Decrease In Arterial Oxygenation Research Articles

Nursing process applied to a preschooler with spinal muscular atrophy and chronic respiratory failure

Introduction: chronic respiratory failure involves changes in the respiratory system, preventing its normal functioning. Inadequate gas exchange leading to the onset of compensatory mechanisms characterized by a sustained decrease in arterial oxygen pressure.Objective: manage the nursing care process for a pediatric patient with spinal muscular atrophy and chronic respiratory failure. Method: a qualitative, descriptive single case study was carried out. Data were collected through the use of observation, physical examination, documented review and interview techniques and the information was organized using the Assessment Guide according to Marjory Gordon's 11 functional health patterns.Results: the 4 altered patterns were identified and 8 nursing diagnoses were formulated (taxonomy II of NANDA I) prioritizing three: deterioration of spontaneous ventilation, ineffective cleaning of the airways and risk of deterioration of skin integrity. Subsequently, the objectives were set and care plans were created (NOC and NIC taxonomy) to then execute a large percentage of said nursing care and finally the NOC indicators were evaluated, differentiating both final and baseline scores. At the end, change scores of +1, +3, +2 were obtained.Conclusions: the nursing care process applied in the preschool was the basis for identifying the present problems and risks, as well as planning the necessary interventions and activities, executing them and evaluating them, in this way it was possible to adequately manage the care. pediatric

Hypoxic White Matter Injury and Recovery After Reoxygenation in Adult Mice: Magnetic Resonance Imaging Findings and Histological Studies.

Cognitive dysfunction and brain white matter (WM) injury have been found in adults exposed to hypoxia. However, the mechanisms underlying these impairments remain unclear, and moreover, it is also unclear whether these impairments are reversible after reoxygenation. In this study, adult male mice were exposed to hypoxia for 15days at a simulated altitude of 4300m and then reoxygenated for 2months. Control mice were raised under normoxic conditions. Mice showed a significant decrease inarterial oxygen saturation (SaO2)and an increase in heart rate and breath rate after hypoxic exposure, and they displayed anxiety-like emotion and impaired cognitions. Hypoxic mice showed decreased brain WM fractional anisotropy(FA) and increased mean diffusion (MD) mainly in the corpus callosum and internal capsule. The reason for the adult brain WM injury was myelin rather than axon. Further, the myelin injury was due to the obstruction of oligodendrocyte precursor cells (OPCs) differentiation and eventually led to behavioral deficits. More importantly, the changes in physiological indicators, behavioral disorders, and WM injury caused by hypoxia can be recovered after reoxygenation. Taken together, our data indicate that adult brain WM injury caused by hypoxia is reversible after reoxygenation and enhancing OPCs differentiation may be a promising therapy for clinical hypoxic diseases associated with brain injury. Schematic diagram of brain WM and behavioral changes induced by hypoxia/reoxygenation in adult mice.

Whole-brain perfusion mapping in mice by dynamic BOLD MRI with transient hypoxia

Non-invasive mapping of cerebral perfusion is critical for understanding neurovascular and neurodegenerative diseases. However, perfusion MRI methods cannot be easily implemented for whole-brain studies in mice because of their small size. To overcome this issue, a transient hypoxia stimulus was applied to induce a bolus of deoxyhemoglobins as an endogenous paramagnetic contrast in blood oxygenation level-dependent (BOLD) MRI. Based on stimulus-duration-dependent studies, 5 s anoxic stimulus was chosen, which induced a decrease in arterial oxygenation to 59%. Dynamic susceptibility changes were acquired with whole-brain BOLD MRI using both all-vessel-sensitive gradient-echo and microvascular-sensitive spin-echo readouts. Cerebral blood flow (CBF) and cerebral blood volume (CBV) were quantified by modeling BOLD dynamics using a partial-volume-corrected arterial input function. In the mouse under ketamine/xylazine anesthesia, total CBF and CBV were 112.0 ± 15.0 ml/100 g/min and 3.39 ± 0.59 ml/100 g (n = 15 mice), respectively, whereas microvascular CBF and CBV were 85.8 ± 6.9 ml/100 g/min and 2.23 ± 0.27 ml/100 g (n = 7 mice), respectively. Regional total vs. microvascular perfusion metrics were highly correlated but a slight mismatch was observed in the large-vessel areas and cortical depth profiles. Overall, this non-invasive, repeatable, simple hypoxia BOLD-MRI approach is viable for perfusion mapping of rodents.

