Hyperventilation Syndrome
Fergus
Hyperventilation Syndrome
Authored by Edward Newton, MD, Vice-Chair, Associate Professor,
Department of Emergency Medicine, Los Angeles County-University of
Southern California Medical Center
Edward Newton, MD, is a member of the following medical societies:
American Academy of Emergency Medicine, American College of Emergency
Physicians, American Medical Association, and Society for Academic
Emergency Medicine
Edited by Robin R Hemphill, MD, Associate Program Director, Assistant
Professor, Department of Emergency Medicine, Vanderbilt University;
Francisco Talavera, PharmD, PhD, Department of Pharmacy, Creighton
University; Paul Blackburn, DO, Program Director, Assistant
Professor, Department of Emergency Medicine, Maricopa Medical Center;
John Halamka, MD, chief Information Officer/CareGroup Healthcare
System, Assistant Professor of Medicine, Department of Emergency
Medicine, Beth Israel Deaconess Medical Center; and Craig Feied, MD,
FACEP, FAAEM, Director of National Center for Emergency Medicine
Informatics, Clinical Associate Professor, Department of Emergency
Medicine, Washington Hospital Center
INTRODUCTION
Background:
Hyperventilation syndrome (HVS) represents a relatively common ED
presentation that most clinicians readily recognize. The syndrome has
defied precise definition and explanation of the underlying
pathophysiology for the past 100 years.
Most simply defined, HVS is a condition in which minute ventilation
exceeds metabolic demands, resulting in hemodynamic and chemical
changes that produce characteristic symptoms.
There is considerable overlap in symptoms between HVS and panic
disorder, although they remain distinct entities. Approximately 50%
of patients with panic disorder and 60% of patients with agoraphobia
manifest hyperventilation as part of their symptomatology, whereas
only 25% of patients with HVS manifest panic disorder.
Pathophysiology:
HVS occurs in acute and chronic forms. Acute HVS accounts for only 1%
of cases but is diagnosed more easily. Chronic HVS can present with a
myriad of respiratory, cardiac, neurologic, or GI symptoms without
any apparent overbreathing by the patient.
Due to the subtlety of the hyperventilation, many patients are
admitted and undergo extensive and expensive testing in an attempt to
discover organic causes of their complaints.
The underlying mechanism by which some patients develop
hyperventilation is unknown, but multiple theories abound. It seems
clear that there is a population in whom certain stressors provoke an
exaggerated respiratory response. Several such stressors have been
identified, including emotional distress, sodium lactate, caffeine,
isoproterenol, cholecystokinin, and CO2.
Infusion of lactate in patients with panic disorder provokes symptoms
of panic in 80% of cases, compared to 10% of controls. Approximately
one half of the lactate responders will develop acute
hyperventilation as part of the panic reaction. Lactate levels are
higher and remain elevated longer in panic patients compared to
controls, suggesting that an abnormal metabolism of lactate is
involved in the pathogenesis, although the abnormality has not been
characterized. Whether the same abnormality is operant in pure HVS is
unknown.
Part of the explanation for HVS lies in the mechanics of breathing.
Normal tidal volumes range from 35-45% of vital capacity at rest.
Hyperinflation of the lungs beyond that level is resisted by the
elastic recoil of the chest wall, and inspiratory volumes beyond this
level are perceived as effort or dyspnea.
Patients with HVS tend to breathe using the upper thorax, rather than
the diaphragm, resulting in chronically overinflated lungs. When
stress induces a need to take a deep breath, it is perceived as
dyspnea. The sensation of dyspnea creates anxiety, which encourages
more deep breathing, and a vicious cycle is created.
Patients with panic disorder have a lower threshold for the fight or
flight response and tend to manifest with primarily psychiatric
complaints, such as fear of death, impending doom, or claustrophobia.
HVS patients tend to focus on somatic complaints related to the
physiologic changes produced by hyperventilation. The initiating
stimulus and the abnormal stress response may be identical in each
group but is expressed differently.
Frequency:
In the US: Up to 10% of patients in a general internal medicine
practice are reported to have HVS as their primary diagnosis,
although equivalent data are not available for ED presentations.
Mortality/Morbidity:
Mortality is extremely rare. A leftward shift in the HbO2
dissociation curve and vasospasm related to low pCO2 may cause
myocardial ischemia in patients with coronary artery disease.
