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Biomedical subjects

S Steen

Publications and source records attributed to S Steen.

At least 55 records · Page 3Linked to original sources

Eliminating the strong pulmonary vasoconstriction caused by Euro-Collins solution.

Single-flush perfusion with Euro-Collins solution (ECS), after pretreatment with prostaglandin E1 or prostacyclin, is at most centers the standard procedure for preservation of lungs for transplantation. In a previous study, we showed that the high potassium content of ECS causes strong pulmonary vasoconstriction at temperatures higher than 20 degrees C. In the present study, five drugs used as pretreatment and added to the perfusate were compared for their ability to counteract ECS-induced constriction of porcine pulmonary arteries: papaverine reduced the vasoconstrictive effect by 92% +/- 4%; nifedipine, by 62% +/- 6%; the thromboxane A2 receptor antagonist daltroban, by 15% +/- 4%; and prostaglandin E1, by 12% +/- 4%. On the other hand, prostacyclin not only failed to reduce ECS-induced vasoconstriction but at the highest concentration tested, enhanced it by 37% +/- 7%. The combination of papaverine (10(-4) mol/L) and nifedipine (10(-6.5) mol/L) was the only pretreatment to abolish ECS-induced vasoconstriction; moreover, it has no adverse effect on endothelial function. Neither prostaglandin E1 nor prostacyclin effectively counteracts ECS-induced vasoconstriction, though they may have other beneficial effects.

Alprostadil↗

Safe lung preservation for twenty-four hours with Perfadex.

The function of six porcine left lung allografts was studied after pulmonary (140 mL/kg) and bronchial (50 mL/kg) artery perfusion with Perfadex (Kabi Pharmacia, Uppsala, Sweden) at room temperature, followed by 24-hour storage of the lungs in an atelectatic state in 6 degrees to 8 degrees C Perfadex, which is a low-potassium-dextran solution. Left lung transplantation was done followed by right pneumonectomy, thereby making all the animals 100% dependent for their survival on the transplanted lungs. The pigs (mean weight = 56 kg, range = 51 to 58 kg, n = 18; 6 donors, 6 recipients, and 6 sham operated) were ventilated with a volume-controlled ventilator (20 breaths/min, 500 mL tidal volume, 8 cm H2O positive end-expiratory pressure, inspired oxygen fraction = 0.5). All the transplanted animals were in good condition throughout the 24-hour observation period with arterial oxygen tensions around 25 kPa (188 mm Hg) and arterial carbon dioxide tensions around 5 kPa (38 mm Hg). The mean pulmonary arterial pressure was around 30 mm Hg, and the pulmonary vascular resistance around 500 dyn.s.cm-5; neither showed any tendency to change with time. After 24 hours the inspired oxygen fraction was increased to 1.0 and the arterial oxygen tension increased to 43.3 +/- 5 kPa (325 +/- 38 mm Hg) (mean +/- standard error of the mean; n = 6). A sham operation (bilateral thoracotomy, right pneumonectomy) was done in 6 pigs, which were followed up for 24 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Efficacy of topical cooling in lung preservation: is a reappraisal due?

The aim of the present study was to test the efficacy of topical cooling as the only viable lung preservation method using the most challenging evaluation method, namely single-lung transplantation followed by immediate contralateral pneumonectomy. Ten domestic pigs (5 donors and 5 recipients) with a mean body weight of 57 kg (range, 53 to 59 kg) were used. After we administered systemic heparin (4 mg/kg), the lungs were harvested and placed in an atelectatic state under cold (8 degrees to 9 degrees C) low-potassium-dextran solution for 12 hours. Left lung transplantation was then done in the recipient pig followed by right pneumonectomy, thus making the recipient 100% dependent on the transplanted donor lung. No operative mortality or morbidity occurred. All animals were in excellent condition throughout the 24-hour observation period. They had normal blood gases which did not differ significantly from the preoperative blood gases obtained from the 5 recipients before transplantation (ie, when they had their own two lungs). A moderate increase (p < 0.05) in pulmonary vascular resistance was seen as compared with sham-operated animals. To conclude, topical cooling to 8 degrees C provides excellent lung preservation for 12 hours in pigs. If similar results can be obtained with other species, the currently accepted 6-hour limit for safe clinical lung preservation may be extended to 12 hours. It seems also warranted to critically reconsider which factors, apart from cooling alone, actually contribute favorably to 12-hour lung preservation.

