Gas Exchange

The two major functions of the lung are taken into consideration during mechanical ventilation: ventilation, the elimination of carbon dioxide (CO₂), and oxygenation, the intake of oxygen (O₂). A clear distinction should be made between the elimination of carbon dioxide and the intake of oxygen, even though these two processes are mechanically coupled during natural, spontaneous breathing and are interrelated at the metabolic level. Each is capable of stimulating ventilation.

Carbon dioxide elimination depends on ventilation, which means the lungs are inflated with non–CO₂-containing gases. The carbon dioxide gas of metabolism enters the alveoli of the lungs, and the CO₂-containing gas is expelled from the lungs on exhalation. As such, the achieved ventilation determines the partial pressure of CO₂ in the arterialized blood (PaCO₂).

Oxygenation is best represented by the partial pressure of oxygen in the arterialized blood (P_AO₂). Predictable improvements in oxygenation can be facilitated by enriching the inspired gas as dictated by the alveolar gas equation:

where P_AO₂ is the partial pressure of alveolar oxygen, FiO₂ is the fraction of inspired oxygen, P_B is barometric pressure, P_H2O is partial pressure of water vapor at 37° C, PaCO₂ is partial pressure of alveolar carbon dioxide, and R is the respiratory quotient. Increased oxygenation also can be accomplished by increases in airway pressure, which can recruit collapsed alveoli and redistribute alveolar fluid. These changes may be largely independent of ventilation.

Carbon Dioxide Equilibrium

The quantity of carbon dioxide produced normally dictates the minute ventilation. With the exception of using cardiopulmonary bypass or an extracorporeal membrane oxygenator (ECMO), no alternative method has proved satisfactory for eliminating carbon dioxide. Breathing is essential. Normally, in the absence of disease, high altitude, and pharmacologic intervention, spontaneous ventilation results in a PaCO₂ of approximately 40 mm Hg. However, the quantitative relationship between CO₂ production and minute ventilation often is poorly understood.

Oxygen Uptake

At rest, the 70-kg adult human has an oxygen consumption of approximately 250 mL/min. Strictly speaking, ventilation is not essential for oxygenation. When the patient is breathing oxygen, the pulmonary reservoir represents approximately 12 minutes worth of metabolic consumption. Furthermore, if a denitrogenated apneic patient is connected to an oxygen supply (apneic oxygenation), oxygenation theoretically is unlimited.¹⁵ In that case, survival is limited by carbon dioxide accumulation, not by hypoxia.

Net Effect of Respiratory Quotient

Respiratory quotient (RQ) is the ratio between carbon dioxide production and oxygen consumption. The production of carbon dioxide, such as 200 mL/min, normally is slightly less than the oxygen consumption, at 250 mL/min (RQ: 200/250 = 0.8). This discrepancy has interesting implications. With an RQ of 0.8, the sum of the arterial partial pressures for carbon dioxide and oxygen (PaO₂ [100] + PaCO₂ [40] = 140 mm Hg) will always be slightly less than the humidified inspired oxygen tension (PiO₂ = 0.21 × [760 − 47] = 149 mm Hg) instead of being exactly equal to it. Because the minute volume inspired is slightly greater than that exhaled, a continuing, small, net inward movement of gas into the lungs is observed. At equilibrium, the partial pressure of nitrogen, or nitrous oxide (N₂O), is slightly greater in the lung than in the inspired gas and, of necessity, this causes an equal reduction in the space that would have been available for the respiratory gases, carbon dioxide, and oxygen.

Interdependence of Ventilator Settings

Many of these respiratory variables are interdependent, such as minute volume, tidal volume, and respiratory rate (V_M = V_T × f). In some ventilators, the tidal volume is determined by dividing the minute volume by the rate:

Tidal volume is also related to the inspiratory flow rate and the inspiratory time:

An inspiratory pause (plateau time [T_plat]) is a part of the inspiratory time. Because the inspiratory pause makes no contribution to the tidal volume, the equation for tidal volume may be modified:

Clinicians are also concerned about the relationship between inspiratory and expiratory time because the I:E ratio and the absolute times T_I and T_E affect ventilation and oxygenation. This ratio and the absolute time of inspiration are related to frequency and may be expressed mathematically.

Frequency determines time of the respiratory cycle (T_c), usually expressed in seconds, by the following relationship:

It follows that 60/f is equal to the inspiratory and expiratory times combined:

The relationship between T_I and T_E is conventionally expressed as the I:E ratio with 1 as the numerator. This ratio may be derived mathematically as follows, where R_I:E equals I:E ratio:

Depending on the manufacturer and the particular model of ventilator, the clinician must choose the R_I:E (I:E ratio), mean Q_I (average inspiratory flow rate), or both. The reader is encouraged to study the manufacturer variations shown in Figures 6-6 to 6-13.

The following example demonstrates how frequency, tidal volume, flow, and I:E ratio are interdependent. Assume that in a 60-kg patient V_T is 600 mL and f equals 10 breaths/min. As such, the cycle time is fixed at 6 seconds.

By choosing an I:E ratio of 1:2, the inspiratory time becomes fixed at 2 seconds, which mandates a mean inspiratory flow rate of 300 mL/sec or 18 L/min (300 mL/sec × 60 sec/min = 18 L/min). Choosing an I:E ratio of 1:1 increases the inspiratory time to 3 seconds, resulting in an inspiratory flow rate of 200 mL/sec or 12 L/min. An I:E ratio of 1:3 reduces the inspiratory time to 1.5 seconds, resulting in an inspiratory flow rate of 400 mL/sec or 24 L/min.

