Changes In Arterial Oxygenation Research Articles

Acute Oxygen-Sensing via Mitochondria-Generated Temperature Transients in Rat Carotid Body Type I Cells.

The Carotid Bodies (CB) are peripheral chemoreceptors that detect changes in arterial oxygenation and, via afferent inputs to the brainstem, correct the pattern of breathing to restore blood gas homeostasis. Herein, preliminary evidence is presented supporting a novel oxygen-sensing hypothesis which suggests CB Type I cell “hypoxic signaling” may in part be mediated by mitochondria-generated thermal transients in TASK-channel-containing microdomains. Distances were measured between antibody-labeled mitochondria and TASK-potassium channels in primary rat CB Type I cells. Sub-micron distance measurements (TASK-1: 0.33 ± 0.04 µm, n = 47 vs TASK-3: 0.32 ± 0.03 µm, n = 54) provided evidence for CB Type I cell oxygen-sensing microdomains. A temperature-sensitive dye (ERthermAC) indicated that inhibition of mitochondrial activity in isolated cells caused a rapid and reversible inhibition of mitochondrial thermogenesis and thus temperature in these microdomains. Whole-cell perforated-patch current-clamp electrophysiological recordings demonstrated sensitivity of resting membrane potential (Vm) to temperature: lowering bath temperature from 37°C to 24°C induced consistent and reversible depolarizations (Vm at 37°C: -48.4 ± 4.11 mV vs 24°C: -31.0 ± 5.69 mV; n = 5; p < 0.01). These data suggest that hypoxic inhibition of mitochondrial thermogenesis may play an important role in oxygen chemotransduction in the CB. A reduction in temperature within cellular microdomains will inhibit plasma membrane ion channels, influence the balance of cellular phosphorylation–dephosphorylation, and may extend the half-life of reactive oxygen species. The characterization of a thermosensory chemotransduction mechanism, that may also be used by other oxygen-sensitive cell types and may impact multiple other chemotransduction mechanisms is critical if we are to fully understand how the CBs, and potentially other oxygen-sensitive cells, respond to hypoxia.

Arterial blood gas measurements during deep open-water breath-hold dives.

Arterial blood gas (ABG) measurements at both maximum depth and at resurfacing prior to breathing have not previously been measured during free dives conducted to extreme depth in cold open-water conditions. An elite free diver was instrumented with a left radial arterial cannula connected to two sampling syringes through a low-volume splitting device. He performed two open-water dives to a depth of 60 m (197', 7 atmospheres absolute pressure) in the constant weight with fins competition format. ABG samples were drawn at 60 m (by a mixed-gas scuba diver) and again on resurfacing before breathing. An immersed surface static apnea, of identical length to the dives and with ABG sampling at identical times, was also performed. Both dives lasted approximately 2 min. Arterial partial pressure of oxygen ([Formula: see text]) increased during descent from an indicative baseline of 15.8 kPa (after hyperventilation and glossopharyngeal insufflation) to 42.8 and 33.3 kPa (dives 1 and 2) and decreased precipitously (to 8.2 and 8.6 kPa) during ascent. Arterial partial pressure of carbon dioxide ([Formula: see text]) also increased from a low indicative baseline of 2.8 kPa to 6.3 and 5.1 kPa on dives 1 and 2; an increase not explained by metabolic production of CO2 alone since [Formula: see text] actually decreased during ascent (to 5.2 and 4.5 kPa). Surface static apnea caused a steady decrease in [Formula: see text] and increase in [Formula: see text] without the inflections provoked by depth changes. Lung compression and expansion provoke significant changes in both [Formula: see text] and [Formula: see text] during rapid descent and ascent on a deep free dive. These changes generally support predictive hypotheses and previous findings in less extreme settings.NEW & NOTEWORTHY Arterial blood gas measurements at both maximum depth and the surface before breathing on the same dive have not previously been obtained during deep breath-hold dives in cold open-water conditions and competition dive format. Such measurements were obtained in two dives to 60 m (197') of 2 min duration. Changes in arterial oxygen and carbon dioxide (an increase during descent, and a decrease during ascent) support previous observations in less extreme dives and environments.

