PubMed Health⌕ Search

Biomedical subjects

A B Groeneveld

Publications and source records attributed to A B Groeneveld.

At least 37 records · Page 2Linked to original sources

Effect of gastric feeding on intragastric P(CO2) tonometry in healthy volunteers.

PURPOSE: The tonometric detection of a high intragastric regional P(CO2) (PrCO2) reflecting an elevated intramucosal P(CO2) can be helpful to diagnose mucosal ischemia, if acid secretion is suppressed to avoid intragastric CO2 production through buffering of acid by bicarbonate in the stomach. It is recommended to perform tonometry in the fasting state, but this may hamper feeding of the critically ill. On the other hand, postfeeding tonometry could serve as a diagnostic stress test because feeding increases mucosal blood flow demand, provided that the meal itself does not hamper diffusion of CO2 from mucosa to tonometer balloon and does not generate intragastric CO2, independently from intramucosal P(CO2). We therefore studied the effect of a standard meal on intragastric PrCO2 tonometry in healthy volunteers with suppression of meal-stimulated gastric acid secretion and, presumably, with an adequate mucosal blood flow reserve. MATERIAL AND METHODS: The gastric juice pH and tonometric PrCO2 were measured in 14 human volunteers, after gastric acid secretion suppression by either ranitidine (100-mg bolus, followed by 25 mg/h i.v., n = 7) or by ranitidine plus pirenzepine (10-mg bolus, followed by 3 mg/h i.v., n=7) to suppress any residual meal-stimulated gastric acid secretion, before and at 30-minute intervals until 120 minutes after oral ingestion of a standard liquid test meal (Pulmocare [Abbott, the Netherlands]; 500 mL, 750 kcal, P(CO2) 5 mm Hg, pH 7.50). RESULTS: The gastric juice pH, which was >4.0 in all individuals throughout the study, and the PrCO2 did not depend on the regimen for gastric acid secretion suppression, and therefore the data were pooled. The PrCO2 (median [range]) after feeding was 69% (56% to 170%) of baseline (42 [37-51] mm Hg) from 0 to 30 minutes (P < .001), 85% (72% to 167%) of baseline from 30 to 60 (P < .05), 97% (57% to 193%) from 60 to 90 minutes, and 112% (97% to 189%) of baseline from 90 to 120 minutes with a rise above baseline in 10 of 14 patients. In vitro, the liquid test meal generated CO2 after adding bicarbonate but not after hydrochloric acid. CONCLUSION: We recommend intragastric tonometry to be performed in the fasting state and discourage tonometry after feeding as a stress test, because a single test meal changes tonometric PrCO2 in a time-dependent manner until 2 hours after gastric feeding of healthy volunteers. The fall in PrCO2 directly after feeding can be attributed to dilution, whereas a rise above baseline in some patients may have been caused, as supported by CO2 production after adding bicarbonate to the test meal in vitro, by CO2 production through buffering of meal-derived acid by gastric bicarbonate, in the absence of stimulated gastric acid secretion by feeding.

Adult↗

Prediction of microbial infection and mortality in medical patients with fever: plasma procalcitonin, neutrophilic elastase-alpha1-antitrypsin, and lactoferrin compared with clinical variables.

Fever suggests the likelihood of severe microbial infection. Abnormal temperature, tachycardia, tachypnea, and abnormal white blood cell counts define the systemic inflammatory response syndrome (SIRS). In 300 hospitalized medical patients with fever, we determined clinical variables and procalcitonin, elastase-alpha1-antitrypsin, and lactoferrin levels in plasma. Of the patients, 71% had clinical infection (by clinical judgment) and 44% had microbial infection (by microbiological testing). SIRS occurred in 95%, and the 28-day mortality rate was 9%. The sensitivity for predicting microbial infection, bacteremia, and mortality was less but the specificity was greater for supranormal procalcitonin, elastase-alpha1-antitrypsin, and lactoferrin levels than for SIRS. The area under the receiver operating characteristic curve (AUC) for microbial infection was higher for procalcitonin and elastase-alpha1-antitrypsin levels than for clinical variables and lactoferrin level. The AUC for bacteremia was also higher for inflammatory factors (>0.70; P < .001) than for clinical variables. The AUC for mortality (P < .05) was 0.79 for the respiratory rate, 0.69 for elastase-alpha1-antitrypsin level, 0.65 for heart rate, 0.61 for procalcitonin level, and 0.60 for white blood cell count. In febrile medical patients, plasma procalcitonin and elastase-alpha1-antitrypsin levels may predict microbial infection and bacteremia better than (and mortality as well as) do clinical symptoms.

