Sinus beat

Torsades de pointes is a specific polymorphic VT that is associated with prolongation of the QT interval in the sinus beats that precede the arrhythmia.13... 

Electrocardiogram from a patient with the long QT syndrome during two episodes of torsade de pointes. The polymorphic ventricular tachycardia is seen at the start of this tracing and spontaneously halts at the middle of the panel. A single normal sinus beat (NSB) with an extremely prolonged QT interval follows, succeeded immediately by another episode of ventricular tachycardia of the torsade type. The usual symptoms would be dizziness or transient loss of consciousness. 

Historically, investigators promoted the concept that patients in the acute phase of MI may have types of PVCs that are predictive of ventricular fibrillation and sudden cardiac death. These types of PVCs were referred to as warning arrhythmias and include frequent ectopy (>5 per minute), multiform configuration (different morphology), couplets (two in a row), and R-on-T phenomenon (PVCs occurring during the repolarization phase of the preceding sinus beat in the... 

FIGURE 6.1 Initiation of atrial fibrillation (AF) with ectopic beats arising from the left superior pulmonary vein (PV). Shown are three surface leads (I, aVF, and VI), five intracardiac electrograms form the coronary sinus (CS prox to CS distal) and five electrograms from a catheter in the left superior PV (PV1 through PV5). After a sinus beat, a premature PV potential appears on PV3, which initiates AF (arrow). 

FIGURE 6.3 Pulmonary vein (PV) isolation. Left panel shows three sinus beats with surface leads aVF, VI, and V6, and ten intracardiac electrograms from the left superior PV (PV-1 through PV-10) before PV isolation. Low amplitude potentials represent atrial activity (small arrow) followed by high amplitude PV potentials (large arrow). Right panels shows elimination of PV potentials after encircling radiofrequency ablation. 

Bigeminy An arrhythmia consisting of normal sinus beats coupled with ventricular extrasystoles, ie, twinned beats ... 

Premature atrial contractions are introduced during sinus rhythm, and the interval between the premature beat and the subsequent sinus beat is measured. This interval will be the sum of conduction time into and out of the sinus node... 

Originate from the His bundle or the AV junction. The impulse may activate the ventricles via the normal pathway. Alternatively the atria may also be activated by retrograde conduction. This is where the impulse travels back up towards the atria instead of down towards the ventricles activating the atria. Junctional pranature beats can be seen on the ECG as they occur before the next normal sinus beat. Often there is no P wave present if the atria and ventricles are depolarised simultaneously, as this is masked by the QRS complex (Fig. 6.3). Alternatively the P wave may be inverted (Fig. 6.4) and can occur either before, or after the QRS complex (Fig. 6.5). 

These conditions consist of regular patterns of premature beats. And can occur in either the atria or ventricles. Atrial bigeminy consists of an atrial premature beat after each sinus beat (Fig. 6.13). Atrial trigeminy involves an atrial premature beat after every second sinus beat. 

Fig. 9.1 ECG changes in QRS complexes and T waves compared with a normal sinus beat...

Junctional (ectopic) beats that occur before normal sinus beats and interrupt the underlying rhythm. 

We examined the effects of selective activation of histamine Hj receptors on coronary hemodynamics in two groups patients with atypical chest pain and normal coronary arteries, and patients with vasospastic angina [48]. Selective Hj receptor stimulation was achieved by infusing histamine intravenously (0.5 pg/kg/min) for 5 min after pretreatment with cimetidine to antagonize the H2 receptors. Heart rate was kept constant (100 beats/min) by coronary sinus pacing. 

Sinus bradycardia is an arrhythmia that originates in the SA node, defined by a sinus rate less than 60 beats per minute (bpm).12... 

Asymptomatic sinus bradyarrhythmias (heart rate less than 60 beats/min) are common especially in young, athletically active individuals. However, some patients have sinus node dysfunction (sick sinus syndrome) because of underlying organic heart disease and the normal aging process, which... 

