- Email: [email protected]
Severe hypercapnia caused by acute heroin overdose
Correspondence
Severe Hypercapnia Caused by Acute Heroin Overdose To the Editor:
0196-0644/$30.00 Copyright © 2004 by the American College of Emergency Physicians.
MAY 2004
43:5
ANNALS OF EMERGENCY MEDICINE
We report a case of hypercapnia apparently caused by acute heroin overdose, which was more severe than any case of hypercapnia previously reported in connection with heroin overdose. An unconscious 51-year-old man brought to the emergency department (ED) by emergency medical services (EMS) technicians had been nauseated, had vomited 3 times, and had “seizures” about a half hour earlier. A friend accompanying the patient said that he drank “a few beers” and sniffed “a lot of dope” about 2 hours before symptoms appeared, at which time he became (and remained) unconscious. He was given 100% oxygen by mask in response to spontaneous respirations. EMSreported vital signs were blood pressure 190/92 mm Hg, pulse rate 110 beats/min, and respiratory rate 8 breaths/ 6 6 5
CORRESPONDENCE
min. According to the friend, the patient had no relevant medical history but occasionally consumed alcohol and tobacco and had smoked “dope” a few times in the past. Physical examination showed blood pressure 180/100 mm Hg, pulse rate 115 beats/min, respiratory rate 8 breaths/min, temperature 99.2°F (37.4°C), normal skin color, skin wetness caused by diaphoresis, and no evidence of physical trauma. He did not respond to verbal stimuli but moved his extremities in response to painful stimuli. Respiratory rate was 8 to 10 breaths/min, and oxygen saturation was 96% after 100% oxygen was given by mask. All other vital signs were normal, and the patient was afebrile. Chest radiograph results were normal, and ECG showed sinus tachycardia at 100 beats/min. The patient’s pupils were constricted but reacted to light. Laboratory examination of arterial blood showed pH 6.79, PaCO2 224 mm Hg, PaO2 176 mm Hg, plasma bicarbonate 33.7 mEq/L (33.7 mmol/L), base excess –6.9, and 97% oxygen saturation. Within the next 5 minutes, blood gas tests were repeated and gave similar results as before. The ethyl alcohol level of 56 mg/dL (12.2 mmol/L) was not high enough to explain existing symptoms and signs. Urine toxicity screening results were positive for opioid substances only. Computed tomographic scan of the head gave normal results. Other laboratory values, including creatine phosphokinase level, were normal. Attempts to intubate were unsuccessful. Because the patient was already deeply sedated by heroin and alcohol, no sedative drugs or rapid sequence intubation were used. The patient had spontaneous breathing with good oxygen saturation and responded well to naloxone. Retesting of arterial blood one-half hour after the patient arrived in the ED showed pH 7.19, PaCO2 86 mm Hg, PaO2 78 mm Hg, plasma bicarbonate 27 mEq/L (27 mmol/L), base excess –0.8, and 97% oxygen saturation. Blood gas values measured 6 hours after the patient arrived in the ED were normal. Results of a second physical examination were normal. The patient responded well neurologically. Absence of lung injury led us to believe that the hypercapnia may have resulted from severe brain stem respiratory center depression. The next day, his condition was normal with no neurologic sequelae. Against medical advice, he left the hospital. At telephone follow-up 10 days later, a relative stated that the patient returned to normal activity without medical sequelae. Hypercapnia has protective effects1-4 against acute respiratory distress syndrome,2 a condition in which death results not from hypoxia (as previously thought) but from multisystem organ failure5; against cardiac ischemia and brain ischemia, especially in stroke, by reducing the
6 6 6
amount of oxygen needed by these organs4; and against inflammation (ie, by reducing oxygen demand of cells and thereby salvaging these cells).1 Hypercapnia may also help patients with head injury by decreasing oxygen demand of the injured brain.4 (This is the basis for so-called permissive hypercapnia.) For this reason, medically induced hyperventilation—commonly recommended for patients with head injury—may not be recommended in the future, when treatment may be designed to keep PaCO2 level high instead of low. However, further studies are needed to confirm these reported protective effects of hypercapnia. In patients with severe hypercapnia, oxygen transport in the lungs occurs by simple diffusion; therefore, oxygenation is well maintained if oxygen is delivered at high concentration,6 as in our case. Rajesh Gupta, MD Department of Emergency Medicine Westchester Medical Center Valhalla, NY Kaiser Permanente Medical Center Fresno, CA Timothy Haydock, MD Department of Internal Medicine Westchester Medical Center Valhalla, NY doi:10.1016/j.annemergmed.2003.11.024
We thank the Kaiser Foundation Hospitals Medical Editing Department for providing editorial assistance. 1. Laffrey JG, Kavanagh BP. Carbon dioxide and the critically ill—too little of a good thing? Lancet. 1999;354:1283-1286. 2. Hickling KG. Lung-protective ventilation in acute respiratory distress syndrome: protection by reduced lung stress or by therapeutic hypercapnia? Am J Respir Crit Care Med. 2000;162:2021-2022. 3. Dries DJ. Permissive hypercapnia. J Trauma. 1995;39:984-989. 4. Brian JE Jr. Carbon dioxide and the cerebral circulation. Anesthesiology. 1998;88:1365-1386. 5. Montgomery AB, Stager MA, Carrico CJ, et al. Causes of mortality in patients with the adult respiratory distress syndrome. Am Rev Respir Dis. 1985;132:485-489. 6. Ayas N, Bergstrom LR, Schwab TR, et al. Unrecognized severe postoperative hypercapnia: a case of apneic oxygenation. Mayo Clin Proc. 1998;73:51-54.
