AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

An understanding of panic disorder (PD) is important for emergency physicians because patients with PD frequently present to the emergency department (ED) with various somatic complaints. As many as 70% of persons with PD are unrecognized as having this condition, and few individuals with PD are referred to mental health professionals.

Persons with PD have a 4-fold higher risk of alcohol abuse and an 18-fold higher risk of suicide than the general population (although some studies suggest that panic disorder itself is not a risk factor for suicide in the absence of other risks, such as affective disorders, substance abuse, eating disorders, and personality disorders). Serious medical problems, such as asthma or cardiac dysrhythmia, or metabolic disturbances, such as hypoglycemia, hypoxia, and thyroid storm, can mimic panic attack.

Following exclusion of somatic disease and other psychiatric disorders, confirmation of the diagnosis with a brief mental status screening examination and initiation of appropriate treatment and referral is time- and cost-effective in these patients who have high rates of medical resource use.

Pathophysiology

PD appears to be a genetically inherited neurochemical dysfunction that may involve autonomic imbalance; allelic polymorphism of the catechol-O-methyltransferase (COMT) gene; increased adenosine receptor function; increased cortisol; diminished benzodiazepine receptor function; and disturbances in serotonin, norepinephrine, gamma-aminobutyric acid, dopamine, cholecystokinin, and interleukin-1-beta. Some theorize that PD may represent a state of chronic hyperventilation and carbon dioxide receptor hypersensitivity. Some epileptic patients have panic as a manifestation of their seizures.

Positron emission tomography (PET) scanning has demonstrated increased flow in the right parahippocampal region and reduced serotonin type 1A receptor binding in the anterior and posterior cingulate and raphe of patients with PD. Magnetic resonance imaging (MRI) has demonstrated smaller temporal lobe volume despite normal hippocampal volume in these patients.

In experimental settings, symptoms can be elicited in people with PD by hyperventilation, inhalation of carbon dioxide, caffeine consumption, or intravenous infusions of sodium lactate, cholecystokinin, isoproterenol, or flumazenil.

The cognitive theory regarding panic is that these patients have a heightened sensitivity to internal autonomic cues (eg, tachycardia).

PD is associated with depression, obsessive-compulsive disorder, specific phobias, social phobia, agoraphobia (ie, fear of being unsafe in public settings), irritable bowel syndrome, migraine, mitral valve prolapse, and alcohol and drug abuse. Individuals with PD also have lower oxygen consumption and exercise tolerance than the general population. They also have reduced heart rate variability and increased QT variability on electrocardiography and may have a higher risk of cardiovascular disease and sudden death.

Frequency

United States

PD has an approximate 1-5% prevalence in the population.

International

Prevalence is similar to that in the United States.

Mortality/Morbidity

• PD can lead to a significant hindrance in lifestyle (many people with agoraphobia are unable to travel alone or be in crowds, malls, or on public transportation), unemployment, depression, substance abuse, and suicide.
• PD is present in 30% of patients with chest pain and normal findings on angiography, 5-40% of persons with asthma, 15% of patients with headache, 20% of patients with epilepsy, 8-15% of individuals in alcohol treatment programs, and 10% of patients in primary care settings.
• PD may be associated with a higher risk of cardiovascular disease and sudden death.
• A variant of PD unrelated to fear (nonfearful panic disorder [NFPD]) is associated with high rates medical resource use (32-41% of patients with PD seeking treatment for chest pain) and poor prognosis.

Sex

Prevalence is higher in females than in males, with a female-to-male ratio of approximately 2:1.

• Panic is more common in women who have never been pregnant and during the postpartum period, but it is less common during pregnancy.

