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Simultaneous chest compressions and ventilation at high airway pressure during cardiopulmonary resuscitation
ABSTRACTS Peter Rosen, M D -
editor
Director of the Division of Emergency Medicine, Denver General Hospital
Frank. J. Baker, II, M D -
assistant editor
Associate Professor and Director, Department of Emergency Medicine, University of Chicago Hospitals and Clinics
Tricyclic antidepressant (TCA) toxicity. Calesnick B, Am Fam Phys 21:104-106, (Jun) 1980. TCAs are the most widely used antidepressants and are present in 10% of hospitalized overdose patients. TCAs have the same chemical structure as phenothiazines, the 0nly difference being the lack of Sand N in the central ring. The most common toxic effects of TCA in decreasing order of incidence are: drowsiness, coma, cardiac a r r h y t h m i a s , convulsions, anticholinergic effects, respiratory depression, delusion, cardiac arrest, respiratory arrest. Tissue levels of TCA are 10 times plasma levels, so plasma level does not reflect tissue level. T h e r a p e u t i c p l a s m a levels are 5-20 ~tgm/dL, toxic levels more t h a n 40 ~gm/dL; 1 mgm/dL is lethal. Sinus tachycardia is the most sensitive sign of toxicity. Of patients treated with TCA, 10%-20% develop a r r h y t h m i a s (PVCS). Delayed overdose complications may occur up to 12 day s following an acute overdose. There are three stages of overdose toxicity: 1) response to pain stimuli and SVT (recovery within 24 hours); 2) convulsive seizures, respiratory deficiency, AV and intraventricular conduction defects (recovery within 24 to 48 hours); 3) respiratory arrest, seizures, hypotension, ventricular a r r h y t h m i a s . T r e a t m e n t is mainly supportive. Dialysis is ineffective. Physostigmine, 2 mgm IV every 20 to 30 m i n u t e s is indicated. Alkalinization with NaHCO3 reduces the unbound TCA in plasma. Cardiac conduction defects are not to be treated by Type I a n t i a r r h y t h m i c s. Glucocorticoids are contraindicated, because they decrease the biotransformation of TCA. ( E d i t o r ' s note: These can be very d e m a n d i n g p a t i e n t s who can rapidly d i s i n t e g r a t e f r o m drowsiness to death. Physostigmine does not appear to reverse the cardiac effects; at present, therapy is supportive with NaHC03 and pressors for hypotension.) DavidBar-Or, MD
drugs, tricyclic antidepressant Simultaneous chest compressions and ventilation at high airway pressure during cardiopulmonary resuscitation. Chandra N, Rudikoff M, Weizfeldt M, Lancet 1:175-178, (Jan) 1980. Ten patients in cardiopulmonary arrest were given conventional CPR alternated with periods of "new CPR," wherein ventilation was given during chest compressions r a t h e r t h a n between compressions. The CPR in both cases was done by a compUterized pneumatic piston device capable of delivering ventilation at different airway pressures. During "new CPR," airway pressures were 60-110 cm H20 during compression, compared with 40-60 cm H20 during ventilation in conventional CPR; chest compression rates were 40/min versus 60/ min. It was found t h a t during ~'new CPR," mean systolic radial a r t e r y p r e s s u r e increased from 40.6_+4.4 m m Hg to 53.1_+3.9 m m Hg, and carotid flow index increased to an average of 252% of values obtained in conventional CPR. The increased blood flow could be attributed to the higher intrathoracic pressures generated by high pressure ventilation d u r i n g chest compressions, because lowering v e n t i l a t i o n
10:8 (August) t981
pressures resulted in a decrease in arterial pressure and carotid flow. The authors caution against routine use of "new CPR" u n t i l f u r t h e r studies can indicate sample complications, and u n t i l adequacy of ventilation in this technique is m o r e thoroughly evaluated. ( E d i t o r ' s note: While the physiologic data are definitely encouraging, more work must be done to demonstrate increased cardiac and cerebral survival. The key to these still lies with early production o f a lifesustaining rhythm, ie, rapid defibrillation.)
