1. Description of the problem
2. Emergency Management
1. Indications for mechanical ventilation
The indications for mechanical ventilation are four-fold, and may be broadly categorized through a mechanistic perspective.
A Type I indication is the result of acute hypoxemic respiratory failure, as one encounters in patients with alveolar filling processes, including hydrostatic pulmonary edema, permeability pulmonary edema (acute respiratory distress syndrome, ARDS) or pneumonia. A Type II indication denotes ventilatory failure as one encounters with alveolar hypoventilation as a result of central nervous system depression, neuromuscular disease, or obstructive lung disease such as asthma or chronic obstructive pulmonary disease. A Type III indication captures those peri-operative encounters wherein atelectasis results in respiratory failure. Finally, Type IV respiratory failure is the consequence of hypoperfusion associated with shock.
In clinical practice, Type I respiratory failure is the most common indication for initiating mechanical ventilation. In an international epidemiologic cross-sectional study, acute hypoxemic respiratory failure accounted for approximately two-thirds of ventilated cases studied. Type II and Type III respiratory failures accounted for approximately 20% and 10% of cases, respectively. Shock, as an etiology requiring the use of mechanical ventilation, was a contributing factor in approximately half of Type I, Type II and Type III cases.
The goals of mechanical ventilation are several-fold. First, one must maintain adequate oxygenation. Second, one must maintain adequate ventilation and also avoid the development of intrinsic positive end-expiratory pressure (PEEP). Third, one must optimize the patient-ventilator interface (i.e., synchrony) by matching the patient’s innate inspiratory time with the mechanical (or set) inspiratory time so as to avoid increasing the work of the respiratory muscles. Fourth, recognizing that mechanical ventilation is a therapeutic modality with inherent risks, one must avoid ventilator-induced lung injury. Last, one must liberate the patient from the assistance of mechanical ventilation as soon as is safe given increased morbidity and mortality associated with prolonged mechanical ventilation use (e.g., ventilator-associated pneumonia).
2. Timing of initiation of mechanical ventilation
The timing of the appropriate initiation of mechanical ventilation is dependent on the patient’s clinical trajectory and is based on the physical examination; supporting objective physiologic data, including arterial blood gas measures; and the patient’s response to therapeutic interventions to improve the physiologic derangement. The objective for the bedside clinician is to avoid the need to urgently or emergently initiate mechanical ventilation, as adverse outcomes are significantly more likely to occur in such circumstances.
3. Modes and phases of mechanical ventilation
There are two modes of mechanical ventilation: pressure pre-set and volume pre-set. Factors that affect which mode to use include:
The indication for initiating mechanical ventilation.
The patient’s respiratory mechanics.
One important distinguishing characteristic between the two modes of ventilation is that a volume pre-set mode of ventilation is a flow-invariable mode, whereas a pressure pre-set mode of ventilation is a flow-variable mode. In other words, in a volume mode, the clinician sets the flow rate for the patient, while in a pressure mode, the flow will vary depending on the patient’s mechanics and drive. When assessing the patient who is asynchronous on the ventilator, this is one important concept to bear in mind, as a failure to provide sufficient flow to meet the needs of the patient may result in asynchrony.
As described by Kapadia, ventilator terminology is complex. To simplify the terminology, Kapadia coined the terms trigger, limit and cycle and described the four-phase concept of mechanical ventilation. The four phases of ventilation are:
The transition from inspiration to expiration.
The transition from expiration to inspiration.
Trigger denotes the pre-set parameter (e.g. flow, pressure or time) which “triggers” the ventilator to initiate inspiration. The trigger signals the transition from expiration to inspiration. The limit denotes the pre-set parameter (volume or pressure) that is not to be exceeded during inspiration. And cycle denotes the pre-set parameter (e.g. flow, pressure, volume or time) that “cycles” the ventilator from inspiration to expiration.
4. Respiratory mechanics
Regardless of the mode selected, an understanding of the principles of respiratory mechanics (compliance and resistance) is essential to understanding the etiology of respiratory failure and to gauge whether the patient’s respiratory condition is improving or deteriorating.
Compliance, the inverse of elastance, is the relationship between volume and pressure (C=∆V/∆P). Compliance measures the recoil pressure of the lungs and chest wall. For reference, a normal compliance is 100 mL/cm H2O and a typical compliance in a supine, ventilated patient is 60 mL/cm H2O.
Static compliance (Cs) is measured with a square inspiratory waveform in a volume assist-control mode of ventilation and is a product of tidal volume (VT), end-inspiratory (plateau [PPL]) pressure and PEEP: CS = VT/ PPL-PEEP.
