Hypoxia and Medicine

Why cellular hypoxia cause bradycardia and abolition of pacemaker activity? Why cellular hypoxia depolarizes the membrane potential causing bradycardia and abolition of pacemaker activity? Because I figure it should accelerate heart rate so called tachycardia?

How does hypoxia cause cardiac arrest? I am a medical student on placement in A&E and recently saw a patient who had a cardiac arrest caused by hypoxia. I was trying to find out the mechanism of this but could find no answers, and no papers. Does anyone know or know of any papers? Thanks

possible causes of hypoxia are? a. too little oxygen in the atmosphere b. too many red blood cells c. taking too many rapid deep breaths d. getting very cold

what can be the possible causes of cyanosis? see i was surprised when i suddenly noticed that i had a mild case of cyanosis this morning.. i just noticed that my fingerpads were a light shade of cyan/bluish green.. not really deep blue.. but still disturbing.. haha.. how is this so? is it because i lack sleep? yesterday i woke up at about 2pm in the afternoon and i was up all night until today.. i only noticed the discoloration on my fingers this morning.. they're almost gone now, only a slight tinge of blue left.. barely visible.. but the bluish color lasted all morning, for a few hours.. can sleep deprivation eventually cause hypoxia of some sort? cause i don't know if it does.. haha.. although i had only been sleepless for a night, a week ago, i was sleepless for about two nights straight, with only naps of about an hour each night.. if that helps.. lol.. so.. theories anyone? or better, any diagnoses coming to mind? haha.. i'd really appreciate anything.. my curiosity about it is killing me just about now.. lol.. thanks a lot guys.. ; )

Can a tight ponytail cause hypoxia? A close friend of mine were hanging out, and she had a ponytail, and she kept making mistakes and was confused. She said she had a headache and I joked around with her saying "your ponytails too tight!". Ever since, when she does something weird or "stupid", I say "your ponytail must be too tight". All of a sudden, I wondered if a ponytail tied too tight could actually cause hypoxia which can cause confusion and etc, all of which she had. Perhaps, if not hypoxia (which I'm skeptical of....seems a bit far-reached) some other ailment? I just wanted to reaffirm that I was more than skeptical in that it could cause hypoxia, seeing as it is not reasonable, rather, what I should have said- "Is it plausible" that it could happened- not that it was likely hypoxia. Also, for some odd reason, I felt that perhaps by a ponytail being so tight that it pulls at the skin drawing blood upwards and somehow affecting the amount of blood circulating and low oxygen would cause a hypoxia of sorts. It wasn't my point in actually stating that hypoxia was the cause. Sorry for the miscommunications!

How long would a coma caused by aquatic hypoxia span? If someone fell into a coma from aquatic hypoxia, would it take a short amount of time, or would it vary like most other cases would? I want to know for a story, and I'd really like even the most vague answers, but really just to know if it could last for up to a few months or indefinitely(weeks, months, years, etc.). Thanks.

Info about lactic acid buildup in muscles? I'm great at developing workout routines. I've been learning as much as I can about how and when to exercise certain muscle groups. Unfortunately, I still know very little about the chemical processes that take place. I know that lactic acid levels build up as muscle use is continued, and that lactic acid is the result of hypoxia. Why does the lack of oxygen cause hypoxia and can anything be done to stave-off lactic acid buildup?

Can you be anaesthetised for a blood test? Weird question I know, but I need a blood test but I'm absolutely terrified of the idea :/ So is it possible to be anaesthetised beforehand or would it affect the blood..? And would a doctor actually do that? Pluuus.. What happens if anaemia is left untreated? I read that if can cause hypoxia which can cause comas and stuff, and now I'm scared. But I'm really way too scared to even think about having the blood test. FML. Thaaaanks <3

Is hypoxia or lack of oxygen causing the mass animal deaths all over the world? I personally think it is hypoxia. What is causing the lack of oxygen or inability to process it I don't know. Is it somehow related to the dispersants that were flooded into the oceans after the gulf oil spill? Maybe the toxins turned gaseous and were absorbed into the atmosphere. Please tell me what you think.

my husband has been told he is hypoxic following a bout of pneumonia. what else might cause this hypoxia? the hosp consultant told him if his blood gas levels do not improve next time he goes to see him then they will have to look for another cause for the hypoxia not the pneumonia. he mentioned among other things leukemia but my husband can't remember what else was mentioned. any ideas? my husband was in hospital two years ago and was told his oxygen sats were low but nothing was done to follow this up. he has not felt completely well since this time. he has been diagnosed with sarcoidosis(levels under control at the moment) and also oesophageal spasms.

oxygen deficiency is called hypoxia.suggest two possible causes of inadequate delivery of oxygen to body? tissues...

Does thumbsucking cause brain hypoxia? as well as holding the blanket up to one's nose and inhalling during 8 hours of sleep?

What would be the effects of a liquid cyanide solution on slightly abraded skin? Would this be fatal, or just cause minor hypoxia? Serious replies from knowledgeable repliers only, please. This is for a fictional story. A character has a small abrasion on their hand, which ends up in a Jim-Jones-style vat of cyanide laced Kool-aid for a few seconds (lethal amounts of cyanide). I know this could allow cyanide into the bloodstream, but would it lead to death like its ingestion would?

The only possible cause of death is hypoxia, right? If you put it really generally, then hypoxia (lack of oxygen) is the only way to die, right? I mean, that's what it comes right down to.

ascending hight altitudes may cause what type of hypoxia ? i have a question in my workbook , the question is : choose : ascending hight altitudes may cause what type of hypoxia 1-stagnant 2-anemic 3-histotoxic. 4-hypoxic

A cardiovascular cause of hypoxia is:? a) Asthma b) Diabetes mellitus c) Dementia d) Anaemia

are you a medical expert? A 10-year old boy is diagnosed with asthma at age 3. His asthma was triggered by upper respiratory infections (URIs) and more recently by dogs. He was hospitalized with hypoxia and began using a long-acting beta agonist twice daily 2 years ago; he took amoxicillin and used an inhaled steroid during URIs only. If you have to educate the parents of the child about the nonallergic asthma, which immune process will best explain this form of asthma; why part of this immune defense process causes hypoxia and which medication has been prescribed to slow down the nonallergic asthma?

what is hypoxia? what is stage one ulcer, and what causes it? what is edema? my grandmother passed away were trying to understand some of the medical reports.

Questions about G Forces and G-LOC? When subjected to high G forces, fighter pilots try to force all their blood to go the brain or else it will all rush to the lower half of their body and cause hypoxia. Why is this so? Why doesn't the blood rush to the upper half of the body? Is it because G force increases weight and makes blood go in the direction of gravity? What if the pilots were upside down? What if they were on their back? Where would the blood rush then?

What affect does hyperventilating have on arterial levels of pCO2? a. It increases pCO2 and may cause acidosis b. It decreases pCO2 and can cause alkalosis c. It causes hypercapnia and hypoxia

how do you know if your hypoxia? i am training for marine recon for another 2 years and i swim subsurface to increase my lung capacity and i really don't want to go hypoxia's cause that would suck what are the symptoms of it and what is it exactly i usually swim 25 meters underwater where i really cant stand not breathing and i have to surface i do this 10 times so i think im okay i don't think im close to hypoxia but if someone can tell me the symptoms of it and if someone can tell me how long do i have to stay underwater before i get it.

can sex cause minor cerebral hypoxia? i feel spaced out for about three days after sex.? in addition to feeling spaced out, my speech/motor functions decline for about the same amount of time after sex. these symptoms are so sever that i'm forced to avoid sex. my doctor is puzzled and wanted to send me to a shrink. i think i'm fucked. i have thalesemia minor so i'm thinking that that may have something to do with it my eeg showed slowed brain waves too which i think may support my theory that i'm not getting enough oxygen to my brain i'm 21 years old and shouldn't have slowed brain waves

how long does hypoxia need to last to cause damage? multiple episodes lasting a few minutes not taking in any more air unable to move/speak excrutiating pain fully conscious..most times near loss of consciousness 1x we have no way of telling what the saturation was..bp is fine 20 years since last incident how long does it take O2 sats to drop significantly when no more O2 is being taken in (trapped under water for example)

What causes the size and shape of the dead zone to vary? Regarding hypoxia and dead zones

AP biology ecology question? Fish kills occur each summer in many central Florida freshwater ecosystems. These are most common in lakes surrounded by citrus groves, farmlands, or extensive development. These fish kills are caused by hypoxia (oxygen depletion) in the ecosystems. Place the order of events that causes the hypoxia. I. Large amounts of nitrates and phosphates draining into the lake or river II. Rapid algae growth III. Rapid bacterial growth on dying bacteria IV. O2 depletion V. Fish death

PLEASE HELP WITH THIS? Not sure how to answer this question? I've got a health project to do at it has to follow this format: Sample Outline on Cerebral Palsy (Question: Why do people get Cerebral Palsy and how can they be helped?) I.Introduction A.Each year more than 10,000 infants are diagnosed with CP B.Definition of CP C.Presentation will describe causes, symptoms and treatments II.Causes A.Hypoxia (lack of oxygen) in the uterus or during birth process B.Illnesses C.Head injury D.Risk Factors 1.Delivery problems 2.Low birth weight & premature birth 3.Multiple births 4.Maternal illnesses III.Types A.Spastic (50%) B.Ataxic (10%) C.Dyskenitic (20%) D.Mixed (20%) IV.Symptoms A.Delayed development of motor skills B.Mental retardation (sometimes) C.Sensory abnormalities D.Spasticity affecting one side of the body, one limb or both arms and legs V.Diagnosis A.MRI of the head B.CT scan of the head C.Hearing screen D.Visual testing E.EEG VI.Treatment A.Types of therapy B.Specialized equipment C.Surgery D.Support groups VII.Ways others can help A.Support groups B.Volunteer work C.Donations to United Cerebral Palsy VIII.Conclusion A.Restatement of thesis B.Call to action My question is "What are the health benefits of owning a pet?" I am not sure how to answer the ways that others can help and the call to action... I am also not sure what to write for the introduction..:(

PLEASE HELP ME? I DON'T UNDERSTAND HOW TO DO THIS? I've got a health project to do at it has to follow this format My question is "What are the health benefits of owning a pet?" I am not sure how to answer the ways that others can help and the call to action... I am also not sure what to write for the introduction..:( Please help??? Sample Outline on Cerebral Palsy (Question: Why do people get Cerebral Palsy and how can they be helped?) I. Introduction A. Each year more than 10,000 infants are diagnosed with CP B. Definition of CP C. Presentation will describe causes, symptoms and treatments II. Causes A. Hypoxia (lack of oxygen) in the uterus or during birth process B. Illnesses C. Head injury D. Risk Factors 1. Delivery problems 2. Low birth weight & premature birth 3. Multiple births 4. Maternal illnesses III. Types A. Spastic (50%) B. Ataxic (10%) C. Dyskenitic (20%) D. Mixed (20%) IV. Symptoms A. Delayed development of motor skills B. Mental retardation (sometimes) C. Sensory abnormalities D. Spasticity affecting one side of the body, one limb or both arms and legs V. Diagnosis A. MRI of the head B. CT scan of the head C. Hearing screen D. Visual testing E. EEG VI. Treatment A. Types of therapy B. Specialized equipment C. Surgery D. Support groups VII. Ways others can help A. Support groups B. Volunteer work C. Donations to United Cerebral Palsy VIII. Conclusion A. Restatement of thesis B. Call to action

Nitrous Oxide/Oxygen Deprivation Damage? In my life I have inhaled 140 balloons full of pure nitrous oxide. Each time I inhaled the contents, then breathed it back into the balloon and repeated the process about four times for about 10-20 seconds without oxygen. Each time I did it my vision blacked out but I remained conscious. I read that vision black outs are a result of severe hypoxia caused by oxygen deprivation and that nitrous oxide displaces oxygen in the blood. What are the chances I did permanent damage to my brain, heart and body?

