Search PubMed⌕ Search

Biomedical subjects

H Blomqvist

Publications and source records attributed to H Blomqvist.

At least 19 recordsLinked to original sources
PubMed1998

Effects of exaggerated lithotomy position on ventilation and hemodynamics during radical perineal prostatectomy.

Ventilation and haemodynamics were studied in nine anaesthetized male patients undergoing perineal prostatectomy in the exaggerated lithotomy position (flexed, head-down position). In the flexed head-down position, as compared to the supine position, there was a significant decrease in arterial oxygen tension (13.1 +/- 2.1 to 11.2 +/- 1.1 kPa, p < 0.001), a significant increase in carbon dioxide tension (4.6 +/- 5.7 to 5.7 +/- 0.2 kPa, p < 0.001) and shunt fraction (7.8 +/- 2.3 to 14.0 +/- 3.0%, p < 0.01). There were also increases in pulmonary wedge pressures (11.3 +/- 2.9 to 17.9 +/- 2.9 mmHg, p < 0.01), mean pulmonary artery pressures (17.6 +/- 3.8 to 25.2 +/- 3.5 mmHg, p < 0.001) and central venous pressures (11.9 +/- 2.1 to 14.7 +/- 2.8, p < 0.05). Mean arterial pressure fell from 92 +/- 14 to 75 +/- 10 mmHg (p < 0.05). Heart rate and cardiac output were unchanged. All these changes had already been seen but to a lesser extent when the patients were positioned in the flexed supine position. When the patients were returned to the supine position following surgery, arterial oxygen tension was returned to baseline values. Mean pulmonary artery, pulmonary capillary wedge and central venous pressures also fell significantly. It is concluded that the extreme exaggerated lithotomy used during surgery results in impaired oxygenation and increased cardiac filling pressures but to acceptable levels in healthy anaesthetized patients. All values returned to normal when patient position was normalized after surgery.

Aged↗
PubMed1998

Forced air warming and intraoperative hypothermia.

OBJECTIVES: To compare a forced air warming system with passive measures to avoid perioperative hypothermia. DESIGN: Prospective open study. SETTING: University hospital, Sweden. SUBJECTS: 28 Patients scheduled for extensive thoracoabdominal operations under standard combined general and regional anaesthesia. MAIN OUTCOME MEASURES: Temperature measured before, repeatedly under anaesthesia and during the operation for up to three hours, and then up to eight hours postoperatively. RESULTS: Three patients were excluded. In the 12 patients who had forced air warming, temperature was preserved, and ranged from a mean (SD) of 36.8 (0.7) degrees C, (95% confidence interval (CI) 36.4 to 37.2) at the start to 36.9 (0.8) degrees C, (95% CI 36.5 to 37.3) after 3 hours. In patients who had conservative passive heat preservation techniques the mean temperature fell significantly perioperatively, from 36.8 (0.6) degrees C (95% CI 36.5 to 37.1) at the start to 35.1 (0.5) degrees C, (95% CI 34.9 to 35.3), after three hours of anaesthesia and surgery. This was a significant fall compared with the temperature in the study group (p < 0.001). CONCLUSION: Forced air warming intraoperatively can preserve normothermia during extensive thoracoabdominal operations.

Aged↗
PubMed1996

Response to nitric oxide inhalation in early acute lung injury.

