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Biomedical subjects

S M Jakob

Publications and source records attributed to S M Jakob.

At least 19 recordsLinked to original sources
PubMed2006

Practical sources of error in measuring pulmonary artery occlusion pressure: a study in participants of a special intensivist training program of The Scandinavian Society of Anaesthesiology and Intensive Care Medicine (SSAI).

BACKGROUND: Physiological data obtained with the pulmonary artery catheter (PAC) are susceptible to errors in measurement and interpretation. Little attention has been paid to the relevance of errors in hemodynamic measurements performed in the intensive care unit (ICU). The aim of this study was to assess the errors related to the technical aspects (zeroing and reference level) and actual measurement (curve interpretation) of the pulmonary artery occlusion pressure (PAOP). METHODS: Forty-seven participants in a special ICU training program and 22 ICU nurses were tested without pre-announcement. All participants had previously been exposed to the clinical use of the method. The first task was to set up a pressure measurement system for PAC (zeroing and reference level) and the second to measure the PAOP. RESULTS: The median difference from the reference mid-axillary zero level was - 3 cm (-8 to + 9 cm) for physicians and -1 cm (-5 to + 1 cm) for nurses. The median difference from the reference PAOP was 0 mmHg (-3 to 5 mmHg) for physicians and 1 mmHg (-1 to 15 mmHg) for nurses. When PAOP values were adjusted for the differences from the reference transducer level, the median differences from the reference PAOP values were 2 mmHg (-6 to 9 mmHg) for physicians and 2 mmHg (-6 to 16 mmHg) for nurses. CONCLUSIONS: Measurement of the PAOP is susceptible to substantial error as a result of practical mistakes. Comparison of results between ICUs or practitioners is therefore not possible.

Calibration↗
PubMed2005

Lack of effect of ranitidine on gastric luminal pH and mucosal PCO2 during the first day in the ICU.

BACKGROUND: Histamine(2) (H(2))-blocking agents can attenuate intragastric CO(2)-production by reducing gastric acid secretion and preventing the interaction between H(+) and bicarbonate. However, gastric acid production may be impaired in acute circulatory failure due to poor mucosal perfusion, and H(2)-blockade could further impair mucosal perfusion. METHODS: Forty patients with acute circulatory and/or respiratory failure, age 61 +/- 16 years (mean +/- SD), APACHE II score 21 +/- 7, and SOFA score 8 +/- 3, received randomly either ranitidine, 50 mg (R) or placebo (P) every 8 h. Gastric intraluminal pH (gpH; antimony probe with external reference electrode) and mucosal pCO(2) (prCO(2), semicontinuous air-tonometry) were measured during 24 h, and blood gases were taken at 6-h intervals. RESULTS: Gastric intraluminal pH was 4.3 +/- 2.4 in P and 5.1 +/- 1.6 in R (NS). Mean prCO(2) was 6.8 +/- 2.7 kPa in P and 7.4 +/- 2.1 kPa in R, and mucosal-arterial pCO(2) gradient (Delta pCO(2)) was 2.2 +/- 2.9 kPa and 2.4 +/- 2.4 kPa, respectively (NS). Within-patient variabilities of gpH and prCO(2) were not influenced by ranitidine. A posthoc analysis revealed that non-survival in R was associated with a low mucosal pHi after 24 h (P = 0.002). This was explained by a low arterial pH but not by differences in gpH or prCO(2). CONCLUSION: In acute respiratory and circulatory failure, H(2) blockade has an inconsistent impact on gpH and does not reduce variabilities of gpH or prCO(2).

Acute Disease↗
PubMed2005

Oxygen extraction in pigs subjected to low-dose infusion of endotoxin after major abdominal surgery.

