HYPERVENTILATION AND PANIC ATTACKS Justin Kenardy, Tian P. S. Oei and Larry Evans
The role of hyperventilation in the aetiology of panic attacks is still unclear. This paper briefly reviewsthe role of hyperventilationand abnormal respiration to panic attacks and examines the experimental evidence. Evidence has been found that physiological variables such as paC02 and pH are involved in the aetiology of panic attacks and panic disorder but the extent and the nature of the involvement of cognitive variables is undetermined. Based on current evidence, there is a needto integratecognitive variables with the physiological framework proposed by the hyperventilation theory. Until clear experimental evidence is produced about the relationships between cognitive and physiologicalfactors, the applicability of hyperventilationin the aetiology and treatment of panic attacks remains in question. Australian and New Zealand Journal of Psychiatry 1990; 24:261-267 Over the past decade, there has been increasing evidence of an association between hyperventilation and the anxiety disorders, in particular the phenomenon of panic attacks [ 1-31. Panic attacks [4] are discrete episodes of intense fear or discomfort and associated physical symptoms which appear to arise unexpectedly. There has been marked interest in panic attacks following their delineation as a form of anxiety amenable to specific pharmacologic treatment [5]. Interest in the relationship of hyperventilation to panic attacks has resulted from investigations of the aetiology and treatment of panic. Although the role of physiological processes in hyperventilation in panic has been formulated [2], the empirical evidence to support this formulation as an explanation of panic, and in particular its relevance to the treatment of panic attacks, is limited. It is therefore the intention of this Department of Psychology, University of Newcastle Justin Kenardy, PhD Anxiety Disorder Clinic, New Farm Clinic, University of Queensland Tian P.S. Oei, PhD Larry Evans, MB, ChB, FRC Psych, FRANZCP Correspond with Dr J. Kenardy, Department of Psychology, University of Newcastle, NSW
paper to review and examine the empirical evidence concerning the application of hyperventilation to the aetiology and treatment of panic attacks. The more obvious respiratory symptoms of dyspnea, breathlessness, and smothering sensations, are among the commonest symptoms of panic attacks reported by 52 - 90% of the sufferers; [6-91. Less obvious expressions of respiratory disturbance such as dizziness, parasthesia, chest pain, palpitations and tachycardia are also reported [ 101. Some or all of these symptoms may be present in acute hyperventilation in all persons but may also be present with panic attacks. Hyperventilation is by definition respiration that is excessive with respect to metabolic needs. It produces changes in the acid-base balance in the blood by producing a fall in hydrogen ion concentrations, causing a state of respiratory alkalosis. The lowering of C02 level (hypocapnia) results in vasoconstriction and, combined with alkalosis (which decreases oxygen reuptake by haemoglobin), cerebral hypoxia, the symptoms of which are dizziness, faintness, and visual disturbances [ 11. It has been suggested that the cardiac system may also adjust to these changes by acute increases in heart rate [ 111. A further effect is a reduction of phosphate and calcium levels in the blood, resulting in symptoms of dizziness, parasthesias, and
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nausea [ 10,191. Concurrent with changes in acid-base balance and C02 levels are changes in bicarbonate levels. The body’s response to these changes is slower than the response to alkalosis and hypocapnia, since it must dispose of bicarbonate by gradual excretion. However it is by this method that alkalosis can be reduced to within normal limits [I]. Thus, a person may be in a chronic hyperventilated state with a lowered partial pressure of C02 in the blood (paCO2) but by virtue of the bicarbonate excretion mechanism have blood pH levels within the normal range [ 1, 2, 101.
The hyperventilated state can be maintained in a chronic way by innocuous respiratory mechanisms such as thoracic breathing [ 1, 21. Thoracic breathing is a style of respiration where the involvement of the diaphragm is limited and thus respiratory efficiency and volume is decreased. The diaphragmatic involvement is restricted largely by tension in the abdominals. Diaphragmatic breathing in contrast is where the diaphragm is allowed to contract and relax freely with respiration. Other mechanisms which can maintain a chronic hyperventilated state are increased respiratory rate [ 131, sighing or an occasional deep breath [2, 101. It is not the chronic hyperventilated state, called “Hyperventilation Syndrome” [ 141, that is said to produce the symptoms of panic, but rather changes from this state produced by acute hyperventilation [ l , 2, 151. Acute hyperventilation in the absence of chronic hyperventilation is not presumed to result in the symptoms of panic. This is because the response to minor changes in ventilation in a person who already has lowered paC02 is said to produce a marked physiological change [ 151. Thus the process of acute hyperventilation should result in a substantial increase in symptoms of rapid respiration and palpitations which feedback on the already imbalanced system. It has been proposed that the abrupt and dramatic nature of these changes will mean that they are perceived as “spontaneous” and potentially life threatening, and that this catastrophic interpretation and the fear associated with it is proposed to be the basis of panic disorder [ 171. This model, which has been called the “hyperventilation model of panic” [ 161, also accounts for the self-limiting nature of panic. Eventually the lowered C02 will be insufficient to stimulate the respiratory reflex, C 0 2 levels will build up and the physiological process will cease with the symptoms abating. Writers in the field have emphasized either the physiological mechanisms of hyperventilation [2,
14, 161 or the cognitive component of the catastrophic interpretation of the symptoms of hyperventilation [ 17,18, 121. However both elements will be examined in this review. Evidence for the role of hyperventilation in panic falls into three general areas: (i) evidence supporting a chronic hyperventilated state in panic patients; (ii) evidence indicating panic-like states associated with acute hyperventilation or its equivalent; (iii) evidence demonstrating changes in panic frequency produced by changes in ventilation. The following will discuss these areas of evidence.
