Alveolar-arterial Oxygen Gradient Research Articles

Evaluation of clinical prognostic factors for interstitial pneumonia in anti-MDA5 antibody-positive dermatomyositis patients

Objectives: We retrospectively investigated clinical prognostic factors for interstitial pneumonia (IP) in anti-melanoma differentiation-associated gene 5 (MDA5) antibody (Ab)-positive dermatomyositis (DM) patients.Methods: Subjects comprised 18 patients with anti-MDA5 Ab-positive DM-IP (9 survivors; 9 deaths).Results: Initial serum albumin levels, ferritin levels, and ground-glass opacity (GGO) scores in the right middle lobes were significantly higher in the death group than in the survivor group (p = .033, .013, and .005, respectively). Initial alveolar-arterial oxygen gradient (P[A-a]O2) was also higher in the death group than in the survivor group (p = .064). Initial serum ferritin, P[A-a]O2, and right middle lobe GGO score were found to significantly relate to death. Survival rates after 24 weeks were significantly lower among patients with an initial ferritin level of ≥450 ng/mL (25%), P[A-a]O2 of ≥30 mmHg (31%), and a right middle lobe GGO score of ≥2 (11%) than each of the others (p = .006, .020, and .002, respectively).Conclusions: An initial serum ferritin level of ≥450 ng/mL, P[A-a]O2 of ≥30 mmHg, and right middle lobe GGO score of ≥2 (GGO ≥5% of the lobe) were identified as poor prognostic factors for anti-MDA5 Ab-positive DM-IP patients.

Pulmonary vascular resistance index during coronary artery bypass surgery with aprotinin

Low pulmonary vascular resistance index (PVRI) reflects favorable redundant pulmonary circulation following coronary artery bypass grafting with cardiopulmonary bypass surgery (CPB). This randomized study investigated whether aprotinin given in different modalities impacts PVRI after coronary artery bypass grafting. A total of 40 patients undergoing coronary artery bypass grafting were randomized to four groups according to aprotinin dose: (1) high dose, (2) early low dose, (3) late low dose, and (4) without aprotinin. Oxygenation index, pulmonary shunt, alveolar-arterial oxygen gradient and PVRI were determined. PVRI was calculated as the transpulmonary pressure gradient divided by cardiac index multiplied by 80. The results showed that PVRI remained relative low in all patients provided aprotinin regardless of treatment dosage; PVRI increased at 4 h after restarting ventilation after CPB in patients without aprotinin as compared with aprotinin (266 ± 137, 266 ± 115, 244 ± 86 vs. 386 ± 121, dynes-s-cm−5, respectively, p = .047). Elevated postoperative PVRI was predictive for patients without aprotinin (AUC 0.668; SE 0.40; p < .0001; CI 0.590–0.746). There were no statistical differences in oxygenation index, pulmonary shunt or alveolar-arterial oxygen gradient between the groups. In conclusion, aprotinin maintains a low PVRI in elective patients with healthy lungs during CPB. We suggest that aprotinin maintains pulmonary arterial endothelial integrity.

Postinduction butorphanol administration alters oxygen consumption to improve blood gases in etorphine-immobilized white rhinoceros

