due to an increase in oxygen consumption (V0 2) and a decrease in carbon dioxide production (VC02), the respiratory quotient (VC02/V02) falls from a normal mean of 0.82 to about 0.65. These changes occur early during hemodialysis and persist at least one hour after dialysis. When alveolar oxygen pressure is calculated from the measured VC02/ Vo2, it decreases; arterial oxygen pressure (Pa02) decreases, and no significant change in the alveolararterial oxygen pressure difference occurs. Our data are consistent with decreased alveolar ventilation and do not support a ventilation-perfusion abnormality which one would expect with microembolization. Bischel and associates, however, do find that the use of filters prevents the significant fall in Pa02 measured after dialysis. The reason for this is unclear and might be best approached by simultaneous measurement of both blood and respiratory gas levels. Joseph M. Letteri, M.D. Joel E. Sherlock, M.D. and James W. Ledwith, M.D., F.C.C.P. Renal and Pulmonary Divisions Nassau County Medical Center State University of New York at Stony Brook REFERENCE
1 Sherlock IE, Yoon Y, Ledwith JW, et al: Respiratory gas exchange during hemodialysis. In Proceedings of the Clinical Dialysis and Transplant Forum (vol 2) ( Schreiner GE, ed). Washington, DC, Georgetown University Press, 1972, pp 171-174
To the Editor: Drs. Letteri, Sherlock, and Ledwith have commented on their observed changes in the alveolar oxygen pressure consequent to changes in the respiratory quotient. Our study was not designed to answer this question; and, indeed, it is most proper to measure the respiratory quotient if one were to point out changes in the alveolar-arterial oxygen pressure difference before, during, or after dialysis. Our study was designed to answer questions on the effect of a filter vs no filter. Our assumption of the respiratory quotient is then a systematic error which is effectively cancelled out by paired analysis. We also note that the article by Sherlock et al' describes the use of a specific commercial model of blood gas analyzer (Instrumentation Laboratories model 313). The function of various commercially available blood gas analyzers has been studied." the results are shown in Table 1. We have repeatedly demonstrated that the speCHEST, 69: 2, FEBRUARY, 1976
Table I-Analysis o] PaO z Data Derived by Various Blood Gas Analyzers Analyzer Radiometer Model BMS-3
Ll.x
a
n
0.7
5.1
260
1.1 1.1
28 74 26 114
Instrumentation Laboratories Model Model Model Corning Model
113 213 313
11.5
4.7 3.7 5.6
165
4.6
4.5
cific model of blood gas analyzer used by Sherlock et al' exceeds the estimate of arterial oxygen pressure (Pa02) by an average of 11.5 mm Hg. Since this specific model of blood gas analyzer was used by these investigators, it is fair to assume that the data for Pa02 reported by Letteri et al are also similarly in excess. Taking this fact into account, correction of their data would then agree with ours. Margaret D. Bischel, M.D. Lutheran General Hospital, Park Ridge, III and John G. Mohler, M.D. Los Angeles County-University of Southern California Medical Center, Los Angeles REFERENCES
1 Sherlock JE, Yoon Y, Ledwith JW, et al: Respiratory gas exchange during hemodialysis. In Proceedings of the Clinical Dialysis and Transplant Forum (vol 2) (S.::hreiner GE, ed ). Washington, DC, Georgetown University Press, 1972, pp 171-174 2 Mohler IG: Devices for blood gas analysis. N Engl J Med 290:632-633, 1974
Ventricular Fibrillation Induced by a Defective Demand Pacemaker To the Editor: Although the occurrence of pacemaker-induced tachycardia or so-called "runaway" pacemakers is a rare event due to the modern design of pacemakers, it still may occur and has been seen in some pacemakers manufactured around 1972. The case we report here is that of a patient who, upon admission to the hospital, presented with a pacemaker rate of 210 beats per minute, which increased to 2,000 beats per minute within five minutes, followed by loss of capture and ventricular fibrillation. CASE REPORT
A 44-year-old man with congenital heart block had a unipolar pacemaker implanted in February 1973 in another hospital. A few months after implantation, the patient devel-
COMMUNICATIONS TO THE EDITOR 247
I