Changes in Arterial Blood Pressure and Oxygen Tension as a Result of Hoisting in Isoflurane Anesthetized Healthy Adult Horses.

Background: In anesthetized adult horses, changes in recumbency can influence the cardiovascular system but how arterial blood pressures and oxygen tension change in isoflurane anesthetized animals as a direct result of hoisting has not been investigated.Objective: To evaluate effects of hoisting on hemodynamic function and pulmonary gas exchange in isoflurane-anesthetized horses.Study Design: Prospective, experimental study.Methods: Six adult horses were anesthetized three times using isoflurane in pure oxygen (inspired fraction 0.9–1.0), and allowed breathing spontaneously in lateral recumbency. After 45 min horses were hoisted using a single hoist-hobble system for 5 min and returned into left lateral recumbency. Heart rate (HR), respiratory rate (RR), and systolic (SAP), diastolic (DAP), and mean arterial blood pressures (MAP) were measured every minute starting from 5 min before to 5 min after hoisting. Arterial blood gas samples were collected before, during, and after hoisting.Results: Significant changes in hemodynamic parameters and PaO2 but not PaCO2 were found between baseline recordings and measurements obtained during and early after hoisting. The MAP decreased within the 1st min of hoisting from a mean of 74 ± 17 mmHg at baseline to 57 ± 20 mmHg (p < 0.05). Thereafter, it rapidly recovered to baseline before continuing to rise to higher than baseline values and then remaining elevated for 5 min after horses were returned into lateral recumbency. Simultaneously, the HR increased by 6–9 beats per min during the initial 3 min of hoisting before returning close to baseline values (p < 0.05). The PaO2 decreased significantly from a mean of 324.9 ±137.0 mmHg at baseline to a mean of 141.3 ± 104.2 mmHg during hoisting (p < 0.001) without recovering any more to baseline values.Clinical significance: Hoisting an adult horse during or at the end of isoflurane anesthesia carries the risk of a precipitous, though short-lived (1–2 min), drop in arterial blood pressures and a persistent decrease in arterial oxygenation. While in systemically healthy animals the observed functional impairments were not life-threatening, they may be more severe in systemically compromised horses.Therefore, arterial blood pressures and oxygenation must be carefully monitored when hoisting sick equine patients during or at the end of inhalant anesthesia.

Halogenated Agent Delivery in Porcine Model of Acute Respiratory Distress Syndrome via an Intensive Care Unit Type Device.

Acute respiratory distress syndrome (ARDS) is a common cause of hypoxemic respiratory failure and death in critically ill patients, and there is an urgent need to find effective therapies. Preclinical studies have shown that inhaled halogenated agents may have beneficial effects in animal models of ARDS. The development of new devices to administer halogenated agents using modern intensive care unit (ICU) ventilators has significantly simplified the dispensing of halogenated agents to ICU patients. Because previous experimental and clinical research suggested potential benefits of halogenated volatiles, such as sevoflurane or isoflurane, for lung alveolar epithelial injury and inflammation, two pathophysiologic landmarks of diffuse alveolar damage during ARDS, we designed an animal model to understand the mechanisms of the effects of halogenated agents on lung injury and repair. After general anesthesia, tracheal intubation, and the initiation of mechanical ventilation, ARDS was induced in piglets via the intratracheal instillation of hydrochloric acid. Then, the piglets were sedated with inhaled sevoflurane or isoflurane using an ICU-type device, and the animals were ventilated with lung-protective mechanical ventilation during a 4 h period. During the study period, blood and alveolar samples were collected to evaluate arterial oxygenation, the permeability of the alveolar-capillary membrane, alveolar fluid clearance, and lung inflammation. Mechanical ventilation parameters were also collected throughout the experiment. Although this model induced a marked decrease in arterial oxygenation with altered alveolar-capillary permeability, it is reproducible and is characterized by a rapid onset, good stability over time, and no fatal complications. We have developed a piglet model of acid aspiration that reproduces most of the physiological, biological, and pathological features of clinical ARDS, and it will be helpful to further our understanding of the potential lung-protective effects of halogenated agents delivered through devices used for inhaled ICU sedation.

