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A demonstration of acute hyperventilation during naturally occurring panic attacks
0005-7967:86
Eehm. Rer Ther. Vol. 24. No. I, PP. 91-94. 1986 Prmted in Great Britain. All rights resewed
$3.00 + 0.00 Press Ltd
CopyrIght 6 1986Perpamon
A demonstration of acute hyperventilation during naturally occurring panic attacks
PAUL M. SALKOVSKIS,‘* HILARY M. C. WARWICK,‘~ DAVID M. CLARKE and D. JULIE WESSELS~$ Departments qf ‘Clinical Psvchology and 2Liaison Psychiatry and “The Renal Unit. The General Irtfirmar> at Leeds, Great George Street. Leeds. England ‘Department of Psychiatry, University of Oxford. Oxford OXI 3(/o,
Engktnd
(Received 12 June 1985)
Summary-Panic attacks and hyperventilation have been linked. although there have not been any demonstrations that patients acutely hyperventilate during naturally occurring panic attacks. A case study is reported in which a patient on renal dialysis showed substantially larger changes in paC02 and blood pH when panic was present than on other occasions. Changes observed in other dialysis patients were similar to those noted during non-panic sessions. INTRODUCrION There is a mounting body of evidence suggesting that hyperventilation, defined as breathing in excess of metabolic requirements, is involved in a variety of anxiety-relate disorders (Clark, 1979; Clark, Salkovskis and Chalkley, 1985; Gibson, 1978; Lum, 1976; Salkovskis, Jones and Clark, 1985bf. In particular. hy~rventilation has been implicated in panic attacks, which are defined as sudden onset episodes of intense anxiety, accompanied by a wide range of distressing bodily sensations. One of the most important implications of this hypothesized link is for treatment. Two recent studies assessed the utility of treatment directed at: (i) demonstration that voluntary hyperventilation reproduces the bodily symptoms characteristic of panic; (ii) the appropriate re-attribution of sensations experienced during panic attacks to hyperventilation and away from catastrophic interpretations; (iii) modification of respiratory and cognitive responses to stress. This treatment was successful in the treatment of panic attacks with and without associated avoidance, and improvements were maintained for up to 2 yr follow-up (Clark er al., 1985; Salkovskis et al., 1985b). One of these studies (Salkovskis et al., 1985b) also demonstrated that resting pC0, was consistently lower in patients experiencing panic attacks than in a group of age- and sex-matched controls, and that treatment resulted in the rapid restoration of patients’ pC0, to normal levels. This suggests that these patients were hyperventilating chronically with resultant renal compensation (Brown, 1953) which maintains pH at normal levels. As the sensations accompanying hyperventilation are mediated by increased pH, such chronic hyperventilation does not produce symptoms. However, the adaptation of the blood-buffe~ng system results in increased sensitivity to changes in ~$0, such as those produced by stressors and exercise. This means that decreases in p,COr will result in relatively larger changes in pH and hence more rapid onset and greater intensity of the bodily sensations of hyperventilation. It is therefore encouraging that one of the effects of treatment was to restore resting p&CO, to normal levels (Salkovskis et al.. 1985). In order to assess the extent to which patients acutely hyperventilate during panic attacks, Salkovskis, Clark and Jones (1985a) carried out a series of single-case experiments with panic patients for whom it seemed likely that hy~rventilation was involved in their attacks. Measures of pC0, were taken in the laboratory both at rest and during a variety of panic-relevant and panic-irrelevant contrived stressors. Results indicated that substantial increases in respiration did indeed take place during stress, and these were specific to the stressors which normally provoked panic in each patient. Furthermore, the degree of hyperventilation meant that these patients were certain to be experiencing some of the bodily symptoms which are produced by respiratory alkalosis. Clearly this demonstration