This situation is complicated somewhat by the selection of an inspiratory pause because the respiratory gases are not in transit into or out of the lungs. Exhalation begins when gases start leaving the lungs, so the inspiratory pause is considered part of the inspiratory phase of the respiratory cycle. When incorporated into the original example, with an I:E ratio of 1:2, the inspiratory time of 2 seconds would result in a mean inspiratory flow rate of 300 mL/sec or 18 L/min. In a situation in which T_plat equals 25%, T_I is selected, and 25% of the original inspiratory time is added to the inspiratory time. This results in a changed I:E ratio. In this example, the inspiratory time is 2 seconds and 25% of the inspiratory time is 0.5 seconds, which results in a total inspiratory time of 2.5 seconds. Superficial calculations of inspiratory flow rate would suggest 240 mL/sec or 14.4 L/min flows. However, the ventilator would continue to deliver the inspiratory flow at 300 mL/sec or 18 L/min. Inspiratory flow is stopped at 2 seconds, achieving the 600 mL tidal volume, but exhalation occurs 0.5 seconds later. As such, the I:E ratio is changed without affecting the tidal volume, respiratory rate, or inspiratory flow rate. This pause at end inhalation allows for a mild increase in mean airway pressure, increased alveolar recruitment, and improved oxygenation (Fig. 6-14).

Primary selection of an inspiratory flow mandates the inspiratory time for the given 600 mL V_T and thus determines the I:E ratio. For example, selecting a flow of 18 L/min (300 mL/sec) mandates an I:E ratio of 1:2 (V_T /Q_I = T_I):

At f = 10, each cycle is 6 seconds. Therefore expiratory time equals 4 seconds. The I:E ratio is 2 seconds relative to 4 seconds, or 1:2.

Some combinations of settings may exceed the capability of the ventilator. For example, a very low flow setting may not be able to deliver the 600 mL within the allotted 6-second cycle time. The alarm “VENT SET ERROR” will appear in the Datex-Ohmeda 7800 ventilator (GE Healthcare, Waukesha, WI) display (Fig. 6-15). In the Datex-Ohmeda 7800, with Q_I equal to 18 L/min, selection of the inspiratory pause of 25% will prolong the T_I to 2.5 seconds, thus changing the I:E ratio to 1:1.4.

Other ventilators allow the selection of the I:E ratio and flow simultaneously. Three situations may result: 1) flow will be inadequate to deliver the selected tidal volume, 2) flow can be increased to create a variable end-inspiratory pause, and 3) flow can be just enough to depress the bellows to the bottom, thus delivering the desired tidal volume without a pause.

The final primary variable is the inspiratory pressure (P_I). This variable can be set on some ventilators as a primary variable if the ventilator is in a pressure mode. In so doing, airway pressure increases very rapidly to the set level and is maintained at that level for the duration of the inspiratory period. This behavior must be distinguished from that of an airway pressure limiter, a passive device that does nothing more than prevent airway pressure (P_AW) from exceeding a certain value. A Venturi ventilator can be set to function like a pressure generator if the flow is set to a high level and the pressure limiter is carefully adjusted to the desired peak airway pressure.

Lung Protection Strategies

Institution of IPPV is associated with the ever-present risk of traumatic lung injury. Barotrauma, or injury related to pressure, can be grossly manifested as a pneumothorax or more subtly as physiologic and pathologic changes related to alveolar overstretching. Volutrauma, injury related to volume, also can cause alveolar overstretching. Damage related to shear stress from the opening and closing of the alveoli, called atelectrauma or shear trauma, can be caused by both pressure- and volume-related changes. Airway irritation that causes patient/ventilator dissynchrony—coughing, bucking, and straining—can result in sharp changes in airway pressure, which can cause lung injury. Usage of PEEP can lessen the injury from shear trauma but also can result in increases in physiologic dead space and reduced cardiac output.

Disease states that affect the uniformity of the lung can increase the risk of lung injury. This happens when small segments of the lung have reductions in compliance compared with their normal counterparts. Previous assumptions about the relatively predictable distribution of the volume, pressure, and perfusion to the lung segments may no longer hold true; nondiseased segments receive a greater share of the tidal volume and effects of the inspiratory pressure and PEEP. As a result, these “good” lung segments can be injured, and physiologic changes related to V/Q mismatch maybe exaggerated. This can be seen in patients with congestive heart failure, pneumonia, and acute respiratory distress syndrome (ARDS).

Large tidal volumes (15 to 20 mL/kg) also have been used during anesthesia to maintain alveolar distension. Although this strategy effectively prevents atelectasis and reduces shunt fraction, it is now recognized as a potential cause of barotrauma. Overdistension of healthy alveoli can cause disruptions of the alveolar-capillary membrane and lead to pulmonary interstitial emphysema and pneumothorax. As already stated, the presence of diffuse lung disease may compound injury to remaining healthy alveoli. Tidal volumes of 6 to 8 mL/kg are now recommended, with the addition of PEEP.^17,18

Complementing the recommendation of normal tidal volumes, safe peak inflation pressures now dominate ventilation strategies. Studies show that maximal alveolar pressures only slightly greater than 30 to 40 cm H₂O may be associated with lung injury.¹⁷ Recent designs of anesthesia ventilators have all incorporated peak airway pressure limiters.

Optimal PEEP recruits collapsed alveoli and maximizes functional residual capacity (FRC). However, increases in PEEP beyond this point may overdistend patent alveoli without further recruitment of others. New strategies analyze static pressure–volume plots to determine optimal PEEP and safe peak inspiratory pressures. Optimal PEEP is usually 5 to 15 cm H₂O.¹⁷

For the past 10 years, clinicians have been reducing tidal volumes even further for patients with acute lung injury (ALI) or ARDS. A landmark paper from the ARDS Network showed a reduction in mortality rate in a group with lower tidal volumes (6 mL/kg) compared with those in a control group (12 mL/kg).²² Ventilator settings that result in injury are attributed to diffuse alveolar damage that causes pulmonary edema, activation of inflammatory cells, local production of inflammatory mediators, and leaks of these mediators into the systemic circulation.²³ Prospective studies are lacking to examine the use of lung protective strategies in the OR for non-ALI patients. The few randomized studies that have been done do not confidently demonstrate benefits in the OR, and some authors still recommend the avoidance of high plateau pressures (>20 cm H₂O) and high tidal volumes (>10 mL/kg) in this patient population. The objective of this strategy is to minimize regional end-inspiratory stretch and thereby reduce alveolar injury and inflammation.²³