Pulmonary Vascular Function and Aerobic Exercise Capacity at Moderate Altitude.

There has been suggestion that a greater "pulmonary vascular reserve" defined by a low pulmonary vascular resistance (PVR) and a high lung diffusing capacity (DL) allow for a superior aerobic exercise capacity. How pulmonary vascular reserve might affect exercise capacity at moderate altitude is not known. Thirty-eight healthy subjects underwent an exercise stress echocardiography of the pulmonary circulation, combined with measurements of DL for nitric oxide (NO) and carbon monoxide (CO) and a cardiopulmonary exercise test at sea level and at an altitude of 2250 m. At rest, moderate altitude decreased arterial oxygen content (CaO2) from 19.1 ± 1.6 to 18.4 ± 1.7 mL·dL, P < 0.001, and slightly increased PVR, DLNO, and DLCO. Exercise at moderate altitude was associated with decreases in maximum O2 uptake (V˙O2max), from 51 ± 9 to 43 ± 8 mL·kg⋅min, P < 0.001, and CaO2 to 16.5 ± 1.7 mL·dL, P < 0.001, but no different cardiac output, PVR, and pulmonary vascular distensibility. DLNO was inversely correlated to the ventilatory equivalent of CO2 (V˙E/V˙CO2) at sea level and at moderate altitude. Independent determinants of V˙O2max as determined by a multivariable analysis were the slope of mean pulmonary artery pressure-cardiac output relationship, resting stroke volume, and resting DLNO at sea level as well as at moderate altitude. The magnitude of the decrease in V˙O2max at moderate altitude was independently predicted by more pronounced exercise-induced decrease in CaO2 at moderate altitude. Aerobic exercise capacity is similarly modulated by pulmonary vascular reserve at moderate altitude and at sea level. Decreased aerobic exercise capacity at moderate altitude is mainly explained by exercise-induced decrease in arterial oxygenation.

Effects of exogenous ubiquitin in a polytrauma model with blunt chest trauma*

To determine whether treatment with the CXC chemokine receptor 4 agonist ubiquitin results in beneficial effects in a polytrauma model consisting of bilateral femur fractures plus blunt chest trauma (Injury Severity Score 18-25). Treatment study. Research laboratory. Seventeen Yorkshire pigs. Intravenous injection of 1.5 mg/kg ubiquitin or albumin (control) at 60 mins after polytrauma. Anesthetized, mechanically ventilated pigs underwent polytrauma, followed by a simulated 60-min shock phase. At the end of the shock phase, ubiquitin or albumin were administered and animals were resuscitated to a mean arterial blood pressure of 70 mm Hg until t=420 mins. After intravenous ubiquitin, ubiquitin plasma concentrations increased 16-fold to 2870±1015 ng/mL at t=90 mins and decreased with t1/2=60 mins. Endogenous plasma ubiquitin increased two-fold in the albumin group with peak levels of 359±210 ng/mL. Plasma levels of the cognate CXC chemokine receptor 4 ligand stromal cell-derived factor-1α were unchanged in both groups. Ubiquitin treatment reduced arterial lactate levels and prevented a continuous decrease in arterial oxygenation, which occurred in the albumin group during resuscitation. Wet weight to dry weight ratios of the lung contralateral from the injury, heart, spleen and jejunum were lower with ubiquitin. With ubiquitin treatment, tissue levels of Interleukin-8, Interleukin-10, Tumor Necrosis Factor α, and stromal cell-derived factor-1α were reduced in the injured lung and of Interleukin-8 in the contralateral lung, respectively. Administration of exogenous ubiquitin modulates the local inflammatory response, improves resuscitation, reduces fluid shifts into tissues, and preserves arterial oxygenation after blunt polytrauma with lung injury. This study further supports the notion that ubiquitin is a promising protein therapeutic and implies CXC chemokine receptor 4 as a drug target after polytrauma.

