Our guest, Eric Steffel, is a paramedic that reached out wanting to discuss active exhalation. It goes by many other names including "external chest compressions" or "lateral chest compressions" as some sources have indicated. We decided not to use the term "compression" though because this can quickly lead to someone thinking this is a chest compression similar to what is performed in cardiopulmonary resuscitation (CPR). Eric prefers "active exhalation" and (understanding its potential limitations) is what we use for this podcast to define this procedure.
Case presentation: 6 y/o male who developed an asthma attack. The patient has a long history of asthma attacks and has been intubation several times in the past. Mother was treating her son and though she could manage this attack at home until his symptoms acutely worsened and she called 911. By the time the ambulance arrived, the patient was obtunded with marked respiratory distress and audible wheezing. Oxygen and albuterol were started before moving to the ambulance. Once in the ambulance, the patient goes apneic and BVM ventilation was initiated with minimal success and dropping O2 sats and bradycardia emerging. Endotracheal Intubation was performed immediately and attempted to place a 5.5 cuffed tube, but ultimately was successful with an uncuffed 5.0 tube. The airway resistance was persistent, and ventilation primarily resulted in air escaping from around the ET tube due to poor lung compliance. ETCO2 waveform was a consistent butt in the low 20’s. Bradycardia eventually evolved to asystole and CPR was started.
Although this particular patient is somewhat rare, the CDC reports show the Asthma patients are increasing which suggest we may continue to see more cases like this. But, when we have these patient’s it is fair to say it seems to always be an uphill battle and can rattle even the experienced provider, especially when the interventions are not having the impact you hoped and the patient condition continued to deteriorate.
Current Treatments & Physiology: Tintinalli (2004, 6th ed. P. 473) discusses the interventions for the severe asthma patient. The typical Beta agonist, Steroids, Magnesium, Ketamine, and Epi as your options to relieve bronchial constriction. But, if the patient develops hypercarbia, acidosis, or become exhausted or confused, Non-invasive positive pressure ventilation or intubation may be required. However, the mechanical ventilation does not relieve the airflow obstruction that exists and merely eliminates the work of breathing and allows the patient to rest while airflow obstruction is resolved.
So even in the worst case, intubation does not offer much to treating the underlying cause and even the supportive measures are tedious to manage. Vent settings to strategically address this situation include decreasing inspiratory time to allow for more expiratory time. In the meantime, reduced TV may be inhibiting the effective delivery of inhaled beta-agonist and IV medications may or may not work in a timely manner. And, as a side note, inline nebs for the intubated patient in the prehospital setting can be tricky or impossible if the service does not carry the right equipment and/or the medic’s not practice assembling it.
The tactic of decreasing inspiratory time and allowing for longer expiratory time is the key. In these patient’s we are passively allowing this process to happen, why not increase is effectiveness by actively exhaling for the patient? I could argue that this concept is as simple as “if a patient is sedated and apneic, then they have an inhalation problem that is solved by providing positive pressure ventilation; whereas, if a patient is air trapping, then they have an exhalation problem that can be solved by providing positive pressure exhalation… or active exhalation”.
Another way to discuss this theory is to highlight the term Diaphragmatic fatigue. I love this term because it really helps to put things into perspective. These patients are or have exhausted the abilities of the diaphragm to exhale; therefore, we should take over exhalation for them. no different than reaching muscle fatigue when doing pushups. You can push yourself until you reach muscle fatigue, then-then soon as you drop to the ground, give it 10 seconds and you can do one more. If someone were to help you or take some weight or resistance away from your repetition, you would theoretically improve. That’s the goal of active exhalation, improve resistance but actively expelling trapped air and reducing the workload or fatigue of the diaphragm.
Description of the procedure: The procedure is very simple, but there are a few things I would like to suggest when doing this to assess for efficacy. First, there is not “preoxygenation” phase to this, if you are doing or considering this procedure, you have already exhausted your oxygenation efforts. Next, try to get the patient on ETCO2 if you have not already. This helps to quantify the CO2 trapping and effectiveness in exhaling it actively. Similar to ETCO2, use a stethoscope. I put the stethoscope under my hand while I’m pushing on the chest so I can listen to the different phases or the auscultatory transition to moving trapped air.
Unconscious: for the unconscious patient place both hands on the chest, one over each lung. This may have to be modified depending on patient size and physiology; however, the goal is to literally squeeze and compress the lungs. Apply constant pressure to the patient’s chest evenly for 8-10 seconds. Duration I typically base on what I am hearing.
