Chapter 4. Mechanical Ventilation

Understanding the importance of ventilator management is a crucial facet of emergency medicine. Emergency physicians are well known for their expertise in emergent airway management, but securing the airway is only a fraction of their role. Mechanical ventilation (MV) is an essential tool for critically ill patients. If not applied correctly, it can worsen the clinical course and increase morbidity and mortality.1 In the past two decades, our understanding of ventilator-induced lung injury (VILI) has resulted in the challenging of conventional practices, such as using lower tidal volumes. With the current crisis of emergency department (ED) overcrowding, critical care patients have increased lengths of stay in the ED and, at times, are boarded for several hours or even days until a bed is available in the intensive care unit (ICU).2,3 The emergency physician must understand critical care topics and the intricacies of MV for heterogeneous patient populations with varying pathologies—no “single setting fits all.” With special consideration of each patient's needs, both patient care and outcomes will improve.

Indications for intubation and institution of MV fall under three basic categories: respiratory failure, airway protection, and anticipation of the clinical course.

The most common indication for MV is respiratory failure. These patients frequently have either hypoventilation or a decreased ability to manage the work of breathing. This can lead to hypoxemia, hypercapnia, or both. Hypoxemia is often defined as a Po2 less than 60 mm Hg. Hypercapnia is defined as an “elevated” Pco2. In contrast to hypoxemia, hypercapnia is difficult to strictly define, as it is a component of hypoventilation directly resulting in elevation of CO2. An exact number is less important than the clinical picture and varies in the literature. In certain populations, such as patients with COPD who chronically retain CO2, a higher baseline Pco2 of 45–55 mm Hg can be well tolerated. An acute rise in CO2 from the patient's baseline will cause lethargy, sleepiness, confusion, and altered mental status. In these hypercapnic patients, the primary action of MV is the promotion of appropriate alveolar ventilation with an end goal of proper CO2 clearance.

Another indication for the institution of MV is to protect the airway from potential aspiration of various etiologies. Common indications include acute intoxication, altered mental status from infection, or massive upper gastrointestinal hemorrhage.

Last, the predicted clinical course will often dictate securing an airway to facilitate either workup or definitive treatment. Patients in a questionable condition may need further diagnostic testing away from the critical resources of the ED, placing them at risk of sudden deterioration “in the hallway of radiology.” These patients should be placed on MV prior to leaving the ED.

There are no absolute contraindications for MV. There are, however, minor adverse effects of MV. The placement of an endotracheal tube takes away the protective functions of the upper airway: gas heating, gas humidification, air filtration, and protection from aspiration. The endotracheal tube decreases effectiveness of removing secretions by expelling them through coughing. There is also loss of speech and an increase in airway resistance.

Appreciation of the fundamental concepts of respiration is essential for the care of a mechanically ventilated patient. The most important parameter one needs to understand and become familiar with is minute ventilation, which is the product of tidal volume and the respiratory rate (Table 4-1). Normal minute ventilation is 5–7 L/min. However, not all of the tidal volume reaches the alveoli because of dead space. Dead space can be anatomic or pathologic. Anatomic dead space exists because gas exchange does not occur in the trachea, larger airways, or ventilator tubing. It is usually estimated as 150 mL or 2.2 mL/kg lean body weight.4 Pathologic dead space exists for reasons of ventilation/perfusion (V/Q) mismatch, shunting, and decreased diffusion across a diseased capillary–alveolar interface. The physician must be aware of the patient's approximate minute ventilation prior to instituting MV to ensure that the ordered ventilation parameters do not create a respiratory pattern that is incompatible with the patient's disease state. Lower minute ventilation will result in hypoventilation with a resulting increase in Pco2. This will directly affect the acid–base balance resulting in an acidemia and may also lead to hypoxemia. In contrast, supranormal minute ventilation will lead to a decrease of Pco2. This will cause an alkalemia and may cause hyperoxygenation, which has been reported to directly result in lung toxicity, although the timing of this toxicity is unclear. This underscores the importance of considering minute ventilation when ordering the initial ventilator settings. Minute ventilation should be adjusted based on the clinical picture rather than a particular number.