of acute hy~rventilation in panic patients remains somewhat ambiguous as contrived (laboratory-induced) stressors were employed and it is important to demonstrate this effect in naturally occurring panic attacks. There are two possible ways of doing this; either by using the newly developed ambulatory monitoring of transcutaneous pC0, (‘p&O,; Hibbert, 1985) or by using more traditional measurement techniques with patients when panic attacks occur in settings which allow the use of such methods. As yet, appropriate methodological studies allowing full validation of ambulatory measures p&O, have not been carried out. More traditional measures have proved difficult to apply as it is in the nature of panic attacks that they seldom occur in settings in which such techniques are possible or justified. However, when settings allow its use, one of the traditional measures, arterial sampling, is particularly informative as it allows the measurement of pH as well as paC02. This is important as the symptoms of hyperventilation, although arising from changes in paC02, have their bodily effect through changes in pH (respiratory alkalosis). The study reported here is of a patient who experienced panic attacks whilst in the later stages of dialysis. These attacks occurred at predictable times, and it is in the nature of dialysis that samples of arterial blood are readily available. This allowed the measurement of paC02 and pH before and during naturaIiy occurring panic attacks and during the course of a respiratory based treatment similar to that used in previous studies. CASE HISTORY
The patient is a 21-yr-old single man who presented with acute on chronic renal failure. His blood urea at that time was 85 mmol/l and dialysis treatment was initiated. Some years previously a routine medical examination had revealed *t:Present addresses: *University of Oxford, Department of Psychiatry. Warneford Hospital, Oxford OX3 7JX. *Bethtern and Maudsiey Hospitals, London; $Hope Hospital, Manchester. England. 91
92
CASE HlST0RtF.S
AND
SHORTER
COMMIJNlCATlONS
proteinuria and haematuria but this had not been investigated. Dialysis treatment was commenced. but over the next 7 yr he had multiple severe complications; treatment with peritoneal dialysis resulted in three laparotomies for peritonitis and suspected bowel perforation. Many attempts were made to site a satisfactory arterio-venous fistula for haemodialysis but eight such fistulae proved unsatisfactory either due to infection or haemorrhage. He sustained a massive bleed from a fistula in his right arm and narrowly avoided amputation. However, 3 yr later the fistula in his leg haemorrhaged and was excised; a popliteal embolus then necessitated above-knee amputation. Aluminium encephalopathy was diagnosed with symptoms of dysarthria, ataxia and grand mal fits and he was hence treated for 3 yr with the chelating agent desferrioxamine. Other complications have also added to the vast number of investigations and periods of hospitalization which he has had to undergo in addition to his routine attendences 3 days each week for haemodialysis. He has had several episodes of septicaemia and pyrexia of unknown origin; cardiac catheterization revealed cardiac failure. He has also been treated for atrial fibrillation and hypertension and has to take several oral drugs daily. During several of these episodes he has been close to death. He had been unable to work since the condition was diagnosed and lived with his widowed mother, approx. 15 miles from the treatment centre. He had few friends, owing to his lengthy periods of hospitalization and was markedly pessimistic about his future prospects. Psychological problems had been prominent throughout his illness. A year after initial presentation a diagnosis of ‘reactive depression’ was made and he was treated with imipramine. Four years later he took an overdose of nitrazepam and received a further course of antidepressants together with a short period of psychiatric inpatient care. In June 1984 he failed to attend for one dialysis session and was again noted to be depressed and withdrawn, expressing suicidal ideas. He was also observed to be increasingly