Case Reports Panic Disorder Associated with Pennanent Pacemaker Implantation JEROME
C.
PETERS, D.O., MARTIN ALPERT. M.D.
BERNARD D. BEITMAN. M.D., MATHEW KUSHNER. M.S. RICHARD WEBEL, M.D.
anic attacks are associated with at least four of the following symptoms: shortness of breath, chest pain, palpitations, dizziness, nausea or abdominal distress, tingling or numbness, unexplained flushing or chilling, trembling, choking, sweating, feelings of depersonalization, the fear of dying, and the fear of going crazy. Panic disorder is diagnosed when the patient experiences at least one panic attack per week for three consecutive weeks. Patients experiencing panic attacks may develop apprehension based on the fear of having an anticipatory anxiety attack which mayor may not impair social or occupational functioning. I The pacemaker syndrome consists of a constellation of symptoms attributable to permanent ventricular pacemaker activation. These include postural hypotension, dizziness, syncope or faintness, breathlessness, chest pain, neck pulsations, generalized lassitude, and weakness. 2 These symptoms are attributable to diminished cardiac output related to a loss of atrioventricular synchrony (atrioventricular dissociation or I: I retrograde ventriculoatrial conduction) or to an absence of atrial activation. Low cardiac output leads to lightheadedness, lethargy with hypotension-inducing apprehension, diaphoresis, and sometimes shock. 3 Such patients also may describe palpitations due to the aforementioned conduction disorders. 4 The patient described in this report originally was misdiagnosed as having the pacemaker syndrome and later was found to have panic disorder, which successfully responded to pharmacotherapy. This case underscores the diffi-
P
VOLUME 31 ' NUMBER 3 • SUMMER 1990
culty of differentiating panic disorder from the pacemaker syndrome and adds evidence to the theory that panic may be triggered by a phobic reaction to real or imagined unpleasant internal bodily sensations. s
Case Report BP was a 29-year-old woman who was hospitalized for evaluation of partial or temporary loss of consciousness. During the month prior to hospitalization, she experienced four such syncopal episodes. These episodes were preceded by a 10- to IS-second period of weakness, diaphoresis, and light-headedness, lasting less than one minute each and followed by a five- to IO-minute period of weakness and giddiness. During the six-month period prior to hospitalization, the patient had experienced one to two episodes per week. Prior to this she had experienced similar episodes three to four times per year for a period of five years, but she had not sought medical attention for these spells. The patient was unable to identify specific exacerbating factors for her syncopal and presyncopal episodes. A physical examination (including postural pulse and blood pressure measurements) showed nothing abnormal except for carotid sinus pressure which variably produced threeReceived January 16. 1989; revised July 5. 1989; accepted July 21. 1989. From the Depanment of Psychiatry and the Division of Cardiology. University Hospital. University of Missouri-Columbia. Columbia. Missouri. Address reprint requests to Dr. Peters. Department of Psychiatry. University of Missouri Hospital and Clinics. # 1 Hospital Drive. Columbia. MO 65201. Copyright © 1990 The Academy of Psychosomatic Medicine.
