Strategies for managing frequently encountered respiratory physiology.
Emergency physicians must be prepared to manage the ventilator in patients with challenging pulmonary physiology. As discussed in parts one and two, keeping Vt (tidal volume) < 6-8 mL/kg, plateau pressure ≤ 30 cm H2O, and rapidly decreasing the FiO2 to prevent the harmful effects of hyperoxia will reduce mortality in intubated patients. This article discusses the strategies of managing challenging, but frequently encountered respiratory physiology such as those with severe obstructive lung disease, stiff lungs (i.e. ARDS), refractory hypoxemia and those with a severe metabolic acidosis.
Obstructive Lung Disease
Asthma and obstructive lung disease in extremis can be frightening to both patients and providers. While many of these patients can be managed successfully with non-invasive bi-level positive pressure ventilation (Ward 2008), some will require intubation and a thoughtful approach to mechanical ventilation. These patients are often profoundly acidotic, stimulating them to breathe rapidly, while their obstructive physiology causes incomplete emptying on exhalation. Together this results in air-trapping, which is seen in the expiratory flow in Figure 1.
High peak pressures (representing proximal airway obstruction, as seen in Figure 2) incomplete expiratory flow and elevated auto-PEEP are the classic ventilator findings of the sick obstructive patient.
Auto-PEEP is measured through performing an expiratory hold to measure end expiratory pressure, here seen as a total PEEP of 16. The PEEP of 16 is a measurement of the entire lung, both large and small airways. The distal, smaller airways are likely closing and “trapping” much higher pressures in the alveoli, which increases your patients’ risk for pneumothorax and barotrauma (Hess 2014). With this total PEEP of 16, the ventilator has been set to deliver a PEEP of 5, which means there is 11 cm H2O of auto-PEEP. Patients with COPD have low levels of auto-PEEP at baseline due to chronic hyperinflation, and usually this is well tolerated. However, with a COPD or asthma, exacerbation can cause auto-PEEP to become dangerously elevated, increasing the risk for barotrauma and decreasing cardiac output, and can result in hypotension and hemodynamic collapse.
When we take care of these patients in the ED or ICU we remember three guiding principles:
- Slow respiratory rate
- Tolerate hypercarbia
- Check for air-trapping
Slow Respiratory Rate: We recommend starting with a tidal volume of 8 mL/kg ideal body weight and a respiratory rate of approximately 10-14 breaths per minute. Many reviews discuss I:E ratios, but we prefer to think about absolute emptying time. The best way to increase the absolute emptying time is to reduce the respiratory rate rather than decreasing the inspiratory time. Decreasing the inspiratory time will increase the peak airway pressures and is not as effective in increasing the emptying time as reducing the respiratory rate. A rate less than 10 does not typically offer additional benefit because of the gas trapped behind occluded airways (Leatherman 2015).
Tolerate Hypercarbia: Respiratory acidosis and hypercarbia are a reflection of increased dead space caused by air trapping and alveolar distention. A pure respiratory acidosis with a pH >7.2 is generally considered safe assuming there is not concomitant severe pulmonary hypertension (Davidson 2016, Leatherman 2015.) While many clinicians will attempt to correct this acidosis through increasing the respiratory rate, this is counterproductive and can be harmful because it will lead to more air trapping and alveolar distention. If the respiratory acidosis is causing systemic effects, we recommend increasing the Vt (even above 8 mL/kg in extreme cases) while keeping a low respiratory rate to maximize alveolar ventilation while preventing air-trapping. The hypercarbia may take days in the ICU to correct, and generally hypercarbia does not kill patients. Hypotension caused by air-trapping and dynamic hyperinflation does.
Check for Air-Trapping: This is done by ensuring the expiratory flow limb of the flow curve reaches zero before a new breath, and by performing an end expiratory hold in a passively breathing patient to assess for auto-PEEP. If you detect a high auto-PEEP (i.e. >5 cm H2O), reduce the respiratory rate. If hypotension is associated with a high auto-PEEP, unplug the patient from the ventilator for 15-20 seconds and then reduce the respiratory rate. See top figure.
Hypoxemia and ARDS
It can be difficult to determine the source of hypoxia in the emergency department, and a large part of the ICU course is often continued work up of the underlying condition. A chest x-ray can provide an avenue to determine appropriate treatment by allowing you to categorize hypoxemic patients into those with unilateral lung disease and those with bilateral lung disease.