Awake: If they are awake, this poses a bigger challenge; however, these patient’s are perhaps the most desirable since we could possibly intervene before they reach fatigue, unconsciousness and/or intubation. Obviously, this will take much more coaxing with the patient. I have not personally performed this on an awake patient; but, I have a single case report where a medic did this for only 3 seconds twice is avoidance of intubation (the kit was out) and reported improved patient status.
Discussion of technique: It could be argued that performing this intervention several times during the patient’s natural or ventilated exhalation phase could be superior to a single, prolonged 8-10 second effort. The argument I offer is the longer the exhalation phase, the more absolute-exhalation is achieved.
Evidence: This is where I would love to throw mounds of research and data out there supporting this technique; however, there isn’t much out there. Actually, I couldn’t find anything specifically on utilizing this technique at all and active exhalation was only sited as the patient actively exhaling using their diaphragm. The studies I found that discussed utilizing active exhalation and pursed-lip breathing as a tactic for lung training in the COPD patient and in infants for bronchopulmonary dysplasia in a similar method as lung training for COPD, but these were not necessarily patient’s with the physiology we are looking to treat in this case and none were in the emergent setting.
At this point, all we have to rely on is anecdotal information. I have used this technique several times in the field and every time I have seen positive results. I respect the possibility of selection bias or coincidence, but there are some measurable results. For example, the auscultated lung sound variance when you transition from regular exhaled air to exhaling trapped air, there has been a clear distinction between these two phases. Next, ETCO2 monitoring. I consistently see is marked an increase in ETCO2 during active exhalation which has been 80, 90, and even above 100. And perhaps the most confirming evidence, the lack of resistance to the next ventilation. Utilizing the manometer on the BVM, I have observed the pressure go from 40-50 cmH2O to around 20-30 cmH2O with the provider reporting an immediate and significant improvement in compliance. Now, this is only a temporizing technique. Unless the bronchial constriction is resolved or improved, over time the air will begin to trap again and this technique may be repeated.
Let's talk Risks: The biggest risk I can think of is the fact that we are pushing on the patient’s chest and increasing intrathoracic pressures for a brief time. The first thing that comes to concern is the potential to cause hypotension that may lead to arrest. Fortunately, in most of these cases, this intervention would be beneficial – hypotension is not a complication unless it is already a peri-arrest situation due to hypoxia. And, we would all agree that cardiac arrest for our patients is bad, but even if the intervention leads to an arrest, the corrective action to oxygenation would potentially be more beneficial and have a positive response as opposed to ventilating an asthmatic patient in arrest. The second risk would be an injury to the lung or chest wall. I want to highlight here that this is NOT a chest compression where we are attempting to compress the heart, we are attempting to compress the lungs. This procedure should not break any cartilage much less bones. That being said, it is reasonable that this procedure could increase the risk of rupturing a bleb and/or breaking a rib, especially in the patient with decalcified bones. Lastly, performing this intervention on a patient that is not air trapped.
Closing Remarks: We can’t ignore the potential benefit of this procedure in the asthma or air trapped patient, especially when you consider the cost $0 and the risks are negligible. If anything, what I hope to see is someone listen to this podcast and runs with it to conduct a mini-trial or study it further. Unfortunately, as we had discussed, we don’t see this patient’s that often, and when we do this procedure easily can become an afterthought as we are cognitively overloaded by troubleshooting interventions that are not improving our patient’s condition.
Case Resolution: After CPR was initiated and Epinephrine was administered as the IO was initiated. I stopped and thought about active exhalation and let everyone know what I was going to do, including interrupting chest compressions. On the count of 3 everyone stopped, I performed active exhalation and watched the monitor in asystole with his ETCO2 increasing over about 8 seconds and peaked to 120. CPR was immediately continued, and the next ventilation was met with little resistance and ETCO2 waveform and value normalized. About 1-2 minutes later, the patient regained pulses and remained unconscious. During transport, ventilation was increasing, and oxygen saturation began to drop as bradycardia presented. Active exhalation was performed with almost immediate improvement hypoxia and bradycardia and avoided re-arresting. The patient was transferred to hospital staff where he was admitted to the ICU.
This was a guest post written by Eric Steffel. If you have a similar topic you want to discuss let us know as we are always looking for guests. You can also let us know what you think by giving us feedback here in the comments section or contacting us on Twitter or Facebook. Remember to look us up on Libsyn and on iTunes. If you have any questions you can also comment below, email at firstname.lastname@example.org, or send a message from the page. We hope to talk to everyone again soon. Until then, continue to provide total care everywhere.
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