Chronic hypewentilation Chronic hyperventilation is associated with a higher resting respiratory rate [15]. Cohen and White [20] found that patients with anxiety neurosis, neurocirculatory asthenia or effort syndrome had a higher resting respiratory rate and minute respiratory volume than healthy controls. Ley [ 131 also found the resting respiration rate to be higher than would be expected in six patients with a history of panic attacks. These patients also demonstrated thoracic breathing patterns and frequent sighs. Rapee [3] assessed resting minute respiratory volume and found a higher volume for 20 panic disorder patients compared to 14 generalized anxiety disorder patients diagnosed according to DSM-111 criteria [21]. This difference was not significant possibly because there was great variability in minute respiratory volumes, with some of the panic disorder patients failing to have low resting minute respiratory volume. Chronic hyperventilation can also be indicated by lowered paC02. Lum [ 11 compared paCO2 levels in 152 normals and 200 patients diagnosed as having hyperventilation syndrome by clinical presentation of abnormal breathing patterns of frequent sighing, thoracic breathing, high baseline respiratory rate. He found lowered levels in more than half of the patients compared to normals. It is difficult in this study to assess the impact of arterial puncture on arousal and therefore paC02. However studies that have examined paC02 in panic disorder compared to other groups have found generally low levels. Rapee [3] found significantly lower paC02 levels in his panic disorder patients compared to the generalized anxiety disorder patients. Leibowitz, el al. [22] measured baseline levels of paCO2, bicarbonate and acid-base balance in 43 panic disorder patients diagnosed using DSM-111
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criteria [21] and 20 age-matched controls. As predicted by the hyperventilation model, panic disorder patients had normal pH compared to controls but had lower venous paCO2 and a lower level of bicarbonate as calculated from pH and paC02 levels. In these two studies heart rate was also assessed and found to be significantly lower in the generalised anxiety disorder and control groups, thus indicating differences not only in respiration but possibly also arousal. This may be a moot point since arousal could drive hyperventilation by leading to higher resting respiration and possibly lower paCO2. However arousal may be determined by the immediate assessment situation or may reflect a baseline and thus a chronically hyperventilated state. The lowered bicarbonate levels and the normal pH in the study by Leibowitz suggests that the differences are related to a chronic hyperventilation. Thus the combination of bicarbonate levels, pH and paC02 seems to provide more complete assessment of chronic hyperventilation. In summary, resting respiratory differences appear to be present in some but not all panic disorder patients compared to normals and generalised anxiety disorder patients. It is worth noting though that there may be overlap in all of these groups since panic attacks can occur in patients with generalised anxiety disorder [ 121 and even in a normal population [23].
Acute hyperventilationand panic Acute changes in ventilation can be produced by relatively brief episodes of voluntary hyperventilation [lo, 241. Anxiety has been reported in response to acute hyperventilation. Clark and Hemsley 1251 found that as well as symptoms of dry mouth, pounding heart, faintness, tingling and feelings of unreality, 19 of the 27 normals who voluntarily hyperventilated also experienced slight increases in self-reported anxiety. Subjects with higher levels of neuroticism reported greater distress in response to hyperventilation, suggesting that those who reported anxiety may have had some susceptibility because of their greater trait anxiety levels. Garsen, van Weenedaal, and Blosmink [26] examined the diagnostic overlap between hyperventilation syndrome diagnosed by interview, response to voluntary hyperventilation and agoraphobia. The investigators found that 17 of the 28 agoraphobics who voluntarily hyperventilated reported that the ex-
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perience was similar to a panic attack. In this study 6 patients failed to complete the voluntary hyperventilation and were excluded from the study. Whether they did not complete the procedure because they were afraid of experiencing a panic attack was not reported. Thus it is difficult to know if any panic attacks would have resulted. In another study of voluntary hyperventilation Bonn, Redhead and Timmons [27] also found that 14 out of 21 agoraphobic patients did not complete a voluntary hyperventilation procedure because of “being overcome with dizziness or other distress”. BOM et af. [27] also asked their subjects to compare usual panic symptoms experienced to those experienced during voluntary hyperventilation. Twenty of the agoraphobic patients reported some symptoms common to both, although their symptoms in panic were generally less severe. Rapee [3] found that panic disorder patients reported significantly more distress, more symptoms and a greater similarity of the experience to usual anxiety than generalised anxiety disorder patients in response to voluntary hyperventilation. Again, however, no patients reported panic attacks in spite of low paC02. No differences were found in minute respiratory volume change, heart rate or paCO2 between the panic and generalised anxiety disorder groups in response to hyperventilation. In explaining the results Rapee suggested that it was environmental cues and cognitive mediation which lead to the non-occurrence of panic attacks. Patients indicated that they did not panic because they knew that they were safe in the environment and that they understood the cause of their symptoms. Gorman et al. [ 191 report one of the few studies were panic disorder patients had panic attacks during voluntary hyperventilation. They found that only 25% [3] of their patients with panic disorder reported experiencing panic attacks during voluntary hyperventilation although again some failed to complete the procedure because of fatigue or distress. In this controlled study blood pH levels were also assessed and found to be similarly high in controls and patients during hyperventilation suggesting that the procedure had produced the same physiological changes in both groups and that the panic attacks resulted from factors other than the physiological changes occurring as a result of hyperventilation. Two studies have examined hyperventilation during panic attacks. Salkovskis, Warwick, Clark and Wessels [28] report a substantial decrease in paCO2 and an
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increase in pH during a panic attack experienced by a patient on renal dialysis. Whilst dialysis in itself does produce mild alkalosis the changes in this patient’s physiology were greater at this time than during other periods of dialysis. Further, prior to the panic attack the patient reported catastrophic thoughts concerned with impending death. The authors suggest that it was the catastrophic cognition that uniquely interacted with the blood chemistry changes to produce further increases in respiration and pH. Hibbert [19] found that some but not all patients show changes in paCO2 during naturally occurring panic attacks assessed using ambulatory measurement. Another procedure which can acutely alter paC02 levels, is direct C02 inhalation. Van den Hout and Griez [30] report that an acute decrease in paC02 and alkalosis follows the first expiration of a single inspiration of a 35% C02/55% 0 2 mixture. Panic-like symptoms were also associated with expirations. Recently Griez, Lousberg, van den Hout, and van den Molen [3 11 employed a double-blind randomized cross-over design to study the effects of single 35% C02/55% 0 2 inhalation on 12 panic disorder patients diagnosed using DSM-111 criteria [21], and 11 controls. The procedure produced significantly more distress than did a control inhalation of air in both patients and controls. Panic patients reported sufficient DSMI11 panic symptoms and anxiety to meet the criteria for a panic attack and many reported a high similarity of the experience to a usual panic. Some patients also reported that the presence of a doctor and the knowledge concerning the duration of the sensations prevented a “fear of losing control”. In an important study Rapee, Mattick, and Murrell [32] compared the effects of an explanation of the consequent symptoms of a single 50% C02/50% 0 2 inhalation versus no explanation on 16 panic disorder and 19 social phobia patients diagnosed using DSM111criteria [21]. The explanation condition created an expectancy of panic by suggesting that symptoms “similar to the physical symptoms which you experience with your panic attacks” would occur. The investigators found no differences in baseline heart rate or state of anxiety and no differences in number of symptoms reported subsequent to inhalation between the explanation and no explanation conditions. However, panic disorder patients in the no explanation group reported significantly more intense symptoms, greater similarity of symptoms to naturally occumng panic attacks, and most important, much more fre-
quent catastrophic cognitions in response to the inhalation than either the panic disorder patients in the explanation condition or the social phobic patients in either condition. The importance of cognitive processes in panic onset is borne out by this study. The results indicate that neither baseline differences nor the effects of a non-specific stressor determine the response to C02 inhalation and change in paC02. Rather, cognitive processes are the most powerful determinants of panic in response to C02. At odds with the hyperventilation theory, is the fact that the breathing of marginally high levels of C02, (up to 5.5%) can also produce panic [19,20,33]. One explanation for the equivalence in responses to the high and low percentage C02 may be that increased paC02 results in an increased respiratory output mediated by central and peripheral acidosis [34]. As the increased respiration proceeds, the peripheral acidosis becomes an alkalosis and the paCO2 decreases leading to effects which are characteristic of panic symptoms [3, 151. Another possibility is that the effects of the low level C02 inhalation are largely mediated by higher baseline levels of arousal which lead to increased respiratory rate in response to the C02 [33]. Inhalation of either 35-50% or 4-5% C02 results in panic attacks in persons with a history of panic. Both procedures produce a hyperventilated state involuntarily, either acutely by lowering paCO2 and causing alkalosis (using 35%-50% C02) or as a part of the homeostatic response to the procedure (5% C02). In contrast voluntary hyperventilation will produce panic symptoms but rarely panic attacks in persons with a history of panic even following changes in the factors proposed as determining a panic attack such as decreased paC02, alkalosis, and the presence of paniclike symptoms. It may be that a panic response is related to the cognitive evaluation of physiological changes. Thus expectancies concerning those changes (e.g. symptoms that accompany the changes) as well as the degree of control (associated with those changes) may account for the responses to symptoms. Hence, panic attacks provoked by voluntary hyperventilation are much less novel and frightening/threatening and more controlled by the subject than C02 inhalation.
