Atropine – an overview sciencedirect topics difference between hypoxia and anoxia

Side effects, contraindications, and precautions

Atropine is contraindicated in patients with known atropine or other belladonna alkaloids hypersensitivity because they may develop an allergic or other adverse reaction, including anaphylaxis. Intense flushing of the face (blush area) and trunk may occur 15 to 20 minutes following parenteral administration of atropine. This is called atropine flush and is not harmful when it occurs. Because of the potential for toxicity, atropine should not be administered in doses exceeding those recommended. Atropine may cause blurred vision, drowsiness, or dizziness.


It should be used with caution in patients with known cardiac disease or a recent myocardial infarction.Difference between hypoxia and anoxia because atropine can alter the heart rate (producing tachycardia), it should be used cautiously in patients with cardiac dysrhythmias, congestive heart failure, coronary artery disease, angina, or other cardiac instability where an increase in heart rate could be detrimental. Atropine should be used with caution during AMI because the drug can potentiate dysrhythmias. In addition, the increase in heart rate caused by atropine increases the oxygen demand on the heart and can exacerbate myocardial ischemia. Increased heart rate is undesirable in patients with hyperthyroidism (thyrotoxicosis) or cardiovascular instability in acute hemorrhage (bleeding).

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A atropine

Atropine acts by blocking the effects of excess concentrations of acetylcholine at muscarinic cholinergic synapses following OP inhibition of ache.Difference between hypoxia and anoxia atropine is the initial drug of choice in acute OP poisoning. Atropine sulfate in combination with an oxime has been used in traditional therapy for intoxication with OP nerve agents as well as with OP insecticides. Atropine can relieve the following symptoms of OP poisoning: sweating, salivation, rhinorrhea, lacrimation, nausea, vomiting and diarrhea, and can help control of bradycardia and circulatory depressions, dilating the bronchi and abolishing bronchorrhea. Atropine does not bind to nicotinic receptors and cannot relieve nicotinic effects of opcs.

Support for an anticonvulsant property of atropine has been presented by mcdonough et al. (1987) who found that atropine pretreatment prevents the development of convulsions and brain damage induced by soman and VX.Difference between hypoxia and anoxia other authors have stated that atropine can only partly block convulsions after exposure to these agents since other transmitter systems (GABA, glutamate) become involved in cholinergic overstimulation in brain ( zilker, 2005; antonijević and stojiljkovic, 2007).

The effects of atropine in OP poisoning are far more complex than muscarinic blockade. In a study in rats, pazdernik et al. (1986) investigated the effect of atropine pretreatment on local cerebral glusose use during seizures induced with soman. Atropine treatment reduced local use of cerebral glucose and brain damage as well. Atropine may be effective in treating acute dystonic reactions and primary position upbeat nystagmus occasionally observed in acute OP poisoning ( heath et al., 1992 ).Difference between hypoxia and anoxia although the clinical efficacy of atropine in OP poisoning is well established, no controlled studies have been published.

The standard dosing of atropine depends on the severity of OP poisoning. The initial dose is usually 2 mg in an adult (0.02 mg/kg in a child) given every 5–10 min until bronchosecretion is cleared and the patient is atropinized (dry skin, sinus tachycardia) which should be maintained during further treatment. The dose may be increased as required. Patients poisoned with ops appear to be resistant to toxic effects of atropine and may require relatively large doses of atropine administered during prolonged periods. According to IPCS (2002) , in severe OP poisoning the total dose of atropine given during 5 weeks of treatment can be as high as 30,000 mg.Difference between hypoxia and anoxia

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Formulations and dose rates

One drop is administered to the affected eye q.6–8 h until the pupil dilates. This usually takes 1–2 d and is dependent on how much intraocular inflammation is present. Once the pupil is dilated, atropine is used as required to maintain dilation. If the eye is inflamed, atropine may be required 2–3 times a day to maintain mydriasis. If inflammation is controlled, then atropine administration may only be required once every second day or twice a week.

The degree of pupillary dilation maintained or achieved by 1 drop of atropine can be used as a guide to how well inflammation is controlled; if the pupil stays dilated with 1 drop of atropine, uveitis is well controlled.Difference between hypoxia and anoxia rapid onset of miosis after atropine administration suggests that inflammation is not well controlled.

In refractory cases subconjunctival atropine can be administered as an epibulbar injection. The dose is 0.05 mg (cats and small dogs) or 0.1 mg (larger dogs). In these cases it is important to increase anti-inflammatory therapy by using subconjunctival depot cortisone injections with the epibulbar atropine injection.