BACKGROUND: Sepsis may impair O(2) extraction due to blood flow redistribution or decreased utilization of the available oxygen. METHODS: We assessed the effect of endotoxemia on systemic and regional O(2) extraction and lactate handling in pigs, randomized to receive either endotoxin (0.4 microg kg(-1) h(-1); n = 10) or saline infusion (controls; n = 9) for 12 h. RESULTS: High baseline regional and systemic O(2) extraction in the endotoxin group (median 56%, range 45-77%) and in the controls (67%, 49-72%) was maintained until the end of the experiment (endotoxin group: 60%, 50-71%; controls: 60%, 50-74%) despite hypotension and a decrease in stroke volume in endotoxic animals. Hepatic lactate exchange decreased during endotoxemia from 14 micromol kg(-1) min(-1) (range 10-28 micromol kg(-1) min(-1)) to 10 (range 3-15) micromol kg(-1) min(-1); P < 0.01), but remained stable in the controls, with 13 micromol min(-1) (4-18 micromol min(-1)) at baseline and 7 micromol min(-1) (3-17 micromol min(-1)) after 12 h of saline infusion. CONCLUSIONS: The high and sustained oxygen consumption and oxygen extraction in this endotoxemic model speak against any major impairment of hepatosplanchnic or systemic oxygen extraction and oxidative metabolism. The reduced hepatic lactate exchange despite an unchanged hepatic lactate influx suggests altered metabolic activities independent of oxygen consumption.

Abdomen↗
PubMed2004

Improved skin flap survival after local heat preconditioning in pigs.

BACKGROUND: Preconditioning induces the expression of heat shock proteins (HSPs), which can help a cell survive an acute episode of stress. Similar to the induction of HSP expression, the cell protection is independent of the type of stress. The aim of this study was to test in a large, randomized animal model, if skin flap survival may be improved by local heat preconditioning and induction of HSP 70. MATERIALS AND METHODS: Twenty-four hours before surgery, a heating blanket was laid on the buttocks of large white pigs. In the preconditioned group (n = 6), the blanket was warmed up to 43 degrees C for 3 x 30 min, whereas it was kept at room temperature in between the heating episodes as well as in the control animals (n = 6). A random pattern skin flap was raised on both sides of the buttocks. Flap survival was measured clinically. Induction of HSP and apoptosis were assessed quantitatively by immunohistochemistry and TUNEL assay, respectively. RESULTS: Preconditioning reduced flap necrosis from 40 +/- 8% of the total flap surface to 7 +/- 14% (P < 0.01). Induction of HSP was significantly higher in the experimental group (79 +/- 12% versus 42 +/- 13%, P < 0.01), whereas apoptosis in healthy flap tissue was reduced from 30 +/- 11 to 11 +/- 6 cells/visual field (P < 0.01). CONCLUSION: In the present study, necrosis and apoptosis rate of skin flaps could be reduced significantly due to local heat preconditioning. Our results suggest that ischemia-related wound healing complications could be diminished with local heat application, a most simple and least invasive method of preconditioning.

Animals↗
PubMed2004

Prevention of acute renal failure--fluid repletion and colloids.

Hypovolemia alone or in conjunction with other factors is a main reason for acute renal failure in critically ill patients. Various crystalloid and colloid solutions are available to correct hypovolemia. Some of them have been implicated in impairment of renal function. Infusion of large amounts of sodium chloride is associated with increased incidence of nausea, vomiting and hyperchloremic metabolic acidosis. While gelatins and HES are preferred colloids in patients with normal kidney function, there is some evidence that the latter are associated with impaired renal function in patients with pre-existing kidney disease. Any hyperoncotic colloid given in large amounts may decrease glomerular filtration, and should therefore be combined with crystalloids.

Acute Kidney Injury↗
PubMed2001

Gut luminal lactate release during gradual intestinal ischemia.