Treatment Interventions aimed at changing respiration effects
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and symptoms have targeted the C02 levels directly through bag re-breathing of C02 [14, 101. Re-breathing expired air is thought to increase paC02 [lo]. Another method is through the alteration of respiration patterns such that diaphragmatic rather than thoracic breathing is performed and the breathing is generally slowed [ 1,2,2 I , 27,28,35] which indirectly increases paC02 by normalising respiration. Lum [15] reported that in a series of over 1000 patients with hyperventilation syndrome, training in altered breathing patterns resulted in 75% of those patients being completely symptom free at 12 months. An integral part of the breathing retaining is an educational component, describing the “pathological” breathing patterns of the patient so that the patient has a rationale for the intervention. Margarian [ 101 uses the experience of voluntary hyperventilation to achieve the same result stating “the importance of this test (voluntary hyperventilation) is to allow recognition by the patient of the association of his symptoms with excessive breathing”. Bonn et al. [27] required all 12 of their agoraphobic subjects to undergo voluntary hyperventilation. For 7 subjects this was followed by breathing retaining prior to standard in vivo exposure. The remaining 5 subjects were given only in vivo exposure. The hyperventilation trial was used to “demonstrate to agoraphobic patients that over-breathing could produce their feared symptoms” and all 12 subjects identified the results of the procedure as similar to past experiences. At a six month follow-up, the group who had been given breathing retraining had improved significantly compared to the in vivo exposure only group on measures of somatic anxiety, panic frequency and respiration rate. Both groups however improved on all measures over time. Bonn et al. [27] discuss the importance of the voluntary hyperventilation procedure suggesting that it gave subjects the realization that they could control their symptoms. The authors did not describe the extent of any explanation with regard to the results of voluntary hyperventilation in the in-vivo exposure alone condition. Furthermore subjects in the breathing retraining condition appear to have training in both global breathing control and re-breathing during panic attacks. Thus it is not possible to determine whether the differences in response at follow-up are due to re-breathing during panic attacks or general slow breathing, since the breathing retraining group had both procedures. This may be important since rebreathing is likely to be more useful in coping with
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panic attacks themselves whereas changes in patterns of breathing are more likely to be associated with global changes in paCO2 and therefore the occurrence of panic attacks. Also the impact of an explanation of symptoms after voluntary hyperventilation cannot be differentiated from the effects of in-vivo exposure. Clark et al. [35] reported the effectiveness of voluntary hyperventilation, an explanation of the process whereby hyperventilation effects panic, and training in slow breathing to control symptoms that are associated with panic attacks. Eighteen patients reported voluntary hyperventilation with their usual panic attacks. These patients were divided into two groups on the basis of having panic attacks in particular situations or independent of situations. The results indicated a significant reduction in panic frequency from baseline to the end of a two-week “pure” (that is with specific non-exposure instruction) respiratory control for both groups. Following the two-week “pure” respiratory treatment, other treatments, self-guided invivo exposure and cognitive behavioural interventions, were used in both groups. At a two-year follow-up both groups maintained low levels of panic frequency. As the authors point out, the study demonstrates only the short-term effects of breathing retraining plus voluntary hyperventilation and explanation on panic frequency. It could not answer any questions concerning the long term effects of the respiratory interventions alone. Another aspect of this study which is open to criticism is the exclusive use of patients whose panic symptoms were similar to the sensations experienced during voluntary hyperventilation. To address these issues Salkovskis and colleagues [28] replicated the previous study with unselected panic patients using measures of paC02 throughout treatment. Again a “pure” respiratory retraining phase was instigated with no exposure instructions. Additionally bag re-breathing was included in the breathing retraining. Panic frequency and intensity dropped significantly over the four-week period compared to an equivalent four-week baseline period. This was maintained over a three-month period. Of greater interest were the paC02 levels which increased to normal levels within two weeks of the breathing retraining being instigated, thus supporting the validity of the respiratory retraining procedure. The breathing retraining used in these studies incorporates a number of elements: (i) controlled exposure to hyperventilation/panic symptoms; (ii) education
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concerning the association between hyperventilation symptoms and hyperventilation generally and panic attacks; (iii) practical applicationof short-termbreathing control in response to panic attacks; and (iv) adjustment of breathing patterns to ameliorate chronic hyperventilation. Whilst the literature contains very little evaluation or even recognition of these separate components of treatment, the overall effectiveness of the treatment seems to be promising. There has been some evidence of the efficacy of exposure to hyperventilation symptoms in the treatment of panic disorder. Griez and van den Hout [36] found that repeated exposureto 35% C02/55% 02 was effective in short-term treatment of panic attacks. The effects of education concerning the association between panic and hyperventilation have never been directly assessed in the literature. The changes in paCO2 reported by Salkovskis et al. [28] provide strong evidence for the effects of the slow breathing training but do not indicate a causal relationship between slow breathing and panic attack frequency. Finally the degree of control given to the patient by the controlled exposure to hyperventilation and the use of the bag re-breathing and also breathing as a control strategy is