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乳酸アシドーシス

著者: 栁内 秀勝 国立国際医療研究センター 国府台病院 糖尿病・内分泌代謝内科

監修: 野田光彦 国際医療福祉大学市川病院 糖尿病・代謝・内分泌内科

著者校正/監修レビュー済:2021/10/13
患者向け説明資料

概要・推奨   

  1. メトホルミン内服中に乳酸アシドーシスを発症した症例に多く認められた特徴としては、腎機能障害、脱水、シックデイ、過度のアルコール摂取、心血管・肺機能障害、手術前後、肝機能障害、高齢者などが挙げられる。高齢者だけでなく、比較的若年者でも少量投与でも、上記の特徴を有する患者で、乳酸アシドーシスの発現が報告されている。経口摂取が困難な患者や寝たきりなど、全身状態が悪い患者には投与しないことは大前提である(推奨度1)。
  1. 乳酸アシドーシス患者の血圧維持を図るためにアドレナリン、ノルアドレナリンは使用せず、ドパミン、ドブタミンを使用することが推奨される(推奨度2)。
  1. メトホルミンによる乳酸アシドーシスの治療に重炭酸透析は有効である(推奨度2)。
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要と
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧
  1. ビタミンB1欠乏による乳酸アシドーシスの治療には100mg以上のビタミンB1の静脈注射が必要である(推奨度1)。
薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
栁内 秀勝 : 未申告[2021年]
監修:野田光彦 : 特に申告事項無し[2021年]

改訂のポイント:
  1. 日本糖尿病学会「メトホルミンの適正使用に関するRecommendation」の2020年改訂を踏まえ、今回改訂を加えた。

病態・疫学・診察

疫学情報・病態・注意事項  
  1. 乳酸アシドーシスは、乳酸が何らかの原因により蓄積して生じるアシドーシスで、致死率が約50%と高く、早急な対応が求められる病態である。
  1. 乳酸アシドーシスの原因は多岐にわたるため、乳酸アシドーシスとしての正確な発症頻度は不明である。
  1. 人体はブドウ糖を細胞質における解糖系で代謝しピルビン酸から乳酸を生成する。酸素が存在する好気的条件下であれば、ピルビン酸はミトコンドリアに入り、ピルビン酸デヒドロゲナーゼの作用によりアセチルCoAに変換された後、クエン酸回路にて代謝される。このクエン酸回路が不具合なく機能していれば乳酸アシドーシスを発症することはない。
 
乳酸産生の代謝経路

ビタミンB1と糖質代謝の関係について示す。
ビタミンB1は、生体内でその活性体であるチアミンピロリン酸(TPP)に変換される。TPPは、ピルビン酸をアセチルCoAに変換するピルビン酸デヒドロゲナーゼ(PDH)の補酵素であり、PDHの活性化には必須の成分である。
ビタミンB1が不足すると、この反応系が阻害される。不足したATP産生を補うために嫌気的解糖が亢進し、ピルビン酸が多量に産生される。このピルビン酸から乳酸が大量に産生されて蓄積し、乳酸アシドーシスが起こると考えられる。
また、ビタミンB1はこのほかにもα-ケトグルタール酸デヒドロゲナーゼや、ペントースリン酸回路のトランスケトラーゼの補酵素としても重要である。
ビタミンB1は、心臓、腎臓、肝臓、脳などのエネルギー代謝活性の高い臓器に高濃度に存在し、その必要量は糖質およびエネルギー量に比例するといわれている。完全静脈栄養(TPN)時には大量の糖質が投与されることから、体内でのビタミンB1の消費量も増大する。
補酵素として機能したビタミンB1は、そのままの形または代謝されて尿中に排泄される。そのため、ビタミンB1欠乏を防止するためには、一定量を常に補給する必要がある。

出典

img1:  著者提供
 
 
 