ObjectiveTo investigate the effects of postinduction butorphanol administration in etorphine-immobilized white rhinoceros on respiration and blood gases. Study designRandomized crossover study. AnimalsA group of six sub-adult male white rhinoceros. MethodsEtorphine, or etorphine followed by butorphanol 12 minutes after recumbency, was administered intramuscularly [2.5 mg etorphine, 25 mg butorphanol (1000–1250 kg), or 3.0 mg etorphine, 30 mg butorphanol (1250–1500 kg)]. Sampling started at 10 minutes after initial recumbency, and was repeated at 5 minute intervals for 25 minutes. Arterial blood gases, limb muscle tremors, expired minute ventilation and respiratory frequency were measured at each sampling point. Calculated values included alveolar–arterial oxygen gradient [P(A-a)O2], expected respiratory minute volume (V˙e), tidal volume (Vt), oxygen consumption (V˙O2) and carbon dioxide production (V˙CO2). ResultsEtorphine administration resulted in an initial median (range) hypoxaemia [arterial partial pressure of oxygen 25.0 (23.0–28.0) mmHg], hypercapnia [arterial partial pressure of carbon dioxide 76.2 (67.2–81.2) mmHg], increased P(A-a)O2 [41.7 (36.6–45.1) mmHg, V˙O2 [11.1 (10.0–12.0) L minute−1] and muscle tremors. Butorphanol administration was followed by rapid, although moderate, improvements in arterial partial pressure of oxygen [48.5 (42.0–51.0) mmHg] and arterial partial pressure of carbon dioxide [62.8 (57.9–75.2) mmHg]. In rhinoceros administered butorphanol, V˙O2 [4.4 (3.6–5.1) L minute−1] and V˙CO2 [4.2 (3.8–4.4) L minute−1] were lower than in those not administered butorphanol. Increased arterial oxygen tension was associated with lower oxygen consumption (p=0.002) which was positively associated with lower muscle tremor scores (p<0.0001). Conclusions and clinical relevanceHypoxaemia and hypercapnia in etorphine-immobilized rhinoceros resulted from an increased [P(A-a)O2] and increased V˙O2 and V˙CO2 associated with muscle tremors. Rather than being associated with changes in V˙e, it appears that improved blood gases following butorphanol administration were a consequence of decreased V˙O2 associated with reduced muscle tremoring.

Comprehensive, noninvasive saturation, oxygen, and pressure index: Does it reflect the severity of acute respiratory illness in neonates on continuous positive airway pressure? a prospective study

Background: The severity of respiratory illness in neonates on invasive ventilatory support is assessed by oxygenation index and alveolar–arterial oxygen gradient (A-aDO2). Both these parameters need arterial blood gas estimation which is an invasive procedure with attendant complications. Neonates with less severe respiratory disease are managed on continuous positive airway pressure (CPAP). The progress of the disease is generally assessed by noting the changes in FiO2and positive end-expiratory pressure (PEEP) provided. Blood gas analysis is done for objectively assess the babies who progress to more severe disease. A noninvasive tool such as saturation, oxygen, and pressure index (SOPI) helps in reducing the need for invasive blood gas estimation. A good correlation of SOPI with A-aDO2can provide near-continuous bedside assessment of the respiratory disease. Objective: To determine the correlation between SOPI and A-aDO2. Materials and Methods: All babies admitted to our neonatal unit requiring CPAP were considered eligible for this study. The adjustments in FiO2, CPAP pressures, and arterial blood gas were done as per unit protocol. A-aDO2was calculated. SOPI was calculated as (PEEP × FiO2)/SpO2. The two values were then correlated. Results: Seventy-five babies were recruited. SOPI correlated positively (r = 0.847) with A-aDO2(P

Intratracheal Instillation of Perfluorohexane Modulates the Pulmonary Immune Microenvironment by Attenuating Early Inflammatory Factors in Patients With Smoke Inhalation Injury: A Randomized Controlled Clinical Trial.

Smoke inhalation injury (SII) is associated with significant morbidity and mortality in burn patients, and effective treatments are lacking. Perfluorocarbons (PFCs) have a protective effect against acute lung injury. We aimed to assess the therapeutic effects of perfluorohexane on burn patients with SII. Patients with burns complicated by moderately severe SII were randomly divided into control (n = 11) and PFC groups (n = 12). The control group received conventional treatment (anti-infection, nutritional support, antishock measures, and supportive treatment). The PFC group received endotracheal perfluorohexane instillation in addition to conventional treatment. On admission and 3 days later, therapeutic effects were evaluated and inflammatory mediators in bronchoalveolar lavage fluid and plasma were analyzed. There was no significant difference between the control and PFC group on admission. After 3 days, perfluorohexane treatment significantly (P < .05) increased lung dynamic compliance, and reduced alveolar-arterial oxygen gradient, Acute Physiology and Chronic Health Evaluation II score, percentage of neutrophils, and levels of interleukin-6, interleukin-8, and tumor necrosis factor alpha in bronchoalveolar lavage fluid; there was no significant change in the control group before and after treatment. Intratracheal instillation of perfluorohexane modulates the pulmonary immune microenvironment and supplements current conventional treatments for burn patients with SII.

