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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acid-base terminology including the sue of SI units is reviewed. The historical reasons why nomograms have been particularly used in acid-base work are discussed. The theoretical basis of the Henderson-Hasselbalch equation is considered. It is emphasized that the solubility of CO2 in plasma and the apparent first dissociation constant of carbonic acid are not chemical constants when applied to media of uncertain and varying composition such as blood plasma. The use of the Henderson-Hasselbalch equation in making hypothermia corrections for PCO2 is discussed. The Astrup system for the in vitro determination of blood gases and derived parameters is described and the theoretical weakness of the base excess concept stressed. A more clinically-oriented approach to the assessment of acid-base problems is presented. Measurement of blood [H+] and PCO2 are considered to be primary data which should be recorded on a chart with in vivo CO2-titration lines (see below). Clinical information and results of other laboratory investigations such as plasma bicarbonate, PO2,P50 are then to be considered together with the primary data. In order to interpret this combined information it is essential to take into account the known ventilatory response to metabolic acidosis and alkalosis, and the renal response to respiratory acidosis and alkalosis. The use is recommended of a chart showing the whole-body CO2-titration points obtained when patients with different initial levels of non-respiratory [H+] are ventilated. A number of examples are given of the use of this [H+] and PCO2 in vivo chart in the interpretation of acid-base data. The aetiology, prognosis and treatment of metabolic alkalosis is briefly reviewed. Treatment with intravenous acid is recommended for established cases. Attention is drawn to the possibility of iatrogenic production of metabolic alkalosis. Caution is expressed over the use of intravenous alkali in all but the severest cases of metabolic acidosis. The role of 2,3-diphosphoglycerate on tissue oxygenation is stressed and use of intravenous sodium phosphate as an alternative to intravenous bicarbonate is mentioned.
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PMID:The physiological assessment of acid-base balance. 23 27

Metabolic acidosis immediately after surgical operation is followed by metabolic alkalosis. Hormonal change by surgical stress and anaerobic glucolysis due to tissue ischemia cause initial lactic acidosis. Later alkalosis may be caused by secondary aldosteronism and bicarbonate production from lactate and citrate supplied by massive infusion and transfusion. Postoperative complications, such as respiratory insufficiency, renal failure and hypovolemic or septic shock, cause acidosis. In the gastrointestinal surgery, acidosis can be caused by starvation and loss of bicarbonate contained in bile, pancreatic juice or intestinal fluid, and alkalosis can be caused by loss of HCl in gastric juice. Severe acidosis can be caused by extracorporeal circulation, hypothermia, low output syndrome or declamping shock in cardioaortic surgery.
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PMID:[Acid-base disturbances in surgical operation]. 143 18

The first 100 liver transplantations at the Mayo Clinic were performed in 83 patients, who required a total of 917 patient days in the intensive-care unit (ICU). The mean duration of stay in the ICU was 5.91 days after liver transplantation and 6.15 days for patients who subsequently required readmission to the ICU. During the immediate postoperative period, hypothermia and hyperglycemia invariably occurred. Later during the initial admission or on readmission to the ICU, there arose the possibility of infections and renal insufficiency. Prompt diagnosis and treatment are necessary for hypertension, hypokalemia, severe metabolic alkalosis, fever, altered mental status, oliguria, and signs of graft failure in liver transplant patients. In our patient series, selective bowel decontamination minimized the occurrence of gram-negative and fungal sepsis, and use of antihypertensive agents and correction of coagulopathies may have decreased the risk of intracranial bleeding in patients with hypertension and clotting defects. Anticipation of potential conditions postoperatively and early implementation of treatment are key factors in the successful ICU management of patients who have undergone liver transplantation.
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PMID:Intensive-care unit experience in the Mayo liver transplantation program: the first 100 cases. 265