Caution with tidal volumes and peak airway pressures is associated with an increased incidence of hypercapnia. Permissive hypercapnia promises to reduce ventilatory complications without adverse effects.¹⁹ Humans seem to tolerate respiratory acidosis well, with an arterial pH of 7.15 and a PaCO₂ of 80 mm Hg. This strategy may be contraindicated in patients with increased intracranial pressure, recent myocardial infarction, pulmonary hypertension, or gastrointestinal bleeding.¹⁹ This is because acute increases in PaCO₂ increase sympathetic activity, cardiac output, pulmonary vascular resistance, and cerebral blood flow and also may impair central nervous system (CNS) function.¹⁹

Inverse ratio ventilation (IRV) originated in the early 1970s as a method to improve oxygenation in neonates with hyaline membrane disease²⁰ and was later extended to adults with ARDS. Although ratios were as high as 4:1, the benefits of this mode depend more on an absolute prolongation of inspiratory time in combination with a decreased peak inspiratory pressure. Typical I:E ratios of 1:2 to 1:4 have been lengthened to 1:1 or greater. The objective is to increase mean airway pressure and minimize peak pressure; the desired outcome is recruitment of collapsed alveoli without overdistension. Mean airway pressure directly corresponds with alveolar recruitment, reduction in shunt fraction, and oxygenation. Clinical evidence supports the contention that shunt fraction is reduced and oxygenation is improved, although modestly.¹⁷ Because pressure control is the desired outcome, this mode of ventilation is more commonly applied with pressure generators. Caution is advised when using IRV because this strategy may not allow adequate alveolar emptying, thus causing “breath stacking” and auto-PEEP. In addition, IRV is contraindicated in obstructive lung disease, such as asthma. It also may cause hypotension from a reduction in venous return since there is a higher inspiratory pressure for a longer portion of the respiratory cycle.

High-frequency ventilation (HFV), defined below, may be an applicable strategy during anesthesia, although some anesthesia ventilators are capable of rates only to 100 breaths/min. The conceptual advantage of HFV is a lower peak airway pressure combined with nonbulk flow of gas to provide a motionless surgical field. This technique has not proven clinically advantageous in patients with respiratory failure, but it is helpful in patients with large pulmonary air leaks. In addition, pulmonary complications in neonates may be reduced with this strategy.²¹

Ventilator Classification

Historically, many different anesthesia ventilators have been produced over the years. Many of them incorporated features that are no longer considered valuable, but these serve in the general description and understanding of ventilator function. Commonly, such things as ventilator mechanisms, cycling parameters, and special clinical features were used to classify anesthesia ventilators.

Control of the Pressure and Flow Waveform During Ventilation

The pattern of ventilation occasionally used has a critical influence on lung function. The most common example in the OR is the hypotension that accompanies hyperventilation. In critical care, greater attention is given to optimizing lung function by appropriate selection of the inspiratory waveform. For example, several advantages have been proposed for using a decelerating waveform: the maximum pressure is minimized, the risk of barotrauma is diminished, alveoli are kept expanded, V/Q ratios are more uniform, and distribution of gas within the lung is facilitated.

Controlled ventilation also tends to affect venous return and cardiac output. To a large extent, the best strategy to optimize cardiac output is the reverse of that which promotes improved lung function. A relatively short inspiratory period, with no time for distribution and no plateau, will have the least effect on the mean intrathoracic pressure and therefore on venous return.

Debate about the potential benefits of variation in the inspiratory waveform has persisted for at least 35 years. The expense and complexity required to achieve such waveforms have been critically discussed since the early 1960s. In the OR, fine control of the inspiratory waveform usually is not provided or needed. To this day, many anesthesia ventilators offer no control of the inspiratory waveform, and the anesthesiologist must occasionally approximate a desired pattern with the equipment available.

Special Ventilator Features

Many other valuable features may be available on a given ventilator. These features are less suitable as tools to classify ventilators, even though they may be critically important when managing a particular patient.

Anesthesia Versus Critical Care Ventilators

Historically, the anesthesiologist was limited in the type of ventilation that could be delivered to a patient. A number of reasons allowed for this limitation: 1) most surgical patients did not have pulmonary disease, 2) widespread use of muscle relaxants enabled complete control of ventilation without patient interaction, 3) the anesthesiologist was immediately available to makes changes in the ventilator settings and/or provide manually assisted ventilation, 4) use was intended for short duration, and 5) recirculation of patient gas was desirable. All these factors focused ventilator design to function only in the control mode.

In contrast, critical care ventilators became far more complex because they were used in different conditions. A trend is now apparent: anesthesia ventilators are are being manufactured to mimic the performance of their critical care counterparts while maintaining the simplicity of complete control. However, critical care ventilators offer ever-increasing complexities of flow and pressure waveforms that may not be needed, desirable, or available in anesthesia ventilators.

Ventilator Performance

Perhaps the most distinguishing characteristic of any ventilator is its performance under extremes of load—in effect, under conditions of very poor compliance. Information regarding performance of individual ventilators may not be readily available in the manufacturer’s literature and is scarcely available in the scientific literature.^28,29 The American National Standards Institute (ANSI) specifies set values for compliance, resistance, and flow within a test lung as the conditions under which breathing machines for patient use should be tested to determine their performance capabilities.³⁰ Although the operator’s manual may specify certain maximum capabilities, these numbers should be regarded as ideal figures under conditions without load. Some manufacturers specify the conditions under which their ventilator is tested, thus giving a basis for reported accuracy data.³¹ One study clearly demonstrates the limitations of anesthesia ventilators when subjected to increasing airway pressures.²⁸ Minute ventilation decreased linearly for some ventilators as airway pressure increased; however, the Siemens 900D maintained its minute volume when the airway pressure was below 60 cm H₂O. This might be attributed to the design of a nonrebreathing system without compression loss in the absorber.

