Tachycardia VT

Three or more premature vennicular beats are termed Ventricular Tachycardia (VT) (Fig. 6.32). On the ECG there is a wide QRS complex and a rate of more than 100 BPM. Due to the rapid contraction of the ventricles, blood does not have sufficient time to flu the ventricle before ejection. A sustained VT is therefore life threatening. 

It can be difficult to teU the difference between a Supra-Ventticular Tachycardia (S VT) and a Ventricular Tachycardia (VT). The wider the QRS complexes the more likely it is to be VT. Another good indicator is the presence of P waves that have no relationship with the QRS complex. VT that turns into VF is considered one of the main causes of sudden cardiac death. Treatment can include implantation of an Automated Internal. 

Cardiac Defibrillator (AICD) that sits in the chest and monitors the heart rhythm. The device is capable of delivering a shock to the patient if it detects a dangerous rhythm that will respond to deflbrillation. 

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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... 

Figure 4.2 Epicardial ECG recorded from an isolated blood-perfused rat heart at the moment of reperfusion. The heart was made regionally ischaemic by occluding a snare around the left anterior descending coronary artery and, after 10 min, reperfused by releasing the snare. Note the rapid onset of ventricular tachycardia (VT) and its subsequent degeneration into ventricular fibrillation (VF). Reproduced with permission from Lawson (1993).

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. 

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). 

Ventricular proarrhythmic effects in patients with atrial fibrillation/flutter A review of the world literature revealed reports of 568 patients treated with oral flecainide for paroxysmal atrial fibrillation/flutter (PAF). Ventricular tachycardia was experienced in 0.4% of these patients. Of 19 patients in the literature with chronic atrial fibrillation (CAF), 10.5% experienced ventricular tachycardia (VT) or ventricular fibrillation (VF). Flecainide is not recommended for use in patients with CAF. Case reports of ventricular proarrhythmic effects in patients treated with flecainide for atrial... 

Verapamil IV- Do not administer concomitantly with IV -adrenergic blocking agents (within a few hours), because both may depress myocardial contractility and AV conduction ventricular tachycardia (VT), because use in patients with wide-complex VT (QRS 0.12 seconds or more) can result in marked hemodynamic deterioration and ventricular fibrillation atrial fibrillation or atrial flutter associated with an accessory bypass tract. 

Deflbrillation is one of the few interventions that has been shown to improve outcome from cardiac arrest. The cardiac arrhythmias commonly associated with sudden collapse are (1) asystole and (2) rapid and ineffective depolarization due to ventricular flbrillation (VF), pulseless ventricular tachycardia (VT), or supraventricular tachycardia with 1 1 ventricular response (as can occur with pre-excitation syndromes). The best strategy is to treat collapsed patients who have a broad-complex tachycardia at once by external Direct Current (DC) defibrillation. 

Electrocardiograms typical of a variety of arrhythmias. SVT, supraventricular tachycardia AFL, atrial flutter AFib, atrial fibrillation VT, ventricular tachycardia VT-TdP, ventricular tachycardia of the torsade de pointes type. 

Contraindications are hypotension, cardiogenic shock, marked bradycardia, second or third degree AV-block, Wolff-Parkinson-White (WPW) syndrome, wide complex tachycardia, VT and uncompensated heart failure. 

Sustained ventricular tachycardia is defined as consecutive premature ventricular contractions lasting more than 30 seconds. Nonsustained ventricular tachycardia (VT) usually self-terminates and lasts for less than 30 seconds. The acute treatment of SuVT depends on the hemodynamic stability and symptoms of the patient. Unstable patients should receive immediate cardioversion. If patients are stable with mild symptoms, they can be treated with IV antiarrhythmics. 

Arrhythmias occur within a few seconds after reperfusion, following ischemic periods of 10-30 min long. They start by a spontaneous stimulus in the reperfused zone and change afterward in a re-entry multiple wavelet type of ventricular tachycardia (VT) or ventricular fibrillation (VF). Extremely short action potential, short refractory period and slow conduction are the main contributing factors. Increased hyperpolarization and elevated intracellular calcium that act negatively on gap conductance impair conduction. Unidirectional conduction is favored by the marked heterogeneity in extracellular potassium, action potential and refractory period. The extra stimulus is initiated in the reperfused zone, probably by early (EAD) and late (DAD) afterdepolirizations. 

Figure 5. Posterior systolic wall thickening (PWT) at baseline, with immediate coronary microcmbolization (ME) and at 5-10 min, 4-6 h and at 2-6 d in chronically instrumented dogs. Between 4-6h and 2 d ventricular tachycardia (VT) did not permit functional measurements. In the placebo-group (cPLA), posterior systolic wall thickening recovered back to baseline values within 5 d, whereas it was back to baseline at 4-6 h in the group receiving methytprednisolone after microembolization (cMP) (by permission from Skyschally ").

