Some info that may help with regards to your query about chronic sinus tachycardia
Sinus arrhythmia is defined as a slight variation in cycling of the sinus rhythm, usually one that exceeds 0.12 seconds between the longest and shortest cycles. Sinus arrhythmia is a normal finding in children and young adults and tends to diminish or disappear with age. Sinus arrhythmia is often somewhat more prominent with fluctuation in the respiratory cycle as heart rate accelerates with inspiration and slows with expiration. The alternating acceleration and deceleration of heart rate with respiration is mainly the result of fluctuations in vagal tone. Sinus arrhythmia may be aggravated by any factor that increases vagal tone.
Sinus tachycardia is defined as sinus rhythm with a rate of greater than 100 beats/min. To be certain that sinus tachycardia is the etiology for a supraventricular tachycardia (tachycardia with its origin in the AV junction, atria or SA node), one must identify a constant single P wave for every QRS complex. Sinus tachycardia usually represents a physiologic response to fever, intravascular volume depletion, hypermetabolism, anxiety or the administration of pharmacologic agents that dramatically increase sinus rate, such as catecholamines. Sinus tachycardia may also be a response to severe emotional distress, fright and strenuous exercise. Other causes may include a response to anemia, CHF, hemorrhage, extensive heart muscle damage associated with a reduction in cardiac output and pulmonary embolism. Physiologically, sinus tachycardia results from either vagal withdrawal and/or endogenous release of catecholamines.
One should not treat sinus tachycardia per se, but instead should be concerned with the reasons for its development. Obviously, if intravascular volume depletion, fright, fever or sepsis is responsible for sinus tachycardia, the preferred approach is to identify the etiology and treat it, expecting the sinus tachycardia to respond to treatment of the basic abnormality. Alternatively if the sinus tachycardia is due to extensive heart muscle damage resulting from an acute MI or severe CHF, efforts must be made to support the pump function of the heart rather than to potentially depress it further with certain pharmacologic interventions. Sinus tachycardia is often an early warning sign of some altered physiologic state that should itself be identified and corrected.
Never "treat" sinus tachycardia: treat the cause of sinus tachycardia.
Summary of ECG criteria
Identify a constant single P wave for every QRS complex
Rate: Greater than 100 beats/min
P waves: Upright in leads I, II and aVF
Sinus bradycardia is the term for a sinus rate of less than 60 beats/min and may be seen in the normal adult population. Sinus bradycardia during exercise, fever or congestive heart failure is abnormal. Persistent rates of less than 45 beats/min are also considered abnormal, and in the absence of drugs such as digitalis, beta-blockers and calcium channel blockers, reflect abnormality in the sinus node. Sinus bradycardia can be present in otherwise normal individuals and is common in well-trained athletes and in most persons during deep sleep. It is part of the normal reaction to vagal stimulation. Sinus bradycardia may also be related to metabolic abnormalities, including hypothermia and myxedema. Nonvagally mediated sinus bradycardia also may occur as a manifestation of organic heart disease, including ischemic heart disease, particularly when the SA node is damaged, as with certain types of acute MI and in association with severe chest pain of acute MI. Sinus bradycardia may also be a complication of myocardial disease in which the SA node is damaged by scarring or infiltrative processes associated with aging as part of a degenerative conduction system process.
Asymptomatic sinus bradycardia requires no treatment. If sinus bradycardia is so extreme, however, that symptoms result, including syncope, congestive heart failure (CHF), angina pectoris and hypertension, and/or if it leads to the development of ventricular ectopic beats (slow sinus rates predispose to re-entry mechanisms), then it should be treated, and in some instances temporary and sometimes permanent ventricular pacing is necessary.
Summary of ECG criteria
Rate: Less than 60 beats/min
P waves: Upright in leads I, II and aVF
Sinus arrest and sinoatrial exit block
Sudden disappearance of sinus P waves for variable intervals can produce different patterns. Since sinus node activity is not recorded on the surface ECG, it is difficult to determine if sinus node automaticity or sinoatrial conduction abnormalities are responsible in a given patient. When PP intervals have a pattern and are a multiple of the basic sinus cycle, the term sinoatrial block is generally used. Both types of sinoatrial block can be diagnosed from the surface ECG. In type I (Wenckebach phenomenon), the PP cycle is progressively shortened until there is a pause and the cycle is repeated. The pause is due to the dropped P wave and measures less than twice the PP cycle. It is similar to the behavior of the RR intervals in type I second-degree AV block. Type II second-degree sinoatrial exit block is characterized by an unexpected drop of the P wave, and the resultant pause is a multiple of the basic sinus cycle. Blocked atrial premature beats sometimes mimic second-degree sinoatrial block. Third-degree sinoatrial exit block cannot be distinguished from sinus arrest when the sinus node ceases to fire. Under such circumstances, subsidiary pacemakers in the AV junction or ventricles may take over.
In theory, sinus arrest cannot be distinguished from complete SA block. In both conditions there is an absence of P waves. However, in patients with complete SA block, the block is frequently associated with atrial or AV junctional escape rhythms, while sinus arrest or pause is usually associated with depression of other potential atrial pacemakers, so that atrial escape is infrequent.
Sinus arrest is an uncommon rhythm disturbance, but is occasionally noted in elderly patients, in those with ischemic heart disease (particularly with acute inferior or true posterior MI), in some patients with myocardial disease, and sometimes with digitalis toxicity. The treatment of SA pause or arrest ordinarily includes administration of atropine or temporary or permanent ventricular pacing. Reasons to pace sinus pause or sinus arrest include the development of an AV junctional or ectopic ventricular pacemaker that is slow enough to result in such problems as syncope, CHF, angina, or frequent ventricular ectopic beats. If the escape AV junctional or ectopic ventricular pacemaker is rapid enough, particularly if the pacemaker is an AV junctional one, it may not be necessary to treat the underlying sinus pause or arrest except to ensure that it is not due to digitalis toxicity and, when possible, to determine its etiology. If this rhythm disturbance is associated with brady- or tachyarrhythmias and appears to be an integral part of the sick sinus syndrome, then pacemaker therapy is indicated. Pacemaker therapy is also indicated when any of the above-mentioned signs or symptoms are a consequence of the slower AV junctional ectopic pacemaker
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