This study investigates the relation between changes in pulse oximeter oxygen saturation (SpO2) and changes in arterial oxygen saturation (SaO2) in the critically ill, and the effects of acidosis and anaemia on precision of using pulse oximetry to predict SaO2.
Patients and methods
Forty-one consecutive patients were recruited from a nine-bed general intensive care unit into a 2-month study. Patients with significant jaundice (bilirubin >40 μmol/l) or inadequate pulse oximetry tracing were excluded.
A total of 1085 paired readings demonstrated only moderate correlation (r= 0.606; P < 0.01) between changes in SpO2 and those in SaO2, and the pulse oximeter tended to overestimate actual changes in SaO2. Anaemia increased the degree of positive bias whereas acidosis reduced it. However, the magnitude of these changes was small.
Changes in SpO2 do not reliably predict equivalent changes in SaO2 in the critically ill. Neither anaemia nor acidosis alters the relation between SpO2 and SaO2 to any clinically important extent.
acidosis; anaemia; arterial oxygen saturation; critical care; pulse oximetry
The objective of this prospective clinical study was to evaluate the accuracy of pulse oximetry and capnography in healthy and compromised horses during general anesthesia with spontaneous and controlled ventilation. Horses anesthetized in a dorsal recumbency position for arthroscopy (n = 20) or colic surgery (n = 16) were instrumented with an earlobe probe from the pulse oximeter positioned on the tip of the tongue and a sample line inserted at the Y-piece for capnography. The horses were allowed to breathe spontaneously (SV) for the first 20 min after induction, and thereafter ventilation was controlled (IPPV). Arterial blood, for blood gas analysis, was drawn 20 min after induction and 20 min after IPPV was started. Relationships between oxygen saturation as determined by pulse oximetry (SpO2), arterial oxygen saturation (SaO2), arterial carbon dioxide partial pressure (PaCO2), and end tidal carbon dioxide (P(et)CO2), several physiological variables, and the accuracy of pulse oximetry and capnography, were evaluated by Bland–Altman or regression analysis. In the present study, both SpO2 and P(et)CO2 provided a relatively poor indication of SaO2 and PaCO2, respectively, in both healthy and compromised horses, especially during SV. A difference in heart rate obtained by pulse oximetry, ECG, or palpation is significantly correlated with any pulse oximeter inaccuracy. If blood gas analysis is not available, ventilation to P(et)CO2 of 35 to 45 mmHg should maintain the PaCO2 within a normal range. However, especially in compromised horses, it should never substitute blood gas analysis.
Pulse oximetry is routinely used to continuously and noninvasively monitor arterial oxygen saturation (SaO2) in critically ill patients. Although pulse oximeter oxygen saturation (SpO2) has been studied in several patient populations, including the critically ill, its accuracy has never been studied in emergency department (ED) patients with severe sepsis and septic shock. Sepsis results in characteristic microcirculatory derangements that could theoretically affect pulse oximeter accuracy. The purposes of the present study were twofold: 1) to determine the accuracy of pulse oximetry relative to SaO2 obtained from ABG in ED patients with severe sepsis and septic shock, and 2) to assess the impact of specific physiologic factors on this accuracy.
This analysis consisted of a retrospective cohort of 88 consecutive ED patients with severe sepsis who had a simultaneous arterial blood gas and an SpO2 value recorded. Adult ICU patients that were admitted from any Calgary Health Region adult ED with a pre-specified, sepsis-related admission diagnosis between October 1, 2005 and September 30, 2006, were identified. Accuracy (SpO2 - SaO2) was analyzed by the method of Bland and Altman. The effects of hypoxemia, acidosis, hyperlactatemia, anemia, and the use of vasoactive drugs on bias were determined.
The cohort consisted of 88 subjects, with a mean age of 57 years (19 - 89). The mean difference (SpO2 - SaO2) was 2.75% and the standard deviation of the differences was 3.1%. Subgroup analysis demonstrated that hypoxemia (SaO2 < 90) significantly affected pulse oximeter accuracy. The mean difference was 4.9% in hypoxemic patients and 1.89% in non-hypoxemic patients (p < 0.004). In 50% (11/22) of cases in which SpO2 was in the 90-93% range the SaO2 was <90%. Though pulse oximeter accuracy was not affected by acidoisis, hyperlactatementa, anemia or vasoactive drugs, these factors worsened precision.
