Ventilator management for most thoracic surgery patients involves two distinct phases: (1) support in the operating room while the patient is undergoing surgery and receiving general anesthesia, and (2) support in the postoperative recovery room or intensive care unit (ICU) as the patient is recovering from surgery. Issues relating to the intraoperative ventilator management of thoracic surgery patients are largely the responsibility of the anesthesiologist and are discussed in Chapter 5. Issues relating to the postoperative management of mechanical ventilation are the responsibilities of the thoracic surgeon and intensivist.

In the transition from the operating room to the recovery room or ICU it is important to appreciate that general anesthesia and thoracic surgery adversely affect nearly all aspects of respiratory physiology. These include anesthetic-related alterations in respiratory drive, reductions in lung volume due to loss of chest wall tone, changes in the ventilation perfusion relationship, and increased airway resistance in the setting of diminished lung volumes. Given the postoperative structural changes in the lung as well as its native state of disease, these alterations may have variable effect on overall function and be unpredictable in duration. They certainly must be taken into account during initial ventilatory management.

The overall approach to mechanical ventilation in the postoperative thoracic surgery patient is similar to that used in the critically ill medical patient. Preexisting lung disease, intraoperative complications, and known physiologic alterations associated with a planned surgery require more innovative approaches.

There are two basic approaches to mechanical ventilation in patients who have undergone thoracic surgery. These are (1) methods used to support postoperative patients who are kept intubated after surgery for a specific indication that is expected to resolve within hours, allowing for rapid discontinuation of ventilator support; and (2) methods used to support patients who develop hypoxic or hypercarbic respiratory failure as a consequence of a primary process that will resolve over a period of days to weeks and may require more gradual weaning.

In most patients, the physiologic alterations caused by anesthesia and thoracic surgery are well tolerated. These patients generally have minimal to mild preexisting pulmonary disease and are either extubated in the operating room or arrive in the postoperative recovery area or ICU ready for extubation with normal Pao₂ and Paco₂ blood gas values on minimal ventilator support. Successful extubation in this group is associated with: (1) intact mental status; (2) reasonable assurance that the patient will have the ability to cough and protect his or her airway; and (3) initiation of an analgesic protocol that optimizes respiratory mechanics without causing undue respiratory depression.

Although mental status is usually simple to assess, often it is not possible to confirm intact recurrent laryngeal nerve (RLN) function before attempting extubation simply by relying on the patient’s ability to cough and swallow secretions. The risk of injury to the RLN is increased in the thoracic surgery population because many procedures involve anatomic dissection or traction on structures near the left mainstem bronchus where the RLN branches from the vagus.¹ Postextubation evaluation revealing a weak voice and ineffective cough should prompt direct laryngoscopic evaluation of the hypopharynx and vocal cords, followed by vocal cord medialization if indicated.²

Several factors contribute to respiratory muscle dysfunction after thoracic surgery. Pain is a major contributor. Thus, selection of an appropriate analgesic regimen is essential for preventing postoperative respiratory failure.³ Studies of respiratory muscle function also have demonstrated that diaphragmatic contractility is compromised by somatic reflex inhibition of the phrenic nerve as a consequence of afferent intercostal stimulation.⁴ Thus analgesic regimens that address both these factors should provide optimal management. Epidural anesthesia with local anesthetic agents (i.e., bupivacaine) accomplishes this objective and can be administered either alone or in combination with opioids. Patient-controlled anesthesia (PCA) also may be an effective adjunct, but care must be taken in titration to minimize the degree of respiratory depression.⁵

A substantial number of patients undergoing thoracic surgery will require ventilator support postoperatively. A successful ventilator strategy for longer-term management involves the following general principles:

1. 
   

   Selecting a mode of ventilation that prevents high airway pressures and optimizes patient-ventilator synchrony.

   
   
2. 
   

   Early weaning of Fio₂ to prevent adsorption atelectasis and limit possible oxygen toxicity, especially in patients receiving medications that have been associated with free-radical lung injury (e.g., bleomycin).

   
   
3. 
   

   Selecting an appropriate sedation/analgesia regimen to ensure patient comfort while permitting periodic assessments of mental status and respiratory function.

   
   
4. 
   

   Initiating nutritional support and deep venous thrombosis prophylaxis.

   
   
5. 
   

   Closely monitoring the intravascular fluid status to prevent development of pulmonary edema, especially in areas of lung tissue that have been manipulated during surgery.

No guidelines exist for selecting the “single best” mode of ventilation for the postoperative thoracic surgery patient. Anecdotal experience indicates that many surgeons select pressure-controlled modes of ventilation in which the user-specified independent variable is airway pressure rather than tidal volume. This ensures that airway pressures will not exceed a known value, thus limiting stress on newly created staple or suture lines. There are no data to indicate that this approach improves respiratory physiology or ICU outcomes in this patient population.⁶ Furthermore, appropriate selection of ventilator parameters using volume-cycled modes can ensure equivalent limiting of airway pressures. Thus, in most instances, user preference and experience will dictate ventilator settings.

