TOC | Pulm
- Mechanical Ventilation
Indications | Settings | Modes | Sedation | Complications
A. Increasing the FIO2
Increasing the FIO2 is indicated when there is dyspnea or hypoxemia (PaO2 < 60 mm Hg).
B. Increasing airway pressure
Increasing airway pressure is required when an increase in FIO2 alone does not adequately treat oxygenation failure (i.e., PaO2 < 60 mm Hg). By maintaining positive airway pressure throughout the respiratory cycle, airways remain open, the FRC increases, and ventilation-perfusion matching improves. Endotracheal intubation is necessary for patients who require positive end-expiratory pressure (PEEP) and for the majority of patients who require continuous positive airway pressure (CPAP).
An alternative, which is occasionally useful, is face-mask CPAP, in which a tight-fitting face mask is put in place and the patient exhales against a device that maintains positive airway pressure. This approach can be useful when less than 10 cm H2O CPAP is required to improve oxygenation and when the work of breathing is not excessive. Face-mask CPAP in patients with cardiogenic pulmonary edema can result in early physiologic improvement and reduce the need for intubation and mechanical ventilation. Gaseous distention of the stomach with emesis and aspiration are potential problems, and therefore face-mask CPAP should not be used in obtunded patients. The mask must be removed periodically to prevent pressure necrosis. Thus, prolonged use for many days is usually impractical. There has been recent interest in the use of nasal positive-pressure ventilation (NPPV) in the setting of acute respiratory failure. However, its clinical value has not been established.
Improving alveolar ventilation
A. Intermittent positive-pressure breathing
When failure to eliminate carbon dioxide is associated with mild acidosis (e.g., pH 7.30-7.35) and the patient is both alert and cooperative, temporizing measures, such as intermittent positive-pressure breathing (IPPB), NPPV, deep breathing, and airway care, may prove beneficial.
IPPB and NPPV may be useful when carbon dioxide retention is due to any of the neuromuscular diseases or chest wall deformities (e.g., amyotrophic lateral sclerosis, severe kyphoscoliosis). IPPB is prescribed by tidal volume (10-12 ml/kg), with a pressure limit of 30-40 cm H2O. Higher pressures may result in a pneumothorax.
B. Endotracheal intubation and mechanical ventilation
More severe degrees of respiratory acidosis, especially with mental status changes, require endotracheal intubation and mechanical ventilator support.
Indications for Mechanical Ventilation is mainly respiratory failure.
1. Blood gas criteria for resp. failure:
PaO2 <55-60 mm Hg on maximum FiO2 by mask; PaCO2 >50 mm Hg and pH <7.30
2. Pulmonary mechanics criteria for resp. failure:
3. Indications other than respiratory failure
Recommended Initial Mechanical Ventilation Settings
Step-by-step setup for the Assist Control Mode
this mode that is most appropriate for initial ventilation of most adult patients in the emergency department or the critical care unit.
1. The recommended working pressure for most adult patients
is 60 cm H2 O. Higher pressures, up to 120 cm H2 O, may be required in
The WORKING PRESSURE adjustment determines the maximum pressure that the ventilator will deliver and provides a secondary safeguard against the inadvertent exposure of the patient to dangerously high pressures. (The primary safeguard is the UPPER PRESSURE LIMIT setting on the ventilator control panel, described in step 12.)
2. The mode selector switch may be turned to either VOLUME CONTROL or VOLUME CONTROL PLUS SIGH. As discussed previously, the sigh function is not recommended.
3. The PRESET INSPIRATORY MINUTE VOLUME control determines the minute volume that the ventilator will deliver if the patient initiates no breaths independently. As discussed previously, not all of the volume that is delivered by the ventilator actually reaches the patient, beause some is lost to compression within the humidifier and the patient tubing. The difference between the preset inspiratory minute volume and the minute volume that the patient actually receives is on the order of 400 to 600 mL/min for a typical adult patient.
4.Either a square wave or an accelerating inspiratory flow pattern may be selected. In most cases, a square wave is the appropriate initial setting (see discussion in the section on inspiratory flow).
5. The BREATHS/MINUTE knob determines the minimum number of breaths that the patient will receive. The patient may trigger the ventilator at a faster rate than the breaths per minute setting, in which case the patient will receive more than the preset inspiratory minute volume.
6. The recommended initial setting is an inspiratory time of 33%
with no pause, resulting in an I:E ratio of 1:2.
The INSPIRATORY TIME PERCENT setting determines the fraction of each respiratory cycle that is spent in inspiration. The PAUSE TIME PERCENT setting may be used to provide a pause at the end of inspiration that is up to 20% of the respiratory cycle. In combination, the inspiratory time percent and pause time percent settings determine the I:E ratio, which may be set anywhere from 1:4 to 4:1.
7. The inspired O2 concentration is set by a control on the air-O2 mixer attached to the right side of the ventilator.
8. The UPPER and LOWER FiO2 ALARM LIMIT controls should be set approximately 6% above and below the desired O2 concentration. When the FiO2 varies outside the set limits, as detected by the internal O2 analyzer on the ventilator, visible and audible alarms are activated.
9. The PARAMETER SELECTOR knob determines which parameter is displayed in the digital readout window on the control panel above the knob. The available parameters include breathing rate (sum of spontaneous and mechanical), actual FIO2 , inspiratory VT, expiratory VT, expired minute volume, peak pressure, pause pressure, and mean airway pressure.
10. If PEEP is required, one sets the desired level by turning the PEEP knob.
11. The UPPER PRESSURE LIMIT knob allows the operator to set a ceiling for airway pressure above which inspiration is terminated, and visible and audible alarms are activated. The limit should be set at approximately 50 cm H2 O initially and should be readjusted with the patient on the ventilator to 10 to 15 cm H2 O above the observed peak pressure. If the upper pressure limit is set above the working pressure (see step 1), inspiration will end when the working pressure is reached, but no alarms will be activated.
12. The TRIGGER SENSITIVITY control determines how much inspiratory effort the patient must make to trigger an assisted ventilator breath. The sensitivity is usually set so that an inspiratory effort of -1 to -3 cm H2 O is required.
13. The EXPIRED MINUTE VOLUME meter at the top left corner of the ventilator control panel has dual scales: from 0 to 40 L/min for adults and from 0 to 4 L/min for children. The proper scale is selected with the INFANTS/ADULTS switch at the lower left corner of the control panel. This switch also sets the scale for the UPPER and LOWER ALARM LIMIT controls (see step 16).
14. The ventilator is now connected to the patient. In addition to observing the clinical response of the patient, one should use the PARAMETER SELECTOR control and EXPIRED MINUTE VOLUME and AIRWAY PRESSURE meters to be sure that the rate, VT, minute volume, FiO2 , and airway pressures are in the desired range.
15. After the patient has been on the ventilator for a few minutes and it has been determined that the patient is receiving an appropriate minute volume, the UPPER and LOWER ALARM LIMIT controls should be set approximately 20% above and below the desired minute volume. When the expired minute volume deviates from this range, visible and audible alarms are activated.
TYPES OF VENTILATORS
Ventilators may be grouped and classified according to a few basic characteristics that describe their operation.
Ventilators are also classified according to the factor that determines when the ventilator cycles from the inspiratory phase to the expiratory phase. Basically, ventilators can be described as pressure-cycled, volume-cycled, or time-cycled.
In pressure-cycled ventilators, the inspiratory phase is terminated, and expiration begins when a preset pressure limit is reached. The tidal volume (VT) received by the patient is not set directly but depends on the set pressure limit and the patient's chest and lung compliance and airway resistance.
As long as the patient's compliance and resistance do not change, the VT will be the same with each breath. If the patient's compliance falls or resistance increases, the VT will also fall, and hypoventilation may result.
Because of the problem of a changing VT caused by changing patient compliance, pressure-cycled ventilators have been largely replaced by volume- or time-cycled ventilators for mechanical ventilation in adults. Pressure-cycled ventilators still have certain advantages, however. They are less expensive than volume- and time-cycled machines. They are more compact and can be run by compressed gas sources without the need for an electrical source, making them well suited for ambulance transport. For reasons discussed later, pressure-cycled machines also remain popular for ventilating infants and neonates.