Unilateral Lung Disease: In the setting of profound hypoxia affecting one lung, such as seen in a unilateral pneumonia, we recommend low tidal volume ventilation. The functional healthy lung has better compliance than the stiff, affected lung and so is at risk for overdistension and volutrauma as it will be receiving a disproportionate amount of the delivered volume. Additionally, when hypoxia is severe we recommend positioning the patient in the lateral decubitus position with the “good” (unaffected) lung down, as this will increase perfusion to the lower lung fields and decrease intrapulmonary shunt, increasing overall oxygenation (Dhainaut 1980).
Bilateral Lung Disease: Hypoxemia with bilateral lung disease should make you think of ARDS. While you will likely not be able to exclude cardiogenic sources of bilateral infiltrates while in the ER, treating the patient as though they have ARDS will still appropriately support those patients that have cardiogenic edema, while providing benefit to those patients that have ARDS. The Berlin criteria that defines ARDS include: onset within one week of an insult; bilateral opacities on chest imaging; respiratory failure not fully explained by cardiac failure or volume overload; and PaO2/FiO2 < 300 mm Hg with PEEP > 5 cm H2O. ARDS is classified by PaO2:FiO2 ratio (P:F) with 200-300 mild, 100-200 moderate, and ≤ 100 severe (JAMA 2012). It is important to think in terms of the P:F ratio because a normal PaO2 can be falsely reassuring. If your patient has a PaO2 of 80 mm Hg while receiving 100% FiO2, the P:F is 80 meeting criteria for severe ARDS. Once ARDS is recognized it can be treated.
The mainstays of ARDS treatment are low Vt ventilation, appropriately higher PEEP, early paralysis, proning and avoidance of hyperoxia. These methods help protect healthy alveoli from barotrauma (injurious high pressures), atelectrauma (injury from opening and closing of alveoli during each breath), and volutrauma (overdistension and stress due to increased volumes). Low Vt ventilation means starting at 6 mL/kg ideal body weight and using plateau pressures to guide titration. If the plateau pressure is above 30 cm H2O the Vt should be incrementally decreased by 1 mL/kg as low as 4 mL/kg (Weingart) (see bottom figure). These protective, low volumes may lead to hypercapnia but a pH of > 7.20 can be tolerated. Most patients with stiff lungs can easily tolerate a respiratory rate of 30-35 without air trapping (Weingart 2016). Hyperoxia is harmful and should be avoided (Massimo 2016, Page 2018), and in ARDS we target an oxygen saturation of 88-95% or PaO2 of 55-80 mm Hg (ARDSnet 2000).
Setting appropriate PEEP can be beneficial to your patients by improving oxygenation through recruiting additional lung, increasing the surface area for gas exchange, redistribution of lung water, and preventing atelectrauma. It should be noted that PEEP does not help everyone- it may worsen oxygenation in about 30% of those with acute lung injury (Tobin 2001). This happens because of overdistension of the healthy, compliant alveoli that are fewer in the diseased lung. PEEP titration techniques include using the driving pressure or using a PEEP table to determine optimal PEEP for your patient. In the ED we favor titrating PEEP based on the ARDSNET PEEP/FiO2 tables (ARDSnet 2000), which can be seen in Table 1 (ARDSnet 2000).
Uptitrate by increments of 2 cm H2O every 15 to 30 minutes until you reach your target based on the PEEP table while watching for any negative effects such as hemodynamic deteriorations or worsening oxygenation.
In those with severe hypoxemia and criteria for severe ARDS we also consider prone positioning and neuromuscular blockade. Neuromuscular blockade and proning have both shown to improve mortality in those with a PaO2:FiO2 ratio < 150 when initiated within the first few days of treatment (Alhazzani 2013, Guerin 2013). Although proning may be difficult in the ED, neuromuscular blockade with adequate sedation would be reasonable in the challenging, severely hypoxemic patients after discussion with the accepting ICU team.
When your patient has high plateau pressure and persistent hypoxemia despite appropriately high PEEP, low Vt and neuromuscular blockade ask for help from your intensivist colleagues and consider sending to a center with ECMO capabilities.