Pulse oximetry overestimates ABG-determined SaO2 by a mean of 2.75% in emergency department patients with severe sepsis and septic shock. This overestimation is exacerbated by the presence of hypoxemia. When SaO2 needs to be determined with a high degree of accuracy arterial blood gases are recommended.
Hypoxemia is common in patients with cirrhosis but the natural history of this syndrome is unknown. This study was conducted to evaluate the natural history of arterial oxygenation in patient with end stage liver cirrhosis.
Sixty eight patients with liver cirrhosis were followed up for 6-12 months. Arterial blood gas (ABG) and pulse oximetry were obtained on day of presentation and follow up.
There were no significant changes in the oxygen saturation by pulse oximetry (SpO2), partial pressure of oxygen (PaO2) and alveolar arterial oxygen gradient (A-a O2) after 6-12 months. Mean arterial oxygen saturation (SaO2) in 46 patients was 95.42±1.92, and after follow up changed to 95.45±2.96. Thirty eight patients had SaO2 > 94% (mean 96.12±1.08 after 6-12 months changed to 95.66±2.58) ; 8 patients had SaO2 = 94 (mean 92.08±1.44 after 6-12 months changed to 94.46±4.47).
There were no significant changes in the SpO2, PaO2 and A-a O2 after 6-12 months.
Blood gas; Cirrhosis; Hypoxemia
Arterial oxygen saturation values (Sao2) from 60% to 98% were measured by the Ohmeda 3700 pulse oximeter with the three types of probe available and compared with values of oxygen saturation estimated from direct arterial sampling (arterial oxygen and carbon dioxide tensions and pH) on 65 occasions. The response time of the oximeter was measured after a sudden rise in inspired oxygen concentration. Artefact rejection was assessed by arterial compression proximal to the probe site, and by simultaneous recordings of overnight Sao2 on opposite hands. The ability to recreate patterns of oscillating Sao2 from the data stored in the oximeter was also investigated. With the best probe system the oximeter measured Sao2, relative to arterial values estimated from Pao2, with a mean (SD) difference of -0.4% (1.8%). The response time was comparable with those of previous oximeters. It was not possible to generate artefactual dips in excess of 2% Sao2, and the dual overnight recordings rarely showed even small dips on one tracing alone. The stored data can recreate oscillating Sao2 signals with wavelengths down to about 35 seconds, but not below. The Ohmeda 3700 pulse oximeter appears to be suitable for unattended overnight recordings of Sao2.
Methemoglobinemia is a rare cause of hypoxemia, characterized by abnormal levels of oxidized hemoglobin that cannot bind to and transport oxygen.
A 62-year-old male underwent bronchoscopy where lidocaine oral solution and Hurricaine spray (20% benzocaine) were used. He developed central cyanosis and his oxygen saturation was 85% via pulse oximetry. An arterial blood gas revealed pH 7.45, PCO2 42, PO2 282, oxygen saturation 85%. Co-oximetry performed revealed a methemoglobin level of 17.5% (normal 0.6–2.5%). The patient was continued on 15 L/minute nonrebreathing face mask and subsequent oxygen saturation improved to 92% within two hours. With hemodynamic stability and improved SpO2, treatment with methylene blue was withheld.
Methemoglobinemia is a potentially lethal condition after exposure to routinely used drugs. Physicians should be aware of this complication for early diagnosis and treatment.
Prompt recognition and treatment of hypoxia is an important part of management in the accident and emergency (A & E) department. Until recently the only reliable method of detecting hypoxia was by estimation of the arterial blood gases (ABG). Continuous monitoring of the arterial oxygen saturation (Sao2) is possible using an infra-red pulse oximeter. This study assessed the usefulness of this instrument in the A&E setting. The Sao2 was measured in 50 patients using a pulse oximeter. In 15 patients simultaneous ABG estimations were obtained. The Sao2 correlated closely with calculated values for Sao2. The use of the oximeter identified 21 patients (42%) with clinically unsuspected hypoxia. The pulse oximeter proved simple to use, accurate and a useful addition to our resuscitation equipment.
