Ventricular contraction

The sinus rhythm is the heart rhythm in which the sinus node generates an electrical impulse that travels through specialized cells (that form a conduction system) and leads to a ventricular contraction. 

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. 

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

The uses of the antiarrhythmic drug are given in the Summaiy Drug Table Antiarrhythmic Drug3. In general these drugp are used to prevent and treat cardiac arrhythmias, such as premature ventricular contractions (PVCs), ventricular tachycardia (VT), premature atrial contractions (PACs), paroxysmal atrial tachycardia (PAT), atrial fibrillation, and atrial flutter. Some of the antiarrhythmic dru are used for other... 

ECG normal sinus rhythm, PR 0.16 s, QRS 0.08 s, QTC 0.38 s, occasional polymorphic premature ventricular contractions, 3 mm ST-segment elevation anterior leads... 

From the AV node, the electrical impulse spreads through the AV bundle or the bundle of His. This portion of the conduction system penetrates the fibrous tissue separating the atria from the ventricles and enters the interventricular septum where it divides into the left and right bundle branches. The bundle branches travel down the septum toward the apex of the heart and then reverse direction, traveling back toward the atria along the outer ventricle walls. This route of conduction of the impulse facilitates ejection of blood from the ventricles. If the impulse were to be conducted directly from the atria to the ventricles, the ventricular contraction would begin at the top of the chambers and proceed downward toward the apex. This would trap the blood at the bottom of the chambers. Instead, the wave of ventricular electrical stimulation and, therefore, contraction moves from the apex of the heart toward the top of the chambers where the semilunar valves are located and ejection takes place. 

Ventricular contraction. This process occurs during ventricular systole. When the ventricular myocardium begins to contract and squeeze down on the blood within the chamber, the pressure increases rapidly. In fact, ven-... 

Premature ventricular complexes, 5 88—89 Premature ventricular contractions, 5 108 Premetallized dyes, 9 215-216, 399-401 29 758-759... 

Exposure at 500,000 ppm induced narcosis in rhesus monkeys within 1 min (Shulman and Sadove 1967). Respiratory depression accompanied by multiple premature ventricular contractions occurred when concentrations exceeded 60%. Blood pressure was said to be increased, but the actual data were not reported. 

In an undated study, HCFC-141b was administered to male SpragueDawley rats at concentrations of 5,000, 10,000, or 20,000 ppm for 30 min (Eger, unpublished data). As exposure continued, bolus intravenous epinephrine, characterized as three times the dose that produced arrhythmias in the same rats anesthetized with halothane, was administered. The dose of epinephrine was defined as a maximum of 12 fig/kg. For this study, three or more premature ventricular contractions was considered an arrhythmic response (Table 4—5). Marked arrhythmias occurred at all concentrations. The author further compared the concentrations of halothane and HCFC-141b that produced arrhythmias with administration of various doses of exogenous epinephrine. The nominal chamber concentration for HCFC-141b did not differ from that of halothane. Furthermore, the arrhythmias were characterized as relatively mild and within acceptable limits for surgical anesthesia in humans. 

The c wave This results from the bulging of the tricuspid valve into the right atrium during ventricular contraction. 

Binds to DNA and prevents separation of the helical strands Affects neuronal transmissions Binds to opiate receptors and blocks pain pathway Acts as central nervous system depressant Inhibits Na/K/ATPase, increases intracellular calcium, and increases ventricular contractibility Blocks the actions of histamine on Hi receptor Blocks ai-adrenergic receptor, resulting in decreased blood pressure Inhibits reuptake of 5-hydroxytryptamine (serotonin) into central nervous system neurons Inhibits cyclooxygenase, inhibition of inflammatory mediators Inhibits replication of viruses or tumor cells Inhibits HIV reverse transcriptase and DNA polymerase Antagonizes histamine effects... 

One of the pollutants known to interfere with cardiovascular development is 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD). TCDD is a persistent, bioaccumulative environmental contaminant, as well as a potent developmental toxicant and human carcinogen [30]. Piscine, avian, and mammalian cardiovascular systems are sensitive to TCDD toxicity, with effects including cardiac enlargement, edema, and several dysfunctions. In zebrafish embryos, these effects include areduction in cardiomyocyte number at 48 hpf, decreased heart size, altered vascular remodeling, pericardial edema, and decreased ventricular contraction culminating in ventricular standstill [31-34]. 

Procainamide is intended for treating paroxysmal atrial tachycardia, atrial fibrillation, prematnre ventricular contraction, and ventricnlar tachycardia. For qnickly reaching therapeutic concentrations, parentemal introdnction of procainamide is preferred over cynidine. Synonyms of this drng are amidoprocaine, cardiorythmine, novocainamide, pronestyl, and others. 

Oral Premature atrial, AV junctional and ventricular contractions paroxysmal atrial (supraventricular) tachycardia paroxysmal AV junctional rhythm atrial flutter paroxysmal and chronic atrial fibrillation established atrial fibrillation when therapy is appropriate paroxysmal ventricular tachycardia not associated with complete heart block maintenance therapy after electrical conversion of atrial fibrillation or flutter. Parenteral When oral therapy is not feasible or when rapid therapeutic effect is required. 

Ventricuiar proarrhythmic effects in patients with atriai fibriiiation/fiutter Flecainide is not recommended for use in patients with chronic atrial fibrillation. Case reports of ventricular proarrhythmic effects in patients treated with flecainide for atrial fibrillation/flutter have included increased premature ventricular contractions (PVCs), ventricular tachycardia (VT), ventricular fibrillation (VF), and death. 

Premature ventricular contractions (PVCs) During conversion or marked reduction in ventricular rate, benign complexes of unusual appearance (sometimes resembling PVCs) may occur after IV verapamil. 

Genera/-Arrhythmias changes in AV conduction ECG changes (most frequently with toxic doses) flushing heart block hot flushes hypertension hypotension orthostatic hypotension palpitations precipitation of CHF premature ventricular contractions stroke sudden death syncope tachycardia. 

PTCA percutaneous transluminal coronary angioplasty PTH parathyroid hormone PTT partial thromboplastin time PUD peptic ulcer disease pulm pulmonary PVC premature ventricular contraction... 

---