Does this scenario causing chest trauma make sense? Let's say someone is playing football when tackled by two offensive players. The force causes him to break two ribs on the left side. One of the ribs penetrate the lung which causes a pulmonary laceration and hemopneumothorax. The hemopneumothorax causes his left lung to collapse, hemoptysis (coughing blood), severe pain, rapid breathing and heart rate, and hypoxia which causes loss of consciousness and a coma. He also has a small pulmonary contusion on the right lung, a severe concussion, a dislocated shoulder and a large hemotoma covering his left side. Does this scenario make sense or am I missing some elements? It is for a story I am beginning and I need to ensure the accuracy of this incident. Thanks so much, I appreciate the help.

why no changes in partial pressure of oxygen in the case of anemia hypoxia? The hypoxemia definition as decreased partial pressure of oxygen excludes decreased oxygen content caused by anemia (decreased content of oxygen binding protein hemoglobin) or other primary hemoglobin deficiency, because they don't decrease the partial pressure of oxygen in blood. this is from wiki.. correct me if I'm wrong. 1) The Hb are independent towards partial pressure of oxygen. but why is that, since Hb decrease,less amount of oxygen carried.but no difference in partial pressure?

Had a back molar extracted a fewdaysago,finding it hard to keep socket clean? My dentist says I have a wisdom yooth growing upward underneath where the molar was - I hadn't expected a wisdom tooth at 50+ - so it must be important to try to keep the area clean, but how? I've tried toothpicks, a fine toothbrush and absolutely loads of swilling and rinsing, but I'm still left with residual gunk (that's the technical term for food that's starting to break down!) and which, more importantly in some ways, makes my breath smell foul and leaves a disgusting taste in my mouth. I've got through more mothwash than you'd believe just trying to get rid of the taste/smell. Has one of you whizzo folks out there any advice to offer me, other than avoiding public places for fear of causing mass hypoxia? Cheers, Denise

Where can I find specific information about brain damage/delirium caused by near-drowning? I can find plenty of information about things like brain hypoxia that causes brain damage and delirium, but have yet to find a specific article/case study/piece of research that suggests any sort of severe/long-lasting delirium as a result of a person nearly drowning. In other words, supporting evidence is abundant, but I can simply not find information on a specific case or study that shows or confirms it. I just have a bunch of information that suggests that a person, after nearly drowning, might experience delirium as a result of brain damage from hypoxia. Can anybody help me out, maybe point me towards a good article or case study or something? Maybe I'm just using the wrong search terms, who knows. (NOTE: The newer the information, of course, the better)

Can Cerebral hypoxia(lack of oxygen to the brain) brain damage be caused by intense exercise?

I'm thinking about humanely euthanizing my male betta, he is suffering, do you think its the right thing to do? I have no idea what is wrong with him. He was in a 10 gallon heated tank but one of his front fins disappeared so he had trouble swimming to the top, and he didnt move at all in the tank. I put him in about a 1 gallon bowl and he still isnt moving. I fed him flakes about 3 days ago he didnt eat them. He isnt eating anything. He looks dead--he used to get excited ALL the time whenever I would come up to him, or at least make eyecontact..but now he just looks dead, but hes not. I feel so bad, hes been like this for about a week or two. His other fin is gone, maybe its fin rot? I thought that could only happen to his long tail. I think its too late for treatment..His front fins are basically gone, and the stubs that are still there are shredded. He looks miserable. I think he had a good life in his 10 gallon tank--I've had him for about 5 months and I'm tired of seeing him suffer, so i'm STRONGLY considering humanely euthanizing him. I was looking up humane ways and found this on a website: "Also known as eugenol, clove oil is a sedative at low doses, but at higher doses it has been recommended by some researchers as an inexpensive way to euthanize fish, particularly small fish. In a container, mix aquarium water with clove oil and mix. When exposed to high concentrations of clove oil, fish quickly lose consciousness and stop breathing, both of which reduce pain. Hypoxia eventually causes death, and once verified, the fish can be removed from the water and clove oil mixture. The required dose for euthanasia is 400 mg/l or more. Clove oil contains some substances believed to be carcinogenic and should be handled with care." Do you think this is good? I didnt know he was suffering from fin rot if thats what it is, and I think its too late, and I just hate seeing him like this. He is always breathing heavily and he looks completely miserable. PLEASE help :( He moved in a different positions and i see 2 white spots on him, one under his eye and one on his stomach. He has ick too...GOD THIS ISNT FAIR I FEEL SO BAD I FEEL LIKE CRYING..

Which of the following is most descriptive of multiple sclerosis? A. Diease in which mylein sheath is gradually replaced by scar tissue B. neuromuscular disorder caused by a deficiency of dopamine C. Brain death due to cerebral hypoxia D. Increased intracranial pressure that causes downward displacement(herniation) of the brain stem thanks

help !! my son has cp and seizures caused by doc but we cant get a lawyer to take the case? need a lawyer here my son is 3 1/2 years old when i was 7 months pregnant i had an appendicitis that the doctor ignored for a week , he even tried to send me home from the hospital when i went in and told me they needed the bed for someone who actually needs it, after 9 hours i finally got him to do bloodwork by saying i would not leave i feel like im dying and then they ended up rushing me to emergency surgery....then 10 days before he was born he quit moving and i went to the ob and he said no big deal and i was like yes it is and begged for a week for them to give me an ultrasound to see if the baby was ok, they wouldnt.... he was born with the cord wrapped around his neck and body - the neurologist says he is disabled because of either the infection went on to long or the cord caused a gradual hypoxia over a period of days.......this is the obs fault ! my son has been tested and does not have a genetic disorder....he has mild cerebal palsy and seizures and cannot talk he will be four in april i had an emergency appendectomy after they wouldnt listen to me for a week, and tried to kick me out of the hospital for 9 hours telling me i had round ligament pain while i wqas throwing up green and orange bile and screaming i was dying....the ob had taken blood work a week before that showed i had an infection but wouldnt pay me any mind - also the cord thing is the ob fault because the neurologist said the reason my baby didnt move for the last ten days was because the cord was wrapped and he wasnt getting enough oxygen... if they had done an ultrasound like i asked them to they could have taken the baby earlier and he would not have suffered as much damage to his brain...either way the obgyn is responsible - they threatened to have securtity take me out of the hospital because they said i was not dying and was only trying to get pain meds - i am not a drug addict! here i was 7 months pregnant and having appendicitis, then after the surgery they didnt monitor the baby either

There is no such thing as an "afterlife" experience, agree? When your heart stops your brain still functions for about 10 minutes. During that time you can have all sorts of hallucinations. Since the oxygen-rich blood is not pumped into your brain anymore you can suffer from cerebral hypoxia which also causes all sorts of hallucinations. So, I don't buy these stories where people "died", saw heaven/hell and then were "returned" back to life. I'm saying people who claimed to have seen afterlife are wrong because they were not actually dead. I'm not making any assumptions. It's common knowledge that the brain is the last organ to stop functioning when a person dies. I'm not denying the possibility of the afterlife. Some people need to read questions more carefully.

your top causes of mortality? so, what do you see in your practice as your top causes of patient death. #1 hypotensive shock. #2 hypovalemia. #3 massive brain stem/brain damage #4 body segmented into parts not compatible with life and decapitation. #5 hypoxia due to pulmonary or airway damage. (gunshots in neck and lungs, barotrauma from over pressure, ect) at least I dont have to see people who smoked and ate them selves to death! :P I'm a Russian military medical technican and these are my top 5 reasons for a death.

Can anxiety and stress cause light-headedness and shortness of breath? I'm generally a pretty anxious person, though today I haven't been worrying that much. However, I do feel a little weird -- almost like when one stands up really fast and gets dizzy, except it's nowhere near as noticeable. Instead, it's just like a background feeling. Could this be from my frequent worrying and stress, even though today I'm not that stressed? Or perhaps it's from fatigue? Any thoughts? I don't wanna end up having hypoxia or something.

Can gas explosions cause oxygen starvation? Is there any kind of domestic gas explosion that can cause oxygen starvation? Could there possibly be a situation during an explosion where a person could get hypoxia? This is for a work of fiction, so I have some artistic license.

can you give me any info on.... hypoxia (fainting), and how fetal hypoxia can affect persons in later life? hi, basically... i suffered from serious carbon monoxide poisoning along with my mother when she was pregnant with me. i was born severely underweight and my mum was given drugs in order to force her to give birth to me to survive. I was roughly 5Ibs. then as I was about 11, i discovered i needed glasses, and this has led to my sight getting worse and worse, and now im nearly 17, and its pretty shite. the opticians told me on three occasions that the arteries and veins int he back of my arms were tiny, incredibly small. i'd also started the frequent passing out stages and being always dizzy once standing up from since I was about 12, till now. it tends to go up and down. could that be a side effect of the carbon monoxide thing? my dads also got severe bowel cancer in his family... i dont know if thats relevant or not, but basically he gets this aswell.. basically, wehnever we go to the toilet, number 2 wise!!!!, if we've got bad stomachs or we're ill, we pass out while going, and its pretty god damn painful and stressing. thats another issue, i went to the doctors and they told me that it could be caused by the bowels pressure squashing nerves or vessels supplying the brain with oxygen and shizz.. thats hypoxia. i am rather underweight, and in general im average heghted but they skinny and light... any advice or stuff, or general info that can help me? cheers :) I MEANT VEINS IN THE BACK OF MY EYES! not arms xD hahaa

Mild Cerebral Hypoxia - would the Urgent Care facility be equipped to test for that? I have symptoms of mild cerebral hypoxia. I've had them before, on and off for over two years, so I'm not concerned that it's a stroke or anything that urgent...however I do have symptoms of a lack of oxygen and it's frustrating and I'm considering going to the Urgent Care facility. We've been there before and it's very ...low tech. I don't want to sit in the ER for hours, that will just stress me out and cost way too much. Does anyone know offhand if there's any common way for the doctor to know oxygen levels to the brain, at a typical urgent care facility? If the cause was blockage in the left carotid artery... would there be a way to test for that? A blood gas would have to be sent out to a lab and take time right?