Pulse oximeter (SaO2P) measurements were compared with direct arterial line oxygen saturation (SaO2) from co-oximeters in 92 instances in 43 patients, and with arterial line oxygen measurements (PaO2) in 169 instances in 81 patients. The mean (SD) absolute difference between SaO2P and SaO2 was 2.6% (2.4) after attempt to correct for the co-oximeter falsely measuring a proportion of fetal haemoglobin as carboxy haemoglobin. For 19 infants and children greater than or equal to 5 months old, who have very little fetal haemoglobin, the mean (SD) absolute difference of 27 comparisons was 1.8% (2.1). Comparison of SaO2P and PaO2 measurements in 46 instances when PaO2 was less than 6.67 kPa showed SaO2 to be less than 90% on 40 occasions. In 24 instances when PaO2 was greater than or equal to 13.3 kPa the SaO2P was greater than or equal to 98% on 22 occasions. In 23 infants undergoing neonatal intensive care, transcutaneous oxygen monitors were compared with arterial PO2 measurements in 60 instances. The mean (SD) absolute difference between PaO2 and transcutaneous oxygen measurements was 1.60 kPa (1.73). Ten of the 60 comparisons had differences greater than 2.67 kPa and three greater than 5.33 kPa (maximum 8.40 kPa). Pulse oximetry is a clinically useful technique for managing oxygenation but further studies are needed to confirm its safety in premature infants at risk of retinopathy of prematurity.
The aim of this study was to examine the potential correlation of sleep characteristics with glucose metabolism in nondiabetic men with obstructive sleep apnea syndrome (OSAS). Included were 31 male patients (mean age 46.7 ±11 years), recently diagnosed with OSAS by full polysomnography. There was a significant correlation of fasting glucose and glycosylated hemoglobin (HbA1c) levels with arousal index (P = 0.047 and P =0.014, respectively). Moreover, HbA1c levels were correlated with apnea hypopnea index (P =0.009), a widely accepted marker of the severity of OSAS, and with percentage of sleep time with saturation of hemoglobin with oxygen as measured by pulse oximetry (SpO2) < 90% (t < 90%) ( P =0.010). Finally, glucose and HbA1c levels showed a significant negative correlation with average SpO2 (P =0.013 and P = 0.012, respectively) and, additionally, glucose levels with minimum SpO 2 (P =0.027) during sleep. In conclusion, severity of OSAS among nondiabetic men is associated with increased HbA1c levels and increased fasting glucose. Thus, severity of OSAS may be an additional marker of cardiovascular risk, as well as of future diabetes, in these subjects. However, further work is needed to confirm the clinical significance of these observations.
obstructive sleep apnea syndrome; glucose metabolism; glycated hemoglobin; sleep disordered breathing
Arterial blood gas tensions, pH, and carboxyhaemoglobin were measured on 322 occasions in 165 patients and the actual oxygen saturation of the haemoglobin (Sao2) was compared with the ear oxygen saturation (SEO2) recorded during the arterial sampling with a Biox IIA ear oximeter. The overall agreement between SEO2 and Sao2 was good, with a mean difference in saturation (SEO2-Sao2) of + 1.5% (SD 3.0). The difference in saturation remained similar at all levels of arterial saturation observed and was unaffected by carboxyhaemoglobin concentration. On four occasions (1% of readings), however, SEO2 and Sao2 differed by more than 10% and such occasional errors might be misleading in clinical practice.
Conventional pulse oximetry uses two wavelengths of light (red and infrared) transmitted through a finger and a photodetector to analyze arterial hemoglobin oxygen saturation and pulse rate. Recent advances in pulse oximetry include: extended analysis of the photo plethysmographic waveform; use of multiple wavelengths of light to quantify methemoglobin, carboxyhemoglobin and total hemoglobin content in blood; and use of electronic processes to improve pulse oximeter signal processing during conditions of low signal-to-noise ratio. These advances have opened new clinical applications for pulse oximeters that will have an impact on patient monitoring and management.
