Sleep Disturbances After Open Heart Surgery
WILLIAM C. ORR, PhD MONTE L. STAHL
Oklahoma City, Oklahoma
From the Veterans Administration Hospital and University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma. This work was supported in part by Grant 1 RO3 MH 25349-01 from the National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland. Manuscript received July 26, 1976, accepted September 8, 1976. Address for reprints: William C. Orr, PhD, Veterans Administration Hospital (183A), 921 NE 13th St., Oklahoma City, Oklahoma 73104.
196
February 1977
This study was designed to document quantitatively the sleep disturbances that occur after open heart surgery and to investigate a group of patients who underwent a thoracic surgical procedure not involving cardiopulmonary bypass. Nine patients were studied, six after open heart surgery and three after partial or complete pneumonectomy. In each patient, sleep patterns were recorded with use of all night polygraphy before and after operation and for up to 5 weeks on follow-up studies. After open heart surgery, patients manifested considerable suppression of electrophysiologic evidence of sleep as well as prolonged suppression of both rapid eye movement and slow wave sleep patterns. In the three patients subjected to thoracotomy these sleep indexes returned to preoperative levels much earlier. Evidence of stage 2 sleep was present in one of the three patients with thoracotomy on the first postoperative night, and in two of the three both rapid eye movement and slow wave sleep returned to preoperative levels by the time of hospital discharge. It is concluded that patients undergoing open heart surgery experience both acute and chronic disruptions of sleep that last well beyond the hospital period of convalescence. These sleep disturbances have considerable relevance for postoperative management.
The management of patients after open heart surgery presents unusually complicated, challenging and sometimes perplexing problems. These problems may be aggravated by the extremely high incidence rate of conditions various authors have termed postoperative psychosis, delirium, psychologic disturbances or psychiatric complications. These disturbances occur in the general surgical population at an estimated incidence rate of about 0.1 percent. 1 The incidence after open heart procedures has been shown to be well over 100 times this rate, ranging from about 13 to more than 50 percent, 2-4 but there are no data on the incidence after thoracotomy procedures without cardiopulmonary bypass. Lazarus and Hagens 5 have referred to these postoperative behavioral complications as the final common pathway for expression of a multiplicity of psychophysiologic variables. The evidence to date rather consistently implicates an organic predisposition resulting from central nervous system compromise during the surgical procedure and environmental and psychologic precipitating factors attributable to the conditions of the intensive care unit and the patient's psychologic status and history. The organic involvement stems primarily from both focal and diffuse damage to the brain. Hill et al., 6 for example, examined the brains of 133 patients who died after open heart surgery; 80 percent had diffuse fat emboli and 31 percent had nonfat emboli. They stated that the most significant factor in the cause of these emboli was the duration of cardiopulmonary bypass, and Tufo et al. 7 reached a similar conclusion. These studies did not include data concerning postoperative behavioral dysfunction.
The American Journal of CARDIOLOGY
Volume 39
SLEEP AFTER OPEN HEART SURGERY--ORR AND STAHL
Perhaps the most consistently indicted nonorganic factor in postoperative behavioral aberrations is sleep deprivation and its consequences. This factor is directly related to the environment of the intensive care unit and the disruptiveness of the constant monitoring required after open heart procedures. Indeed, Lazarus and Hagens 5 have described this experience as a "unique form" of psychologic torture, and Dlin et al. s have noted that, in view of the importance of sleep in the healing process, it is ironic that the intensive care unit is ideally suited to ensure prolonged sleep deprivation. In line with this thinking are the results of Blachly and Starr, 3 who reported frequent clearing of the sensorium of delirious patients after a prolonged sleep. Previous studies 9,1° of electrophysiologic sleep patterns have documented severe and prolonged disturbances of sleep in patients after open heart surgery. However, these studies have not included long-term follow-up data investigating the possibility of delayed rapid eye movement (REM) rebound and they have not included control subjects undergoing thoracotomy without cardiopulmonary bypass. This study was designed to document further the sleep disturbances in such patients and to investigate patients who underwent a thoracic surgical procedure not involving cardiopulmonary bypass.
% 20
STAGE REM THORACOTOMY of® 7 O
=8
0°9 J° //o 0
~--~ I
1 %
I I ./ /
I
I
I
I
I
I
1
2
3
4
5
6
7
~ 31
OPEN HEART
I
I
8. 9
O
20 /O ~ •
II 2
p-
.
o0 i
i
Methods
1
The subjects studied were nine male volunteer patients from the thoracic surgery service at the Veterans Administration Hospital. Informed consent was obtained in all cases. Six subjects had open heart surgery and three partial or complete pneumonectomy (Table I). All patients received a
I
2
/','/
2
i
-D
i
I
I
i
I
i
i
1
2
3
4
5
6
7
i
8
,
//Z
9 10 14
i
1
2
FIGURE 1. REM sleep stages (percent of each recording session) in patients after thoracotomy (top) and open heart surgery (bottom). The numbers within the graphs indicate case numbers; those at the bottom of the graphs indicate recordings before (left) and early (center) and late (right) after operation.
TABLE I S u m m a r y of Nine Cases Case no.
Age (yr)
Procedure
Time on CP bypass (min)
Anesthetic Agents
Duration of Operation (min)
Psych®tropic Medications
A. Patients With Open Heart Surgery 1
42
Aortocoronary bypass
75
2
50
Aortocoronary bypass
158
3
54
Aortocoronary bypass
114
4
47
Aortocoronary bypass
187
5
50
Aortocoronary bypass
158
6
43
Aneurysm repair
30
Morphine, nitrous oxide, sodium Pent®thai ® Morphine, nitrous oxide, sodium Pent®thai Morphine, nitrous oxide, sodium Pent®thai Morphine, nitrous oxide, sodium Pent®thai Morphine: nitrous oxide, sodium Pent®thai Morphine, nitrous oxide, sodium Pent®thai
208
Percodan®(2), EmpirinO(3F)
250
Morphine( 1,2), Percodan®(7), Dalmane®(7), Empirin(3F) None
227 395 410 135
Nembutal®(1 ), morphine(1,2,4), Valium®(1,8,10,14,F) Morphine(2,3), Valium(3~7,F), Dalmane(7,F), Tylenol®(F) Morphine( 1), Valium (1), Percodan(4,6,F), Dalmane(P)
B. Patients With Thoracotomy 7
76
Partial pneumonectomy
0
8
43
Complete pneu monectomy
0
8
67
Partial pneumonectomy
0
Flu®thane, nitrous oxide, sodium Pent®thai Flu®thane, nitrous oxide Hal®thane, nitrous oxide, sodium Pent®thai
195
Morphine(2,4)
195
Demerol( 1,2), Percodan (6), Dalmane(6) Morphine(1,2,5), Oemerol( I ), Valium(1 )
170
CP = cardiopulmonary; F = medication given on the follow-up study. Numbers indicate the postoperative study during which the drug was taken; P = medication given preoperatively.