The middle cerebral artery blood velocity response to acute normobaric hypoxia occurs independently of changes in ventilation in humans

What is the central question of this study? Does the ventilatory response to moderate acute hypoxia increase cerebral perfusion independently of changes in arterial oxygen tension in humans? What is the main finding and its importance? The ventilatory response does not increase middle cerebral artery mean blood velocity during moderate isocapnic acute hypoxia beyond that elicited by reduced oxygen saturation. Hypoxia induces ventilatory, cardiovascular and cerebrovascular adjustments to defend against reductions in systemic oxygen delivery. We aimed to determine whether the ventilatory response to moderate acute hypoxia increases cerebral perfusion independently of changes in arterial oxygenation. Eleven young healthy individuals were exposed to four 15min experimental conditions: (1) normoxia (partial pressure of end-tidal oxygen, =100mmHg), (2) hypoxia ( =50mmHg), (3) normoxia with breathing volitionally matched to levels observed during hypoxia (hyperpnoea; =100mmHg) and (4) hypoxia ( =50mmHg) with respiratory frequency and tidal volume volitionally matched to levels observed during normoxia (i.e., restricted breathing (RB)). Isocapnia was maintained in all conditions. Middle cerebral artery mean blood velocity (MCA Vmean ), assessed by transcranial Doppler ultrasound, was increased during hypoxia (58±12cm/s, P=0.04) and hypoxia + RB (61±14cm/s, P<0.001) compared to normoxia (55±11cm/s), while it was unchanged during hyperpnoea (52±13cm/s, P=0.08). MCA Vmean was not different between hypoxia and hypoxia + RB (P>0.05). These findings suggest that the hypoxic ventilatory response does not increase cerebral perfusion, indexed using MCA Vmean , during moderate isocapnic acute hypoxia beyond that elicited by reduced oxygen saturation.

Do Cheyne and Stokes have an important message for modern‐day patients with heart failure? Yes, they do

Do <scp>C</scp>heyne and <scp>S</scp>tokes have an important message for modern‐day patients with heart failure? <scp>Y</scp>es, they do

Changes in arterial oxygenation after portal decompression in Budd-Chiari syndrome patients with hepatopulmonary syndrome.

To evaluate the changes in arterial oxygenation after portal decompression in Budd-Chiari syndrome (BCS) patients with hepatopulmonary syndrome (HPS). From June 2014 to June 2015, all patients with BCS who underwent balloon angioplasty or transjugular intrahepatic portosystemic shunt (TIPS) creation at our institution were eligible for inclusion in this study. Arterial blood gas analysis was performed with the patient in an upright position and breathing room air at 2-3days and 1 and 3months after the procedure. Eleven patients with HPS and 14 patients without HPS were included in this study. The procedure was technically successful in 24 patients. One patient with HPS had technically unsuccessful TIPS creation. Reobstruction or TIPS dysfunction was not detected in any patient within 3months after the procedure. For patients with HPS, the alveolar-arterial oxygen gradient (A-aO2) remained comparable to baseline 2-3days after the procedure (-3.2 ± 11.9mmHg; p = .412), significantly improved 1month after the procedure (-11.7 ± 6.4mmHg; p < .001), and then returned to baseline 3months after the procedure (-1.3 ± 12.5mmHg; p = .757). For patients without HPS, the A-aO2 remained comparable to baseline at all three time points after the procedure (+1.4 ± 8.3mmHg, +3.5 ± 8.1mmHg, and +1.3 ± 8.2mmHg; p = .543, p = .137, and p = .565). Arterial oxygenation transiently improves after portal decompression in BCS patients with HPS. • Intrapulmonary vascular dilation and hepatopulmonary syndrome are common in patients with Budd-Chiari syndrome. • Arterial oxygenation transiently improves after portal decompression in Budd-Chiari syndrome patients with hepatopulmonary syndrome.

