Morbidly obese patients
Optimising pre-oxygenation by nasopharyngeal oxygen insufflation
By Professor Anis Baraka MD FRCA (Hon), Chairman of the Anaesthesiology Department at the American University of Beirut, Lebanon
Prof. Anis Baraka is Vice President of the World Federation of Anaesthesiologists and WFSA Representative to the Regional Commission of the United Nations. The professor has published hundreds of scientific papers and is also Editor-in-Chief of the Middle East Journal of Anaesthesiology and reviewer for various specialist journals
In morbidly obese patients, oxyhaemoglobin desaturation during apnoea following standard pre-oxygenation is significantly reduced compared with non-obese patients. This is hazardous, since morbid obesity may be associated with increased risk of difficult tracheal intubation. The rapid haemoglobin desaturation during apnoea may be attributed to increased oxygen consumption associated with reduced oxygen reserve. The FRC, which is the main oxygen store, is decreased with obesity secondary to the increased mass of the chest and abdomen. Also, the supine position further decreases the FRC, due to cephalad displacement of the diaphragm by the abdominal contents, and hence the tidal volume of the obese may fall within the closing capacity. Whereas the FRC of normal patients decreases by around 20% following induction of anaesthesia, it decreases by approximately 50% in morbidly obese patients, causing micro-atelectasis resulting in ventilation/perfusion (V/Q) mismatch, with a subsequent increase of alveolar-arterial oxygen gradient. Also, the intrapulmonary shunt in the obese patient is 10-20% compared with 2-5% in the non-obese (Fig 1).
Fig 1: Morbidly obese patient with low FRC due to cephalad displacement of the diaphragm
The head-up position has been recommended to optimise pre-oxygenation in a pregnant woman, as well as in morbidly obese patients. The head-up position during pre-oxygenation in morbidly obese patients has been shown to prolong the mean time of desaturation by about 50s. Also, the application of continuous positive airway pressure (CPAP) during pre-oxygenation has been suggested to optimise pre-oxygenation in the morbidly obese, on the assumption that CPAP will increase FRC. However, CPAP only resulted in an insignificant increase of the mean time to desaturate to 90%, as the FRC will return to pre-CPAP levels once the patient is anesthetised and the CPAP mask is removed.
In critically ill patients, Baillard et al showed that pressure support ventilation in the ICU ensured improved oxygen saturation before, during and after endotracheal intubation as compared with the standard pre-oxygenation. In our department, we use non-invasive ventilatory support in the form of BiPAP to optimise pre-oxygenation in the morbidly obese patient having acute lung injury. Potential adverse effects of non-invasive BiPAP include gastric insufflation, distension and aspiration. However, there are no reported cases of barotrauma or serious haemodynamic changes associated with non-invasive BiPAP.
Nasopharyngeal oxygen insufflation can optimise pre-oxygenation in the morbidly obese. Following pre-oxygenation, the morbidly obese patients desaturate rapidly during the apnoeic period following traditional pre-oxygenation to a SpO2 of 95% in a mean time of 145(27)s. In addition, correlation of BMI with the time to desaturation showed an inverse linear correlation i.e. the higher the BMI, the shorter the time to desaturation (Fig 2).
Fig 1: Morbidly obese patient with low FRC due to cephalad displacement of the diaphragm
In 1956, H M Holmdahl introduced the term apnoeic diffusion oxygenation, which is achieved by pre-oxygenation with 100% oxygen followed by oxygen insufflation during subsequent apnoea. During the apnoea, oxygen is extracted from the FRC into the blood at a rate of about 250 ml.min-1 to maintain metabolic oxygen consumption. However, due to the high solubility of carbon dioxide in blood, it is only added to the alveolar space at a rate of 10 ml.min-1, resulting in a net gas flow from the alveoli to the blood at about 240 ml.min-1. Hence, a subatmospheric pressure is produced in the alveoli, and the ambient oxygen is drawn ‘en masse’ into the lungs and maintains oxygenation. This explains the delay of hypoxemia in morbidly obese patients when pre-oxygenation is followed by nasopharyngeal oxygen insufflation.
In conclusion, in the morbidly obese patients traditional tidal volume pre-oxygenation is followed by a rapid oxyhaemoglobin desaturation during the subsequent apnoea, with a significant negative correlation between the time to oxyhaemoglobin desaturation and body mass index. However, when nasopharyngeal oxygen insufflation followed pre-oxygenation using 5 litre/min, the onset of oxyhaemoglobin desaturation during the subsequent apnoea is significantly delayed.
This article was published on 03/01/2008
.jpg&contenttype=jpeg)