Compliance is a measure of the distensibility of the respiratory system. It is the inverse relationship between the change in volume (ΔV) accommodated per change in pressure (ΔP) (Table 4-1). Total compliance is a sum of the chest wall and lung compliances. Decreased compliance is seen in pulmonary/chest wall edema, pulmonary fibrosis, pneumonia, or increased intra-abdominal pressure, whereas increased compliance is seen in emphysema and sarcoidosis. Ventilator settings should be tailored in patients with abnormal compliance to ensure adequate oxygenation and minimize the risk of VILI.

Resistance is the amount of pressure needed to achieve a given amount of airflow. It is mainly a function of the larger airways because velocity is inversely proportional to area and the smaller airways exist in parallel, rather than in series.

These concepts affect two important variables of MV: peak inspiratory pressure (PIP) and plateau pressure (Pplat). Both are easily measured on the ventilator (see Figure 4-1).

The PIP is a dynamic pressure measurement during maximal end inspiration. It is influenced by both airway resistance and lung compliance. This pressure only reflects upper airway pressure and not transalveolar pressure. Next, if an end-inspiratory pause is applied after maximal inflation, the airway pressure decreases and then reaches a steady state. This resulting value is the Pplat. Elasticity is often associated with Pplat, but this pressure measurement is a function of the total compliance and reflects the mean airway pressure of all of the airways. A respiratory therapist can assist the physician in obtaining these values if one does not have the expertise or time.

Pplat is the force the lung experiences at the alveoli, not PIP. Thus, Pplat has been used as marker of transalveolar pressure. This surrogate value is solely an estimation of transalveolar pressure. Elevated pressures greater than 30 cm H2O, according to a study conducted by the Acute Respiratory Distress Syndrome (ARDS) Network, have shown a significant increase in mortality (further discussed below).1 Consideration of the Pplat leads to significant changes in clinical decision making.

The PIP and Pplat become instrumental during ventilatory therapy. Anticipation and direct action of abnormal pressures can identify the likely cause of the problem. First, one looks at the PIP. A decrease in PIP is due to an air leak, inadvertent change of the ventilator settings, or extubation. The upper limit of normal of PIP is 35 cm H2O. When the PIP is increased, the physician should reflexively check the Pplat. A normal Pplat indicates that there is increased airway resistance due to either bronchospasm or an obstruction reducing the endotracheal tube diameter. These obstructions can be caused by biting, kinking, or twisting of the tube. They may also be caused by blood or foreign bodies such as mucus plugs and aspiration. An elevated Pplat indicates decreased lung and chest wall compliance. This can be due to pneumothorax, gas trapping (also known as auto–positive end-expiratory pressure [PEEP]), atelectasis, or any of the previously mentioned medical conditions associated with decreased compliance. Careful attention and proper alarm settings for PIPs will alert the astute physician to potential problems.

The primary goal of MV is oxygenation and ventilation, but of equal importance is the avoidance injury to the already compromised lung tissue. Damage caused by MV is termed VILI. VILI is a current, discrete term that encompasses and replaces older terms and misconceptions. Its mechanisms are mainly 2-fold: shear and strain stresses.

First, repetitive collapsing and inflation of alveoli produces a shear stress that can tear the thin, fragile alveolar–capillary interface (atelectrauma). It has been confirmed that high end-inspiratory pressures and volumes can lead to alveolar–capillary permeability alterations, nonhydrostatic pulmonary edema, and tissue injury similar to acute lung injury (ALI) and ARDS.5

Second, strain in the form of overdistension can lead to alveolar fracture and rupture (barotrauma/volutrauma). Additional effects of alveolar rupture can stem from the liberation of inspired air into the various spaces around the lung: pleural cavity (pneumothorax), mediastinum (pneumomediastinum), or simply the pulmonary parenchyma (pulmonary interstitial emphysema).