February 1977
The American Journal of CARDIOLOGY
Volume 39
197
SLEEP AFTER OPEN HEART SURGERY--ORR AND STAHL
complete neurologic evaluation preoperatively as well as dally bedside neurologic examinations (including evaluation of sensorium, reflexes, pupils and extraocular muscles) while in the intensive care unit. Recordings in each patient were made with use of all night polygraphy both before and after operation. To minimize adaptation to the recording conditions, all subjects were monitored in their own private ward room rather than in the sleep laboratory. Recordings used two channels of the electroencephalogram with leads C3 and C4 (International 10-20 system), two channels of eye movement recorded from the outer canthus of each eye, one channel of muscle activity recorded from the chin and the electrocardiogram. Recordings were made preoperatively (1 to 2 nights), postoperatively in the intensive care unit (3 to 4 nights), after return to the ward (2 to 3 nights) and, in three patients, at a follow-up examination 2 to 5 weeks postoperatively (1 night each). Monitoring was not performed in any patient the night before operation or on the first night after discharge from the intensive care unit and return to the ward. It was believed that 1 night should be allowed for readaptation to the ward environment. Results
Preoperative and early postoperative sleep data: Data from the analyzed sleep variables are presented in Table II and rapid eye movement (REM) sleep data are illustrated graphically in Figure 1. The preoperative data showed, in general, some minor alterations in sleep patterns such as an increase in waking and stage 1, and a slight suppression of stages 3 and 4 (slow wave sleep). These data are not considered grossly abnormal, 11 especially in light of the high level of anxiety normally present in preoperative patients. Among patients studied on 2 nights preoperatively, sleep patterns did not differ significantly on the 2 nights. Thus, any alteration of sleep patterns due to adaptation to the recording conditions is believed to be minimal. All but one patient who had open heart surgery (Case 6) showed a total absence of electrophysiologic evidence of sleep (12 to 14 hertz spindles in the electroencephalogram) until the 2nd postoperative night. In nearly all instances, records taken on the 1st postoperative night showed a preponderance of low voltage mixed frequency electroencephalographic activity throughout most of the night. Considerable muscle artifact appeared across all recording channels. These electrophysiologic signs are indicative of both cortical and somatic arousal. Short episodes of stage 1 sleep (generally accepted as a transitional stage from wakefulness to sleep) were interspersed throughout the night. These were characterized by rolling eye movements in the eye movement recordings, an increase in theta activity (4 to 7 hertz) in the electroencephalogram and an overall decrease in muscle artifact. Five of the six patients with open heart surgery showed no evidence of R E M sleep until the 4th postoperative night (although Patients 2 and 6 had no recordings on their 3rd postoperative night). Follow-up data: Because of the small number of subjects in the thoracotomy group, meaningful comparisons with the patients who had open heart surgery are limited. It is clear that the electrophysiologic indicators of sleep as well as REM and slow wave sleep were acutely suppressed in patients after thoracotomy. In two
198
February 1977
The American Journal of CARDIOLOGY
of these three patients (Cases 7 and 8), both R E M and slow wave sleep had returned to control levels by the time of discharge from the hospital. In contrast, Patients 1, 2 and 5 in the open heart surgery group had evidence of R E M suppression 2 to 4 weeks after hospital discharge (Fig. 1). At 5 weeks, R E M sleep in Patient 5 had returned to the preoperative level. At 3 weeks, Patient 6, who had the shortest cardiopulmonary bypass and surgical times, had a slightly elevated R E M time compared with preoperative data. Follow-up monitoring revealed considerable suppression of slow wave sleep in two of four patients (Cases 1 and 5). In Case 5, this was still evident in the 5 week follow-up study. In Patient 2, there was some evidence of slow wave sleep rebound 4 weeks after discharge. Fbllow-up data were not obtainable in the patients who underwent thoracotomy. Neurologic and psychiatric findings: No patient demonstrated signs of focal or diffuse neurologic deficits preoperatively, and none had a history of significant psychiatric illness or sleep disturbance. Postoperatively, no patient had any evidence of neurologic dysfunction or signs of postoperative psychosis or delirium. Subjectively, all patients reported considerable difficulty sleeping. They found it especially difficult to compensate for nocturnal sleep disturbances by napping during the day and uniformly attributed their difficulty to persistent disruptions by nurses and the con~stant activity of the intensive care unit during the normal operating hours. This indicates that most of the patient's sleep was concentrated during the nocturnal hours. Discussion
These data substantiate the belief that severe postoperative sleep disturbances occur after both open heart surgery and thoracotomy. Our findings are in essential agreement with previous reports of extensive deprivation and fragmentation of sleep during the postoperative period after open heart surgery. With regard to REM sleep, our results are most in accord with those of Elwell et al., 9 who reported virtually complete suppression of R E M sleep in the immediate postoperative period with a relative suppression continuing "well into convalescence." These data apply to recordings made on the 4 consecutive nights subsequent to discharge from the recovery room. Our three patients who underwent thoracotomy provided a striking contrast, showing evidence of spindling sleep (stage 2) as well as R E M sleep by the 1st and 2nd postoperative nights, respectively. The comparatively rapid recovery of preoperative sleep patterns in this group is documented by the return, in two of our three patients, to preoperative sleep patterns by the time of hospital discharge. Open heart versus thoracotomy data: Direct comparison of the data from our patients with open heart surgery and thoracotomy is complicated by the use of cardiopulmonary bypass and the generally longer operative times in the former group. However, the data from Case 6 (open heart surgery) and Case 7 (thoracotomy) provide an interesting comparison. Both patients had similar operative times, and both were dis-
Volume 39
SLEEP AFTER OPEN HEAR~" SURGERY--ORR AND STAHL
dure is a crucial determinant in the persistence of postoperative sleep disturbances. In spite of considerable REM suppression in the patients with open heart surgery, in the immediate postoperative period none, with the possible exception of Case 6, had evidence of REM rebound in the follow-up
charged from the hospital at approximately the same time. In both patients preoperative levels of REM and slow wave sleep had returned by the time of the last recording, which was always within 24 to 36 hours of the time of hospital discharge (Table II). These findings suggest that thetotal duration of the operative proce-
TABLE II Sleep Stages (percent of records) and Recording Time (minutes) in Nine Patients Before, During and After Operation Preoperative Study
Postoperative Study
Follow-Up Study
Case no.