Linda Wahby, MD
cardiopulmonary resuscitation Bacterial intracranial aneurysms. Frazee JG, Cahan LD, Winter J, J Neurosurg 53:633-641, 1980. The authors review 13 cases of bacterial intracranial aneurysms presenting at one university center over a 23-year period. Five patients had known heart disease (four involving the mitral valve), and nine p a t i e n t s had possible predisposing factors such as dental work, urological surgery, bronchitis, and prolonged labor. The diagnosis of bacterial endocarditis was made within two days of admission in all patients and preceded the diagnosis of intracranial bacterial aneurysm in all but one case, with an average time interval of 18 days. Presenting characteristics were sudden onset of coma in six patients, focal neurological findings in six patients, and sudden severe headache in one. Diagnostic studies included positive blood cultures in 11 patients, CAT scans in six patients (five of which were helpful), and serial angiography in 12. Angiography revealed multiple aneurysms in some cases. Repeat studies revealed resolution, enlargement, or new appearances of aneurysms. Of 19 aneurysms, 15 were middle cerebral. Signs and symptoms prior to aneurysmal hemorrhage were sudden severe headache in six patients, focal neurological deficits in six, and seizures in one. Treatment of these 13 patients included antibiotics alone in eight (six of the eight died) and surgery in five (all of whom lived, two being classified as "normal" and three as ~Misabled").
Steve Cooley, MD
aneurysm, bacteria/, intracranial Controlled clinical trial of methylprednisolone in patients with chronic bronchitis and acute respiratory insufficiency. Algert RK, Martin TR, Lewis SW, Ann ~ntern Med 92:753-758, (Jun) 1980. The authors p r e s e n t the results of a randomized, doubleblind, prospective study to d e t e r m i n e t h e efficacy of intravenous methylprednisolone in the t r e a t m e n t of patients with chronic obstructive pulmonary disease and acute respiratory insufficiency. P a t i e n t s who m e t the strict requirements for inclusion in the study were treated with nasal oxygen, i n h a l e d i s o p r o t e r e n o l , i n t r a v e n o u s a m i n o p h y l l i n e , antibiotics, and either methylprednisolone 0.5 mg/kg or a placebo every six hours for 72 hours. Patients were moni-
Ann Emerg Med
451/75
editor
Director of the Division of Emergency Medicine, Denver General Hospital
Frank. J. Baker, II, M D -
assistant editor
Associate Professor and Director, Department of Emergency Medicine, University of Chicago Hospitals and Clinics
Tricyclic antidepressant (TCA) toxicity. Calesnick B, Am Fam Phys 21:104-106, (Jun) 1980. TCAs are the most widely used antidepressants and are present in 10% of hospitalized overdose patients. TCAs have the same chemical structure as phenothiazines, the 0nly difference being the lack of Sand N in the central ring. The most common toxic effects of TCA in decreasing order of incidence are: drowsiness, coma, cardiac a r r h y t h m i a s , convulsions, anticholinergic effects, respiratory depression, delusion, cardiac arrest, respiratory arrest. Tissue levels of TCA are 10 times plasma levels, so plasma level does not reflect tissue level. T h e r a p e u t i c p l a s m a levels are 5-20 ~tgm/dL, toxic levels more t h a n 40 ~gm/dL; 1 mgm/dL is lethal. Sinus tachycardia is the most sensitive sign of toxicity. Of patients treated with TCA, 10%-20% develop a r r h y t h m i a s (PVCS). Delayed overdose complications may occur up to 12 day s following an acute overdose. There are three stages of overdose toxicity: 1) response to pain stimuli and SVT (recovery within 24 hours); 2) convulsive seizures, respiratory deficiency, AV and intraventricular conduction defects (recovery within 24 to 48 hours); 3) respiratory arrest, seizures, hypotension, ventricular a r r h y t h m i a s . T r e a t m e n t is mainly supportive. Dialysis is ineffective. Physostigmine, 2 mgm IV every 20 to 30 m i n u t e s is indicated. Alkalinization with NaHCO3 reduces the unbound TCA in plasma. Cardiac conduction defects are not to be treated by Type I a n t i a r r h y t h m i c s. Glucocorticoids are contraindicated, because they decrease the biotransformation of TCA. ( E d i t o r ' s note: These can be very d e m a n d i n g p a t i e n t s who can rapidly d i s i n t e g r a t e f r o m drowsiness to death. Physostigmine does not appear to reverse the cardiac effects; at present, therapy is supportive with NaHC03 and pressors for hypotension.) DavidBar-Or, MD
