Manual of Emergency Airway Management, 3rd Edition

37.Mechanical Ventilation

Michael F. Murphy

Peter M. C. DeBlieux

Introduction

Initiating mechanical ventilation is a common task and required skill set for all emergency physicians. The etiologies for respiratory failure are expansive, and the choice between invasive and noninvasive mechanical ventilation can be a challenging clinical decision. This chapter focuses on those patients requiring invasive mechanical ventilation following endotracheal intubation and introduces the concepts essential for the initiation of invasive mechanical ventilation. Chapter 38 focuses on respiratory distress and the institution of noninvasive mechanical ventilation.

Spontaneous ventilation draws air into the lungs (negative pressure), whereas mechanical ventilation pushes it in (positive pressure). In either case, the amount of negative or positive pressure required to deliver the breath (tidal volume) must overcome resistance to airflow. Positive-pressure ventilation alters normal pulmonary physiology by decreasing venous return to the thorax, changing ventilation-perfusion matching in the lung, and increasing airway pressures.

Terminology of Mechanical Ventilation

The following terms are used in mechanical ventilation:

· Tidal volume (V_t). The tidal volume is the volume of a single breath. It is usually in the range of 7 to 8 mL/kg ideal body weight (IBW). Smaller tidal volumes 6 mL/kg IBW with more rapid rates are used in those patients with diffuse infiltrates to prevent excessive airway pressures and to avoid ventilator-induced lung injury (VILI). Such patients with multilobar disease, severe congestive heart failure, adult respiratory distress syndrome (ARDS), or limited healthy lung units should receive these smaller tidal volumes. In reactive lung diseases, the use of permissive hypercapnia and low respiratory rates (RRs; 8–10 breaths per minute) combined with low tidal volumes (6–7 mL/kg IBW) promotes a prolonged expiratory time and diminishes the risk of hyperinflation.

· RR or frequency (f). The usual starting RR is 12 to 20 breaths per minute in the adult. It is much higher in neonates, infants, and small children, and in those conditions where carbon dioxide production is accelerated (e.g., fever, acidosis, other hypermetabolic conditions). The non–gas-exchanging parts of the respiratory system (dead space) constitute a fixed volume of each tidal breath. The remainder of the volume in each breath participates in gas exchange and constitutes alveolar ventilation. Rapid RRs and small tidal volumes risk ventilating little more than dead space, a particular risk in infants and small children. The tradeoff here is rate versus volume (alveolar ventilation).

· Fractional concentration of inspired oxygen (F_iO₂). This ranges from the concentration of oxygen in room air (0.21 or 21%) to that of pure oxygen (1.0 or 100%). When initiating mechanical ventilation, start with a F_iO₂ of 100% and wean the oxygen based on pulse oximetry.

· Inspiratory flow rate (IFR). The IFR is the speed that a tidal volume breath is delivered during inspiration. In an adult, this is typically set at 60 L/minute. During cases of reactive airways disease, the peak IFR may be increased to 90 to 120 L/minute to enhance expiratory time and diminish dynamic hyperinflation.

· Positive end-expiratory pressure (PEEP). PEEP offers a static pressure to the airways during inspiratory and expiratory efforts, and is typically set at 5 cm H₂O. PEEP increases functional residual capacity, total lung volumes, and total lung pressures. When a patient is unable to meet oxygenation goals using a F_iO₂ of 100% then PEEP can be progressively increased to reach oxygenation goals. Excessive PEEP can cause VILI and alter hemodynamics in patients with limited cardiopulmonary reserve. After a short time, air hunger and fatigue become appreciable. The same thing happens to a patient breathing spontaneously through an endotracheal tube (ETT), especially a small one.

· Ventilation mode. There are a variety of modes applicable in invasive mechanical ventilation, and the key to understanding the differences between these modes centers on three variables: the trigger, the limit, and the cycle. The trigger is the event that initiates inspiration: either patient effort or machine-initiated positive pressure. The limit refers to the airflow parameter that is regulated during inspiration, either airflow rate or airway pressure. The cycle terminates inspiration: either a set volume is delivered (volume cycled ventilation), a pressure is delivered over a set time period (pressure cycled ventilation [PCV]), or the patient ceases inspiratory efforts (pressure support [PS] ventilation). The best mode in a given circumstance depends on the needs of the patient.

