Packing blackout

I think they are just saying that the release of myoglobin supports their theory or findings that packing blackout can cause "a serious cardiac incident if the lungs are excessively overinflated by glossopharyngeal insufflation."
I'm gonna guess that myoglobin is released for recovery of lung and respiratory related injuries to aid in O2 transportation and storage after being injured.

It sounds like they are suggesting that the myoglobin concentration is raised by mechanical damage to heart tissue that is trying to pump, but is being blocked by the overinflated lungs. My understanding is that myoglobin is intracellular, so it shouldn't be in the serum.
Anybody know more about it?
Howard

The myoglobin is intracellular and should not be in the serum. When the myocardial cells (heart muscle cells) are damaged, myoglobin is released from the intracellular fluid into the blood. This indicates that cells were actually damaged by the incident. That's why the increase in myoglobin concentration in serum (in addition to the asystolic periods) is of concern.

I haven't been able to read more than the abstract, however, only CK-MB or TnT are the real biomarkers for damage to the heart. Further, the ECG should also be able to show disturbances, which haven't been described by the authors in the abstract. CK elevation can have different explanations, I should read the whole article to review if other causes then the packing black-out can have cause this, including the severity of the described asystole.

This will be a post with very detailed info regarding cardiac biomarkers and ECG. Maybe of interest to some, but I guess not to everyone...
The "medicine uninterested reader" can jump to the last paragraph of this post for the summary...


Rik, I agree that serum elevations of CK-MB and TnT have higher specificity for myocardial damage than myoglobin. But also myoglobin is released during myocardial damage, even though a rise in myoglobin may also be found in conditions related to skeletal muscle damage. However, it is most unlikely that skeletal muscle could have been adversely affected by the packing blackout, i.e. skeletal muscle is unlikely to be the origin of the myoglobin release in this specific case. Also, myoglobin is the one of these three biomarkers that increases first in serum (myoglobin has a high sensitivity in the early phase, but a lower specificity). Already 40 min after the incident we saw increases in myoglobin. CK-MB and TnT needs 2-4 h after a damage to be detectable and have their peaks in serum 24-48 h after. Unfortunately we were unable to get a blood sample from this diver the day after to measure CK-MB and TnT, which would have been most interesting. Instead we had to settle with reporting what we were able to observe.

Concerning the ECG, about 4 s into the apnea and 6-7 s before the packing blackout, without any preceding sinus bradycardia, a ventricular extrasystole occurred. Immediately following this, the normal sinus rhythm changed to sinus arrest with nodal escape, including two periods of asystole with R–R intervals of 6.6 and 7.3 s. An arterial blood pressure recording confirmed the periods of asystole (with blood pressure quickly falling from 120-140/80-90 mmHg before the apnea to below 70/35 mmHg during the nodal escape beat following directly after the onset of the packing blackout).

That a packing blackout could be associated with dysrhythmia and increased myoglobin had never been described before. But I guess that is understandable as most freedivers are not connected to an ECG-recorder or has blood drawn for analysis of cardiac biomarkers everytime they pack...
Not that I think that this happens everytime you pack, not even with every packing blackout, but it may be of interest knowing that it may happen so that it can be included in a risk evaluation.


The main conclusion from this case is that susceptible individuals may be put at risk of a serious cardiac incident if the lungs are excessively overinflated by the use of packing (besides the other risks that may be associated with packing; air embolism, pneumomediastinum, increased risk for pulmonary edema?).

/Johan