Respiratory Function and Acid-Base Status in Accidental Hypothermia Assessed by Arterial Blood Gas Analysis

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Respiratory Function and Acid-Base Status in Accidental Hypothermia Assessed by Arterial Blood Gas Analysis Original Article Respiratory Function and Acid-base Status in Accidental Hypothermia Assessed by Arterial Blood Gas Analysis Michio OKADAand Fumiaki NISHIMURA To study the respiratory function and acid-base status in hypothermia, we retrospectively reviewed data of arterial blood gas analysis obtained from 63 patients with accidental hypothermia on admission. Twenty- nine showed acidemia and 16 showed alkalemia. The following results were obtained from 57 patients in whom blood gas analysis was performed in room air. PaCO2was 46 mmHgor more in 2 and 34 mmHgor less in 46. Most of the patients exhibiting acidemia had metabolic acidosis except 2 with severe pneumonia or subdural hematoma. PaCO2was low even in the patients with alkalemia. PaO2 was 60 mmHgor less in 8, of whom7 had pneumonia, and 70 mmHgor more in most of the patients without pneumonia. Wefound that patients with accidental hypothermia generally showed a respiratory function proportionate to their decreased metabolism or hyperventilation, and most of the patients with acidemia exhibited metabolic acidosis. Key words: Metabolic acidosis, Respiratory acidosis Accidental hypothermia is not an uncommon In an attempt to clarify the respiratory function and condition and is often associated with acidosis and acid-base status in patients with accidental hypo- can result in a high mortality (1-7). Although the thermia, a retrospective study of the arterial blood initial respiratory response to hypothermia is one of gas analysis data of patients with accidental stimulation, the respiration begins to become hypothermia, including many without pneumonia shallow and the rate decreases as the core or circulatory failure, was carried out. temperature drops to below approximately 32°C (8). PATIENTS AND METHODS However, in the hypothermic state, metabolism also decreases, and an 8°C drop in body temperature Wereviewed retrospectively the data of arterial causes a 50%decrease in the production of carbon blood gas analysis, which had been performed dioxide (9, 10). Thus, to manage patients with immediately after admission in 63 of the 74 patients accidental hypothermia, it is important to know with accidental hypothermia whowere admitted to whether this reduction in respiratory function is Tokyo Metropolitan Charity Hospital. Wemoni- proportional to the decreased rate of metabolism, tored the core body temperature with a thermometer or not. As it is difficult to assess the effects of placed in the rectum, and defined hypothermia as hypothermia on the respiratory function in man this a core body temperature of 34.0°C or lower. The issue is still controversial; the changes that occur hypothermia occurred by exposure to cold weather during induced hypothermia under general as a result of alcohol intoxication or weakness anesthesia largely reflect the mechanical ventilation, secondary to underlying diseases. Although the and in patients with accidental hypothermia, the duration of exposure to cold weather could not be findings are often complicated by changes produced determined in most of the patients, it was estimated by coexisting pneumonia, or circulatory failure (1). to range from a few hours to a few days. Manyof From the Department of Internal Medicine, Tokyo Saiseikai Central Hospital, Tokyo Received for publication September 4, 1989; Accepted for publication July 27, 1990 This work originated from the Department of Internal Medicine, Tokyo Saiseikai Central Hospital, Tokyo, Japan Reprint requests should be addressed to Michio Okada, MD,Second Department of Internal Medicine, School of Medicine, Kyorin University, 6-20-2 Shinkawa, Mitaka 181, Japan 500 Jpn J Med Vol 29, No 5 (September, October 1990) Blood Gas in Accidental Hypothermia the patients were alcoholics and/or poorly nourished A 7i .. vagrants. Their mean age was 52 years. Although more detailed clinical data from these 74 patients can be found in a previous study (7), the important 7.2- . à"à" : "à""à" data concerning the underlying causes of hypo- thermia in 63 patients in this study is included here. Q7.aà" à" Thirty-one patients were under the influence of alcohol, 18 had pneumonia or pulmonary tuber- 6.8 culosis, 4 had head injuries, 3 had diabetic 6.6 ketoacidosis and 2 had drug intoxication. Ta 26 28 30 32 34 The arterial blood gas analysis was carried out Q BODY TEMPERATURECc) by percutaneous puncture of the brachial or femoral b 60r arteries. At the time of blood gas analysis, 3 patients had 50 been treated by assisted respiration and 3 patients by oxygen administration. In the remaining 57 patients, the blood gas analysis was performed in I3°- à" ,à" "'*{ room air. PaO2, PaCO2 and pH were determined