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 Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 46  |  Issue : 2  |  Page : 93-98

Pulse oximetry in comparison to arterial blood oxygen saturation in children with bronchial asthma coming to the emergency room


1 Department of Emergency Medicine, Faculty of Medicine, Tanta University, Tanta, Egypt
2 Department of Pediatrics, Faculty of Medicine, Tanta University, Tanta, Egypt
3 Department of Internal Medicine, Faculty of Medicine, Tanta University, Tanta, Egypt
4 Department of Cardiothoracic Surgery, Faculty of Medicine, Tanta University, Tanta, Egypt

Date of Submission28-Jun-2017
Date of Acceptance26-Jul-2017
Date of Web Publication31-Oct-2018

Correspondence Address:
Ramy R El-Sberbihy
Resident at Department of Emergency Medicine, Faculty of Medicine, Tanta University, 32 Ebn Elfared Street, Tanta, El-Gharbia
Egypt
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DOI: 10.4103/tmj.tmj_64_17

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  Abstract 


Background Bronchial asthma is currently defined as a chronic inflammatory disorder of the airways. Hypoxia is a universal finding in acute exacerbations of asthma. However, respiratory failure with PaO2 below 60 mmHg or PaCO2 above 45 mmHg occurs in no more than one-third of patients. Pulse oximetry allows noninvasive measurement of arterial oxygen saturation (SpO2), without the risks associated with arterial puncture.
Aim The aim of this study was to evaluate pulse oximetry as a valid tool to predict respiratory failure in children with acute severe attack of bronchial asthma as compared with the standard arterial blood gas (ABG) analysis.
Patients and methods The study was carried out on 50 children, 30 of them were patients with acute bronchial asthma and 20 of them were healthy controls. All patients and controls were subjected to the following: Full history taking, clinical examination such as pulse oximetry and investigations which included chest radiography, echocardiography, and ABG analysis.
Results There was no significant difference between asthmatic and control groups regarding age, sex, weight, and height. We found that respiratory rate and heart rate was higher in asthmatic patients than controls. We demonstrated a negative correlation between PaCo2 and SPO2 and between PaO2 and PaCO2, and a positive correlation between SaO2 and SPO2 and between PaO2 and SPO2. Oxygen saturation measured by pulse oximetry (SpO2) was greater than oxygen saturation measured by the ABG analyzer, but this difference was not statistically significant.
Conclusion Arterial oxygen saturation measured by pulse oximetry can be used as a tool to diagnose respiratory failure in an emergency setting where ABG facility in not available.

Keywords: arterial blood gas, bronchial asthma, pulse oximetry


How to cite this article:
El-Sberbihy RR, El-Ezz AA, El-raouf YM, Taha AM. Pulse oximetry in comparison to arterial blood oxygen saturation in children with bronchial asthma coming to the emergency room. Tanta Med J 2018;46:93-8

How to cite this URL:
El-Sberbihy RR, El-Ezz AA, El-raouf YM, Taha AM. Pulse oximetry in comparison to arterial blood oxygen saturation in children with bronchial asthma coming to the emergency room. Tanta Med J [serial online] 2018 [cited 2018 Nov 18];46:93-8. Available from: http://www.tdj.eg.net/text.asp?2018/46/2/93/244689




  Introduction Top


Bronchial asthma is currently defined as a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation is associated with airway hyper-responsiveness [1],[2].

Airway obstruction in bronchial asthma is mainly caused by the following four mechanisms: contraction of bronchial smooth muscles, edema of the airway walls, mucous plugging of the bronchioles, and the lung remodeling, as its responses to a variety of stimuli, such as allergens and nonspecific triggers and infections [3].

Asthma is characterized by completely or partially reversible airway obstruction, which may improve spontaneously or may subside only after specific therapy [3].

Hypoxia is a universal finding in acute exacerbations of asthma but respiratory failure with a partial pressure of oxygen (PaO2) below 8 kPa (60 mmHg) or a raised partial pressure of carbon dioxide tension (PaCO2) above 6 kPa (45 mmHg) occurs in no more than a third of patient. Cyanosis is a late sign of respiratory failure in severe asthma and indicates a very severe life-threatening attack [4].

Clinical features of less pronounced respiratory failure are unreliable and therefore guidelines recommend that arterial blood gas (ABG) tensions should be measured in all patients presenting to hospital with acute severe asthma [5].

Pulse oximetry allows noninvasive measurement of arterial oxygen saturation (SPO2), without the risks associated with arterial puncture [6].

