Sinus tachycardia causes

Propranolol is indicated in the management of a variety of cardiac rhythm abnormalities that are totally or partially due to enhanced adrenergic stimulation. In selected cases of sinus tachycardia caused by anxiety, pheochromocytoma, or thyrotoxicosis, (3-blockade will reduce the spontaneous heart rate. 

A. Cardiotoxic effects of the type la agents include sinus bradycardia sinus node arrest or asystole PR, QRS, or QT interval prolongation sinus tachycardia (caused by anticholinergic effects) polymorphous ventricular tachycardia (torsade de pointes) and depressed myocardial contractility, which, along with alpha-adrenergic or ganglionic blockade, may result in hypotension and occasionally pulmonary edema. 

In overdose, the antihistamines cause convulsions, hallucinations, excitement, ataxia, incoordination, and athetosis. On exam patients may exhibit fixed, dilated pupils with a flushed face, sinus tachycardia, urinary retention, dry mouth, and fever. At high doses the patient can become comatose, which is often followed by cardiorespiratory collapse and death within 2 to 18 hours (Babe and Serafin, 1996). Treatment of overdose is mainly supportive, with efforts to manage the anti-colinergic effects. 

Nausea and vomiting because of CTZ stimulation, which can be minimized by starting with a lower dose. It also causes confusion, hallucinations, delusions and other behavioural effects. Certain cardiovascular effects such as palpitation, postural hypoten-sion, sinus tachycardia and ventricular arrhythmias have also been reported. 

Sympathomimetic effects (from NA re-uptake inhibition) and antimuscarinic effects can cause a sinus tachycardia. Postural hypotension may occur as a result of sympatholytic al-adrenoceptor antagonism. With overdoses of these drugs, there is a reduced re-uptake of catecholamines, resulting in arrhythmias and hypertension. Tricyclic compounds have a high... 

In addition to sinus tachycardia and tremor, vomiting is common after overdose. Hypotension, tachycardia, hypokalemia, and hyperglycemia may occur, probably owing to B2-adrenergic activation. The cause of this activation is not fully... 

In addition to sinus tachycardia and tremor, vomiting is common after overdose. Hypotension, tachycardia, hypokalemia, and hyperglycemia may occur, probably due to -adrenergic activation. The cause of this activation is not fully understood, but the effects can be ameliorated by the use of B-blockers (see below). Cardiac arrhythmias include atrial tachycardias, premature ventricular contractions, and ventricular tachycardia. In severe poisoning (eg, acute overdose with serum level > 100 mg/L), seizures often occur and are usually resistant to common anticonvulsants. Toxicity may be delayed in onset for many hours after ingestion of sustained-release tablet formulations. 

In terms of its potential for inducing cardiac dysrhythmias, cannabis is most likely to cause palpitation due to a dose-related sinus tachycardia. Other reported dysrhythmias include sinus bradycardia, second-degree atrioventricular block, and atrial fibrillation. Also reported are ventricular extra beats and other reversible electrocardiographic changes. 

TCAs have been reported to cause arrhythmias, prolongation of conduction time, orthostatic hypotension, sinus tachycardia, and heart failure, especially in the diseased heart... 

The most readily observable change in cardiac function is sinus tachycardia, which occurs to a greater or lesser extent in more patients and which correlates weakly or inconsistently with plasma concentrations (4,17,18). The mechanism may be related to both central and peripheral effects on cholinergic and adrenergic systems, but is not simply a reflex response to hypotension (4). The presence of tachycardia can serve as an indirect measure of compliance (4), but it is seldom a cause for concern, except in individuals who anxiously monitor their own physiological functions. 

The toxic events of terbutaline overdose follow its -adrenergic agonist activity. The effects of terbutaline overdose are usually mild and benign however, they can be prolonged. Cardiovascular effects are usually limited to a sinus tachycardia and widened pulse pressure. Although there may be a drop in diastolic pressure, the systolic pressure is maintained by increased cardiac output from the tachycardia. Evidence of myocardial ischemia after terbutaline overdose has been infrequently reported. Transient hypokalemia may occur, caused by a shift of extracellular potassium to the intracellular space. A transient metabolic acidosis can be seen due to increased lactate production. Restlessness, agitation, and tremors are common in terbutaline overdose. 

Pre-hospital mortality in acute myocardial infarction is approximately 20-30% (Braunwald, Zipes and Libby, 1998 Fiol, 2001). More than half of these deaths occur within the first hour and are generally caused by sudden death due to primary VF. This is generally triggered by a PVC with R/T phenomenon in the setting of autonomic nervous system (ANS) dysfunction (sinus tachycardia) (Figure 8.32A Adgey et al, 1982). In the thrombolytic era, this phenomenon has already been mentioned to be less frequent (Chiladakis et al, 2000). Furthermore, in ambulatory patients, primary VF only explains 10% of all sudden death cases, with sustained ventricular tachycardia leading to VF be-... 

The common supraventricular tachycardias that often require drug treatment are (1) atrial fibrillation or atrial flutter, (2) paroxysmal supraventricular tachycardia, and (3) automatic atrial tachycardias. Other common supraventricular arrhythmias that usually do not require drug therapy include premature atrial complexes (PACs), wandering atrial pacemaker, sinus arrhythmia, and sinus tachycardia. As an example, PACs rarely cause symptoms and never cause hemodynamic compromise, and therefore, drug therapy usually is not... 

Sinus tachycardia Increased SA automaticity results in a sinus rhythm in excess of 100 beats per minute. Sinus tachycardia is usually not pathological and is caused by simple anxiety or stimulants (caffeine, amphetamines). 

An allocryptopine isomer, probably differing from allocryptopine in the positions of the methylenedioxy and the methoxyl groups, has been called fagarine II (35). This substance was found to increase the amount of electric current necessary to provoke fibrillation and cause sinus tachycardia, due, at least in part, to an antivagal action (50). 

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