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Premature Beat

The atria can also be activated retrogradely and sometimes P waves can appear inverted (upside down) merged with the ectopic T wave. The T waves of the ventricular premature beats are usually defected in the opposite direction to the intrinsic rhythm, and also appear odd in appearance. [Pg.83]


The process of reentry is depicted in Fig. 6-3.4 Under normal circumstances, when a premature impulse is initiated, it cannot be conducted in either direction down either pathway because the tissue is in its absolute refractory period from the previous beat. A premature impulse may be conducted down both pathways if it is only slightly premature and arrives after the tissue is no longer refractory. However, when refractoriness is prolonged down one of the pathways, a precisely timed premature beat may be conducted down one pathway, but cannot be conducted in either direction in the pathway with prolonged refractoriness because the tissue is still in its absolute refractory period (Fig. 6-3, panel la).4 When the third condition for reentry is present, that is, when the velocity of impulse conduction in the other pathway is slowed, the impulse traveling forward down the other pathway still cannot be conducted. However, because the impulse in the other pathway is traveling so slowly, by the time it circles around and travels upward down the other pathway, that pathway is no longer in its absolute refractory period, and now the impulse may travel upward in that pathway. In other words,... [Pg.111]

Characteristic feature a "long-short" initiating sequence, which occurs as a result of a ventricular premature beat followed by a compensatory pause, which is followed by the first beat of the torsades de pointes. [Pg.129]

Proarrhythmia Mexiletine can worsen arrhythmias it is uncommon in patients with less serious arrhythmias (freguent premature beats or nonsustained ventricular tachycardia) but is of greater concern in patients with life-threatening arrhythmias, such as sustained ventricular tachycardia. [Pg.454]

It is indicated in prevention of atrial arrhythmia, atrial fibrillation or flutter, paroxysmal supraventricular tachycardia, ventricular premature beats and ventricular tachycardia. [Pg.191]

Ventricular and supraventricular tachycardia (especially those due to re-entry phenomena), atrial fibrillation and flutter (can convert recent-onset fibrillation or flutter to sinus rhythm) Paroxysmal supraventricular tachycardia, atrial or ventricular premature beats, atrial fibrillation, or flutter (slows ventricular rate)... [Pg.157]

Caffeine is derived by extraction of coffee beans, tea leaves, and kola nuts. It is also prepared synthetically. Much of the caffeine of commerce is a by-product of decaffeinized coffee manufacture. The compound is purified by a series of recrystallizations. Caffeine finds use in medicine and in soft drinks. Caffeine is also available as the hydrobromide and as sodium benzoate, winch is a mixture of caffeine and sodium benzoate, containing 47-50% anhydrous caffeine and 50-53% sodium benzoate. This mixture is more soluble in water than pure caffeine. A number of nonprescription (pain relief) drugs contain caffeine as one of several ingiedients. Caffeine is a known cardiac stimulant and in some persons who consume significant amounts, caffeine can produce ventricular premature beats. [Pg.50]

FIGURE 19.4 Relationsliip behA een plasma concentrations of tocainide and suppression of ventricular premature beats (VPBs) for four representative patients. The relationship betwreen VPB frequency and tocainide concentrations shown by the solid curves was obtained from a nonlinear least-squares regression analysis of the data using Equation 19.10. The estimate of n for each patient can be compared with the shape of the tocainide concentration-antiarrhythmic response curve. (Reproduced with permission from Meffin PJ, Winkle RA, Blaschke TF, Fitzgerald J, Harrison DC. Clin Pliarmacol Ther 1977 22 42-57.)... [Pg.306]

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. [Pg.502]

These are common after myocardial infarction. Their particular significance is that the R-wave (ECG) of an ectopic beat, developing during the early or peak phases of the T-wave of a normal beat, may precipitate ventricular tachycardia or fibrillation (the R-on-T phenomenon). About 80% of patients with myocardial infarction who proceed to ventricular fibrillation have preceding ventricular premature beats. Lignocaine (lidocaine) is effective in suppression of ectopic ventricular beats but is not often used as its addition increases overall risk. [Pg.509]

Klotz U, Muller-Seydlitz PM, Heimburg P. Lorcainide infusion in the treatment of ventricular premature beats (VPB). Eur J Clin Pharmacol 1979 16(l) l-6. [Pg.2166]

ST-segment depression observed in V1-V3 is even more striking in the ventricular premature beats (first QRS in V1-V3). [Pg.105]

