Fall In PaO2 Research Articles

Lung ultrasonography for detection of atelectasis in adults undergoing robot assisted laparoscopic pelvic surgeries

Introduction: Robot-assisted laparoscopic pelvic surgeries are minimally invasive techniques that require the patient to be placed in the steep Trendelenburg position. Pneumoperitoneum further increases the risk of postoperative pulmonary complications. We used lung ultrasound score (LUSS) to detect post-operative atelectasis in this subset of patients.
 Methodology: Patients aged 18 to 70 y with ASA physical status I/II undergoing robot assisted pelvic surgeries in steep Trendelenburg position were enrolled. Patients were mechanically ventilated with 50% oxygen in air with a tidal volume of 6 to 8 ml/kg in volume control mode to maintain an end tidal carbon dioxide at 35−45 mmHg with positive end-expiratory pressure (PEEP) of 5 cmH2O. Ultrasonographic assessment was done; before induction (A), after extubation (F), 12 h (G) and 24 h after surgery (H) by dividing chest into 12 regions.
 Results: A total of 1152 cine-loops acquired during the study period in 32 patients were analyzed. Incidence of postoperative atelectasis was 87.5% and each lung ultrasound examination required 12.35 ± 4.68 min. Statistically significant fall in PaO2 was recorded at extubation from baseline and intra-operative values (P < 0.0001). Statistically significant difference was established between change in baseline and post-extubation LUSS to the total volume of fluid given (P = 0.002).
 Conclusion: A high incidence (87.5%) of atelectasis in adults after robot assisted laparoscopic pelvic surgeries was detected using lung ultrasound score. Lung oxygenation decreased significantly after steep Trendelenburg position and extubation. The observed statistical difference in total IV fluids administered between patient subgroups who showed increased ultrasound signs of lung edema from the A period to the F period, although suggestive of association, is no evidence of causation.
 Abbreviations: ARISCOT- Assess Respiratory Risk in Surgical patients in Catalonia; LUS- Lung Ultrasound; LUSS- Lung Ultrasound Score; OR- Operating room; PEEP- Positive End-Expiratory Pressure
 Key words: LUSS; Lung ultrasound score; Pneumoperitoneum; Robotic Surgery; Ultrasonography
 Citation: Sethi S, Kathuria R, Samra T, Saini V, Toshkhani D, Kushal P. Lung ultrasonography for detection of atelectasis in adults undergoing robot assisted laparoscopic pelvic surgeries. Anaesth. pain intensive care 2023;27(4):573−578; DOI: 10.35975/apic.v27i4.1503
 Received: October 28, 2021; Reviewed: June 06, 2022; Accepted: September 17, 2022

CARDIAC ARRHYTHMIA AND HEMODYNAMIC EFFECTS DURING FIBEROPTIC BRONCHOSCOPY

Background: Arterial hypoxaemia is the commonest complication, since respiratory depressant drugs are used for premedication, and the airway is also partially occluded by the bronchoscope. The study is therefore designed to nd out the changes in arterial oxygen tension during FOB along with effect on central hemodynamics, electrocardiographically. Objectives: · To nd out the changes in arterial oxygen tension during FOB. · To study the effects of beroptic bronchoscopy on central hemodynamics, electrocardiographically. Methods: 100 patients aged 20 years and above undergoing FOB were evaluated for the arterial oxygen tension and cardiac rhythm changes at KNCH, Jodhpur. Results: All patients developed a fall in PaO2 following FOB which was highly signicant but hypoxaemia was noted only in 18 cases. There was a uniform rise in heart rate in all the patients after FOB which was statistically signicant. There was slight sinus tachycardia in most of the cases although E.C.G. indicated no major arrhythmias. There was no signicant change in pH level. Mean of SBP and mean of DBP was statistically signicant. Conclusion: All patients showed a decline in arterial PaO2 after FOB which was highly signicant. There was slight sinus tachycardia in most of cases. FOB itself does not endanger the patients with any signicant or serious complications.