Animals↗

Pulmonary vascular resistance related to endothelial function after lung transplantation.

In 8 donor pigs, flush perfusion was performed with a low-potassium-dextran solution. Ring segments were taken from a small intralobar pulmonary artery in the right lung immediately after perfusion and after 24 hours of cold storage for studies in organ baths. Stable vasoconstriction was induced with the thromboxane mimic U-46619, and acetylcholine was used to induce endothelium-dependent relaxation. The maximum relaxation was significantly reduced after flush perfusion compared with fresh nonperfused controls, and a significant additional reduction was seen after the 24-hour storage period. The left donor lung was transplanted into a recipient after 24 hours of cold storage. Contralateral pneumonectomy was then performed, making the recipient entirely dependent on the transplanted lung for survival. All 8 pigs were in good condition throughout the 24-hour observation period, with arterial oxygen tension of around 165 mm Hg (range, 80 to 275 mm Hg; inspired oxygen fraction, 0.5) and pulmonary vascular resistance of around 450 dyne.s.cm-5 (range, 260 to 730 dyne.s.cm-5). The maximum endothelium-dependent relaxation for each donor was checked for correlation to pulmonary vascular resistance and to systolic, mean, and diastolic pulmonary artery pressures as recorded at 4-hour intervals. Regression analyses showed arterial oxygen tension to be unrelated to pulmonary vascular resistance and endothelial dysfunction to be unrelated to pulmonary artery pressure but to correlate to pulmonary vascular resistance, this correlation being significant after reperfusion for 16 hours (p < 0.05) and highly significant after 24 hours (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Nitric oxide gives maximal response after coronary artery bypass surgery.

The dose-response to inhalation of nitric oxide (NO) after coronary artery bypass surgery was studied in seven patients with normal preoperative lung function and chest radiograms. During postoperative controlled ventilation with PEEP 5 and 10 cmH2O, the patients inhaled NO in concentrations of 2 to 25 ppm, in random order, for 6 to 10 minutes. Hemodynamic and oximetric data were analyzed before, 5 minutes after start of the NO inhalation, and 5 minutes after the cessation. The response was the same at all concentrations; mean pulmonary artery pressure decreased by 11 +/- 1% (P < 0.05) and pulmonary vascular resistance decreased by 22 +/- 2% (P < 0.05). Systemic hemodynamics did not change, but oximetric parameters tended to improve. Changes in PEEP did not affect the response. It is concluded that, in patients who have undergone coronary artery bypass grafting, inhalation of 2 to 25 ppm NO causes a dose-independent decrease in pulmonary artery pressure and pulmonary vascular resistance. In order to investigate the dose-response curve, concentrations lower than 2 ppm of NO must be used.

Aged↗

Filling of a model left ventricle studied by colour M mode Doppler.

OBJECTIVE: It has been proposed that the early diastolic flow pattern inside the left ventricle reflects ventricular diastolic function. The flow pattern often divides into two phases towards the apex. The aim of this study was to examine the hydrodynamic nature of this phenomenon. METHODS: A rubber balloon representing the ventricle was connected to a reservoir representing the atrium, both filled with anticoagulated blood. Rigid "mitral" orifices 20 mm long and 15-40 mm in diameter were used. Surrounding the ventricle was a water filled chamber to which suction could be applied. The colour M mode Doppler sample beam coincided with the ventricular long axis. Colour M mode measures velocity at multiple sites along the beam simultaneously. The timing and magnitude of the velocities were analysed digitally. The filling was also qualitatively studied by ultrasonic two dimensional sector scanning. RESULTS: At the start of the filling, blood moved simultaneously at all levels, behaving as a fluid column. This was denoted "phase I". A flow wave then propagated from the mitral orifice towards the apex, called "phase II". This was found to represent a ring vortex, with blood velocities twice its propagation velocity [ratio 2.1(SEM 0.016)]. The ratio between the velocity time integrals of phase II and phase I decreased progressively from 51(15) to 0.41(0.14) when mitral orifice diameter was increased in 5 mm steps from 15 mm to 40 mm (p < 0.001). The propagation velocity correlated strongly with peak transmitral blood velocity, r = 0.95, p < 0.001. The flow patterns resembled patterns recorded in patients. CONCLUSIONS: The two phases of the filling pattern represented the motion of a blood column and the propagation of a ring vortex, respectively. Mitral orifice size determined which phase dominated the flow pattern.