In volume-cycled ventilators, inspiration is terminated and expiration begins when a preset VT is delivered. The gas is usually delivered from a compressible bellows. Since the introduction of the Puritan-Bennett MA-1 volume ventilator in 1968, volume ventilators have become the standard for mechanical ventilation in adults. They have an important advantage over pressure-cycled ventilators: delivery of a relatively constant VT despite changes in the patient's compliance. Even with volume-cycled machines, however, the delivered VT falls slightly if the patient's compliance falls.
This is because although a constant volume is delivered from the ventilator bellows, as the patient's lungs become stiffer, more of this gas is lost to expansion of the ventilator tubing. This phenomenon becomes very important in infants. The compliance of the child's chest and lungs may be less than the compliance of the ventilator tubing, and more gas will go to expansion of the tubing than to ventilation of the patient.
Most modern volume-cycled ventilators have adjustable secondary pressure limits such that when the airway pressure exceeds the set limit, inspiration is terminated. Thus, volume-cycled ventilators may function as pressure-cycled ventilators when the pressure limit is set at a low enough level.
In time-cycled ventilators, inspiration is terminated and expiration begins after a preset time has elapsed. The VT that is delivered is determined by the integral of the inspiration flow-inspiratory time curve. Time-cycled ventilators resemble volume-cycled machines in that they deliver a relatively constant VT despite changes in the patient's compliance. They may also function as pressure-limited ventilators when the secondary pressure limits are adjusted. Time-cycled ventilators are becoming increasingly popular. They allow great flexibility in adjustment of the inspiratory-to-expiratory ratio, and their internal circuitry is such that they can be manufactured at a lower cost than most volume-cycled machines.
After rate, VT, and FiO2 have been set, the next priority is to set the mode of ventilation.
Controlled Ventilation Mode
Assist Control Mode
IMV and SIMV Mode
Pressure Support Mode
The acronym PEEP is used to denote positive end-expiratory pressure in
a patient who is receiving assisted ventilation. In this mode, airway
pressure is positive not only at end expiration but also throughout the
respiratory cycle. When using PEEP, the ventilator can be in the control,
assist control, IMV, SIMV, or pressure support modes.
Theoretically, PEEP improves oxygenation by keeping alveoli open during expiration. What is known is that it leads to improved oxygenation and narrowing of the A-aDO2 in most patients.
A generally accepted indication for PEEP is failure to achieve adequate oxygenation (i.e., PaO2 <60 mm Hg) with safe levels of inspired O2 (i.e., FiO2 = 0.50).
A conservative approach is to use a level of PEEP that is just enough to provide adequate arterial oxygenation with an FiO2 <50%. In patients requiring higher FiO2 levels, PEEP may be started at 5 cm H2 O and may be increased in increments of 3 to 5 cm H2 O at 15-minute intervals. At each new level, pulse and blood pressure, static compliance, peak airway pressure, arterial blood gas tension, and cardiac output should be measured and recorded. The pulmonary artery wedge pressure (PAWP) should probably also be measured, although it may not accurately reflect left ventricular filling pressure in patients on PEEP. The FiO2 can usually be gradually turned down as PEEP is increased and the A-aDO2 narrows. Most patients exhibit a fall in cardiac output at levels of PEEP above 12 to 15 cm H2 O. This drop is due in part to decreased venous return and can be at least partially overcome by expansion of intravascular volume. Diminished myocardial blood flow at higher levels of PEEP may also contribute to diminished cardiac output. A useful method of determining when a fall in cardiac output negates the effect of a rise in PaO2 is to calculate the peripheral O2 delivery at different levels of PEEP. One can calculate the peripheral O2 delivery by multiplying the cardiac output by the arterial O2 content as follows: O2 delivery to periphery = cardiac output × arterial O2 content
The O2 content C (expressed in milliliters of O2 per 100 mL of blood) equals the product:
Measurement of static compliance also has been advocated as a means of determining the optimal level of PEEP. One small study found that the best PEEP (from the point of view of O2 delivery to the periphery ) coincided with the level at which static compliance was highest, usually in the range of 6 to 12 cm H2 O.
Dual Synchronous Ventilation
Sedation and Paralysis
Whereas many patients adapt readily to mechanical ventilation and synchronize
their own breathing with the ventilator breaths, other
patients "fight the machine." By coughing,
bucking, and breathing out of phase with the ventilator, they generate high
peak airway pressures and increase their O2 consumption and CO2 production.
When their airway pressures exceed the peak pressure limits, they receive
less than the prescribed VT, and hypoventilation results.
In such cases, a complication or a mechanical problem
must first be ruled out. One should check the inspired O2 concentration with
an O2 analyzer to be sure that the set FiO2 is really being delivered. While
the patient is being "bagged" by hand, increased resistance to inflow of
air, suggesting a plugged or kinked endotracheal tube, can be sensed. Malposition
of the endotracheal tube and pneumothorax should be ruled out by auscultation
and a chest film. The patient should
be suctioned to remove any large airway obstruction due to mucus, blood,
or other debris. Other causes for agitation,
such as hypotension or pain, should be considered. If coherent,
the patient should be reassured.
When all of these measures have been taken, no complication or malfunction has been found, and the patient continues to fight the ventilator, sedation should be considered.
Diazepam is a useful drug in this setting. Diazepam acts rapidly and provides excellent relaxation, sedation, and amnesia. The usual starting dose in adults is 2.5 to 5.0 mg IV, given at a rate of 2.5 mg/min. Because the main side effect is respiratory depression, much larger doses, up to 1 mg/kg, can be given in a mechanically ventilated patient, although some cardiac depression occurs at very high doses (>3 mg/kg).
An alternative to diazepam is morphine sulfate. Morphine is usually given in 2- to 4-mg increments IV and titrated to effect. As with diazepam, the main side effect of morphine is respiratory depression, which is not a problem in the mechanically ventilated patient with a secure airway. The drug also causes a small drop in blood pressure, probably a result of peripheral vasodilation rather than a direct cardiac depressant effect.  Morphine is also known to cause histamine release, which could theoretically lead to increased bronchospasm.  Whether this effect is of clinical significance is unknown. Advantages of morphine over diazepam are that it is a potent analgesic and its effect is readily reversible with naloxone.
When sedation and analgesia are ineffective in preventing the patient from fighting the ventilator, a paralyzing drug may be used. Pancuronium bromide is the drug of choice for inducing paralysis in ventilator patients. Pancuronium is a nondepolarizing blocker of neuromuscular transmission. The main side effects of the drug are a mild increase in pulse and blood pressure, although it has also been reported to cause severe hypertension, ventricular dysrhythmias, and anaphylactic reactions on rare occasions .
Pancuronium is preferred over d-tubocurarine, which commonly causes hypotension, and the depolarizing agent succinylcholine, which is short acting and causes fasciculations and cholinergic side effects.
The dose of pancuronium is 0.02 to 0.06 mg/kg IV. Paralysis occurs
within 1 to 3 minutes and lasts 1 to 2 hours, after which time repeated doses
may be given.
Paralysis induced by pancuronium can be reversed by neostigmine, 0.06 to 0.08 mg/kg IV up to a total of 2.5 mg.
Physostigmine should not be used for reversal, because it crosses the blood-brain barrier and may induce seizures. Atropine, 0.01 to 0.02 mg/kg up to a total of 1 mg, should be given in the same syringe to block the cholinergic side effects of neostigmine. Paralysis with pancuronium has been reported to be particularly effective in asthmatics.
It is important to remember that although a patient who is paralyzed with
pancuronium or other newer agents may appear asleep and calm,
the drug pancuronium has no sedative or analgesic
properties. A paralyzed patient must
be given liberal doses of sedatives and analgesics at regular intervals.