Structural and Physiological Age-Associated Changes in Aging Lungs

The tissues of the lungs undergo changes with age that lead to an increase in alveolar size without any destruction of alveolar walls. This lowers the alveolar surface tension and so reduces the elastic recoil of the lungs, which in turn causes a reduction in maximum achievable flow in the airways during the breathing cycle. Muscle performance diminishes with age and the chest wall becomes stiffer, which together lead to an increased residual volume and also counter the possible increase in total lung capacity (TLC) from the reduced elastic recoil. Exercise performance falls with age, with a small decrease in arterial oxygenation that stabilizes over the age of 70 years. Predicting lung function for the elderly is not easy, and basing clinical decisions on percent of predicted may lead to age, sex, and height bias. Focusing on what function remains can allow survival predictions to guide decisions on treatment options.

Treatment of anesthesia-induced lung collapse with lung recruitment maneuvers

Summary General anesthesia causes atelectasis and airway closure in dependent areas of the lung. Both kinds of collapse induce a deterioration of gas exchange characterized by a decrease in arterial oxygenation and an increase in dead space. The severity of this lung dysfunction is proportional to the amount of collapsed tissue that depends on anesthesia, surgical and patient's factors. Lung collapse can be partially prevented by decreasing FiO 2 and/or by applying CPAP during the induction of anesthesia. However, only lung recruitment maneuvers can resolve atelectasis completely. These recruitment maneuvers are ventilatory strategies aimed to restore the normal aeration of the lungs. The maneuvers consist in a brief and controlled increase in airway pressure to open up those pulmonary areas with collapse. Afterward, the lungs are ventilated with a protective strategy setting keeping the lungs open in time with enough positive-end expiratory pressure and low driving pressure. This article describes the physiological and clinical background of lung recruitment maneuvers applied during the intra-operative period.

Protective role of Coenzyme Q10in two models of rat lung injury

Ischaemia-reperfusion injury is a life-threatening complication of lung transplantation. Attempts to ameliorate this injury have included optimization of donor management and improving techniques of lung preservation. However, few investigators have sought to pretreat potential recipients. Coenzyme Q(10) (CoQ(10)) is a potent antioxidant and cellular energizer that has been shown to protect the heart against injury. However, its protective effect in the lung is unknown. We therefore set out to study the impact of Coenzyme Q(10) pretreatment in a model of mild and severe lung injury. We evaluated the impact of CoQ(10) in a two-stage laboratory study. In the first stage, in order to measure the magnitude of increase in tissue and plasma CoQ(10) following oral therapy we administered high-dose oral CoQ(10) to rats (n = 6). In the second stage we evaluated the impact of CoQ(10) in the rat lung (n = 10) that was subjected to 230 min of normoxic lung injury or 90 min of warm ischaemia and 120 min of reperfusion in a model of lung transplantation. High-dose oral CoQ(10) for 7 days produced a 15-fold increase in plasma and a 3-fold increase in lung CoQ(10). In the normoxic lung, the injury-induced rise in peak airway pressure was reduced by CoQ(10) treatment at 90 min (P = 0.037) and at 120 min (P = 0.005) without any change in arterial oxygen. In the lung subjected to severe ischaemia-reperfusion injury, CoQ(10) did not reduce the injury-induced increase in peak airway pressure (P = 0.599) nor the decrease in arterial oxygen (P = 0.844). However, CoQ(10) markedly reduced the increase in tumour necrosis factor-alpha in ischaemic compared with normoxic lung (P = 0.027). The effect of CoQ(10) pretreatment is insufficient to protect the lung against severe ischaemia-reperfusion as may occur in lung transplantation. However, in the setting of less severe pulmonary injury as in anaesthesia and non-transplant surgery, CoQ(10) may have a protective role.