drugs, tricyclic antidepressant Simultaneous chest compressions and ventilation at high airway pressure during cardiopulmonary resuscitation. Chandra N, Rudikoff M, Weizfeldt M, Lancet 1:175-178, (Jan) 1980. Ten patients in cardiopulmonary arrest were given conventional CPR alternated with periods of "new CPR," wherein ventilation was given during chest compressions r a t h e r t h a n between compressions. The CPR in both cases was done by a compUterized pneumatic piston device capable of delivering ventilation at different airway pressures. During "new CPR," airway pressures were 60-110 cm H20 during compression, compared with 40-60 cm H20 during ventilation in conventional CPR; chest compression rates were 40/min versus 60/ min. It was found t h a t during ~'new CPR," mean systolic radial a r t e r y p r e s s u r e increased from 40.6_+4.4 m m Hg to 53.1_+3.9 m m Hg, and carotid flow index increased to an average of 252% of values obtained in conventional CPR. The increased blood flow could be attributed to the higher intrathoracic pressures generated by high pressure ventilation d u r i n g chest compressions, because lowering v e n t i l a t i o n
10:8 (August) t981
pressures resulted in a decrease in arterial pressure and carotid flow. The authors caution against routine use of "new CPR" u n t i l f u r t h e r studies can indicate sample complications, and u n t i l adequacy of ventilation in this technique is m o r e thoroughly evaluated. ( E d i t o r ' s note: While the physiologic data are definitely encouraging, more work must be done to demonstrate increased cardiac and cerebral survival. The key to these still lies with early production o f a lifesustaining rhythm, ie, rapid defibrillation.)
Linda Wahby, MD
cardiopulmonary resuscitation Bacterial intracranial aneurysms. Frazee JG, Cahan LD, Winter J, J Neurosurg 53:633-641, 1980. The authors review 13 cases of bacterial intracranial aneurysms presenting at one university center over a 23-year period. Five patients had known heart disease (four involving the mitral valve), and nine p a t i e n t s had possible predisposing factors such as dental work, urological surgery, bronchitis, and prolonged labor. The diagnosis of bacterial endocarditis was made within two days of admission in all patients and preceded the diagnosis of intracranial bacterial aneurysm in all but one case, with an average time interval of 18 days. Presenting characteristics were sudden onset of coma in six patients, focal neurological findings in six patients, and sudden severe headache in one. Diagnostic studies included positive blood cultures in 11 patients, CAT scans in six patients (five of which were helpful), and serial angiography in 12. Angiography revealed multiple aneurysms in some cases. Repeat studies revealed resolution, enlargement, or new appearances of aneurysms. Of 19 aneurysms, 15 were middle cerebral. Signs and symptoms prior to aneurysmal hemorrhage were sudden severe headache in six patients, focal neurological deficits in six, and seizures in one. Treatment of these 13 patients included antibiotics alone in eight (six of the eight died) and surgery in five (all of whom lived, two being classified as "normal" and three as ~Misabled").
Steve Cooley, MD
aneurysm, bacteria/, intracranial Controlled clinical trial of methylprednisolone in patients with chronic bronchitis and acute respiratory insufficiency. Algert RK, Martin TR, Lewis SW, Ann ~ntern Med 92:753-758, (Jun) 1980. The authors p r e s e n t the results of a randomized, doubleblind, prospective study to d e t e r m i n e t h e efficacy of intravenous methylprednisolone in the t r e a t m e n t of patients with chronic obstructive pulmonary disease and acute respiratory insufficiency. P a t i e n t s who m e t the strict requirements for inclusion in the study were treated with nasal oxygen, i n h a l e d i s o p r o t e r e n o l , i n t r a v e n o u s a m i n o p h y l l i n e , antibiotics, and either methylprednisolone 0.5 mg/kg or a placebo every six hours for 72 hours. Patients were moni-
Ann Emerg Med
451/75