Hospital personnel should treat the patient as if fully awake, talking to
the patient in a reassuring manner and avoiding bedside discussion of the
case. Finally, the patient must be continually observed and ventilator
function and alarms must be checked frequently, because the patient will
be entirely unable to breathe independently should the ventilator fail.
Potential Complications of Mechanical Ventilation
Complications related to endotracheal or tracheostomy tube
Complications resulting from machine malfunction and operator error
KP-BF Tracheostomy Management Protocol 10-1999
Abbreviations Used in This Chapter
A-aDO2 - Alveolar-arterial oxygen difference
CPAP - Continuous positive airway pressure
f - Respiratory rate or frequency
FEV1 - Forced expiratory volume in 1 second
FiO2 - Percent oxygen content of inspired gas
IMV - Intermittent mandatory ventilation
MVV - Maximum voluntary minute volume
PACO2 - Alveolar carbon dioxide tension
PaCO2 - Arterial carbon dioxide tension
PAO2 - Alveolar oxygen tension
PaO2 - Arterial oxygen tension
VC - Vital capacity
VT - Tidal volume
Ventilation Beyond the Intensive Care Unit. ACCP Consens Statement- CHEST
113(5): May, 1998 Supplement]
[Mechanical Ventilation. ACCP Consensus Statement. Chest 104 1833-59, 1993]
Roberts: Clinical Procedures in Emergency Medicine, 3rd ed., Copyright © 1998
2010 Ventilator Settings
REF: Merck Manuals Online 2007
Overview of Mechanical Ventilation
Mechanical ventilation can be noninvasive, involving various types of face masks, or invasive, involving endotracheal intubation. Selection and use of appropriate techniques require an understanding of respiratory mechanics.
There are numerous indications for endotracheal intubation and mechanical ventilation (see Table 1: Respiratory and Cardiac Arrest: Situations Requiring Airway Control) but, in general, mechanical ventilation should be considered when there are clinical or laboratory signs that the patient cannot maintain an airway or adequate oxygenation or ventilation. Concerning findings include respiratory rate > 30/min, inability to maintain arterial O2 saturation > 90% with fractional inspired O2 (Fio2) > 0.60, and PaCO2 of > 50 mm Hg with pH < 7.25. The decision to initiate mechanical ventilation should be based on clinical judgment that considers the entire clinical situation and should not be delayed until the patient is in extremis.
Normal inspiration generates negative intrapleural pressure, which creates a pressure gradient between the atmosphere and the alveoli, resulting in air inflow. In mechanical ventilation, the pressure gradient is the result of increased (positive) pressure of the air source.
Peak airway pressure is measured at the airway opening (Pao) and is routinely displayed by mechanical ventilators. It represents the total pressure needed to push a volume of gas into the lung and is composed of pressures resulting from inspiratory flow resistance (resistive pressure), the elastic recoil of the lung and chest wall (elastic pressure), and the alveolar pressure present at the beginning of the breath (positive end-expiratory pressure [PEEP]see also Fig. 1: Respiratory Failure and Mechanical Ventilation: Components of airway pressure during mechanical ventilation, illustrated by an inspiratory-hold maneuver.). Thus:
Resistive pressure is the product of circuit resistance and airflow. In the mechanically ventilated patient, resistance to airflow occurs in the ventilator circuit, the endotracheal tube, and most importantly, the patient's airways. Note that even when these factors are constant, an increase in airflow increases resistive pressure.
Components of airway pressure during mechanical ventilation, illustrated by an inspiratory-hold maneuver.
PEEP = positive end-expiratory pressure.
Elastic pressure is the product of the elastic recoil of the lungs and chest wall (elastance) and the volume of gas delivered. For a given volume, elastic pressure is increased by increased lung stiffness (as in pulmonary fibrosis) or restricted excursion of the chest wall or diaphragm (eg, tense ascites, massive obesity). Because elastance is the inverse of compliance, high elastance is the same as low compliance.
End-expiratory pressure in the alveoli is normally the same as atmospheric pressure. However, when the alveoli fail to empty completely because of airway obstruction, airflow limitation, or shortened expiratory time, end-expiratory pressure may be positive relative to the atmosphere. This pressure is called intrinsic PEEP or autoPEEP to differentiate it from externally applied (therapeutic) PEEP, which is set by adjusting the mechanical ventilator or by adding a mask to the airway that applies positive pressure throughout the respiratory cycle.
Any elevation in peak airway pressure (eg, > 25 cm H2O) should prompt measurement of the end-inspiratory pressure (plateau pressure) by an end-inspiratory hold maneuver to determine the relative contributions of resistive and elastic pressures. The maneuver keeps the exhalation valve closed for an additional 0.3 to 0.5 sec after inspiration, delaying exhalation. During this time, airway pressure falls from its peak value as airflow ceases. The resulting end-inspiratory pressure represents the elastic pressure once PEEP is subtracted (assuming the patient is not making active inspiratory or expiratory muscle contractions at the time of measurement). The difference between peak and plateau pressure is the resistive pressure.
Elevated resistive pressure (eg, > 10 cm H2O) suggests the endotracheal tube has been kinked or plugged with secretions or the presence of an intraluminal mass, increased intraluminal secretions, or bronchospasm. An increase in elastic pressure (eg, > 10 cm H2O) suggests decreased lung compliance from edema, fibrosis, or lobar atelectasis; large pleural effusions, pneumothorax or fibrothorax; extrapulmonary restriction as may arise from circumferential burns or other chest wall deformity, ascites, pregnancy, or massive obesity; or a tidal volume too large for the amount of lung being ventilated (eg, a normal tidal volume being delivered to a single lung because of malpositioning of the endotracheal tube).
Intrinsic PEEP can be measured in the passive patient through an end-expiratory hold maneuver. Immediately before a breath, the expiratory port is closed for 2 sec. Flow ceases, eliminating resistive pressure; the resulting pressure reflects alveolar pressure at the end of expiration (intrinsic PEEP). A nonquantitative method of identifying intrinsic PEEP is to inspect the expiratory flow tracing. If expiratory flow continues until the next breath, or the patient's chest fails to come to rest before the next breath, intrinsic PEEP is present. The consequences of elevated intrinsic PEEP include increased inspiratory work of breathing and decreased venous return, which may result in decreased cardiac output and hypotension.
The demonstration of intrinsic PEEP should prompt a search for causes of airflow obstruction (eg, airway secretions, bronchospasm); however, a high minute ventilation (> 20 L/min) alone can result in intrinsic PEEP in a patient with no airflow obstruction. If the cause is airflow limitation, intrinsic PEEP can be reduced by shortening inspiratory time (ie, increasing inspiratory flow) or reducing the respiratory rate, thereby allowing a greater fraction of the respiratory cycle to be spent in exhalation.
Means and Modes of Mechanical Ventilation
Mechanical ventilators are typically volume or pressure cycled; some newer models combine features of both. Because pressures and volumes are directly linked by the pressure-volume curve, any given volume will correspond to a specific pressure, and vice versa, regardless of whether the ventilator is pressure or volume cycled.
Adjustable ventilator settings differ with mode but include respiratory rate, tidal volume, trigger sensitivity, flow rate, waveform, and inspiratory/expiratory (I/E) ratio.
In this mode, which includes assist-control (A/C) and synchronized intermittent mandatory ventilation (SIMV), the ventilator delivers a set tidal volume. The resultant airway pressure is not fixed but varies with the resistance and elastance of the respiratory system and with the flow rate selected.
A/C ventilation is the simplest and most effective means of providing full mechanical ventilation. In this mode, each inspiratory effort beyond the set sensitivity threshold triggers delivery of the fixed tidal volume. If the patient does not trigger the ventilator frequently enough, the ventilator initiates a breath, ensuring the desired minimum respiratory rate.
SIMV also delivers breaths at a set rate and volume that is synchronized to the patient's efforts. In contrast to A/C, however, patient efforts above the set respiratory rate are unassisted, although the intake valve opens to allow the breath. This mode remains popular, despite the fact that it neither provides full ventilator support as does A/C nor facilitates liberating the patient from mechanical ventilation.