Animals↗

Effects of hypothermia with and without buffering in hypercapnia and hypercapnic hypoxemia.

Anesthetized, paralyzed and mechanically ventilated pigs were hypoventilated to extreme hypercapnia (PaCO2 approximately 20 kPa) at FiO2 0.5, and allotted to receive hypothermia (approximately 31.5 degrees C) and buffer infusion, (HB-group, n = 6) or to a hypothermic control group (H-group, n = 6). The HB-group had higher arterial pH (7.34 vs 7.09, P < 0.01) and plasma bicarbonate (58.8 vs 35.4 mmol.l-1, P < 0.01) than the controls, but lower mean pulmonary arterial pressure (MPAP), (16 vs 23 mmHg (2.1 vs 3.1 kPa), P < 0.01) and pulmonary vascular resistance (PVR), (512 vs 699 dyn.s.cm-5 (5120 vs 6990 microN.s.cm-5), P < 0.05). Mixed venous PO2 (PVO2) was lower in the HB-group (5.1 vs 6.8 kPa, P < 0.01), as well as serum potassium (2.8 vs 3.7 mmol.l-1, P < 0.01) and ionized calcium (1.01 vs 1.29 mmol.l-1, P < 0.01). Subsequently, the inspired oxygen fraction (FiO2) was decreased stepwise (0.3, 0.25, 0.21, 0.15, 0.10) at 30 min intervals. At FiO2 0.3, the HB-group had lower PVO2 (6.6 vs 7.8 kPa, P < 0.01), O2 half saturation tension (3.6 vs 4.2 kPa, P < 0.01), MPAP (17 vs 25 mmHg (2.3 vs 3.3 kPa, P < 0.01) and PVR (598 vs 793 dyn.s.cm-5 (5980 vs 7930 microN.s.cm-5, P < 0.05) compared with the controls, but higher arterial O2 saturation (95.3 vs. 88.6%, P < 0.01) and O2 content (17.7 vs 15.7 ml.100 ml-1, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Lung mechanics, gas exchange and central circulation during treatment of intra-abdominal hemorrhage with pneumatic anti-shock garment and intra-aortic balloon occlusion. An experimental study in pigs.

Standardized intra-abdominal hemorrhage was induced in 7 anesthetized pigs. The resulting hypovolemic shock was treated with pneumatic anti-shock garment (PASG) followed by intra-aortic balloon occlusion. The effects of this treatment on circulation, lung mechanics and gas exchange were studied. Hemorrhage was induced by pulling out sutures introduced in the inferior caval vein. We found that the use of PASG partially restored mean arterial blood pressure from 44 +/- 6 to 66 +/- 6 mm Hg. When intraaortic balloon occlusion was added, the arterial pressure returned to basal levels. Cardiac output fell severely due to the hemorrhage from 3.7 +/- 0.2 to 1.3 +/- 0.2 liters/min and could not be restored during the treatment. A severe fall in total lung compliance was recorded after inflation of the PASG from 18.6 +/- 0.9 to 10 +/- 0.7 ml/cm H2O, this was accompanied by a fall in alveolar ventilation. These findings emphasize the severe restriction in lung function that occurred during treatment with PASG. Both parameters returned to near normal values when the PASG was deflated and the intra-aortic balloon was inflated. Pulmonary vascular resistance increased by more than 400% and remained high during the study period. There was no change in arterial PO2, however the fall in mixed venous PO2 caused by hemorrhage was reversed at the end of the treatment. Indirect monitoring of cerebral function by continuous EEG showed a decreased voltage during the hemorrhage, this was reversed by the combined treatment. We conclude that the outlined treatment makes it possible to restore central hemodynamics and preserve cerebral function at least for a short period of time until definite surgical treatment can be performed. However, severe restriction on lung mechanics, especially when PASG was inflated, makes it probable that ventilatory support can be necessary in such cases.

Abdomen↗

Endothelium-dependent relaxation in pulmonary arteries after lung preservation and transplantation.