A Possible Case of Neurogenic Pulmonary Edema in a Sheep following Intracranial Surgery

Abstract Objective: To describe presentation, treatment and outcome of a sheep that developed acute respiratory distress after intracranial surgery. Case summary: A 3-year-old female crossbred sheep weighing 64 kg was anaesthetized for intracranial surgery as a part of a research project. Premedication and induction of anesthesia were uneventful as well as tracheal intubation. Anesthesia was maintained with isoflurane in a 50% mixture of oxygen and air, fentanyl (5-15 μg kg-1h-1) and lidocaine (1.8 mg kg-1h-1). During anesthesia, an increased alveolar-arterial oxygen gradient was calculated on the basis of arterial blood gas analysis: inspiratory fraction of oxygen was increased and a recruitment manoeuvre was performed. After 210 minutes of anesthesia, the sheep was let recover with oxygen supplementation under monitoring of pulse-oxymetry, capnography, inspired and expired oxygen, temperature and invasive blood pressure. At tracheal extubation no signs of regurgitation or aspiration were noticed. Twenty-five minutes later, the sheep showed deterioration of neurological status and clonic seizure responsive to diazepam. After transient tachycardia, blood pressure rose acutely and sinus bradycardia followed. Severe tachypnea started in few minutes accompanied by loud respiratory noises and harsh diffuse crackles on both sides of the thorax. Foamy blood nasal exudates discharged from the nostrils. Neurogenic pulmonary edema as a sequel of increased intracranial pressure was suspected and treated with intravenous mannitol (0.5 gkg-1) and furosemide (4 mgKg-1). Hypoxemia was successfully managed with oxygen supplementation. Motor and cognitive functions improved progressively and were deemed normal within 12 hours from the episode, when arterial partial pressure of oxygen was 11.7 kPa (88 mmHg) at room air. New information provided: Severe pulmonary complications may be observed after iatrogenic neurological injury in sheep. Neurogenic pulmonary edema should be taken into account among the differential diagnoses of abrupt respiratory distress following seizure.

The Impact of Hypoxaemia on the Outcome in Liver Cirrhosis.

Prognostic factors for poor evolution are critical in the setting of limited access to liver transplantation for patients with cirrhosis. We aimed to investigate the impact of hypoxaemia on the outcome in cirrhosis and the evolution of arterial oxygen tension during long-term follow-up in these patients. Consecutive cirrhotic patients were prospectively enroled and followed-up in our tertiary referral center. Clinical features, biological tests, arterial blood gases, NT-proBNP levels, pulse oximetry measurements, 12-lead ECG, and transthoracic contrast echocardiography were documented on enrolment. The main outcomes were death and decompensation due to liver disease. 87 cirrhotic patients were included in the analysis and followed-up for a mean of 16 months. At enrolment, 27 (31%) patients were hypoxaemic, 19 had hepatopulmonary syndrome (HPS), but only 6 of those who were sampled at follow-up had persistent hypoxaemia. During the study period, 22 patients died of liver-related complications. Nine of them (41%) were hypoxaemic on enrolment but none had severe hypoxaemia. Hypoxaemia present at enrollment was not a risk factor for death (p=0.29) or decompensation of liver disease (p=0.7). A higher MELD score at baseline or increase during follow-up was a risk factor for death (p=0.02) and correlated with the presence of hypoxaemia. Normalization of the arterial oxygen levels was accompanied by a significant decrease in NT-proBNP (83 pg/ml vs 0 pg/mL, p=0.023). Mild and moderate hypoxaemia was frequent in our patients but was not associated with adverse outcome in cirrhosis. Repeated arterial blood gas sampling is advisable, especially in patients diagnosed with hepatopulmonary syndrome.

