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Biomedical subjects

L Bindslev

Publications and source records attributed to L Bindslev.

At least 37 records · Page 2Linked to original sources
PubMed1987

Hypoxia-induced vasoconstriction in human lung exposed to enflurane anaesthesia.

The degree of hypoxic pulmonary vasoconstriction was studied in eight subjects during enflurane anaesthesia and was compared with that during intravenous pentobarbital anaesthesia in the same subjects. The lungs were ventilated separately with the aid of a double-lumen endobronchial catheter. After preoxygenation of both lungs for 30 min, during intravenous anaesthesia, the right lung (test lung) was rendered hypoxic by ventilation with 6% O2 in nitrogen. The left lung (control lung) was ventilated continuously with 100% oxygen. Cardiac output (QT) was determined by thermodilution, and the distribution of blood flow between the lungs was assessed from the elimination of a continuously infused, poorly soluble inert gas (SF6). The hypoxic challenge resulted in a reduction of the distribution of perfusion to the test lung from 57% to 36% of QT. Mean pulmonary arterial pressure increased by 37% and pulmonary vascular resistance of the test lung doubled. Arterial oxygen tension decreased from 45.9 to 9.5 kPa. Administration of enflurane to an end-tidal concentration of 2% to both lungs caused no significant change in the distribution of the pulmonary blood flow, PVR, or any other circulatory variable. The arterial blood gases remained unaltered. When the hypoxic challenge was discontinued, all variables returned towards control values. The findings suggest that the inhalational anaesthetic enflurane does not reduce the hypoxic vasoconstrictor response in the human lung.

Abdomen↗
PubMed1986

Effect of lignocaine and nitrous oxide on hypoxic pulmonary vasoconstriction in the dog constant-flow perfused left lower lobe preparation.

The effects of lignocaine hydrochloride on hypoxic pulmonary vasoconstriction in the presence and absence of nitrous oxide were examined during constant-flow perfusion of the left lower lobe. Lignocaine had no effect on lobar pulmonary vascular resistance during lobar ventilation with oxygen or 7% oxygen in nitrogen. The substitution of nitrous oxide for nitrogen diminished the hypoxic vasoconstrictor response, whilst the subsequent infusion of lignocaine during 7% oxygen in nitrous oxide increased the response to a value which was not significantly different from that produced by 7% oxygen in nitrogen alone.

Animals↗
PubMed1986

Reversal of nitrous oxide-induced depression of hypoxic pulmonary vasoconstriction by lignocaine hydrochloride during collapse and ventilation hypoxia of the left lower lobe.

The blood flow to the left lower lobe (QL), and total (QT) pulmonary blood flow, were measured in 10 open-chest dogs using electromagnetic flowmeters. Ventilation of the left lower lobe with 7% oxygen in nitrogen produced a greater reduction in QL/QT (41%) than lobar ventilation with 7% oxygen in nitrous oxide (33%). Lobar collapse reduced QL/QT by 65%, but there was no change in QL/QT when 50% nitrous oxide was administered to the right lung. The i.v. infusion of lignocaine hydrochloride during ventilation of the lobe with 7% oxygen in nitrogen produced no change in QL/QT. However, lignocaine infusion during lobar ventilation with 7% oxygen in nitrous oxide produced a further reduction in QL/QT to a value which was not significantly different from that observed during ventilation with 7% oxygen in nitrogen. Lignocaine had no effect on QL/QT during lobar collapse whether the right lung was ventilated with 50% oxygen in nitrogen or 50% oxygen in nitrous oxide. It is concluded that lignocaine reverses the depression of hypoxic pulmonary vasoconstriction produced by lobar ventilation with nitrous oxide.

Animals↗
PubMed1985

Hypoxic pulmonary vasoconstriction in the human lung: effect of repeated hypoxic challenges during anesthesia.