Pulmonary hypertension is frequently seen after lung transplantation. To study how the release of the endothelium-dependent relaxing factor is affected by lung preservation and transplantation, porcine pulmonary arteries were investigated in organ baths. The arteries (1 mm in diameter) were taken from fresh nonperfused lungs (group I), lungs immediately after flush-perfusion with a low-potassium-dextran solution (group II), non-perfused lungs stored for 12 hours in low-potassium-dextran solution (group III), flush-perfused lungs stored for 12 hours in low-potassium-dextran solution (group IV), and group IV lungs after left lung transplantation and right pneumonectomy followed by 24 hours of reperfusion (group V). Stable contractions were induced with the thromboxane A2 analogue U-46619. Acetylcholine was used to stimulate the release of endothelium-dependent relaxing factor. In vessel segments where the endothelium had been removed, acetylcholine elicited no response. In segments with intact endothelium, acetylcholine induced concentration-dependent relaxation; the maximum relaxation obtained was 91% +/- 3% (I), 86% +/- 3% (II), 85% +/- 3% (III), 69% +/- 5% (IV), and 69% +/- 9% (V). Relaxation was significantly reduced in groups IV (p < 0.01) and V (p < 0.05) as compared with group I. Stable moderate pulmonary hypertension was present in all the transplanted lungs throughout the 24-hour observation period. It is concluded that the endothelium-mediated relaxation is significantly reduced after flush perfusion combined with 12 hours of storage in low-potassium-dextran solution. Lung transplantation, followed by 24 hours of reperfusion did not further impair the endothelium-dependent relaxation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Safe pulmonary preservation for 12 hours with low-potassium-dextran solution.

The function of porcine left lung allografts was studied after perfusion with (150 mL/kg) and storage for 12 hours in a 4 degrees to 6 degrees C low-potassium-dextran solution (Perfadex; Kabi Pharmacia AB, Uppsala, Sweden). After a left lung transplantation, an artificial lung in the form of venoarterial extracorporeal membrane oxygenation was established. The artificial lung has a "biological" heparin-coated surface (Carmeda AB, Stockholm, Sweden), and there is no need for systemic anticoagulation. Immediately thereafter, pneumonectomy of the normal right lung was done. All the animals were weaned from the artificial lung within 1 hour after the pneumonectomy. Six animals were followed up for 24 hours. They were in good condition throughout the 24-hour observation period with arterial oxygen tensions around 200 mm Hg (inspired oxygen fraction = 0.4) and arterial carbon dioxide tensions around 40 mm Hg. This study demonstrates a reliable method for continuous evaluation of the function of a transplanted lung immediately after transplantation and over the ensuing postoperative period. Safe 12-hour lung preservation can be obtained with the low-potassium-dextran solution Perfadex.

Animals↗

Effects of hypothermia in hypercapnia and hypercapnic hypoxemia.

Anesthetized, paralyzed and mechanically ventilated pigs were hypoventilated to extreme hypercapnia (PaCO2 approximately 20 kPa) at FiO2 0.5, and allotted to a hypothermic group (31.5 +/- 0.1 degrees C, n = 6) or a control group (39.6 +/- 0.2 degrees C, n = 6). Compared with the controls, the hypothermic animals had higher PaO2 (19.2 vs 15.6 kPa, P < 0.05), SaO2 (97.2 vs 89.3%), SvO2 (78.7 vs 68.2%), end-tidal O2 (34.5 vs 24.8 kPa) and arterial pH (7.01 vs 6.91), (P < 0.01), but lower PvO2 (7.0 vs 10.2 kPa) and PaCO2 (13.2 vs 23.5 kPa), (P < 0.01). Hypothermia reduced O2 delivery (DO2), O2 consumption (VO2) and CO2 production by 40-45% (P < 0.05), but O2 extraction ratio, i.e. VO2.DO(2)-1 x 100(%), did not differ between groups. Hypothermic animals had lower heart rate (127 vs 223 beats.min-1, P < 0.05) and cardiac output (2.5 vs 3.9 l.min-1, P < 0.01). Subsequently, the inspired oxygen fraction (FiO2) was decreased stepwise (0.3, 0.25, 0.21, 0.15, 0.10) at 30-min intervals. At FiO2 0.3, the hypothermic group had higher PaO2 (10.0 vs 5.7 kPa), SaO2 (91.3 vs 28.5%), PvO2 (5.8 vs 3.4 kPa), SvO2 (70.7 vs 10.3%), end-tidal O2 (16.7 vs 8.5 kPa), O2 delivery (344 vs 155 ml.min-1), arterial pH (7.02 vs 6.94) and systemic vascular resistance (3850 vs 1652 dyn.s.cm-5 (38,500 vs 16,520 microN.s.cm-5)) compared with the controls (P < 0.01), while PaCO2 was lower (12.4 vs 22.7 kPa), as well as O2 extraction ratio (23 vs 63%) and O2 half saturation tension (4.3 vs 8.0 kPa) (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of buffering in hypercapnia and hypercapnic hypoxemia.