High PEEP in acute respiratory distress syndrome: quantitative evaluation between improved arterial oxygenation and decreased oxygen delivery

BackgroundPositive end-expiratory pressure (PEEP) is widely used to improve oxygenation and prevent alveolar collapse in mechanically ventilated patients with the acute respiratory distress syndrome (ARDS). Although PEEP improves arterial oxygenation predictably, high-PEEP strategies have demonstrated equivocal improvements in ARDS-related mortality. The effect of PEEP on tissue oxygen delivery is poorly understood and is difficult to quantify or investigate in the clinical environment. MethodsWe investigated the effects of PEEP on tissue oxygen delivery in ARDS using a new, high-fidelity, computational model with highly integrated respiratory and cardiovascular systems. The model was configured to replicate published clinical trial data on the responses of 12 individual ARDS patients to changes in PEEP. These virtual patients were subjected to increasing PEEP levels during a lung-protective ventilation strategy (0–20 cm H2O). Measured variables included arterial oxygenation, cardiac output, peripheral oxygen delivery, and alveolar strain. ResultsAs PEEP increased, tissue oxygen delivery decreased in all subjects (mean reduction of 25% at 20 cm H2O PEEP), despite an increase in arterial oxygen tension (mean increase 6.7 kPa at 20 cm H2O PEEP). Changes in arterial oxygenation and tissue oxygen delivery differed between subjects but showed a consistent pattern. Static and dynamic alveolar strain decreased in all patients as PEEP increased. ConclusionsIncremental PEEP in ARDS appears to protect alveoli and improve arterial oxygenation, but also appears to impair tissue oxygen delivery significantly because of reduced cardiac output. We propose that this trade-off may explain the poor improvements in mortality associated with high-PEEP ventilation strategies.

Protamine Administration Via the Ascending Aorta May Prevent Cardiopulmonary Instability.

The method of protamine administration may influence adverse reactions. The authors investigated the effects of 3 different methods of protamine administration on cardiopulmonary function. Prospective, randomized clinical study. Single university hospital. Human volunteer patients. Ninety-five patients undergoing cardiac surgery were randomized prospectively into 3 groups. Group central vein control (CVC) and group central vein (CV) received protamine via a central vein over 10 minutes and 2 minutes, respectively. Group ascending aorta (AA) received protamine via the ascending aorta over 2 minutes. Hemodynamic parameters were assessed at 7 intraoperative time points, and pulmonary parameters were assessed at 4 intraoperative time points. The groups were similar regarding preoperative demographics, intraoperative care, and baseline cardiopulmonary function. However, both the CVC and CV groups exhibited decreased blood pressure and impaired pulmonary oxygenation after protamine administration; these changes were not observed in the AA group. Within-group changes in mean arterial blood pressure after protamine administration were significant in the AA group (mean increase 6.5 mmHg; p = 0.01) but not in the CVC (mean decrease 3.1 mmHg, p = 0.13) or CV (mean decrease 4.3 mmHg, p = 0.14) groups. Within-group changes in arterial oxygenation after protamine administration were significant in the CVC (mean decrease 85 mmHg; p<0.001) and CV (mean decrease 47 mmHg; p = 0.009) groups but not in the AA group (mean decrease 8 mmHg; p = 0.82). The results indicated that administration of protamine via the ascending aorta may be the preferred route. The potential ability of administering protamine via the ascending aorta to prevent cardiopulmonary instability in patients undergoing cardiac surgery deserves further clinical investigation.

Acrolein inhalation alters arterial blood gases and triggers carotid body-mediated cardiovascular responses in hypertensive rats

Context: Air pollution exposure affects autonomic function, heart rate, blood pressure and left ventricular function. While the mechanism for these effects is uncertain, several studies have reported that air pollution exposure modifies activity of the carotid body, the major organ that senses changes in arterial oxygen and carbon dioxide levels, and elicits downstream changes in autonomic control and cardiac function.Objective: We hypothesized that exposure to acrolein, an unsaturated aldehyde and mucosal irritant found in cigarette smoke and diesel exhaust, would activate the carotid body chemoreceptor response and lead to secondary cardiovascular responses in rats.Materials and methods: Spontaneously hypertensive (SH) rats were exposed once for 3 h to 3 ppm acrolein gas or filtered air in whole body plethysmograph chambers. To determine if the carotid body mediated acrolein-induced cardiovascular responses, rats were pretreated with an inhibitor of cystathionine γ-lyase (CSE), an enzyme essential for carotid body signal transduction.Results: Acrolein exposure induced several cardiovascular effects. Systolic, diastolic and mean arterial blood pressure increased during exposure, while cardiac contractility decreased 1 day after exposure. The cardiovascular effects were associated with decreases in pO2, breathing frequency and expiratory time, and increases in sympathetic tone during exposure followed by parasympathetic dominance after exposure. The CSE inhibitor prevented the cardiovascular effects of acrolein exposure.Discussion and conclusion: Pretreatment with the CSE inhibitor prevented the cardiovascular effects of acrolein, suggesting that the cardiovascular responses with acrolein may be mediated by carotid body-triggered changes in autonomic tone. (This abstract does not reflect EPA policy.)