Six patients, ages 29-58 yr, were investigated during barbiturate and fentanyl anesthesia. After intubation with a double-lumen bronchial catheter, one lung was ventilated continuously with 100% O2, and the other was rendered hypoxic during three 15-min periods by ventilation with 95% N2 + 5% O2, with intervening 15-min periods of oxygen ventilation. Cardiac output was determined by thermodilution, and the distribution of blood flow between the lungs was assessed from the excretion of a continuously infused poorly soluble gas (SF6). The first hypoxic challenge resulted in a 10% increase in cardiac output (QT) and a reduction in the fractional perfusion of the test lung from 57% to 31% of QT. The pulmonary artery mean pressure increased by 54%, and the vascular resistance of the test lung increased threefold. The venous admixture increased from 19% to 40% of QT, whereas the inert gas shunt remained unaltered at 15% (inert gases also being eliminated by nitrogen-ventilated areas). The arterial oxygen tension decreased from 353 mmHg to 79 mmHg. On resumption of the control state, central hemodynamics and gas exchange returned to the initial values. The second and third hypoxic challenges resulted in reductions in the fractional perfusion of the test lung to 35% and 37% of QT. All other variables were altered to the same degree as during the first challenge. The authors conclude that hypoxic challenge of one lung in an intravenously anesthetized human subject elicits a maximum vasoconstrictor response within the first 15 min, and this response cannot be potentiated by repeated challenges.

Adult↗
PubMed1985

Hypoxic pulmonary vasoconstriction in the human lung: the effect of prolonged unilateral hypoxic challenge during anaesthesia.

The influence of time on the pulmonary vasoconstrictor response to hypoxia was studied in six subjects during general anaesthesia and artificial ventilation prior to elective surgery. The lungs were intubated separately with a double-lumen bronchial catheter. After preoxygenation of both lungs for 30 min, the test lung was rendered hypoxic for 60 min by ventilation with 5% O2 in N2, with the control lung still being ventilated with 100% O2. Cardiac output was determined by thermodilution, and the distribution of blood flow between the lungs was assessed from the excretion of a continuously infused poorly soluble gas (SF6). The fractional perfusion of the test lung decreased from 53% to 25% of cardiac output within the first 15 min of unilateral hypoxia. The pulmonary artery mean pressure increased by 14% and the pulmonary vascular resistance (PVR) of the test lung increased by 54%. Venous admixture increased from 21% to 39% of cardiac output, while the "true" shunt was maintained at about 15%. Arterial oxygen tension (Pao2) fell from 45 kPa to 12 kPa. Prolonging the unilateral hypoxic challenge caused no further change in the redistribution of the pulmonary blood flow, but cardiac output and pulmonary artery mean pressure continued to increase to 40%-50% above control values after 1 h of hypoxia. The PVR of the test lung remained unchanged. The findings suggest that there is an immediate vasoconstrictor response to hypoxia in the human lung and that there is no further potentiation or diminution, of the response during a 60-min period of hypoxia.

Adult↗
PubMed1985

Hypoxic pulmonary vasoconstriction in man: effects of hyperventilation.

The pulmonary vasoconstriction response to hypoxia was studied in eight anaesthetized supine subjects. One lung was made hypoxic while the other was ventilated with 100% oxygen. This was achieved by separating the tidal gas-distribution to the lungs by means of a double-lumen tracheal catheter. The hypoxic pulmonary vasoconstriction (HPV) response was estimated from the blood flow diversion away from the hypoxic lung. Blood flow distribution between the lungs was calculated from the regional expired carbon dioxide production, assuming regional carbon dioxide production to be proportional to blood flow. The subjects were studied during six different conditions. Firstly, when ventilated with 100% oxygen to both lungs at a PaCO2 of about 6 kPa. Secondly, with 100% oxygen to the left lung and 5% oxygen in nitrogen to the right (test) lung. The ratio between carbon dioxide output from right and left lung was calculated. These measurements were repeated during two states of hyperventilation (PaCO2 of about 4.5 kPa and 3.5 kPa, respectively) with and without hypoxia (conditions 3-6). During normoventilation, blood flow distribution between the lungs was equal. During hypoxia, blood flow distribution to the hypoxic lung decreased by 35% of the pre-hypoxic value. Furthermore, a decrease in arterial oxygen tension from 51.5 +/- 4.5 to 11.5 +/- 2.1 kPa was observed. During excessive hyperventilation (PaCO2 3.2 +/- 0.2 kPa), blood flow distribution to the hypoxic right lung decreased by only 10% of its pre-hypoxic value. A further decrease in arterial oxygen tension to 8.5 +/- 1.8 kPa was observed. This decrease in PaO2 was possibly due to an increased venous admixture caused by an abolished HPV response. It is concluded that hyperventilation counteracts hypoxic pulmonary vasoconstriction in man.