agitated towards the end of each dialysis session. At this point a referral was made to the Liaison Psychiatry Department. During the last hour of dialysis he complained of ‘tight feelings’ in his head and chest associated with tachycardia, palpitations and parasthesiae. He was afraid to let go of the bed frame, thinking he would die if he did so. He described difficulty in breathing and was obviously markedly hyperventilating when observed during these episodes. Analysis of blood gases during the last hour of dialysis (as panic symptoms were reaching their maximum level) showed a substantial drop in p,CO,. confirming this observation (see Fig. 2). It became clear that he had realized that previous serious complications. such as his amputation, had occurred during the summer months. He was unable to recall a summer in which he had not had to spend lengthy periods in hospital. He felt that the frightening sensations he was experiencing during the last hour of dialysis were indicative of some new disaster-becoming more certain of this as the summer months progressed and symptoms worsened. His experience of the symptoms closely resembled sensations he recalled from periods when he had been close to death. Reassurance had proven ineffective and, if anything, made him more distressed [see Warwick and Salkovskis (1985) for a discussion of the role of reassurance in medical settings]. Similarly, attempts at treatment using parenteral benzodiazepines had been unsuccessful. The failure of these interventions had served to confirm his fears. Treatment commenced with a 2 min period of voluntary hyperventilation whilst in the position he adopted during dialysis, but away from the machine. The symptoms he experienced were identical to those experienced when on the machine. This dramatic demonstration formed the basis of a discussion in which the patient was encouraged to interpret the bodily sensations he experienced as being a result of stress-induced hyperventilation, rather than being indicative of the more catastrophic things he feared. He was also taught the use of slow, shallow breathing in a pattern incompatible with hyperventilation, and the use of appropriate cognitive strategies relating to his fears. These interventions were immediately effective in reducing panic attack frequency. as shown in Fig. I. Improvement in self-ratings of anxiety and depression were also noted, acco ipanied by normalization of blood gas and pH changes accompanying dialysis. Figure 2 shows the changes inp,COz and pH which, after treatment, closely matched those observed in other dialysis patients. DISCUSSION
During panic attacks experienced by this patient, paC02 dropped and pH increased by greater amounts and to more extreme levels than observed at times when panic was not experienced or in control patients. Treatment rapidly abolished all symptoms and paC02 and pH remained normal in subsequent sessions. At the start of dialysis, patients are often in metabolic acidosis which is accompanied by a compensatory decrease in paC02. During the course of acetate-buffered haemodialysis. the metabolic acidosis is corrected and eventually the respiratory change would also be expected to correct; however. during dialysis itself, mild hyperventi!ation often occurs (Kliger. 1985; Salvadeo, Pezzagno, Segagni, Galli, Villa.
z 5
2 i+ :: L3
.-.-.-.-.-.,
2 t2 0 z
I.
’
> d0
i
3
I
! I 1
I 2
I 3
I 4
.
\ .-.-.-.-.
11’1 5
6
7
I 6
I 9
/\ I I I 10 11 12
.-.-.-.-.-.-r’+. / I I I , I I 13 14 15 16 17 18 19 Y&-J 33
WEEKS
Fig. I. Frequency of panic attacks. The dashed vertical line indicates the point where respiratory control was started. This treatment duration was only 2 weeks (4 sessions). It should be noted that the patient received treatment for other, non-panic-related problems over a longer period of time.
CASE
HISTORIES
AND
SHORTER
93
COMMUNICATIONS
5.50
T-
5.25 l5.00
$ a”
i
5.75 4.50 4.25 -
L
4.00 3.75
0-s
Controis
_m
Case--panic
b-4
Case --no
panic
t
w
I 7.31
I
I1
7.33
7.35
II 137
239
1
11 241
7.43
z45
I 247
I 249
I 7.51
I 253
II 255
7.57
J 7.59
PH
Fig. 2. paCO, (kPa) and pH at start of dialysis (open symbols) and end of dialysis (closed symbols).