1
2
1
2
3
4
5
W/1 2 REM SWS Min
... ... . .. . . . ..
15.8 45.8 24.8 13.6 397
100.0 0.0 00 0.0 378
100.0 0.0 0.0 00 382
85.7 14.3 0.0 0.0 416
. .. ... ... ... ...
35.6 52.7 11.6 0.1 270
2
W/1 2 REM SWS Min
28.4 51.6 15.6 4.4 390
42.4 36.5 16.5 4.6 332
100•0 0.0 0.0 00 389
92.1 7.9 00 0.0 353
3
W/1 2 REM SWS Min
... ... . . . ... ...
23•3 50.8 224 3.5 417
100.0 00 0.0 0.0 337
80.8 17.9 1.3 0.0 366
56.6 36.4 7.0 0.0 407
55.4 41.0 3.5 0.1 367
4
W/1 2 R EM SWS Min
26.6 64.2 6.3 2.9 350
13.0 61.0 25.5 05 364
100.0 0.0 0.0 00 379
99.7 0.3 0.0 0.0 381
62.2 37.4 0.0 0.4 340
52.1 45.7 0.0 2.2 305
W/1 2 REM SWS Min
24.6 49•5 18.2 7.7 441
29.3 46.4 15.4 8.9 480
100.0 0.0 0.0 0.0 360
100.0 0.0 0•0 0.0 329
100.0 0.0 0.0 0.0 304
97.6 2.4 0.0 00 302
W/1 2 BEM SWS Min
. .
11.3 73.5 14.8 0.4 473
978 2.2 0.0 0.0 395
76.7 23.3 00 0 •0 381
. .. ... . . .. ..
21.7 62.3 16.0 0 •0 460
. • ... . .
. •. ... ,• . . . ...
6
7
8
9
14
16.2 70.4 12.8 0.6 428
2
(2 wks) 19.2 61.1 19.0 0.7 496
19.3 74.2 5.0 1.5 417
24.3 63.8 11.4 0.5 434
1
(4 wks) 42 6 33.4 10.6 13.4 437
15.9 72.4 9.7 2.0 397
14.5 69.5 15.9 0.1 395 42.2 47 1 10.6 0.1 340
. . .. .. .
33.0 57 3 8.8 0.9 347 (3 wks) 29.1 64.4 6.3 02 474
89 •6 10.4 0.0 0.0 247 21.2 59.7 19.0 0.1 441
(5 wks) 28.1 55.3 14.0 2.6 414
(3 wks) 19.9 55.0 25.0 0.1 477
17.0 60.5 22.0 0.5 462
Patients With Thoracotomy 7
9*
W/1 2 REM SWS Min
29.0 51.6 18.3 1.1 433
33•3 47.1 19.6 0.0 435
... . . ... . .
100 0 0.0 0.0 0.0 265
97.5 2.5 0.0 0.0 397 52.6 47.4 0.0 0.0 384
W/1 2 REM SWS Min
33.8 41.3 15.8 91 402
72.0 28.0 0.0 0.0 300
75.2 247 0.0 0.1 384
W/1 2 REM SWS Min
15.1 75.4 9.1 0.4 427
100.0 0.0 0.0 0.0 414
94.7 0.0 5.2 0.0 325
•
•
79.9 16.0 4.1 0.0 381
•. •. •. .. .
44.0 37.7 17.0 1.3 438
29.6 50.8 11.5 8.1 430
.
.
.
.
.
•
* Patient died of a presumed pulmonary embolus before completion of sleep study• Min = total recording time in m i n u t e s ; R E M = rapid eye movement sleep stage;SWS = slow wave sleep (stage 3 and 4 ) ; W / 1 stages 1 and 2.
February 1977
The American Journal of C A R D I O L O G Y
.
,
.
.