Adult↗
PubMed1985

Lung and chest wall mechanics during differential ventilation with selective PEEP.

Eight patients free from cardio-pulmonary disease and with a mean age of 46 years were studied during general anaesthesia in the lateral position. Measurements of hemithoracic mechanics were made during four different modes of ventilation: 1. Conventional ventilation (free distribution of ventilation) with no positive end-expiratory pressure (PEEP) (CV), 2. differential ventilation (50% of ventilation to each lung) with no PEEP (DV:0), and 3 and 4. DV with selective PEEP of 0.8 and 1.6 kPa, respectively, to the dependent lung only (DV:8, DV:16). During CV, 60% of ventilation was distributed to the non-dependent lung. Non-dependent hemithoracic compliance was 64% greater and inspiratory resistance 39% lower than those of the dependent hemithorax. No significant differences between the two hemithoraces were noted during DV:0, but on application of selective PEEP the compliance of the dependent hemithorax increased and its resistance decreased. With DV:16, the compliances of the two hemithoraces were essentially equal, as were their resistances. Selective PEEP caused a larger volume increase in the dependent lung than general PEEP. Selective PEEP reduced the volume of the non-dependent lung but only by 1/3 of the simultaneous increase in that of the dependent lung. Oesophageal pressure increased only slightly on selective inflation of the dependent lung, and remained negative within the 21 volume range studied. It is suggested that the altered mechanics of the dependent lung during selective PEEP result in a more even distribution of the inspired gas within that lung.

Adult↗
PubMed1984

Ventilation and perfusion of each lung during differential ventilation with selective PEEP.

Lung perfusion was studied in 10 patients (mean age 58 yr) in the lateral position during enflurane anesthesia. They were ventilated through a double-lumen endotracheal catheter: 1) by one ventilator with free distribution of ventilation between the lungs, with no (zero) end-respiratory pressure (ZEEP); 2) as above but with a general positive end-expiratory pressure (PEEP) of 9 cmH2O; or 3) by two ventilators with equal distribution of ventilation between the lungs and with a selective PEEP of 8 cmH2O to the dependent lung only. Total ventilation was on average 8 l/min (BTPS) throughout the study. During the first method, 34% of ventilation was distributed to the dependent and 66% to the nondependent lung. Cardiac output (thermodilution) was 4.5 l/min, 57% being distributed to the dependent lung as assessed by iv boli of Xenon 133. During the second method, ventilation was assumed to be distributed equally between the lungs. Cardiac output was decreased to 3.8 l/min, and the dependent lung received 81% of lung blood flow. During the third method, cardiac output was significantly greater than during the second method (4.1 l/min), 51% passing to the dependent lung. Peak and end-inspiratory airway pressures were 5-18 cm H2O lower during selective than during general PEEP. Arterial oxygen tension was significantly greater during the third method than during either of the other ventilator settings and the alveolar-arterial oxygen tension difference was almost halved compared with the first method. It is concluded that differential ventilation with selective PEEP improves ventilation-perfusion matching and thus oxygenation.

Adult↗
PubMed1983

Differential ventilation in acute bilateral lung disease. Influence on gas exchange and central haemodynamics.

Eight patients with acute respiratory failure (ARF) due to diffuse and rather uniform lung disease were intubated with a double-lumen bronchial tube and ventilated in the lateral decubital position by two synchronized ventilators. Ventilation of each lung was individually adjusted to match the expected regional blood flow (differential ventilation). When ventilation with equal volumes (i.e. 50% of tidal volume to each lung) was performed, a 19% reduction of venous admixture (P less than 0.001) and a 22% increment in arterial oxygen tension (P less than 0.001) were seen. Comcomitantly, the cardiac output increased by 17% (P less than 0.001), to which a reduced pulmonary vascular resistance may have contributed. The net result was a 14% increment of the oxygen availability (P less than 0.001). An attempt to go further, giving 2/3 of the tidal ventilation to the dependent lung, was made on six of the patients. However, this ventilatory pattern did not further improve the gas exchange and also had detrimental effects on the haemodynamics. It is concluded that differential ventilation with equal tidal volumes in the lateral position can substantially improve gas exchange and central haemodynamics in patients with ARF due to diffuse lung disease.