OBJECTIVE: To evaluate the dose response of inhaled nitric oxide (NO) on gas exchange and central haemodynamics in patients with early acute lung injury (ALI). DESIGN: Prospective, multicentre clinical study. SETTING: General ICUs in university and regional hospitals. PATIENTS: 18 Patients with early ALI according to specified criteria. INTERVENTIONS: During controlled ventilation an inhalation system was used to deliver NO (1000 ppm in N2) and O2/air to the low pressure fresh gas inlet of a Siemens 900C ventilator. Haemodynamics and pulmonary gas exchange variables were measured at baseline and at stepwise increased inspiratory NO concentrations of 0.1, 0.3, 1, 3, 10, 30 and 100 ppm, each dose being maintained for 15 min. Dose testing was repeated the next day, and the response to prolonged (2 h) NO inhalation at 1 and 10 ppm was also tested. MEASUREMENTS AND RESULTS: Inhalation of NO produced a significant increase in PaO2 (P < 0.0025). The degree of response, as well as the optimal NO dose varied in individual patients and between different days. Venous admixture (QVA/QT) was reduced (P < 0.02) from 38% (31-46%) to 33% (26-41%). In our patients with early acute lung injury and only a moderate elevation in pulmonary arterial pressure NO inhalation did not reduce mean pulmonary artery pressure significantly, being 27.0 (21-30) mmHg at baseline and 26.0 (21-30) mm Hg at 100 ppm. CONCLUSIONS: This study shows that improvements in arterial oxygenation in response to inhaled NO may show great inter- as well as intraindividual variability, and that improvements in arterial oxygenation occur without any measurable lowering of the pulmonary artery pressure.

Administration, Inhalation↗
PubMed1996

Hypertonic-hyperoncotic solution increases canine lymph flows.

BACKGROUND: Hypertonic-hyperoncotic solutions (HHS) have attracted a lot of interest in the treatment of various forms of hypovolaemic conditions during the last decade. It has been speculated that HHS might even be of therapeutic value in normo- and hypervolaemic conditions by mobilising extravascular fluid. METHODS: We studied thoracic and abdominal lymphatic flows and circulatory response following the administration of a single bolus injection of hypertonic-hyperoncotic solution, 10% dextran 60 in 7.2% saline (HHS), in a nonhypovolaemic canine model. A modified surgical procedure for collecting thoracic lymph is also presented. RESULTS: Both thoracic and abdominal lymph flow increased significantly by approximately 50% after administration of HHS. Cardiac output and calculated pulmonary capillary hydrostatic pressure increased. CONCLUSION: Hypertonic-hyperoncotic solution given intravenously as a single injection increased both thoracic and abdominal lymph flows in the initially normovolaemic animal.

Animals↗
PubMed1995

Evaluation of a knowledge-based decision-support system for ventilator therapy management.

Evaluation of knowledge-based systems differs from that of conventional systems in terms of verification and validation techniques. Furthermore, evaluating medical decision-support systems is difficult because the field is thus far comparatively unexplored. This paper presents an evaluation of a medical knowledge-based system called VentEx that supports decision-making in the management of ventilator therapy. Real patient data from 1300 hours of patient care involving 12 patients with 6 diagnoses are used to validate the knowledge base. The results range from 4.5% to 15.6% disagreement between the setting recommendations produced by VentEx and a gold standard, and 22.2% disagreement for recommendations for weaning. A comparison between the standard and two physicians showed that VentEx produced advice of the same quality as the physicians.

Databases, Factual↗
PubMed1995

Clinical application of differential ventilation with selective positive end-expiratory pressure in adult respiratory distress syndrome.

Differential ventilation in the lateral position with positive end-expiratory pressure (PEEP) selectively applied to the dependent lung (DVSP) has been shown to reduce venous admixture and improve oxygenation without compromising cardiac output in short term studies of patients with acute respiratory failure. We have applied this ventilation technique as a long-term treatment in severe adult respiratory distress syndrome (ARDS) in an open clinical trial. Eleven patients with ARDS of varying aetiology were treated with DVSP for a total of 34 days. Median duration of conventional ventilatory therapy before start of DVSP was 5 days (1 to 18 days), inspiratory oxygen fraction (FIO2) was 0.61 +/- 0.16 (mean +/- s.d.), resulting in a mean arterial oxygen tension (PaO2) of 7.1 +/- 2.1 kPa (PaO2/FIO2 = 11 +/- 4 kPa). A gradual improvement in gas exchange was seen during the first 24 h of DVSP such that PaO2 increased to 8.4 +/- 1.4 with a decreased FIO2 (0.52 +/- 0.14) resulting in an increased PaO2/FIO2 (16 +/- 5 kPa). Five out of the eleven patients survived. No major complication was noted using DVSP as a method. We found a steady improvement in gas exchange over the first 24 hours in most patients. However, mortality rate was no lower than expected. Drawbacks with DVSP were increased demand on staff and difficulties with adequate endo-bronchial suctioning.