Role of splenic reservoir monocytes in pulmonary vascular monocyte accumulation in experimental hepatopulmonary syndrome.

Background and AimPulmonary monocyte infiltration plays a significant role in the development of angiogenesis in experimental hepatopulmonary syndrome (HPS) after common bile duct ligation (CBDL). Hepatic monocytes are also increased after CBDL, but the origins remain unclear. Splenic reservoir monocytes have been identified as a major source of monocytes that accumulate in injured tissues. Whether splenic monocytes contribute to monocyte alterations after CBDL is unknown. This study evaluates monocyte distributions and assesses effects of splenectomy on monocyte levels and pulmonary vascular and hepatic abnormalities in experimental HPS.MethodsSplenectomy was performed in CBDL animals. Monocyte levels in different tissues and circulation were assessed with CD68. Pulmonary alterations of HPS were evaluated with vascular endothelial growth factor‐A (VEGF‐A) levels, angiogenesis, and alveolar–arterial oxygen gradient (AaPO2). Liver abnormalities were evaluated with fibrosis (Sirius red), bile duct proliferation (CK‐19), and enzymatic changes.ResultsMonocyte levels increased in the lung and liver after CBDL and were accompanied by elevated circulating monocyte numbers. Splenectomy significantly decreased monocyte accumulation, VEGF‐A levels, and angiogenesis in CBDL animal lung and improved AaPO2 levels. In contrast, hepatic monocyte levels, fibrosis, and functional abnormalities were further exacerbated by spleen removal.ConclusionsSplenic reservoir monocytes are a major source for lung monocyte accumulation after CBDL, and spleen removal attenuates the development of experimental HPS. Liver monocytes may have different origins, and accumulation is exacerbated after depletion of splenic reservoir monocytes. Tissue specific monocyte alterations, influenced by the spleen reservoir, have a significant impact on pulmonary complications of liver disease.

CT Scan Does Not Differentiate Patients with Hepatopulmonary Syndrome from Other Patients with Liver Disease

BackgroundHepatopulmonary syndrome (HPS) is defined by liver dysfunction, intrapulmonary vascular dilatations, and impaired oxygenation. The gold standard for detection of intrapulmonary vascular dilatations in HPS is contrast echocardiography. However, two small studies have suggested that patients with HPS have larger segmental pulmonary arterial diameters than both normal subjects and normoxemic subjects with cirrhosis, when measured by CT. We sought to compare CT imaging-based pulmonary vasodilatation in patients with HPS, patients with liver dysfunction without HPS, and matching controls on CT imaging.MethodsWe performed a retrospective cohort study at two quaternary care Canadian HPS centers. We analyzed CT thorax scans in 23 patients with HPS, 29 patients with liver dysfunction without HPS, and 52 gender- and age-matched controls. We measured the artery-bronchus ratios (ABRs) in upper and lower lung zones, calculated the “delta ABR” by subtracting the upper from the lower ABR, compared these measurements between groups, and correlated them with clinically relevant parameters (partial pressure of arterial oxygen, alveolar-arterial oxygen gradient, macroaggregated albumin shunt fraction, and diffusion capacity). We repeated measurements in patients with post-transplant CTs.ResultsPatients had significantly larger lower zone ABRs and delta ABRs than controls (1.20 +/- 0.19 versus 0.98 +/- 0.10, p<0.01; and 0.12 +/- 0.17 versus -0.06 +/- 0.10, p<0.01, respectively). However, there were no significant differences between liver disease patients with and without HPS, nor any significant correlations between CT measurements and clinically relevant parameters. There were no significant changes in ABRs after liver transplantation (14 patients).ConclusionsBasilar segmental artery-bronchus ratios are larger in patients with liver disease than in normal controls, but this vasodilatation is no more severe in patients with HPS. CT does not distinguish patients with HPS from those with uncomplicated liver disease.