System Compliance and Compression of Gas

As previously stated, gas compression and compliance volume losses caused by expanding hoses explain why delivered tidal volumes are frequently less than desired. Loss of tidal volume is greatest and most variable in machines that have an external ventilator connected to a circuit that includes a soda lime absorber and a humidifier. This is because the compressible volume is large, there is a greater total length of compliant breathing hose, and the change in pressure during each breath affects the gas in the entire circuit, including the bellows. The total volume of the gas that may be compressed in the circuit often exceeds 6 L. The amount lost due solely to gas compression may then be calculated; for every 10 cm H₂O pressure, approximately 1% of the compressible volume is lost from the circuit. Boyle’s law (P₁V₁ = P₂V₂) explains this phenomenon. Boyle’s law can be applied such that the resultant volume (V₂) is calculated by knowing the original volume (V₁) and pressure (P₁) and the secondary pressure (P₂). For example, if compression of V₁ (6000 mL) increases the pressure 10 cm H₂O (1%) above atmospheric pressure (P₁ = 1000 cm H₂O and P₂ = 1010 cm H₂O), the resultant volume (V₂) will be 5941 mL, or approximately 1% less. This would equal a loss of 120 mL at 20 cm H₂O for a 6 L system. Next, the amount lost due to expansion of the system must be calculated by using compliance specifications from the manufacturers of the ventilator and the breathing hose. These losses typically are overcome by default of FGF, which at 3 L/min would add 100 mL to the circuit during a 2-second period of inspiration.

As the complexity of ventilators has increased, their ability to deliver the intended volume has improved. New designs with fresh gas decoupling do not contribute any fresh gas to the delivered inspiratory volume; they have low-volume, noncompliant metallic manifolds, they calculate and sequentially compensate for circuit and patient compliance and gas compression losses, and they may subtract the breathing hose volume compensation from the measured exhaled volume to report an actual exhaled volume.

Atmospheric Pressure Variations

At least one anesthesia ventilator (Siemens Servo 900B) has been tested under hyperbaric conditions (1 to 3 atm), which cause increases in gas density, resistance to flow, and dead space ventilation.^32,33 Minute ventilation was found to decrease linearly as atmospheric pressure increased, but the ventilator functioned well as long as compensation was made to restore the minute ventilation.³⁴ Different ventilators have variable outputs in flight because of lower barometric pressures, but they may be used under these conditions during military emergencies. Their performance is determined by the type of control circuit, fluidic or electronic, and the method of powering the ventilator because gas density decreases at increased altitude. Differences in the mass versus volume of gas used to control these units are responsible for the alterations in function.³⁵ In general, effective ventilation at abnormal ambient pressure depends on providing the patient’s usual minute volume. Carbon dioxide continues to be eliminated at the usual partial pressure but is accompanied by either a smaller or greater mass of other gases.

Mode Conversion

With the appearance of pressure generator capabilities within the OR, the opportunities for conversion from flow to pressure generator systems will increase. The clinician should first record the tidal volume and frequency; peak, mean and plateau airway pressures; PEEP; and I:E ratios while in flow mode. The emphasis of the conversion is on the maintenance of plateau pressure because inspiratory, peak, and plateau pressures are merged into the square-wave airway pressure profile. Whether desired and set inspiratory pressure is absolute or whether it is a set pressure above PEEP should be noted. Leaving PEEP and frequency the same, the inspiratory time—and therefore the I:E ratio—should now be set to equal the total inspiratory time from the flow generator mode, accounting for inspiratory pause. Next, a change in modes must be initiated and the new parameters are measured; mean airway pressure should be slightly higher, considering the new airway pressure profile. Minor increases in set inspiratory pressure usually are necessary to match tidal volume.²⁷ For convenience, some modern ventilator designs are able to apply an algorithm automatically on conversion from a volume to pressure mode, or vice versa.

Controlled Breathing Modes

In controlled breathing modes of ventilation, the patient cannot contribute any effort toward the work of breathing. Such situations commonly occur with nondepolarizing neuromuscular blocking agents, such as pancuronium. The variable to be controlled—fixed, targeted, or limited—defines the mode.

Assisted and Supported Modes

In assisted and supported modes of ventilation, both the patient and the ventilator can contribute to the work of breathing. At times, the patient may be doing some or most of the work of breathing; at other times, the ventilator may contribute little to the work of breathing or the ventilator may be doing it all. These modes were developed as a solution for the pulmonary recovery of critically ill patients. As a group, these patients typically required long-standing intubation and mechanical ventilation. In the OR, these modes may allow augmentation of the patient’s breathing effort while anesthetized. When native breathing can occur, the patient’s effort is assisted, supported, or synchronized with mechanical breathing. Because the mechanical effort occurs while the patient is attempting to breathe, patient-ventilator dissynchrony is minimized, which in turn decreases coughing, bucking, and straining during surgery. The transition from effortless breathing to spontaneous breathing during an anesthetic emergency is commonly associated with risks of hypoxemia, hypercarbia, and dissynchrony. It is believed that these modes facilitate this transition by synchronizing with the patient’s effort while maintaining minimum set minute ventilation.

Spontaneous Breathing Without Assistance or Support

All anesthesia ventilators allow spontaneous ventilation without mechanical assistance or support. The use of a ventilator in this fashion allows continuous monitoring of respiratory parameters while the patient generates all the work of breathing. Pressure, volume, flow, and respiratory rate can be monitored for all phases of anesthetic management in which the patient spontaneously breathes. In steady state, only two possible conditions can occur to change respiratory parameters: the airway pressure can start and end at atmospheric pressure, the so-called flow-by mode, or positive pressure can be applied to the airway during breathing, the continuous positive airway pressure (CPAP) mode.

CPAP mode is more easily accepted in the ICU as a mode of breathing because it can be set on the ventilator. The CPAP number represents the airway pressure between exhalation and inhalation, when the gas flow within the airway is zero. When the patient inhales, a relative negative pressure is created within the airway compared with the set CPAP number, and gas flows into the patient. On exhalation, the airway pressure exceeds the set CPAP number and causes airway gases to exit the patient. As such, the airway pressure appears to oscillate around the set CPAP number.