A case of delayed detection of esophageal intubation is described. Preoxygenation and pulse oximetry were used, and the first indication of tube misplacement was arterial desaturation indicated by the pulse oximeter. The combination of preoxygenation and pulse oximetry may contribute to delays in early detection of endotracheal tube misplacement for the following reasons: (1) preoxygenation results in a pulmonary reservoir of oxygen sufficient to maintain arterial hemoglobin saturation for an extended period of time; and (2) the maintenance of normal arterial saturations for an extended period after inadvertent esophageal tube placement may lead the practitioner to initially seek other causes of declining oxygen saturations. Although pulse oximetry is an acknowledged advance in patient monitoring, it must not be utilized as an early indication of correct endotracheal tube placement.
Since the invention of pulse oximetry by Takuo Aoyagi in the early 1970s, its use has expanded beyond the perioperative care into neonatal, paediatric and adult intensive care units (ICUs). Pulse oximetry is one of the most important advances in respiratory monitoring as its readings (SpO2) are used clinically as an indirect estimation of arterial oxygen saturation (SaO2). Sensors were placed frequently on the sole, palm, ear lobe or toes in addition to finger. On performing an extensive Medline search using the terms “accuracy of pulse oximetry” and “precision of pulse oximetry”, limited data were found in congenital heart disease patients in the immediate post-corrective stage. Also, there are no reports and comparative data of the reliability and precision of pulse oximetry when readings from five different sensor locations (viz. finger, palm, toe, sole and ear) are analysed simultaneously. To fill these lacunae of knowledge, we undertook the present study in 50 infants and children with cyanotic heart disease in the immediate post-corrective stage.
Accuracy; bias; precision; co-oximeter; pulse oximetry; SpO2; SaO2
Hepatopulmonary syndrome (HPS) is a rare complication of liver diseases of different etiologies and may indicate a poor prognosis. Therefore, a simple non-invasive screening method to detect HPS would be highly desirable. In this study pulse oximetry was evaluated to identify patients with HPS.
In 316 consecutive patients with liver cirrhosis (n = 245), chronic hepatitis (n = 69) or non-cirrhotic portal hypertension (n = 2) arterial oxygen saturation (SaO2) was determined using a pulse oximeter. In patients with SaO2 ≤92% in supine position and/or a decrease of ≥4% after change from supine to upright position further diagnostic procedures were performed, including contrast-enhanced echocardiography and perfusion lung scan.
Seventeen patients (5.4%) had a pathological SaO2. Four patients (1.3%) had HPS. HPS patients had a significant lower mean SaO2 in supine (89.7%, SD 5.4 vs. 96.0%, SD 2.3; p = 0.003) and upright position (84.3%, SD 5.0 vs. 96.0%, SD 2.4; p = 0.001) and had a lower mean PaO2 (56.2 mm Hg, SD 15.2 vs. 71.2 mm Hg, SD 20.2; p = 0.02) as compared to patients without HPS. The mean ΔSaO2 (difference between supine and upright position) was 5.50 (SD 7) in HPS patients compared to non-HPS patients who showed no change (p = 0.001). There was a strong correlation between shunt volume and the SaO2 values (R = -0.94).
Arterial SaO2 determination in supine and upright position is a useful non-invasive screening test for HPS and correlates well with the intrapulmonary shunt volume.
Pulse oximetry data such as saturation of peripheral oxygen (SpO2) and pulse rate are vital signals for early diagnosis of heart disease. Therefore, various pulse oximeters have been developed continuously. However, some of the existing pulse oximeters are not equipped with communication capabilities, and consequently, the continuous monitoring of patient health is restricted. Moreover, even though certain oximeters have been built as network models, they focus on exchanging only pulse oximetry data, and they do not provide sufficient device management functions. In this paper, we propose an advanced pulse oximetry system for remote monitoring and management. The system consists of a networked pulse oximeter and a personal monitoring server. The proposed pulse oximeter measures a patient's pulse oximetry data and transmits the data to the personal monitoring server. The personal monitoring server then analyzes the received data and displays the results to the patient. Furthermore, for device management purposes, operational errors that occur in the pulse oximeter are reported to the personal monitoring server, and the system configurations of the pulse oximeter, such as thresholds and measurement targets, are modified by the server. We verify that the proposed pulse oximetry system operates efficiently and that it is appropriate for monitoring and managing a pulse oximeter in real time.