Prevalence, Severity, and Prognostic Effect of Hepatopulmonary Syndrome in Liver Transplant Candidates.

Hepatopulmonary syndrome (HPS) is commonly encountered in the setting of end-stage liver disease (ESLD). Past studies have reported conflicting results in terms of demonstrating an association between HPS and mortality. The aim of this study was to determine the prevalence of HPS in patients with ESLD referred for assessment of transplantation suitability. In addition, we investigated survival rates in the setting of HPS, with and without liver transplantation. The medical records of 524 consecutive patients with ESLD evaluated for potential liver transplantation were retrospectively reviewed. HPS was defined by a reduced partial pressure of oxygen or an elevated alveolar-arterial oxygen gradient and the presence of intrapulmonary vascular dilatation on contrast-enhanced echocardiography. In total, 57 subjects (12%) fulfilled the diagnostic criteria of HPS; 88% of these had mild to moderate HPS. For patients with HPS, the overall survival rates at 1 and 3 years were 95% and 92%, respectively. Liver transplants were received by 245 patients (53%), 26 of whom had HPS. For transplant recipients with HPS, the overall survival rates at 1 and 3 years were 96% and 91%, respectively, compared to 85% and 80% in subjects without HPS. Post-transplantation survival in patients with and without HPS did not differ significantly (HR=0.489, 95% CI: 0.153-1.564; p=0.228). This study demonstrated a high prevalence of IPVD and HPS among patients who were potential candidates for liver transplantation. HPS was mild to moderate in the majority of those affected and had no significant effect on overall survival.

Le syndrome hépato-pulmonaire

Hepatopulmonary syndrome (HPS) is defined by the association of portal hypertension, increased alveolar-arterial oxygen gradient and intrapulmonary vascular dilations. Pathophysiological mechanisms of hypoxemia are characterized by ventilation-perfusion mismatch, oxygen diffusion limitation between alveolus and the centre of the dilated capillary, and right-to-left shunting. An excess of vasodilator molecules (like nitric monoxide) and proangiogenic factors (like VEGF) play an important role in the occurrence of HPS. Symptoms of HPS are not specific and dominated by a progressive dyspnea in upright position. Pulse oximetry is a simple non-invasive screening test but only detect the most severe forms of HPS. Medical treatment is disappointing and only liver transplantation may lead to resolution of HPS. Survival following liver transplantation is promising when hypoxemia is not severely decreased.

Effect of positive end-expiratory pressure on intraoperative pulmonary function in patients undergoing urological retroperitoneal laparoscopic surgery in mode of protective ventilation

Objective To evaluate the effect of positive end-expiratory pressure (PEEP) on intraoperative pulmonary function in the patients undergoing urological retroperitoneal laparoscopic surgery in the mode of protective ventilation. Methods Forty patients of both sexes, aged 30-64 yr, with body mass index of 16-29 kg/m2, of American Society of Anesthesiologists physical status Ⅰ or Ⅱ, scheduled for elective retroperitoneal laparoscopic ureterolithotomy, were randomly divided into 2 groups (n=20 each) using a random number table: control group (group C) and PEEP group (group P). After induction of general anesthesia, the patients were endotracheally intubated.Intermittent positive pressure ventilation (tidal volume [VT] 6 ml/kg, respiratory rate [RR] 12 breaths/min, inspiratory/expiratory ratio [I∶E] 1∶2, fraction of inspired oxygen 50%) was performed from the end of intubation until the onset of pneumoperitoneum.After the onset of pneumoperitoneum, the patients were ventilated (VT 6 ml/kg, RR 22 breaths/min, I∶E 1.0∶1.5), and the end-tidal pressure of carbon dioxide was maintained at 35-45 mmHg in group C. After the onset of pneumoperitoneum, the patients were ventilated (VT 6 ml/kg, RR 22 breaths/min, I∶E 1.0∶1.5, PEEP 5 cmH2O), and the end-tidal pressure of carbon dioxide was maintained at 35-45 mmHg in group P. At 5 min before pneumoperitoneum (T1), at 10, 30 and 60 min of pneumoperitoneum (T2-4), immediately after the end of pneumoperitoneum (T5), and at 5 min before extubation (T6), arterial blood samples were collected for blood gas analysis.Peak airway pressure and mean airway pressure were also recorded.Dynamic lung compliance, oxygenation index, respiratory index, dead space fraction and alveolar-arterial oxygen gradient were calculated. Results Compared with group C, mean airway pressure was significantly higher at T2-4, oxygenation index was significantly higher at T3, alveolar-arterial oxygen gradient difference was significantly lower at T3 and T6, and respiratory index was significantly lower at T6 (P 0.05). Conclusion PEEP (5 cmH2O) can improve the intraoperative pulmonary function in the patients undergoing urological retroperitoneal laparoscopic surgery in the mode of protective ventilation. Key words: Positive-pressure respiration; Respiratory function tests; Laparoscopy; Urologic surgical procedures