Morbidity - Certain patients are psychologically disabled by their
symptoms, and many patients carry false diagnoses. The real danger
with HVS is that they will suffer complications from unneeded
investigations (eg, angiography) or treatment (eg, thrombolytics). It
may be extremely difficult to withhold such therapy in a patient with
crushing chest pain, dyspnea, and/or suggestive electrocardiogram
(ECG) changes.
One study reported a series of 45 patients with chest pain who had
normal coronaries on angiography. These patients were ultimately
diagnosed as HVS. Over a 3.5-year average follow-up, 67% of patients
had made subsequent ED visits for chest pain, and 40% of patients had
been readmitted to rule out myocardial infarction.
Consequently, not only does HVS produce severe and genuine discomfort
for the patient, it also accounts for considerable medical expense in
excluding more serious pathology.
Sex:
A female preponderance of HVS cases exist, ranging from 2:1-7:1.
Age:
The peak age of incidence is from 15-55 years; however, cases have
been reported in all age groups, except infancy.
CLINICAL
History:
Patients with acute HVS may present with great agitation and anxiety.
Most commonly, the history is sudden onset of chest pain, dyspnea, or
neurologic symptoms (eg, dizziness, weakness, paresthesias) following
a stressful event.
Patients with chronic HVS present with similar symptoms of recurrent
chest pain, dyspnea, or neurologic deficits but usually have had
numerous similar presentations in the past.
Acute hyperventilation
Patients often present dramatically with agitation, hyperpnea and
tachypnea, chest pain, dyspnea, wheezing, dizziness, palpitations,
tetanic cramps (carpopedal spasm), paresthesias, generalized
weakness, and syncope.
The patient often complains of a sense of suffocation. An emotionally
stressful precipitating event often can be identified.
Cardiac symptoms
The chest pain associated with HVS usually has atypical features,
but, occasionally, it closely resembles typical angina. It tends to
last longer (hours vs. minutes), often is relieved rather than
provoked by exercise, is tender to palpation, and is unrelieved by
nitroglycerine.
HVS should be suspected in young patients without cardiac risk
factors who present with chest pain, particularly if associated with
paresthesias and carpopedal spasm. However, this diagnosis should be
reached cautiously because many other potentially serious causes
should be considered.
ECG changes are common and include prolonged QT interval, ST
depression or elevation, and T wave inversion.
In older patients, who may have coexistent coronary artery stenosis,
the vasospasm induced by hypocarbia may be sufficient to provoke
myocardial injury.
A high incidence of HVS occurs among patients with mitral valve
prolapse, and the chest pain associated with MVP may be due to
hyperventilation.
Prinzmetal's angina is associated strongly with HVS, but the chest
pain associated with this syndrome would normally be expected to
respond to nitrates or calcium channel blockers.
Central nervous system (CNS) symptoms
CNS symptoms occur because hypocapnia causes reduced cerebral blood
flow (CBF). CBF decreases 2% for every mm Hg decrease in pCO2.
Symptoms of dizziness, weakness, confusion, and agitation are common.
Patients may report symptoms of depersonalization and visual
hallucinations.
Rarely, syncope or seizure may be provoked by hyperventilation.
Paresthesias occur more commonly in the upper extremity and are
usually bilateral.
Unilateral paresthesias are left-sided in approximately 80% of the
cases.
Perioral numbness is very common.
GI symptoms, such as bloating, belching, flatus, and epigastric
pressure, may result from aerophagia.
Dry mouth occurs with mouth breathing and anxiety.
Metabolic changes
Acute metabolic changes result from intracellular shifts and
increased protein binding of various electrolytes during respiratory
alkalosis.
Acute hypocalcemia can result in carpopedal spasm, muscle twitching,
positive Chvostek's and Trousseau's signs, and prolonged QT interval.
Hypokalemia tends to be less pronounced but can produce generalized
weakness.
Acute hypophosphatemia is common and may contribute to paresthesias
and generalized weakness.
Chronic hyperventilation
The diagnosis of chronic HVS is much more difficult because the
hyperventilation usually is not clinically apparent.
Often, these patients have had extensive medical investigations and
have been assigned several misleading diagnoses.
Two thirds of the patients with chronic HVS have a persistently low
pCO2 with compensatory renal excretion of HCO3, resulting in a near
normal pH.