The end-inspiratory (or plateau PPL) pressure is related to static compliance through the following relationship and is measured after a 0.5 second inspiratory pause (i.e., no flow): P = VT/CS+PEEP. As the relationship dictates, as the static compliance decreases, the plateau pressure will increase. Given that the distending pressure at total lung capacity is approximately 37 cm of water and given evidence that outcomes are improved in patients with acute lung injury if PPL is maintained at less than 30 cm of water, efforts should be made to maintain the PPL at less than 30 cm of water. When the PPL is elevated, an evaluation for lung (e.g. pulmonary edema, pneumonia, atelectasis), chest wall (e.g. edema, obesity, pleural disease, abdominal compartment syndrome), or intrinsic-PEEP, or a combination thereof, is warranted.
Resistance is the relationship between pressure and flow, depicted in the equation R=∆P/flow. On volume assist-control, with a flow rate set at 60L/minute in square waveform (i.e. 1L/second), resistance is proportional to the difference between the peak inspiratory pressure and the plateau pressure (R=PPIP – PPL/1L/second). A normal resistance is less than 10 cm of water/L/second. Examples of conditions associated with an elevated resistance include: obstructive pulmonary disease (e.g. asthma, COPD) and functional obstruction of the endotracheal tube or airway (e.g. secretions, foreign body).
In sum, the airway opening pressure is a product of the resistance pressure, the elastance pressure (i.e. inverse of compliance), and PEEP, and the ability to measure each of these components serially is critical to assessing the ventilated patient.
5. Initial ventilator settings
Choosing the initial ventilator settings is a complex process that requires the clinician to synthesize data regarding the patient’s comorbid conditions (e.g. chronic obstructive pulmonary disease, congestive heart failure) and the patient’s present clinical status and cause of respiratory failure.
Using a systematic approach, the process of selecting the initial ventilator settings will ensure that the patient is appropriately oxygenated and ventilated, while simultaneously assuring that the patient is synchronous with the ventilator and avoiding the deleterious consequences of mechanical ventilation (e.g. ventilator-induced lung injury).
The initial settings selected include the:
Limit (or mode).
Minute ventilation (the product of rate and tidal volume).
Oxygenation parameters (FiO2 and mean alveolar pressure, which includes positive end-expiratory pressure [PEEP]).
Trigger (flow or pressure)
There exist two standard choices for triggering in patients capable of initiating their own breath, flow or pressure-sensing triggers.
A standard flow trigger is 1-2 liters/minute. The primary benefit of a flow trigger is that it requires less work to initiate; however, a flow trigger is susceptible to auto-triggering. For example, the cardiac oscillations of a hypovolemic patient can result in intra-thoracic pressure perturbations that are detected as patient-initiated flow (i.e. auto-triggering).
Two additional scenarios where this can have adverse consequences include: (1) concluding that a patient with a cervical spine injury has the ability to initiate a breath when they have no spontaneous respiration; and (2) development of respiratory alkalosis in a patient in septic shock who is triggering the ventilator to deliver a rate in excess of 35 breaths per minute and consequent development of dynamic hyperinflation, which exacerbates hemodynamic compromise.
As such, we recommend a pressure trigger of 1-2 centimeters of water. Ideally, the pressure-sensing site would be located in the trachea to lessen patient work-of-breathing. In modern ventilators, however, the pressure-sensing site is located within the airway circuit (the endotracheal tube or the inspiratory or expiratory limb of the circuit).
Whether a volume or pressure mode of ventilation is chosen is clinician-specific and without clear evidence that one mode is superior to another. In reality, as demonstrated in the 2000 cross-sectional international study by Esteban et al, both modes are commonly used.
See Table 1.
The two chief volume pre-set modes of mechanical ventilation are assist-control and synchronized intermittent mandatory ventilation (SIMV). In volume assist-control ventilation, the spontaneously breathing patient will trigger a ventilator-delivered pre-set tidal volume. The limit of the breath is set by the clinician; nevertheless, the presence of a demand valve permits the tidal volume to exceed the limit if so demanded by the patient. Inspiration ceases, as does the breath cycle, once the tidal volume limit has been exceeded.
The airway pressure is dependent on the patient’s mechanics (e.g. compliance). As a volume pre-set mode of ventilation, it is a flow-invariable mode in that the flow can not exceed the set flow rate. The inspiratory time is a by-product of the set flow rate, respiratory rate and tidal volume.