PEAK EXPIRATORY FLOW RATE CHANGES AND HYPOXEMIA DURING FIBEROPTIC BRONCHOSCOPY

Background: Arterial hypoxaemia is the common complication, since respiratory depressant drugs are used for premedication, and the airway is also partially occluded by the bronchoscope. The study is therefore designed to nd out the changes in arterial oxygen tension and PEFR during FOB. Objectives: Ÿ To nd out the changes in arterial oxygen tension and in peak expiratory ow rate during FOB. Methods: 100 patients aged 20 years above undergoing FOB were evaluated for the arterial oxygen tension and peak expiratory ow rate changes at KNCH, Jodhpur. Results: All patients developed a fall in PaO2 following FOB but hypoxemia was noted only in 18 cases. The change in PEFR after FOB, no signicant statistical difference could be observed on statistically comparison. Conclusion: All patients showed a decline in arterial PaO2 after FOB which was highly signicant. FOB itself does not causes any signicant or serious complications.

HYPOXEMIA AND LUNG MECHANICS DURING FIBEROPTIC BRONCHOSCOPY

Background: Arterial hypoxaemia is the common complication, since respiratory depressant drugs are used for premedication, and the airway is also partially occluded by the bronchoscope. The study is therefore designed to nd out the changes in arterial oxygen tension and PFTduring FOB. Objectives: To nd out the changes in arterial oxygen tension and pulmonary function tests during FOB. Methods: One hundred patients aged 20 years above undergoing FOB were evaluated for the arterial oxygen tension and pulmonary function tests changes at KNCH, Jodhpur. Results: All patients developed a fall in PaO2 following FOB but hypoxemia was noted only in 18 cases. Bronchial washing, punch biopsy and brush biopsy did contribute to hypoxemia signicantly. The pulmonary functions which include change in V.C, FVC, FEV1 and PEFR after FOB, no statistical difference could be observed on statistically comparison. Conclusion: All patients showed a decline in arterial PaO2 after FOB which was highly signicant. FOB itself does not cause any signicant or serious complications.

An observational study to find out changes in arterial oxygen tension during fiberoptic bronchoscopy

Background: Arterial hypoxaemia is the commonest complication, since respiratory depressant drugs are used for premedication, and the airway is also partially occluded by the bronchoscope. The study is therefore designed to find out the changes in arterial oxygen tension during (FOB) along with effect on central hemodynamics, pre and post procedure ECG and PFT. Objectives were to find out the changes in arterial oxygen tension during FOB, to study the effects of FOB on central hemodynamics, electrocardiographically and pulmonary function tests.Methods: One hundred patients aged 20 years undergoing FOB were evaluated for the arterial oxygen tension and cardiac rhythm changes at KNCH, Jodhpur during 12 months study period from 2019 to 2020.Results: All patients developed a fall in PaO2 following FOB but hypoxaemia was noted only in 18 cases. Bronchial washing, punch biopsy and brush biopsy did contribute to hypoxaemia significantly. There was a uniform rise in heart rate in all the patients after FOB which was statistically significant. There was slight sinus tachycardia in most of the cases although ECG indicated no major arrhythmias. The pulmonary functions which include change in VC, FVC, FEV1 and PEFR after FOB, on statistically comparison no statistical difference could be observed. There was no significant change in PaCO2 level and pH level. Mean of SBP and mean of DBP was statistically significant.Conclusions: All patients showed a decline in arterial PaO2 after FOB which was highly significant. There was slight sinus tachycardia in most of cases. FOB itself does not endanger the patients with any significant or serious complications.