and 2 = sleep
Volume 39
199
SLEEP AFTER OPEN HEART SURGERY--ORR AND STAHL
evaluations. In the study of Johns et al., I° the patients appeared to return to normal preoperative levels of R E M sleep and also had no evidence of R E M rebound. That study included one patient who had postoperative delirium and was studied during a 3 week period of convalescence. Influence of psychoti-opic drugs: Data describing alterations in sleep patterns should be considered in the light of the known sensitivity of sleep variables to the effects of various drugs, particularly psychotropic compounds. Because of the variety of such drugs these patients received, the cause of alterations in sleep patterns must be interpreted with considerable caution. Patients received both REM sleep-suppressant narcotic compounds, such as morphine, and slow wave sleepsuppressant benzodiazapine compounds, such as diazepam and flurazepam (Table I). 12-14 It is of interest that in Patient 3, who received no psychotropic medications postoperatively, R E M and slow wave sleep alterations were similar to those of other patients who had open heart surgery. Thus, although drugs undoubtedly alter postoperative sleep patterns, the operative procedure itself and conditions in the intensive care unit can also substantially disrupt sleep patterns. Aithough there was little evidence of R E M rebound in these patients, one must be aware of risks in precipitously withdrawing psychotropic medications. 15 Alterations in brain metabolism: The extended suppression of both R E M and slow wave sleep after open heart surgery is compatible with the view that these patients have a disturbance in brain amine metabolism. This inference is based on the striking difference between the recovery recordings in our patients and those reported in the classic sleep deprivation studies, which showed an immediate slow wave sleep rebound followed by R E M sleep rebound. 16 In addition, the postoperative suppression of R E M sleep resembles the pattern seen after the withdrawal of drugs that greatly alter central nervous system metabolism. Wyatt et al., 17 for example, gave para-chlorophenylalanine (a serotonin inhibitor) to patients with carcinoid syndromes, and found patterns of prolonged R E M suppression after drug withdrawal. R E M inhibition lasted for up to several weeks in three of the four patients studied and no compensatory rebound was seen. This pattern is quite similar to that in our six patients with open heart surgery. Similar patterns have been reported with the administration of lithium carbonate to patients with affective disorders. Is It is hypothesized, then, that
the open heart surgical procedure results in a significant alteration in brain metabolism as reflected by the extended suppression of R E M sleep and absence of R E M rebound. These factors could contribute to the development of the postoperative psychotic reaction occasionally seen in these patients. Influence of the intensive care unit--clinical observations: From nighttime observations and patient reports, it is clear that much of the acute postoperative sleep deprivation in these patients was attributable to the location of the patient in the intensive care unit (directly in the flow of all traffic in and out of the unit) and to frequent disturbances required for monitoring of vital signs, respirator adjustments and administration of medications. Even the slightest disruption (for example, adjustment of an intravenous drip infusion) was sufficient to awaken the patient from sleep, as documented by electroencephalographic changes. Such arousals may have considerable clinical significance because there are several reports 19-m indicating that transitional periods from waking to sleep are especially provocative of ventricular arrhythmias. In addition, Wellens et al. 22 have reported a case of persistent ventricular fibrillation upon arousal from sleep by an auditory stimulus. Moreover, in our study there were frequent unnecessary awakenings due to a general lack of awareness by the intensive care unit staff of noise levels, lighting conditions and other factors that would be conducive to sleep. For example, all lights would often be on until well after midnight. These factors can easily be corrected by a concerted staff effort to alter the environment of the intensive care unit at night so as to effect optimal sleeping conditions. It would be of interest to evaluate further the effect of presumed optimal sleeping conditions on postoperative sleep deprivation to include a group of control subjects receiving similar degrees of sleep disturbance in an environment (perhaps simulated) outside of the intensive care unit. Acknowledgment
We acknowledge with much appreciation the support and encouragement of Dr. Lazar J. Greenfield, former chief of the surgical service at the Veterans Administration Hospital, Oklahoma City. The study would not have been accomplished without the outstanding cooperation and support of the nursing staff of the surgical intensive care unit of that hospital. We also acknowledge the valuable contribution of Cindy Gruenau to all aspects of this study, and thank Dr. Thomas Whitsett for many helpful comments on the preparation of this manuscript.
References 1. Knox SJ: Severe psychiatric disturbances in the postoperative period--a five-year survey of Belfast hospitals. J Ment Sci 107: 1078-1098, i961 2. Egerton N, Kay JH: Psychological disturbances associated with open-heart surgery. Am J Psychiatry 110:433-439, 1964 3. Blachly PH, Starr A: Post-cardiotomy delirium. Am J Psychiatry 121:371-375, 1964 4. Heller SS, Frank KA, Maim JR, et al: Psychiatric complications of open-heart surgery. N Engl J Med 282:1015-1020, 1970
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5. Lazarus NR, Hagens JH: Prevention of psychosis following open-heart surgery. Am J Psychiatry 124:1190-1195, 1968 6. Hill JD, Aguilar MJ, Baranco A, et al: Neuropathological manifestations of cardiac surgery. Ann Thorac Surg 7:409-419, 1969 7. Tufo HM, Ostfeld AM, Shekelle R: Central nervous system dysfunction following open-heart surgery. JAMA 212:1333-1340, 1970 8. Dlin BM, Rosen H, Dlckstein K, et al: The problems of sleep and
Volume 39
SLEEP AFTER OPEN HEART SURGERY--ORR AND STAHL
9.
10. 11. 12.
13. 14. 15.
rest in the intensive care unit. Psychosomatics 12:155-163, 1971 Elwell EL, Frankel BL, Snyder F: A polygraphic sleep study of five cardiotomy patients. Presented at the Annual Meeting of the Association for the Psychophysiological Study of Sleep, Jackson Hole, Wyoming, 1974 Johns MW, Large AA, Mastedon JP, et al: Sleep and delirium after open-heart surgery. Br J Surg 61:377-381, 1974 Williams RL, Karacan I, Hursch CJ: EEG of Human Sleep. New York, Wiley & Sons, 1974 Borenstein P, Cujo P: Influence of barbiturates and benzodiazepine on the sleep EEG. In, Modern Problems in Pharmacopsychiatry (Turan I, ed). Basel, Karger, 1974, p 182-192 Kay DC, Eisensteln RB, Jasinski DR: Morphine effects on human REM states, waking state and non-REM sleep. Psychopharmacologia 14:404-416, 1969 Kales A, Kales J: Evaluation, diagnosis, and treatment of clinical conditions related to sleep. JAMA 213:2229-2235, 1970 Kales A, Malstrom EJ, Scharf MB, et ah Psychophysiological and biochemical changes following use and withdrawal of hypnotics.
16. 17. 18. 19. 20. 21. 22.
February 1977
In, Sleep Physiology and Pathology (Kales A, ed). Philadelphia, JB Lippincott, 1969, p 331-344 Kales A, Tan TL, Kollar EG, el ah Sleep patterns following 205 hours of sleep deprivation. Psychosom Med 32:189-200, 1970 Wyatt RJ, Engelman K, Kupfer DJ, el ah Effects of para-chlorophenylalanine on sleep in man. Electroencephalogr Clin Neurophysiol 27:529-532, 1969 Kupfer DJ, Reynolds CF, Weiss BL, el ah Lithium carbonate and sleep in affective disorders. Arch Gen Psychiatry 30:79-84, 1974 Rosenblatt G, Hartman E, Zwilling G: Cardiac irritability during sleep. J Psychosom Res 17:129-134, 1973 Lester B, Block R, Gunn CG: The relation of cardiac arrhythmias to phases of sleep (abstr). Clin Res 17:456, 1969 Smith R, Johnson L, Rothfeld D, et ah Sleep and cardiac arrhythmias. Arch Intern Meal 130:751-753, 1972 Wellens HJ, Vermeulen A, Durrer O: Ventricular fibrillation occurring on arousal from sleep by auditory stimuli. Circulation 46: 661-665, 1972
The American Journal of CARDIOLOGY
Volume 39
201
WILLIAM C. ORR, PhD MONTE L. STAHL
Oklahoma City, Oklahoma
From the Veterans Administration Hospital and University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma. This work was supported in part by Grant 1 RO3 MH 25349-01 from the National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland. Manuscript received July 26, 1976, accepted September 8, 1976. Address for reprints: William C. Orr, PhD, Veterans Administration Hospital (183A), 921 NE 13th St., Oklahoma City, Oklahoma 73104.
