Bilateral Tension Pneumothorax: Harder To Diagnose

Tension pneumothorax is a life-threatening emergency. We all know the signs of tension pneumothorax:

  • unilateral breath sounds (breath sounds absent on affected side),
  • thorax may be hyperresonant,
  • jugular venous distention,
  • tracheal deviation to the opposite side,
  • maximum heart sounds shifted to the opposite side, and often
  • tachycardia
  • hypotension

However diagnosis is more difficult if the patient is suffering from bilateral tension pneumothoraces. We think about bilateral tension pneumothorax occurring with trauma cases. Yet the three cases I’ve seen in my career were complications of intubation and emergency airway management.

Case 1

The 14 month old in Kenya during a volunteer medical trip was scheduled to have his cleft lip repaired as one of the last cases of the day. We had already done 10 children in that OR and the case was starting at about 9 pm. The hospital was poor and this was 1986. The only monitors we had were blood pressure, pulse, and a small, portable, one lead EKG. We did not have pulse oximetry or end-tidal CO2 available in the hospital.

I was working with a Kenyan anesthetic assistant, similar to an OR tech. I induced the child, started the IV and intubated without difficulty. At that point I turned my back to the patient. My assistant pushed the flush button on the anesthesia machine to rapidly refill the ventilation bag. What I didn’t know was that the anesthesia machine, a type I had never seen before, had a flush button that you could rotate and lock in the on position, producing continuous 30 liter per minute flow. When my assistant hit the button from an angle, he accidentally locked it on.

The next thing I heard was a loud hissing sound and when I looked down the ventilation bag was hugely distended. I quickly disconnected the circuit, turned off the flush, and checked the patient. Everything appeared fine. Good bilateral breath sounds, good heart tones, good blood pressure. I breathed a sigh of relief and we started surgery.

Starting about forty minutes into the case, I noticed that the child was more tachycardic than I expected, in the 120s. Giving a fluid bolus didn’t correct this. I was assisting his spontaneous ventilation but he seemed to be breathing shallowly and more and more quickly at about 40 breaths per minute, despite being deeply anesthetized. I was feeling uneasy but the blood pressure was fine and bilateral breath sounds were equal, although faint. The child’s dark black skin and the dim lighting in the room did not show any discernible cyanosis.

Sixty minutes into the case the child arrested, developing pulseless electrical activity. We started CPR. Breath sounds were equal, but terribly wheezy and very faint. Lung compliance was poor. Remembering the circuit over-pressurization at the beginning of the case, I worried about bilateral tension pneumothoraces. We needled both chest cavities and released a huge amount of free air from both. The pulse came back and the child stabilized. We then placed formal chest tubes.

Case 2

During a difficult intubation in the ICU, one of my colleagues inserted a bougie to assist with passage of the endotracheal tube. As he slowly advanced the tube over the bougie, one of the nurses assisting us suddenly pushed the bougie in deeper in an attempt to help. Unfortunately the tip of the bougie was pushed deep enough to penetrate the carina. Both lungs instantly collapsed and the patient went into cardiogenic shock. Emergent placement of Thora-Vents into both chest cavities quickly improved blood pressure and stabilized the patient. To read a discussion of the complications of using bougie, and how to safely avoid trachea trauma click here.

Case 3

A patient with a tracheostomy arrived in the emergency department with respiratory failure and developed ventricular tachycardia. During CPR and defibrillation, the tracheostomy tube was dislodged and then replaced. After defibrillation, VTach was converted to sinus tachycardia, but the patient then developed pulseless electrical activity. Unfortunately, during replacement of the tracheostomy tube during chest compressions, the tip of the tracheostomy tube created a false passage in the posterior wall of the trachea, with air subsequently dissecting down and causing bilateral tension pneumothoraces. The emergency room physicians quickly diagnosed tension pneumothorax using the ultrasound machine. Thora-Vents were placed and the patient stabilized.

Let’s review what happens physiologically with tension pneumothorax.