This form of mechanical ventilation includes pressure control ventilation (PCV), pressure support ventilation (PSV), and several noninvasive modalities applied via a tight-fitting face mask. In all of these, the ventilator delivers a set inspiratory pressure. Hence, tidal volume varies depending on the resistance and elastance of the respiratory system. In this mode, changes in respiratory system mechanics can result in unrecognized changes in minute ventilation. Because it limits the distending pressure of the lung, this mode can theoretically benefit patients with acute lung injury/acute respiratory distress syndrome (ALI/ARDS); however, no clear clinical advantage over A/C has been shown.
Pressure control ventilation is similar to A/C; each inspiratory effort beyond the set sensitivity threshold delivers full pressure support maintained for a fixed inspiratory time. A minimum respiratory rate is maintained.
In pressure support ventilation, a minimum rate is not set; all breaths are triggered by the patient. Pressure is typically cut off when back-pressure causes flow to drop below a certain point. Thus, a longer or deeper inspiratory effort by the patient results in a larger tidal volume. This mode is commonly used to liberate patients from mechanical ventilation by letting them assume more of the work of breathing. However, no studies indicate that this approach is more successful.
Noninvasive positive pressure ventilation (NIPPV)
NIPPV is the delivery of positive pressure ventilation via a tight-fitting mask that covers the nose or both the nose and mouth. Because of its use in spontaneously breathing patients, it is primarily applied as a form of PSV, although volume control can be used.
NIPPV can be given in the form of continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BIPAP). In CPAP, constant pressure is maintained throughout the respiratory cycle with no additional inspiratory support. With BIPAP, the physician sets both the expiratory positive airway pressure (EPAP) and the inspiratory positive airway pressure (IPAP), with respirations triggered by the patient. Because the airway is unprotected, aspiration is possible, so patients must have adequate mentation and airway protective reflexes and no imminent indication for surgery or transport off the floor for prolonged procedures. NIPPV should be avoided in patients who are hemodynamically unstable or those with evidence of impaired gastric emptying, such as occurs with ileus, bowel obstruction, or pregnancy. In such circumstances, the swallowing of large quantities of air may result in vomiting and life-threatening aspiration. Indications for conversion to endotracheal intubation and conventional mechanical ventilation include the development of shock or frequent arrhythmias, myocardial ischemia, and transport to a cardiac catheterization laboratory or surgical suite where control of the airway and full ventilatory support are desired. Obtunded patients and those with copious secretions are not good candidates. Also, IPAP must be set below esophageal opening pressure (20 cm H2O) to avoid gastric insufflation.
NIPPV can be used in the outpatient setting. For example, CPAP is often used for patients with obstructive sleep apnea (see Sleep Apnea: Obstructive Sleep Apnea), whereas BIPAP can be used for those with concomitant central sleep apnea (see Sleep Apnea: Central Sleep Apnea) and obstructive sleep apnea or for chronic ventilation in patients with progressive neuromuscular diseases.
Ventilator settings are tailored to the underlying condition, but the basic principles are as follows.
Tidal volume and respiratory rate set the minute
Too high a volume risks overinflation; too low a volume risks atelectasis. Too high a rate risks hyperventilation and respiratory alkalosis along with inadequate expiratory time and autoPEEP; too low a rate risks inadequate minute ventilation and respiratory acidosis. A tidal volume of 8 to 10 mL/kg ideal body weight (see Respiratory Failure and Mechanical Ventilation: Initial Ventilator Management in ALI/ARDS) is usually appropriate, although some patients with normal lung mechanics (particularly those with neuromuscular disease) benefit from tidal volumes on the high end of this range to prevent atelectasis, whereas patients with ALI/ARDS or acute exacerbations of COPD or asthma may require lower volumes (see Respiratory Failure and Mechanical Ventilation: Mechanical ventilation in ALI/ARDS). Ideal body weight (IBW) rather than actual body weight is used to determine the appropriate tidal volume for patients with lung disease receiving mechanical ventilation:
Sensitivity adjusts the level of negative pressure required to trigger the ventilator. A typical setting is 2 cm H2O. Too high a setting will cause weak patients to be unable to trigger a breath. Too low a setting may lead to overventilation by causing the machine to auto-cycle. Patients with high levels of autoPEEP may have difficulty inhaling deeply enough to achieve a sufficiently negative intra-airway pressure.
The ratio of the time spent in inhalation versus that spent in exhalation (I:E ratio) can be adjusted in some modes of ventilation. A normal setting for patients with normal mechanics is 1:3. Patients with asthma or COPD exacerbations should have ratios of 1:4 or even more to limit the degree of autoPEEP.
The inspiratory flow rate can be adjusted in some modes of ventilation (ie, either the flow rate or the I:E ratio can be adjusted, not both). The inspiratory flow should generally be set at about 60 L/min but can be increased up to 120 L/min for patients with airflow limitation to facilitate having more time in exhalation, thereby limiting autoPEEP.
Fio2 is initially set at 1.0 and is subsequently decreased to the lowest level necessary to maintain adequate oxygenation.
PEEP can be applied in any ventilator mode. PEEP increases end-expired lung volume and reduces airspace closure at the end of expiration. Most patients undergoing mechanical ventilation may benefit from the application of PEEP at 5 cm H2O to limit the atelectasis that frequently accompanies endotracheal intubation, sedation, paralysis, and/or supine positioning. Higher levels of PEEP improve oxygenation in disorders such as cardiogenic pulmonary edema and ARDS. PEEP permits use of lower levels of Fio2 while preserving adequate arterial oxygenation. This may be important in limiting the lung injury that may result from prolonged exposure to a high Fio2 (= 0.6). PEEP increases intrathoracic pressure and thus may impede venous return, provoking hypotension in the hypovolemic patient, and may overdistend portions of the lung, thereby causing ventilator-associated lung injury (VALI). By contrast, if PEEP is too low, it may result in cyclic airspace opening and closing, which in turn may also cause VALI from the resultant repetitive shear forces.
Mechanical ventilation is typically done with the patient in the semi-upright position. However, in patients with ALI/ARDS, prone positioning may result in better oxygenation primarily by creating more uniform ventilation. Uniform ventilation reduces the amount of lung that has no ventilation (ie, the amount of shunt), which is generally greatest in the dorsal and caudal lung regions, while having minimal effects on perfusion distribution.
Although many investigators advocate a trial of prone positioning in patients with ALI/ARDS who require high levels of PEEP (eg, > 12 cm H2O) and Fio2 (eg, > 0.6), trials have not shown any improvement in mortality with this strategy. Prone positioning is contraindicated in patients with spinal instability or increased intracranial pressure. This position also requires concerted effort by the ICU staff to avoid complications, such as dislodgement of the endotracheal tube or intravascular lines.
Sedation and comfort
Although some patients tolerate mechanical ventilation via endotracheal tube without sedatives, most require continuous IV administration of sedatives (eg, propofol, lorazepam, midazolam) and analgesics (eg, morphine, fentanyl) to minimize stress and anxiety. These drugs also can reduce energy expenditure to some extent, thereby reducing CO2 production and O2 consumption. Doses should be titrated to the desired effect, guided by standard sedation/analgesia scoring systems. Patients undergoing mechanical ventilation for ALI/ARDS typically require higher levels of sedation and analgesia. The use of propofol for longer than 24 to 48 h requires periodic monitoring of serum triglyceride levels.
Neuromuscular blocking agents are now rarely used in patients undergoing mechanical ventilation because of the risk of prolonged neuromuscular weakness and the need for continuous heavy sedation. Exceptions include failure to tolerate some of the more sophisticated and complicated modes of mechanical ventilation and to prevent shivering when cooling is used after cardiac arrest.
Complications and safeguards
Complications can be divided into those resulting from endotracheal intubation, from mechanical ventilation itself, or from prolonged immobility and inability to eat normally.
The presence of an endotracheal tube causes risk of sinusitis (which is rarely of clinical importance), ventilator-associated pneumonia (see Pneumonia: Hospital-Acquired Pneumonia), tracheal stenosis, vocal cord injury, and rarely tracheal-esophageal or tracheal-vascular fistula. Purulent tracheal aspirate in a febrile patient who has an elevated WBC count > 48 h after ventilation has begun suggests ventilator-associated pneumonia.
