A 58 year-old female presents to a local emergency department with weakness and difficulty breathing. She has a history of asthma and chronic obstructive pulmonary disease (COPD). A portable chest x-ray taken in the ED reveals bilateral infiltrates, consistent with pneumonia. Clinically, she is breathing at a rate of 24 breaths per minute with use of accessory muscles, her heart rate is 126 beats per minute and her blood pressure is 98/44. Pulse oximetry on high flow oxygen via mask reads 88 percent. She was given inhaled nebulized bronchodilators, an IV crystalloid infusion and transported to the intensive care unit (ICU). After a brief trial of BiPAP, her condition quickly deteriorated and she was promptly intubated and placed on a ventilator.
Upon the transport team’s arrival, they found the following ventilator settings:
- Assist Control (volume) mode at a respiratory rate of 16 breaths/min
- I:E ratio 1:3.7
- 1.0 fiO2
- Tidal Volume (Vt) 460 ml (PIP 44 cmH2O)
- PEEP of 20 cmH2O
- Minute Ventilation 11 liters per minute
An arterial blood gas drawn just prior to the transport team’s arrival included:
pH | 7.44 |
PaCO2 | 61 |
PaO2 | 78 |
HCO3- | 36 |
SaO2 | 83% |
What the above ABG is showing is a compensated respiratory acidosis. The compensatory part of this ABG (the high HCO3-) takes a long time to get to this level as compensation occurs in the kidneys. A mixed respiratory acidosis and metabolic acidosis would occur in the acute setting. If the pH were abnormally low in this case, we would have an acute problem on top of our chronic issue.
Management prior to, and during transport
The paramount issue in this flight was the hypoxia (as evidenced by a P/F ratio of 78. Remember that the P/F ratio is the PaO2 by ABG divided by the FiO2. In this case, the PaO2 was 78 mmHg and the FiO2 was 1.0. Diagnosis for Acute Lung Injury occurs at a P/F ratio at or below 200). Therefore, managing the patient’s hypoxia and not the respiratory acidosis took priority. The crew managed the patient’s evolving Acute Respiratory Distress Syndrome (ARDS)3.
Ventilatory management in this case included:
- An initial “recruitment maneuver” (inspiratory hold at 40 cmH2O pressure for 25 seconds) in order to attempt to increase the number of alveoli available for gas exchange2.
- Clamping the ETT between ventilator circuit manipulations (to prevent “derecruitment”).
- Pressure control ventilation at a rate of 24 breaths per minute. Peak Inspiratory Pressures were kept at 35-40 cmH2O for a return tidal volume (Vte) of 450 ml. Minute ventilation with this remained at 11 liters per minute and mean airway pressure was at 31 cmH2O2.
- PEEP 20 cmH2O
- 1.0 fiO2
- I:E ratio eventually transitioned (with manipulation of respiratory rate and inspiratory time) to 1:1 and eventually 1.5:1 to further increase surface area for gas exchange. This was titrated for an SpO2 > 88 percent.
The above interventions improved oxygen saturations from the low 80 percent’s to the low 90 percent’s. The patient received low dose vasopressor support in the form of norepinephrine to keep mean arterial pressure > 65 mmHg and artificially address the increased intrathoracic pressures intentionally generated3.
Arterial Blood Gas measurements taken just prior to transport included:
pH | 7.38 |
PaCO2 | 72 |
PaO2 | 88 |
HCO3- | 35 |
SaO2 | 93% |
Again, not a dramatic change in an ongoing and chronic condition. Reversing hypoxia for a safe transport was the goal that was achieved with somewhat success in this instance. One question later asked by a staff member in the ICU of the referring center was “I am not sure that I understand your ventilator settings. This patient has COPD. Where does the COPD management come in?” The answer is that in this case it doesn’t. Remember that permissive hypercapnia is standard in attempts to manage profound hypoxia3. Had this patient had a COPD exacerbation and had not been suffering from an acute lung injury secondary to her pneumonia, ventilator strategies may have included:
- Lengthening the expiratory time
- Permissive hypercapnia
- Assessing autopeep and addressing this issue in the event of hemodynamic compromise due to dynamic hyperinflation1.
Conclusion
Ventilator management is a foundational skill of any critical care transport team. As the acuity of our patient population increases, so must our proficiency in assisting with gas exchange. Some of the aforementioned techniques, while evidence based, may not be consistent with local protocols. As always, a transport team’s individual care standards take precedence in transport.
References
1. Mughal MM, Minai OA, Culver DA and Arroliga AC. Auto-positive End-expiratory Pressure: Mechanisms and Treatment. Cleveland Clinic Journal of Medicine 72(9). 2005. 801-809
2. Papadakos PJ and Lachmann B. The Open Lung Concept of Alveolar Recruitment Can Improve Outcome in Respiratory Failure and ARDS. The Mount Sinai Journal of Medicine 69(1&2); January/March 2002 (73-77).
3. http://www.ardsnet.org/. NIH National Heart Lung and Blood Institute. Accessed January 11, 2011.