Mechanics of Breathing

To inhale, the muscles between the ribs (intercostal muscles) and the diaphragm contract. Contraction of the intercostal muscles lifts the ribs upward and outward, increasing the volume of the chest cavity. As the diaphragm contracts, it moves downward, further expanding the chest cavity. When the volume of a container increases, the pressure inside goes down. A good analogy is using a syringe. When you pull the syringe plunger, the chamber inside becomes larger, the pressure inside goes down, and the fluid is drawn into the chamber. Like liquid, air is also a fluid. Chest expansion lowers the pressure inside the chest cavity, the intrathoracic pressure, below atmospheric pressure. If the airway is open, air flows into the lungs until the two pressures are again equal.

Illustration of the mechanics of breathing showing Airflow in and out of the lungs depends on changes in air pressure inside the thoracic cavity and an open airway.

Airflow in and out of the lungs depends on changes in air pressure inside the thoracic cavity and an open airway.

When we exhale, normal elastic recoil of our chest wall compresses the rib cage. The diaphragm relaxes. The chest cavity becomes smaller. When volume decreases, pressure increases. Think of pushing the plunger on our syringe inward. As intrathoracic pressure rises higher than atmospheric pressure it pushes the remaining air (minus some of its oxygen and now containing CO2) out through the unobstructed airway.

The lungs are elastic.  As the chest wall expands, air flows into and inflates the lungs like a balloon — although in this case the balloon is composed of millions of tiny balloons like a sponge. These air sacs are called alveoli. The volume of an average breath, the tidal volume, thus generated is about 8 ml/kg and can be as high as 10-15 ml/kg with maximum expansion of the chest.

Pathophysiology of Pneumothorax

Holes in the lungs or chest wall can alter the mechanics. Open pneumothorax results when a penetrating chest wound enables air to rush in and collapse the lung. Closed pneumothorax results when air leaks from a lung (or a perforated esophagus) into an intact chest cavity.

With an open pneumothorax, expansion of the chest cavity can’t effectively decrease intrathoracic pressure. Depending on the severity, the lung may only partially expand, or not expand at all.

When the chest wall expands in the presence of closed pneumothorax, air follows the path of least resistance and fills the thoracic space. The lung itself can’t expand very well because the air around it compresses it. This is expecially true with manual ventilation, when air continues to be forced into the thoracic cage around the lung despite building intrathoracic pressure. If intrathoracic pressure gets high enough, it flattens the lung, shifts the remaining chest contents, such as the heart, to the other side, and prevents blood return. This life-threatening situation is called a tension pneumothorax.

Illustration showing how increased intrathoracic pressure shifts the heart and lungs to the left in a right sided tension pneumothorax .

Right tension pneumothorax with heart and lungs shifted to the left.

chest X ray of Left tension pneumothorax, with heart and trachea shifted to the right.

Left tension pneumothorax, with heart and trachea shifted to the right.

Tension Pneumothorax

With tension pneumothorax, the intrathroacic organs are compressed to the point of failure by the increased air pressure. Respiratory failure results from inability of the affected lung to fill. However the over-pressurized air pushes the unaffected lung to the other side, compressing it so it too cannot fill.

  • breath sounds are absent on the affected side, but also very poor on the unaffected side
  • trachea deviates away from the affected side.
  • thorax on affected side may be hyperresonant

Circulatory failure results from the increased pressure inside the chest cavity obstructing blood flow leaving of the heart as well as impeding blood flow returning to the heart from outside the chest.

  • hypotension
  • jugular venous distention
  • tachycardia
  • shift of the mediastinum (with shift of the maximally heart heart sounds)
  • potential subcutaneous emphysema

Bilateral Tension Pneumothorax

Spontaneous bilateral pneumothorax is rare, estimated at 1.4-6% of pneumothoraces. They can occur with trauma, tumor, and iatrogenic causes (1).

Bilateral tension pneumothorax can be difficult to diagnose. Breath sounds are often poor, but they tend to be equally poor on both sides. The trachea and the mediastinum may not shift, as the lungs and heart are pinned and compressed midline between the two overpressurized chest cavities.

CXR showing severe compression of heart and both lungs by bilateral tension pneumothorax

CXR showing severe compression of heart and both lungs by bilateral tension pneumothorax. (

To diagnose bilateral tension pneumothorax you have to have a high index of suspicion. Whenever there is deterioration in the patient’s oxygenation or ventilatory status, the chest should be re-examined and tension pneumothorax ruled out. If you don’t think about a diagnosis, you will never make the diagnosis.