On the anesthesia machine, the CPAP setting is manually dialed with the adjustable pressure-limiting (APL) valve. (Modern valves are now pressure regulators and not pressure resistors.) End exhalation occurs as a fleeting moment on an anesthesia monitor between exhalation and inhalation, which is why most clinicians use peak exhalation pressures as a guide for CPAP when administering an anesthetic. Unless there is vigorous exhalation, the difference between peak exhalation pressure and the end exhalation pressure is only 1 to 2 cm H₂O. In the ICU, the end exhalation pressure correlates to the set CPAP because the ICU ventilators are able to distinguish between peak exhalation pressure and end exhalation pressure.

Confusion regarding this mode commonly occurs if a subatmospheric pressure is generated during a vigorous inhalation. The trough pressure created at maximal inspiratory effort is confused with the terminology peak inspiratory pressure, in which the word peak is taken to mean “the highest.” Most clinicians use the term peak to refer to maximal flow or maximal effort. Thus the term peak inspiratory pressure means the highest airway pressure when positive pressure ventilation is used to generate a breath and the lowest airway pressure achieved when spontaneous ventilation occurs.

CPAP during anesthesia may serve in alveolar recruitment and facilitate oxygenation. On the pressure-volume curve, CPAP can shift function to the right and allow the best compliance characteristics of the lung to be manifested. In doing so, patients may be able to generate a better tidal volume for a given generated pressure. However, as with all conditions that increase airway pressure, CPAP increases intrathoracic pressure, which in turn decreases venous return and cardiac output. Also, patients with obstructive lung physiology may incur air trapping and worsening oxygenation and ventilation. Flow-by mode is generally used immediately before extubation; and use at this time allows the clinician to judge native respiratory effort and respiratory parameters most consistent with successful extubation.

Other Modes of Ventilation

7900 Smartvent

The Datex-Ohmeda 7900 Smartvent is designed around the bag-in-a-bottle configuration. As such, two different gas circuits are used in ventilation. When the ventilator is in use, the driving-gas circuit uses high-pressure air or oxygen (flow-generator classification) to squeeze a visible ascending bellows; this bellows is housed in a clear, hard plastic case and is under microprocessor control. The gas contained inside the bellows is part of the patient circuit.

When the bellows is pushed, the gas contained within it is pushed through the carbon dioxide adsorber. This gas mixes with the fresh gas flow just prior to entering the inspiratory limb of the patient circuit on its way to the patient (Fig. 6-22). On exhalation, used gases pass down the expiratory limb of the patient circuit and back to the bellows. Unidirectional valves, just prior to the inspiratory limb and immediately following the exhalational limb of the patient circuit, ensure one-way gas flow through the entire patient circuit (Fig. 6-23).

The drive gas can be either oxygen or air. This is set up by the service technician when the ventilator is first installed; the gas comes from either the anesthesia machine pipeline or cylinder supply. If a cylinder is used to power the ventilator, it will use up the gas supply faster than would be predicted from the flowmeter settings. The gas being used to drive the ventilators can be seen by pushing the menu key, selecting setup/calibration, then selecting about ventilator.

During exhalation, both exhalational gases from the patient and absorber gases being pushed retrograde by the fresh gas flow fill the bellows. Also during exhalation, when the bellows is filled and the pressure exceeds 2.5 cm H₂O, an internal mechanical valve within the bellows assembly opens and redirects the patient circuit gas to the scavenger system (Fig. 6-24). This must occur because gas is constantly being added to the system by the fresh gas flow.

Basic ventilator modes available include spontaneous breathing (Figs. 6-25 and 6-26) with or without CPAP and VCV. Certain GE Healthcare products may include PCV, SIMV, and PSV (Pro series) modalities as a standard build or as an option. The SIMV mode is a volume mode with the ability to deliver PSV between breaths. Interestingly, the PSV Pro mode has an apnea back-up mode using SIMV in pressure mode, with the ability to conduct PSV breaths between controlled breaths. Once the apnea alarm has been triggered, SIMV (pressure) with PSV will be delivered until the PSV Pro mode is selected through the menu system or the ventilator is turned off and on by using the ventilator/bag selector. This ventilator is equipped with electronic PEEP.

The 7900 Smartvent is also capable of providing tidal volume compensation from circuit feedback. This helps provide consistent delivery of set tidal volumes by automatically adjusting for changes in fresh gas flows; changing lung compliance; small system leaks; or compression losses in the ventilator, patient circuit, absorber, or bellows. The manufacturer claims accurate volume delivery to 20 mL of set tidal volume when available. When present, the compensation requires a few breaths to reach a compensated volume.

The set tidal volume range is 20 to 1500 mL for VCV and SIMV (volume) modes. Users may set an inspiratory pause for modes with volume breaths. In PCV modes, inspired pressure can be set from 5 to 60 cm H₂O and from 2 to 40 cm H₂O in PSV modes. For VCV and PCV, the respiratory rate can be set from 4 to 100 breaths/min, and the I:E ratio may be adjusted from 2:1 to 1:8 in increments of 0.5. The inspiratory time may be set to 0.2 to 5 seconds for SIMV and PSV Pro modes. In addition, the flow trigger for PSV Pro can be adjusted. In SIMV modes the observational window period, called a trigger window by GE Healthcare, can be adjusted.

GE Healthcare claims less than a 7% and 9% deviation in tidal volume delivery and monitoring, respectively, when set tidal volumes are above 210 mL. Accuracy is improved in delivery and monitoring at lower set tidal volumes. Pressure delivery and monitoring is accurate to ±3 and ±2 cm H₂O, respectively, and delivery of PEEP is accurate to ±1.5 cm H₂O.

Among the common adjustable alarms are tidal volume (low and high) and minute volume (low and high). In addition, four pressure alarms include high pressure, low pressure, negative pressure, and sustained pressure; an apnea alarm and a FiO₂ alarm (low and high) are also adjustable. The priorities of ventilator alarms are low, medium, and high. Low-priority alarms are sounded only once, as a single tone; as priority increases, multiple alarm tones are repeated until disabled by the user or the problem resolves.

