FUNDAMENTALS OF MECHANICAL VENTILATION

CHAPTER 86 FUNDAMENTALS OF MECHANICAL VENTILATION



Mechanical ventilation is often required to manage trauma or critical illness, whether for airway protection, administration of general anesthesia, or management of acute respiratory failure (ARF) (Table 1). New technology now provides several modes by which a patient may be ventilated, with the goals of improved gas exchange, better patient comfort, and rapid liberation from the ventilator. Moreover, noninvasive positive-pressure ventilation permits some cases of ARF to be managed without insertion of an artificial endotracheal airway, and some patients who are extubated with marginal reserves to avoid reintubation. Nearly all ventilators can be set to allow full support of the patient on the one hand, and periods of exercise on the other. Thus, the choice of ventilator settings is a matter of physician preference for the majority of patients (Table 2). Controlled ventilation with suppression of spontaneous breathing leads rapidly to respiratory muscle atrophy; therefore modes of assisted ventilation are preferred wherein machine-delivered breaths are triggered by the patient’s own inspiratory efforts. Basic modes of assisted ventilation include assist-control ventilation (ACV), synchronized intermittent mandatory ventilation (SIMV), and pressure support ventilation (PSV).


Table 1 General Indications for Mechanical Ventilation













Table 2 Glossary of Basic Terminology of Mechanical Ventilation



























Control: regulation of gas flow



Cycling: ventilator switching from inhalation to exhalation after volume or pressure target (or limit) has been reached



Triggering: causes the ventilator to cycle to inhalation



Breaths: cause the ventilator to cycle from inhalation to exhalation



Flow pattern: constant, decelerating, or sinusoidal



Mode (breath pattern)





Most patients are started on mechanical ventilation for management of ARF, during which the work necessary to initiate a breath increases by a factor of four to six. The most common reason to initiate mechanical ventilation is to decrease the work of breathing by the patient. Additional potential benefits of mechanical ventilation include improved gas exchange, enhanced coordination between support and the patient’s own efforts, resting of respiratory muscles, prevention of deconditioning, and prevention of iatrogenic lung injury while promoting healing. However, unless settings are chosen carefully to synchronize with the patient’s own central respiratory drive, mechanical ventilation can cause an increase in work. Regardless of the mode chosen, all mechanical ventilation is a modification of the manner in which positive pressure is applied to the airway, and the interplay of the mechanical support and the patient’s own efforts.



NONINVASIVE VENTILATION


Ventilatory support delivered without establishing an endotracheal airway is “noninvasive ventilation” (NIV). Noninvasive ventilation was administered previously with intermittent negative pressure, but the current technique utilizes positive-pressure ventilation delivered through a nasal or face mask, and usage is expanding in the management of acute and chronic respiratory failure and possibly for some patients with heart failure.


Putative benefits of NIV are numerous, owing to avoidance of the complications of endotracheal intubation. Noninvasive ventilation preserves swallowing, feeding, speech, cough, and physiologic air warming and humidification by the nasooropharynx. Nonintubated patients communicate more effectively, require less sedation, and are more comfortable. In addition, patients are often able to continue with standard oral nutrition. Noninvasive ventilation eliminates complications such as trauma with tube insertion, mucosal ulceration, aspiration, infection (e.g., pneumonia, sinusitis), and dysphagia after extubation.


In a randomized, prospective trial following pulmonary resection of 48 patients with acute hypoxemic respiratory insufficiency, Auriant et al. compared standard invasive mechanical ventilation with nasal mask NIV. The need for postoperative reintubation and mortality were clearly reduced in patients receiving NIV as a part of respiratory support. Similarly, Squadrone et al. randomized 209 patients with respiratory failure in the postanesthesia care unit after major abdominal surgery to oxygen alone, or with continuous positive airway pressure (CPAP) via a mask. Patients who received oxygen plus CPAP had a significantly lower intubation rate, and also lower rates of pneumonia, infection, and sepsis.







MODES OF MECHANICAL VENTILATION





Positive End-Expiratory Pressure


Although it is a ubiquitous form of ventilatory support, positive end-expiratory pressure (PEEP) can be confusing because the positive pressure is actually applied throughout the respiratory cycle and is more correctly termed CPAP. Using PEEP accomplishes three goals: prevention of alveolar derecruitment by restoring FRC, which is decreased in acute lung injury (ALI) and atelectasis, to the physiologic range; protection against injury during phasic opening and closing of atelectatic units; and assisting cardiac performance during heart failure, by increasing mean intrathoracic pressure.


