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Biomedical subjects

H Stjernström

Publications and source records attributed to H Stjernström.

At least 19 recordsLinked to original sources
PubMed1998

Parathyroid hormone and ionized calcium levels are related to the severity of illness and survival in critically ill patients.

BACKGROUND: The present study explores serum parathyroid hormone (PTH) and blood ionized calcium (Ca2+) levels in relation to the severity of disease and mortality in the intensive care unit (ICU). METHODS: In a pilot study, 37 consecutive critically ill patients admitted to the ICU were studied with determinations of serum PTH and total serum calcium within the first 24 h. In a following prospective study, patients suffering from sepsis (n = 13) or subjected to major surgery (n = 13) were investigated daily for 1 week with determinations of serum PTH and ionized calcium (Ca2+). Severity of disease was assessed by the APACHE II score and hospital mortality was recorded. RESULTS: In the pilot study, serum PTH levels were elevated (> 55 ng L-1) in 38% of the patients and were not related to serum calcium but showed a significant relationship to the APACHE II score (r = 0.39, P < 0.05). In the prospective study, serum PTH was elevated in 69% of the patients in both groups at inclusion, and 6 days later 87% of the septic and 37% of the surgery patients still showed elevated levels. Hypocalcaemia was more commonly seen in the septic patients [mean Ca2+ 1.03 +/- 0.08 (SD) mmol L-1] than in the surgical patients (1.14 +/- 0.06 mmol L-1) at inclusion. Both PTH and Ca2+ levels were significantly related to the APACHE II score (r = 0.46, P < 0.03, and r = -0.54, P < 0.009, respectively). Furthermore, PTH levels were significantly increased in non-survivors (n = 5) compared with survivors (mean 161 +/- 51 vs. 79 +/- 51 ng L-1, P < 0.005). CONCLUSION: Hypocalcaemia and increased levels of PTH were common findings in critically ill patients. These alterations in calcium homeostasis were related to the severity of disease and increased PTH levels were associated with a poor outcome.

APACHE↗
PubMed1996

[Ventilation-perfusion ratio in patients with acute respiratory insufficiency].

UNLABELLED: Acute respiratory failure is characterised by mismatch of ventilation with perfusion (VA/Q). The multiple inert gas elimination technique (MIGET) is a complex method which allows the description of a virtually continuous distribution of VA/Q ratios. We investigated VA/Q relationships in patients admitted to the intensive care unit due to acute respiratory failure and thus requiring for mechanical ventilation. METHOD: Eight patients (mean APACHE 11 = 22 +/- 4) who suffered from acute pneumonia (n = 4), traumatic lung contusion (2), toxic lung failure (1) or massive bilateral atelectasis (1) were investigated by MIGET within 3 days after the begin of mechanical ventilation. A mixture of six inert gases, dissolved in isotonic saline, was infused continuously. Arterial and mixed venous blood samples and expired gas samples were obtained and analysed by gas chromatography. Blood-gas partition coefficients were determined, and the ratios of retention and excretion were calculated. The data were transformed in a 50-compartment model of blood flow and ventilation against VA/Q ratio. We assessed the amount of intrapulmonary shunt (VA/Q = 0), low VA/Q regions (VA/Q = 0.005-0.1), normal VA/Q regions (VA/Q = 0.11-10), high VA/Q regions (VA/Q = 11-100) and dead space ventilation (VA/Q > 100). Furthermore, we calculated the logarithmic standard deviation of pulmonary perfusion distribution (logSDQ). RESULTS: In all patients we found moderate to severe intrapulmonary shunt and VA/Q mismatching. The data are expressed as median values and ranges. Inert-gas-measured shunt was 21% (3-45.5%), whereas low VA/Q regions were little affected. Normal VA/Q regions ranged from 41.5% to 96.0% (median 76.8%). The amount of alveolar dead space ventilation was 28% (19.7-41.8%). Median logSDQ (normal range 0.3-0.6) was calculated to be 0.855 (0.540-1.490). In patients presenting with moderate lung injury (Murray score < 3), a moderate increase in shunt and a moderate VA/Q mismatch were observed. In contrast, patients with severe lung failure and critically decreased oxygenation (Murray score > 3) were characterised by massive shunting and VA/Q mismatching. Additionally, low VA/Q and high VA/Q compartments and an increase in dead space ventilation was found in these patients. CONCLUSIONS: The impairment of oxygenation in patients with acute respiratory failure is due to several pathophysiological mechanisms: increase in intrapulmonary shunt, VA/Q-mismatching and dead space ventilation, according to the severity of lung failure. We conclude from our results that the prevention and/or reduction of non-ventilated lung areas (atelectasis) is an outstanding therapeutic strategy in the treatment of patients with acute respiratory failure. From this point of view, several techniques of systemic changes in body position should be integrated as supportive therapeutic strategies.