Adolescent↗

Predicting outcome after cardiac surgery: comparison of global haemodynamic and tonometric variables.

To compare how outcome can be predicted from global haemodynamic compared with regional perfusion-related variables (gastric intramucosal pH (pHi) and intramucosal-arterial PCO2 difference (delta PCO2)), we measured global haemodynamics, gastric pHi and delta PCO2 in 68 haemodynamically compromised patients after cardiac surgery on admission to the intensive care unit (ICU) and 12 h later. Overall mortality rate in the ICU was 19.1%. In non-survivors, mean arterial pressure on admission (P = 0.03) and at 12 h (P = 0.02) was lower, and mean pulmonary artery pressure on admission (P = 0.006) and at 12 h (P = 0.004) was higher than in survivors. Gastric pHi on admission and at 12 h did not differ between non-survivors and survivors (7.37 (SD 0.1) vs 7.39 (0.09), and 7.37 (0.1) vs 7.41 (0.09), respectively). delta PCO2 on admission and at 12 h did not differ between non-survivors and survivors (0.52 (0.52) kPa vs 0.47 (1.01) kPa and 0.59 (0.7) kPa vs 0.62 (0.9) kPa, respectively). Our data showed that global, routinely monitored, haemodynamic variables are better early predictors of outcome after cardiac surgery than regional, tonometric variables. This conclusion does not support hypoperfusion of the gastrointestinal tract as an early determinant of outcome after cardiac surgery.

Adult↗

Continuous cardiac output in septic shock by simulating a model of the aortic input impedance: a comparison with bolus injection thermodilution.

BACKGROUND: To compare continuous cardiac output obtained by simulation of an aortic input impedance model to bolus injection thermodilution (TDCO) in critically ill patients with septic shock. METHODS: In an open study, mechanically ventilated patients with septic shock were monitored for 1 (32 patients), 2 (15 patients), or 3 (5 patients) days. The hemodynamic state was altered by varying the dosages of dopamine, norepinephrine, or dobutamine. TDCO was estimated 189 times as the series average of four automated phase-controlled injections of iced 5% glucose, spread equally over the ventilatory cycle. Continuous model-simulated cardiac output (MCO) was computed from radial or femoral artery pressure. On each day, the first TDCO value was used to calibrate the model. RESULTS: TDCO ranged from 4.1 to 18.2 l/min. The bias (mean difference between MCO and TDCO) on the first day before calibration was -1.92 +/- 2.3 l/min (mean +/- SD; n = 32; 95% limits of agreement, -6.5 to 2.6 l/min). The bias increased at higher levels of cardiac output (P < 0.05). In 15 patients studied on two consecutive days, the precalibration ratio TDCO:MCO on day 1 was 1.39 +/- 0.28 (mean +/- SD) and did not change on day 2 (1.39 +/- 0.34). After calibration, the bias was -0.1 +/- 0.8 l/min with 82% of the comparisons (n = 112) < 1 l/min and 58% (n = 79) < 0.5 l/min, and independent of the level of cardiac output. CONCLUSIONS: In mechanically ventilated patients with septic shock, changes in bolus TDCO are reflected by calibrated MCO over a range of cardiac output values. A single calibration of the model appears sufficient to monitor continuous cardiac output over a 2-day period with a bias of -0.1 +/- 0.8 l/min.

Adult↗

Circulating endothelin and nitrate-nitrite relate to hemodynamic and metabolic variables in human septic shock.