Comparison of two different techniques of fibreoptic intubation

The application of analgesics and sedatives during fibreoptic intubation (FOI) may result in a transient decrease in arterial oxygen saturation.This study evaluates two different techniques of FOI and respective effects on procedural duration, arterial oxygen saturation, and coughing by the patient. Thirty-four patients received a standardized conscious sedation with fentanyl (1.5 microg kg(-1)) and midazolam (12.5 microg kg(-1)).All patients were randomly allocated to one of the following techniques: the 'vaporization' (VAP) technique included four applications of 2 ml lidocaine 2% administered through the working channel of the fibrescope supplying an oxygen flow of 3 l min(-1); the 'standard' (STAN) technique included the insufflation of 3 l(-1) min oxygen via a nasal probe and two applications of 4 ml of lidocaine 2%, each followed by a maximum of 2 min to take effect. FOI was successful in all patients (STAN 15; 'vaporization' 17 patients). The overall intubation time interval was significantly (P < 0.001) shorter in the VAP group. There was no difference in oxygen saturation between the two groups prior to the start of FOI, but a significant (P = 0.008) decrease in oxygen saturation levels was detected in the STAN group after completion of FOI. Patients in the VAP group coughed less; a significant difference in the number of coughs (P = 0.036) was found during the application of lidocaine into the proximal trachea. The VAP technique decreases overall intubation time, increases the oxygen saturation of the patient until completion of the intubation, and reduces cough.

Effects of medetomidine, l–methadone, and their combination on arterial blood gases in dogs

ObjectiveTo investigate the influence of l–methadone on medetomidine–induced changes in arterial blood gases and clinical sedation in dogs. Study designProspective experimental cross–over study (Latin square design). AnimalsFive 1–year–old purpose bred laboratory beagle dogs of both sexes. MethodsEach dog was treated three times: medetomidine (20 μg kg−1 IV), l–methadone (0.1 mg kg−1 IV) and their combination. Arterial blood was collected for blood gas analysis. Heart and respiratory rates were recorded, and clinical sedation and reaction to a painful stimulus were scored before drug administration and at various time points for 30 minutes thereafter. ResultsArterial partial pressure of oxygen decreased slightly after medetomidine administration and further after medetomidine/l–methadone administration (range 55.2–86.7 mmHg, 7.4–11.6 kPa, at 5 minutes). A slight increase was detected in arterial partial pressure of carbon dioxide after administration of l–methadone and medetomidine/l–methadone (42.6 ± 2.9 and 44.7 ± 2.4 mmHg, 5.7 ± 0.4 and 6.0 ± 0.3 kPa, 30 minutes after drug administration, respectively). Arterial pH decreased slightly after administration of l–methadone and medetomidine/l–methadone. Heart and respiratory rates decreased after administration of medetomidine and medetomidine/l–methadone, and no differences were detected between the two treatments. Most dogs panted after administration of l–methadone and there was slight sedation. Medetomidine induced moderate or deep sedation, and all dogs were deeply sedated after administration of medetomidine/l–methadone. Reaction to a noxious stimulus was strong or moderate after administration of methadone, moderate or absent after administration of medetomidine, and absent after administration of medetomidine/l–methadone. Conclusions and clinical relevanceAt the doses used in this study, l–methadone potentiated the sedative and analgesic effects and the decrease in arterial oxygenation induced by medetomidine in dogs, which limits the clinical use of this combination.

Dietary flaxseed enhances antioxidant defenses and is protective in a mouse model of lung ischemia-reperfusion injury

Dietary flaxseed (FS) is a nutritional whole grain with high contents of omega-3 fatty acids and lignans with anti-inflammatory and antioxidant properties. We evaluated FS in a murine model of pulmonary ischemia-reperfusion injury (IRI) by dietary supplementation of 0% (control) or 10% (treatment) FS before IRI. Mice fed 0% FS undergoing IRI had a significant decrease in arterial oxygenation (Pa(O(2))) and a significant increase in bronchoalveolar lavage (BAL) protein compared with sham-operated mice. However, mice fed 10% FS undergoing IRI had a significant improvement in both Pa(O(2)) and BAL protein compared with mice fed 0% FS undergoing IRI. In addition, oxidative lung damage was decreased in 10% FS-supplemented mice undergoing IRI, as assessed by malondialdehyde levels. Immunohistochemical staining of lungs for iPF(2alpha)-III F(2) isoprostane, a measure of lipid oxidation, was diminished. FS-supplemented mice had less reactive oxygen species (ROS) release from the vascular endothelium in lungs in an ex vivo model of IRI, and alveolar macrophages isolated from FS-fed mice had significantly reduced ROS generation in response to oxidative burst. Pulmonary microvascular endothelial cells produced less ROS in a flow cessation model of ischemia when preincubated with purified FS lignan metabolites. Pharmacological inhibition of heme oxygenase-1 (HO-1) resulted in only a partial reduction of FS protection in the same model. We conclude that dietary FS is protective against IRI in an experimental murine model and that FS affects ROS generation and ROS detoxification via pathways not limited to upregulation of antioxidant enzymes such as HO-1.