APACHE↗
PubMed1995

Lactate metabolism and hypocarbic hyperventilation. An experimental study in piglets.

Hyperventilation has been reported to increase blood lactate levels. Uncertainty exists as to whether high lactate levels are caused by increased peripheral release or decreased hepatic uptake. Seven piglets were investigated during controlled normoventilation and 13 piglets during controlled hyperventilation. Blood was drawn from catheters in the femoral artery and vein and in the hepatic vein. Blood flow was measured in the femoral artery by an electromagnetic flow meter and in the splanchnic area by indocyanine green extraction. In addition, repeated muscle biopsies from the hind limb and back muscles were taken. The mean PaCo2 was 5.4 in the normoventilated and 3.5 kPa in the hyperventilated group. The average hind limb oxygen uptake was the same in both groups. The arterial blood lactate concentration was significantly higher (P = 0.03) in the hyperventilated group (2.6 mmol.l-1) as compared to the normoventilated group (1.5 mmol.l-1). However, the release of lactate from the hind limb, and the muscular content of lactate were the same in both groups. Similar and unchanged skeletal muscle contents of glucose-6-phosphate, fructose-1,6-diphosphate, alpha-glycerophosphate, pyruvate, citrate and ATP were recorded in both groups. The splanchnic region did not take up or release lactate at normal PaCO2, but released lactate after 120 minutes of hyperventilation. The results indicate that the increased concentration of lactate during hypocarbic hyperventilation was not caused by an increased peripheral release from the skeletal muscles of the pig but could be caused by an altered splanchnic turn-over of lactate.

Adenosine Triphosphate↗
PubMed1994

The effects of different intravenous feeding regimens on the rates of synthesis of alpha1-antitrypsin after surgery.

The effects of two nutritional regimens on the synthesis of alpha-1 antitrypsin were investigated postoperatively in gynaecological cancer patients. Total parenteral nutrition (TPN) or a hypocaloric amino acid mixture was administered on the day of surgery and continued for 3 days. The rate of synthesis of alpha-1 antitrypsin was estimated by a computer model from serial plasma concentrations of this protein and a reference protein, albumin. The hypocaloric amino acid mixture resulted in a more negative nitrogen balance than that produced during administration of TPN containing the same amount of nitrogen but more non-protein energy. Urinary excretion of 3-methylhistidine was significantly greater (p = 0.017) in the hypocaloric amino acid group (350 +/- 40 mumol/day; mean +/- SE) on the third postoperative day, as compared to the TPN group (240 +/- 20 mumol/day). In spite of this the synthesis of alpha-1 antitrypsin was apparently greater in the hypocaloric amino acid than in the TPN group. The accumulated plasma appearance rate of alpha-1 antitrypsin was significantly higher (p = 0.0465) in HAA group, at 70 h it was 490 +/- 40 compared to 400 +/- 20 times the pre-operative synthesis in the TPN group.

Journal Article↗
PubMed1994

Central and regional blood flow during hyperventilation. An experimental study in the pig.