The respiratory alkalosis can be maintained with occasional deep
sighing respirations, which are observed often in patients with
chronic HVS.
When faced with an additional stress that provokes hyperventilation,
the physiologic acid base reserve is less, and these patients become
symptomatic more readily than non-HVS patients.
Many of these patients suffer from obsessive-compulsive disorders,
experience sexual and marital difficulties, and have poor adaptations
to stress.
Chronic HVS patients may have symptoms that mimic virtually any
serious organic disorder, but usually they will have atypical
features of these diseases.
Physical:
Acute hyperventilation
Obvious tachypnea, hyperpnea
Chest wall tenderness, particularly in the upper thorax, due to
ligamentous and muscle fatigue in the chest wall
Carpopedal spasm
Acute hypocarbia causes reduced ionized calcium and phosphate levels,
resulting in involuntary contraction of the feet or, more commonly,
the hands.
Chvostek's or Trousseau's signs may be positive due to hypocalcemia.
Wheezing may be heard due to bronchospasm from hypocarbia.
Tremor, mydriasis, pallor, tachycardia, and other manifestations of
anxiety
Evidence of depersonalization, hallucination
Chronic HVS
Hyperventilation is usually not apparent.
Frequent sighing respirations; 2-3 per minute
Chest wall tenderness
Characteristically, multiple complaints without much supporting
physical evidence of disease
Causes:
The cause of HVS is unknown, but it appears that affected persons
have an abnormal respiratory response to stress, sodium, lactate, and
other chemical and emotional triggers, thereby resulting in excess
minute ventilation and hypocarbia.
The incidence of HVS in first-degree relatives is increased compared
with the general population, but no clear genetic factors have been
identified.
DIFFERENTIALS
Acute Respiratory Distress Syndrome
Asthma
Atrial Fibrillation
Atrial Flutter
Cardiomyopathy, Dilated
Cardiomyopathy, Restrictive
Chronic Obstructive Pulmonary Disease and Emphysema
Costochondritis
Diabetic Ketoacidosis
Hyperthyroidism, Thyroid Storm and Graves' Disease
Hyperventilation Syndrome
Metabolic Acidosis
Methemoglobinemia
Myocardial Infarction
Panic Disorders
Pleural Effusion
Pneumonia, Bacterial
Pneumothorax, Iatrogenic, Spontaneous and Pneumomediastinum
Pneumothorax, Tension and Traumatic
Pulmonary Embolism
Respiratory Distress Syndrome, Adult
Smoke Inhalation
Venous Air Embolism
Withdrawal Syndromes
WORKUP
Lab Studies:
Acute HVS
The diagnosis of acute HVS is clinical. Obtaining an arterial blood
gas (ABG) is not necessary to document hypocarbia and alkalosis,
although it may be useful if the diagnosis is unclear.
Recognition of the typical constellation of dyspnea, agitation,
dizziness, atypical chest pain, tachypnea and hyperpnea,
paresthesias, and carpopedal spasm in a young, otherwise healthy
patient is sufficient to make the diagnosis.
Pulse oximetry
Measurement of a normal O2 saturation is useful in eliminating
hypoxia as a cause of hyperventilation.
ABG
An ABG is indicated if acidosis is suspected.
ABG sampling will confirm chronic (compensated) respiratory alkalosis
in a majority of cases. The pH in these cases is near normal, with a
low pCO2 and low HCO3.
Other tests
Toxicology screen
D-Dimer assay
Imaging Studies:
Imaging studies are not indicated when the diagnosis of HVS is clear.
In less obvious cases of HVS, if imaging studies are done, they will
be normal.
Chest radiography is indicated for patients at high risk for cardiac
or pulmonary pathology or when an abnormality is encountered on
physical examination that suggests chest pathology.
Other Tests:
ECG
TREATMENT
Prehospital Care:
Because many potentially serious causes of respiratory distress or
chest pain exist, it is prudent to transport patients with these
complaints for a more complete evaluation than is available in the
field.
Rebreathing into a paper bag is not recommended in the field or the
ED unless more serious etiologies have been excluded. Deaths have
occurred in patients with acute myocardial infarction (MI) when this
technique was applied erroneously.