An SPO2 cutoff value of up to 92% indicates respiratory failure in chronic obstructive pulmonary disease patients [7]. We therefore aimed to determine whether ABG estimation was necessary in all patients presenting with acute severe asthma or whether oxygen saturation as measured by pulse oximetry (SPO2) was a safe and reliable alternative in predicting those in respiratory failure and therefore need more intensive management is warranted [8].


  Aim and objectives Top


The aim of this study was to evaluate pulse oximetry as a valid tool to predict respiratory failure in children with acute severe attack of bronchial asthma as compared with the standard ABG analysis.


  Patients and methods Top


After approval from the ethics committee, an informed consent was obtained from parents of all participants in this research. This study was carried out on 50 children [group I (30) patients with acute severe bronchial asthma and group II (20) healthy controls]. Patients presented with acute severe attack of bronchial asthma and were recruited from The Emergency Unit, Pediatrics Department, Tanta University Hospitals over a period of 1 year. The Control children were 20 healthy children, of matched age and sex who had no history or symptoms of chest troubles. These control children were companions with children presented with severe acute asthma.

Inclusion criteria

Patients aged 5–12 years, with significant symptoms of bronchial asthma were included.

Exclusion criteria

Patients aged less than 5 years and more than 12 years, children presented with congenital chest and lung anomalies, congenital or acquired heart diseases, and syndromatic patients and children with systemic, metabolic or genetic diseases, and with psychological problems were excluded.

All patients underwent full history taking. Full clinical examination with special emphasis on body weight, height, and BMI. The most useful physical findings were wheezing and silent chest on auscultation. Other physical findings as tachypnea, tachycardia, hyperinflated chest, using of accessory muscles, and intercostal retraction. Pulse oximetry (SPO2) was conducted. Laboratory investigations included complete blood count, random blood sugar, ABG analysis, and spirometry (when possible). Patients underwent examination by chest radiography to exclude any complications or local precipitating cause. Echocardiography was done on all patients to exclude congenital heart disease.

We examined our patients and control children for vital sings and pulse oximetry. The finger probe of the oximeter (Nihon Kohden model BSM-2301K, Shinjuku-ku, Tokyo, Japan) with serial number 22 648, and made in Japan was placed on the index finger of the opposite arm from which the arterial sample had been taken. Arterial blood sample was obtained from the radial artery following confirmation of collateral vessel flow by Allen’s test. The modified Allen test was performed as follows: firm occlusive pressure was held on both the radial artery and the ulnar artery. The patient was asked to clench the fist several times until the palmar skin was blanched, then to unclench the fist. Overextension of the hand or wide spreading of the fingers was avoided, because it might cause false-normal results. The pressure on the ulnar artery was released while occlusion of the radial artery was maintained. The time required for palmar capillary refill was noted. The test was then repeated, but this time the radial artery was released while the ulnar artery remains compressed.

We used a syringe (GEM Easy Draw; Smiths Medical ASD, Inc., Keene, USA) for ABG analysis. Its contents were 3 cm3 luer slip aspirator, 113 IU (N) units heparin, and luer tip cap. Its patch number was 24330063.


  Results Top


Statistical presentation and analysis of the present study was conducted, using the mean, SD, and χ2-test by SPSS, version 21. Values of P less than 0.05 were considered significant.

We found that the respiratory rate was significantly higher in the asthmatic group than control patients (41.5±12.2, 25.1±2.3, respectively) (P=0.000). We also found that the heart rate was significantly higher in the asthmatic group than controls (147.7±15 and 79.4±4.6, respectively) (P=0.000) (significant, P<0.05) ([Figure 1]).
Figure 1 Comparison between the studied groups as regards heart rate and respiratory rate.

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Our work showed that SPO2 was significantly lower in the asthmatic group than control patients (89.2±6.3 and 98.6±1.2, respectively) (P=0.000), SaO2 was significantly lower in the asthmatic group than control patients (87.4±7.3 and 98.5±0.7, respectively) (P=0.000) ([Figure 2]).
Figure 2 Comparison between the studied groups as regards SPO2 and SaO2.

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We demonstrated that PH was significantly lower in the asthmatic group than control patients (7.3±0.1 and 7.4±0.02, respectively) (P=0.002). The PaO2 was also significantly lower in the asthmatic group than control patients (57.9±9.8 and 96.9±1, respectively) (P=0.000). The PaCO2 was significantly higher in the asthmatic group than control patients (46.5±12.1 and 38.2±1.6, respectively) (P=0.001) ([Figure 3]).
Figure 3 Comparison between the studied groups as regards pH, PaO2, and PaCO2.

