Effectiveness of positive end-expiratory pressure, decreased fraction of inspired oxygen (FiO2) and vital capacity recruitment maneuver on prevention of pulmonary atelectasis in patients undergoing general anesthesia: a systematic review protocol

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Abstract

Review question/objective

The objectives of this systematic review are to systematically review and synthesize research literature in order to identify the most effective interventions used by anesthesia providers in the reduction of pulmonary atelectasis. This review aims to answer the following specific question: In patients undergoing general anesthesia, what are the effects of peak end expiratory pressure (PEEP), a decreased fraction of inspired oxygen (FiO2) delivery, and/or the use of a recruitment maneuver on the development of post-operative pulmonary atelectasis? More specifically, the objectives are to identify: The effectiveness of PEEP, a decreased FiO2 delivery, and/or the use of a recruitment maneuver on the development of post-operative pulmonary atelectasis in patients undergoing general anesthesia.

Background

General anesthesia is associated with impaired oxygenation and pulmonary atelectasis has been identified as a major cause.4 Atelectasis is the collapse of the lung's air sacs, known as alveoli, in all or part of the lungs. The effect of decreased FiO2, the use of PEEP and a vital capacity recruitment maneuver to prevent post-operative atelectasis has been studied within the anesthesia community. However, the implications for anesthesia practice regarding these interventions have not been well defined. A common practice among anesthesia providers is to perform general anesthesia without the use of PEEP or a vital capacity maneuver and a 100% FiO2 enduring the course of the anesthetic. A cursory review of the literature reveals that randomized clinical trials do exist regarding post-operative atelectasis and these interventions individually.8,9 Clinical trials on this subject have been conducted and are currently in progress.3 However, there is no systematic review to reveal data about the proposed interventions and their effect of post-operative pulmonary atelectasis. This review's purpose is to provide data on use of PEEP, decreased FiO2, and/or a recruitment maneuver during general anesthesia in reducing the development of post-operative pulmonary atelectasis.

Background

Central to this review are the key terms: PEEP and FiO2 as well as ventilation/perfusion ratio (Va/Q), partial pressure of oxygen dissolved in arterial blood (PaO2), functional residual capacity (FRC), and pulmonary vascular resistance (PVR). For the purposes of this review, these terms are defined as follows:

Background

Positive end expiratory pressure, or PEEP, is used when oxygenation is not adequately maintained with mechanical ventilation alone. Positive end expiratory pressure has many well documented supportive benefits including: decreased shunting and dead space ventilation while improving functional residual capacity, compliance and arterial oxygenation.2 Shunt and dead space are terms used to describe extreme situations where either blood flow (perfusion) does not meet air flow (ventilation) in the lung. As a result, gas exchange cannot occur. More specifically, shunt is that part of the cardiac output that returns to the left side of the heart without being ventilated and oxygentated.7 The fraction of inspired oxygen, or FiO2 is the percentage of oxygen delivered in the gas mixture administered to the patient.2 Ventilation/perfusion ratio is the match between capillary perfusion and alveolar ventilation - which must be very well executed. The ventilation/perfusion ratio is ideally equal to one.2 Functional residual capacityis the volume of gas which is left in the lungs at the end of a passive exhalation.2 Pulmonary vascular resistance, or PVR, increases with the incidence of any disease process that restricts pulmonary blood flow. Examples include chronic lung disease, pulmonary embolus, alveolar hypoxia, acidosis, hypoxemia and many vasoactive drugs.2

Background

Two reasons to prevent the formation of pulmonary atelectasis are a decrease in lung compliance and a decrease in the PaO2.7 Research has demonstrated the occurrence of atelectasis formation in the most dependent parts of the lung in 90% of patients undergoing general anesthesia within minutes of induction.4 In addition, general anesthesia causes an increase in intrapulmonary shunt. This shunting can impair oxygenation and is directly correlated with the formation of atelectasis. Three causes of atelectasis will be discussed including compression, gas reabsorption and pulmonary surfactant impairment.4

Background

The intrathoracic and abdominal cavities are separated by the diaphragm, which when functioning normally, generates differential pressures in these two cavities. However, when general anesthesia is induced the work of the diaphragm is disabled as it relaxes and moves cephalad. This inhibits the maintenance of these two distinct cavity pressures causing the dependent lung to actually crush the adjacent lung causing compression atelectasis. There is a difference in diaphragmatic displacement between the anesthetized spontaneously breathing patient and the patient receiving positive-pressure ventilation with paralysis.3,4The spontaneously breathing patient is able to overpower the weight of the abdominal contents by generating enough active tension. The paralyzed patient; however, has a passive diaphragm that gets displaced to the upper nondependent portion of the chest cavity by positive pressure ventilation. Lastly, the reduction in FRC may also be attributed to the loss of intercostal muscle function which contributes to the development of atelectasis as well.5

Background

The second cause of atelectasis, reabsorption atelectasis, occurs by two pathways. The first occurs after complete airway obstruction causing a gas pocket to collect and eventually collapse distal to the obstruction. The second occurs without airway obstruction and deals with low ventilation and perfusion ratios (Va/Q) in the zones of the lungs.5 As FiO2 is increased the PaO2 increases and oxygen moves from the alveoli to the capillary blood at an expedited rate. This efflux of oxygen out of the alveoli causes alveolar collapse and the lung tissue to become progressively smaller. To review, atelectasis is mostly likely to occur with a high FiO2 and a low Va/Q2.2

Background

The third and last cause of atelectasis deals with pulmonary surfactant impairment during general anesthesia. Surfactant acts as a lubricant for the alveoli and is produced by alveolar type 2 cells. It prevents alveolar collapse by reducing alveolar surface tension and prohibits small alveolus from emptying into larger alveoli with a lower surface tension. This would result in a single alveolus and surfactant is the reason this phenomenon does not occur.5 General anesthesia decreases the production of surfactant; therefore, making patients more susceptible to alveolar collapse during this time. This mechanism is considered to be of least importance in the formation of perioperative atelectasis as compression and absorption are credited with the most involvement.4

Background

A recruitment maneuver is performed by the anesthetist by inflating the patient's lungs to an airway pressure of 40cm H2O.This increased airway pressure must be maintained for duration of seven to eight seconds. This maneuver, also named a vital capacity maneuver, functions to re-expand all previously collapsed lung tissue. The recruitment maneuver functions to increase the patient's lung volumes and restore their pulmonary function to a pre-anesthesia state. However, when the recruitment maneuver is followed by a FiO2 of 1.0, the formation of new atelectasis occurs within 10 minutes. In summary, the recruitment maneuver should be followed with a moderate FiO2 in order to eliminate atelectasis formation and shunting. Therefore, this will lessen the need for an increased FiO2 prior to the patient's extubation.5

Background

The adverse effects of perioperative atelectasis include decreased lung compliance, impairment of oxygenation, increased PVR, and development of lung injury. These effects can persist into the post-operative period and last for two days causing an impact on patient recovery.5 Atelectasis formation in the perioperative patient is liable to be a cause of infection and a contributor to pulmonary complications. This occurrence increases the length of hospitalization which in turn increases health care cost. In addition, patient satisfaction with their overall surgical and anesthesia experience is dampened in light of this preventable occurrence.6 In conclusion, it is of utmost importance for the anesthesia provider to reverse the effects or prevent the formation of perioperative atelectasis in order to prevent pulmonary complications in the postoperative patient.

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