Complications of ongoing mechanical ventilation itself include pneumothorax, O2 toxicity, hypotension, and VALI.
If acute hypotension develops in the mechanically ventilated patient, particularly when accompanied by tachycardia and/or a sudden increase in peak inspiratory pressure, tension pneumothorax must always be considered; patients with such findings should immediately have a chest examination and a chest x-ray (or immediate treatment if examination is confirmatory). More commonly, however, hypotension is a result of sympathetic lysis from sedatives or opioids used to facilitate intubation and ventilation. Hypotension can also be caused by decreased venous return from high intrathoracic pressure in patients receiving high levels of PEEP or in those with high levels of intrinsic PEEP from asthma or COPD. If there are no physical findings suggestive of tension pneumothorax, and ventilation-related causes of hypotension are a possible etiology, pending a portable chest x-ray, the patient may be disconnected from the ventilator and gently bagged manually at 2 to 3 breaths/min with 100% O2 while fluids are infused (eg, 500 to 1000 mL of 0.9% saline in adults, 20 mL/kg in children). An immediate improvement suggests a ventilation-related cause, and ventilator settings should be adjusted accordingly.
Relative immobility increases the risk of venous thromboembolic disease, skin breakdown, and atelectasis.
Most hospitals have standardized protocols to reduce complications. Elevating the head of the bed to > 30° decreases risk of ventilator-associated pneumonia, and routine turning of the patient every 2 h decreases the risk of skin breakdown. All patients receiving mechanical ventilation should receive deep venous thrombosis prophylaxis, either heparin 5000 units sc bid to tid or low molecular heparin or, if heparin is contraindicated, sequential compression devices. To prevent GI bleeding, patients should receive an H2 blocker (eg, famotidine 20 mg enterally or IV bid) or sucralfate (1 g enterally qid). Proton pump inhibitors should be reserved for patients with a preexisting indication or active bleeding. Routine nutritional evaluations are mandatory, and enteral tube feedings should be initiated if ongoing mechanical ventilation is anticipated. Finally, the most effective way to reduce complications of mechanical ventilation is to limit its duration. Daily sedation vacations and spontaneous breathing trials help determine the earliest point at which the patient may be liberated from mechanical support.
Last full review/revision August 2007 by Brian K. Gehlbach, MD; Jesse Hall, MD
E-Medicine 2010 http://emedicine.medscape.com/article/810126-overview
Author: Allon Amitai, MD, International Emergency Medicine Fellow, Rhode Island Hospital; Consulting Staff, Memorial Hospital of Rhode Island; Doctoring Preceptor, Brown University Medical School
Coauthor(s): Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center; Daniel M Joyce, MD, Consulting Staff, Department of Emergency Medicine, Saint Vincent's and Saint Mary's Medical
Initial ventilator settings in various disease states.
Introduction to Ventilator Management
Intubation, with subsequent mechanical ventilation, is a common life-saving intervention in the emergency department (ED). Given the increasing length of stay of ventilated patients in EDs, it is necessary for emergency practitioners to have a good understanding of techniques to optimize mechanical ventilation and minimize complications.
Many different strategies of positive-pressure ventilation are available; these are based on various permutations of triggered volume-cycled and pressure-cycled ventilations and are delivered at a range of rates, volumes, and pressures. Poor ventilatory management can inflict serious pulmonary and extrapulmonary damage that may not be immediately apparent.
Because many of the effects of ventilator-induced lung injury are delayed and not seen while patients are in the ED, much of our understanding of the adverse consequences of volutrauma, air-trapping, barotrauma, and oxygen toxicity has come from the critical care literature. While the fundamental principles underlying mechanical ventilatory support have changed little over the decades, much progress has been made in our understanding of the secondary pathophysiologic changes associated with positive-pressure ventilation.
Ventilatory strategies have been devised for different disease processes to protect pulmonary parenchyma while maintaining adequate gas exchange, and they may be responsible for the increased rates of survival for pathologies such as acute respiratory distress syndrome (ARDS). Several recent clinical trials have demonstrated that optimizing ventilatory parameters reduces overall duration of mechanical ventilation and organ failure. Additionally, an upsurge in utilization of noninvasive ventilation has permitted many patients to avoid the risks and complications of tracheal intubation.1,2
Modes of Mechanical Ventilation
1. Volume-cycled mode
Inhalation proceeds until a set tidal volume (TV) is delivered and is followed by passive exhalation. A feature of this mode is that gas is delivered with a constant inspiratory flow pattern, resulting in peak pressures applied to the airways higher than that required for lung distension (plateau pressure). Since the volume delivered is constant, applied airway pressures vary with changing pulmonary compliance (plateau pressure) and airway resistance (peak pressure).
Because the volume-cycled mode ensures a constant minute ventilation, it is a common choice as an initial ventilatory mode in the ED. A major disadvantage is that high airway pressures may be generated, potentially resulting in barotrauma. Close monitoring and use of pressure limits are helpful in avoiding this problem. Note that ventilators set to volume-cycled mode function well as monitors of patients' pulmonary compliance, which will be decreased in physiological states such as worsening ARDS, pneumothorax, right mainstem intubation, chest-wall rigidity, increased intra-abdominal pressure, and psychomotor agitation ("fighting the vent"). These pathophysiological states increase peak pressure and should be considered whenever pressure alarms are sounded.
In pressure-cycled settings, by contrast, such states result only in reduced delivered volumes and may not trigger alarms. Given that the airway resistance and pulmonary compliance of the critical ED patient is unknown and potentially unstable, the authors recommend the volume-cycled mode for initial ventilation of most patients.
2. Pressure-cycled mode
A set peak inspiratory pressure (PIP) is applied, and the pressure difference between the ventilator and the lungs results in inflation until the peak pressure is attained and passive exhalation follows. The delivered volume with each respiration is dependent on the pulmonary and thoracic compliance.
A theoretical advantage of pressure-cycled modes is a decelerating inspiratory flow pattern, in which inspiratory flow tapers off as the lung inflates. This usually results in a more homogeneous gas distribution throughout the lungs. However, no definite evidence exists that this results in a reduction of the rate of ventilator-induced lung injury or overall mortality. Nevertheless, pressure-cycled ventilation has achieved considerable popularity in the intensive care setting for management of patients with ARDS, whose lungs are most likely to be characterized by a broad range of alveolar dysfunction and are also most vulnerable to the effects of barotrauma and volutrauma.
A major disadvantage is that dynamic changes in pulmonary mechanics may result in varying tidal volumes. This necessitates close monitoring of minute ventilation and limits the usefulness of this mode in many emergency department patients. However, newer ventilators can provide volume-assured pressure-cycled ventilation, which increase peak pressures as needed to deliver a preset minimum tidal volume.
3. High-frequency oscillatory support
In this ventilatory strategy, ultra-high respiratory rates (180-900 breaths per minute) are coupled with tiny tidal volumes and high airway pressures. This is a commonly accepted ventilatory setting for premature infants and has now also been used in small critical care unit studies on patients with ARDS, with reports of improving oxygenation and lung recruitment.3
While this setting cannot currently be recommended for routine ED use, it may in the future be found appropriate for the management of patients with ARDS.
Types of support
Most ventilators can be set to apply the delivered tidal volume in a control mode or a support mode.
Methods of Ventilatory Support
1. Continuous mandatory ventilation
Breaths are delivered at preset intervals, regardless of patient effort. This mode is used most often in the paralyzed or apneic patient because it can increase the work of breathing if respiratory effort is present. Continuous mandatory ventilation (CMV) has given way to assist-control (A/C) mode because A/C with the apneic patient is tantamount to CMV. Many ventilators do not have a true CMV mode and offer A/C instead.