Age

• Although panic can occur in people at any age, the average age of onset, as with most anxiety disorders, is in the third decade of life, and it usually occurs between the ages of 18 and 45 years.
• PD has a bimodal age of onset, with patients with late-onset PD having less mental health use, lower comorbidity and hypochondriasis, and better coping behavior.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• Patients who experience panic attack report a spontaneous sudden onset of fear or discomfort, typically reaching a peak within 10 minutes.
• Attacks are associated with a constellation of systemic symptoms, including the following (4 or more of these are needed for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition [DSM-IV] criteria):
• • Palpitations, pounding heart, or accelerated heart rate
  • Sweating
  • Trembling or shaking
  • Shortness of breath or feeling of smothering
  • Choking sensation
  • Chest pain or discomfort
  • Nausea or abdominal distress
  • Feeling dizzy, unsteady, lightheaded, or faint
  • Derealization (ie, feeling of unreality) or depersonalization (ie, being detached from oneself)
  • Fear of losing control or going crazy
  • Fear of dying
  • Paresthesias (ie, numbness or tingling sensations)
  • Chills or hot flashes
• During the episode, patients have the urge to flee or escape and have a sense of impending doom (as though they are dying from a heart attack or suffocation).
• Other symptoms may include headache, cold hands, diarrhea, insomnia, fatigue, intrusive thoughts, and ruminations.
• Patients with PD have recurring episodes of panic, with the fear of recurrent attack resulting in significant behavioral changes (eg, avoiding situations or locations) and worry about the implications of the attack or its consequences (eg, losing control, going crazy, dying).
• PD may result in changes in personality traits, characterized by the patient becoming more passive, dependent, or withdrawn.
• DSM-IV criteria include 4 or more attacks in a 4-week period or 1 or more attacks followed by at least 1 month of fear of another.
• Agoraphobia, present in 30% of persons with PD, establishes the diagnosis.
• Assess precipitating events, suicidal ideation or plan, phobias, agoraphobia, and obsessive-compulsive behavior.
• Exclude involvement of alcohol, illicit drugs (eg, cocaine, amphetamine, phencyclidine, amyl nitrate, lysergic acid diethylamide [LSD], yohimbine, 3,4-methylenedioxymethamphetamine [MDMA, ecstasy]), cannabis, and medications (eg, caffeine, theophylline, sympathomimetics, anticholinergics).
• Consider symptomatology of other medical disorders, which may manifest with anxiety as a primary symptom.
• • Angina and myocardial infarction (eg, dyspnea, chest pain, palpitations, diaphoresis)
  • Cardiac dysrhythmias (eg, palpitations, dyspnea, syncope)
  • Mitral valve prolapse
  • Pulmonary embolus (eg, dyspnea, hyperpnea, chest pain)
  • Asthma (eg, dyspnea, wheezing)
  • Hyperthyroidism (eg, palpitations, diaphoresis, tachycardia, heat intolerance)
  • Hypoglycemia
  • Pheochromocytoma (eg, headache, diaphoresis, hypertension)
  • Hypoparathyroidism (eg, muscle cramps, paresthesias)
  • Transient ischemic attacks (TIAs)
  • Seizure disorders
• Consider other mental illnesses that may result in panic attacks, including schizophrenia, manic disorder, depressive disorder, posttraumatic stress disorder, phobic disorders, and somatization disorder.
• Assess family history of panic or other psychiatric illness.

Physical

• The patient may have an anxious appearance.
• Tachycardia and tachypnea are common; blood pressure and temperature may be within the reference range.
• Cool clammy skin may be observed.
• Hyperventilation may be difficult to detect by observing breathing because respiratory rate and tidal volume may appear normal.
• • Patients may have frequent sighs or difficulty with breath holding.
  • Reproduction of symptoms with overbreathing is unreliable.
  • Chvostek sign, Trousseau sign, or overt carpopedal spasm may be present.
• Mental status screening is essential for diagnosis. Standardized examinations include the following:
• • Primary Care Evaluation of Mental Disorders (PRIME-MD)
  • Mobility Inventory for Agoraphobia (MIA)
  • The Agoraphobia Cognitions Questionnaire (ACA)
  • The Body Sensations Questionnaire (BSQ)
• The remaining examination findings are typically normal in PD. However, remember that PD is largely a diagnosis of exclusion, and attention should be focused on the exclusion of other disorders.