Adolescent↗
PubMed1993

Inhaled nitric oxide selectively reverses human hypoxic pulmonary vasoconstriction without causing systemic vasodilation.

BACKGROUND: Nitric oxide (NO), an endothelium-derived relaxing factor, acts as a local vasodilator. The authors examined the effects of NO on pulmonary and systemic circulation in human volunteers. METHODS: Nine healthy adults were studied awake while breathing 1) air, 2) 12% O2 in N2, 3) followed by the same mixture of O2 and N2 containing 40 ppm of NO. Pulmonary artery and radial artery pressures were monitored. RESULTS: The PaO2 decreased from 106 +/- 4 (mean +/- standard error of the mean) while breathing air (21% O2) to 47 +/- 2 mmHg after 6 min of breathing 12% O2. Concomitantly, the pulmonary artery mean pressure (PAP) increased from 14.7 +/- 0.8 mmHg to 19.8 +/- 0.9 mmHg, and the cardiac output (CO) increased from 6.1 +/- 0.4 to 7.7 +/- 0.6 L/min. After adding 40 ppm NO to the inspired gas while maintaining the FIO2 at 0.12, the PAP decreased (P < 0.01, by analysis of variance) to the level when breathing air while the PaO2 and PaCO2 were unchanged. The dilation (or recruitment) of pulmonary vessels produced by inhaling NO during hypoxia was not accompanied by any alteration in the systemic vascular resistance or mean arterial pressure (MAP). The authors also examined the effects of inhaling NO while breathing air. Breathing 40 ppm NO in 21% O2 for 6 min produced no significant changes of PAP, CO, PaO2, MAP, or central venous pressure. Plasma endothelinlike immunoreactivity concentrations did not change either during hypoxia or hypoxia with NO inhalation. CONCLUSIONS: Inhalation of 40 ppm NO selectively induced pulmonary vasodilation and reversed hypoxic pulmonary vasoconstriction in healthy humans without causing systemic vasodilation.

Administration, Inhalation↗
PubMed1993

Enhanced pneumonia resolution by inhalation of nitric oxide?

We present a patient with severe bacteraemic pneumococcal pneumonia associated with severe hypoxaemia, where nitric oxide (NO) 15-40 ppm was added to the inspired gas. Nitric oxide therapy improved gas exchange, reduced pulmonary vasoconstriction and peak airway pressure. The patient survived. We observed an unexpected rapid and complete disappearance of bilateral pulmonary infiltrates during the first 120 h of the 7-day NO inhalation period.

Administration, Inhalation↗
PubMed1993

The leukotriene-receptor antagonist MK-0679 blocks airway obstruction induced by inhaled lysine-aspirin in aspirin-sensitive asthmatics.

Drugs which block the action or formation of the cysteinyl leukotrienes (LTC4, LTD4 and LTE4) inhibit asthmatic responses evoked by allergen, exercise and cold dry air. The purpose of this study was to determine whether the specific leukotriene-receptor antagonist MK-0679 could block the airway obstruction induced by aspirin (acetylsalicylic acid (ASA)) in aspirin-intolerant asthmatics. Eight asthmatics (mean age 45 yrs), with an average history of asthma and ASA-sensitivity of about 10 yrs duration, were subjected to bronchial provocation with lysine-ASA. Baseline ASA-sensitivity was first determined in an open prestudy session by inhalation of cumulative doses of lysine-ASA to establish the dose of ASA decreasing forced expiratory volume in one second (FEV1) by 20% (PD20). Rechallenge with lysine-ASA was performed on two different occasions, 1 h after oral administration of placebo, or 750 mg of MK-0679, under double-blind conditions, in a randomized, cross-over design. Leukotriene formation was estimated by the measurement of urinary LTE4. The lysine-ASA challenge was highly reproducible (geometric mean for group PD20 being identical for the open prestudy and the placebo session), and was associated with a post-challenge increase in urinary LTE4. In contrast, after MK-0679, there was a rightward shift in the dose response relationship for all eight subjects (median shift being 4.4 fold), with three of the subjects failing to produce a 20% decrease in FEV1 despite inhalation of the highest dose of lysine-ASA feasible to deliver.(ABSTRACT TRUNCATED AT 250 WORDS)

Aspirin↗
PubMed1992

Influence of positive end-expiratory pressure on extravascular lung water during the formation of experimental hydrostatic pulmonary oedema.

