Atropine Flashcards
Atropine overdose clinical presentation
The clinical picture of a high (toxic) dose of atropine may be remembered by an old mnemonic device that summarizes the symptoms:
Hot as a hare since the patient will have a high temperature and decreased sweating,
Mad as a hatter since the patient will experience confusion and delirium
Red as a beet since the patient will have tachycardia and a flushed face
Dry as a bone because of the decrease in secretions, thirsty
Blind as a bat since the patient will have a very blurry vision.
eicosanoids
Prostaglandins and related compounds are collectively known as eicosanoids
Most are produced from arachidonic
The eicosanoids are considered “local hormones.”
They have specific effects on target cells close to their site of formation.
Atropine as a respiratory stimulant
Although mild vagal excitation occurs due to the paradoxical effect of atropine, the increased respiratory rate and (sometimes) increased depth of respiration produced by Atropine are more probably the result of bronchiolar dilatation. Accordingly, Atropine is an unreliable respiratory stimulant and large or repeated doses may depress respiration.
Effect on circulation
when Atropine is given alone, the effect on blood vessels and blood pressure is not constant nor striking. why? because most vascular beds lack cholinergic innervation.
however, Atropine, in clinical doses, completely counteracts the peripheral vasodilation and sharp fall in blood pressure caused by choline esters
In toxic and occasionally in therapeutic doses, atropine can dilate cutaneous blood vessels, especially those in the blush area (atropine flush). This may be a compensatory reaction permitting the radiation of heat to offset the atropine-induced rise in temperature that can accompany inhibition of sweating.
Effect on eyes
Atropine blocks the cholinergic responses of the pupillary sphincter muscle of the iris and the ciliary muscle controlling lens curvature.
Thus, they dilate the pupil (mydriasis) and paralyze accommodation (cycloplegia).
The wide pupillary dilation results in photophobia; the lens is fixed for far vision, near objects are blurred, and objects may appear smaller than they are.
The normal pupillary reflex constriction to light or upon convergence of the eyes is abolished.
These effects can occur after either local or systemic administration of Atropine.
However, conventional systemic doses of atropine (0.6 mg) have little ocular effect.
Locally applied atropine produces ocular effects of considerable duration; accommodation and pupillary reflexes may not fully recover for 7-12 days.
Muscarinic receptor antagonists administered systemically have little effect on intraocular pressure except in patients predisposed to angle-closure glaucoma, in whom the pressure may occasionally rise dangerously. The rise in pressure occurs when the anterior chamber is narrow and the iris obstructs outflow of aqueous humor into the trabeculae.
Why relatively large doses are needed for atropine to have an effect on GI motility
Relatively large doses are needed to
produce such inhibition. This probably can be explained by the ability of the enteric nervous system to regulate motility independently of parasympathetic control; parasympathetic nerves serve only to modulate the effects of the enteric nervous system.
Effect of atropine on other smooth muscles
Urinary Tract. Muscarinic antagonists decrease the normal
tone and amplitude of contractions of the ureter and
bladder, and often eliminate drug-induced enhancement
of ureteral tone. However, this inhibition cannot be
achieved in the absence of inhibition of salivation and
lacrimation and blurring of vision
Biliary Tract. Atropine exerts a mild antispasmodic
action on the gallbladder and bile ducts in humans.
However, this effect usually is not sufficient to
overcome or prevent the marked spasm and increase in
biliary duct pressure induced by opioids. The nitrates are more effective than atropine in this respect.
how to treat atropine intoxication
In cases of full-blown atropine poisoning, the syndrome may last 48 hours or longer. Intravenous injection of the anticholinesterase agent physostigmine may be used for confirmation. If physostigmine does not elicit the expected salivation, sweating, bradycardia, and intestinal hyperactivity, intoxication with atropine or a related agent is almost certain. Depression and circulatory collapse are evident only in cases of severe intoxication; the blood pressure declines, convulsions may ensue, respiration becomes inadequate, and death due to respiratory failure may follow after a period of paralysis and coma. Measures to limit intestinal absorption should be initiated without delay if the poison has been taken orally. For symptomatic treatment, slow intravenous injection of physostigmine rapidly abolishes the delirium and coma caused by large doses of atropine, but carries some risk of overdose in mild atropine intoxication. Since physostigmine is metabolized rapidly, the patient may again lapse
into coma within 1-2 hours, and repeated doses may be needed (Chapter 10). If marked excitement is present and more specific treatment is not available, a benzodiazepine is the most suitable
agent for sedation and for control of convulsions. Phenothiazines or agents with antimuscarinic activity should not be used, because their antimuscarinic action is likely to intensify toxicity. Support of respiration
and control of hyperthermia may be necessary. Ice bags andalcohol sponges help to reduce fever, especially in children
Scopalamine and reducing motion sickness
As an antiemetic, scopolamine probably blocks neural pathways from the vestibular nuclei in the inner ear to the brain stem and from the reticular formation to the vomiting center. Because acetylcholine mediates impulses from the inner ear, scopolamine is an effective antiemetic in motion sickness. Scopolamine is a poor choice, however, for treating nausea/vomiting in other settings since neural pathways not mediated by acetylcholine are involved. High doses of scopolamine produce symptoms of antimuscarinic toxicity such as restlessness, disorientation, irritability, and hallucinations
DDI with nitroglycerin
Discussion The labeling for sublingual nitroglycerin tablets states that anticholinergic agents may impair the dissolution of the nitroglycerin sublingual tablets due to decreased salivary secretions, which is a known side effect of anticholinergic agents.1 The labeling recommends that patients should consider actions to increase saliva production (chewing gum and use of artificial saliva products are recommended in sublingual nitroglycerin labeling as examples of such actions).