Causes

Triggers of panic can include the following:

• Injury (eg, accidents, surgery)
• Illness
• Interpersonal conflict or loss
• Use of cannabis (can be associated with panic attacks, perhaps because of breath-holding)
• Use of stimulants, such as caffeine, decongestants, cocaine, and sympathomimetics (eg, amphetamine, MDMA)
• Certain settings, such as stores and public transportation (especially in patients with agoraphobia)

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Pheochromocytoma
Huntington chorea

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Arterial blood gas analysis is useful in confirming hyperventilation (respiratory alkalosis) and excluding hypoxemia or metabolic acidosis. The presence of hypoxemia with hypocapnia or a widened alveolar-arterial (A-a) gradient should increase the suspicion of pulmonary embolus.
• Electrolyte analysis is unnecessary, although several abnormalities may be present in the setting of hyperventilation.
• • Serum phosphorus and ionized calcium may be diminished in patients with hyperventilation and carpopedal spasm, Chvostek sign, or Trousseau sign.
  • The serum calcium level may be within the reference range.
• Other laboratory studies may be necessary to exclude other medical disorders, as follows:
• • Serum electrolytes to exclude hypokalemia and acidosis
  • Serum glucose to exclude hypoglycemia
  • Cardiac enzymes in patients suspected of acute coronary syndromes
  • Serum hemoglobin in patients with near-syncope
  • Thyroid-stimulating hormone (TSH) in patients suspected of hyperthyroidism
  • Urine toxicology screen for amphetamines, cocaine, and phencyclidine in patients suspected of intoxication
  • D-dimer assay to exclude pulmonary embolism

Imaging Studies

• Chest radiography is useful in excluding other causes of dyspnea with chest pain.

Other Tests

• Room air pulse oximetry values are within the reference range or at the upper limit of the reference range.
• End-tidal capnography values are typically less than 30 torr during hyperventilation.
• Electrocardiography (ECG) should be inspected for signs of ventricular preexcitation (short PR and delta wave), long QT interval in patients with palpitations, and for ischemia, infarction, or pericarditis patterns in patients with chest pain.
• Outpatient Holter monitoring or transtelephonic event recording is rarely necessary but should be considered in patients with palpitations associated with syncope or near-syncope.
• Patients who may be at risk for pulmonary embolus require appropriate testing (eg, ventilation-perfusion [V/Q] scanning, duplex Doppler/ultrasonography, spiral CT scanning, pulmonary angiography).

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Prehospital Care

• Supplemental oxygen and cardiac monitoring are recommended for patients experiencing dyspnea or chest pain.

Emergency Department Care

• Patients with chest pain, dyspnea, palpitations, or near-syncope should be placed on oxygen and in a supine or Fowler position; monitor them with pulse oximetry, ECG, and frequent vital signs (including one set of orthostatic vital signs, when possible).
• Patients with PD may require frequent reassurance and explanation. Many may benefit from social service intervention.
• A major component of therapy involves education that the symptoms are neither from a serious medical condition nor from a mental deficiency but rather from a chemical imbalance in the fight or flight response. This alone may allow a 30-50% placebo response rate.
• The ED staff must listen effectively and remain empathic and nonargumentative. Statements made by healthcare staff such as, "It's nothing serious," and "It's related to stress," are frequently misinterpreted as implying lack of understanding and concern.
• Intravenous medication (eg, Ativan 0.5 mg IV q20min) may be necessary in patients with PD who, as a result of subsequent poor impulse control, pose a risk to themselves or to those around them.
• Patients with PD are probably best served by referral to a psychiatrist, before beginning anxiolytic medications, because the psychiatrist can establish a constructive rapport with them and follow their needs on a long-term basis.
• • Institution of treatment for PD in the ED is appropriate in a very limited subset of patients with PD who are very motivated, cooperative, possess an understanding of the psychological nature of their disorder, and whose symptomatology is elicited as a response to a temporary stress.
  • In such cases, pharmacotherapy with an oral benzodiazepine for no longer than 1 week may be appropriate.

