Arrhythmia adrenaline

Halogenated hydrocarbons depress cardiac contractility, decrease heart rate, and inhibit conductivity in the cardiac conducting system. The cardiac-toxicity of these compounds is related to the number of halogen atoms it increases first as the number of halogen atoms increases, but decreases after achieving the maximum toxicity when four halogen atoms are present. Some of these compounds, e.g., chloroform, carbon tetrachloride, and trichloroethylene, sensitize the heart to catecholamines (adrenaline and noradrenaline) and thus increase the risk of cardiac arrhythmia. 

Antidepressants are used in the treatment of neuropathic pain and headache. They include the classic tricyclic compounds and are divided into nonselective nor-adrenaline/5-HT reuptake inhibitors (e.g., amitriptyline, imipramine, clomipramine, venlafaxine), preferential noradrenaline reuptake inhibitors (e.g., desipramine, nortriptyline) and selective 5-HT reuptake inhibitors (e.g., citalopram, paroxetine, fluoxetine). The reuptake block leads to a stimulation of endogenous monoaminer-gic pain inhibition in the spinal cord and brain. In addition, tricyclics have NMDA receptor antagonist, endogenous opioid enhancing, Na+ channel blocking, and K+ channel opening effects which can suppress peripheral and central sensitization. Block of cardiac ion channels by tricyclics can lead to life-threatening arrhythmias. The selective 5-HT transporter inhibitors have a different side effect profile and are safer in cases of overdose [3]. 

Inhalation of certain hydrocarbons, including some anesthetics, can make the mammalian heart abnormally sensitive to epinephrine, resulting in ventricular arrhythmias, which in some cases can lead to sudden death (Reinhardt et al. 1971). The mechanism of action of cardiac sensitization is not completely understood but appears to involve a disturbance in the normal conduction of the electrical impulse through the heart, probably by producing a local disturbance in the electrical potential across cell membranes. The hydrocarbons themselves do not produce arrhythmia the arrhythmia is the result of the potentiation of endogenous epinephrine (adrenalin) by the hydrocarbon. 

It may produce tachypnoea and bradycardia and sensitizes the myocardium to adrenaline and cardiac arrhythmias can occur probably due to hypoxic release of adrenaline. 

Restlessness, anxiety, tremor, headache. Both adrenaline and noradrenaline cause sudden increase in blood pressure, precipitating sub-arachnoid haemorrhage and occasionally hemiplegia, and ventricular arrhythmias. May produce anginal pain in patients with ischemic heart disease. 

These result from over-stimulation of the sympathetic nervous system anxiety, sweating, tachycardia, arrhythmia, hypertension, myocardial ischaemia, headache, cerebral haemorrhage, pulmonary oedema. Adrenaline may cause pupillary dilatation which must be distinguished from pupillary dilatation due to other causes, e.g. severe brain injury. 

When adrenaline is administered during halothane anaesthesia there is an increased risk of arrhythmia. 

Tricyclic antidepressants + directly acting sympathomimetic amines (e.g. noradrenaline, adrenaline) —> hypertension and arrhythmias due to enhancement of the sympathomimetic effects. 

Dose. For local anaesthesia, the total dose of lignocaine hydrochloride by injection should not exceed 300 mg (4.5 mg/kg), unless administered with adrenaline. For ventricular arrhythmias, initally 50 to 100 mg intravenously, followed by an infusion. 

Accidental overdose with adrenaline occurs occasionally. It is rationally treated by propranolol to block the cardiac p effects (cardiac arrhythmia) and phentolamine or chlorpromazine to control the a effects on the peripheral circulation that will be prominent when the P effects are abolished. Labetalol (a + p block) would be an alternative. P-adrenoceptor block alone is hazardous as the then unopposed a-receptor vasoconstriction causes (severe) hypertension (see Phaeochromocytoma, p. 494). Use of antihypertensives of most other kinds is irrational and some may also potentiate the adrenaline. 

Less selective adrenoceptor agonists such as adrenaline (epinephrine), ephedrine, isoetharine, isoprenaline and orciprenaUne are less safe, being more likely to cause cardiac arrhythmias, a-adrenoceptor activity contributes to bronchoconstriction but a-adrenoceptor antagonists have not proved effective in practice. 

In addition to drugs in these classes, others may be used for certain arrhythmias. Digoxin may be used for treatment of atrial fibrillation, adrenaline for asystolic cardiac arrest, atropine for sinus bradycardia, methacholine (rarely) for supraventricular tachycardia, magnesium salts for ventricular arrhythmias, and calcium salts for ventricular arrhythmia due to hyperkalaemia. 

Adrenaline (epinephrine) is a cardiac irritant that increases the risk of arrhythmias. For more details, see Chapter 37. 