Patients with sickle cell disease usually have mild hypoxaemia and their oxyhaemoglobin dissociation curve is shifted to the right. It follows that oxygen saturation in sickle cell disease should be lower than normal. Most subjects in this clinic had normal oxygen saturation by pulse oximetry, however. To improve the understanding of this paradox, arterialised capillary oxygen tension (PO2) and oxygen saturation were compared with simultaneously measured pulse oximeter saturation in 20 children with sickle cell disease. In addition, the PO2 at 50% haemoglobin saturation (P50) was compared with saturation measured by pulse oximetry in all 20 patients. It was found that saturation measured by pulse oximetry was, on the whole, similar to that calculated from the sampled blood. Individual deviations were not random, however, and were partly explained by differences in P50 values. It is concluded that pulse oximetry gives variable results in patients with sickle cell disease and should be used with caution to predict arterial saturation in this patient group.
Changes in oxygenation occur during one-lung ventilation (OLV) due to intrapulmonary shunt. Although arterial oxygenation is generally adequate, there are no studies evaluating the effect of these changes on cerebral oxygenation.
MATERIALS AND METHODS:
Cerebral oxygenation (rSO2), heart rate (HR), blood pressure (BP), oxygen saturation (SaO2), and end-tidal carbon dioxide (ETCO2) were prospectively monitored during OLV in adults. Cerebral oxygenation was monitored using near infrared spectroscopy. No clinical decisions were made based on the rSO2 value. BP and HR were the inspired oxygen concentration was adjusted as needed to maintain the SaO2 ≥ 95%.
The study cohort included 40 adult patients. 18,562 rSO2 values were collected during OLV. The rSO2 was ≥ baseline at 3,593 of the 18,562 data points (19%). The rSO2 was 0-9 ≤ baseline in 7,053 (38%) of the readings, 10-19 ≤ baseline in 4,084 (22%) of the readings, and 20-29 ≤ baseline in 3,898 (21%) of the readings. 2,599 (14%) of the rSO2 values were less than 75% of the baseline value. Thirteen patients (32.5%) had at least one rSO2 value that was less than 75% of the baseline. Eight patients (20%) had rSO2 values less than 75% of baseline for ≥ 25% of the duration of OLV. These patients were older (63.7 ± 10.2 vs 54.6 ± 9.8 years, P<0.025), weighed more (95.8 ± 17.4 vs 82.6 ± 14.6 kgs, P=0.038), and were more likely to be ASA III vs II (7 of 8 versus 25 of 32, relative risk 1.75) than the remainder of the cohort.
Significant changes in rSO2 occur during OLV for thoracic surgical procedures. Future studies are needed to determine the impact of such changes on the postoperative course of these patients.
Cerebral oxygenation; near infrared spectroscopy; one-lung ventilation; thoracic surgery; thoracoscopy
Pulse oximetry is commonly used to monitor oxygenation in neonates, but cannot detect variations in hemoglobin. Venous and arterial oxygen saturations are rarely monitored. Few data are available to validate measurements of oxygen saturation in neonates (venous, arterial, or pulse oximetric).
To validate oxygen saturation displayed on clinical monitors against analyses (with correction for fetal hemoglobin) of blood samples from neonates and to present the oxyhemoglobin dissociation curve for neonates.
Seventy-eight neonates, 25 to 38 weeks’ gestational age, had 660 arterial and 111 venous blood samples collected for analysis.
The mean difference between oxygen saturation and oxyhemoglobin level was 3% (SD 1.0) in arterial blood and 3% (SD 1.1) in venous blood. The mean difference between arterial oxygen saturation displayed on the monitor and oxyhemoglobin in arterial blood samples was 2% (SD 2.0); between venous oxygen saturation displayed on the monitor and oxyhemoglobin in venous blood samples it was 3% (SD 2.1) and between oxygen saturation as determined by pulse oximetry and oxyhemoglobin in arterial blood samples it was 2.5% (SD 3.1). At a Pao2 of 50 to 75 mm Hg on the oxyhemoglobin dissociation curve, oxyhemoglobin in arterial blood samples was from 92% to 95%; oxygen saturation was from 95% to 98% in arterial blood samples, from 94% to 97% on the monitor, and from 95% to 97% according to pulse oximetry.