Consultations

• Consult a cardiologist for patients with abnormal ECG findings, ventricular dysrhythmia, abnormal cardiac examination, or risk factors for ischemic heart disease.
• Consult a chemical dependence treatment specialist in cases of significant intoxication or withdrawal.
• Refer all patients with PD for psychiatric or mental health follow-up care and to support groups.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Aside from IV medications required to treat acute anxiety states in the ED, the use of pharmacotherapy for patients with PD should, in most instances, be deferred to the primary physician or psychiatrist who is monitoring the patient long term. Benzodiazepines are optimal for ED and outpatient abortive therapy because of their immediate antipanic effects. Selective serotonin reuptake inhibitors (SSRIs) are becoming first-line preventive agents in PD because of a better safety profile.

Tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs) are used in refractory cases. Coexisting disorders may influence medication choice (eg, MAOIs, clonazepam, or SSRIs for social phobia; SSRIs or Anafranil for obsessive-compulsive disorder; TCAs for depression). Beta-blockers, clonidine, and buspirone, although promising in theory, have had poor efficacy in PD. Newer agents such as bupropion (Wellbutrin), nefazodone (Serzone), mirtazapine (Remeron), and the serotonin norepinephrine reuptake inhibitors (SNRIs) venlafaxine (Effexor) and duloxetine (Cymbalta) have not been FDA approved for use in PD.

Olanzapine (Zyprexa) may be effective in combination with an SSRI in SSRI-resistant PD cases.

Drug Category: Benzodiazepines

These should not be prescribed to patients who have a history of alcohol and/or drug abuse or emotional dependence. Most common side effects are sedation, somnolence, memory impairment, and poor coordination.

Alprazolam has been studied best and is an effective agent with a rapid (20-min) onset and short (12- to 15-h) half-life. An extended-release formulation is now available for patients on long-term therapy or during the initial titrating phase of an SSRI or TCA. Lorazepam has also been used but is more habituating and results in depression in some patients. Some psychiatrists think that the longer-acting benzodiazepines (eg, diazepam, clonazepam) also have advantages.

Benzodiazepine dependence occurs in as many as 30% of long-term users (>8 wk). Many think that after 6 months they should be slowly tapered (over several weeks to months) to avoid withdrawal and precipitating panic. Withdrawal symptoms include anxiety, insomnia, tremor, impaired concentration, lethargy, dysphoria, headaches, gastrointestinal disturbances, dizziness, photophobia, and hyperacusis. Concomitant therapy with TCAs, SSRIs, antiepileptics, or propranolol may be beneficial, although the withdrawal symptoms do not predict success of eventual discontinuation.

Drug Name	Diazepam (Valium)
Description	Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Individualize dosage and increase cautiously to avoid adverse effects.
Adult Dose	2-10 mg PO bid/qid
Pediatric Dose	<6 months: Not recommended >6 months: 1-2.5 mg PO tid/qid initially, increase gradually prn and as tolerated
Contraindications	Documented hypersensitivity; narrow-angle glaucoma
Interactions	Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohol, and MAOIs
Pregnancy	D - Unsafe in pregnancy
Precautions	Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)

Drug Category: Triazolopyridine agents

The mechanism of antidepressant action of this class of drugs is not fully understood in humans. They are not MAOIs and, unlike amphetamine-type drugs, do not stimulate the CNS.

Drug Category: Selective serotonin reuptake inhibitors

May take from 2-6 weeks to become effective and can result in initial anxiogenic effects, especially with higher doses. Therefore, initial doses should be lower than doses used to treat depression, and they should be titrated up over several weeks. Patients may require concomitant therapy with benzodiazepines for the first several weeks. SSRIs are uniquely effective in PD coexisting with obsessive-compulsive disorder. Sertraline (Zoloft) may be better tolerated than paroxetine (Paxil). Fluvoxamine (Luvox), fluoxetine (Prozac), citalopram (Celexa), and escitalopram (Lexapro) are also effective. Common adverse effects include gastrointestinal problems, headache, dry mouth, insomnia, nervousness, agitation, and difficulty reaching orgasm.

Paroxetine (Paxil) may increase the suicide risk in children and adolescents with major depressive disorder. If paroxetine is discontinued, as with all SSRIs, tapering should occur over several weeks.

