- •
Respiratory failure is a frequent disease process encountered in the emergency department.
- •
There is significant need for improvement in the care of patients on mechanical ventilation. If not contraindicated, lung-protective ventilation strategies should be used.
- •
Patient specific disease pathophysiology is important to consider when treating patients that are difficult to oxygenate, ventilate or when Pao2, Paco2, and/or pH can only be maintained at unsafe ventilator settings.
Lung-protective Ventilation Strategies and Adjunctive Treatments for the Emergency Medicine Patient with Acute Respiratory Failure
Section snippets
Key points
Epidemiology/statement of the problem
Acute respiratory failure (ARF) requiring MV is a common clinical scenario. Wunsch and colleagues1 suggested that approximately 3% of all hospital admissions in the United States require invasive MV. MV costs approximately $27 billion dollars nationally.1 Nearly one-third of patients who are placed on MV die in the hospital and among survivors only 30% are discharged home after their admission.1 Recent data suggest opportunities for improvement because many patients in the ED and intensive care
Pathophysiology
Breathing is essential for homeostasis. In critically ill patients the demands for oxygen supply and carbon dioxide removal are often increased. This increased demand can be superimposed on prior impaired cardiopulmonary reserve. In ARF the cardiopulmonary system fails to oxygenate or ventilate adequately or inefficient breathing mechanics put excessive loads on the cardiopulmonary system. MV is used to offload respiratory muscle work and assist in oxygen delivery and ventilation.
Oxygenation and hyperoxia
Most oxygen is carried by hemoglobin molecules in red blood cells. MV is often used to correct hypoxemia (low oxygen saturation) to improve total blood oxygen content. In emergent situations it is beneficial to increase the fraction of inspired oxygen (Fio2) to increase blood oxygen content. Increased Fio2 should only be considered as a temporary fix because there are downsides to high concentrations of Fio2.
First, in patients with normal lungs, supernormal Fio2 concentrations lead to hyperoxia
Oxygen delivery and heart-lung interactions
Placing a critically ill patient on MV can have serious untoward effects on cardiac output (CO) and oxygen delivery and can lead to adverse events if not appropriately anticipated and managed proactively.11 In conditions associated with high afterload, MV can be beneficial by decreasing the force opposing left ventricular contraction and left ventricular transmural wall pressure.11 In preload-dependent states (hypovolemic and distributive shock) and diseases with right ventricular (RV)
Hypoxemia
Hypoxemia is low arterial oxygen saturation. There are multiple physiologic mechanisms for hypoxemia: hypoventilation (airway obstruction or sedative overdose), low Fio2 or low partial pressure of O2 (high altitude), diffusion-limited processes (interstitial lung disease), ventilation/blood flow (V/Q) mismatch (COPD), shunt (pulmonary edema), and low venous oxygen content (shock).14 During MV, persistent hypoxemia can usually be attributed to a combination of shunt physiology and low venous
Ventilation and hypercapnea
Effective MV must provide for adequate CO2 excretion and O2 saturation while not exposing the patient to excessive airway pressures (barotrauma) or tidal volumes (Tv) (volutrauma). The clearance of CO2 depends on the relationship between CO2 production and alveolar ventilation (Va)17:Paco2 ≈ (CO2 production)/(Va).Va = minute ventilation (Vm) − Dead space ventilation (Vds).
The typical MV adjustment to hypercarbia is to increase the Vm by increasing the respiratory rate (RR) or Tv. In most
ARDS and lung-protective ventilation
ARDS was first described by Ashbaugh and colleagues19 in 1967. They described 12 patients with a diffuse alveolar infiltrative chest radiograph pattern that manifested acute onset of tachypnea, hypoxemia, and cyanosis that was refractory to oxygen therapy. ARDS was defined in 1994,20 and this definition was revised in 2012 (the Berlin definition21) to address some limitations of the earlier definition. The major changes and new ARDS criteria are as follows:
- 1.
The term acute lung injury was
Selection of optimal tidal volume
The mainstays of LPVS are to (1) limit tidal volume; (2) limit end-inspiratory plateau pressure (Pplat); (3) provide adequate PEEP to keep the lung open and prevent alveolar collapse, and (4) limit Fio2.30
The optimal Tv for patients without ARDS who require MV is not known.30, 31, 32 Animal data suggest that normal Tv for mammals is 6.3 mL/kg.33 Data from ARDSNet25 as well as multiple additional trials27, 28, 29 suggest that Tv greater than 10 mL/kg IBW is harmful. Lellouche and colleagues27
Limiting inspiratory Pplat
An additional goal of LPVS is to limit airway pressure to avoid barotrauma. The inspiratory hold or Pplat estimates the pressure distending the alveolus. This maneuver is done by pausing the flow of air at the end of inspiration. There is no definitive safe Pplat.34 In ARDS, the goal should be a Pplat less than 30 cm H2O.25 Hager and colleagues,34 in their analysis of the ARDSNet data, saw improved outcomes with lower Pplat values. Whether this was causal or coincidental and whether a lower P
Selection of optimal PEEP and open lung recruitment
As stated earlier, most oxygenation problems that occur on MV are secondary to shunt physiology. Shunts are caused by pulmonary (pneumonia, pulmonary contusion, pulmonary edema, and so forth) or cardiac (patent foramen oval, atrial or ventricular septal defects) causes.