OBJECTIVES: Gut ischemia induced by occlusion of the superior mesenteric artery (SMA) results in release of lactate into the gut lumen. We studied the threshold of SMA flow reduction that leads to increased gut luminal lactate during stepwise reduction in SMA blood flow. DESIGN AND SETTING: A randomized, controlled animal experiment in a university experimental research laboratory. INTERVENTIONS: Anesthetized, normoventilated, normovolemic domestic pigs were randomized to ischemia ( n=7) and sham groups ( n=7). SMA blood flow was reduced stepwise at 15-min intervals by 22%, 44%, 66%, and 88% and kept constant thereafter for 60 min. MEASUREMENTS AND RESULTS: Jejunal luminal microdialysate lactate and mucosal pCO(2) were measured every 15 min. The luminal lactate increased over the upper normal limit of 0.2 mmol/l at a median SMA blood flow of 9.6 ml kg(-1) min(-1) (range 7.5-23.7). In five of seven animals the increase in luminal lactate was preceded by or accompanied by an increase in the mucosal-arterial pCO(2) gradient. CONCLUSIONS: There is a threshold of SMA blood flow below which gut luminal lactate increases, indicating mucosal anaerobic metabolism. Measurement of gut luminal lactate by microdialysis can be used to assess the adequacy of gut perfusion and the onset of anaerobic metabolism.

Animals↗
PubMed2001

Splanchnic perfusion during hemodialysis: evidence for marginal tissue perfusion.

OBJECTIVE: Splanchnic perfusion may be compromised during hemodialysis because of hypovolemia, inflammatory response, and blood flow redistribution. The aim of this study was to assess the response of splanchnic blood flow and oxygen transport to hemodialysis. DESIGN: A prospective clinical study. SETTING: A mixed medical-surgical intensive care unit in a university hospital. PATIENTS: Nine patients with acute renal failure. INTERVENTIONS: A 4-hr period of hemodialysis. MEASUREMENTS AND MAIN RESULTS: Systemic (via a pulmonary artery catheter), hepatosplanchnic, and femoral (via dye dilution) blood flow and gastric mucosal Pco2 were measured before, during, and 2 hrs after hemodialysis. During hemodialysis, despite unchanged arterial blood pressure, cardiac output and stroke volume decreased from 3.0 +/- 1.0 L/m2/min (mean +/- sd) to 2.3 +/- 0.7 L/m2/min (p =.02), and from 38 +/- 16 mL/m2/min to 28 +/- 12 mL/m2/min (p =.01), respectively. Splanchnic but not femoral blood flow decreased from 0.9 +/- 0.3 L/m2/min to 0.7 +/- 0.2 L/m2/min (p =.02). The blood flows returned to baseline values after dialysis without need for therapeutic interventions. Gastric mucosal-arterial Pco2 gradients were high before dialysis (35 +/- 23 torr [4.6 +/- 3.1 kPa]) and did not change. Renin but not atrial natriuretic peptide concentration increased during hemodialysis from 13 +/- 13 microg/L to 35 +/- 40 microg/L and decreased afterward to baseline values (13 +/- 13 microg/L; p =.01). Whereas interleukin 6 tended to decrease, tumor necrosis factor alpha increased during hemodialysis from 74 +/- 24 pg/mL to 86 +/- 31 pg/mL and continued to increase after hemodialysis to 108 +/- 66 pg/mL (p =.022). CONCLUSION: Hemodialysis and fluid removal in normotensive patients with acute renal failure may result in a reduction of systemic and splanchnic blood flow that is undetectable using traditional clinical signs. In contrast to what is observed in hypovolemia, the changes in regional blood flow are rapidly reversible after hemodialysis.

Acute Kidney Injury↗
PubMed2001

Metabolic changes after cardiac surgery.

The metabolic changes that occur after cardiac surgery result from a complex interaction between the effects of surgery and extracorporeal circulation per se, the inflammatory response to surgical trauma and extracorporeal circulation, perioperative use of hypothermia, the cardiovascular and neuroendocrine responses characteristic to cardiac surgery, and the drugs and blood products used to support circulation during and after operation. These changes include among others increased oxygen consumption and energy expenditure and increased secretion of insulin, growth hormone, adrenocorticotrophic hormone, cortisol, epinephrine and norepinephrine. Other changes include decreased total-Trijodthyronine levels, hyperglycemia, hyperlactatemia, increased glutamate, aspartate and free fatty acid concentrations, hypokalemia, an increased production of inflammatory cytokines and increased consumption of complement and adhesion molecules. There is evidence that better control of metabolic abnormalities improves the patients' outcome.