Further, the body's immune system contributes to VILI. This injury to the lung induces the production of inflammatory mediators (cytokines and products of the endothelium and arachidonic acid pathways) that infiltrate the bloodstream through the compromised alveolar–capillary interface and produce injurious effects distant to the lungs. This process of multiorgan injury is called biotrauma.6,7

The more severe the preventilation abnormalities are, the more severe potential VILI can be.8 In one study, repetitive collapse and reopening of terminal units did not injure healthy lungs, although it did decrease compliance and alter gas exchange.9 However, other studies illustrate the increased susceptibility of diseased lungs to the adverse effects of MV.

Based on animal data, Pplat >35 cm H2O is concerning for VILI. This has led to the concept and strategy of “lung-protective ventilation.”10 Subsequently, the ARDS Network conducted a landmark multicenter, randomized study illustrating that a lung-protective strategy with reduced tidal volumes of 6 mL/kg predicted body weight (PBW; see Table 4-1) showed a significant decrease of days on a ventilator and decrease in mortality when Pplat was less than 30 cm H2O versus traditional tidal volumes of 12–15 mL/kg PBW.1 Tidal volumes of 12–15 mL/kg PBW are detrimental to the general population. Presently, no exact volume recommendation has been defined in the literature except in ALI/ARDS.

To ensure proper minute ventilation with lower tidal volumes, higher respiratory rates should be used and then adjusted. Clear benefit to the patient was demonstrated in spite of hypoventilation, introducing the concept of permissive hypercapnia. Permissive hypercapnia is the acceptance of hypoventilation and resultant CO2 retention caused by reduced tidal volumes selected to prevent VILI. The retention and breakdown of CO2 then leads to acidemia. A pH greater than 7.2 has been shown to be well tolerated.11 Although hypercapnia as a beneficial lung-protective strategy is clear in animal studies, the precise contribution of hypercapnia in human populations remains heavily debated.

After the airway has been secured, physicians must decide on the mode, target, and variable settings in their orders. This discussion will begin with the four common basic modes of ventilation that most ventilators can deliver: assist/control (A/C), intermittent mandatory ventilation (IMV), pressure support ventilation (PSV), and continuous positive airway pressure (CPAP), all of which can be volume or pressure targeted. Figure 4-2 provides a graphic representation of how the patient and ventilator interact with the different modes of ventilation.

A/C is a combination of two types of MV. Assist mode allows the patient to spontaneously initiate a fully assisted, machine-delivered tidal volume, whereas control mode (or control mechanical ventilation [CMV]) provides ventilation without regard to patient effort. CMV alone has an application solely in deeply sedated or paralyzed patients.

In A/C mode, the ventilator monitors the circuit for the patient to trigger a ventilator-assisted spontaneous breath. In the absence of that trigger, the ventilator automatically cycles, delivering set tidal volume machine breaths at a predetermined rate (Figure 4-3). All breaths in A/C mode receive the set tidal volume; the patient can have a varying rate but the tidal volume is always the set TV. A/C mode is appropriate for apneic, pharmacologically paralyzed and deeply sedated patients, as well as patients with hypoventilation, respiratory muscle fatigue, and those requiring therapeutic hyperventilation.

Settings: For A/C mode, the primary settings are respiratory rate, tidal volume, and fraction of inspired oxygen (FiO2), with or without PEEP.