The influence of positive end-expiratory pressure (PEEP) on extravascular lung water measured with the double-indicator dilution technique (EVLWi) has been studied during formation of hydrostatic pulmonary oedema in a canine model. The oedema was created by elevating the mean pulmonary artery pressure (PAP) to 30 mmHg (4.0 kPa) by inflation of a left atrial balloon, and a simultaneous intravenous saline infusion of 15 ml.kg-1.h-1. All dogs were ventilated with zero end-expiratory pressure (ZEEP) until the initial EVLWi had increased by 50%. In one group (n = 5) a PEEP of 10 cmH2O (1.0 kPa) was applied and the dogs were studied for a further 4 h and in the other group (n = 5) ZEEP was maintained throughout the study. During the first 2 h after ZEEP/PEEP application EVLWi increased from 13.7 +/- 2.1 to 20.2 +/- 1.2 ml.kg-1 with ZEEP ventilation and from 13.6 +/- 1.2 to 18.6 +/- 1.9 ml.kg-1 with PEEP ventilation. EVLWi remained unchanged during the last 2 h in both groups. The gas exchange improved with PEEP, arterial oxygen tension increased from 30.4 +/- 8.9 kPa to 38.6 +/- 2.5 kPa (P less than 0.01), and the shunt fraction decreased from 6.0 +/- 3.8% to 1.2 +/- 0.8% (P less than 0.001). There were significant differences (P less than 0.01) in both PaO2 and shunt fraction between the ZEEP and PEEP groups throughout the study. In conclusion, positive end-expiratory pressure improves gas exchange but does not protect against increasing extravascular lung water during the creation of hydrostatic pulmonary oedema.

Animals↗
PubMed1992

Effect of antithrombin concentrate on haemostatic variables in critically ill patients.

In a controlled pilot study of 32 critically ill patients, we have attempted prospectively to identify laboratory variables which can be used to select and monitor patients on antithrombin (AT) therapy. Patients with plasma AT levels less than 70% of normal were randomized to receive (AT group) or not to receive AT concentrate (non-AT group). The groups did not differ in median age, sex, median APACHE II and TISS scores, number of days spent in the Intensive Care Unit or mortality rate. At the time of inclusion all patients had activated coagulation and fibrinolysis demonstrated as high levels of soluble fibrin, thrombin-antithrombin complexes and fibrin-D-dimers (twice, four and ten times the upper reference range, respectively). In the AT group these levels decreased faster and the prothrombin complex concentration increased more rapidly to normal (i.e. the prothrombin time decreased). The level of C-reactive protein which was high in both groups on inclusion (139 and 98 mg/l, respectively) decreased by 40% in the AT group but did not change in the control group. Our study indicates that laboratory variables normalize faster in seriously ill patients who have activated coagulation and fibrinolysis when they receive AT concentrate and that the variables mentioned above seem to be useful for monitoring the treatment.

Aged↗
PubMed1992

Influence of hypertonic-hyperoncotic solution and furosemide on canine hydrostatic pulmonary oedema resorption.