Activation of the nitric oxide (NO) pathway over that of endothelin in the vessel wall, as judged from circulating endothelin and nitrate-nitrite (NN) levels, may partly account for the hypotension associated with vasodilation, diminished catecholamine sensitiveness and O2 extraction, and lactic acidemia in human septic shock. In a prospective study, 14 consecutive patients with septic shock and a pulmonary artery catheter in place were included. For 3 days after admission, serial measurements of hemodynamic variables and plasma levels of endothelin and NN were done. The patients had a hyperdynamic circulation. Except for a higher final blood lactate level and more treatment with vasoconstricting catecholamines in nonsurvivors, global hemodynamic and O2-related variables did not differ between outcome groups. On the day of admission, circulating endothelin and NN levels were elevated and related to elevated levels of tumor necrosis factor-alpha and interleukin-6. The levels of endothelin increased in time in nonsurvivors as compared with survivors. The NN levels declined in survivors but not in nonsurvivors. The systemic vascular resistance indices (SVRI), global O2 extraction ratios, and blood lactate levels directly related to the endothelin levels. SVRI and global O2 extraction ratios inversely, and the lactate blood levels directly, related to NN levels, and the hemodynamic and metabolic parameters related directly to the ratio between endothelin and NN plasma levels on the days of the study. The vessel wall factors did not relate to the creatinine levels. The results suggest that the hemodynamic and metabolic peripheral abnormalities of human septic shock are mediated in part by cytokine-activated endothelin and NO systems in the vessel wall. They also suggest that increased production rather than diminished renal clearance accounts for elevated levels of NN and endothelin and that the latter are associated with a poor outcome.

Adult↗

Increased gastric PCO2 during exercise is indicative of gastric ischaemia: a tonometric study.

BACKGROUND: Diagnosis of gastric ischaemia is difficult and angiography is an invasive procedure. Angiographic findings may not correlate with clinical importance. AIMS: To investigate whether tonometric measurement of intragastric PCO2 during exercise can be used to detect clinically important gastric ischaemia. METHODS: Fourteen patients with unexplained abdominal pain or weight loss were studied. Splanchnic angiography served as the gold standard. Three patients were studied again after a revascularisation procedure. Gastric PCO2 was measured from a nasogastric tonometer, with 10 minute dwell times, and after acid suppression. Gastric and capillary PCO2 were measured before, during, and after submaximal exercise of 10 minutes duration. RESULTS: Seven patients had normal angiograms; seven had more than 50% stenosis in the coeliac (n=7) or superior mesenteric artery (n=4). Normal subjects showed no changes in tonometry. In patients with stenoses, the median intragastric PCO2 (PiCO2) at rest was 5.2 kPa (range 4.8-11.2) and rose to 6.4 kPa (range 5.7-15.7) at peak exercise; the median intragastric blood PCO2 gradient increased from 0.0 kPa (range -0.8 to 5.9) to 1.7 kPa (range 0.9 to 10.3; p<0.01). Only two subjects had abnormal tonometry at rest; all had supernormal values at peak exercise. The PCO2 gradient correlated with clinical and gastroscopic severity; in patients reexamined after revascularisation (n=3), exercise tonometry returned to normal. CONCLUSION: Gastric tonometry during exercise is a promising non-invasive tool for diagnosing and grading gastrointestinal ischaemia and evaluating the results of revascularisation surgery for symptomatic gastric ischaemia.

Adult↗

The clinical host response to microbial infection in medical patients with fever.

STUDY OBJECTIVES: Predictors among demographic, clinical, and laboratory variables for a microbial (nonviral/nonchlamydial) infection in hospitalized medical patients with new onset of fever (temperature > or =38.0 degrees C axillary or > or =38.3 degrees C rectal) were analyzed and compared with the criteria for the systemic inflammatory response syndrome (SIRS), including an abnormal body temperature and WBC count, tachypnea and tachycardia, and sepsis, defined as SIRS and the presence of a clinical infection. DESIGN: A prospective cohort study. SETTING: Department of internal medicine at a university hospital. PATIENTS: In 300 hospitalized medical patients with new onset of fever, demographic, clinical, and laboratory variables were obtained during the first 2 days after inclusion, and peak and nadir values, when appropriate, were taken. Microbiologic results for 7 days were collected. Clinical information was used to decide on the presence of a clinical infection. MEASUREMENTS AND RESULTS: One hundred thirty-three of 300 patients (44%) had a microbial infection: 26% suffered from local microbial infection only, 9% from bacteremia only, and 9% had bloodstream plus local microbial infections. Patients with a microbial infection had a higher World Health Organization performance score at home (p<0.05), higher peak body temperature (p<0.001), higher nadir and peak WBC counts (p<0.05), lower nadir platelet count (p<0.01), higher peak alanine and aspartate aminotransferases (p<0.01), and lower nadir albumin (p<0.001) levels in blood during the first 2 days after inclusion than those without infection. Using multivariate techniques, predictors for microbial infection or bacteremia alone, independent of age, sex, underlying disease, and clinical infection, were peak temperature, peak WBC count, and nadir platelet count and albumin level. In contrast, conventional SIRS/sepsis definitions and criteria predicted microbial infection less well, mainly because tachypnea and tachycardia were of no predictive value. CONCLUSIONS: In febrile medical patients, microbial infection can be predicted with use of easily obtained clinical and laboratory variables, including peak temperature, peak WBC count, and nadir platelet count and albumin level within the first 2 days. The new model predicted microbial infection better than conventional SIRS/sepsis criteria. This may help to improve the clinical recognition of the systemic host response to microbial infection and to refine SIRS/sepsis definitions.

