Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The necessity of providing alkalizing therapy after re-establishment of the local circulation was studied in 10 otherwise healthy patients with intermittent claudication. No such necessity was found in providing stable peroperative circulation, normo- to slight hypothermia, adequate infusions, and normal acid-base values prior to arterial clamping. It is pointed out that alkalosis can cause circulatory problems that are just as serious as those occurring with acidosis; therefore the routine use of alkalizing agents during vascular surgery is inadvisable. Should unstable circulatory parameters occur and hypoperfusion be suspected, then repeated control of the acid-base values is indicated.
 ...
PMID:Acid-base status before and after arterial clamping. 1 71

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.
 ...
PMID:The physiological assessment of acid-base balance. 23 27

It is reported on the successful treatment of a 60-year-old female patient with extreme accidental hypothermia (body temperature 24 degrees C). Cardiac and pulmonary complications could be commanded by intensiv-therapeutic measures. As interesting findings at the time of hospitalisation are exhibited the Osborn-wave in the ECG (first description in a clinical case), the alkalosis (pH 7.52) and a good diuresis (60 ml/min). The prognosis of the accidental hypothermia depends on the duration of the chilling, the rapid transfer under control of a physician into an intensive therapy facility, optimal control and therapy of cardio-vascular and respiratory system, the time of re-warming and the previous injuries as well as the concomitant diseases. The time of re-warming is of importance especially in asystolia and in ventricular fibrillation, in order to reach the defibrillation threshold of 26.6 degrees C. The forms of re-warming (combination of inner and outer re-warming) are to be chosen individually and according to the possibilities. They do not play the role expected for the prognosis. A repeated examination of the patient described after 14 months showed normal according to age organic functions without late lesions.
 ...
PMID:[Accidental hypothermia--case contribution to the clinical aspects and therapy]. 106 95

We investigated the effect of 30 degrees C whole body hypothermia on neuronal injury, astroglial reactivity and intracellular pH in rats subjected to 15 min of forebrain ischemia. Experimental groups included: (1) normothermic ischemia (n = 8), ischemia induced under 37 degrees C body temperature, (2) hypothermic ischemia (n = 6), ischemia induced under 30 degrees C body temperature. Cerebral intracellular pH was measured using in vivo 31P NMR spectroscopy over 7 days. Neuronal injury and astrocytic reactivity were evaluated using hematoxylin and eosin staining, and immunoreactivity to glial fibrillary acidic protein, respectively. Normothermic animals revealed significant alkalosis (P less than 0.01) at 48 h after ischemia compared to the pre-ischemic value. No significant intracellular pH change was detected after ischemia in the hypothermic group. Ischemic neuronal injury was prevented in the hypothermic animals, compared to the severe neuronal injury found in the normothermic animals (P less than 0.01). The marked astrocytosis of normothermic animals was significantly inhibited in the hypothermic animals (P less than 0.01). Our data indicate, that hypothermia significantly inhibits neuronal injury as well as post-ischemic alkaloids and astrocytosis, induced by 15 min of forebrain ischemia in the rat.
 ...
PMID:Neuronal damage, glial response and cerebral metabolism after hypothermic forebrain ischemia in the rat. 138 61

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.
 ...
PMID:[Acid-base disturbances in surgical operation]. 143 18

Effects of pH and PaCO2 on cerebral as well as systemic hemodynamics and oxygen consumption were investigated during moderate hypothermia under 0.5% halothane anesthesia. Twenty-seven adult mongrel dogs were cooled to 28 degrees C (brain temperature) with a surface cooling method. They were divided into 3 groups, pH-stat (pH 7.35 n = 9), alpha-stat (pH 7.48 n = 9), and alkalosis (pH 7.70 n = 9). During hypothermia cardiac index fell to 74%, 56%, and 45%, and cerebral blood flow to 54%, 42%, and 36% in pH-stat, alpha-stat and alkalosis groups, respectively. Cerebral and systemic oxygen consumptions decreased to approximately 54% and 47%, respectively in all groups. Cerebrospinal fluid pH rose from 7.36 precooling to 7.49 (pH-stat), 7.53 (alpha-stat), and 7.72 (alkalosis). We concluded from these results that pH-stat and alpha-stat management have no significant effect on either hemodynamics or metabolism during moderate hypothermia but alkalosis management has deleterious effects because of the alkalinity itself and of the hyperventilation by which the alkalosis is induced.
 ...
PMID:[Optimal pH and PaCO2 during moderate hypothermia]. 157 16

We tested the hypotheses that hypoxic toads (Bufo marinus) in a thermal gradient would select a lower than normal temperature and that this behavioral response would be beneficial. Under normoxic conditions, selected body temperature was 24.2 +/- 3.6 degrees C. When inspired O2 was 10% or less, mean selected temperature decreased to 15.3 +/- 2.4 degrees C. The theoretical advantages of hypoxia-induced hypothermia we tested include (1) a reduction of oxygen uptake (VO2) by a Q10 effect; (2) increased arterial saturation (SaO2), (3) a decreased ventilatory response, and (4) a decreased stress response. Gas exchange, hematocrit, hemoglobin, SaO2, PaO2 and pH were measured at 25 degrees C (normal preferred temperature) and 15 degrees C (hypoxia preferred temperature) in toads breathing normoxic or hypoxic gas mixtures. During graded hypoxia at 15 degrees C, SaO2 was significantly increased and VO2 was significantly reduced compared with 25 degrees C. Graded hypoxia did not significantly affect VO2 at 25 degrees C, despite evidence for increased ventilation at that temperature (increased pH and respiratory exchange ratio, RE). At 15 degrees C, graded hypoxia had a significant effect on VO2 only at an inspired O2 of 4%. Increased RE with hypoxia was significant at 25 degrees C but not at 15 degrees C. Hematocrit and [hemoglobin] rose significantly during graded hypoxia at 25 degrees C but did not change at 15 degrees C. Toads exposed to 10% O2 (the value that elicits behavioral hypothermia) showed a significant respiratory alkalosis at 25 degrees C but not at 15 degrees C. Likewise, hypoxia caused a significant drop in SaO2 and PO2 at 25 degrees C. Cooling to 15 degrees C during hypoxia caused a significant rise in SaO2 but no change in PaO2. In conclusion, behavioral hypothermia is a beneficial response to hypoxia in Bufo marinus.
 ...
PMID:Physiological significance of behavioral hypothermia in hypoxic toads (Bufo marinus). 194 Jul 67

