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Objective: Because hyperventilation has figured prominently in theories of panic disorder (PD) but not of social phobia (SP), we compared predictions regarding diagnosis-specific differences in psychological and physiological measures before, during, and after voluntary hyperventilation., Method: Physiological responses were recorded in 14 patients with PD, 24 patients with SP, and 24 controls during six cycles of 1-minute of fast breathing alternating with 1 minute of recovery, followed by 3 minutes of fast breathing and 10 minutes of recovery. Speed of fast breathing was paced by a tone modulated at 18 cycles/minute, and depth by feedback aimed at achieving an end-tidal pCO2 of 20 mm Hg. These values were reached equally by all groups., Results: During fast breathing, PD and SP patients reported more anxiety than controls, and their feelings of dyspnea and suffocation increased more from baseline. Skin conductance declined more slowly in PD over the six 1-minute fast breathing periods. At the end of the final 10-minute recovery, PD patients reported more awareness of breathing, dyspnea, and fear of being short of breath, and their pCO2s, heart rates, and skin conductance levels had returned less toward normal levels than in other groups. Their lower pCO2s were associated with a higher frequency of sigh breaths., Conclusions: PD and SP patients report more distress than controls to equal amounts of hypocapnia, but PD differ from SP patients and controls in having slower symptomatic and physiological recovery. This finding was not specifically predicted by hyperventilation, cognitive-behavioral, or suffocation alarm theories of PD.

Objective: Because breath holding causes arterial pCO2 to increase, we used it to test the hypothesis that in panic disorder (PD) a biological suffocation monitor is pathologically sensitive., Method: Nineteen patients with PD, 17 with generalized anxiety disorder (GAD), and 22 normal controls took deep breaths on signal and held them until a release signal was given 30 seconds later. This was repeated 12 times separated by 60-second normal breathing periods., Results: PD patients reported having had in the past more symptoms of shortness of breath when anxious, and more frequent frightening suffocation experiences than the other groups. However, increases in self-rated anxiety between periods of normal breathing and periods of breath holding were similar in all three groups. Skin conductance, blood pressure, and T-wave amplitude reactions to breath holdings were also similar, but heart rate acceleration upon taking a deep breath was greater in GAD patients. Before and after individual breath holdings, end-tidal pCO2 was lower in PD patients than in normal controls; GAD patients were intermediate. Inspiratory flow rate did not differ between groups., Conclusions: Our physiological results provide no direct support for an overly sensitive suffocation alarm system in PD. Lower pCO2 may be due to anxiety causing hyperventilation in patients prone to panic.

Response to sodium lactate infusions has been proposed as an experimental model and a biologic marker for panic attacks. Several authors have claimed that patients suffering from panic attacks, but not normal controls, "panic" in response to lactate. A careful review of methods and results of 13 studies, however, reveals serious methodologic problems, lack of specificity and sensitivity, and a failure to consider cognitive variables. When baseline differences are ruled out, the responses of patients and controls may not differ. So far, response to lactate cannot be interpreted as a model and marker for panic attacks and does not provide evidence for their underlying biologic distinctness from other types of anxiety. Known biologic mechanisms do not sufficiently explain the effects of lactate. Instead, an interaction of peripheral physiologic changes, past experience, environmental cues, and their appraisal as threatening or dangerous seems to be a more appropriate model.

There has been considerable speculation about a possible relationship between panic disorder and mitral valve prolapse syndrome (MVP), although empirical results have been highly inconsistent. Some studies report low frequencies of 0-8%, others high frequencies of 24-35% "definite" MVP in panic patients (average across 17 studies: 18% of panic patients, 1% of normal controls). Elevated prevalences of MVP were also reported for generalized anxiety disorder, bipolar affective disorder, and anorexia nervosa. Studies of MVP patients generally failed to find elevated prevalence of panic compared to other cardiac patients or normal controls (averages across seven studies: 14%, 10%, and 8%, respectively). Inconsistent results may be due to widely different diagnostic criteria for MVP, low reliability of this diagnosis, inadequate control groups, "non-blind" ratings of panic or MVP, and sampling bias in both patient and control populations. These problems as well as the great variations in the published results preclude any final judgment. If there is concomitance between MVP and panic, it is small and primarily involves subjects with milder or reversible variants of MVP. At present it seems most justified, however, to assume co-morbidity in highly symptomatic individuals rather than a functional relationship.