The Tachycardias

2 The VEGM R wave morphology during sinus tachycardia and normal sinus rhythm is typically the.  

So how can the ICD differentiate sinus tachycardia from VT Most ICDs can be programmed in their VT zones with a discriminator commonly referred to as sudden onset. This can be used to help limit delivery of therapy for sinus tachycardia. Sudden onset tries to take advantage of the fact that sinus tachycardia, as opposed to VT, typically does not initiate in a sudden fashion. Other SVTs, however, can typically initiate in a sudden manner. In any case, an ICD may rarely deliver therapy for sinus tachycardia simply by the fact that a sustained rate criteria has been met should such a function be programmed on (it is actually quite common for both a sudden onset and sustained duration feature to be programmed on simultaneously). 

A comparison of R wave width may suggest an SVT when the tachycardia and baseline measurements are similar. Conversely a significant increase in width may suggest VT. The baseline width is developed from a sampling of many R waves during the patient s normal rhythm. The sampling is commonly from R waves as recorded by the shocking coils. 

As such, these discriminators can be considered for helping to differentiate sinus tachycardia (or any other SVT for that matter) from VT. This is particularly relevant in single chamber ICDs (dual chamber ICDs may not have such features available). However, the phenomenon of BBA during SVT can fool such discriminators. 

As an SVT causes signal input below the atrio-ventricular (AV) node at progressively more rapid rates one of the bundle branches may cease conducting temporarily due to its refractory period being reached. What can happen then is the R wave morphology recorded by the ventricular defibrillator lead may change due to the alteration in ventricular activation. 

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The cardiovascular adverse effects associated with quinidine therapy are hypotension and tachycardia, both of which are related to its a-adrenoceptor blocking actions. The tachycardia may be a reflex adjustment to the fall in blood pressure or may also be a direct action of the dmg on sympathetic nerve terminals leading to an increased release of NE. Quinidine also produces ringing in the ears (cinchonism) (1,2). 

Supraventricular tachycardias may cause a variety of clinical manifestations ranging from no symptoms to minor palpitations and/or irregular pulse to severe and even life-threatening symptoms. Patients may experience dizziness or acute syncopal episodes symptoms of HF anginal chest pain or, more often, a choking or pressure sensation during the tachycardia episode. 

Ditran is intermediate between atropine and scopolamine with respect to heart rate changes, with a slight dip below baseline at the low dose of 50 mcg/kg (Fig. 65). Peak FIR elevation occurs at about 30 min, somewhat later than both atropine and scopolamine. The tachycardia is short-lived, with recovery at 5-6 hours. No doubt, the short duration of Ditran was an advantage when used by Ostfeld et al. in their Ditran coma therapy, which was perhaps inspired by Forrer s atropine coma therapy introduced a few years earlier. 

Wolff-Parkinson-White syndrome In several cases, the tachycardia was replaced by a severe bradycardia requiring a demand pacemaker after propranolol administration with as little as 5 mg. 

Cardiovascular Effects. Infoimation regarding cardiovascular eiJects in humans following inhalation exposure to chlorine dioxide is limited to a single account of tachycardia that developed in a woman several hours after having been exposed to an unknown concentration of chlorine dioxide that had triggered respiratory effects severe enough to force her to leave the area where she had been bleaching dried flowers (Elkins 1959). The tachycardia was likely secondary to the primary respiratory effects. 

C. Nitroglycerin can increase heart rate via an increase in sympathetic tone to the heart due to an excessive decrease in blood pressure propranolol would block the p-receptors responsible for the tachycardia. Propranolol does not decrease preload, and its effect to decrease afterload would exacerbate the decrease in afterload produced by nitroglycerin. Propranolol does not increase myocardial contractile force and could actually increase the incidence of vasospasm by unmasking a-adrenocep-tors in the coronary blood vessels. 

Although there is no doubt that amphetamines or other psychomotor stimulants induce an initial euphoria, there is considerable doubt that they can serve as long-lasting antidepressants. Cocaine, for example, produces a euphoria almost immediately after i.v. injection and within a few minutes after intranasal administration, but the euphoria, as well as the tachycardia, decrease at a slightly faster rate than the level of plasma cocaine. A second dose given 1 hour later fails to produce a similar level of euphoria or tachycardia, suggesting a rapid tachyphylaxis. 

As with most data for reboxetine, this information primarily comes from summary papers rather than primary sources (473, 474). With this caveat, the adverse-effect profile of reboxetine is consistent with its pharmacology as an NSRI. Thus, it is similar to that of desipramine and maprotiline but without the risk of serious CNS (i.e., seizures, delirium) or cardiac (i.e., conduction disturbances) toxicity. The most common adverse effects of reboxetine are dry mouth, constipation, urinary hesitancy, increased sweating, insomnia, tachycardia, and vertigo. Whereas the first three adverse effects are commonly called anticholinergic, they are well known to occur with sympathomimetic drugs as well. In other words, these effects can be either the result of decreased cholinergic tone or increased sympathetic tone, although they tend to be more severe with the former than the latter. In contrast to TCAs, reboxetine does not directly interfere with intracardiac conduction. The tachycardia produced by reboxetine, however, can be associated with occasional atrial or ventricular ectopic beats in elderly patients. 

