Let's have a serious discussion about carbon monoxide poisening
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Let's have a serious discussion about carbon monoxide poisening
id talk about mine but im too tired
sorry im smoking a cig give me five mins .......................
is that french?Quote:
Originally posted by samsamsamsam@5 March 2004 - 23:27
Let's have a serious discussion about carbon monoxide poisening
http://www.bridgernet.com/~thefamily.../lightbulb.gif
Here's an idea!! STFU!!
Good pointQuote:
Originally posted by kaiweiler@6 March 2004 - 02:50
http://www.bridgernet.com/~thefamily.../lightbulb.gif
Here's an idea!! STFU!!
http://www.singersoutdoors.co.uk/pag...fork-spoon.jpg
it kills :ghostface:
I would say pretty serious since you cant smell it.
Get a carbon monoxide detector just in case. You might not wake up the next morning from your sleep. :)
Cars omit carbon minoxide
In 1913, Brauer introduced the term "arterial air embolism" to describe the symptom complex following entry of air into the arterial circulation (1). Hyperbaric oxygen (HBO2) reduces the volume of gas bubbles and increases the diffusion gradient of the embolized gas, thereby reducing the morbidity and mortality of those afflicted with arterial air emboli.
Gas embolism occurs when gases enter or enucleate in the vasculature (venous or arterial) embolizing in sufficient volume to compromise the function of an organ or body part. The available investigations indicate that this occlusive process results in varying degrees of ischemia in the affected areas (2-4). Even very early accounts cite air embolus as a cause of neurologic dysfunction (5,6). In addition to being a well-docinnented complication of diving (7-10), air emboli are probably even more prevalent from other causes.
Air emboli may occur as a result of surgical procedures. The first report of gas embolism in the medical literature was a descriptive account of an embolic process which occurred during the extirpation of a tumor from the neck (11). The medical literature recounts a large number of mortalities and permanent residual impairments from air emboli arising from surgical invasion of the vasculature (12,13). It has been proposed that the most common cause of death during an operation where there has been vascular invasion is air embolism (14). Neurosurgery performed in the sitting position may give rise to air embolism (15-17). Even a surgical procedure as simple as a burr hole can give rise to an air embolus (18). Gas embolism is ubiquitous enough in cardiovascular surgery to give credence to the statement "air is the bane of cardiac surgery" (19). Other procedures in cardiovascular surgery whereby gas may be introduced include the cardiopulmonary bypass device (20,21) and angioplasty (22,23). Air emboli in the heart may lead to intracardiac gas entrapment (24,25) and retrograde air embolization into the coronary arteries (26).
Arthroplasties (27) and arthroscopies have been noted as sources of gas embolism. Gas embolism as a complication of total hip replacement can occur when the cement is forced into an air-filled femoral shaft (28). Air emboli may also occur during endoscopy. This generally occurs when gas is used to clear a space within which to visualize a target with the endoscope (29). Biopsy through a bronchoscope (30) or thorascope (31) has been reported to cause gas embolism. Death from gas embolism has also been observed in liver transplantation (32). Life support equipment such as intra-aortic balloons have been the source of massive gas embolism (33-35). Laser usage carries the hazard of gas embolism when gases are liberated adjacent to open blood vessels (36-38).
Air emboli have been associated with diagnostic monitoring procedures involving the use of cannulae or needles. The flow of gas at a pressure gradient of 4 mmHg through a Swan-Ganz introducer is sufficient to induce a fatal air embolus in an adult patient (39). The injection of contrast fluids or the insertion of intravascular catheters for monitoring or therapy are potential sources of gas embolism (40-46). The use of biopsy needles presents potential risks for air emboli (47,48). Infusion pumps for intravenous fluid maintenance have been the cause of unfortunate outcomes (49).
Air emboli may occur in nonsurgical patients. Rupture of the lung can result from overexpansion of the lung in the respirator-dependeit patient (50,5 1). Air eniboli may also occur during hemodialysis where the loss of continuity of the dialyzing membrane is lost and air enters the circulation (52,53). The incidence of this potential complication seems to be diminishing due to the use of bubble detectors with automated turn off systems. Air embolism can occur during injection of fluids or gases into a tissue space or organ (54,55).