Mechanical hyperventilation not only reduces brain oedema after neurotrauma but also affects the central and systemic circulation. We have, in pigs, measured blood flow in the pulmonary artery, the portal vein and in the femoral artery, as well as estimated the splanchnic blood flow and studied the relative perfusion using the microsphere technique in normo- and hypocarbia during intermittent positive pressure ventilation. A normoventilated control group did not change in cardiac output, portal vein blood flow, splanchnic blood flow and femoral arterial blood flow. Hyperventilation was performed to a PCO2 of 3.0 +/- 0.1 kPa. We found that in pigs ventilated with high tidal volume skeletal muscle blood flow did not change during the first 60 min of hyperventilation but gradually decreased thereafter. Blood flow to the cerebellum decreased soon after the induction of hyperventilation, whereas the cerebral blood flow did not decrease until the second hour of hyperventilation. Cardiac output, splanchnic perfusion and portal vein blood flow all decreased. Myocardial perfusion and arterial blood flow to spleen and kidney decreased while pancreatic and liver arterial blood flows were unaffected. It is concluded that mechanical hyperventilation with low frequency and large tidal volumes reduces the flow to most tissues, where the relative decrease according to microsphere measurements is most pronounced in skeletal muscles, heart muscle and cerebellum. However, the changes in cardiac output and splanchnic blood flow were not observed when hyperventilation was induced by increased frequency, keeping the tidal volume constant.

Animals↗
PubMed1993

Chemical monitoring of intensive care patients using intravenous microdialysis.

The objective of the study was to evaluate intravenous microdialysis for monitoring of plasma lactate, pyruvate, glucose, creatinine, urea, adenosine, inosine and hypoxanthine in intensive care patients. Microdialysis probes (O.D. 0.9 mm; membrane length 20 mm) were inserted into major veins and perfused with Ringer's solution. Dialysis samples were collected from 4 patients with septic shock in 60 min fractions during 24 h. At the end of every hour a venous blood plasma sample was drawn from the corresponding contralateral vein for comparison. Microdialysate values of all metabolites closely followed the changes in the corresponding blood samples. The in vivo recovery of the probe type used was close to 100% for lactate, creatinine, and urea, and about 90% for glucose. It is concluded that intravenous microdialysis sampling is a suitable method for continuous bedside monitoring of important metabolites in intensive care patients.

Aged↗
PubMed1992

Gas exchange as monitored in mixed venous and arterial blood during experimental cardiopulmonary resuscitation.

Nineteen anaesthetized piglets were investigated. After catheterization and a stabilization period, ventricular fibrillation was induced with a transthoracic DC shock, after which a 10-min period of cardiopulmonary resuscitation (CPR) took place. CPR included manual chest compression and mechanical ventilation with pure oxygen. After 1 min of CPR, an infusion of alkaline buffer was begun and completed within 5 min. A total of 50 mmol of either sodium bicarbonate (n = 6) or tris buffer mixture (n = 7) were given. These two groups were compared with a third control group (n = 6) receiving the same volume of normal saline. After 8 min of CPR all animals were given 0.5 mg adrenaline i.v., and after 10 min DC shocks were used to revert the heart back to normal sinus rhythm. Our results demonstrate that blood flow and not ventilation is the limiting factor for the efficient disposal of CO2 during CPR. This also applied when the demand for CO2 transport was increased by administration of sodium bicarbonate. The respiratory exchange ratio increased 1.9-fold, indicating that the transport of carbon dioxide was less affected than that of oxygen. The estimated alveolo-arterial oxygen tension difference, shunt, and overall ventilation/perfusion ratio increased, creating an inverse hyperbolic relationship between arterial PCO2 and PO2. The difference between mixed venous and arterial PCO2 correlated well to the mixed venous PCO2, implying more efficient pulmonary elimination of PCO2 when the mixed venous PCO2 was high. Pulmonary gas exchange during CPR appears to be independent of alkaline buffer therapy in the form of sodium bicarbonate or tris buffer mixture.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Effects of alkaline buffer administration on survival and myocardial energy metabolism in pigs subjected to ventricular fibrillation and closed chest CPR.

