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Biomedical subjects

G Hedenstierna

Publications and source records attributed to G Hedenstierna.

At least 19 recordsLinked to original sources
PubMed2003

Nitric oxide increases dramatically in air exhaled from lung regions with occluded vessels.

BACKGROUND: We observed dramatic changes in exhaled nitric oxide concentration (DeltaNOE) during wedge measurements, and hypothesised that occlusion and redistribution of pulmonary blood flow affects NOE. METHODS: We inflated the balloon of the pulmonary artery catheter and measured NOE and central hemodynamics in closed chest anesthetised pigs (n = 11) ventilated with hyperoxic gas (fraction of inspired oxygen [FIO2] = 0.5), before and during lung injury, and in open chest anesthetised pigs (n = 17) before and during left lower lobar (LLL) hypoxia (FIO2 0.05), and during hyperoxic (FIO2 0.8) ventilation of the other lung regions (HL). RESULTS: In the closed chest pigs NOE increased from 2.0 (0.9) to 3.4 (2.0) p.p.b. (P < 0.001) during wedge, and returned to 2.0 (1.0) p.p.b. when the balloon was deflated. The increase in mean pulmonary artery pressure (MPaP) during wedge was small and insignificant (P > 0.07). When the balloon was inflated in the right pulmonary artery in the open chest pigs, the perfusion of the HL decreased from 2.57 (0.58) to 2.34 (0.55) l min(-1) (P < 0.001), and NOEHL increased from 2.5 (0.9) to 6.2 (3.2) p.p.b. (P < 0.001). The perfusion of the LLL increased from 0.33 (0.26) to 0.54 (0.34) l min(-1) (P < 0.001), and NOELLL decreased from 1.7 (0.6) to 1.5 (0.5) p.p.b. (P < 0.001). Neither lung injury nor LLL hypoxia had any influence on DeltaNOE (P > 0.07) during wedge. The correlation coefficient (R2) was 0.66 between changes in regional blood flow and DeltaNOE, and 0.37 between changes in MPaP and DeltaNOE. CONCLUSIONS: Nitric oxide concentration increases dramatically from lung regions with occluded vessels, whereas changes in MPaP have minor effects on NOE. This is an important fact to consider when comparing NOE within or between studies, and indicates a possible marker of diseases with occluded lung vessels.

Anesthesia↗
PubMed2003

Hyperosmolarity decreases the relaxing potency of sodium nitroprusside on guinea-pig trachea by the release of superoxide anions.

UNLABELLED: Increased osmolarity of the airway surface has been shown to abolish the airway relaxant effects of inhaled nitric oxide in rabbits in vivo and in guinea-pig trachea in vitro. AIM: In this study, we used a guinea-pig tracheal perfusion method to investigate whether superoxide anions, which rapidly react with nitric oxide, could be responsible for the reduced effect of nitric oxide in hyperosmolar airways. METHODS: Guinea-pig tracheas were constricted with carbachol (CCh) and then subjected to the nitric oxide donor sodium nitroprusside (SNP) under isoosmolar or hyperosmolar conditions. Hyperosmolarity was created by increasing the NaCl concentration of the buffer on the epithelial side of the airway. RESULTS: The relaxation produced by SNP was significantly less following hyperosmolar challenge, with a relaxation by 31 +/- 7% in hyperosmolar conditions as compared to 53 +/- 6% under normal isoosmolar conditions (P<0.05). The experiment was then performed in the presence of superoxide dismutase (SOD) that reduces levels of superoxide anions. SOD restored the relaxing potency of SNP in hyperosmolar conditions back to normal, to 46 +/- 5%. CONCLUSION: This study shows that superoxide anions are responsible for the reduced relaxing potency of the nitric oxide donor SNP following an intraluminal hyperosmolar challenge in guinea-pig trachea in vitro. The finding may form the basis for new treatment of patients not responding to treatment with inhaled nitric oxide.

Animals↗
PubMed2003

Good short-term agreement between measured and calculated tracheal pressure.