1. Seri al tracings ob ta ined sho rt ly afte r ad mission to hospital. Tracin g 1 (lead aVR; pap er speed, 25 mm/sec ) sho ws p acemaker firing at rat e of 260 beats per minute, with 1: 1 ve ntricu lar ca ptu re. Tracing 2 ( lead 3 ) shows pa cemaker rat e increased to 320 beat s per minute, with 2 : 1 ventric ular resp onse . Tracin g 3 is co nt inuous strip whi ch depicts sudde n transiti on from pa cemak er rat e of 750 beats per minute and 3: I ve ntricu lar resp on se to ve ry rapid pacemaker firing rat e, resembling 60- Hz int erfer en ce, and loss of ca p ture. Tracing 4 ( paper speed, 50 mm /sec ) reveals pacemaker sp iking at rat e of 35 beats per sec ond (2, 100 beat s pe r minute) and supe rimposed electroca rd iog rap hic complexes. Sh ortly th er eafter , pati ent devel op ed ve ntr icular fibrillation. FIG UHE
ope d pain and /luid ac cumulation in th e ge ne rator pocket. Th ese symptoms were treated co nse rvative ly, and th e patient did fairl y well until about four days prior to admission, wh en he first noticed p alpitations. On th e morning of admission , th e pati enb noted lightheadedness and again comp laine d of palpitations, for whi ch he co nsu lted a nurse at his pla ce of emp loyme nt. His ra te was not ed to be extre me ly rapid, and th e patient wa s transferred to our hospital. Up on arri va l, th e patient was anxious, cold, and clamm y with a systoli c blood p ressure of 70 mm Hg . Th e pulse was th read y. An electrocard iogram revealed an artifi cial pacemaker rhythm at a rat e of 2 10 beats per minute with 1: 1 ventricu lar resp onse, whi ch di d not resp ond to ches t stimulation to overd rive it. At this point th e patient was transferred imm ediatel y to th e oper ating room, and while his ches t was bein g prep ar ed for pacemaker removal, th e pa cemak er rat e increased to 2,000 beats per minute with loss of ventricul ar ca p ture ( Fig 1 ). Imm ediat ely th er eafter , th e card iac monitor reveal ed ve ntri cular fibrill ati on. Wh ile card iopu lmonary resuscitation was tak ing place, th e pacemaker ge nera to r was removed , and th e wires were di sconn ect ed and attach ed to an exte rn al pulse ge nera tor, with per sisten ce of th e ve ntr icula r fibrill ati on . At the third attem pt at elec tr ica l ca rdiove rsio n, th e patient reverted to his underl ying rhy th m of thi rd-degree atr iove ntri cul ar b lock . This rhythm was eas ily ca ptu re d by an exte r-
248 COMMUNICATIONS TO THE EDITOR
nal ge ne ra to r until a new perman ent unit was implanted sho rtly th er eafter. Th e patient recover ed un eventfully. Th e failing pacem aker was a Biotronik model IDP44 (serial number , 56 358 ). It was note d to have a red oxide in vario us areas of the seam of th e metal case, with evi de nce of leakage at th ese points ma nifest ed by th e form ati on of a crus t. DISCUSSION
Although th e occurren ce of runaway pacemakers is a rare event in recent years, it is still a condition whi ch should be conside red wh en pati ents who ha ve permanent artificial pacemakers complain of palpitations or when an y rate increase is noticed on follow up visits. Run away pacemakers show an increase in rate to very fast levels in a relatively short period of tim e, as was not ed in this case. This mod e of failure is associate d with a ver y high mortality, whi ch has been reported to be between 24 and 50 percent. 1-3 According to th e manufacturer of thi s particul ar pacemaker , the ca talyst used to harden the epoxy resin s used for enca psula tion of th e units pro ved to be def ecti ve, allowing leakage of bod y fluids
CHEST, 69: 2, FEBRUARY, 1976
through the defective epoxy resins into the circuitry. Another postulated mode of malfunction in this case is the swelling of the epoxy resin due to this leakage, with consequent breakage of some electronic components. Pacemakers from another manufacturer (Cordis Corp., written communication, December 1974) also showed evidence of excessive moisture penetration through the epoxy encapsulation, but apparently the only abnormality noted so far is the progressive slowing of the paced rate and we are not aware of pacemaker tachycardia occurring in units manufactured by this company. In another instance (Food and Drug Administration recalls T-1l9-5 to T-122-5, T-133-5 to T-137-5, and T-163-5), pacemakerinduced tachycardia was produced by electrolytic leakage from the batteries. All of these problems have already been corrected by the manufacturers for the new units. We, therefore, strongly recommend that pacemaker-regulated patients who complain of palpitations should be immediately. examined for the possibility of pacemaker-induced tachycardia and that any documented rate increase, although minimal, should raise the suspicion of this condition and cause the generator to be replaced immediately.