1. This study aimed at enhancing the clearance of experimental hydrostatic pulmonary oedema in dogs using hypertonic-hyperoncotic solution (HHS) and furosemide. 2. Anaesthetized dogs (n = 20) were mechanically ventilated with a positive end-expiratory pressure of 10 cmH2O (1.0 kPa). 3. Hydrostatic pulmonary oedema was induced by inflating a balloon inserted into the left atrium and simultaneously infusing isotonic saline rapidly. Oedema formation was terminated by deflating the balloon and reducing the infusion rate. 4. Four groups were studied: A, control; B, furosemide; C, HHS and D, HHS+furosemide. HHS, 6 ml kg-1, was given as a bolus injection and furosemide, 1 mg kg-1, intravenously as a bolus followed by an infusion of 0.5 mg kg-1 h-1. All dogs were studied for 4 h. 5. Serum osmolarity, plasma colloid oncotic pressure and diuresis in groups C and D (HHS groups) substantially increased; haemoglobin concentration decreased and pulmonary arterial wedge pressure remained constant. 6. Despite the combination of these factors favouring fluid flux from the extravascular to the intravascular compartment, extravascular lung water measured with the double indicator dilution technique decreased no faster in the HHS groups than in the two other groups (from over 26 to approximately 19 ml kg-1 in groups A, C and D and to 14.7 in group B (only furosemide)). 7. This was confirmed by postmortem gravimetric measurements of extravascular lung water; A, 11.0 +/- 5.7; B, 9.7 +/- 3.3; C, 10.5 +/- 3.1 and D, 10.6 +/- 1.8 g kg-1. 8. We speculate that mechanisms other than effective Starling gradients and enhanced diuresis might define a maximal rate of pulmonary oedema clearance.

Animals↗
PubMed1991

Thoracic lymph drainage in the dog: evaluation of a new model.

A new model for selective sampling of thoracic lymph flow (TLF) and abdominal lymph flow (TDA) in the dog was assessed to ascertain whether there were extrathoracic contributions of lymph to the TLF. Inflating a right atrial balloon in 4 dogs and a left atrial balloon in 2 dogs indicated good separation between TLF and TDA. Data on total lymph protein and albumin clearance before and after oleic acid induced pulmonary oedema in an additional 5 dogs indicated that TLF and TDA drained two differing regions. Our data demonstrate that this lymph preparation provides a sample of thoracic lymph flow with no major extrathoracic lymph contamination. We also propose an alternative method to test for extrathoracic contributions to thoracic lymph, by the application of positive end-expiratory pressure, thereby replacing right atrial balloon inflation.

Albumins↗
PubMed1991

Effects of pleural fluid and positive end-expiratory pressure on the measurement of extravascular lung water by the double-indicator dilution technique.

The reliability of the double-indicator dilution technique (dye/cold) for measuring extravascular lung water (EVLW) has been studied in lung-healthy dogs after pleural fluid injection of saline (up to 20 ml/kg) during mechanical ventilation at zero and 10 cmH2O (1.0 kPa) end-expiratory pressure (ZEEP and PEEP, respectively). Pleural fluid injection had no effect on EVLW at either ZEEP or PEEP. PEEP induced changes in cardiac output, and reduced both the intravascular (dye) and the thermal indicator volumes, but with no effect on the calculated EVLW. It is concluded that pleural fluid up to 20 ml/kg and ventilation with PEEP of 10 cmH2O (1.0 kPa) do not affect the reliability of the double-indicator dilution technique for measuring extravascular lung water in the dog.

Animals↗
PubMed1991

Furosemide, when used in combination with positive end-expiratory pressure, facilitates the resorption of extravascular lung water in experimental hydrostatic pulmonary oedema.

The study aimed to establish whether furosemide given intravenously improved resorption of hydrostatic pulmonary oedema in 14 dogs mechanically ventilated with positive end-expiratory pressure (PEEP). Hydrostatic pulmonary oedema was created by simultaneous inflation of a left atrial balloon and rapid intravenous infusion of isotonic saline. The hydrostatic process was terminated by deflating the balloon and reducing the infusion rate. A PEEP of 10 cmH2O (1.0 kPa) was applied in all animals; in seven, furosemide was administered (diuretic group), 1 mg/kg intravenously as a bolus followed by an infusion of 0.5 mg/kg per hour, while the remaining seven dogs served as a control group. All dogs were studied for a period of 4 h. The extravascular lung water measured with the double indicator dilution technique was 28.3 +/- 3.8 (diuretic group) and 28.2 +/- 6.8 ml/kg (control group) during maximum oedema. It was reduced to 16.4 +/- 2.2 (diuretic group) vs 19.8 +/- 3.7 ml/kg (control group) after 4 h of resorption, P less than 0.05. Postmortem gravimetric values of extravascular lung water were 9.1 +/- 3.4 (diuretic group) vs 12.6 +/- 5.0 g/kg (control group). In the diuretic group the urinary output increased threefold, and haemoglobin and serum protein concentrations were higher than in the control group. There was a significantly greater decrease in cardiac output and central blood volume in the diuretic group. In conclusion, furosemide given intravenously improved lung fluid resorption in hydrostatic pulmonary oedema, probably by increasing the plasma colloid osmotic pressure.