BACKGROUND: Tracheal pressure (P(tr)) is required to measure the resistance of the tracheal tube and the breathing circuit. P(tr) can either be measured with a catheter or, alternatively, calculated from the pressure-flow data available from the ventilator. METHODS: Calculated P(tr) was compared with measured P(tr) during controlled ventilation and assisted spontaneous breathing in 18 healthy and surfactant-depleted piglets. Their lungs were ventilated using different flow patterns, tidal volumes (V(T)) and levels of positive end-expiratory pressure. RESULTS: In terms of the root mean square error (RMS), indicating the average deviation of calculated from measured P(tr), the difference between calculated and measured P(tr) was 0.6 cm H(2)O (95%CI 0.58-0.65) for volume-controlled ventilation; 0.73 cm H(2)O (0.72-0.75) for pressure support ventilation; and 0.78 cm H(2)O (0.75-0.80) for bi-level positive airway pressure ventilation. CONCLUSION: The good agreement between calculated and measured P(tr) during varying conditions, suggests that calculating P(tr) could help setting the ventilator and choosing the appropriate level of support.

Air Pressure↗
PubMed2002

Gas exchange during intense exercise in Standardbreds with earlier Rhodococcus equi pneumonia.

It is not known if pulmonary function and gas exchange during exercise are altered after pyogranulomatous pneumonia caused by Rhodococcus equi infection in the foal. The aim was to evaluate whether pulmonary gas exchange during high intensity exercise was altered in mature Standardbreds with a history of R. equi pneumonia as foals. In 7 foals, R. equi pneumonia was confirmed and treated. At age 3 years, when these horses were subjected to professional training, an inclined treadmill exercise test including 4 speeds was performed. Samples were collected when a steady state in VO2 was obtained. Red cell volume, heart rate, respiratory rate, and systemic and pulmonary mean arterial pressures were measured and cardiac output calculated. Oxygen and carbon dioxide tensions in arterial and mixed venous blood were analysed. The alveolar ventilation and the alveolar-arterial oxygen tension difference were determined. Pulmonary gas exchange was assessed and the ventilation-perfusion distribution, VA/Q, was estimated by the multiple inert gas elimination technique. Ventilation-perfusion mismatch and shunt were determined and diffusion limitation calculated. The gas exchange in Standardbred trotters previously infected with R. equi and successfully treated was not compromised during intense treadmill exercise compared with reference values for healthy, fit Standardbreds. We conclude that adult Standardbreds trotters with diagnosed R. equi pneumonia as foals, can achieve an adequate gas exchange at a workload close to VO2peak.

Actinomycetales Infections↗
PubMed2002

Airway closure, atelectasis and gas exchange during anaesthesia.

Pulmonary gas exchange is regularly impaired during general anaesthesia with mechanical ventilation. This results in decreased oxygenation of blood. Major causes are collapse of lung tissue (atelectasis) and airway closure. Collapsed lung tissue is present in 90% of all subjects, both during spontaneous breathing and after muscle paralysis, and whether intravenous or inhalational anaesthetics are used. Airway closure is also common and increases in magnitude with increasing age of the patient. There are correlation between the amount of atelectasis and pulmonary shunt and between airway closure and perfusion of poorly ventilated lung regions (low VA/Q). Atelectasis and airway closure explain as much as 74% of gas exchange impairment in routine anaesthesia. A major cause of atelectasis is the pre-oxygenation during induction of anaesthesia. Lowering the inspired O2 concentration to 80% suffices to avoid almost all atelectasis. Airway closure and low VA/Q can only be prevented by raising the FRC level by PEEP or by other means.

Airway Obstruction↗
PubMed2001

Ventilation-perfusion distributions in different porcine lung injury models.