  1. 酸素が存在しないような嫌気的条件下であれば最終産物は乳酸のみである。ブドウ糖の炭素数は6個で乳酸の炭素数は3個であるため、ブドウ糖1個が解糖系に入り乳酸に変化すると乳酸は2個生成されることになる。
  1. 嫌気的条件下では、ブドウ糖からピルビン酸という解糖系にのみ依存しATPの供給を補おうとするため乳酸の蓄積が発生する。
  1. 解糖系では、2分子のNAD+(酸化型ニコチンアミドアデニンジヌクレオチド)がNADH(還元型ニコチンアミドアデニンジヌクレオチド)に変換される。クエン酸回路が円滑に機能している状態であればNADHがNAD+に変換されるが、クエン酸回路に障害があるとNADHが蓄積する。NADHの蓄積は、ピルビン酸から乳酸への変換を促進し、さらに乳酸の蓄積をもたらす。
 
  1. 乳酸アシドーシスは入院中の患者の代謝性アシドーシスの主要な原因である(推奨度1S)。(参考文献:[1][2]
  1. さまざまな代謝性アシドーシスを来す疾患の入院中に発症する頻度を検討し、乳酸アシドーシスの頻度が高いことが明らかになっている。
問診・診察のポイント  
  1. 食事歴(ビタミンB1欠乏)、アルコール歴、薬剤歴(メトホルミン、イソニアジドなど)、輸血歴、危険な性交渉歴(肝炎、ヒト免疫不全ウイルス[HIV]感染など)、家族歴(先天性代謝異常など)
  1. 食欲不振、吐き気、嘔吐、下痢、腹痛といった消化器症状および倦怠感、筋肉痛の有無(初期症状)

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文献 

著者: P A Gabow
雑誌名: Kidney Int. 1985 Feb;27(2):472-83.
Abstract/Text
PMID 2581012  Kidney Int. 1985 Feb;27(2):472-83.
著者: Jeffrey A Kraut, Nicolaos E Madias
雑誌名: Clin J Am Soc Nephrol. 2007 Jan;2(1):162-74. doi: 10.2215/CJN.03020906. Epub 2006 Dec 6.
Abstract/Text The serum anion gap, calculated from the electrolytes measured in the chemical laboratory, is defined as the sum of serum chloride and bicarbonate concentrations subtracted from the serum sodium concentration. This entity is used in the detection and analysis of acid-base disorders, assessment of quality control in the chemical laboratory, and detection of such disorders as multiple myeloma, bromide intoxication, and lithium intoxication. The normal value can vary widely, reflecting both differences in the methods that are used to measure its constituents and substantial interindividual variability. Low values most commonly indicate laboratory error or hypoalbuminemia but can denote the presence of a paraproteinemia or intoxication with lithium, bromide, or iodide. Elevated values most commonly indicate metabolic acidosis but can reflect laboratory error, metabolic alkalosis, hyperphosphatemia, or paraproteinemia. Metabolic acidosis can be divided into high anion and normal anion gap varieties, which can be present alone or concurrently. A presumed 1:1 stoichiometry between change in the serum anion gap (DeltaAG) and change in the serum bicarbonate concentration (DeltaHCO(3)(-)) has been used to uncover the concurrence of mixed metabolic acid-base disorders in patients with high anion gap acidosis. However, recent studies indicate variability in the DeltaAG/DeltaHCO(3)(-) in this disorder. This observation undercuts the ability to use this ratio alone to detect complex acid-base disorders, thus emphasizing the need to consider additional information to obtain the appropriate diagnosis. Despite these caveats, calculation of the serum anion gap remains an inexpensive and effective tool that aids detection of various acid-base disorders, hematologic malignancies, and intoxications.

PMID 17699401  Clin J Am Soc Nephrol. 2007 Jan;2(1):162-74. doi: 10.22・・・
著者: R A Kreisberg
雑誌名: Ann Intern Med. 1980 Feb;92(2 Pt 1):227-37.
Abstract/Text The roles of changes in cellular redox, interorgan lactate flux and balance, and quantitative aspects of lactate metabolism in the pathogenesis of lactic acidosis are discussed. Altered metabolism of pyruvate is central to the development of lactic acidosis and hyperlactatemia. Lactic acidosis occurs as a result of a relative or absolute imbalance in lactate production and utilization. Lactate utilization for oxidative purposes and for the resynthesis of glucose is essential for the maintenance of acid-base balance. Because of its role in lactate homeostasis the liver may play a central role in acid-base balance. Impairment of hepatic utilization of lactate may produce lactic acidosis.