The FRC is the lung’s physiologic reserve; loss of chest wall or lung compliance (the rate of change of volume in response to pressure) causes reduced FRC. The FRC is the volume of gas that remains in the lungs at the end of a normal tidal breath (∼2.5 liters); gas exchange does occur. At FRC, the tendency for the lungs to collapse is balanced by the tendency for the chest wall to move outward. A small vacuum in the pleural space assists in maintaining equilibrium, which is lost when pneumothorax is present.


The FRC is determined by the compliance of the lung and chest wall. Anything that constrains chest wall expansion reduces its compliance; likewise, anything that reduces lung volume reduces lung compliance. The FRC is composed of two volumes, the expiratory reserve volume (ERV) and the residual volume (RV). Below FRC, exhalation is active; lung tissue must be compressed to express gas. The RV (∼1 liter in adults) is the point where no more gas can be expressed from the lungs regardless of the pressure applied, because alveolar pressure exceeds atmospheric pressure and the gradient along the airway is reversed. Being filled with gas and coated with surfactant, alveoli are difficult to compress, but airways are compressible. When intrathoracic pressure exceeds pressure in the small airways, “dynamic airway collapse” occurs and gas is trapped in alveoli. Airway collapse increases the work of breathing and leads to ventilation-perfusion (V/Q) mismatch. Collapsed airways are difficult to reinflate, leading to a huge increase in the work of breathing and oxygen consumption.


The concept behind PEEP is to increase FRC; in essence, to allow alveoli to deflate only to the point just above where inflation remains easy (called the lower inflection point of the pressure–volume curve). The patient requires sufficient PEEP to prevent alveolar derecruitment, but not so much PEEP that alveolar overdistension, dead space ventilation from collapse of the alveolar microcirculation, or hypotension due to reduced right ventricular preload, right ventricular output, and ultimately cardiac output occur.


Auto-PEEP is caused by gas trapped in alveoli at end-expiration. This gas is not in equilibrium with the atmosphere and is at positive pressure, increasing the work of breathing. In patients with obstructive airways disease, increased bronchial tone leads to resistance to both inhalation and exhalation. Shortening of E (e.g., small airways disease, mucus plugging, pressure-controlled ventilation with inverted I:E) results in gas trapping at end-expiration, hyperinflation, and increased intrathoracic pressure, which abolishes the alveolar pressure gradient. Auto-PEEP can be ameliorated by lengthening E, shortening I, or decreasing the respiratory rate.


The ideal level of PEEP is controversial (Table 3). It may be that which prevents derecruitment of the majority of alveoli, while causing minimal overdistension; alternatively, application of PEEP is a recruitment maneuver, arguing for higher pressures to be applied to overcome alveolar collapse. Applying PEEP to put the majority of lung units on the favorable part of the pressure–volume curve will maximize gas exchange and minimize overdistention, but is easier said than done because the lower inflection point is sometimes indistinct. Undoubtedly, the combination of PEEP and low VT prevents volutrauma, but the exact amount of PEEP to apply is controversial. The reason for this is hysteresis—the tendency of the lungs, due to surfactant, to exist at higher volumes in exhalation than in inhalation.


Table 3 Protocol Summary for Institution of Mechanical Ventilation for Acute Lung Injury/Acute Respiratory Distress Syndrome







Initial ventilator settings















PEEP, Positive end-expiratory pressure.


Adapted from Nathens AB, Johnson JL, Mine JP, et al. Inflammation and the Host Response to Injury Investigators: Inflammation and the host response to injury, a large-scale collaborative project: patient-oriented research core—standard operating procedures for clinical care. I. Guidelines for mechanical ventilation of the trauma patient. J Trauma 59:764–769, 2005.



Ventilator “Bundle”


Care of the patient who requires mechanical ventilation is more than just a matter of providing ventilation and oxygenation. Such patients are often critically ill and at risk of numerous complications, not all of which are related directly to acute respiratory failure or mechanical ventilation. Therefore, it is important for the clinician to bear in mind the total patient. The patient may be at prolonged bed rest, and at risk for deconditioning, venous thromboembolic complications, and the development of pressure ulcers. Neurologic compromise from disease or sedative/analgesic drugs may impair the sensorium sufficiently that the patient cannot protect his or her airway, increasing the risk of pulmonary aspiration of gastric contents. Oversedation may be one component aspect of prolonged mechanical ventilation, which is a definite risk factor for development of ventilator-associated pneumonia (VAP). Prolonged mechanical ventilation (>48 hours) is itself a marker of critical illness, specifically the development of stress-related gastric mucosal hemorrhage, a rare but serious (∼50% mortality) harbinger of adverse outcomes of critical illness.


