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PubMed2005

Nocturnal hypoxemia after lobectomy for lung cancer.

BACKGROUND: Although nocturnal episodic hypoxemia after major abdominal surgery has been reported, the condition of nocturnal oxygen saturation after lung surgery is largely unknown. We evaluated nocturnal oxygen saturation during the perioperative period after lobectomy for lung cancer. This study also compared the postoperative course of nocturnal oxygen saturation after standard lobectomy with posterolateral thoracotomy and lobectomy with video-assisted thoracic surgery. METHODS: Twenty-one consecutive patients who had undergone lobectomy for lung cancer by either the posterolateral thoracotomy approach (n = 11) or the video-assisted thoracic surgery approach (n = 10) were studied. Fifteen consecutive patients who had undergone gastrectomy for gastric cancer were also studied. Overnight oxygen saturation was measured on the third and 14th postoperative days. RESULTS: The frequency of hypoxemia in the lobectomy group was higher than that in the gastrectomy group (p = 0.043). The frequency of hypoxemia on the 14th postoperative day (p = 0.009) and the severity of hypoxemia on the third and 14th postoperative days (p = 0.041, 0.046) for the video-assisted thoracic surgery approach were lower than those for the posterolateral thoracotomy approach. In terms of mean arterial oxygen saturation, heart rate, forced vital capacity, and forced expiratory volume in 1 second, there were no statistically significant differences between the video-assisted thoracic surgery group and the posterolateral thoracotomy group. CONCLUSIONS: Video-assisted thoracic surgery lobectomy was superior in terms of early postoperative nocturnal oxygen saturation. We conclude that the video-assisted thoracic surgery approach is more beneficial than the posterolateral thoracotomy approach for high-risk patients.

Aged↗

PubMed2004

Hypoxemia and blunted hypoxic ventilatory responses in mice lacking heme oxygenase-2.

Heme oxygenase (HO) catalyzes physiological heme degradation and consists of two structurally related isozymes, HO-1 and HO-2. Here we show that HO-2-deficient (HO-2(-/-)) mice exhibit hypoxemia and hypertrophy of the pulmonary venous myocardium associated with increased expression of HO-1. The hypertrophied venous myocardium may reflect adaptation to persistent hypoxemia. HO-2(-/-) mice also show attenuated ventilatory responses to hypoxia (10% O2) with normal responses to hypercapnia (10% CO2), suggesting the impaired oxygen sensing. Importantly, HO-2(-/-) mice exhibit normal breathing patterns with normal arterial CO2 tension and retain the intact alveolar architecture, thereby excluding hypoventilation and shunting as causes of hypoxemia. Instead, ventilation-perfusion mismatch is a likely cause of hypoxemia, which may be due to partial impairment of the lung chemoreception probably at pulmonary artery smooth muscle cells. We therefore propose that HO-2 is involved in oxygen sensing and responsible for the ventilation-perfusion matching that optimizes oxygenation of pulmonary blood.

Animals↗

PubMed2006

Significance of hypoxemia screening in candidates for liver transplantation: our experience.

Hepatopulmonary syndrome (HPS) is recognized as one of the causes of hypoxemia in patients with chronic liver disease. This complication is responsible for increased mortality and increased perioperative risk in liver transplantation candidates. Recent data from the literature suggest extending the screening for HPS to all candidates for liver transplantation. The aim of this retrospective study was to evaluate the incidence of hypoxemia among a population of patients awaiting liver transplantation. Using pulse oximetry as a screening tool for hypoxemia, 39 of 198 patients (20%) were hypoxemic. The results of this study confirmed the importance of screening for hypoxemia among patients awaiting liver transplantation. In these patients, a more accurate evaluation of respiratory function should be performed to confirm or exclude the diagnosis of HPS.

Humans↗

PubMed1994

Cerebral metabolism during sustained hypoxemia in preterm fetal sheep.

