Ventricular abnormality

Andreasen, N.C., Swayze, V.I.I., Flaum, M., Alliger, R., and Cohen, G. (1990) Ventricular abnormalities in affective disorder clinical and demographic correlates. Am J Psychiatry 147 893-900. 

These dm are primarily used in the treatment of hypertension (see the Summary Drug Table Adrenergic Blocking Drugs also see Chap. 39) and certain cardiac arrhythmias (abnormal rhythm of the heart), such as ventricular arrhythmias or supraventricular tachycardia They are used to prevent reinfarction in patients with a recent myocardial infarction (1—4 weeks after MI). Some of these dm have additional uses, such as the use of propranolol for migraine headaches and nadolol for angina pectoris. 

Cardiac-changes in pulse rate or rhythm electrocardiographic changes, such as bradycardia, tachycardia, premature ventricular contractions, bigeminal (two beats followed by a pause), or trigeminal (three beats followed by a pause) pulse. Other arrhythmias (abnormal heart rhythms)also may be seen. 

Hypertrophic cardiomyopathy (HCM) is characterized by abnormal left ventricular thickening. The left ventricular septum is the most common site of involvement. Pathologically, the disease is characterized by myocardial fiber disarray. The myocardium may exhibit extensive scarring and disorganization of interstitial and intercellular tissue (Elstein et al., 1992). The severity of HCM depends on the age of the patient, as well as the extent of the disarray. Patients with HCM have variable... 

Wall motion abnormalities or left ventricular dilation with stress echocardiography are indicative of IHD. 

Abnormal initiation of electrical impulses occurs as a result of abnormal automaticity. If the automaticity of the SA node increases, this results in an increased rate of generation of impulses and a rapid heart rate (sinus tachycardia). If other cardiac fibers become abnormally automatic, such that the rate of initiation of spontaneous impulses exceeds that of the SA node, other types of tachyarrhythmias may occur. Many cardiac fibers possess the capability for automaticity, including the atrial tissue, the AV node, the Purkinje fibers, and the ventricular tissue. In addition, fibers with the capability of initiating and conducting electrical impulses are present in the pulmonary veins. Abnormal atrial automaticity may result in premature atrial contractions or may precipitate atrial tachycardia or atrial fibrillation (AF) abnormal AV nodal automaticity may result in junctional tachycardia (the AV node is also sometimes referred to as the AV junction). Abnormal automaticity in the ventricles may result in ventricular premature depolarizations (VPDs) or may precipitate ventricular tachycardia (VT) or ventricular fibrillation (VF). In addition, abnormal automaticity originating from the pulmonary veins is a precipitant of AF. 

Automaticity of cardiac fibers is controlled in part by activity of the sympathetic and parasympathetic nervous systems. Enhanced activity of the sympathetic nervous system may result in increased automaticity of the SA node or other automatic cardiac fibers. Enhanced activity of the parasympathetic nervous system tends to suppress automaticity conversely, inhibition of activity of the parasympathetic nervous system increases automaticity. Other factors may lead to abnormal increases in automaticity of extra-SA nodal tissues, including hypoxia, atrial or ventricular stretch [as might occur following long-standing hypertension or after the development of heart failure (HF)], and electrolyte abnormalities such as hypokalemia or hypomagnesemia. 

Ventricular premature depolarizations occur as a result of abnormal ventricular automaticity, as a result of enhanced activity of the sympathetic nervous system and altered electro-physiologic characteristics of the heart during myocardial ischemia and following myocardial infarction. 

Premature ventricular complexes (PVCs) are common ventricular rhythm disturbances that occur in patients with or without heart disease and may be elicited experimentally by abnormal automaticity, triggered activity, or reentrant mechanisms. 

Ventricular tachycardia (VT) is defined by three or more repetitive PVCs occurring at a rate greater than 100 beats/min. It occurs most commonly in acute myocardial infarction (MI) other causes are severe electrolyte abnormalities (e.g., hypokalemia), hypoxemia, and digitalis toxicity. The chronic recurrent form is almost always associated with underlying organic heart disease (e.g., idiopathic dilated cardiomyopathy or remote MI with left ventricular [LV] aneurysm). 

Type II drugs include /Tadrenergic antagonists clinically relevant mechanisms result from their antiadrenergic actions. /3- Blockers are most useful in tachycardias in which nodal tissues are abnormally automatic or are a portion of a reentrant loop. These agents are also helpful in slowing ventricular response in atrial tachycardias (e.g., AF) by their effects on the AV node. 

