Blood ethanol

Figure 4. Levels of blood ethanol in fire death victims.

Both THC and ethanol increase reaction time, and produce decrements in standing steadiness and psychomotor coordination (Belgrave et al. 1979). Whereas the peak effects of ethanol appeared quickly and wore off quickly (after 280 minutes), THC s effects were slower in onset and longer in duration. The effects of combined THC and ethanol are additive and not synergistic, and THC did not alter blood-ethanol levels. Other studies have shown an interaction between ethanol and THC on psychomotor skills necessaiy for driving, although there were no interactions on the subjective "high," heart rate acceleration, or THC plasma concentration (Perez-Reyes et al. 1988). 

The best-known exception to exponential kinetics is the elimination of alcohol (ethanol), which obeys a linear time course (zero-order kinetics), at least at blood concentrations > 0.02 %. It does so because the rate-limiting enzyme, alcohol dehydrogenase, achieves half-saturation at very low substrate concentrations, i.e at about 80 mg/L (0.008 %). Thus, reaction velocity reaches a plateau at blood ethanol concentrations of about 0.02 %, and the amount of drug eliminated per unit of time remains constant at concentrations above this level. 

The metabolism of most drugs or chemicals is proportional to the concentration in the blood, which allows a half-life to be calculated. Ethanol is different its metabolism is relatively constant over time and does not increase with rising blood ethanol concentrations. Metabolism is proportional to body weight thus the bigger you are, the higher the rate of ethanol metabolism, but on average ethanol is metabolized at a rate of 120 mg/kg per hour or about 1 oz (30 ml) in 3 hours. 

Management of methanol and ethylene glycol poisoning is similar. Symptomatic support of respiration and circulation is augmented by correction of metabolic acidosis with intravenous bicarbonate infusion, and control of seizures with diazepam. Ethanol inhibits the metabolism of methanol and ethylene glycol to the toxic metabolites, and can give time for further treatment. The goal is to maintain blood ethanol concentrations between 100 and 150 mg per decilitre, sufficient to saturate alcohol... 

Normally, 90 to 98% of an ingested dose of ethanol is metabolized by the liver. Most of the remaining 2 to 10% is excreted unchanged in the urine and expired air. The ethanol content in the urine is normally about 130% of the blood concentration and is quite constant the expired air contains about 0.05% of the blood ethanol level, a concentration that also is remarkably consistent. 

The most important goals in the treatment of acute alcohol intoxication are to prevent severe respiratory depression and to prevent aspiration of vomitus. Even with very high blood ethanol levels, survival is probable as long as the respiratory and cardiovascular systems can be supported. The average blood alcohol concentration in fatal cases is above 400 mg/dL however, the lethal dose of alcohol varies because of varying degrees of tolerance. 

H2 antagonists compete with creatinine and certain drugs (eg, procainamide) for renal tubular secretion. All of these agents except famotidine inhibit gastric first-pass metabolism of ethanol, especially in women. Although the importance of this is debated, increased bioavailability of ethanol could lead to increased blood ethanol levels. 

In fact, small amounts of morphine, 6-acetylmorphine, codeine, and thebaine, all opiate compounds, have been found in mammalian brain877 878 and have presumably arisen by the same pathway observed in plants (Fig. 25-10). However, there is no cross reactivity between morphine and alcohol in addicted mice,879 and acetaldehyde is probably not the addictive agent. Acetaldehyde is very reactive and may be responsible for much of the damage caused by ethanol.880 At a blood ethanol concentration of 20 mm a person is legally intoxicated, and large amounts of acetaldehyde may be formed and react with many amines, nucleotides, proteins, etc. Ethanol blocks glutamatergic NMDA receptors and... 