What are the effects of hypoxia at birth? Lets say a baby is born with the umbilical cord wrapped around it's neck and not breathing. If that baby is revitalized, has it suffered from hypoxia? If it has, what are the long term effects the child could have? I know of a child who was born like this, he is a-sexual, anti-social and has very strange behaviour plus he's extremely apathetic and has no "close" relationships, but this person is very intelligent, with no signs of brain issues other than ADD, Chronic insomnia, poor immune system and occasional light headedness. I'm just wondering if this is all caused from his birth experience. This is more for curiosity than anything else. Oh and the mother smoked while pregnant and who knows what else she did.

Will my new, 6-week-old puppy be able to fly in a plane safely? (an air-pressure and potty question)? A friend told me that the change in air pressure within a plane cabin during flight could cause the puppy to get pressure sickness and ultimately hypoxia (which is caused by a lack of sufficient air), which can lead to death. I have to fly on June 11th, by which time, the puppy will be 6 weeks old. I plan on an in-cabin flight for the puppy. No cargo for her. The ride should be no more than 4 hours cumulatively, with one, one-hour stop-over. Most airlines require that a puppy be at least 8 weeks old before flying, but some do not. It would make sense that these airlines have such an age restriction to protect themselves from liability or to protect the puppy itself. Has anyone flown a puppy as young as 6 weeks? Why does the age restriction exist for so many airlines? Is it dangerous to fly a puppy younger than 8 weeks (and why)? Also, how long does it take for a puppy to pass food?

Need help answering this question...Describe the impact of flight & time zone changes on physiology.? I need to include the following: Causes, symptom's and effects of: Hypoxia Hyperventilation Dehydration Circadian Rhythm Effects of time zone changes on the body clock (Jet lag) I am studying Cabin Crew and trying to finish the last of my assignment and got a little stuck. Any help would be appreciated. Thanks in advance Sarah x

Pulseless electrical activity? Do you have an idea of how hypoxia(low oxygen) may cause pulseless electrical activity?

is acquired brain injury and traumatic brain injury the same thing? i am doing a project on acquired brain injury, but whenever i google it i get results to traumatic brain injury... i was wondering if tbi is a type of abi. i understand that tbi is from an external force, like bumping your head. i also understand that abi is caused by things like hypoxia, strokes and ischemia. but when i look on wikipedia tbi is mentioned in the abi category. i cannot make a mistake on this or i lose huge marks in my class. 20% of my final mark in chronic health care is on this one project!

cardiac arrest:science and practice of resuscitation? i've read this book at a medical library at the UCONN library at Farmington, CT a few years ago. I came across some information about bradyasystolic rhythms and it mentioned that hypoxia and hybercarbia(high carbon dioxide) frequently cause bradyasystole by directly depressing cardiac pacemaker function and by causing increasing parasympathetic discharge. do you know how they cause both ? the textbook was a 1996 edition.

Why does atelectasis cause opacification on chest x-ray? I don't understand why a collapse of the alveoli (from obstructive or non-obstructive causes) will cause the lobe to "white-out." Found a possible explanation here http://www.pharmpedia.com/Atelectasis that states that pulmonary edema follows hypoxia in the collapsed lung. Does this mean that in atelectasis, the lung is actually filled with fluid and that's why it appears white on xray?

Birds fall from sky. Whats the reason? Here's the story below...what do you think? n five days wildlife experts and forestry officers have picked up more than 1,000 dead turtle doves and other birds including pigeons. Yesterday alone, 300 corpses were recovered. The incident in the town of Faenza in northern Italy comes after a series of similar cases in the US and Sweden. All the birds had a blue tinge to their beaks. Scientists say this indicates poisoning or hypoxia – lack of oxygen which causes confusion. Millions of dead fish have also washed up on river banks and coasts in Arkansas and Texas and in New Zealand. The turtle dove incident is the largest to hit Europe so far. Fifty jackdaws were found dead in Sweden. Faenza forestry official Dr Anna Mazzini said: “My opinion is that it is probably food poisoning.” Yesterday a local newspaper wrote: “Let’s hope it is poisoning. That would be easier to deal with than a sign the world is ending.” Read more: http://www.express.co.uk/posts/view/221846/Mystery-as-1-000-birds-fall-from-skyMystery-as-1-000-birds-fall-from-sky#ixzz1AQVunOfM

Is it possible the evidence is stacking up? Have you ever thought about this before? Question to believers. It has been noted in the medical field that there are explanations for religious experiences: abnormalities in the temporal lobe It has also been noted that you can induce out of body experiences by stimulating the right angular gyrus the cause of near death experiences: hypoxia Could it be that the god stuff is all in your head? gunner..hahaha..cute :)

How many cigarettes (in a row) would it take for you to die? Firstly, I don't smoke, so please no 'omg ur ruining ur life!' answers. I am interested in knowing the possible toxicity of cigarette smoke in relation to a normal person? Even simple over-the-counter drugs like aspirin have recorded lethal dosages (generally .2g/kg-.5g/kg), but I have been unable to find the 'lethal dosage' of cigarettes, if there is one? I would imagine it is kind of hard to find a lethal dose of cigarettes since there are many factors involved, but for the fun of it, let's say a man starts smoking, and just doesn't stop, I would imagine eventually tar build up in his throat would eventually cause asphyxiation, other chemicals that replace oxygen would cause him to die from hypoxia (as we see in Carbon Monoxide poisoning), or simply poison from one of the other thousands of lethal chemicals in cigarettes? how long before he/she would 'over dose' on cigarettes?

I just discovered that a childhood friend has some sort of brian disease/disorder that caused her to regress? She is at the mental capacity of a 7/8 year old. I am so sad and confused. What could have possibly caused this? She was FINE at the age of 16!... by 18 she had started to regress... now at the age of 22, she is mentally back to our days of dress up. ANY ideas???.. she did not have a stroke, and suffered no hypoxia of any kind... no car accident either.

Can a 21 year old sue for birth trauma 21 years ago, that caused her brain damage? given new understanding of interpreting fetal heart monitoring and such? This case showed fetal distress, hypoxia, she was in special ed her whole life, but at the time they said it wasn't the cause...now some experts DO, does it matter? If men can sue 30 years after sexual abuse, without proof other than what they say, can't she with all the medical records? Thanks

Has anyone here had a? near death experience? What did it feel like? FYI: Cerebral hypoxia (lack of oxygen in the brain) causes your pineal gland to release the neurotransmitter dimethyltriptamine (DMT). This is why some kids enjoy choking each other to the point of passing out. DMT is the same neurotransmitter that causes you to dream. A hydroxylated alkaloid of this neurotransmitter is the active ingredient in "magic" mushrooms.

Do people really take near death experiences seriously? Being a cardio-vascular patient, I've had a few. Lack of oxygen to the brain causes some really messed up hallucinations sometimes. How can anyone consider these hypoxia induced dreams as meaningful? Some even put enough stock in it to consider it some kind of "proof" of the supernatural. During my stroke last year, I saw a blond in a bikini smiling at me....... turned out to be a fat guy with a crash cart ready to defib. lol DcubeD: the blog was funny, and the child is adorable (almost as cute as mine) ;) lol

opioid overdose? do you know how hypoxia from an heroin overdose may cause hypotension late in the course of opioid poisoning. i read it in the Goodman & Gillman pharmacology book.

Do hyperventilation and the resulting hypocapnia cause brain damage? I was recently diagnosed with Hyperventilation Syndrome. I never faint from over-breathing, but I do experience tingling in my hands, lightheadedness and dizziness. Hyperventilation causes hypocapnia (a reduced amount of CO2 in the bloodstream, and thus vasoconstriction in the brain), but can this lead to permanent brain damage? From what I have researched, it seems that hypocapnia can lead to cerebral hypoxia, and thus kill off brain tissue. I did not think to ask my doctor when I was with her, so maybe a doctor could answer my question on here before I have to schedule another appointment. Thanks; I appreciate it!

lack of oxygen to brain at night? ive had this problem for over a year now. When im lying down on my bed about to sleep, i get these weird episodes where i feel like half-fainted and my heart has stopped, and afterwords my heart beat becomes stronger and faster and blood rushes to my head. Tis happens a couple times at night and only at night. Could this be hypoxia, where im not getting adequate amount of oxygen to my brain? please tell me what's causing this and has it caused brain damage?

Does this football injury make sense with this scenario? Let's say that someone is playing football and ends up getting tackled with enough force to cause two broken ribs, a dislocated shoulder, and a severe concussion. Let's say that as a result of two broken ribs, the lung on the left side gets penetrated causing a pulmonary laceration. The pulmonary laceration causes a hemopneumothorax, which causes severe breathing complications. The person would be coughing blood as a result of the hemothorax and wouldn't be able to breath properly because of the collapsed lung caused by the pneumothorax. Since the person isn't getting proper oxygen, they would suffer from hypoxia and loss consciousness after several minutes. Does this all make sense and what would be the course of action at a high school football practice? Let's say one of the other plays decides to give CPR and oxygenate the person while the ambulance is arriving. When the ambulance arrives they would insert an endotracheal tube to help the the person breath until they get to the hospital, where they would insert a chest tube to reinflate the collapsed lung. Does this make sense, and if not, how could I correct it? I know I have already asked this, but I didn't get much feedback. I am hoping more people will be on and able to answer this question. I need to know if it at all possible, I am using this idea for my story.

Does thumbsucking cause brain hypoxia? as well as holding the blanket upto ones nose and inhalling during 8 hours of sleep? what are the side effects?

