Arterial Carbon Dioxide Levels Research Articles

Diaphragm paralysis in primary systemic amyloidosis

A patient with primary (AL) systemic amyloidosis developed mononeuropathy multiplex complicated by diaphragmatic failure. High dose melphalan and autologous stem cell transplantation did not ameliorate neuropathy or diaphragm dysfunction. Nocturnal non-invasive ventilation lowered arterial carbon dioxide levels and improved daytime dyspnea. This is the first case associating AL amyloid-induced neuropathy with diaphragm dysfunction.

190 The Effect of Tidal Volume and Peep on Co2 and Oxygenation During Resuscitation of Very Premature Lambs

Background: Over-ventilation causing low arterial carbon dioxide levels (PaCO2) has been associated with the development of neonatal chronic lung disease and adverse outcomes. This may occur very soon after birth.Aim: To investigate the effect on PaCO2 and oxygenation of very premature lambs resuscitated with different tidal volumes and PEEP.Methods: Anaesthetised lambs delivered at 126 days gestation were randomised to 15 min resuscitation with 3 regimes: (1) Laerdal resuscitation bag (B) with 100% oxygen and no PEEP, (2) fixed tidal volume (VT) of 5 mL/kg, or (3) VT of 10 mL/kg, both delivered with a Babylog 8000 ventilator in volume guarantee mode with 8 cm H2O PEEP and variable FiO2. Frequent blood gases were measured and VT, mean airway pressure (Paw), minute volume (MV), ventilation rate (VR), respiratory system compliance (Crs) and alveolar/arterial oxygen difference (AaDO2) were recorded.Results: Twenty lambs were studied. B (1) was associated with more variable VT and peak inspiratory pressures (PIP) compared to fixed tidal volumes (2 and 3). The lambs ventilated with 10 mL/kg were over-ventilated, those ventilated with 5 mL/kg were slightly under-ventilated. Those ventilated with the Laerdal bag had a mean VT of 7.5 mL/kg and were normocarbic. The different tidal volumes had little effect on oxygenation. PEEP improved oxygenation. The table shows the values at 15 minutes expressed as mean and SEM.Table 1Full size tableConclusion: Very premature lambs can be effectively resuscitated from birth using volume guarantee ventilation. Within minutes of birth different tidal volumes had a large effect on PaCO2 and no effect on oxygenation. Studies are needed to determine the appropriate tidal volume for resuscitating very premature infants to maintain acceptable levels of PaCO2.

Optimum cardiopulmonary resuscitation for basic and advanced life support: a simulation study.

Optimum cardiopulmonary resuscitation (CPR) for both basic and advanced cardiac life support depends on a compromise between the number of chest compressions delivered and the amount of ventilation provided. This study used theoretical models of blood flow and both arterial and venous blood gas values to investigate the influence of different compression to ventilation ratios on CPR efficiency, as well as the effects of different inspired oxygen concentrations. With mouth-to-mouth ventilation, greater numbers of compressions between each ventilation provided progressively greater blood flow. However, a greater the number of compressions, reduced the arterial oxygen levels and carbon dioxide clearance. There was an optimum ratio, in terms of both oxygen delivery and carbon dioxide clearance, of around 20:1 compressions to ventilation. Optimum oxygen delivery was 0.19 L/min at 20:1, which was better than the oxygen delivery for standard CPR based on a ratio of 15:2 (0.13 L/min). When patients were ventilated with supplemental oxygen (either 50 or 85%) the lungs rapidly became saturated with oxygen, and oxygen delivery depended more on blood flow. Higher numbers of compressions provided greater oxygen delivery, but at the cost of increasing hypercarbia, which is thought to affect resuscitation success rates adversely. The simulation results suggested ratios around 20:1 would be the best compromise between blood flow, oxygen delivery (0.25 L/min) and avoidance of hypercarbia. The best results were provided by continuous chest compressions and simultaneous, asynchronous ventilation in an intubated patient. Arterial and venous oxygen and carbon dioxide levels were well maintained, with very good oxygen delivery (0.32 L/min). Intubation with continuous chest compressions and asynchronous ventilation can therefore significantly improve the quality of CPR as a whole, and not just ventilation.