Heart disease is the leading cause of death in the United States and is responsible for approximately 870,000 deaths per year (1). Sudden cardiac death (SCD) is responsible for almost half of these deaths, claiming 350,000 to 400,000 lives per year (2). SCD is defined by the World Health Organization as death due to any cardiac disease that occurs out of hospital, in an emergency room, or a patient who is dead on arrival to a care facility. Of note, the death must occur within one hour after the onset of symptoms. The majority of SCD is likely arrhythmic in etiology. In women, up to 88% of sudden cardiac arrests may be due to arrhythmic causes (3). Of SCD due to cardiac arrhythmias, greater than 80% of events are due to ventricular tachycardia (VT) and ventricular fibrillation (VF), with the remainder due to bradyarrhythmias and asystole (4). Coronary artery disease (CAD), manifesting acutely as ischemic ventricular arrhythmias or chronically as scar-mediated... 

ABBREVIATIONS DAD, delayed afterdepolarization HAD, early afterdepolarization WPW, Wolff-Parkinson-White PSVT, paroxysmal supraventricular tachycardia VT, ventricular tachycardia VF, ventricular fibrillation. 

Tachycardias are generally classified as ventricular or supraventricular. Ventricular tachycardia (VT) is due to primary ventricular dysfunction and is often acutely dangerous. Supraventricular tachycardia (SVT) is almost never immediately dangerous and does not necessarily respond to ICD therapy hence, the treatment of SVT by an ICD is generally considered undesirable. The discrimination subsystem identifies rhythms that are sufficiently fast to treat (tachycardia), but are not ventricular in origin (SVT). Again, the bias of the device is to overtreat because the erroneous treatment of SVT is considered preferable to failure to treat a potentially lethal Ventricular. 

Ventricular tachycardia (VT) is the result of uncontrolled electrical activity in the ventricle. This activity may be coordinated or uncoordinated. The definitive therapy for Ventricular is external stimulation by an electric field sufficiently large to reset the electrical activity of most ventricular cells. This ends the previous (uncontrolled) electrical activity and allows the reestablishment of normal cardiac activity. As explained earlier, this requires depolarization of a critical mass of tissue by a high-voltage discharge. When high-voltage therapy is delivered, an attempt is made to synchronize the delivery with a detected R-wave. A synchronized shock is termed cardioversion, whereas an unsynchronized shock is termed defibrillation because VF has no coherent electrical activity, and therefore no basis for synchronization (Figure 15.6). 

Fig. 20.2 Detection and therapy parameters for an ICD. Top Detection parameters. As programmed the ICD defines ventricular tachycardia (VT) as 12 beats greater than 150 bpm and ventricular fibrillation (VF) as 12 of 16 beats greater than 188 bpm. An optional fast ventricular tachycardia (FVT) zone has not been programmed on. Bottom Therapies for ventricular fibrillation are a first shock at 24 J and subsequent shocks at 35 J. Therapies for ventricular tachycardia are two pacing sequences followed by cardioversion attempts at 15,35,35, and 35 J. Pacing for bradycardia is set at 40 bpm.

Cardiac arrhythmias are any abnormahty or perturbation in the normal activation sequence of the myocarchum. Some earher studies showed beneficial effects of garlic in cardiac arrhythmias. Garhc powder (1 % corresponding to Kwai/Sapec added to a standard chow for a 10-week period) significantly reduces the incidence of ventricular tachycardia (VT) and fibrillation (VF) in isolated perfused rat heart... 

Veno-occlusive disease (VOD), 373 Veno-occlusive liver disease, 1387 Venous hypertension, 3968 Venous-lymphatic disraders, 3968 Ventricular arrhythmias, 945, 1516 Ventricular tachycardia (VT), 3683 Vepris, 724 Veratridine, 57 Verbaiaceae, 4095 Vermifuge, 3477 Vemmiia, 3529 Verlehrale hosts, 1266 Verticine, 1171, 1189 Verticinone, 1171, 1189 Vertigo, 3724... 

Antiarrhythmic EGb-761 Dose-dependently reduction in ventricular flbrillation (VF) and ventricular tachycardia (VT) in the hearts of rats [26]... 

Cardiovascular Chronic aluminium exposure associated with cardiotoxic manifestations is rather rarely reported. A recent case study reported Mobitz type I second-degree atrioventricular block and nonsustained ventricular tachycardia (VT) following chronic occupational aluminium exposure [4 ]. 

Represents a serious threat of subsequent ventricular fibrillation (VF) or tachycardia (VT). This is because the premature beat occurs during the T wave of the previous beat. As the cells are stiU recovering from depolarisation and not yet fully repolarised. Another potential complication of R on T phenomenon is torsade de pointes (twisting about a point), a form of polymorphic VT so named due its spindle like appearance (Fig. 6.12). 

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