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Serious circulatory deficiency during external chest compression for asthma attack
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5. Krasnow AZ, Bloomfiled DK: Artifacts in portable electrocardiographic monitoring. Am Heart J 1976;91:349-357 6. Kanz KA, Russ W, Assal J, et al: Performance of automated external defibrillators under electromagnetic fields and noise of high-voltage power. Scientific session of the American Heart Session, Atlanta. Circulation 1999;100:1312 (abstr 1641). 7. Santucci PA, Haw J, Trohman RG, et al: Interference with an implantable defibrillator by an electronic antitheft-surveillance device. N Engl J Med 1998;339:1371-1374 8. Occhetta E, Plebani L, Bortnik M, et al: Implantable cardioverter defibrillators and cellular telephones: Is there any interference? Pacing Clin Electrophysiol 1999;22:983-989 9. Groh WJ, Boschee SA, Engelstein ED, et al: Interactions between electronic article surveillance systems and implantable cardioverter defibrillators. Circulation 1999;100:387-392
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SERIOUS CIRCULATORY DEFICIENCY DURING EXTERNAL CHEST COMPRESSION FOR ASTHMA ATFACK
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FIGURE 1. Fifty and 3 Hz current power carried by the rails mimicking 180 beats/min regular QRS complexes rhythm in a clinically dead patient. power is likely to interfere with medical devices such as automated defibrillators. So physicians should be aware of the potential for these interferences. FRI~DI~RIC LAPOSTOLLE, M D FLORENCE POMMERIE, M D JEAN CATINEAU, M D
SAMU 93, HOpital Avicenne Bobigny, France
FR~Dr2PdCADNET,MD, PD MARC WENZEK, M D
SNCF Paris, France References
1. Chase C, Brady W J: Artifactual electrocardiographic change mimicking clinical abnormalities on the ECG. Am J Emerg Med 2000;18:312-316 2. Knight BP, P e l o s i F, Michaud GF, e t al: Brief report: Clinical consequences of electrocardiographic artifact mimicking ventricular tachycardia. N Engl J Med 1999;341:1270-1274 3. Boyd EG: A solution to difficult power frequency interference on ECG recordings. Pacing Clin Electrophysiol 1985;8:17-24 4. Sander A, Voss A, Griessbach G: An optimized filter system for eliminating 50 Hz interference from high resolution ECG. Biomed Tech (Berl) 1995;40:82-87
To the E d i t o r : - - To palliate asthmatic respiratory deficiency, external chest compression (ECC), a respiratory physiotherapy in which the ribcage is compressed using the palms of the hands synchronized with expiration to facilitate exhausting of entrapped alveolar gas, 1-2 has been performed in addition to drug therapies for dilating bronchus. The effectiveness of ECC for palliation of severe asthma and bronchospasms has been reported previously. 3-4 Because there are rarely complications, ECC is not considered to be a risky procedure. 1-2 However, we experienced a case of ECC-induced serious circulatory deficiency, suggesting that ECC may be harmful in some cases. A 7-year-old boy (body weight 21 kg) was taken to an emergency department because of a severe asthma attack with expiratory wheezing and cyanosis (SpO 2, 70 %). He was unconscious (Glasgow Coma Scale, 7) but not in shock (blood pressure, 92/66 mmHg; heart rate, 144 beats/min). Initial therapies, including oxygen inhalation, isoproterenol aerosol, aminophylline (100 mg IV), methylpredonizolone (500 mg IV), and epinephrine (0.5 mg SC), did not palliate the expiratory deficiency. Endotracheal intubation and manual pressure support ventilation (PIP, 40-70 cmH20; FiO 2, 1.0) with isoflurane inhalation (1%-3%) were therefore performed. Blood oxygenation was maintained (PaO 2, 156.3 mmHg), but high PaCO 2 (143.1 mmHg) and respiratory acidosis (pH, 6.910) remained. Excessively expanded lungs and a compressed mediastinum were seen in a radiograph (Fig 1 ). Because the asthma attack became further aggravated, ECC was performed and then expiration was immediately improved. However, about 2 rain after the start of ECC, a sequence of wide QRS tachycardia, short-term bradycardia, and cardiac arrest occurred (Fig 2A). With immediate resuscitation; external cardiac massage and administration of epinephrine (1 mg IV), the heart beat soon recovered (blood pressure, 84/62 mmHg; heart rate, 135 beats/min; Fig. 2B). Deterioration of both expanded lungs and compressed mediastinum were seen in a radiograph at that time (Fig 3 ). Because the expiratory deficiency was reaggravated several minutes later, ECC was performed again. About 1 rain after the start of ECC, expiration improved but the sequence