BACKGROUND: Acute lung injury is characterized by hypoxemia which may be caused by hypoventilation, ventilation-perfusion (V(A)/Q) mismatch, intrapulmonary shunting and oxygen diffusion impairment. The multiple inert gas elimination technique (MIGET) allows analysis of these four causes of hypoxemia and is therefore the most comprehensive approach to investigate blood gas abnormalities. Using MIGET, we studied whether specific patterns of gas exchange abnormalities occur in different lung injury models and whether gas exchange abnormalities can be related to pathogenic aspects of lung injury. METHODS: Lung injury was induced with oleic acid injection, endotoxin infusion or repeated lung lavage in groups of 6 mechanically ventilated pigs. RESULTS: PaO2 decreased and PaCO2 increased significantly in all three lung injury models, but gas exchange was more impaired in the oleic acid and lavage, as compared to the endotoxin group. Shunt was the major cause of hypoxemia in our lung injury models, whereas V(A)/Q mismatch contributed to venous admixture only after oleic acid injection and lung lavage. Oxygen diffusion limitation was not observed. Although alveolar ventilation was maintained after induction of lung injury, hypercapnia developed due to an increase of the ventilatory mean towards higher V(A)/Q ratios, increased shunt and increased carbon dioxide production. CONCLUSIONS: Shunt and ventilation-perfusion mismatch fully explain the gas exchange disturbances observed in our lung injury models. Although V(A)/Q distributions can be related to pathogenic aspects of the three study groups, we did not observe specific V(A)/Q patterns which allow diagnosis of the type of lung injury from a recovered V(A)/Q distribution.

Animals↗
PubMed2001

Ventilatory support by continuous positive airway pressure breathing improves gas exchange as compared with partial ventilatory support with airway pressure release ventilation.

UNLABELLED: In acute lung injury, airway pressure release ventilation (APRV) with superimposed spontaneous breathing improves gas exchange compared with controlled mechanical ventilation. However, the release of airway pressure below the continuous positive airway pressure (CPAP) level may provoke lung collapse. Therefore, we compared gas exchange and hemodynamics using a crossover design in nine pigs with oleic acid-induced lung injury during CPAP breathing and APRV with a release pressure level of 0 and 5 cm H(2)O. At an identical minute ventilation (V(E) 8 L/min) spontaneous breathing averaged 55%, 67%, and 100% of V(E) during the two APRV modes and CPAP, respectively. Because of the concept of APRV, mean airway pressure was highest during CPAP and lowest during APRV with a release pressure of 0 cm H(2)O. Shunt was reduced to almost half during CPAP (6.6% of Q(t)) compared with both APRV-modes (13.0% of Q(t)). Cardiac output and oxygen consumption, in contrast, were similar during all three ventilatory settings. Thus, in our lung injury model, CPAP was superior to partial ventilatory support using APRV with and without positive end-expiratory pressure. This may be attributable to beneficial effects of spontaneous breathing on gas exchange as well as to rapid lung collapse during the phases of airway pressure release below the CPAP level. These findings may suggest that the amount of mechanical ventilatory support using the APRV mode should be kept at the necessary minimum. IMPLICATIONS: Oxygenation is better with continuous positive airway pressure breathing than with partial mechanical ventilatory support using airway pressure release ventilation. Therefore, mechanical ventilatory support achieved by a cyclic release of airway pressure during APRV should be kept at the minimum level that enables enough ventilatory support for patients to avoid respiratory muscle fatigue.

Anesthesia↗
PubMed2001

Pulmonary vasoconstriction during regional nitric oxide inhalation: evidence of a blood-borne regulator of nitric oxide synthase activity.