Condensation of circuit humidity could foul the normal function of the variable-orifice flow sensors located at the proximal inspiratory and distal exhalation limb of the patient circuit, especially if the clinician does not interpose a disposable heat and moisture exchanger (HME). This problem is magnified in a cold OR; such a malfunction may be heralded by various flow senor alarms, such as check flow, exp reverse flow, insp reverse flow, and Vte > Insp Vt. A new flow sensor design purportedly minimizes this condensation problem. In addition, holes or perforations in the ventilator bellows may cause the entrainment of driving gas into the bellows. The resulting dilution of the anesthetic agent can cause patient awareness, and the use of air as the drive gas may cause the unintentional delivery of a gas mixture with a lower than expected oxygen concentration, which could lead to hypoxia. Many clinicians appreciate being able to see the ventilator bellows because it affords early detection of ventilator malfunction, disconnect, and circuit leak.

E-vent

The E-vent ventilator deviates from common ventilator designs of the past 40 years by the use of a piston and electrical motor to generate airway pressures, gas flows, and tidal volumes. This system is used in all of the current Dräger Medical workstations. As this piston ventilator produces pressures close to, or only moderately above, airway pressure to move gases, it fits the pressure generator classification of ventilators. Again, its classification as a pressure generator does not exclude its ability to provide reliable, constant flow at fixed volumes (VCV) or constant pressure (PVC) ventilation. Once calibrated, the movements of the piston within the cylinder are well defined and allow precise calculations of the delivered tidal volume, especially in low FGF states.

The ventilator is typically located in front of the unidirectional inspiratory valve of the inspiratory limb of the circuit. The reported advantage of this comes from decreasing the compressible gas volume on the inspiratory side of the circuit. In doing so, the accuracy of the delivered ventilator breath is increased. When the ventilator is cycled, the emptying piston ventilator closes a fresh gas decoupler upstream from the ventilator, which causes two separate events to occur. First, the piston gases are pushed into the inspiratory limb of the circuit to the patient, while the computer closes the PEEP/P_max value in the expiratory circuit. At the same time, the closed fresh gas decoupler valve diverts FGF through the carbon dioxide absorber retrograde to the reservoir bag. The reservoir bag is not adjusted by the APL valve because this is automatically bypassed in the mechanical ventilation mode (Fig. 6-27). On exhalation, gases from the patient and exhalation limb exit the circuit and pass through the unidirectional expiratory valve and PEEP/P_max valve. These gases combine directly with the residual and fresh reservoir bag gas before passing over the CO₂ absorber with retraction of the piston. Thus, the mixed gases from the reservoir bag, CO₂ absorber, and fresh gas inflow all join together as the piston cylinder fills (Fig. 6-28).

The most basic E-vent ventilator and workstation are provided with a spontaneous mode of breathing (Figs. 6-29 and 6-30) with or without CPAP and VCV. Some models offer as standard or optional modes PCV, PSV, and SIMV (volume) with PSV. The supported breathing mode allows support by pressure (PSV) or volume breaths (AV).

The fresh gas decoupler valve affords the ventilator volume and pressure delivery without interference from the FGF, which improves ventilator accuracy. Some workstations are equipped with an automated start-up procedure that checks the compliance of the circuit before use. In addition, some models can adjust initial ventilator settings based on patient age and weight.

The E-vent ventilator can provide respiratory frequencies from 3 to 80 breaths/min, and the I:E ratio can be adjusted from 1:4 to 5:1. Tidal volumes between 20 and 1400 mL are attainable. In pressure modes, peak pressure can be adjusted to 70 cm H₂O, and the inspiratory time window for SIMV can vary from 0.3 to 6.7 seconds. The inspiratory flow in pressure mode can achieve 150 L/min in some workstations; the flow trigger for PSV can be adjusted from 0.3 to 15 L/min, and maximum deliverable PEEP is 20 cm H₂O. Similar standard alarms are provided compared with the previous manufacturer; however, tones and screen warnings may differ.

An advantage over the gas-driven bellows configuration described above is the motor-driven piston. Because the motor is electrically driven, no oxygen or air is required for its function, which can reduce the costs of compressed and wasted gases. However, the ventilator can fail as a result of worn motor parts. The ventilator piston returning to the filled position could cause negative pressure in the system, with a flat reservoir bag, were it not for negative-pressure entrainment valves. Also, if the reservoir bag were to be torn or removed, or if system leaks occurred, room air could be entrained and thereby dilute the gases to be delivered, causing hypoxia and patient awareness. Some clinicians dislike the workstation design that encloses the ventilator piston within the machine because it occludes the visible function of the ventilator; however, new software displays have been designed that enhance the “visibility” of the piston by revealing its function.

General Concerns with Airway Pressure

Complications of mechanical ventilation have been reviewed by Keith and Pierson.⁴¹ One problem associated with the use of an anesthesia ventilator is overpressurization of the airway, which can occur in several situations: 1) when the patient coughs against the ventilator, 2) when the ventilator’s settings are excessive for the first breath, or 3) when the oxygen flush button is depressed during the inspiratory phase. A pressure limit control is available on contemporary anesthesia ventilators; this should be appropriately set because the internal overpressure protection devices may not open until a pressure high enough to cause a pneumothorax is reached. Problem 3 is eliminated by fresh gas–decoupled circuitry.

Some problems arise even during proper operation of the ventilator, such as 1) hypothermia and drying of secretions, usually avoided by using disposable HMEs; 2) hypercarbia or hypocarbia as a result of setting the ventilator incorrectly; 3) hypotension secondary to excessive tidal volume, excessive minute ventilation, or excessive PEEP or auto-PEEP, all of which can reduce preload; 4) barotrauma from excessive transpulmonary pressure; 5) hidden airflow obstruction, particularly from mucous plugging, mainstem intubation, tracheal tube cuff herniation, or bronchospasm; 6) hypoxemia from inadequate ventilator settings; and 7) electromagnetic interference with electronically controlled microprocessors.⁴¹

As a general rule, when machine malfunction impairs the safe delivery of anesthetic gases, the patient should be immediately disconnected from the anesthesia machine, and a back-up ventilation system should be used instead.

