Tachycardia and

Propanidid. Propanidid [1421-14-3] (Epontol), C gH2yNO, (7) a derivative of the propyl ester of homo vanillic acid, has been in clinical use in Europe for a number of years. Its main advantage is rapid onset of action and a fast recovery which, like etomidate, is because of rapid metaboHsm by esterases rather than redistribution (108). Excretion is rapid 75 to 90% of the dmg is eliminated as metaboUtes within two hours. Propanidid side effects include hypotension, tachycardia, and hyperventilation followed by apnea, as well as excitatory side effects such as tremor and involuntary muscle movement (109). 

Aerosol adniinistration of isoproterenol produces a prompt (2—5 minutes) intense bronchodilatation of relatively short (1 h) duration. The lack of P2-selectivity leads, in many cases, to tachycardia and blood pressure elevation. Also, use of isoproterenol, like all other known P-agonists, results in a down-regulation, or desensitization, of P-adrenergic receptors. This desensitization is only partial, and after time (depending on dose, patient, and agent), a stable, less responsive state is achieved in which P-agonists remain effective. Isoproterenol has been widely used for many years. 

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). 

OC-Adrenoceptor Blockers. Nonselective a-adrenoceptor blockers (Table 6), such as phentolamine, which block both a - and a2 adrenoceptors, produce vasodilation by antagonizing the effects of endogenous norepinephrine. They also produce severe tachycardia and have been replaced by selective a -adrenoceptor blockers, such as prazosin, terazosin, and doxazosin, which do not usually cause severe tachycardia. 

There are at least 13 primary types of K+ channels known. In addition, within each type there are several subtypes. The best known chemical classes of potassium channel openers are nicorandil, piaacidil, and cromakalim. They are aU potent smooth muscle relaxants. PharmacologicaUy, they behave as classical vasodilators, lowering blood pressure and causiag tachycardia and fluid retention. 

Piaacidil has a short half-life and most human studies were carried out ia slow-release formulatioas. The reductioa ia blood pressure produced by piaacidil is accompanied by tachycardia and fluid retention. Plasma catecholamines and renin activity are iacreased. Other side effects are headache, di22iaess, and asthenia. 

Propranalol hydrochloride (5-l-isopropylamino-3-(l-naphthyloxy)-2-propanol HCl) [4199-10-4] M 295.8, m 192°, 193-195 , [a] +25° (c 1, EtOH) pK 9.5. See preceding entry for physical properties. The is the active isomer which blocks isoprenaline tachycardia and is a (i-adrenergic blocker. [Leclerc et al. Trends Pharmacol Sci 2 18 7987 Howe and Shanks Nature 210 1336 7966.]... 

Presently, only adenosine itself is approved for clinical use. It is used widely in the treatment of supraventricular tachycardia and in cardiac stress imaging to assess coronary artery disease [5]. Other agonists and antagonists and an allosteric modulator of the Ai receptor are in clinical trials for a variety of indications. 

Non-selective P-adrenergic receptor antagonists (e.g. propranolol) can suppress tachycardia and tremor in patients with hyperthyroidism or tremor caused by... 

The acute adverse effects of the organic nitrates as well as molsidomine are directly related to their therapeutic vasodilation as they can cause orthostatic hypotension, tachycardia and throbbing headache. 

The amide local anaesthetic lidocaine may also be used as an antianhythmic for ventricular tachycardia and exra-systoles after injection into the blood circulation. Drugs with high lipid solubility such as bupivacaine cannot be used for these purposes because their prolonged binding to the channel may induce dysrhythmias or asystolic heart failure [3]. Systemically applied lidocaine has also been used successfully in some cases of neuropathic pain syndromes [4]. Here, electrical activity in the peripheral nervous system is reduced by used-dependent but incomplete sodium channel blockade. 

Drowsiness is the most common reaction seen with the use of skeletal muscle relaxants. Additional adverse reactions are given in die Summary Drug Table Drugp Used to Treat Musculoskeletal Disorders. Some of the adverse reactions tiiat may be seen with the administration of diazepam include drowsiness, sedation, sleepiness, letiiargy, constipation or diarrhea, bradycardia or tachycardia, and rash. 

The tricyclics can cause cardiac-related adverse reactions such as tachycardia and heart block. For this reason, the nurse gives these drugs with caution to the person with preexisting cardiac disease and to the elderly. 

Use of oral decongestants may result in tachycardia and other cardiac arrhythmias, nervousness, restlessness, insomnia, blurred vision, nausea, and vomiting. 

Warning sgns of a fluid and electrolyte imbalance include dry mouth, thirst, weakness lethargy, drowsiness restlessness muscle pains or cramps confuson, gastrointestinal disturbances hypotenson, oliguria, tachycardia, and seizures... 

The symptoms of hypothyroidism and hyperthyroidism are given in Table 51-1. A severe form of hyperthyroidism, called thyrotoxicosis or tiiyroid storm, is characterized by high fever, extreme tachycardia, and altered mental status. Thyroid hormones are used to treat hypothyroidism and antithyroid... 

Cardiovascular Effects. Both tachycardia and bradycardia were noted among 18 agricultural workers in India who applied endosulfan without protective equipment (both dermal and inhalation exposures probably occurred) (Chugh et al. 1998). 

In the setting of a sustained loss of myocardium, a number of mechanisms aid the heart when faced with an increased hemodynamic burden and reduced CO. They include the following the Frank-Starling mechanism, tachycardia and increased afterload, and cardiac hypertrophy and remodeling (Table 3-2).5,7... 

Tachycardia and increased contractility (due to SNS activation) Increase cardiac output Increased MV02 Shortened diastolic filling time P,-Receptor down-regulation, decreased receptor sensitivity Precipitation of ventricular arrhythmias Increased risk of myocardial cell death... 

There is a paucity of clinical trial evidence comparing the benefit of diuretics to other therapies for symptom relief or long-term outcomes. Additionally, excessive preload reduction can lead to a decrease in CO resulting in reflex increase in sympathetic activation, renin release, and the expected consequences of vasoconstriction, tachycardia, and increased myocardial oxygen demand. Careful use of diuretics is recommended to avoid overdiuresis. Monitor serum electrolytes such as potassium, sodium, and magnesium frequently to identify and correct imbalances. Monitor serum creatinine and blood urea nitrogen daily at a minimum to assess volume depletion and renal function. 

Current data suggest little benefit on clinical outcomes beyond symptom relief for calcium channel blockers in the setting of ACS.43 Moreover, the use of first-generation shortacting dihydropyridines, such as nifedipine, should be avoided because they appear to worsen outcomes through their negative inotropic effects, induction of reflex sympathetic activation, tachycardia, and increased myocardial ischemia.43 Therefore, calcium channel blockers should be avoided in the acute management of MI unless there is a clear symptomatic need or a contraindication to p-blockers. 

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