2. Assist-control ventilation
The ventilator delivers preset breaths in coordination with the respiratory effort of the patient. With each inspiratory effort, the ventilator delivers a full assisted tidal volume. Spontaneous breathing independent of the ventilator between A/C breaths is not allowed. As might be expected, this mode is better tolerated than CMV in patients with intact respiratory effort.
3. Intermittent mandatory ventilation
With intermittent mandatory ventilation (IMV), breaths are delivered at a preset interval, and spontaneous breathing is allowed between ventilator-administered breaths. Spontaneous breathing occurs against the resistance of the airway tubing and ventilator valves, which may be formidable. This mode has given way to synchronous intermittent mandatory ventilation (SIMV).
4. Synchronous intermittent mandatory ventilation
The ventilator delivers preset breaths in coordination with the respiratory effort of the patient. Spontaneous breathing is allowed between breaths. Synchronization attempts to limit barotrauma that may occur with IMV when a preset breath is delivered to a patient who is already maximally inhaled (breath stacking) or is forcefully exhaling.
The initial choice of ventilation mode (eg, SIMV, A/C) is institution and practitioner dependent. A/C ventilation, as in CMV, is a full support mode in that the ventilator performs most, if not all, of the work of breathing. These modes are beneficial for patients who require a high minute ventilation. Full support reduces oxygen consumption and CO2 production of the respiratory muscles. A potential drawback of A/C ventilation in the patient with obstructive airway disease is worsening of air trapping and breath stacking.
When full respiratory support is necessary for the paralyzed patient following neuromuscular blockade, no difference exists in minute ventilation or airway pressures with any of the above modes of ventilation. In the apneic patient, A/C with a respiratory rate (RR) of 10 and a TV of 500 mL delivers the same minute ventilation as SIMV with the same parameters.
5. Pressure support ventilation
For the spontaneously breathing patient, pressure support ventilation (PSV) has been advocated to limit barotrauma and to decrease the work of breathing. Pressure support differs from A/C and IMV in that a level of support pressure is set (not TV) to assist every spontaneous effort. Airway pressure support is maintained until the patient's inspiratory flow falls below a certain cutoff (eg, 25% of peak flow). With some ventilators, there is the ability to set a back-up IMV rate should spontaneous respirations cease.
PSV is frequently the mode of choice in patients whose respiratory failure is not severe and who have an adequate respiratory drive. It can result in improved patient comfort, reduced cardiovascular effects, reduced risk of barotrauma, and improved distribution of gas.
6. Noninvasive ventilation
The application of mechanical ventilatory support through a mask in place of endotracheal intubation is becoming increasingly accepted and used in the emergency department. Considering this modality for patients with mild-to-moderate respiratory failure is appropriate. The patient must be mentally alert enough to follow commands. Clinical situations in which it has proven useful include acute exacerbation of chronic obstructive pulmonary disease (COPD) or asthma, decompensated congestive heart failure (CHF) with mild-to-moderate pulmonary edema, and pulmonary edema from hypervolemia. It is most commonly applied as continuous positive airway pressure (CPAP) and biphasic positive airway pressure (BiPAP). BiPAP is commonly misunderstood to be a form of pressure support ventilation triggered by patient breaths; in actuality, BiPAP is a form of CPAP that alternates between high and low positive airway pressures, permitting inspiration (and expiration) throughout.
Reviews of the literature have shown noninvasive positive-pressure ventilation to be beneficial for COPD, reducing the rate of tracheal intubations as well as length of stay.2 Their benefit increases with increasing severity of disease. In patients with mild cases of COPD and CHF who would not otherwise require ventilatory support do not benefit from noninvasive positive-pressure ventilatory support. The use of noninvasive positive-pressure ventilation has been less well studied in asthma, but, in one small randomized trial, it reduced hospital admission rates.4
Adverse Consequences of Mechanical Ventilation
The deterioration of intubated patients to multiorgan failure has been observed for decades. In recent years, however, much progress delineating the adverse effects of positive-pressure ventilation has been made.5 In 1993, Tremblay et al demonstrated increased cytokine and inflammatory mRNA expression in a high-stress ventilatory model, showing that increasing volumes and reducing PEEP resulted in higher tumor necrosis alpha serum concentrations. Further research over the 1990s demonstrated a cascade of systemic inflammatory effects of biochemical pulmonary injury contributing to distal organ dysfunction.6
Barotrauma may result in pulmonary interstitial emphysema, pneumomediastinum, pneumoperitoneum, pneumothorax, and/or tension pneumothorax. High peak inflation pressures (>40 cm H2 O) are associated with an increased incidence of barotrauma. However, note that separating barotrauma from volutrauma is difficult, since increasing barometric pressure is usually accompanied by increasing alveolar volume.
Experimental models of high peak inflation pressures in animals with high extrathoracic pressures have not demonstrated direct alveolar damage from increased pressure without increased volume as well. Thus, saying that high airway pressures result in alveolar overdistention (volutrauma) and accompanying increased microvascular permeability and parenchymal injury might be more accurate. Alveolar cellular dysfunction occurs with high airway pressures. The resultant surfactant depletion leads to atelectasis, which requires further increases in airway pressure to maintain lung volumes.
High-inspired concentrations of oxygen (fraction of inspired oxygen [FiO2] >0.5) result in free-radical formation and secondary cellular damage. These same high concentrations of oxygen can lead to alveolar nitrogen washout and secondary absorption atelectasis.
It has been theorized that pulmonary biophysical and biomechanical injury in the presence of bacterial lung infections contributes to bacterial translocation and bacteremia.
The heart, great vessels, and pulmonary vasculature lie within the chest cavity and are subject to the increased intrathoracic pressures associated with mechanical ventilation. The result is a decrease in cardiac output due to decreased venous return to the right heart (dominant), right ventricular dysfunction, and altered left ventricular distensibility.
The decreased cardiac output from reduction in right ventricular preload is more pronounced in the hypovolemic patient and in those with a low ejection fraction.
Exaggerated respiratory variation on the arterial pressure waveform is a clue that positive-pressure ventilation is significantly affecting venous return and cardiac output. In the absence of an arterial line, a good pulse oximetry waveform can be equally instructive. A reduction in the variation after volume loading confirms this effect. These effects will most frequently be seen in patients with preload-dependent cardiac function (that is, operating on the right side of the Starling curve) and in hypovolemic patients or in those with otherwise compromised venous return.
Increased alveolar-capillary permeability secondary to pulmonary inflammatory changes may, alternatively, contribute to increased cardiac output.
For patients with Swan-Ganz catheterization in place for whom cardiac output may be measured (usually in the ICU setting), PEEP studies may be performed. This is performed by adjusting PEEP, monitoring oxygenation by peripheral oxygen saturation or arterial oxygen measurement via blood gas sampling, and measuring the associated cardiac output. The process is repeated at various PEEP settings, and the results are recorded. The practitioner can then review the results and determine the optimal PEEP for that patient at that time. This procedure is not generally performed in the ED but underlies the association of ventilation strategy and cardiac output.
Renal, hepatic, and gastrointestinal effects
Positive-pressure ventilation is responsible for an overall decline in renal function with decreased urine volume and sodium excretion.
Hepatic function is adversely affected by decreased cardiac output, increased hepatic vascular resistance, and elevated bile duct pressure.
The gastric mucosa does not have autoregulatory capability. Thus, mucosal ischemia and secondary bleeding may result from decreased cardiac output and increased gastric venous pressure.
Indications For Mechanical Ventilation
The principal indications for mechanical ventilation are airway protection and respiratory failure.
A compromised airway, or an airway at risk of compromise, may be identified by physical examination and ancillary testing.
Respiratory failure in the ED is almost always-and most appropriately-a clinical diagnosis. The decision to intubate and mechanically ventilate or to institute noninvasive ventilation support is generally made purely on clinical grounds without delay for laboratory evaluation.
Respiratory failure may also be easily identified with laboratory or pulmonary function data. Obtaining a PaCO2 is useful to confirm respiratory failure when a broader differential diagnosis exists-for example, obtunded patients who may be hypercarbic but might have a reversible metabolic or toxicological etiology for their conditions-but adequate stabilization and ventilation of these patients should not be delayed to wait for laboratory results.