SIMV is a dual mode of ventilation capable of providing graded levels of support. Similar to assist-control, SIMV delivers a pre-set tidal volume when the ventilator detects the patient triggering a breath during the synchronization interval, an interval dependent on the specified respiratory rate. Between synchronized breaths, spontaneous breaths are supported at a specified level of pressure support.
Pressure-control ventilation (PCV) is a pressure pre-set mode of ventilation. The trigger options are flow, pressure or time. The limit is the sum of the set inspiratory pressure and PEEP. The tidal volume delivered is dependent on the patient’s mechanics. The breath cycles based on the set inspiratory time (or set inspiratory to expiratory ratio, I:E) and respiratory rate.
The clinician needs to be cognizant that the I:E and respiratory rate permit expiratory flow to cease. If expiratory flow is present at the time that the breath cycles, dynamic hyperinflation gradually develops as intrinsic PEEP increases. As a new functional residual capacity is set with each stacked breath, the patient is at increased risk for hypotension secondary to decreased pre-load and increased afterload, barotrauma, and increased work of breathing as the pressure trigger threshold is raised as a result of intrinsic PEEP.
Pressure support ventilation (PSV) is a mode that permits the spontaneously breathing patient to trigger a supported breath to a pre-set pressure limit. As with PCV, volume is dependent on the patient’s mechanics, their effort, and the duration of inspiratory flow. The breath cycles at the pre-set proportion of the terminal peak expiratory flow rate (TPEFR). The expiratory sensitivity is commonly set at 25% of the TPEFR. While evidence supports that PSV is a more comfortable mode of ventilation, there is no evidence that outcomes are improved by the use of one mode of ventilation compared to another.
Biphasic intermittent positive airway pressure (BiPAP) and airway pressure release ventilation (APRV) are two advanced pressure pre-set modes of ventilation which permit spontaneous respirations in the non-paralyzed patient through the use of an open circuit during the extended inspiratory time interval. Oxygenation is improved through recruitment achieved through higher mean alveolar pressures via the sustained inspiratory time. The proposed advantage of permitting spontaneous respirations include patient comfort, improved gas exchange and improved cardiac output; nevertheless, improvement in survival has not been demonstrated with either of these modes.
Regardless of the mode chosen, clinicians need to be mindful of the importance of minimizing ventilator-induced lung injury by limiting both pressure and volume. The physiologic rationale for what are injurious volumes and pressures stems from the observation that spontaneous tidal volume is approximately 5 mL/kg predicted body weight and the observation that the distending pressure at total lung capacity is 37 cm of water.
Based on the physiologic principle that ventilator-set volumes and pressures should approximate normal physiologic conditions, several randomized controlled trials of patients with acute lung injury and acute respiratory distress syndrome (ALI/ARDS) compared the outcomes of patients receiving lung-protective ventilation strategies to patients receiving higher volumes (and pressures). The tidal volume and mean plateau (end-inspiratory) pressure differences achieved differed by study, with the three studies (including the largest ARDSNet trial) achieving the greatest differences finding a mortality benefit in patients randomized to a lung protective ventilation strategy.
As such, the general consensus is to use a lung protective ventilation strategy in patients with severe, hypoxemic respiratory failure (e.g., ALI/ARDS), to consider its use in patients at risk of developing ALI, and to avoid injurious high volumes and high pressures in all patients managed on a mechanical ventilator.
A primary goal of mechanical ventilation is to ensure oxygenation. In patients with evidence of acute, hypoxemic respiratory failure, adequate oxygenation is ensured through the placement of an endotracheal tube through which an appropriate fraction of inspired oxygen (FiO2) is delivered at an appropriate mean alveolar pressure. The mean alveolar pressure is a product of the inspiratory time and pressure (or tidal volume in volume mode of ventilation) and the end-expiratory time and pressure. An equally important goal is to minimize oxygen toxicity.
As such, the general recommendation is to maintain oxyhemoglobin saturation at or greater than 90%, which correlates with a partial pressure of arterial oxygen (PaO2) goal of at least 60 mm Hg. This strategy serves to avoid the steep portion of the oxyhemoglobin dissociation curve, where a shift to the left would result in a linear decline in saturation.
The pathophysiologic rationale for avoiding oxygen toxicity dates to a number of animal studies in the mid-20th century in which animals were exposed to 100% FiO2 and, upon necropsy, were observed to have hyaline membranes consistent with ARDS, and to human experimental data in which healthy volunteers exposed to high oxygen concentrations for 24 hours developed pulmonary edema and were observed to have decreased vital capacity. The proposed pathophysiologic mechanism is one of injury induced by free radical formation.