196
February 1977
This study was designed to document quantitatively the sleep disturbances that occur after open heart surgery and to investigate a group of patients who underwent a thoracic surgical procedure not involving cardiopulmonary bypass. Nine patients were studied, six after open heart surgery and three after partial or complete pneumonectomy. In each patient, sleep patterns were recorded with use of all night polygraphy before and after operation and for up to 5 weeks on follow-up studies. After open heart surgery, patients manifested considerable suppression of electrophysiologic evidence of sleep as well as prolonged suppression of both rapid eye movement and slow wave sleep patterns. In the three patients subjected to thoracotomy these sleep indexes returned to preoperative levels much earlier. Evidence of stage 2 sleep was present in one of the three patients with thoracotomy on the first postoperative night, and in two of the three both rapid eye movement and slow wave sleep returned to preoperative levels by the time of hospital discharge. It is concluded that patients undergoing open heart surgery experience both acute and chronic disruptions of sleep that last well beyond the hospital period of convalescence. These sleep disturbances have considerable relevance for postoperative management.
The management of patients after open heart surgery presents unusually complicated, challenging and sometimes perplexing problems. These problems may be aggravated by the extremely high incidence rate of conditions various authors have termed postoperative psychosis, delirium, psychologic disturbances or psychiatric complications. These disturbances occur in the general surgical population at an estimated incidence rate of about 0.1 percent. 1 The incidence after open heart procedures has been shown to be well over 100 times this rate, ranging from about 13 to more than 50 percent, 2-4 but there are no data on the incidence after thoracotomy procedures without cardiopulmonary bypass. Lazarus and Hagens 5 have referred to these postoperative behavioral complications as the final common pathway for expression of a multiplicity of psychophysiologic variables. The evidence to date rather consistently implicates an organic predisposition resulting from central nervous system compromise during the surgical procedure and environmental and psychologic precipitating factors attributable to the conditions of the intensive care unit and the patient's psychologic status and history. The organic involvement stems primarily from both focal and diffuse damage to the brain. Hill et al., 6 for example, examined the brains of 133 patients who died after open heart surgery; 80 percent had diffuse fat emboli and 31 percent had nonfat emboli. They stated that the most significant factor in the cause of these emboli was the duration of cardiopulmonary bypass, and Tufo et al. 7 reached a similar conclusion. These studies did not include data concerning postoperative behavioral dysfunction.
The American Journal of CARDIOLOGY
Volume 39
SLEEP AFTER OPEN HEART SURGERY--ORR AND STAHL
Perhaps the most consistently indicted nonorganic factor in postoperative behavioral aberrations is sleep deprivation and its consequences. This factor is directly related to the environment of the intensive care unit and the disruptiveness of the constant monitoring required after open heart procedures. Indeed, Lazarus and Hagens 5 have described this experience as a "unique form" of psychologic torture, and Dlin et al. s have noted that, in view of the importance of sleep in the healing process, it is ironic that the intensive care unit is ideally suited to ensure prolonged sleep deprivation. In line with this thinking are the results of Blachly and Starr, 3 who reported frequent clearing of the sensorium of delirious patients after a prolonged sleep. Previous studies 9,1° of electrophysiologic sleep patterns have documented severe and prolonged disturbances of sleep in patients after open heart surgery. However, these studies have not included long-term follow-up data investigating the possibility of delayed rapid eye movement (REM) rebound and they have not included control subjects undergoing thoracotomy without cardiopulmonary bypass. This study was designed to document further the sleep disturbances in such patients and to investigate patients who underwent a thoracic surgical procedure not involving cardiopulmonary bypass.
% 20
STAGE REM THORACOTOMY of® 7 O
=8
0°9 J° //o 0
~--~ I
1 %
I I ./ /
I
I
I
I
I
I
1
2
3
4
5
6
7
~ 31
OPEN HEART
I
I
8. 9
O
20 /O ~ •
II 2
p-
.
o0 i
i
Methods
1
The subjects studied were nine male volunteer patients from the thoracic surgery service at the Veterans Administration Hospital. Informed consent was obtained in all cases. Six subjects had open heart surgery and three partial or complete pneumonectomy (Table I). All patients received a
I
2
/','/
2
i
-D
i
I
I
i
I
i
i
1
2
3
4
5
6
7
i
8
,
//Z
9 10 14
i
1
2
FIGURE 1. REM sleep stages (percent of each recording session) in patients after thoracotomy (top) and open heart surgery (bottom). The numbers within the graphs indicate case numbers; those at the bottom of the graphs indicate recordings before (left) and early (center) and late (right) after operation.
TABLE I S u m m a r y of Nine Cases Case no.
Age (yr)
Procedure
Time on CP bypass (min)
Anesthetic Agents
Duration of Operation (min)
Psych®tropic Medications
A. Patients With Open Heart Surgery 1
42
Aortocoronary bypass
75
2
50
Aortocoronary bypass
158
3
54
Aortocoronary bypass
114
4
47
Aortocoronary bypass
187
5
50
Aortocoronary bypass
158
6
43
Aneurysm repair
30
Morphine, nitrous oxide, sodium Pent®thai ® Morphine, nitrous oxide, sodium Pent®thai Morphine, nitrous oxide, sodium Pent®thai Morphine, nitrous oxide, sodium Pent®thai Morphine: nitrous oxide, sodium Pent®thai Morphine, nitrous oxide, sodium Pent®thai
208
Percodan®(2), EmpirinO(3F)
250
Morphine( 1,2), Percodan®(7), Dalmane®(7), Empirin(3F) None
227 395 410 135
Nembutal®(1 ), morphine(1,2,4), Valium®(1,8,10,14,F) Morphine(2,3), Valium(3~7,F), Dalmane(7,F), Tylenol®(F) Morphine( 1), Valium (1), Percodan(4,6,F), Dalmane(P)
B. Patients With Thoracotomy 7
76
Partial pneumonectomy
0
8
43
Complete pneu monectomy
0
8
67
Partial pneumonectomy
0
Flu®thane, nitrous oxide, sodium Pent®thai Flu®thane, nitrous oxide Hal®thane, nitrous oxide, sodium Pent®thai
195
Morphine(2,4)
195
Demerol( 1,2), Percodan (6), Dalmane(6) Morphine(1,2,5), Oemerol( I ), Valium(1 )
170
CP = cardiopulmonary; F = medication given on the follow-up study. Numbers indicate the postoperative study during which the drug was taken; P = medication given preoperatively.