Cardiac Surgical Procedures↗
PubMed2001

Effects of systemic arterial hypoperfusion on splanchnic hemodynamics and hepatic arterial buffer response in pigs.

The hepatic arterial buffer response (HABR) tends to maintain liver blood flow under conditions of low mesenteric perfusion. We hypothesized that systemic hypoperfusion impairs the HABR. In 12 pigs, aortic blood flow was reduced by cardiac tamponade to 50 ml. kg(-1). min(-1) for 1 h (short-term tamponade) and further to 30 ml. kg(-1). min(-1) for another hour (prolonged tamponade). Twelve pigs without tamponade served as controls. Portal venous blood flow decreased from 17 +/- 3 (baseline) to 6 +/- 4 ml. kg(-1). min(-1) (prolonged tamponade; P = 0.012) and did not change in controls, whereas hepatic arterial blood flow decreased from 2 +/- 1 (baseline) to 1 +/- 1 ml. kg(-1). min(-1) (prolonged tamponade; P = 0.050) and increased from 2 +/- 1 to 4 +/- 2 ml. kg(-1). min(-1) in controls (P = 0.002). The change in hepatic arterial conductance (DeltaC(ha)) during acute portal vein occlusion decreased from 0.1 +/- 0.05 (baseline) to 0 +/- 0.01 ml. kg(-1). min(-1). mmHg(-1) (prolonged tamponade; P = 0.043). In controls, DeltaC(ha) did not change. Hepatic lactate extraction decreased, but hepatic release of glutathione S-transferase A did not change during cardiac tamponade. In conclusion, during low systemic perfusion, the HABR is exhausted and hepatic function is impaired without signs of cellular damage.

Animals↗
PubMed2000

IBIS data library: clinical description of the Finnish database. Improved Monitoring for Brain Dysfunction during Intensive Care and Surgery.

Improved monitoring of brain function in intensive care and surgery is a project aiming to develop methods of biosignal processing and interpretation, in order to characterise critical events during anaesthesia and cardiac surgery, effect of anaesthesia regimen, neurophysiological findings of different sedation levels, arousal from post-anaesthesia sedation, post-cardiopulmonary bypass brain dysfunction and early brain dysfunction in patients with multiple organ failure. A data library was collected in the three participating hospitals. This is a description of the data library from the University Hospital of Kuopio, Finland, which includes data from 40 patients after cardiac surgery and from seven patients with multiple organ dysfunction. This project demonstrates that active neuromonitoring can be performed in the intensive care unit without interference with the normal treatment and care. The presented database may serve other scientific workers as a reference for a typical spectrum of perioperative data with respect to severity of disease, length of cardiopulmonary bypass, postoperative levels of sedation and length of hospital stay in cardiac surgery patients, and for types of diseases and outcome in patients with multiple organ dysfunction.

Adult↗
PubMed2000

Quantification of haemodynamic response to auditory stimulus in intensive care.

Measuring effects of sensory stimuli on haemodynamics could provide information about the interplay between central and autonomous nervous system (ANS). However, ANS response to sensory stimulus has received little attention. In this paper we present a signal processing scheme to extract the responses of heart rate and systemic arterial pressure on auditory stimulus in intensive care patients (N=5). In short, the effect of mechanical ventilation is rejected by optimal linear modelling. Other disturbances are attenuated by filtering and efficient rejection of outlying sweeps of data. The results show identifiable responses on three out of five cases. The response characteristics may be explained by synchronisation of spontaneous variability in systemic arterial pressure to auditory stimulus.

Acoustic Stimulation↗
PubMed2000

Assessment of the adequacy of systemic and regional perfusion after cardiac surgery.