Adrenaline is contraindicated in cases of diabetes, hyperthyroidism, serious heart arrhythmias and coronary insufficiency or in combination with beta-blockers or monoamine oxidase (MAO) inhibitors. Lidocaine with adrenaline has a very rapid onset of action. Its duration of action is longer than that of lidocaine without adrenaline. However, inadvertent injection of a lidocaine-adrenaline solution into the vessels located near the nerve trunks increases the heart rate (immediate sinus tachycardia at over 130 beats per minute, spontaneously reversible in around 15 minutes) and increases ventricular excitability (risk of fibrillation). It can trigger angina attacks that may lead to a heart attack. It is therefore preferable not to use adrenaline before a full-face phenol peel. 

K., Yoshiya, I., 1996. Anti arrhythmic of rilmenidine on adrenaline-induced arrhythmia via central imidazoline receptors in halothane anaesthetized dogs. Br. J. Pharmacol. 117, 1744-1748. 

Halothane is known to cause arrhythmias and it has been suggested that it may increase susceptibility to the adverse cardiac effect of beta-agonist bronchodilators, which can cause arrhythmias. Note that beta agonists such as terbutaline are sympathomimetics (see Table 24.1 , (p.879)), like adrenaline (epinephrine), which has also been shown to cause arrhythmias in the presence of halothane (see Anaesthetics, general + Inotropes and Vasopressors , p.99). 

Patients anaesthetised with inhalational anaesthetics (particularly cyclopropane and halothane, and to a lesser extent desflurane, enflurane, ether, isoflurane, methoxyflurane, and sevoflurane) can develop cardiac arrhythmias if they are given adrenaline (epinephrine) or noradrenaline (norepinephrine), unless the dosages are very low. Children appear to be less susceptible to this interaction. file addition of adrenaline to intrathecal tetracaine enhances the sedative effects of propofol. 

Children appear to be much less susceptible to these effects than adults. A retrospective study of 28 children found no evidence of arrhythmia during halothane anaesthesia with adrenaline doses of up to 8.8 micrograms/kg, and a subsequent study in 83 children (aged 3 months to 17 years) found that 10 micrograms/kg doses of adrenaline were safe. ... 

Phenylephrine is a sympathomimetic, and as such may carry some risk of potentiating arrhythmias if it is used with inhalational anaesthetics such as halothane -see Anaesthetics, general + Inotropes and Vasopressors , p.99. However, it is considered that it is much less likely than adrenaline (epinephrine) to have this effect, since it has primarily alpha-agonist activity. ... 

Two children and one adult patient undergoing general anaesthesia developed arrhythmias shortly after nasal application of a paste containing cocaine 25% and adrenaline (epinephrine) 0.18%. All 3 patients received doses of cocaine that exceeded the maximum dose (1.5 mg/kg) currently recommended in the BNF for healthy adults. 

Cocaine has sympathomimetic actions (tachycardia, peripheral vasoconstriction, and hypertension). Combined use with sympathomimetics such as adrenaline increases these effeets, and the risk of life-threatening arrhythmias. This risk may be further inereased if halothane anaesthesia is used (two of the above patients reeeived halothane ). See also Anaesthetics, general + Anaesthetics, local , p.92 and Anaesthetics, general + Ino-tropes and Vasopressors , p.99. 

The use of adrenaline with topical cocaine is controversial. Some consider that the addition of adrenaline is of doubtful value and that the combination should not be used, especially in the form of a concentrated paste. However, others consider the combination to be safe and useful. Whether or not adrenaline is combined with cocaine, the BNF considers that topical cocaine should be used only by those skilled in the precautions needed to minimise absorption and the consequent risk of arrhythmias. Note also that the use of local anaesthetics containing adrenaline should be avoided in patients who abuse cocaine, unless it is certain that they have not used cocaine for at least 24 hours. ... 

Patients taking tricyclic antidepressants show a grossly exa er-ated response (hypertension, cardiac arrhythmias, etc.) to parenteral noradrenaline (norepinephrine), adrenaline (epinephrine) and to a lesser extent to phenylephrine. Case reports suggest that this interaction only occurs rarely with local anaesthetics containing these vasoconstrictors. 

Treatment is nonspecific and should be directed to promote recovery from an anesthetic agent. In treating persons suffering toxic effects caused by exposure to halo-genated solvents, the use of epinephrine (adrenalin) and similar drugs must be avoided because they may produce cardiac arrhythmias, including ventricular fibrillation. 

Mrs A was admitted for minor day case surgery, expecting to return home later that day. A surgeon requested a weak solution of adrenaline to induce a blood free field, but was given a stronger solution than requested. As soon as the liquid was applied the patient developed a serious cardiac arrhythmia, the operation was terminated and she was transferred to the Intensive Therapy Unit, where she gradually recovered. 

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