Advanced techniques in mechanical ventilation


Key points

  • Mechanical ventilation (MV) must support gas exchange and promote patient comfort while minimizing lung injury due to elevated airway pressures.

  • Protective, low tidal volume ventilation reduces morbidity and mortality rates in patients following acute respiratory distress syndrome (ARDS).

  • Pressure-controlled ventilation (PCV) determines inhaled tidal volumes via a preset inspiratory pressure and intrinsic respiratory mechanics.

  • Airway pressure release ventilation (APRV) allows for spontaneous and nonspontaneous ventilation and may reduce patient-ventilator asynchrony and overall work of breathing.

  • Permissive hypercapnia allows CO 2 concentrations to increase in conjunction with reduced tidal volumes in order to decrease airway pressures and prevent barotrauma.

  • Proportional assist ventilation (PAV) varies gas flow in response to patient demand as a form of synchronized partial ventilatory assistance (closed-loop model).

  • Neurally adjusted ventilator assist delivers support in proportion to respiratory drive, which is measured via electrical activity of the diaphragm (EAdi).

  • Administration of nitric oxide (NO) or surfactant has theoretical advantages for improving oxygen exchange but is used sparingly outside the neonatal population.

  • Additional methods of ventilatory support that may benefit select patient populations include extracorporeal membrane oxygenation (ECMO), high-frequency oscillatory ventilation (HFOV), positive end-expiratory pressure (PEEP), and prone positioning.

  • COVID-19 pneumonia has posed new and unique challenges with the need to incorporate advanced techniques in MV as well as innovative means of ventilatory support.

Modern positive-pressure MV emerged more than 50 years ago. The primary goal is to assist patients who cannot maintain adequate exchange of oxygen and carbon dioxide between the alveolar air spaces and capillaries. Clinical experience has taught that assisting gas exchange is but one important function of MV. Yet, the complications associated with invasive mechanical ventilation are well documented, including (1) lung injury from high positive airway pressures, referred to as ventilator-induced lung injury (VILI). To attempt to avoid VILI methods for noninvasive ventilation, such as bilevel positive airway pressure (BiPAP), have emerged as useful alternatives to endotracheal intubation. Additionally, mortality accrues as the duration of mechanical ventilation increases. Thus, a broad knowledge of mechanical ventilation strategies that limit the total number of ventilator days lowers not only morbidity, but also mortality.

The science of ventilator management is advancing rapidly. Clinicians can now support critically ill patients who otherwise would have died owing to human knowledge and experience and machine limitations. This chapter focuses on innovations in ventilatory support and introduces some newer technologies that may provide benefits to patients with acute respiratory failure (ARF) secondary to ARDS. Further, this chapter seeks to address MV strategies in patients with COVID-19 pneumonia.

Impaired oxygenation in acute respiratory distress syndrome (ARDS)

Over the last several years, the term “acute lung injury” (ALI) has been abandoned. Thus, ARDS is now classified as mild, moderate, and severe based on Pao 2 /Fio 2 ratios (mild = Pao 2 /Fio 2 of 200–300, moderate = Pao 2 /Fio 2 of 100–200, and severe = Pao 2 /Fio 2 < 100 on mechanical ventilation with a PEEP of 5). Patients with ARDS are difficult to oxygenate because of hyperreactive airways, alveolar edema, and inflammation. This condition is characterized pathologically by increased permeability of the alveolar-capillary barrier and accelerated influx of neutrophils. Alveolar edema and inflammation in ARDS are heterogeneous, and matching of ventilation and perfusion varies throughout the different lung regions. It is recognized that MV can increase lung inflammation, exacerbate tissue injury due to barotrauma, and increase morbidity and mortality.

Ventilator-induced lung injury

VILI results from excessive mechanical stresses causing alveolar overdistention, usually from high tidal volumes (V t ) and airway pressures. Alveolar overdistention induces a local pulmonary and systemic proinflammatory cytokine response. Limiting alveolar overdistention and phasic alveolar recruitment and derecruitment of lung tissue ( atelectrauma ) can reduce inflammation. Experimental and clinical data suggest that the proinflammatory response driving VILI is attenuated by protective, low V t ventilation tactics. New modes of MV are designed specifically to minimize iatrogenic injury, and this approach is now a fundamental tenet of modern critical care ( Table 1 ).

TABLE 1
Modes of Ventilation
Ventilatory Mode/Strategy Advantages Disadvantages
Volume-controlled ventilation Predetermined respiratory rate and tidal volume Barotrauma, stacking of breaths
Low tidal volume ventilation Lower airway pressures, decreased mortality rate Hypoventilation, hypoxemia
Pressure-controlled ventilation Predetermined airway pressures, less barotrauma Hypoventilation, hypoxemia
Inverse-ratio ventilation Increases alveolar recruitment Auto-PEEP, barotrauma
Airway pressure release ventilation Predetermined airway pressure, allows for spontaneous breathing, can improve oxygenation Hypoventilation
Permissive hypercapnia Allows for lower tidal volumes and MVV and airway pressures Increased ICP, arrhythmias
Proportional assist ventilation Decreases patient-ventilator asynchrony, adapts to respiratory mechanics No predetermined tidal volume, requires measurable inspiratory drive
Adaptive support ventilation Predetermined minute ventilation Higher tidal volumes
Neurally adjusted ventilatory assist Decreases patient-ventilator asynchrony Requires invasive monitor to measure electrical activity of diaphragm
Mandatory minute ventilation Predetermined minute ventilation, allows spontaneous breathing Atelectasis, variable airway pressures
Extracorporeal membrane oxygenation Avoids mechanical lung stress Requires cardiopulmonary bypass with anticoagulation
High-frequency oscillatory ventilation Allows for lower tidal volumes Higher mean airway pressures, requires heavy sedation
Prone positioning Decreases V/Q mismatch Pressure sores, increased sedation, inadvertent extubation
ICP, Intracranial pressure; PEEP, positive end-expiratory pressure.