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Atropine

Atropine is primarily effective in treating the muscarinic effects of OP poisoning, especially in its effects on bronchial secretions, it has no effect on the neuromuscular junctions. Atropine crosses the blood-brain barrier and counters the effects of excess ach on the extrapyramidal system.Difference between hypoxia and anoxia thus, atropinization is the most important mode of treatment during acute cholinergic crisis and can be achieved with the judicious use of atropine. As many as 30 dose schedules of atropine have been cited by different authors. Atropinization, once achieved, should be maintained for 3 to 5 days, depending upon the compound involved. The endpoint of atropinization is pulmonary secretions. Tachycardia and mydriasis must not be used to limit or to stop subsequent doses of atropine. According to the most frequently cited schedule, the recommendation is to begin IV atropine at 2 to 5 mg in adults or 0.05 mg/kg in children. This should be given for 3 to 5 minutes until pulmonary secretions clear. 150 an alternative to repeated doses of atropine is a continuous infusion (0.02–0.08 mg/kg/hour) after the initial bolus has been given. 150 glycopyrrolate (robinul) may be considered as an alternative to atropine when the patient develops too much central anticholinergic delirium or agitation.Difference between hypoxia and anoxia glycopyrrolate does not enter the brain and so will not cause toxic delirium, but it does not dry up secretions as effectively as atropine.

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Atropine

Atropine acts by blocking the effects of excess concentrations of ach at muscarinic cholinergic synapses after OP inhibition of ache. Atropine is the initial drug of choice in acute OP poisoning that can relieve the following symptoms of OP poisoning: sweating; salivation; rhinorrhea; lacrimation; nausea; vomiting; and diarrhea. It can also help control bradycardia and circulatory depressions and dilating of the bronchi, and it can abolish bronchorrhea. Atropine does not bind to nicotinic receptors and cannot relieve nicotinic effects of OP compounds.Difference between hypoxia and anoxia in addition, there is evidence regarding the anticonvulsant properties of atropine in poisoning with soman and VX ( mcdonough et al., 1987; zilker, 2005).

The standard dosing of atropine depends on the severity of OP poisoning. The initial dose is usually 2 mg in an adult (0.02 mg/kg in a child) administered every 5–10 min until hyperatropinization (flushing, dryness of the mouth, nose, lungs, and the skin, heart rate 80–100/min, normal blood pressure, mydriasis). The dose may be increased as required. Patients poisoned with ops appear to be resistant to the toxic effects of atropine and may require relatively large doses of atropine administered during prolonged period of time. According to IPCS (2002) in severe OP poisoning, the total dose of atropine given during 5 weeks of treatment can be as high as 30,000 mg.Difference between hypoxia and anoxia

In an open-label, randomized clinical trial, abedin et al. (2012) compared the efficacy and safety of conventional bolus doses of atropine with individual incremental doses for atropinization followed by atropine infusion for management of OP poisoning. It was concluded that rapid incremental dose atropinization, followed by atropine infusion reduced mortality and morbidity from OP poisoning and shortened the length of the total hospital stay and recovery. They recommended that incremental atropine and infusion should become the treatment of choice for OP poisoning.

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Atropine and scopolamine

Atropine (0.02 mg/kg) and scopolamine (0.01 mg/kg) both have CNS effects, although the sedating effect of scopolamine is 5 to 15 times greater than atropine.Difference between hypoxia and anoxia scopolamine possesses two to three times more potent antisialagogue action than atropine. Atropine and scopolamine decrease the ability to sweat and thus may cause a slight increase in temperature. 1512 atropine and scopolamine have equipotent cardiovascular accelerator properties. The dose for both anticholinergics in infants to speed the heart rate is greater doses per kilogram than adults. 1513 anticholinergics are appropriate in specific situations, such as to diminish secretions preoperatively, to block laryngeal and vagal reflexes, to treat or prevent the bradycardia associated with succinylcholine, and to treat the bradycardia of anesthetic-induced myocardial depression, the muscarinic effects of neostigmine, and the oculocardiac reflex.Difference between hypoxia and anoxia atropine is painful when administered intramuscularly. When it is administered as a premedicant, it does not block laryngeal reflexes. Atropine is much more effective in blocking the laryngeal reflexes when it is given intravenously. Although some data suggest that children with down syndrome are more susceptible to the cardiac effects of atropine, 1514 our clinical experience and that of others do not support this notion. 1515, 1516 because some children with down syndrome have narrow-angle glaucoma, atropine must be administered cautiously because it might worsen the glaucoma. 1515, 1516 atropine may be administered orally, rectally, and via the trachea. Oral atropine may blunt the hypotensive response to potent inhalation agents during induction of anesthesia in infants younger than 3 months of age. 1517 when administered via the trachea, atropine is rapidly absorbed, producing physiologic effects. 1518–1521

difference between hypoxia and anoxia

In clinical practice, scopolamine is usually limited to those situations in which its sedative effect, combined with that of morphine, will be most advantageous, such as during cardiac surgery. It is also very useful as an adjuvant to ketamine anesthesia because of its antisialagogue and central sedative effects. The central sedative effects of both atropine and scopolamine may be antagonized with physostigmine. Many centers no longer routinely administer anticholinergic medications as part of the premedication because they are painful, the optimal effect may not coincide with induction of anesthesia, and current potent inhalation agents produce fewer secretions and infrequent bradycardia.

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difference between hypoxia and anoxia

Atropine

Atropine represents the cornerstone of the treatment for poisoning by anticholinesterase. Other available drugs, such as reactivators of inhibited ache, which are very effective, should be considered, in principle, as valid adjuncts to atropine administration.