Emergency Department Care:
ED treatment of HVS is often ineffective. Techniques of rebreathing
into a paper bag are no longer recommended because significant
hypoxia and death have been reported.
In patients who are hyperventilating for organic reasons (eg,
pulmonary edema, metabolic acidosis), increasing pCO2 and decreasing
O2 may be disastrous.
In addition, paper bag rebreathing is often unsuccessful in reversing
the symptoms of HVS because patients have difficulty complying with
the technique and because CO2 itself may be a chemical trigger for
anxiety in these patients.
Once life-threatening conditions have been eliminated, simple
reassurance and an explanation in layman's terms of how
hyperventilation produces the patient's symptoms is usually
sufficient to terminate the episode.
Provoking the symptoms by having the patient voluntarily
hyperventilate for 3-4 minutes often convinces the patient of the
diagnosis but is time-consuming and often ineffective.
Most patients with HVS tend to breathe using the upper thorax and
have hyperinflated lungs throughout the respiratory cycle.
Physically compressing the upper thorax and having the patient exhale
maximally will decrease hyperinflation of the lungs
Instructing the patient to breathe abdominally, with the diaphragm,
often will lead to improvement in dyspnea and eventually will correct
many of the associated symptoms.
The patient should be instructed in the technique of diaphragmatic
breathing and referred to a specialist who can reinforce this
approach.
Use of benzodiazepines for stress relief and for resetting the
trigger for hyperventilation is effective but may require prolonged
treatment.
Although acute chemical sedation may be effective and humane in
selected severe cases, prolonged use of these medications should not
be initiated in the ED.
Stress reduction therapy, beta-blockers, tricyclic antidepressants,
and breathing retraining have all proven effective in reducing the
intensity and the frequency of episodes of hyperventilation, and the
patient should be referred to an appropriate therapist to implement
these techniques over the long term.
Consultations: Consultation usually is not required. The patient can
be referred to the primary physician or to a therapist to help
control this disease.
MEDICATION
Benzodiazepines are effective in reducing stress that may provoke HVS
and are thought to reset the CNS response to a variety of
"panic-ogens".
Beta blockade and tricyclic antidepressants have been reported to
reduce the frequency and the severity of episodes of
hyperventilation.
Drug Category:
Benzodiazepines
- These agents are useful in the treatment of hyperventilation
resulting from anxiety and panic attacks. By binding to specific
receptor-sites, these agents appear to potentiate the effects of
gamma-aminobutyrate (GABA) and facilitate inhibitory GABA
neurotransmission and other inhibitory transmitters.
Drug Name Alprazolam (Xanax)
- It is indicated for the treatment of anxiety and management of
panic attacks.
Adult Dose 0.25-0.5 mg tid
Average dose proven effective is 0.5-4 mg/d
Pediatric Dose < 18 years: Not established
Contraindications Documented hypersensitivity; patients diagnosed
with severe respiratory depression, narrow angle glaucoma, and
preexisting hypotension
Interactions Carbamazepine and disulfiram decrease the effects of
this medication when administered concurrently. Conversely, the
toxicity of alprazolam increases when it is administered concurrently
with cimetidine, lithium, contraceptives, and CNS depressants
(including alcohol).
Pregnancy D - Unsafe in pregnancy
Precautions Withdrawal symptoms, including seizures, have occurred 18
h to 3 d following the abrupt discontinuation of the drug.
Drug Name Lorazepam (Ativan)
- It is a sedative hypnotic in the benzodiazepine class that has a
short onset of effect and a relatively long half-life.
By increasing the action of GABA, a major inhibitory neurotransmitter
in the brain, it may depress all levels of the CNS, including limbic
and reticular formation.
Adult Dose 1-10 mg/d divided bid/tid
Pediatric Dose 0.05 mg/kg/dose q4-8h
Contraindications Documented hypersensitivity; patients with
preexisting CNS hypotension, depression, and narrow angle glaucoma.
Interactions The toxicity of benzodiazepines in the CNS increases
when used concurrently with alcohol, phenothiazines, barbiturates,
and MAO inhibitors.
Pregnancy D - Unsafe in pregnancy
Precautions Use caution in patients diagnosed with renal or hepatic
impairment, myasthenia gravis, organic brain syndrome, or Parkinson's
disease.
Drug Category:
Serotonin reuptake inhibitors
- These agents are useful in treating hyperventilation associated
with anxiety.
