SPECIFIC ARRHYTHMIAS - sinus nodal rhythm disturbances
Normal sinus rhythm refers to impulse formation beginning in the sinus node and, in adults, having a rate of between 60 and 100 beats per minute. The P wave is upright in leads 1,2, and aV> and negative in lead aVR. The rate of sinus nodal discharge is under autonomic control and increases with sympathetic and decreases with parasympathetic stimulation. Sinus tachycardia refers to a tachycardia of sinus origin with a rate exceeding 100 beats per minute. Sinus tachycardia occurs with stresses such as fever, hypotension, thyrotoxicosis, anemia, anxiety, exertion, hypovolemia, pulmonary emboli, myocardial ischemia, congestive heart failure, shock, drugs (e.g., atropine, catecholamines, thyroid, alcohol, caffeine), or inflammation. Therapy should be focused on the cause of the tachycardia. If the sinus tachycardia must be treated directly, propranolol may be used. Sinus bradycardia refers to sinus node discharge at a rate less than 60 beats per minute. The P wave contour is normal, but sinus arrhythmia is often present. Sinus bradycardia frequently occurs in young adults, especially well-trained athletes, and is common at night. Sinus bradycardia can be produced by a variety of conditions, including eye manipulation, increased intracranial pressure, myxedema, hypothermia, sepsis, fibrodegenerative changes, vagal stimulation, or vomiting, and the administration of parasympathomimetic drugs, beta-adrenergic blocking drugs, or amiodarone. It occurs commonly in the acute phase of myocardial infarction, espedaily inferior myocardial infarction. Treatment of asymptomatic sinus bradycardia is usually not necessary. If cardiac output is low or tachyarrhythmias occur owing to the slow heart rate, atropine or, if necessary, isoproterenol may be effective. There is no drug that effectively and safely increases the heart rate over a long period of time, and therefore electrical pacing is the treatment of choice chronically if symptomatic sinus bradycardia is present.
Sinus arrhythmia refers to phasic variation in the sinus cycle length by greater than 10 per cent. P wave morphology is normal. Respiratory sinus arrhythmia occurs when the PP interval shortens during inspiration as a result of reflex inhibition of vagal tone and lengthens during expiration. Nonrespiratory sinus arrhythmia refers to sinus arrhythmia not associated with the respiratory cycle. Symptoms are unusual and treatment not necessary.
In sinus pause (sinus arrest) and sinoatrial exit block, a sudden unexpected failure of a P wave occurs. In sinoatrial exit block, the PP interval surrounding the absent P wave is a multiple of the P to P intervals, implying that the sinus impulse was generated but did not propagate through the perinodal tissue to the atrium. If no such cycle relationship can be found, the term sinus pause or sinus arrest is employed. Acute myocardial infarction, degenerative fibrotic changes, digitalis toxicity, or excessive vagal tone can produce sinus arrest or exit block. Therapy involves searching for the underlying etiology. Patients are not treated if they are asymptomatic. If they are symptomatic and the arrhythmia is not reversed by correcting the underlying etiologies, pacing is employed.
Wandering atrial pacemaker involves a transfer of the dominant pacemaker from the sinus node to latent pacemakers in other atrial sites or in the AV junction. The change from one pacemaker focus to another occurs gradually, associated with a change in the RR interval, PR interval, and P wave morphology. Treatment is usually not necessary except if symptoms occur from bradyar-rhythmias.
The hypersensitive carotid sinus syndrome is characterized by cessation of atrial activity due to sinus arrest or sinoatrial exit block with light pressure over the carotid baroreceptors. In addition, AV block may be observed. Adequate junctional or ventricular escape complexes may not occur. Cardioinhibitory carotid sinus hypersensitivity is arbitrarily defined as ventricular asystole exceeding three seconds during carotid sinus stimulation. Vasodepressor carotid sinus hypersensitivity is defined as a fall in systolic blood pressure of 30 to 50 mm Hg without cardiac slowing, usually with reproduction of a patient’s symptoms. The treatment in symptomatic patients is pacemaker implantation (to include at least a ventricular lead, since the sinus node slowing is usually also associated with AV block). Neither atropine nor pacing prevents the vasodepressor manifestations of carotid sinus hypersensitivity. Severe vasodepressor carotid sinus hypersensitivity occasionally requires denervation of the carotid sinus.
The sick sinus syndrome is applied to a variety of sinus nodal and AV nodal abnormalities that occur alone or in combination. They include [1) persistent spontaneous sinus bradycardia not caused by drugs and inappropriate to the physiological circumstances, (2) sinus arrest or exit block, (3) combinations of sinus and AV conduction disturbances, and (4) alternation of paroxysms of atrial tachyarrhythmias with periods of slow atrial and ventricular rates (bradycardia/ tachycardia syndrome]. The sick sinus syndrome may be associated with AV nodal or His-Purkinje conduction disturbances. If symptoms are present from bradyarrhythmias, pacemaker implantation is appropriate. Pacing for the symptomatic brady-arrhythmia combined with drug therapy for the tachyarrhythmia is often needed.
Sinus nodal re-entrant tachycardia accounts for 5 to 10 per cent of paroxysmal supraventricular tachycardias. Its mechanism is presumed to be re-entry within the sinus node and the peri-nodal tissues, giving rise to a tachycardia, usually with a rate of 130 to 140 beats per minute and containing P waves very similar to sinus P waves. AV block may occur without affecting the tachycardia. Vagal activation may slow and then abruptly terminate the tachycardia by its action on sinus nodal tissue. Tachycardia may be induced and terminated at electrophysiological study with premature atrial stimulation. Treatment with propranolol, verapamil, or digitalis is effective therapy
- PHYSICAL EXAMINATION
- TESTS OF HEPATIC FUNCTION
- Uremic Osteodystrophy
- CHRONIC RENAL FAILURE
- CLINICAL SYMPTOMS OF ESOPHAGEAL DISEASE
- AV JUNCTIONAL RHYTHM DISTURBANCES
- Hematuria
- Multiple Myeloma
- C. MALABSORPTION
- Bretylium Tosylate
- Nephrotic Glomerulopathies
- PHYSIOLOGY OF THE PULMONARY CIRCULATION
- Idiopathic Pulmonary Fibrosis
- Diagnosis
- ACUTE AND CHRONIC HEPATITIS - DEFIRILTIORI
- ENDOSCOPIC PROCEDURES
- DIAGNOSTIC TECHNIQUES AND THEIR INDICATIONS - IMAGING PROCEDURES
- THE SLEEP APNEA SYNDROME
- SCREENING TESTS OF HEPATOBILIARY DISEASE
- SUDDEN CARDIAC DEATH
- MULTIVALVULAR DISEASE
- Polycystic Kidney Disease (PKD)
- CLINICAL PRESENTATION
- Urinalysis, Renal ‘Tubular Function, and Urine Flow Rate
- ACUTE PANCREATITIS
- CLASSIFICATION OF THE MALABSORPTION SYNDROMES
- ETIOLOGY OF GASTROINTESTINAL BLEEDING
- APPROACH TO THE PATIENT WJTH SUSPECTED MALDIGESTION AND/OR MALABSORPTION
- Renal Glycosuria
- CARDIOVASCULAR RESPONSE TO EXERCISE
- OTHER THERAPEUTIC MODALITIES
- Alterations in Glomerular Hemodynamics, Parathyroid Hormone Metabolism, and Systemic Arterial Blood Pressure
- Bartter’s Syndrome
- ENVIRONMENTAL DAMAGE OF THE EXTREMITIES
- Procainamide