Adrenaline shock

L-Tyrosine metabohsm and catecholamine biosynthesis occur largely in the brain, central nervous tissue, and endocrine system, which have large pools of L-ascorbic acid (128). Catecholamine, a neurotransmitter, is the precursor in the formation of dopamine, which is converted to noradrenaline and adrenaline. The precise role of ascorbic acid has not been completely understood. Ascorbic acid has important biochemical functions with various hydroxylase enzymes in steroid, dmg, andhpid metabohsm. The cytochrome P-450 oxidase catalyzes the conversion of cholesterol to bUe acids and the detoxification process of aromatic dmgs and other xenobiotics, eg, carcinogens, poUutants, and pesticides, in the body (129). The effects of L-ascorbic acid on histamine metabohsm related to scurvy and anaphylactic shock have been investigated (130). Another ceUular reaction involving ascorbic acid is the conversion of folate to tetrahydrofolate. Ascorbic acid has many biochemical functions which affect the immune system of the body (131). 

Epinephrine (adrenalin) 0.1 to 0.5 mg may be given by subcutaneous or intramuscular injection. Hypotension and shock may be treated with fluids and vasopressors. Bronchodilators are given to relax the smooth muscles of the bronchial tubes. Antihistamines may be given to block the effects of histamine. 

Adrenaline, when administered to humans at 20 ug. per min. levels, caused increases in pulmonary ventilation of 13 to 153 per cent. The percentage increases in oxygen consumption resulting from the same administration were 19 to 56 per cent.30 Noradrenaline at the same level caused increases in pulmonary ventilation of 39 to 70 per cent and changes in oxygen consumption from -23 percent up to +31 per cent. Funkenstein, et al.,31 have tabulated the differences in the pharmacological action of these two substances and have adduced good evidence that two different types of psychotic patients tend to secrete excessive amounts, respectively, of the two types of hormones. Those who appear to secrete excess epinephrine-like hormone are more likely, at better than the 0.01 level of probability, to be benefited by electric shock therapy. If there are, as indicated, wide... 

Adrenaline (epinephrine) is a sympathomimetic agent that causes bronchodilatation. It is used to relieve bronchospasm in anaphylactic shock reactions. Histamine, kinins and prostaglandins, such as prostaglandin E2, are inflammatory mediators. In response to allergic stimuli, inflammatory mediators may cause bronchoconstrictions. Guaifenesin is an expectorant preparation that increases bronchial secretions to promote the expulsion of the mucus coughed up. 

Dopamine is an intermediate product in the biosynthesis of noradrenaline. Furthermore it is an active transmitter by itself in basal ganglia (caudate nucleus), the nucleus accumbens, the olfactory tubercle, the central nucleus of the amygdala, the median eminence and some areas in the frontal cortex. It is functionally important, for example in the extra-pyramidal system and the central regulation of emesis. In the periphery specific dopamine receptors (Di-receptors) can be found in the upper gastrointestinal tract, in which a reduction of motility is mediated, and on vascular smooth muscle cells of splanchnic and renal arteries. Beside its effect on specific D-receptors, dopamine activates, at higher concentrations, a- and -adrenoceptors as well. Since its clinical profile is different from adrenaline and noradrenaline there are particular indications for dopamine, like situations of circulatory shock with a reduced kidney perfusion. Dopamine can dose-dependently induce nausea, vomiting, tachyarrhythmia and peripheral vasoconstriction. Dopamine can worsen cardiac ischaemia. 

Noradrenaline and adrenaline are the classic catecholamines and neurotransmitters in the sympathetic nervous system. Noradrenaline stimulates the following subtypes of adrenoceptors P, a, U2. It has positive inotropic and chronotropic activities as a result of /3i-receptor stimulation. In addition, it is a potent vasoconstrictor agent as a result of the stimulation of both subtypes (ai,a2) of a-adrenoceptors. After intravenous infusion, its effects develop within a few minutes, and these actions disappear within 1-2 minutes after stopping the infusion. It may be used in conditions of acute hypotension and shock, especially in patients with very low vascular resistance. It is also frequently used as a vasoconstrictor, added to local anaesthetics. Adrenaline stimulates the following subtypes of adrenoceptors /3i, P2, oil, 0L2. Its pharmacological profile greatly resembles that of noradrenaline (see above), as well as its potential applications in shock and hypotension. Like noradrenaline, its onset and duration of action are very short, as a result of rapid inactivation in vivo. Both noradrenaline and adrenaline may be used for cardiac stimulation. Their vasoconstrictor activity should be kept in mind. A problem associated with the use of /3-adrenoceptor stimulants is the tachyphylaxis of their effects, explained by the /3-adrenoceptor downregulation, which is characteristic for heart failure. 