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In patients presented with acute severe asthmatic form a negative correlation between PaCO2 and SPO2 (R=−0.48, P=0.006), and between PaO2 and PaCO2 (R=−0.65, P=0.000) was found, but a positive correlation between SaO2 and SPO2 (R=0.98, P=0.000) and between PaO2 and SPO2 (R=0.7, P=0.000) was detected ([Figure 4],[Figure 5],[Figure 6],[Figure 7]).
Figure 4 Correlation between PaCO2 and SPO2 in the asthmatic group.

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Figure 5 Correlation between SaO2 and SPO2 in the asthmatic group.

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Figure 6 Correlation between SPO2 and PaO2 in the asthmatic group.

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Figure 7 Correlation between PaCO2 and PaO2 in the asthmatic group.

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  Discussion Top


The differences in the incidence of respiratory alkalosis and respiratory acidosis in asthmatic attack could be ascribed to the magnitude of airway obstruction, as hypocapnia is described in patients with mild airway obstruction and hypercapnia in patients with severe airway obstruction [9].

Patients with respiratory acidosis have been described as more hypoxemic and with evidence of greater airflow obstruction compared with those without respiratory acidosis [9].

The aim of this study was to evaluate pulse oximetry as a valid tool to predict respiratory failure in children with acute severe attack of bronchial asthma as compared with the standard ABG analysis.

This study was carried out on 50 children. Thirty patients with acute severe bronchial asthma and 20 healthy controls.

Our study demonstrated that heart rate in asthmatic patients was significantly higher and the same for respiratory rate (P=0.000).

This result was in agreement with Harvey et al. [10], who reported that heart rate and respiratory rate were higher and oxygen saturation was lower in children with acute bronchial asthma.

The results of this study revealed that the mean of oxygen saturation values measured by pulse oximetry (SPO2) was greater than those measured by the ABG analyzer system (SPO2=89.2±6.3%, SaO2=87.4±7.3%, correlation coefficient=0.98, P=0.000). But this difference was not statistically significant (P=0.3).

Razi et al. [11], do not go hand in hand with our study as they found that the mean of oxygen saturation values measured by the ABG analyzer (SaO2) system were greater than those measured by pulse oximetry (SPO2): SaO2=89.14±8.60%, SPO2=88.39±9.13%; correlation coefficient=0.935, P<0.05.

Razi and colleagues also reported that in 22 of the hypoxemic patients, the mean of SaO2 and SPO2 were 74.40±10.24 and 70.63±9.13%, respectively; r=0.856, P<0.05. As patients were defined nonhypoxemic based on SPO2 values, the mean of SPO2 and SaO2 were 94.37±2.18 and 94.17±3.71%, respectively; there was high correlation coefficient between these groups, r=0.95, P<0.00 [11].

Also, in the previous study, there were significant differences between pulse oximetry results (SPO2) and ABG values (SaO2) in the limit of SPO2<80% (P=0.003), while there was no significant difference between the two methods in the limit of SPO2≥80% (P=0.105) and SPO2≥90% (P=0.590) [11].

In another way, our results might be in agreement with Razi et al. [11], as the difference between SaO2 and SPO2 in our study was not statistically significant.

Webb and colleagues reported that pulse oximetry is poorly calibrated at low saturations and generally less accurate and less precise than at normal saturations. Nearly 30% of values reviewed by them were erroneous by more than 5% at a saturation of less than 80% [12].

Moreover, Chiappini and colleagues, stated a significant difference between SpO2 and SaO2 values in patients with respiratory failure. SpO2 values were lower than SaO2 (90.58±5.45 vs. 92.14±5.79%) in patients with respiratory failure [13], which is not consistent with our results.

Many studies have been conducted regarding the accuracy of oxygen saturation values measured by the different pulse oximeters now available [14].

In a study of Hannhart and colleagues, the accuracy of six types of pulse oximeters was compared with SaO2 in hypoxemic patients. The bias (mean SpO2−SaO2 difference) and the error in precision (SD of the differences) were both below 4% for two kinds of instruments and remained below 1.2 and 3% for the other [15].

However, in patients with abnormal cardiac index, the pulse oximeter measurements exceeded the actual oxygen saturation (SaO2) by up to 7% [16], which is not the situation for our patients with normal cardiac index.

In another study, Kelly et al. [17] reported that there had not been sufficient agreement for oxygen saturation measured by pulse oximetry to replace the analysis of an ABG sample in the clinical evaluation of oxygenation in emergency patients.

Reynolds and colleagues explained the limited performance of pulse oximeters at low saturations. One is the slight variations in the output wavelength of the light-emitting diodes which generate proportionally larger errors at low saturations. Another is the generation of proportionally larger errors in the measurement of transmitted red light versus the infrared light at low saturations because of the large extinction coefficient of reduced hemoglobin [18].

