Department of Psychiatry,
Columbia University, New York
Abstract : A carbon dioxide
hypersensitivity theory of panic has been
posited. We hypothesize more broadly that a
physiologic misinterpretation by a suffocation
monitor misfires an evolved suffocation alarm
system. This produces sudden respiratory
distress followed swiftly by a brief
hyperventilation, panic, and the urge to flee.
Carbon dioxide hypersensitivity is seen as due
to the deranged suffocation alarm monitor. If
other indicators of potential suffocation
provoke panic this theoretical extension is
supported. We broadly pursue this theory by
examining Ondine's curse as the physiologic and
pharmacologic converse of panic disorder,
splitting panic in terms of symptomatology and
challenge studies, reevaluating the role of
hyperventilation, and reinterpreting the
contagiousness of sighing and yawning, as well
as mass hysteria. Further, the phenomena of
panic during relaxation and sleep, late luteal
phase dysphoric disorder, pregnancy, childbirth,
pulmonary disease, separation anxiety, and
treatment are used to test and illuminate the
suffocation false alarm theory.
.......
CHRONIC HYPERVENTILATION DURING PANIC
DISORDER
Chronic hyperventilation causes both low
PCO2 and bicarbonate levels. These normalize
during panic remission ,76 suggesting that
chronic hyperventilation does not cause panic,
but rather it adaptively compensates for a
lowered suffocation alarm threshold by keeping
PCO2 below the triggering range.
Chronic hyperventilation might entail a
vicious circle if hypocapnia produced a
deafferentation hypersensitivity, thus further
decreasing the alarm threshold. However, chronic
hyperventilation effects on carbon dioxide
sensitivity are markedly variable, so this
remains an interesting possibility.'
SIGHS AND
YAWNS
AS COMPENSATORY ADAPTATIONS
Chronic hyperventilation as an adaptive
hypocapnia inducing mechanism is consonant with
frequent sighing, a venerable feature of
neurosis. A feeling of respiratory oppression
precedes sighing. The deep inspiration that
initiates a sigh, triple the normal tidal
volume, abruptly lowers PCO2 and relieves
respiratory distress. Therefore, chronic
hyperventilation and sighing may adaptively keep
PCO2 below a depressed suffocation alarm
threshold. (It is arresting that frequent
extreme yawning inspirations often accompany
increased sighing, indicating a common
function.) A sigh or yawn may serve as a
bioanalytical test for high ambient carbon
dioxide. If, on deep inhalation, the PCO2 failed
to fall sufficiently, an asphyxiai cue would be
detected.
That suffocation serves as a particularly
traumatic unconditional stimulus was made plain
by Sanderson et al and Campbell et al. These
investigators gave alcoholic volunteers an
injection of succinyicholine, producing a
"harrowing" period of 90 to 130 seconds in which
they were unable to move or breathe while
remaining conscious. A tone, to which they had
previously been habituated, was played during
the apnea.
After the paralysis, many took occasional
deep breaths that led to an immediate
suppression of respiration for 12 to 15 seconds.
Curiously this re-creation of the traumatic
stimulus was not aversive. This becomes
comprehensible if the sighs served as ambient
carbon dioxide bioassays. Since the sigh-induced
apneas diagnosed a safe low carbon dioxide
environment they were safety signals, although
they should be anxiogenic by conditioning
theory. The potency and specificity of the
suffocation stimulus is indicated by the marked
resistance to extinction of these subjects
sighing.
The mysterious contagious effects of yawns
and sighs are well known. Observed acute
inspirations may be interpreted as tests of
increased ambient carbon dioxide or efforts to
overcome breathlessness. Thus, observing
another's yawn incites ones' own yawning test
without any relevant cognition, thus resembling
an ethologic fixed action pattern.
PANIC DURING RELAXATION AND
SLEEP
Panics occur during relaxation' and
deepening nonrapid eye movement s1eep despite
lack of danger cues or cognitions. However, both
states cause sharply increasing PCO2, especially
in those with chronic hyperventilation.
If sensitivity to increasing PCO2 incites
panics during relaxation and sleep, then those
who panic during deepening sleep should also be
likely to panic during relaxation. Mellman and
Uhdde have shown this.
Ley suggests that patients who panic during
sleep are chronic hyperventilators with
diminished buffer. Therefore, minor nocturnal
ventilatory reductions cause hypercapnic
respiratory acidosis, which incites
hyperventilation, swinging into hypocapnia that
triggers panic.
However, even given that nocturnal panickers
chronically hyperventilate, carbon dioxide
increase due to nocturnal ventilatory reduction
might lead only to a compensatory tidal volume
increase, producing eucapnia rather than
hypocapnia. Ley's model does not account for
overshoot. Further, even given overshoot, it
does not follow that acute hypocapnia produces
panic since controlled studies indicate
hypocapnic hyperventilation is
insufficient.
In our model, hyperpnea, hypocapnia, and
alkalosis are consequences of panic rather than
causal antecedents. If nocturnal carbon dioxide
challenges were panicogenic prior to respiratory
alkalosis onset, this would resolve this
disagreement.
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Hyperventilation-induced alterations in the
level of consciousness with
electroencephalographic slowing have been
documented repeatedly. Over the past 5 years,
three children presented with
hyperventilation-stereotyped attacks that
impressed us as being extremely unusual, both
clinically and electroencephalographically.
These attacks we have termed
'pseudoabsences.'
In contrast to the striking ictal discharges
of typical or atypical absences, the
concomitants of pseudoabsences resemble but a
mere accentuation of the hyperventilation
buildup.
It should be stressed, however, that:
(1) electroencephalographically, the
sinusoidal slow waves of pseudo-absences are of
higher voltage, more widely distributed, and
distinctly slower than those encountered with
the usual hyperventilation buildup.
(2) clinically, concomitantly with the
appearance of these slower waves, the child
stops breathing, stares, fails to obey simple
commands, and may exhibit automatic movements
such as yawning, swallowing, and
smiling.
Seconds after cessation of overbreathing,
the electroencephalogram reverts gradually to a
more normal appearance. The child then begins
spontaneously to hyperventilate again, as if
resuming activity where he had left off. The
same sequence of events recurs repeatedly, the
second and subsequent attacks being precipitated
by much shorter bouts of hyperventilation than
the initial one.
