Alcohol and road traffic

• 45% of car accidents are caused at an
alcoholemy of <1.0g%
• some countries have a kind of tolerance of
alcoholemy: eg. Ireland tolerates an
alcoholemy of 1.0g%

• The alcohol is dangerous because its effects:
– negative psichological (optimism, exagerated
selfconfidence, reduced selfcriticism and
– physiological (reflex deprimation)
– sensorial (diminuation of visual field, difficulties in
estimating the distances and speed of the
comming vehicles)

• Reaction time at noticing an obstacle is 0.75 s,
at alcoholemy level this value is three times
• The braking distance at 100 km/h is 75 m ->
will become 225 m
• 0.5g% alcoholemy doubles the risks of car
accident, it will double at every 0.5g%

• The alcoholometry estimates the alcohol level in the
organism by measuring its concentration in the expired
• It is a chemical reaction of oxidation -> „the
alcoholometer becomes green” (it contains bichromat
of potassium)
• This permits only sanctions, it has not the character of
an evidence at the justice
• Modern alcoholometers are based on one of the
properties of the alcohol: the intensity absorbtion of
infrared light is directly proportional with the
concentration of alcohol in the expired air

60 g%o 2.1 l alveolar air contains the same ammount of alcohol as 1 ml blood blood/alcohol in expired air =1/2100 Blood Expired Air 0.00 g%o .40 g%o 1.• 2.00 g%o 1.20 g%o 0.80 g%o 0.

O. acute intoxication with ethanol. acute and chronic intoxication with alcohol.Alcohology notions • Chemically the alcohols conatin C. therapeutic use of alcohol • Many of there problems have medico-legal and major juristic implications . H and have the capacity to bind directly with acids • The alcohols are largely used in many domains • We are interested in the per os use of alcoholic drinkables. nutritive value of alcohol.

plum brandy (ţuică) Industrial alcoholic drinks fermentation of a must or potato or cereal’s juice B. Classification of alcoholic drinks and their nutritive values A. The way of preparation Examples Fermented alcoholic drinks direct fermentation of the sugar grape wine. Ammount of alcohol Strong alcoholic drinks 25-30% alcohol plum brandy. cogniac. whisky Medium strength alcoholic drinks 8-12% alcohol wine Light alcoholic drinks 1-9% alcohol beer. rom.1. some fruit juices . cogniac. beer Distilled alcoholic drinks distillation of fermentated drinks brandy.

• As calory source the alcohol can cover some of these kind of necessity: – In Germany it covers 8% – In France it covers 10% • It can cover 50%. but the avitaminoses are cauzed by the alcohol’s reduced ammount of vitamins .

2. Therapeutic use of alcohol • Solvent for drugs • Reduces transpiration. decreases the meteorism and colicas • In inhalation it decreases the pulmonary edema by decreasing the superficial tension • Sedative and anesthetic .) • It is used in ganglionar alcoholisation • Increases the apetite. good extern desinfectant (in 70% conc.

Pharmacokinetiks and pharmacodynamics I. triciclic antidepressants slows down the absorbtion – Diseases of the stomach . neuroleptics.mucosa) by diffusion – Also at the buccal mucosa – Small cantities in the lungs • Absorbtion speed in the gastric and duodenal mucosa depends of: – The concentration of the alcohol in the ingested drink – Speed and rhytm of ingestion – The absence or presence of food in the stomac and their type: • Fat. proteins and milk slow the absorbtion • Anti-cholinergics. Absorbtion – Ethanol is rapidly absorbed from the gastrointestinal tract (gastric – 20% .1.and duodenal – 80% .I.

• At the begining of the ingestion the absorbtion speed is high (expecially strong drinks) then slows down -> the absorbtion may last 2-6 hours • Following the ingestion on an empty stomach. peak levels occur in ¾ to 2 hours • Ethanol rapidly distributes into the body water and equilibrates very rapidly with it target organs .

Alcoholemy – Reaches the vena portae and liver -> is distributed in the organism’s liquids: extra.2.Distribution of the alcohol in the organism.and intracellular fluids – Repartisation in tissues is done based on the tissue’s water and fat content -> more water – more alcohol – The alcohol concentration in plasma is bigger than in RBC so the alcohol determination is done on anticoagulated blood – The concentration is bigger in arterial blood than in venous .I.