Pressure-dependent NOS activation contributes to endothelial hyperpermeability in a model of acute heart failure

Aims: Acute increases in left ventricular end diastolic pressure (LVEDP) can induce pulmonary edema (PE). The mechanism(s) for this rapid onset edema may involve more than just increased fluid filtration. Lung endothelial cell permeability is regulated by pressure-dependent activation of nitric oxide synthase (NOS). Herein, we demonstrate that pressure-dependent NOS activation contributes to vascular failure and PE in a model of acute heart failure (AHF) caused by hypertension.Methods and results: Male Sprague–Dawley rats were anesthetized and mechanically ventilated. Acute hypertension was induced by norepinephrine (NE) infusion and resulted in an increase in LVEDP and pulmonary artery pressure (Ppa) that were associated with a rapid fall in PaO2, and increases in lung wet/dry ratio and injury scores. Heart failure (HF) lungs showed increased nitrotyrosine content and ROS levels. L-NAME pretreatment mitigated the development of PE and reduced lung ROS concentrations to sham levels. Apocynin (Apo) pretreatment inhibited PE. Addition of tetrahydrobiopterin (BH4) to AHF rats lung lysates and pretreatment of AHF rats with folic acid (FA) prevented ROS production indicating endothelial NOS (eNOS) uncoupling.Conclusion: Pressure-dependent NOS activation leads to acute endothelial hyperpermeability and rapid PE by an increase in NO and ROS in a model of AHF. Acute increases in pulmonary vascular pressure, without NOS activation, was insufficient to cause significant PE. These results suggest a clinically relevant role of endothelial mechanotransduction in the pathogenesis of AHF and further highlights the concept of active barrier failure in AHF. Therapies targetting the prevention or reversal of endothelial hyperpermeability may be a novel therapeutic strategy in AHF.

The use of Transnasal Humidified Rapid-Insufflation Ventilatory Exchange (THRIVE) for pre-oxygenation in neurosurgical patients: a randomised controlled trial.

This study explored the use of high-flow nasal oxygen (HFNO) in both pre-oxygenation and apnoeic oxygenation in adults who were intubated following a non-rapid sequence induction. Fifty patients were randomised to receive pre-oxygenation via a standard facemask or the Transnasal Humidified Rapid-Insufflation Ventilatory Exchange (THRIVE) device. After five minutes of pre-oxygenation, induction and muscle relaxant agents were given. While waiting for complete paralysis, patients in the standard facemask group received bag-mask ventilation (BMV), whereas patients in the HFNO group received apnoeic oxygenation via the THRIVE device. Serial blood samples for arterial blood gas analysis were taken. Baseline patient and airway characteristics were similar. The median PaO₂ after pre-oxygenation was 357 (interquartile range [IQR] 324-450 [range 183-550]) mmHg in the facemask group, compared to 471 (IQR 429-516 [range 185-550]) mmHg in the HFNO group (<i>P</i>=0.01). The median arterial partial pressure of oxygen (PaO₂) in the HFNO group decreased after a period of apnoeic oxygenation, and was significantly lower when compared to patients who received BMV in facemask group. The arterial carbon dioxide partial pressure (PaCO₂) level after complete paralysis was significantly higher in the HFNO group when compared to the facemask group (median 52 [IQR 48-55 {range 40-65}] versus median 43 [IQR 40-48 {range 35-63}] mmHg, <i>P</i>=0.0005 and <i>P</i>=0.004 respectively). There were no differences in the time to muscle paralysis and time to intubation. Seven patients required use of airway adjuncts during BMV in the facemask group, compared to none in the HFNO group (<i>P</i>=0.004). No complications were observed in either group. HFNO produces a higher PaO₂ after pre-oxygenation and safe PaO₂ during intubation. However, the subsequent fall in PaO₂ and rise in PaCO₂ indicates that it is not as effective as BMV in maintaining oxygenation and ventilation following neuromuscular blockade.

Efficiency and Efficacy of Two Techniques of Preoxygenation during Modified Rapid Sequence Intubation.

