Arrhythmia cardiac

The most important potential complication of phenol-based peels is cardiotoxicity. Phenol is directly toxic to myocardium. Studies in rats have shown a decrease in myocardial contraction and in electrical activity following systemic exposure to phenol [i6]. Since fatal doses ranged widely in these studies, it seems that individual sensitivity of myocardium to this chemical exists. In humans neither sex/age nor previous cardiac history/blood phenol levels are accurate predictors for cardiac arrhythmia susceptibility [17]. [Pg.85]

After application of peeling solution, there is a quick absorption of phenol from the skin surface to the circulation [18]. Seventy-five percent of phenol is excreted directly through kidney or detoxified by liver. The other 25% is metabolized to CO and water. [Pg.85]

Phenol blood levels measured after application of 3 ml of 50% solution of phenol is 0.68 mg/dl, while in patients who survived accidental oral ingestion of phenol, a level of 23 mg/ dl was found. Application of phenol to one cosmetic unit is equivalent to the application of phenol into a nail matrix for matrixectomy. [Pg.85]

In humans cardiac arrhythmias have been recorded in 23% of patients when full-face peel was performed in less than 30 min. These arrhythmias included tachycardia, premature ventricular beats, bigeminy, atrial and ventricular tachycardia [19]. [Pg.85]

Therefore, full-face phenol-based peel should always be performed under full cardiopulmonary monitoring. The average lag time for the onset of the arrhythmias was 17.5 min from the beginning of the peel, and they are usually not delayed for more than 30 min after the peel. Cardiac arrhythmias are more common while applying the solution on the thin skin of eyelids. In this area skin absorption is maximal therefore, application should be performed extremely cautiously. If arrhythmia occurs, the application of phenol should be stopped until [Pg.85]

FIGURE 23-2 Schematic representation of the conduction system of the heart. Conduction normally follows the pathways indicated by the dashed lines. Impulses originate in the sinoatrial node and are transmitted to the atrioventricular node. Impulses are then conducted from the atrioventricular node to the ventricles by the bundle of His and bundle branches. [Pg.323]

Regardless of what the initiating factor is in producing arrhythmias, the mechanism underlying a disturbance in cardiac rhythm can be attributed to one of the three basic abnormalities listed below.5 [Pg.323]

Abnormal impulse generation. The normal automatic rhythm of the cardiac pacemaker cells has been disrupted. Injury and disease may directly render the SA and AV cells incapable of maintaining normal rhythm. Also, cells that do not normally control cardiac rhythm may begin to compete with pacemaker cells, thus creating multiple areas of automaticity. [Pg.323]

Abnormal impulse conduction. The conduction of impulses throughout the myocardium has been interrupted. Various diseases and local damage may result in the delay or failure of an action potential to reach certain areas. These conduction impairments or heart blocks can prevent a smooth and synchronous contraction, thus creating an abnormal rhythm. [Pg.323]

Simultaneous abnormalities of impulse generation and conduction. A combination of both previously listed factors may cause cardiac arrhythmias. [Pg.323]

Cardiac arrhythmias are an important cause of morbidity and mortality approximately 400,000 people per year die from myocardial infarctions (MI) in the United States alone. Individuals with MI exhibit some form of dysrhythmia within 48 h. Post-mortem examinations of MI victims indicate that many die in spite of the fact that the mass of ventricular muscle deprived of its blood supply is often quite small. These data suggest that the cause of death is ventricular fibrillation and that the immediate availability of a safe and efficacious antiarrhythmic agent could have prolonged a number of Hves. The goals of antiarrhythmic therapy are to reduce the incidence of sudden death and to alleviate the symptoms of arrhythmias, such as palpitations and syncope. Several excellent reviews of the mechanisms of arrhythmias and the pharmacology of antiarrhythmic agents have been pubflshed (1,2). [Pg.110]

Cardiac arrhythmias or dysrhythmias are disturbances of the normal regular rhythm which may be caused by an abnormality in the site of impulse generation, its rate or regularity, or its propagation or conduction (1,2). The more commonly encountered cardiac arrhythmias are... [Pg.112]

Adverse reactions to digoxin include anorexia, vomiting, diarrhea, dizziness, headaches, visual disturbances, and cardiac arrhythmias. Allergic reaction such as urticaria, skin emptions, fever, and edema have been reported (87). [Pg.120]

The Cardiac Arrhythmia Pilot Study (CAPS) Investigators, Am. J. Cardiol 61, 501 (1988). [Pg.146]

The Cardiac Arrhythmia Suppression Trial (CAST) Investigators, W. Engl J. Med. 321, 406 (1989). [Pg.146]

Like many organic solvents, including hexane, heptane, ben2ene, xylene, toluene, gasoline, and particularly some of the other chlorinated and fluorinated solvents, methylene chloride may cause cardiac arrhythmias in the presence of elevated epinephrine when inhaled at concentrations as high as 20,000 ppm (36). [Pg.521]

Ingestion of large amounts of trichloroethylene may cause Hver damage, kidney malfunction, cardiac arrhythmia, and coma (38) vomiting should not be induced, but medical attention should be obtained immediately. [Pg.25]

Hypokalemia. Hypokalemia associated with thia2ide diuretic therapy has been knpHcated in the increased incidence of cardiac arrhythmias and sudden death (82). Several large clinical trials have been conducted in which the effects of antihypertensive dmg therapy on the incidence of cardiovascular complications were studied. The antihypertensive regimen included diuretic therapy as the first dmg in a stepped care (SC) approach to lowering the blood pressure of hypertensive patients. [Pg.212]