Pogglo, Piazza, Bovio, Picardi, Petrella and Bigi, 1983). It is suggested that hyperventilation, and the transient dialysis-induced metabolic alkalosis produce bodily symptoms. Such symptoms do not usually precipitate panic attacks during dialysis, because the sensations are usually attributed to the medical procedures involved, particularly if they predictably occur towards the end of regular dialysis. In this case, however, the symptoms were interpreted in a particularly threatening and specific fashion (‘dialysis itself is about to kill me’) and hence resulted in an increase in anxiety. This anxiety itself led to further increase in respiration (Clark et al., 1985) and would therefore have further increased pH and symptoms and so on, round in a vicious circle. The rapid and complete response to the treatment used is consistent with this view of events, particularly when considered in the context of the failure of treatment by supportive psychotherapy and parenteral benzodiazepines. It seems likely that cognitive change was important-the patient’s belief that the sensations were symptoms of serious physical complications was weakened by their exact reproduction during voluntary hyperventilation whilst not undergoing dialysis. The implications of this report are three-fold. Firstly. knowledge of such cognitiv~physiolo~~l interactions is likely to be increasingly important as cognitive-behavioural treatments are used more frequently in renal units (Nichols and Springford, 1984). The treatment described here is medically more acceptable in patients with renal failure than is parenteral benzodiazepine, the previous treatment of choice (Viederman and Rusk, 1977). Secondly, Hampl, Klopp, Michels, Mahiout. Schilling, Wolfgruber, Schiller, Hanefeld and Kessel (1983) have proposed a link between decrease in paCOZ and dialysis disequilibrium syndrome. Some investigation of the possible contribution of psychophysiological factors to this problem would appear to be indicated. Thirdly, we have hypothesized elsewhere (Clark, 1979; Clark et al., 1985; Salkovskis et al., l985b) that, when anxious, some patients hyperventilate and that the resulting respiratory alkalosis is responsible for the somatic symptoms which form the basis of panic attacks when the patient interprets the symptoms in a catastrophic fashion. TO our knowledge, this is the first report of direct measurement of pBC02 and pH during naturally occurring panic and therefore fulfils a necessary condition of the model. Aekno~ledgements-The
All correspondence
authors are grateful to Dr Turney and Dr Storer for help and support with this case. should be addressed to P. M. Salkovskis. REFERENCES
Brown E. B. (1953) The physiological effects of hyperventilation. PhTsiol. Rea. 33, 445. Clark D. M. (1979) Therapeutic aspects of increasing pCOZ by ~havioral means. Unpublished M. Phil. Thesis, Univ. of London. Clark D. M., Salkovskis P. M. and Chalkley A. J. (1985) Respiratory control as a treatment for panic attacks. J. Behac. Ther. exp. Psychiat. 16, 23-30.
Gibson H. B. (1978) A form of behaviour therapy for some states diagnosed as “affective disorder”. Behao. Res. Ther. 16, 191-195.
Hampl H., Klopp H. W., Michels N., Mahiout A. Schilling H., Wolfgruber M., Schiller R., Hanefeld F. and Kessel M. (1983) Electroencephalogram investigations of the disequilibrium syndrome during bicarbonate and acetate dialysis. In Proceedings of rhe European Dialysis and Transplant Associafion, Vol I9 (Edited by Davison A. M. and Guillou P. J.). Pitman. London. Hibbert G. A. (1985) The diagnosis of hyperventilation using ambulatory carbon-dioxide monitoring. In Proceedings CJ/ the 15th European Conference of Psychosamaric Research (Edited by Lacey H. and Sturgeon J.). Libby, London. Kliger A. S. (1985) Complications of dialysis, haemodialysis, peritoneal dialysis and CAPD. In Ffuid, Electrolytes and Acid-Base Disorder, Vol. II (Edited by Arieff A. I. and Defronzo R. A.). Churchill-Livin~tone, New York. Lum L. C. (1976) The syndrome of habitual chronic hyperventillation. In Modern Trends in Psychosomatic Medicine, Vol. 3 (Edited by Hill 0. W.). Butterworths, London. Nichols K. A. and Springford V. (1984) The psycho-social stressors associated with survival by dialysis, Eehav. Res. Ther. 22, 563-574.
Salkovskis P. M., Clark D. M. and Jones D. R. 0. (1985a) A psychosomatic mechanism in anxiety attacks: the role of hy~~entilation in social anxiety and cardiac neurosis. In Proceedings ofthe flh European Conference on Psych~somQric Research (Edited by Lacey H. and Sturgeon J.). Libby, London.