The skin and subcutaneous fat provide little insulation in hot weather but very effective insulation in...? cold weather due to what? READING 3 VASODILATION AND VASOCONSTRICTION: During times of thermal stress, heat must be dissipated into the environment or contained within the body. The body's temperature is monitored and controlled by special neurons in the hypothalamus that respond to the temperature of the surrounding blood. This has been demonstrated by experiments which found that when implanted electrodes are used to change the temperature of the hypothalamus, the body's temperature-regulating mechanisms are fully activated, even though the temperature of the rest of the body is unchanged. When the temperature of the hypothalamus is above 37 �C, the heat loss mechanisms, such as vasodilation and sweating are activated, and when the temperature is below 37 �C, the heat conserving and heat generating mechanisms, such as vasoconstriction and shivering, are activated [12]. The body uses changes in blood circulation and changes in the thickness of the skin to control heat loss under different temperature conditions. The rate of heat conductance to the surrounding environment is influenced by the "countercurrent" system of blood flow [13]. This employs two systems of venous blood flow in the limbs: the deep venea and peripheral veins. In addition, subcutaneous fat enhances the control of insulation achieved by changes of peripheral blood flow [14,15]. In a cold environment most of the venous return from arms and legs is through the deep venea comitantes that receive heat from blood flowing through the arteries and thereby minimizes heat loss. Thus heat conductance to the periphery is low, yet actual blood flow to the limbs may be high, protecting tissues of the limbs from cold injury and hypoxia. In a hot environment most of the venous blood flow returns through the peripheral veins, and because they are close to the surface, heat loss to the environment is increased. By this pathway, external heat loss is maximized with high conductance [13]. When the blood vessels of the skin are dilated, the subcutaneous fat can have little effect, since warm blood is moving through to the surface, where heat exchange with the surrounding can take place [14]. The dermis-epidermis combination changes effective thickness by virtue of involuntary, lateral muscle movements which govern the depth of blood capillaries carrying the heat energy to be thrown away: in the cold these capillaries retract, thus increasing the effective thickness of the insulation [15]. After vasoconstriction of the blood vessels at the dermis-epidermis, this shunt no longer exists, and heat exchange must take place through the fat [14]. A. Capillary retraction B. Lateral muscle movements C. Vasoconstriction D. All of the above causes the skin and subcutaneous fat to insulate effectively in cold weather.

Can you please summarize this... in English? OK, I am supposed to be doing research on some topics, but, medical websites like to use humongous words... I was wondering if any doctors or anyone could translate this into language a 14 y/o would understand... Or, can you please just give me the gist of each paragraph? Thanks! Amyotrophic lateral sclerosis (ALS) is a disease of unknown cause characterized by slowly progressive degeneration of upper motor neurons (UMNs) and lower motor neurons (LMNs). The UMN findings include hyperreflexia and spasticity. They result from degeneration of the lateral corticospinal tracts in the spinal cord. The LMN findings include weakness, atrophy, and fasciculations. They are a direct consequence of muscle denervation. ALS is eventually fatal because of respiratory muscle weakness. Aspiration pneumonia and medical complications of immobility contribute to morbidity. _________________________________________________ Lower motor neuron signs include weakness, atrophy, fasciculations, and depressed reflexes. Fasciculations are observed with the muscle at rest. Upper motor neuron signs include an upper motor neuron pattern of weakness (greatest in the extensors of the arm and flexors of the leg), spastic bulbar and limb muscles, hyperreflexia, and extensor plantar responses. A hyperreflexic jaw jerk helps to confirm upper motor neuron involvement causing dysarthria and dysphagia. Tendon reflexes are paradoxically brisk. In patients with pseudobulbar palsy, emotional incontinence may cause the patient to over-react to sad or funny things. The patient is aware of the lack of control. Cognitive impairment, if present, most often is observed in patients with bulbar involvement. Muscle cramps are common for patients with lower motor neuron involvement, while patients with upper motor neuron dysfunction can have clonus or painful extensor spasms. Ocular, sensory, or autonomic dysfunction occurs only very late in the disease course, usually in patients living with ventilatory support. The key finding in an involved limb is the combination of lower and upper motor neuron dysfunction with a weak, atrophic, fasciculating muscle occurring in combination with increased tone and hyperreflexia. * Lower motor neuron signs include atrophy and fasciculations. * Upper motor neuron (ie, corticospinal tract) signs include spasticity and hyperactive tendon reflexes and may include the Babinski sign. * No loss of anal sphincter tone occurs. Cardiac and smooth muscle are not involved. * The course is progressive, and initial symptoms primarily are those of weakness. * Weakness often is asymmetric and begins in the legs, arms, or oropharyngeal muscles with approximately equal frequency. Masticatory weakness occurs late. Ultimately, weakness becomes symmetrical. * Ocular musculature is not involved. * Muscle atrophy and weight loss almost always are recognized by the time the patient seeks medical treatment. * Fasciculations may be quite widespread and active. Surprisingly, the patient often ignores this symptom. * Patients may have inappropriately active tendon reflexes and weak, wasted, twitching muscles. * Muscle cramps are common. * Dysarthria, exaggeration of motor expressions, and emotional lability (pseudobulbar affect) may occur when the disease process involves the corticobulbar projections to the brainstem. * Decubitus ulcers are rare. * Hypoxia or cardiac arrhythmias are the most common cause of death in patients with ALS. The primary cause of death among patients electing to use ventilatory support is pulmonary infection.

How do I comfort my friend, I'm in tears myself? Hey, so my friend (she's in 7th grade) has a 10 year old sister and she's having some problems. If you'd like, read the super long email below sent from her mom. If not, I'll sum it up at the bottom. They'll be a dash-line where it ends. Tia was born full-term 10 years ago last month (March). She was slightly jaundiced but otherwise healthy. We took her home and returned when she was 3 days old due to her choking and slightly turning blue after she nursed and while she slept. Our oldest daughter had moderate to severe GERD so we were very familiar with the symptoms and assumed Tia had the same problem. The doctors agreed and put her on medication and an apnea monitor. At 2 weeks of age Tia was hospitalized for Jaundice. At 6 weeks she was hospitalized for RSV. Tia was again hospitalized for RSV when she was around 18 months old. She continued to cough, choke, gag and vomit massive amounts of mucous and slept in 15 minute increments. We lived in and out of emergency rooms, hospitals and doctors offices. She has even been rushed by ambulance from the doctor’s office to the hospital. Over the entire 10 year span Tia has had 2 sleep studies, she has been scoped 3 times, checking all of her airways, tonsils, adenoids, lungs, scarring, etc., she has had 2 MRI’s, 2 EEG’s, 2 EKG’s, 2 Cystic Fibrosis tests (she was borderline), countless x-rays, allergy tests, immune tests and so on. She has been on every nebulized drug available, she has been on numerous steroids and antibiotics and nothing works, no inhalers, no allergy meds, nothing! She spent 3 days with an oximeter attached to her which indicated she has intermittent hypoxia…but why. No one can find the cause of Tia’s breathing problems, her constant dips in oxygen, her lack of oxygen while sleeping. The sleep tests confirmed she is not getting enough oxygen but that there is no obstruction, she does not have Apnea. We have countless videos of her odd breathing while she is asleep….the doctors are alarmed by what they see and hear but again, cant figure out what is causing it. Once Tia clears and starts breathing again she is no longer blue and shows no sign whatsoever of being ill or having problems. (note: there have been times where Tia was seen by various specialists while she was sick and experiencing the breathing problems. They would always try things like Albuterol, Pulmicort, Symbacort….and the list goes on….and nothing would help. 2nd note: Tia has done much better over the past couple of years where she sleeps and has less frequent nights like last night *read below* We thought..hoped she might be outgrowing this problem but sadly she is not.) Last night was an extremely chaotic stressful night. Tia was fine, took a bath, brushed her teeth and went to bed. She has been recuperating from what the doctors initially thought might be whooping cough but she was not congested and she was only coughing a few times per day. Shortly after she went to bed I could hear some really odd sounds coming from her room….sort of a grumbling. When I went in I found Tia blue in the face struggling to get air. She was coughing, choking and she was completely congested. I screamed for my husband and the two of us raced to try everything we have learned to do in the past to help her breathe. Last night was the worst in 10 years. If we had been asleep, in the shower or both downstairs where we didn’t hear her…..she would have been gone. Thankfully that is not the case, I had the phone in my hand to call 911 but we were able to help her clear her airways and then she was fine. I took her to the doctors today and after giving him the details he said that was very consisted with Cyanotic Episodes and that we should immediately call 911, don’t take any chances. The only reason we were hesitant to call is because we have done that so many times in the past and they end up not doing anything for her. They give her a breathing treatment and call it a day. This has broken us financially, this has broken us physically and has broken us mentally. We are exhausted. BUT, we have not lost our determination to figure out what this child needs! (*note: the doctor is not convinced it was whooping cough because her symptoms have resembled whooping cough all of her life. It isn’t possible that she had whooping cough 4-6 times per year….is it?) Tomorrow we go back to the Pulmonologist and in a week we go back to the Neurologist at the MIND clinic an hour away. Please, I beg of you, if you know anyone or have experienced anything like this yourself and know what it is or what we can do to help her…please please please contact us! There has got to be an answer out there somewhere…there just has to be! She has suffered long enough…..more importantly, we don’t want to lose our little girl! Can you help us? ------------------------------------------------------- Well, there. I'm in tears. But here's how to sum it up for the people who didn't read i OMG I guess it was too long and Y!A cut it off Suming it up: My friends sister Tia had trouble breathing as a baby, and it's coming back. The doctors just said it was a 'whooping cough' but it wasn't. Last night her mom heard a growling noise from Tia's room and came in to find Tia blue-faced and choking. The doctors have put her on practically everything, but nothings working. I'm not looking for answers on how to help, I'm just looking for how to help my friend get through this, it's hurt it really bad emotionally.