Positive end-expiratory pressure (PEEP)
Despite multiple trials to determine the optimal level of PEEP, it is unclear what the optimal level is. As Esteban demonstrated in the 2000 international study of ventilator use, PEEP levels employed are relatively modest, with a median PEEP of 5 and an interquartile range of 5-6. Several recent trials tested the theory that an open-lung approach, including recruitment maneuvers (e.g. 40 cm of water pressure for 40 seconds), would improve outcomes.
The physiologic rationale for the use of recruitment maneuvers is that high levels of PEEP do not recruit the lung, but rather maintain recruitment achieved through increased mean alveolar pressure. All three recent trials failed to achieve a mortality benefit; however, oxygenation was consistently improved in the higher PEEP groups and a higher PEEP strategy (with or without recruitment maneuvers) appeared to be safe.
A reasonable initial inspiratory flow is 60 liters/minute. It is important to recognize that in certain disease states, such as in patients with septic shock, the flow demand can exceed 80-100 liters/minute. The optimal flow waveform (square-wave vs. decelerating ramp) is controversial and often patient-specific. Importantly, a square-wave ramp is required to measure respiratory mechanics.
An important and often unrecognized phenomenon is that as flow is increased (e.g. in the asynchronous patient), the respiratory rate increases. For example, an increase from 60 to 90 liters per minute was associated with an increase respiratory rate of 41% in an experimental trial. This effect on respiratory frequency is due to the effect that changes in flow have on ventilator inspiratory time. It is important to recognize that the expiratory time may be shortened as respiratory rate increases, and intrinsic PEEP may develop as a result.
In the spontaneously breathing, physiologic state, the I:E approximates 1:2. In patients with chronic obstructive pulmonary disease, the expiratory time is prolonged so as to permit return to functional residual capacity; as a result, the I:E can exceed 1:5 and the clinician needs to be cognizant of the potential for intrinsic PEEP to develop if the patient is tachypneic or when the inspiratory time is set too long. In hypoxemic patients, the inspiratory time may be lengthened to optimize mean alveolar pressure so as to “recruit” the lung, with the resultant risk of intrinsic PEEP as previously discussed. This practice is known as “inverse ratio ventilation.”
The I:E can be set directly or indirectly by selecting the inspiratory time (in conjunction with the respiratory rate), given the relationship between inspiratory time, tidal volume, flow and rate. For example, at a tidal volume of 1 liter, and an inspiratory rate of 60 liters/minute (or 1 liter/second), the inspiratory time is 1 second. In a patient breathing 20 times per minute, the I:E = 1:2.
The respiratory rate is guided by the patient’s innate minute ventilation requirements and their physiologic state, which is ascertained through an assessment of the patient’s physiologic data (e.g. respiratory mechanics, arterial blood gas measures). Minute ventilation is a product of tidal volume and respiratory rate. The respiratory rate should be set slightly lower than the pre-intubation respiratory rate; failure to approximate the set respiratory rate to the patient’s required respiratory rate could result in an acute decompensation should the patient’s drive to breathe be abolished through pharmacologic means (e.g. sedation).
In summary, a reasonable starting point for the initial ventilator settings are as suggested by Lanken et al:
Trigger (pressure with set sensitivity of -2 cm of water).
Limit (volume-limited assist control ventilatory mode).
Cycle (adjusted to maintain adequate minute ventilation for the specific patient).
Tidal volume (selected to minimize volutrauma and barotrauma).
FiO2 (1.00 initially and then titrated down over the next several hours to the level that maintains oxyhemoglobin saturation >=90-92%).
Inspiratory flow (60 liters/minute and titrated to patient’s needs/comfort).
Inspiratory time (1:2 ration and then titrated to optimize oxygenation and ventilation).
Respiratory rate (slightly below the pre-intubation rate).
Special considerations for nursing and allied health professionals.
What's the evidence?
Hall, Schmidt, Wood. Principles of Critical Care. (An authoritative reference on the pathophysiology of respiratory failure and mechanical ventilation.)
Esteban, A, Anzueto, A, Alia, I. “How is mechanical ventilation employed in the Intensive Care Unit?”. Am J Respir Crit Care Med. vol. 161. 2000. pp. 1450-8. (An international point prevalence study that provides a snapshot of how MV is employed.)
Esteban, A, Anzueto, A, Frutos, F. “Characteristics and outcomes in adult patients receiving mechanical ventilation: A 28-day international study”. JAMA. vol. 287. 2002. pp. 345-55.