Ultrasound is increasingly considered more sensitive than chest X ray in diagnosing pneumothorax. This link leads to the Sonosite video lecture on using ultrasound to diagnose pneumothorax

Treatment is immediate needle decompression by inserting a large-bore (eg, 14 or 16 gauge) needle into the 2nd intercostal space in the midclavicular line (2). Air will usually gush out. Because needle decompression causes a simple pneumothorax, tube thoracostomy should be done immediately thereafter. However, needle decompression is not without complication. Reported complications include vessel injury and hemothorax, lung laceration, and air embolism. always consider confirming with ultrasound or chest Xray if you can quickly proceed without jeopardizing the patient.

An Anesthesia Machine Risk For Barotrauma

A common denominator in the 3 cases I describe is human error. As we approach the start of the new year with a class of brand new anesthesia trainees, let me point out one potential risk for barrotrauma: over-pressurizing the anesthesia circuit of the anesthesia machine.

This rather humorous picture is an anesthesia machine inadvertently left in test mode for several minutes, with the pop-off valve set to 20 mmHg and 10 liter flow.

picture of an anesthesia machine with Ventilation bag left overinflated during a machine check, with 10 liter flow and the pop-off set at 20mmHg demonstrating barotrauma risk

Ventilation bag left overinflated during a machine check, with 10 liter flow and the pop-off set at 20mmHg demonstrating a potential risk of barotrauma following intubation.

This potential safety issue can cause pneumothorax in our anesthetized patients if we’re not careful. Technically 20 mmHg is not that high a pressure, but I think we can all agree that the ventilation bag is distended to the extent that if this was a pair of lungs, there might be serious trauma.

Anesthesia providers often turn the oxygen flows to 10 liters during induction in order to allow the bag to fill rapidly while we mask ventilate. This allows us to make and break the mask seal repeatedly as we give IV medications and adjust inhalational agent flows, yet still rapidly ventilate again. After placement of the cuffed endotracheal tube, the provider quickly reduces flows after intubation to avoid overpressurizing the circuit.

However, it is very common for me to have to remind new trainees to open their pop-off valves after intubation to avoid over-pressurization of a circuit still receiving 10 liter flow into an endotracheal tube. My experience in Kenya makes me hyper-vigilant of circuit pressure with my students. I’m hoping that by sharing this experience, I can make you hyper-vigilant as well.

May The Force Be With You

Christine Whitten MD, author of
Anyone Can Intubate, A Step By Step Guide
Pediatric Airway Management; A Step By Step Guide

  1. Taegum K, Bae JS, Yuk YS. Life-Threatening Simultaneous Bilateral
    Spontaneous Tension Pneumothorax. Korean J Thorac Cardiovasc Surg 2011;44:253-256
  2. Brohi, K. (London, UK, July 01, 2006)The diagnosis and management of tension pneumothorax. Retrieved from URL:

Button to see inside or buy the book Pediatric Airway Management: A Step-by-Step Guide by Christine Whitten    Button link to see inside or buy the book Anyone Can Intubate, A Step By Step Guide to Intubation and Airway Management, 5th edition on amazon

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Anatomic Dead Space Affects Hypoventilation

Understanding anatomic dead space is important to recognizing subtle hypoventilation. Hypoventilation from sedation, pain medications, anesthesia in the immediate postoperative period is common. The most obvious sign is slowing of the rate of breathing. A more subtle sign is that tidal volume becomes shallower. Having a tidal volume close to, or smaller than the patient’s dead space can lead to significant hypercarbia, hypoxia, and respiratory failure. This article discusses the concept of dead space and it’s clinical use in recognizing hypoventilation and preventing hypoxia and hypercarbia. Continue reading


When I was training, we used nitrous oxide on just about every anesthetic. It was easy to use. It was inexpensive. It didn’t tend to effect hemodynamics so it was useful in less stable patients when combined with an opioid. It helped speed induction through the second gas effect. It was not metabolized so renal and liver insufficiency were of less concern.

