Atrial fibrillation causes

Schoonderwoerd BA, Smit MD, Pen L, Van Gelder IC. New risk factors for atrial fibrillation causes of not-so-lone atrial fibrillation. Europace 2008 10 668—73. 

Atrial fibrillation causes pooling of the blood in the atria, which could lead to the development of a blood clot, and the client is prescribed Coumadin to decrease the probability of developing a thrombus/embolus. Green, leafy vegetables are high in vitamin K, which is the antidote for Coumadin overdose and should be limited in the client s diet. 

Atrial fibrillation Irregular and rapid atrial contraction, resulting in a quivering of the atria and causing an irregular and inefficient ventricular contraction... 

Duration of atrial fibrillation/atrial flutter >48 h or unknown, o Electrical or chemical cardioversion in a patient without adequate anticoagulation may cause embolization of atrial thrombi. 

O Atrial fibrillation may be caused by both abnormal impulse formation and abnormal impulse conduction. Traditionally, AF was believed to be initiated by premature impulses initiated in the atria. However, it is now understood that in many patients AF is triggered by electrical impulses generated within the pulmonary veins.20 These impulses initiate the process of reentry within the atria, and AF is believed to be sustained by multiple reentrant wavelets operating simultaneously within the atria.21 Some believe that, at least in some patients, the increased automaticity in the pulmonary veins may be the sole mechanism of AF and that the multiple reentrant wavelet hypothesis may be incorrect.21 However, the concept of multiple simultaneous reentrant wavelets remains the predominant hypothesis regarding the mechanism of AF. 

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. 

Atrial fibrillation (most important and treatable cardiac cause of stroke)... 

Common precipitating factors that may cause a previously compensated patient to decompensate include noncompliance with diet or drug therapy, coronary ischemia, inappropriate medication use, cardiac events (e.g., MI, atrial fibrillation), pulmonary infections, and anemia. 

The a wave This is caused by atrial contraction and is, therefore, seen before the carotid pulsation. It is absent in atrial fibrillation and abnormally large if the atrium is hypertrophied, for example with tricuspid stenosis. Cannon waves caused by atrial contraction against a closed tricuspid valve would also occur at this point. If such waves are regular they reflect a nodal rhythm, and if irregular they are caused by complete heart block. 

Atrial fibrillation Peak digoxin body stores larger than the 8 to 12 mcg/kg required for most patients with heart failure and normal sinus rhythm have been used for control of ventricular rate in patients with atrial fibrillation. Titrate doses of digoxin used for the treatment of chronic atrial fibrillation to the minimum dose that achieves the desired ventricular rate control without causing undesirable side effects. Data are not available to establish the appropriate resting or exercise target rates that should be achieved. 

Another important, in fact more convincing indication for the use of digoxin is atrial fibrillation, in particular when occurring after cardiac surgery. The beneficial effect of digoxin is caused by impairment of the AV conduction, leading to the dissociation of the electrical activities of the atria and the ventricles. The inotropic effect, although weak, is potentially useful. 

Management of hypothyroidism consists of identifying the underlying cause and then providing thyroid hormone replacement to normalize thyroid sta-ms. The goal of treatment is to reduce semm TSH levels to normal, which for most assays is roughly between 0.5 and 3 mU/1. Oversuppression of TSH levels is probably not advisable, as overtreatment may predispose to cardiac arrhythmias (particularly atrial fibrillation), and may have subtle effects on bone mineral density. 

Ipecac syrup is prepared from the dried rhizome and roots of Cephaelis ipecacuanha or Cephaelis acuminata, plants from Brazil and Central America that have the alkaloid emetine as their active principal ingredient. It acts directly on the CTZ and also indirectly by irritating the gastric mucosa. Ipecac is cardiotoxic if absorbed and can cause cardiac conduction disturbances, atrial fibrillation, or fatal myocarditis. If emesis does not occur, gastric lavage using a nasogastric tube must be performed. 

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. 

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. 

Diltiazem appears to be similar in efficacy to verapamil in the management of supraventricular arrhythmias, including rate control in atrial fibrillation. An intravenous form of diltiazem is available for the latter indication and causes hypotension or bradyarrhythmias relatively... 

Adenosine causes flushing in about 20% of patients and shortness of breath or chest burning (perhaps related to bronchospasm) in over 10%. Induction of high-grade atrioventricular block may occur but is very short-lived. Atrial fibrillation may occur. Less common toxicities include headache, hypotension, nausea, and paresthesias. 

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. 

Budesonide for collagenous colitis caused Cushing s syndrome in a patient with chronic renal insufficiency taking amiodarone for paroxysmal atrial fibrillation (477). 

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). 

A 62-year-old woman with paroxysmal atrial fibrillation who had taken amiodarone 300 mg/day had a serum sodium concentration of 120 mmol/1 with a normal serum potassium and a reduced serum osmolality (240 mmol/kg) the urinary sodium concentration was 141 mmol/1 and the urine osmolality 422 mmol/kg (25). There was no evident cause of inappropriate secretion of ADH and within 5 days of withdrawal of amiodarone the serum sodium concentration had risen to 133 mmol/ 1 and rose further to 143 mmol/1 14 days later. There was no rechallenge and no recurrence of hyponatremia during the next 6 months. Another case has been reported (28). 

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... 

The risk of embolism associated with mechanical heart valves is 2 to 6% per patient per year despite anticoagulation and is highest with valves in the mitral position. Warfarin therapy (INR 2.5 to 3.5) is recommended in these patients. The addition of enteric-coated aspirin (100 mg/d) to warfarin (INR 3.0 to 4.5) in high-risk patients (preoperative atrial fibrillation, coronary artery disease, history of thromboembolism) with mechanical valves decreases the incidence of systemic embolism and death from vascular causes (1.9 vs. 8.5% per year), but increases the risk of bleeding. 

These agents appear to be similar in efficacy to verapamil in the management of supraventricular arrhythmias, including rate control in atrial fibrillation. An intravenous form of diltiazem is available for the latter indication and causes hypotension or bradyarrhythmias relatively infrequently. Bepridil also has action potential- and QT-prolonging actions that theoretically may make it more useful in some ventricular arrhythmias but also create the risk of torsade de pointes. Bepridil is only rarely used, primarily to control refractory angina. 

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. 

Clinical effects A large number of randomized, doubleblind, placebo-controlled trials have shown that the longterm use of (3 blockers improves the clinical status in patients with HF (22-32) (Table 2) and the ACC/AHA guidelines (II) recommend that (3 blockers should be routinely prescribed to all patients with asymptomatic LV dysfunction or stable HF caused by LV systolic dysfunction (unless they have a contraindication or have been shown to be intolerant to treatment with these drugs). (3 blockers should also be used in patients with HF and preserved LV systolic function, particularly when those patients have hypertension, coronary artery disease (CAD) and/or atrial fibrillation. 

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