A 24-year-old male was admitted to the emergency department of St Alphonsus Regional Medical Center, Boise, Idaho, a regional trauma center, on February 14, 2001. He had been the lone, unrestrained victim of a motor-vehicle accident and had sustained numerous injuries, including a closed head injury with severe facial injuries and missing teeth. He had fractures of the first three ribs on the right side and several other orthopedic injuries. He had been orally intubated by paramedics with an 8-mm endotracheal tube. A chest radiograph found the tube to be in the right main stem bronchus; the radiograph also showed pulmonary edema and left lower lobe contusion. The endotracheal tube was withdrawn to the appropriate position, and other diagnostic and resuscitative efforts continued in the emergency department.

Initial tests for this patient showed these values: hemoglobin, 6.4 g/dL; glucose, >500 mg/dL (the patient was diabetic); anion gap, within normal limits; Pao2, 165 mm Hg; pH, 7.19; Paco2, 30 mm Hg; bicarbonate, 19 mmol/L; and oxygen saturation, 97%, while the patient was manually ventilated using 100% oxygen. His heart rate, blood pressure, and pulse-oximetry (Spo2) results were noted to be labile. He was taken to the operating room for initial facial repairs and placement of an intraparenchymal pressure monitor. His intracranial pressures were reported to range from 11 to 40 mm Hg. The patient continued to be unstable and was transferred to the intensive care unit (ICU) for further evaluation and stabilization. In the ICU, he began using synchronous intermittent mandatory ventilation at 20 breaths per minute with a tidal volume of 650 mL (approximately 10 mL/kg), a fraction of inspired oxygen of 1, positive end-expiratory pressure (PEEP) of 8 cm H2O, pressure support of 15 cm H2O, and a peak flow of 70 L/min with a decelerating flow pattern. Endotracheal suction produced significant amounts of bright red blood and clotted blood. The patient was evaluated by a pulmonologist/critical care physician who inserted a left subclavian flow-directed pulmonary artery catheter to assist in the evaluation of the patient’s fluid status. The patient had received multiple infusions of fresh frozen plasma, packed red blood cells, and platelets, as well as 9 L of normal saline. Despite this fluid replacement, his systolic pressures varied between 80 and 190 mm Hg, reportedly depending on his state of agitation.

figure 1Figure 1. The flow-versus-time graphic waveform resembles the simulated pattern.

Shortly after placement of the flow-directed catheter, the patient’s Spo2 dropped to 80%, and he was observed to be exhaling forcefully. Peak pressures during mandatory breaths ranged from 30 to 50 cm H2O, and he occasionally triggered pressure supported breaths that delivered minimal volume. The ventilator was disconnected and he was manually ventilated with 100% oxygen. Repeated suction produced only a moderate amount of secretions. After his Spo2 returned to normal, the ventilator was reconnected; the flow-versus-time graphic waveform resembled the simulated pattern shown in Figure 1.

What does the flow-versus-time graphic waveform indicate? The inspiratory portion of the graphic waveform is unremarkable, since the shape is determined by the set values of tidal volume, flow rate, and flow waveform; however, the expiratory portion of the flow-versus-time graph is abnormal. The shape of this curve is consistent with a variable intrathoracic obstruction.1 There is an initial burst of expiratory flow, followed by an abrupt deceleration to a relatively fixed expiratory flow rate. Normally, expiratory flow gradually decelerates, generating a form similar to an exponential decay curve.

What steps would be appropriate to determine the cause of the abnormal waveform? It was apparent that there was significant expiratory obstruction of the endotracheal tube. This facility frequently secures endotracheal tubes with a twill tie, which is knotted to incorporate a bite block. These ties can be too tight, causing increased airway resistance. The tie and bite block were visually inspected, and were deemed not to be the cause of the resistance. A suction catheter was once again passed with little difficulty, with lavage and suction producing only moderate bloody secretions. The flow-versus-time waveform was unchanged after suction, indicating that the obstruction was essentially unchanged. The lead RCP wondered whether the endotracheal tube’s cuff had herniated over the end of the tube and, upon feeling the pilot balloon and finding it quite firm, decided to check the cuff pressure. The pressure was elevated, and although it was adjusted to 24 cm H2O, the expiratory obstruction continued. It appeared that bronchoscopy might be necessary to determine the actual cause of the expiratory obstruction, but the patient continued to be unstable. The pulmonologist decided to sedate and paralyze the patient in an attempt to control both blood pressure and intracranial pressure more effectively. When the patient stopped his forceful exhalation, the expiratory flow obstruction disappeared.

There are several factors that may have contributed to this patient’s hemodynamic instability, and elevated airway pressures. It is possible that the placement of the flow-directed catheter led to the development of a tension pneumothorax. The patient’s percussion note was not hyperresonant on the left, which was the side on which the catheter was placed. A chest radiograph obtained after catheter placement was negative for pneumothorax. Of course, one would not expect such alterations in the flow-versus-time curve due to pneumothorax. Since there appeared to be significant obstruction during the expiratory phase of ventilation, it would be appropriate to measure the resulting level of auto-PEEP. Auto-PEEP can contribute to hemodynamic instability through increasing intrathoracic pressure and reducing venous return.2 In a patient with a closed head injury and intracranial hypertension, it is especially important to maintain adequate mean arterial blood pressure and, therefore, adequate cerebral perfusion pressure. Although the ventilator that was used has an expiratory hold control, a measurement of auto-PEEP could not be made due to the patient’s active inspiration and expiration. In retrospect, if a measurement had been made, it is possible that it would have significantly underestimated the patient’s actual end-expiratory alveolar pressure due to apparently severe obstruction between the alveoli and the site of measurement of airway pressure (at the ventilator). Intrathoracic pressures would probably have been very high due to the combination of air trapping and forced expiration.

Unfortunately, it is impossible to say specifically what caused this level of expiratory obstruction. It is possible that clotted blood or (less likely) a herniated endotracheal tube cuff generated a ball-valve type of obstruction of the endotracheal tube, although it was not possible to demonstrate such findings. Paralysis terminated the obstruction, and this is similar to the results that one would expect in a case of tracheomalacia. The patient had no previous medical, surgical, or trauma history that would lead to the development of such a condition, and no airway trauma was identified during the trauma work-up.

A tracheostomy was performed on this patient 2 days after admission, in association with his facial repairs and in anticipation of his probable long-term requirements for airway maintenance. No mention was made in the operative notes of any abnormalities of his airway (or of the endotracheal tube, upon its removal). After the tracheostomy, his ventilator was changed to one without graphic waveform displays, and no further problems were documented. The patient expired shortly thereafter due to the sequelae of his injuries.

Jeffrey M. Anderson, RRT, is director of clinical education and associate professor, Department of Respiratory Therapy, Boise State University, Idaho; Lonny J. Ashworth, RRT, is professor of the department; and Lisa Crystal, RRT, is a staff therapist, St Alphonsus Regional Medical Center, Boise.

1. Wanger J. Pulmonary Function Testing: A Practical Approach. Philadelphia: Williams & Wilkins; 1992.
2. Pepe PE, Marini JJ. Occult positive end-expiratory pressure in mechanically ventilated patients with airflow obstruction: the auto-PEEP effect. Am Rev Respir Dis. 1982;126:166-170.