However, with all of the more recent investigation into reasons for cognitive dysfunction or decline in infants and the elderly following anesthesia, a lot more is now known about the pharmacologic disadvantages of nitrous oxide (1, 2, 3). Continue reading

Communication In A Crisis: A Case of Respiratory Depression In A Child:

When I’m teaching communication in a crisis to my Perioperative/OR nurses, I often recount the story of what happened during one particular child’s recovery years ago. This case, involving a 2 year old child who developed respiratory depression in the recovery room, demonstrates how good communication in a crisis, including the ability to challenge an authority figure, can improve patient safety and allow collaborative teamwork in a crisis management situation. Continue reading

Close Call In Honduras With A Nosebleed

I recently visited Honduras with a Head and Neck surgical team where we had a close call with a potential airway obstruction due to a blood clot. The case illustrates how a provider should never make assumptions, because if those assumptions are wrong, you can endanger your patient.

After a long day in the OR, while we were packing up to leave, a nurse from the ward ran in and said that one of the patient’s who had had a septoplasty that day for chronic sinusitis was bleeding. I immediately started setting up the OR again while our surgeon went over to the ward. Continue reading

Intubation With Airway Bleeding and Massive Emesis

During intubation, any liquid in the mouth that obscures the view of larynx not only hinders visualization, it risks aspiration. We’re used to being able to rapidly suction the mouth clear or secretions, blood, or vomit and then have a clear view of the larynx. But sometimes, either because of continued profuse airway bleeding or massive emesis, fluid continues to accumulate while we’re watching. How can you manage this situation and successfully intubate? Here I describe two cases, one involving blood and the other massive emesis, that required intubation through a large puddle of fluid. I offer tips and tricks to assist you in your future emergency management. Continue reading

Avoiding Pediatric Drug Errors

Pediatric drug errors are unfortunately common. The literature states that medication errors occur in 5% to 27% of all pediatric medication orders, a very sobering number. Considering that many of these errors occur in the smallest, and therefore most vulnerable, of our little patients, the potential impact is especially great.

For the last 3 months, I’ve been teaching critical event training classes for our OR and Perioperative RNs, Anesthesia MDs and CRNAs, and OR techs in preparation for opening our new hospital in San Diego. Several of the scenarios involved pediatric cases. As part of that process, I’ve been reviewing with my providers ways to avoid the potentially deadly problem of pediatric drug dosing errors as well as ways to avoid them. Let’s discuss some of the ways to make pediatric medication administration safer. Continue reading

Ventilation Perfusion Mismatch

Alveolar gas exchange depends not only on ventilation of the alveoli but also on circulation of blood through the alveolar capillaries. In other words it depends both on ventilation and perfusion. This makes sense. You need both oxygen in the alveoli, and adequate blood flow past alveoli to pick up oxygen, other wise oxygen cannot be delivered. When the proper balance is lost between ventilated alveoli and good blood flow through the lungs, ventilation perfusion mismatch is said to exist.

The ventilation/perfusion ratio is often abbreviated V/Q. V/Q mismatch is common and often effects our patient’s ventilation and oxygenation. There are 2 types of mismatch: dead space and shunt.

Imbalance between perfusion and ventilation is called ventilation perfusion mismatch. This illustration compares shunt, the perfusion of poorly ventilated alveoli; and Physiologic dead space: the ventilation of poor perfused alveoli.

Shunt is perfusion of poorly ventilated alveoli. Physiologic dead space is ventilation of poor perfused alveoli.

This article will describe how dead space is different from shunt. It will help you understand how you can use these concepts to care for your patient. Continue reading

Help! My Anesthesia Machine’s Not Working!

There is nothing quite as scary as being in the middle of administering an anesthetic and having your anesthesia machine fail. In my 36 years of anesthesia practice I’ve had this happen to me a few times. Knowing how to quickly troubleshoot your machine, and knowing how to protect your patient are important, potentially life-saving skills. It helps to have thought through the steps to rescue the situation before it happens to you.