Nineteen anaesthetized piglets were investigated. After characterization and a stabilization period, ventricular fibrillation was induced by a transthoracic DC shock, after which a 10-min period of cardiopulmonary resuscitation (CPR) took place. CPR included manual chest compression and mechanical ventilation with pure oxygen. After 1 min of CPR an infusion of alkaline buffer was begun and was completed within 5 min. A total of 50 mmol of one of two different buffer solutions was given, either sodium bicarbonate (n = 6) or tris buffer mixture (n = 7). These two groups were compared with a third control group (n = 6) receiving the same volume of normal saline. After 8 min of CPR all animals were given 0.5 mg adrenaline i.v., and after 10 min DC shocks were used to return the heart to normal sinus rhythm. If this procedure was successful, the heart was rapidly (within 15 s) stopped again by another DC shock. Myocardial biopsies were then taken immediately in all animals. Successful CPR was more frequent in the animals given normal saline or tris buffer mixture and no effect was seen in the group given sodium bicarbonate. Survival was statistically correlated to low myocardial content of creatine phosphate and low base excess values in blood. Such parameters as myocardial content of ATP or ACP (adenylate charge potential) had no direct correlation to survival. Sodium bicarbonate induced significantly higher base excess and PCO2 values, while the tris buffer mixture seemed to have a greater alkalizing effect intracellularly. We consider it probable that the poor results regarding survival after experimental CPR combined with a rapid infusion of sodium bicarbonate were a result of the excessive alkalosis created in combination with the higher resulting PCO2. Indirect evidence was given that a slightly alkaline pH also intracellularly supported critical reactions including ATPases essential for cellular survival.

Animals↗
PubMed1990

Total and net muscle protein breakdown in infection determined by amino acid effluxes.

The present investigation was undertaken to study whether, in human infection of varying severity, peripheral 3-methylhistidine efflux and urinary excretion are associated with net protein degradation and to estimate the protein synthesis rate from the combined effluxes of 3-methylhistidine, tyrosine, and phenylalanine. Quadruplicate femoral arteriovenous differences of 3-methylhistidine, tyrosine, and phenylalanine were multiplied by leg plasma flow in 15 infected patients. Leg effluxes for 3-methylhistidine, tyrosine, and phenylalanine were -0.074 +/- 0.011, -2.57 +/- 0.43, and -3.17 +/- 0.44 mumol/min, respectively. There was a significant linear relationship (P less than 0.01) between the effluxes of tyrosine and phenylalanine and the efflux and urinary excretion of 3-methylhistidine. A significant release of tyrosine and phenylalanine was observed in patients studied at the 3-methylhistidine level seen in normal healthy subjects. It is concluded that in infection 1) there is an increased breakdown of skeletal muscle protein and a reduced rate of protein synthesis, with the latter being relatively more important in patients with mild disease; and 2) urinary 3-methylhistidine excretion is associated with net skeletal muscle protein degradation for the patient group studied.

Abdomen↗
PubMed1989

Splanchnic and peripheral release of 3-methylhistidine in relation to its urinary excretion in human infection.

The present investigation was undertaken in order to determine the release of 3-methylhistidine (3MH) from the splanchnic region and from the leg, and the contributions these make to the increase in urinary 3MH excretion in infection. Thirteen febrile patients with infection were investigated. After an overnight fast, hepatic vein, femoral vein, and radial artery catheterizations were performed. Splanchnic and leg blood flows were determined by dye dilution technique. Plasma 3MH was analyzed by a modified HPLC method. The release of 3MH from the leg was 0.064 +/- 0.007 mumol/min (+/- SE) and from the splanchnic region 0.012 +/- 0.013 mumol/min. These releases of 3MH constitute 27% +/- 2% and 8% +/- 6% of the individual urinary excretions, respectively. With increasing degree of catabolism, measured as individual 3MH increase above baseline excretion or as the 3MH to creatinine ratio (3MH:Cr), the relative contribution to urinary excretion from the leg was increased (individual increase, P = 0.08; 3MH:Cr, P less than 0.01). Since this contribution was not decreased in the more catabolic patients, as would have been expected if the increase in urinary 3MH originated elsewhere, it is concluded that skeletal muscle is the source, and these results thus validate the use of urinary 3MH excretion as a marker of myofibrillar protein catabolism in infected patients.

