危重患者高浓度静脉补钾的安全性和疗效研究

目的 探讨高浓度钾微量泵入治疗危重患者低钾血症的安全性及有效性.方法 128例合并低钾血症的危重患者[内生肌酐清除率(CCr)＞0.5 ml/s且每小时尿量＞50 ml]被随机分为治疗组和对照组,各64例.治疗组和对照组补钾浓度分别为1 208 mmol/L(相当于质量分数为9%的KCl溶液)、201 mmol/L(相当于1.5%的KCI溶液),补钾速度相同.均进行严密监测与血钾浓度监测,血钾正常时停止补钾.结果 治疗组和对照组补钾时间比较差异无统计学意义[(15.55±3.22)h比(14.18±4.93)h,P＞0.05];治疗组补钾的液体量明显低于对照组[(124.36±25.79)ml比(680.83±36.70)ml,P＜0.01].两组治疗过程中均未发生明显血流动力学变化、高钾血症或急性心功能不全.两组患者肾功能是否正常对补钾时间无明显影响.补钾前血钾浓度与补钾量有一定相关性(相关系数r=-0.259,P＜0.01).结论 高浓度钾微量泵入治疗危重患者低钾血症可以在短时间内纠正低钾血症,是安全有效的.肾功能轻度异常但无少尿及无尿的患者也可以在严密监测下高浓度补钾.     

Lowering of glucose in critical care: a randomized pilot trial

BACKGROUND: Similar to cardiac surgery patients, medical-surgical critically ill patients may benefit from intensive insulin therapy. The objectives of this pilot trial were to evaluate the feasibility of a randomized trial of intensive insulin therapy with respect to (a) achieving target glucose values in the 2 ranges of 5 to 7 and 8 to 10 mmol/L and (b) uncovering problems with the protocol in anticipation of a larger trial. SETTING: The trial was conducted in a 15-bed medical-surgical university-affiliated intensive care unit (ICU). METHODS: We included patients older than 18 years, expected to be in ICU for more than 72 hours, with a glucose value of more than 10 mmol/L within 48 hours of ICU admission. Exclusion criteria were diabetic ketoacidosis, severe hepatic failure or hepatic resection, pancreatitis, glucose of less than 2.2 mmol/L on admission to hospital, insulin infusion on admission to ICU, planned withdrawal of life support, and inability to obtain informed consent. Patients underwent concealed random allocation to a target glucose range of 5 to 7 or 8 to 10 mmol/L using pretested algorithms of insulin infusions. Dedicated glucometer measurement of arterial glucose values was calibrated daily to values measured in the laboratory. RESULTS: We enrolled 20 patients with a mean (SD) Acute Physiology and Chronic Health Evaluation (APACHE) II score of 32 (10.2); 14 were insulin-dependent pre-ICU, and all were medical admissions. Mean glucose values were different in the 2 groups (7.1 +/- 2.6 vs 9.4 +/- 2.1 mmol/L, P < .001). Although the intensive insulin therapy group had more glucose measurements performed than the control group, a similar proportion of values were within the target range (682 [42.4%] of 1607 values in the 5- to 7-mmol/L range; 250 [38.7%] of 660 values in the 8- to 10-mmol/L range, P = .35). Glucose values of less than 2.5 mmol/L developed 7 times in 5 patients, 4 of whom were in the intensive insulin therapy group; however, no adverse consequences were documented. As expected, there were no differences in clinically important outcomes. CONCLUSIONS: In this pilot trial of ICU patients with high illness severity, glucose values were in the 2 target ranges only 40% of the time, using well-accepted initiation and maintenance insulin infusion algorithms. A large randomized trial of glycemic control is feasible in this population to examine clinically important outcomes, but will require refined insulin algorithms and more comprehensive behavior change strategies to achieve target values.     