Das and colleagues studied pulse oximeter bias based on sensor location. Unfortunately, only eight children had oxygen saturations of less than 90%. However, in their small sample size, SpO2 was always greater than SaO2 [19], which could explain our findings in part.

Torres et al. [20] showed poor pulse oximeter accuracy with 77 patients with SaO2 samples <90%.

In our work, we found a negative correlation between PaCO2 and SPO2 (R=−0.48, P=0.006), a positive correlation between SaO2 and SPO2 (R=0.98, P=0.000), a positive correlation between PaO2 and SPO2 (R=0.7, P=0.000), and a negative correlation between PaO2 and PaCO2 (R=−0.65, P=0.000).

Lee and colleagues showed that PaCO2 levels can affect the accuracy and reliability of SPO2 measurements. Agreement between SaO2 and SPO2 decreases as PaCO2 increases, regardless of the grade of associated hypoxemia. Moreover, in a large series of determinations their study also confirmed that SPO2 correlates poorly with SaO2 when PaO2 is low, particularly when it is less than 54 mmHg (7.20 kPa) [9].

West showed that the mechanism by which abnormal blood carbon dioxide levels can affect the agreement between SaO2 and SPO2 measurements is unknown. Pulse oximetry provides instantaneous, in-vivo determination of oxygen saturation by measuring the arterial blood light absorption at two specific wavelengths, 660 nm (red) and (940) nm (infrared), to distinguish between deoxygenated and oxygenated hemoglobin, whereas co-oximetry uses at least four different wavelengths of light for ABG analysis. In normal conditions, ∼5% of carbon dioxide in arterial blood and 30% in venous blood were transported in a hemoglobin-bound form, as carbaminohemoglobin [21].

Hampson explained that it is reasonable to hypothesize that the presence of elevated PaCO2 levels can alter the wavelength reading of the pulse oximeter because of increases in the amount of carbaminohemoglobin when the carbon monoxide levels are elevated, or because of an increase in red blood cell osmolarity, which can induce changes in cell morphology. Another possible explanation might be that the venous blood pulsatility index is larger in the context of a vasodilated dynamic circulation, owing to an increase in the PaCO2 [22].

O’Connor and colleagues, who studied patients with hypoxemia, reported that a decrease in PaCO2 to levels below the first tertile [PaCO2<42 mmHg (5.60 kPa)] also affected agreement between SaO2 and SPO2. Under these conditions, SPO2 underestimates SaO2, although the magnitude of the discrepancy is smaller than when PaCO2 levels are elevated [23].

Also, Hanning and colleagues showed that SPO2 correlates poorly with SaO2 when PaO2 is low. These findings are similar to the reported results demonstrating that most pulse oximeters are accurate to ±4% in patients when SaO2 is above 70% [24].In a study by Ross and colleagues, pulse oximetry accurately reflects arterial oxygenation in most of the ranges (≥90%) that we deal with outside of the ICU. However, the findings suggest that clinicians can consider it in the 80–90% range and consider making decisions more on the basis of arterial oxygen readings if patient saturations are less than 90% on pulse oximetry. It is also worth remembering that pulse oximetry is affected by perfusion and may differ among patients of different skin hues [25].

Tremper and colleagues reported that while the response time of the pulse oximeter is generally fast, there may be a significant delay between a change in alveolar oxygen tension and a change in the oximeter reading. It is possible for arterial oxygen to reach dangerous levels before the pulse oximeter alarm is activated [26].

Delay in response is related to sensor location. Desaturation is detected earlier when the sensor is placed more centrally. Lag time will be increased with poor perfusion and a decrease in blood flow to the site monitored. Performance of a neural block may cause the lag time to decrease while venous obstruction, peripheral vasoconstriction, hypothermia, and motion artifacts delay detection of hypoxemia. Increasing the time over which the pulse signals are averaged also increases the delay time [26].

Limitations of our study can explain our different results from those obtained by others. The first limitation was lack of subgroup analysis of patients with different levels of O2 saturations. A second limitation was lack of subgroup analysis of correlation of SaO2 and SPO2 at different PaCO2 level and between SPO2 and different PaCO2 levels. A third limitation was the absence of measurement of carboxyhemoglobin in our patients and we did not consider the effect of site of measurement of SPO2 on the accuracy of SPO2 and the accuracy of correlation between SPO2 and SaO2. A fourth limitation was the missed role of PaO2 as a factor which could affect SaO2–SPO2 relationship.


  Conclusion Top


Arterial oxygen saturation measured by pulse oximetry can be used as a tool to diagnose respiratory failure in an emergency setting where the ABG facility in not available.

Acknowledgements

All authors had equal role in the design, work, statistical analysis, and manuscript writing.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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