Coughing, choking... anyway to solve it? Below is all about my friend's sister. They are desperate for anything that may help them. If you know of anything, PLEASE answer below Tia was born full-term 10 years ago last month (March). She was slightly jaundiced but otherwise healthy. We took her home and returned when she was 3 days old due to her choking and slightly turning blue after she nursed and while she slept. Our oldest daughter had moderate to severe GERD so we were very familiar with the symptoms and assumed Tia had the same problem. The doctors agreed and put her on medication and an apnea monitor. At 2 weeks of age Tia was hospitalized for Jaundice. At 6 weeks she was hospitalized for RSV. Tia was again hospitalized for RSV when she was around 18 months old. She continued to cough, choke, gag and vomit massive amounts of mucous and slept in 15 minute increments. We lived in and out of emergency rooms, hospitals and doctors offices. She has even been rushed by ambulance from the doctor’s office to the hospital. Over the entire 10 year span Tia has had 2 sleep studies, she has been scoped 3 times, checking all of her airways, tonsils, adenoids, lungs, scarring, etc., she has had 2 MRI’s, 2 EEG’s, 2 EKG’s, 2 Cystic Fibrosis tests (she was borderline), countless x-rays, allergy tests, immune tests and so on. She has been on every nebulized drug available, she has been on numerous steroids and antibiotics and nothing works, no inhalers, no allergy meds, nothing! She spent 3 days with an oximeter attached to her which indicated she has intermittent hypoxia…but why. No one can find the cause of Tia’s breathing problems, her constant dips in oxygen, her lack of oxygen while sleeping. The sleep tests confirmed she is not getting enough oxygen but that there is no obstruction, she does not have Apnea. We have countless videos of her odd breathing while she is asleep….the doctors are alarmed by what they see and hear but again, cant figure out what is causing it. Once Tia clears and starts breathing again she is no longer blue and shows no sign whatsoever of being ill or having problems. (note: there have been times where Tia was seen by various specialists while she was sick and experiencing the breathing problems. They would always try things like Albuterol, Pulmicort, Symbacort….and the list goes on….and nothing would help. 2nd note: Tia has done much better over the past couple of years where she sleeps and has less frequent nights like last night *read below* We thought..hoped she might be outgrowing this problem but sadly she is not.) Last night was an extremely chaotic stressful night. Tia was fine, took a bath, brushed her teeth and went to bed. She has been recuperating from what the doctors initially thought might be whooping cough but she was not congested and she was only coughing a few times per day. Shortly after she went to bed I could hear some really odd sounds coming from her room….sort of a grumbling. When I went in I found Tia blue in the face struggling to get air. She was coughing, choking and she was completely congested. I screamed for my husband and the two of us raced to try everything we have learned to do in the past to help her breathe. Last night was the worst in 10 years. If we had been asleep, in the shower or both downstairs where we didn’t hear her…..she would have been gone. Thankfully that is not the case, I had the phone in my hand to call 911 but we were able to help her clear her airways and then she was fine. I took her to the doctors today and after giving him the details he said that was very consisted with Cyanotic Episodes and that we should immediately call 911, don’t take any chances. The only reason we were hesitant to call is because we have done that so many times in the past and they end up not doing anything for her. They give her a breathing treatment and call it a day. This has broken us financially, this has broken us physically and has broken us mentally. We are exhausted. BUT, we have not lost our determination to figure out what this child needs! (*note: the doctor is not convinced it was whooping cough because her symptoms have resembled whooping cough all of her life. It isn’t possible that she had whooping cough 4-6 times per year….is it?) Tomorrow we go back to the Pulmonologist and in a week we go back to the Neurologist at the MIND clinic an hour away.

Premature Infant Neurological condition? An infant is born two months early due to abruptio placenta and is later diagnosed with mild spastic cerebral palsy approximately two years later. Due to the early birth, his lungs were under-developed and could not sustain the needed oxygen levels needed for life on their own. Therefore there was no gas exchanges in the lungs from the moment of the complication to the time of being placed in an incubator. During that time, He suffered cerebral hypoxia (lack of oxygen in the brain), which caused damage to the motor cortex, the cause of the Cerebral Palsy. How long would it take for the child to develop Cerebral Palsy due to the lack of oxygen under these conditions? How long does it take from start to finish, for a lack of oxygen in the body to cause enough damage in the motor cortex to initiate Cerebral Palsy? What is the possible chance (percentage) of legally dieing on the table (so to speak) and being resuscitated again under these conditions? Does anybody know? The child was me (I'm 32 now). I've got mild right spastic hemiplegia and paralysis. No, no one (family) seems to know the answers or seems to give a crap about it and I've got very little paperwork from the doctors, so accurate information is a bit scarce on the birth. So I'm just trying for basic generalizations. I know it seems silly to ask these types of questions after the damage has already been done but I cannot seem to shake it, no matter how hard I try.

heroin overdose? do you know what heart rate changes may occur in a heroin overdose and do you how hypoxia in heroin overdose (due to decreased respiratory drive) may cause hypotension late in the course of the intoxication ?

can anyone answer these accurately? Too much nitrogen in the waters of Long Island Sound (or any body of water) can cause excessive algae growths called blooms. What problems are associated with algae blooms? Some nitrogen entering the Sound is from natural sources, but human activities increased by 400 percent the amount of nitrogen entering the Sound. What are the sources of nitrogen from human activities? In 1990 a project was undertaken, by various agencies in New York (NY) and Connecticut (CT), to reduce nitrogen loads from human activities. Examine the two graphs near the bottom right of the page. Based on the information in those graphs make two statements about the way things are looking or going as a result of the efforts made in that project. Write one statement that comes from the interpretation of each graph. a. Nitrogen from Sewage Treatment Plants: b. Area and Duration of Hypoxia: Now look for some detailed information in each graph and write one statement of fact from each graph. For example: In the year 2002, the total nitrogen fell to its lowest point; about 144,000 lbs per day. Based on the trends shown in the graph, Nitrogen from Sewage Treatment Plants, what would you expect to happen in the year 2005? Explain your answer.

Medical ppl help! Just to clarrify a few points...(note if u cant answer any pls dont post to say look it up)? 1) T1 and T2 resp failiure are characterised by hypoxia and hypercarbia respectively... Does this mean certain resp conditions can only cause T1 or T2 - if so which ones... (I mean eg- asthma can obviously cause T1 resp fail, but I guess it could cause T2 as well?could it?) 2) Adrenaline is the same as epinephrine right? Just a different name isnt it? (I ask cos someone said adrenaline was the natural version of epinephrine - is that right?) 3) A MAP of above 65 is req to avoid renal failiure.. Does this mean kidneys are first to go in inadequate perfusion? 4) RE: Sepsis - one can be 'septic' if they have only 1 infection that affects the SIRS score adequately? t/f? (cos I thought that sepsis ((before)) that sepsis req more than 1 infection?) 5) Where are cardiac pacing wires inserted in the heart? And do they ever stay 'paced' on these wires for prolonged periods of time? Thanks in advance, just wanted to clarrify a few questions, feel free to answer even 1or2 if u can thanks

which of the following is correct...? 21.In the ischemia hypoxia stage of shock, which of the following is the dominating humoral factor that can cause vascular constriction of microcirculation ( ) A. AngiotensinⅡ ↑ B. Vasopressin ↑ C. Catecholamine ↑ D. MDF ↑ E. TXA2 ↑

i need a doctors help pleaseon my sillborns post mortam results? i have been reading the post mortam of by still born baby which i lost in March this year . i need help with medical words i will write word for word and could some one help please? the pathologist noted that there were abnormal utero-placental perfusion with villous crowding and fibrin disposition. the pathologist made a diagnosis of idiopathic ante partrum hypoxia. when i went for the verbal results they said they did not know what caused his death just lack of oxygen . some help with these medical words would be greatfully apreciated thank you dont know why some one gave you the thumbs down .. at least ur trying to help. i have asked doctors why my son died they said oh just lack of oxygen

How does rice enhance ripening in fruits? hi! i am currently doing a science project that revolves around the tradition of putting mangoes in rice tins to enhance its ripening. I need to explain why it happens, and test out if it is really true. although after several researches on the internet, i haven't really found anything concrete or leading me directly to the reason. possible reasons is that the rice induced with ACC synthase leads to ethylene production (which ripens fruits), but according to it "In rice, ethylene production is greatly enhanced by hypoxia because of the induction of ACC' synthase. The enhanced ethylene production is thought to be responsible for the increase in intemodal length" I tried to search if rice produced ethylene normally (like after harvest when we commercially buy it), but i can't find anything. link to rice&ACCsynthase website: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC300938/pdf/mbc00098%2D0017.pdf apparently, abscisic acid (a plant hormone) also hastens fruit ripening, and it is also found in rice (the exact reason i am really not sure). but if it is a hormone, it can't possibly cause other fruits to ripen? link to abscisic acid in rice website: http://www.plantcell.org/cgi/reprint/2/6/503.pdf anyone knows why rice cause fruits to ripen faster? thanks alot!

Would it be right to do an ED thoracotomy on a concious person? Let us take the following cenerio as an example where this might occurs: An MVA-blunt trauma patient is admitted to the ED with chest trauma and X-rays reveal an thoracic aortic aneurysm. An average adult has about 5L of blood and average cardiac output is about 5L meaning that if the aorta rupture the person would bleed to death in about a minute. For the minute he would still have perfusion to the brain and be concious. After brain perfusion and cerebral blood pressure drops as the patient is bleeding out, pyramidal cells of the cortex, which are very sensitive to hypoxia start to die, although it is general accepted that the process is reversible if the time < 6 minutes. If the rupture was to occur in the ED, can perform an ED thoracotomy to cross-clamp the aorta before the patient actually losses conciousness to preserrve as much perfusion to the brain as possible. It would be a painful procesudre but it was cause less permanent damage to the brain? Sometime you gotta weight pain vs. benefit

Which one is worse, waterboarding or? waterboarding description Waterboarding is slow-motion suffocation with enough time to contemplate the inevitability of blackout and expiration. Usually the person goes into hysterics on the board. For the uninitiated, it is horrifying to watch. If it goes wrong, it can lead straight to terminal hypoxia - meaning, the loss of all oxygen to the cells. The lack of physical scarring allows the victim to recover and be threatened with its use again and again. Call it "Chinese water torture," "the barrel," or "the waterfall." It is all the same. OR With forceps, the doctor turns the baby around in the womb to be positioned feet first. The baby’s legs are pulled out into the birth canal. The baby is alive at this point. . The abortionist delivers the baby’s entire body, except for the head, which remains inside the birth canal. The baby’s hands and feet move The abortionist stabs the scissors into the base of the baby’s skull. The scissors are spread to enlarge the opening. The suction catheter is then inserted and the brains are sucked out, causing the skull to collapse. The head slides out easily. Im sorry if this offends you but I've heard about all the phony outrage I can stand. Which one is worse? Jenny - Cases similar to what you've stated represent only about 5% of the partial birth abortions that have been performed. For the most part they weren't done for (rape / incest / life of the mother) this is a fact. If you need info on this my email is open. For the one who said this proceedure is illegal, you and I both know that this is No Thanks to Obama! I know his record and this and even worse would still be legal if it was up to him. Tell me, are you claiming credit for the fact that it's now illegal? How did you vote? Btw it's interesting that none on your side can simply answer the question (which is worse?). Thanks people, some real good answers. We'll see if they're honest enough to let this one stand. On this site, experience tells me no but maybe they'll surprise us.