Adult↗
PubMed1989

Evaluation of urinary 3-methylhistidine excretion in infection by measurements of 1-methylhistidine and the creatinine ratios.

When 3-methylhistidine (3MH) excretion is used as an indicator of myofibrillar protein catabolism, there are restricting factors, such as meat intake, incorrect 24-h urine collections, and a large interindividual variation in basal excretion. 1-Methylhistidine (1MH) was previously suggested as an indicator of meat intake. We studied the basal urinary excretion of 1MH and whether this was influenced by infection and we compared the use of 3MH vs the 3MH:creatinine ratio (3MH:Cr) in detecting changes during infection. The basal excretion of 1MH was 84.9 mumol/24 h and its creatinine molar ratio (1MH:Cr) was 7.4 x 10(-3) with no change during infection. Because 1MH:Cr was significantly increased in 4 of 14 patients, their 3MH values were considered influenced by meat intake and thus discarded. Among the remaining 10 patients, 9 showed a significant individual increase in 3MH:Cr during infection compared with only 4 in 3MH. This was due to a higher precision in 3MH:Cr despite the concomitant significant increase in urinary creatinine excretion.

Adolescent↗
PubMed1989

Exchange of 3-methylhistidine in the splanchnic region in human infection.

This investigation was undertaken to determine the splanchnic exchange of 3-methylhistidine (3MH) in infection. Hepatic vein, femoral vein, and radial artery catheterizations were performed in 12 febrile patients with infections of varying severity. Differences in arteriovenous 3MH, analyzed by high-performance liquid chromatography, were multiplied by the plasma flows, determined by a dye dilution technique. The mean splanchnic efflux was 0.062 +/- 0.180 mumol/min (mean +/- SD) with uptake occurring in five patients. The splanchnic uptake was significantly (p less than 0.001) correlated with the urinary 3MH excretion and the peripheral release from the leg. It is concluded that in human infection, splanchnic 3MH release is low and in patients with high rates of myofibrillar catabolism there may even be an uptake. The urinary 3MH excretion is still a marker of myofibrillar protein breakdown because it correlates well with the release from the leg, regardless of whether the patient has a splanchnic uptake or a release.

Chromatography, High Pressure Liquid↗
PubMed1987

Carbon dioxide production during mechanical ventilation.

Because of large stores of CO2 in different body tissues, metabolic change cannot be detected by measuring gas exchange until the CO2 stores have adapted to the new situation. Similarly, changes in the CO2 stores not due to metabolic alterations, may lead to error in gas exchange measurements. We studied CO2 production (VCO2) and oxygen consumption (VO2) in mechanically ventilated ICU patients, where CO2 stores were altered by: a) changing minute ventilation by 15%, b) reducing body temperature, and c) changing the level of sedation. Expired gases went through a mixing chamber and were analyzed continuously by a mass spectrometer. Signals from this instrument, together with gas-volume signals from the ventilator, were fed to a computer for calculation of VO2 and VCO2. Twenty to 120 min were required to reach a stable level, depending on the patient's size and circulatory response. Similar results were obtained by computer simulation using a five-compartment model of CO2 stores. These experiments indicate that measuring VO2 (for calculation of metabolic respiratory quotient [RQ]) in ventilated patients should occur after the patients maintain a 60-min period of stable body temperature and awareness. Ventilatory variables should not be changed substantially during the 90-min period before gas sampling. Cardiac output and muscle blood flow should not have changed 2 to 3 h before measuring RQ. If muscle blood flow is low, the stable periods for body temperature and ventilatory variables should be increased.

Carbon Dioxide↗
PubMed1987

The influence of epidural analgesia on the splanchnic exchange of amino acids during upper abdominal surgery.