BACKGROUND: Inhaled nitric oxide (INO) is thought to cause selective pulmonary vasodilation of ventilated areas. The authors previously showed that INO to a hyperoxic lung increases the perfusion to this lung by redistribution of blood flow, but only if the opposite lung is hypoxic, indicating a more complex mechanism of action for NO. The authors hypothesized that regional hypoxia increases NO production and that INO to hyperoxic lung regions (HL) can inhibit this production by distant effect. METHODS: Nitric oxide concentration was measured in exhaled air (NO(E)), NO synthase (NOS) activity in lung tissue, and regional pulmonary blood flow in anesthetized pigs with regional left lower lobar (LLL) hypoxia (fraction of inspired oxygen [FIO2] = 0.05), with and without INO to HL (FIO2 = 0.8), and during cross-circulation of blood from pigs with and without INO. RESULTS: Left lower lobar hypoxia increased exhaled NO from the LLL (NO(E)LLL) from a mean (SD) of 1.3 (0.6) to 2.2 (0.9) parts per billion (ppb) (P < 0.001), and Ca2+-dependent NOS activity was higher in hypoxic than in hyperoxic lung tissue (197 [86] vs. 162 [96] pmol x g(-1) x min(-1), P < 0.05). INO to HL decreased the Ca2+-dependent NOS activity in hypoxic tissue to 49 [56] pmol x g(-1) x min(-1) (P < 0.01), and NO(E)LLL to 2.0 [0.8] ppb (P < 0.05). When open-chest pigs with LLL hypoxia received blood from closed-chest pigs with INO, NO(E)LLL decreased from 2.0 (0.6) to 1.5 (0.4) ppb (P < 0.001), and the Ca2+-dependent NOS activity in hypoxic tissue decreased from 152 (55) to 98 (34) pmol x g(-1) x min(-1) (P = 0.07). Pulmonary vascular resistance increased by 32 (21)% (P < 0.05), but more so in hypoxic (P < 0.01) than in hyperoxic (P < 0.05) lung regions, resulting in a further redistribution (P < 0.05) of pulmonary blood flow away from hypoxic to hyperoxic lung regions. CONCLUSIONS: Inhaled nitric oxide downregulates endogenous NO production in other, predominantly hypoxic, lung regions. This distant effect is blood-mediated and causes vasoconstriction in lung regions that do not receive INO.

Administration, Inhalation↗
PubMed2001

Cardiorespiratory effects of automatic tube compensation during airway pressure release ventilation in patients with acute lung injury.

BACKGROUND: Spontaneous breaths during airway pressure release ventilation (APRV) have to overcome the resistance of the artificial airway. Automatic tube compensation provides ventilatory assistance by increasing airway pressure during inspiration and lowering airway pressure during expiration, thereby compensating for resistance of the artificial airway. The authors studied if APRV with automatic tube compensation reduces the inspiratory effort without compromising cardiovascular function, end-expiratory lung volume, and gas exchange in patients with acute lung injury. METHODS: Fourteen patients with acute lung injury were breathing spontaneously during APRV with or without automatic tube compensation in random order. Airway pressure, esophageal and abdominal pressure, and gas flow were continuously measured, and tracheal pressure was estimated. Transdiaphragmatic pressure time product was calculated. End-expiratory lung volume was determined by nitrogen washout. The validity of the tracheal pressure calculation was investigated in seven healthy ventilated pigs. RESULTS: Automatic tube compensation during APRV increased airway pressure amplitude from 7.7+/-1.9 to 11.3+/-3.1 cm H2O (mean +/- SD; P < 0.05) while decreasing trans-diaphragmatic pressure time product from 45+/-27 to 27+/-15 cm H2O x s(-1) x min(-1) (P < 0.05), whereas tracheal pressure amplitude remained essentially unchanged (10.3+/-3.5 vs. 10.1+/-3.5 cm H2O). Minute ventilation increased from 10.4+/-1.6 to 11.4+/-1.5 l/min (P < 0.001), decreasing arterial carbon dioxide tension from 52+/-9 to 47+/-6 mmHg (P < 0.05) without affecting arterial blood oxygenation or cardiovascular function. End-expiratory lung volume increased from 2,806+/-991 to 3,009+/-994 ml (P < 0.05). Analysis of tracheal pressure-time curves indicated nonideal regulation of the dynamic pressure support during automatic tube compensation as provided by a standard ventilator. CONCLUSION: In the studied patients with acute lung injury, automatic tube compensation markedly unloaded the inspiratory muscles and increased alveolar ventilation without compromising cardiorespiratory function and end-expiratory lung volume.

Adult↗
PubMed2001

Endothelin-1 and nitric oxide synthase in short rebound reaction to short exposure to inhaled nitric oxide.