Here I describe how I learned this lesson the hard way on a volunteer medical mission to rural Honduras. When my machine failed, I was poorly prepared and this forced crisis management that I could easily have avoided with a little forethought and preparation.
Continue reading

Codeine Risk In Children, Especially Those With Sleep Apnea

Although the initial FDA warnings about potentially fatal overdose from codeine in children were released in 2012, I’m recently discovered that a few of my surgeon and nursing colleagues were still unaware of the potential risks. Therefore I thought it might be helpful to bring up the topic so people can remind their own colleagues of the risks of codeine in children.

Codeine must be used with extreme caution, if at all, in young children or pregnant women because of variants in the enzymes some patient’s use to metabolize the drug. Continue reading

Alert: We May All Be Over-Inflating Our LMA Cuffs!


Since its invention, the Laryngeal Mask Airway, or LMA, has become quite valuable as a surgical airway alternative to intubation. When I first started in anesthesia, the only way to avoid intubation during surgery was to manually assist ventilation with a bag-valve-mask attachment. Cases that went on for hours often resulted in cramped fingers, and sometimes progressively poorer ventilation over time as the hand holding the mask became overly tired. A poor mask seal could potentially cause the stomach to distend with air, pushing up the diaphragms, limiting tidal volume, and increasing the risk of aspiration. The LMA has changed anesthesia so much that residents now find it challenging to find cases to practice their masking skills.

However, the LMA is so commonly used, and so apparently safe, that it’s easy to become complacent. Research is showing that it’s apparently very common for us to over-inflate our LMA cuffs — to the potential harm of our patients. Continue reading

Potential Tongue Ischemia with LMA Supreme

When we place anything in the mouth, be it an endotracheal tube, oral airway or LMA, we are typically extremely careful to protect the teeth. We take care to avoid cutting the lips with the teeth. But we often take the safety of the tongue for granted. I recently recognized a potential problem while using an LMA supreme that could have caused tongue ischemia if not corrected. Let we show you what happened so you can be on guard with your own patients.  Continue reading

Apneic Oxygenation: Increase Your Patient’s Margin Of Safety During Intubation

While breathing room air, oxygen saturation drops precipitously to below 90% within about a minute of the start of apnea in the average healthy adult. As we saw in a previous blog post, preoxygenation is one of the most important safety measures we can use prior to induction of anesthesia and in preparation for intubation. Adequate preoxygenation can more than double the time to hypoxia during open airway apnea, allowing more time for intubation to occur. However, increasing the time to critical hypoxia from 1 minute to 2 or 3 minutes with preoxygeation, as important as that is, can still be too short if the intubation turns out to be truly challenging. Apneic oxygenation is an easy technique to increase the time to desaturation significantly. However you have to know how to optimally provide it in order to safeguard your patient  Continue reading

Preoxygenation Can More Than Double The Time To Hypoxia During Apnea

While breathing room air, oxygen saturation drops precipitously to below 90% within about a minute of the start of apnea in the average healthy adult. One of the most important safety measures we use in anesthesia is to preoxygenate our patients prior to induction of anesthesia and in preparation for intubation. This is especially true if we are planning a rapid sequence induction. Adequate preoxygenation can more than double the time to hypoxia during apnea, allowing more time for intubation to occur.

Preoxygenation increases the margin for safety. It treats any pre-existing hypoxemia in the critically ill patient. It also postpones the onset of hypoxia while the patient is apneic during the intubation attempt. This becomes especially important if the intubation attempt becomes difficult and prolonged.

Speed of onset of hypoxia with apnea depends on metabolic rate and on the actual amount of oxygen available in the patient’s functional residual capacity. To see how preoxygenation can effect this let’s review some physiology. Continue reading

Don’t Withhold Oxygen From That CO2 Retainer

There is often a great deal of confusion about how to manage the care of a patient with COPD because of unwarranted, and incorrect, concern that all patients with COPD are CO2 retainers. This fear of causing CO2 retention sometimes causes providers to withhold or withdraw oxygen inappropriately. Understanding some of the respiratory physiology behind CO2 retention will allow you to make more informed decisions. Let’s start at the beginning. Some of this material comes from my book Anyone Can Intubate, 5th Edition. Continue reading

To Extubate, Or Not to Extubate, That Is The Question

Assessing extubation criteria, and then deciding when to extubate a patient safely can sometimes be a difficult decision.