IMV combines periods of control ventilation with spontaneous breathing. Spontaneous breaths generate a tidal volume proportional to the patient's efforts, that is, no ventilator assistance. The intermittent mandatory breaths are the set amount (rate) of fully assisted breaths delivered by the machine. Currently, IMV has been replaced by synchronized IMV (SIMV). In SIMV, intermittent mandatory breaths are synchronized with spontaneous breaths to preclude breath stacking (Figure 4-4). In patients who are not spontaneously breathing, SIMV is identical to A/C ventilation (Figure 4-5). For each of the nonmandatory, spontaneous breaths, the patient is forced to generate the entire work of breathing. For this reason, it is the authors' opinion that SIMV should always be paired with PSV (discussed next) to decrease the work of breathing.

Settings: Similar to A/C mode, the physician sets an IMV rate, tidal volume, and FiO2s to determine a minimum minute ventilation as well as the optional PEEP and PSV.

PSV augments spontaneous breathing with a set inspiratory pressure while the patient determines the tidal volume and respiratory rate; thus, PSV is a mode of partial ventilator support. The negative pressure generated by the patient opens a valve that delivers a preset pressure. To keep the pressure constant, the ventilator adjusts the flow rate. When the machine detects the end of inspiration, the pressure support terminates and the patient is allowed to exhale spontaneously. As well as augmenting spontaneous breathing, PSV provides assistance to overcome the resistance of the tubing of the ventilator circuit. It is the authors' recommendation that PSV always be added to SIMV.

Settings: The physician sets the PSV generally between a range of 0 and 35 cm H2O with an average starting value of 5–10 cm H2O and FiO2, with or without PEEP. It is essential to set a rate alarm in those patients who are ventilated by PSV alone because there is no guaranteed minute ventilation.

CPAP is another mode for spontaneous breathing patients. Patients who are able to generate an acceptable minute ventilation can undergo a trial of CPAP. It is frequently used as a weaning mode. CPAP should equal the amount of PEEP, between 2 and 5 cm H2O, to prevent loss of alveolar recruitment, atelectasis, and hypoxia. CPAP is also added to decrease the work of breathing (Figure 4-6). The recommended CPAP is 5–10 cm H2O.

After a mode has been selected, the mechanism of breath delivery must be determined: inflating the lungs to a predetermined either volume or pressure. Over the years, various terms have been used for the type of mechanically delivered breath: targeted, controlled, and cycled. These terms are all interchangeable. For ease of discussion, the term “target” will be used hereafter.

Volume-targeted MV delivers a set tidal volume regardless of the pressures needed to do so. Throughout lung inflation, the gas in a volume-assisted breath exerts different pressures in the proximal airways than in the alveoli. The pressure in the proximal airways is a function of resistance; the higher the resistance, the more the pressure needed to deliver the set volume to the lungs. In disease states where compliance is decreased, increased pressures are required to achieve the desired tidal volume.

The other option is pressure-targeted ventilation. The ventilator will deliver variable or intermittent flow to maintain a predetermined inspiratory pressure that is generally equivalent to or lower than Pplat to achieve gas delivery. This setting aims to distribute adequate pressures and reduce alveolar overdistension. This can be achieved through precise tailoring.12 Given that the pressure is constant resulting in variable tidal volumes, the patient may experience hypoventilation due to variations in minute ventilation. Hence, any alteration in the respiratory circuit such as endotracheal tube/airway resistance or lung compliance can lead to hypoventilation. This variability requires more monitoring such as tidal volume and minute ventilation alarms, evaluation of respiratory circuit, and decision making by the physician.

Pressure-targeted ventilation is mainly reserved for patients with increased Pplat and is recommended to limit VILI or allow healing in ALI/ARDS. All things considered, pressure-targeted ventilation is an option worth considering for specific scenarios. Currently, no study exists stating that one mode is superior to another; however, physician familiarity with a specific mode is more important than modality.

Oxygenation is mainly a function of FiO2 and PEEP. Increasing the PEEP decreases intrapulmonary shunting and increases alveolar recruitment. An increase in FiO2 supplies the substrate for those two advantages. One approach is to set the FiO2 at 1.0 and increase the PEEP in increments of 2–3 cm H2O every 10–15 minutes until oxygenation goals are met.