Animals↗
PubMed1991

Does PEEP facilitate the resolution of extravascular lung water after experimental hydrostatic pulmonary oedema?

The effect of mechanical ventilation with positive end-expiratory pressure on the resolution of hydrostatic pulmonary oedema created by temporary left atrial balloon inflation was studied in mechanically ventilated dogs. Immediately after the hydrostatic process was terminated, by deflating the left atrial balloon, the animals were ventilated for 4 h with zero end-expiratory pressure (ZEEP, n = 6) or with a positive end-expiratory pressure (PEEP, n = 6) of 1.0 kPa (10 cmH2O). Gas exchange and extravascular lung water content (EVLW) with the double indicator dilution technique (dye/cold) were studied and gravimetric determination of lung water was made postmortem. EVLW decreased from 31.6 +/- 7.3 mean +/- SD ml.kg.1 during maximal oedema to 14.5 +/- 2.1 ml.kg.1 (p less than 0.001) 4 h after deflation of the left atrial balloon in dogs ventilated with ZEEP. The corresponding values in dogs ventilated with PEEP were a reduction in EVLW from 28.0 +/- 4.1 to 20.7 +/- 4.0 ml.kg.1 (p less than 0.01) (mean decrease 7.3 +/- 4.0 ml.kg.1). EVLW was significantly higher after 4 h on PEEP than after ZEEP (p less than 0.01). Gravimetric values at the end of the experiment were 12.4 +/- 2.8 ml.kg.1 (ZEEP) and 14.7 +/- 4.5 ml.kg.1 (PEEP) (NS). Oxygenation improved in both groups during the resolution of oedema with a more evident and early effect in the PEEP group. It is concluded that mechanical ventilation with PEEP of 1.0 kPa (10 cmH2O) in the resolution phase after experimental hydrostatic oedema improves oxygenation but retards the resolution of oedema.

Animals↗
PubMed1990

Lung fluid balance evaluated by the rate of change of extravascular lung water content.

Lung fluid balance was studied in 27 mongrel dogs by measuring changes in extravascular lung water content (EVLW). The expression delta EVLWi, which is the difference in EVLWi per kilo bodyweight per hour between two measurement occasions, was used as an estimate of the rate of change of EVLW. EVLW was measured by a double-indicator dilution technique (EVLWi) using iced glucose and indocyanine green. In addition, EVLW was determined at the end of each experiment with gravimetric technique (EVLWg), which enabled the calculation of a regression equation between EVLWi and EVLWg. Delta EVLWi was calculated repeatedly during an 8-h period of mechanical ventilation (MV) with no application of a positive end-expiratory pressure (n = 5), during an 8-h period with a positive end-expiratory pressure (PEEP) of 10 cmH2O (1.0 kPa) (n = 5), during the development of oleic acid (OA)-induced pulmonary oedema (n = 7), and hydrostatic pulmonary oedema (left atrial balloon inflation) (n = 9). An increase of EVLW was seen during PEEP 8 h (mean 35%) and after induction of OA and hydrostatic oedema (mean 300%), but no change was found during MV without PEEP. The regression equation was EVLWi = 5.5 + 0.97 x EVLWg (P = 0.001, r = 0.90). OA-induced oedema caused a mean maximum delta EVLWi of 5.1 ml/kg/h, indicating capillary leakage which, however, was self-limiting within 2 h after OA injection. In hydrostatic oedema there was a maximum delta EVLWi of 16.0 ml/kg/h. Delta EVLWi was negative after deflation of the left atrial balloon, indicating reabsorption of oedema.

Animals↗