Drug Name	Sertraline (Zoloft)
Description	Selectively inhibits presynaptic serotonin reuptake. Also has a weak inhibitory effect on norepinephrine and dopamine neuronal reuptake.
Adult Dose	25 mg PO qd; increase to 50 mg PO qd after 1 wk
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	Increases toxicity of MAOIs, diazepam, tolbutamide, and warfarin
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Caution in preexisting seizure disorders and in those that have experienced a recent MI, unstable heart disease, and hepatic or renal impairment

Drug Name	Fluvoxamine (Luvox)
Description	Potent selective inhibitor of neuronal serotonin reuptake. Does not significantly bind to alpha-adrenergic, histamine, or cholinergic receptors and, thus, has fewer adverse effects than tricyclic antidepressants.
Adult Dose	50 mg/dose PO hs initially; increase dose in 50-mg increments q4-7d, as tolerated, until maximum therapeutic benefit achieved; divide total daily dose into 2 doses; if doses are unequal, administer larger dose hs; not to exceed 300 mg/d
Pediatric Dose	<8 years: Not established 8-17 years: 25 mg PO initially as single daily dose hs; increase dose in 25-mg increments PO q4-7d as tolerated, until maximum therapeutic benefit achieved; divide total daily doses >50 mg into 2 doses; if not equal, administer larger dose hs; not to exceed 200 mg/d
Contraindications	Documented hypersensitivity; current use of MAOIs or use in previous 2 wk
Interactions	Risk of a hypertensive crisis increases with coadministration with MAOIs; potentiates effect of triazolam and alprazolam, and thus, when taking them concurrently, dose should be reduced by at least 50%; also reduce the dose of theophylline by one third and monitor plasma levels if taking concurrently with fluvoxamine; alcohol, cimetidine, sertraline, phenothiazines, and warfarin increase toxicity of fluvoxamine
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in liver dysfunction, cardiovascular disease, history of seizures, or suicidal tendencies

Drug Name	Fluoxetine (Prozac)
Description	Selectively inhibits presynaptic serotonin reuptake with minimal or no effect in the reuptake of norepinephrine or dopamine.
Adult Dose	5-10 mg/d PO qam; increase after several wk by 20 mg/d; not to exceed 80 mg/d
Pediatric Dose	<18 years: Not established; initial doses of 20 mg/d in children 6-14 y have been used >18 years: Administer as in adults
Contraindications	Documented hypersensitivity; use of MAOIs or use in the last 2 wk
Interactions	Increases toxicity of diazepam and trazodone by decreasing clearance; also increases toxicity of MAOIs and highly protein bound drugs
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Caution in hepatic impairment and history of seizures; MAOIs should be discontinued at least 14 d before initiating therapy

Drug Category: Tricyclic antidepressants

These agents have the advantages of once daily dosing, low risk of dependence, and no dietary restrictions. However, they are discontinued in 35% of cases because of adverse effects, such as blurred vision, dry mouth, dizziness, weight gain, gastrointestinal disturbance, agitation, insomnia, headache, and decreased libido or ability to orgasm. TCAs must be started in low doses to avoid amphetaminelike stimulation and can require up to 8-12 weeks for treatment response.

Drug Name	Desipramine (Norpramin)
Description	May increase synaptic concentration of norepinephrine in CNS by inhibiting reuptake by presynaptic neuronal membrane. May have effects in the desensitization of adenyl cyclase, down-regulation of beta-adrenergic receptors, and down-regulation or serotonin receptors.
Adult Dose	10-250 mg/d PO
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; narrow-angle glaucoma; recent postmyocardial infarction; current use of MAOIs or fluoxetine or use in the previous 2 wk
Interactions	Decreases antihypertensive effects of clonidine but increases effects of sympathomimetics and benzodiazepines; effects increase with phenytoin, carbamazepine, and barbiturates
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in cardiovascular disease, conduction disturbances, seizure disorders, urinary retention, hyperthyroidism, and patients receiving thyroid replacement