Anesthetized, paralyzed and mechanically ventilated pigs were exposed to extreme hypercapnia (PaCO2 approximately 20 kPa) at FiO2 0.4 for 480 min, with (n = 6) or without (n = 6) continuous infusion of isotonic buffers (bicarbonate and trometamol). Arterial pH was higher in buffered animals than controls, 7.21 +/- 0.01 vs 7.01 +/- 0.01 (mean +/- s.e.mean, P < 0.01). Serum osmolality and PaCO2 did not differ between groups throughout the experiment. The hemodynamic response to hypercapnia was attenuated in the buffered group, who had lower heart rate, 133 +/- 6 vs 189 +/- 12 min-1 (P < 0.01), mean arterial pressure (MAP) 109 +/- 4 vs 124 +/- 4 mmHg (14.5 +/- 0.5 vs 16.5 +/- 0.5 kPa) (P < 0.05), mean pulmonary arterial pressure 16 +/- 1 vs 23 +/- 1 mmHg (2.1 +/- 0.1 vs 3.1 +/- 0.1 kPa) (P < 0.01), and pulmonary vascular resistance (PVR) 249 +/- 21 vs 343 +/- 20 dyn s.cm-5 (2490 +/- 210 vs 3430 +/- 200 microN.s.cm-5) (P < 0.01), compared with the control group. Subsequently, both groups were exposed to hypercapnic hypoxemia by stepwise increases in FiO2 (0.15, 0.10, 0.05) at 30-min intervals, while FiCO2 was kept at 0.2. PVR increased in both groups (P < 0.05) but, except for heart rate, all hemodynamic differences between the groups disappeared during hypoxia. At FiO2 0.15, buffered animals had higher arterial oxygen saturation (73 +/- 5%) than the controls (55 +/- 5%), (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Imbalance↗

Twenty-four-hour heparin-free veno-right ventricular ECMO: an experimental study.

Platelets and coagulation factors were studied during 24-hour heparin-free veno-right ventricular extracorporeal membrane oxygenation (ECMO) in 6 healthy pigs. An endpoint attached and covalently bonded heparin-coated ECMO system was used in these experiments. The veno-right ventricular ECMO supplied the total lung function of the animals, and after 24 hours, all the animals were successfully weaned from ECMO. Lung function and central hemodynamics were not affected by the procedure. Because all the animals showed a significant reduction in plasma volume, the concentration of measured coagulation variables was corrected both for plasma volume changes and for hemodilution. The platelet count and the plasma-free hemoglobin level were not significantly altered by ECMO. Similarly, the prothrombin complex, antithrombin, thrombin-antithrombin complex, factor XII, and the urinary excretion of 2,3-dinor-thromboxane B2 were not significantly altered. Fibrinogen and fibrin monomer increased significantly, whereas von Willebrand factor was significantly decreased after ECMO. In summary, 24-hour heparin-free veno-right ventricular total extracorporeal lung assistance does not affect the platelets and the coagulation system significantly in healthy juvenile pigs.

Animals↗

Endothelium-mediated relaxation in transplanted aorta.