Background:Apneic mass movement of oxygen by applying continuous positive airway pressure (CPAP) is possible only when the airway is kept patent which helps to reduce the rate of desaturation.Aims:The aim of this study was to check the efficiency of preoxygenation and apneic oxygenation by assessing the drop in partial pressure of arterial oxygen (PaO2) during apnea with and without keeping an oropharyngeal airway to maintain the patency of airway.Settings and Design:This prospective observational study was conducted at a tertiary care center.Materials and Methods:Sixty patients undergoing robotic and laparoscopic-assisted surgeries requiring modified rapid sequence intubation were recruited for the study. In Group A, CPAP was not applied during preoxygenation and oropharyngeal airway was not used, but oxygen was administered at 5 L/min during the apnea. In Group B, CPAP of 5 cmH2O was maintained during preoxygenation and after induction an oropharyngeal airway was inserted. Patients in both the groups were induced and paralyzed following standardized anesthesia protocol.Statistical Analysis Used:Chi-square test, independent t-test, and ANCOVA were used as applicable.Results:Group B showed significantly higher mean PaO2 levels after preoxygenation (525.3 ± 42.5 vs. 500.8 ± 51) and at 90 s of apnea (494.8 ± 42.6 vs. 368.6 ± 98.4) as compared to Group A. The fall in PaO2 was significantly lower in Group B. The rise in partial pressure of arterial carbon dioxide was comparable in both groups.Conclusion:Preoxygenation with CPAP of 5 cmH2O followed by apneic oxygenation with CPAP keeping the airway patent with an oropharyngeal airway results in significantly higher PaO2 after preoxygenation and slower reduction in PaO2 during apnea.

P131 Fitness to fly assessment in patients with neuromuscular disease

IntroductionPatients with neuromuscular disorders (NMD) can develop ventilatory impairment due to respiratory muscle weakness but despite disability, many travel by air. The British Thoracic Society (BTS) recommends hypoxic challenge test...

Not sleeping well can damage your heart

Obstructive sleep apnea (OSA) is characterized by recurrent obstruction of the pharyngeal airway during sleep, and results in episodes of intermittent hypoxia. Regardless of the presence of daytime symptoms, OSA is an independent risk factor for cardiovascular disease and increased mortality.1 A number of studies have shown that development of OSA correlates with increasing weight. The prevalence of OSA among obese patients has been reported, and substantial improvement was achieved by weight reduction.2 Regarding the pathophysiology of OSA, an anatomically small pharyngeal airway is a prerequisite factor leading to OSA. This smaller airway size always worsens with increasing body fat and obesity.3 When luminal size is narrower, it makes the airway vulnerable to collapse. An individual with OSA is able to compensate for this modified anatomy by increasing the activity of the upper airway muscles during the time that he or she is awake. However, with the onset of sleep, this compensation is lost and airway obstruction occurs. Even short periods of apnea can induce a rise in PaCO2, a fall in PaO2, and increased ventilatory effort against an occluded airway. Therefore, patients with OSA experience repetitive episodes of hypoxia during transient cessation of breathing that promote inflammation and oxidative stress. In addition to direct fat deposits within the airway walls, the upper airway size may be smaller in obese patients because of a reduced lung volume.3

Regulation of cerebral blood flow in mammals during chronic hypoxia: a matter of balance