Changes in systemic, hepatosplanchnic and femoral blood flow and liver function after cardiac surgery were studied in 17 patients from April to October 1995. Blood flows were measured every 3 h and gastric mucosal PCO2 (by tonometry) every hour from arrival in the intensive care unit until extubation. Cardiac output and systemic oxygen consumption increased from 2.83 (0.68) litres min-1 m-2 to 3.17 (0.57) litres min-1 m-2 and from 126 (18) ml min-1 m-2 to 135 (44) ml min-1 m-2, respectively (mean (SD), P = 0.028 and P = 0.019, respectively, baseline vs 6 h). The fraction of cardiac output distributed to the splanchnic region decreased from 0.25 (0.06) to 0.20 (0.04) (P = 0.004) while splanchnic oxygen extraction increased from 0.43 (0.15) to 0.50 (0.12) (P = 0.019). Femoral blood flow increased from 0.18 (0.07) litres min-1 m-2 to 0.23 (0.09) litres min-1 m-2, (P = 0.006, baseline vs 3 h) but femoral oxygen consumption did not change. Changes in blood flow were not reflected by venous-arterial PCO2 gradients. Initially high glutathione transferase alpha concentrations decreased and indocyanine green extraction was well preserved. We conclude that the predominant increase in peripheral blood flow and the increased oxygen uptake in certain regions of the body may increase the risk of a mismatch between splanchnic perfusion and metabolic demands. This mismatch was not associated with impaired liver function or cellular integrity.

Aged↗
PubMed2000

Jejunal and gastric mucosal perfusion versus splanchnic blood flow and metabolism: an observational study on postcardiac surgical patients.

OBJECTIVES: To evaluate the association between changes in total splanchnic and mucosal perfusion, assessed either by gastric tonometry or jejunal laser Doppler flowmetry in postcardiac surgical patients. DESIGN: A prospective, observational study. SETTINGS: A general intensive care unit in a tertiary care center. PATIENTS: Twelve, postoperative cardiac surgery patients were studied. INTERVENTIONS: Patients were treated according to clinical routine. Total splanchnic blood flow (indocyanine green extraction), jejunal mucosal perfusion (laser Doppler flowmetry), gastric mucosal-arterial PCO2 gradients, and splanchnic lactate uptake were studied during four 30-min measurements periods, each separated by a period of 1 hr. MEASUREMENTS AND MAIN RESULTS: There was no consistent association between either total splanchnic and local mucosal perfusion or between gastric and jejunal perfusion as assessed by two different techniques. The PCO2 gradient increased from 0.73+/-0.21 kPa to 1.15+/-0.30 kPa (p < .05), and splanchnic oxygen extraction increased from 40%+/-9% to 49%+/-14% (p < .01). CONCLUSIONS: In this observational study on postcardiac surgical patients, local mucosal perfusion did not reflect total splanchnic blood flow and vice versa. Either changes in gastric and jejunal mucosal perfusion were different or increasing tissue metabolism was responsible for the observed lack of association between tonometry, laser Doppler flowmetry, and total splanchnic blood flow. Increasing mucosal arterial PCO2 gradient and splanchnic oxygen extraction may reflect a mismatch between splanchnic perfusion and metabolic demands.

Adult↗
PubMed2000

Prevention of systemic hyperlactatemia during splanchnic ischemia.