My aunt just had a seizure, can someone tell me why? She was sitting on a trampaline, not jumping, just sitting. Watching everyone. When she started to think of something, a number actually, she couldn't remember and then flew back into a seizure. She had 2 grand Mal Seizures that day. One on the trampaline, leaving her scared and thinking she was in the desert and the other when she was in the hospital. I know that the doctors treated her and everything but they can find an underlying cause of what happened. She is horribly depressed and she doesn't want her life to be like this. She suffers from Short term memory loss, dehydration, and extreme sleepiness. Please if you could even mention something that would be helpful. I mentioned Cerebral Hypoxia, but no one listens to me. I hope that if someone could help, i could convince someone to do something about this because she is Horribly depressed. Thanks so much.

Chem Help please! pleeeaasseee!!? 1. The reaction for the decomposition of PCl5 to chlorine and PCl3 is shown below. PCl5(g) ↔ PCl3(g) + Cl2(g) If the equilibrium concentrations are [PCl5] = 1.0 M, [PCl3] = 0.10 M, [Cl2] = 0.10 M, what is the value of the equilibrium constant? A) 1.0 × 10^-4 B) 1.0 × 10^2 C) 2.0 × 10^-2 D) 10 × 10^-2 E) 1.0 × 10^-2 2.For the reaction of carbon with carbon dioxide to make carbon monoxide, the reaction is as follows. C(s) + CO2(g) ↔ 2CO(g) Adding additional C(s) to the reaction container will cause ______ to occur. A) no change in the amounts of CO and CO2 B) a decrease in the amount of CO C) the formation of more CO2 and a decrease in the amount of CO D) the formation of more CO2 E) the formation of more CO 3.If the amount of oxygen available to the blood decreases significantly, what happens to the individual involved? A) Acclimatization results B) Anemia results C) Oxygen poisoning results D) Nitrogen narcosis results E) Hypoxia results

Does thumbsucking cause brain hypoxia? as well as holding the blanket upto ones nose and inhalling during 8 hours of sleep?

Does this football injury make sense with this scenario? Let's say that someone is playing football and ends up getting tackled with enough force to cause two broken ribs, a dislocated shoulder, and a severe concussion. Let's say that as a result of two broken ribs, the lung on the left side gets penetrated causing a pulmonary laceration. The pulmonary laceration causes a hemopneumothorax, which causes severe breathing complications. The person would be coughing blood as a result of the hemothorax and wouldn't be able to breath properly because of the collapsed lung caused by the pneumothorax. Since the person isn't getting proper oxygen, they would suffer from hypoxia and loss consciousness after several minutes. Does this all make sense and what would be the course of action at a high school football practice? Let's say one of the other plays decides to give CPR and oxygenate the person while the ambulance is arriving. When the ambulance arrives they would insert an endotracheal tube to help the the person breath until they get to the hospital, where they would insert a chest tube to reinflate the collapsed lung. Does this make sense, and if not, how could I correct it? Thanks so much. :) Is it POSSIBLE that this scenario could occur in football, though? Even if it is like a one-time freak accident? Is it remotely legit?

lack of oxygen to brain at night? ive had this problem for over a year now. When im lying down on my bed about to sleep, i get these weird episodes where i feel like half-fainted and my heart has stopped, and afterwords my heart beat becomes stronger and faster and blood rushes to my head. Tis happens a couple times at night and only at night. Could this be hypoxia, where im not getting adequate amount of oxygen to my brain? please tell me what's causing this and has it caused brain damage? Also if oyu have sleep apnea can you ge a feeling of being almost fainted and kinda out of ur body feeling?

Cerebral Hypoxia: Can it lead to secondary issues later in life? Can cerebral hypoxia, caused at birth, lead to cerebral or cerebral arterial issues (i.e. brain tumor, weak arterial walls or stroke) later in life? Thank you Crypto... Very indepth answer. It laid to rest my main concerns. I appreciate that very much.

How does hypoxia cause cell damage?

why does pulmonary edema cause hypoxia and cyanosis? Would like a simple but detailed explanation

What cause coagulative necrosis apart from hypoxia environment?

Is death caused by hypoxia (induced by helium, nitrogen, etc) painless?

severe hypoxia? Can severe hypoxia cause bradydysrhythmias (slow rhythms) more often than ventricular fibrillation and why?

Can you have hypoxia without any symptoms? What would they be caused by? thanks :)

how can people SUDDENLY faint? i often wonder about people who pretend to fall out. but if fainting is due to a panic that causes hypoxia..shouldn't this take at least 1 minute? Also have you seen someone faint?...if so...what do you think

Anyone have histotoxic hypoxia? what caused it?

Post Concussion shock(hypoxea), if some-one suffers hypoxia,posthead neck/ injury for unspecified time ,? What is the prognosis if that person survives, can this cause permanent disability.Usually known as secondary injury(assault), when with head injury/concussion.

DOCTORS OR NURSES HELP!!!? How does hypoxia causes hypotension?

Ladies, what if a guy said this to you? Ladies what if a guy walked right up to you and looked you right in the eye and said: "I hope you know CPR to keep oxygenated blood flowing to my vital organs or have a defibrillator to terminate my cardiac arrhythmia, because your beauty took my breath away, causing cerebral hypoxia and a myocardial infarction." Would you give him your number?

About Cerebral Palsy? Causes - Cytomegalovirus, Hypoxia, Hypoglycemia, PROM

a question for paramedics? do you know why hypoxia typically causes bradydysrhythmias rather than ventricular fibrillation?

bradyasystolic rhythms? how do you think severe hypoxia may cause bradyasystolic rhythms? is it a direct effect on the heart itself or an indirect effect on the heart?

respiratory shock? do you know how hypoxia may cause blood pressure to drop causing shock?

cardiac irritability? do you know how hypoxia irritates the heart causing PVCs ?

what should i do if people pick on me but they don't understand why i look like this? i have mobius syndrome {Möbius syndrome (also spelled Moebius) is an extremely rare congenital neurological disorder which is characterized by facial paralysis and the inability to move the eyes from side to side. Most people with Möbius syndrome are born with complete facial paralysis, which means they cannot close their eyes or form facial expressions. Limb and chest wall abnormalities sometimes occur with the syndrome. Most people with Möbius syndrome have normal intelligence, and others should take care not to confuse their lack of facial expression with dullness or unfriendliness. It is named for Paul Julius Möbius, a neurologist who first described the syndrome in 1888.[1]Möbius syndrome results from the underdevelopment of the VI and VII cranial nerves.[2] The VI cranial nerve controls lateral eye movement, and the VII cranial nerve controls facial expression. People with Möbius syndrome are born with facial paralysis and the inability to move their eyes laterally. Often, the upper lip is retracted due to muscle shrinkage.[3] Occasionally, the cranial nerves V and VIII are affected.[4] If cranial VIII is affected, the person experiences hearing loss. It is estimated that there are, on average, 2 to 20 cases of Möbius syndrome per million births.[5][6] Although its rarity often leads to late diagnosis, infants with this disorder can be identified at birth by a "mask-like" lack of expression that is detectable during crying or laughing and by an inability to suck while nursing because of paresis (palsy) of the sixth and seventh cranial nerves. Also, because a person with Möbius syndrome cannot follow objects by moving their eyes from side to side, they turn their head instead. Other symptoms that sometimes occur with Möbius syndrome are: Limb abnormalities—clubbed feet, missing fingers or toes Chest-wall abnormalities (Poland Syndrome) Crossed eyes (strabismus) Difficulty in breathing and/or in swallowing Corneal erosion resulting from difficulty in blinking Children with Möbius syndrome may have delayed speech because of paralysis of the lips. However, with speech therapy, most people with Möbius syndrome can develop understandable speech.[7] Möbius syndrome has been linked to increased occurrence of the symptoms of autism.[8] However, some children with Möbius syndrome are mistakenly labeled as mentally retarded or autistic because of their expressionless faces, strabismus, and frequent drooling.Treatment There is no single course of medical treatment or cure for Möbius syndrome. Treatment is supportive and in accordance with symptoms. If they have difficulty nursing, infants may require feeding tubes or special bottles to maintain sufficient nutrition. Physical, occupational, and speech therapy can improve motor skills and coordination and can lead to better control of speaking and eating abilities. Often, frequent lubrication with eye drops is sufficient to combat dry eye that results from impaired blinking. Surgery can correct crossed eyes, protect the cornea via tarsorraphy, and improve limb and jaw deformities. Sometimes called "smile surgery" by the media, muscle transfers grafted from the thigh to the corners of the mouth can be performed to provide the ability to smile. Although "smile surgery" may provide the ability to smile, the procedure is complex and can take twelve hours for each side of the face. Also, the surgery cannot be considered a "cure" for Möbius syndrome, because it does not improve the ability to form other facial expressions. [edit] Living with Möbius syndrome Many people with Möbius syndrome lead full lives and experience personal and professional success.[9] Facial expression is important in social interaction, and other people may have difficulty recognizing the emotions of people with Möbius. A person with Möbius syndrome who cannot smile may appear unfriendly or disinterested in a conversation. However, friends and family who are familiar with the person with Möbius syndrome learn to recognize other signals of emotion such as body language, and they sometimes report forgetting that the person has facial paralysis altogether.[10] People with Möbius syndrome can use alternative methods to communicate emotion—such as body language, posture, and vocal tone.[11]Pathological picture The causes of Möbius syndrome are poorly understood. Möbius syndrome is thought to result from a vascular disruption (temporary loss of bloodflow) in the brain during prenatal development.[12] There could be many reasons that a vascular disruption leading to Möbius syndrome might occur. Most cases do not appear to be genetic. However, genetic links have been found in a few families. Some maternal trauma may result in impaired or interrupted blood flow (Ischemia) or lack of oxygen (Hypoxia) to a developing fetus. Some cases are associated with reciprocal translocation between chromosomes or maternal illness. In the majority of cases of Möbius syndrome in which autosomal

how can DIC cause organ dysfunction? hypoxia hemorrhage nutrition deficient necrosis

What percentage of babies are born with the umbilical cord around the neck causing hypoxia? And needing artificial respiration

Biology Questions NEed HelP FAST! please? Cilia that line the walls of air passageways a.move the inspired air to the alveoli b. move the expired air to the nasal cavity c. moisten the expired air d. clean the inspired air 2. The exchange of gass that occurs at an alveolus depends on a. elevated blood pressure b. mucus carrying dissolved oxygen c. concentration gradients d. bronchioles closing during expiration 3. Critical Thinking Oxygen deficiency is called hypoxia. Suggest two possible causes of inadequate delivery of oxygen to body tissue Sorry for asking too much questions... but i hav a test on thursday and i dont know these PLEASE HELP THank YOU SO MUCH!

