[shortnurse75]

LZone, on Sep 13 2008, 11:38 AM, said:

I never heard of it but how about spontaneous pneumomediastinum?

I googled on day 1 and thought of this too. But I was n't sure since he wasn't SOB.

[Mike MacKinnon]

So....

Do you take the chance of needling the chest? Or wait and see what happens?

Why can you hear bilateral breath sounds?

Generally I would not needle a chest in a conscious patient, would you in this case?

Whats the worst thing that could happen if you do not needle the chest and the outcome?

Whats the worst case if you do needle the chest, afterall, noone can say he "didnt" have a pneumo after that eh?

[Gila]

No, I needle him. So, I put a little hole in his chest wall. I do not think he will tolerate the current situation much longer. He potentially buys the farm if we continue to delay. Regarding lungs sounds, I have seen a fair number roll through the ER having what I though were bilateral breath sounds, only to find out they had a large pneumo after an x-ray was completed. Clinically, this guy is presenting like a pneumo.

[Flightgypsy]

I don't think I would needle him with the vital signs we have been given so far unless things have drastically changed. Update on the vitals, Mike?
Besides if it is pneumomediastinum needling him in the usual places won't really achieve much and may just make it worse. If you think it is a pneumothorax on one side, which side are you going to needle, both? Does one side sound hyperresonant to percussion if we are not already on the go and can hear? Any other signs starting to happen such as dysphonia, dysphagia or SQ emphysema?

I would only needle if he developed severe hemodynamic compromise in which case I would start on the right if I have no clues for which side the tension might be on. I would also err a little closer to the sternum then usual maybe. I wouldn't wait until he was pulseless to needle but would wait until I was seeing more hemodynamic compromise. What if it isn't a pneumo after all and he is still having a MI? Giving him a pneumo might be the last straw his stressed heart might be able to handle. (Just playing the devil's advocate here ).

If he develops severe enough hemodynamic compromise I don't think you have to worry too much about him being too conscious but hopefully the Fentanyl we have given him will blunt it somewhat. Once he is stable again then give him more analgesics.

I have needled a conscious patient with a flail chest. He was in so much pain anyway he barely reacted to the needle. We had also given some fentanyl as well.

[jbflightnurse]

I'm with flightgypsy....I don't think I'd needle him. I'm not convinced that its a pneumo. And yes...good point...why can we hear bilat breath sounds?

[Flightgypsy]

I'm not sure about bilateral breath sounds as it is conceivable for breath sounds to be transferred to the other side as someone noted. Also with a pneumomediastinum you should still have bilateral breath sounds unless the lungs are totally squished and then you wouldn't have any of the other life signs either.

Just a thought.

[Speed]

Quote

Do you take the chance of needling the chest? Or wait and see what happens?

Within the next five minutes or so you may be able to get a better picture, or you may be able to start reassessing now and feel more confident. He is getting more short of breath rather quickly. So you have to think that it's expanding. You would expect to see the NIBP drop and start losing lung sounds even though they've been unremarkable so far. I would be leaning towards decompressing it.

Quote

Why can you hear bilateral breath sounds?

Maybe there wasn't enough air trapped yet? Maybe you were hearing the right lung resonate to the left wall?


Generally I would not needle a chest in a conscious patient, would you in this case?

Sure. Not saying it's right but thousands of residents put in chest tubes without adequate local anesthesia (in too big of a hurry). A painless chest tube is possible, but this is an emergent situation.


Whats the worst thing that could happen if you do not needle the chest and the outcome?

He could become hypoxic, seize, anoxal brain injury, hemodynamic compromise from a lack of LV filling, and lose his LV pre-load from the infarct. The loss of his pre-load may not kill him now, but could sure limit his quality of life (old man fast).


Whats the worst case if you do needle the chest, afterall, noone can say he "didnt" have a pneumo after that eh

Noscomial pneumothorax, vessel laceration with hemothorax (or you could "way remotely" introduce free air into central circulation/emboli/CVA), shock & arrest, denervation of the left chest wall, inadvertent puncture of the pericardium with the possibility of lacerating a coronary vessel (MI) or myocardium leading to a tamponade (highly unlikely with proper technique).

[Mike MacKinnon]

Huhu

WICKED assessment flightgypsy!

The right side is hyperresonant to percussion.

If you wanted to needle him now you could by using a little lido and localizing the area before you put the needle in, or (as many said) if you wait just a bit it wont matter.


So end result, you have 3 choices.

1) Wait till he passes out (which he will eventually)
2) give some fent which blunts the pain and results in him passing out quicker
3) local and needle awake.

So you needle him and he almost instantly gets better.