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SLEEP AFTER OPEN HEART SURGERY--ORR AND STAHL
complete neurologic evaluation preoperatively as well as dally bedside neurologic examinations (including evaluation of sensorium, reflexes, pupils and extraocular muscles) while in the intensive care unit. Recordings in each patient were made with use of all night polygraphy both before and after operation. To minimize adaptation to the recording conditions, all subjects were monitored in their own private ward room rather than in the sleep laboratory. Recordings used two channels of the electroencephalogram with leads C3 and C4 (International 10-20 system), two channels of eye movement recorded from the outer canthus of each eye, one channel of muscle activity recorded from the chin and the electrocardiogram. Recordings were made preoperatively (1 to 2 nights), postoperatively in the intensive care unit (3 to 4 nights), after return to the ward (2 to 3 nights) and, in three patients, at a follow-up examination 2 to 5 weeks postoperatively (1 night each). Monitoring was not performed in any patient the night before operation or on the first night after discharge from the intensive care unit and return to the ward. It was believed that 1 night should be allowed for readaptation to the ward environment. Results
Preoperative and early postoperative sleep data: Data from the analyzed sleep variables are presented in Table II and rapid eye movement (REM) sleep data are illustrated graphically in Figure 1. The preoperative data showed, in general, some minor alterations in sleep patterns such as an increase in waking and stage 1, and a slight suppression of stages 3 and 4 (slow wave sleep). These data are not considered grossly abnormal, 11 especially in light of the high level of anxiety normally present in preoperative patients. Among patients studied on 2 nights preoperatively, sleep patterns did not differ significantly on the 2 nights. Thus, any alteration of sleep patterns due to adaptation to the recording conditions is believed to be minimal. All but one patient who had open heart surgery (Case 6) showed a total absence of electrophysiologic evidence of sleep (12 to 14 hertz spindles in the electroencephalogram) until the 2nd postoperative night. In nearly all instances, records taken on the 1st postoperative night showed a preponderance of low voltage mixed frequency electroencephalographic activity throughout most of the night. Considerable muscle artifact appeared across all recording channels. These electrophysiologic signs are indicative of both cortical and somatic arousal. Short episodes of stage 1 sleep (generally accepted as a transitional stage from wakefulness to sleep) were interspersed throughout the night. These were characterized by rolling eye movements in the eye movement recordings, an increase in theta activity (4 to 7 hertz) in the electroencephalogram and an overall decrease in muscle artifact. Five of the six patients with open heart surgery showed no evidence of R E M sleep until the 4th postoperative night (although Patients 2 and 6 had no recordings on their 3rd postoperative night). Follow-up data: Because of the small number of subjects in the thoracotomy group, meaningful comparisons with the patients who had open heart surgery are limited. It is clear that the electrophysiologic indicators of sleep as well as REM and slow wave sleep were acutely suppressed in patients after thoracotomy. In two
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of these three patients (Cases 7 and 8), both R E M and slow wave sleep had returned to control levels by the time of discharge from the hospital. In contrast, Patients 1, 2 and 5 in the open heart surgery group had evidence of R E M suppression 2 to 4 weeks after hospital discharge (Fig. 1). At 5 weeks, R E M sleep in Patient 5 had returned to the preoperative level. At 3 weeks, Patient 6, who had the shortest cardiopulmonary bypass and surgical times, had a slightly elevated R E M time compared with preoperative data. Follow-up monitoring revealed considerable suppression of slow wave sleep in two of four patients (Cases 1 and 5). In Case 5, this was still evident in the 5 week follow-up study. In Patient 2, there was some evidence of slow wave sleep rebound 4 weeks after discharge. Fbllow-up data were not obtainable in the patients who underwent thoracotomy. Neurologic and psychiatric findings: No patient demonstrated signs of focal or diffuse neurologic deficits preoperatively, and none had a history of significant psychiatric illness or sleep disturbance. Postoperatively, no patient had any evidence of neurologic dysfunction or signs of postoperative psychosis or delirium. Subjectively, all patients reported considerable difficulty sleeping. They found it especially difficult to compensate for nocturnal sleep disturbances by napping during the day and uniformly attributed their difficulty to persistent disruptions by nurses and the con~stant activity of the intensive care unit during the normal operating hours. This indicates that most of the patient's sleep was concentrated during the nocturnal hours. Discussion
These data substantiate the belief that severe postoperative sleep disturbances occur after both open heart surgery and thoracotomy. Our findings are in essential agreement with previous reports of extensive deprivation and fragmentation of sleep during the postoperative period after open heart surgery. With regard to REM sleep, our results are most in accord with those of Elwell et al., 9 who reported virtually complete suppression of R E M sleep in the immediate postoperative period with a relative suppression continuing "well into convalescence." These data apply to recordings made on the 4 consecutive nights subsequent to discharge from the recovery room. Our three patients who underwent thoracotomy provided a striking contrast, showing evidence of spindling sleep (stage 2) as well as R E M sleep by the 1st and 2nd postoperative nights, respectively. The comparatively rapid recovery of preoperative sleep patterns in this group is documented by the return, in two of our three patients, to preoperative sleep patterns by the time of hospital discharge. Open heart versus thoracotomy data: Direct comparison of the data from our patients with open heart surgery and thoracotomy is complicated by the use of cardiopulmonary bypass and the generally longer operative times in the former group. However, the data from Case 6 (open heart surgery) and Case 7 (thoracotomy) provide an interesting comparison. Both patients had similar operative times, and both were dis-
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SLEEP AFTER OPEN HEAR~" SURGERY--ORR AND STAHL
dure is a crucial determinant in the persistence of postoperative sleep disturbances. In spite of considerable REM suppression in the patients with open heart surgery, in the immediate postoperative period none, with the possible exception of Case 6, had evidence of REM rebound in the follow-up
charged from the hospital at approximately the same time. In both patients preoperative levels of REM and slow wave sleep had returned by the time of the last recording, which was always within 24 to 36 hours of the time of hospital discharge (Table II). These findings suggest that thetotal duration of the operative proce-
TABLE II Sleep Stages (percent of records) and Recording Time (minutes) in Nine Patients Before, During and After Operation Preoperative Study
Postoperative Study
Follow-Up Study
Case no.