94
CASE
HISTORIES
AND
SHORTER
COMMUNICATIONS
Salkovskis P. M.. Jones D. R. 0. and Clark D. M. (1985b) Respiratory control in the treatment of panic attacks: replication and extension with concurrent measurement of behaviour and pC0,. Br. J. Ps&ior. In press. Salvadeo A., Pezzagno G., Segagni S., Galli F., Villa G.. Poggio F.. Piazza V., BOVIO G.. Picardi L.. Petrella E. and Blgi L. (1983) Respiratory response of acetate dialysis and bicarbonate dialysis. In Proceed&s of the European Diulrsiv and Trun.~p/unf A~sociafibn, vol. 19 (Edited by davison A. M. and Guillbu P. J.). Pitmany London. Viederman M. and Rusk G. H. (1977) Appropriate use of psychotropic drugs in physical illness. Primq~ Cure 4, 60 I-606. Warwick H. M. C. and Salkovskis P. M. (1985) Reassurance. Br. med. J. 290, 1028.
Eehm. Rer Ther. Vol. 24. No. I, PP. 91-94. 1986 Prmted in Great Britain. All rights resewed
$3.00 + 0.00 Press Ltd
CopyrIght 6 1986Perpamon
A demonstration of acute hyperventilation during naturally occurring panic attacks
PAUL M. SALKOVSKIS,‘* HILARY M. C. WARWICK,‘~ DAVID M. CLARKE and D. JULIE WESSELS~$ Departments qf ‘Clinical Psvchology and 2Liaison Psychiatry and “The Renal Unit. The General Irtfirmar> at Leeds, Great George Street. Leeds. England ‘Department of Psychiatry, University of Oxford. Oxford OXI 3(/o,
Engktnd
(Received 12 June 1985)
Summary-Panic attacks and hyperventilation have been linked. although there have not been any demonstrations that patients acutely hyperventilate during naturally occurring panic attacks. A case study is reported in which a patient on renal dialysis showed substantially larger changes in paC02 and blood pH when panic was present than on other occasions. Changes observed in other dialysis patients were similar to those noted during non-panic sessions. INTRODUCrION There is a mounting body of evidence suggesting that hyperventilation, defined as breathing in excess of metabolic requirements, is involved in a variety of anxiety-relate disorders (Clark, 1979; Clark, Salkovskis and Chalkley, 1985; Gibson, 1978; Lum, 1976; Salkovskis, Jones and Clark, 1985bf. In particular. hy~rventilation has been implicated in panic attacks, which are defined as sudden onset episodes of intense anxiety, accompanied by a wide range of distressing bodily sensations. One of the most important implications of this hypothesized link is for treatment. Two recent studies assessed the utility of treatment directed at: (i) demonstration that voluntary hyperventilation reproduces the bodily symptoms characteristic of panic; (ii) the appropriate re-attribution of sensations experienced during panic attacks to hyperventilation and away from catastrophic interpretations; (iii) modification of respiratory and cognitive responses to stress. This treatment was successful in the treatment of panic attacks with and without associated avoidance, and improvements were maintained for up to 2 yr follow-up (Clark er al., 1985; Salkovskis et al., 1985b). One of these studies (Salkovskis et al., 1985b) also demonstrated that resting pC0, was consistently lower in patients experiencing panic attacks than in a group of age- and sex-matched controls, and that treatment resulted in the rapid restoration of patients’ pC0, to normal levels. This suggests that these patients were hyperventilating chronically with resultant renal compensation (Brown, 1953) which maintains pH at normal levels. As the sensations accompanying hyperventilation are mediated by increased pH, such chronic hyperventilation does not produce symptoms. However, the adaptation of the blood-buffe~ng system results in increased sensitivity to changes in ~$0, such as those produced by stressors and exercise. This means that decreases in p,COr will result in relatively larger changes in pH and hence more rapid onset and greater intensity of the bodily sensations of hyperventilation. It is therefore encouraging that one of the effects of treatment was to restore resting p&CO, to normal levels (Salkovskis et al.. 1985). In order to assess the extent to which patients acutely hyperventilate during panic attacks, Salkovskis, Clark and Jones (1985a) carried out a series of single-case experiments with panic patients for whom it seemed likely that hy~rventilation was involved in their attacks. Measures of pC0, were taken in the laboratory both at rest and during a variety of panic-relevant