This study compares the vasodilating effect of endothelium-derived relaxing factors (EDRFs) in free arterial grafts with that in their normal control vessels. The infrarenal aorta of Sprague-Dawley rats was transplanted into the same position in other inbred recipient rats. A Krebs buffer solution (4 degrees C) served as the preservation solution. The ischemic time for the grafts (n = 8) was 42 +/- 1 minutes. Two grafts were studied after 3 days and six grafts, after 60 days. Ring segments were cut from all vessels, and isometric contractions were recorded in organ baths. The vessel segments were constricted with noradrenaline, a thromboxane A2 mimic (U-46619), or prostaglandin F2 alpha. Concentration-response curves with acetylcholine, which was used as the endothelium-stimulating substance causing release of EDRFs, were obtained. The patency of the grafts was 100%. Acetylcholine induced relaxation in all vessel segments with intact intima, whereas no relaxation was seen when the endothelium was manually removed. No significant differences were found between the grafts and the normal control vessels. Histology of the 60-day grafts showed elastomuscular arteries without intimal thickening and a media consisting of eight to ten muscle layers interrupted by five to six elastic lamellae. Scanning electron microscopy showed no major differences between normal endothelium and the endothelium of 3-day or 60-day grafts. This study indicates that free elastomuscular arterial grafts, in which the morphology of the intima is preserved, will retain their full ability to release EDRFs.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Combined use of hypothermia and buffering in the treatment of critical respiratory failure.

A 20-year-old male, recovering from post-traumatic ARDS, subsequently developed pneumonia with extreme hypercapnia (PaCO2 max 19.4 kPa) and hypoxemia (PaO2 min 5.1 kPa), in spite of maximal mechanical ventilation. Hypothermia was induced by surface cooling, reducing the body temperature from 40 degrees C to a mean of 33.3 degrees C. Buffer infusion (1375 mmol) during the first 2 days increased base excess from 3 to 22 mmol/l and pH from 7.16 to a median value of 7.30. Active cooling was discontinued on day 11. Weaning from the ventilator was possible 9 days later and the patient subsequently recovered fully. Combined use of hypothermia and buffering might offer an alternative to extracorporeal lung assist (ECLA) and facilitate a reduction of barotrauma and oxygen toxicity during mechanical ventilation.

Adult↗

Venoarterial extracorporeal membrane oxygenation--how safe is it? Evaluation with a new experimental model.

This study was undertaken to find out if about 25% right cardiac output is sufficient for preservation of lung function during prolonged periods of venoarterial extracorporeal membrane oxygenation. Six healthy pigs weighing 57 kg were subjected to 18-hour venoarterial extracorporeal membrane oxygenation. During this period 1200 ml/min venous blood was delivered to the lungs through the pulmonary artery with the help of a separate roller pump and with use of the animal's own right ventricle to generate the pulse. Animals were observed for 6 hours after weaning from the venoarterial extracorporeal membrane oxygenation. At the sixth hour after extracorporeal membrane oxygenation, arterial oxygen tension, venous oxygen tension, lung compliance, and cardiac output had decreased significantly. Pulmonary vascular resistance and pulmonary clearance of technetium 99m-diethylenetriamine pentaacetic acid increased significantly also. The systemic arterial and venous carbon dioxide tensions, pH, and the base excess remained unchanged, as did the blood pressure and the systemic vascular resistance. Histopathology of the lung specimens revealed focal alveolar wall thickening and alveolar capillary congestion. The major portion of the pulmonary parenchyma looked normal. Alterations in pulmonary parameters cited were, to a major extent, explained on the basis of the experimental protocol followed and were believed to be reversible. This study suggests that about 25% of the systemic cardiac output should be diverted into the pulmonary artery for prevention of irreversible physiologic and histopathologic changes in the lungs during 18-hour normothermic venoarterial extracorporeal membrane oxygenation in healthy juvenile pigs.

Animals↗

Total extracorporeal lung assist--a new clinical approach.

Total extracorporeal lung assist (ECLA) requires a bypass flow approaching cardiac output. Recirculation of venous blood through the oxygenator is minimized with a veno-right ventricular cannulation technique which separates venous drainage from returned oxygenated blood. A case of posttraumatic ARDS was treated with surface-heparinized veno-right ventricular ECLA for 35 days. Cardiac output was stabilized by means of sedation, hypothermia (35 degrees C) and beta blockers (pulse rate less than 90) in order to match the maximal venous drainage achieved (5.5 l/min). A bypass flow around 85% of cardiac output resulted in mean arterial PO2 values between 9-13.6 kPa without any contribution from the lungs. Low platelet counts and a marked bleeding tendency complicated treatment, even though no heparin was used during the last 24 days of ECLA. Weaning from the ventilator was accomplished 2 months after ECLA. Lung function tests show constant improvement.

Adult↗