AltitudeOmics: The Integrative Physiology of Human Acclimatization to Hypobaric Hypoxia and Its Retention upon Reascent

An understanding of human responses to hypoxia is important for the health of millions of people worldwide who visit, live, or work in the hypoxic environment encountered at high altitudes. In spite of dozens of studies over the last 100 years, the basic mechanisms controlling acclimatization to hypoxia remain largely unknown. The AltitudeOmics project aimed to bridge this gap. Our goals were 1) to describe a phenotype for successful acclimatization and assess its retention and 2) use these findings as a foundation for companion mechanistic studies. Our approach was to characterize acclimatization by measuring changes in arterial oxygenation and hemoglobin concentration [Hb], acute mountain sickness (AMS), cognitive function, and exercise performance in 21 subjects as they acclimatized to 5260 m over 16 days. We then focused on the retention of acclimatization by having subjects reascend to 5260 m after either 7 (n = 14) or 21 (n = 7) days at 1525 m. At 16 days at 5260 m we observed: 1) increases in arterial oxygenation and [Hb] (compared to acute hypoxia: PaO2 rose 9±4 mmHg to 45±4 while PaCO2 dropped a further 6±3 mmHg to 21±3, and [Hb] rose 1.8±0.7 g/dL to 16±2 g/dL; 2) no AMS; 3) improved cognitive function; and 4) improved exercise performance by 8±8% (all changes p<0.01). Upon reascent, we observed retention of arterial oxygenation but not [Hb], protection from AMS, retention of exercise performance, less retention of cognitive function; and noted that some of these effects lasted for 21 days. Taken together, these findings reveal new information about retention of acclimatization, and can be used as a physiological foundation to explore the molecular mechanisms of acclimatization and its retention.

Effect of Intravenous Infusion of Dexmedetomidine Combined with Inhalation of Isoflurane on Arterial Oxygenation and Intrapulmonary Shunt During Single-Lung Ventilation

To investigate the changes in arterial oxygenation and intrapulmonary shunt during one-lung ventilation (OLV) with intravenous infusion of dexmedetomidine combined with isoflurane inhalation. ASA I-II 60 patients aged 18-70 year, undergoing OLV during elective thoracic surgery were randomly allocated to two groups: (1) isoflurane + saline (group NISO, n = 30) and (2) isoflurane + dexmedetomidine (group DISO, n = 30). After induction, anesthesia was maintained with intravenous infusion of remifentanil 0.1-0.2 μg kg(-1) min(-1) and inhalation isoflurane (1.0-2.0%). In addition, anesthesia was maintained with intravenous infusion of dexmedetomidine 0.7 μg kg(-1) h(-1) in DISO group and saline 0.25 ml kg(-1) h(-1) in NISO group. Bispectral Index values were maintained within 40-60 by changing the concentration of isoflurane in all groups. Arterial blood gas samples and central venous blood gas samples were taken as follows: during two-lung ventilation before OLV and during the first 40 min of OLV. 45 Patients completed the study, with 23 patients in DISO group and 22 patients in NISO group. The two groups were comparable in terms of demographic variables, hemodynamic, PaO2, Qs/QT, end expiration isoflurane and BIS levels during the operation. Compared with patients in the group NISO, there were significant increases with PaO2, significant decrease with Qs/QT, significant decrease with end expiration isoflurane, and significant decrease with HR in the group DISO during the first 40 min of OLV (P < 0.05). Dexmedetomidine infusions decrease the requirement for isoflurane, decrease intrapulmonary shunt, and moderate the change in PaO2 and may be useful in managing OLV.