Using the principles of evidence-based medicine, several “best practices” have been combined into a “ventilator bundle” to optimize the outcomes of mechanical ventilation. The bundle consists of four maneuvers: Keeping the head of the patient’s bed up at least 30 degrees from level at all times unless contraindicated medically; prophylaxis against venous thromboembolic disease; prophylaxis against stressrelated gastric mucosal hemorrhage; and a daily “sedation holiday” to assess for readiness to liberate from mechanical ventilation through assessment of a trial of spontaneous breathing. Careful adoption and adherence to all facets of the bundle can decrease the substantial risk of VAP, along with other maneuvers such as adherence to the principles of infection control.



Routine Settings


Ventilator settings are based on the patient’s ideal body mass and medical condition. The risk of oxygen toxicity from prolonged exposure to a fraction of inspired oxygen (FIO2) greater than 60% is minimized by using the lowest FIO2 that can oxygenate arterial blood satisfactorily (e.g., arterial oxygen tension [PaO2] of 60 mm Hg or an oxygen saturation [SaO2] of 88%) (see Table 3).


The normal lung (e.g., during general anesthesia) may be ventilated safely with VT 8–10 ml/kg for prolonged periods. Historically, critically ill patients with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) have been ventilated with VT 10–15 ml/kg of ideal body mass, which is now considered inappropriate due to convincing data from experiments indicating that alveolar overdistention can produce endothelial, epithelial, and basement membrane injuries associated with increased microvascular permeability and iatrogenic lung injury (VILI). Direct monitoring of alveolar volume is not feasible. A reasonable substitute is to estimate peak alveolar pressure as obtained from the plateau pressure (Pplat) measured in a relaxed patient by occluding the ventilator circuit briefly at end-inspiration. In patients with pulmonary dysfunction, there is a growing tendency to reduce the VT delivered to 4–6 ml/kg or less in order to achieve a Pplat no higher than 35 cm H2O. The incidence of VILI increases markedly when Pplat is high. Low VT ventilation may lead to an increase in PaCO2. Acceptance of elevated CO2 tension in exchange for controlled alveolar pressure is termed “permissive hypercapnia.” It is important to focus on pH rather than PaCO2 if this approach is employed. If the pH falls below 7.25, increase VE or administer NaHCO3.


The f that is set depends on the mode. With ACV, the backup rate should be about four breaths per minute less than the patient’s spontaneous rate to ensure that the ventilator will continue to supply adequate VE should the patient have a sudden decrease in spontaneous breathing. With SIMV, the rate is typically high at first and then decreased gradually in accordance with patient tolerance.


An inspiratory flow rate of 60 l/min is used with most patients during ACV and SIMV. In patients with chronic obstructive pulmonary disease, better gas exchange may be achieved at a flow rate of 100 l/min, probably because the resulting increase in E allows for more complete emptying of trapped gas. If the flow rate is insufficient to meet the patient’s requirements, the patient will strain against his or her own pulmonary impedance and that of the ventilator, with a consequent increase in the work of breathing.


In the ACV, SIMV, and pressure control modes (discussed in the next chapter), the patient must lower airway pressure below a preset threshold (usually minus 1–2 cm H2O) in order to trigger the ventilator to deliver a tidal breath. In most situations, this is straightforward; the more negative the sensitivity the greater the effort demanded of the patient. When auto-PEEP is present, the patient must lower alveolar pressure by the amount of auto-PEEP in order to have any impact on airway opening pressure, and then further by the trigger amount to initiate a breath, increasing dramatically the work of breathing. Flow triggering systems have been used to reduce the work of triggering the ventilator. In contrast to the usual approach in which the patient must open a demand valve in order to receive assistance, continuous flow systems maintain a high continuous flow, and then further augment flow when the patient initiates a breath. These systems reduce the work of breathing slightly below that present using conventional demand valves, but do not solve the triggering problem when breath stacking occurs.

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Jul 7, 2016 | Posted by in CRITICAL CARE | Comments Off on FUNDAMENTALS OF MECHANICAL VENTILATION

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