The result was that this pt was doing crack resulting in spontaneous pneumo which became a tension. He is clearly in great shape and young so compensated well. The vital signs were not changing much because of the crack itself (acting as a stimulant). You not seeing the HTN only because the pressure on the inferior vena cava is limiting preload. The EKG is showing you this pattern because there is ischemia in the right atrium d/t compression. He is able to compensate his sats because he is young. Filling one lung (in the absence of lung Ds) is enough to keep his sats up. He became slightly tachypenic to increases exchange further compensating for the loss of a lung. His body does something called hypoxic pulmonary vasoconstriction (HPV) which constricts the arteries and veins on the affected lung which significantly decreases the V:Q mismatch and so helps him compensate further as the blood volume is shunted to the left lung where the exchange is still taking place.

Freaky eh?

[Speed]

Ah, right side. So was the RCA being compressed? By just the lung? This has got to be rare. What would V3R-V6R have looked like? Why the R wave anomaly on the left?

[EDMEDIC]

another great case, Mike....brian

[Mike MacKinnon]

Well, not really RCA compression but the whole right side of the heart was compressed resulting in inability to move coronary blood through to feed the atrium. There are actually a number of case studies published on this very thing. Odd eh?

As for a right sided EKG, id expect to see exactly the opposite. Depression in II III AVF and elevation on the precordial leads. Hard to say for sure tho.

R wave on the left is likely unrelated to the case and more related to the EKG i used for the case (older person), tho it shouldnt really throw anyone off Unless it was left sided probably wouldnt see low voltage.

Speed, on Sep 14 2008, 10:05 AM, said:

Ah, right side. So was the RCA being compressed? By just the lung? This has got to be rare. What would V3R-V6R have looked like? Why the R wave anomaly on the left?

[rfdsdoc]

Thanks Mike!
Always learn something with your cases.
The EKG was in fact a complete distraction!
I am bit surprised about the bilateral breath sounds given the tension pneumo.
well done to the flight crew for picking it up before they got flying!
It would have been very hard to figure out the diagnosis inflight.
We carry a Sonosite 180 portable ultrasound and it would have been more helpful for me than the EKG in making the diagnosis .

And he WAS taking speed!

cheers for the teaching !

[rfdsdoc]

Here's the article I think you got the EKG from, Mike?

I found a Japanese letter to this article reporting something similar.

And the article reports a LEFT tension pneumothorax so can we necessarily say the EKG would look the same for a right sided one?

It all seems a bit theoretical (the explanation of the EKG changes) and what is described is interesting but to me goes to show that basic history and examination is the CORE of your clinical skills.

I would shudder to think if people started doing routine EKGs to diagnose a pneumothorax!

Anyway great teaching case, thanks mate!

Minh

Chest. 1999;115:1742-1744.)
© 1999 American College of Chest Physicians

New ECG Changes Associated With a Tension Pneumothorax*
A Case Report
Brian Strizik , MD and Robert Forman , MD
* From the Division of Cardiology, Department of Medicine, Albert Einstein College of Medicine, Jack D. Weiler Hospital, Bronx, NY.



Abstract
TOP
Abstract
Introduction
Case Report
Discussion
References


This case report reveals new ECG changes associated with a left tension pneumothorax, specifically, PR-segment elevation in the inferior leads and reciprocal PR-segment depression in the aVR lead. A mechanism of atrial injury and/or ischemia is proposed as the cause, and the ECG changes associated with a left tension pneumothorax are briefly reviewed.


Key Words: atrial injury • atrial ischemia • ECG • PR segment • tension pneumothorax


Introduction
TOP
Abstract
Introduction
Case Report
Discussion
References


The ECG manifestations of a tension pneumothorax have been well described. For a left tension pneumothorax, these include a rightward shift of the mean frontal QRS axis, reduced precordial R-wave voltage, decreased and/or alternating QRS amplitude (electrical alternans), or precordial T-wave inversions.1 Commonly, two or three of the above are present, and less often, all four are present. We present a case of ECG manifestations that have not been reported before (to our knowledge), such as PR-segment elevation and depression associated with a left tension pneumothorax. These ECG changes were transient, and they promptly reverted to the baseline on relief of the tension.


Case Report
TOP
Abstract
Introduction
Case Report
Discussion
References


An 82-year-old woman presented with acute onset of shortness of breath and left-sided chest pain. Her medical history was significant for > 80 pack-years of smoking and GI bleeding from diverticulosis. On presentation to the emergency department, her BP was 140/80 mm Hg, with a pulse rate of 148 beats/min and a respiratory rate of 34 breaths/min. Her oxygen saturation, as measured by pulse oximetry, was 94%. On physical examination, she was in mild respiratory distress, she was without jugular venous distention, and she had diminished breath sounds in both lung fields. An ECG revealed atrial fibrillation with a ventricular response of 150 beats/min. She was placed on a regimen of 100% oxygen with the use of a face mask and was given IV diltiazem, which slowed her heart rate to 80 beats/min. Her mental status and oxygen saturation then progressively declined. On emergent intubation, her symptoms and oxygenation improved. However, she suddenly became hypotensive, and her oxygenation saturation dropped once again. Results of her physical examination at this time were remarkable for absent breath sounds over the left lung and distended neck veins. The chest radiograph (Fig 1 ) showed a 100% left tension pneumothorax. The ECG (Fig 2 ) showed a bizarre pattern of sinus tachycardia at 100 beats/min with a first-degree atrioventricular block, 8 mm of PR-segment elevation, which particularly occurred in the inferior leads (II, III, and aVF) and was accompanied by PR-segment depression in the aVR lead, very low-amplitude r waves in the precordial QRS complexes, and an isoelectric QRS complex in V6. A chest tube was immediately placed in the patient, and the pneumothorax and bizarre ECG manifestations (Fig 3 ) were resolved. In addition, there was a marked increase in the R-wave amplitude in the precordial leads, a shift in the horizontal axis toward normal, and resolution of the PR segments to the baseline. The patient subsequently died from pneumonia and sepsis 4 weeks later.