Pron pozisyonda PEEP uygulamasının solunum mekaniği ve arteriyel oksijenizasyon üzerine etkileri

Objectives: To evaluate the changes in arterial oxygenation and vital parameters by applying 10cm HO positive end-expiratory pressure (PEEP) to patients undergoing lumbar spine surgery in the prone position. Patients and Method: According to The American Society of Anesthesiologists (ASA) status I-II, 40 patients, scheduled for lumbar discectomy in the prone position were enrolled in the study. During the anesthesia induction and after intubation they were ventilated with intermittent positive pressure ventilation (IPPV) mode, 60%NO-40%O, 4L.min flow and 0.7-1.0 minumum alveolar concentration (MAC) sevoflurane. The patients were randomized into 2 groups. PEEP value was set at 0 cm HO in PEEP 0 group and at 10 cm HO in PEEP 10 group. Respiratory rate 10/min, inspiration-expiration ratio 1:2 and tidal volume 8ml.kgwere kept constant. Blood gas samples were obtained 10 min after induction and 15-30-45-60-75-90 min after prone positioning. Vital parameters, dynamic compliance and side effects were recorded. Results: Mean blood pressure was statistically low in PEEP 10 group at the prone positioning, compared to the other periods (p<0.05). Pulse rate in both groups was significantly low during the prone period compared to other periods (p<0.05). PaO and compliance were statistically high in PEEP10 group at the prone position as compared to the PEEP 0 group (p<0.05).Conclusion: In our opinion, applying 10 cm HO PEEP to patients undergoing spine surgery in the prone position is a beneficial implementation.

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Introduction: Retinal oximetry allows for non-invasive measurement of arterial and venous oxygenation of the central circulation so that oxygen utilization can be efficiently monitored. Hypothesis: We sought to determine whether changes in mixed venous oxygen saturation (SvO2) were reflected in the retinal venous oxygen saturation (SrvO2) during progressive hypoxia and recovery from hypoxic insult. Methods: One domestic swine weighing 53kg was anesthetized, intubated, and kept under general anesthesia with isoflurane. Arterial and venous sheaths were placed via femoral cutdown, and a Swan-Ganz catheter was placed into the pulmonary artery. The placement of all lines was confirmed via waveform. The eye was sutured open to facilitate oximetry measurements and was kept hydrated with a balanced salt solution which was instilled throughout the experiment. All retinal oximetry measurements were performed using the ROx-3 retinal oximeter, a scanning laser ophthalmoscope, using the blue-green minima technique. Mixed venous blood saturation was measured by Swan-Ganz catheter. The animal was given a high-nitrogen, low-oxygen gas mixture and measurements were recorded and retinal images recorded at intervals determined by changes in arterial oxygenation as measured by pulse oximeter (SpO2). When SpO2 reached 60% or hemodynamic instability occurred the animal was placed on 100% oxygen and allowed to recover fully, with additional measurements recorded during re-oxygenation. The animal was euthanized at the end of the experimental period. Results: Four successive hypoxic insults were performed for a total of 187 measurements, with SpO2 ranging from 98% to 60%, SvO2 from 73% to 18%, and SrvO2 93% to 21%. Linear regression demonstrated an association between SrvO2 and SvO2 for each insult. Bland-Altman analysis revealed mean difference (SD) of -3.64(16.7), 6.29(14.2), -6.09(17.8), and -5.99(14.9) between SrvO2 and SvO2 for each hypoxic insult. Conclusions: SrvO2 correlates with SvO2 during progressive hypoxic insult and recovery from that insult. Funding: Emergency Medicine Departmental Pilot Grant.