Alveolar overdistention secondary to elevated airway pressures or high V t is referred to as barotrauma or volutrauma . As such, peak and plateau airway pressures and V t are critical parameters to monitor during MV. The Acute Respiratory Distress Syndrome Network (ARDSnet) trial is a landmark study that highlighted the lethal consequences of high V t and airway pressures in patients requiring MV. In this randomized, multicenter trial, patients with what was then termed acute lung injury (ALI) received either traditional ventilation with initial V t of 12 mL/kg and plateau pressures of 50 cm H 2 O or less or lower V t of 6 mL/kg and plateau pressures of 30 cm H 2 O or less. The trial was stopped early because of a statistically significant survival advantage in the lower V t group.

In addition to demonstrating improved outcomes following ALI/ARDS with lower V t , the ARDSnet trial found that ventilating patients with a lower V t results in less circulatory, coagulation, and renal failure. The lower V t group also had greater reductions in plasma interleukin 6 concentration. Taken together, these findings suggest a reduced systemic inflammatory response to VILI.

Alternatives to conventional mechanical ventilation

Pressure-controlled ventilation

Most conventional MV is volume cycled, in which the desired V t is determined by a setting on the ventilator. Airway pressures depend on the volume of gas delivered and the patient’s underlying respiratory mechanics. PCV is a unique modality in that inspiratory pressure is set beforehand, and the V t delivered to the patient is dependent on airway resistance and lung compliance. Inspiratory airway pressure increases early in the respiratory cycle and is maintained throughout the delivery phase. The inspiratory flow decreases exponentially during lung inflation in order to keep the airway pressure at the preselected value. This flow pattern can improve gas exchange, and it is believed to be the major benefit of PCV. PCV is a nonspontaneous modality and requires no active patient participation. The primary disadvantage of PCV is that V t depends on airway pressures and mechanical properties of the lungs. For example, with a constant peak airway pressure, inflation volume will decrease as airway resistance increases or lung compliance decreases. Inflation volumes can vary substantially during PCV. In patients with ARDS and damaged, noncompliant lungs, PCV can result in hypoventilation and hypoxemia.

A recent randomized controlled trial compared targeted low airway pressures (plateau pressure < 30 cm H 2 O) with an ARDSnet (low V t ) control ventilation strategy in 20 patients with ARDS. There were no significant differences in duration of ventilation, duration of intensive care unit (ICU) stay, or duration of hospital stay between groups. The treatment group had significantly lower systemic proinflammatory cytokine concentrations, which could result in less organ damage. Additional larger studies are needed to evaluate differences in mortality rate.

Open lung ventilation

The concept of “open lung” ventilation refers to preventing repetitive opening and closing of alveoli, which may maximize gas exchange and prevent atelectrauma and associated proinflammatory cytokine production. Atelectasis occurs most often during exhalation when gas exits the lungs. Delivering higher gas pressures during exhalation via PEEP is one method of preventing alveolar collapse. Recent studies examined the effects of “open lung” ventilation and recruitment strategies combined with PCV and low V t on outcomes in patients with ARDS. Villar et al conducted a multicenter, randomized controlled trial comparing high PEEP and low V t ventilation with conventional V t (9–11 mL/kg) ventilation and observed significant reductions in ICU and hospital mortality rate and ventilator-free days in the high PEEP/low V t group. It is unclear whether the survival benefits resulted from low V t , high PEEP, or both. To address this question, Meade et al conducted a multicenter, randomized study comparing low V t ventilation with a combined approach of low V t , high PEEP, and recruitment maneuvers in patients with ARDS. The authors did not observe any differences in all-cause hospital mortality rate but found that the experimental group had lower rates of refractory hypoxemia and death with refractory hypoxemia. The additive benefits of an “open lung” approach to low V t ventilation require further evaluation.

Inverse-ratio ventilation

Inverse-ratio ventilation (IRV) is a combination of PCV (hence, PC-IRV), when the ratio of inspiratory time (I) and expiratory time (E) is adjusted. It is often the first modality attempted after conventional MV fails ( Fig. 1 ). A normal I:E ratio is 1:4. Decreasing the inspiratory flow rate can increase I and I:E to 2:1 or even 4:1. Increasing I can improve alveolar recruitment by preventing alveolar collapse. Studies of PC-IRV in ARDS demonstrate improvements in oxygenation. The early use of PC-IRV can facilitate tapering of high fractions of inspired oxygen (Fio 2 ) and decreasing high PEEP and peak inspiratory pressures (PIPs). A potential drawback to PC-IRV is stacking of breaths (auto-PEEP), with resulting alveolar hyperinflation, high airway pressures, and barotrauma. Increased transthoracic pressures from auto-PEEP can reduce cardiac output (Q) via decreased central venous return. To date, there are no prospective randomized studies comparing mortality rate differences between conventional and IRV.

FIGURE 1, Hierarchical ventilator management in a patient with acute respiratory distress syndrome (ARDS). ECMO, Extracorporeal membrane oxygenation; PBW, predicted body weight; PCV, pressure-controlled ventilation; PEEP, positive end-expiratory pressure; V t , tidal volume.

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