Hepatopulmonary Syndrome and Liver Transplantation: A Recent Review of the Literature.

A severe and common pulmonary vascular complication of liver disease is hepatopulmonary syndrome (HPS). It is a triad of liver dysfunction and/or portal hypertension, intrapulmonary vascular dilatations, and increased alveolar-arterial oxygen gradient. Prevalence varies according to various study groups from 4%–47%. While the most common presenting symptom of HPS is dyspnea, it is usually asymptomatic, and thus all liver transplant candidates should be screened for its presence. Pulse oximetry is a useful screening method, but arterial blood gas examination is the gold standard. If there is an abnormal P (A-a)O2 gradient, microbubble transthoracic echocardiography should be done for diagnosis. Outcome is unpredictable, and there is currently no effective medical therapy. The only effective therapy is considered to be liver transplantation. Complete resolution of HPS after liver transplantation is seen within a year in most HPS patients.

A Study of Gas-Exchange Variability in the Hepatopulmonary Syndrome

The hepatopulmonary syndrome (HPS) is a rare condition defined as the triad of cirrhosis, intrapulmonary vascular dilatations (IPVDs), and abnormal gas-exchange. Recently, there has been controversy in the scientific literature regarding the criterion for abnormal gas-exchange that should be used in this syndromic definition. Although current expert recommendations call for an alveolar-arterial oxygen gradient cutoff of &gt;20 mm Hg (a low threshold cutoff), other authors have suggested higher threshold cutoffs. In our clinical experience, we have noted significant variability in the alveolar-arterial oxygen gradient over time among patients with possible HPS. Our objectives were to characterize and formally describe this variability in order to propose a new, more stable diagnostic cutoff. We analyzed longitudinal gas-exchange data over five years from 58 patients who were referred to the Toronto HPS Clinic. Each patient had an average of 4.19 visits on file. Using the expert recommended cutoffs, we found that 20.69% of patients fluctuate above or below the threshold for abnormal gas-exchange despite stability of clinical symptoms. Using a stricter two-visit partial pressure of arterial oxygen cutoff of &lt;80mm Hg, no patients fluctuate above or below the cutoff. The stricter cutoff also has stronger correlations with clinical indicators of disease progress and severity. The currently recommended cutoffs for abnormal gas-exchange in HPS patients may not be the best threshold to establish a stable diagnosis and distinguish patients with respect to disease progress and severity.

Hepatopulmonary syndrome: What we know and what we would like to know.