Acute Disease↗
PubMed1983

Selective PEEP in acute bilateral lung disease. Effect on patients in the lateral posture.

Seven patients with acute respiratory failure due to diffuse and fairly uniform lung disease were studied during mechanical ventilation in the lateral decubital position with: (a) zero end-expiratory pressure (ZEEP) through a double-lumen oro-bronchial tube to permit a recording of the ventilation to each lung; (b) bilateral positive end-expiratory pressure (PEEP) of 1.2 kPa, with maintenance of ventilation distribution between lungs as observed during ZEEP; (c) selective PEEP of 1.2 kPa, applied to the dependent lung only, with ventilation as during ZEEP; and (d) conventional PEEP of 1.2 kPa applied to both lungs through a single-lumen tube, with free distribution of ventilation between the lungs. During ZEEP, 69% of ventilation was distributed to the non-dependent and 31% to the dependent lung; cardiac output was 6.51 X min-1, venous admixture (QS/QT) 40% and arterial oxygen tension (PaO2) 8.3 kPa. With bilateral PEEP, functional residual capacity (FRC) increased by 0.331, cardiac output was reduced to 5.11 X min-1 and venous admixture to 32%. PaO2 increased to 10.1 kPa. With selective PEEP the dependent lung FRC increased by 0.211 and the FRC of the non-dependent lung decreased by 0.081. Cardiac output increased to 6.11 X min-1, which was no longer significantly different from that during ZEEP. Venous admixture remained at the same level as with bilateral PEEP.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1982

Regional differences in lung function during anaesthesia and intensive care: clinical implications.

Anaesthesia and most frequently acute respiratory failure are accompanied by a lowered functional residual capacity (FRC). This lowering promotes airway closure in dependent lung units and forces ventilation to non-dependent regions. Perfusion, on the other hand, is forced towards dependent lung units. A ventilation-perfusion mismatch is created and hypoxaemia may develop. General PEEP counters airway closure, but impedes cardiac output and forces perfusion further to dependent regions. In addition, barotrauma may occur. Improved matching of ventilation and perfusion can be achieved by: (1) positioning the subject in the lateral posture; (2) ventilating each lung separately in proportion to its perfusion (differential ventilation); and (3) applying PEEP only to the dependent lung (selective PEEP). Because of less overall intrathoracic pressure and lung expansion, interference with the total lung blood flow and the danger of barotrauma should be less than with general PEEP. Improved gas exchange with a 50-100% increase in PaO2 has been observed in a limited number of patients with acute bilateral lung disease studied so far during differential ventilation and selective PEEP.

Anesthesia↗
PubMed1981

Distribution of inspired gas to each lung in anesthetized human subjects.

The distribution of ventilation in man during halothane anesthesia was studied in a two-compartment lung model in which each lung was ventilated separately by means of a double-lumen tracheal tube. Eight subjects were studied prior to scheduled surgery. Tidal volume distribution was even between the lungs in the supine position (horizontal distribution) as was distribution of dynamic lung compliance, resistance and dead space. The vertical distribution was assessed when the patient was in the left lateral position. Dependent dynamic lung compliance and dead space were lower and lung resistance was higher than in the non-dependent lung. These factors favoured a non-dependent lung ventilation and, moreover, caused a re-distribution from dependent to non-dependent lung during an end-inspiratory pause (EIP), thus increasing the inhomogeneity of ventilation. The application of a positive end-expiratory pressure (PEEP) of 10 cmH2O improved dependent ventilation and abolished redistribution between the lungs. In conclusion, uneven distribution of dynamic lung compliance and lung resistance causes inhomogeneous ventilation distribution, favouring the non-dependent lung. An EIP enhances and a PEEP reduces the inhomogeneity of ventilation.

Adult↗
PubMed1981

Ventilation-perfusion distribution during inhalation anaesthesia. Effects of spontaneous breathing, mechanical ventilation and positive end-expiratory pressure.

