 3+4 stage (‘%) Minimum arterial 0, saturation at night (%) Mean arterial 0, saturation at night (‘Z,) Time under 90% 0, saturation at night (min)
Mean f SD
Range
35&24 40 f 24 404 f I 89 f 12 16+ 12 693 18 16114
O-98 5-98 203-509 499100 O-72 13-100 O-84
7oi
13
41-99
9oi
8
57-99
123 f 130
o-497
50, ^
40
I
p : -0.1
.
P= 0.3
.
.
Results We studied 109 consecutive patients (99 male) with a mean age of 54 f 11 years. Each patient had at least one (mean 3; range l-7) of the following clinical features: a history of loud snoring, unsatisfying nocturnal sleep, disturbed sleep, changes of mood in the last months, morning headache, excessive day-time somnolence, cardiovascular disease and/ or polycythaemia. Table 1 presents their anthropometric. blood gas and spirometric data. Overall, patients were mildly obese and showed normal spirometry and day-time arterial blood gases, although wide inter-individual variation existed (Table 1). Table 2 shows the polysomnographic data. By definition, all patients had an AH1 greater than 5 h ~ ‘_ Mean AI was 35 h ~ ’ ( & 24) and mean AH1 was 40 h - ’ ( f 24) (Table 2). There was no significant
Number
of apnoeas
(h-l)
FIG. 1. Lack of relationship between the number of apnoeas h ’ and the number of hypopnoeas h - ’ in all the patients studied.
relationship between the AI and the AH1 @: - 0.1; P=O.3) (Fig. 1). Therapeutic decision based upon the AI alone led to conservative treatment (diet and sleep hygiene) in 32 cases and to active treatment in 77 patients (76 CPAP and one
1030
M. CARRERA
ET AL
surgery). When the same patients were evaluated using the AHI, conservative treatment was indicated in 28 cases and active treatment in 81 individuals @=0.36, P>O.3). Only in four out of the 109 patients studied (3.7%) therapeutic decision changed by considering the AHI. All four patients had an AI lower than 20 h - ’ (15, 7, 3 and 9 h - ’ . Their AH1 was 22, 10, 46 and 17 h-i, respectively. Combined with their clinical data, this change was considered a requirement for active treatment (CPAP). These four patients represent 11% of patients with an AI<20 h- ‘.
Discussion This investigation sought to assess the impact upon therapeutic decision of the most commonly used definition of hypopnoea (reduction of airflow of 50% or more accompanied by decreased blood oxygen saturation of 4% or more) (5). This is the definition recommended by the Agency for Health Care Policy and Research (3). Our results show that it has a minor clinical impact because, by considering the presence of hypopnoeas, a change in therapeutic decision occurred only in 3.7% of the patients. A recent study, has shown that there is enormous variability of the definition of hypopnoea among different laboratories (5). There is no consensus on the degree of airflow reduction required to categorize an event as hypopnoea, or on how to measure it, or if hypopnoea has to be defined as a function of the reduction in airflow or thoracoabdominal movements, or even on what neurological events (sleep fragmentation, change of frequency in electroencephalograph) (9) should be associated with airflow reduction in order to consider it as clinically significant. Consequently, many laboratories use their own definition of hypopnoea, making comparison of the results difficult and, more importantly, without having a clear knowledge of the real outcome of each definition. Our results apply to a particular definition of hypopnoea. Although this is the definition most commonly used in different laboratories (5), our results can not be extrapolated directly to all definitions currently in use. Within this conceptual frame though, our study underscores the small clinical impact of this definition and suggests that, if hypopnoeas really have to be incorporated into clinical judgement, other definitions should be evaluated. Our current records do not allow us to explore other alternatives in the population investigated herein. Previous studies (10) have shown that hypopnoeas can: (1) induce transitory awakenings (arousals) that fragment sleep and causes day-time sleepiness (10,ll); (2) associate intrathoracic pressure changes due to partial occlusion of the upper airway that lead to cardiocirculatory and haemodynamics disturbances (12); and (3) stimulate the sympathetic nervous system (13,14). The definition of hypopnoea evaluated in the present study does not include any of these potential consequences of hypopnoea. Given its small impact on clinical practice, we suggest that any future definition would probably need to include some of these neurological and/or cardiovascular parameters (9). Several methodological limitations should be considered. On the one hand, the possibility that we had mistaken
hypopnoeas for apnoeas. We believe that this is unlikely because, we used standard methodology (see Methods), and the number of hypopnoeas we observed was similar to that reported previously (1.516). On the other, we can not completely exclude some intra-observer variability in the therapeutic decision chosen. However, we think that this is probably minor because the short duration of the study (18 months) allowed us not to change the therapeutic protocol used. Further, this was easy to follow but rigid enough as to minimize this potential effect. In summary, our study shows that the most commonly used definition of hypopnoea (Agency for Health Care and Research) (3) has a small impact on therapeutic decision in patients with an AH1 greater than 5 h - ‘. We suggest the need to develop new definitions of hypopnoea that incorporate other variables (neurophysiological, cardiovascular) of potential relevance (9). From our results, it is also clear that the impact of any new definition has to be assessed rigorously in terms of its clinical outcome.
Acknowledgement The authors thank N. J. Douglas useful comments and criticisms.
(Edinburgh,
U.K.) for his
References 1. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993; 328: 123G-1235. 2. Block AJ, Boysen PG, Wynne JW, Hunt LA. Sleep apnea, hypopnea and oxygen desaturation in normal subjects. N Engl J Med 1979; 300: 513-517. 3. Agency for Health Care Policy and Research. Polysomnogrphy and Sleep Disorders Centers: Health Technology Assessment Reports. 1991, Number 4. US Dept of Health and Human Services, Public Health Service publication No. 92-0027, 1992. 4. Marin JM, ArLn X, Barbe F et al. Normativa sobre diagnaostico y tratamiento de apnea obstructiva de1 suetno (SAOS). Recomenaciones Sociedad Espafiola de Neumologia y Cirugia Toracica (SEPAR), No. 14. Ediciones Doyma S.A. Barcelona 1993: 13-14. 5. Moser NJ, Phillips BA, Berry DT, Harbison L. What is hypopnea anyway? Chest 1994; 105: 426428. 6. Rechtschaffen A, Kales A. Manual of standarized terminology, techniques and scoring system for the sleep stages of human subjects. Washington, D.C. U.S. Government Printing Office, 1968: 204. 7. Douglas NJ, Thomas S, Jan MA. Clinical value of polysomnography. Lancet 1992; 339: 347-350. 8. Rota J, Sanchis J, Agust-Vidal A et al. Spirometric reference values from a Mediterranean population. Bull Eur Physiopathiol Respir 1986; 22: 217-224. 9. Collard P, Dury M, Delguste P et al. Movement arousals and sleep-related disordered breathing in adults. Am J Respir Crit Care Med 1996; 154: 454459.
HYPOPNOEAS
10. Gould GA, Whyte F, Rhind GB et al. Sleep hypopnea syndrome. Am Rev Respir Dis 1988; 137: 895898. 11. Shepard JW. Excessive daytime sleepiness, upper airway resistance, and nocturnal arousals. Chest 1993; 104: 665-666. 12. Morgan BJ, Denahan T, Ebert TJ. Neurocirculatory consequences of negative intrathoracic pressure vs asphyxia during voluntary apnea. J Appl Physiol 1993; 74: 2967-2992. 13. Baylor P, Mouton A. Increased norepinephire variability in patients with sleep apnea syndrome. Am J Med 1995; 99: 61 l-661.
AND THERAPY IN OSAS
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