Extubation Criteria

We all know the common extubation criteria:

  • recovery of airway reflexes and response to command;
  • inspiratory capacity of at least 15 ml/kg;
  • no hypoxia, hypercarbia, or major acid/base imbalance;
  • no cardiopulmonary instability;
  • signs of intact muscle power;
  • absence of retraction during spontaneous respiration;
  • absence of a distended stomach.

In other words, you want your patient to be stable, able to breathe without help, and able to protect the airway.

However, sometimes the decision is not so easy. Here I describe a case of a patient who met some but not all of the criteria for extubation. The reason turned out to be due to a rare complication: plugging of the endotracheal tube. However, getting to that solution required working through the extubation algorithm.  Continue reading

Ventilate and Intubate But Don’t Forget Communicate

Failure to communicate, and making assumptions rather seeking true facts,  can endanger your patient. Many years ago I was participating in a volunteer medical mission to Kenya when I learned a valuable lesson in communication which I often share with my students. In this case, multiple providers made bad assumptions about what the others knew that led to a potentially dangerous situation involving intubation.
Continue reading

Avoiding Medication Errors

Humans are fallible and unfortunately medication errors can occur easily. On my hospital’s wards, and indeed on most hospital wards, when medications are drawn up, the nurse must check the medications, dosage and labeling with another nurse before administering the medication. In fact, in my hospital the pharmacist also checks all of the orders to make sure allergies and other drug conflicts have not been overlooked. This is a wonderful safety feature, but it’s time consuming and labor intensive.

In the OR, during anesthesia, things are happening quickly – too quickly to have a second person constantly checking each medication draw. The anesthesia provider is drawing and administering the medications solo. That added responsibility means we have to be extra vigilant. There are many things that can predispose to medication error

A Mistake From My Own Past

Picture of multiple syringes and vials on a work station

It’s easy to grab the wrong syringe if your work station is not organized.

It can happen to anyone, even me. About twenty five years ago I was giving a routine “local with sedation” anesthetic in a healthy patient. One of the CRNAs came in to see if I needed anything. As I was talking to my colleague, my patient said he was still nervous. I told the patient, who had already received some valium, that I would give him a “little more medicine that would help him relax“. At that point I accidentally picked up the 5 ml anectine syringe rather than the 5 ml valium syringe. Continue reading

Use Of A Nasal Airway To Assist Ventilation During Fiberoptic Intubation

Attaching a nasal airway to a breathing circuit as a tool to assist or control ventilation is a very helpful trick to have in challenging airway management situations.

Illustration of An alternate means of ventilation — insert an endotracheal tube connector into a nasal airway as in a. Place the nasal airway, close the opposite nostril and mouth. Ventilate as in b.

An alternate means of ventilation — insert an endotracheal tube connector into a nasal airway as in a. Place the nasal airway, close the opposite nostril and mouth. Ventilate as in b.

The Case

Many years ago I was taking care of a 40 y.o. man had Ludwig’s Angina, a serious, potentially life-threatening cellulitis infection of the tissues of the floor of the mouth, often occurring in an adult with a dental infection. Continue reading

How Does Hypoventilation Cause Hypoxemia?

I often find that my students sometimes confuse oxygenation and ventilation as the same process. In reality they are really very different. Ventilation exchanges air between the lungs and the atmosphere so that oxygen can be absorbed and carbon dioxide can be eliminated. Oxygenation is simply the addition of oxygen to the body. You must understand the difference to understand how hypoventilation causes hypoxia.

If you hyperventilate with room air, you will lower your arterial carbon dioxide content (PaCO2) significantly, but your oxygen levels won’t change much at all. On the other hand, if  you breathe a high concentration of oxygen, but don’t increase or decrease your respiratory rate, your arterial oxygen content (PaO2) will greatly increase, but your PaCO2 won’t change.

Ventilation changes PaCO2. Oxygenation changes PaO2.

Why do we need to understand this? Let’s look at some common examples. Along the way we will painlessly use the Alveolar Gas Equation to explain two common scenarios:

  • how hypoventilation causes hypoxia,
  • why abruptly taking all supplemental oxygen away from a carbon dioxide retainer will hurt them.

Continue reading