Respiratory-induced changes in the partial pressures of arterial carbon dioxide (PaCO2) and oxygen (PaO2) play a major role in cerebral blood flow (CBF) regulation. Elevations in PaCO2 (hypercapnia) lead to vasodilatation and increases in CBF, whereas reductions in PaCO2 (hypocapnia) lead to vasoconstriction and decreases in CBF. A fall in PaO2 (hypoxia) below a certain threshold (<40-45 mmHg) also produces cerebral vasodilatation. Upon initial exposure to hypoxia, CBF is elevated via a greater relative degree of hypoxia compared with hypocapnia. At this point, hypoxia-induced elevations in blood pressure and loss of cerebral autoregulation, stimulation of neuronal pathways, angiogenesis, release of adenosine, endothelium-derived NO and a variety of autocoids and cytokines are additional factors acting to increase CBF. Following 2-3 days, however, the process of ventilatory acclimatization results in a progressive rise in ventilation, which increases PaO2 and reduces PaCO2, collectively acting to attenuate the initial rise in CBF. Other factors acting to lower CBF include elevations in haematocrit, sympathetic nerve activity and local and endothelium-derived vasoconstrictors. Hypoxia-induced alterations of cerebrovascular reactivity, autoregulation and pulmonary vascular tone may also affect CBF. Thus, the extent of change in CBF during exposure to hypoxia is dependent on the balance between the myriad of vasodilators and constrictors derived from the endothelium, neuronal innervations and perfusion pressure. This review examines the extent and mechanisms by which hypoxia regulates CBF. Particular focus will be given to the marked influence of hypoxia associated with exposure to high altitude and chronic lung disease. The associated implications of these hypoxia-induced integrative alterations for the regulation of CBF are discussed, and future avenues for research are proposed.

Oxidative stress in patients on mechanical ventilation

The appearance and intensity of oxidative stress were analyzed in the course of mechanical ventilation and parameters that could point toward potential lung damage. In three time intervals on day 1, 3 and 7 of mechanical ventilation, parameters such as: triglycerides, cholesterol, lactate, serum lactic dehydrogenase, acid-base balance and lipid peroxidation products--thiobarbituric acid reactive substances, were followed in 30 patients with head injuries. A decrease in the level of partial oxygen pressure (PaO2) (p < 0.01) and PaO2/FiO2 index (p < 0.05) in arterial blood was recorded on day 3 of mechanical ventilation. This was accompanied with an increase in alveolar-arterial difference (AaDO2) (p < 0.05), thiobarbituric acid reactive substances (p < 0.001) and lactic dehydrogenase (p < 0.001) comparing to day 1 of mechanical ventilation. The patients with initial PaO2 > 120 mmHg, had significant increase of thiobarbituric acid reactive substances and AaDO2 (p < 0.05) and fall of PaO2 (p < 0.001) on day 3 of mechanical ventilation. Oxidative stress and lipid peroxide production are increased during third day of mechanical ventilation leading to disruption of oxygen diffusion through alveolar-capillary membrane and reduction of parameters of oxygenation.

Échanges gazeux pulmonaires pendant l’exercice musculaire chez le sujet sain

The modifications of gas exchange on exercise reflect the consequences of the control and limits of adaptation of the respiratory apparatus to the mechanical loads imposed on the muscles and the oxygen requirements of the organism. In the majority of cases, even if the thoraco-pulmonary apparatus is perfectly adapted to the increase in these requirements, the balance between the metabolic demands of the tissues and the pulmonary supply appears difficult to satisfy beyond certain limits without hypoxaemia, particularly in those subjects with a low ventilatory response to exercise. Based on the populations reported in the literature the functional limits of the control of the thoraco-pulmonary system and the possible modifications of the structures of the lung are discussed for each of these mechanisms. At certain levels of duration and intensity of exercise there is an increase in the alveolar-arterial oxygen gradient [P(A-a)O2] associated inconsistently with a fall in PaO2. It is mainly the use of inert gas techniques that has established over many years the respective roles of the different possible patho-physiological mechanisms: shunt, unequal distribution of VA/Q ratios, limitation of alveolar-capillary diffusion and its components. The inequalities of VA/Q increase at low levels of exercise but beyond certain levels of VO2 limitation of oxygen diffusion may develop. In effect, particularly in subjects capable of high levels of exercise, the interaction between diminished transit time of the red cells in the pulmonary capillaries and possible delay in equilibration of partial pressures between the blood and gas phases may create a limitation of diffusion. This added to the inequalities of distribution of VA/Q and reduction in PVO2 leads, in certain subjects, to a transitory exercise induced hypoxaemia. New techniques of investigation seem to be necessary to clarify the sources of the observed changes and the development of modifications of pulmonary structure that establish the functional limits of the lungs on exercise. It remains to demonstrate the true impact of these anomalies on the limitation of human performance.