Copyright © 2001 by W.B. Saunders Company 0735-6757/01/1902-0022535.00/0 doi:10.1053/ajem.2001.21310
170
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 19, Number 2 • March 2001
ered again. However, we then found that cautious trials of weak ECC transiently decreased blood pressure and heart rate. Therefore, we terminated ECC and the patient's respiratory effort with vecuronium, and we started pressure control ventilation. Severe respiratory deficiency thereafter remained, but there was no more circulatory trouble. No neurologic deficiency was observed during these episodes. Thereafter, symptoms of the asthma attack were gradually palliated by administration of aminophylline and methylpredonizolone. Administration of vecuronium and isoflurane was stopped after 24 hours, and it required 5 days for the weaning from the artificial ventilation. The respiratory symptoms were mostly palliated, but weak expiratory wheezing remained for 20 days. The experience of this case indicates that ECC has a harmful potency eliciting circulating deficiency. Circulatory deficiency appeared while performing ECC, and weak circulatory deficiency was elicited by subsequent cautious trials of weak ECC. At these times, the mediastinum was strongly compressed by the excessively expanded lungs, and expiration was deteriorated. These findings strongly suggest that decreases in venous return and cardiac output 5 induced by increased intrathoracic pressure and pulmonary vascular resistance, which are elicited by the addition of asthmatic alveolar hyperextension, the patient's expiratory effort, and the direct physical effect of ECC compressing the thorax, are the main causes of the circulatory deficiency. From these facts, we regard this circulatory deficiency as a complication of ECC. Because hemodynamic impairment is often occurred in mechanically ventilated asthma and chronic obstructive pulmonary disease patients with high airway pressure, 6-7 there is a potential risk of circulatory deficiency while performing ECC. It has been reported that a decrease in cardiac output elicited by mechanical ventilation with pulmonary hyperinflation, a simulated asthmatic
FIGURE 1. Chest radiograph showing expanded lungs and a compressed mediastinum. of tachycardia, bradycardia ,and cardiac arrest, which appeared similar to that observed just before, was occurred again. With immediate external cardiac massage and administration of epinephrine (0.2 mg IV), heart beat soon recov-
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FIGURE 2. Electrocardiograms showing wide QRS bradycardia observed just before the initial cardiac arrest (A-l), subsequent induction (A-2) and recovery (B-l) of cardiac arrest under external cardiac massage, and subsequent wide QRS bradycardia seen immediately after the initial cardiac arrest (B-2).
CORRESPONDENCE
171
References 1. Fisher MM, Bowey CJ, Ladd-Hudson K: External chest compression in acute asthma: A preliminary study. Crit Care Med 1989; 17:686-687 2. Watts Jh Thoracic compression for asthma. Chest 1984; 86: 505 3. Burton A, Champion P: External chest compression in acute severe asthma. Anaesth Intensive Care 1991; 19:470 4. Eason J, Tayler D, Cottam S, et al: Manual chest compression for total bronchospasm. Lancet. 1991; 337:366 5. Fewell JE, Abendschein DR, Carlson CJ: Continuous positivepressure ventilation decreases right and left ventricular end-diastolic volumes in the dog. Circ Res 1980; 46:125-132 6. Rosengarten PL, Tuxen DV, Dziukas L, et al: Circulatory arrest induced by intermittent positive pressure ventilation in a patient with severe asthma. Anaesth Intensive Care 1991 ; 19:118-121 7. Rogers PL, Schlichtig R, Miro A, et al: Auto-PEEP during CPR. An "occult" cause of electromechanical dissociation? Chest 1991; 99:492-493 8. Van der Touw T, Tully A, Amis TC: Cardiorespiratory consequences ofexpiratory chest wall compression during mechanical ventilation and severe hyperinflation. Crit Care Med 1993; 21 : 19081914
VERTEBRAL ARTERY DISSECTION AND PONTINE INFARCT AFTER CHIROPRACTIC MANIPULATION
FIGURE 3. Chest radiograph showing more intensely expanded lungs and a compressed mediastinum than those seen before resuscitation (see Fig 1).