Adolescent↗

Electrical impedance tomography in the assessment of extravascular lung water in noncardiogenic acute respiratory failure.

STUDY OBJECTIVES: To establish the value of electrical impedance tomography (EIT) in assessing pulmonary edema in noncardiogenic acute respiratory failure (ARF), as compared to the thermal dye double indicator dilution technique (TDD). DESIGN: Prospective clinical study. SETTING: ICU of a general hospital. PATIENTS: Fourteen ARF patients. INTERVENTIONS: In order to use the TDD to determine the amount of extravascular lung water (EVLW), a fiberoptic catheter was placed in the femoral artery. MEASUREMENTS AND MAIN RESULTS: Fourteen consecutive ARF patients receiving mechanical ventilation were measured by EIT and TDD. EIT visualizes the impedance changes caused by the ventilation in two-dimensional image planes. An impedance ratio (IR) of the ventilation-induced impedance changes of a posterior and an anterior part of the lungs was used to indicate the amount of EVLW. For the 29 measurements in 14 patients, a significant correlation between EIT and TDD (r = 0. 85; p < 0.001) was found. The EIT reproducibility was good. The diagnostic value of the method was tested by receiver operator characteristic analysis, with 10 mL/kg of EVLW considered as the upper limit of normal. At a cutoff level of the IR of 0.64, the IR had a sensitivity of 93%, a specificity of 87%, and a positive predictive value of 87% for a supranormal amount of EVLW. Follow-up measurements were performed in 11 patients. A significant correlation was found between the changes in EVLW measured with EIT and TDD (r = 0.85; p < 0.005). CONCLUSION: We conclude that EIT is a noninvasive technique for reasonably estimating the amount of EVLW in noncardiogenic ARF.

Acute Disease↗

Reliable gastric tonometry after coronary artery surgery: need for acid secretion suppression despite transient failure of acid secretion.

OBJECTIVE: To study the need for suppression of gastric acid secretion for reliable intragastric partial pressure of carbon dioxide (PCO2) tonometry by evaluating the effect of an oral dose of sodium bicarbonate before and after administration of the H2-blocker ranitidine to mimic CO2 generation following the buffering of acid by bicarbonate in patients after cardiac surgery. DESIGN: Prospective, open, non-randomized clinical study. SETTING: Cardiothoracic intensive care unit at a university hospital. PATIENTS: 10 patients after elective coronary artery bypass surgery. INTERVENTIONS: An oral dose of 500 mg sodium bicarbonate before and after acid secretion suppression by 100 mg ranitidine as an intravenous bolus given at approximately 3 h after surgery (day 0) and on the first postoperative day (day 1). MEASUREMENTS AND RESULTS: Intragastric PCO2 (iPCO2; tonometry), gastric juice pH (aspirate) and arterial blood gas values were measured. On day 0, the iPCO2 was 25 +/- 5 mmHg before and 31 +/- 5 mmHg after the bicarbonate dose, 29 +/- 5 mmHg after ranitidine infusion, and 31 +/- 5 mmHg after the bicarbonate dose following the ranitidine infusion (NS). On day 1, the basal iPCO2 was 32 +/- 4 mmHg and it increased to 56 +/- 25 mmHg following bicarbonate (p < 0.01). After ranitidine, the iPCO2 was 33 +/- 4 mmHg before and 40 +/- 14 mmHg after bicarbonate (NS). Basal gastric juice pH was > 4 in nine of ten patients on day 0 and > 4 in seven of ten patients on day 1. CONCLUSIONS: Pharmacological suppression of gastric acid secretion is mandatory for reliable iPCO2 tonometry after cardiopulmonary bypass surgery, even when gastric acid secretion is transiently inhibited. In fact, gastric acid secretion was inhibited immediately after surgery, but returned on the first postoperative day in most patients, as judged from the bicarbonate back titration of gastric acid, even when gastric juice pH was relatively high.

