3D concept rendering of COPD lung disease. (Shutterstock/CI Photos)
Mechanical ventilation in the critical care transport environment is rarely as straightforward as matching a patient’s disease to an algorithm or guideline. This is especially true for severe obstructive lung diseases.
I am saying “severe” here because we are going to be talking about patients who are in extremis. They progressed to the degree that they required intubation and management with a ventilator. This did not solve any problems, and in fact added complexity to an already complicated situation.
While the foundational ventilator strategy for chronic obstructive pulmonary disease (COPD) and asthma might appear deceptively simple on paper, applying those settings without understanding the underlying mechanics and architectural difficulties can be a pathway to hemodynamic collapse. To successfully manage the flow-obstructed patient, clinicians must look past the rigid guidelines and to the actual physiology.
This is Part 1 of a two-part series where we are going to pull apart the architectural differences of obstructive lung diseases, explore the physiological traps of positive pressure ventilation, and discuss why understanding the “why” matters far more than the “how.”
Pulling It Apart
An important thing to do when evaluating various approaches to mechanical ventilation for patients with obstructive lung problems is to pull apart COPD and asthma. The “how” may generally be the same in how we set up the ventilator, but the “why” could not be more different.
That “why” may shift our focus away from one treatment modality to another that better addresses the physiologic difficulty. Both COPD and asthma fall under the umbrella of “obstructive lung disease” and share some characteristics, but there are some key differences that can inform treatment decisions. Most of those differences can be attributed to lung architecture.
Architecture
Airflow limitation is the problem that patients contend with for both diseases, but how it manifests is completely different.1-3 The lung architecture is different between the two.3
Inflammation and destruction of lung tissues (alveolar walls) are the emphysematous hallmarks of COPD, while narrowing of the lumen in the large and small airways is characteristic of asthma. Asthma adds the issues of mucus plugs to the bronchoconstriction.1-3
They both create the same primary problem—expiratory flow issues—but in different ways.
COPD = Compliance Problem
COPD is not a compliance problem like that of acute respiratory distress syndrome (ARDS), where the lungs are quite non-compliant (commonly referred to as “stiff”), but just the opposite. The lungs of a COPD patient are rather compliant.
Due to a loss of elasticity, their lungs can accommodate a significant amount of volume.2 The problem is that because the lungs have lost their elastic recoil, the patients simply do not have enough time to fully exhale before taking their next breath.2-4
This results in chronic hyperinflation that creates even more inflammation and damages increasingly more alveoli.2-4 This problem is exponentially more difficult to address once the patient is in distress.
For the COPD patient suffering primarily from an emphysema presentation, the once passive process of exhalation has slowly become an active process.3 Adding to the difficulty with exhalation, the COPD patient’s smaller airways collapse during exhalation, having lost their strength and elasticity as well. When these small passages collapse, air is trapped in the alveoli.
Asthma = Resistance Problem
The asthmatic has the opposite problem. They still have the issues with airflow (in and out), but it is due to narrowed airways secondary to bronchoconstriction, inflammation, and mucus production.3-4
Their lung tissues (read: alveoli) and air passages are mostly structurally intact, and they generally have adequate recoil for exhalation.3-4 The structural problem is primarily the narrow airways that reduce the amount of airflow out of the lungs.
In the most severe cases, airflow into the lungs can be restricted as well. The patient must forcefully exhale to clear volume from their lungs, but in distress, they are often breathing at a rate that demands the next inhalation before the exhalation of the previous breath is complete.4-5
Foundational Management Strategy
The core pathology is expiratory flow limitation; therefore, our focus to overcome that is to prolong the expiratory time as long as possible (1:4/1:5). We also must deliver ventilation in a manner that avoids dynamic hyperinflation while avoiding acute lung injury. Doing all of this while delivering optimal minute volume for gas exchange can be tricky.
The ventilator tidal volume is set to the larger end of the range at 8 milliliters per kilogram of the patient’s ideal body weight; this is to help maintain adequate minute ventilation and maximize the inspiratory time (inhaling) to expiratory time (exhaling) (I:E) ratio.1,5-6
The smaller the tidal volume used, the higher the rate will be to deliver proper minute ventilation. The higher the rate, the shorter the cycle time and therefore the shorter the I:E ratio. This highlights the importance of focusing on the respiratory rate and total cycle time.