• Ethanol blood concentration may be used to estimate the level of ethanol in the brain • The equilibrium between the concentration of ethanol in the blood and in the expired air is attained rapidly .

Alcoholemy curve .

• Alocoholemy reaches the maximum level after 30-120 mins from ingestion • Alcohol concentration in any tissue results from: diffusion speed / oxidation speed • The time and values of maximum levels of alcohol varies – depends in the same time of the detoxification processes • Based on the nature of the alcohol the period when the alcoholemy is at maximum level varies from 30 mins to 90 mins • Around 90-95% of absorbed alcohol is oxidated. respiration. saliva and sweat . the rest 510% is eliminated in the urine.

90 g/o alcoholemy.• 1 g%o alcoholemy is reached by ingestion of 1g alcohol/kg • Concetrated alcoholic drinks are absorbed quickly • At an adult with average weight 45 g ingerated alcohol (as whisky) with empty stomac results a 0. but in case of aliment consumption the alcoholemy would be approximatelly half of this value .65 – 0.

• Consumed aliments and their type influences the alcoholemy: – Fat and sugar flattens the curve – Proteins lowers the alcoholemy – Ingestion of a greater cantity of fruits results a 0.48g%o alcoholemy – At diabetics the alcoholemy may be much greater after the ingestion of the same alcohol as a healthy person .

3. it will end in 24 hours after the ingestion. being dependent of many fators (also constitutional) • The ethil-oxidation coeficiency is constant for the same person . Elimination of the alcohol or post-absorbtion phase • Ethil-oxidation coeficiency: cantity of oxidated alcohol on minute/kg body • The elimination is low at the begining of the absorbtion period.I.

but it can ameliorate the clinical signs of alcoholic inhibition • Barbiturates does NOT modify the alcoholemy. but worsens the clinical signs of alcoholic inbibition • Morphine decreases the alcoholemy • Hipothermia (cold) influences the speed of oxidation .• Biological factors which influences the alcoholemy: – Trauma: cranio-cerebral trauma with coma slows down the oxidation -> the alcoholemy level increases – Vomiting: empties the stomac -> reduces the alcoholemy – The capacity of oxidation increases by aging – Drugs: • Caffeine does NOT modify the alcoholemy.

6g) • Women eliminates more alcohol than men • Urine/alcohol in blood=1.• The elimination of the alcohol is cantitatively proportional with its concentration in the blood • The curve is different in small alcoholemies and huge alcoholemies • An adult eliminates 6.30-1.5-2% of the ingerated alcohol is eliminated in the lungs: in the lungs the organism eliminates 1g alcohol/hour (if the alcoholemy and hiperventilation are raised .6-10.40 • Concentration of alcohol in blood/alveolar air=1/2000 • The smell of alcohol is from the aromatic substances • 0.33 g alcohol/h (3.

000 ml/hour (0.43g/1000ml/hour .15g/1000ml/hour • At chronic alcoholists the elimination rate is 0.27g/1000ml/hour (0.15g/1.11 – 0. so juridically it is considered that tha elimination rate is 0.16-0.18 g/1000ml/hour women • It has huge variations.• Mean value of metabolic rate at the descending phase is: – 0.22 g/1000ml/hour) men – 0.

The Michaelis constant is the substrate concentration at which the reaction rate is half of Vmax. .• Elimination can be appreciated with MichaelsMenten equation: dC = Vmax C dt Km + C Where the elimination rate (dC/dt) depends on the maximum elimination rate (Vmax). Michaelis constant (Km)and concentration.

4. also at microsomal level and catalase-peroxidase system I.I.4.1. • Most of it is in the liver and participate in the process of transforming the ethanol in the liver • Codehydrase – is a coenzyme which is a NAD (nikotineadenine-dinucleotide) which is the receptor of H . Alcohol-dehidrogenase (ADH) • Large specificity enzyme including the steroid’s dehidrogenase and a megaoxidation of fatty acids. Metabolisation process of the alcohol Absorbtion -> oxidation (quick process) – in liver through the ADH (alcohol-dehidrogenase system).

The oxidation process in the liver • 1st phase: alcohol -> acetic-aldehide (the alcohol loses 2H) • 2nd phase: acetic-aldehide -> acetate – The 1st phase is catalised by the ADH which is in the hepatic citosole. it cannot be found in the blood – In the kidney the concentration of ADH is very high -> can assure the degradation of alcohol until CO2 and H2O – ADH is a metalic (Zn++) ezyme. which is incorporated through biosynthesis -> element which gives possibility to form an active complex of enzyme-coenzyme (the coenzyme is is phosphorilated-NAD) .