Drug Name	Clomipramine (Anafranil)
Description	Affects serotonin uptake while it affects norepinephrine uptake when converted into its metabolite desmethylclomipramine.
Adult Dose	25-100 mg/d PO
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; recent MI; use of MAOIs within 14 d
Interactions	Barbiturates, phenytoin, and carbamazepine decrease effects; increases effects of anticholinergics, sympathomimetics, alcohol, and CNS depressants; toxicity of MAOIs increases
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in severe cardiopulmonary or renal impairment and in persons unable to metabolize sorbitol

Drug Category: Monoamine oxidase inhibitors

They are effective in patients with social phobia. Advantages of MAOIs are low risk of dependence and less anticholinergic effect than TCAs. Disadvantages are the higher number of adverse effects, including sexual difficulty, hypotension, weight gain, dry mouth, tachycardia, insomnia, drowsiness, headache, weakness, and constipation.

Drug Name	Tranylcypromine (Parnate)
Description	Also effective in PD. Binds irreversibly to MAO, thereby reducing monoamine breakdown and enhancing synaptic availability.
Adult Dose	30-60 mg/d PO
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; pheochromocytoma; hepatic or renal disease; cardiovascular disease; cerebrovascular defect
Interactions	Increases effects and/or toxicity of barbiturates and CNS depressants; toxicity increases when taken concurrently with fluoxetine, disulfiram, levodopa, sympathomimetics, and tyramine-containing foods
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in hyperactive or hyperexcitable disorders and glaucoma

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Inpatient treatment is necessary in patients with suicidal ideation and plan, serious alcohol or sedative withdrawal symptoms, or when the differential includes other medical disorders that warrant admission (eg, unstable angina, acute myocardial ischemia).
  

Further Outpatient Care

• Follow-up care by a chemical dependence treatment specialist is recommended when indicated.
• Patients with ventricular dysrhythmias, abnormal findings on ECG, abnormal findings on cardiac examination, or significant risk factors for heart disease should be referred to a cardiologist.
• All patients with PD should be referred to a psychiatrist, psychologist, or other mental health professional. Free information is available to patients and physicians from the National Institute of Mental Health (NIMH) by calling 1-800-64-PANIC or by writing to the following address:

  NIMH
  Room 7C-02
  5600 Fishers Ln
  Rockville, MD 20857

• Cognitive behavioral therapy (CBT), with or without pharmacotherapy, is the treatment of choice, and it should be considered for all patients. CBT has higher efficacy and lower cost, dropout rates, and relapse rates than pharmacological treatments.
• • Patients meet with therapists for 1-3 hours per week for at least 8-12 weeks.
  • Cognitive restructuring involves substituting positive thoughts (eg, patients can tell themselves that they are only feeling a little uneasiness or that their feelings will soon be gone) for the maladaptive thoughts that accompany panic (eg, feeling that they are going to die or are having a heart attack).
  • Behavioral therapy involves various relaxation techniques and breathing retraining. Guided imagery and hypnotic suggestion may also be beneficial.
  • Capnometry feedback-assisted breathing training therapy can be used to prevent hypocapnia and stabilize the respiratory rate.
  • Interoceptive exposure involves encouraging patients to induce internal sensations (eg, dizziness, increased heart rate, lightheadedness) by spinning, exercising, or rapid breathing and to interpret these as normal bodily sensations.
  • Instructions for finding a cognitive behavioral therapist can be found at Paniccure.com.

In/Out Patient Meds

• Although pharmacotherapy for PD should generally be deferred to the follow-up psychiatrist, in a very limited subset of patients with PD in the ED, alprazolam (Xanax) as an abortive and/or prophylactic agent may be instituted for a brief course of treatment (generally no longer than 1 wk.)
• Most patients are started on long-term (eg, 6 mo) therapy with SSRIs, TCAs, or MAOIs after consultation with their primary physician or psychiatrist.

Transfer

• Transfer to an acute psychiatric facility may be necessary for suicidal or homicidal patients.