Effects of potassium supplementation on the recovery of thyrotoxic periodic paralysis

Potassium supplements have been recommended to hasten recovery and prevent cardiopulmonary complications in patients with thyrotoxic periodic paralysis (TPP). However, this recommendation has not yet been proven efficacious. Thirty-two patients with acute attacks of TPP over a 3-year-period were divided into 2 groups. Group A (n = 12) was a control group treated with normal saline infusion 125 mL/hr only. Group B (n = 20) received intravenous KCl administration at a rate of 10 mmol/hr in normal saline 125 mL/hr. During the attack and for 6 hours after muscle recovery, hemodynamics were continuously recorded and muscle strength and plasma K(+) concentration were measured hourly. The sex, age, muscle strength, thyroid function, biochemical values including plasma K(+) levels, as well as the time from attack to therapy (3.6 +/- 1.6 v 3.3 +/- 1.0 hr) were not significant between the 2 groups. However, recovery time was significantly shorter in the KCl group than the control (6.3 +/- 3.8 v 13.5 +/- 7.5 hr, P < .01). Rebound hyperkalemia greater than 5.5 mmol/L occurred in 40% patients receiving KCl. The dose of KCl administered and peak K(+) concentration were positively correlated (r = 0.85, P < .001). In conclusion, KCl therapy proves to help the recovery of paralysis in TPP associated with rebound hyperkalemia. KCl supplementation should be given as small as possible (<10 mmol/hr) to avoid rebound hyperkalemia unless there are cardiopulmonary complications.     

Inadequate aldosterone response to hyperkalemia during angiotensin converting enzyme inhibition in chronic renal failure

To assess the mechanism involved in hyperkalemia during angiotensin converting enzyme inhibition with captopril in chronic renal failure, captopril, 150 mg/day, was administered to 16 patients with hypertension with plasma creatinine levels between 1.6 and 12.4 mg/dl. After 4 weeks of therapy, plasma potassium levels increased from 3.9 +/- 0.1 to 5.5 +/- 0.2 mEq/L (P less than 0.001) and the final plasma potassium levels correlated with plasma creatinine levels (r = 0.67; P less than 0.01). In six patients with plasma creatinine levels greater than or equal to 3 mg/dl, aldosterone excretion decreased after 4 weeks of captopril, from 7.5 +/- 3.1 to 1.8 +/- 0.5 micrograms/24 hr, whereas plasma renin activity increased from 0.6 +/- 0.2 to 4.4 +/- 1.1 ng/ml/hr (P less than 0.05). This was associated with increases in plasma potassium levels from 3.9 +/- 0.2 to 5.4 +/- 0.4 mEq/L (P less than 0.005) and a significant reduction in fractional excretion of potassium from an average of 34% to 25%. No significant changes in plasma creatinine levels were observed during therapy. There was a significant positive correlation between aldosterone excretion and the potassium excretion fraction (r = 0.53; P less than 0.01). Increases in plasma potassium levels were not able to increase aldosterone excretion, although the greater the plasma potassium level attained, the smaller the reduction in aldosterone excretion (r = 0.47; P less than 0.05). Our results indicate that adequate aldosterone production is essential to preserve potassium homeostasis in chronic renal failure. Moreover, angiotensin II appears necessary for an adequate aldosterone response to potassium stimulation.     

Intravenous phosphate in the intensive care unit: more aggressive repletion regimens for moderate and severe hypophosphatemia

OBJECTIVE: To evaluate efficacy and safety of aggressive correction of hypophosphatemia with intravenous potassium phosphate in the ICU. DESIGN AND SETTING: Randomized interventional prospective study in the medical and surgical ICU of a tertiary university hospital. PATIENTS: Critically ill patients with hypophosphatemia between June and November 1998. MEASUREMENTS AND RESULTS: Patients with moderate hypophosphatemia (<0.65 and >0.40 mmol/l; n=37) were randomized into two groups: group 1 received 30 mmol potassium phosphate intravenously in 50 ml saline over 2 h, and group 2 received 30 mmol potassium phosphate in 100 ml saline over 4 h. Patients with severe hypophosphatemia (<0.40 mmol/l; n=10) were also randomized into two groups: group 3 received 45 mmol potassium phosphate intravenously in 100 ml saline over 3 h, and group 4 received 45 mmol potassium phosphate in 100 ml saline over 6 h. Electrolytes, blood gas, renal function were monitored until day 3; urine was collected during and until 6 h after infusions. The overall efficacy of the protocols was 98% by the end of the infusion. There was no statistical difference in phosphate values between groups at the end of infusion or at 24 h. No adverse events were noted; one patient had an increase in serum potassium to 6.1 mmol/l. Phosphaturia in all groups was elevated as evidenced by fractional excretion above 20%. CONCLUSIONS: More rapid administration of large potassium phosphate boluses is effective and safe for correcting hypophosphatemia in ICU patients with preserved renal function if baseline serum potassium is below 4 mmol/l.     