Atrial Septostomy Decreases Sympathetic Overactivity in Pulmonary Arterial Hypertension

We have reported previously that the sympathetic nervous system is activated in patients with pulmonary arterial hypertension (PAH), and that this is only partly explained by a decrease in arterial oxygenation. Possible causes for increased muscle sympathetic nerve activity (MSNA) in patients with PAH include right atrial distension and decreased cardiac output. Both may be improved by atrial septostomy, but this intervention also further decreases arterial oxygenation. In the present study, we wanted to investigate the effect of atrial septostomy on MSNA in patients with PAH. We recorded BP, heart rate (HR), arterial O2 saturation (SaO2), and MSNA before and after atrial septostomy in PAH patients (mean [+/- SE] age, 48 +/- 5 years) and in closely matched control subjects. Measurements were also performed after septostomy, while SaO2 was brought to the preprocedure level by supplemental O2 therapy. Compared to the control subjects (n = 10), the PAH patients (n = 11) had a lower mean BP (75 +/- 2 vs 96 +/- 3 mm Hg, respectively; p < 0.001), lower mean SaO2 (92 +/- 1% vs 97 +/- 0%, respectively; p < 0.001), increased mean HR (84 +/- 4 vs 68 +/- 3 beats/min; p < 0.01), and markedly increased mean MSNA (76 +/- 5 vs 29 +/- 2 bursts per minute; p < 0.001). Atrial septostomy decreased mean SaO2 (to 85 +/- 2%; p < 0.001) and mean MSNA (to 69 +/- 4 bursts per minute; p < 0.01), but did not affect HR or BP. Therapy with supplemental O2 did not affect MSNA, BP, or HR. The decrease in MSNA was correlated to the decrease in right atrial pressure (r = 0.62; p < 0.05). Atrial septostomy in PAH patients decreases sympathetic hyperactivity despite an associated decrease in arterial oxygenation, and this appears to be related to decreased right atrial distension.

A Comparison of the Effects of Isoflurane Verus Propofol Anesthesia on Blood Gas Parameters during One Lung Ventilation for Lung Surgery

Background: During one-lung ventilation (OLV) for thoracic surgery, hypoxic pulmonary vasoconstriction (HPV) may reduce venous admixture and ameliorate the decrease in arterial oxygenation by diverting blood from the non-ventilated to the ventilated lung. Volatile anesthethics are the drugs of choice in thoracic surgery despite numerous experimental data showing their inhibiting effect on the HPV. The object of the present study was to compare the effects of propofol with those of isoflurane on oxygenation & shunt during two lung ventilation (TLV) and OLV in human volunteers.Methods: Thirty patients who needed OLV for an elective thoracic surgery were randomly assigned to receive either isoflurane (1 MAC isoflurane + fentanyl + vecuronium, n = 15) or propofol (2-3g/ dl propofol + fentanyl + vecuronium, n = 15) with 100% oxygen in separate groups. Systemic hemodynamic data was recorded, and blood gas values were obtained 30 min after the start of TLV (TLV-30) and 30, 45 and 60 min after the start of OLV (OLV-30, 45, 60) in the lateral position. Results: A significant reduction in PaO2 and increase in shunt fractions at all study times after the start of OLV compared with TLV were observed in both groups at OLV-30, 45 and 60. Percent changes of PaO2 and shunt of OLV-60 to those of TLV-30 were less in the propofol group than the isoflurane group. Other blood gas data (SaO, S￣ｖO, PaCO, P￣ｖCO, pH, Hb, CaO2 and C￣ｖO) and systemic hemodynamics (mean arterial blood pressure, heart rate and central venous pressure) were not different after the start of OLV compared with TLV in either group. Conclusions: TIVA with propofol was superior than isoflurane anesthesia in terms of arterial blood oxygenation and pulmonary shunting during OLV for lung surgery.