Resting fluctuations in arterial carbon dioxide induce significant low frequency variations in BOLD signal

Carbon dioxide is a potent cerebral vasodilator. We have identified a significant source of low-frequency variation in blood oxygen level-dependent (BOLD) magnetic resonance imaging (MRI) signal at 3 T arising from spontaneous fluctuations in arterial carbon dioxide level in volunteers at rest. Fluctuations in the partial pressure of end-tidal carbon dioxide (P et CO 2 ) of ±1.1 mm Hg in the frequency range 0–0.05 Hz were observed in a cohort of nine volunteers. Correlating with these fluctuations were significant generalized grey and white matter BOLD signal fluctuations. We observed a mean (±standard error) regression coefficient across the group of 0.110 ± 0.033% BOLD signal change per mm Hg CO 2 for grey matter and 0.049 ± 0.022% per mm Hg in white matter. P et CO 2 -related BOLD signal fluctuations showed regional differences across the grey matter, suggesting variability of the responsiveness to carbon dioxide at rest. Functional magnetic resonance imaging (fMRI) results were corroborated by transcranial Doppler (TCD) ultrasound measurements of the middle cerebral artery (MCA) blood velocity in a cohort of four volunteers. Significant P et CO 2 -correlated fluctuations in MCA blood velocity were observed with a lag of 6.3 ± 1.2 s (mean ± standard error) with respect to P et CO 2 changes. This haemodynamic lag was adopted in the analysis of the BOLD signal. Doppler ultrasound suggests that a component of low-frequency BOLD signal fluctuations is mediated by CO 2-induced changes in cerebral blood flow (CBF). These fluctuations are a source of physiological noise and a potentially important confounding factor in fMRI paradigms that modify breathing. However, they can also be used for mapping regional vascular responsiveness to CO 2.

Hemoglobin Level Is an Important Determinant of Acid-Base Status in Hemodialysis Patients

Background/Aims: We studied the relationship between hemoglobin (Hb), which is a major buffer of blood, and arterial blood total carbon dioxide (tCO₂) levels in maintenance hemodialysis (HD) patients. We also evaluated the difference between the tCO₂ measured with a standard Hb value of 15 g/dl, and that assayed with an actual Hb level entered into an analyzer. Methods/Results: In 105 patients the predialysis tCO₂ level of 21.4 ± 2.84 mEq/l inversely correlated with the Hb level of 9.5 ± 1.78 g/dl (r = –0.358, p = 0.0002). This indicated that the rise in Hb from 6 to 14 g/dl could result in a decrease of about 5 mEq/l in the tCO₂ level. In 20 patients the tCO₂ level measured at the Hb of 15 g/dl was 21.0 ± 2.47 mEq/l, and higher (p = 0.009) than that of 20.8 ± 2.45 mEq/l estimated at the actual Hb. The difference between these two measurements was inversely associated with the Hb level (r = –0.579, p = 0.007). The measurement of tCO₂at the unadjusted Hb slightly underestimated the degree of acidosis when the actual Hb level was < 11.5 g/dl. Conclusion: The degree of anemia and, to some extent, laboratory technique should always be considered when interpreting changes in arterial blood acid-base balance in maintenance HD patients.

Carbonic anhydrase inhibitors for hypercapnic ventilatory failure in chronic obstructive pulmonary disease.