Kapadia, F. “Mechanical ventilation: simplifying the terminology”. Postgrad Med. vol. 74. 1998. pp. 330-5. (A basic review of MV.)
“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. vol. 342. 2000. pp. 1301-8. (The landmark study that proved the survival benefit with lung protective ventilation using low tidal volumes and constrained inspiratory pressures.)
Hager, DN, Krishnan, JA, Hayden, DL. “Tidal volume reduction in patients with acute lung injury when plateau pressures are not high”. Am J Respir Crit Care Med. vol. 172. 2005. pp. 1241-5. (Re-analysis of the ARMA trial [above] that provides support for the notion that it is important to keep tidal volume at 6 ml/kg PBW even if the plateau pressure is low.)
Imanaka, H, Nishimura, M, Takeuchi, M, Kimball, WR, Yahagi, N. “Autotriggering caused by cardiogenic oscillation during flow-triggered mechanical ventilation”. Crit Care Med. vol. 28. 2000. pp. 402-7. (An interesting description of how cardiac motion can trigger the ventilator.)
Tobin, MJ, Lodato, RF. “PEEP, auto-PEEP, and waterfalls”. Chest. vol. 96. 1989. pp. 449-51. (A wonderful editorial commentary about PEEP using the waterfall analogy.)
Girault, C, Leroy, J, Bonmarchand, G. “Comparative physiologic effects of noninvasive assist-control and pressure support ventilation in acute hypercapnic respiratory failure”. Chest. vol. 111. 1997. pp. 1639-48.
Groeger, JS, Levinson, MR, Carlon, GC. “Assist control versus synchronized intermittent mandatory ventilation during acute respiratory failure”. Crit Care Med. vol. 17. 1989. pp. 607-12.
Chiumello, D, Pelosi, P, Calvi, E. “Different modes of assisted ventilation in patients with acute respiratory failure”. Eur Respir J. vol. 20. 2002. pp. 925-33.
Seymour, CW, Frazer, M, Reilly, PM. “Airway pressure release and biphasic intermittent positive pressure ventilation: are they ready for prime time?”. J Trauma. vol. 62. 2007. pp. 1298-309. (A nice review of this poorly understood mode of MV for ARDS.)
Gajic, O, Dara, SI, Mendez, JL. “Ventilator-associated lung injury in patients without acute lung injury at the onset of mechanical ventilation”. Crit Care Med. vol. 32. 2004. pp. 1817-24.
Nash, G, Bowen, JA, Langlinais, PC. “Respirator lung: a misnomer”. Arch Path. vol. 21. 1971. pp. 234-40.
Comroe, JH, Dripps, RD, Dumke, PR. “Oxygen toxicity: the effect of inhalation of high concentrations of oxygen for twenty-four hours on normal mean at sea level and at a simulated altitude of 18,000 feet”. JAMA. vol. 128. 1945. pp. 710-7. (One of the first demonstrations in man showing that high concentrations of oxygen can cause biologic derangements in the human lung.)
Pelosi, P, Goldner, M, McKibben, A. vol. 164. 2001. pp. 122-30.
“Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome”. vol. 351. 2004. pp. 327-36. (A follow up study to the ARMA trial that failed to show any benefit to using a high PEEP ventilation strategy, set by an adjusted FiO2/PEEP table.)
Mercat, A, Richard, JCM, Vielle, B. “Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome”. JAMA. vol. 299. 2008. pp. 646-55.
Meade, MO, Cook, DJ, Guyatt, GH. “Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome”. JAMA. vol. 299. 2008. pp. 637-45.
Corne, S, Gillespie, D, Roberts, D. “Effect of inspiratory flow rate on respiratory rate in intubated ventilated patients”. Am J Respir Crit Care Med. vol. 156. 1997. pp. 304-8. (Study showing that increasing inspiratory flow rate can increase respiratory rate in MV subjects.)
Laghi, F, Karamchandani, K, Tobin, MJ. “Influence of ventilator settings in determining respiratory frequency during mechanical ventilation”. Am J Respir Crit Care Med. vol. 160. 1999. pp. 1766-70.
Tharratt, RS, Allen, RP, Albertson, TE. “Pressure control inverse ratio ventilation in severe adult respiratory failure”. Chest. vol. 94. 1988. pp. 755-62. (This manuscript describes the mode and its theoretical benefits.)
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- 1. Description of the problem
- 2. Emergency Management
- 3. Diagnosis
- Special considerations for nursing and allied health professionals.
- What's the evidence?