Hypoxia and Medicine

Brain anoxia and reperfusion iojury?

I have come to know the following happens during a cardiac arrest. 1) Anoxia during cardiac causes exitotoxosis due to the ischeamic cascase. This is evident here... http://en.wikipedia.org/wiki/Ischemic_cascade So why are there no covulsion during a cardiac arrest no matter how long it lasts? 2) Reperfusion injury where reoxygenation starts using the built up glutamate store in the brain to over-exite the brain. This is evident here... http://en.wikipedia.org/wiki/Reperfusion_injury But I do not hear much about patients convulsing then. They may be having a very long form of atonic convulsions during cardiac arrest or reperfusion injury, but how would we know? http://en.wikipedia.org/wiki/Atonic_seizure Do you know if they do, and if they do not why, because reading all the stuff it says about ishemic cascades, it does not add up with what really happens to cardiac arrest patients. What is it that I am missing here, explain in detial? CREED

Public Comments

1. contact a doctor
2. Convulsions, or seizures, are generated by sustained, uncontrolled, inappropriate electrical activity of the brain. On the whole, you're not going to get a whole lot of that in an ischemic episode: no oxygen, no conversion of glucose (or other molecules) to energy, no sustained electrical activity. No sustained, uncontrolled, abnormal electrical activity, no seizure. Hardly that simple, but hey, it's pretty close. What the anoxia (and hypoxia, in the penumbra, or rim, of inadequately perfused tissue around the stuff that isn't getting anything) does is trigger the release of compounds that try to cause an increase in the local blood flow. (A lot of these compounds are pre-formed and stored, requiring little or no energy use to release) The same thing is going to happen with ischemia that doesn't progress to frank anoxia. When the circulation gets back to normal (for whatever reason) these chemicals are going to cause a massive delivery of oxygen to the cells. One of the major events is a sudden calcium influx into the neurons--which can kill the neuron. Dead neuron equals no significant electrical activity in the neuron; go figure. The consumption of the glutamate generates chemical byproducts that can be irritating, and there are highly oxidizing compounds produced during the re-oxygenation, but again, these damage neurons rather than generate bizarre electrical activity. I've been at, oh, something over 200 cardiac arrests; people don't seize because there just isn't enough blood flow to produce the seizure activity--either at the brain level, or at the muscular level, frankly. Believe me, in over 200 cardiac arrests, I've never seen one seize. No one I know has ever seen it, either, except when the seizure (or its cause) causes the cardiac arrest... I think I've given you the information you've missed: seizure activity takes energy, and in a cardiac arrest, there's pretty well not enough of it to drive the activity. Hope that helps