On withdrawal of inhalation of nitric oxide (INO) administered after lung injury, pulmonary artery pressure (PAP) and arterial oxygen tension (Pa(O(2))) may deteriorate more than before INO (rebound response). In this study, we investigated the possible roles of endothelin (ET)-1 and nitric oxide (NO) synthase (NOS) activity in the short rebound reaction to short-term inhalation of NO. Twenty-six anesthetized mechanically ventilated piglets were given endotoxin infusion. Twelve animals then received INO (30 parts per million) for two 30-min periods. Nine controls were not given NO. Measurements were made of blood gases and hemodynamic parameters, lung tissue ET-1 expression and NOS activity, and plasma ET-1 concentration. INO decreased PAP and increased Pa(O(2)), but INO withdrawal caused a short rebound reaction with an increase in PAP. Lung tissue expression and plasma concentration of ET-1 increased during INO, and plasma ET-1 increased further after its withdrawal. Activity of constitutive NOS decreased during INO, whereas that of inducible NOS was unchanged. Upregulation of ET-1 and downregulation of NOS activity may have influenced the short rebound reaction to short-term INO.

Administration, Inhalation↗
PubMed2001

Assessment of respiratory system mechanics by artificial neural networks: an exploratory study.

We evaluated 1) the performance of an artificial neural network (ANN)-based technology in assessing the respiratory system resistance (Rrs) and compliance (Crs) in a porcine model of acute lung injury and 2) the possibility of using, for ANN training, signals coming from an electrical analog (EA) of the lung. Two differently experienced ANNs were compared. One ANN (ANN(BIO)) was trained on tracings recorded at different time points after the administration of oleic acid in 10 anesthetized and paralyzed pigs during constant-flow mechanical ventilation. A second ANN (ANN(MOD)) was trained on EA simulations. Both ANNs were evaluated prospectively on data coming from four different pigs. Linear regression between ANN output and manually computed mechanics showed a regression coefficient (R) of 0.98 for both ANNs in assessing Crs. On Rrs, ANN(BIO) showed a performance expressed by R = 0.40 and ANN(MOD) by R = 0.61. These results suggest that ANNs can learn to assess the respiratory system mechanics during mechanical ventilation but that the assessment of resistance and compliance by ANNs may require different approaches.

Animals↗
PubMed2001

An animal model of response and nonresponse to inhaled nitric oxide in endotoxin-induced lung injury.

STUDY OBJECTIVE: Oxygenation may be improved in 40 to 60% of ARDS patients by inhalation of nitric oxide (NO). We have studied the response to inhaled NO in porcine acute lung injury 4 h and 6 h after onset of a 2-h endotoxin infusion (30 microg/kg/h), hypothesizing that a responder may change to a nonresponder over time and with progression of lung injury. DESIGN: Animal study. SETTING: Experimental laboratory in a university hospital. INTERVENTIONS AND MEASUREMENTS: We studied eight pigs under general anesthesia (mean weight, 26.2 kg) receiving mechanical ventilation adjusted to normocapnia, with a fraction of inspired oxygen (FIO(2)) of 0.5 to 1.0. Blood gases, endotoxin concentration, and central hemodynamics were measured hourly, and ventilation-perfusion (/) relationships were assessed by multiple inert gas elimination technique before and after inhalation of NO. NO was delivered at 40 ppm for 10 min at 4 h and 6 h of endotoxin exposure. RESULTS: Seven of eight pigs were responders to NO at 4 h, defined as a > or = 20% increase in oxygenation index (PaO(2)/FIO(2)) [223 +/- 43 to 330 +/- 56 mm Hg; p = 0.001]. The same pigs exhibited a > or = 20% fall in mean pulmonary artery pressure (39.4 +/- 2.2 to 30.0 +/- 2.1 mm Hg; p < 0.001). The response correlated to the perfusion to "normal /" regions (r = - 0.82) and negatively to shunt and dead space ventilation (r = 0.76 and r = 0.87, respectively). At 6 h, seven of eight pigs were nonresponders, despite unaltered hemodynamics and gas exchange. Correlations at 4 h between physiologic variables and response to NO were abolished. The logarithmic SDs of the perfusion distribution, a measure of the degree of / mismatch, increased significantly from 4 to 6 h (p = 0.04). CONCLUSION: Response to inhaled NO is abolished over time in endotoxin-induced ARDS pig lungs. The response seems to be related to the degree of / mismatch, which may indicate an important role of hypoxic pulmonary vasoconstriction.

Administration, Inhalation↗
PubMed2001

Effects of phlebotomy on haemodynamic characteristics during exercise in standardbred trotters with red cell hypervolaemia.