What have you learned from Winston Kayanan about global warming? Looks like no reaction yesterday which means that you are all clueless in the same manner as France & Europe and also speechless from the standpoint of the stunned world. This SUDDEN DEATH phenomenon can happen again and elsewhere, like Greece, California, Australia, Indonesia, etc.. Since world's mind is directed to UN's wrong objective (GHG reduction) than the right path (O2 replenishment), global warming & its repercussions (disasters & death) will NEVER go away. No matter how much the world reduce CO2, there is nothing to stop the magnitude (being cumulative). The world invented all sorts of carbon reduction technologies and conceptualized mitigation & adaptation programs but no technologies to break CO2 and regenerate O2 other than the failing plant forest (due to droughts & fires). Let us follow then the lyrics of a song in the 70's "What goes up, must come down. Spinning wheel got to go round." CONTINUATION: Two months later after my diagnosis, the European Environment Agency (EEA) came up with their own version in a press release sometime November 2003 as a case of OZONE POLLUTION, staying longer for a time (days) as reported. But, from what I can reason & argue, ozone is lighter than oxygen and oxygen is lighter than carbon dioxide and therefore, ozone pollution, I believe, was a WILD GUESS for ozone gas which is abundantly traceable in industrial zones (closer to factory workers than older people at home), immediately ascends up (in milliseconds to seconds) rather than move laterals or stay longer for days. Given this, it was not ozone that caused the deaths but rather heavy concentration of carbon dioxide &/or carbon monoxide (with less oxygen) persisted in some areas. As elderly people (with poor health) were mostly affected by the temporary loss or shortage of oxygen (known as hypoxia), they were easily vulnerable to major complications of organ's dysfunction unlike younger people as the least likely to succumb for they could still tolerate in those short periods of oxygen loss. Tomorrow, excerpts from the same letter: Gauge the power & strength of Philippines' implantation technology vs. UNFCCC's Plant Forest Scheme & Nobel Prize winner - African woman, planting 30,000,000 trees in 20 years.

bradyasystolic rhythms? how do you think severe hypoxia may cause bradyasystolic rhythms? is it a direct effect on the heart itself or an indirect effect on the heart?

Congestive Heart Failure as a complication of Leukemia? If someone could share his/her idea about the pathophysiology for this complication, it would be very helpful. My idea is that the uncontrollable proliferation of WBCs supresses the production as well as the maturation of RBCs and also that of the platelets. Eventually, this causes severe anemia if prolonged. Anemia and presence of immature RBCs, eventually, would cause tissue hypoxia and as the body's compensatory mechanism, the heart would try to increase the cardiac output to respond to increased in body's metabolic demand. This event increases the myocardial workload which would eventually cause the heart to fail causing decreased myocardial contractility. Is this all? I think I'm missing something. What are the other physiologic changes in a person with cancer (Chronic Myelogenous Leukemia to be exact) that would precipitate congestive heart failure (right-sided) ?

A 90% Cancer Cure Diet using Flaxseed Oil & Cottage Cheese?

A 90% Cancer Cure Diet using Flaxseed Oil & Cottage Cheese?

Why do some people think ADHD is fake? Hi, I work aiding a scientific research team in performing various sleep research. I haveno opinion on overmedication of children for ADHD as that is an entirely different subject, but yes, ADHD is real. One of our most recent studies about sleep apnea involved raising rats and subjecting them to intermittent hypoxia to simulate untreated sleep apnea in human children. Rats who were subjected to hypoxia all grew up to manifest symptoms of ADHD. Further investigation revealed that intermittent hypoxia (simulating untreated sleep apnea in children) results in damage to the dopaminergic system in the brain, which causes deficits in working memory and hyperactivity. This dopaminergic system damage caused a functional impairment in the brain's ability to release dopamine from the presynaptic nerve terminals. Treatment with amphetamines potentiated the release of DA from these terminals and temporarily relieved the symptoms of ADHD. I see a lot of posters calling it fake. It isn't! And just for the record, though it isn't my speciality, I believe that many symptoms of ADHD can be remedied after the patient uses a CPAP or other device to aid breathing overnight. Medication can be lessened or even removed.

