patients considered to have only the hyperventilation syndrome. Patients with ischaemic heart disease reported difficulty speaking, air hunger, breathing through the nose or panting, sighing and pareasthesia. Patients with HVS alone reported palpitations/heart pounding, upper chest breathing, trouble swallow- ing and tingling.

The Goldberg 60 item questionnaire was administered to detect concom- itant psychiatric coping problems. The mean score was 13.9 & 11.3 (> 12 =‘case’). Patients who did not hyperventilate (i.e. either had P,,CO, > 30 or Beumer and Hardonk slope < 1.5) scored si~n;fic~~tly higher ( p < 0.001) than those who had adopted a hyperventilation pattern of breathing.

7 further patients were studied in a similar fashion with chest pain and normal coronary arteriograms. None of these patients had resting hypocapnia but 417 had a slope > 1.5 and 5 reproduced chest pain.

Conclusions

(1) Hyperventilation and ischaemic heart disease are not mutually exclusive. (2) Hyperventilation may mimic symptoms of ischaemic heart disease and

its recognition and treatment in this group of patients may reduce the need for arteriography, drugs and even surgery.

(3) The high incidence of hyperventilation and coping problems in this group of patients with IDH suggest that both should be searched for more diligently (Freeman and Nixon, in press).

References

Freeman, L.J. and Nixon, P.G.F. (in press). Dynamic causes in Angina Pectoris. American Heart

Journal. Legg, CR., Cheridan, K. and Timmons, B.H. (1981). Hyperventilation symptoms: A factor

analytic study. Proceeding of the 4th International Symposium of Respiratory Psychophysi-

ology, Southanlp~on.

THE ROLE OF HYPERVENTILATION IN PANIC DISORDER

AND AGORAPHOBIA

Ronald LEY

Srrtre Unwersity of New York at Alban)t, A#u~~y, NY 12222. U.S.A

The thesis of this paper (Ley, 19852~; in press) is that the panic attacks which underlie agoraphobia are caused by the mis~ttribution of the symptoms

H. Folgering, ed. / Respwatoty psychophysiology abstract, 1985 175

produced by hyperventilation. The sequence of conditions which are assumed

to lead to panic disorder is as follows:

(1) ‘Sensitive’ individuals (persons who maintain a normally high level of anxiety together with a normally low threshold for the elicitation of fear) under prolonged periods of stress which produce a relatively constant state of anxiety, are more likely than others to become chronic hyperventilators. Thus, if hyperventilation underlies the panic attacks that lead to agoraphobia, it would be expected that agoraphobes maintain a higher resting respiration rate than that found in the normal population of adults. This expectation was confirmed in a study by Ley (1985b). (2) The chronic hyperventilator does not connect the somatic complaints produced by hyperventilation with dysfunctional breathing. The increased blood pH and decreased arterial tension may produce the somatic complaints (the hyperventilation syndrome) at a relatively low level of intensity which may be tolerated for relatively long periods of time. (3) The relationship between blood pH (and PCO,) is a positively accelerating exponential function in which relatively large increases in pH (e.g. 7.4 to 7.6) and/or relatively large decreases in PCO, (e.g. 40 to 20 mmHg) lead to relatively small increments in the intensity of the symptoms of hypocapnea; whereas relatively small increases in pH beyond 7.6 and/or small decreases in PCO, beyond 20 mmHg, lead to dramatic changes in the frequency and intensity of the symptoms of hypocapnea. Chief among these symptoms are dyspnea and heart palpitations, the intensity of which leads the sufferer to believe that death is imminent, that he is about to suffocate or die of heart failure. (4) The critical points of an upper threshold of tolerance for the symptoms of hypocapnea are pH beyond 7.6 and/or PCO, beneath 20 mmHg. The symp- toms of hypocapnea increase rapidly in intensity to the point where tolerance gives way to alarm and fear. Exceeding this threshold marks the onset of the panic attack. (5) The sudden onset of the intense symptoms of hypocapnea (especially dyspnea and heart palpitations) frighten the sufferer and thereby activate the sympathetic nervous system which increases heart rate and drives the inter- costal muscles of the thorax, thereby increasing respiration rate. This subse- quent increase in respiration rate will in turn lead to an even greater dissipa- tion of carbon dioxide, which will result in a greater rise in pH and a greater decline in PCO,, and an increase in the intensity of the symptoms of hypo- capnea. The panic attack will in this way grow in intensity until events occur which lead to a reduction in blood alkalosis and an increase in arterial tension. (6) The cause of dyspnea (a primary source of fear in panic attacks) is the same agent that leads to termination of the attack. With excessive loss of CO,, the respiratory reflex center of the medulla is dampeneded while at the same time

the intercostal muscles are weakened by an insufficient supply of oxygen. Under such circumstances, even extreme efforts to increase respirstion rate will not be effective, Dyspnea will br experienced. but the rate of dissipation of CO, will decline, thus providing time for the build up of CO,, and consequent deciine in pH and rise in X0,. If the rise in pH and decline in PCO, is markedly sudden. the panic attack will be terminated by loss of consciousness. (‘7) Ignorance or misattribution of the cause of the panic attack will make the sufferer fearful that subsequent attacks will occur when he is vulnerabIe, Thus, he will adapt to this contingency by engaging in agoraphobic behaviours. namely, avoiding threatening situations and seeking ‘safe’ places and the

company of ‘safe’ people.

In a recent study, Bonn, Readhead and Timmons (1984) reported a con- trolled experiment in which agoraphobia was successfully treated by means of

breathing retraining,

References

Bonn, J.A.. Readhead, C.P. and Timmons, B.H. (1964). Enhanced adaptive behnviuural wspons~

in agoraphobic patients pretreated with breathing retraining. The Lancet, 22. 665469.

K.&y. R. (1985a). RlooJ, breath and fears: A h~p~n~e~t~latj~r~ theory of panic attacks and agoraphobia. Clinical Psychology, Review, 5.

Izy, R. (1985b). Agoraphobia. the panic attack. and the hyperventilation syndrome. Behaviour

Research and Therapy, 23, 79-81.

Ley, R. (In press). Panic disorder: A hyperventilation interpretation. In: Michelson, I.. and Ascher, M. (Eds.). Cognitive-Behal~iourat Assessment and Treatment oE Anxiety Disorderx. Guitdford:

New York.

ACTION AND INTERACTION OF RESPIRATORY MUSCLES

Recent progress had led to a better insight in how the respiratory muscles interact and how they move the chest wall. Tt is now general’ty accepted that quiet breathing in the norm& subject requires a coordinated ~ntr~~t~on of the diaphragm, the parasternaf intercostafs and the scaieness. Contraction of either of those muscles alone causes important distortion of the chest wall and hence, is less efficient, Attempts to change the inspiratory muscle coordination vofuntarily, often cause changes which are considerably more complicated than expected. Voluntary attempts to breathe with the diaphragm alone for example