PMID 6766289  Ann Intern Med. 1980 Feb;92(2 Pt 1):227-37.
著者: N E Madias
雑誌名: Kidney Int. 1986 Mar;29(3):752-74.
Abstract/Text
PMID 3702227  Kidney Int. 1986 Mar;29(3):752-74.
著者: M Fulop, M Horowitz, A Aberman, E R Jaffe
雑誌名: Ann Intern Med. 1973 Aug;79(2):180-6.
Abstract/Text
PMID 4726533  Ann Intern Med. 1973 Aug;79(2):180-6.
著者: M H Weil, A A Afifi
雑誌名: Circulation. 1970 Jun;41(6):989-1001.
Abstract/Text
PMID 5482913  Circulation. 1970 Jun;41(6):989-1001.
著者: J D Lalau, P F Westeel, X Debussche, H Dkissi, M Tolani, B Coevoet, B Temperville, A Fournier, J Quichaud
雑誌名: Intensive Care Med. 1987;13(6):383-7.
Abstract/Text Lactic acidosis in diabetics on metformin therapy is rare but still associated with poor prognosis. The authors report here five cases. Three patients were initially with a cardiovascular collapse and all had an acute renal failure. Sodium bicarbonate haemodialysis therapy led to a dramatic improvement. Consciousness and hemodynamic status recovered rapidly. Severe metabolic and blood gases derangements were also rapidly corrected. Plasma metformin removal, appreciated by repeated blood samplings in 3 cases, was satisfactory. All patients survived. However, blood metformin levels remained abnormally high at the end of the dialytic therapy. In conclusion, (1) bicarbonate dialysis is an adequate treatment of lactic acidosis observed in diabetic patients treated with metformin since it rapidly corrects the acid-base disorders and partially removes metformin; (2) the sole accumulation of metformin is not sufficient to explain lactic acidosis since this latter might be corrected in spite of persisting high levels of blood metformin.

PMID 2822788  Intensive Care Med. 1987;13(6):383-7.
著者: D Heaney, A Majid, B Junor
雑誌名: Nephrol Dial Transplant. 1997 May;12(5):1046-7.
Abstract/Text
PMID 9175069  Nephrol Dial Transplant. 1997 May;12(5):1046-7.
著者: M E Coghlan, J P Sommadossi, N C Jhala, W J Many, M S Saag, V A Johnson
雑誌名: Clin Infect Dis. 2001 Dec 1;33(11):1914-21. doi: 10.1086/323783. Epub 2001 Oct 24.
Abstract/Text We retrospectively investigated the clinical and histopathologic features of hospitalized patients infected with human immunodeficiency virus who had symptomatic lactic acidosis syndrome at a university teaching hospital during 1995-2000. Twelve patients were identified, 11 during 1998-2000; of these, 5 died with rapid progression to otherwise unexplained multiple-organ failure. All had extensive prior exposure to nucleoside analog reverse-transcriptase inhibitors (NRTIs). At presentation, the most commonly identified NRTI component of antiretroviral regimens was stavudine plus didanosine. Eleven patients presented with abdominal pain, nausea, and/or emesis. Eight patients had prior acute weight loss (mean [+/-SD], 12+/-5.3 kg). Median venous plasma lactate levels were > or =2-fold greater than the upper limit of normal (2.1 mmol/L). Serum transaminase levels were near normal limits at presentation. Histopathologic studies confirmed hepatic macrovesicular and microvesicular steatosis in 6 patients. Concurrent chemical pancreatitis was identified in 6 patients. The increasing number of cases identified during the study period suggests that physicians better recognize symptomatic lactic acidosis and/or that cumulative NRTI exposure may increase the risk for this syndrome.