Drug Name Paroxetine (Paxil)
- It is the alternate DOC. It is a potent selective inhibitor of
neuronal serotonin reuptake. It has a weak effect on norepinephrine
and dopamine neuronal reuptake.
Adult Dose 40 mg/d qd
Pediatric Dose < 18 years: Not established
Contraindications Avoid use in patients with documented
hypersensitivity to this drug or related products.
Avoid its concurrent administration with MAO inhibitors, or
administering within 14 d of discontinuing a MAO inhibitor.
Interactions Phenobarbital and phenytoin decrease the effects of this
medication. Conversely, alcohol, cimetidine, sertraline,
phenothiazines, and warfarin increase the toxicity of paroxetine.
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Use cautiously in patients with a history of seizures,
mania, renal disease, and cardiac disease.
Drug Category:
Tricyclic antidepressants
- These agents are a complex group of drugs that have central and
peripheral anticholinergic effects, as well as antianxiety effects,
and block the active reuptake of norepinephrine and serotonin.
Drug Name Doxepin (Sinequan)
- It increases the concentration of serotonin and norepinephrine in
the CNS by inhibiting their reuptake by the presynaptic neuronal
membrane. These effects are associated with a decrease in anxiety
symptoms.
Adult Dose 30-150 mg/d hs or divided bid/tid; titrate the dose to
effect
Pediatric Dose < 12 years: Not recommended
> 12 years: 25-50 mg/d hs or bid/tid; increase gradually to 100 mg/d
Contraindications Documented hypersensitivity; avoid use in patients
with urinary retention or glaucoma, and during the acute recovery
phase following MI
Interactions TCAs may enhance the effects of anticholinergic
medications.
Barbiturates may lower the serum levels of TCAs.
Charcoal can prevent TCA absorption, thereby reducing their
effectiveness or toxicity.
Cimetidine can increase TCA levels in patients taking cimetidine.
Ranitidine may be an alternative.
It can increase blood pressure to dangerous levels and can cause a
hypertensive crisis in patients receiving concurrent TCAs. Avoid
coadministration.
TCAs may increase the half-life or bioavailability of dicumarol,
possibly resulting in increased anticoagulation effects.
Disulfiram and TCA coadministration may result in acute organic brain
syndrome. The bioavailability of the antidepressant may be increased.
TCAs may antagonize the antihypertensive action of guanethidine by
inhibiting uptake into adrenergic neurons. Avoid this combination
when possible.
Haloperidol may increase serum concentrations of TCAs.
Levodopa absorption may be delayed and its bioavailabilitydecreased
by TCAs. Hypertensive episodes have also occurred.
MAOIs should not be given with or immediately following TCAs. Such
combinations can produce seizures, sweating, coma, hyperexcitability,
hyperthermia, tachycardia, tachypnea, headache, mydriasis, flushing,
confusion, hypotension, disseminated intravascular coagulation, and
death. At least 7-10 days should pass between MAOI discontinuation
and TCA institution.
Oral contraceptives inhibit the hepatic metabolism of TCAs and may
increase their plasma levels.
Phenothiazines may increase serum TCA levels by inhibiting hepatic
metabolism.
Smoking may increase the metabolic biotransformation of TCAs.
Pregnancy C - Safety for use during pregnancy has not been
established.
Precautions Perform baseline and periodic leukocyte and differential
counts and LFTs. Discontinue therapy if neutropenia is evident.
Prior to initiating large doses of TCAs and at appropriate intervals
thereafter, monitor ECG. Monitor patients with cardiovascular
disease.
Elderly patients and patients with cardiac disease or a history of
cardiac disease can develop cardiac abnormalities with TCAs.
TCAs may increase the hazards of electroconvulsive therapy.
FOLLOW-UP
Further Inpatient Care:
Inpatient care is not indicated, but many patients with chronic HVS
are admitted because their symptomatology resembles many serious
organic problems and because a simple way to confirm the diagnosis in
the ED is not available.
Further Outpatient Care:
Patients should be referred to a consultant psychiatrist,
psychologist, or family physician with expertise and interest in
managing HVS. Some physiotherapists and respiratory therapists have
extensive experience in retraining patients in proper breathing
techniques and should be consulted (if available).