Atropine is a muscarinic receptor antagonist that prevents the effects of acetylcholine by blocking its binding to muscarinic cholinergic receptors ( brown and taylor, 1996). It is a racemic mixture of active 1-hysocyamine and inactive d-hysocyamine that should be stored at 15–30°C and protected from light. Freezing should be avoided. The shelf life is 24 months from the date of manufacture if it is kept under the recommended conditions ( heath and meredith, 1992).Difference between hypoxia and anoxia

Pharmacokinetic data about atropine are limited. The kinetics of distribution of atropine seem to be dose dependent: about 20% of the drug is bound in plasma and two phases, with apparent half-lives of 1 and 140 min, respectively, have been identified after intravenous injection ( hinderling et al., 1985). However, for practical purposes, the reported plasma half-lives after both intravenous and intramuscular injections, varying between 1.3 and 4.3 h, should be considered. Differences are due to assay methods and to a considerable intra- and interindividual variability ( adams et al., 1982; kanto and klotz, 1988; kentala et al., 1990). In children and in the elderly, the plasma half-life may be longer.Difference between hypoxia and anoxia the reported apparent volume of distribution is quite large (2–3.5 liter kg −1 ), implying significant intra- and extracellular binding and partitioning of the drug. In children, higher volumes of distribution than in adults have been reported. About 50% of atropine is eliminated unchanged in the urine. There is no correlation between plasma levels and maximal pharmacological effects after intravenous injections ( adams et al., 1982 ); therefore, the dose of atropine cannot be titrated by means of plasma concentration. For practical purposes, however, one should consider that the effects of intravenous atropine begin within 3–4 min and are maximal about 12–16 min after injection.

Atropine is less effective in blocking certain muscarinic effects (for example, effects on the gastrointestinal and urinary tracts) than others effects (for example, effects on the heart and the salivary glands).Difference between hypoxia and anoxia atropine has no effect on nicotinic symptoms, and central muscarinic effects may be undetectable, perhaps reflecting the difficulty of penetration of atropine into the CNS, which can be achieved only by large doses ( taylor, 1996a).

Caution should be exercised in the use of atropine in hypoxic patients because it may cause ventricular fibrillation due to the increased myocardial oxygen demand brought about by the increased heart rate produced by atropine ( massumi et al., 1972 ). Therefore, in severe cases of OP poisoning, anoxia should be corrected before atropine is administered ( durham and hayes, 1962 ). However, when arterial oxygen has been normalized, there is no reason to avoid the use of atropine because of the suggested risk of ventricular fibrillation ( kecik et al., 1993).Difference between hypoxia and anoxia

Atropine is preferably given intravenously, although the intramuscular route is also effective. Satisfactory absorption also can be achieved by inhalation, and the pharmacokinetic characteristics are similar to those that occur after intramuscular injection ( harrison et al., 1986 ). However, atropine administration by inhalation has not been tested in cases of OP poisoning. Although several dosage regimens have been proposed and some caution was suggested in the dosage of atropine ( de kort et al., 1988 ), the best clinical approach is to administer doses of atropine large enough to achieve clinical evidence of atropinization, that is, flushing, dry mouth, changes in pupil size, bronchodilation and increased heart rate.Difference between hypoxia and anoxia if such signs are undetected, the dose of atropine is assumed to be insufficient and it must be increased ( barr, 1966). A mild degree of atropinization should be maintained for at least 48 h and withdrawal of atropine should be very carefully monitored because relapse can occur, particularly when ops are stored in fat (see section 72.1.3.1 ). In case of relapse, atropinization should be immediately reestablished. In patients with mild cholinergic signs, it is appropriate to start with a test dose of atropine (1 mg in the adult and 0.01 mg kg −1 in children, intravenously). If signs of atropinization occur rapidly, severe poisoning is unlikely, although observation of the patient for at least 24 h is mandatory.Difference between hypoxia and anoxia in moderately to severely poisoned adult patients, 2–5 mg of atropine should be given intravenously and repeated every 10–20 min (0.02–0.05 mgkg −1 in children at the same intervals). Continuous intravenous infusion may be required in severe cases. Because patients poisoned with ops are tolerant to the effects of atropine, quite large doses of the drug have been used in cases of severe and prolonged poisoning ( golsousidis and kokkas, 1985; lotti et al., 1986). In a case of dimethoate poisoning, 30 g of atropine were given over 35 days with maximum daily dosage of 3.5 g ( le blanc et al., 1986 ). Indicated dosages of atropine in accord with the severity of the clinical picture are summarized in table 72.6 .Difference between hypoxia and anoxia overdosage with atropine is rarely serious in OP poisoned patients. On the contrary, patients frequently die because of insufficient atropine. When massive tachycardia is produced by atropine, it may be corrected by propanolol ( valero and golan, 1967 ), thus avoiding the need to reduce the amount of atropine. It has also been suggested that using a combination of atropine and glycopyrrolate might offer an advantage over atropine alone, inasmuch as tachycardia could be avoided and adequate antimuscarinic effects still could be provided ( tracey and gallagher, 1990), and that glucopyrrolate may better alleviate some signs of cholinergic overstimulation ( choi et al., 1998).

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