Carbonic anhydrase inhibitors such as acetazolamide cause a mild metabolic acidosis and may stimulate breathing. Some patients with severe chronic obstructive pulmonary disease (COPD) develop chronic hypercapnic ventilatory failure. In theory, they may benefit from use of these drugs with a fall in arterial carbon dioxide level (PCO2) and a rise in arterial oxygen (PO2). To determine the effectiveness and safety of acetazolamide in the treatment of hypercapnic ventilatory failure due to COPD SEARCH STRATEGY: The Cochrane Register of Controlled Clinical Trials was searched along with Medline, Embase, Central and CINAHL for relevant randomised control trials. Trials were included in the review provided they were placebo controlled, carried out in patients with stable chronic ventilatory failure due to COPD. Data were extracted and analysed by two reviewers (PJ and MG) and agreement was reached by consensus. Where data could be aggregated they were analysed using a fixed efefcts model and reported as a weighted mean difference (WMD) and its associated 95% confidence interval (95% CI). Four trials were included in the review. Of these, two were randomised parallel studies, one was a crossover study and the other had a sequential design. A total of 84 patients were involved. Study quality was mixed and the studies were short (typically two weeks). All studies showed a similar direction and size of effect. In the randomised parallel studies, acetazolamide caused a metabolic acidosis and produced a non-significant fall in PCO2 (WMD -0.41 kPa; 95% CI -0.91, 0.09; N=2) and a significant rise in PO2 (WMD 1.54 kPa; 95% CI 0.97, 2.11; N=2). One study reported an improvement in sleep but there were no data concerning outcomes such as health status, symptoms, exacerbation rate, hospital admissions or deaths. Side effects were reported infrequently. Acetazolamide can produce a small increase in arterial PO2 and fall in PCO2. These conclusions are drawn from a few small short studies that were not all of high quality. It is not known whether this physiological improvement is associated with clinical benefit.

Ocular Hemodynamics during Isometric Exercise

The autoregulatory capacity of the human retina is well documented, but the pressure–flow relationship of the human choroid is still a matter of controversy. Recent data, using laser Doppler flowmetry to measure choroidal blood flow, indicate that the choroid has some autoregulatory potential, whereas most data using other techniques for the assessment of choroidal hemodynamics indicate that the choroidal pressure–flow curve is linear. We used a new laser interferometric technique to characterize choroidal blood flow during isometric exercise. Twenty healthy subjects performed squatting for 6 min during normocapnia and during inhalation of 5% CO2 and 95% air. Ocular fundus pulsation amplitude, flow velocities in the ophthalmic artery, intraocular pressure, and systemic hemodynamics were measured in 2-min intervals. To gain information on choroidal blood flow fundus pulsation amplitude was corrected for changes in flow pulsatility using data from the ophthalmic artery and for changes in pulse rate. Ocular perfusion pressure was calculated from mean arterial pressure and intraocular pressure. The ocular pressure–flow relationship was calculated by sorting data according to ascending ocular perfusion pressure values. In a pilot study in 6 healthy subjects comparable ocular pressure flow relationships were obtained when choroidal blood flow was assessed with the method described above and with laser Doppler flowmetry. In the main study isometric exercise caused a significant increase in mean arterial pressure (56%, P < 0.001), pulse rate (84%, P < 0.001), and intraocular pressure (37%, P 0.004), but decreased fundus pulsation amplitude (−36%, P < 0.001). Significant deviations from baseline choroidal blood flow were observed only at ocular perfusion pressures >69% during normocapnia and 70% during hypercapnia. Our data indicate that during isometric exercise the choroid has a high capacity to keep blood flow constant despite changes in perfusion pressure and that this pressure–flow relationship is not altered by moderate changes in arterial carbon dioxide levels.

