Cocaine Beta blockers

BETA-BLOCKERS COCAINE Risk of hypertensive crisis Cocaine produces both alpha- and beta-adrenergic agonist effects selective beta-blockade leads to unopposed alpha-agonism (vasoconstriction) Avoid concurrent use... 

Thyroid supplement Blood pressure medications Beta blockers Thiazide diuretics Alpha methyl DOPA Appetite suppressants Phentermine Sibutramine Other Alcohol Caffeine Cocaine Nicotine... 

Doping substances include most of the drugs already discussed in the previous sections (e.g., drugs of abuse like amphetamines, cocaine, opiates pharmaceutical drugs like diuretics, beta-blockers, etc.) and, in most cases, the described methods may be extended to doping control applications. 

Clinically important, potentially hazardous interactions with albuterol, alpha-blockers, amitriptyline, amoxapine, atenolol, beta-blockers, carteolol, chlorpromazine, clomipramine, cocaine, desipramine, doxepin, ephedra, ergotamine, furazolidone, halothane, imipramine, insulin detemir, MAO inhibitors, metoprolol, nadolol, nortriptyline, oxprenolol, penbutolol, phenelzine, phenoxybenzamine, phenylephrine, pindolol, prazosin, propranolol, protriptyline, sympathomimetics, terbutaline, thioridazine, timolol, tranylcypromine, tricyclic antidepressants, trimipramine, vasopressors... 

B. Toxicodynamics Toxicodynamics is a term used to denote the injurious effects of toxins, ie, their pharmacodynamics. A knowledge of toxicodynamics can be useful in the diagnosis and management of poisoning. For example, hypertension and tachycardia are typically seen in overdoses with amphetamines, cocaine, and antimuscarinic drugs. Hypotension with bradycardia occurs with overdoses of calcium channel blockers, beta-blockers, and sedative-hypnotics. Hypotension with tachycardia occurs with tricyclic antidepressants, phenothiazines, and theophylline. Hyperthermia is most frequently a result of overdose of drugs with antimuscarinic actions, the salicylates, or sympathomimetics. Hypothermia is more likely to occur with toxic doses of ethanol and other CNS depressants. Increased respiratory rate is often a feature of... 

B. Specific drugs and antidotes. There is no specific antidote. Although propranolol was previously recommended as the dmg of choice for treatment of cocaine-induced hypertension, it may in fact produce paradoxic worsening of hypertension because of blockade of beta-2-mediated vasodilation propranolol (see p 496) or esmoioi (p 443) may be used in combination with a vasodilator such as phentoiamine (p 487). Cardioselective beta-blockers may be used alone for treatment of tachyarrh 4hmias. 

Propranolol reduces the clearance of bupivacaine and so theoretically the toxicity of bupivacaine may be increased. There has been a single report of enhanced bupivacaine cardiotoxicity in a patient also receiving metoproioi and digoxin. The coronary vasoconstriction caused by cocaine is increased by propranolol. Beta blockers may interact with adrenaline (epinephrine)-containing local anaesthetics. 

A study in 30 patients being evaluated for chest pain found that 2 mg/kg of a 10% intranasal solution of cocaine reduced coronary sinus flow hy about 14% and coronary artery diameter by 6 to 9%. The coronary vascular resistance increased by 22%. The addition of propranolol 400 micrograms/minute by intracoronary infusion, (to a total of 2 mg) reduced coronary sinus flow by a further 15% and increased the coronary vascular resistance by 17%. The probable reason is that the cocaine stimulates the alpha-receptors of the coronary blood vessels causing vasoconstriction. When the beta-receptors are blocked by propranolol, the resultant unopposed alpha-adrenergic stimulation may lead to enhanced coronary vasoconstriction (see also Beta blockers + Inotropes and Vasopressors , p.848). The clinical importance of these frndings is uncertain but the authors of the report suggest that beta blockers should be avoided in patients with myocardial ischaemia or infarction associated with the use of cocaine. ... 

Even long-term use of beta-blockers in cocaine users continues to generate debate. In a retrospective study over 10 years. 

Singavarapu A, Zolty R. Long-term beta-blocker use is associated with increased risk of myocardial infarction among cocaine users. J Am Coll Cardiol 2010 55(10A) 1213-97. 

Three typical STA procedures are presented here, one for the detection of most of the basic and neutral drugs in urine after acid hydrolysis, LLE, and acetylation [1,2,10,23,25,39 59] one for the detection of doping relevant stimulants, beta-blockers, beta agonists, and narcotics after enzymatic hydrolysis, SPE, and combined TFA and TMS derivatization [8] and one for automated screening of barbiturates, benzodiazepines, antidepressants, morphine, and cocaine in blood after SPE and trimethylsilylation [7,14]. 

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