Mechanical Ventilation in Severe Metabolic Acidosis
Metabolic acidosis, as seen with DKA and salicylate toxicity, is a significant stimulus for tachypnea and a high minute ventilation. The patient is compensating for their acidosis by blowing off their CO2. The post intubation time is dangerous! During this time the patient is still paralyzed and sedated, not allowing them to compensate by breathing rapidly themselves. Do your best to match the patient’s pre-intubation minute ventilation through giving the patient appropriate volumes (starting at 8 mL/kg) and a respiratory rate like that of their pre-intubation. They will require a repeat blood gas shortly after intubation, to ensure that you are adequately ventilating and not allowing worsening of their underlying acidosis. Once the paralytic has worn off some patients may be most comfortable setting their own respiratory rate in a pressure support mode. Others may require deep sedation to allow for synchrony with a set rapid respiratory rate and a safe Vt ~ 8 mL/kg. With a faster set rate watch for air trapping in the flow waveform and avoid breath stacking.
Providing excellent care to intubated patients in the ED will save lives. When taking care of obstructive lung disease remember three principles: slow respiratory rate, tolerate hypercarbia, and check for air-trapping. These patients will need to be adequately sedated and potentially paralyzed for ventilator compliance. When taking care of hypoxemic patients, first identify if it is a unilateral or bilateral process. Refractory hypoxemia in the setting of unilateral disease should be treated with low Vt ventilation and positioning with the “good lung” down to decrease the intrapulmonary shunt. Hypoxemia in a patient with a bilateral process should alert you to the possibility of ARDS and cue you to initiate low Vt ventilation in the ED, increase PEEP according to the ARDSnet tables, and provide appropriate sedation and sometimes paralysis to improve vent synchrony. In ventilating patients with profound metabolic acidosis try to match their pre- and post-intubation minute ventilation and check a blood gas soon after intubation. Finally, as we stated in parts I and II, all patients will benefit from keeping Vt < 6-8 mL/kg, plateau pressure ≤ 30 cm H2O, and rapidly decreasing the FiO2 to prevent the harmful effects of hyperoxia.
1.Hess, D. Respiratory Mechanics in Mechanically Ventilated Patients. Respiratory Care Nov 2014 59:11
2. Davidson C et al. BTS/ICS guideline for the ventilatory management of acute hypercapnic respiratory failure in adults. Thorax 2016;71:ii1–ii35. doi:10.1136/thoraxjnl-2015-208209
3. Weingart, S. Managing Initial Mechanical Ventilation in the Emergency Department. Ann Emerg Med. 2016; 68:614-617.
4. Ward, NS and Dushay, KM. Clinical concise review: Mechanical ventilation of patients with chronic obstructive pulmonary disease Crit Care Med 2008; 36:1614–1619)
5. The ARDS Definition Task Force. Acute Respiratory Distress Syndrome: The Berlin Definition. JAMA. 2012;307(23):2526-2533. doi:10.1001/jama.2012.5669
6. Fuller BM, Mohr NM, Skrupky L, Fowler S, Kollef MH, Carpenter CR. The use of inhaled prostaglandins in patients with ARDS: A systemic review and meta-analysis. Chest. 2015;147(6):1510-1522.
7. Alhazzani et al. Neuromuscular blocking agents in acute respiratory distress syndrome: a systematic review and meta-analysis of randomized controlled trials. Crit Care. 2013;17(2):R43.
8. Guerin et al. Prone positioning in severe acute respiratory distress syndrome. N Engl J Med. 2013;368:2159-2168.
9. Dhainaut JF, Bons J, Bricard C, Monsallier JF. Improved oxygenation in patients with extensive unilateral pneumonia using the lateral decubitus position. Thorax. 1980;35:792-793.
10. The ARDS Network. Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome. N Engl J Med 2000; 342:1301-8.
11. Massimo Girardis et al. Effect of Conservative vs Conventional Oxygen Therapy on Mortality Among Patients in an Intensive Care Unit: The Oxygen-ICU Randomized Clinical Trial. JAMA. 2016; 316(15):1583-1589
12. Page et al. Emergency Department Hyperoxia Is Associated with an Increased Mortality in Mechanically Ventilated Patients: A Cohort Study. Critical Care (2018) 22:9
13. Leatherman J. Mechanical ventilation for severe asthma. Chest. 2015 Jun;147(6):1671-1680.