• Rate: 15mg/h .

• The acetate transforms in acetil-coenzyme A which oxidates in Krebs cycle • Micro-somal system: 20% of the alcohol is burned • The catalase-peroxidase system intervines in high alcoholemies .

due to acetaldehyde accumulation because of the alcohol dehydrogenises increasing or acetaldehyde dehydrogenises diminution. This is a state due to the hallucinogen effect of acetaldehye.• In some of the oriental people there is an immediate hypersensitivity to alcohol ingestion. but is different from the pathological drunkenness . named „oriental reaction” or „flash reaction”.

0 – 3.50 g%o none. 1.5 g%o obvious intoxication 3.50 . 0. somnolence. memory.1.Simptomatoloy of acute ethilic intoxication Entrance ways: •orally (by ingestion) – the most common way •inhalation – very rarely Alcoholemy level Intoxication signs <0.cardio-respirator stop . atention.0 g%o none.0 – 1.5 g%o may appear signs 2.5 g%o very advanced condition of intoxication.0 – 2. coma >4.0 g%o death . motiliy. rationality tulburancy. subconscious condition.

reducing their activity – The depressant action begins in the superior parts of the brain (the most developed) amd goes down through the bulb – If only superior parts of the brain are affected. the behavior will be more primitive and understained – which seems to be a false simulator efect (the inferior parts of the brain being controlled byy the superior parts due to their inhibition .Simptomatology • Actions on the CNS – Acute doses of ethanol depress the excitability at all levels of the CNS enhancing GABA neurotransmission – Ethyl-alcohol determines a state of hypoxia to the neural cells.

folic acid. thiamine and vit B12 • Accumulation of fat in the liver and cirrhosis • Cancer of the liver and of the GI tract • Effects on kidney – Produces diuresis – inhibits the antidiurethic hormone .• Actions on gastrointestinal tract – Chronic alcoholic is associated with • Malabsorption of fat.

tachicardia. psycho-motor exaltation. euphoria. Until an amount of 1g%o .Ethanol intoxication • The ethanol intoxication is produced in 3 clinical phases: 1.excitation of intellectual functions. nystagmus. vasodilatation. the sensation of warmth . diminished reflex activity. decreased reaction speed. midriasis. perspiration.

guidance and motricity It is also called the medico-legal phase.50 %oProfound psycho-sensorial disturbances. . because in this phase are commited many antisocial acts and accidents.2. Alcohol level between 1 – 2. The disturbances affects the intelligence.

Increased heart and respiratory rhytm . Vestibulo-labirintial disturbances are present. attention. memory are altered. intelectualrationalment functions. words are incoherent. Vomiting and hiccups are indicating the involment of the medulla oblongata.• The alcohol is the intelligence’s poison: the autocritics is abolished. absurd. also agression. Instincts and passions are takeing control.

0 g%o alcoholemy decrease in alkaline reserves -> marked acidosis. hypothermia.Lethal dose: 300-500 ml (equivalent to about a litre of whisky) if taken in less than an our . Comatose phase – above 3. coma . hypothermia.3.Death is caused by the respiratory depression. decrease of the ureea level in blood. profound sleep. hipercholesterolaemia. anesthesia. hypotension. hypoglycemia .

abdominal pain.• Death can also be caused by an acute methabolic decompensation of alcoholic ketoacidosis (AKA) or alcoholic lacticacidosis (ALA) type • Common simptoms: nausea. tachicardia and Kussmaul type respiration . vomiting.

• Normal values of ketonic bodies: 2.5 mg/l . with decreased release of insulin -> increased lipolysis -> increase of ketonic bodies.Alcoholic ketoacidosis (AKA) • Excessive ingestion of alcohol increases the NADH/NAD+ ratio which inhibits the gluconeogenesis and utilisation of free fatty acids. Simultaniously decreased ingestion of carbohidrates causes a depletion of glycogen and reduction of gluconeogenesis.3 – 3.