condition, was exacerbated by rib cage compression in dogs. s This finding supports our hypothesis regarding the mechanism inducing circulatory deficiency in the present case. However, such a serious circulatory deficiency as a complication of ECC has not been reported. 1-2 Because EEC was executed by a skilled physiotherapist in the present case, it is unlikely that the complication was caused by poor technique in the execution of ECC. We assume that the increased intrathoracic pressure-induced decrease in venous return appeared more intensely in the present case than the average. Even though this circulatory complication is extremely rare, care should be taken when performing ECC considering the seriousness of circulatory complication, especially. EICHI NARIMATSU,MD, PHD SATOSHINAR& MD
Asr~ KITa,MD YOSHIHIKO KURIMOTO,MD YASUFUMIASAI, MD, PHD
Sapporo Medical University Department of Traumatology and Critical Care Medichze Sapporo Japan AKIRA ISHIKAWA,PHD,RPT
Sapporo Japan
To the Editor:-- Chiropractic has grown exponentially since its inception in this country in 1896. Every year, there are more than 10 million patients who visit a chiropractor for a variety of ailments, resulting in an average of 125 million visits annually. ~ Spinal manipulation has proven helpful to many patients for a variety of complaints, and deserves a place in the therapeutic armamentarium for the treatment of musculoskeletal disorders. Chiropractic is one of the most popular alternative therapies in the United States, and there is a public perception that injuries sustained from spinal manipulation are insignificant, as well as rare. We report a case of a left pontine infarct with vertebral artery dissection, sustained after a chiropractic spinal manipulation in a previously healthy young woman. A 33-year-old woman in good health presented to a chiropractor for treatment of a headache of several week duration. While undergoing manipulative therapy, she noted the acute onset of right-sided hemiplegia. Paramedics responding to the chiropractor's office found the patient to be alert with normal vital signs (blood pressure of 132/76 mmHg, heart rate of 86 beats/rain, and a respiratory rate of 20 breaths/min). They noted complete fight-sided hemiplegia, and transported her to a nearby hospital in full cervical spine precautions. On arrival to the emergency department, the patient remained hemiplegic, and complained of a severe headache. The patient was also suffering from severe vertigo, as well as tinnitus. Her vital signs remained relatively unchanged. Physical examination revealed a well-appearing patient who was alert and cooperative. Her head and neck showed no obvious signs of trauma, and were held midline with a cervical collar. Pupils were 4 mm, equal, and reacted briskly
Copyright © 2001 by W.B. Saunders Company 0735-6757/01/1902-0023535.00/0 doi:l 0.1053/ajem.2001.21351
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5. Krasnow AZ, Bloomfiled DK: Artifacts in portable electrocardiographic monitoring. Am Heart J 1976;91:349-357 6. Kanz KA, Russ W, Assal J, et al: Performance of automated external defibrillators under electromagnetic fields and noise of high-voltage power. Scientific session of the American Heart Session, Atlanta. Circulation 1999;100:1312 (abstr 1641). 7. Santucci PA, Haw J, Trohman RG, et al: Interference with an implantable defibrillator by an electronic antitheft-surveillance device. N Engl J Med 1998;339:1371-1374 8. Occhetta E, Plebani L, Bortnik M, et al: Implantable cardioverter defibrillators and cellular telephones: Is there any interference? Pacing Clin Electrophysiol 1999;22:983-989 9. Groh WJ, Boschee SA, Engelstein ED, et al: Interactions between electronic article surveillance systems and implantable cardioverter defibrillators. Circulation 1999;100:387-392
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SERIOUS CIRCULATORY DEFICIENCY DURING EXTERNAL CHEST COMPRESSION FOR ASTHMA ATFACK
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f
....