PMID 11692304  Clin Infect Dis. 2001 Dec 1;33(11):1914-21. doi: 10.108・・・
著者: Mina John, Simon Mallal
雑誌名: Curr Opin Infect Dis. 2002 Feb;15(1):23-9.
Abstract/Text Hyperlactatemia associated with use of nucleoside analogue reverse transcriptase inhibitors (NRTIs) is not a single entity but a spectrum of abnormalities. The spectrum reflects varying degrees of derangement in systemic homeostasis in the face of primary drug effects on lactate load. Lactic acidosis, characterized by metabolic acidosis, blood lactate above 5 mmol/l, hepatic steatosis and high mortality, represents the extreme end of this spectrum where there is complete decompensation. Partially compensated states of lactate excess have now been described, ranging from less fulminant symptomatic hyperlactatemia with hepatic steatosis to chronic or intermittent low-grade hyperlactatemia without acidosis, steatosis or any symptoms. At a population level, average venous lactate concentrations do rise following treatment with NRTIs but stabilize long term in the majority of cases. The average increase in systemic lactate turnover that is required to maintain such compensated blood levels is not known and research into this may provide insights into the extent of incipient mitochondrial toxicity associated with chronic NRTI use. At a tissue-specific level, it is not known which tissues or organs (liver, fat, other) are the predominant contributors to an increase in systemic lactate load, nor whether the primary defect is one of increased production, decreased elimination or both.

PMID 11964902  Curr Opin Infect Dis. 2002 Feb;15(1):23-9.
著者: M H Mokrzycki, C Harris, H May, J Laut, J Palmisano
雑誌名: Clin Infect Dis. 2000 Jan;30(1):198-200. doi: 10.1086/313594.
Abstract/Text Type "B" lactic acidosis has been described in patients receiving the nucleoside analogs zidovudine, didanosine, and fialuridine. Lactic acidosis has also been described in 4 patients receiving combination therapy with stavudine and lamivudine. We describe the development of chronic type "B" lactic acidosis in 3 patients receiving stavudine as a single agent and in 2 patients receiving combination therapy with stavudine and either lamivudine or delavirdine, a nonnucleoside analog. All patients presented with abdominal pain, vomiting, and hepatic steatosis. Other signs of mitochondrial toxicity included pancreatitis and myopathy (2 cases). The mean duration of stavudine therapy was 9.4 months, and the mean observed peak lactate level+/-SD was 10.3+/-5 mmol/L. After discontinuation of stavudine treatment, lactic acidosis improved in 4 patients after 4-60 weeks, and 1 patient died. Evaluations for other causes of lactic acidosis, including hypoxemia, malignancy, sepsis, and cardiogenic shock, were negative.

PMID 10619755  Clin Infect Dis. 2000 Jan;30(1):198-200. doi: 10.1086/3・・・
著者: K D Miller, M Cameron, L V Wood, M C Dalakas, J A Kovacs
雑誌名: Ann Intern Med. 2000 Aug 1;133(3):192-6.
Abstract/Text BACKGROUND: An association between use of zidovudine and didanosine and a rare but life-threatening syndrome of hepatic steatosis, lactic acidosis, and myopathy has been reported.
OBJECTIVE: To describe the syndrome of hepatic steatosis, lactic acidosis, and myopathy in four patients taking stavudine.
DESIGN: Case series.
SETTING: A community hospital in Washington, D.C., and National Institutes of Health Clinical Center, Bethesda, Maryland.
PATIENTS: Two men and two women with HIV-1 infection who were taking stavudine presented with lactic acidosis and elevated levels of aminotransferases. All patients required intensive care.
MEASUREMENTS: Levels of lactic acid, alanine aminotransferase, aspartate aminotransferase, amylase, and lipase; computed tomography of the abdomen; liver biopsy (two patients); and muscle biopsy (two patients).
RESULTS: Histologic findings consistent with mitochondrial injury confirmed the diagnosis of hepatic or muscle abnormality.
CONCLUSION: Because hepatic steatosis may be life-threatening, physicians should consider it as a possible cause of elevated hepatic aminotransferase levels among patients taking stavudine.