OBJECTIVE: The purpose of this study was to determine the effect of sustained hypoxia with resulting metabolic acidosis on cerebral metabolism in the preterm ovine fetus. STUDY DESIGN: Twelve fetal sheep were studied at 0.75 of gestation during a normoxic control period, after 1 and 8 hours of sustained hypoxemia, and again after a 1-hour recovery period. Cerebral arteriovenous differences were analyzed for oxygen content, blood gases and pH, glucose, and lactate. Cerebral blood flow was measured with the microsphere technique. RESULTS: Induced hypoxemia resulted in a variable degree of fetal acidemia that was entirely metabolic. Although cerebral oxidative metabolism was well maintained throughout the study, cerebral glucose consumption was variably increased when measured after 1 hour of sustained hypoxemia, with a subsequent decrease after 1 hour of recovery. Although lactate was neither consumed nor produced during the control period, by 8 hours of hypoxic study a significant efflux of lactate from the brain was evident, which continued into the recovery period. CONCLUSION: Sustained hypoxemia results in an increase in the anaerobic metabolism of glucose by the preterm fetal brain independent of any change in cerebral oxidative metabolism, which may give rise to an accumulation of lactic acid and contribute to neurologic impairment.

Animals↗

PubMed1999

Prediction of hypoxemia and mechanical ventilation after lung resection for cancer.

BACKGROUND: Hypoxemia usually occurs after thoracotomy, and respiratory failure represents a major complication. METHODS: To define predictive factors of postoperative hypoxemia and mechanical ventilation (MV), we prospectively studied 48 patients who had undergone lung resection. Preoperative data included, age, lung volume, force expiratory volume in one second (FEV1), predictive postoperative FEV1 (FEV1ppo), blood gases, diffusing capacity, and number of resected subsegments. RESULTS: On postoperative day 1 or 2, hypoxemia was assessed by measurement of PaO2 and alveolar-arterial oxygen tension difference (A-aDO2) in 35 nonventilated patients breathing room air. The other patients (5 lobectomies, 9 pneumonectomies) required MV for pulmonary or nonpulmonary complications. Using simple and multiple regression analysis, the best predictors of postoperative hypoxemia were FEV1ppo (r = 0.74, p < 0.001) in lobectomy and tidal volume (r = 0.67, p < 0.01) in pneumonectomy. Using discriminant analysis, FEV1ppo in lobectomy and tidal volume in pneumonectomy were also considered as the best predictive factors of MV for pulmonary complications. CONCLUSIONS: These results suggest that the degree of chronic obstructive pulmonary disease in lobectomy and impairment of preoperative breathing pattern in pneumonectomy are the main factors of respiratory failure after lung resection.

Adult↗

PubMed1997

Liver transplantation for severe hypoxemia caused by patent ductus venosus.

The authors describe the case of a 9-year-old girl who underwent liver transplantation because she suffered from severe hypoxemia caused by patent ductus venosus (PDV). Generally, severe hypoxemia (PaO2 < 50 mm Hg in room air or < 300 mm Hg in pure oxygen) is not an indication for liver transplantation because the hypoxemia may not be improved, and may lead to a fatal outcome. PDV, which is associated with mild liver dysfunction, is not an indication for liver transplantation by itself. But in our patient, most of the mesenteric venous flow directly entered the systemic circulation through the PDV just like the portosystemic shunt, and this caused the pulmonary arteriovenous shunt and hypoxemia. Thus, the authors operated on the patient in an attempt to restore her pulmonary function. Nitric oxide (10 to 20 ppm) was added to the inhaled gas to dilate the functional pulmonary capillaries and to deliver sufficient oxygen after the transplantation. Although the patient suffered various complications after the operation, the final results were excellent.

Angiography, Digital Subtraction↗

PubMed1986

Effects of chronic in utero hypoxemia on rat neonatal pulmonary arterial structure.

Idiopathic persistent pulmonary hypertension of the newborn infant (PPHN) is characterized by intrauterine structural remodeling of the pulmonary arterial bed, consisting of precocious development of muscle in intraacinar arteries, proliferation of adventitial connective tissue, and sometimes medial hypertrophy of preacinar arteries. To evaluate whether gestational hypoxemia causes these changes, we studied pulmonary arterial structure in two groups of newborn rats: one control, the other exposed to hypoxemia produced by maternal hypoxia during the second half of gestation. Morphometric analysis of the pulmonary arterial bed was performed after barium injection into the pulmonary arteries and formol saline expansion of the air spaces. Birth weight was similar in each group. Hematocrit was elevated in the hypoxemia group (51% +/- 1.0% vs 46% +/- 0.8%, P less than 0.005). The structure of preacinar and intraacinar arteries was similar and normal in both groups. Chronic fetal hypoxemia in the rat does not produce the pulmonary arterial structural changes identified in fatal cases of PPHN in human infants.

Animals↗

PubMed1998

Role of hypoxemia and hypercapnia in acute cardiovascular response to periodic apneas in sedated pigs.