Hypotension, tachycardia, tachypnea, confusion, and oliguria are common symptoms. Myocardial and cerebral ischemia, pulmonary edema (cardiogenic shock), and multisystem organ failure often follow. Significant hypotension (systolic blood pressure [SBP] less than 90mmHg) with reflex sinus tachycardia (greater than 120 beats/min) and increased... 

Ivabradine is used in the treatment of angina in patients in normal sinus rhythm. It acts on the sinus node resulting in a reduction of the heart rate. It is contraindicated in severe bradycardia (heart rate lower than 60 beats/ minute), cardiogenic shock, acute myocardial infarction, moderate-to-severe heart failure, immediately after a cerebrovascular accident, second and third-degree heart block and patients with unstable angina or a pacemaker. Side-effects include bradycardia, first-degree heart block, ventricular extrasystoles, headache, dizziness and visual disturbances, including blurred vision. 

Sinus bradycardia. An abnormally low sinoatrial impulse rate (<60/min) can be raised by parasympatholytics. The quaternary ipratropium is preferable to atropine, because it lacks CNS penetrability (p. 107). Sympathomimet-ics also exert a positive chronotropic action they have the disadvantage of increasing myocardial excitability (and automaticity) and, thus, promoting ectopic impulse generation (tendency to extrasystolic beats). In cardiac arrest epinephrine can be used to reinitiate heart beat... 

Sinus tachycardia (resting rate >100 beats/min). p-Blockers eliminate sympathoexcitation and decrease cardiac rate. 

Sinus bradycardia Sinus bradycardia (heart rate less than 50 beats/min) occurred in 13% of patients receiving sotalol in clinical trials, and led to discontinuation in about 3%. Bradycardia itself increases risk of torsade de pointes. 

Contraindications Cardiogenic shock, MI with a heart rate less than 45 beats/minute or systolic BP less than 100 mm Hg, overt heart failure, second- or third-degree heart block, sinus bradycardia... 

Bradycardia can be due to depressed sinus automaticity and AV block. Bradyarrhythmias manifest as slow heart rate (less than 50 to 60 beats per minute in sleep). Depressed SA nodal automaticity lead to missing beats and bradycardia. AV block can be due to high vagal activity and side effect of certain drugs e.g. digitalis and P-blockers. 

The most common adverse effects are hypotension and bradycardia, which are usually easily managed unless there is preexisting heart disease. Dubovsky et al. (389) reported severe cardiotoxicity when verapamil was combined with lithium in two elderly patients. One had a profound bradycardia with a heart rate of 36 beats/minute another, who had a sinus bradycardia and atrioventricular ectopy, developed an acute myocardial infarction and died. 

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)... 

Electrocardiographic record showing digitalis-induced bigeminy. The complexes marked NSR are normal sinus rhythm beats an inverted T wave and depressed ST segment are present. The complexes marked PVB are premature ventricular beats and are the electrocardiographic manifestations of depolarizations evoked by delayed oscillatory afterpotentials as shown in Figure 13-5. 

Vomiting is common in patients with digitalis overdose. Hyperkalemia may be caused by acute digitalis overdose or severe poisoning, whereas hypokalemia may be present in patients as a result of long-term diuretic treatment. (Digitalis does not cause hypokalemia.) A variety of cardiac rhythm disturbances may occur, including sinus bradycardia, AV block, atrial tachycardia with block, accelerated junctional rhythm, premature ventricular beats, bidirectional ventricular tachycardia, and other ventricular arrhythmias. 

The acute phase of ischemia is followed by 3-6 h of predominantly sinus rhythm. Thereafter, the number of ventricular ectopic beats increases. In the subacute phase of infarction (12-24 h) ventricular arrhythmias often occur. One of the mechanisms involved is reinfarction. If there is no acute reinfarction involved, these arrhythmias have been suggested to originate from surviving strands of Purkinje fibers in the subendocardium. The predominant mechanism has been postulated to be abnormal automaticity in these fibers. These fibers exhibit an increased sensitivity for catecholamines. In some cases a combination of focal activity and reentry in these fibers may be possible. 

Sick sinus syndrome Severe bradycardia (<50 beats/min) periods of sinus arrest... 

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