Low exogenous lactate clearance as an early predictor of mortality in normolactatemic critically ill septic patients

OBJECTIVE: To evaluate the prognostic value of lactate clearance and lactate production in severely ill septic patients with normal or mildly elevated blood lactate concentration.DESIGN Prospective, observational study. SETTING: Nineteen-bed mixed medicosurgical intensive care unit. PATIENTS: Fifty-six patients with severe sepsis and blood lactate concentration <3 mmol/L. MEASUREMENTS AND MAIN RESULTS: Lactate metabolism was evaluated in all patients. Lactate clearance was measured by modeling the change in arterial blood lactate over time induced by an infusion of 1 mmol/kg sodium lactate for 15 mins. Lactate production was calculated as the product of lactate clearance times the blood lactate concentration before the infusion. Outcome was taken to be mortality at 28 days after the beginning of the septic episode. A logistic regression model taking into account different risk factors was constructed. Among the 56 patients, 17 (30.3%) died before the 28th day. Basal blood lactate concentration was not different between survivors and nonsurvivors, whereas lactate clearance and production were higher in survivors (0.86 +/- 0.32 vs. 0.58 +/- 0.18 L/hr/kg, p < .005, and 1.19 +/- 0.63 vs. 0.89 +/- 0.24 mmol/hr/kg, p = .055, respectively). An increase in blood lactate 45 mins after the end of the lactate infusion (Deltalact-T60) > or = 0.6 mmol/L was predictive of 28-day mortality with 53% sensitivity and 90% specificity. Multivariate analysis showed that only three factors were independently and significantly correlated with 28-day mortality: presence of more than two organ failures (odds ratio, 27; p = .04), age >70 yrs (odds ratio, 5.7; p = .032), and Deltalact-T60 > or =0.6 mmol/L (odds ratio, 14.2; p = .042). CONCLUSION: Low lactate clearance in severely ill septic patients with normal or mildly elevated blood lactate is predictive of poor outcome independently of other known risk factors such as age and number of organ failures.     

Comparison of continuous versus intermittent furosemide administration in postoperative pediatric cardiac patients.

OBJECTIVE: To compare the effects of furosemide administered by intermittent iv infusion vs. continuous iv infusion on urine output, hemodynamic variables, and serum electrolyte concentrations. DESIGN: Prospective, randomized trial. SETTING: Pediatric ICU. PATIENTS: Postoperative pediatric cardiac patients. INTERVENTIONS: Patients were assigned to either the continuous iv infusion or the intermittent infusion groups. The intermittent group received 1 mg/kg iv of furosemide every 4 hrs to be increased by 0.25 mg/kg iv every 4 hrs to a maximum of 1.5 mg/kg iv if the urine output was less than 1 mL/kg.hr. The continuous infusion group received an initial furosemide dose of 0.1 mg/kg iv (minimum 1 mg) followed by an iv infusion rate of 0.1 mg/kg.hr of furosemide to be doubled every 2 hrs to a maximum of 0.4 mg/kg.hr if the urine output was less than 1 mL/kg.hr. MEASUREMENTS AND MAIN RESULTS: Demographic variables, fluids, electrolyte and inotropic requirements were the same in both groups. A significantly (p = .045) lower daily dose of furosemide (4.90 +/- 1.78 vs. 6.23 +/- 0.62 mg/kg.day) in the continuous iv infusion group produced the same 24-hr urine volume as that of the intermittent group. There was more variability in urine output in the intermittent group as well as more urinary losses of sodium (0.29 +/- 0.15 vs. 0.20 +/- 0.06 mmol/kg.day, p = .0007) and chloride (0.40 +/- 0.20 vs. 0.30 +/- 0.12 mmol/kg.day, p = .045). CONCLUSION: Furosemide administered by continuous iv infusion is advantageous in the post-operative pediatric patient because of a more controlled and predictable urine output with less drug requirement and less urinary loss in sodium and chloride.     