Administration, Oral↗

Complement activation in patients with sepsis is in part mediated by C-reactive protein.

The involvement of C-reactive protein (CRP) in the activation of complement in patients with sepsis was investigated. In 104 patients with infections of varying severity, circulating levels of CRP-complement complexes, which are specific indicators for CRP-mediated complement activation, were assessed. Complement-CRP complexes were increased in almost all patients and correlated significantly with levels of C3a (r = .59; P < .001) and C-reactive protein (r = .76; P < .001). In addition, they correlated with levels of secretory phospholipase A2 (r = .59; P < .001). Levels of complement-CRP complexes in patients with a pneumococcal type of infection were similar to those in patients with other types of infections. Complement-CRP complexes were significantly higher in patients with shock (P = .01) and in patients who died (P = .03). These results demonstrate that part of the complement activation in patients with sepsis is independent from a direct interaction with microorganisms but rather results from an endogenous mechanism involving CRP.

C-Reactive Protein↗

Catheter deadspace: a source of error during tonometry.

Tonometry of PCO2 is a promising method for assessing the oxygen supply to demand ratio of the gastrointestinal mucosa in critically ill patients. A balloon-tipped tonometer is introduced into the stomach or sigmoid colon, and saline is instilled into the balloon. After a time to allow partial equilibration with intraluminal PCO2, saline is aspirated and PCO2 is measured. Intermittent instillation and aspiration of saline allows serial PCO2 measurements, provided correction factors are used to calculate the PCO2 value expected at full equilibration from the PCO2 values measured after short dwell times. The technique is not yet widely applied, partly because of methodological controversies. We evaluated the role of the catheter deadspace as a source of error during PCO2 tonometry. The increase in PCO2 in sigmoid-type tonometers with a normal length (normal tonometer (NT)) and in those with a 50% increase in length and thus deadspace (extended tonometer (ET)), in a saline bath at a PCO2 of 4.8 kPa was assessed. Saline dwell times were 10, 20, 30, 45, 60 and 90 min and the time-dependent PCO2 increase was determined at deadspace PCO2 values of approximately 4.0 and 8.0 kPa following contamination of the catheter deadspace after immersion in saline baths at PCO2 values of 4.8 and 9.6 kPa, respectively, before each measurement cycle. In another experiment, the tonometer was rinsed between measurement cycles to remove deadspace saline containing carbon dioxide and to obviate contamination of instilled saline. PCO2 was measured in a blood-gas analyser, taking into account measurement bias in saline. Failure to remove deadspace saline between measurement cycles resulted in an overestimation of 10% and 6% for the NT and 16% and 10% for the ET, at saline dwell times of 10 and 20 min, respectively, at a deadspace PCO2 of approximately 4.0 kPa. At a deadspace PCO2 of approximately 8.0 kPa, PCO2 was overestimated by 17%, 11% and 5% for the NT and 31%, 20% and 11% for the ET, at dwell times of 10, 20 and 30 min, respectively. Rinsing the NT/ET resulted in accurate assessment of PCO2 at all dwell times, but the dwell time-dependent increase in PCO2 was slightly slower in the ET, particularly at 10 min, after a sink effect of the increased deadspace. Hence, a previously unrecognized deadspace effect caused error during PCO2 tonometry, particularly with short dwell times. This potentially large error can be avoided by rinsing the tonometer before each measurement cycle, allowing accurate PCO2 tonometry even at 10-min saline dwell times, provided that correction factors are used that are specific for catheter size. These findings may help to widen the clinical applicability of tonometry.

Carbon Dioxide↗

Characteristics of time-dependent PCO2 tonometry in the normal human stomach.