1
2
1
2
3
4
5
W/1 2 REM SWS Min
... ... . .. . . . ..
15.8 45.8 24.8 13.6 397
100.0 0.0 00 0.0 378
100.0 0.0 0.0 00 382
85.7 14.3 0.0 0.0 416
. .. ... ... ... ...
35.6 52.7 11.6 0.1 270
2
W/1 2 REM SWS Min
28.4 51.6 15.6 4.4 390
42.4 36.5 16.5 4.6 332
100•0 0.0 0.0 00 389
92.1 7.9 00 0.0 353
3
W/1 2 REM SWS Min
... ... . . . ... ...
23•3 50.8 224 3.5 417
100.0 00 0.0 0.0 337
80.8 17.9 1.3 0.0 366
56.6 36.4 7.0 0.0 407
55.4 41.0 3.5 0.1 367
4
W/1 2 R EM SWS Min
26.6 64.2 6.3 2.9 350
13.0 61.0 25.5 05 364
100.0 0.0 0.0 00 379
99.7 0.3 0.0 0.0 381
62.2 37.4 0.0 0.4 340
52.1 45.7 0.0 2.2 305
W/1 2 REM SWS Min
24.6 49•5 18.2 7.7 441
29.3 46.4 15.4 8.9 480
100.0 0.0 0.0 0.0 360
100.0 0.0 0•0 0.0 329
100.0 0.0 0.0 0.0 304
97.6 2.4 0.0 00 302
W/1 2 BEM SWS Min
. .
11.3 73.5 14.8 0.4 473
978 2.2 0.0 0.0 395
76.7 23.3 00 0 •0 381
. .. ... . . .. ..
21.7 62.3 16.0 0 •0 460
. • ... . .
. •. ... ,• . . . ...
6
7
8
9
14
16.2 70.4 12.8 0.6 428
2
(2 wks) 19.2 61.1 19.0 0.7 496
19.3 74.2 5.0 1.5 417
24.3 63.8 11.4 0.5 434
1
(4 wks) 42 6 33.4 10.6 13.4 437
15.9 72.4 9.7 2.0 397
14.5 69.5 15.9 0.1 395 42.2 47 1 10.6 0.1 340
. . .. .. .
33.0 57 3 8.8 0.9 347 (3 wks) 29.1 64.4 6.3 02 474
89 •6 10.4 0.0 0.0 247 21.2 59.7 19.0 0.1 441
(5 wks) 28.1 55.3 14.0 2.6 414
(3 wks) 19.9 55.0 25.0 0.1 477
17.0 60.5 22.0 0.5 462
Patients With Thoracotomy 7
9*
W/1 2 REM SWS Min
29.0 51.6 18.3 1.1 433
33•3 47.1 19.6 0.0 435
... . . ... . .
100 0 0.0 0.0 0.0 265
97.5 2.5 0.0 0.0 397 52.6 47.4 0.0 0.0 384
W/1 2 REM SWS Min
33.8 41.3 15.8 91 402
72.0 28.0 0.0 0.0 300
75.2 247 0.0 0.1 384
W/1 2 REM SWS Min
15.1 75.4 9.1 0.4 427
100.0 0.0 0.0 0.0 414
94.7 0.0 5.2 0.0 325
•
•
79.9 16.0 4.1 0.0 381
•. •. •. .. .
44.0 37.7 17.0 1.3 438
29.6 50.8 11.5 8.1 430
.
.
.
.
.
•
* Patient died of a presumed pulmonary embolus before completion of sleep study• Min = total recording time in m i n u t e s ; R E M = rapid eye movement sleep stage;SWS = slow wave sleep (stage 3 and 4 ) ; W / 1 stages 1 and 2.
February 1977
The American Journal of C A R D I O L O G Y
.
,
.
.