and panic-irrelevant contrived stressors. Results indicated that substantial increases in respiration did indeed take place during stress, and these were specific to the stressors which normally provoked panic in each patient. Furthermore, the degree of hyperventilation meant that these patients were certain to be experiencing some of the bodily symptoms which are produced by respiratory alkalosis. Clearly this demonstration of acute hy~rventilation in panic patients remains somewhat ambiguous as contrived (laboratory-induced) stressors were employed and it is important to demonstrate this effect in naturally occurring panic attacks. There are two possible ways of doing this; either by using the newly developed ambulatory monitoring of transcutaneous pC0, (‘p&O,; Hibbert, 1985) or by using more traditional measurement techniques with patients when panic attacks occur in settings which allow the use of such methods. As yet, appropriate methodological studies allowing full validation of ambulatory measures p&O, have not been carried out. More traditional measures have proved difficult to apply as it is in the nature of panic attacks that they seldom occur in settings in which such techniques are possible or justified. However, when settings allow its use, one of the traditional measures, arterial sampling, is particularly informative as it allows the measurement of pH as well as paC02. This is important as the symptoms of hyperventilation, although arising from changes in paC02, have their bodily effect through changes in pH (respiratory alkalosis). The study reported here is of a patient who experienced panic attacks whilst in the later stages of dialysis. These attacks occurred at predictable times, and it is in the nature of dialysis that samples of arterial blood are readily available. This allowed the measurement of paC02 and pH before and during naturaIiy occurring panic attacks and during the course of a respiratory based treatment similar to that used in previous studies. CASE HISTORY
The patient is a 21-yr-old single man who presented with acute on chronic renal failure. His blood urea at that time was 85 mmol/l and dialysis treatment was initiated. Some years previously a routine medical examination had revealed *t:Present addresses: *University of Oxford, Department of Psychiatry. Warneford Hospital, Oxford OX3 7JX. *Bethtern and Maudsiey Hospitals, London; $Hope Hospital, Manchester. England. 91
92
CASE HlST0RtF.S
AND
SHORTER
COMMIJNlCATlONS
proteinuria and haematuria but this had not been investigated. Dialysis treatment was commenced. but over the next 7 yr he had multiple severe complications; treatment with peritoneal dialysis resulted in three laparotomies for peritonitis and suspected bowel perforation. Many attempts were made to site a satisfactory arterio-venous fistula for haemodialysis but eight such fistulae proved unsatisfactory either due to infection or haemorrhage. He sustained a massive bleed from a fistula in his right arm and narrowly avoided amputation. However, 3 yr later the fistula in his leg haemorrhaged and was excised; a popliteal embolus then necessitated above-knee amputation. Aluminium encephalopathy was diagnosed with symptoms of dysarthria, ataxia and grand mal fits and he was hence treated for 3 yr with the chelating agent desferrioxamine. Other complications have also added to the vast number of investigations and periods of hospitalization which he has had to undergo in addition to his routine attendences 3 days each week for haemodialysis. He has had several episodes of septicaemia and pyrexia of unknown origin; cardiac catheterization revealed cardiac failure. He has also been treated for atrial fibrillation and hypertension and has to take several oral drugs daily. During several of these episodes he has been close to death. He had been unable to work since the condition was diagnosed and lived with his widowed mother, approx. 