Mechanical ventilation is indicated for both hypercapnic respiratory failure and hypoxemic respiratory failure. It is also indicated for treatment of certain critical conditions such as correction of life-threatening acidemia in the setting of salicylate intoxication, for intentional hyperventilation in the setting of major head injury with elevated intracranial pressure, for suspicion of clinical brain herniation from any cause, or for a patient in critical condition with cyclic antidepressant toxicity.
Laboratory Criteria for Mechanical Ventilation
|Blood gases||PaO2 <55 mm Hg|
|PaCO2 >50 mm Hg and pH <7.32|
|Pulmonary function tests||Vital capacity <10 mL/kg|
|Negative inspiratory force <25 cm H2 O|
|FEV1 <10 mL/kg|
Clinical Criteria for Mechanical Ventilation
Other Criteria for Mechanical Ventilation
No absolute contraindications exist to mechanical ventilation. The need for mechanical ventilation is best made early on clinical grounds. A good rule of thumb is if the practitioner is thinking that mechanical ventilation is needed, then it probably is. Waiting for return of laboratory values can result in unnecessary morbidity or mortality.
Guidelines for Ventilator Settings
1. Mode of ventilation
The mode of ventilation should be tailored to the needs of the patient. In the emergent situation, the practitioner may need to order initial settings quickly. SIMV and A/C are versatile modes that can be used for initial settings. In patients with a good respiratory drive and mild-to-moderate respiratory failure, PSV is a good initial choice.
2. Tidal volume
Observations of the adverse effects of barotrauma and volutrauma have led to recommendations of lower tidal volumes than in years past, when tidal volumes of 10-15 mL/kg were routinely used.
An initial TV of 5-8 mL/kg of ideal body weight is generally indicated, with the lowest values recommended in the presence of obstructive airway disease and ARDS. The goal is to adjust the TV so that plateau pressures are less than 35 cm H2 O.
3. Respiratory rate
A respiratory rate (RR) of 8-12 breaths per minute is recommended for patients not requiring hyperventilation for the treatment of toxic or metabolic acidosis, or intracranial injury. High rates allow less time for exhalation, increase mean airway pressure, and cause air trapping in patients with obstructive airway disease. The initial rate may be as low as 5-6 breaths per minute in asthmatic patients when using a permissive hypercapnic technique.
4. Supplemental oxygen therapy
The lowest FiO2 that produces an arterial oxygen saturation (SaO2) greater than 90% and a PaO2 greater than 60 mm Hg is recommended. No data indicate that prolonged use of an FiO2 less than 0.4 damages parenchymal cells.
5. Inspiration/expiration ratio
The normal inspiration/expiration (I/E) ratio to start is 1:2. This is reduced to 1:4 or 1:5 in the presence of obstructive airway disease in order to avoid air-trapping (breath stacking) and auto-PEEP or intrinsic PEEP (iPEEP). Use of inverse I/E may be appropriate in certain patients with complex compliance problems in the setting of ARDS.
6. Inspiratory flow rates
Inspiratory flow rates are a function of the TV, I/E ratio, and RR and may be controlled internally by the ventilator via these other settings. If flow rates are set explicitly, 60 L/min is typically used. This may be increased to 100 L/min to deliver TVs quickly and allow for prolonged expiration in the presence of obstructive airway disease.
7. Positive end-expiratory pressure (PEEP)
PEEP has several beneficial effects and may be clinically underutilized. Research underway is examining the utility of high (>10 cm H2 O) PEEP in disease states ranging from COPD/asthma to ARDS. PEEP has been found to reduce the risk of atelectasis trauma and increase the number of "open" alveoli participating in ventilation, thus minimizing V/Q mismatches. However, note that in disease states such as ARDS, the degree to which alveoli function has been compromised varies tremendously within the lungs and there is no single "ideal" PEEP appropriate for all alveoli; rather, a compromise PEEP must be selected.
One obvious beneficial effect of PEEP is to shift lung water from the alveoli to the perivascular interstitial space. It does not decrease the total amount of extravascular lung water. This is of clear benefit in cases of cardiogenic as well as noncardiogenic pulmonary edema. An additional benefit of PEEP in cases of CHF is to decrease venous return to the right side of the heart by increasing intrathoracic pressure.
Applying physiologic PEEP of 3-5 cm H2 O is common to prevent decreases in functional residual capacity in those with normal lungs. The reasoning for increasing levels of PEEP in critically ill patients is to provide acceptable oxygenation and to reduce the FiO2 to nontoxic levels (FiO2 <0.5). The level of PEEP must be balanced such that excessive intrathoracic pressure (with a resultant decrease in venous return and risk of barotrauma) does not occur.
With assisted ventilation, the sensitivity typically is set at -1 to -2 cm H2 O. The development of iPEEP increases the difficulty in generating a negative inspiratory force sufficient to overcome iPEEP and the set sensitivity. Newer ventilators offer the ability to sense by inspiratory flow instead of negative force. Flow sensing, if available, may lower the work of breathing associated with ventilator triggering.
Monitoring During Ventilatory Support
Cardiac monitor, blood pressure, and pulse oximetry (SaO2) are recommended. The authors' practice with stable patients is to titrate down FiO2 to the minimum value necessary to maintain maximal SaO2. An arterial blood gas (ABG) measurement is frequently obtained 10-15 minutes after the institution of mechanical ventilation. The measured arterial PaO2 should verify the transcutaneous pulse oximetry readings and direct the reduction of FiO2 to a value less than 0.5. The measured PaCO2 can suggest adjustments of minute ventilation but should be interpreted in light of the patient's overall acid-base status. For example, full correction of PaCO2 in a chronically hypercarbic COPD patient will lead to unopposed metabolic alkalosis.
Reasonable alternatives to arterial blood gas measurement in more stable patients include measuring the venous blood gas, which will give values close to arterial pH and PaCO2 or monitoring an end-tidal CO2.
Peak inspiratory and plateau pressures should be assessed frequently, although it should be recognized that both pressures will be increased by extrapulmonary pressure, for example from stiff chest walls or a distended abdomen, and do not reflect the true risk of barotrauma. In general, however, parameters may be altered to limit pressures to less than 35 cm H2 O. Expiratory volume is checked initially and periodically (continuously if ventilator is capable) to ensure that the set tidal volume is delivered. Any indication of an air leak must prompt a search for underinflated tube cuffs, open tubing ports, or worsening pneumothorax. In patients with airway obstruction, monitor auto-PEEP.
Initial Ventilator Settings in Various Disease States
In the ED setting, patients frequently require full respiratory support. For most ED patients who are paralyzed as a component of rapid-sequence induction, CMV and A/C are good choices as an initial ventilatory mode. SIMV may be better tolerated in nonparalyzed patients with obstructive airway disease and an intact respiratory effort. PSV can be used when respiratory effort is intact and respiratory failure is not severe.
Noninvasive ventilation (CPAP, BiPAP) can be used effectively in many cases of severe COPD and CHF to avoid tracheal intubation. Initial ventilator settings are guided by the patient's pulmonary pathophysiology and clinical status. Adjustments can then be made to limit barotrauma, volutrauma, and oxygen toxicity. CPAP and BiPAP require alert, cooperative patients capable of independently maintaining their airways and are contraindicated in the presence of facial trauma.
Asthma and COPD
Hypoxia can generally be corrected through a high FiO2, but patients with airway obstruction are at risk of high airway pressures, breath stacking leading to intrinsic PEEP, barotrauma, and volutrauma. To minimize intrinsic PEEP, it is recommended that expiratory flow time be increased as much as possible. Permissive hypercapnia enables a low respiratory rate of 6-8 breaths per minute to be used, as well as an increased I:E ratio of 1:1.5 or 1:2.