PMID 10906833  Ann Intern Med. 2000 Aug 1;133(3):192-6.
著者: Vicente Falcó, Dolors Rodríguez, Esteban Ribera, Esteban Martínez, José Maria Miró, Pere Domingo, Ruth Diazaraque, José R Arribas, Juan J González-García, Francesc Montero, Lluis Sánchez, Albert Pahissa
雑誌名: Clin Infect Dis. 2002 Mar 15;34(6):838-46. doi: 10.1086/339041. Epub 2002 Feb 13.
Abstract/Text Lactic acidosis is a rare but often fatal complication reported in some human immunodeficiency virus (HIV)-infected patients treated with nucleoside-analogue reverse-transcriptase inhibitors. We report a series of 12 patients with HIV infection treated with nucleoside analogues who developed unexplained metabolic acidosis. We have also reviewed 60 additional published cases. The aim of the present study is to describe the clinical picture, prognostic factors, and final outcome for nucleoside-associated lactic acidosis. The mortality rate is high: 33% for our patients, and 57% for the patients described in the literature. In the multivariate analysis, a lactate serum level of >10 mM (odds ratio [OR], 13.23; 95% confidence interval [CI], 2.96-59.25) was the only factor associated with higher mortality. The administration of specific therapy with cofactors against acidosis was associated with a lower mortality (OR, 0.17; 95% CI, 0.04-0.73). We conclude that specific therapy with cofactors may improve the outcome for patients with this syndrome.

PMID 11850865  Clin Infect Dis. 2002 Mar 15;34(6):838-46. doi: 10.1086・・・
著者: K Brinkman
雑誌名: AIDS. 2001 Apr 13;15(6):795-7.
Abstract/Text
PMID 11371695  AIDS. 2001 Apr 13;15(6):795-7.
著者: E B Marliss, J L Ohman, T T Aoki, G P Kozak
雑誌名: N Engl J Med. 1970 Oct 29;283(18):978-80. doi: 10.1056/NEJM197010292831807.
Abstract/Text
PMID 4990419  N Engl J Med. 1970 Oct 29;283(18):978-80. doi: 10.1056/・・・
著者: H J Adrogué, N E Madias
雑誌名: N Engl J Med. 1998 Jan 1;338(1):26-34. doi: 10.1056/NEJM199801013380106.
Abstract/Text
PMID 9414329  N Engl J Med. 1998 Jan 1;338(1):26-34. doi: 10.1056/NEJ・・・
著者: R J Velez, B Myers, M S Guber
雑誌名: JPEN J Parenter Enteral Nutr. 1985 Mar-Apr;9(2):216-9.
Abstract/Text Total parenteral nutrition is one of the most important recent advances in medicine. The delivery of total parenteral nutrition, however, can be associated with a broad spectrum of complications ranging from mechanical (catheter related) to metabolic. We have recently seen a previously unreported complication of total parenteral nutrition - three patients maintained on total parenteral nutrition, who did not receive vitamins and experienced the acute onset of life-threatening metabolic acidosis with pH values as low as 6.70. All responded promptly and completely to the administration of intravenous thiamine, and thus were probably examples of acute beriberi. Acute beriberi is a well-documented syndrome which usually occurs in nutritionally compromised individuals outside the hospital setting who lack thiamine in their diet. Without thiamine, glucose cannot enter the Krebs cycle in order to be completely oxidized for energy production and therefore, accumulates as lactic acid. This lactic acidosis is refractory to any treatment except thiamine and will result in cardiovascular collapse if the vitamin is not administered.

PMID 3921738  JPEN J Parenter Enteral Nutr. 1985 Mar-Apr;9(2):216-9.
著者: S M Forsythe, G A Schmidt
雑誌名: Chest. 2000 Jan;117(1):260-7.
Abstract/Text Lactic acidosis often challenges the intensivist and is associated with a strikingly high mortality. Treatment involves discerning and correcting its underlying cause, ensuring adequate oxygen delivery to tissues, reducing oxygen demand through sedation and mechanical ventilation, and (most controversially) attempting to alkalinize the blood with IV sodium bicarbonate. Here we review the literature to answer the following questions: Is a low pH bad? Can sodium bicarbonate raise the pH in vivo? Does increasing the blood pH with sodium bicarbonate have any salutary effects? Does sodium bicarbonate have negative side effects? We find that the oft-cited rationale for bicarbonate use, that it might ameliorate the hemodynamic depression of metabolic acidemia, has been disproved convincingly. Further, given the lack of evidence supporting its use, we cannot condone bicarbonate administration for patients with lactic acidosis, regardless of the degree of acidemia.