Lactobacillus rhamnosus HN001 Attenuates Allergy Development in a Pig Model

BackgroundProbiotics have been studied as immunomodulatory agents of allergy. Several human probiotic trials tracking the development of eczema and other forms of allergy have yielded inconsistent results. A recent infant study demonstrated that pre and postnatal Lactobacillus rhamnosus HN001 (HN001) supplementation decreased the prevalence of eczema and IgE associated eczema. However, the influence of HN001 on the incidence of wheeze, asthma, and/or other allergic manifestations has yet to be reported.ObjectiveThis study was conducted to determine the effects of the probiotic HN001 on the development of allergic lung disease in a pig model.MethodsAllergy was induced by a series of subcutaneous and intratracheal sensitizations with Ascaris suum allergen (ASA) during a six week time frame in post-weanling pigs supplemented daily with HN001, or without supplementation. One week following final sensitization intradermal skin tests and respiratory challenges were conducted.ResultsIn response to intradermal and respiratory challenges, ASA-sensitized pigs fed HN001 had less severe skin flare reactions, smaller increases in pleural pressure, and trends towards lower changes in arterial oxygen and carbon dioxide partial pressure levels compared to control pigs. The frequency of ASA-specific IFN-γ-secreting peripheral blood mononuclear cells, as well as the amount of IL-10 produced by ASA-specific cells, was of greater magnitude in probiotic-fed pigs compared to control animals. These observations suggest that differences in clinical responses to the allergen challenges may be related to probiotic-induced modulation of Th1 (IFN-γ) and regulatory (IL-10) cytokine expression.ConclusionsProbiotic supplementation decreased the severity of allergic skin and lung responses in allergen-sensitized pigs with a corresponding increase in IFN-γ expression. A similar correlation between certain allergic responses and increased IFN-γ expression has been reported in human clinical studies of allergy; this pig model of allergy may be indicative of potential probiotic modulation of allergic lung disease in humans.

A model investigation of the impact of ventilation–perfusion mismatch on oxygenation during apnea in preterm infants

Ventilation–perfusion ( V/ Q) mismatch is a prominent feature of preterm infants and adults with lung disease. V/ Q mismatch is known to cause arterial hypoxemia under steady-state conditions, and has been proposed as the cause of rapid arterial oxygen desaturation during apnea. However, there is little evidence to support a role for V/ Q mismatch in the dynamic changes in arterial oxygenation that occur during apnea. Using a mathematical model, we quantified the effect of V/ Q mismatch on the rate of desaturation during apnea to ascertain whether it could lead to rates of up to 10% s –1 as observed in preterm infants. We used a lung–body model for the preterm infant that incorporated 50 parallel alveolar–capillary units that were ventilated and perfused with the severity of V/ Q mismatch ( σ) defined conventionally according to σ=S.D. of the distribution of V/ Q ratios. Average desaturation rate 10 s from apnea onset was strongly elevated with worsening V/ Q mismatch as a result of an earlier desaturation of low V/ Q units compared with high V/ Q units. However, V/ Q mismatch had little impact after apnea onset, with peak desaturation rate only substantially increased if mismatching caused a lowered resting arterial O 2 saturation. In conclusion, V/ Q mismatch causes a more immediate onset of desaturation during apnea, and therefore places preterm infants and adults with lung disease at risk of hypoxemic dips. However, V/ Q mismatch does not accelerate desaturation rate beyond apnea onset and cannot, therefore, explain the rapid desaturation observed during recurrent apnea in preterm infants.

A comparison of the MIGET and a simple model of pulmonary gas exchange

The multiple inert gas elimination technique (MIGET) [1] is the reference technique for assessing pulmonary gas exchange, but is not routinely used in clinical practice. The purpose of this study was to assess whether a simpler model of gas exchange, identifiable from clinical data, could simulate the effects of changing ventilator settings on arterial oxygenation in a comparable way to MIGET. Seven pigs were studied prior to and following lung damage with oleic acid, and at a range of ventilator settings. The MIGET and simple models were fitted to inert gas data, as described previously [2], and then used to simulate changes in arterial oxygenation on varying FiO2. Model simulations performed using MIGET and the simple model are comparable, the MIGET model simulating PaO2 values on average 0.22 kPa ± 0.59 (SD) higher than the simple model. Model simulations are also accurate with a difference between model simulated and measured values of PaO2 of 0.33 kPa ± 1.48 (SD) for the MIGET model, and 0.12 kPa ± 1.33 (SD) for the simple model. For oleic acid lung damage, the simple model provides a description of arterial oxygenation which is comparable to the MIGET over the clinically relevant range of PaO2.