Five Standardbred trotters with red cell hypervolaemia (RCHV) were compared before and after removal of approximately 22% (36 ml/kg bwt) of the total blood volume in order to evaluate the haemodynamic responses, haemorheological alterations and oxygen transport during exercise to fatigue. Data were recorded during submaximal exercise at 4 different speeds on a treadmill and then during continued running at the highest speed step until fatigue. Oxygen uptake (VO2), pulmonary artery pressure (PAP), systemic artery pressure (SAP), heart rate (HR), haematocrit and haemoglobin concentrations (Hb) were measured. Arteriovenous O2 content difference (C(a-v)O2), pulmonary vascular resistance (PVR) and total systemic resistance (TSR) were calculated. Whole blood and plasma viscosity and erythrocyte aggregation tendency were determined with a rotational viscometer. Endoscopy was performed after exercise. ANOVA was used for statistical analysis. Phlebotomy resulted in a decrease in haematocrit and Hb during the course of exercise. Blood and plasma viscosity were lower and erythrocyte aggregation tendency was higher after phlebotomy. Throughout exercise, including submaximal work and continued running to fatigue, PAP, SAP, PVR, TSR and C(a-v)O2 were lower after phlebotomy. HR was higher after phlebotomy during submaximal exercise. Oxygen delivery and VO2 were lower after phlebotomy in the period from submaximal exercise to fatigue. Run time to fatigue was shorter after phlebotomy. Four horses showed exercise-induced pulmonary haemorrhage (EIPH) before phlebotomy and the degree of bleeding was diminished but not abolished after phlebotomy. The reductions in PVR, TSR, PAP and SAP after phlebotomy were probably a result of reduced blood viscosity. In conclusion, although a 22% reduction in blood volume improved the haemodynamic and haemorheological parameters and the degree of EIPH, it was found that RCHV trotters have to rely on high oxygen delivery to the working muscles for maintenance of maximal performance.

Animals↗
PubMed2001

Thallium-201 myocardial imaging at rest in male orienteers and other endurance athletes.

During the period 1979 to 1992, 16 sudden unexpected cardiac deaths were known to have occurred in young Swedish orienteers. Autopsy indicated myocarditis to be the most frequent finding, most often combined with extensive myocardial fibrosis. The aim of the present investigation was to explore whether young male orienteers show a higher frequency than other young elite endurance athletes (controls) in the occurrence of Thallium-201 myocardial perfusion defects at rest, suggestive of fibrosis evoked by myocarditis. Thallium-201 perfusion abnormalities at rest were more frequently found in the controls than in the orienteers (26% vs. 12%, p=0.03). Uneven Tl-201 perfusion was associated with left ventricular mass (r=0.32, r=0.24, p<0.01, p=0.02) and body weight (r=0.30, r=0.31, p<0.01, p=0.03) in orienteers and controls, respectively. Echocardiographic left ventricular wall motion abnormalities were found in 11 athletes (9 orienteers and 2 controls) but only two displayed an abnormal Thallium-201 perfusion scan at rest. Perfusion abnormalities at rest did not occur more frequently in the orienteers but were commonly found in both groups of apparently healthy athletes making it futile to discern abnormals from normals. Thallium-201 perfusion aberrations were not associated with left ventricular wall motion abnormalities obtained by echocardiography.

Adult↗
PubMed2000

Hyperosmolarity-induced relaxation and prostaglandin release in guinea pig trachea in vitro.

In this study, a tracheal perfusion apparatus was used to investigate the nature of the relaxing factor released by hyperosmolarity on the epithelial side of guinea pig trachea. NaCl induced concentration-dependent relaxation. This relaxation was not affected when the trachea was preincubated with a vasoactive intestinal peptide (VIP) receptor antagonist or with the nitric oxide synthesis inhibitor N(G)-monomethyl-L-arginine (L-NMMA). When the prostaglandin synthesis was prevented by preincubation with the phospholipase A(2)-inhibitor quinacrine, or the cyclooxygenase inhibitor indomethacin, the maximal relaxation induced by NaCl was suppressed by 50% (P<0.05). Moreover, the prostaglandin E(2) concentration was four times higher (P<0.05) in the organ bath during the relaxations, whereas the nitric oxide concentration remained unchanged. In conclusion, increased osmolarity on the airway surface leads to the release of prostaglandins, which are involved in part in the hyperosmolarity-induced relaxation of airway smooth muscle. This might be relevant for asthmatic patients since prostaglandin may modulate the bronchoconstrictive response to hyperosmolar stimuli and exercise.