PMID 10631227  Chest. 2000 Jan;117(1):260-7.
著者: D J Cooper, K R Walley, B R Wiggs, J A Russell
雑誌名: Ann Intern Med. 1990 Apr 1;112(7):492-8.
Abstract/Text STUDY OBJECTIVE: To determine whether correction of acidemia using bicarbonate improves hemodynamics in patients who have lactic acidosis.
DESIGN: Prospective, randomized, blinded, crossover study. Each patient sequentially received sodium bicarbonate and equimolar sodium chloride. The order of the infusions was randomized.
SETTING: Intensive care unit of a tertiary care hospital.
PATIENTS: Fourteen patients who had metabolic acidosis (bicarbonate less than 17 mmol/L and base excess less than -10) and increased arterial lactate (mean, 7.8 mmol/L). All had pulmonary artery catheters and 13 were receiving catecholamines.
MEASUREMENTS AND MAIN RESULTS: Sodium bicarbonate (2 mmol/kg body weight over 15 minutes) increased arterial pH (7.22 to 7.36, P less than 0.001), serum bicarbonate (12 to 18 mmol/L, P less than 0.001), and partial pressure of CO2 in arterial blood (PaCO2) (35 to 40 mm Hg, P less than 0.001) and decreased plasma ionized calcium (0.95 to 0.87 mmol/L, P less than 0.001). Sodium bicarbonate and sodium chloride both transiently increased pulmonary capillary wedge pressure (15 to 17 mm Hg, and 14 to 17 mm Hg, P less than 0.001) and cardiac output (18% and 16%, P less than 0.01). The mean arterial pressure was unchanged. Hemodynamic responses to sodium bicarbonate and sodium chloride were the same. These data have more than 90% power of detecting a 0.5 L/min (7%) change in mean cardiac output after administration of sodium bicarbonate compared with that after sodium chloride. Even the 7 most acidemic patients (mean pH, 7.13; range, 6.90 to 7.20) had no significant hemodynamic changes after either infusion.
CONCLUSIONS: Correction of acidemia using sodium bicarbonate does not improve hemodynamics in critically ill patients who have metabolic acidosis and increased blood lactate or the cardiovascular response to infused catecholamines in these patients. Sodium bicarbonate decreases plasma ionized calcium and increases PaCO2.

PMID 2156475  Ann Intern Med. 1990 Apr 1;112(7):492-8.
著者: M L Weisfeldt, A D Guerci
雑誌名: JAMA. 1991 Oct 16;266(15):2129-30.
Abstract/Text
PMID 1656109  JAMA. 1991 Oct 16;266(15):2129-30.
著者: F Kette, M H Weil, M von Planta, R J Gazmuri, E C Rackow
雑誌名: Circulation. 1990 May;81(5):1660-6.
Abstract/Text We investigated the effects of carbon dioxide-producing and carbon dioxide-consuming buffers on intramyocardial pH and on cardiac resuscitability. In 29 pigs, intramyocardial pH was continuously measured with a glass electrode advanced into the midmyocardium of the posterior left ventricle through a diaphragmatic window. Ventricular fibrillation (VF) was electrically induced by alternating current applied to the epicardium of the left ventricle. After 3 minutes of VF, precordial compression was begun and continued for an interval of 8 minutes. Sodium bicarbonate (a carbon dioxide-generating buffer), Carbicarb (a carbon dioxide-consuming buffer), and hypertonic sodium chloride (control solution) were infused into the right atrium during cardiac resuscitation. Defibrillation was attempted by transthoracic direct-current shock after 11 minutes of VF. Intramyocardial pH progressively decreased from an average value of 7.26 before VF to 6.87 before infusion of buffers. Systemic circulation and great cardiac vein pH significantly increased after administration of the two buffer agents. However, intramyocardial pH continued to decline to an average of 6.62 after 11 minutes of VF, and this decline was not altered by either buffer solution or by the saline control. As in previous studies, resuscitability was closely related to coronary perfusion pressure at the time of direct-current countershock but not to pH. Accordingly, the rationale of reversing acidosis by the administration of these buffer agents is not supported. Even more important, neither carbon dioxide-consuming nor carbon dioxide-producing buffers altered myocardial acidosis or improved myocardial resuscitability under controlled experimental conditions of cardiac arrest.

PMID 2158865  Circulation. 1990 May;81(5):1660-6.

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