Effects of Fluid Resuscitation on Cardiovascular Performance After Posttraumatic Pneumonectomy

: Several factors have been implicated in the high-mortality rate of posttraumatic pneumonectomy. In this study, we evaluated the hemodynamic and echocardiographic changes induced by pneumonectomy and fluid resuscitation after hemorrhagic shock. : Fourteen dogs were bled to a target mean arterial pressure of 40 mmHg. The animals were assigned to two groups: control (no fluid resuscitation) and lactated Ringer's (3 x shed blood volume). The left pulmonary hilum was cross clamped, and the animals were observed for 60 minutes. Systemic hemodynamics was evaluated using Swan-Ganz, arterial catheter, and ultrasonic flow probe. Systemic O2-derived variables were calculated. Ejection fraction was determined by two-dimensional echocardiography. : Fluid resuscitation improved the mean arterial pressure and systemic oxygen delivery. After pneumonectomy, no significant increase in right ventricular pressure was observed in the LR group. No signs of major ventricular dilation or changes in arterial oxygenation were observed. : Our data suggest that pneumonectomy is not associated with early pulmonary hypertension; gentle fluid resuscitation improves cardiovascular performance and is not associated with an increase in right ventricular pressure.

Influence of arousal threshold and depth of sleep on respiratory stability in man: analysis using a mathematical model

We examined the effect of arousals (shifts from sleep to wakefulness) on breathing during sleep using a mathematical model. The model consisted of a description of the fluid dynamics and mechanical properties of the upper airways and lungs, as well as a controller sensitive to arterial and brain changes in CO(2), changes in arterial oxygen, and a neural input, alertness. The body was divided into multiple gas store compartments connected by the circulation. Cardiac output was constant, and cerebral blood flows were sensitive to changes in O(2) and CO(2) levels. Arousal was considered to occur instantaneously when afferent respiratory chemical and neural stimulation reached a threshold value, while sleep occurred when stimulation fell below that value. In the case of rigid and nearly incompressible upper airways, lowering arousal threshold decreased the stability of breathing and led to the occurrence of repeated apnoeas. In more compressible upper airways, to maintain stability, increasing arousal thresholds and decreasing elasticity were linked approximately linearly, until at low elastances arousal thresholds had no effect on stability. Increased controller gain promoted instability. The architecture of apnoeas during unstable sleep changed with the arousal threshold and decreases in elasticity. With rigid airways, apnoeas were central. With lower elastances, apnoeas were mixed even with higher arousal thresholds. With very low elastances and still higher arousal thresholds, sleep consisted totally of obstructed apnoeas. Cycle lengths shortened as the sleep architecture changed from mixed apnoeas to total obstruction. Deeper sleep also tended to promote instability by increasing plant gain. These instabilities could be countered by arousal threshold increases which were tied to deeper sleep or accumulated aroused time, or by decreased controller gains.

Changes in Arterial Oxygenation and Self-Reported Oxygen Use after Lung Volume Reduction Surgery

Lung volume reduction surgery (LVRS) is inconsistently reported to improve arterial oxygenation in patients with chronic obstructive pulmonary disease. We studied the effects of surgery on oxygenation in a large cohort and identified predictors of postoperative oxygenation improvement. We evaluated oxygenation in 1,078 subjects with chronic obstructive pulmonary disease enrolled in the National Emphysema Treatment Trial after LVRS compared with medical control subjects, including arterial blood gases, use of supplemental oxygen during treadmill walking, and self-reported use of oxygen during rest, exertion, and sleep. Pa(O(2)) breathing room air was equal in medical and surgical subjects at baseline (64.8 vs. 65.0 mm Hg, P = not significant), but lower in medical subjects at 6 months (63.6 vs. 70.0 mm Hg, P < 0.001), 12 months (63.9 vs. 68.7 mm Hg, P < 0.001), and 24 months (62.4 vs. 68.0 mm Hg, P < 0.001). Fewer medical subjects required oxygen for treadmill walking at baseline compared with surgical subjects (46 vs. 53%, P = 0.02). However, more medical subjects required oxygen for this activity at 6 months (49 vs. 33%, P < 0.001), 12 months (50 vs. 36%, P < 0.001), and 24 months (52 vs. 42%, P = 0.02). Self-reported oxygen use was greater in medical than in surgical subjects at 6, 12, and 24 months. Multivariate modeling of preoperative characteristics showed baseline oxygenation status was the best predictor of postoperative oxygenation. LVRS increases Pa(O(2)), and decreases treadmill and self-reported use of oxygen for up to 24 months post-procedure. Clinical trial registered with www.clinicaltrials.gov (NCT 00000606).