Epinephrine (adrenaline) should be given every 3-5 min whilst the patient remains in cardiac arrest, immediately if the patient has an initially non-shockable rhythm (asystole or pulseless electrical activity) but delayed until before the third shock for shockable rhythms. Continued administration of epinephrine (adrenaline), cardiac massage, and DC shock may be required for several cycles. 

Once Rachel was hospitalized the doctors put her on Prozac. The trial of Prozac was short, however, because it made her so sick to her stomach. The replacement, Well-butrin, was even worse it threw her into anaphylactic shock. Shortly after taking the medication she noticed hives on her body. A nurse dismissed the symptom, insisting that it could not be caused by the medication. But Rachel woke up the next morning covered with hives, and she was not breathing well. Fortunately, shots of adrenaline and epinephrine solved the problem. 

Ebstein R, Belmaker R, Grunhaus L, et al Lithium inhibition of adrenaline-stimulated adenylate cyclase in humans. Nature 259 411-413, 1976 Ebstein RP, Hermoni M, Belmaker RH The effect of lithium on noradrenahne-in-duced cyclic AMP accumulation in rat brain inhibition after chronic treatment and absence of supersensitivity. J Pharmacol Exp Ther 213 161-167, 1980 Ebstein RP, Lerer B, Shlaufman M, et al The effect of repeated electroconvulsive shock treatment and chronic lithium feeding on the release of norepinephrine from rat cortical vesicular preparations. Cell Mol Neurobiol 3 191-201, 1983 Ebstein RP, Moscovich D, Zeevi S, et al Effect of lithium in vitro and after chronic treatment on human platelet adenylate cyclase activity prosreceptor modification or second messenger signal amplification. Psychiatry Res 21 221-228, 1987 Eccleston D, Cole AJ Calcium-channel blockade and depressive illness. Br J Psychiatry 156 889-891, 1990... 

Epinephrine, commonly referred to as adrenaline, is an amine secreted in increased amounts during times of stress (Figure 15.21). Adrenaline increases the heart rate and blood pressure, releases sugar stored in the liver, and constricts blood vessels. It is sometimes administered to people in shock or during periods of acute asthma attacks. 

Adrenaline is used in cardiac resuscitation to convert asystole prior to defibrillation. It is also used in acute hypotensive emergencies and low cardiac output states, especially in severe sepsis or following extracorporeal circulation in cardiac surgery. In anaphylactic shock the combination of powerful a (vasoconstriction) and 32 (bronchodilatation) effects may be life-saving (Appendix AAGBI protocol). Adrenaline is also used to relieve bronchoconstriction in bronchial asthma and status asthmaticus. Dose... 

The reaction may be either local or systemic. Symptoms vary from mild irritation to sudden death from anaphylactic shock. Treatment usually involves intramuscular injection of adrenaline (epinephrine), antihistamines and corticosteroids. 

If treatment is delayed and shock has developed, adrenaline 500 micrograms should be given i.v. by slow injection at a rate of 100 micrograms/min (1 ml/min of the Dilute 1 in... 

Adrenaline is used in anaphylactic shock because its mix of actions, cardiovascular and bronchial, provide the best compromise for speed and simplicity of use in an emergency it may also stabilise mast cell membranes and reduce release of vasoactive autacoids (see p. 280). Patients who are taking nonselective p-blockers may not respond to adrenaline (use salbutamol i.v.) and indeed may develop severe hypertension (see below). 