PEEP may benefit some asthmatic patients by reducing the work of breathing and maintaining open airways during expiration, but its effects are difficult to predict and must be carefully monitored. Patients with asthma and COPD are at particular risk of barotraumatic progression to tension pneumothorax, a complication that can initially appear similar to runaway intrinsic PEEP. These conditions may be distinguished by temporary detachment of the patient from positive-pressure ventilation; if exhalation results in a recovery of pulse or normal blood pressure, the diagnosis is intrinsic PEEP.
CPAP and BiPAP will benefit some asthmatics and many patients with COPD. These patients will require careful monitoring as they can easily deteriorate from hypercarbia, intrinsic PEEP, or respiratory exhaustion. Nevertheless, a Cochrane Database Systematic Review analysis of trials including patients with severe COPD exacerbations demonstrated that the use of noninvasive positive-pressure ventilation absolutely reduced the rate of endotracheal intubation by 59% (95% confidence interval [CI] of relative risk [RR]: 0.33-0.53), the length of hospital stay by 3.24 days (95% CI: 2.06-4.44 days), and the risk of mortality by 48% (95% CI of RR: 0.35-0.76).2
Acute respiratory distress syndrome
ARDS lungs are typically irregularly inflamed and highly vulnerable to atelectasis as well as barotrauma and volutrauma. Their compliance is typically reduced, and their dead space increased. The standard of care for the ventilatory management of patients with ARDS changed dramatically in 2000 with the publication of a large multicenter, randomized trial comparing patients with ARDS initially ventilated with either the traditional tidal volume of 12 mL/kg or a lower TV of 6 mL/kg. This trial was stopped early because the lower tidal volume was found to reduce mortality by an absolute 8.8% (P=0.007). Intriguingly, plasma interleukin 6 concentrations decreased in the low TV group relative to the high TV group (P <0.001), suggesting a decrease in lung inflammation.7
The authors recommend initiating ventilation of patients with ARDS with A/C ventilation at a tidal volume of 6 mL/kg, with a PEEP of 5 and initial ventilatory rate of 12, titrated up to maintain a pH greater than 7.25. There is not yet adequate evidence to routinely recommend PEEP greater than 5 cm H2 O, but, in appropriately monitored circumstances, it may be attempted. Intrinsic PEEP may occur in patients with ARDS at high ventilatory rates and should be watched for and treated by reducing the rate of ventilation under direct observation until plateau pressures decrease. The authors recommend a target plateau pressure of less than 30 cm H2 O. Once a patient has been stabilized with adequate tidal volumes at a plateau pressure of less than 30 cm H2 O, considering a trial of pressure-cycled ventilation is reasonable.
Several recruitment maneuvers have been devised to increase the proportion of alveoli ventilated in ARDS. These techniques typically attempt short-term increased PEEP or volume to open occluded or collapsed alveoli. Gattinoni et al, for example, found that among ARDS patients undergoing whole-lung CT, applying 45 cm H2 O PEEP recruited a mean of 13% new lung tissue.8 The National Heart, Lung, and Blood Institute ARDS Clinical Trial Network, however, in a randomized comparison of high and low PEEP among 549 patients with ARDS, found no statistical difference in the outcomes of death rates and time spent intubated.9
Small, nonrandomized studies have evaluated the effects of prone positioning and kinetic therapy in ARDS/ALI. In a study of trauma and general surgery patients, Davis et al demonstrated shorter durations of intubation and reduced mortality among their kinetic prone therapy group, but this study was not randomized.10
Permissive hypercapnia is a ventilatory strategy that has won particular favor in the management of patients with ARDS and COPD/asthma who would otherwise require dangerously high tidal volumes and airway pressures. In patients without contraindications such as head injury, cerebrovascular accident (CVA), elevated intracranial pressure, or cardiovascular instability, permissive hypercapnia has permitted much decreased tidal volumes, airway pressures, and respiratory rates, though evidence for a decrease in mortality rates is incomplete.11 The typically recommended target pH is 7.25.
Noninvasive ventilatory strategies have met with little success in the treatment of patients with ARDS. The authors recommend great caution and close monitoring if noninvasive positive pressure ventilation (NIPPV) is attempted among patients with ARDS.
In trials of NIPPV among patients with undifferentiated hypoxemia, the presence of pneumonia or ARDS was associated with significantly increased risk of failure. Some subgroups of patients with ARDS may benefit from NIPPV; however, Antonelli et al demonstrated greater success in applying noninvasive positive pressure ventilation to patients with lower simplified acute physiology scores and higher PaO2/FiO2 ratios.12
Congestive heart failure
CHF responds very well to positive-pressure ventilation, which serves the dual role of opening alveoli and reducing preload. Many patients with CHF benefit from a trial of noninvasive CPAP or BiPAP. Some of these patients will clinically improve so rapidly that admitting services may request discontinuation of noninvasive ventilatory support, but great caution must be maintained if this is attempted, as fluid may unpredictably reaccumulate, resulting in hypoxia and respiratory failure.
Intubated patients usually manage to adequately oxygenate. PEEP can be increased as tolerated to improve oxygenation and reduce preload. However, in some patients, cardiac output can be particularly dependent on preload and such patients may easily develop postintubation hypotension. Management of this common complication includes a combination of fluid therapy, discontinuation of nitroglycerin or other medical therapies, and, if necessary, medical or mechanical hemodynamic support interventions.
Traumatic brain injury
Hyperventilation was traditionally recommended in the management of severe traumatic brain injury, but recent studies have demonstrated poor outcomes thought to be secondary to excessive cerebral vasoconstriction and reduced cerebral perfusion. However, retrospective data have demonstrated decreased mortality among traumatic brain injury ventilated to PCO2 between 30 and 39 mm Hg, though this has not been prospectively validated.13
Ventilator Troubleshooting - Managing Complications in the ED
The complications most commonly encountered in the emergency department include hypoxia, hypotension, high pressure alarms, and low exhaled volume alarms.
High pressure alarms are triggered when resistance to ventilation is high. This may occur secondary to reduced lung elasticity or airway obstruction, or extrinsic compression. Thus, patients should be evaluated for pneumothorax, bronchospasm, elevated abdominal pressure, mainstem intubation, tube plugs or kinks, tube biting, dynamic hyperinflation/air trapping, psychomotor agitation, and worsening pulmonary compliance secondary to progressive pulmonary disease. Tube suctioning and adequate patient sedation are recommended after other causes of obstruction are ruled out. Comparison of peak pressures with plateau pressures may be helpful in identifying the location of resistance, especially if graphical representation of airway pressures is available.
Plateau pressure can be measured by applying a brief inspiratory pause after ventilation. It better reflects the risk of barotrauma than peak inspiratory pressure, but it is not in itself necessarily dangerous; if pleural pressure is elevated secondary to a stiff chest wall or high abdominal pressure, transpulmonary pressure (plateau pressure - pleural pressure) will be low, minimizing the risk of bleb or alveolar rupture.
Low exhaled volume alarms are triggered by air leaks. These are most frequently secondary to ventilatory tubing disconnect from the patient's tracheal tube but will also occur in the event of balloon deflation or tracheal tube dislodgement. Tube placement, balloon inflation, and connection to the ventilator should be carefully verified.
Hypoxia after intubation may occur secondary to hypoventilation, worsening cardiac shunting, inadequate FiO2, mainstem intubation, aspiration, tube dislodgement, or pulmonary edema. The causes of high airway pressures and low exhaled volumes described above can result in hypoxia if they cause hypoventilation. Despite the use of numerous safety precautions, cases are occasionally documented of ventilators being connected to compressed air or nitrous oxide rather than oxygen. Increasing FiO2 and adjusting ventilatory settings to increase PEEP or respiratory rate are useful first steps after excluding equipment failure and mechanical causes of hypoxia.
Hypotension after intubation is usually attributable to diminished central venous blood return to the heart secondary to elevated intrathoracic pressures. This can be treated with fluid infusions and/or adjustment of ventilatory settings to lower intrathoracic pressure (reducing PEEP, tidal volume, and, if air trapping is suspected, respiratory rate). Hypotension may also be secondary to vasovagal reaction to intubation, rapid sequence induction, sedation, and tension pneumothorax.
Initial ventilator settings in various disease states.