Most of us learned that hypotension is our main indication that a pneumothorax has progressed to a tension pneumothorax. What does the research say thus far?......IT DEPENDS! The presentation of a tension pneumothorax depends on the answer to one simple question: "Is the patient breathing on their own or not?" Before diving into the research, let's review some pathophysiology.
Tension Physiology
A pneumothorax can develop due to traumatic and non-traumatic causes. Either way, the pleura that surrounds our lungs has an opening. This opening acts like a one-way valve into the pleura. Normally the pressure inside our pleural space is slightly negative compared to the pressure inside our lungs. The volume of a gas likes to move from an area of high pressure to low pressure (Boyles Law). Air begins to accumulate in the pleural space increasing the pressure around the lung with each breath. This causes increased work of breathing, dyspnea, and progressive hypoxia as the patient tries to compensate. Eventually the lung collapses and this pressure is exerted on vital organs in the mediastinum, the heart and the greater vessels. This results in a decrease in cardiac output due to decreased cardiac filling and ultimately can lead to cardiac arrest (obstructive shock).
Research & Evidence
Research in regard to tension pneumothorax presentation is scarce. Due to this being a life-threatening condition that can develop suddenly during the resuscitation of complex patients, only observational/retrospective studies could be found. In some cases, a randomized control trial (RCT) is not feasible/difficult to conduct. Sometimes the best studies we are going to get will not be RCTs but observational studies. This topic I think is a great example of that. Keeping that in mind, lets dive in!
Back in 1963, a study was conducted using dogs and they were looking at cardiopulmonary effects of a pneumothorax in anesthetized dogs versus awake. First off yes, these people are a**holes for using dogs. Long story short they found that large pneumothoraxes increased the respiratory rate and work of breathing in both the awake and sedated canines. However, "In contrast, the arterial blood oxygen saturation fell, pulmonary artery pressure rose, and carbon monoxide diffusing capacity was reduced in anesthetized dogs despite greatly increased respiratory minute volume and alveolar ventilation. (Kilburn)" In other words, the awake dogs were able to compensate longer than the sedated dogs before seeing the same cardiopulmonary collapse.
Fast forward to 1997 as study was conducted looking at ventilated swine and progressive increases in pneumothorax and its effects on: heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), mean intrapleural pressure (MIP), oxygen saturation (O2%), arterial blood gas (ABG), and cardiac output (C.O.) (Barton et al.). The study concluded that in ventilated swine: "We conclude that the findings of this study support the alternative hypothesis that significant hypoxemia occurs early and precedes hypotension in ventilated animals with TP. (Barton et al.)"
In 2005 an article was written discussing that the clinical presentation of a tension pneumothorax. In this article they discuss their method for reviewing the current literature and concluded that "The differences in the pathophysiology and presentation of TPT between awake and ventilated patients have been mentioned by other authors but deserve increased emphasis. TPT should not be taught as if it was a single entity. (Leigh-Smith and Harris)"
Obtained from: "Tension Pneumothorax -- Time for a Rethink" Article
This brings us to the meta-analysis conducted in 2014, which was focusing in on clinical presentation of a tension pneumothorax. Two physicians independently searched for incidences on tension pneumothorax that had data on clinical presentation and found a total of 183 cases; among the 183 included cases, 86 (47.0%) were breathing unassisted and 97 (53.0%) receiving assisted ventilation (Roberts et al.). Here is the breakdown of the clinical presentation between the two:
Obtained from: “Clinical Presentation of Patients With Tension Pneumothorax.”
Looking at this data we see that hypotension is significantly more common in the assisted ventilations group. I love that they used MAP instead of some arbitrary systolic number. The authors discuss another important difference between these two groups; the assisted ventilation group often had a sudden cardiopulmonary collapse (within minutes) where the unassisted group had a much slower onset of signs of cardiopulmonary collapse (Roberts et al.). The authors of this meta-analysis created a table where they tried to quantify the differences between the two groups. I find this table to be a great visual of the differences.
Obtained from: “Clinical Presentation of Patients With Tension Pneumothorax.”
This studies final conclusion: "The reported clinical presentation of tension pneumothorax depends on the ventilatory status of the patient. This may have implications for improving the diagnosis and treatment of this uncommon yet catastrophic clinical condition. (Roberts et al.)"
Final Thoughts
Clinical presentation of a tension pneumothorax is dependent on the ventilatory status of our patients (assisted VS unassisted). Why is this the case? The meta-analysis discussed above offers a great explanation but let me simplify it. We have essentially a one-way valve that lets air into the pleura. When a patient is breathing unassisted, they are using the intercostal muscles and diaphragm (negative pressure), this allows air in during the inspiratory phase of ventilation but not expiratory. This could explain the reason their cardiopulmonary collapse is more delayed. Now looking at the assisted ventilation patients, we are pushing air into their lungs (positive pressure), this creates much higher intrathoracic pressures. In this case we could have continued air movement into the pleura through not only the inspiratory phase but also the expiratory phase of ventilation. Tension physiology sets in suddenly as the pressure is exerted on not only the ipsilateral lung but also the mediastinum (heart & greater vessels). This could explain why hypotension is more commonly seen in patients who are receiving assisted ventilation.
Although the research is observational/retrospective it is the best research method for this specific topic; RCT is not really feasible here. Knowing that, I believe this evidence to be sufficient enough to show we do have varying clinical presentations of tension pneumothorax and that it depends on the patient's ventilatory status.
On a side note, ultrasound could be a valuable tool to increase our sensitivity and specificity of identifying a tension pneumothorax, especially in patients breathing unassisted. However, it is just a tool, and our clinical gestalt is key here.
Putting it all together when do we have a tension pneumothorax that needs immediate decompression:
Unassisted Ventilation (Delayed Onset):
- Clinical suspicion with
- SEVERE DYSPNEA & increased work of breathing and
- HYPOXIA (SpO2 <90%) despite high flow oxygen
Assisted Ventilation (Rapid Onset):
- Clinical suspicion with
- Immediate drop in SpO2 and/or HYPOTENSION
What are your thoughts on these studies? Let us know!
Take Care!
- Tyler
References:
Barton, E D et al. “The pathophysiology of tension pneumothorax in ventilated swine.” The Journal of emergency medicine vol. 15,2 (1997): 147-53. doi:10.1016/s0736-4679(96)00312-5
KILBURN, K H. “Cardiorespiratory effects of large pneumothorax in conscious and anesthetized dogs.” Journal of applied physiology vol. 18 (1963): 279-83. doi:10.1152/jappl.1963.18.2.279
Leigh-Smith, Simon, and Tim Harris. “Tension Pneumothorax--time for a Re-think?” Emergency Medicine Journal, vol. 22, no. 1, BMJ, Dec. 2004, pp. 8–16. https://doi.org/10.1136/emj.2003.010421.
Roberts, Derek J., et al. “Clinical Presentation of Patients With Tension Pneumothorax.” Annals of Surgery, vol. 261, no. 6, Lippincott Williams and Wilkins, June 2015, pp. 1068–78. https://doi.org/10.1097/sla.0000000000001073.
Sahota, Ruchi Jalota. “Tension Pneumothorax.” StatPearls - NCBI Bookshelf, 28 Nov. 2022, www.ncbi.nlm.nih.gov/books/NBK559090/#article-27373.s3.
Shakespeareanddarwin. “Boyle’s Law, Pneumothorax and Imperator Furiosa.” Shakespeare and Darwin, 12 Nov. 2022, shakespeareanddarwin.wordpress.com/2019/07/03/boyles-law-pneumothorax-and-imperator-furiosa.
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