Arterial blood lactate increases as a result of poor tissue perfusion. In splanchnic hypoperfusion, increased hepatic lactate uptake may delay increases in arterial blood lactate. We hypothesized that during isolated reduction of mesenteric blood flow, maintaining systemic blood volume and flow by fluid resuscitation may prevent systemic hyperlactatemia and therefore mask splanchnic ischemia. In a randomized study, 7 pigs were subjected to 4 h of splanchnic hypoperfusion by reducing the superior mesenteric artery blood flow to 4 +/- 0.8 mL/kg min [mean +/- standard deviation (SD)]. Seven pigs served as controls. Fluid was administered in order to keep the pulmonary artery occlusion pressure at 5 to 8 mm Hg. Cardiac output, portal vein, superior mesenteric, and hepatic arterial blood flow were measured every 30 min. Arterial, mixed venous, hepatic, portal, and mesenteric venous blood lactate, and jejunal mucosal pCO2 were measured at baseline and thereafter at 30-min intervals. The initial decrease in portal venous blood flow in the ischemic animals was subsequently counterbalanced by increasing hepatic arterial blood flow from 2 +/- 1 mL x kg(-1) x min(-1) at baseline to 11 +/- 4 mL x kg(-1) x min(-1) [after 4 h of ischemia; mean +/- standard deviation (SD), P = 0.02]. Jejunal mucosal- and mesenteric vein-arterial pCO2 gradients increased in the ischemic group from 11 +/- 8 mm Hg to 73 +/- 5 mm Hg (P = 0.02), and from 10 +/- 4 mm Hg to 44 +/- 8 mm Hg, respectively (P = 0.02). Mesenteric and portal venous lactate increased in the ischemic animals from 1.1 +/- 0.3 mmol/L to 4.2 +/- 1.0 mmol/L (P = 0.02), and from 1.0 +/- 0.2 mmol/L to 1.6 +/- 0.3 mmol/L, respectively (P = 0,03). While mesenteric lactate production and hepatic lactate uptake increased in parallel in the ischemic animals from 5 +/- 6 micromol x kg(-1) x min(-1) to 14 +/- 5 micromol x kg(-1) x min(-1) (P = 0.04), and from 14 +/- 7 micromol x kg(-1) x min(-1) to 24 +/- 6 micromol x kg(-1) x min(-1), respectively (P = 0.02), hepatic venous and arterial lactate, and apparent splanchnic lactate uptake and extraction did not change. We conclude that the hepatic lactate uptake increases in response to hepatic lactate influx. Systemic hyperlactatemia and increased hepatic venous lactate concentrations are late consequences of mesenteric hypoperfusion if hypovolemia is prevented. The net exchange of lactate across the splanchnic region does not reflect hepato-portal lactate kinetics in this animal model of intestinal hypoperfusion.

Animals↗
PubMed2000

Splanchnic perfusion in intensive care patients.

Splanchnic vasoregulation is poorly understood. The tissue perfusion in the splanchnic region may be compromised in critically ill patients both because of the underlying disease and therapeutic interventions. Inadequate perfusion, dysoxia, and ischemia-reperfusion may trigger and modify an inflammatory response which may itself cause deterioration of the splanchnic perfusion.

Critical Care↗
PubMed1999

The Haldane effect--an alternative explanation for increasing gastric mucosal PCO2 gradients?

When venous oxygen saturation increases as a result of increased blood flow, changes in venous blood PCO2 and carbon dioxide content may differ because of the Haldane effect. The Haldane effect may also explain increases in gastric mucosal-arterial PCO2 gradient despite major increases in splanchnic blood flow. We re-analysed data from 22 patients after cardiac surgery who were randomized to receive either dobutamine or placebo, and a separate group of patients who received dobutamine for low cardiac output (n = 6). Three different values of gastric mucosal oxygen extraction at baseline were assumed (0.3, 0.5 and 0.7). In nine of 14 patients with both increasing splanchnic blood flow and mucosal-arterial PCO2 gradient, an equal increase in mucosal and total splanchnic blood flow, oxygen consumption and carbon dioxide production together with the Haldane effect would have caused an increase in mucosal-arterial PCO2 gradients from a mean value of 0.53 (SD 0.88) kPa at baseline to 0.68-0.82 (0.89-0.90) kPa (P < 0.01). In the remaining patients, disproportionate changes in flow and metabolism must have been involved in addition to the Haldane effect. We conclude that whenever major changes in mucosal tissue oxygen extraction are likely to occur, an increase in the mucosal-arterial PCO2 gradient may be explained in part or completely by the Haldane effect, and may therefore not reflect worsening perfusion.

Carbon Dioxide↗