In addition, there are obstetrical and gynecological sources of gas embolism. Women attempting to abort pregnancies by catheterizing the cervical os and injecting air into the uterus have come to untimely deaths due to gas embolism (56). This can also occur during the course of a therapeutic abortion (57,58). The sex act, wherein the sex partner forcefully blows into the vagina, performed during pregnancy has a noted morbidity and mortality due to air emboli (59-63). It would also appear that gas embolism is not an uncommon occurrence during Cesarean delivery (64).
Air emboli may also result from traumatic injuries. Gunshot wounds of the head are a potential source of air emboli (65). Penetrating chest injuries may lead to air emboli. This injury compromises the patient by disrupting the non-nal architecture of the lung, thereby allowing air to gam access to the arterial side of the heart (66-68). Ventilatory support should be undertaken with caution as a positive over-pressure incident may cause a problem (69,70). Blast injury may cause air emboli by exposure of the vascular to the concussive wave (71-73). Fractures may lead to air emboli by opening the vasculature within the bone matrix, thus allowing access of air into circulation (74,75). Autotransfusion devices used to recycle blood during trauma surgery may be another source of gas embolism (76).
The generally accepted belief that small amounts of gases that enter the venous circulation will be filtered out in the pulmonary bed must be qualified. A significant percentage of the population has a pro patent foramen ovale. Its presence, or the presence of a pulmonary shunt may allow lethal amounts of gas to gain entrance to the arterial circulation (77-80).
The role of gas embolism in the pathogenesis of serious decompression illness was clearly demonstrated in animal models (81,82) and confirmed in (83). Lastly, gas embolism may result when scuba diving, from breath holding during ascent of less than 10 feet of fresh or sea water (84,85). This occurs despite the fact that the pressure is insufficient to create a dissolved gas load of sufficient quantity to bubble during ascent. This unanticipated event is due to pulmonary over pressure which tears the pulmonary membrane and allows gas to enter the pulmonary veins.
The repressurization treatment for gas embolism has not changed since first reported for "caisson" disease in 1854 (86). The success of this mode of treatment has been substantiated by its successful use in large numbers of patients (87,88). Hyperbaric oxygen therapy has been noted by Rivera (89) to be most effective when initiated early. Further improvement is encouraged by repetitive applications of HBO2. Since gas bubbles have been known to persist for several days, there are many reports noting success when HBO2 treatments were begun after delays of hours to days (12,40,45,62,90). Therefore, a trial of HBO2 therapy is indicated even for those patients presenting to a hyperbaric unit hours to days after the inciting event. It is speculated that delayed signs and symptoms of central nervous system (CNS) injury occur after reactive edema surrounds and expands in the distally dependent nervous tissue supplied by an occluded vessel (91).
Oxygen under pressure was first used successfully on a series of patients by Yarbrough and Behnke (92). Their work was expanded by Workman (93). All practitioners agree that the combination of pressure and an appropriate gas mixture (to create a proper gas diffusion gradient) are the cornerstone for the treatment of air emboli (13,94-96). The efficacy and action of the different available treatment protocols have been reviewed by Peirce (97). Basic research with animal models indicates that the major objective benefit to the CNS may be achieved at shorter exposure times and at lower pressures when using oxygen dm previously appreciated (98-101). These data may represent only a short-term improvement from enhanced oxygen delivery to an ischemic area, although in all likelihood after removing the enucleated or embolized gas, the coagulative state about the bubbles will remain for longer periods of time (102,103). Opinion (104,105) that advocates HBO2, in a repetitive fashion for the treatment of air emboli to further improve the long-term result has been confirmed by the U.S. Navy Experimental Diving Unit (106).
Hyperbaric oxygen is the primary treatment for air embolism. It reduces the mortality rate and remediates the development of permanent neurological damage. Treatment modalities range from long high-pressure dives using mixed gas schedules to those employing lower pressure oxygen schedules. The protocol or tables chosen should be those with which the supervising practitioner is familiar and with which the available equipment is most compatible.
DISCUSS!!! NOW!!!!
YoCarMon
In a brief review of what we know and do not know about earth's climate and our ability to model it, Kump (2002) correctly notes that the direct contributions of CO2 and other greenhouse gases to global warming "are relatively small." When fed into modern-day climate models, however, these inducements to warming are strongly amplified, so much so, in fact, that the ultimate increase in temperature predicted by the models is "well in excess" of the direct effects produced by the greenhouse gases themselves. This result seems highly suspicious; and as we shall see from further study of Kump's review, there are many good reasons to question it.