ANNALS OF EMERGENCY MEDICINE
43:5
MAY 2004
Severe Hypercapnia Caused by Acute Heroin Overdose To the Editor:
0196-0644/$30.00 Copyright © 2004 by the American College of Emergency Physicians.
MAY 2004
43:5
ANNALS OF EMERGENCY MEDICINE
We report a case of hypercapnia apparently caused by acute heroin overdose, which was more severe than any case of hypercapnia previously reported in connection with heroin overdose. An unconscious 51-year-old man brought to the emergency department (ED) by emergency medical services (EMS) technicians had been nauseated, had vomited 3 times, and had “seizures” about a half hour earlier. A friend accompanying the patient said that he drank “a few beers” and sniffed “a lot of dope” about 2 hours before symptoms appeared, at which time he became (and remained) unconscious. He was given 100% oxygen by mask in response to spontaneous respirations. EMSreported vital signs were blood pressure 190/92 mm Hg, pulse rate 110 beats/min, and respiratory rate 8 breaths/ 6 6 5
CORRESPONDENCE
min. According to the friend, the patient had no relevant medical history but occasionally consumed alcohol and tobacco and had smoked “dope” a few times in the past. Physical examination showed blood pressure 180/100 mm Hg, pulse rate 115 beats/min, respiratory rate 8 breaths/min, temperature 99.2°F (37.4°C), normal skin color, skin wetness caused by diaphoresis, and no evidence of physical trauma. He did not respond to verbal stimuli but moved his extremities in response to painful stimuli. Respiratory rate was 8 to 10 breaths/min, and oxygen saturation was 96% after 100% oxygen was given by mask. All other vital signs were normal, and the patient was afebrile. Chest radiograph results were normal, and ECG showed sinus tachycardia at 100 beats/min. The patient’s pupils were constricted but reacted to light. Laboratory examination of arterial blood showed pH 6.79, PaCO2 224 mm Hg, PaO2 176 mm Hg, plasma bicarbonate 33.7 mEq/L (33.7 mmol/L), base excess –6.9, and 97% oxygen saturation. Within the next 5 minutes, blood gas tests were repeated and gave similar results as before. The ethyl alcohol level of 56 mg/dL (12.2 mmol/L) was not high enough to explain existing symptoms and signs. Urine toxicity screening results were positive for opioid substances only. Computed tomographic scan of the head gave normal results. Other laboratory values, including creatine phosphokinase level, were normal. Attempts to intubate were unsuccessful. Because the patient was already deeply sedated by heroin and alcohol, no sedative drugs or rapid sequence intubation were used. The patient had spontaneous breathing with good oxygen saturation and responded well to naloxone. Retesting of arterial blood one-half hour after the patient arrived in the ED showed pH 7.19, PaCO2 86 mm Hg, PaO2 78 mm Hg, plasma bicarbonate 27 mEq/L (27 mmol/L), base excess –0.8, and 97% oxygen saturation. Blood gas values measured 6 hours after the patient arrived in the ED were normal. Results of a second physical examination were normal. The patient responded well neurologically. Absence of lung injury led us to believe that the hypercapnia may have resulted from severe brain stem respiratory center depression. The next day, his condition was normal with no neurologic sequelae. Against medical advice, he left the hospital. At telephone follow-up 10 days later, a relative stated that the patient returned to normal activity without medical sequelae. Hypercapnia has protective effects1-4 against acute respiratory distress syndrome,2 a condition in which death results not from hypoxia (as previously thought) but from multisystem organ failure5; against cardiac ischemia and brain ischemia, especially in stroke, by reducing the
6 6 6
amount of oxygen needed by these organs4; and against inflammation (ie, by reducing oxygen demand of cells and thereby salvaging these cells).1 Hypercapnia may also help patients with head injury by decreasing oxygen demand of the injured brain.4 (This is the basis for so-called permissive hypercapnia.) For this reason, medically induced hyperventilation—commonly recommended for patients with head injury—may not be recommended in the future, when treatment may be designed to keep PaCO2 level high instead of low. However, further studies are needed to confirm these reported protective effects of hypercapnia. In patients with severe hypercapnia, oxygen transport in the lungs occurs by simple diffusion; therefore, oxygenation is well maintained if oxygen is delivered at high concentration,6 as in our case. Rajesh Gupta, MD Department of Emergency Medicine Westchester Medical Center Valhalla, NY Kaiser Permanente Medical Center Fresno, CA Timothy Haydock, MD Department of Internal Medicine Westchester Medical Center Valhalla, NY doi:10.1016/j.annemergmed.2003.11.024
We thank the Kaiser Foundation Hospitals Medical Editing Department for providing editorial assistance. 1. Laffrey JG, Kavanagh BP. Carbon dioxide and the critically ill—too little of a good thing? Lancet. 1999;354:1283-1286. 2. Hickling KG. Lung-protective ventilation in acute respiratory distress syndrome: protection by reduced lung stress or by therapeutic hypercapnia? Am J Respir Crit Care Med. 2000;162:2021-2022. 3. Dries DJ. Permissive hypercapnia. J Trauma. 1995;39:984-989. 4. Brian JE Jr. Carbon dioxide and the cerebral circulation. Anesthesiology. 1998;88:1365-1386. 5. Montgomery AB, Stager MA, Carrico CJ, et al. Causes of mortality in patients with the adult respiratory distress syndrome. Am Rev Respir Dis. 1985;132:485-489. 6. Ayas N, Bergstrom LR, Schwab TR, et al. Unrecognized severe postoperative hypercapnia: a case of apneic oxygenation. Mayo Clin Proc. 1998;73:51-54.
ANNALS OF EMERGENCY MEDICINE
43:5
MAY 2004