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Effects of Anaesthesia Techniques and Drugs on Pulmonary Function

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Effects of Anaesthesia Techniques and Drugs on Pulmonary Function Review Article Effects of anaesthesia techniques and drugs on pulmonary function Address for correspondence: Vijay Saraswat Dr. Vijay Saraswat, Department of Anaesthesiology, Apollo Hospitals, Nashik, Maharashtra, India Apollo Hospitals, Nashik, Maharashtra, India. E‑mail: drvsaraswat@gmail. ABSTRACT com The primary task of the lungs is to maintain oxygenation of the blood and eliminate carbon dioxide through the network of capillaries alongside alveoli. This is maintained by utilising ventilatory reserve capacity and by changes in lung mechanics. Induction of anaesthesia impairs pulmonary functions by the loss of consciousness, depression of reflexes, changes in rib cage and haemodynamics. All drugs used during anaesthesia, including inhalational agents, affect pulmonary functions directly by acting on respiratory system or indirectly through their actions on other systems. Volatile anaesthetic agents have more pronounced effects on pulmonary functions compared to intravenous induction agents, leading to hypercarbia and hypoxia. The posture of the patient also leads to major changes in pulmonary functions. Anticholinergics and neuromuscular blocking agents have little effect. Analgesics and Access this article online sedatives in combination with volatile anaesthetics and induction agents may exacerbate Website: www.ijaweb.org their effects. Since multiple agents are used during anaesthesia, ultimate effect may be DOI: 10.4103/0019‑5049.165850 different from when used in isolation. Literature search was done using MeSH key words ‘anesthesia’, ‘pulmonary function’, ‘respiratory system’ and ‘anesthesia drugs and lungs’ in Quick response code combination in PubMed, Science Direct and Google Scholar filtered by review and research articles sorted by relevance. Key words: Anticholinergic agents, benzodiazepines, compliance, dead space, functional residual capacity, general anaesthesia, induction agents, neuromuscular blocking agents, ventilation perfusion ratio, volatile anaesthetic agents INTRODUCTION EFFECT OF GENERAL ANAESTHESIA The primary function of the lungs is to provide an Effect on upper airway adequate gas exchange for maintaining normal oxygen GA causes relaxation of jaw and pharyngeal muscles content in blood and eliminate carbon dioxide. This is and leads to posterior displacement of tongue. Loss of achieved by optimising lung volumes to meet higher cough reflex along with increased secretions results in metabolic demand during the peri‑operative period. airway obstruction, laryngospasm and bronchospasm. General anaesthesia (GA) per se causes respiratory Patients with hyperreactive airways are more prone to [1] impairment and both oxygenation and elimination complications. Tracheal intubation protects airway of carbon dioxide are affected. The factors affecting pulmonary function include loss of consciousness, This is an open access article distributed under the terms of the Creative Commons Attribution‑NonCommercial‑ShareAlike 3.0 License, which allows mode of ventilation (spontaneous or mechanical), others to remix, tweak, and build upon the work non‑commercially, as long as the posture of patient, actions of anaesthetic agents and author is credited and the new creations are licensed under the identical terms. drugs, used during anaesthesia on respiratory smooth For reprints contact: [email protected] muscles and secretions. Literature search was done using MeSH key words in PubMed, Science Direct and How to cite this article: Saraswat V. Effects of anaesthesia Google Scholar filtered by review and research articles techniques and drugs on pulmonary function. Indian J Anaesth sorted by relevance. 2015;59:557‑64. © 2015 Indian Journal of Anaesthesia | Published by Wolters Kluwer - Medknow 557 Saraswat: Anaesthesia and pulmonary function but increases the dead space, and delivery of dry gases Effects of pre‑oxygenation may affect pulmonary function, especially in younger The higher oxygen concentration, used during patients. pre‑oxygenation, leads to faster gas adsorption and consequently collapse of alveoli and atelectasis. As Effect on volumes alveolar ventilation decreases, PaCO2 increases and Anaesthesia causes respiratory impairment by mismatch displaces oxygen from the alveoli, consequently, in alveolar ventilation (Va) and perfusion (Q). GA increasing shunt fraction and hypoxia. Ventilation with abolishes the sigh reflex with rapid onset of atelectasis PEEP reduces the atelectasis, but oxygenation need not in the majority of the patients. Irrespective of mode improve, because blood flow may shift to remaining of ventilation (spontaneous or mechanical), there atelectatic tissue. Application of PEEP of 40 cm is loss of muscle tone and dose‑dependent decrease H2O recruits almost all collapsed lung and the lung in minute ventilation (MV) as a result of decrease remains open if ventilation is with moderate oxygen in respiratory rate or tidal volume (VT) or both.