345
Case Reports
to five-second periods of asystole and sinus bradycardia (30-50 beats per minute) with marked hypotension and reproduction of symptoms. Her resting electrocardiogram. chest x-ray. 24-hour ambulatory electrocardiogram. treadmill exercise test. and echocardiogram (M-mode and two-dimensional) were normal. Cardiac electrophysiology studies including sinus node function tests. a His' bundle electrogram. and programmed stimulation (atrial and ventricular) were also normal. On the basis of these findings. she was diagnosed as having autonomic hyperactivity with secondary carotid sinus hypersensitivity (cardioinhibitory and vasodepressor forms). A Medtronic 7000A unipolar ventricular demand pacemaker was implanted via the transvenous route. Over the ensuing four months she developed several complications related to pacemaker implantation. After being asymptomatic for one month. she again developed episodes of faintness. Pacemaker evaluation demonstrated a failure to maintain a paced heart rate due to electrode malposition. Repositioning of the electrode in the right ventricular apex resulted in normal pacing and sensing. One month later a pacemaker evaluation showed a failure to sense. and attempts to attain appropriate sensing thresholds by external reprogramming and repositioning of the electrode were unsuccessful. Shonly thereafter. the ventricular demand pacemaker and transvenous electrode were removed. and she subsequently underwent operative attachment of electrodes and implantation of a Medtronic 7000A ventricular demand pacemaker via the epicardial route. Thereafter. the syncopal and presyncopal episodes. as described above. abated. One month later she developed precordial pleuritic chest pain associated with a pericardial friction rub and was diagnosed as having postpericardiotomy pericarditis. Her symptoms resolved over the ensuing month following the initiation of oral ibuprofen. Shonly after the resolution of pericarditis. the patient developed spells that were qualitatively different from those experienced prior to pacemaker implantation. These spells. which typically lasted 10 to 30 minutes. were characterized by palpitations, fullness in the anterior chest, dizziness. paresthesias in the hands and feet. rapid breathing. diaphoresis. and a feeling of impending doom. Because of the serious complications associated with pacemaker implantation. the patient became quite concerned about pacemaker function. She eventually became convinced that her new spells were related directly to pacemaker activation. At this point her physicians were 346
considering the diagnosis of pacemaker syndrome as an explanation for her symptoms. To funher clarify this issue, a 24-hour ambulatory Holter monitoring was repeated. during which time the patient had three symptomatic episodes as described above. The underlying cardiac rhythm was predominantly of sinus origin with minimal rate changes and no sinus arrhythmia. There were brief periods of paced rhythm with normal capture and sensing. There were neither premature beats nor tachyarrhythmias. She remained in normal sinus rhythm during the symptomatic episodes. with rates ranging from 75 to 85 beats per minute. As a result of these spells. and despite a lack of correlation of symptoms with pacemaker activation or dysfunction, the patient entered into self-imposed seclusion in her home. fearing an attack in public. Inasmuch as no organic cause for her spells could be identified. she was referred for psychiatric evaluation. On evaluation the patient met the criteria of DSM-III-R for panic disorder with agoraphobia. Mental status evaluation demonstrated a neatly groomed female who displayed good eye-hand interaction. Her affect was anxious with neutral mood. Thought flow was well organized. and content centered on denial of emotional problems as the cause of her attacks. She strongly believed that her spells were of cardiac origin. Family history and past medical history were negative for psychiatric interventions. Clonazepam. in doses of I mg orally, three times a day. rapidly eliminated her panic attacks. The initial goal of psychotherapy was to develop a cognitive behavioral exploration into the anxiety-provoking events that resulted in her panic attacks. This was facilitated by demonstrating a lack of association between the panic attacks and pacemaker activation. The second goal of psychotherapy was to redirect the patient's perception to realize the difference between environmental anxiety and the anxiety of her panic attacks.
Discussion
This case demonstrates the difficulty in clinically distinguishing the pacemaker syndrome from panic disorder due to the overlap in symptoms. and it underscores the importance of seeking psychiatric consultation in such patients. Moreover. in that she displayed a cardiac awareness which heightened her fear of cardiac dysfunction. this patient's clinical and psychiatric course sugPSYCHOSOMATICS
Case Reports
gests that unpleasant internal bodily sensations (real or imagined) may serve as a trigger for panic attacks. The notion that distressing autonomic and physical sensations can trigger panic attacks has led investigators to postulate that internal stimuli can be perceived as a change in bodily state, rather than as an external event. s Prior studies consistently have shown that a belief that bodily function changes have occurred can lead to increased anxiety and physiologic arousal in patients with panic disorder. Patients suffering from panic disorder have a more genuine fear of bodily sensations and become more anxious when they believe physiological changes have occurred, as noted by Ehlers et aI. and Barlow in their extensive works. 6 .7 The implications of this case are intriguing, particularly since opinion is divided concerning the etiology of panic disorder. Biologically oriented theorists have speculated that panic attacks result from some unknown metabolic dysfunction or disease. 8 Conversely, cognitive theorists have suggested that panic attacks result from misinterpretation of bodily sensations. 7 The patient under discussion believed that her "pacemaker speIls" were due to cardiac dysfunction, resulting from actual pacemaker activation. However, the results of the ambulatory electrocardiographic monitoring did not substantiate an association between pacemaker activa-
tion and the onset of the panic attacks. Ehlers et al. previously demonstrated that panic anxiety can be induced in anxiety-prone patients (but not in normal patients) by convincing them that they had experienced an abrupt increase in heart rate even when such had not occurred.6 Thus, rather than being a post-hoc explanation of panic, the perception of changes in internal bodily sensations, which are interpreted as dangerous, have the potential to initiate panic in susceptible individuals. In summary, this case supports prior work suggesting that panic attacks may be triggered by unpleasant internal bodily stimuli (real or imagined). This case also illustrates the difficulty in clinically distinguishing the pacemaker syndrome from panic disorder due to the overlap of symptoms of shortness of breath, dizziness, apprehension, palpitations, and chest discomfort or pain. Panic disorder should be considered as a possible diagnosis when patients with a permanent cardiac pacemaker develop speIls similar to those experienced by the patient described in this report. It is believed by the authors that anxiety disorders are likely in pacemaker patients and that the consequences of not diagnosing such a disorder can lead to major medical interventions which compound the fears and stressors placed upon cardiac patients. Psychiatric evaluation is recommended for such individuals if an organic cause of symptoms cannot be identified.