The safety limits for pulse oximeters are higher and narrower in neonates (95%-97%) than in adults, and clinical guidelines for neonates may require modification.
Arterial oxygen saturation (SaO2) and partial arterial pressure of carbon dioxide (PaCO2) are important respiratory parameters in critically ill neonates. A sensor combining a pulse oximeter with the Stow-Severinghaus electrode, required for the measurement of peripheral oxygen saturation (SpO2) and transcutaneous partial pressure of carbon dioxide (PtcCO2), respectively, has been recently used in neonatal clinical practice (TOSCA500ÒRadiometer). We evaluated TOSCA usability and reliability in the delivery room (DR), throughout three different periods, on term, late-preterm, and preterm neonates. During the first period (period A), 30 healthy term neonates were simultaneously monitored with both TOSCA and a MASIMO pulse oximeter. During the second period (period B), 10 healthy late-preterm neonates were monitored with both TOSCA and a transcutaneous device measuring PtcCO2 (TINAÒ TCM3, Radiometer). During the third period (period C), 15 preterm neonates were monitored with TOSCA and MASIMO after birth, during stabilization, and during transport to the neonatal intensive care unit (NICU). Blood gas analyses were performed to compare transcutaneous and blood gas values. TOSCA resulted easily and safely usable in the DR, allowing reliable noninvasive SaO2 estimation. Since PtcCO2 measurements with TOSCA required at least 10 min to be stable and reliable, this parameter was not useful during the early resuscitation immediately after birth. Moreover, PtcCO2 levels were less precise if compared to the conventional transcutaneous monitoring. However, PtcCO2 measurement by TOSCA was useful as trend-monitoring after stabilization and during transport to NICU.
oxygen saturation; partial pressure of carbon dioxide; pulse oximeter; delivery room; TOSCA sensor; neonate
Arterial oxygen saturation (SpO2) was monitored postoperatively with pulse oximetry in 72 dental patients. Intravenous general anesthesia was employed in 57 patients. All of these patients received supplemental oxygen intraoperatively, and of these, 29 received supplemental oxygen postoperatively. Fifteen patients received only local anesthesia without supplemental oxygen and served as the control group. Continuous pulse oximetry revealed 43 episodes of arterial oxygen desaturation (SpO2 decreases greater than 3% from baseline) in patients who did not receive postanesthesia supplemental oxygen and eight episodes of desaturation in patients who did receive postanesthesia oxygen. Patients with a smoking history had more episodes of desaturation than did nonsmokers in the group that received general anesthesia and breathed room air postoperatively. The total amount of methohexital administered had no significant effect on the number of patients with desaturation episodes. These observations emphasize the need for postoperative oxygen for patients who undergo general anesthesia for outpatient oral and maxillofacial surgery.
The pulse oximeter, a medical device capable of measuring blood oxygen saturation (SpO2), has been shown to be a valuable device for monitoring patients in critical conditions. In order to incorporate the technique into a wearable device which can be used in ambulatory settings, the influence of motion artifacts on the estimated SpO2 must be reduced. This study investigates the use of the smoothed psuedo Wigner-Ville distribution (SPWVD) for the reduction of motion artifacts affecting pulse oximetry.
The SPWVD approach is compared with two techniques currently used in this field, i.e. the weighted moving average (WMA) and the fast Fourier transform (FFT) approaches. SpO2 and pulse rate were estimated from a photoplethysmographic (PPG) signal recorded when subject is in a resting position as well as in the act of performing four types of motions: horizontal and vertical movements of the hand, and bending and pressing motions of the finger. For each condition, 24 sets of PPG signals collected from 6 subjects, each of 30 seconds, were studied with reference to the PPG signal recorded simultaneously from the subject's other hand, which was stationary at all times.
Results and Discussion
The SPWVD approach shows significant improvement (p < 0.05), as compared to traditional approaches, when subjects bend their finger or press their finger against the sensor. In addition, the SPWVD approach also reduces the mean absolute pulse rate error significantly (p < 0.05) from 16.4 bpm and 11.2 bpm for the WMA and FFT approaches, respectively, to 5.62 bpm.