Untoward effects of both E and NE (usually to a lesser degree) are anxiety, headache, cerebral hemorrhage (from vasopressor effects), cardiac arrhythmias, especially in presence of digitaUs and certain anesthetic agents, and pulmonary edema as a result of pulmonary hypertension. The minimum subcutaneous lethal dose of E is about 4 mg, but recoveries have occurred after accidental overdosage with 16 mg subcutaneously and 30 mg intravenously, followed by immediate supportive treatment. [Pg.360]

Ipecac is prepared from the dried roots and rhizomes of Cephaelis ipecacuanha (Brot.) A. Rich, and contains the alkaloids emetine [483-18-1] (17) and cephaeJine [483-17-0] (18) in a ratio between 2 1 and 4 1. It has been used extensively in cough preparations and is beheved to act by gastric reflex stimulation. Toxic effects include vomiting, irritation of the gastrointestinal tract, and cardiac arrhythmias (19). Ipecac symp is available over-the-counter in the United States only in 30-mL containers for use as an emetic in treating poisonings. [Pg.520]

Several chemical compounds can have an adverse effect on the heart and the vascular system. The effect may first appear as a transient change in the cardiac function. However, prolonged exposure increases the risk of permanent effects. Occasionally, functional effects such as cardiac arrhythmias may even lead to death. Furthermore, in many cases the effects of chemicals... [Pg.295]

Compounds Causing Cardiovascular Toxicity Alcohols are the most important compounds causing vascular toxicity. Ethanol depresses cardiac muscle and attenuates its contractivity when the concentration of ethanol in the blood exceeds 0.75 mg/100 mL. Ethanol also causes arrhythmias, and a metabolite of ethanol, acetaldehyde, also depresses the heart. Furthermore, high concentrations of acetaldehyde cause cardiac arrhythmias. The cardiovascular toxicity of methanol is about the same as that of ethanol, whereas al cohols with longer chains are more toxic than ethanol. [Pg.297]

Halogenated hydrocarbons depress cardiac contractility, decrease heart rate, and inhibit conductivity in the cardiac conducting system. The cardiac-toxicity of these compounds is related to the number of halogen atoms it increases first as the number of halogen atoms increases, but decreases after achieving the maximum toxicity when four halogen atoms are present. Some of these compounds, e.g., chloroform, carbon tetrachloride, and trichloroethylene, sensitize the heart to catecholamines (adrenaline and noradrenaline) and thus increase the risk of cardiac arrhythmia. [Pg.297]

Some metals, such as cadmium, cobalt, and lead, are selectively car-diotoxic. They depress contractivity and slow down conduction in the cardiac-system. They may also cause morphological alterations, e.g., cobalt, which was once used to prevent excessive foam formation in beers, caused cardiomyopathy among heavy beer drinkers. Some of the metals also block ion channels in myocytes. Manganese and nickel block calcium channels, whereas barium is a strong inducer of cardiac arrhythmia. [Pg.297]

Many local anesthetics have a selective depressant action on heart muscle when given system cally. This is useful in t.reatment of cardiac arrhythmias, and a 1 idocaine-1 ike drug with this kind of action is tocainide (2). ... [Pg.55]

Facilitates GI transit/mechanical intestinal allodynia Cardiac arrhythmia... [Pg.171]

Selective AR agonists are undergoing clinical trials for cardiac arrhythmias and pain (Ai) cardiac imaging and inflammation (A2a) colon cancer, rheumatoid arthritis, psoriasis, and dry eye (A3). Selective AR antagonists are either in or advancing toward clinical trials for kidney disorders (Ax) Parkinson s disease (A2a) diabetes and asthma (A2B) cancer and glaucoma (A3). [Pg.27]

Antidepressants Noradrenaline/5-HT transporters Na+, K+ channels l Noradrenaline/ 5-HT reuptake l Na+ currents t K+ currents l Excitability of peripheral and central neurons Cardiac arrhythmia, myocardial infarction, sedation, nausea, dry mouth, constipation, dizziness, sleep disturbance, blurred vision... [Pg.76]

Andersen s syndrome is a rare disorder characterized by periodic paralysis, cardiac arrhythmias, and dysmorphic features. [Pg.79]

Antiarrhythmic drugs are substances that affect cardiac ionic channels or receptors, thereby altering the cardiac action potential or its generation or propagation. This results in changes of the spread of activation or the pattern of repolarization. Thereby, these drugs suppress cardiac arrhythmia. [Pg.96]

The Cardiac Arrhythmia Suppression Trial Investigators (1991) Mortality and morbidity in patients receiving encainide, flecainide or placebo. New Engl J Med 324 781... [Pg.102]

Cardiac arrhythmia with a rapid and irregular activity in different areas within the upper chambers (atria) of the heart is also known as atrial fibrillation. [Pg.236]

Ca2+ is an important intracellular second messenger that controls cellular functions including muscle contraction in smooth and cardiac muscle. Ca2+ channel blockers inhibit depolarization-induced Ca2+ entry into muscle cells in the cardiovascular system causing a decrease in blood pressure, decreased cardiac contractility, and antiarrhythmic effects. Therefore, these drugs are used clinically to treat hypertension, myocardial ischemia, and cardiac arrhythmias. [Pg.295]

A disease predisposing those affected to severe cardiac arrhythmia. The term long QT syndrome refers to an abnormality found in the electrocardiograms of the patients a long QT interval caused by a prolonged... [Pg.386]

Hyperkalemia is an excess of potassium in the blood. Clinical symptoms are muscle weakness and cardiac arrhythmias. It is caused by, e.g., hyperaldosteronism and angiotensin-converting enzyme (ACE) inhibitors. [Pg.607]

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