Some clinicians use adrenaline, in preference to noradrenaline plus dobutamine, on the basis that its powerful a and p effects are appropriate in the setting of septic shock it may exacerbate splanchnic ischaemia and lactic acidosis. 

Co-administration of beta-blockers has been associated with an increased risk of severe allergic drug reactions and reduces the effect of adrenaline in the immediate treatment of anaphylactic shock. The mechanism involves changes in the regulation of anaphylactic mediators (281). 

A 44-year-old woman chewed a castor bean seed and within minutes developed urticaria, drowsiness, Quincke s edema, and extreme hypotension. Her anaphylactic shock was treated with adrenaline, intravenous glucocorticoids, antihistamines, and intravenous fluids. She quickly recovered and a subsequent blood test demonstrated CAP-RAST to castor beans. 

An anaphylactic reaction with shock after a 10th dose of fluorouracil 900 mg intravenously was reported in a 60-year-old man with colorectal adenocarcinoma (124). Two minutes after his 10th dose of fluorouracil, he became cyanotic and collapsed, with a rapid thready pulse of 120. His blood pressure was 30/0 mmHg. Adrenaline 1 1000, 1 ml, was given, with immediate and prompt signs of recovery. Within 25 minutes, his blood pressure, pulse, and skin color had returned to normal. 

In severe reactions, intravenous glucocorticoids are usually given on an empirical basis, with oxygen as required. Non-cardiogenic hypotensive shock usually responds best to fluid replacement, but vasopressors are occasionally required. Adrenaline is primarily... 

For acute anaphylaxis, immediate treatment is essential, with adrenaline followed by intravenous histamine Hi receptor antagonists, glucocorticoids, fluids, and electrolytes. In view of the frequency of cardiac dysrhythmias and conduction disturbances in patients with anaphylactic shock, they should immediately be monitored (198,199). 

Quinuronium sulfate is a bitter, white to yellow, crystalline powder that is usually available as a stable 5% aqueous solution. This compound is effective in the treatment of B. caballi infections but is associated with relapses, making it more effective for premunition than for the elimination of infection. One treatment consists of two doses of a 5% solution of quinuronium sulfate, administered s.c. at 0.3mg/kg, 6h apart. Quinuronium sulfate has a narrow margin of safety and overdosing produces parasympathomimetic effects including tremors, salivation, urination and defecation. These signs usually respond to treatment with atropine, epinephrine (adrenaline) and calcium gluconate. The interval between treatments should not be shorter than 2 weeks and should preferably be 3 months because sensitization occurs, which results in shock, with a profound drop in blood pressure, and death. 

Procaine, on the other hand, is an ester-type local anesthetic when it is injected into the organism, it is transformed into N,N-diethylaminoethanol and para-amino-benzoic acid (PABA) when the ester link that binds these two components of procaine is broken. PABA is a well-known allergen. Methyl para-hydroxybenzoate, whose structure is similar to that of PABA, is also called PAB or methylparaben. It is a preservative that binds, like a hapten, to the immunoglobulin E (IgE) on the surface of mast cells and basophils and maybe the cause of the few cases of anaphylactic shock that have been described. Other patients may be allergic to metabisulfite conservative, found in preparations containing adrenaline (epinephrine). 

Another consideration is that an insect bite or a plant exposure may trigger an allergic reaction, even deadly anaphylactic shock, which may require the immediate administration of a histamine-countering drug such as epinephrine (adrenalin) or Benadryl . 

Radiographers who inject contrast agents must be trained in emergency treatment of severe adverse reactions and basic life support. The most severe adverse reaction is anaphylactic shock. This is treated as an emergency with adrenaline, atropine and oxygen. Antihistamines, aminophylline, salbutamol and corticosteroids may also be necessary. 

Antivenoms (usually made by injecting a tolerant animal with the venom) are the best therapy with adrenaline required in cases of anaphylactic shock. Antibiotics, corticosteroids, ice-packs and rest can be used as supportive therapy while oxygen, mechanical ventilation and intravenous fluid support may be needed in severe cases and atropine may be useful in reducing salivation. Severe hypertension and tachycardia may respond to P-blockers most reports suggest that benzodiazepines are useful sedatives. 

---