unknown. Hence the mechanisms by which breathing retraining effects panic attacks are largely unexplored. Generally the evidence reviewed here suggests that cognitive factors, particularly those concerned with expectancy and control may be influential in treatment. The evidence describing the association between hyperventilation and panic attacks would suggest that the physiological processes involved in panic attacks could be hyperventilation. It must be remembered though, that the evidence concerning hyperventilation is equivocal in every case of panic. For example not every person with panic disorder has a low paC02 [3]. Similarly, acute hyperventilationdoes not necessarily precipitate or coincide with panic attacks [29, 191. Finally, treatment that employs hyperventilation as a model of panic physiology generally incorporates factors concerning expectancy, control and learning. Cognitive factors probably play an important, if not, necessary part in those cases where hyperventilation processes are involved in panic attacks [32]. The relative importance of the cognitive and physiological processes in panic is as yet unknown. Ley [2] would emphasise the physiological processes, stating that increases in symptoms of hyperventilation and hypocapnea defines the occurrence of panic. In con-
trast the data of Rapee and colleagues [32] indicates that merely experiencinga physiologicalchange, even one similar to that produced by hyperventilation does not result in a panic attack. It is likely that the evaluation of a particular pattern of symptoms leads to a panic attack and mediates conditioned responses of fear and panic. Thus both cognitive and physiological components may be involved in the panic attacks [37, 381. Furthermore respiratory mechanisms during panic fail to account adequately for factors that precede the naturally occurring panic attack. Nonspecific factors which can lead to hyperventilation include being startled or surprised, experiencing an emotional reaction such as anger, activity where overbreathing may occur such as sexual activity, lecturing or driving amongst other activities [2]. The variability in this list indicates that within the hyperventilation theory there is still much doubt as to what actually provokes panic, and why persons who are susceptible to panic should experience panic attacks at the particular instant they do. In summary, hyperventilation provides a plausible model for the physiological processes that underlie panic attacks but requires the incorporation of a cognitive component to explain panic attacks. In an analysis of panic attacks it would be desirable to assess the physiological parameters directly associated with hyperventilation such as paC02 and pH. Since the recent treatment advances of Clark and his colleagues [28,35], it is tempting for practitioners in this field to embrace the concepts and techniques following from hyperventilation theory as applied to panic attacks. Panic disorder is a difficult condition to treat and the mechanics of hyperventilation provide a solid and plausible explanation. The real danger here is that hyperventilationwill be assumed to be the cause of panic disorder. This review of the literature does not support this assumption at all. Panic attacks and hyperventilation are not the same. The clinician must be cautious in making assumptions covering hyperventilation as the model for panic. To take an approach that exclusivelyemphasiseshyperventilationmay lead the clinician up a blind alley where alternative models to understand the physiological components of panic become unavailable. Instead, hyperventilation should be considered as only one possible explanation for some of the physiologicalcomponents.Clark [ 181 and Barlow [12] describe other approaches such as vestibular stimulation through spinning the patient in a chair, visual stimulation through observing grids, and
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exposure to increases in heart rate through exercise. Furthermore,the importance of the interaction of cognitive and physiologicalcomponents in treatment cannot be underemphasised.
Acknowledgement This paper was supported by grants from the NHMRC, Social Sciences Research grants, and Australia Institute of Health to Drs Oei and Evans, and a University of Queensland Postgraduate Scholarship to Dr Kenardy.
References 1. Lum LC. The syndrome of habitual chronic hyperventilation. In: O.W. Hill ed. Modern Trends in Psychosomatic Medicine 1976; 3. 2. Ley R. Blood, breath and fears: a hyperventilation theory of panic attacks and agoraphobia. Clinical Psychology Review 1985;5:27 1285. 3. Rapee RM. Differential response to hyperventilation in panic and generalized anxiety disorder. Journal of Abnormal Psychology 1986;24-28. 4. American Psychiatric Association. Diagnostic and statisticalmanual of mental disorders. Washington, DC: Author. 3rd ed. rev. 1987. 5 . Klein D. Anxiety reconceptualized. In: DF Klein, J Rabkin, eds. Anxiety: New research and changing concepts. New York: Raven Press. 1981. 6. Wheeler ED, White PD, Reed EW, Cohen ME. Neurocirculatory asthenia (anxiety neurosis, effort syndrome, Neurasthenia). Journal of the American Medical Association 1950 142:878-889. 7. Anderson DJ, Noyes R, Crowe RR. A comparison of panic disorder and generalised anxiety disorder. American Journal of Psychiatry 1984; 141572-575. 8. Barlow DH, Vermilyes JA, Blanchard J, Vermilyes BB, Dinardo PA, Cerny JA. The phenomenon of panic. Journal of Abnormal Psychology 1985;94:320-328. 9. Noyes R, Clancy J, Garvey M, & Anderson D. Is agoraphobia a variant of panic disorder or a separate illness? Journal of Anxiety Disorders 1987;1:3-13. 10. Magarian GJ. Hyperventilation syndromes: infrequently recognized common expressions of anxiety and stress. Medicine 1982;61:219-236. 11. Gelder MG. Panic attacks: new approaches to an old problem. British Journal of Psychiatry 1986;149:346-352. 12. Barlow DM. Anxiety and its disorders. New York: Guilford. 1988. 13. Ley R. Agoraphobia, the panic attack and the hyperventilation syndrome. Behaviour Research and Therapy 1985;23:79-81. 14. Rice RL. Symptom patterns of the hyperventilation syndrome. American Journal of Medicine 1950;8:69 1-700. 15. Lum LC. Hyperventilation and anxiety state. Journal of the Royal Society of Medicine 1981;74: 1-4. 16. Ley R. Panic disorder and agoraphobia: fear of fear or fear of the symptoms produced by hyperventilation? Journal of Behaviour Therapy and Experimental Psychiatry 1987;18:305-316. 17. Clark DM. A cognitive approach to panic. Behaviour Research and Therapy 1986;4:461-470.
