Sinus arrhythmia causes

There is a similar high prevalence of peripheral neuropathy (34%) in the pediatric population infected with HIV (Araujo et al. 2000). The frequency of IDP in the HIV-infected population is unknown but is thought to be rare (Wulff et al. 2000). In an outpatient population of HIV positive patients, mononeuritis multiplex and lumbosacral polyradiculopathy were found in less than 1% of patients with AIDS (Fuller et al. 1993). HIV-associated autonomic nervous system dysfunction is also not uncommon as up to 66% of patients have papillary involvement and 15% have sympathetic and parasympathetic involvement causing orthostatic hypotension and respiratory sinus arrhythmia (Gluck et al. 2000). 

Acute digoxin poisoning causes initial nausea and vomiting and hyperkalaemia because inhibition of the Na, K" -ATPase pump prevents intracellular accumulation of potassium. The ECG changes (see Table 24.1) of prolonged use of digoxin may be absent. There may be exaggerated sinus arrhythmia, bradycardia and ectopic rhythms with or without heart block. 

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... 

A. To control excessive sinus tachycardia or ventricular arrhythmias caused by catecholamine excess (eg, theophylline or caffeine), sympathomimetic drug intoxication (eg, amphetamines, pseudoephedrine, or cocaine), or excessive myocardial sensitivity (eg, chloral hydrate, freons, or chlorinated and other hydrocarbons). 

Sometimes the rhythm will be irregular with all waves present (PQRST). A 10 % variance is considered quite normal. In the case of sinus arrhythmia the rhythm is irregular and corresponds to the respiratory cycle. This is caused by the heart rate inaeasing during inspiration. This is often found in the elderly, children or fit people, and causes no symptoms. 

Treatment of sinus bradycardia is only necessary in patients who become symptomatic. If the patient is taking any med-ication(s) that may cause sinus bradycardia, the drug(s) should be discontinued whenever possible. If the patient remains in sinus bradycardia after discontinuation of the drug(s) and after five half-lives of the drug(s) have elapsed, then the drugs(s) can usually be excluded as the etiology of the arrhythmia. In certain circumstances, however, discontinuation of the medication(s) may be undesirable, even if it may be the cause of symptomatic sinus bradycardia. For example, if the patient has a history of myocardial infarction or HF, discontinuation of a (3-blocker is undesirable, because (3-blockers have been shown to reduce mortality and prolong life in patients with those diseases, and the benefits of therapy with... 

Sick sinus syndrome Use sotalol only with extreme caution in patients with sick sinus syndrome associated with symptomatic arrhythmias, because it may cause sinus bradycardia, sinus pauses, or sinus arrest. 

WARNING Long-acting p2-agonists may t risk of asthma-related death Uses COPD maint Action LA p2-agonist, relaxes airway smooth muscles Dose 15 meg neb bid, 30 meg/d max Caution [C, ] w/ CV Dz, X Contra Not for acute asthma component hyp sensitivity peds w/ phenothiazines Disp Meg neb SE Chest/back pain, D, sinusitis, leg cramps, dyspnea, rash, flu-synd, t BP, arrhythmias, heart block J-K EMS Monitor ECG for arrhythmias, heart block, and hypokalemia (flattened T waves) t risk of acute asthma attack, treat w/ shortacting p-agonist OD May cause CP, palpitations, muscle tremors and cramps, and syncope symptomatic and supportive... 

Mechanism of Action An antiarrhythmicthat prolongs both atrial and ventricular action potential duration and increases the atrial and ventricular refractory period. Activates slow, inward current (mostly of sodium), produces mild slowing of sinus node rate and AV conduction, and causes dose-related prolongation of QT interval. Therapeutic Effect Converts arrhythmias to sinus rhythm. 

Depression or cardiac excitability and contractility may cause AV block, ventricular arrhythmias, or cardiac arrest. Symptoms of local anesthetic CNS toxicity, such as dizziness, tongue numbness, visual impairment or disturbances, and muscular twitching appear to occur before cardiotoxiceffects. Cardiotoxic effects include angina, QT prolongation, PR prolongation, atrial fibrillation, sinus bradycardia, hypotension, palpitations, and cardiovascular collapse. 

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. 

This is the amide analogue of procaine hydrochloride. It has an active metabolite with significant class III activity. Procainamide is particularly effective in the treatment of lifethreatening ventricular arrhythmias unresponsive to other therapies. It is also used to maintain sinus rhythm following cardioversion. Intravenous administration can cause hypotension, mainly due to peripheral vasodilatation, and it should not be given faster than 50 mg-min-1. It should be given intravenously as a bolus of 100 mg over 2-5 min, followed by an infusion of 30-90 pg-kg-l-min-1. 

This is a class IB drug used primarily for the emergency treatment of ventricular arrhythmias. It has little effect on sinus node automaticity but depresses normal and abnormal forms of automaticity in Purkinje fibres. It is generally ineffective against supraventricular and accessory pathway-induced (e.g. WPW syndrome) arrhythmias. Lidocaine is relatively safe and free from adverse cardiovascular side effects. It causes minimal cardiodepression, although high doses can cause heart block. The most common side effect is a dose-related CNS toxicity. It is given intravenously as a bolus of 1 mg-kg-1 followed by an infusion of 20-50 pg-kg-l-min-1. 

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... 

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. 

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. 

Succinylcholine may cause tachycardia, cardiac arrhythmias, and hypertension, which is brought about by stimulation of the sympathetic ganglia. It may also provoke bradycardia, caused by stimulation of muscarinic receptor sites in the sinus node of the heart. This effect is more pronounced following a second dose of succinylcholine. The bradycardia may be blocked by thiopental, atropine, and ganglionic blocking agents. 

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