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r
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,
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,
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FIGURE 1. Fifty and 3 Hz current power carried by the rails mimicking 180 beats/min regular QRS complexes rhythm in a clinically dead patient. power is likely to interfere with medical devices such as automated defibrillators. So physicians should be aware of the potential for these interferences. FRI~DI~RIC LAPOSTOLLE, M D FLORENCE POMMERIE, M D JEAN CATINEAU, M D
SAMU 93, HOpital Avicenne Bobigny, France
FR~Dr2PdCADNET,MD, PD MARC WENZEK, M D
SNCF Paris, France References
1. Chase C, Brady W J: Artifactual electrocardiographic change mimicking clinical abnormalities on the ECG. Am J Emerg Med 2000;18:312-316 2. Knight BP, P e l o s i F, Michaud GF, e t al: Brief report: Clinical consequences of electrocardiographic artifact mimicking ventricular tachycardia. N Engl J Med 1999;341:1270-1274 3. Boyd EG: A solution to difficult power frequency interference on ECG recordings. Pacing Clin Electrophysiol 1985;8:17-24 4. Sander A, Voss A, Griessbach G: An optimized filter system for eliminating 50 Hz interference from high resolution ECG. Biomed Tech (Berl) 1995;40:82-87
To the E d i t o r : - - To palliate asthmatic respiratory deficiency, external chest compression (ECC), a respiratory physiotherapy in which the ribcage is compressed using the palms of the hands synchronized with expiration to facilitate exhausting of entrapped alveolar gas, 1-2 has been performed in addition to drug therapies for dilating bronchus. The effectiveness of ECC for palliation of severe asthma and bronchospasms has been reported previously. 3-4 Because there are rarely complications, ECC is not considered to be a risky procedure. 1-2 However, we experienced a case of ECC-induced serious circulatory deficiency, suggesting that ECC may be harmful in some cases. A 7-year-old boy (body weight 21 kg) was taken to an emergency department because of a severe asthma attack with expiratory wheezing and cyanosis (SpO 2, 70 %). He was unconscious (Glasgow Coma Scale, 7) but not in shock (blood pressure, 92/66 mmHg; heart rate, 144 beats/min). Initial therapies, including oxygen inhalation, isoproterenol aerosol, aminophylline (100 mg IV), methylpredonizolone (500 mg IV), and epinephrine (0.5 mg SC), did not palliate the expiratory deficiency. Endotracheal intubation and manual pressure support ventilation (PIP, 40-70 cmH20; FiO 2, 1.0) with isoflurane inhalation (1%-3%) were therefore performed. Blood oxygenation was maintained (PaO 2, 156.3 mmHg), but high PaCO 2 (143.1 mmHg) and respiratory acidosis (pH, 6.910) remained. Excessively expanded lungs and a compressed mediastinum were seen in a radiograph (Fig 1 ). Because the asthma attack became further aggravated, ECC was performed and then expiration was immediately improved. However, about 2 rain after the start of ECC, a sequence of wide QRS tachycardia, short-term bradycardia, and cardiac arrest occurred (Fig 2A). With immediate resuscitation; external cardiac massage and administration of epinephrine (1 mg IV), the heart beat soon recovered (blood pressure, 84/62 mmHg; heart rate, 135 beats/min; Fig. 2B). Deterioration of both expanded lungs and compressed mediastinum were seen in a radiograph at that time (Fig 3 ). Because the expiratory deficiency was reaggravated several minutes later, ECC was performed again. About 1 rain after the start of ECC, expiration improved but the sequence
Copyright © 2001 by W.B. Saunders Company 0735-6757/01/1902-0022535.00/0 doi:10.1053/ajem.2001.21310
170
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 19, Number 2 • March 2001
ered again. However, we then found that cautious trials of weak ECC transiently decreased blood pressure and heart rate. Therefore, we terminated ECC and the patient's respiratory effort with vecuronium, and we started pressure control ventilation. Severe respiratory deficiency thereafter remained, but there was no more circulatory trouble. No neurologic deficiency was observed during these episodes. Thereafter, symptoms of the asthma attack were gradually palliated by administration of aminophylline and methylpredonizolone. Administration of vecuronium and isoflurane was stopped after 24 hours, and it required 5 days for the weaning from the artificial ventilation. The respiratory symptoms were mostly palliated, but weak expiratory wheezing remained for 20 days. The experience of this case indicates that ECC has a harmful potency eliciting circulating deficiency. Circulatory deficiency appeared while performing ECC, and weak circulatory deficiency was elicited by subsequent cautious trials of weak ECC. At these times, the mediastinum was strongly compressed by the excessively expanded lungs, and expiration was deteriorated. These findings strongly suggest that decreases in venous return and cardiac output 5 induced by increased intrathoracic pressure and pulmonary vascular resistance, which are elicited by the addition of asthmatic alveolar hyperextension, the patient's expiratory effort, and the direct physical effect of ECC compressing the thorax, are the main causes of the circulatory deficiency. From these facts, we regard this circulatory deficiency as a complication of ECC. Because hemodynamic impairment is often occurred in mechanically ventilated asthma and chronic obstructive pulmonary disease patients with high airway pressure, 6-7 there is a potential risk of circulatory deficiency while performing ECC. It has been reported that a decrease in cardiac output elicited by mechanical ventilation with pulmonary hyperinflation, a simulated asthmatic
FIGURE 1. Chest radiograph showing expanded lungs and a compressed mediastinum. of tachycardia, bradycardia ,and cardiac arrest, which appeared similar to that observed just before, was occurred again. With immediate external cardiac massage and administration of epinephrine (0.2 mg IV), heart beat soon recov-
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FIGURE 2. Electrocardiograms showing wide QRS bradycardia observed just before the initial cardiac arrest (A-l), subsequent induction (A-2) and recovery (B-l) of cardiac arrest under external cardiac massage, and subsequent wide QRS bradycardia seen immediately after the initial cardiac arrest (B-2).