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18. Clark DM, Salkovskis PM. Cognitive therapy for panic attacks: Treatment manual. Unpublished manuscript, 1986. 19. Gorman JM, Askanazi J, Liebowitz MR, Fyer AJ,Stein J, Kinney JM, Klein DF. Response to hyperventilation in a group of patients with panic disorder. American Journal of Psychiatry 1984; 141,7:857-86 1. 20. Cohen, ME, White, P.D. Life situations, emotions and neurocirculatory asthenia. Psychosomatic Medicine 1951; 13:335-337. 2 1. American Psychiatric Association. Diagnostic and Statistical manual of mental disorders. Washington D.C.: Author, 3rd ed. 1980. 22. Liebowitz, MR, Gorman, JM, Fyer, AJ, Levitt, M, Dillon D, Levy G, Appleby IL, Anderson S, Palij M, Davies, SO, Klein DF. Lactate provocation of panic attacks-11. Biochemical physiological findings. Archives of General Psychiatry 1985;42:709-719. 23. Norton GR, Doward J, Cox BJ. Factors associated with panic attacks in nonclinical subjects. Behavior Therapy 1986;17:239-252. 24. Compernolle T, Hoogduin K, Joele L. Diagnosis and treatment of the hyperventilation syndrome. Psychosomatics 1979;20:6 12625. 25. Clark DM, Hemsley DR. The effects of hyperventilation: individual variability and its relation to personality. Journal of Behaviour Therapy & Experimental Psychiatry 1982; 13:41-47. 26. Garsen B, van Weenedaal W, Blosmink, R. Agoraphobia and the hyperventilation syndrome. Behaviour Research and Therapy 1982;21:643-649. 27. Bonn JA, Readhead CPA, Timmons BA. Enhanced adaptive behavioural response in agoraphobic patients pretreated with breathing retraining. Lancet 1984; 1:665-669. 28. Salkovskis PM, Wanvick M, Clark D, Wessels J. A demonstration of acute hyperventilation during naturally occumng panic attacks. Behaviour Research and Therapy 1986;24:91-94. 29. Hibbert GA. The diagnosis of hyperventilatioii using ambulatory carbon dioxide monitoring. Proceedings of the 15th European conference for Psychosomatic Research, London: John Libby, 1986. 30. van den Hout MA & Griez E. Peripheral panic symptoms occur during changes in alveolar carbon dioxide. Comprehensive Psychiatry 26:381-387. 3 1. Griez EJL, Lousberg H, van den Hout MA, van den Molen DM. COz vulnerability in panic disorder. Psychiatry Research 1987;20:87-95. 32. Rapee RM, Mattick R, Murrell E. Cognitive mediation in the affective component of spontaneous panic attacks. Journal of Behavior Therapy and Experimental Psychiatry 1987; 17:245-253. 33. Ehlers A, Margraf J, Roth WT.Interaction of expectancy and physiological stressors in a laboratory model of panic. In: Hellhammer D, Florin I, eds. Neuronal control of bodily function basic and clinical aspects: Vol 11, Gottingen: Hogrefe. 1987. 34. Vander AJ, Sherman JN, Lucian0 DS. Human physiology: The mechanisms of body function. New York: McGraw-Hill, 1986. Comprehensive Psychiatry 1985;26:38 1-387. 35. Clark DM, Salkovskis PM, Chalkley, A.J. Respiratory control as a treatment for panic attacks. Journal of Behaviour Therapy and Experimental Psychiatry 1985;13:41-47. 36. Griez E, van den Hout MA. COZ inhalation in the treatment of panic attacks. Behaviour Research & Therapy 1986;24: 145-150. 37. Kenardy J, Evans L, Oei TPS. The importance of cognition in panic attacks. Behavior Therapy 1988;19:471-483. 38. Kenardy J, Evans L, Oei TPS. Cognition and heart rate in panic disorders during everyday activity. Journal of Anxiety Disorders 1989;3:33-43.
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The role of hyperventilation in the aetiology of panic attacks is still unclear. This paper briefly reviewsthe role of hyperventilationand abnormal respiration to panic attacks and examines the experimental evidence. Evidence has been found that physiological variables such as paC02 and pH are involved in the aetiology of panic attacks and panic disorder but the extent and the nature of the involvement of cognitive variables is undetermined. Based on current evidence, there is a needto integratecognitive variables with the physiological framework proposed by the hyperventilation theory. Until clear experimental evidence is produced about the relationships between cognitive and physiologicalfactors, the applicability of hyperventilationin the aetiology and treatment of panic attacks remains in question. Australian and New Zealand Journal of Psychiatry 1990; 24:261-267 Over the past decade, there has been increasing evidence of an association between hyperventilation and the anxiety disorders, in particular the phenomenon of panic attacks [ 1-31. Panic attacks [4] are discrete episodes of intense fear or discomfort and associated physical symptoms which appear to arise unexpectedly. There has been marked interest in panic attacks following their delineation as a form of anxiety amenable to specific pharmacologic treatment [5]. Interest in the relationship of hyperventilation to panic attacks has resulted from investigations of the aetiology and treatment of panic. Although the role of physiological processes in hyperventilation in panic has been formulated [2], the empirical evidence to support this formulation as an explanation of panic, and in particular its relevance to the treatment of panic attacks, is limited. It is therefore the intention of this Department of Psychology, University of Newcastle Justin Kenardy, PhD Anxiety Disorder Clinic, New Farm Clinic, University of Queensland Tian P.S. Oei, PhD Larry Evans, MB, ChB, FRC Psych, FRANZCP Correspond with Dr J. Kenardy, Department of Psychology, University of Newcastle, NSW
paper to review and examine the empirical evidence concerning the application of hyperventilation to the aetiology and treatment of panic attacks. The more obvious respiratory symptoms of dyspnea, breathlessness, and smothering sensations, are among the commonest symptoms of panic attacks reported by 52 - 90% of the sufferers; [6-91. Less obvious expressions of respiratory disturbance such as dizziness, parasthesia, chest pain, palpitations and tachycardia are also reported [ 101. Some or all of these symptoms may be present in acute hyperventilation in all persons but may also be present with panic attacks. Hyperventilation is by definition respiration that is excessive with respect to metabolic needs. It produces changes in the acid-base balance in the blood by producing a fall in hydrogen ion concentrations, causing a state of respiratory alkalosis. The lowering of C02 level (hypocapnia) results in vasoconstriction and, combined with alkalosis (which decreases oxygen reuptake by haemoglobin), cerebral hypoxia, the symptoms of which are dizziness, faintness, and visual disturbances [ 11. It has been suggested that the cardiac system may also adjust to these changes by acute increases in heart rate [ 111. A further effect is a reduction of phosphate and calcium levels in the blood, resulting in symptoms of dizziness, parasthesias, and
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nausea [ 10,191. Concurrent with changes in acid-base balance and C02 levels are changes in bicarbonate levels. The body’s response to these changes is slower than the response to alkalosis and hypocapnia, since it must dispose of bicarbonate by gradual excretion. However it is by this method that alkalosis can be reduced to within normal limits [I]. Thus, a person may be in a chronic hyperventilated state with a lowered partial pressure of C02 in the blood (paCO2) but by virtue of the bicarbonate excretion mechanism have blood pH levels within the normal range [ 1, 2, 101.
