Also, other intervening factors such as fever or sepsis can further increase oxygen demand and carbon dioxide production. Atelectasis is common after general anaesthesia [8] and even after spinal anaesthesia [9] and will contribute to ventilation perfusion mismatch and resultant hypoxemia. Sedative effects from subanaesthetic doses of inhalational Nec-1s nmr agents or opioid analgesia can

depress respiration and the ability of the body to oxygenate the blood and eliminate carbon dioxide. The urge to cough can be depressed by opioid analgesics, together with the impaired mucociliary clearance mechanism of the respiratory epithelium from general anaesthesia [10] can predispose the patient to develop pneumonia. Therefore, the anaesthesiologist has to evaluate the likelihood the patient can adequately compensate for these adverse factors by increasing their respiratory effort without developing exhaustion. Preoperative pulmonary assessment: what do we look

for? In the preoperative evaluation of pulmonary risk, the anaesthesiologist is required to determine the likelihood in the postoperative period that the patient can adequately oxygenate the blood, eliminate carbon dioxide, cough adequately selleck compound to expel lung secretions and to meet the increased oxygen demand. Clinical assessment is of paramount importance although not always possible from the uncooperative patient; however, much information can still be gleaned from the patient’s general appearance. Those who appear frail, pale, cyanotic and tachypneic are less likely to sustain a prolonged increase respiratory effort. Certain physiological parameters may give an indication of the likelihood of developing postoperative

pulmonary complications. Room-air saturation of below 90% represents an important finding as from this point a small decrement of partial pressure will lead to a large decrease in saturation. Those with low haemoglobin will have a reduced oxygen carrying capacity. Some objective parameters may be associated with the possibility Molecular motor of CO2 retention. These include a reduced FEV1 of between 27% and 47% of predicted [11, 12], forced vital capacity of less than 1.7 L [13]. A patient with a peak expiratory flow rate of less than 82 L/min would probably have difficulty generating an effective cough to clear sputum [14]. An estimation of the patient’s maximal breathing capacity (MBC) in comparison to the patient’s baseline minute volume may provide an insight into their respiratory reserve. The MBC may be approximated by multiplying their FEV1 by 35, with healthy people being able to sustain a minute volume of 50% to 60% of their MBC [15, 16]. Acute chest infection or exacerbation of chronic lung condition presents a dilemma as the condition may or may not be improved with ongoing immobility.