Tachycardia atropine

Atropine is absorbed orally and crosses the placental barrier, whereupon it causes fetal tachycardia. Atropine has been used to examine the functional integrity of the placenta. 

Atropine is absorbed orally and crosses the placental barrier, whereupon it causes fetal tachycardia. Atropine has been used to examine the functional integrity of the placenta. Atropine toxicity is characterized by dry mouth, burning sensation in the mouth, rapid pulse, mydriasis, blurred vision, photophobia, dry and flushed skin, restlessness, and excitement. 

Atropine is the classic anticholinergic bronchodila-tor. It antagonizes acetylcholine, resulting in reduced intracellular cyclic guanosine monophosphate (cGMP) and smooth muscle relaxation. In horses, the therapeutic index of atropine is narrow and the duration of action is short (0.5-2.0 h). Adverse systemic effects associated with parenteral atropine administration include mydriasis, ileus, dry mucous membranes, blurred vision, excitement and tachycardia. Atropine is not suitable for routine administration to horses with recurrent airway obstruction. 

The main effect of atropine on the heart is the alteration of the rate. At low doses, the rate is slowed (bradycardia) without a change in blood pressure or cardiac output. Higher doses cause an increase in pulse rate (tachycardia). Atropine may be used in the initial treatment of a myocardial infarction or high-grade atrioventricular block. 

A. Patients with hypertension, tachyarrhythmias, thyrotoxicosis, congestive heart failure, coronary artery disease, and other illnesses, who might not tolerate a rapid heart rate. Patients with severe cholinesterase inhibitor poisoning are often tachycardia. Atropine should not be withheld and may lower heart rate (by improving oxygenation). Glycopyrrolate may also be helpful (due to its lessened propensity to cause a tachycardia). 

Dilated pupils, xerostomia, gastrointestinal hypomotility, tachycardia atropine and scopolamine may cause disorientation and ataxia... 

Adverse effects with atropine therapy include dry mouth, myosis, loss of visual accommodations, constipation, and urinary retention. The dmg can also produce flushing, hyperthermia, delirium, tachycardia, and exacerbate glaucoma (85). 

Supraventricular bradycardia is treated by implantation of a pacemaker device or has been treated pharmacologically with atropine. Supraventricular paroxysmal tachycardia is treated with aj marine or praj marine. Supraventricular tachyarrhythmias or AV reentrant arrhythmia typically can be terminated using adenosine. 

Cardiovascular system—palpitations, bradycardia (after low doses of atropine), tachycardia (after higher doses of atropine)... 

THE PATIENT WITH HEART BLOCK. The patient receiving atropine for third-degree heart block is placed on a cardiac monitor during and after administration of the drug. The nurse watches the monitor for a change in pulse rate or rhythm. Tachycardia, other cardiac arrhythmias, or failure of the drug to increase the heart rate must be reported to the primary health care provider immediately because other dm or medical management may be necessary. 

Monitor for adverse effects of medications, such as atropine (dry mouth, mydriasis, urinary retention, and tachycardia). 

The answer is local anesthetic properties it can block the initiation or conduction of a nerve impulse. It is biotransformed by plasma esterases to inactive products. In addition, cocaine blocks the reuptake of norepinephrine. This action produces CNS stimulant effects including euphoria, excitement, and restlessness Peripherally, cocaine produces sympathomimetic effects including tachycardia and vasoconstriction. Death from acute overdose can be from respiratory depression or cardiac failure Cocaine is an ester of benzoic acid and is closely related to the structure of atropine. 

The answer is e, (Katzungf p JI . High concentrations of atropine block all parasympathetic function. The patient usually presents with an array of symptoms and signs that include dry mouth, dilated pupils, tachycardia, red and hot skin, and delirium. Hyperthermia may occur, particularly in very young children. 

The answers arc 488-d, 489-h. (Katzang, pp 108-112, 1020.) Atropine blocks muscarinic cholinergic transmission in the brain and in the autonomic nervous system. The result is dry mouth, thirst, dry and hot skin, tachycardia, urinary retention, ataxia, restlessness, excitement, and hallucinations, followed by stupor, delirium, respiratory depression, coma, and death. 