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Figure 1. Chest radiograph showing a 100% left tension pneumothorax.







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Figure 2. ECG revealing marked PR-segment elevation in the inferior leads and PR-segment depression in the aVR lead in a patient with a 100% left tension pneumothorax.







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Figure 3. ECG demonstrating resolution of the PR-segment changes following relief of the left tension pneumothorax.





Discussion
TOP
Abstract
Introduction
Case Report
Discussion
References


Numerous mechanisms have been proposed whereby a tension pneumothorax may cause ECG changes. Simple displacement of the heart has been reported to cause only minor changes.2 ,3 Others have proposed that rotation around the posteroanterior or longitudinal axis causes shifts in the heart's axis as well as loss of anterior forces and precordial R waves.4 ,5 Air within the thoracic cavity has also been suggested as a cause of the ECG changes.6 Although both Lewis2 and Dieuaide et al3 have shown that changes caused by air in the thoracic cavity are minimal, others have said that it is the combination of retrosternal air and rotation around the longitudinal axis of the heart that causes the ECG changes.5
Our case represents the unique finding of the PR-segment elevation in inferior leads with reciprocal PR-segment depression in the aVR lead. After an exhaustive search of the literature, we found that this has never been reported (to our knowledge) in conjunction with a pneumothorax, with or without tension. We propose that the mechanism behind the PR-segment changes is atrial ischemia or injury.

Some ECG changes that have been reported to occur in a left tension pneumothorax have been attributed to a "cor pulmonale theory," which says that a sudden rise in intrathoracic pressure increases pulmonary vascular resistance, which, in turn, leads to a decrease in coronary blood flow and an increase in inward pericardial force.1 The ECG changes attributed to this theory were ventricular in origin, and they included loss of R-wave7 and T-wave inversions1 ; however, no P-wave changes were noted. We propose that a combination of inward pericardial force and atrial injury was the mechanism behind the very marked PR-segment elevations in the inferior leads and the PR-segment depression in the aVR lead in our patient. With the sudden rise in intrathoracic pressure in a left tension pneumothorax, the heart rotates clockwise and rightward, leaving the inferior surface and the left atrium in close proximity to the collapsed lung. With air under tension, force is placed on the collapsed lung, which translates into force also being placed on the heart; consequently, the blood flow of the left atrial branch of the circumflex artery may be jeopardized, or the direct pressure that is placed on the left atrium could lead to atrial injury. This would persist only if the tension remained unrelieved. Although our patient's cardiac enzyme levels were normal, the "ischemic" period only lasted for 15 to 20 min, and at least 45 min is necessary to elicit permanent myocardial damage. In support of our theory that the heart was displaced rightwardly and rotated clockwise are the ECG manifestations of electrical neutrality seen in lead 1 and the positive ECG forces seen in the inferior leads. This phenomenon is transient, and it is reversed by releasing the tension. As this happens, the affected left lung expands, the compressive or injurious forces on the epicardial surface are released, blood flow is restored, and the ECG changes revert to the baseline.

The mechanism we have proposed is highly speculative and theoretical, and it has not been verified scientifically. We encourage readers to communicate with us about their own interpretation via the correspondence column or e-mail.

[jbflightnurse]

GREAT case Mike. Always a great learning opportunity. I still can't figure out breath sounds with that significant tension pneumo. huh......

Thanks again.

[JPatterson]

I know that for people that are tall and thin and for smaller pneumo's, you will still have bilateral breath sounds because you would still have enough lung volume in that side of the chest to make the difference barely or not noticeable. I also think that we would have seen the answers to some of our questions earlier to make this dx faster if the pt was right in front of us. We could have seen JVD, retractions, chest expansion/exertion, WOB. All of which would have made us look harder at resp. before cardiac.
The other thing that you need to remember is that in small pneumos (even small symptomatic ones causing CP) high flow O2 can correct them due to gaseous diffusion. This can be important when you have a pt present like a pneumo (non-tension) and at the receiving facility, they do not significantly prove to on X-ray (longer transports). Of course they would be less or asymptomatic at that point.
Sorry if this is scattered...long night
JP