[2] concentration (<40%) but recollapses within a few Simultaneously, there is fall in functional residual minutes if ventilation is with 100% oxygen.[8] However, capacity (FRC) and forced expiratory volume in 1 recent study has found no significant difference in s (FEV1) leading to alveolar collapse and increase in oxygenation index or FRC between patients given 80% shunts. Alveolar recruitment manoeuvres, followed by and 30% oxygen for approximately 5 h.[9] positive end‑expiratory pressure (PEEP) which limits the shunts, may reduce post‑operative pulmonary Effect on dead space The distribution of pulmonary blood flow is altered complications and improve patient outcomes.[3] during anaesthesia due to increased mismatch of Effects on functional residual capacity ventilation to perfusion ratios (Va/Q ratio). Pulmonary Anaesthesia leads to fall in FRC despite maintaining blood flow distribution is primarily determined by spontaneous breathing and irrespective of anaesthetic gravity. Although anatomical dead space remains used (intravenous [IV] or inhalational).[4,5] FRC unchanged, alveolar dead space increases as a result (approximately 3L in normal person) falls by 0.8– of perfusion of non‑ventilated and poorly ventilated lung areas. Pulmonary perfusion alters during 1.0 L by a change in position from upright to supine change from upright to supine, sitting and lateral due to upward pressure from abdominal contents decubitus positions, which are not matched by and more cephalad position of the diaphragm. altered ventilation. Hence, an increased mismatching Induction of GA further decreases it by 0.4–0.5 L due of ventilation to perfusion develops. This includes to relaxation of diaphragm and intercostal muscles, the lung regions with high Va/Q ratio (ventilation of which further moves the diaphragm up. The resultant non‑perfused or poorly perfused areas) or ‘dead space volume is close to residual volume. The muscle ventilation’ and regions with low Va/Q ratios (poor paralysis and mechanical ventilation does not cause ventilation in highly perfused areas) or ‘shunt’ (due any further reduction in FRC. As FRC approaches to atelectasis). Dead space ventilation impairs CO closing capacity, small airways collapse resulting in 2 elimination whereas shunt impairs oxygenation. The atelectasis and consequently hypoxia. Atelectasis shunt may increase about 5%, which has a profound occurs in approximately 90% of the patients effect on arterial oxygenation. The increase in inspired undergoing anaesthesia. FRC increases significantly in oxygen concentration (FiO ) may improve oxygenation [6] 2 the 30° head‑up position in comparison with supine. to a small degree. PEEP applied during anaesthesia may increase FRC; however, patients with high intra‑abdominal Effect on ventilatory response pressure (IAP) may require PEEP higher than IAP.[7] Anaesthesia depresses movements of intercostal muscles, alters the shape and motion of chest wall and FRC is also reduced in neonates, elderly, obesity, diminish rib cage excursion affecting lung mechanics smokers, pregnancy, abdominal distension and patients and consequent decrease in FRC and ventilatory with respiratory diseases even before induction of response to CO2. PaCO2 is the predominant factor anaesthesia. Total static compliance (both lung and controlling ventilation. Any rise in PaCO2 is detected chest walls) is also reduced, which may be due to by peripheral (carotid bodies) and central (medullary) decrease in FRC. FRC remains unaffected during chemoreceptor with resultant increase in ventilation. ketamine anaesthesia as muscle tone is maintained.[8] Acidosis also stimulates ventilation via the peripheral 558 Indian Journal of Anaesthesia | Vol. 59 | Issue 9 | Sep 2015 Saraswat: Anaesthesia and pulmonary function chemoreceptors. This ventilatory response to carbon Va/Q ratio by delivering adequate MV and limiting dioxide is blunted by all anaesthetic drugs (except atelectasis. ether) resulting in hypercarbia. Anaesthesia also reduces the sensitivity of carotid and aortic body Naitoh et al. reported a significant decrease in FEV1 chemoreceptors to hypoxia, which increases MV by upon changing position from sitting to six recumbent sympathetic nervous system stimulation. However, positions. Rib cage motion was restricted in all at low concentrations of anaesthetic agents (≤0.2), recumbent positions (left retroversion at a 45° tilt, hypercapnic ventilatory response is not significant. It right retroversion at a 45° tilt and right anteversion at is probable that it is more resistant to the effects of a 45° tilt), but not
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