Ventilation-perfusion (VA/Q) ratios were studied by means of an inert gas elimination technique in healthy subjects with an average age of 51 years in the supine posture (a) when awake, (b) during inhalational anaesthesia, spontaneously breathing, (c) during mechanical ventilation, and (d) when a positive end-expiratory pressure (PEEP) was applied. In the awake subject a bimodal distribution of VA/Q was recovered in most patients, one mode centered around the ratio of 1 and another, smaller mode, within low VA/Q-regions. Any shunt was less than 3% of cardiac output. With anaesthesia and spontaneous breathing, the low VA/Q mode was reduced and the shunt increased to an average of 6.2%. With mechanical ventilation, the major VA/Q mode was widened while the shunt was further increased in 4 of 10 subjects (mean 8.6%). With PEEP, the shunt was reduced and a new mode within high VA/Q-regions appeared. The shunt and low VA/Q-regions appeared. The shunt and low VA/Q-regions may be explained in terms of airway closure while the high VA/Q mode with PEEP may be attributed to the development of a zone I.

Adult↗
PubMed1981

Pressure-volume and airway closure relationships in each lung in anaesthetized man.

Airway closure, functional residual capacity (FRC) and transpulmonary pressure-volume curves were assessed for each lung separately in the anaesthetized subject by means of a double lumen tracheal catheter. In the supine position airway closure occurred synchronously in the two lungs and 0.2-0.31 above FRC. The pressure- volume curves in both lungs were rather similar and critical closing pressure (CP) was approximately 3 cmH2O in each lung. In the left lateral posture, FRC was increased in the non-dependent and reduced in the dependent lung, while closing capacity (CC) remained unaltered. Airway closure was asynchronous and discontinuous between the two lungs. This was caused by the non-linear transpulmonary pressure-volume curve in the lungs, in conjunction with the vertical pleural pressure gradient. An interpulmonary "pendelluft" phenomenon was observed in the left lateral posture, increasing inhomogeneity of ventilation. It may depend on regional differences in compliance.

Adult↗
PubMed1981

Airway closure in each lung of anesthetized human subjects.

Airway closure and functional residual capacity (FRC) were assessed for each lung separately in the anesthetized subject by means of a double-lumen tracheal catheter. Airway closure was studied by argon-bolus and nitrogen-washout techniques, and FRC was calculated from single-breath nitrogen washout. Recordings were done with subjects in the supine and lateral postures. In the supine position, closing capacity (CC) exceeded FRC in each lung. Airway closure occurred synchronously in the two lungs. Argon CC was 0.05-0.1 liter larger than nitrogen CC of either lung. Minor gas trapping occurred during the vital capacity (VC) maneuver, so that inspired VC exceeded expired VC by 3%. In the left lateral posture, CC remained unaltered in either lung, whereas FRC was markedly increased in the nondependent and reduced in the dependent lung. Airway closure occurred asynchronously in the two lungs, and its distribution was discontinuous between them. Onset of airway closure in the dependent lung caused an early (60% VC) upstroke on the overall tracer gas recording (sampling of mixed expirate at the mouth), whereas onset of airway closure in the nondependent lung caused an additional upstroke at 10% VC. Gas trapping was more marked in the dependent lung than in the supine position, but some gas was released (expired VC greater than inspired VC) n the nondependent lung.

Adult↗
PubMed1980

Airway closure during anaesthesia, and its prevention by positive end expiratory pressure.

Airway closure, functional residual capacity (FRC) and the transpulmonary pressure volume relationship of each lung were studied in the anaesthetized subject in the supine and the left lateral positions. In the supine posture, FRC was of approximately the same size in each lung as was closing capacity (CC). CC exceeded FRC in either lung. In the left lateral position, FRC was increased by 0.91 in the non-dependent lung and was reduced by 0.21 in the dependent lung, while CC was unaltered in either lung. Consequently, FRC exceeded CC in the non-dependent lung and was further lowered beneath CC in the dependent lung. Airway closure did not occur in the non-dependent lung until an average of 0.51 of gas had been expelled after the dependent lung had ceased to empty. The addition of positive end-expiratory pressure (PEEP) in the range 0.5-2 kPa, increased FRC more in the non-dependent than the dependent lung. The findings suggest that airway closure is evenly distributed in the horizontal level, while it has a discontinuous distribution between the dependent and non-dependent lung. Moreover, the increase in lung volume caused by PEEP has a distribution that is by no means ideal for the purpose of countering airway closure.

Adult↗