Hepatopulmonary syndrome (HPS) is characterized by abnormalities in blood oxygenation caused by the presence of intrapulmonary vascular dilations (IPVD) in the context of liver disease, generally at a cirrhotic stage. Knowledge about the subject is still only partial. The majority of the information about the etiopathogenesis of HPS has been obtained through experiments on animals. Reported prevalence in patients who are candidates for a liver transplantation (LT) varies between 4% and 32%, with a predominance of mild or moderate cases. Although it is generally asymptomatic it does have an impact on their quality of life and survival. The diagnosis requires taking an arterial blood gas sample of a seated patient with alveolar-arterial oxygen gradient (AaO2) ≥ 15 mm Hg, or ≥ 20 mm Hg in those over 64 years of age. The IPVD are identified through a transthoracic contrast echocardiography or a macroaggregated albumin lung perfusion scan ((99m)Tc-MAA). There is currently no effective medical treatment. LT has been shown to reverse the syndrome and improve survival rates, even in severe cases. Therefore the policy of prioritizing LT would appear to increase survival rates. This paper takes a critical and clinical look at the current understanding of HPS, as well as the controversies surrounding it and possible future research.

Factors Determining the Choice of Surgical Procedure in Elderly Patients with Non-Small Cell Lung Cancer

In the elderly patients, optimal surgical treatment can be difficult to achieve, because of comorbidity. Therefore, we aimed to clarify the preferred surgical management in this patient group. A retrospective study was conducted between April 2008 and March 2015 that included patients with non-small cell lung cancer (NSCLC) aged ≥ 75 years. We included 44 patients who underwent partial resection (n = 20) or lobectomy (n = 24). There were no significant differences between the two groups on most variables, except for some character. Survival analysis revealed a significant difference in overall survival (OS) between the two groups; however, no significant differences existed in the disease-free survival or in the OS for stage I disease. Postoperative complications led to poor prognoses. Cox regression analysis revealed statistical significance for the Brinkman Index, the ratio of the pulmonary artery diameter to the ascending aorta diameter (PA:A), and the alveolar-arterial oxygen gradient. Only the PA:A ratio remained significant after multivariate analysis, with a higher ratio associated with better survival. In elderly patients with NSCLC, surgical resection should not be denied because of age alone. However, partial resection should be favored to lobectomy when possible.

Intraoperative cell salvage during cardiac surgery is associated with reduced postoperative lung injury.

In addition to its blood-sparing effects, intraoperative cell salvage may reduce lung injury following cardiac surgery by removing cytokines, neutrophilic proteases and lipids that are present in cardiotomy suction blood. To test this hypothesis, we performed serial measurements of biomarkers of the integrity of the alveolar-capillary membrane, leucocyte activation and general inflammation. We assessed lung injury clinically by the duration of postoperative mechanical ventilation and the alveolar arterial oxygen gradient. Serial measurements of systemic plasma concentrations of interleukin-6 (IL-6), myeloperoxidase, elastase, surfactant protein D (SP-D), Clara cell 16 kD protein (CC16) and soluble receptor for advanced glycation endproducts (sRAGEs) were performed on blood samples from 195 patients who underwent cardiac surgery with the use of a cell salvage (CS) device (CS, n = 99) or without (CONTROL, n = 96). Postoperative mechanical ventilation time was shorter in the CS group than in the CONTROL group [10 (8-15) vs 12 (9-18) h, respectively, P = 0.047]. The postoperative alveolar arterial oxygen gradient, however, was not different between groups. After surgery, the lung injury biomarkers CC16 and sRAGEs were lower in the CS group than in the CONTROL group. Biomarkers of systemic inflammation (IL-6, myeloperoxidase and elastase) were also lower in the CS group. Finally, mechanical ventilation time correlated with CC16 plasma concentrations. The intraoperative use of a cell salvage device resulted in less lung injury in patients after cardiac surgery as assessed by lower concentrations of lung injury markers and shorter mechanical ventilation times.