The cardiorespiratory effects of reducing body temperature to 30 degrees C (by packing in ice) and subsequent metabolic alkalosis (by infusion of NaHCO3) were studied in six anesthetized, paralyzed, and artificially ventilated (FIO2 = 0.4) dogs. Heart rate decreased from 135 +/- 6 beats/min (mean +/- S.E.) at 37 degrees C to 84 +/- 4 at 30 degrees C; it increased to 96 +/- 4 after 2 h alkalosis. Cardiac output decreased from 1.84 +/- 0.14 to 0.66 +/- 0.08 l/min and then increased to 0.83 +/- 0.07. pHa increased, as expected on cooling, from 7.41 +/- 0.07 to 7.49 +/- 0.03; with bicarbonate it increased to 7.79 +/- 0.03. PaCO2 decreased on cooling from 32.9 +/- 1.4 to 21.7 +/- 1.2 torr, increasing with bicarbonate to 27.9 +/- 1.4 torr. VO2 decreased from 104.9 +/- 5.1 ml . min-1 . m-2 at 37 degrees C to 51.3 +/- 2.0 at 30 degrees C; with alkalosis it increased by 16.2% to 59.6 +/- 3.3 ml . ml-1 . m-2, an increase identical to that seen in normothermic alkalosis. Thus, the mechanism of the alkalosis-induced increase in oxygen consumption is not suppressed by the decrease in VO2 seen in hypothermia, and the increase in VO2 appears to be a consequence of the change in relative alkalinity rather than the increase in pH.
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PMID:Cardiorespiratory effects of hypothermia and bicarbonate alkalosis. 677 49

Hypokalemic periodic paralysis is a rare genetic disorder characterized by recurrent attacks of skeletal muscle weakness with associated hypokalemia which is precipitated by stress, cold, carbohydrate load, infection, glucose infusion, hypothermia, metabolic alkalosis, anesthesia, and steroids. We encountered one such incidence of prolonged recovery after general anesthesia, which on further evaluation revealed a case of hypokalemic paralysis. The key to successful management of such a patient was vigilant pre-operative evaluation, perioperative monitoring, and aggressive treatment of hypokalemia when it occurs.
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PMID:Hypokalemic periodic paralysis. 2383 4

We present the case of a 36-year-old man with type-1 diabetes who was hospitalized with diabetic ketoacidosis (DKA). On admission, he had hypothermia, hypokalemia and combined metabolic and respiratory alkalosis, in addition to hyperglycemia. Hypothermia, hypokalemia and metabolic alkalosis, with a concurrent respiratory alkalosis, are not commonly seen in DKA. After admission, intravenous infusion of 0.45% saline was administered, which resulted in the development of pure metabolic acidosis. After starting insulin infusion, hypokalemia and hypophosphatemia became evident and finally resulted in massive rhabdomyolysis. Hyperkalemia accompanying oliguric acute kidney injury (AKI) warranted initiation of hemodialysis (HD) on Day-five. On the 45th hospital day, his urine output started to increase and a total of 22 HD sessions were required. We believe that in this case severe dehydration, hypothermia and hypokalemia might have contributed to the initial symptoms of DKA as well as the prolongation of AKI.
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PMID:Hypothermia and hypokalemia in a patient with diabetic ketoacidosis. 2602 32

The various complications of continuous renal replacement therapy (CRRT) are mostly preventable. Hemodynamic disturbances are dominated by hypotension due to the modification of volume status, myocardial dysfunction, cardiac arrhythmia, or modification of systemic vascular resistances, which are correlated with body temperature changes. Metabolic complications remain at the forefront and have profoundly changed with the use of regional citrate anticoagulation (RCA). RCA may lead to two distinct situations: citrate overload and citrate accumulation, respectively, responsible for metabolic alkalosis and metabolic acidosis. Electrolyte imbalance is also a classic occurrence with RCA. The chelation of cations by citrate results in hypocalcemia and hypomagnesemia in case of inappropriate substitution. Hemorrhagic complications have been drastically reduced mostly for two reasons: the use of systematic ultrasound guidance for the insertion of dialysis catheters and the use of RCA instead of systemic heparin anticoagulation. Hypothermia induced by CRRT and complications associated with prolonged bed rest are also better controlled today. Finally, the removal of undesired substances remains a major issue, especially when it comes to antibiotics, vitamins and micronutrients, molecules for which the intake should be adapted in case of CRRT.
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PMID:Clinical Complications of Continuous Renal Replacement Therapy. 2959 22