Search

Current guidelines for the provision of safe anaesthesia from the World Health Organization and the World Federation of Societies of Anaesthesiologists (WFSA) are unachievable in a majority of low and middle-income countries (LMICs) worldwide. Current guidelines for anaesthesia and patient safety provisions from the WHO and WFSA are compared with local ability to achieve these recommendations in LMICs. Influential international organizations have historically published anaesthesia guidelines, but for the most part, without impacting substantial documentable changes or outcomes in low-income environments. This analysis, and subsequent recommendations, reviews the effectiveness of existing strategies for international guidelines, and proposes practical, step-wise implementation of patient safety approaches for LMICs.

In 1978, Drs. R Knill and A. Gelb published the results of a study to measure the effect of subanesthetic levels of halothane on the ability of fit volunteers to respond to sustained hypoxia, and to determine how long potentially hazardous levels of halothane persist after a brief non-complex surgical procedure in healthy patients. The purpose of this commentary is to highlight the historical context of their findings and the impact of their work on our modern day practice of anesthesia.In six fit male volunteers, steady states of halothane reduced the ventilatory response to normocapnic hypoxemia (PETO2 40 mmHg) by ~ 50% at 0.05 MAC and by 70% at 0.10 MAC without affecting resting levels of ventilation. Subjects remained easily rousable and coherent with full memory of events. Symptoms of hypoxemia were markedly reduced or totally absent during hypoxic periods. In five patients recovering from dental procedures (mean duration 59 min), 0.10 MAC halothane levels persisted in the recovery room for approximately one hour.Patients emerging from a brief (about one hour) halothane anesthetic, although appearing conscious, may have a hazardous degree of depression of the usually protective ventilatory response to hypoxemia for about one hour in the recovery room. Both the symptoms and signs of hypoxemia will be substantially reduced during this emergence phase, enhancing the risk that severe hypoxic episodes may go unrecognized.Gelb AW, Knill RL.Subanaesthetic halothane: Its effect on regulation of ventilation and relevance to the recovery room. Can Anaesth Soc J 1978; 25: 488-94.

Using a radiologic technique, the position and pattern of movement of the diaphragm have been evaluated in three adult volunteers, both awake and anesthetized, during spontaneous ventilation and with muscle paralysis and mechanical ventilation. Studies were made with the subjects in supine and left lateral decubitus positions with tidal and large-volume breaths. Positive end-expiratory pressure (PEEP) was added in studies of two subjects. During spontaneous ventilation awake or anesthetized, because of regional mechanical advantages, the dependent part of the diaphragm had the greatest displacement despite the higher intraabdominal pressure in this region. Paralysis, awake or anesthetized, caused a cephalad shift of the end-expiratory position of the diaphragm that was disproportionately large in dependent regions. It also reversed the pattern of diaphragmatic displacement. The passive diaphragm was displaced preferentially in nondependent zones where abdominal pressure is least. Consequently, PEEP could not restore the diaphragm to its awake functional residual capacity position, and large breaths also could not duplicate the pattern of displacement achieved spontaneously.

Efforts to minimize ventilator-induced lung injury in adults with hypoxemic respiratory failure have recently focused on the potential role of high-frequency oscillatory ventilation (HFOV). However, HFOV has been studied in newborns with hypoxemic respiratory failure for nearly 3 decades. In this brief review, we attempt to summarize key physiological principles learned from this cumulative neonatal/pediatric experience with HFOV.

Both ventilator pattern and neutrophil activation influence lung injury in adult respiratory distress syndrome (ARDS). We therefore questioned whether ventilator pattern independently affects neutrophil accumulation and function in early ARDS. Thirty-five New Zealand White rabbits were anesthetized, paralyzed, and prepared using sterile techniques. Fifteen surfactant-depleted animals were randomized and ventilated for 4 h using high-frequency oscillatory ventilation (HFO) at 15 Hz with an inspired O2 fraction = 1.0 and arterial PO2 (PaO2) > 400 Torr (a pattern known to reverse atelectasis) or conventional mechanical ventilation (CMV) with PaO2 = 80–100 Torr (a pattern with some atelectasis despite positive end-expiratory pressure). Eight normal animals on CMV with PaO2 > 400 Torr served as a reference group (NorCMV). NorCMV animals progressively increased circulating polymorphonuclear neutrophil (PMN) numbers and had minor pressure-volume curve alterations but no other significant changes. Lavaged CMV animals developed the characteristic gas exchange and marked pressure-volume curve abnormalities of ARDS. Circulating PMNs remained constant but developed decreased chemotactic activity, whereas lung neutrophil numbers increased significantly (P = 0.0002) and had substantially enhanced chemiluminescence (P = 0.0003 vs. NorCMV animals). Although lavaged HFO animals accumulated an intermediate number of lung neutrophils (lung myeloperoxidase > NorCMV animals; P = 0.003), the chemiluminescence and chemotaxis of these PMNs were the same as in cells from NorCMV animals. We concluded that both the degree of neutrophil activation and lung injury can be minimized by preventing cyclic alveolar/airway expansion and collapse in the surfactant-deficient lung by use of appropriate ventilator patterns.

Mechanical ventilators have only two functions: to provide a flux to eliminate carbon dioxide from those who will not or cannot breathe and to establish an adequate gas-exchanging volume to reduce shunting. The concept of volume recruitment to reduce shunting goes back at least to Mead and Collier in 1959,1 who showed that without periodic inflations there was a progressive fall in compliance during prolonged mechanical ventilation. Much of the subsequent history of mechanical ventilation in acute lung disease has really been the search for better methods of volume recruitment. The lung has to be inflated past the pressure at which atelectatic lung begins to open and be maintained above its closing pressure (that pressure below which alveoli and airways start to close again).