CORRESPONDENCE
171
References 1. Fisher MM, Bowey CJ, Ladd-Hudson K: External chest compression in acute asthma: A preliminary study. Crit Care Med 1989; 17:686-687 2. Watts Jh Thoracic compression for asthma. Chest 1984; 86: 505 3. Burton A, Champion P: External chest compression in acute severe asthma. Anaesth Intensive Care 1991; 19:470 4. Eason J, Tayler D, Cottam S, et al: Manual chest compression for total bronchospasm. Lancet. 1991; 337:366 5. Fewell JE, Abendschein DR, Carlson CJ: Continuous positivepressure ventilation decreases right and left ventricular end-diastolic volumes in the dog. Circ Res 1980; 46:125-132 6. Rosengarten PL, Tuxen DV, Dziukas L, et al: Circulatory arrest induced by intermittent positive pressure ventilation in a patient with severe asthma. Anaesth Intensive Care 1991 ; 19:118-121 7. Rogers PL, Schlichtig R, Miro A, et al: Auto-PEEP during CPR. An "occult" cause of electromechanical dissociation? Chest 1991; 99:492-493 8. Van der Touw T, Tully A, Amis TC: Cardiorespiratory consequences ofexpiratory chest wall compression during mechanical ventilation and severe hyperinflation. Crit Care Med 1993; 21 : 19081914
VERTEBRAL ARTERY DISSECTION AND PONTINE INFARCT AFTER CHIROPRACTIC MANIPULATION
FIGURE 3. Chest radiograph showing more intensely expanded lungs and a compressed mediastinum than those seen before resuscitation (see Fig 1).
condition, was exacerbated by rib cage compression in dogs. s This finding supports our hypothesis regarding the mechanism inducing circulatory deficiency in the present case. However, such a serious circulatory deficiency as a complication of ECC has not been reported. 1-2 Because EEC was executed by a skilled physiotherapist in the present case, it is unlikely that the complication was caused by poor technique in the execution of ECC. We assume that the increased intrathoracic pressure-induced decrease in venous return appeared more intensely in the present case than the average. Even though this circulatory complication is extremely rare, care should be taken when performing ECC considering the seriousness of circulatory complication, especially. EICHI NARIMATSU,MD, PHD SATOSHINAR& MD
Asr~ KITa,MD YOSHIHIKO KURIMOTO,MD YASUFUMIASAI, MD, PHD
Sapporo Medical University Department of Traumatology and Critical Care Medichze Sapporo Japan AKIRA ISHIKAWA,PHD,RPT
Sapporo Japan
To the Editor:-- Chiropractic has grown exponentially since its inception in this country in 1896. Every year, there are more than 10 million patients who visit a chiropractor for a variety of ailments, resulting in an average of 125 million visits annually. ~ Spinal manipulation has proven helpful to many patients for a variety of complaints, and deserves a place in the therapeutic armamentarium for the treatment of musculoskeletal disorders. Chiropractic is one of the most popular alternative therapies in the United States, and there is a public perception that injuries sustained from spinal manipulation are insignificant, as well as rare. We report a case of a left pontine infarct with vertebral artery dissection, sustained after a chiropractic spinal manipulation in a previously healthy young woman. A 33-year-old woman in good health presented to a chiropractor for treatment of a headache of several week duration. While undergoing manipulative therapy, she noted the acute onset of right-sided hemiplegia. Paramedics responding to the chiropractor's office found the patient to be alert with normal vital signs (blood pressure of 132/76 mmHg, heart rate of 86 beats/rain, and a respiratory rate of 20 breaths/min). They noted complete fight-sided hemiplegia, and transported her to a nearby hospital in full cervical spine precautions. On arrival to the emergency department, the patient remained hemiplegic, and complained of a severe headache. The patient was also suffering from severe vertigo, as well as tinnitus. Her vital signs remained relatively unchanged. Physical examination revealed a well-appearing patient who was alert and cooperative. Her head and neck showed no obvious signs of trauma, and were held midline with a cervical collar. Pupils were 4 mm, equal, and reacted briskly
Copyright © 2001 by W.B. Saunders Company 0735-6757/01/1902-0023535.00/0 doi:l 0.1053/ajem.2001.21351