The role of ventilation is to maintain adequate Pco2 and, therefore, pH. This is manipulated primarily by controlling respiratory rate and tidal volume. The goal is to keep the pH between 7.3 and 7.4. Rate has a greater influence on Pco2 than tidal volume; however, an increase in either will cause a decrease in the pH.

Finally, the physician must determine the remaining variables. These variable settings most commonly found on a ventilator are PEEP, FiO2, respiratory rate, tidal volume, and inspiration flow rate and time. Although recommendations will be made regarding initial settings, there are numerous scenarios in which variations should be considered (discussed later in this chapter). As the patient's condition changes, the settings may need to be adapted as well.

Positive pressure applied at the end of expiration is PEEP. Its main function is to overcome the tendency of alveolar collapse, especially in states of decreased compliance. It is usually set between 3 and 8 cm H2O, which has become a standard setting for some. However, PEEP can have adverse consequences as well, since it increases the intrathoracic pressure. Increased intrathoracic pressure impedes venous return and decreases preload, leading to systemic hypotension. Thus, caution should be exercised with PEEP values greater than 8 cm H2O. At times, however, greater values are needed for adequate oxygenation.

FiO2 is usually set at 1.0 (100% oxygen) initially, but the general recommendation is to titrate it down shortly thereafter to maintain a Pao2 greater than 60 mm Hg or SpO2 greater than 92% to prevent the theoretical risk of oxygen toxicity.

Normal respiratory rate is 8–12 breaths/min but ventilators are usually set at 10–14 breaths/min. This may need to be increased when utilizing reduced tidal volumes. Normal tidal volume in a healthy adult without respiratory distress is 5–8 mL/kg PBW (Table 4-1). Tidal volumes have historically been set at 10–15 mL/kg PBW. In a 70-kg patient, this is 700–1,050 mL. Assuming a 1 L tidal volume, the first 150 mL goes to the dead space and 850 mL to the patient's alveoli. If the respiratory rate is 10, this produces a minute ventilation of 8.5 L/min. In the ARDS Network trial, it was learned that lower tidal volumes decreased the incidence of VILI and barotrauma. In that study, the tidal volume goal for lung-protective ventilation was 4–6 mL/kg PBW. In another study, it was shown that tidal volumes greater than 9 mL/kg PBW are a risk factor for development of VILI.13 The ideal tidal volume should lie somewhere in between the old logic and the ARDS Network trial. Thus, the authors recommend an initial value of 8–10 mL/kg PBW as needed.

Normal physiologic inspiratory to expiratory (I:E) ratio is approximately 1:3, whereas patients on MV typically are set to 1:2. This can be manipulated by changing the respiratory rate, tidal volume, and the inspiration time or flow rate. This becomes important in reactive airway diseases.

An assisted breath can be triggered by a timer on the ventilator or by patient effort. One of the two factors can be used to sense patient effort. A decrease in airway pressure can be the trigger detected by the ventilator that causes a breath to be given. This threshold pressure is usually set at a level of −1 to −2 cm H2O and is commonly used in MV today. It is worth noting that most patients on MV have PEEP. This adds to the total amount of force needed to trigger a breath. For example, if the trigger pressure is −2 cm H2O and the PEEP is 5 cm H2O, the patient must generate a pressure of −7 cm H2O, a considerable amount of force from a patient in respiratory failure. Ventilators can also deliver a breath based on the amount of inspiratory flow. Generally a setting of 2 L/min is used because this amount does not generate significant airway pressures and should require less effort by the patient.14

Although respiratory failure is the most common indication for MV, its causes are numerous, and thus it is optimally treated in various ways based on the specific etiology.