Exposure of brown trout, Salmo trutta, to a sub-lethal concentration of copper in soft acidic water: effects upon muscle metabolism and membrane potential

Brown trout acclimated to soft water and exposed for 96 h to a sub-lethal concentration of copper at low pH (0.08 μmol l −1 Cu, pH 5) have a lower critical swimming speed than fish from copper-free water at neutral pH. This loss of performance is not due to difficulties in oxygen transfer resulting from gill damage since arterial oxygen and carbon dioxide levels remain unaffected. Both red and white muscle showed some metabolic disruptions consistent with local hypoxia, namely a high lactate concentration at rest and, in the white muscle, depletion of glycogen and phosphocreatine. However, a putative role of increased blood viscosity following haematological changes in reducing the supply of oxygen to the tissues is not supported by the current study. Haematocrit, haemoglobin and plasma protein concentrations were not affected by this treatment and a lack of further change in variables such as lactate at the onset of exercise led one to look for an alternative explanation for the effects of copper and low pH upon tissue metabolites. Ammonia concentration, both in the plasma and muscles, is significantly higher in trout exposed to copper and low pH. Ammonia plays a role in the regulation of a number of metabolic pathways and could contribute to the altered metabolic status of these fish. In addition, ammonium ions are known to cause electrophysiological disruptions, particularly the displacement of K + in ion exchange mechanisms that could lead to the observed loss of swimming performance. Using the measured distribution of ammonia between intracellular and extracellular compartments to estimate membrane potential of resting muscle, a significant depolarisation is predicted in both red and white muscle of fish exposed to copper and low pH.

Breathlessness in humans activates insular cortex.

Dyspnea (shortness of breath, breathlessness) is a major and disabling symptom of heart and lung disease. The representation of dyspnea in the cerebral cortex is unknown. In the first study designed to explore the central neural structures underlying perception of dyspnea, we evoked the perception of severe 'air hunger' in healthy subjects by restraining ventilation below spontaneous levels while holding arterial oxygen and carbon dioxide levels constant. PET revealed that air hunger activated the insular cortex. The insula is a limbic structure also activated by visceral stimuli, temperature, taste, nausea and pain. Like dyspnea, such perceptions underlie behaviors essential to homeostasis and survival.

Cerebral blood volume and blood flow at varying arterial carbon dioxide tension levels in rabbits during propofol anesthesia.

There are little data on the effects of propofol on cerebral blood volume (CBV). We studied the effects of changes in PaCO(2) on CBV and cerebral blood flow (CBF) during propofol anesthesia in eight New Zealand white rabbits. We also investigated the effects of propofol over time on CBV and CBF during normocapnia (control group). At normocapnia, the mean (+/- SD) CBV and CBF values were 2.41 +/- 0.68 mL/100 g and 56 +/- 28 mL/100 g/min, respectively,. When PaCO(2) was reduced from 41 to 27 mm Hg, no significant change in either CBV or CBF was observed (P > 0.10). However, increasing PaCO(2) from 41 to 58 mm Hg resulted in a 30% increase in CBV (3.08 +/- 0.86 mL/100 g, P < 0.05) and a 91% increase in CBF (97 +/- 39 mL/100 g/min, P < 0.01). In the control group, there were no significant changes in CBV and CBF (P > 0.10) during 2 h of propofol anesthesia. These results indicate that, during propofol anesthesia, cerebrovascular reactivity of blood flow and blood volume is maintained during hypercapnia but is markedly diminished during hypocapnia. During propofol anesthesia in rabbits with normal brains, a reduction in the arterial carbon dioxide level may not always be accompanied by a reduction in brain blood flow and blood volume.

A Management Guideline for Obesity-Hypoventilation Syndromes

A survey of our pulmonary service revealed little consensus as to the definition, work-up, and management of hypoventilation, more often encountered in the presence of obesity. If hypoventilation is defined by an arterial carbon dioxide level above 45mmHg, 22% of artrial blood gas samples over a 5-month period met this criterium, suggesting a high Oany-causeO prevalence. This article presents the rationale and explanation for a management protocol for obesity-hypoventilation that is currently being assessed in the VA Medical Center and Case Western Reserve University training program in Pulmonary and Critical Care Medicine.

Leptin prevents respiratory depression in obesity.