References I. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. 3rd Edition. Re,'ised. Washington. DC. American Psychiatric Association. 1987. pp 235-238 2. Kenny RA. Sutton R: Pacemaker syndrome. Br Med J 293:902-903.1986 3. Ausubel K. Furman S: The pacemaker syndrome. Ann Intern Med 103:420-429. 1983 4. Mitsui T. Mizuno A. Hasegawa A. et al: Atrial rate as an indicator for optimal pacing rate and the pacemaking syndrome. Ann Cardiol AngeioI20:371-379. 1971 5. Clark OM. Salkoviskis PM. Chalkley AJ: Respiratory
VOLUME31·NUMBER3·SUMMER 1990
control as a treatment for panic attacks. J Behav Ther Exp Psychiatry 16:23-30. 1985 6. Ehlers A. Margraf J. Roth W. et al: Amdety induced by false hean rate feedback in patients with panic disorder. Behav Res Ther 26: I-II. 1988 7. Barlow DH: A psychological model of panic. in Anxiety Disorders: Theory. Diagnosis. and Treatment. Edited by Shaw BF. Cashman F. Segal ZV. et aI. New York. Plenum Press. 1986 8. Margraf J. Ehlers A. Roth WT: Biological models of panic disorder and agoraphobia: a review. Behav Res Ther 24:553-576.1986
347
C.
PETERS, D.O., MARTIN ALPERT. M.D.
BERNARD D. BEITMAN. M.D., MATHEW KUSHNER. M.S. RICHARD WEBEL, M.D.
anic attacks are associated with at least four of the following symptoms: shortness of breath, chest pain, palpitations, dizziness, nausea or abdominal distress, tingling or numbness, unexplained flushing or chilling, trembling, choking, sweating, feelings of depersonalization, the fear of dying, and the fear of going crazy. Panic disorder is diagnosed when the patient experiences at least one panic attack per week for three consecutive weeks. Patients experiencing panic attacks may develop apprehension based on the fear of having an anticipatory anxiety attack which mayor may not impair social or occupational functioning. I The pacemaker syndrome consists of a constellation of symptoms attributable to permanent ventricular pacemaker activation. These include postural hypotension, dizziness, syncope or faintness, breathlessness, chest pain, neck pulsations, generalized lassitude, and weakness. 2 These symptoms are attributable to diminished cardiac output related to a loss of atrioventricular synchrony (atrioventricular dissociation or I: I retrograde ventriculoatrial conduction) or to an absence of atrial activation. Low cardiac output leads to lightheadedness, lethargy with hypotension-inducing apprehension, diaphoresis, and sometimes shock. 3 Such patients also may describe palpitations due to the aforementioned conduction disorders. 4 The patient described in this report originally was misdiagnosed as having the pacemaker syndrome and later was found to have panic disorder, which successfully responded to pharmacotherapy. This case underscores the diffi-
P
VOLUME 31 ' NUMBER 3 • SUMMER 1990
culty of differentiating panic disorder from the pacemaker syndrome and adds evidence to the theory that panic may be triggered by a phobic reaction to real or imagined unpleasant internal bodily sensations. s
Case Report BP was a 29-year-old woman who was hospitalized for evaluation of partial or temporary loss of consciousness. During the month prior to hospitalization, she experienced four such syncopal episodes. These episodes were preceded by a 10- to IS-second period of weakness, diaphoresis, and light-headedness, lasting less than one minute each and followed by a five- to IO-minute period of weakness and giddiness. During the six-month period prior to hospitalization, the patient had experienced one to two episodes per week. Prior to this she had experienced similar episodes three to four times per year for a period of five years, but she had not sought medical attention for these spells. The patient was unable to identify specific exacerbating factors for her syncopal and presyncopal episodes. A physical examination (including postural pulse and blood pressure measurements) showed nothing abnormal except for carotid sinus pressure which variably produced threeReceived January 16. 1989; revised July 5. 1989; accepted July 21. 1989. From the Depanment of Psychiatry and the Division of Cardiology. University Hospital. University of Missouri-Columbia. Columbia. Missouri. Address reprint requests to Dr. Peters. Department of Psychiatry. University of Missouri Hospital and Clinics. # 1 Hospital Drive. Columbia. MO 65201. Copyright © 1990 The Academy of Psychosomatic Medicine.