Kump begins by stating - and, again, rightly so - that earth's climate system is complex, "with numerous feedback mechanisms (interdependent cause-effect relationships) that create indirect effects that are more difficult to predict" than direct effects. Indeed, the preeminence of this complexity permeates his entire commentary. In his very next sentence, for example, Kump again rightly states that any climatic transition to new states "may involve counterintuitive transients." A little further into his essay, he also correctly notes "it is difficult to predict the extent of amplification or damping of the external forcings by internal feedbacks."
Other uncertainties, in Kump's words, result "from the coarseness of the gridded representation of spatially continuous physical processes that numerical models must adopt, especially as it affects our ability to predict cloud cover and rainfall." He also notes "the possibility that the models are missing key climate feedbacks, with biotic processes perhaps being neglected most." As one specific example, he again correctly notes that "most models neglect the potentially critical role that marine algae play in the formation and reflectivity of clouds over the remote ocean."
In spite of these many acknowledged shortcomings, Kump still tries to make a case for believing in model predictions. He says, for example, that "the 400,000-year Vostok ice-core record of atmospheric pCO2 and temperature would seem to provide the ideal demonstration [our italics] that CO2 drives climate." Yet he goes on to admit, with respect to this record, that "cause and effect is difficult to assign." Based on other palaeoclimatic data sets from the more distant geologic past, Kump also says "there are good reasons [our italics] to suspect that atmospheric pCO2 has been a primary climate driver." But he admits in the very same sentence that "the evidence is not conclusive." Are these the things one would imagine would be said about "the ideal demonstration" that CO2 drives climate, or about "good reasons" for believing in this presumption? We think not.
In summing up the gist of the palaeoclimatic evidence near the end of his essay, Kump claims, yet again, that there is "general support for the notion than an increase in atmospheric pCO2 will cause global warming." But he admits, yet again, that this relationship "is neither linear nor in phase on all timescales." And he further admits that "proxy indicators of global warmth do not always coincide with proxy indications of elevated pCO2, and when they do, as in the Late Pleistocene, there is no lead-lag relationship from which one might hope to assign cause and effect." Hence, we ask, yet again: Is this the stuff of what convincing arguments are made? We think not.
Nevertheless, Kump seems to think so, claiming that these observations give us "an elevated confidence in the models." For us, however, they do just the opposite. But he has an amazing answer for this problem. "Fortunately," he says, "improved models ... are on the horizon, and should be adequate to support policy decisions concerning the reduction of fossil-fuel CO2 emissions."
Well, we surely hope improved models are on the horizon. But on what basis should we believe they will "support policy decisions concerning the reduction of fossil-fuel CO2 emissions"? As deficient as Kump has convinced us current models are, why should we not at least consider the possibility that new and improved models might suggest a more neutral position, i.e., that there is no need to reduce anthropogenic CO2 emissions? Or the possibility that future models might suggest the earth would not suffer from even greater CO2 emissions? Or that the earth might even benefit from them?
From what Kump has revealed about climate model deficiencies and inadequacies, none of these possibilities can be ruled out. Nevertheless, Kump - and many others - have clearly eliminated them from their thinking. Hence, we can only presume they do so on a basis other than science and logic.
We need more trees!!
Oh shit, thats carbon dioxide :rolleyes:
actually, algae is the world's number one converter of carbon dioxide to oxygen
ok when i commit suicide i will make sure there is none aroundQuote:
Originally posted by DarthInsinuate@6 March 2004 - 14:35
actually, the algae is the world's number one converter of carbon dioxide to oxygen
I donate my aquarium!!!Quote:
Originally posted by DarthInsinuate@6 March 2004 - 16:35
actually, algae is the world's number one converter of carbon dioxide to oxygen
YoLgae
Carbon Monoxide poisoning mimics the symptoms of other serious diseases. :ph34r:
Ask Gemby. :)
:blink:Quote:
Originally posted by bigboab@6 March 2004 - 19:43
Carbon Monoxide poisoning mimics the symptoms of other serious diseases. :ph34r:
Ask Gemby. :)