When Anxiety Attacks: Treating Hyperventilation and Panic
Aaron Rubin, MD; C. Mark Chassay, MD
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In Brief: The athlete who panics or hyperventilates requires immediate stabilization and assessment to rule out more serious diagnoses. Repeated attacks may indicate panic disorder, which can be treated effectively with a combination of psychological and pharmacologic therapy. Drug options include selective serotonin reuptake inhibitors, benzodiazepines, tricyclic antidepressants, and monoamine oxidase inhibitors.
Athletes may experience panic and hyperventilation attacks with little or no warning. While these are not life-threatening, rapid assessment is necessary to differentiate benign episodes from more serious events. The team physician must also be aware of treatment options for these disorders, since appropriate treatment may prevent future emergencies.
A 40-year-old male triathlete had participated in over 45 triathlons in 13 years. He was a very strong swimmer and had surfed before his triathlon career; he felt he had very strong ocean skills. Over a period of 4 years, he had three episodes in which he felt that he had "let my imagination get away from me" and began to "second-guess my ability." These episodes occurred during the swimming portion of the triathlons: With the combination of cold water and people pushing and swimming over his back, he contemplated dropping out. He felt out of control and began to hyperventilate. During these episodes, his heart pounded, and his monitor recorded heart rates up to 180 beats per minute. After waiting 2 to 3 minutes, he was able each time to talk himself out of his panic and complete the race. He was diagnosed as having panic attacks, but not panic disorder. He has continued to compete.
Athletes are often anxious before competition; such performance anxiety is not considered abnormal unless it progresses to panic attack. In hyperventilation and panic attack, the athlete typically expresses strong emotions in vivid physical terms.
Hyperventilation is defined as a higher rate of ventilation than necessary to meet the demands of the body. This leads to a decrease in the alveolar and arterial Pco2 and an increased pH in the blood and cerebrospinal fluid, or a respiratory alkalosis. Episodes are generally self-limiting, but if they last long enough, symptoms such as dizziness, blurred vision, tingling, stiff muscles, trembling, cold extremities, and shivering can occur (1). Other complaints while hyperventilating include carpopedal spasm, tetany, and anxiety (2).
The relationship between panic attack and hyperventilation has been difficult to establish. Hyperventilation was previously considered an underlying cause of panic attack. Recently, however, investigators measuring Pco2 to test directly the temporal relationship between panic and hyperventilation were able to detect decreased Pco2 during only 1 of 24 panic attacks (1). This seems to dismiss hyperventilation as a mechanism leading to panic attack.
However, hyperventilation occurs in a substantial number of panic attacks; it also causes many of the same symptoms as occur in panic attack. Nonetheless, hyperventilation is not considered a criterion for diagnosing panic attack (3).
A panic attack is a discrete period of intense fear or discomfort occurring in an unexpected way. The panic attack may arise in a situation that
For diagnostic purposes, a panic attack is defined as an episode in which at least 4 of the 13 symptoms (table 1) develop suddenly and increase in intensity within 10 minutes. Associated but nondiagnostic symptoms may also be present (table 2). Most attacks last less than 1 hour, but they may persist for several hours in rare cases. A limited-symptom attack is one of lower intensity or one in which fewer than 4 of the diagnostic symptoms are present.
Panic disorder is defined as four panic attacks in 1 month, or an attack followed by at least 1 month of persistent fear of having another attack. Not all individuals who have panic attacks go on to develop panic disorder. Many patients seek care because they feel something is wrong with their body. Reassurance, supportive therapy, including mental health counseling, and education about the normal course and triggers for an attack may prevent the progression to panic disorder.
Panic disorder has been reported in 1% to 3% of the general population (3). Thirty-four percent of college students and 20% of primary care patients have met the criteria for panic disorder at some time (4). Age at onset is typically late adolescence to mid-30s; for a smaller percentage of patients, the disorder develops in childhood or after age 45.
Differential diagnosis of panic disorder includes anxiety disorder caused by general medical conditions such as hyperthyroidism, hyperparathyroidism, pheochromocytoma, vestibular dysfunction, seizure disorders, and cardiac conditions, especially arrhythmias like supraventricular tachycardia (3). Angina and myocardial infarction may share with panic disorder the symptoms of palpitations, sweating, chest pain, nausea, and fear of dying. Appropriate history, exam, and laboratory testing should be undertaken to rapidly differentiate these serious conditions from panic disorder.
The diagnosis of panic attack may also be colored by the viewpoint of particular specialists. Cardiologists consider mitral valve prolapse, labile hypertension, hyperdynamic beta-adrenergic state, and atypical chest pain. Pulmonologists think of hyperventilation syndrome. Neurologists may be consulted to explain dizziness. Clearly, the patient benefits from the diagnosis of the underlying panic disorder.
Certain drugs can lead to substance-induced anxiety disorder, which could be confused with panic disorder. Cocaine, "crack," amphetamines, caffeine, and other stimulants can lead to panic feelings as an effect of the drug. Withdrawal from depressants (alcohol, barbiturates, marijuana) may also lead to panic attacks. In addition, anabolic steroids have been implicated in behavior changes that could be confused with panic attacks. Recognizing underlying drug use is important but difficult, and requires an index of suspicion on the part of the physician. The physician should also be aware that other anxiety disorders and psychotic disorders can resemble panic disorders.
The immediate intervention for both hyperventilation and panic attack is to stabilize these athletes by helping them relax and overcome immediate panic and anxiety. Techniques include calm reassurance and removal from the stressful situation.
The traditional treatment for hyperventilation is having the patient breathe heavily into a paper bag. The rationale is that rebreathing into the bag increases Pco2 and decreases respiratory alkalosis. This technique may be helpful as a relaxation and breathing control exercise.