The effects of hypoxemia and hypercapnia in acute cardiovascular response to periodic non-obstructive apneas were explored in seven preinstrumented, sedated paralyzed and ventilated pigs under three conditions: room air breathing (RA), O2 supplementation (O2), and supplementation with O2 and CO2 (CO2). EEG monitoring showed no arousal under any conditions. RA apneas increased mean arterial pressure (MAP, from baseline 95.9 +/- 4.5 to late apnea 124.4 +/- 7.8 Torr, P < 0.01), left ventricular end-diastolic pressure, end-diastolic and end-systolic myocardial fiber lengths and systemic vascular resistance, but decreased cardiac output (CO, 3.09 +/- 0.34-2.37 +/- 0.26 L/min, P < 0.01), heart rate (HR, 115.1 +/- 7.5-102.0 +/- 7.8 bpm, P < 0.01), and stroke volume (SV, 29.6 +/- 0.7 21.1 +/- 1.8 ml, P < 0.01). 02 apneas produced similar decreases in HR (114.0 +/- 11.8-105.4 +/- 8.7 bpm, P < 0.05) as with RA apneas, but smaller increases in MAP (94.5 +/- 1.8-103.4 +/- 2.8 Torr, P < 0.01) and in the variables of pre- and after-load. CO and SV remained unchanged with O2 apneas. CO2 was associated with higher MAP, CO, and HR at baseline relative to RA, but similar cardiovascular response during apneas in direction and magnitude to those of O2 apneas. We conclude that in this model hypoxemia is a major but not the sole determinant of the pressor response during apneas. Hypercapnia cannot explain the pressor response seen when hypoxemia is abolished. The HR fall during apneas is independent of hypoxemia, hypercapnia and the pressor response.

Acute Disease↗

PubMed1992

Evidence against participation of V2 receptors in the increase of cerebral blood flow during hypoxemia in the rat.

Cerebral blood flow (CBF) and cerebral utilization of oxygen (CMRO2) were studied in anesthetized and artificially ventilated rats during normoxemia and hypoxemia before and during intravenous infusion of a selective blocker of V2 vasopressinergic receptors (d(CH2)5 [D-Ile2,Abu4] AVP, 15 micrograms/kg per hour i.v.). CBF was measured by means of the intracarotid 133-Xe injection method. CMRO2 was calculated from the oxygen arteriovenous difference using the Fick principle. Infusion of V2 antagonist did not influence CBF, CMRO2 or blood pressure (BP) during normoxia. It also did not change the response of cerebral circulation to hypoxemia. Increase in CBF and decrease in cerebrovascular resistance (CVR) during hypoxemia were similar during the infusion of V2 blocker or without it. However, the decrease in BP observed during hypoxemia in the control group of rats was prevented in the group of animals which were infused with V2 blocker.

Angiotensin Receptor Antagonists↗

PubMed1998

Chronic hypoxemia causes extracellular glutamate concentration to increase in the cerebral cortex of the near-term fetal sheep.

Fetal hypoxia is an important cause of neurologic morbidity and mortality. Hypoxia-induced increase in extracellular glutamate concentration can lead to excitotoxic neuronal death in adults. The objective of this study was to test whether chronic fetal hypoxemia increases extracellular glutamate concentration in the unanesthetized intact cerebral cortex of the near-term fetal sheep. Microdialysis probes were implanted into the parasagittal parietal cortex and periventricular white matter of near-term fetal sheep. At 124 +/- 1 days of gestation, extracellular glutamate concentration was determined before and during 24 h of fetal hypoxemia. Chronic hypoxemia was produced by tightening a vascular occluder placed around the maternal common iliac artery. Larger decreases in fetal arterial oxygen content were associated with larger increases in extracellular glutamate concentration in the parietal cortex (Kendall's tau = 0.81, N = 7, p = 0.005). No such relationship was detected in the periventricular white matter. Chronic hypoxemia increases extracellular glutamate concentration in the intact cerebral cortex of the unanesthetized near-term fetal sheep.

Animals↗

PubMed1997

The vulnerability of the fetal sheep brain to hypoxemia at mid-gestation.