Cross-Infection

Infection risk related to the anesthesia ventilator and circuit was evaluated in the early 1980s. Several authors have studied the risk of cross-infection arising from the use of ventilators and anesthesia circuits. Cross-infection cases have been reported in which the repeated use of the same piece of airway equipment transferred infection among patients.⁴² Carbon dioxide absorbers cannot be regarded as a barrier to the transmission of bacteria. Indeed, bacteria such as Pseudomonas have been cultured from soda lime absorbers.⁴³ Nevertheless, with the older type of nondisposable circuits, adequate infection control was achieved by washing with suitable decontamination fluids.⁴⁴ The subsequent widespread introduction of disposable circuits has obviated the need for such decontamination; bacteria are not disseminated during quiet breathing, nor does the machine or circuit disseminate organisms.^45,46

The concern caused by human immunodeficiency virus (HIV) and the even greater risk posed by hepatitis B or C transmission warrant vigilance about controlling cross-contamination in all aspects of anesthesia care. Precautions that prevent cross-contamination appear to offer appropriate safety for airway equipment and anesthesia delivery systems. The use of disposable circuits appears to afford patients adequate safety, although actual sterility is hard to achieve. The GE Healthcare bellows and canister system is easily disassembled and autoclavable; however, the absorber manifold is interposed between the circuit and bellows. Similar to other anesthesia circle breathing systems, it cannot be cleaned effectively without disassembly by trained technicians. The entire Dräger breathing manifold and system are easily removed and autoclavable, which has recently been recommended for the preparation of the machine in patients susceptible to malignant hyperthermia.

Preoperative Procedures

The 1993 check-out recommendations from the United States Food and Drug Administration (FDA)⁴⁷ should be used as a generic checklist for ascertaining the proper function of a ventilator. Specific manufacturer recommendations should always be consulted. The FDA list states that backup manual ventilation must be immediately available and must be tested. These resuscitators typically have a one-way valve that must be properly installed and competent to provide positive-pressure ventilation. The scavenger system and ventilator relief valve (pop-off valve) should be tested together to verify that excess gas will be released once the bellows is full to prevent any distension or sustained pressure. Then, with minimal or no flow, the bellows should remain filled to ascertain a proper seal of the relief valve, proper seating of the bellows, and no holes in the bellows. Next, when the ventilator is activated with a test lung (a second reservoir bag at the patient “Y”) and no FGF, the bellows should not lose volume. If it does, the ventilator relief valve may not be sealing under pressure. Furthermore, the volume delivered and motion of the test lung should be appropriate for the set parameters, or a leak in the drive gas circuit should be considered. In the active test mode, external pressure applied to the test lung should appropriately activate the pressure limit safety feature and high-pressure alarm.

Since the 1993 FDA recommendations were made, new check-out procedures have been required to adapt to the changing anesthesia delivery systems. Further, a single check-out procedure is no longer applicable to the various equipment designs. Updated recommendations were developed in 2008 by a multidisciplinary subcommittee of the American Society of Anesthesiologists (ASA) Committee on Equipment and Facilities.⁴⁸ The check-out design guideline is also supported as educational information by the FDA’s Office of Device Evaluation. Sample check-out procedures have been submitted and approved for inclusion in the ASA library by the ASA Committee on Equipment and Facilities.⁴⁹

Intraoperative Procedures

Vigilance should be maintained whenever a ventilator is in operation. When mechanical ventilation is selected in older workstations, it is essential to change from manual to mechanical ventilation on the ventilator selection switch. The ventilator and pressure limit must be appropriately set for each patient, and the first ventilator-delivered breath must be observed, carefully watching for chest expansion, proper cycling, peak pressure, I:E ratio, airway pressure waveform, plateau pressure, inspiratory pause, and tidal volume before and after adjusting the FGF. Is the bellows compression complete, and does it completely return during exhalation? Is the inspiratory flow adequate to meet ventilatory settings? Once ventilation is established, reset the minute volume and minimum airway pressure alarms, the pressure limiter, PEEP, and the peak airway pressure alarm according to the patient’s unique parameters. Listen to breath sounds, despite capnography, to see if they are coincident with, and appropriate for, ventilator sounds. Follow end-tidal carbon dioxide and pulse oximetry as measures of ventilation, breathing circuit valve function, and proper alveolar expansion.

1. Baker A.B. Early attempts at expired air respiration, intubation and manual ventilation. In: Atkinson R.S., Boulton T.B., eds. The history of anaesthesia. London: Royal Society of Medicine; 1987:372–374.

2. Gordon A.S. History and evolution of modern resuscitation techniques. In: Gordon A.S., ed. Cardiopulmonary resuscitation conference proceedings. Washington, DC: National Academy of Sciences; 1966:7–32.

3. Vesalius A. De humani corporis fabrica libri septem. Basileae: Ex Off. Ioannis Oporini; 1543.

4. Mushin W.W., Rendell-Baker L. The principles of thoracic anaesthesia. Oxford: Blackwell; 1953. pp 28–30

5. O’Dwyer J. Fifty cases of croup in private practice treated by intubation of the larynx, with a description of the method and of the dangers incident thereto. Med Rec. 1887;32:557–561.

6. Fell G.E. Forced respiration. JAMA. 1891;16:325–330.

7. Hochberg L.A. Thoracic surgery before the 20th century. New York: Vantage Press; 1960. 684–697

8. Tuffier T., Hallion L. Intrathoracic operations with artificial respiration by insufflation. C R Soc Biol (Paris). 1896;48:951.

9. Matas R. Artificial respiration by direct intralaryngeal intubation with a new graduated air-pump, in its applications to medical and surgical practice. Am Med. 1902;3:97–103.

10. Drinker P., Shaw L. An apparatus for the prolonged administration of artificial respiration. J Clin Invest. 1929;7:229.

11. Mushin W.W., Rendell–Baker L., Thompson P.W., et al. Automatic ventilation of the lungs. Oxford, UK: Blackwell Scientific; 1980.

12. Magill I.W. Development of endotracheal anaesthesia. Proc R Soc Med. 1928;22:83–88.

13. Lassen H.C.A. A preliminary report on the 1952 epidemic of poliomyelitis in Copenhagen with special reference to the treatment of acute respiratory insufficiency. Lancet. 1953;1:37–41.