· Control mode ventilation (CMV)

· Assist control (AC)

· PCV

· Synchronized intermittent mandatory ventilation (SIMV) and PS

· Continuous positive airway pressure (CPAP)

Ventilation Modes

· CMV. CMV is almost exclusively relegated to the operating room in sedated and paralyzed patients, but an understanding of this mode's limits helps in appreciating the support level of the other modes. In CMV, all breaths are triggered, limited, and cycled by the ventilator. The clinician sets the tidal volume, RR, IFR, PEEP, and F_iO₂. The ventilator then delivers the prescribed V_t (the cycle) at the set IFR (the limit). Even if the patient wanted to initiate an additional breath, the machine would not respond. The analogy is sucking on an empty bottle. In addition, if the patient has not completely exhaled before initiation of the next breath, the machine would generate the required pressure to deliver the full V_t breath. For these reasons, CMV is only employed in those patients who are sedated and paralyzed.

· AC. AC mode is the preferred mode for patients in respiratory distress. The clinician sets the V_t, RR, IFR, PEEP, and F_iO₂. In contrast to all other modes, the trigger that initiates inspiration can be either the patient's effort or elapsed time interval. When either occurs, the ventilator delivers the prescribed tidal volume. The ventilator synchronizes set RRs with patient efforts, and if the patient is breathing at or above the set RR, then all breaths are patient initiated. The work of breathing (WOB) is primarily limited to the patient's effort in triggering the ventilator, and altering the sensitivity sets this threshold.

· SIMV and PS. SIMV is commonly misunderstood and can lead to excessive WOB on the patient's part. The physician sets the V_t, RR, IFR, PEEP, and F_iO₂. The trigger that initiates inspiration depends on the patient's RR relative to the set RR. When the patient is breathing at or below the set RR, the trigger can be the patient's effort or elapsed time. In these cases, the WOB is similar to an AC mode. If the patient is breathing above the set RR, the ventilator does not assist the patient's efforts. In these instances, the patient's WOB can be excessive due to resistance of the ETT, ventilator circuit, and inherent lung disease. In these additional breaths over the set RR, the patient's effort dictates the size of the tidal volume.

The WOB detailed previously can be limited through the addition of PS to the SIMV mode. PS is positive inspiratory pressure applied during patient-initiated breaths that exceed the set RR. The WOB and tidal volume in this mode depend on the degree of PS; patient effort; and resistance of the ETT, ventilator circuit, and inherent lung disease. Insufficient PS is associated with high RR and low V_t, also known as rapid, shallow breathing. Typically, RR is the best marker for the appropriate level of PS. RR should be maintained at <30 breaths per minute and ideally below 24 breaths per minute.

· CPAP. CPAP is not a true mode of assisted mechanical ventilation. It is equivalent to PEEP and facilitates inhalation by reducing pressure thresholds to initiate airflow. It provides positive airway pressure throughout the respiratory cycle. This static, positive pressure is maintained constant during inhalation and exhalation. In a fashion similar to SIMV, PS can be added to CPAP to function as an assisted form of ventilation. In the CPAP-PS mode, the patient initiates and terminates each breath, dictating the RR with the WOB and tidal volume dependent on the degree of PS; patient effort; and resistance of the ETT, ventilator circuit, and inherent lung disease. This mode should never be used in patients that may have apneic episodes because of the lack of a backup rate.

Ventilator Tidal Volume Delivery

Volume Cycled Ventilation

In this method of delivering a breath, the operator sets the tidal volume of each breath. The pressure required to deliver this volume varies, depending on the compliance and resistance of the lungs, the flow rate selected, the size and length of the ETT, and other minor factors as discussed previously. In adults, the initial peak flow is usually set to 60 L/minute.

With volume cycled ventilation (VCV), one is also able to determine the flow characteristics of the delivered breaths. The waveform may be square or decelerating (Fig. 37-1). Choosing a square wave results in the tidal volume being delivered at the constant peak flow selected throughout inspiration. This waveform usually generates a higher peak pressure than the decelerating waveform, but has the advantage of a shorter inspiratory time and more time for expiration. A decelerating flow wave causes inspiration to be initiated at the selected peak flow and then decelerates linearly as the breath is delivered. Because resistance to flow normally increases as the breath is delivered, the decelerating waveform generally results in lower peak inspiratory pressures (PIPs). However, this approach increases the inspiratory time, at the expense of expiratory time, potentially trapping gas in the lung (stacking breaths) and leading to a continuous buildup of pressure called auto-PEEP. For this reason, the peak flow setting for decelerating flow wave is usually higher than that used in a square wave flow pattern. Auto-PEEP may lead to overdistension and rupture of alveoli (VILI), as well as decreased venous return and cardiac output. Most mechanical ventilators measure auto-PEEP. When setting up the ventilator, one can switch back and forth from one waveform to another in attempting to determine which offers better synchrony for the patient.