Our aim was to test the hypothesis that a brief episode of hypoxemia near mid-gestation in fetal sheep will result in damage to the fetal brain with the extent and type of damage in any particular region being related to the developmental processes occurring at the time of the insult. Hypoxemia was induced, sufficient to reduce arterial O2 content by approximately 50%, by restricting utero-placental blood flow in 14 chronically catheterised fetuses for 6 h or 12 h at 84 days of gestation (term 145-8 days). Age-matched fetuses (n = 14; 4 operated and 10 unoperated) were used as controls. Fetuses were killed 7 days after being exposed to hypoxemia, and brains removed for histological analysis at the light and ultrastructural levels. Body weights of hypoxemic fetuses did not differ significantly from controls but brain weights were significantly reduced both in absolute terms and when expressed in relation to body weight (P < 0.05). Most fetuses exposed to hypoxemia sustained no gross brain damage. However, in one hypoxemic fetus from a multiple pregnancy there was extensive leucomalacia in the cortical white matter; mild focal damage was seen in another 8 hypoxemic fetuses. In the cerebral cortex (frontal lobe) the surface folding index was significantly reduced (P < 0.05) in hypoxemic fetuses compared to controls suggesting that gyral formation had been delayed. In these fetuses there were also degenerating neurons in the deeper cortical layers. In the hippocampus of hypoxemic fetuses there was a delay (P < 0.05), compared to controls, in the migration of cells from the germinal layer to the pyramidal layer in the CA1 region, and decreases (P < 0.05) in the density (area1) of neurons in the pyramidal layer and in the width of stratum oriens. In the cerebellum of hypoxemic fetuses there was a decrease (P < 0.05), compared to controls, in the density (area1) of mitotic bodies in the external granule cell layer. However, there were no significant differences in the number of pyknotic cells in this layer, in the density of Purkinje cells, in their somal area, or in the width of the external granule cell or molecular layers. There was an increase (P < 0.05) in the proportion of the brain parenchyma occupied by blood vessels in both the hippocampus and cortex of hypoxemic fetuses compared to controls. This study has shown that an hypoxemic insult near mid-gestation can result, one week later, in white matter damage and in neuronal death in the hippocampus and to a lesser extent in the cerebral cortex and cerebellum. It can also retard neuronal migration and the growth of neural processes in the hippocampus where development is well established at this age. Such brain damage could result in less than optimal neuronal connectivity and could affect function postnatally.

Animals↗

PubMed1988

Dialysis leukopenia, hypoxemia, and anaphylatoxin formation: effect of membrane, bath, and citrate anticoagulation.

The goal of these prospective studies was to determine the effect of different dialyzer membranes and dialysate composition on leukopenia and hypoxemia during hemodialysis with citrate anticoagulation. Significant early leukopenia was found with a cuprophane membrane, while a cellulose acetate membrane was associated with mild early leukopenia. Bath composition had no effect. Bicarbonate dialysate, compared with acetate, eliminated hypoxemia in cellulose acetate membranes and reduced its degree and duration with cuprophane. Membrane composition had no effect on hypoxemia during acetate dialysis. The findings indicate that leukopenia is directly and exclusively related to membrane composition while hypoxemia only relates in part to membrane effects. Serial determinations of complement components C3a and C5a showed significant increases in parallel with leukopenia during heparin anticoagulation, but the anaphylatoxin concentration changes were dissociated during dialysis with citrate anticoagulation. The concentrations of anaphylatoxins C3a and C5a appear not to be directly related to dialysis-induced leukopenia. The dissociation between anaphylatoxin concentrations and leukopenia may be related to changes in generation or unmasked changes in leukocyte response. Citrate anticoagulation may provide a useful probe for further studies on membrane-leukocyte interactions in vivo.

Acetates↗

PubMed2003

Fetal hypoxemia on a molecular level: adaptive changes in the hypothalamic-pituitary-adrenal (HPA) axis and the lungs.