Figure 4.54 (A) Preoperative ECG of a 58-year-old patient without heart disease. (B) In a postoperative period the patient suffered from massive pulmonary embolism with the ECG showing an AQRS pointing sharply to the right, complete right bundle branch block with the ST-segment elevation in some leads and sinus tachycardia. The P wave is visible in the majority of leads with occasional premature beats. (C) Patient died within minutes the ECG in agonic rhythm. Figure 4.54 (A) Preoperative ECG of a 58-year-old patient without heart disease. (B) In a postoperative period the patient suffered from massive pulmonary embolism with the ECG showing an AQRS pointing sharply to the right, complete right bundle branch block with the ST-segment elevation in some leads and sinus tachycardia. The P wave is visible in the majority of leads with occasional premature beats. (C) Patient died within minutes the ECG in agonic rhythm.
Figure 8.25 Exercise test of a patient with doubtful precordial pain and frequent (A) ventricular and (B) supraventricular premature beats. Observe that ST-segment depression was little evident in sinus rhythm complexes, while it was very significant in premature complexes (see V3 and V4 in (B) and V5 and V6 in (A)). (C) The patient presented severe three-vessel disease. Figure 8.25 Exercise test of a patient with doubtful precordial pain and frequent (A) ventricular and (B) supraventricular premature beats. Observe that ST-segment depression was little evident in sinus rhythm complexes, while it was very significant in premature complexes (see V3 and V4 in (B) and V5 and V6 in (A)). (C) The patient presented severe three-vessel disease.
Figure 8.26 Other example of exercise test in a patient with ischaemic heart disease that demonstrated the presence of significant ST-segment changes in premature beats (see V3-V4) that were not so evident in normal sinus complexes. Figure 8.26 Other example of exercise test in a patient with ischaemic heart disease that demonstrated the presence of significant ST-segment changes in premature beats (see V3-V4) that were not so evident in normal sinus complexes.
Ventricular premature beats, atrial premature beats, atrial arrhythmias, conduction abnormalities all may occur... [Pg.460]

Ruberman W, Weinblatt E, Goldberg JD, et al. Ventricular premature beats and mortality after myocardial infarction. N Engl J Med 1977 297 750-757. [Pg.355]

Serious untoward effects are unusual if dosing is appropriate and the patient is carefully monitored during initial treatment. Levothyroxine replacement in athyrotic hypothyroid patients restores systolic and diastolic left ventricular performance within 2 weeks, and the use of levothyroxine may increase the frequency of atrial premature beats, but not necessarily ventricular premature beats. Excessive doses of... [Pg.1385]

Automaticity is the ability of cardiac tissue fibers to depolarize spontaneously. This enables them to contract again without external nerve stimulation. It is not surprising that digitalis affects this ability profoundly. When digitalis causes an increase in the rate of spontaneous depolarization during diastole of the ventricle, automaticity is increased at the pacemaker site. This may result in premature beats that increase as higher doses reduce excitability. [Pg.474]

The frequency and reproducibility of arrhythmia should be established prior to initiating therapy because inherent variability in the occurrence of arrhythmias can be confused with a beneficial or adverse drug effect. Techniques for this assessment include recording cardiac rhythm for prolonged periods or evaluating the response of the heart to artificially induced premature beats. [Pg.591]

Dogs were instrumented to examine the cardiac changes occurring for a month after intravenous administration of 2 LD50 of soman.113 Atropine and diazepam were administered shortly after soman exposure to control seizure activity. During the study period, there was an increased frequency of episodes of bradycardia with ventricular escape, second- and third-degree heart block, and independent ventricular activity (single premature beats,... [Pg.156]

C. Differential diagnosis. Rule out the following possible causes of ventricular premature beats, ventricular tachycardia, or ventricular fibrillation ... [Pg.14]

Eight patients with ventricular tachycardia treated with disopyramide 600 mg to 2 g daily had a 54% fall in their serum disopyramide levels (from a mean of 3.99 to 1.82 micrograms/mL) when they were also given phenytoin 200 to 600 mg daily for a week. Two of the patients who responded to disopyramide and underwent Hotter monitoring showed a 53- and 2000-fold increase in ventricular premature beat frequency as a result of this interaction. ... [Pg.253]


See other pages where Premature Beat is mentioned: [Pg.286]    [Pg.125]    [Pg.131]    [Pg.4]    [Pg.5]    [Pg.81]    [Pg.302]    [Pg.509]    [Pg.252]    [Pg.1320]    [Pg.323]    [Pg.324]    [Pg.325]    [Pg.335]    [Pg.486]    [Pg.216]    [Pg.289]    [Pg.298]    [Pg.36]    [Pg.57]    [Pg.440]    [Pg.86]    [Pg.1083]    [Pg.584]    [Pg.594]   
See also in sourсe #XX -- [ Pg.79 , Pg.80 , Pg.83 , Pg.84 , Pg.85 , Pg.86 , Pg.87 , Pg.96 , Pg.104 , Pg.111 ]




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Atrial premature beats

Beats

Junctional premature beats

Ventricular premature beats

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