Pressure Cycled Ventilation

PCV should not be confused with PS ventilation, described previously. The limit during PCV is a set airway pressure. Instead of V_t, the cycle during PCV is a set inspiratory time (Ti). Some other PCV ventilator models require a RR and inspiratory to expiratory (I:E) ratio to be set. Ti is then calculated by the ventilator based on these settings. The clinician specifies an inspiratory pressure and an inspiratory-expiratory (I/E) ratio predicted to give a reasonable rate and tidal volume, based on the patient's expected resistance and compliance. Tidal volume varies breath to breath based on lung compliance, patient effort, and airways resistance.

In this method of delivering a breath, the peak flow of the administered tidal breath and the flow waveform vary according to the patient's resistance and compliance. Early in inspiration the ventilator generates a flow rate that is sufficiently rapid to reach the preset pressure, automatically alters the flow rate to stay at that pressure, and cycles off at the end of the predetermined inspiratory time. The flow waveform created by this method is a decelerating pattern (Fig. 37-2). A normal I/E ratio is 1:2. If the RR is 10 breaths per minute evenly distributed over the minute, each cycle of inspiration and expiration is 6 seconds. With an I/E ratio of 1:2, inspiration is 2 seconds, and expiration is 4 seconds.

The I/E ratio is usually determined by simply observing the pressure and flow waveforms on the ventilator monitor, especially the termination of flow at the end of expiration to avoid generating auto-PEEP (Fig. 37-3). The inspiratory pressure is selected, and then the inspiratory time is adjusted by watching the monitor so that when the end inspiratory flow approaches zero, inspiration is terminated and expiration begins. Short inspiratory times lead to low tidal volumes and hypoventilation; long ones may increase mean intrathoracic pressure and compromise hemodynamic function. PCV has been used in reactive airways disease patients, infants, and neonates, and in some transport ventilators.

Initiating Mechanical Ventilation

The patient who is spontaneously breathing possesses a complex series of physiological feedback loops that control the volume of gas moved into and out of the lungs each minute (minute ventilation). They automatically determine the RR and the volume of each breath necessary to effect gas exchange and maintain homeostasis. The patient who is entirely dependent on a ventilator has no such “servocontrol” mechanism and must rely on the individuals setting the ventilatory parameters to meet their needs adequately. In the past, this meant frequent blood gas determinations. Now we rely on noninvasive techniques such as pulse oximetry and end-tidal carbon dioxide monitoring.

A certain amount of ventilation is required each minute (minute ventilation or minute volume) to remove the carbon dioxide produced by metabolism and delivered to the lungs by the circulatory system each minute. This minute volume approximates 100 mL/kg, provided the metabolic rate is normal. Febrile patients, for instance, produce 25% more carbon dioxide each minute than the same patients when they are afebrile. Minute ventilation would need to increase by 25% to accommodate for this increase, guided by arterial blood gases or end-tidal carbon dioxide monitoring.

In general, we recommend the following settings in an adult:

· Mode—AC

· V_t—7 to 8 mL/kg

· f—12 to 20 breaths per minute

· F_iO₂—1.0

· PEEP—5.0 cm

· IFR—60 L/minute

The vast majority of patients are easily ventilated, and this formula produces reasonable arterial blood gas tensions. Larger tidal volumes and lower rates delivering the same minute ventilation are acceptable, provided the volume/pressure tradeoff is adequate. Similarly, faster rates and smaller tidal volumes are acceptable, provided the rate/dead space ventilation tradeoff is accounted for.

High airway pressures and volumes are real risks to lung injury in mechanical ventilation. The many faces of VILI (pneumothorax, pneumomediastinum, etc.) are visible outcomes of high airway pressures and excessive volumes. This airway pressure is also transmitted directly to the intrathoracic compartment compressing the great veins and the right atrium, and when averaged over the respiratory cycle, is known as the mean intrathoracic pressure. This pressure compromises cardiac output and may in severe situations, such as that with the ventilated asthmatic, produce a pulseless electrical activity rhythm. Mean airway pressure exceeding 30 cm of water pressure places patients at risk for VILI. The same applies to mean intrathoracic pressure and venous return.

For some patients, the most perplexing task in establishing adequate mechanical ventilation is trading off rate, volume, and pressure. Ventilating the asthmatic is a good example. The tidal volume has to be sufficient, at a given rate, to provide reasonable minute ventilation, preventing severe acidosis pH <7.2 in permissive hypercapnia. One wants the inspiratory part of the cycle to be short (i.e., high IFR) to allow maximum time for expiration and avoid starting the next inspiration before expiration is complete (stacking breaths). Meanwhile, the rate has to be slow enough to allow reasonable time for expiration and appropriate emptying of trapped volume. The dilemma is how to give a big enough tidal volume 6 to 7 cc/kg IBW, quickly, and without developing excessive pressure. Deliberate hypoventilation (permissive hypercapnia) is one strategy used to attenuate the risks of high airway pressures and dynamic hyperinflation. However, this is one case where attention to detail can make a material difference:

· Use as large an ETT as possible.