Ethanol has a range of acute effects, normally expressed as a function of percent blood ethanol. In general, these effects are related to central nervous system depression. Mild effects such as decreased inhibitions and slowed reaction times begin to appear at about 0.05% blood ethanol. Most individuals are clinically intoxicated at a level of 0.15 to 0.3% blood ethanol in the 0.3 to 0.5% range, stupor may be produced and at 0.5% and above, coma and often death occur. 

ADH activity and to enhance the bioavailability of ethanol, with a resulting increase in blood ethanol levels. This exaggeration by certain drugs is particularly important for social drinkers, who commonly take several small drinks, but experience a cumulative effect on blood alcohol levels. 

Ethanol is frequently taken at the same time as other drugs and can intensify the action of depressant drugs. A blood-ethanol determination assists in distinguishing this from normal alcoholic intoxication it is also useful in the clinical assessment of unconscious patients admitted with head injuries and smelling of drink. Children are particularly at risk from hypoglycaemia which may follow ingest-ion of alcohol. 

Alcohol clearly affects eye movement. Both smooth pursuit movements and saccades are impaired when blood ethanol concentrations reach the range of 60 to 100 mg/dl. There is a direct linear relationship between blood alcohol concentration and a reduction in smooth-pursuit movement velocity. At a blood ethanol concentration of 80 mg/dl, the capacity of the eyes to track objects moving across the visual fields is impaired by 25%. 

Inhibiting methanol metabolism. Ethanol, which occupies the dehydrogenase enzymes in preference to methanol, competitively prevents metabolism of methanol to its toxic products. A single oral dose of ethanol 1 ml/kg (as a 50% solution or as the equivalent in gin or whisky) is followed by 0.25 ml/kg/h orally or i.v., aiming to maintain the blood ethanol at about... 

CabaUeria J, Baraona E, Rodamilans M, Lieber CS. Effects of cimetidine on gastric alcohol dehydrogenase activity and blood ethanol levels.. Gastroenterology 1989 96(2 Pt 1) 388-92. 

Seitz HK, Bosche J, Czygan P, Veith S, Simon B, Kommerell B. Increased blood ethanol levels following cimetidine but not ranitidine. Lancet 1983 1(8327) 760. 

Once peak blood ethanol levels are reached, disappearance is linear, with a 70 kg man metabolizing 7-10 g of alcohol per hour. 

Another complicating factor in the interpretation of postmortem toxicology results is the phenomenon known as postmortem production. This phenomenon is most applicable to blood alcohol levels after a fatality has occurred. Postmortem production can account for measurable blood ethanol levels after a fatality that may have no connection to prior exposure to alcohol. Postmortem ethanol production can result from a number of sources that include the existence of large numbers of appropriate microorganisms in improperly preserved bodies, or from bodies that suffered severe trauma at death. In any case, the forensic toxicologist attempting to offer an interpretation of these results should carefully consider these facts. 

The blood ethanol peak was delayed by about 45 min by acarbose, and the fall in blood ethanol was significantly retarded (Jandrain et al., 1988). 

Alcohol distributes into the aqueous compartments of blood, and because the water content of serum ( 98%) is greater than that of whole blood ( 86%), results indicating higher alcohol levels are obtained with serum. Experimentally the serum whole blood ethanol ratio is 1.14 (1.09 to 1,18) and varies slightly with hematocrit.Several states have enacted laws that define intoxication while driving a motor vehicle under the influence of alcohol based on whole blood ethanol concentrations. Some states do not specify the specimen type. Therefore laboratories that perform alcohol determinations should make clear the choice of specimen. 

This device was evaluated and determined to provide results in agreement with those for breath or venous blood ethanol.The Q.E.D. is suited for on-site use in the emergency department, in the workplace, and potentially at the roadside. It is approved by the DOT for alcohol screening. Although designed for measurement of alcohol in saliva, the Q.E.D. provides accurate measurements for serum ethanol as weU. ... 

Winek CL, Carfagna M. Comparison of plasma, serum, and whole blood ethanol concentrations. J Anal Toxicol 1987 11 267-8. 

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