High protein diet complements resin therapy of familial hypercholesterolemia.

The intermediate-term effects on plasma lipoprotein lipids of substituting meat and dairy protein for carbohydrate in the diets of five subjects (three women, two men) with familial hypercholesterolemia receiving cholestyramine (mean dose, 18 g/d) were studied. Subjects were randomly allocated to either the high or low protein diets (mean 27 versus 10% of energy as protein, 25% as fat, and 48 versus 65% as carbohydrate) for 4 to 5 weeks and then switched to the other diet for another 4 to 5 weeks. Mean fasting plasma HDL cholesterol rose significantly by 17 +/- 3% (1.11 +/- 0.12 vs 0.95 +/- 0.11 mmol/L, p less than 0.005, n = 5), whereas total triglycerides fell by 23 +/- 2% (1.7 +/- 0.3 vs 2.2 +/- 0.3 mmol/L, p less than 0.005, n = 5), VLDL triglycerides fell by 28 +/- 5% (0.88 +/- 0.15 vs 1.18 +/- 0.19 mmol/L, p less than 0.02, n = 5), VLDL cholesterol fell by 32 +/- 7% (0.39 +/- 0.08 vs 0.56 +/- 0.09 mmol/L, p less than 0.01, n = 5), the ratio of LDL cholesterol: HDL cholesterol by 19 +/- 5% (4.7 +/- 0.7 vs 5.7 +/- 0.7, p less than 0.05) and that of total cholesterol: HDL cholesterol by 16 +/- 5% (6.6 +/- 0.5 vs 8.0 +/- 0.7, p less than 0.05) on the high versus low protein diet. Increasing dietary protein intake at the expense of carbohydrate may be useful in treating hypoalphalipoproteinemia and/or hypertriglyceridemia in patients with familial hypercholesterolemia.     

Amino acid alterations and encephalopathy in the sepsis syndrome

OBJECTIVE: To evaluate the role of amino acid profiles in septic encephalopathy. DESIGN: Retrospective analysis. SETTING: Medical wards and medical ICU of a university hospital. PATIENTS: Patients with infections and normal mental status were compared with patients with septic shock and altered sensorium. INTERVENTIONS: Plasma amino acid levels and Acute Physiology and Chronic Health Evaluation (APACHE II) scores were determined. MEASUREMENTS AND MAIN RESULTS: Patients with septic shock and altered sensorium had higher circulating concentrations of ammonia (425 +/- 55 vs. 127 +/- 7 mmol/L) and the aromatic amino acids phenylalanine (122 +/- 19 vs. 74 +/- 3 mmol/L) and tryptophan (97 +/- 7 vs. 32 +/- 13 mmol/L), and lower levels of the branch-chain amino acid isoleucine (48 +/- 7 vs. 68 +/- 5 mmol/L) than patients with infections and normal sensorium (p less than .05). Aromatic amino acid levels correlated with APACHE II scores (R2 = .4, p less than .001) and mortality. APACHE II scores were higher in the septic shock patients (30 +/- 2 vs. 8 +/- 1, p less than .001), and these patients had a higher mortality rate (71% vs. 12%, p less than .01). Patients with septic shock who died had higher levels of ammonia (524 +/- 58 vs. 227 +/- 40 mmol/L, p less than .05) and sulfur-containing amino acids (172 +/- 31 vs. 61 +/- 7 mmol/L, p less than .05) than patients who survived. CONCLUSIONS: Plasma amino acid profiles appear to be important in septic encephalopathy and the severity of septic disease.     