Alcoholic lacticacidosis (ALA) • It is determined by the increase of the NADH/NAD+ ratio with the increase of lactate or piruvate. ALA cand be triggered by hypothermia. Diagnosis is put when the sum of glucose + lactate in the vitreous humour is bigger than 300mg/dl . At alcoholics. Major causes are malnutrition and thiamine deficiency at chronic alcoholics. diminished gluconeogenesis and decrease of hepatic reconversion of lactate.

1 Measuring/Dosage of the alcohol in the expired air: – Henry’s law: at a given temperature. the mass of gas disolved in the volume of a liquid is proportional with the pressure exerted of the gas on the liquid – Ratio of alcohol: 1/2000 -> 1ml blood contains as much alcohol as 2000 ml alveolar air – Alcohol tests! .Laboratory diagnosis • 1.

• 1. Measuring/Dosage of the alcohol in the blood: – Cromatography. like Nicloux method – The official method in Romania is the CORDEBARD method (the nitro-chromic oxidation) – it needs at least 10 ml venous blood for determinatios .2. titrimetry – based on the property of alcohol that it can be oxidated by a sulfo-cromic mixture.

Interpreting the results and some medicolegal problems regarded to the alcoholemy a. if the alcoholemy is multiplied with the R factor and the weight of the body.70.• 1. the total cantity of alcohol is obtained . Factor R – WIDMARK – to calculate the total cantity of alcohol in the organism: concentration of alcohol in organism (whole body) alcoholemy normal value= 0.3.

Practically the determination of the total ammount of ingested alcohol depends of many factors. but using this formula we can deduce: alcoholemy (g%o) x body weight (kg) .

• Taking in consideration the ethil-oxidation factor (0.• Another problem is calculating the alcoholemy for the moment when the traffic happening was produced. knowing the time elapsed until taking the blood sample. (IML Bucuresti) .18 g%o/h) this is possible for a 5-6 hours period.12 – 0.

Calculation of the alcoholemy based on the ingestion datas (without lab exam of the blood sample): alcohol conc. with full stomac in 90-120 mins (based on the way of consuption and type of alcohol . In blood g%o= A/B A= ingested alcohol B=body weight - A= TxVxd/100 d=alcohol density – 0.1.8 When more types of alcohol are consumed A will be the sum of each type In case of strong alcohols the value increases with 30% Maximum level of alcoholemy with empty stomac is reached in 30 mins.

Retrospective calculation of the alcoholemy . when from the traffic event and blood sample had passed an interval of time (more then 30-60 mins) .2.This is effectuated for the eliminatory phase of alcohol.

The alcoholemy value is given by the relation: alcoholemy g%o = alcohol conc.15 g%o/hour T=time between traffic event and blood sample It is done max. g%o + BxT B=coeficiency of ethil-oxidation 0. 7-8 hours retroactive – above this period it has only informative value .

hypoglycemia. hypovitaminosis • Maintaning respiratory tracts open • Metadoxine has been used with succes – accelerates the urinary elimination of ethanol and acetaldehyde .Treatment • Symptomatic • Correction any physiological dysfunctions. as possible acid-basic or electrolytic disorders.

25% of the accidents are the drivers’ fault and 10.Alcohol and traffic accidents • Traffic accidents: 250000 death/year. injuries/year – 40% remains with infirmities • In Romania 58. 10 mill.2 % are caused by alcohol .

38. is punished with 1-5 years of imprisonment. The right of driving an automibile is suspended in case of: driving an automobile under the influence of alcoholic drinks. Driving an automobile on public roads by a person who has in his blood an alcohol inhibition above the legal limit (alcoholemy >0.41.8g%o) .8 g%o) or which is in drunkennes condition.• Legislative problems: – Art. – Evasion from taking biological samples to determine the alcoholemy is punished with 1-5 years of imprisonment – Art..(>0.

– Medical examination of the driver to determine the condition of alcoholic intoxication – The alcoholtest is a way of sorting. dependending of the alcoholemy: green it >0. it is based on oxidation (sulpho-chromic content of the tube) of the expired alcohol with the alveolar air. which manifests in changing the colour (green.40 g%o alcoholemy) – The legal limit of infractionality in Romania is >0.80 g%o .

• Juridical regime in alcoholism: – In acute volunteer drunkennes the person has responsability for his acts – Intentioned drunkennes (drinks „to make courage”) is an agravant factor – Acute accidental drunkenness excuses the person from the responsability for his acts – In pathological drunkenness there is no responsability for the persons acts – Psychotic manifestations of chronic alcoholics does not involve penal liability .