Rectal Temperature Correction Overestimates the Frequency of Exercise-Induced Hypoxemia

Exercise-induced hypoxemia (EIH) occurs in an uncertain proportion of endurance trained athletes. Whereas blood gas measurements must be corrected for core temperature at the time of sampling, the commonly used rectal temperature readings may not be the most appropriate. Ten males [mean peak oxygen uptake, (.-)VO(2peak), 65.4 +/- 7.0 mL x kg x min] performed incremental treadmill exercise from rest to exhaustion with radial artery blood samples collected at the end of each 2-min workload for gas analysis. The thermogenic effect of exercise was monitored with rectal, arterial blood, and esophageal temperature probes, and the values obtained at all three sites, simultaneous with blood sampling, were used to correct the standard blood gas measurements made at 37 +/- C. The mean increase in rectal temperature across exercise (1.4 +/- 0.4 +/- C) was approximately half that recorded in radial arterial blood (2.3 +/- 0.5+/- C) and the esophagus (2.4 +/- 0.5 degrees C). In consequence, the uncorrected fall in PaO2 across exercise of 15.4 +/- 8.2 mm Hg was reduced to 8.4 +/- 7.7 mm Hg when corrected for rectal temperature, and to 2.9 +/- 7.4 and 2.1 +/- 8.8 mm Hg when corrected for arterial blood and esophageal temperatures. Using a fall of > or = 10 mm Hg as the index of EIH, the proportion in the 10 subjects in the present study fell from 80% (uncorrected) through 50% (rectal correction) to 20% (arterial blood and esophageal corrections). When correcting arterial blood gas values for the thermogenic effects of exercise, the proportion of athletes meeting the definition of EIH depends on the site of core temperature measurement.

Tachypnea.

Tachypnea.

Effects of exhaustive endurance exercise on pulmonary gas exchange and airway function in women.

Seventeen fit women ran to exhaustion (14 +/- 4 min) at a constant speed and grade, reaching 95 +/- 3% of maximal O(2) consumption. Pre- and postexercise lung function, including airway resistance [total respiratory resistance (Rrs)] across a range of oscillation frequencies, was measured, and, on a separate day, airway reactivity was assessed via methacholine challenge. Arterial O(2) saturation decreased from 97.6 +/- 0.5% at rest to 95.1 +/- 1.9% at 1 min and to 92.5 +/- 2.6% at exhaustion. Alveolar-arterial O(2) difference (A-aDO(2)) widened to 27 +/- 7 Torr after 1 min and was maintained at this level until exhaustion. Arterial PO(2) (Pa(O(2))) fell to 80 +/- 8 Torr at 1 min and then increased to 86 +/- 9 Torr at exhaustion. This increase in Pa(O(2)) over the exercise duration occurred due to a hyperventilation-induced increase in alveolar PO(2) in the presence of a constant A-aDO(2). Arterial O(2) saturation fell with time because of increasing temperature (+2.6 +/- 0.5 degrees C) and progressive metabolic acidosis (arterial pH: 7.39 +/- 0.04 at 1 min to 7.26 +/- 0.07 at exhaustion). Plasma histamine increased throughout exercise but was inversely correlated with the fall in Pa(O(2)) at end exercise. Neither pre- nor postexercise Rrs, frequency dependence of Rrs, nor diffusing capacity for CO correlated with the exercise A-aDO(2) or Pa(O(2)). Although several subjects had a positive or borderline hyperresponsiveness to methacholine, this reactivity did not correlate with exercise-induced changes in Rrs or exercise-induced arterial hypoxemia. In conclusion, regardless of the degree of exercise-induced arterial hypoxemia at the onset of high-intensity exercise, prolonging exercise to exhaustion had no further deleterious effects on A-aDO(2), and the degree of gas exchange impairment was not related to individual differences in small or large airway function or reactivity.