Aminophylline inhibits renal vasoconstriction produced by intrarenal hypertonic saline

An intrarenal infusion of hypertonic saline to sodium-depleted dogs causes an acute reduction in renal blood flow (RBF) which has been postulated to be due to tubuloglomerular feedback (TGF). Adenosine has been suggested as a mediator of TGF, as adenosine receptor blockade with methylxanthines inhibits TGF. In order to test further the hypothesis that the renal response to hypertonic saline is mediated by TGF, the RBF response to intrarenal hypertonic saline infusions have been investigated in sodium-depleted dogs before and after either an infusion of vehicle or an intrarenal infusion of aminophylline. Aminophylline (2.5 mg/min), at a dose which did not change basal RBF or responses to bolus doses of angiotensin II, inhibited the responses to intrarenal bolus doses of adenosine. In control dogs (n = 5), a 10-min intrarenal infusion of hypertonic saline significantly (P less than .05) reduced RBF both before (-27 +/- 4%) and during (-16 +/- 9%) an infusion with aminophylline vehicle. In a second group of animals (n = 5), an intrarenal hypertonic saline infusion reduced RBF before (-33 +/- 8%; P less than .05), but not during an intrarenal aminophylline infusion (2.5 mg/min). We conclude that aminophylline inhibits the renal vascular response to hypertonic saline and that the renal response to hypertonic saline might be mediated by intrarenal adenosine release.     

Osmoregulation of thirst and vasopressin secretion in insulin-dependent diabetes mellitus

1. Osmotically stimulated thirst and vasopressin release were studied during infusions of hypertonic sodium chloride and hypertonic D-glucose in euglycaemic clamped diabetic patients and healthy controls. 2. Infusion of hypertonic sodium chloride caused similar elevations of plasma osmolality in diabetic patients (288.0 +/- 1.0 to 304.1 +/- 1.6 mosmol/kg, mean +/- SEM, P less than 0.001) and controls (288.6 +/- 0.9 to 305.7 +/- 0.6 mosmol/kg, P less than 0.001), accompanied by progressive increases in plasma vasopressin (diabetic patients, 0.9 +/- 0.3 to 7.7 +/- 1.5 pmol/l, P less than 0.001; controls 0.5 +/- 0.1 to 6.5 +/- 1.0 pmol/l, P less than 0.001) and thirst ratings (diabetic patients 1.0 +/- 0.2 to 7.1 +/- 0.5 cm, P less than 0.001; controls 1.8 +/- 0.4 to 8.0 +/- 0.5 cm, P less than 0.001) in both groups. 3. Drinking rapidly abolished thirst and vasopressin secretion before major changes in plasma osmolality occurred in both diabetic patients and healthy controls. 4. There were close and significant correlations between plasma vasopressin and plasma osmolality (diabetic patients, r = +0.89, controls r = +0.93) and between thirst and plasma osmolality (diabetic patients r = +0.95, controls r = +0.97) in both diabetic patients and healthy controls during hypertonic saline infusion. 5. Hypertonic D-glucose infusion caused similar elevations in blood glucose in diabetic patients (4.0 +/- 0.2 to 20.1 +/- 1.2 mmol/l, P less than 0.001) and healthy controls (4.3 +/- 0.1 to 19.3 +/- 1.2 mmol/l, P less than 0.001) but did not change plasma vasopressin or thirst ratings.(ABSTRACT TRUNCATED AT 250 WORDS)     

Supraventricular tachycardia treated with continuous infusions of propranolol

Because oral therapy is often contraindicated in hospitalized patients we assessed the safety and efficacy of continuous intravenous propranolol infusions in nine patients with refractory supraventricular tachycardia. Standard pharmacokinetic formulas predicted a loading dose (52.2 +/- 38.3 micrograms/kg), steady-state plasma concentration, and the initial maintenance dose (16.1 +/- 16.2 micrograms/kg/hr; range 6.1 to 56.0 micrograms/kg/hr) to control heart rate. Subsequent maintenance doses (3.9 to 74.9 micrograms/kg/hr) were determined by clinical response. Heart rate decreased from 146 +/- 22 to 98 +/- 16 beats/min (p less than 0.0001). This decrease persisted throughout the infusion. Measured propranolol levels (28 +/- 21 ng/ml) did not differ significantly from the predicted levels (23 +/- 17 ng/ml). The duration of the infusion averaged 97 +/- 77 hours. A side effect, transient wheezing, occurred in only one patient. This resolved when the infusion rate was decreased. We conclude that continuous propranolol infusions appear safe and effective in treating these patients with supraventricular tachycardia.     