345
Case Reports
to five-second periods of asystole and sinus bradycardia (30-50 beats per minute) with marked hypotension and reproduction of symptoms. Her resting electrocardiogram. chest x-ray. 24-hour ambulatory electrocardiogram. treadmill exercise test. and echocardiogram (M-mode and two-dimensional) were normal. Cardiac electrophysiology studies including sinus node function tests. a His' bundle electrogram. and programmed stimulation (atrial and ventricular) were also normal. On the basis of these findings. she was diagnosed as having autonomic hyperactivity with secondary carotid sinus hypersensitivity (cardioinhibitory and vasodepressor forms). A Medtronic 7000A unipolar ventricular demand pacemaker was implanted via the transvenous route. Over the ensuing four months she developed several complications related to pacemaker implantation. After being asymptomatic for one month. she again developed episodes of faintness. Pacemaker evaluation demonstrated a failure to maintain a paced heart rate due to electrode malposition. Repositioning of the electrode in the right ventricular apex resulted in normal pacing and sensing. One month later a pacemaker evaluation showed a failure to sense. and attempts to attain appropriate sensing thresholds by external reprogramming and repositioning of the electrode were unsuccessful. Shonly thereafter. the ventricular demand pacemaker and transvenous electrode were removed. and she subsequently underwent operative attachment of electrodes and implantation of a Medtronic 7000A ventricular demand pacemaker via the epicardial route. Thereafter. the syncopal and presyncopal episodes. as described above. abated. One month later she developed precordial pleuritic chest pain associated with a pericardial friction rub and was diagnosed as having postpericardiotomy pericarditis. Her symptoms resolved over the ensuing month following the initiation of oral ibuprofen. Shonly after the resolution of pericarditis. the patient developed spells that were qualitatively different from those experienced prior to pacemaker implantation. These spells. which typically lasted 10 to 30 minutes. were characterized by palpitations, fullness in the anterior chest, dizziness. paresthesias in the hands and feet. rapid breathing. diaphoresis. and a feeling of impending doom. Because of the serious complications associated with pacemaker implantation. the patient became quite concerned about pacemaker function. She eventually became convinced that her new spells were related directly to pacemaker activation. At this point her physicians were 346
considering the diagnosis of pacemaker syndrome as an explanation for her symptoms. To funher clarify this issue, a 24-hour ambulatory Holter monitoring was repeated. during which time the patient had three symptomatic episodes as described above. The underlying cardiac rhythm was predominantly of sinus origin with minimal rate changes and no sinus arrhythmia. There were brief periods of paced rhythm with normal capture and sensing. There were neither premature beats nor tachyarrhythmias. She remained in normal sinus rhythm during the symptomatic episodes. with rates ranging from 75 to 85 beats per minute. As a result of these spells. and despite a lack of correlation of symptoms with pacemaker activation or dysfunction, the patient entered into self-imposed seclusion in her home. fearing an attack in public. Inasmuch as no organic cause for her spells could be identified. she was referred for psychiatric evaluation. On evaluation the patient met the criteria of DSM-III-R for panic disorder with agoraphobia. Mental status evaluation demonstrated a neatly groomed female who displayed good eye-hand interaction. Her affect was anxious with neutral mood. Thought flow was well organized. and content centered on denial of emotional problems as the cause of her attacks. She strongly believed that her spells were of cardiac origin. Family history and past medical history were negative for psychiatric interventions. Clonazepam. in doses of I mg orally, three times a day. rapidly eliminated her panic attacks. The initial goal of psychotherapy was to develop a cognitive behavioral exploration into the anxiety-provoking events that resulted in her panic attacks. This was facilitated by demonstrating a lack of association between the panic attacks and pacemaker activation. The second goal of psychotherapy was to redirect the patient's perception to realize the difference between environmental anxiety and the anxiety of her panic attacks.