Time required for partial pressure of arterial oxygen equilibration during mechanical ventilation after a step change in fractional inspired oxygen concentration.

To determine the time required for the partial pressure of arterial oxygen (PaO2) to reach equilibrium after a 0.20 increment or decrement in fractional inspired oxygen concentration (FIO2) during mechanical ventilation. A multi-disciplinary ICU in a university hospital. Twenty-five adult, non-COPD patients with stable blood gas values (PaO2/FIO2 > or = 180 on the day of the study) on pressure-controlled ventilation (PCV). Following a baseline PaO2 (PaO2b) measurement at FIO2 = 0.35, the FIO2 was increased to 0.55 for 30 min and then decreased to 0.35 without any other change in ventilatory parameters. Sequential blood gas measurements were performed at 3, 5, 7, 9, 11, 15, 20, 25 and 30 min in both periods. The PaO2 values measured at the 30th min after a step change in FIO2 (FIO2 = 0.55, PaO2[55] and FIO2 = 0.35, PaO2[35]) were accepted as representative of the equilibrium values for PaO2. Each patient's rise and fall in PaO2 over time, PaO2(t), were fitted to the following respective exponential equations: PaO2b + (PaO2[55]-PaO2b)(1-e-kt) and PaO2[55] + (PaO2[35]-PaO2[55])(e-kt) where "t" refers to time, PaO2[55] and PaO2[35] are the final PaO2 values obtained at a new FIO2 of 0.55 and 0.35, after a 0.20 increment and decrement in FIO2, respectively. Time constant "k" was determined by a non-linear fitting curve and 90% oxygenation times were defined as the time required to reach 90% of the final equilibrated PaO2 calculated by using the non-linear fitting curves. Time constant values for the rise and fall periods were 1.01 +/- 0.71 min-1, 0.69 +/- 0.42 min-1, respectively, and 90% oxygenation times for rises and falls in PaO2 periods were 4.2 +/- 4.1 min-1 and 5.5 +/- 4.8 min-1, respectively. There was no significant difference between the rise and fall periods for the two parameters (p > 0.05). We conclude that in stable patients ventilated with PCV, after a step change in FIO2 of 0.20, 5-10 min will be adequate for obtaining a blood gas sample to measure a PaO2 that will be representative of the equilibrium PaO2 value.

Ventilatory effects of radiographic contrast media.

Respiratory adverse reactions have been reported with the use of contrast media. This study investigates the effects of different radiographic contrast media (RCM) on ventilation and blood gases. Tidal volume and respiratory rate of male Wistar rats anaesthetised with Inactin (100 mg kg-1 intraperitoneally), were measured continuously by integration of tracheal airflow. Contrast media (diatrizoate 370, ioxaglate 320 and iopromide 300) or mannitol controls matched for volume, pH and osmolarity (4 ml kg-1) were administered via a jugular cannula (n > or = 6 per group). Carotid artery blood was sampled at 2, 7, 12, 17, 25 and 30 min post-injection for PaO2, PaCO2 and pH. Systemic blood pressure was monitored from the same cannula. No significant reduction was observed in minute ventilation (tidal volume x respiratory rate per minute) with any of the contrast media. All contrast media and control solutions produced a fall in PaO2 within 4 min; returning to basal levels at 10 min (diatrizoate 35.6% (p < 0.05), ioxaglate 15.2% (p < 0.02), iopromide 16.2% (p < 0.01); controls: 17.3% (p < 0.01), 13.5% (p < 0.02) and 12.0% (NS), respectively). The fall in PaO2 induced by diatrizoate was significantly (p < 0.05) larger in comparison to the other groups. Ioxaglate, iopromide and their mannitol controls induced a comparable fall in PaO2. There was a concurrent rise in PaCO2 and fall in pH that reached significance for diatrizoate (p < 0.01). The changes in blood gases with RCM administration cannot be explained by changes in ventilation and may be due to an effect on pulmonary perfusion.