Respiratory rates are generally between 10 and 12 breaths per minute for these patients, which allows for an I:E ratio of 1:4 to 1:5 while still delivering proper minute ventilation.5-6 This setting has the single largest positive impact for ensuring the safety of obstructive lung disease patients receiving mechanical ventilatory support.5-6
Setting positive end-expiratory pressure (PEEP) for these patients varies in support in the literature. Some authors say that zero PEEP is acceptable since the patients already have a large amount of intrinsic PEEP (PEEPi) and therefore there is the possibility of making the picture worse with extrinsic PEEP.2,5,7
Others recommend setting PEEP at 5 cm H₂O to start, or 50 to 80 percent of the measured PEEPi.5 Plateau pressure (Pplat) still needs to be measured to ensure there is no hyperinflation of the alveoli (stay tuned for part 2 to dive deeper into this).5-7
While the vent may be the star of the show, do not neglect the use of pharmacologic therapies such as inhaled bronchodilators. Continuous administration via a supplied air breathing apparatus is a mainstay of obstructive lung disease care.5
IV bronchodilators can be considered as well. Their use is no more effective than inhaled beta agonists.5 Magnesium sulfate, corticosteroids, and anticholinergic therapy are all still needed to assist with improving airflow and relief of bronchoconstriction.5
Conclusion
Ultimately, the ventilator management of a flow-obstructed patient is a delicate, high-stakes balancing act. Whether the crew is working to address the floppy, over-compliant architecture of emphysematous COPD or the high resistance of acute asthma, the result is a potentially lethal expiratory flow limitation.
The foundational strategy is focused on ensuring that the patient has ample time to exhale. But a well-intended hyper-focus on a single parameter, such as lowering the peak inspiratory pressure or peak airway pressure, only creates new and more dangerous problems.
It is important to remember that we cannot successfully manage these patients by treating the ventilator and responding to every beep and bloop it generates; we have to treat physiology. By respecting the mechanical disadvantages inherent to obstructive diseases, we can begin to safely manipulate the respiratory cycle.
In Part 2, we will build on this physiological foundation and explore how to separate the true clinical “signals” from the distracting “noise” from the nearly guaranteed pressure alarms that the patients will generate.
References
1. Demoule A, Brochard L, Dres M, Heunks L, Jubran A, Laghi F, Mekontso-Dessap A, Nava S, Ouanes-Besbes L, Peñuelas O, Piquilloud L, Vassilakopoulos T, Mancebo J. How to ventilate obstructive and asthmatic patients. Intensive Care Med. 2020 Dec;46(12):2436-2449. doi: 10.1007/s00134-020-06291-0. Epub 2020 Nov 9. PMID: 33169215; PMCID: PMC7652057.
2. Jubran A. Setting positive end-expiratory pressure in the severely obstructive patient. Curr Opin Crit Care. 2024 Feb 1;30(1):89-96. doi: 10.1097/MCC.0000000000001131. Epub 2023 Dec 8. PMID: 38085854; PMCID: PMC11141232.
3. Jeffery PK. Remodeling in asthma and chronic obstructive lung disease. Am J Respir Crit Care Med. 2001 Nov 15;164(10 Pt 2):S28-38. doi: 10.1164/ajrccm.164.supplement_2.2106061. PMID: 11734464.
4. Sköld CM. Remodeling in asthma and COPD–differences and similarities. Clin Respir J. 2010 May;4 Suppl 1:20-7. doi: 10.1111/j.1752-699X.2010.00193.x. PMID: 20500606.
5. Mein SA, Ferrera MC. Management of Asthma and COPD Exacerbations in Adults in the ICU. CHEST Crit Care. 2025 Mar;3(1):100107. doi: 10.1016/j.chstcc.2024.100107. Epub 2024 Nov 8. PMID: 40330435; PMCID: PMC12054689.
6. MacIntyre NR. Acute Hypercapnic Respiratory Failure in COPD. Respir Care. 2023 Jul;68(7):973-982. doi: 10.4187/respcare.10560. PMID: 37353327; PMCID: PMC10289623.
7. Gayen S, Dachert S, Lashari BH, Gordon M, Desai P, Criner GJ, Cardet JC, Shenoy K. Critical Care Management of Severe Asthma Exacerbations. J Clin Med. 2024 Feb 1;13(3):859. doi: 10.3390/jcm13030859. PMID: 38337552; PMCID: PMC10856115.
Cody Winniford is a flight paramedic and base manager in Baltimore, MD. He has a passion for sharing his professional experience in EMS and management. Cody’s clinical and leadership development background spans both military and civilian settings and has served in several capacities as a leader and prehospital clinician. He specializes in air medical and critical care transport, as well as organizational development and leadership development. He is an active speaker on various leadership and clinical topics and is an established and successful educator for prehospital clinicians of all levels. He has a passion for human performance improvement and the mental health and performance aspects of prehospital care.