The development of diseases in later life, such as diabetes type II, hypertension and cardiovascular disease, is linked to abnormal intrauterine conditions that reduce birth weight. Obviously, fetal development can be disturbed so profoundly, that fetal programming is changed permanently. We have examined the effects of hypoxia, or more precisely hypoxemia, on the fetal hypothalamic-pituitary-adrenal (HPA) axis and lungs using molecular biology techniques in order to elucidate the underlying mechanisms. Chronically catheterized fetal sheep were subjected to a hypoxemia (48 h) without change in arterial pH or paCO2. Major changes occurred, although the degree of hypoxemia was just moderate. There was a transient increase in the fetal plasma ACTH-concentrations with an upregulation of the cortisol-concentrations, which was more pronounced in the older, hypoxemic fetuses (134-136 days of gestation) than in the younger, hypoxemic animals (126-130 days of gestation; term is 145 days). There was an unique, differential regulation for pro-opiomelanocortin messenger RNA (mRNA), the precursor molecule of e.g. ACTH, in the pars distalis and pars intermedia of the pituitary gland. This finding supported the increased bioactivity besides the increased concentrations for ACTH. Simultaneously, there was an increase in the mRNAs of the ACTH-receptor and of the steroid-synthesizing enzymes in the fetal adrenal gland of the older, hypoxemic fetuses. No changes in the fetal plasma androstenedione-concentrations were observed. Clearly, there was a selective increase of the cortisol-synthesis. Growth and maturation of the fetal lung might also have been affected, because of the increase in surfactant-protein A mRNA in the older, hypoxemic animals and the decrease in the insulin-like growth factor-I and its binding protein-5 mRNA in the younger, hypoxemic fetuses. In summary, even a moderate degree of hypoxemia was shown to affect the different levels of fetal organism profoundly, offering a pathophysiological basis for changes in fetal development.

Adrenal Glands↗

PubMed2001

The ability of pulse oximetry to screen for hypoxemia and hypercapnia in patients breathing room air.

This study was designed to determine whether high room-air pulse oximetry can rule out hypoxemia or moderate hypercapnia. Based on retrospective analysis of 513 arterial blood gas results, oxygen saturation cutpoints were derived. Coincidentally, a room-air oxygen saturation (RAO2 sat) value of 96% was selected as a cutpoint to screen for both hypoxemia (PaO2 < 70 mm Hg) and moderate hypercapnia (PaCO2 > 50 mm Hg). These tests were validated prospectively by using a convenience sample of 213 Emergency Department patients in whom room-air arterial blood gas sampling was ordered. To detect hypoxemia, the sensitivity of RAO(2) sat < or = 96% was 1.0 [0.95-1.0, 95% confidence interval (CI)] and specificity was 0.54 (0.45-0.64, 95% CI). To detect hypercapnia, the sensitivity of RAO(2) sat < or = 96% was 1.0 (0.7-1.0) and specificity was 0.31 (0.25-0.38, 95% CI). We concluded that RAO(2) sat > or = 97% rules out hypoxemia and may also rule out moderate hypercapnia.

Adult↗

PubMed1997

Does significant arterial hypoxemia alter vital signs?

STUDY OBJECTIVE: To determine the cardiovascular and respiratory effects of arterial hypoxemia in adult volunteers. DESIGN: Prospective, subject-controlled. SETTING: University-affiliated hospital. SUBJECTS: 16 awake, unsedated, unanesthetized adult volunteers. INTERVENTIONS: Inspired oxygen concentration (FIO2) was decreased in decrements to reduce pulse oximeter values to a range of 95% to 90%, 89% to 85%, 84% to 80%, and 79% to 70%. MEASUREMENTS AND MAIN RESULTS: Heart rate (HR), blood pressure (BP), respiratory rate (RR), arterial blood pH, gas tensions, and oxyhemoglobin saturation were determined during normoxia and each level of oxyhemoglobin desaturation. FIO2 was reduced from 21% to 10%. Arterial blood oxyhemoglobin saturation and oxygen tension ranged from 100% to 71% and 103 to 35 mmHg, respectively. There were no significant changes in RR, BP, or HR during the study. CONCLUSIONS: HR, BP, and RR are not reliable indicators of arterial hypoxemia in awake volunteers. If this finding is also true for sedated or anesthetized patients, then continuous monitoring with pulse oximetry should be used whenever patients are at risk for arterial hypoxemia. Stable HR, BP, and RR may not eliminate the possibility of significant arterial hypoxemia and impending catastrophic events.

Adult↗

PubMed1998

Fetal brain injury following prolonged hypoxemia and placental insufficiency: a review.