Psychological treatment for panic disorders includes behavioral, cognitive, assertive, relaxation, mental imaging, and desensitization therapies (5). During counseling, the physician should discuss the stresses that precipitate their disorder, the strength of their social support, and their self-esteem level. Although exercise and sports are a healthy relaxation and coping mechanism for many, athletes often place themselves in situations that would lead to panic in many individuals. If the attacks cannot be controlled by these methods, drug therapy is indicated.
The goal of drug therapy is to prevent attacks; it can also facilitate psychological therapy. Effective drugs for treating panic disorder (table 3) (5-7) include selective serotonin reuptake inhibitors (SSRIs), high-potency benzodiazepines, tricyclic antidepressants (TCAs), and monoamine oxidase inhibitors (MAOIs) (8). In addition, low-potency benzodiazepines and beta-blockers have been used with some success.
Selective serotonin reuptake inhibitors. The newest class of medicines to be found effective in the treatment of panic disorder and attacks is the SSRIs (fluoxetine, fluvoxamine, paroxetine, and sertraline) (6). The advantages of SSRIs include a lack of dependency and safer side effect profiles than other drug classes used in treating panic disorder.
Benzodiazepines. High-potency benzodiazepines such as alprazolam have been effective in treating panic disorder (6), particularly the short-term management of panic attacks. Patients can, however, become physically dependent on benzodiazepines within 2 weeks, making the potential for abuse the primary concern with this class of agents. Originally, low-potency benzodiazepines were not thought to aid in the treatment of panic disorder, but recent studies have shown that this subclass can also be helpful (9). Because of the slower onset of therapeutic effect, low-potency benzodiazepines have slightly less abuse potential.
The major side effects of all benzodiazepines are sedation and psychomotor impairment; additional side effects include fatigue, ataxia, slurred speech, and amnesia. Physicians are somewhat hesitant to prescribe higher and more frequent doses for panic attacks, but many patients with debilitating symptoms may need larger doses for adequate therapeutic blockade. However, a higher dose in the athlete can increase psychomotor impairment, diminishing an athlete's performance.
Tricyclic antidepressants. Traditionally, TCAs have been the first pharmacologic treatment for panic disorder. Imipramine has been most widely used, followed by the less studied TCAs such as amitriptyline, desipramine, and nortriptyline (6,10). Clomipramine, a recently developed TCA approved for obsessive-compulsive disorders, may prove effective for panic disorder (9). The major advantage of this class of medicines is its lack of habituation over prolonged use.
However, TCAs exhibit antihistaminic, anticholinergic, sedative, and orthostatic hypotensive side effects, as well as increased risk for heat illness (5). These numerous side effects, particularly the slowing of cardiac conduction time, are potentially dangerous in the athlete. All tricyclics can slow both atrial and ventricular depolarization and therefore cause increased PR, QRS, and QT intervals as well as decreased T wave amplitude (10). This slow post-AV nodal conduction (similar to that caused by group I antiarrhythmic drugs) can become a bundle branch block in well-conditioned athletes or a complete heart block in patients with preexisting bundle branch blocks.
Monoamine oxidase inhibitors. MAOIs are effective in treating panic disorder, but required lifestyle changes and potentially lethal drug interactions make this class of drugs less desirable (11). Their use should be limited to treating disease resistant to other medications. To avoid a sympathomimetic crisis characterized by headache, diaphoresis, mydriasis, hypertension, neuromuscular excitation, and cardiac dysrhythmia, patients on MAOIs must forgo foods that contain high amounts of tyramine, such as cheese. The need for a sudden change in diet can cause even more stress for the patient (12).
Beta-blockers. Beta-blockers are not first-line agents. The beta-blocker propranolol is mostly used to treat symptoms that are adrenergically mediated. If used in high doses to diminish symptoms or quell stage fright, beta-blockers should be tapered to prevent a rebound effect (13).
Maintenance and tapering. Once an effective dosage of a drug without unacceptable side effects is reached and the patient's panic attacks have ceased, the patient should be kept on maintenance therapy for 6 to 12 months. Then, drug tapering is recommended, though SSRIs do not generally require this. Benzodiazepines are more difficult to taper because of a higher reported rebound of panic attacks (14) and occasionally a transient, mild-to-moderate withdrawal syndrome. Tapering benzodiazepines quite slowly over at least 8 weeks is recommended (5). The addition of carbamazepine or TCAs to benzodiazepines can decrease rebound panic attacks and even help to rapidly taper the regimen over 4 to 7 days (10).
Panic disorder is a recurring condition often precipitated by stressful life events. Between 30% and 90% of patients will relapse within 1 year (10). Because psychotherapy improves self-esteem and coping mechanisms, combining psychotherapy and medication can help diminish recurrence. With careful attention from their primary care physician, athletes suffering from panic disorder can return to play with confidence—and without anxiety.
Dr Rubin is the clinical director and Dr Chassay is a graduate of the Kaiser Permanente/SPORT fellowship program in Fontana, California. Dr Rubin is a fellow of the American Academy of Family Physicians and the American College of Sports Medicine. Dr Chassay is team physician for women's athletics at the University of Texas at Austin. Dr Howe is a team physician at Western Washington University in Bellingham, Washington, and an editorial board member of The Physician and Sportsmedicine. Address correspondence to Aaron Rubin, MD, Kaiser Permanente Family Medicine Residency Program, 9961 Sierra Ave, Fontana, CA 92335; address e-mail to [email protected].
The authors thank Gerry Vuchetich for his photographic assistance.