15 miles from the treatment centre. He had few friends, owing to his lengthy periods of hospitalization and was markedly pessimistic about his future prospects. Psychological problems had been prominent throughout his illness. A year after initial presentation a diagnosis of ‘reactive depression’ was made and he was treated with imipramine. Four years later he took an overdose of nitrazepam and received a further course of antidepressants together with a short period of psychiatric inpatient care. In June 1984 he failed to attend for one dialysis session and was again noted to be depressed and withdrawn, expressing suicidal ideas. He was also observed to be increasingly agitated towards the end of each dialysis session. At this point a referral was made to the Liaison Psychiatry Department. During the last hour of dialysis he complained of ‘tight feelings’ in his head and chest associated with tachycardia, palpitations and parasthesiae. He was afraid to let go of the bed frame, thinking he would die if he did so. He described difficulty in breathing and was obviously markedly hyperventilating when observed during these episodes. Analysis of blood gases during the last hour of dialysis (as panic symptoms were reaching their maximum level) showed a substantial drop in p,CO,. confirming this observation (see Fig. 2). It became clear that he had realized that previous serious complications. such as his amputation, had occurred during the summer months. He was unable to recall a summer in which he had not had to spend lengthy periods in hospital. He felt that the frightening sensations he was experiencing during the last hour of dialysis were indicative of some new disaster-becoming more certain of this as the summer months progressed and symptoms worsened. His experience of the symptoms closely resembled sensations he recalled from periods when he had been close to death. Reassurance had proven ineffective and, if anything, made him more distressed [see Warwick and Salkovskis (1985) for a discussion of the role of reassurance in medical settings]. Similarly, attempts at treatment using parenteral benzodiazepines had been unsuccessful. The failure of these interventions had served to confirm his fears. Treatment commenced with a 2 min period of voluntary hyperventilation whilst in the position he adopted during dialysis, but away from the machine. The symptoms he experienced were identical to those experienced when on the machine. This dramatic demonstration formed the basis of a discussion in which the patient was encouraged to interpret the bodily sensations he experienced as being a result of stress-induced hyperventilation, rather than being indicative of the more catastrophic things he feared. He was also taught the use of slow, shallow breathing in a pattern incompatible with hyperventilation, and the use of appropriate cognitive strategies relating to his fears. These interventions were immediately effective in reducing panic attack frequency. as shown in Fig. I. Improvement in self-ratings of anxiety and depression were also noted, acco ipanied by normalization of blood gas and pH changes accompanying dialysis. Figure 2 shows the changes inp,COz and pH which, after treatment, closely matched those observed in other dialysis patients. DISCUSSION
During panic attacks experienced by this patient, paC02 dropped and pH increased by greater amounts and to more extreme levels than observed at times when panic was not experienced or in control patients. Treatment rapidly abolished all symptoms and paC02 and pH remained normal in subsequent sessions. At the start of dialysis, patients are often in metabolic acidosis which is accompanied by a compensatory decrease in paC02. During the course of acetate-buffered haemodialysis. the metabolic acidosis is corrected and eventually the respiratory change would also be expected to correct; however. during dialysis itself, mild hyperventi!ation often occurs (Kliger. 1985; Salvadeo, Pezzagno, Segagni, Galli, Villa.
z 5
2 i+ :: L3
.-.-.-.-.-.,
2 t2 0 z
I.
’
> d0
i
3
I
! I 1
I 2
I 3
I 4
.
\ .-.-.-.-.
11’1 5
6
7
I 6
I 9
/\ I I I 10 11 12
.-.-.-.-.-.-r’+. / I I I , I I 13 14 15 16 17 18 19 Y&-J 33
WEEKS
Fig. I. Frequency of panic attacks. The dashed vertical line indicates the point where respiratory control was started. This treatment duration was only 2 weeks (4 sessions). It should be noted that the patient received treatment for other, non-panic-related problems over a longer period of time.
CASE
HISTORIES
AND
SHORTER
93
COMMUNICATIONS
5.50
T-
5.25 l5.00
$ a”
i
5.75 4.50 4.25 -
L
4.00 3.75
0-s
Controis
_m
Case--panic
b-4
Case --no
panic
t
w
I 7.31
I
I1
7.33
7.35
II 137
239
1
11 241
7.43
z45
I 247
I 249
I 7.51
I 253
II 255
7.57
J 7.59
PH
Fig. 2. paCO, (kPa) and pH at start of dialysis (open symbols) and end of dialysis (closed symbols).