Human obesity leads to an increase in respiratory demands. As obesity becomes more pronounced some individuals are unable to compensate, leading to elevated arterial carbon dioxide levels (PaCO2), alveolar hypoventilation, and increased cardiorespiratory morbidity and mortality (Pickwickian syndrome). The mechanisms that link obesity and hypoventilation are unknown, but thought to involve depression of central respiratory control mechanisms. Here we report that obese C57BL/6J-Lepob mice, which lack circulating leptin, also exhibit respiratory depression and elevated PaCO2 (> 10 mm Hg; p < 0. 0001). A role for leptin in restoring ventilation in these obese, mutant mice was investigated. Three days of leptin infusion (30 microg/d) markedly increased minute ventilation (V E) across all sleep/wake states, but particularly during rapid eye movement (REM) sleep when respiration was otherwise profoundly depressed. The effect of leptin was independent of food intake, weight, and CO2 production, indicating a reversal of hypoventilation by stimulation of central respiratory control centers. Furthermore, leptin replacement in mutant mice increased CO2 chemosensitivity during non-rapid eye movement (NREM) (4.0 +/- 0.5 to 5.6 +/- 0.4 ml/min/%CO2; p < 0.01) and REM (-0.1 +/- 0.5 to 3.0 +/- 0.8 ml/min/%CO2; p < 0.01) sleep. We also demonstrate in wild-type mice that ventilation is appropriately compensated when obesity is diet-induced and endogenous leptin levels are raised more than tenfold. These results suggest that leptin can prevent respiratory depression in obesity, but a deficiency in central nervous system (CNS) leptin levels or activity may induce hypoventilation and the Pickwickian syndrome in some obese subjects. O'Donnell CP, Schaub CD, Haines AS, Berkowitz DE, Tankersley CG, Schwartz AR, Smith PL. Leptin prevents respiratory depression in obesity.

Quantification and distribution of cerebral emboli during cardiopulmonary bypass in the swine: the impact of PaCO2.

Patients undergoing cardiac surgery have a substantial incidence of neurologic complications related to cerebral embolization during cardiopulmonary bypass. The purpose of this study was to determine if adjustments in the arterial carbon dioxide (PaCO2) level can reduce cerebral and ocular embolization. Twenty pigs underwent cardiopulmonary bypass at 38 degrees C. At either hypercarbia (PaCO2 = 50-55 mmHg, group H, n = 10) or hypocarbia (PaCO2 = 25-30 mmHg, group L, n = 10), an embolic load of 1.2 x 10(50 67-microm orange fluorescent microspheres was injected into the aortic cannula. Before and after embolization, cerebral and ocular blood flows were determined at normocapnia using 15-microm fluorescent microspheres. After cardiopulmonary bypass was completed, the eyes were enucleated and brain tissue samples were collected. Microspheres were isolated and the fluorescence was measured. In groups H and L, the mean PaCO2 values at embolization were 52+/-3 mmHg and 27+/-2 mmHg, respectively (P < 0.0001). Total and regional embolization were significantly less in hypocapnia than in hypercapnic animals: 142% more emboli were detected in the brain in group H than in group L (P < 0.0001). Cerebral blood flow after embolization was unchanged in both groups. Similarly, fewer ocular emboli occurred in hypocapnic animals than in hypercapnic animals (P = 0.044), but in contrast to the brain, ocular blood flow decreased significantly in both groups after embolization. Cerebral embolization is determined by the PaCO2 at the time of embolization. In cardiopulmonary bypass practice, reductions in PaCO2 during periods of embolic risk may reduce the risk for brain injury.

Effects of a Protective-Ventilation Strategy on Mortality in the Acute Respiratory Distress Syndrome

PASSOS AMATO, MARCELO BRITTO; VALENTE BARBAS, CARMEN SILVIA; MEDEIROS, DENISE MACHADO; MAGALDI, RICARDO BORGES; PAULA PINTO SCHETTINO, GUILHERME DE; LORENZI-FILHO, GERALDO; KAIRALLA, RONALDO ADIB; DEHEINZELIN, DANIEL; MUNOZ, CARLOS; OLIVEIRA, ROSELAINE; TAKAGAKI, TERESA YAE; RIBEIRO CARVALHO, CARLOS ROBERTO Author Information