The hyperventilated state can be maintained in a chronic way by innocuous respiratory mechanisms such as thoracic breathing [ 1, 21. Thoracic breathing is a style of respiration where the involvement of the diaphragm is limited and thus respiratory efficiency and volume is decreased. The diaphragmatic involvement is restricted largely by tension in the abdominals. Diaphragmatic breathing in contrast is where the diaphragm is allowed to contract and relax freely with respiration. Other mechanisms which can maintain a chronic hyperventilated state are increased respiratory rate [ 131, sighing or an occasional deep breath [2, 101. It is not the chronic hyperventilated state, called “Hyperventilation Syndrome” [ 141, that is said to produce the symptoms of panic, but rather changes from this state produced by acute hyperventilation [ l , 2, 151. Acute hyperventilation in the absence of chronic hyperventilation is not presumed to result in the symptoms of panic. This is because the response to minor changes in ventilation in a person who already has lowered paC02 is said to produce a marked physiological change [ 151. Thus the process of acute hyperventilation should result in a substantial increase in symptoms of rapid respiration and palpitations which feedback on the already imbalanced system. It has been proposed that the abrupt and dramatic nature of these changes will mean that they are perceived as “spontaneous” and potentially life threatening, and that this catastrophic interpretation and the fear associated with it is proposed to be the basis of panic disorder [ 171. This model, which has been called the “hyperventilation model of panic” [ 161, also accounts for the self-limiting nature of panic. Eventually the lowered C02 will be insufficient to stimulate the respiratory reflex, C 0 2 levels will build up and the physiological process will cease with the symptoms abating. Writers in the field have emphasized either the physiological mechanisms of hyperventilation [2,
14, 161 or the cognitive component of the catastrophic interpretation of the symptoms of hyperventilation [ 17,18, 121. However both elements will be examined in this review. Evidence for the role of hyperventilation in panic falls into three general areas: (i) evidence supporting a chronic hyperventilated state in panic patients; (ii) evidence indicating panic-like states associated with acute hyperventilation or its equivalent; (iii) evidence demonstrating changes in panic frequency produced by changes in ventilation. The following will discuss these areas of evidence.
Chronic hypewentilation Chronic hyperventilation is associated with a higher resting respiratory rate [15]. Cohen and White [20] found that patients with anxiety neurosis, neurocirculatory asthenia or effort syndrome had a higher resting respiratory rate and minute respiratory volume than healthy controls. Ley [ 131 also found the resting respiration rate to be higher than would be expected in six patients with a history of panic attacks. These patients also demonstrated thoracic breathing patterns and frequent sighs. Rapee [3] assessed resting minute respiratory volume and found a higher volume for 20 panic disorder patients compared to 14 generalized anxiety disorder patients diagnosed according to DSM-111 criteria [21]. This difference was not significant possibly because there was great variability in minute respiratory volumes, with some of the panic disorder patients failing to have low resting minute respiratory volume. Chronic hyperventilation can also be indicated by lowered paC02. Lum [ 11 compared paCO2 levels in 152 normals and 200 patients diagnosed as having hyperventilation syndrome by clinical presentation of abnormal breathing patterns of frequent sighing, thoracic breathing, high baseline respiratory rate. He found lowered levels in more than half of the patients compared to normals. It is difficult in this study to assess the impact of arterial puncture on arousal and therefore paC02. However studies that have examined paC02 in panic disorder compared to other groups have found generally low levels. Rapee [3] found significantly lower paC02 levels in his panic disorder patients compared to the generalized anxiety disorder patients. Leibowitz, el al. [22] measured baseline levels of paCO2, bicarbonate and acid-base balance in 43 panic disorder patients diagnosed using DSM-111
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criteria [21] and 20 age-matched controls. As predicted by the hyperventilation model, panic disorder patients had normal pH compared to controls but had lower venous paCO2 and a lower level of bicarbonate as calculated from pH and paC02 levels. In these two studies heart rate was also assessed and found to be significantly lower in the generalised anxiety disorder and control groups, thus indicating differences not only in respiration but possibly also arousal. This may be a moot point since arousal could drive hyperventilation by leading to higher resting respiration and possibly lower paCO2. However arousal may be determined by the immediate assessment situation or may reflect a baseline and thus a chronically hyperventilated state. The lowered bicarbonate levels and the normal pH in the study by Leibowitz suggests that the differences are related to a chronic hyperventilation. Thus the combination of bicarbonate levels, pH and paC02 seems to provide more complete assessment of chronic hyperventilation. In summary, resting respiratory differences appear to be present in some but not all panic disorder patients compared to normals and generalised anxiety disorder patients. It is worth noting though that there may be overlap in all of these groups since panic attacks can occur in patients with generalised anxiety disorder [ 121 and even in a normal population [23].