Pogglo, Piazza, Bovio, Picardi, Petrella and Bigi, 1983). It is suggested that hyperventilation, and the transient dialysis-induced metabolic alkalosis produce bodily symptoms. Such symptoms do not usually precipitate panic attacks during dialysis, because the sensations are usually attributed to the medical procedures involved, particularly if they predictably occur towards the end of regular dialysis. In this case, however, the symptoms were interpreted in a particularly threatening and specific fashion (‘dialysis itself is about to kill me’) and hence resulted in an increase in anxiety. This anxiety itself led to further increase in respiration (Clark et al., 1985) and would therefore have further increased pH and symptoms and so on, round in a vicious circle. The rapid and complete response to the treatment used is consistent with this view of events, particularly when considered in the context of the failure of treatment by supportive psychotherapy and parenteral benzodiazepines. It seems likely that cognitive change was important-the patient’s belief that the sensations were symptoms of serious physical complications was weakened by their exact reproduction during voluntary hyperventilation whilst not undergoing dialysis. The implications of this report are three-fold. Firstly. knowledge of such cognitiv~physiolo~~l interactions is likely to be increasingly important as cognitive-behavioural treatments are used more frequently in renal units (Nichols and Springford, 1984). The treatment described here is medically more acceptable in patients with renal failure than is parenteral benzodiazepine, the previous treatment of choice (Viederman and Rusk, 1977). Secondly, Hampl, Klopp, Michels, Mahiout. Schilling, Wolfgruber, Schiller, Hanefeld and Kessel (1983) have proposed a link between decrease in paCOZ and dialysis disequilibrium syndrome. Some investigation of the possible contribution of psychophysiological factors to this problem would appear to be indicated. Thirdly, we have hypothesized elsewhere (Clark, 1979; Clark et al., 1985; Salkovskis et al., l985b) that, when anxious, some patients hyperventilate and that the resulting respiratory alkalosis is responsible for the somatic symptoms which form the basis of panic attacks when the patient interprets the symptoms in a catastrophic fashion. TO our knowledge, this is the first report of direct measurement of pBC02 and pH during naturally occurring panic and therefore fulfils a necessary condition of the model. Aekno~ledgements-The
All correspondence
authors are grateful to Dr Turney and Dr Storer for help and support with this case. should be addressed to P. M. Salkovskis. REFERENCES
Brown E. B. (1953) The physiological effects of hyperventilation. PhTsiol. Rea. 33, 445. Clark D. M. (1979) Therapeutic aspects of increasing pCOZ by ~havioral means. Unpublished M. Phil. Thesis, Univ. of London. Clark D. M., Salkovskis P. M. and Chalkley A. J. (1985) Respiratory control as a treatment for panic attacks. J. Behac. Ther. exp. Psychiat. 16, 23-30.
Gibson H. B. (1978) A form of behaviour therapy for some states diagnosed as “affective disorder”. Behao. Res. Ther. 16, 191-195.
Hampl H., Klopp H. W., Michels N., Mahiout A. Schilling H., Wolfgruber M., Schiller R., Hanefeld F. and Kessel M. (1983) Electroencephalogram investigations of the disequilibrium syndrome during bicarbonate and acetate dialysis. In Proceedings of rhe European Dialysis and Transplant Associafion, Vol I9 (Edited by Davison A. M. and Guillou P. J.). Pitman. London. Hibbert G. A. (1985) The diagnosis of hyperventilation using ambulatory carbon-dioxide monitoring. In Proceedings CJ/ the 15th European Conference of Psychosamaric Research (Edited by Lacey H. and Sturgeon J.). Libby, London. Kliger A. S. (1985) Complications of dialysis, haemodialysis, peritoneal dialysis and CAPD. In Ffuid, Electrolytes and Acid-Base Disorder, Vol. II (Edited by Arieff A. I. and Defronzo R. A.). Churchill-Livin~tone, New York. Lum L. C. (1976) The syndrome of habitual chronic hyperventillation. In Modern Trends in Psychosomatic Medicine, Vol. 3 (Edited by Hill 0. W.). Butterworths, London. Nichols K. A. and Springford V. (1984) The psycho-social stressors associated with survival by dialysis, Eehav. Res. Ther. 22, 563-574.
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