Mechanical ventilation has evolved dramatically in the last 100 years, revolutionizing the concept of intensive care. Mechanical ventilation can be provided as either negative pressure ventilation (iron lung, cuirass shell, or rocking bed) or more commonly as positive pressure inflation by using an endotracheal tube or mask (known as noninvasive positive pressure ventilation). Positive pressure ventilation is also classified as manual (hand bag valve mask) or mechanical. The latter is provided by transport, critical care, and neonatal/pediatric ventilators.

There are many models of commercially available ventilators and it is important for the physician to understand the core components of these devices (Fig. 7-1). The most widely used system is positive pressure ventilation, which is administered through an endotracheal tube.⁷ Positive pressure ventilation requires the following components: an oxygen source (if O₂ mixture above 21% is needed), a mixing chamber, a compressor, an electronically controlled inspiratory valve, a ventilator circuit (with inhalation, “Y” connector, and exhalation limb), and an exhalation valve to form a closed circuit. The core of the apparatus is a computer, which controls the manner in which the ventilator breaths are triggered, cycled, and limited. These parameters are organized as preset modes. The computer also monitors pressure and flow sensors, providing a feedback and safety system. The array of information generated by the computer is displayed on a monitor in tabular or graphic format. In this way, the clinician can adjust the patient’s ventilatory strategy based on the patient’s clinical status while minimizing potential harm.

Commonly used modes available on most commercial ventilators include assist/control, pressure-controlled ventilation (PCV), pressure-support ventilation (PSV), and continuous positive airway pressure (CPAP). The setup and operation of these modes are described below.

When choosing ventilator settings, the mode refers specifically to the manner in which ventilator breaths are triggered, cycled, and limited. The trigger, either an inspiratory effort or a time-based signal, defines what the ventilator senses to initiate an assisted breath. Cycle refers to the factors that determine the end of inspiration. For example, in volume-cycled ventilation, inspiration ends when a specific tidal volume is delivered to the patient. Other types of cycling include pressure cycling, time cycling, and flow cycling. Limiting factors are operator-specified values, such as airway pressure, that are monitored by transducers internal to the ventilator circuit throughout the respiratory cycle. If the specified values are exceeded, inspiratory flow is immediately stopped, and the ventilator circuit is vented to atmospheric pressure or the specified positive end-expiratory pressure (PEEP). A list of types of assessments that should be considered for a patient undergoing mechanical ventilation are provided in Table 7-1.

In assist/control mode ventilation (ACMV), an inspiratory cycle is initiated either by the patient’s breathing effort or, if no patient effort is detected within a specified time window, by a timer signal within the ventilator based on user-specified parameters. Every breath delivered, whether patient- or timer-triggered, consists of the operator-specified tidal volume. Ventilatory rate is determined either by the patient or by the operator-specified backup rate, whichever is of higher frequency (Fig. 7-2). ACMV is used commonly for initiation of mechanical ventilation because it ensures a backup minute ventilation in the absence of an intact respiratory drive and allows for synchronization of the ventilator cycle with the patient’s inspiratory effort.

Problems can arise when ACMV is used in patients with tachypnea resulting from nonrespiratory or nonmetabolic factors such as anxiety, pain, or airway irritation. Respiratory alkalemia may develop and trigger myoclonus or seizures. Dynamic hyperinflation may occur if the patient’s respiratory mechanics are such that inadequate time is available for complete exhalation between inspiratory cycles. This can limit venous return, decrease cardiac output, and increase airway pressures, predisposing to barotrauma. ACMV is not effective for weaning patients from mechanical ventilation because it provides full ventilator assistance on each patient-initiated breath.

PCV can be used to provide ventilator support either with ACMV triggering (PCV-ACM) or SIMV triggering (PCV-SIMV). In contrast to conventional ACMV or SIMV, which are volume-cycled and pressure-limited, PCV-ACM and PCV-SIMV are time-cycled and pressure-limited. During the inspiratory phase, a given pressure is imposed at the airway opening, and the pressure remains at this user-specified level throughout inspiration (Fig. 7-3). Since inspiratory airway pressure is specified by the operator, tidal volume and inspiratory flow rate are dependent rather than independent variables and are not user-specified. PCV is used commonly for patients with documented barotrauma because airway pressures can be limited, as well as for postoperative thoracic surgical patients, in whom the stress across a fresh suture line can be limited. When PCV is used, minute ventilation and tidal volume must be monitored; minute ventilation is varied by the user through changes in rate or in the pressure-controlled value.

PCV with the use of a prolonged inspiratory time is frequently applied to patients with severe hypoxemic respiratory failure. This approach, called pressure-controlled inverse inspiratory-to-expiratory ratio ventilation (PCIRV), increases mean distending pressures without increasing peak airway pressures. It is thought to work in conjunction with PEEP to open collapsed alveoli and improve oxygenation. In acute lung injury (ALI), PCIRV may be associated with fewer deleterious effects than conventional volume-cycled ventilation, which requires higher peak airway pressures to achieve an equivalent reduction in shunt fraction, but there are no convincing data to show that PCIRV improves outcomes in ALI or adult respiratory distress syndrome.^8,9