Critical care nurses should understand the concepts of mechanical ventilation (MV), as an effective management strategy for patients requiring MV that can influence morbidity and mortality in the ICU environment. A classic study by Gajic and colleagues¹ demonstrated that injudicious MV resulted in damage to the pulmonary tissue in as little as 30 minutes. This tissue injury created an alveolar inflammatory response resulting in poor lung function.¹ Integrating evidence-based knowledge and skill related to MV is necessary to maximize the benefits of this intervention in the support of critically ill patients.

Effective management of patients requiring MV depends on the clinician’s knowledge of normal pulmonary physiology and mechanics of breathing. The pulmonary system is a low-pressure system that serves two essential physiologic functions: oxygenation and ventilation. Both of these processes require effective pulmonary function paired with adequate perfusion of the lungs. Breathing naturally, without the assistance of MV, is achieved by negative inspiratory force mechanics. During inspiration the diaphragm and accessory muscles contract, generating a negative pressure, pulling air in. Relaxation of the diaphragm and other muscles allows air to passively leave the lungs. An intact circulation surrounding the alveoli, matched to functional alveoli, results in optimal diffusion of oxygen (O₂) and carbon dioxide (CO₂).

Inspiratory assistance with MV completely “flips” the natural mechanics of negative pressure inspiration. MV breaths are delivered by positive pressure, thereby “pushing” air into the lungs. Pulmonary surfactant is a mixture of lipids and proteins that line the alveolus lowering surface tension and maintains alveolar surface area for effective gas exchange in the healthy lung.³ Pulmonary disease, inflammatory triggers, and the positive pressure mechanics of MV disrupt the balance of surfactant necessary to maintain open alveoli.⁴ Disruption in the surfactant–alveoli interface causes atelectasis that results in a ventilation/perfusion mismatch. A pulmonary shunt is described as a diffusion or perfusion impairment resulting in decreased oxygenated blood returning into arterial circulation.⁵

To maximize oxygenation and ventilation for the patient requiring MV, open lung strategies are implemented. Lachmann first described open lung protective therapies in 1992.⁶ Open lung strategy refers to employing modes of ventilation that minimize alveolar loss through positive pressure and include the recruitment of collapsed alveoli.⁷ This is typically achieved in MV by (1) adjusting the positive end-expiratory pressure (PEEP) to avoid alveolar collapse, (2) using a low peak inspiratory pressure (PIP) to deliver effective breaths, and (3) employing decelerating air flow patterns.^4,7,8 Decelerating air flow patterns refer to the speed of the gas delivered during inspiration and the slow release of the gas, distributing air more effectively as the chest fills before expiration⁹ (Fig. 1). This flow pattern is considered more physiologic in nature, contributing to better alveoli gas distribution.^4,7–9 Advanced MV modes that incorporate open lung strategies deliver decelerating air flow breaths predominantly using pressure-regulated modes rather than volume (ie, size of tidal volume). Newer and more sophisticated pressure modes of MV have been found to be more effective in maintaining an open lung for maximal alveolar function.^4,9

Fig. 1 Decelerating flow waveform. Abbreviations: EXP, expiration; INSP, inspiration; S, seconds; V˙, flow.

(Image used by permission from Nellcor Puritan Bennett LLC, Boulder, Colorado, doing business as Covidien.)

The lung is a low-pressure system. By changing the mechanics of breathing during MV to positive pressure, intrathoracic pressures are increased; that is, more force is exerted within the thoracic space than normal. This increased intrathoracic pressure can result in symptoms of hemodynamic instability, notably reduction in cardiac output. Pushing air into the pulmonary system via MV also causes mechanical trauma to the lung, known as barotrauma. In fact, the greater the application of pressure to deliver a breath, the worse the barotrauma (ie, lung damage).^8,10,11 Volutrauma, on the other hand, refers to lung damage caused by high tidal volumes. A combination of high tidal volumes and high pressures increases the stress on the pulmonary system and compound tissue injury and barotrauma.⁸ This tissue insult activates proinflammatory cytokines, triggering an intrapulmonary inflammatory cascade, referred to as biotrauma.^8,12 Cyclic opening and closing of alveoli caused by ineffective MV exacerbates biotrauma and ventilator induced lung injury (VILI).⁸

Management of patients on MV attempts to provide effective oxygenation and ventilation with the least amount of pulmonary trauma. This can be accomplished through various advanced modes and settings utilized in mechanical ventilation. MV modes that employ lower tidal volumes, decelerating pressure regulated breaths, and effective PEEP are necessary to minimize VILI and are considered lung protective strategies.^4,8–10

Management of patients on MV requires that the critical care nurse appreciate the treatment goals for the intervention as well as the underlying pulmonary disorder(s) (ie, disease/systemic pathology, oxygenation, ventilation or mixed pulmonary disorder). Disturbances in O₂ and CO₂ exchange include both oxygenation and ventilation impairments: apnea, acute or impending ventilatory failure, severe hypoxemia, and respiratory muscle fatigue.¹³

Diffusion concentration gradients perpetuate the movement of both O₂ and CO₂ across the alveolar–capillary membrane. Factors interfering with effective diffusion can originate from disruption of the alveoli, the capillaries surrounding the alveoli, or the insterstitium. Pulmonary edema, inflammation, vasoconstriction, poor ventilation, and poor oxygenation are disruptive to adequate gas diffusion. When factors interfere with effective diffusion through poor ventilation, poor perfusion, or a combination of these factors, deoxygenated hemoglobin returns to the circulatory system, resulting in a physiologic shunt. The most common causes of shunt occur in acute respiratory distress syndrome (ARDS), atelectasis, pneumonia, pulmonary edema, pulmonary embolus, and intracardiac right-to-left flow shunts.