14. Bjork V.O., Engstrom C.G. The treatment of ventilatory insufficiency after pulmonary resection with tracheostomy and prolonged artificial ventilation. J Thorac Surg. 1955;30:356–367.

15. Frumin M.J., Epstein R.M., Cohen G. Apneic oxygenation in man. Anesthesiology. 1959;20:789–798.

16. Chatburn R.L. Classification of mechanical ventilators. In: Tobin M.J., ed. Principles and practice of mechanical ventilation. New York: McGraw-Hill, 1994.

17. MacIntyre N.R. New modes of mechanical ventilation. Clin Chest Med. 1996;17:411–421.

18. Slutsky A.S. Mechanical ventilation. American College of Chest Physicians’ consensus conference. Chest. 1993;104:1833–1859.

19. Feihl R., Perret C. Permissive hypercapnia: how permissive should we be? Am J Respir Crit Care Med. 1994;150:1722–1737.

20. Marcy T.W. Inverse ratio ventilation. In: Tobin M.J., ed. Principles and practice of mechanical ventilation. New York: McGraw-Hill; 1994:319–331.

21. Schwartz D.E., Katy J.A. Delivery of mechanical ventilation during general anesthesia. In: Tobin M.J., ed. Principles and practice of mechanical ventilation. New York: McGraw-Hill, 1994.

22. Acute Respiratory Distress Network. 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(18):1301–1308.

23. Schultz M.J., Haitsma J.J., Slutsky A.S., Gajic O. What tidal volumes should be used in patients without acute lung injury? Anesthesiology. 2007;106(6):1226–1231.

24. ASTM. Standard specification for ventilators intended for use during anesthesia, F1101–90. West Conshohocken, PA: American Society for Testing and Materials; 1990.

25. Marini J.J., Ravenscraft S.A. Mean airway pressure: physiologic determinants and clinical importance. Part 1. Physiologic determinants and measurements. Crit Care Med. 1992;20:1461–1472.

26. Marini J.J., Ravenscraft S.A. Mean airway pressure: physiologic determinants and clinical importance. Part 2. Clinical implications. Crit Care Med. 1992;20:1604–1616.

27. McKibben A.W., Ravenscraft S.A. Pressure-controlled and volume-cycled mechanical ventilation. Clin Chest Med. 1996;17:395–410.

28. Marks J.D., Schapera A., Kraemer R.W., Katz J.A. Pressure and flow limitations of anesthesia ventilators. Anesthesiology. 1989;71:403–408.

29. Marks J.D., Katz J.A., Schapera A., Kraemer R.W. Evaluation of a new operating room ventilator: the Ohmeda 7810. Anesthesiology. 1989;71(3A):A463. (abstract)

30. ANSI. American National Standard for Breathing Machines for Medical Use, ANSI Z79.7. New York: American National Standards Institute; 1976.

31. Ohmeda 7900 Ventilator operations and maintenance manual. Madison, WI: Ohmeda, The BOC Group; 1996.

32. Salzano J.V., Camporesi E.M., Stolp B.W., Moon R.E. Physiologic responses to exercise at 47 and 66 ATA. J Appl Physiol. 1984;57:1055.

33. Nunn J.F., ed. Nunn’s applied respiratory physiology, ed 4, Oxford/Boston: Butterworth-Heinemann, 1993.

34. Mielke L., Breinbauer B., Kling M., et al. The use of the Servo 900 B for ventilation in hyperbaric chambers [abstract]. Anesth Analg. 1996;82:S315.

35. Thomas G., Brimacombe J. Function of the Dräger Oxylog ventilator at high altitude. Anaesth Intens Care. 22, 1994. 276–228

36. Rouby J.J., Viars P. Clinical use of high frequency ventilation. Acta Anaesthesiol Scand Suppl. 1989;33:134–139.

37. Majewski A., Telmanik S., Arrington V. High frequency oscillatory ventilation. Va Med Q. 1994:230–232. Fall

38. Malina J.R., Nordström S.G., Sjöstrand U.H. Wattwil, LM: Clinical evaluation of high-frequency positive-pressure ventilation (HFPPV) in patients scheduled for open-chest surgery. Anesth Analg. 1981;60:324–330.

39. Heres E.K., Shulman M.S., Krenis L.J., Moon R. High-frequency ventilation with a conventional anesthetic ventilator during cardiac surgery. J Cardiothorac Vasc Anes. 1995;9:63–65.

40. Tessler M.J., Ruiz-Neto P.P., Finlayson R., Chartrand D. Can anesthesia ventilators provide high-frequency ventilation? Anesth Analg. 1994;79:563–566.

41. Keith R.L., Pierson D.J. Complications of mechanical ventilation: a bedside approach. Clin Chest Med. 1996;17:439–451.

42. Walter C.W. Cross-infection and the anesthesiologist, twelfth annual Baxter-Travenol lecture. Anesth Analg. 1974;53:631–644.

43. Dryden G.E. Uncleaned anesthesia equipment. JAMA. 1975;233:1297–1298.

44. Nielsen H., Jacobsen J.B., Stokke D.B., et al. Cross-infection from contaminated anaesthetic equipment. Anaesthesia. 1980;35:703–708.

45. du Moulin G.C., Hedley-Whyte J. Bacterial interactions between anesthesiologists, their patients, and equipment. Anesthesiology. 1982;57:37–41.

46. du Moulin G.C., Saubermann A.J. The anesthesia machine and circle system are not likely to be sources of bacterial contamination. Anesthesiology. 1977;47:353–358.

47. Morrison J.L. FDA Anesthesia Apparatus Checkout Recommendations. American Society of Anesthesiologists Newsletter. 1993;1994(58):25–28.

48. Recommendations for Pre-Anesthesia Checkout Procedures. Sub-Committee of ASA Committee on Equipment and Facilities. 2008. Accessed online at. http://www.asahq.org/clinical/FINALCheckoutDesignguidelines02-08-2008.pdf

49. American Society of Anesthesiologists. Sample checkout procedures. Available at http://www.asahq.org/clinical/checklist.htm.