Obstructive lung diseases such as asthma and COPD are commonly encountered in the ED. When medical therapy fails or the clinical condition deteriorates (severe hypoxia, hypercapnia, or acidosis), intubation and MV may be the only life-saving options. The specifics of MV in these patients primarily revolve around the prevention of a gas trapping phenomenon called intrinsic PEEP (also termed auto-PEEP or dynamic hyperinflation). By definition, obstructive lung disease involves problems that result in prolonged exhalation exhibited by their decreased FEV1. If the ventilator delivers a breath before the patient is able to exhale back down to baseline, breath stacking occurs. This breath stacking phenomenon increases lung volumes, placing the patient at risk of pneumothorax. The gas trapping of intrinsic PEEP results in a higher alveolar pressure. In a patient not on MV, this increases the work required by the respiratory muscles to generate the negative intrathoracic pressure for inhalation that leads to worsening respiratory failure. Regardless of MV, intrinsic PEEP also causes decreased venous return that leads to hypotension, thereby increasing morbidity and mortality.

To begin, outcomes can be improved by optimizing preintubation volume status. Induction agents as well as auto-PEEP from bag–mask ventilation for preoxygenation can lead to hypotension. A 500-mL to 1-L crystalloid bolus can abate these adverse issues.15 Also, ventilator settings can be adjusted to prevent auto-PEEP. To prevent breath stacking, a lower respiratory rate (6–10 breaths/min), an increased flow rate (around 80–100 L/min initially), and lower tidal volumes (5–7 mL/kg PBW) should be employed to increase the I:E ratio. However, these changes are not without consequences. The reduction in minute ventilation with a decreased respiratory rate and tidal volume does lead to hypercapnia, which in turn leads to a respiratory acidosis. The consequences of hypercapnia can be increased cerebral blood flow (and subsequent increase in intracranial pressure [ICP]), myocardial depression, arrhythmias, and abnormal cellular metabolism. Overall, these decreases in arterial pH are generally well tolerated and much less harmful than the complications of auto-PEEP. The pH may require intervention when it is less than 7.15–7.20 with sodium bicarbonate or tromethamine (an alternative alkalinizing agent known as THAM), but some physicians tolerate these values and continue to monitor for adverse consequences of the acidosis. Hypercapnia can be a powerful central stimulus to increase respiratory rate. This response is usually blunted with medications such as opiates or other sedatives. The response may be so strong as to require chemical paralysis. However, paralytics should be used with caution in conjunction with steroids because of the relation of the steroid-induced neuropathies.16

Another cause of shortness of breath that usually requires MV in the ED is ARDS and the similar ALI. The American–European Consensus Conference, in the absence of a biopsy, defines these diseases with four criteria: (1) acute onset, (2) bilateral patchy airspace disease on chest x-ray, (3) without evidence of increased left atrial pressures (pulmonary capillary wedge pressure <18 mm Hg), and (4) Pao2/FiO2 ≤200 for ARDS or Pao2/FiO2 ≤300 for ALI. As previously discussed, the ARDS Network trial utilized “lung-protective ventilation” with a lower TV of 6 mL/kg PBW; respiratory rates of 18–22 breaths/min and oxygenation goals were met by initially setting the FiO2 and PEEP high (1.0 and 24, respectively) and decreasing them incrementally. If oxygenation suffers at any point, there is a mortality benefit to increase PEEP before the FiO2 is augmented.

MV has hemodynamic consequences, as well as apparent pulmonary effects. The following properties are important in patients with cardiogenic shock and severe pulmonary edema, when PEEP should be used judiciously to titrate oxygen concentrations. The positive pressure generated by MV increases intrathoracic pressure. This increased intrathoracic pressure decreases preload by decreasing venous return to the heart and compressing the right atrium. This decreases cardiac distensibility, inhibiting ventricular filling and compressing the pulmonary artery. The resulting increased pulmonary artery resistance dilates the right ventricle and inhibits the filling of the left ventricle as well. Inversely, the extrinsic pressures decrease afterload, improving cardiac output by assisting ventricular emptying. The exact mechanisms of these effects remain controversial.17 The variable that determines which effect predominates is the intravascular volume. If a patient has a decreased intravascular volume, the preload effects dominate, decreasing cardiac output. If the volume is within normal limits, the afterload effects dominate, increasing cardiac output.4 These properties are important in MV of patients with cardiogenic shock and severe pulmonary edema, when PEEP should be used judiciously to titrate oxygen concentrations.