Splanchnic turnover of plasma amino acids was studied in 10 patients given thoracic epidural analgesia combined with general anaesthesia for elective cholecystectomy. Ten other patients given only general anaesthesia for cholecystectomy served as a control group. All patients received an infusion of glucose during the investigation. The total concentration of amino acids in arterial plasma did not change in the patients given epidural analgesia but decreased by approximately 15% in the non-epidural group. In both groups splanchnic uptake of amino acids increased during surgery and was found to be more than doubled in the early postoperative period. The addition of epidural analgesia to general anaesthesia did not modify the splanchnic uptake of amino acids during surgery and in the immediate (2 h) postoperative period.

Abdomen↗
PubMed1986

The influence of abdominal surgical trauma on the exchange of blood-borne amino acids in the human leg.

Associated with surgical trauma is an increased release of gluconeogenic substrates from the periphery. The present study was undertaken to investigate the peripheral exchange of blood and plasma amino acids as well as some other gluconeogenic substrates (lactate and glycerol) in connection with abdominal surgery. Measurements of leg blood flow and femoral arterio-venous substrate differences were made before, during and immediately after elective cholecystectomy. Blood and plasma concentrations of most amino acids except alanine decreased during and immediately after surgery. Simultaneously there was an increased release of several of the amino acids as well as lactate and glycerol from the leg. The total release of plasma amino acids from one leg in the immediate postoperative period was about 2.5 times as high as before surgery. The turnover rates of amino acids as well as the changes in turnover rates were comparable whether the calculations were made from plasma or whole blood concentrations. At the end of surgery there was a high peripheral uptake of 3-hydroxybutyrate concomitant with a low release of amino acids.

Journal Article↗
PubMed1986

The exchange of blood-borne amino acids in the leg during abdominal surgical trauma: effects of glucose infusion.

The exchange of plasma amino acids and glucose, lactate, glycerol and 3-hydroxybutyrate in the leg was studied in otherwise healthy patients undergoing elective cholecystectomy. Seven patients were given a constant intravenous infusion of glucose at a rate of 1.1 mmol/min throughout the study. Seven other patients who received normal saline only served as a control group. Measurement of leg blood flow and arterio-femoral venous differences of amino acids and other energy metabolites were made on four occasions: (I) before surgery, (II) 10 min after skin incision, (III) at the end of surgery, and (IV) 30 min after the end of anaesthesia. The release of amino acids from the leg was comparable in the two groups before and during the early part of surgery. At the end of surgery the release of several individual amino acids, as well as the total release of amino acids, from the leg was higher in the patients given glucose infusion compared with the control patients. The infusion of glucose prevented the intraoperative rise in arterial levels and uptake of 3-hydroxybutyrate in the leg. A high release of amino acids at the end of surgery was thus associated with low arterial levels of 3-hydroxybutyrate while the reverse pattern was seen in the control patients. These effects of glucose infusion were qualitatively different from those seen in uninjured postabsorptive man.

3-Hydroxybutyric Acid↗
PubMed1986

Effect of extradural analgesia on glucose metabolism and gluconeogenesis. Studies in association with upper abdominal surgery.

Concentrations of glucose and gluconeogenic substrates across the splanchnic circulation were studied in 20 patients undergoing cholecystectomy with general anaesthesia. In 10 patients, general anaesthesia was administered alone, and in 10 general anaesthesia was combined with thoracic extradural analgesia. All patients received a constant i.v. infusion of glucose. Blood glucose concentration increased markedly in the general anaesthesia group in contrast to a moderate and shortlived increase in the patients given extradural analgesia, in whom the splanchnic release of glucose tended to be lower. The splanchnic uptake of glycerol was lower in the patients given extradural analgesia, while the uptake of lactate and the increase in alanine uptake was similar in both groups. Plasma catecholamine and serum cortisol concentrations were higher in the group receiving general anaesthesia alone, while serum growth hormone concentration was higher after surgery in the extradural group. The addition of extradural blockade to general anaesthesia suppresses the increase in blood glucose concentration--and this may be related to a reduced splanchnic release of glucose combined with an increased peripheral uptake.

Abdomen↗