Cardio-vascular and ventilatory effects of prostaglandin E 2 in the European eel Anguilla anguilla

Prostaglandin E2 (PGE2) injection caused an initial decrease in heart rate (HR) (55%), cardiac output (QC) (55%), ventral (VAP, 40%) and dorsal (DAP, 60%) aortic pressures, associated with a marked gill vasoconstriction (100%) and a systemic vasodilation (30%) while cardiac stroke volume (CSV) remained unchanged. It was followed by a progressive recovery of HR, DAP, and vascular resistances to control values while VAP, QC, and CSV significantly increased (20%, 40%, and 40%, respectively). Bradycardia was abolished either by atropine treatment or bilateral section of the cardiac vagus, suggesting that bradycardia could be the consequence of a vagal mechanism triggered by a central action of PGE2. The increase in QC is due to the increase in CSV, which suggests a positive inotropic action of PGE2. Infusion with PGE2 (10−9 to 10−5 mol · l−1) did not cause any significant effect on the branchial vasculature in vitro, but when the preparation was pre-treated with adrenaline (10−8 mol · l−4), a dose-related vasoconstrictory response to PGE2 (10−9 to 10−5 mol · l−1) occurred. A significant rise (25%) in gill vascular resistance was observed in vivo after treatment with the β-blocker propranolol (2.0 mg · kg−1), suggesting the existence of a vasodilatory β-adrenergic control of the branchial vasculature. PGE2 caused an apnea followed by a simultaneous tachypnea (50%) and decrease in ventilatory amplitude (40%). The resulting decrease in ventilatory water flow (Qw) was accompanied by a fall in arterial O2 tension (Pa O2). Under steady Qw in curarized eels, an initial fall in Pa O2 was still observed during the PGE2-induced gill vasoconstriction. It is concluded that PGE2 could play a role in the regulation of gas exchanges and blood circulation in particular environmental conditions which require an impairment of gill respiration and a redistribution of blood to the benefit of the systemic vascular bed.

A Placebo-Controlled Trial of Prostacyclin in Acute Respiratory Failure in COPD

Although patients with COPD often have elevated pulmonary artery pressures (PAP) and pulmonary vascular resistance (PVR), it is uncertain whether treatment of this pulmonary hypertension is beneficial. We evaluated the extent of pulmonary hypertension in 16 patients with severe COPD complicated by acute respiratory failure and pulmonary hypertension. We assessed the hypothesis that the vasodilator prostacyclin (PGI2) would reduce PVR and improve systemic O2 transport. Patients with a COPD exacerbation requiring mechanical ventilation, and mean PAP greater than 30 mm Hg, were randomized to receive PGI2 or placebo, in addition to conventional therapy. Randomization to PGI2 or placebo therapy occurred 1 to 12 h after intubation, while the patient was mechanically ventilated. An optimal PGI2 dose (2 to 12 ng/kg/min, IV) was established in an initial dose-ranging study and then this dose was infused continuously for 48 h. PGI2 initially reduced PVR, but this effect dissipated within 24 h, indicating the development of tachyphylaxis. Tolerance to the adverse effects of PGI2 (tachycardia, hypotension, flushing, and headache) also developed over time. PGI2 treatment was associated with a significant fall in PaO2 but no increase in systemic oxygen transport. PGI2 proved to be a nonselective vasodilator that caused mild hypoxemia. Despite acute respiratory failure, pulmonary hypertension is mild in patients with severe COPD receiving mechanical ventilation and IV PGI2 is not beneficial in such patients.