Neutrophil number and interleukin-8 and elastase concentrations in bronchoalveolar lavage fluid correlate with decreased arterial oxygenation after cardiopulmonary bypass.

Atelectasis is a major cause of decreased arterial oxygenation after cardiopulmonary bypass (CPB). There is a close relationship between atelectasis and inflammatory responses. We therefore tested the hypothesis that neutrophil number and the concentrations of proinflammatory cytokines and elastase in plasma and bronchoalveolar lavage fluid correlate with changes in arterial oxygenation. Bronchoalveolar lavage was performed just after the induction of anesthesia and at the end of surgery in 80 patients undergoing CPB. Peripheral blood was sampled simultaneously. Arterial oxygenation was quantified by PaO(2)/fraction of inspired oxygen (FIO(2)) and intrapulmonary shunt (Q(s)/Q(t)). PaO(2)/FIO(2) and Q(s)/Q(t) decreased significantly at the end of surgery, whereas neutrophil number, interleukin (IL)-6, IL-8, tumor necrosis factor-alpha, and elastase concentrations in the lavage fluid increased significantly. The increase in neutrophil count from the lavage fluid correlated significantly with the increases in IL-8 and elastase concentrations. The increase in neutrophil number and IL-8 and elastase concentrations in the lavage fluid correlated significantly with PaO(2)/FIO(2) and Q(s)/Q(t) at the end of surgery. In contrast, none of the plasma values correlated with these variables. Significant correlation between immune mediators and decreased arterial oxygenation suggests that inflammatory responses in the distal airway are strongly related to a decrease in arterial oxygenation after CPB.

Percutaneous balloon dilatation of the atrial septum: immediate and midterm results.

To assess the effectiveness of atrial septostomy by percutaneous balloon dilatation in patients with congenital heart defects or primary pulmonary hypertension. Twenty three patients (15 boys, eight girls; aged 10 days to 10 years; 17 with congenital heart defects and six with primary pulmonary hypertension), all haemodynamically unstable under optimal medical treatment, underwent atrial septostomy by percutaneous balloon dilatation. The balloon catheter entered the left atrium through a patent foramen ovale (n = 14) or via transseptal puncture in cases with an intact atrial septum (n = 9). The size of the balloons used ranged from 13 to 18 mm. There were no complications. The interatrial communication (mm) increased (P < 0.05) after dilatation and remained unchanged (P = NS) during a 16.6 (13.8) month follow up (2 (1.7) v 8.8 (1.4) v 8.2 (1.1), respectively). Transatrial gradient (mm Hg) fell and arterial oxygenation (%) improved both in patients with transposition (6.3 (0.8) v 0.8 (1) (P = 0.0001) and 40.6 (4.2) v 76.5 (4.8) (P = 0.0001), respectively) and in those with mitral atresia (13.4 (1.9) v 2 (1.4) (P = 0.0001) and 77.1 (3.9) v 81.5 (4.2) (P = 0.008), respectively). There were two failures, one early and one late, both in the group of patients with mitral atresia or stenosis. A decrease in arterial oxygenation (94.8 (1.5) v 83 (2.4), P = 0.004) and an increase in left atrial pressure (6.8 (0.9) v 8.3 (1.2), P = 0.02) and cardiac index (2.3 (0.2) v 3.1 (0.2) l/min/m2, P = 0.002) was observed in patients with primary pulmonary hypertension. Percutaneous balloon dilatation is an effective and safe procedure for creating an adequate interatrial communication that can be used as an alternative to blade septostomy.

Antagonism of detomidine with tolazoline in isoflurane-anaesthetised ponies

The effects of tolazoline (4.0 mg/kg iv) antagonism of detomidine (0.02 mg/kg iv) were evaluated in isoflurane-anaesthetised, ventilated ponies. Each of 6 ponies received both tolazoline and saline treatment during separate anaesthetic episodes only (no surgery was performed). Detomidine administration produced an increase in blood pressure, decrease in heart rate and decrease in PaO2 Tolazoline treatment transiently increased heart rate while blood pressure returned to baseline after both treatments. Arterial oxygenation decreased further after tolazoline treatment while oxgenation recovered towards baseline with saline treatment. No other cardiopulmonary effects were detected. Recovery from anaesthesia tended to be more rapid when detomidine was antagonized. The potential benefit of antagonizing detomidine-induced bradycardia with tolazoline, during isoflurane anaesthesia should be weighed against the potential to produce a decrease in arterial oxygenation. The mechanism for this effect is not clear.