Cardiopulmonary parameters in propofol- or thiopental-anesthetized dogs induced to pulmonary hypertension by serotonin

ABSTRACTThe cardiopulmonary changes in propofol- or thiopental-anesthetized dogs induced to pulmonary hypertension (PH) were evaluated. Twenty adult animals were randomly assigned to two groups: propofol group (PG) and thiopental group (TG). In PG, propofol was used for induction (8(0.03mg.kg-1) and anesthesia maintenance (0.8mg.kg-1.minute-1), while, in TG, thiopental was used (22±2.92mg.kg-1; 0.5mg.kg-1.minute-1, respectively). Mechanical ventilation using time cycle was started. PH was induced by administration of serotonin (5HT) (10µg.kg-1 and 1mg.kg-1.hour-1) through a thermodilution catheter positioned in the pulmonary artery. The measurements were performed before administration of 5HT (T0), after 30 minutes (T30), then at 15-minute intervals (T45, T60, T75 and T90). No differences between groups were registered for systolic (sPAP) and mean pulmonary arterial pressure (mPAP), mean arterial pressure (MAP), total peripheral resistance index (TPRI) and pulmonary vascular resistance index (PVRI). In PG, sPAP and mPAP increased from T30. While in TG, sPAP and mPAP increased from T75. In PG, heart rate (HR) increased from T30, in which PG was higher than TG. The TPRI values decreased from T30 in PG, and in TG, at T45, T60 and T90. In PG, at T0, PVRI was lower than at other times. In PG, arterial partial pressures of oxygen (PaO2) decreased from T60 and alveolar-arterial oxygen gradient (PA-aO2) increased at T60. In TG, at T0 PaO2 was higher than at T30, T45, T60 and T90, while PA-aO2 at T0 was lower than at T90. From T30 to T90, TG showed higher PaO2 means and lower arterial partial pressures of carbon dioxide (PaCO2) values when compared to PG. In PG, from T30, PaCO2 increased, while in TG this parameter was stable. In conclusion, thiopental anesthesia attenuated the cardiopulmonary changes resulting from serotonin-induced PH, probably by attenuation of vasoconstriction and bronchoconstriction.

Lung perfusion imaging in hepatopulmonary syndrome using 99mTc macroaggregated albumin

Hepatopulmonary syndrome is a serious pulmonary vascular complication in patients with chronic liver disease. It constitutes a triad of chronic liver disease, increased alveolar-arterial oxygen gradient, and evidence of intrapulmonary shunt (IPS). The diagnosis of IPS can be made by bubble echocardiography, technetium-99m-labeled macroaggregated albumin (99mTc-MAA) scintigraphy or pulmonary arteriography. Though echocardiography is a sensitive screening test, MAA scintigraphy can also quantify the extent of shunting.

330 Hepatopulmonary syndrome may mask cystic fibrosis

Clinically significant hepatobiliary manifestations of CF are reported to occur in 15–30% of children and cirrhosis is reported in 5–10% of pediatric populations. A 7 year-old boy consultated to pediatric pulmonology clinic with chronic cough, decreased exercise tolerance for six months and cyanosis for 15 days, in terms of hepatopulmonary syndrome. He was under investigation because of hepatosplenomegaly for one year. Physical examination demonstrated tachypnea, mild clubbing, orthodeoxia (saturation 81–82% in the upright position and 86–88% in the supine position) and common crepitan crackles on the auscaltation. On abdominal examination hepatosplenomegaly were present. The calculated alveolar-arterial oxygen gradient was 43 mmHg. Chest x-ray and CT demonstrated dilated peripheral vasculature and bronchiectasis. Liver function tests, coagulation profiles, serum ceruloplasmin, alpha-1 antitrypsin, antinuclear antibodies, anti smooth muscle antibody were all normal. Endoscopy of upper gastrointestinal tract showed no esophageal varices. Liver biopsy findings resulted as cirrhotic liver showing signs of ascending cholangitis. But definitive diagnosis was not determined for one year. Contrast-enhanced echocardography with agitated saline was compatible with intrapulmonary shunting. Although patient denied recurrent lower respiratory tract infection, diarrhea, malnutrition, CF was diagnosed with p.G85E (c.254G>A), p.I148T (c443T>C) mutation. Cystic fibrosis should be investigated in cirrhotic patients with respiratory signs. Hepatosplenomegaly may be the first sign of CF.