Experimental studies have documented changes in drug response caused by increases or decreases in the number of receptor sites or by alterations in the efficiency of coupling of receptors to distal effector mechanisms. In some cases, the change in receptor number is caused by other hormones for example, thyroid hormones increase both the number of 3 receptors in rat heart muscle and cardiac sensitivity to catecholamines. Similar changes probably contribute to the tachycardia of thyrotoxicosis in patients and may account for the usefulness of propranolol, a 3-adrenoceptor antagonist, in ameliorating symptoms of this disease. 

For example, because an adequate dose of hydralazine causes a significant decrease in peripheral vascular resistance, there will initially be a drop in mean arterial blood pressure, evoking a strong response in the form of compensatory tachycardia and salt and water retention (Figure 11-5). The result is an increase in cardiac output that is capable of almost completely reversing the effect of hydralazine. The addition of a B-blocker prevents the tachycardia addition of a diuretic (eg, hydrochlorothiazide) prevents the salt and water retention. In effect, all three drugs increase the sensitivity of the cardiovascular system to each other s actions. 

A 14-month-old boy began convulsing 40 minutes after taking an unknown medication. The convulsions lasted for 20 minutes. He became cyanotic with a heart rate of 130/minute and a temperature of 38°C. He was treated with oxygen, intravenous benzodiazepines, and dipyrone, but continued to have isolated ventricular extra beats, hypertension, and tachycardia. The serum and urine concentrations of MDMA 8 hours after ingestion were 0.591 and 1477 mg/1 respectively. After 12 hours, the tachycardia and hypertension resolved and the child was discharged 9 days later with no residual symptoms. 

This report provided no data to enable the reader to Judge whether the tachycardia that followed the various doses of atropine was dose-related data on heart rate are provided only after the single dose of 3 mg. The mean heart rate In the 20 men before exposure to atropine was 75.8 beats/mln. At 15 aln after Injection, the mean was 116.8 beats/mln. After another 15 min. the mean was 117.8 beats/mln. Thereafter, the heart rate decreased gradually, the mean at 7-8 h after the Injection being 66.1 beats/mln. The mean was below that during the control period from the third hour to the eighth hour after Injection ... 

Their heart rates were Increased markedly for more than 24 h after Injection, but the peak of the tachycardia ( f85E) occurred about 12 h after Injection. This dose was the only one chat resulted In pupil dilatation, by about 2 mm. 

Flecainide slows conduction in all cardiac cells including the anomalous pathways responsible for the Wolff-Parkinson-White (WPW) syndrome. Together with encainide and moricizine, it underwent clinical trials to establish if suppression of asymptomatic premature beats with antiarrhythmic drugs would reduce the risk of death from arrhythmia after myocardial infarction. The study was terminated after preliminary analysis of 1727 patients revealed that mortality in the groups treated with flecainide or encainide was 7.7% compared with 3.0% in controls. The most likely explanation for the result was the induction of lethal ventricular arrhythmias possibly due to ischaemia by flecainide and encainide, i.e. a proarrhythmic effect. In the light of these findings the indications for flecainide are restricted to patients with no evidence of structural heart disease. The most common indication, indeed where it is the drug of choice, is atrioventricular re-entrant tachycardia, such as AV nodal tachycardia or in the tachycardias associated with the WPW syndrome or similar conditions with anomalous pathways. This should be as a prelude to definitive treatment with radiofrequency ablation. Flecainide may also be useful in patients with paroxysmal atrial fibrillation. 

A 75-year-old man who had had coronary bypass surgery was given an intravenous infusion of adenosine for stress testing (25). After 1 minute he developed a three-beat run of wide-complex tachycardia, followed by a 20-second run of a regular wide-complex tachycardia at a rate of 115/minute. There was left bundle branch block, and the tachycardia ended spontaneously. Adenosine infusion was continued and some ventricular extra beats with the same configuration occurred. In this case there was impaired perfusion of the left ventricle. 

A 74-year-old man had a tachycardia of 145/minute during infusion of milrinone after an operation for repair of an abdominal aortic aneurysm (15). The tachycardia was controlled by esmolol on one occasion and more impressively by metoprolol on a second occasion. However, the hemodynamic effects of mikinone were not altered by beta-blockade. 

When salbutamol is used to arrest premature labor, effective doses are likely to produce mild fetal tachycardia (for example an increase of 20/minute) (23). In one case, supraventricular tachycardia occurred in the fetus in the 34th week of pregnancy after the mother had been treated with salbutamol digoxin with and without propranolol was ineffective, but amiodarone controlled the tachycardia (24). 

Salbutamol has additive effects with theophylline, which can potentiate the hypokalemic effect (SEDA-17, 164). In 14 healthy volunteers, theophylline increased salbu-tamol-induced hjrpokalemia and in some individuals there was profound hypokalemia (less than 2.5 mmol/1) (35). Combining theophylline with salbutamol increased the tachycardia resulting from the salbutamol infusion. Salbutamol infusion caused a fall in diastolic and a rise in systolic blood pressure, which was not altered by theophylline. 

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