Deterrence/Prevention

• CBT with cognitive restructuring, relaxation techniques, breathing exercises, hypnotic suggestion, and interoceptive exposure may prevent recurrence.
• Pharmacotherapy and dietary modification with inositol supplementation and use of herbal preparations (eg, valerian) may prevent recurrence.
• Exercise is effective in preventing panic recurrence.
• Patients who have give a high importance to religion and religious practices have improved panic symptoms and fewer recurrences.
• Internet-based cognitive behavioral therapy and virtual reality exposure therapy are promising.

Complications

• Patients with PD are reluctant to believe their symptoms are not life threatening and have a high rate of ED use if education, treatment, and follow-up care are incomplete.
• Because of a reluctance to use medications (related to a fear of losing control), patients with PD are frequently noncompliant. Patients with PD also have a 4-fold increased risk of medication adverse effects.
• Benzodiazepine abuse is rare. It is less likely to occur in patients without history of chemical dependence or emotional dependence.
• • Benzodiazepine abuse is suggested by escalating dose consumption over time.
  • Because PD is usually a chronic disorder, sole reliance on habituating drugs (benzodiazepines) is discouraged.
  • Benzodiazepine dependence can occur in 30% of patients on long-term therapy longer than 8 weeks.
  • Benzodiazepine withdrawal can precipitate panic. The primary physician should gradually taper doses over several weeks or months.
• Individuals with PD have a suicide rate 18 times higher than the population.
• The rate of substance abuse (especially stimulants, cocaine, and hallucinogens) in persons with PD is 7-28%, a risk 4-14 times greater than that of the population.
• Pregnant mothers with PD are more likely to have infants of smaller birth weight for gestational age.
• Panic patients are nearly twice as likely to develop coronary artery disease, and those with known coronary disease can experience myocardial ischemia during their panic episodes.

Prognosis

• Long-term prognosis is usually good, although the risk of coronary artery disease is nearly doubled. In patients with coronary disease, panic can induce myocardial ischemia. The risk of sudden death may also theoretically be increased due to reduced heart rate variability and increased QT interval variability.
• Appropriate pharmacological therapy and cognitive-behavioral therapy, individually or in combination, are effective in more than 85% of cases.

Patient Education

• Information regarding PD and support groups can be obtained from the NIMH (see Further Outpatient Care).
• Advise patients with PD to avoid nicotine, sympathomimetic or anticholinergic drugs, caffeine, and alcohol.
• Dietary modification with inositol supplementation or herbal preparations (eg, valerian) may be effective in preventing recurrence. Such herbal supplementation should be deferred until after the patient has discussed it with the psychiatrist or primary care provider that is responsible for the follow-up and long-term care of the patient.
• For excellent patient education resources, visit eMedicine's Mental Health and Behavior Center and Anxiety Center. Also, see eMedicine's patient education articles Panic Attacks, Anxiety, and Palpitations.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Persons with PD are no less likely (and perhaps even twice as likely) to have coronary artery disease than the general population.
• Approximately 44% of ED patients with PD have a history of coronary disease.
• Exclude acute coronary syndromes in patients with risk factors, history, and ECG findings before labeling the event as panic.
• Patients with supraventricular tachycardia have the potential to be misclassified as having PD (in more 50% of cases), and PD may be missed if event monitoring is not obtained.
• As many as 10-20% of patients with PD have had a suicide attempt.
• As many as 7-28% of patients with PD have a history of substance abuse.
• Many of the symptoms of an anxiety attack correspond with symptomatology found in life-threatening medical disorders (eg, pulmonary embolus). Remember that panic disorder is a diagnosis of exclusion.
• Patients with PD are twice as likely as the population to use alternative therapies. Use of dietary supplements (eg, herbs) should be discussed to avoid drug interactions.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Bakker A, van Balkom AJ, van Dyck R. Selective serotonin reuptake inhibitors in the treatment of panic disorder and agoraphobia. Int Clin Psychopharmacol. Aug 2000;15 Suppl 2:S25-30. [Medline].
• Baldwin DS, Birtwistle J. The side effect burden associated with drug treatment of panic disorder. J Clin Psychiatry. 1998;59 Suppl 8:39-44; discussion 45-6. [Medline].
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Article Last Updated: Feb 7, 2007