The results suggested that the SPWVD approach could potentially be used to reduce motion artifact on wearable pulse oximeters.
Pulse oximetry is widely used in critical care medicine to noninvasively estimate arterial hemoglobin oxygen saturation. Despite the obvious benefits of using pulse oximetry to detect life threatening desaturations, it is unknown how well pulse oximetry is able to predict the finer graduations of arterial oxygenation needed for clinical decision making. A computerized protocol was developed for the use of pulse oximetry to classify arterial oxygenation into four fuzzy categories and tested in a prospective clinical trial which compared the oxygenation category assigned by the protocol to one assigned by a respiratory therapist. In 3,742 classifications from 15 patients over a seven month period, the protocol showed 96% agreement with the therapists in the direction of therapy and 75% agreement with the oxygenation classes assigned by the therapists.
Pulmonary disease in mice induced by influenza virus was monitored by measurement of oxygen saturation (SaO2) in blood with a pulse oximeter. The SaO2 declined in inverse proportion to the viral inoculum. The known antiviral agent ribavirin inhibited the SaO2 decline, prevented death, lowered lung consolidation, and reduced the level of recoverable virus. Pulse oximetry is an effective means of monitoring murine influenzal disease and can be used in the study of potential antiviral drugs.
In cirrhotic patients, in addition to hepatocytes and Kuppfer cells dysfunction circulatory anatomic shunt and ventilation/perfusion (VA/ Q) ratio abnormalities can induce decrease in partial pressure of oxygen in arterial blood (PaO2), in oxygen saturation of hemoglobin (SaO2) as well as various acid-base disturbances. We studied 49 cases of liver cirrhosis (LC) with ascites compared to 50 normal controls. Causes were: posthepatic 37 (75.51%), alcoholic 7 (14.24%), cardiac 2 (4.08%), and cryptogenic 3 (6.12%). Complications were: upper gastrointestinal bleeding 24 (48.97), hepatic encephalopathy 20 (40.81%), gastritis 28 (57.14%), hepatoma 5 (10.2%), renal hepatic syndrome 2 (4.01%), HbsAg (+) 24 (48.97%), and hepatic pleural effusions 7 (14.28%). Average PaO2 and SaO2 were 75.2 mmHg and 94.5 mmHg, respectively, compared to 94.2 mmHg and 97.1 mmHg of the control group, respectively (p value in both PaO2 and SaO2 was p<0.01). Respiratory alkalosis, metabolic alkalosis, metabolic acidosis, respiratory acidosis and metabolic acidosis with respiratory alkalosis were acid-base disturbances observed. In conclusion, portopulmonary shunt, intrapulmonary arteriovenous shunt and VA/Q inequality can induce a decrease in PaO2 and SaO2 as well as various acid-base disturbances. As a result, pulmonary resistance is impaired and patients more likely succumb to infections and adult respiratory distress syndrome.
liver cirrhosis; ascites; acid base disturbances; hepatopulmonary syndrome
Objective: To study whether lower arterial oxygen saturation (SaO2) and chronic obstructive pulmonary disease (COPD) are associated with cerebral white matter lesions and lacunar infarcts.
Methods: We measured SaO2 twice with a pulse oximeter, assessed the presence of COPD, and performed MRI in 1077 non-demented people from a general population (aged 60–90 years). We rated periventricular white matter lesions (on a scale of 0–9) and approximated a total subcortical white matter lesion volume (range 0–29.5 ml). All analyses were adjusted for age and sex and additionally for hypertension, diabetes, body mass index, pack years smoked, cholesterol, haemoglobin, myocardial infarction, and left ventricular hypertrophy.
Results: Lower SaO2 was independent of potential confounders associated with more severe periventricular white matter lesions (score increased by 0.12 per 1% decrease in SaO2 (95% confidence interval 0.01 to 0.23)). Participants with COPD had more severe periventricular white matter lesions than those without (adjusted mean difference in score 0.70 (95% confidence interval 0.23 to 1.16)). Lower SaO2 and COPD were not associated with subcortical white matter lesions or lacunar infarcts.
Conclusion: Lower SaO2 and COPD are associated with more severe periventricular white matter lesions.