Using the Human Patient Simulator to Test the Efficacy of an Experimental Emergency Percutaneous Transtracheal Airway

As clinicians continue to gain experience with the use of emergency cricothyrotomy, a need exists to continue to explore methods to perfect both the technique and the equipment used. The clinician in the austere military environment may be forced to be innovative in the design of such a device. A combination of commonly used disposable intravenous equipment for emergency cricothyrotomy is described. Its efficacy for the maintenance of oxygen saturation, arterial oxygen levels, and arterial carbon dioxide levels was determined using the Human Patient Simulator from Medical Education Technologies, Inc. The emergency airway device was compared with the needle cricothyrotomy technique. The control profile for the return of acceptable oxygen saturation and arterial oxygen levels was more closely matched by the emergency airway device than by the needle cricothyrotomy technique.

Effects of moderate, central fluid percussion traumatic brain injury on nitric oxide synthase activity in rats.

Experimental traumatic brain injury (TBI) damages cerebral vascular endothelium and reduces cerebral blood flow (CBF). The nitric oxide synthase (NOS) substrate, L-arginine, prevents CBF reductions after TBI, but the mechanism is not known. This study examined the possibility that post-traumatic hypoperfusion is due to reductions in the substrate sensitivity of NOS which are overcome by L-arginine. Isoflurane-anesthetized rats were prepared for TBI (midline fluid-percussion, 2.2 atm), sham-TBI, or no surgery (control), and were decapitated 30 min after injury or sham injury. The brains were removed and homogenized or minced for measurements of crude soluble or cell-dependent stimulated NOS activity, respectively. Baseline arterial oxygen, carbon dioxide, pH, or hemoglobin levels did not differ among control, sham, or TBI groups. Total cortical soluble NOS activity in TBI-treated rats was not significantly different from either untreated or sham groups when 0.45 microM or 1.5 microM L-arginine was added. Also, there were no differences in cell-dependent NOS activity among the three groups stimulated by 300 microM N-methyl-D-aspartate, 50 mM K+, or 10 microM ionomycin. These data suggest that TBI reduces CBF by a mechanism other than altering the substrate specificity or activation of nNOS.

SHORT COMMUNICATION: The effect of raised inspired carbon dioxide on normal retinal vascular development in the neonatal rat

PURPOSE. Raised arterial carbon dioxide levels have been suggested as a risk factor for retinopathy of prematurity (ROP). We investigated the effect of raised inspired CO 2 on normal postnatal vasculogenesis in the neonatal rat retina. METHODS. One hundred fifty newborn rat pups were divided among 15 mothers (n = 10 for each litter). Five litters were exposed to low CO 2 (0.2%), 5 litters exposed to 6%, and 5 litters to 10% CO 2. On day 7 of life the rats were sacrificed and the total retinal and vascularized retinal areas analyzed. RESULTS. The vascularized retinal area and ratio of vascularized to total retinal area were reduced in rats exposed to 6% and 10% CO 2. CONCLUSIONS. Raised inspired CO 2 was associated with retardation of normal retinal vascular development and increased peripheral avascular area in neonatal rats. Raised CO 2 may be a risk factor for the development of abnormal neovascularization such as in ROP.

Correlation of end-tidal CO2 measurements to arterial Paco2 in nonintubated patients