Patents with brain injury, encephalopathy, and increased ICP commonly need MV due to respiratory failure and for airway protection. The goal with these patients is to maintain adequate cerebral perfusion pressure. Although hypercapnia and acidosis can compromise cerebral blood flow, prophylactic hyperventilation has been shown to be deleterious in patients with head injuries and is no longer recommended.18 Settings should focus on adequate oxygenation, normalizing pH, and hemodynamic stability. If a patient deteriorates secondary to worsening neurologic pathology, hyperventilation can be instituted briefly to allow time for other therapies to take effect. This application of hyperventilation should not extend past 1–2 hours.

It is essential to establish a quick and logical approach to the unstable patient on MV when the ventilator alarms are sounding and the patient is hemodynamically compromised. VILI, MV-induced cardiovascular collapse, and patient-ventilator dyssynchrony are the primary concerns.

The first critical action is to disconnect the ventilator tubing from any patient in the presence of ventilator alarms and cardiovascular collapse. Removing the ventilator from the equation limits the number of variables in solving this life-threatening challenge and immediately eliminates it as a primary culprit. Ventilations with a bag–valve system can confirm endotracheal tube placement with an end-tidal CO2 device, estimate the degree of airway resistance, and observe the chest or abdomen rise with each ventilation. These steps eliminate immediate threats of extubation, endotracheal tube obstruction, and increased airway resistance. If an end-tidal CO2 device and auscultation are not sufficient in detecting appropriate tube placement, direct visualization is the gold standard. If evidence of extubation is discovered, the tube should be removed and the patient must be ventilated with bag–valve mask applying high-flow oxygen to achieve appropriate oxygenation prior to reintubation.

Endotracheal tube obstructions due to mucus plug, blood clot, or aspirate are quickly deduced utilizing airway intubating stylets (gum elastic bougie) and require prompt extubation and reintubation. Increased airway resistance and difficulty during bag–valve ventilations are linked to increased airway resistance and reduced compliance. The differential in these cases includes elevation in intrinsic PEEP, pneumothorax, main stem intubation, and worsening reactive airway disease. Utilization of bedside ultrasound or portable chest x-ray can quickly identify the etiology of the reduced compliance in most of these cases. Emergent diagnosis of tension pneumothorax and immediate intervention with needle thoracostomy can be life saving.

Caution should be maintained for patients with reactive airway disease and dynamic hyperinflation or intrinsic PEEP. Rescue ventilations can further exacerbate this condition if ventilations are too fast (greater than 10 breaths/min), or too large (more than 500 mL tidal volume). Limiting the rate and size of the tidal volume breaths increases the expiratory time and permits enhanced lung emptying of trapped volume present in intrinsic PEEP. As previously stated, a crystalloid bolus of 500 mL to 1 L should be administered over 5–15 minutes with consideration for appropriate sedation.

It is critical for providers to understand that the diagnosis of patient agitation causing patient-ventilator dyssynchrony should be one of the exclusions. Treating the unstable, agitated patient on MV with paralysis or heavy sedation without applying a quick and logical approach to exclude other life-threatening causes can be a preterminal event. When the respiratory demands of the patient are not met by MV, patient-ventilator dyssynchrony occurs, and it is one of the more common problems of MV.19 Physiologic issues, such as neurologic derangements, hypoxia, and hypercapnia, need to be investigated primarily. Lastly, dyssynchrony can also be an issue of inadequate sedation—again a diagnosis of exclusion. One study has shown that adequate postintubation anxiolysis and analgesia is commonly overlooked by emergency physicians.20