The role of the anesthesiologist in myocardial protection is to optimize myocardial oxygen balance during the perioperative period. Nonpharmacological steps that can be taken to achieve this revolve around maintaining a satisfactory hemoglobin concentration and oxyhemoglobin saturation through maximizing ventilation. In addition, alkalosis and hypothermia should be prevented since they cause a left shift of the oxyhemoglobin dissociation curve, thus interfering with tissue oxygen delivery. Hypocarbia increases coronary vascular resistance. Blood volume must be adequate with an optimal hemoglobin concentration. Pharmacological measures should also be used, and it is important to continue through the perioperative period any previously administered cardioactive drugs. Furthermore, in the prebypass period, tachycardia may not be controlled by anesthetics; unless the tachycardia is paroxysmal, beta blockers are the drugs of choice. Depending on the cause, diastolic hypotension also needs to be treated either with volume, vasoconstrictors, or inotropes. Likewise, major hypertension can produce increased demand and, again depending on the cause, either anesthetics, vasodilators, beta blockers, or calcium blockers may be useful. Finally, myocardial ischemia without obvious cause probably should be treated with nitroglycerin or calcium blockers. During surgery, the effect of the anesthetic drugs on myocardial oxygen balance is important.
 ...
PMID:Myocardial protection: what the anesthesiologist does. 213 51

Extracorporeal circulation (ECC), with its shock-like pulmonary perfusion, leads to pathomorphologic and functional pulmonary changes, the postperfusion syndrome. This study investigated the effects of different types of ventilation during ECC on postoperative pulmonary function and the resulting pulmonary blood gas changes. METHOD. Thirty patients scheduled for aortocoronary bypass surgery were studied. Patients with pre-operative left ventricular end-diastolic pressures exceeding 15 mmHg or signs of right ventricular failure, pulmonary hypertension, or pre-existing pulmonary disease were excluded. The patients were randomly assigned to one of the following three groups: Group 1 (n = 10): static pulmonary inflation during ECC, PEEP 5-10 cm H2O, F1O2 1.0; Group 2 (n = 10): low-frequency ventilation during ECC, rate 10/min, PEEP 5 cm 5H2O, F1O2 1.0; Group 3 (n = 10): medium-frequency ventilation during ECC, rate 120/min, PEEP 5 cm 5H2O, F1O2 1.0. The measurements were made under relative steady-state conditions before the start of surgery and postoperatively after an equilibrium phase of at least 15 min. During ECC using a bubble oxygenator (Bentley BOS 10 S) in moderate hypothermia, blood was aspirated from the pulmonary artery during inflation of the wedge balloon and blood gases were analyzed. Postoperative changes in pulmonary function were evaluated by venous admixture (QVA/Qt); changes in pulmonary vascular resistance after ECC were determined using the pulmonary pressure-flow relationship. RESULTS. In group 1, QVA/Qt rose significantly from 9.6 +/- 2.9% preoperatively to 13.6 +/- 3.5% postoperatively (P less than 0.05, t-test for paired samples). In groups 2 and 3, postoperative QVA/Qt was significantly lower than preoperative QVA/Qt (P less than 0.05; group 2: preoperative 11.9 +/- 3.5%, postoperative 8.1 +/- 2.6%; group 3: preoperative 11.9 +/- 3.0%, postoperative 7.8 +/- 3.2%; Fig. 1). The postoperative pulmonary pressure-flow relationship changed similarly in all three groups (Fig. 2). During ECC, blood aspirated from the pulmonary artery during inflation of the wedge balloon was fully oxygenated with a hematocrit approximating that of arterial blood. In ventilated patients, pO2 during ECC was higher in pulmonary arterial blood than in arterial blood. Pulmonary ventilation during ECC did not lead to pulmonary arterial alkalosis. CONCLUSIONS. Pulmonary ventilation during ECC can prevent a post-operative increase in venous admixture. ECC-related pulmonary vascular changes were not affected by ventilation. Middle-frequency ventilation offers no advantage over low-frequency ventilation during ECC, except that the operating field is more quiet.
 ...
PMID:[Lung inflation or mechanical ventilation in extracorporeal circulation?]. 251 76

Massive transfusion is a potentially serious problem associated with a number of complications, including changes in coagulation factor and platelet concentration, nonmechanical bleeding, hypothermia, pulmonary dysfunction, hypokalemia and hyperkalemia, hypocalcemia, hypomagnesemia, acidosis and alkalosis, immune suppression, blood transfusion reactions, and transmission of infectious diseases. The pathophysiology and management of massive transfusion are reviewed in this article.
 ...
PMID:Massive transfusion. 333 32


1 2 3 4 Next >>