Acute hyperventilationand panic Acute changes in ventilation can be produced by relatively brief episodes of voluntary hyperventilation [lo, 241. Anxiety has been reported in response to acute hyperventilation. Clark and Hemsley 1251 found that as well as symptoms of dry mouth, pounding heart, faintness, tingling and feelings of unreality, 19 of the 27 normals who voluntarily hyperventilated also experienced slight increases in self-reported anxiety. Subjects with higher levels of neuroticism reported greater distress in response to hyperventilation, suggesting that those who reported anxiety may have had some susceptibility because of their greater trait anxiety levels. Garsen, van Weenedaal, and Blosmink [26] examined the diagnostic overlap between hyperventilation syndrome diagnosed by interview, response to voluntary hyperventilation and agoraphobia. The investigators found that 17 of the 28 agoraphobics who voluntarily hyperventilated reported that the ex-
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perience was similar to a panic attack. In this study 6 patients failed to complete the voluntary hyperventilation and were excluded from the study. Whether they did not complete the procedure because they were afraid of experiencing a panic attack was not reported. Thus it is difficult to know if any panic attacks would have resulted. In another study of voluntary hyperventilation Bonn, Redhead and Timmons [27] also found that 14 out of 21 agoraphobic patients did not complete a voluntary hyperventilation procedure because of “being overcome with dizziness or other distress”. BOM et af. [27] also asked their subjects to compare usual panic symptoms experienced to those experienced during voluntary hyperventilation. Twenty of the agoraphobic patients reported some symptoms common to both, although their symptoms in panic were generally less severe. Rapee [3] found that panic disorder patients reported significantly more distress, more symptoms and a greater similarity of the experience to usual anxiety than generalised anxiety disorder patients in response to voluntary hyperventilation. Again, however, no patients reported panic attacks in spite of low paC02. No differences were found in minute respiratory volume change, heart rate or paCO2 between the panic and generalised anxiety disorder groups in response to hyperventilation. In explaining the results Rapee suggested that it was environmental cues and cognitive mediation which lead to the non-occurrence of panic attacks. Patients indicated that they did not panic because they knew that they were safe in the environment and that they understood the cause of their symptoms. Gorman et al. [ 191 report one of the few studies were panic disorder patients had panic attacks during voluntary hyperventilation. They found that only 25% [3] of their patients with panic disorder reported experiencing panic attacks during voluntary hyperventilation although again some failed to complete the procedure because of fatigue or distress. In this controlled study blood pH levels were also assessed and found to be similarly high in controls and patients during hyperventilation suggesting that the procedure had produced the same physiological changes in both groups and that the panic attacks resulted from factors other than the physiological changes occurring as a result of hyperventilation. Two studies have examined hyperventilation during panic attacks. Salkovskis, Warwick, Clark and Wessels [28] report a substantial decrease in paCO2 and an
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increase in pH during a panic attack experienced by a patient on renal dialysis. Whilst dialysis in itself does produce mild alkalosis the changes in this patient’s physiology were greater at this time than during other periods of dialysis. Further, prior to the panic attack the patient reported catastrophic thoughts concerned with impending death. The authors suggest that it was the catastrophic cognition that uniquely interacted with the blood chemistry changes to produce further increases in respiration and pH. Hibbert [19] found that some but not all patients show changes in paCO2 during naturally occurring panic attacks assessed using ambulatory measurement. Another procedure which can acutely alter paC02 levels, is direct C02 inhalation. Van den Hout and Griez [30] report that an acute decrease in paC02 and alkalosis follows the first expiration of a single inspiration of a 35% C02/55% 0 2 mixture. Panic-like symptoms were also associated with expirations. Recently Griez, Lousberg, van den Hout, and van den Molen [3 11 employed a double-blind randomized cross-over design to study the effects of single 35% C02/55% 0 2 inhalation on 12 panic disorder patients diagnosed using DSM-111 criteria [21], and 11 controls. The procedure produced significantly more distress than did a control inhalation of air in both patients and controls. Panic patients reported sufficient DSMI11 panic symptoms and anxiety to meet the criteria for a panic attack and many reported a high similarity of the experience to a usual panic. Some patients also reported that the presence of a doctor and the knowledge concerning the duration of the sensations prevented a “fear of losing control”. In an important study Rapee, Mattick, and Murrell [32] compared the effects of an explanation of the consequent symptoms of a single 50% C02/50% 0 2 inhalation versus no explanation on 16 panic disorder and 19 social phobia patients diagnosed using DSM111criteria [21]. The explanation condition created an expectancy of panic by suggesting that symptoms “similar to the physical symptoms which you experience with your panic attacks” would occur. The investigators found no differences in baseline heart rate or state of anxiety and no differences in number of symptoms reported subsequent to inhalation between the explanation and no explanation conditions. However, panic disorder patients in the no explanation group reported significantly more intense symptoms, greater similarity of symptoms to naturally occumng panic attacks, and most important, much more fre-
quent catastrophic cognitions in response to the inhalation than either the panic disorder patients in the explanation condition or the social phobic patients in either condition. The importance of cognitive processes in panic onset is borne out by this study. The results indicate that neither baseline differences nor the effects of a non-specific stressor determine the response to C02 inhalation and change in paC02. Rather, cognitive processes are the most powerful determinants of panic in response to C02. At odds with the hyperventilation theory, is the fact that the breathing of marginally high levels of C02, (up to 5.5%) can also produce panic [19,20,33]. One explanation for the equivalence in responses to the high and low percentage C02 may be that increased paC02 results in an increased respiratory output mediated by central and peripheral acidosis [34]. As the increased respiration proceeds, the peripheral acidosis becomes an alkalosis and the paCO2 decreases leading to effects which are characteristic of panic symptoms [3, 151. Another possibility is that the effects of the low level C02 inhalation are largely mediated by higher baseline levels of arousal which lead to increased respiratory rate in response to the C02 [33]. Inhalation of either 35-50% or 4-5% C02 results in panic attacks in persons with a history of panic. Both procedures produce a hyperventilated state involuntarily, either acutely by lowering paCO2 and causing alkalosis (using 35%-50% C02) or as a part of the homeostatic response to the procedure (5% C02). In contrast voluntary hyperventilation will produce panic symptoms but rarely panic attacks in persons with a history of panic even following changes in the factors proposed as determining a panic attack such as decreased paC02, alkalosis, and the presence of paniclike symptoms. It may be that a panic response is related to the cognitive evaluation of physiological changes. Thus expectancies concerning those changes (e.g. symptoms that accompany the changes) as well as the degree of control (associated with those changes) may account for the responses to symptoms. Hence, panic attacks provoked by voluntary hyperventilation are much less novel and frightening/threatening and more controlled by the subject than C02 inhalation.