The echocardiogram is the single most useful evaluation procedure because it can identify abnormalities of the pericardium, myocardium, or heart values and quantify the left ventricular ejection fraction (LVEF) to determine if systolic or diastolic dysfunction is present. 

Cardiopulmonary examination may reveal an abnormal heart rate or rhythm, left ventricular (LV) hypertrophy, precordial heave, third and fourth heart sounds, and rales. 

Radionuclide angiocardiography is used to measure ejection fraction (EF), regional ventricular performance, cardiac output, ventricular volumes, valvular regurgitation, asynchrony or wall motion abnormalities, and intracardiac shunts. 

Echocardiography is useful if the history or physical findings suggest valvular pericardial disease or ventricular dysfunction. In patients unable to exercise, pharmacologic stress echocardiography (e.g., dobutamine, dipyridamole, or adenosine) may identify abnormalities that would occur during stress. 

Serotonin (5-HT) abnormalities. Schizophrenic patients with abnormal brain scans have higher whole blood 5-HT concentrations, and these concentrations correlate with increased ventricular size. 

Inhalation of certain hydrocarbons, including some anesthetics, can make the mammalian heart abnormally sensitive to epinephrine, resulting in ventricular arrhythmias, which in some cases can lead to sudden death (Reinhardt et al. 1971). The mechanism of action of cardiac sensitization is not completely understood but appears to involve a disturbance in the normal conduction of the electrical impulse through the heart, probably by producing a local disturbance in the electrical potential across cell membranes. The hydrocarbons themselves do not produce arrhythmia the arrhythmia is the result of the potentiation of endogenous epinephrine (adrenalin) by the hydrocarbon. 

Report 957-77, E.I. du Pont de Nemours and Co., Newark, DE. Test species/Strain/Sex/Number male beagle dogs (1-2 per exposure group) Exposure route/Concentrations/Durations Inhalation 2,600, 5,200, 10,000, and 21,600 ppm for 10 min (the cardiac sensitization test is a 10-min test) epinephrine dose at 8 g/kg. The cardiac sensitization test is based on the observation that some halocarbons make the mammalian heart abnormally sensitive to epinephrine, resulting in ectopic beats and/or ventricular fibrillation, which may result in death. 

Gamouras, G.A., Monir, G., Plunkitt, K., Gursoy, S. and Dreifus, L.S. (2000) Cocaine abuse repolarization abnormalities and ventricular arrhythmias. The American Journal of the Medical Sciences, 320, 9-12. 

Thomas, S.H.L., Drugs, QT interval abnormalities and ventricular arrhythmias, Adverse Drug React. Toxicol. Rev., 13, 77-102,1994. 

Somatomedins are insulin-like polypeptide hormones that should be used with caution in diabetic patients since adjustment of antidiabetic therapy may be required. Before initiating therapy, a baseline ECG is recommended and, if abnormalities are identified, regular ECG monitoring during treatment is required. Somatomedins may cause tachycardia, cardiomegaly, ventricular hypertrophy and changes in blood glucose levels as side-effects. 

The ICH guideline lists the assessment of effects on blood pressure, heart rate and ECG. In vivo, in vitro and/or ex vivo evaluations, including methods for electrical repolarisation and conductance abnormalities, should also be considered. These abnormalities can be associated with risks for fatal ventricular arrhythmias called Torsade de pointes. 

Electrical cardioversion It may be desirable to reduce the dose of digoxin for 1 to 2 days prior to electrical cardioversion of atrial fibrillation to avoid the induction of ventricular arrhythmias, but physicians must consider the consequences of increasing the ventricular response if digoxin is withdrawn. If digitalis toxicity is suspected, delay elective cardioversion. If it is not prudent to delay cardioversion, select the lowest possible energy level to avoid provoking ventricular arrhythmias. Lab test abnormalities Periodically assess serum electrolytes and renal function (serum creatinine concentrations) the frequency of assessments will depend on the clinical setting. 

Cardiovascular - Ang na pectoris aggravated, arrhythmia, arrhythmia atrial, atrial fibrillation, bradycardia, bundle branch block, cardiac failure, extrasystole, heart murmur, heart sound abnormal, hypertension, hypotension. Ml, palpitation, Q-wave abnormality, tachycardia, ventricular tachycardia (5% or less). 

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