The typical treatment of hypoxemia from pulmonary shunts is to attempt to recruit collapsed lung units by increasing PEEP. The optimal PEEP settings, or even the best method to go about choosing PEEP, are controversial.35, 36 To
Adjunctive maneuvers
Multiple new and promising developments that focus on non-MV adjunctive treatment measures for patients with refractory ARDS and respiratory failure have recently been developed. These treatments may find a role in the EM management of ARDS and severe respiratory failure. Further information on each can be found in references.38, 42, 43
Neuromuscular blocking agents
Neuromuscular blocking agents (NMBAs) are used in patients with severe respiratory failure to facilitate ventilator synchrony.44 A patient who is bucking the ventilator can be exposed to barotrauma, volutrauma from breath stacking, and other serious complications (eg, tube dislodgment). NMBAs have been used to facilitate ventilator synchrony and are associated with improvements in P/F ratio.31 The rational for this benefit is not fully clear because NMBAs seem to help even in patients who do
Inhaled pulmonary vasodilators
Inhaled nitric oxide (INO) and inhaled prostacyclin (IP) are the inhaled pulmonary vasodilators (IPVs) currently used for salvage therapy in refractory hypoxemia. The reader is encouraged to read a more in-depth review from the clinics series.46 IPVs work by improving blood flow to ventilated lung units and decreasing shunt magnitude. In many cases this leads to an improvement, albeit transient (24–96 hours), in oxygenation.42, 43, 46
In addition to better V/Q matching, IPV may be beneficial in
Prone positioning
Prone positioning (PP) involves rotating the patient from the standard supine position to a face-down or prone position. When supine, the inferior and posterior portions of the lung can become atelectatic from compression by the heart, thorax, and diaphragm. Atelectasis can worsen gas exchange, decrease compliance, and increase the risk for volutrauma because the Tv prescribed is now directed to a smaller lung volume. PP in some individuals allows reexpansion of these posterior lung units.
Extracorporeal membrane oxygenation
The use of venovenous extracorporeal membrane oxygenation (ECMO) in severe ARDS and refractory hypercarbic respiratory failure has gained renewed interest after recent encouraging data from the United Kingdom56 and from experience with ARDS during the 2009 H1N1 pandemic.57 Work from the late twentieth century showed dismal survival23 and no benefit in patients with ARDS treated with ECMO58 but improvements in technology have made this a potential modality for severe ARDS.
ECMO has risks and
Summary
Respiratory failure is a frequent disease process encountered in the ED. Better care can lead to better outcomes for patients on MV.61 If not contraindicated, LPVS should be used. It is important to consider disease pathophysiology when formulating treatment strategies in patients that are difficult to oxygenate or ventilate, or when Pao2, PaCo2, and pH can only be maintained with unsafe ventilator settings. If MV adjustments do not produce the expected clinical outcome then different treatment
References (61)
- et al.
Balancing the risks and benefits of oxygen therapy in critically III adults
Chest
(2013) - et al.
Rising Paco2 in the ICU: using a physiologic approach to avoid cognitive biases
Chest
(2011) - et al.
Acute respiratory distress in adults
Lancet
(1967) - et al.
Low tidal volume ventilation should be the routine ventilation strategy of choice for all emergency department patients
Ann Emerg Med
(2012) - et al.
Low tidal volume should not routinely by used for emergency department patients requiring mechanical ventilation
Ann Emerg Med
(2012) - et al.
Chest
(2012) Counterpoint: should positive end-expiratory pressure in patients with ARDS be set based on oxygenation? No
Chest
(2012)- et al.
Severe hypoxemic respiratory failure part 1–ventilatory strategies
Chest
(2010) - et al.
Severe hypoxemic respiratory failure part 2—nonventilatory strategies
Chest
(2010) - et al.
Inhaled nitric oxide and inhaled prostacyclin in acute respiratory distress syndrome: what is the evidence?
Crit Care Clin
(2011)
Dose-response to inhaled aerosolized prostacyclin for hypoxemia due to ARDS
Chest
Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial
Lancet
The epidemiology of mechanical ventilation use in the United States
Crit Care Med
Mechanical ventilation and acute lung injury in emergency department patients with severe sepsis and septic shock: an observational study
Acad Emerg Med
Mechanical ventilation in the emergency department: a call to action in a resource-constrained era
Acad Emerg Med
Association between early hyperoxia and worse outcomes after traumatic brain injury
Arch Surg
Pulmonary oxygen toxicity: early reversible changes in human alveolar structures induced by hyperoxia
N Engl J Med
Development of fine structural damage to alveolar and capillary lining cells in oxygen-poisoned rat lungs
J Cell Biol
Hyperoxia increases H2O2 production by brain in vivo
J Appl Physiol (1985)
Association between hyperoxia and mortality after stroke: a multicenter cohort study
Crit Care Med
Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality
JAMA
Emergency oxygen use
BMJ
Interactions between respiration and systemic hemodynamics. Part II: practical implications in critical care
Intensive Care Med
The role of venous return in critical illness and shock—part I: physiology
Crit Care Med
Role of the venous return in critical illness and shock: part II—shock and mechanical ventilation
Crit Care Med
Pulmonary pathophysiology, the essentials
Hypoxemia due to increased venous admixture: influence of cardiac output on oxygenation
Predicting dead space ventilation in critically ill patients using clinically available data
Crit Care Med
The American-European Consensus Conference on ARDS: definitions, mechanisms, relevant outcomes, and clinical trial coordination
Am J Respir Crit Care Med
Acute respiratory distress syndrome
JAMA
Cited by (0)
Disclosure: None.