Hydrochloric acid infusion for treatment of metabolic alkalosis associated with respiratory acidosis

Hypercapnia due to respiratory failure can be more severe when accompanied by coexistent metabolic alkalosis. We therefore tested the hypothesis that hydrochloric acid (HCl) infusion could improve PaCO2 in 15 critically ill patients admitted with mixed respiratory acidosis and metabolic alkalosis, and a pH of between 7.35 and 7.45. HCl was infused at a constant rate of 25 mmol/h until the bicarbonate concentration decreased less than 26 mmol/L, or until the pH decreased less than 7.35 (initial pH greater than 7.40) or 7.30 (initial pH less than 7.40). Administration of 170 +/- 53 mmol of HCl decreased the bicarbonate concentration from 34 +/- 3 to 25 +/- 2 mmol/L (p less than .001), the pH from 7.41 +/- 0.03 to 7.33 +/- 0.02 (p less than .001), and the PaCO2 from 54 +/- 8 to 48 +/- 8 torr (p less than .001). Postinfusion PaCO2 could be predicted accurately from the initial status of the patients (r = .95, p less than .001) except in one patient with fixed hypercapnia. PaCO2 increased from 77 +/- 19 to 94 +/- 24 torr (p less than .001) and PaO2/PAO2 increased from 59 +/- 17 to 66 +/- 17% (p less than .001). The effects of HCl were still present 12 h after the end of the infusion. No complications related to the acid infusion were noted. These results indicate that, even in the absence of alkalemia, active correction of metabolic alkalosis by HCl infusion can improve CO2 and oxygen exchange in critically ill patients with mixed respiratory acidosis and metabolic alkalosis.     

Risk factors of ventricular fibrillation during rapid amphotericin B infusion.

Amphotericin B causes reversible concentration-dependent loss of intracellular potassium in vitro and hyperkalemic ventricular arrhythmias in dogs. Hyperkalemic ventricular arrhythmias associated with amphotericin B infusion have not been well documented in humans. Ventricular fibrillation with progressive hyperkalemia (up to 8 to 8.4 meq/liter) occurred twice in an anuric patient during rapid infusion of high-dose amphotericin B (1.4 mg/kg over 45 min). The peak amphotericin B concentration in serum at the end of infusion was 6.7 micrograms/ml. Prolonged infusion (3 h) and concurrent hemodialysis each prevented the development of hyperkalemia and ventricular arrhythmia. In two anuric patients receiving 4-h infusions of amphotericin B during dialysis (0.7 and 1.0 mg/kg), peak amphotericin B concentrations in serum were lower, 1.6 +/- 0.1 and 2.7 +/- 0.7 micrograms/ml, respectively; serum potassium levels were maintained in the normal range; and venous access for outpatient therapy was convenient. Peak concentrations of amphotericin B in serum were also lower (1.7 +/- 0.7 micrograms/ml) in eight patients with normal renal function who received lower doses (0.7 +/- 0.2 mg/kg) over 45 min; there were only slight increases in the serum potassium level (from 3.9 +/- 0.9 to 4.4 +/- 0.6 meq/liter, P less than 0.05). We recommend that rapid infusion of amphotericin B not be used in patients with impaired potassium excretion unless accompanied by hemodialysis and careful potassium monitoring.     

Effect of filtration volume of continuous venovenous hemofiltration in the treatment of patients with acute renal failure in intensive care units