Animals↗
PubMed2000

Functional lung unit in the pig.

To study the size of the vessels supplying the functional lung unit, polystyrene beads of uniform diameter were injected intravenously in anaesthetised pigs and subsequent gas exchange abnormalities were studied using the multiple inert gas elimination technique. Beads of different sizes, ranging from 63 to 262 microm, were used, each pig receiving beads of only one size. Successive 0.25 g boli of beads (cumulative dose 1.0-1.5 g) increased shunt (from 3% baseline to 20% of cardiac output) and pulmonary artery mean pressure (from 26 to 45 mmHg) and decreased arterial P(O(2)) (from 96 to 43 mmHg) and cardiac output from 2.8 to 2.2 L min(-1) with no differences according to bead sizes. The dispersion of the ventilation dist ribution (log SDV), normal at 0.39 before beads, increased progressively with bead size from 0.48 (63 microm to 0.91 (262 microm). The 63 microm beads were lodged in vessels associated with respiratory bronchioles and smaller airways, whereas larger beads were positioned in vessels associated with non-respiratory airways. A linear correlation analysis between log SDV and bead size showed that 59 microm beads produce a log SDV that is 2 SEM above mean baseline log SDV. These findings suggest that the functional lung unit in this species (with no collateral ventilation) is smaller than in a species of the same size and with collateral ventilation (dog) in whom occlusion of 124 microm or larger diameter vessels is required to increase log SDV.

Animals↗
PubMed2000

Atelectasis formation during anesthesia: causes and measures to prevent it.

Pulmonary gas exchange is regularly impaired during general anaesthesia with mechanical ventilation. This results in decreased oxygenation of blood. A major cause is collapse of lung tissue (atelectasis), which can be demonstrated by computed tomography but not by conventional chest x-ray. Collapsed lung tissue is present in 90% of all subjects, both during spontaneous breathing and after muscle paralysis, and whether intravenous or inhalational anaesthetics are used. There is a correlation between the amount of atelectasis and pulmonary shunt. Shunt does not increase with age. In obese patients, larger atelectatic areas are present than in lean ones. Finally, patients with chronic obstructive lung disease may show less or even no atelectasis. There are different procedures that can be used in order to prevent atelectasis or to reopen collapsed lung tissue. The application of positive end-expiratory pressure (PEEP) has been tested in several studies. On the average, arterial oxygenation does not improve markedly, and atelectasis may persist. Further, reopened lung units re-collapse rapidly after discontinuation of PEEP. Inflation of the lungs to an airway pressure of 40 cm H2O, maintained for 7-8 seconds (recruitment or "vital capacity" manoeuvre), re-expands all previously collapsed lung tissue. During induction of anaesthesia, the use of a gas mixture, that includes a poorly absorbed gas such as nitrogen, may prevent the early formation of atelectasis. During ongoing anaesthesia, pulmonary collapse reappears slowly if a low fraction of oxygen in nitrogen is used for the ventilation of the lungs after a previous VC-manoeuvre. On the other hand, ventilation of the lungs with pure oxygen results in a rapid reappearance of atelectasis. Thus, ventilation during anaesthesia should be done if possible with a moderate fraction of inspired oxygen (FIO2, e.g. 0.3-0.4). Alternatively, if the lungs are ventilated with a high inspiratory fraction of oxygen, the use of PEEP may be considered. In summary, atelectasis is present in most humans during anaesthesia and is a major cause of impaired oxygenation. Avoiding high fractions of oxygen in inspired gas during induction and maintenance of anaesthesia may prevent formation of atelectasis. Finally, intermittent "vital capacity"-manoeuvres together with PEEP reduces the amount of atelectasis and pulmonary shunt.

Anesthesia, General↗