To determine the accuracy of end-tidal carbon dioxide levels as a measure of arterial carbon dioxide levels in nonintubated patients presenting to an emergency department for care. A prospective, cross-sectional analysis. University hospital ED. Nonintubated adult patients presenting to the ED for care of a variety of problems. Patients who had arterial blood gas samples taken as part of their ED evaluation were asked to breathe normally through an endotracheal tube adapter or a modified nasal cannula connected to a side port sampling capnometer while a sample for arterial blood gas was drawn from the radial artery. End-tidal carbon dioxide levels (mm Hg) were recorded at the time of arterial blood gas sampling. The difference between end-tidal carbon dioxide and PaCO2 was tested with the paired t-test at a significance level of .05. The correlation of end-tidal carbon dioxide to PaCO2 was tested in all patients and in subgroups using simple linear regression. Seventy-six patients were enrolled. In all patients, end-tidal carbon dioxide was 3.5 mm Hg lower than PaCO2 and correlated well with PaCO2 (r2 = .772). In patients with hypocapnia, there was no significant difference between end-tidal carbon dioxide and PaCO2 (P = .17), and the correlation of end-tidal carbon dioxide to PaCO2 was stronger (r2 = .838). In patients with a respiratory or metabolic acidosis, the difference between end-tidal carbon dioxide and PaCO2 was 6 mm Hg (P = .005), but end-tidal carbon dioxide correlated well to PaCO2 (r2 = .899). Measurements of end-tidal carbon dioxide concentrations correlate well with PaCO2 values in nonintubated patients presenting with a variety of conditions to EDs. End-tidal carbon dioxide measurements may be sufficient measures of PaCO2 in selected patients and obviate the need for repeat arterial blood gas determination. Further study is warranted.

Optimal ventilatory patterns in periodic breathing.

The goal of this study was to determine whether periodic breathing (PB), which is highly prevalent during sleep at high altitudes, imposes physiological penalties on the respiratory system in the absence of any accompanying disease. Using a computer model of respiratory gas exchange, we compared the effects of a variety of PB patterns on the chemical and mechanical costs of breathing to those resulting from regular tidal breathing. Although PB produced considerable fluctuation in arterial blood gas tensions, for the same cycle-averaged ventilation, higher arterial oxygen saturation and lower arterial carbon dioxide levels were achieved. This result can be explained by the fact that the combination of large breaths and apnea in PB leads to a substantial reduction in dead space ventilation. At the same time, the savings in mechanical cost achieved by the respiratory muscles during apnea partially offset the increase during the breathing phase. Consequently, the "pressure cost," a criterion based on mean inspiratory pressure, was elevated only slightly, although the average work rate of breathing increased significantly. We found that, at extreme altitudes, PB patterns with clusters of 2 to 4 large breaths that alternate with apnea produce the highest arterial oxygenation levels and lowest pressure costs. The common occurrence of PB patterns with closely similar features has been reported in sleeping healthy sojourners at extreme altitudes. Taken together, these findings suggest that PB favors a reduction in the oxygen demands of the respiratory muscles and therefore may not be as detrimental as it is generally believed to be.

Analysis of the Hemodynamic and Ventilatory Effects of Laparoscopic Cholecystectomy

Laparoscopic cholecystectomy uses carbon dioxide, a highly diffusable gas, for insufflation. With extended periods of insufflation, patient arterial carbon dioxide levels may be adversely altered. Patients were selected for laparoscopic cholecystectomy using the same criteria as for open cholecystectomy. Twenty patients (group 1) had normal preoperative cardiopulmonary status (American Society of Anesthesiologists class I), while 10 patients (group 2) had previously diagnosed cardiac or pulmonary disease (class II or III). Demographic, hemodynamic, arterial blood gas, and ventilatory data were collected before peritoneal insufflation and at intervals during surgery. Patients with preoperative cardiopulmonary disease demonstrated significant increases in arterial carbon dioxide levels and decreases in pH during carbon dioxide insufflation compared with patients without underlying disease. Results of concurrent noninvasive methods of assessing changes in partial arterial pressures of carbon dioxide (end-tidal carbon dioxide measured with mass spectrographic techniques) may be misleading and misinterpreted because changes in partial arterial pressures of carbon dioxide are typically much smaller than changes in arterial blood levels and, unlike arterial gas measurements, do not indicate the true level of arterial hypercarbia. During laparoscopic cholecystectomy, patients with chronic cardiopulmonary disease may require careful intraoperative arterial blood gas monitoring of absorbed carbon dioxide.