Critical Care in the ED: Mechanical Ventilation, Sepsis, Neurological Hypertensive Emergencies, and Pressors in Shock
The tremendous overlap between the specialties of emergency medicine and critical care medicine is particularly apparent in the initial resuscitation of critically ill patients—a vulnerable population in which the early period of care has significant impact on outcomes.
Positive End-Expiratory Pressure. Previous recommendations for ventilation in respiratory failure called for large TVs (ie, 10 to 15 mL/kg), partly out of concern that smaller volumes would promote distal airway collapse, thereby increasing the amount of lung that received blood but not air, consequently worsening overall oxygenation.11 Although administering such large volumes has clearly proved harmful, the valid concern about distal airway collapse can be addressed in part by adjustments to PEEP, which acts to “stent” open airways after most of the tidal breath has left the airways.
Positive end-expiratory pressure, however, is not without risks.12 Blood from the rest of the body will encounter resistance returning to a thoracic cavity persistently inflated by positive pressure, and this decrease in preload may contribute to hypotension. Similarly, a weak right ventricle may struggle to push blood into the compressed pulmonary vasculature, increasing the cardiac workload and further compromising hemodynamics.13 In general, PEEP should be set as low as the maintenance of adequate oxygenation permits. The NHLBI ARDS guidelines provide a table on balancing PEEP and the fraction of inspired O2 (FiO2), as well as hypotension, in refractory hypoxemic patients—with the limitation on PEEP set by the patients’ pulmonary compliance (plateau pressures, discussed next).8
After making these selections, several parameters must be monitored closely. Those most relevant to lung-protective ventilation are the peak airway pressure and, most importantly, the plateau pressure. Numerous animal studies now demonstrate serious lung injury in both healthy and diseased lungs from high peak pressures (defined as a plateau pressure >30 cm water [H2O]).14,15 A high-pressure alarm sounding on the ventilator must be promptly addressed by an evaluation for easily reversible causes, such as tube obstruction, pneumothorax, breath stacking, pulmonary edema, or pleural effusions. A full discussion of the causes of elevated peak and plateau pressures is beyond the scope of this review, but if the plateau pressures remain consistently high, a reduction in TV may be necessary.
,Step II: Maintaining Normoxia
As a severely hypoxic patient will rapidly decompensate with progression to death, a host of monitoring devices are used to alert the nurse or physician that O2 levels have fallen below the normal range. Strategies to manage refractory hypoxia in the ventilated patient are complex. For most patients, 100% FiO2 is initiated immediately after intubation to increase the safety of the procedure, but there is animal evidence that high O2 levels promote inflammatory responses, and human data suggest hyperoxia can be deleterious to long-term outcomes, particularly following cardiac arrest and stroke.16,17 A persistent O2 saturation of 100% on pulse oximetry or a supraphysiologic partial pressure of O2 (PaO2) on an arterial blood gas (defined as >200 mm Hg) may actually cause the patient more harm than good. Therefore, the fraction of inspired O2 should be titrated to maintain normoxia. The ARDS protocol, for example, targets an O2 saturation of 88% to 95% and a PaO2 of 55 to 80 mm Hg.8
Step III: Maintaining Acid-Base Balance
The basic principles of acid-base physiology should be familiar to EPs. When a patient is sedated and the airway secured, the primary means by which blood pH is maintained is now in the hands of the intubating physician. Patients with respiratory failure may have compensated for a preexisting derangement in their blood pH. If the preexisting condition is not recognized and ventilator settings are not maintained appropriately, they may be vulnerable to developing another derangement. Even on settings that allow the patient to breathe over a set rate, the sedation required to tolerate an endotracheal tube may cause significant respiratory depression, making it impossible for the patient to auto-regulate the respiratory component of acid-base homeostasis (ie, by hyperventilation).
As in the discussion of RR, TVs are “fixed” based on low-TV lung-protective ventilation. Therefore, changing the patient’s set RR is the easiest method to adjust the partial pressure of CO2 (PaCO2), and consequently address any respiratory acidosis. An increase in the RR will increase the patient’s minute ventilation, leading to a decrease in serum PaCO2 levels, whereas a decrease in the RR will have the converse effect. It is important to obtain an arterial blood-gas reading shortly after intubation and to continue to monitor the impact of any ventilator titrations on the patient’s acid-base status.
Studies of “permissive hypercapnia” in ARDS patients have shown that prioritizing lung-protective ventilator settings, even at the expense of a normal CO2, reduce mortality.1,18 Even in situations where it is not necessary to maintain hypercapnia for lung-protective settings, the hypercapnia appears to have beneficial effects.19-21 No upper limits on hypercapnia have been established, and even extreme levels have been associated with successful patient outcomes.22 However, a study by Hickling et al23 demonstrated that an initial trial of lung-protective ventilation demonstrated benefit from unbuffered hypercarbia and acidosis, reporting an average CO2 level of 66 and a pH of 7. These guidelines should be appropriate for use in the ED.