OBJECTIVE: We evaluated the variable Kt/V, which has become established in the therapy of end-stage renal disease in acute renal failure, to assess the influence of the filtration volume of continuous venovenous hemofiltration on Kt/V. We measured the variables of acid-base balance and uremia control. DESIGN: Prospective interventional pilot study. SETTING: Medical intensive care unit of a university hospital. PATIENTS: Fifty-six patients with acute renal failure and continuous venovenous hemofiltration treatment. INTERVENTIONS: The patients were consecutively treated with a filtration volume of either 1 L/hr (group 1) or 1.5 L/hr (group 2). MEASUREMENTS AND MAIN RESULTS: Patients with a filtration volume of 1.5 L/hr achieved a Kt/V of 0.8 per day, which was significantly higher than in the patient group treated with 1 L/hr (0.53, p <.05). The filtration volume of 1.5 L/hr led to a markedly better control of blood urea nitrogen concentrations, 69.3 +/- 6.6 mg/dL vs. 52.1 +/- 5.2 (p <.05), and to a much quicker and longer lasting compensation of acidosis. Both groups had acidotic pH at the beginning of therapy (group 1, 7.29 +/- 0.02; group 2, 7.29 +/- 0.02, nonsignificant). In group 2, a significantly higher pH value than in group 1 was measured after 24 hrs of continuous venovenous hemofiltration (p < .001; 7.39 +/- 0.02 vs. 7.31 +/- 0.02). The pH values in group 1 did not normalize until after 4 days. The filtration volume of 1.5 L/hr led to a quicker increase in bicarbonate concentrations after 24 hrs of therapy (group 1, 2.8 +/- 3.2 mmol/L; group 2, 6.5 +/- 3.1 mmol/L, p <.001). CONCLUSIONS: The standardized urea clearance Kt/V is a valuable tool in the treatment of acute renal failure. Higher Kt/V levels were associated with a better control of uremia and acid-base balance. However, there were no differences in the clinical course, patient survival, percentage of patients with or without renal failure who were transferred from the intensive care unit, or Acute Physiology and Chronic Health Evaluation III scores.     

A direct relationship between ionized calcium and arterial pressure among patients in an intensive care unit

Serum ionized calcium (Ca+2), creatinine, magnesium, phosphate, and arterial pH were measured in patients on admission to the medical ICU (MICU). Patients were classified into three groups: a) hypotensive (n = 38), those who received vasopressor support for frank hypotension; b) hypertensive (n = 21), those who required vasodilator therapy; and c) normotensive (n = 53), those who required neither vasopressor nor vasodilator therapy. Analysis of variance revealed that only Ca+2, creatinine, and arterial pH differed among the three groups. The difference in Ca+2 persisted when analysis of variance was repeated with creatinine as a covariate. Hypotensive patients had a significantly (p less than .05) lower mean Ca+2 (1.04 +/- 0.13 mmol/L) than normotensive patients (1.13 +/- 0.10 mmol/L), who in turn had a significantly (p less than .05) lower Ca+2 than hypertensive patients (1.18 +/- 0.09 mmol/L). Ca+2 correlated with mean arterial pressure at the time of serum collection (n = 118; r = .43; p less than .01), independent of any other variable. Vasopressor support was required in 41% of hypocalcemic patients in comparison to 14% of normocalcemic patients (p less than .01). Vasodilator therapy was required for 34% of normocalcemic patients, compared to 7.5% of hypocalcemic patients (p less than .01). There appears to be a clinically significant association between hypotension and hypocalcemia. This association may or may not be causal.     

Hypertonic Saline Treatment of Severe Hyperkalemia in Nonnephrectomized Dogs

OBJECTIVES: To determine whether a hypertonic saline bolus improves cardiac conduction or plasma potassium levels more than normal saline infusion within 15 minutes of treatment for severe hyperkalemia. Previously with this model, 8.4% sodium chloride (NaCl) and 8.4% sodium bicarbonate (NaHCO(3)) lowered plasma potassium equally effectively. METHODS: This was a crossover study using ten conditioned dogs (14-20 kg) that received, in random order, each of three intravenous (IV) treatments in separate experiments at least one week apart: 1) 2 mmol/kg of 8.4% NaCl over 5 minutes (bolus); 2) 2 mmol/kg of 0.9% NaCl over one hour (infusion); or 3) no treatment (control). Using isoflurane anesthesia and ventilation (pCO(2) = 35-40 torr), 2 mmol/kg/hr of IV potassium chloride (KCl) was infused until conduction delays (both absent p-waves and >/=20% decrease in ventricular rate in 相似文献   

Comparison of plasma glucose and plasma free insulin during CSII and intensified conventional insulin therapy