DDI with Potassium chloride
Discussion Solid oral dosage forms of potassium chloride are contraindicated in patients with impaired gastric emptying (e.g., due to the effects of drugs such as many anticholinergics) due to the risks of gastric and intestinal irritation and ulceration associated with prolonged contact between these solid dosage forms and the gastrointestinal mucosa. slowed gastrointestinal motility due to the effects of anticholinergic drugs
DDI with Thalidomide
Thalidomide itself is associated with frequent drowsiness and somnolence. With medications that cause CNS depression, we will have additive CNS depression and thus additive sedative effect.
Adverse reactions
Xerostomia (dry mouth) is the most frequent adverse effect following transdermal administration of scopolamine, occurring in about 67% of patients. Xerostomia has also been reported with the use of the injectable and ophthalmic formulations.
Warning/precautions
Patients with a known hypersensitivity to belladonna alkaloids can experience an allergic reaction including anaphylaxis with scopolamine.
The anticholinergic effects of scopolamine may be significant and are additive with other anticholinergic medications. This is especially true for the older adult, but may also occur with any patient. Consider the anticholinergic burden of all applicable medication therapies and consider the potential for additive side effects. 30354
Scopolamine is contraindicated in patients with closed-angle glaucoma because the drug can induce cycloplegia and mydriasis, which would result in increased intraocular pressure. Scopolamine should be avoided in open-angle glaucoma. The anticholinergic effects of scopolamine may make the eyes dry. This can cause an increased lens awareness, or blurred vision for wearers of contact lenses. The use of lubricating drops may be necessary, or in severe cases discontinued use of contact lenses while using scopolamine skin patches.
Scopolamine use should be avoided in patients with urinary tract obstruction or bladder neck obstruction due to prostatic hypertrophy because it can cause urinary retention via its antimuscarinic effects on the ureters and bladder.
Scopolamine should be avoided in patients with GI obstruction because its antimotility effects can exacerbate this disease state and can cause paralytic ileus. Scopolamine is not recommended for use in patients with severe ulcerative colitis because it decreases GI motility and can exacerbate the condition. Scopolamine is not recommended for use in patients with adynamic ileus, and toxic megacolon because it further decreases intestinal motility and exacerbates these conditions. Scopolamine should be used cautiously in patients with gastroesophageal reflux disease (GERD) or hiatal hernia associated with reflux esophagitis. Antimuscarinics decrease gastric motility and relax the lower esophageal sphincter. These effects promote gastric retention and aggravate reflux in these patients.
Scopolamine should be used with caution in patients with asthma or chronic obstructive pulmonary disease (COPD) because of its effects on bronchial smooth muscle and bronchial secretory glands.
Scopolamine should be used with caution in patients with myasthenia gravis or autonomic neuropathy because the drug competes with the small amount of acetylcholine that has potential to act in the body.
Scopolamine should be avoided in patients with coronary artery disease or congestive heart failure because it can increase heart rate, which would increase the oxygen demand on the heart. Scopolamine should be used with caution in patients with hyperthyroidism because these patients may be at an increased risk of suffering adverse effects, especially in the heart. Scopolamine should be used with caution in patients with hypertension since the drug has some actions on the heart and can exacerbate this condition. Scopolamine is not recommended for use in patients with cardiac arrhythmias because it can potentiate arrhythmias by blocking the vagal inhibition of the SA node.
Scopolamine should be used with caution in patients with hepatic disease because the drug can accumulate to toxic levels in the body.
Scopolamine should be used with caution in patients with renal impairment because of an increased likelihood of CNS adverse effects.
ndNMBA Adverse effect Prolonged paralysis
Prolonged paralysis—Prolonged paralysis following drug discontinuation results from accumulation of drug or active metabolites, or an acute myopathy, often in the setting of renal or hepatic insufficiency especially with NMBAs that are dependent upon renal clearance –pancuronium, pipecuronium, and tubocurarine – accumulate in patients with renal insufficiency if they are not properly
dose-adjusted to peripheral nerve stimulation (PNS) response. Affected patients have flaccid areflexic tetraplegia