Discussion
This case demonstrates the difficulty in clinically distinguishing the pacemaker syndrome from panic disorder due to the overlap in symptoms. and it underscores the importance of seeking psychiatric consultation in such patients. Moreover. in that she displayed a cardiac awareness which heightened her fear of cardiac dysfunction. this patient's clinical and psychiatric course sugPSYCHOSOMATICS
Case Reports
gests that unpleasant internal bodily sensations (real or imagined) may serve as a trigger for panic attacks. The notion that distressing autonomic and physical sensations can trigger panic attacks has led investigators to postulate that internal stimuli can be perceived as a change in bodily state, rather than as an external event. s Prior studies consistently have shown that a belief that bodily function changes have occurred can lead to increased anxiety and physiologic arousal in patients with panic disorder. Patients suffering from panic disorder have a more genuine fear of bodily sensations and become more anxious when they believe physiological changes have occurred, as noted by Ehlers et aI. and Barlow in their extensive works. 6 .7 The implications of this case are intriguing, particularly since opinion is divided concerning the etiology of panic disorder. Biologically oriented theorists have speculated that panic attacks result from some unknown metabolic dysfunction or disease. 8 Conversely, cognitive theorists have suggested that panic attacks result from misinterpretation of bodily sensations. 7 The patient under discussion believed that her "pacemaker speIls" were due to cardiac dysfunction, resulting from actual pacemaker activation. However, the results of the ambulatory electrocardiographic monitoring did not substantiate an association between pacemaker activa-
tion and the onset of the panic attacks. Ehlers et al. previously demonstrated that panic anxiety can be induced in anxiety-prone patients (but not in normal patients) by convincing them that they had experienced an abrupt increase in heart rate even when such had not occurred.6 Thus, rather than being a post-hoc explanation of panic, the perception of changes in internal bodily sensations, which are interpreted as dangerous, have the potential to initiate panic in susceptible individuals. In summary, this case supports prior work suggesting that panic attacks may be triggered by unpleasant internal bodily stimuli (real or imagined). This case also illustrates the difficulty in clinically distinguishing the pacemaker syndrome from panic disorder due to the overlap of symptoms of shortness of breath, dizziness, apprehension, palpitations, and chest discomfort or pain. Panic disorder should be considered as a possible diagnosis when patients with a permanent cardiac pacemaker develop speIls similar to those experienced by the patient described in this report. It is believed by the authors that anxiety disorders are likely in pacemaker patients and that the consequences of not diagnosing such a disorder can lead to major medical interventions which compound the fears and stressors placed upon cardiac patients. Psychiatric evaluation is recommended for such individuals if an organic cause of symptoms cannot be identified.
References I. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. 3rd Edition. Re,'ised. Washington. DC. American Psychiatric Association. 1987. pp 235-238 2. Kenny RA. Sutton R: Pacemaker syndrome. Br Med J 293:902-903.1986 3. Ausubel K. Furman S: The pacemaker syndrome. Ann Intern Med 103:420-429. 1983 4. Mitsui T. Mizuno A. Hasegawa A. et al: Atrial rate as an indicator for optimal pacing rate and the pacemaking syndrome. Ann Cardiol AngeioI20:371-379. 1971 5. Clark OM. Salkoviskis PM. Chalkley AJ: Respiratory
VOLUME31·NUMBER3·SUMMER 1990
control as a treatment for panic attacks. J Behav Ther Exp Psychiatry 16:23-30. 1985 6. Ehlers A. Margraf J. Roth W. et al: Amdety induced by false hean rate feedback in patients with panic disorder. Behav Res Ther 26: I-II. 1988 7. Barlow DH: A psychological model of panic. in Anxiety Disorders: Theory. Diagnosis. and Treatment. Edited by Shaw BF. Cashman F. Segal ZV. et aI. New York. Plenum Press. 1986 8. Margraf J. Ehlers A. Roth WT: Biological models of panic disorder and agoraphobia: a review. Behav Res Ther 24:553-576.1986
347