In/Out Patient Meds:
Several medications, including benzodiazepines, tricyclic
antidepressants, and beta-blockers, are effective in reducing the
frequency and the severity of hyperventilation; however, these agents
require prolonged use and are best managed by a consultant on an
ongoing outpatient basis, rather than sporadic prescriptions
following an ED visit.
Complications:
Complications are related mainly to invasive procedures and
investigations (eg, angiography) or to symptoms produced indirectly
by hyperventilation (eg, injuries sustained in a fall during a
syncopal episode due to hyperventilation).
Prognosis:
Patients with chronic HVS experience multiple exacerbations
throughout their lives.
Children who experience acute hyperventilation often will continue
this pattern into adulthood.
Many patients have associated disorders (eg, agoraphobia) that may
predominate the clinical picture.
Management of these underlying disorders will affect the course of
hyperventilation.
Patients who are treated with breathing retraining, stress reduction
therapy, and various medications (eg, beta blockers, benzodiazepines,
tricyclics) experience significant reductions in the frequency and
the severity of exacerbations.
Patient Education:
Patients should have the underlying pathophysiology explained in
layman's terms and be instructed in the technique of deflating the
upper chest followed by controlled diaphragmatic breathing.
MISCELLANEOUS
Medical/Legal Pitfalls:
Hyperventilation can be a symptom of serious underlying pathology,
including pulmonary embolism, asthma and other respiratory disorders.
Particular care must be exercised when considering a diagnosis of HVS
in an elderly person or in those with existent co-morbid disease.
TEST QUESTIONS
CME Question 1:
Which of the following is most accurate with regard to acute
hyperventilation syndrome?
A: Characteristic ABG findings of respiratory alkalosis are essential
to make the diagnosis.
B: Having the patient rebreathe into a paper bag is a safe and
effective method of relieving symptoms.
C: Hypocalcemia produced by hyperventilation commonly results in
torsades des pointes.
D: It is less common than chronic hyperventilation syndrome.
E: Unilateral paresthesias do not occur with hyperventilation and
suggest a focal CNS lesion.
The correct answer is D: Acute hyperventilation syndrome is estimated
to account for only 1% of the cases. The diagnosis is clinical, and
an ABG is not required to make the diagnosis, although it may be
helpful in confusing cases. Hypocalcemia occurs, but torsades has not
been reported in association with acute hyperventilation syndrome.
Unilateral paresthesias occur in up to 10% of cases of HVS and are
usually left-sided.
CME Question 2:
All of the following statements are correct EXCEPT:
A: Benzodiazepines are effective in controlling symptoms of HVS, and
they should be prescribed routinely.
B: It is associated with obsessive-compulsive disorder, agoraphobia,
and panic disorder.
C: Once established, respiratory alkalosis can be maintained with
occasional sighing respirations.
D: Patients with chronic hyperventilation syndrome have abnormal
mechanics of breathing, using the upper thorax rather than the
diaphragm.
E: Tricyclic antidepressants are effective in decreasing the
frequency and the severity of episodes of hyperventilation.
The correct answer is A: Benzodiazepines may be necessary in a
minority of severe cases but are not prescribed routinely in the ED.
Pearl Question 1 (T/F):
Hypoxia is the most serious entities to be considered in the
differential diagnosis of hyperventilation?
The correct answer is True: 1. Hypoxia: asthma/COPD, CHF, acute MI,
pulmonary embolus, pneumothorax, pleural effusion, and
pneumoniaOthers are:2. Metabolic acidosis: (MUDPILES) especially DKA,
salicylate toxicity, alcohols, and shock
Pearl Question 2 (T/F):
ST elevation or depression may be associated with acute
hyperventilation syndrome.
The correct answer is True: Others are T wave inversion and prolonged
QT interval.
Pearl Question 3 (T/F):
Myocardial or cerebral ischemia (shift of HbO2 dissociation curve,
vasospasm may be provoked by hyperventilation?
The correct answer is True: Others are seizure and syncope.
Pearl Question 4 (T/F):
The typical ABG findings in patients with chronic hyperventilation
syndrome are chronic compensated respiratory alkalosis.
The correct answer is True: Chronic compensated respiratory
alkalosis: normal or minimally elevated pH, low pCO2, and low HCO3
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Cowley DS, Roy-Byrne PP: Hyperventilation and panic disorder. Am J
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