It is well-established that severe, acute episodes of hypoxemia can damage the brain before birth, but the effects of more sustained hypoxemia are less well understood. We have used fetal fetal sheep in a series of studies aimed at determining the effects of prolonged hypoxemia, induced by placental insufficiency of differing severity and duration, on fetal brain structure. Restriction of placental, and hence fetal, growth by carunclectomy caused impaired development of neural processes and connections in the hippocampus, cerebellum, and visual cortex; neuronal migration and neuronal numbers did not appear to be affected. Twenty days of placental insufficiency during late gestation induced by umbilicoplacental embolisation also caused abnormalities in brain structure; the cerebellum, which develops late in gestation, was particularly affected. In the cortex, there was evidence of white matter lesions, an increase in the size of capillaries and a proliferation of astroglia. We also examined the effects of shorter periods of hypoxemia (6-12 hr) near mid-gestation on brain structure; fetuses were allowed to recover for 7 or 35 days after the hypoxemic challenge. The major changes were mild focal damage in the cortical white matter, a reduction in the number of Purkinje cells, a delay in the growth of neural processes in the cerebellum and proliferation of blood vessels. The hippocampus was also affected, in particular the areal density of pyramidal cells was reduced. The use of several classes of pharmacological agents with the potential to protect neurons from hypoxemic injury is discussed in relation to the developing brain.

Animals↗

PubMed2004

Neonatal electrocortical brain activity and cerebral tissue oxygenation during non-acidotic, normocarbic and normotensive graded hypoxemia.

OBJECTIVE: Neonates are commonly exposed to isolated hypoxemic episodes. In order to identify the risk of this, we correlated cerebral oxygen delivery and electrocortical brain activity during isolated graded and repetitive hypoxemia in 1-week-old piglets. METHODS: Six halothane-anesthetized piglets were subjected to two episodes of graded hypoxemia of 45 min duration. The fractional concentration of inspired oxygen (FiO(2)) was stepwise decreased at 15 min intervals from 0.21 to 0.15, 0.10 and 0.05. A second identical hypoxemic event was induced after 1 h of normoxemia (FiO(2) 0.21). Mean arterial pressure (MAP) and pH were maintained at baseline values during the whole experiment. We measured near infrared spectroscopy parameters (cerebral oxidized cytochrome aa(3) (Cytaa3), total hemoglobin (tHb: oxy- +deoxyhemoglobin)) corresponding to cerebral blood volume (CBV), carotid blood flow (Q(car)), intra-arterial oxygen saturation (SaO(2)), and mean maximal EEG amplitude and relative spectral power. RESULTS: Delta (delta) power increased significantly and the EEG amplitude dropped below 10 and 5 microV at the end of the first and the second hypoxemic period (PaO(2) 2.68+/-1.08 (P<0.05) and 2.87+/-0.58 kPa, respectively). Both EEG variables normalized during recovery (FiO(2) 0.21). Q(car), CBV and Cytaa3 were not changed. CONCLUSION: Acute isolated hypoxemia has to be sustained to induce neuronal hypofunction in normotensive animals. Hypoxic hypoxemia led to acute changes in neuronal activity, whereas cellular oxygenation remained unaffected.

Animals↗

PubMed1998

Influence of pulse oximeter settings on the frequency of alarms and detection of hypoxemia: Theoretical effects of artifact rejection, alarm delay, averaging, median filtering or a lower setting of the alarm limit.

OBJECTIVE: The potential benefit of a reduced frequency of false pulse oximeter low oxyhemoglobin saturation (SpO2) alarms is that the attention of personnel is only directed to patients who experience hypoxemia. The present study was undertaken to better understand the effects of different settings of the pulse oximeter on false (artifact) and true (hypoxemia) alarms. METHODS: Using the original SpO2 data of 200 postoperative patients, we calculated off-line the effects of five methods (artifact rejection, alarm delay (2-44 s, 2 s increments), averaging (10-90 s), median filtering (10-90 s) and decreasing the alarm limit from 90% to 85%) on the number of (true- and false) alarms. RESULTS: 830 episodes of hypoxemia (SpO2 < or = 90%) and 73 episodes of severe hypoxemia (SpO2 < or = 85%) occurred. With a SpO2 alarm limit of 90%, the alarm was triggered 1535 times (830 true, 705 false). Artifact rejection reduced alarms by almost 50%. An alarm delay of 6 s or an averaging or median filtering epoch of 10 s resulted in an alarm reduction of almost 50%. No differences were found in the reduction of alarms between averaging and median filtering. Changing the alarm limit to 85% reduced the number of alarms by 82%. A similar reduction of alarms was obtained with either an alarm delay of 18 s or an averaging or median filtering epoch of 42 s. However, an alarm limit of 85% reduced the number of false alarms less than the other three algorithms (p < 0.01). CONCLUSIONS: The data from the present study suggest that in order to effectively suppress false alarms caused by pulse oximeter artifacts, it may be preferable to use a longer filtering epoch of approximately 40 s, rather than to decrease the lower alarm limit.

Artifacts↗