· Cut the ETT to minimize the length.

· RR of 8 to 10 breaths per minute.

· V_tof 6 to 7 cc/kg IBW.

· Adjust the peak flow (90 to 120 L/minute) in an attempt to prolong the expiratory phase.

For details and discussion on specific disorders and initiating mechanical ventilation for those conditions, refer to Section 6 of this book.

Tips and Pearls

· Have a respiratory therapist (RT) review the features of ventilators available for use in your particular emergency department. Make sure that your RT is familiar with the ARDSnet protocol, plateau pressure measurements, and the concept of permissive hypercapnia.

· When a ventilator alarms, know how to take a patient off the ventilator and resume bag ventilation until an RT can return. To do this, you must be able to turn the ventilator on and off and know how to silence the alarms. These minimal steps will preserve calm until the RT can respond. Bag ventilation can be used to deal with temporary problems and provides the additional feedback of “feel.”

· Understand the typical resistance and compliance characteristics of the various respiratory disorders. This information may help predict specific tidal volumes and rates for your patients.

· Use AC mode in totally apneic patients and in those patients displaying respiratory distress to diminish the WOB. Use SIMV-PS for patients without evidence of respiratory distress.

· Always disconnect the patient from the breathing circuit and bag-mask ventilation during transport. The circuit is heavy and may drag the ETT out, especially in infants and children.

Evidence

1. Does PIP correlate with lung injury? The PIP is a function of the ventilator circuitry, ETT, peak flow, and the patient's lung compliance, and does not accurately reflect the risk of VILI. The risk for VILI is best represented by the plateau pressure, measured at the end of inspiration when an inspiratory pause is set. This pause allows for equilibration of pressures between the ventilator and the individual lung units, creating the plateau pressure. The plateau pressure correlates best with the risk of VILI and the current recommendation is to maintain the plateau pressure <30 cm H₂O. Plateau pressures >30 cm H₂O are best managed by reducing either tidal volumes or PEEP.

2. What is permissive hypercapnia, and is there evidence that it is safe? Permissive hypercapnia is the technique of ventilating patients with reactive airways disease that manifest dynamic hyperinflation, also known as auto-PEEP or intrinsic PEEP. The concept is based on prolonging expiratory time in hopes of promoting improved lung emptying and reduced pressures. The technique requires low RRs in the 8 to 10 breaths-per-minute range, coupled with a reduced tidal volume of 6 cc/kg/IBW and an elevated peak IFR of 80 to 120 L/minute. This intentional hypoventilation will promote a longer expiratory time and reduce dynamic hyperinflation. Patients will often require significant sedation and possible paralysis to maintain sufficient bradypnea. The consequence of this technique is an elevation in PCO₂ and a reduction in pH, with the goal of maintaining the pH >7.2 (1,2,3).

3. What is the current ventilator management strategy to limit lung injury in ARDS? ARDSnet protocol strives for using reduced tidal volume breaths in patients with diffuse lung injury or ARDS. In such clinical scenarios, tidal volume breaths travel predominantly to healthy, nondiseased lung units. The goal in limiting tidal volumes to 6 cc/kg/IBW is to prevent overdistension of the remaining functional lung units, preventing further VILI and an escalation of the inflammatory cascade within the lungs. The initial ARDSnet protocol compared 6 cc/kg to 12 cc/kg, and subsequent studies have compared 6 cc/kg to 10 cc/kg with similar dramatic results in mortality reduction and fewer ventilator days (4,5,6,7,8).

References

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2. Williams TJ, Tuxen DV, Scheinkestel CD, et al. Risk factors for morbidity in mechanically ventilated patients with acute severe asthma. Am Rev Respir Dis 1992;146:607–615.

3. Leatherman JW, McArthur C, Shapiro RS. Effect of prolongation of expiratory time on dynamic hyperinflation in mechanically ventilated patients with severe asthma. Crit Care Med 2004;32:1542–1545.

4. Bower RG, Shanholtz CB, Fessler HE, et al. Prospective, randomized, controlled clinical trial comparing traditional versus reduced tidal volume ventilation in acute respiratory distress syndrome. Crit Care Med 1999;27:1492–1498.

5. Stewart TE, Meade MO, Cook DJ, et al. Evaluation of a ventilatory strategy to prevent barotrauma in patients at high risk for acute respiratory distress syndrome. N Engl J Med 1998;338:355–361.

6. Donahoe M. Basic ventilator management: lung protective strategies. Surg Clin North Am 2006;86:1389–1408.

7. The Acute Respiratory Distress Syndrome Network Authors. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000;342:1301–1308.

8. Girard TD, Bernard GR. Mechanical ventilation in ARDS: a state-of-the-art review. Chest 2007;131(3):921–929.