this communication. We believe that the title of this editorial, "The Atypical Adams-Stokes Attack," although original and attention-getting, is also slightly misleading. The title conveys the impression that in cases with bradycardia-tachycardia syndrome or sick sinus syndrome, the nature of the cerebral manifestations, such as vertigo, blackout, or syncope, is "atypical," ie, different from the manifestations encountered in the course of transient atrioventricular block, which is the classic cause of Adams-Stokes attacks; however, the contrary is true. The type of neurologic manifestation is similar, if not identical, both in patients with the aforementioned "atypical attack" and in patients with transient atrioventricular block. This similarity makes the differential diagnosis even more difficult and makes the use of newer diagnostic methods, such as Holter monitoring, mandatory.' Therefore, in our humble opinion the title of the editorial should read "Atypical Causes of AdamsStokes Attacks." Interestingly, this editorial appeared in the same issue as your own excellent editorial- devoted to the art of medical writing, which stressed the importance of clear definitions of the message of a scientilic paper.
Raul Chirife, M.D. William S. Frankl, M.D. Rolando Mendizabal, M.D. and Manuel R. Estioko, M.D., F.C.C.P. Departments of Medicine and Surgery Medical College of Pennsylvania, Philadelphia
Shlomo Stern, M.D. and Dan Tzivoni, M.D. Hebrew University-Hadassah Medical School Jerusalem, Israel ----~_._----
Reprint requests: Dr. Stern, c/o Hrulassah. Medical Organization, P.o.B. 499, Jerusalem, Israel
Reprint requests: Dr. Chirife, 3300 Henry Ave, Philadelphia 19129 REFERENCES
1 Harper R, Peter T, Hunt D, et al: Runaway pacemaker rhythm after 36 hours of electrical inactivity. Br Heart J 36:610, 1974 2 Furman S, Escher DJW, Solomon N: Experiences with myocardial and transvenous implanted cardiac pacemakers. Am J CardioI23:66-72, 1969 3 Ector H, Stroobandt R, Lemmens A, et al: Successful treatment of pacemaker-induced ventricular fibrillation. Chest 66:733-734, 1974
Atypical Causes of Adams-Stokes Attacks To the Editor: As the mentioned but unidentified "Israeli group" of the editorial by Cosby and Giddings entitled "The Atypical Adams-Stokes Attack" (Chest 67:2-3, 1975), we take the liberty of commenting briefly on
CHEST, 69: 2, FEBRUARY, 1976
REFERENCES
1 Tzivoni D, Stern S: Pacemaker implantation based on ambulatory ECG monitoring in patients with cerebral symptoms. Chest 67 :274-278, 1975 2 Soffer A, Weinberg SL: Flexibility in medical writing ( editorial). Chest 67: 5-7, 1975
Contents of Journal To the Editor: I have had a subscription to your journal, Chest, for several years and would like to commend you on the steady increase I have noted in its quality. It is a difficult thing to balance off articles in both cardiac and pulmonary disease to the satisfaction of either specialty, but I think you are doing an excellent job. Martin 1. Broder, M.D. Director, Cardiac Care Unit Cuyahoga County Hospital Cleveland COMMUNICATIONS TO THE EDITOR 249