and 2 = sleep
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SLEEP AFTER OPEN HEART SURGERY--ORR AND STAHL
evaluations. In the study of Johns et al., I° the patients appeared to return to normal preoperative levels of R E M sleep and also had no evidence of R E M rebound. That study included one patient who had postoperative delirium and was studied during a 3 week period of convalescence. Influence of psychoti-opic drugs: Data describing alterations in sleep patterns should be considered in the light of the known sensitivity of sleep variables to the effects of various drugs, particularly psychotropic compounds. Because of the variety of such drugs these patients received, the cause of alterations in sleep patterns must be interpreted with considerable caution. Patients received both REM sleep-suppressant narcotic compounds, such as morphine, and slow wave sleepsuppressant benzodiazapine compounds, such as diazepam and flurazepam (Table I). 12-14 It is of interest that in Patient 3, who received no psychotropic medications postoperatively, R E M and slow wave sleep alterations were similar to those of other patients who had open heart surgery. Thus, although drugs undoubtedly alter postoperative sleep patterns, the operative procedure itself and conditions in the intensive care unit can also substantially disrupt sleep patterns. Aithough there was little evidence of R E M rebound in these patients, one must be aware of risks in precipitously withdrawing psychotropic medications. 15 Alterations in brain metabolism: The extended suppression of both R E M and slow wave sleep after open heart surgery is compatible with the view that these patients have a disturbance in brain amine metabolism. This inference is based on the striking difference between the recovery recordings in our patients and those reported in the classic sleep deprivation studies, which showed an immediate slow wave sleep rebound followed by R E M sleep rebound. 16 In addition, the postoperative suppression of R E M sleep resembles the pattern seen after the withdrawal of drugs that greatly alter central nervous system metabolism. Wyatt et al., 17 for example, gave para-chlorophenylalanine (a serotonin inhibitor) to patients with carcinoid syndromes, and found patterns of prolonged R E M suppression after drug withdrawal. R E M inhibition lasted for up to several weeks in three of the four patients studied and no compensatory rebound was seen. This pattern is quite similar to that in our six patients with open heart surgery. Similar patterns have been reported with the administration of lithium carbonate to patients with affective disorders. Is It is hypothesized, then, that
the open heart surgical procedure results in a significant alteration in brain metabolism as reflected by the extended suppression of R E M sleep and absence of R E M rebound. These factors could contribute to the development of the postoperative psychotic reaction occasionally seen in these patients. Influence of the intensive care unit--clinical observations: From nighttime observations and patient reports, it is clear that much of the acute postoperative sleep deprivation in these patients was attributable to the location of the patient in the intensive care unit (directly in the flow of all traffic in and out of the unit) and to frequent disturbances required for monitoring of vital signs, respirator adjustments and administration of medications. Even the slightest disruption (for example, adjustment of an intravenous drip infusion) was sufficient to awaken the patient from sleep, as documented by electroencephalographic changes. Such arousals may have considerable clinical significance because there are several reports 19-m indicating that transitional periods from waking to sleep are especially provocative of ventricular arrhythmias. In addition, Wellens et al. 22 have reported a case of persistent ventricular fibrillation upon arousal from sleep by an auditory stimulus. Moreover, in our study there were frequent unnecessary awakenings due to a general lack of awareness by the intensive care unit staff of noise levels, lighting conditions and other factors that would be conducive to sleep. For example, all lights would often be on until well after midnight. These factors can easily be corrected by a concerted staff effort to alter the environment of the intensive care unit at night so as to effect optimal sleeping conditions. It would be of interest to evaluate further the effect of presumed optimal sleeping conditions on postoperative sleep deprivation to include a group of control subjects receiving similar degrees of sleep disturbance in an environment (perhaps simulated) outside of the intensive care unit. Acknowledgment
We acknowledge with much appreciation the support and encouragement of Dr. Lazar J. Greenfield, former chief of the surgical service at the Veterans Administration Hospital, Oklahoma City. The study would not have been accomplished without the outstanding cooperation and support of the nursing staff of the surgical intensive care unit of that hospital. We also acknowledge the valuable contribution of Cindy Gruenau to all aspects of this study, and thank Dr. Thomas Whitsett for many helpful comments on the preparation of this manuscript.
References 1. Knox SJ: Severe psychiatric disturbances in the postoperative period--a five-year survey of Belfast hospitals. J Ment Sci 107: 1078-1098, i961 2. Egerton N, Kay JH: Psychological disturbances associated with open-heart surgery. Am J Psychiatry 110:433-439, 1964 3. Blachly PH, Starr A: Post-cardiotomy delirium. Am J Psychiatry 121:371-375, 1964 4. Heller SS, Frank KA, Maim JR, et al: Psychiatric complications of open-heart surgery. N Engl J Med 282:1015-1020, 1970
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5. Lazarus NR, Hagens JH: Prevention of psychosis following open-heart surgery. Am J Psychiatry 124:1190-1195, 1968 6. Hill JD, Aguilar MJ, Baranco A, et al: Neuropathological manifestations of cardiac surgery. Ann Thorac Surg 7:409-419, 1969 7. Tufo HM, Ostfeld AM, Shekelle R: Central nervous system dysfunction following open-heart surgery. JAMA 212:1333-1340, 1970 8. Dlin BM, Rosen H, Dlckstein K, et al: The problems of sleep and
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SLEEP AFTER OPEN HEART SURGERY--ORR AND STAHL
9.
10. 11. 12.
13. 14. 15.
rest in the intensive care unit. Psychosomatics 12:155-163, 1971 Elwell EL, Frankel BL, Snyder F: A polygraphic sleep study of five cardiotomy patients. Presented at the Annual Meeting of the Association for the Psychophysiological Study of Sleep, Jackson Hole, Wyoming, 1974 Johns MW, Large AA, Mastedon JP, et al: Sleep and delirium after open-heart surgery. Br J Surg 61:377-381, 1974 Williams RL, Karacan I, Hursch CJ: EEG of Human Sleep. New York, Wiley & Sons, 1974 Borenstein P, Cujo P: Influence of barbiturates and benzodiazepine on the sleep EEG. In, Modern Problems in Pharmacopsychiatry (Turan I, ed). Basel, Karger, 1974, p 182-192 Kay DC, Eisensteln RB, Jasinski DR: Morphine effects on human REM states, waking state and non-REM sleep. Psychopharmacologia 14:404-416, 1969 Kales A, Kales J: Evaluation, diagnosis, and treatment of clinical conditions related to sleep. JAMA 213:2229-2235, 1970 Kales A, Malstrom EJ, Scharf MB, et ah Psychophysiological and biochemical changes following use and withdrawal of hypnotics.
16. 17. 18. 19. 20. 21. 22.
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In, Sleep Physiology and Pathology (Kales A, ed). Philadelphia, JB Lippincott, 1969, p 331-344 Kales A, Tan TL, Kollar EG, el ah Sleep patterns following 205 hours of sleep deprivation. Psychosom Med 32:189-200, 1970 Wyatt RJ, Engelman K, Kupfer DJ, el ah Effects of para-chlorophenylalanine on sleep in man. Electroencephalogr Clin Neurophysiol 27:529-532, 1969 Kupfer DJ, Reynolds CF, Weiss BL, el ah Lithium carbonate and sleep in affective disorders. Arch Gen Psychiatry 30:79-84, 1974 Rosenblatt G, Hartman E, Zwilling G: Cardiac irritability during sleep. J Psychosom Res 17:129-134, 1973 Lester B, Block R, Gunn CG: The relation of cardiac arrhythmias to phases of sleep (abstr). Clin Res 17:456, 1969 Smith R, Johnson L, Rothfeld D, et ah Sleep and cardiac arrhythmias. Arch Intern Meal 130:751-753, 1972 Wellens HJ, Vermeulen A, Durrer O: Ventricular fibrillation occurring on arousal from sleep by auditory stimuli. Circulation 46: 661-665, 1972
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