Atrial tachycardia causes

Vomiting is common in patients with digitalis overdose. Hyperkalemia may be caused by acute digitalis overdose or severe poisoning, whereas hypokalemia may be present in patients as a result of long-term diuretic treatment. (Digitalis does not cause hypokalemia.) A variety of cardiac rhythm disturbances may occur, including sinus bradycardia, AV block, atrial tachycardia with block, accelerated junctional rhythm, premature ventricular beats, bidirectional ventricular tachycardia, and other ventricular arrhythmias. 

Digitoxin and related drugs are used as cardiac stimulants, causing a positive inotropic effect. Thus, they increase the strength and intensity of the contractions and so are used in the treatment of heart failure. Because they slow the electrical conduction between atria and ventricles, they can also be used in the treatment of atrial fibrillation, atrial tachycardia, and atrial flu ter. 

Sun, H., Gaspo, R., Eeblanc, N., and Nattel, S. (1998). Cellular Mechanisms of Atrial Contractile Dysfunction Caused by Sustained Atrial Tachycardia. Circulation 98(7) 719—27. 

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. 

One of the more serious complications of magnesium deficiency is cardiac arrhythmias. Premature atrial complexes, atrial tachycardia and fibrillation, ventricular premature complexes, ventricular tachycardia, and ventricular fibrillation may be associated with magnesium deficiency. These effects maybe partly caused by the hypokalemia, renal wasting, and intracellular depletion of potassium caused by hypomagnesemia. 

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... 

Factors that commonly precipitate cardiac arrhythmias include hypoxia, electrolyte disturbances (especially hypokalemia), myocardial ischemia, and certain drugs (Table 34-1). For example, theophylline can cause multifocal atrial tachycardia, while torsades de pointes can arise not only during therapy with action potential-prolonging antiarrhythmics but also with other drugs, including erythromycin (see Chapter 46) pentamidine (see Chapter 40) and some antipsy-chotics, notably thioridazine (see Chapter 18). 

Is characterized by the presence of three or more atrial premature beats, and an atrial rate of between 140 and 250 BPM (Fig. 6.19). P waves, best seen in leads II or Vi are sometime present and usually hidden in the preceding T waves. The rhythm is regular. Atrial Tachycardia can also cause loss of atrial kick and a reduced cardiac output if sustained. 

RED FLAG At toxic levels, digoxin may cause numerous arrhythmias, including paroxysmal atrial tachycardia with block, AV block, atrial and junctional tachyarrhythmias, and ventricular arrhythmias. 

Atrial fibrillation leads to the development of HF, as a result of tachycardia-induced cardiomyopathy.25 Atrial fibrillation increases the risk of mortality approximately two-fold compared to that in patients without AF 23 the causes of death are likely stroke or HF. 

Verapamil (Class IV antiarrhythmic drug) is an effective agent for atrial or supraventricular tachycardia. A Ca++ channel blocker, it is most potent in tissues where the action potentials depend on calcium currents, including slow-response tissues such as the SA node and the AV node. The effects of verapamil include a decrease in heart rate and in conduction velocity of the electrical impulse through the AV node. The resulting increase in duration of the AV nodal delay, which is illustrated by a lengthening of the PR segment in the ECG, reduces the number of impulses permitted to penetrate to the ventricles to cause contraction. 

Disturbances of cardiac rhythm (e.g., tachycardia, atrial fibrillation, ventricular flutter, and A-V or intraventricular block) are the most frequent causes of death. Thus, management of cardiac function is critical. If the patient survives the early phase, recovery without sequelae is probable, and vigorous resuscitative measures are important. A major clinical problem is determining when a patient is no longer in danger. Many patients with mild overdose have been hospitalized... 

Supraventricular tachycardia is the major arrhythmia indication for verapamil. Adenosine or verapamil are preferred over older treatments (propranolol, digoxin, edrophonium, vasoconstrictor agents, and cardioversion) for termination. Verapamil can also reduce the ventricular rate in atrial fibrillation and flutter. It only rarely converts atrial flutter and fibrillation to sinus rhythm. Verapamil is occasionally useful in ventricular arrhythmias. However, intravenous verapamil in a patient with sustained ventricular tachycardia can cause hemodynamic collapse. 

Overdosage of levothyroxine causes increased metabolism resulting in increased heat production, with increased sweating and weight loss despite normal or even increased appetite. Accidental or suicidal injection of large amounts of thyroid hormones is exceptional (67). Clinical symptoms do not necessarily correlate well with plasma T4 concentrations and range from anxiety, confusion, or coma to tachycardia, atrial fibrillation, and angina. At least three lethal cases have been reported (SEDA-8, 371). 

Calcium channel blockers decrease the rate of discharge of the SA node and inhibit conduction velocity through the AV node.5 These drugs are most successful in treating arrhythmias caused by atrial dysfunction, such as supraventricular tachycardia and atrial fibrillation.15,39... 

Cardiovascular Effects. No studies were located regarding cardiovascular effects of various forms of aluminum following intermediate- or chronic-duration oral exposure in humans. Acute-duration oral exposure to aluminum phosphide has been shown to cause tachycardia, hypotension, cardiovascular electrocardiographic abnormalities, subendocardial infarction, and transient atrial fibrillation in persons who either ingested it accidentally or in suicide attempts (Chopra et al. 1986 Khosla et al. 1988). However, toxicity was probably due to the formation of highly toxic phosphine gas rather than to aluminum exposure. 

Digoxin (see p. 158) shortens the refractory period in atrial and ventricular myocardial cells while prolonging the effective refractory period and diminishing conduction velocity in Purkinje fibers. Digoxin is used to control the ventricular response rate in atrial fibrillation and flutter. At toxic concentrations, digoxin causes ectopic ventricular beats that may result in ventricular tachycardia and fibrillation. [Note This arrhythmia is usually treated with lidocaine or phenytoin.]... 

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. 

The authors reviewed the biphasic effect of marijuana on the autonomic nervous system. At low to moderate doses it causes increased sympathetic activity, producing a tachycardia and increase in cardiac output blood pressure therefore increases. At high doses it causes increased parasympathetic activity, leading to bradycardia and hypotension. They thought that this patient most probably had adrenergic atrial flutter. 

Altered rate of automatic discharge or abnormality of the mechanism by which an impulse is generated from a centre in the nodes or conducting tissue, is one cause of cardiac arrhythmia, e.g. atrial fibrillation, flutter or tachycardia. 

Ajmaline occasionally causes cardiac dysrh5dhmias (SEDA-17, 219). Of 1995 patients who were given ajmaline 1 mg/kg intravenously during an electrophysiological study, 63 developed a supraventricular tachydysrhythmia (atrial flutter, fibrillation, or tachycardia), and seven an atrioventricular re-entrant tachycardia (2). Those most at risk were older patients, those with underlying cardiac disease, and those with a history of dysrhythmias or sinus node dysfunction. 

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