with a blood gas analyzer (M 175, Corning), and 20à"'à">." ' à"'" corrected for body temperature according to the 10- 8 Kelman and Nunn formula: ty« - -, _-i , pHt = pH37-0.015(t-37) 24 26 28 30 32 34 PO2t = PO2eA(t"37) BODY TEMPERATURECc) PCO t = PCO e10-044^37^ Fig. 1-A. Arterial pH and body temperature (A = 0.012+0.062 [i-e-^ioo-o. sat^ on admission in 63 patients. B. PaCO2and body temperature on admission in 57 patients in whom where pHt, PCO2t, and PO2t = pH, PCO2 and blood gas analysis was performed in roomair. PO2 corrected for body temperature (t), and t = body temperature at which the arterial blood gas temperature. Of 8 patients in whomthe hypothermia analysis was performed. The electrode temperature appeared to have contributed largely to death, 6 was maintained at 37°C. showed acidemia, but none had alkalemia. For statistical comparisons, the unpaired t test Weinvestigated PaCO2,PaO2, and the relation was employed, p <0.05 was considered significant. between PaCO2 and pH in 57 patients after ex- cluding the 6 who had been treated by assisted RESULTS respiration (3 patients) or oxygen administration (3 The body temperature of the 63 patients on patients) by the time of blood gas analysis. There admission ranged from 24.1°C to 33.8°C (mean, was no apparent association between PaCO2and 29.8°C). Pneumonia was observed in 18 patients. body temperature (Fig. 1-B). PaCO2 was 46 mmHg Assisted respiration was required immediately after or more in 2 patients, 34.1-45.9 mmHgin 9, and admission before blood gas analysis in 3 patients: 34 mmHgor less in 46 patients. One patient with this was due to severe pneumoniain one patient, to a PaCO2of 60.3 mmHghad severe pneumonia, a cessation of breathing following ventricular fibrilla- pH of7.08 and a PaO2 of 16.8 mmHg. The same tion in another, and to ataxic respiration induced patient was also suffering from drug intoxication. by intracranial hemorrhage in the third. No patients Another patient with a PaCO2 of 48.3 mmHgwas required assisted respiration due to impaired in a deep comaon admission, and died from acute respiratory function caused by the hypothermia. subdural hematomaon the day. There were no The arterial pHwas less than 7.36 in 29 patients records about his respiratory status on admission. and more than 7.44 in 16 (Fig. 1-A). There appeared Evaluation of the relation between pH and to be no definite association between pH and body PaCO2indicated base deficit in all the patients with Jpn J Med Vol 29, No 5 (September, October 1990) 501 Okada and Nishimura acidemia (Fig. 2). PaCO2 was also decreased in patients with a normal pH showed a decreased most of them. Only the 2 above-mentioned patients PaCO2 and base deficit. exhibited an increase in PaCO2. Seven patients were Anemia with a hemoglobin value of 10 g/dl or within the range of acute base deficit suggesting in- less was observed in 13 patients on admission (Fig. adequate compensationfor metabolic acidosis by 2). All of these patients revealed a pH of 7.36 or hyperventilation. PaCO2and pHin 3 patients with moreand were in a state of acute or chronic diabetic keto-acidosis was 10.1, 14.9 and ll.6 hypocapnia. In 10 patients with a PaO2 level of 70 mmHg, and 6.88, 6.92 and 6.86, respectively. All mmHgor less, the extent of decrease in PaO2was 3 patients were between acute and chronic base not associated with the severity of metabolic acidosis deficit. In all the patients with alkalemia, PaCO2 (Fig. 2). The base excess was -17.2±8.3 was decreased. About half of them with alkalemia (mean± lSD) in 20 patients with a systolic blood showed a normal base excess, and the remaining half pressure of 80 mmHg or less and -7.86±6.8 were in a state of base deficit. None of them ex- (mean ± 1SD) in 37 patients with that of more than hibited an abnormal base excess. Most of the 80 mmHg; more severe metabolic acidosis was Paco2 .^ BASE EXCESS EXTRACELL. mm"9\ ri^^^^^^^^*\ BASE EXCESS 150" ^/C^ +5 +10\+20\+30 mmol/l 140- a/\\° \ \+15\+25\ 130" &F-*\ \ \\\\\ -120" <^\10 \ \ \a\\\ no- T 4 \ \°\ \\VvAoA \ \ \.\\YVt^\V\ 5°- -25 \ ^V" \ °\r^\<#\V\\\ -£å å v\PLASMAHXDRQGENCARBONATE XlNQRM^L _/\ \ \\\ ° \ / à"«? / \ *å \ \ I à"* \/ l\/ \ \ \ '5" \ \/ à"o V \ \ \ -30 V ^ /\ \ \ \ ! \o #6.9 7.0 ^7.1 d/\: 7.2 7.3 |7.4?V\\ 7.5 7.6 7.7 PLASMA pH ACIDEMIA NORMAL ALKALEMIA i i i t Fig. 2. Acid-base balance in 57 patients with accidental hypothermia. Closed symbols = Twenty patients with a systolic blood pressure of 80 mmHgor less, Boxes = Thirteen patients who had anemia with a hemoglobin value of 10 g/dl or less, * = Ten patients with a PaO2 level of 70 mmHgor less. 502 Jpn J Med Vol 29, No 5 (September, October 199G) Blood Gas in Accidental Hypothermia patient. He died from severe pneumonia. (p<0.001)observed in (Fig.the patients2). with a lower blood pressure DISCUSSION Nodefinite association was found between PaO2 and body temperature (Fig.
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