Please read this? Neurologic complications of cocaine, amphetamine, and their derivatives By: Douglas J Lanska MD MS MSPH FAAN Veterans Affairs Medical Center Great Lakes VA Healthcare System, Tomah, WI Department of Neurology University of Wisconsin, Madison, WI Abuse of certain illicit drugs can be complicated by ischemic stroke, intracerebral or subarachnoid hemorrhage, and other neurologic complications (Mathew and Wilson 1991; Baquero and Alfaro 1994; Auer et al 2002). Such agents include the sympathomimetic drugs cocaine and amphetamine, and their derivatives, including "crack," methamphetamine ("meth" or "crystal" or "speed"), "ecstasy," and "eve." Cocaine and amphetamine are strong risk factors for stroke in adolescents and young adults in most (Kaku and Lowenstein 1990; Petitti et al 1998), but not all (Qureshi et al 1997; 2001) epidemiological studies. There are multiple pathophysiological mechanisms for the cerebrovascular diseases related to use of these drugs, including vasospasm, altered platelet function, excitotoxicity, hyperthermia, and acute severe hypertension, which can cause endothelial disruption, loss of cerebral autoregulation, and hemorrhage. In many cases with abuse of such drugs, intracerebral hemorrhage is associated with an underlying vascular malformation (Klonoff et al 1989; Levine et al 1991; Daras et al 1994; Konzen et al 1995; Fessler et al 1997; McEvoy et al 2000; Auer et al 2002). In addition, individuals who abuse such drugs are also potentially susceptible to particulate embolization (from contaminants injected with intravenous drug abuse), cardiac arrhythmias, mycotic aneurysms, and endocarditis. Synergistic vasoconstrictive effects may occur with combined use of sympathomimetic agents in both human reports (Lambrecht et al 1993; Vallee et al 1993) and animal models (Wang et al 1990). Interestingly, basilar artery vasospasm has been produced in animal models by combined administration of cocaine and amphetamine (Wang et al 1990) and basilar artery thrombosis has been reported with combined abuse of cocaine and "ecstasy," an amphetamine derivative (Vallee et al 1993). Cocaine. Cocaine (benzoylmethylecgonine) is a potent sympathomimetic and CNS stimulant derived from the leaves of the shrub Erythroxylon coca, which grows primarily on the slopes of the Andes mountains in South America (Klein et al 2000; Lange and Hillis 2001). Cocaine is administered by inhalation (of smoked "crack," ie, the freebase or alkaloidal form which can be smoked), intranasally ("snorting"), and intravenously ("mainlining"), or less commonly orally ("chewing"; it is poorly absorbed by the gastrointestinal tract), intramuscularly, intravaginally, sublingually, or rectally. Cocaine hydrochloride is a water-soluble powder or granule that is readily absorbed through all mucous membranes, but that decomposes when heated, whereas alkaloidal or freebase cocaine is heat-stable and can be smoked. Alkaloidal or freebase cocaine is known as "crack" because of the popping sound that it produces when heated. Crack cocaine is the most potent and most addictive form of the drug, and smoking it can deliver cocaine to the circulation within seconds to minutes producing a short-lasting euphoria or "high." Although cocaine itself is metabolized by plasma and liver cholinesterases and is detectable in blood or urine only for several hours after use, cocaine metabolites can be detected in blood or urine for 24 to 36 hours after use, and in hair for weeks or months. Cocaine is frequently abused by adolescents and young adults in the United States (Brown et al 1992; Moliterno et al 1994; Hollander 1995; Lange and Hilllis 2001). Particularly since 1983, with the introduction of "crack" (alkaloidal or freebase form of cocaine), use of cocaine in the United States has increased dramatically (Daras et al 1994). Twenty three to 30 million Americans have used cocaine at least once (including reportedly over 30% of men and 20% of women between ages 26 and 34 years), and 2 to 5 million use it regularly (Moliterno et al 1994; Hollander 1995; Lange and Hillis 2001). Cocaine is responsible for approximately 30% of all drug-related visits to emergency rooms (Hollander 1995; Lange and Hillis 2001). When given systemically, cocaine's effects are mediated through modulation of synaptic transmission (Lange and Hillis 2001). Cocaine causes powerful sympathomimetic effects by blocking presynaptic reuptake of norepinephrine, epinephrine, and dopamine, while also stimulating the presynaptic release of norepinephrine, causing excess amounts of these neurotransmitters to stimulate the corresponding postsynaptic receptors, particularly alpha receptors peripherally (Hollander 1995; Lange and Hillis 2001). The pathogenesis of cocaine-related neurologic complications is heterogeneous, and depends in part on the dose administered and the form of cocaine used (Levine et al 1991). Abuse of alkaloidal ("crack") cocaine results in approximately equal frequencies of ischemic and hemorrhagic strokes, while cocaine hydrochloride is much more likely to be associated with hemorrhagic stroke (approximately 80% of the time) (Levine et al 1991). Cardiovascular, neurologic, and psychiatric complications are common with cocaine abuse (Moliterno et al 1994; Hollander 1995; Lange et al 2001; Kloner and Rezkalla 2003). Acute toxicity is dose-related and characterized by sympathomimetic effects, including acute and possibly profound hypertension, headache, tachycardia, hyperthermia, cardiac arrhythmias, and possibly seizures (Klein et al 2000). In some cases, profound acute toxicity occurs from rupture of packets of cocaine that have been ingested or inserted into the vagina or rectum by drug smugglers ("body packers" or "mules") (Levine et al 1990; Klein et al 2000). Cocaine, especially recent use of cocaine, is the illicit drug used most frequently in drug-related strokes (Kaku and Lowenstein 1990); the relative risk for stroke among drug abusers is 6.5 compared with nondrug abusers, and this increased to 49.4 for patients whose symptoms began within 6 hours of drug administration (Kaku and Lowenstein 1990). The higher potency of crack compared with cocaine hydrochloride has been associated with a marked increase in the frequency of cocaine-related strokes (Klonoff et al 1989; Daras et al 1994). Stroke may follow the use of cocaine by any route of administration (Klonoff et al 1989). Cocaine can produce severe cerebral vasospasm, multifocal or diffuse cerebral ischemia, ischemic and hemorrhagic stroke, intracerebral hemorrhage (particularly in the basal ganglia, but also in the deep cerebral hemispheres and the brainstem), subarachnoid hemorrhage, seizures, movement disorders, dizziness, anxiety, paranoia, hallucinations, insomnia, confusional states, stupor and coma, and possibly vasculitis (Klonoff et al 1989; Meza et al 1989; Nalls et al 1989; Sloan et al 1991; Brown et al 1992; Sloan and Mattioni 1992; Daras et al 1994; Reeves et al 1995; Nolte et al 1996; Johnson 1998a; Klein et al 2000; Broderick et al 2003; Buttner et al 2003; Vallee et al 2003; Bolouri and Small 2004). Cocaine is a major risk factor for aneurismal subarachnoid hemorrhage in young people (Levine et al 1987; 1990; 1991; Devore and Tucker 1988; Klonoff et al 1989; Rowley et al 1989; Strickland et al 1993; Daras et al 1994; Nolte et al 1996; Herning et al 1999; Broderick et al 2003). It is thought that cocaine induces a sudden rise in systemic arterial pressure, which precipitates vasospasm, endothelial disruption, disruption of cerebral autoregulation, with resultant intracranial hemorrhage, often in association with underlying aneurysms or arteriovenous malformations (Klonoff et al 1989; Levine et al 1991; Daras et al 1994; Konzen et al 1995; Fessler et al 1997). Indeed, chronic cocaine use appears to induce earlier clinical presentations in patients with incidental neurovascular abnormalities compared to similar non-cocaine users (Fessler et al 1997). Evidence for a true vasculitides is not compelling and most studies have failed to find any indication of vasculities, suggesting that the pathologic findings are a consequence of pharmacodynamic effects of cocaine and not a cocaine-induced vasculopathy (Nolte and Gelmann 1989; Nolte et al 1996). There is also a significantly increased risk of ischemic changes in the cerebral white matter and insular subcortex white matter (Bartzokis et al 1999a; 1999b). In some cases, vascular imaging and histopathologic studies suggest vasospasm of large arteries produced secondary intravascular thrombosis (Konzen et al 1995). Cocaine administration is associated with dose-dependent global and regional reductions in brain blood flow (Wallace et al 1996; Johnson et al 1998a), likely due to an immediate and brief period of vasoconstriction or vasospasm (Strickland et al 1993; Konzen et al 1995; Herning et al 1999). Cocaine-induced vasospasm can be partially blocked with calcium channel antagonists (Johnson et al 1998b; 2001). Chronic cocaine use can produce sustained brain perfusion deficit and persistent neuropsychological changes with deficits in attention, concentration, new learning, visual and verbal memory, word production, and visual-motor integration (Strickland et al 1993). Other manifestations of cerebral ischemia can result from direct embolization of foreign material injected with the drug diluents; mycotic aneurysms; as well as primary cardiac problems, including cardiac arrest (even in young patients), cardiac arrhythmias, cardiomyopathy with associated atrial or ventricular thrombus, aortic dissection, and endocarditis resulting from intravenous drug abuse (Kaku and Lowenstein 1990; Petty et al 1990; Sauer 1991; Sloan and Mattioni 1992; Moliterno et al 1994; Hollander 1995; Neiman et al 2000; Lange and Hillis 2001; Lange et al 2001; Kloner and Rezkalla 2003; Bolouri and Small 2004). Cocaine use during pregnancy can produce fetal hypoxia, intracerebral hemorrhage, and congenital malformations (Heier et al 1991; Brown et al 1992; King et al 1995). In a retrospective case-control study, maternal cocaine use was significantly associated with increased risks of neonatal stroke and congenital malformations (particularly neural tube defects), attributed to cocaine-induced vasospasm in the third and first trimesters, respectively (Heier et al 1991). Transcranial Doppler ultrasound studies of newborns who were exposed to cocaine in utero demonstrate increased flow velocities in intracranial arteries consistent with the vasoconstrictive effects of cocaine (King et al 1995). The mechanisms of cocaine-related cerebrovascular disease remain somewhat controversial, with several explanations proposed with varying degrees of support from human studies and animal models (Muir and Eliis 1993; Daras et al 1994; Kosten 1998; Buttner et al 2003; Fandino et al 2003). Proposed pathophysiologic contributors (not necessarily mutually exclusive) include pharmacologically-induced vasospasm, rapid transient increases in systemic blood pressure, disruption of cerebrovascular autoregulation (particularly with increasing levels of acute or hyperacute hypertension), impaired endothelium-dependent vasorelaxation, apoptosis of cerebral vascular muscle cells, arteritis, myocardial infarction with cardiac arrhythmias, impaired hemostatis, increased platelet aggregation, decreased global and regional cerebral blood flow, and cocaine-induced cerebral excitotoxicity (Kelley et al 1993; Muir and Ellis 1993; Daras et al 1994; Havranek et al 1996; Heesch et al 2000; Buttner et al 2003; Fandino et al 2003; Su et al 2003; Bolouri and Small 2004). Cocaine-induced vasospasm is thought to be mediated by endothelin-1, an extremely potent, 21-amino acid vasoconstrictor peptide produced by vascular endothelial cells; endothelin receptor antagonists can block cocaine-induced vasospasm in animal models (Fandino et al 2003). Cerebral vascular smooth muscle cells can undergo rapid apoptosis in response to cocaine, which may contribute to cerebral microvascular damage and strokes (Su et al 2003). In addition, work in animal models suggests that some of the adverse neurologic complications of cocaine use are medicated by changes in calcium or magnesium concentrations in vascular smooth muscle cells or brain, including precipitation of cerebral vasospasm by rapid elevation of intracellular free calcium and depletion of magnesium in vascular smooth muscle cells (Altura and Gupta 1992; Altura et al 1993; 1997; Zhang et al 1996). Amphetamine and derivatives, including methamphetamine and "ecstasy." Amphetamine is another potent sympathomimetic drug that can cause a wide variety of vascular complications, including stroke, aneurismal rupture, and myocardial infarction, similar to the case with cocaine (Chen et al 2003). Methamphetamine (aka: meth, crystal, speed) is a derivative of amphetamine that also acts as a CNS stimulant. Amphetamine and methamphetamine are administered in several ways (eg, orally, or by injection, smoking, or snorting). Prolonged use at high levels can produce dependence. Methamphetamine was widely used clinically in the 1950s and 1960s for treatment of depression and obesity (Anglin et al 2000). Until the late 1980s, methamphetamine use was endemic in California and relatively restricted to that state, but use has subsequently broadened with increased use, particularly in the Midwest (Anglin et al 2000). Approximately 2% of the US population have tried methamphetamine at some point in their lives. "Ecstasy" and "eve" are newer drugs of abuse, being ring-substituted amphetamines (3,4-methylenedioxymethyl-amphetamine, or MDMA, and 3,4-methylenedioxyethylamphetamine, or MDEA, respectively) that have greatly increased in popularity in the United States in the last decade. Neurologic and psychiatric complications of amphetamine, methamphetamine, and other amphetamine derivatives are similar to those seen with cocaine, and include ischemic and hemorrhagic strokes, anxiety, paranoia, hallucinations, and insomnia (Lambrecht et al 1993; Perez et al 1999). In some cases, intracranial hemorrhage occurs in the setting of underlying vascular malformations (Auer et al 2002). Pathological studies have suggested multiple pathophysiological mechanisms of brain and other organ damage, including perivascular hemorrhagic and hypoxic changes similar to those of heat stroke and other forms of hyperthermia (Milroy et al 1996). References: Altura BM, Gebrewold A, Altura BT, Gupta ARK. Magnesium protects against cocaine-indiced hemorrhagic stroke in a rat model: a 31P-NMR in-vivo study. Front Biosci 1997;15:a9-12. Altura BM, Gupta RK. Cocaine induces intracellular free Mg deficit, ischemia and stroke as observed by in-vivo 31P-NMR of the brain. Biochim Biophys Acta 1992;1111:271-4. Altura BM, Zhang A, Cheng TP, Altura BT. Cocaine induces rapid loss of intracellular free Mg2+ in cerebral vascular smooth muscle cells. Eur J Pharmacol 1993;246:299-301. Anglin MD, Burke C, Perrochet B, Stamper E, Dawud-Noursi S. History of the methamphetamine problem. J Psychoactive Drugs 2000;32:137-41. Auer J, Berent R, Weber T, Lassnig E, Eber B. Subarachnoid hemorrhage with "Ecastsy" abuse in a young adult. Neurol Sci 2002;23:199-201. Baquero M, Alfaro A. Progressive bleeding in spontaneous thalamic hemorrhage. Neurologia 1993;9:364-7. Bartzokis G, Beckson, Hance DB, et al. Magnetic resonance imaging evidence of "silent" cerebrovascular toxicity in cocaine dependence. Biol Psychiatry 1999b;45:1203-11. Bartzokis G, Goldstein IB, Hance DB, et al. The incidence of T2-weighted MR imaging signal abnormalies in the brain of cocaine-dependent patients is age-related and region-specific. AJNR Am J Neuroradiol 1999a;20:1628-35. Bolouri MR, Small GA. Neuroimaging of hypoxia and cocaine-induced hippocampal stroke. J Neuroimaging 2004;14:290-1. Broderick JP, Viscoli CM, Brott T, et al. Major risk factors for aneurismal subarachnoid hemorrhage in the young are modifiable. Stroke 2003;34:1375-81. Buttner A, Mall G, Penning R, Sachs H, Weis S. The neuropathology of cocaine abuse. Leg Med 2003;(5 Suppl 1):S240-2. Chen HJ, Liang CL, Lu K, Liu CC. Rapidly growing internal carotid artery aneurysm after amphetamine abuse: case report. Am J Forensic Med Pathol 2003;24:32-4. Daras M, Tuchman AJ, Koppel BS, Samkoff LM, Weitzner I, Marc K. Neurovascular complications of cocaine. Acta Neurol Scand 1994;90:124-9. Devore RA, Tucker HM. Dysphagia and dysarthria as a result of cocaine abuse. Otolaryngol Head Neck Surg 1988;98:174-5.