High-frequency jet ventilation vs continuous positive airway pressure for differential lung ventilation in patients undergoing resection of thoracoabdominal aortic aneurysm

Twenty patients, scheduled for surgical resection of thoracoabdominal aortic aneurysm were divided into two groups according to the type of differential lung ventilation used during graft replacement of the descending thoracic aorta. In the high-frequency jet ventilation (HFJV) group of ten patients, HFJV was applied to the left lung once collapsed and retracted by the surgeon, the patient lying in the right lateral decubitus and being intubated by a Carlens' tube. In the continuous positive airway pressure (CPAP) group of ten patients, CPAP was applied to the left lung at the same mean airway pressure as HFJV (1 kPa). Before anaesthetic induction, an arterial and a Swan-Ganz catheter were inserted for cardiovascular monitoring. The same anaesthetic technique using fentanyl 6 micrograms.kg-1, flunitrazepam 0.02 mg.kg-1 and pancuronium 0.1 mg.kg-1 was used for each patient. Haemodynamic and respiratory measurements were made; 15 min after positioning the patients in the right lateral decubitus using two-lung ventilation; 15 min after collapse and retraction of the left lung using one-lung ventilation and 15 min after using differential lung ventilation with CPAP or HFJV. Left lung collapse with conventional one-lung ventilation induced a dramatic decrease in arterial oxygenation: PaO2/FIO2 ratio decreased from 43 +/- 6 kPa to 20 +/- 8 kPa, alveolo-arterial oxygen difference increased from 24 +/- 7 kPa to 72 +/- 11 kPa and pulmonary shunt increased from 17 +/- 2% to 37 +/- 3%. Whereas differential lung ventilation with CPAP did not improve any of the respiratory parameters measured, differential lung ventilation with HFJV, significantly increased PaO2/FIO2 ratio to 41 +/- 14 kPa.(ABSTRACT TRUNCATED AT 250 WORDS)

Intravenously Administered Atrial Natriuretic Factor in Patients With COPD: Effects on Ventilation-Perfusion Relationships and Pulmonary Hemodynamics

The potent pulmonary vasodilating property of atrial natriuretic factor (ANF) may alter gas exchange in patients with COPD. We examined the hemodynamic and gas exchange responses to intravenous infusion of ANF (0.01 and 0.03 ng/min/kg body weight) in eight stable patients with COPD studied during spontaneous breathing, using the inert gas elimination technique. When compared with baseline, ANF infusion was associated with a dose-dependent decrease in pulmonary artery pressure (from 27.3 +/- 2.5 to 23.9 +/- 1.8 and 20.2 +/- 1.7 mm Hg, respectively) and a dose-dependent increase in blood flow perfusing poorly ventilated and unventilated units (VA/Q < 0.1: from 5.80 +/- 2.05 to 7.25 +/- 2.5 and 12.0 +/- 5.4 percent of total blood flow, respectively; p = 0.02). However, PaO2 remained unchanged (70.2 +/- 3.6, 68.1 +/- 3.8 65.4 +/- 3.5 mm Hg, respectively) because of a significant increase in minute ventilation (VE) from 8.6 +/- 0.8 to 9.6 +/- 0.8 and 10.3 +/- 0.7 L/min (p < 0.002). Six additional COPD patients receiving intravenously administered ANF at the same dosages were studied during controlled mechanical ventilation using right heart catheterization. In these patients, pulmonary vasodilation was associated with a significant increase in venous admixture (from 12.7 +/- 2.4 to 14.4 +/- 2.9 and 17.5 +/- 3.5 percent of total blood flow, respectively; p < 0.02), and a dose-dependent reduction in arterial PO2 (from 117 +/- 17 to 110 +/- 15 and 96.4 +/- 8.8 mm Hg, respectively; p < 0.05). The present results show that ANF infusion is associated with alterations in the VA/Q relationship in patients with COPD. However, a decrease in arterial oxygenation may be prevented by an increase in VE.