Factors that affect PCO2 measurement in balloon saline during gastrointestinal tonometry are unclear. They include carbon dioxide diffusion rate, correction factors for calculation of equilibrium PCO2 from measurements at saline dwell times that are shorter than needed for full equilibration, role of blood-gas analyser bias during ex vivo PCO2 measurements in saline, and normal values for intragastric PCO2 (PiCO2) and intramucosal pH (pHi) at equilibrium, and their differences from blood values. In a laboratory study, normal PCO2 changes in a saline-filled tonometer balloon placed in a saline bath at constant PCO2 were described by a non-linear model, with a half-time of mean 4.4 min and 95% equilibration at mean 83 min. In a study in 20 healthy volunteers, PiCO2 build up in a saline-filled tonometer balloon placed in the stomach, measured at dwell times of 10, 20, 30 and 60 min, was slightly (P < 0.05) slower than in vitro, with a half-time of mean 5.8 min and 95% equilibration at mean 110 min. Correction factors to derive equilibrium PiCO2 at short dwell times and independently from blood-gas analyser bias were calculated. The factors differed (P < 0.05) from those currently provided by the manufacturer. Normal threshold values (mean) were: equilibrium PiCO2 < or = 6.6 kPa, pHi > or = 7.33, PiCO2 to blood PCO2 difference < or = 1.1 kPa and pH difference > or = -0.06. PiCO2 did not differ from, and was directly related to, blood PCO2. These values provide a reference base for other studies and show that gastric mucosal PCO2 depends on alveolar ventilation if blood flow is adequate.

Adult↗

The 67gallium-transferrin pulmonary leak index in patients at risk for the acute respiratory distress syndrome.

OBJECTIVE: To determine the occurrence and clinical importance of increased pulmonary microvascular permeability in patients at risk for acute respiratory distress syndrome (ARDS). DESIGN: Prospective, cohort study. SETTING: Medical and surgical intensive care unit (ICU) and department of nuclear medicine of a university hospital. PATIENTS: Thirteen consecutive patients at risk for ARDS with sepsis (n = 4), multiple trauma (n = 3), hemorrhagic pancreatitis (n = 5), and near-drowning (n = 1), admitted into the ICU. All patients were intubated and mechanically ventilated in the course of the study. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The 67gallium-transferrin pulmonary leak index (PLI) (upper limit of normal in patients scheduled for major surgery 14.7 x 10(-3)/min) was measured within 24 hrs of admission. In addition, radiographic, gas exchange, and ventilatory variables allowing calculation of the Lung Injury Score, were obtained on the day of the PLI (day 0) and from days 1 to 7. Patients were followed until discharge or death in the ICU. No patient developed ARDS (Lung Injury Score of >2.5 in the absence of congestive heart failure) and all but four patients survived. The PLI (median [range]) was 18.5 (7.0 to 81.9) x 10(-3)/min and was supranormal in 8 of 13 patients (p < .001 vs. normal). The PLI correlated with the Simplified Acute Physiology Score (SAPS) II (r[s] = .79, p < .01) and was higher in nonsurvivors than in survivors (p < .05), with a tendency for a higher SAPS II in the nonsurvivors. On day 0, the chest radiographic score of alveolar abnormalities was 0 (0 to 4), indicating absence of radiographic abnormalities in most patients. Also, on day 0, the median PaO2/FIO2 ratio was 257 (range 119 to 460). The Lung Injury Score on day 0 was 1.0 (0 to 2.0), which is consistent with mild acute lung injury in all but one patient. In the course of time, the oxygenation ratio was lower and the Lung Injury Score was higher in nonsurvivors than in survivors, particularly for the Lung Injury Score on days 1 and 2. The PLI correlated directly with the Lung Injury Score on days 0 and 1. On day 0, the PLI correlated inversely with the oxygenation ratio. On the last evaluable day of the first ICU week, the PLI correlated directly with the Lung Injury Score and the positive end-expiratory pressure level. The duration of mechanical ventilation tended to be longer in patients with a supranormal PLI. CONCLUSIONS: In this small population, 61% of patients at risk for ARDS and with only mild respiratory changes exhibited increased microvascular permeability in the lungs at ICU admission. Increased permeability may be an early marker of acute lung injury and its clinical features, and may be associated with a relatively complicated respiratory course during the first week after admission, even in the absence of progression to ARDS. Finally, increased pulmonary microvascular permeability may be associated with severe underlying disease and ultimate mortality in the ICU.

Adult↗