Treatment Interventions aimed at changing respiration effects
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and symptoms have targeted the C02 levels directly through bag re-breathing of C02 [14, 101. Re-breathing expired air is thought to increase paC02 [lo]. Another method is through the alteration of respiration patterns such that diaphragmatic rather than thoracic breathing is performed and the breathing is generally slowed [ 1,2,2 I , 27,28,35] which indirectly increases paC02 by normalising respiration. Lum [15] reported that in a series of over 1000 patients with hyperventilation syndrome, training in altered breathing patterns resulted in 75% of those patients being completely symptom free at 12 months. An integral part of the breathing retaining is an educational component, describing the “pathological” breathing patterns of the patient so that the patient has a rationale for the intervention. Margarian [ 101 uses the experience of voluntary hyperventilation to achieve the same result stating “the importance of this test (voluntary hyperventilation) is to allow recognition by the patient of the association of his symptoms with excessive breathing”. Bonn et al. [27] required all 12 of their agoraphobic subjects to undergo voluntary hyperventilation. For 7 subjects this was followed by breathing retaining prior to standard in vivo exposure. The remaining 5 subjects were given only in vivo exposure. The hyperventilation trial was used to “demonstrate to agoraphobic patients that over-breathing could produce their feared symptoms” and all 12 subjects identified the results of the procedure as similar to past experiences. At a six month follow-up, the group who had been given breathing retraining had improved significantly compared to the in vivo exposure only group on measures of somatic anxiety, panic frequency and respiration rate. Both groups however improved on all measures over time. Bonn et al. [27] discuss the importance of the voluntary hyperventilation procedure suggesting that it gave subjects the realization that they could control their symptoms. The authors did not describe the extent of any explanation with regard to the results of voluntary hyperventilation in the in-vivo exposure alone condition. Furthermore subjects in the breathing retraining condition appear to have training in both global breathing control and re-breathing during panic attacks. Thus it is not possible to determine whether the differences in response at follow-up are due to re-breathing during panic attacks or general slow breathing, since the breathing retraining group had both procedures. This may be important since rebreathing is likely to be more useful in coping with
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panic attacks themselves whereas changes in patterns of breathing are more likely to be associated with global changes in paCO2 and therefore the occurrence of panic attacks. Also the impact of an explanation of symptoms after voluntary hyperventilation cannot be differentiated from the effects of in-vivo exposure. Clark et al. [35] reported the effectiveness of voluntary hyperventilation, an explanation of the process whereby hyperventilation effects panic, and training in slow breathing to control symptoms that are associated with panic attacks. Eighteen patients reported voluntary hyperventilation with their usual panic attacks. These patients were divided into two groups on the basis of having panic attacks in particular situations or independent of situations. The results indicated a significant reduction in panic frequency from baseline to the end of a two-week “pure” (that is with specific non-exposure instruction) respiratory control for both groups. Following the two-week “pure” respiratory treatment, other treatments, self-guided invivo exposure and cognitive behavioural interventions, were used in both groups. At a two-year follow-up both groups maintained low levels of panic frequency. As the authors point out, the study demonstrates only the short-term effects of breathing retraining plus voluntary hyperventilation and explanation on panic frequency. It could not answer any questions concerning the long term effects of the respiratory interventions alone. Another aspect of this study which is open to criticism is the exclusive use of patients whose panic symptoms were similar to the sensations experienced during voluntary hyperventilation. To address these issues Salkovskis and colleagues [28] replicated the previous study with unselected panic patients using measures of paC02 throughout treatment. Again a “pure” respiratory retraining phase was instigated with no exposure instructions. Additionally bag re-breathing was included in the breathing retraining. Panic frequency and intensity dropped significantly over the four-week period compared to an equivalent four-week baseline period. This was maintained over a three-month period. Of greater interest were the paC02 levels which increased to normal levels within two weeks of the breathing retraining being instigated, thus supporting the validity of the respiratory retraining procedure. The breathing retraining used in these studies incorporates a number of elements: (i) controlled exposure to hyperventilation/panic symptoms; (ii) education
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concerning the association between hyperventilation symptoms and hyperventilation generally and panic attacks; (iii) practical applicationof short-termbreathing control in response to panic attacks; and (iv) adjustment of breathing patterns to ameliorate chronic hyperventilation. Whilst the literature contains very little evaluation or even recognition of these separate components of treatment, the overall effectiveness of the treatment seems to be promising. There has been some evidence of the efficacy of exposure to hyperventilation symptoms in the treatment of panic disorder. Griez and van den Hout [36] found that repeated exposureto 35% C02/55% 02 was effective in short-term treatment of panic attacks. The effects of education concerning the association between panic and hyperventilation have never been directly assessed in the literature. The changes in paCO2 reported by Salkovskis et al. [28] provide strong evidence for the effects of the slow breathing training but do not indicate a causal relationship between slow breathing and panic attack frequency. Finally the degree of control given to the patient by the controlled exposure to hyperventilation and the use of the bag re-breathing and also breathing as a control strategy is unknown. Hence the mechanisms by which breathing retraining effects panic attacks are largely unexplored. Generally the evidence reviewed here suggests that cognitive factors, particularly those concerned with expectancy and control may be influential in treatment. The evidence describing the association between hyperventilation and panic attacks would suggest that the physiological processes involved in panic attacks could be hyperventilation. It must be remembered though, that the evidence concerning hyperventilation is equivocal in every case of panic. For example not every person with panic disorder has a low paC02 [3]. Similarly, acute hyperventilationdoes not necessarily precipitate or coincide with panic attacks [29, 191. Finally, treatment that employs hyperventilation as a model of panic physiology generally incorporates factors concerning expectancy, control and learning. Cognitive factors probably play an important, if not, necessary part in those cases where hyperventilation processes are involved in panic attacks [32]. The relative importance of the cognitive and physiological processes in panic is as yet unknown. Ley [2] would emphasise the physiological processes, stating that increases in symptoms of hyperventilation and hypocapnea defines the occurrence of panic. In con-
trast the data of Rapee and colleagues [32] indicates that merely experiencinga physiologicalchange, even one similar to that produced by hyperventilation does not result in a panic attack. It is likely that the evaluation of a particular pattern of symptoms leads to a panic attack and mediates conditioned responses of fear and panic. Thus both cognitive and physiological components may be involved in the panic attacks [37, 381. Furthermore respiratory mechanisms during panic fail to account adequately for factors that precede the naturally occurring panic attack. Nonspecific factors which can lead to hyperventilation include being startled or surprised, experiencing an emotional reaction such as anger, activity where overbreathing may occur such as sexual activity, lecturing or driving amongst other activities [2]. The variability in this list indicates that within the hyperventilation theory there is still much doubt as to what actually provokes panic, and why persons who are susceptible to panic should experience panic attacks at the particular instant they do. In summary, hyperventilation provides a plausible model for the physiological processes that underlie panic attacks but requires the incorporation of a cognitive component to explain panic attacks. In an analysis of panic attacks it would be desirable to assess the physiological parameters directly associated with hyperventilation such as paC02 and pH. Since the recent treatment advances of Clark and his colleagues [28,35], it is tempting for practitioners in this field to embrace the concepts and techniques following from hyperventilation theory as applied to panic attacks. Panic disorder is a difficult condition to treat and the mechanics of hyperventilation provide a solid and plausible explanation. The real danger here is that hyperventilationwill be assumed to be the cause of panic disorder. This review of the literature does not support this assumption at all. Panic attacks and hyperventilation are not the same. The clinician must be cautious in making assumptions covering hyperventilation as the model for panic. To take an approach that exclusivelyemphasiseshyperventilationmay lead the clinician up a blind alley where alternative models to understand the physiological components of panic become unavailable. Instead, hyperventilation should be considered as only one possible explanation for some of the physiologicalcomponents.Clark [ 181 and Barlow [12] describe other approaches such as vestibular stimulation through spinning the patient in a chair, visual stimulation through observing grids, and
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exposure to increases in heart rate through exercise. Furthermore,the importance of the interaction of cognitive and physiologicalcomponents in treatment cannot be underemphasised.
Acknowledgement This paper was supported by grants from the NHMRC, Social Sciences Research grants, and Australia Institute of Health to Drs Oei and Evans, and a University of Queensland Postgraduate Scholarship to Dr Kenardy.
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