The presence of a shunt is further appreciated when critical care clinicians calculate alveolar–arterial (A–a) gradients, shunted blood flow-to-total blood flow ratio (Q_s/Q_t), arterial to alveolar ratio (Pao₂/PAo₂), or ratio of Pao₂ to fraction of inspired oxygen (F_io₂) (P/F).¹⁴ Normal physiologic shunt equates to 2% to 5% of the cardiac output via the cardiac venous circulation. Shunting can be estimated noninvasively by examining P/F relationship. Clinical concerns are present when P/F are 300 mm Hg or lower. Oxygen Index (OI) calculation also incorporates the measurement of the severity of oxygenation impairment in combination with the mean airway pressure (mP_aw). OI has been classically utilized in the pediatric population, but is gaining momentum in the adult population as a predictor of respiratory outcome. An OI of 20 or greater is associated with increased mortality. A P/F of 100 mm Hg or less and an OI of 30 or greater are considered measures of severe pulmonary dysfunction and a failure of conventional ventilation, which may necessitate lung protective MV modes of ventilation.¹⁵ It is clinically important to conceptualize the underlying cause and complexity of a pulmonary shunt to identify which lung protective mode of MV may be most beneficial to the patient.

Traditionally, MV included principles of delivering breaths based on volume (eg, size of breath) or pressure. Volume modes would trigger inspiration and the cycling of breaths was based on programmed tidal volume, rate, and time that were believed to provide optimal ventilation. Classic strategies of ventilation (eg, CMV, AC, SIMV, IMV) were programmed irrespective of pulmonary compliance. Although these classic volume modes continue to be used in the short-term management of patients requiring MV support, they have been less effective in providing open lung protective ventilation in critically ill patients.⁹ Newer modes of MV based on pressure principles rather than volume provide lower tidal volumes, decelerating air flow patterns, and pressure and maintain open lung ventilation.

Historically higher tidal volume breaths, defined as 10 to 15 mL/kg, were calculated from either actual or predicted body weight to determine the tidal volume setting. Advances in clinical research have demonstrated adverse effects from high tidal volumes shifting this practice. Current practice accepts usage of lower tidal volumes defined as 4 to 8 mL/kg.

A large multicenter research study known as the Acute Respiratory Distress Syndrome Network study (ARDS Net) examined tidal volume (low vs high) in the treatment of patients with ARDS.^15,16 This study defined low tidal volume as 4 to 8 mL/kg and high tidal volume as 12 mL/kg. Patients with ARDS and acute lung injury (ALI) were randomized to receive either high (control group) or low (treatment group) tidal volumes. The study was stopped after the enrollment of 861 patients because of decreased mortality and decreased ventilator days noted in the treatment group (ie, patients receiving low tidal volumes). Findings from this study described that lower tidal volumes protect the lungs from excessive stretch, improving patient outcomes.¹⁶

A process of incorporating lung protective strategies into clinical practice supports the use of ideal body weight (IBW) as opposed to actual or daily body weight. Tidal volume calculations based on IBW usage at 4 to 8 mL/kg, maintaining plateau pressures at 30 cm of H₂O or lower and incorporating moderate levels of PEEP (ie, 5–15 cm of H₂O).¹⁷ However, if alveolar derecruitment persists, as evidenced by episodes of refractory hypoxemia, careful consideration should be exercised in adjusting to higher levels of PEEP (ie, 15–24 cm H₂O).¹⁴ Excessive alveolar stretch has been shown to cause barotrauma and further compromise atelectatac regions of the lung. The use of lung protective strategies in critical care has been shown to offer a survival benefit, a decrease in ventilatory days, and is currently considered the standard of care¹⁵ (Fig. 2).

Fig. 2 NIH NHLBI ARDS Clinical Network, mechanical ventilation protocol summary. Available at: http://www.ardsnet.org/system/files/Ventilator%20Protocol%20Card.pdf.

Beyond the ARDS Net study, there was a recent randomized controlled trial comparing lower tidal volume usage (4–8 mL/kg) versus historically larger tidal volumes (10–15 mL/kg) in patients who do not meet the clinical criteria for ALI. The trial was stopped prematurely because of increased rates of ALI in the higher tidal volume group.¹⁸ These findings support the usage of lower tidal volumes at 4 to 8 mL/kg, calculated from IBW for all mechanically ventilated patients.

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