Atropine generally increases heart rate, but it may briefly and mildly decrease it initially, due to Ml receptors on postganglionic parasympathetic neurons. Larger doses of atropine produce greater tachycardia, due to M2 receptors on the sinoatrial node pacemaker cells. There are no changes in blood pressure, but arrhythmias may occur. Scopolamine produces more bradycardia and decreases arterial pressure, whereas atropine has little effect on blood pressure (Vesalainen et al. 1997 Brown and Taylor 1996). 

Ditran is intermediate between atropine and scopolamine with respect to heart rate changes, with a slight dip below baseline at the low dose of 50 mcg/kg (Fig. 65). Peak FIR elevation occurs at about 30 min, somewhat later than both atropine and scopolamine. The tachycardia is short-lived, with recovery at 5-6 hours. No doubt, the short duration of Ditran was an advantage when used by Ostfeld et al. in their Ditran coma therapy, which was perhaps inspired by Forrer s atropine coma therapy introduced a few years earlier. 

The side effects of tricyclic antidepressants are largely attributable to the ability of these compounds to bind to and block receptors for endogenous transmitter substances. These effects develop acutely. Antagonism at muscarinic cholinoceptors leads to atropine-like effects such as tachycardia, inhibition of exocrine glands, constipation, impaired micturition, and blurred vision. 

Specific treatment starts with the administration of atropine sulphate, a competitive antagonist of acetylcholine at muscarinic receptors. Sufficient atropine should be given to control hypersecretion and produce tachycardia and pupillary dilation. Very large doses of atropine are required atropine sulphate 2-A mg should be given intravenously every few minutes during the first hour, and then by continuous infusion. Patients may require up to 500 mg intravenously during the first day, and treatment may be needed for days. 

The reflex nature of the bradycardia induced by parenterally administered norepinephrine can readily be demonstrated by administration of atropine, a choli-noreceptor antagonist. Atropine abolishes the compensatory vagal reflexes. Under conditions of vagal blockade, the direct cardiac stimulatory effects of norepinephrine are unmasked. There is marked tachycardia, an increase in stroke volume, and as a consequence, a marked increase in cardiac output (Fig. 10.4). 

Atropine can be used in the differential diagnosis of S-A node dysfunction. If sinus bradycardia is due to extracardiac causes, atropine can generally elicit a tachy-cardic response, whereas it cannot elicit tachycardia if the bradycardia results from intrinsic causes. Under certain conditions, atropine may be useful in the treatment of acute myocardial infarction. Bradycardia frequently occurs after acute myocardial infarction, especially in the first few hours, and this probably results from excessive vagal tone. The increased tone and bradycardia... 

C. Atropine will not directly paralyze the respiratory muscles. However, it can prevent the detection of early signs of an overdose of neostigmine, which can quickly progress to a depolarizing block of skeletal muscle and paralysis of the respiratory muscles. Dry mouth, ocular disturbances, and tachycardia are common side effects of atropine given alone, but these effects are less likely to occur with competition between atropine and the increase in the synaptic ACh produced by inhibition of AChE by neostigmine. 

Atropine initially decrease the heart rate due to stimulation of vagal centre followed by tachycardia due to peripheral vagal block on SA node. It also shortens effective refractory period of AV node and facilitates AV conduction. In therapeutic doses, atropine completely blocks the peripheral vasodilatation and decrease in blood pressure produced by cholinergic agents. 

Heart rate In CHF patients, the heart rate is decreased. Digitalis produce a decrease in heart rate by stimulation of vagus. The vagal effect is probably evoked by sensitization of carotid baroreceptors, and by direct stimulation of vagal centre. The vagal action can be blocked by atropine but after full digitalising dose the effect can not be blocked by atropine and it is due to its direct cardiac action. In CHF patients, the sympathetic activity is increased as a compensatory phenomenon which leads to tachycardia. Digitalis decreases the... 

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