Near-infrared spectroscopy to monitor cerebral oxygen saturation in single-ventricle physiology

Near-infrared spectroscopy monitors cerebral oxygen saturation. This parameter parallels jugular venous oxygen saturation and reflects the balance between cerebral oxygen supply and demand. Experience with near-infrared spectroscopy in univentricular physiology is limited. This study explores the relationship between cerebral oxygen saturation, jugular venous oxygen saturation, and other variables of cerebral perfusion in a model of univentricular physiology. Univentricular physiology was created in newborn piglets by means of an aortopulmonary shunt, echocardiography-guided atrial septostomy, tricuspid valve avulsion, and pulmonary artery occlusion. Intra-aortic balloon inflation was used to increase afterload. Cerebral oxygen saturation monitoring (INVOS 5100; Somanetics Corp, Troy, Mich), physiologic recordings, and stable-isotope microsphere determination of cerebral blood flow were performed at baseline and after conversion to univentricular physiology (30 minutes, 120 minutes, and during afterload augmentation). Univentricular physiology resulted in lower cerebral oxygen saturation, arterial oxygen content, jugular venous oxygen saturation, and cerebral oxygen delivery. Afterload augmentation increased cerebral oxygen saturation, arterial oxygen content, and jugular venous oxygen saturation, whereas cerebral oxygen delivery was unaffected because of lower cerebral blood flow. Cerebral oxygen saturation predicted jugular venous oxygen saturation, arterial oxygen saturation, and arterial oxygen content. No association was found with cerebral oxygen delivery, which decreased in parallel with cerebral oxygen saturation when the single-ventricle physiology model was established but failed to increase during afterload augmentation. This study shows that in univentricular physiology cerebral oxygen saturation correlates well with jugular venous oxygen saturation, arterial oxygen saturation, and arterial oxygen content. However, our findings suggest that in singe-ventricle physiology changes in cerebral oxygen saturation need to be interpreted in the context of changes in arterial oxygenation.

Feasibility and Results of Awake Thoracoscopic Resection of Solitary Pulmonary Nodules

General anesthesia with single-lung ventilation is considered mandatory for thoracoscopic pulmonary resection. We assessed in a randomized study the feasibility and results of awake thoracoscopic resection of solitary pulmonary nodules. Between March 2001 and February 2003, 60 patients were randomized into two 30-patients arms: a general anesthesia arm entailing double-lumen intubation and thoracic epidural anesthesia (control group); and an awake arm entailing sole thoracic epidural anesthesia at T4-T5 (awake group). Anesthesia time; operative time; global operating room time; patient satisfaction with the anesthesia and technical feasibility scored into 4 grades (from 1 = poor to 4 = excellent); visual analog pain score (VAS), nursing care (number of patient calls per day), 24 hours changes in arterial oxygenation (DeltaPaO2), and hospital stay were assessed. There was no mortality. There was no difference in technical feasibility between the groups although 2 patients in the awake group required conversion to thoracotomy due to severe adhesions. Other 2 patients in each group required conversion due to unexpected lung cancer requiring lobectomy. Comparisons of awake versus control group results showed that in the awake group, anesthesia satisfaction score was greater (4 vs 3, p = 0.04), whereas DeltaPaO2 (-3 mm Hg vs -6.5 mm Hg, p = 0.002); nursing care (2.5 calls per day vs 4 calls per day, p = 0.0001), and hospital stay (2 days vs 3 days, p = 0.02) were significantly reduced. In our study, awake thoracoscopic resection of solitary pulmonary nodules proved safely feasible. It resulted in better patient satisfaction, less nursing care and shorter in-hospital stay than procedures performed under general anesthesia.