The plasma glucose and plasma free insulin profiles of six totally insulin-dependent diabetic patients were compared during periods of 4 days in hospital under a conventional insulin therapy (ICIT) comprising 4 daily injections of regular insulin and under continuous subcutaneous insulin infusion (CSII). Two profiles of prandial insulin administration with CSII were compared: a rectangular (R) and an exponential wave (E) in which 50% of the dose was given rapidly followed by an exponential decrease. In both cases, the basal infusion rate was increased by 30-50% between 5 a.m. and 8 a.m. Mean circadian blood glucose was equally good with ICIT: R and E: 7.0 +/- 0.9, 7.3 +/- 1.0, and 7.1 +/- 1.0 mmol/L, respectively. In five patients, fasting plasma glucose was higher with ICIT than with R and E (12.7 +/- 1.8 versus 6.9 +/- 1.0 and 6.8 +/- 0.8 mmol/L, respectively; t test: P less than 0.05; Wilcoxon: P = 0.06). Mean plasma free insulin level was significantly higher (t test: P less than 0.005; Wilcoxon: P less than 0.05) with ICIT (0.46 +/- 0.04 nmol/L) than with R (0.37 +/- 0.04 nmol/L) or E (0.36 +/- 0.05 nmol/L), although the daily doses were similar. In conclusion, CSII leads to a better glycemic control than ICIT, since it appears to prevent the morning rise of blood glucose.     

Amino acid losses during continuous high-flux hemofiltration in the critically ill patient

Total amino acid losses were measured daily in the ultrafiltrate collected from eight patients with acute renal failure treated by continuous high-flux venovenous hemofiltration. All patients had type-1 respiratory failure and required mechanical ventilation. Four patients also suffered cardiogenic shock and were dependent on two or more inotropic drugs; the other four had Escherichia coli septicemia. All patients received identical daily parenteral nutrition as a continuous infusion. The overall mean serum amino acid values were greater in the group with cardiogenic shock (180 +/- 36 [SEM] mumol/L) compared to those with septicemia (131 +/- 26 mumol/L; p less than .05). The daily ultrafiltrate losses of amino acids were also greater, 4.2 +/- 0.7 mmol/24 h (1.1 g N) compared to 2.1 +/- 0.3 mmol/24 h (0.6 g N, p less than .05). For all patients there was a positive correlation between the serum amino acid value and ultrafiltrate loss (r = .84, p less than .001). However, the slopes of the regression curves for the two groups differed (p less than .001), suggesting that for the same plasma value the ultrafiltrate loss was greater for those patients with cardiogenic shock.     

Intravenous insulin nomogram improves blood glucose control in the critically ill

OBJECTIVE: To improve control of blood glucose concentrations in critically ill patients through use of a bedside, nurse-managed, intravenous insulin nomogram. DESIGN: Retrospective, before-after cohort study. SETTING: Fifteen-bed mixed medical/surgical intensive care unit in a tertiary, teaching hospital. PATIENTS: A total of 167 intensive care unit patients requiring intravenous insulin infusions during two 9-month periods. INTERVENTION: The sliding scale group was treated using ad hoc sliding scale infusion therapy. The intervention group was treated using a dosing nomogram that allowed the nurse to adjust the insulin infusion rate based on current glucose concentration and concurrent insulin infusion rates. The adjustments were made independent of physician input. MEASUREMENTS AND MAIN RESULTS: Time from initiating the insulin infusion to initial control of glucose concentration (<11.5 mmol/L) was determined. Effectiveness of glucose control was determined retrospectively by measuring the area under the curve of blood concentrations >11.5 mmol/L versus time of insulin infusion, divided by total duration of insulin infusion. The median time to initial control of glucose (<11.5 mmol/L) was 4 hr (range 1-38 hr) for the baseline and 2 hr (range 1-22 hr) for nomogram group (p =.0004). The median area under the curve of glucose concentration divided by duration of insulin infusion was 0.9 (range 0.0-5.9) for sliding scale group and 0.3 (range 0.0-11.1) for nomogram (p =.0001), without any increase in the frequency of episodes of hypoglycemia. CONCLUSION: Use of an insulin nomogram in critically ill patients improves control of blood glucose concentrations and is safe.