Basic and Bedside Electrocardiography, 1st Edition (2009)

Chapter 14. Sinus Tachycardia

Electrocardiogram Findings

·   Sinus tachycardia: Sinus tachycardia refers to impulses that originate from the sinus node with a rate that exceeds 100 beats per minute (bpm). The 12-lead electrocardiogram (ECG) is helpful in identifying the presence of sinus tachycardia as well as excluding other causes of tachycardia such as supraventricular tachycardia (SVT), atrial flutter, and atrial fibrillation.

·   ECG findings: The classic ECG finding of sinus tachycardia is the presence of sinus P wave in front of every QRS complex with a PR interval of ≥0.12 seconds. The morphology of the P wave in the 12-lead ECG differentiates a sinus P wave from a P wave that is not of sinus origin.

o    Frontal plane: Because the sinus node is located at the upper right border of the right atrium close to the entrance of the superior vena cava, the sinus impulse spreads from right atrium to left atrium and from top to bottom in the direction of 0° to 90°, resulting in upright P waves in leads I, II, and aVF (Fig. 14.1). The axis of the sinus P wave is approximately 45° to 60°; thus, the P wave is expected to be upright in lead II. The hallmark of normal sinus rhythm therefore is a positive P wave in lead II. If the P wave is not upright in lead II, the P wave is probably ectopic (not of sinus node origin).

o    Horizontal plane: In the horizontal plane, the sinus node is located at the posterior and right border of the right atrium. Thus, the impulse travels anteriorly and leftward causing the P waves to be upright in V3 to V6 (Fig. 14.2). This was previously discussed in Chapter 7, Chamber Enlargement and Hypertrophy.

Figure 14.1: Sinus Tachycardia. Because the sinus node is located at the upper border of the right atrium, activation of the atria is from right to left and from top to bottom (arrows) resulting in upright P waves in leads I, II, and aVF. RA, right atrium; LA, left atrium.

Pathologic Sinus Tachycardia

·   Sinus tachycardia: Sinus tachycardia accelerates and decelerates gradually and is a classic example of a tachycardia that is nonparoxysmal. Sinus tachycardia usually has an identifiable cause, which could be physiologic, such as exercise, emotion, fear, or anxiety. The underlying condition may be pathologic, such as acute pulmonary embolism, acute pulmonary edema, thyrotoxicosis, infection, anemia, hypotension, shock, or hemorrhage. It may be due to the effect of pharmacologic agents such as atropine, hydralazine, epinephrine, norepinephrine and other catecholamines.

·   Pathologic sinus tachycardia: Although sinus tachycardia is appropriate and physiologic, it should be differentiated from other types of sinus tachycardia that are not associated with any identifiable cause. These other types of tachycardia are primary compared with normal sinus tachycardia, which is secondary to an underlying condition or abnormality. Sinus tachycardia without an identifiable cause is abnormal and can occur in the following conditions.

o    Inappropriate sinus tachycardia: This type of sinus tachycardia is not associated with any underlying condition and no definite causes can be identified.

Very often, the rate of the tachycardia is inappropriately high at rest or during physical activity. Increase in sinus rate during exercise is very often out of proportion to the expected level of response. The sinus tachycardia is due to enhanced automaticity of the cells within the sinus node.

o    Postural orthostatic tachycardia syndrome (POTS): This is similar to inappropriate sinus tachycardia except that the tachycardia is initiated by the upright posture and is relieved by recumbency. In POTS, there should be no significant orthostatic hypotension or autonomic dysfunction because sinus tachycardia becomes appropriate when these entities are present.

o    Sinoatrial reentry: This tachycardia is a type of SVT resulting from re-entry where the sinus node is part of the reentrant pathway. When this occurs, the P waves resemble that of sinus tachycardia. It is paroxysmal in contrast to the other types of sinus tachycardia that are nonparoxysmal. This tachycardia will be discussed in more detail under SVT from sinoatrial reentry.

Figure 14.2: Sinus Tachycardia. Twelve-lead electrocardiogram showing sinus tachycardia. Sinus tachycardia is identified by the presence of upright P waves in leads I, II, and aVF and also in V3 to V6. The axis of the P wave is closest to lead II, which is the most important lead in identifying the presence of sinus rhythm.

Sinus Tachycardia

·   The 12-lead ECG alone cannot differentiate physiologic sinus tachycardia from sinus tachycardia that is pathologic and inappropriate because the ECG findings of these two clinical entities are identical. The diagnosis of pathologic sinus tachycardia therefore is based on additional clinical information demonstrating that the sinus tachycardia is not associated with any underlying condition. Continuous monitoring is often helpful in demonstrating that the tachycardia is inappropriate. It is also helpful in showing that the sinus tachycardia can be paroxysmal and can be precipitated or terminated by premature atrial complexes, suggesting that the tachycardia is due to sinoatrial reentry.

·   The following ECG shows sinus tachycardia (Fig. 14.2). The P waves are upright in leads I, II, and aVF and in V3 to V6. Each P wave is in front of the QRS complex with a PR interval of ≤0.12 seconds.

Summary of ECG Findings

·   Sinus P waves are present with a rate >100 bpm.

·   The sinus P waves precede each QRS complex with a PR interval ≥0.12 seconds.

·   The morphology of the P wave should be upright in leads I, II, and aVF and in V3 to V6.

Mechanism

·   The sinus impulse arises from the sinus node, which contains automatic cells with pacemaking properties. Pacemaking cells exhibit slow spontaneous diastolic depolarization during phase 4 of the action potential (see Chapter 1, Basic Anatomy and Electrophysiology). The sinus node has the fastest rate of spontaneous depolarization occurring more than one per second. As a result, the rhythm originating from the sinus node is the most dominant and is the pacemaker of the heart.

·   The rate of the sinus node is usually modified by a number of stimuli, most notably sympathetic and parasympathetic events, but it could also be influenced by other conditions such as stretch, temperature, and hypoxia. It responds appropriately to physiologic as well as pathologic stimuli. When the sinus tachycardia is inappropriate, it may be due to enhance firing rate of the automatic cells in the sinus node or autonomic regulation of the sinus node may be abnormal with increased response to sympathetic stimuli or decreased response to parasympathetic influences.

·   Pacemaker cells are not localized to a specific area, but are widely distributed throughout the sinus node. Cells with faster rates occupy the more cranial portion, whereas cells with slower rates occupy the more caudal portion of the sinus node. During sinus tachycardia, the impulses do not originate from a single stationary focus, but migrate from a caudal area to a more cranial location as the rate of the tachycardia increases. This shift in the origin of the sinus impulse to a more cranial location may change the morphology of the P wave, resulting in a P wave axis that is slightly more vertical (toward 90°) during faster heart rates and slightly more horizontal (toward 0°) during slower sinus rates. This change in the origin of the impulse during sinus tachycardia has clinical and therapeutic implications. Patients with inappropriate sinus tachycardia, where the primary abnormality is due to inappropriate increase in automaticity in the sinus node cells and are refractory to medical therapy, may respond to selective ablation of certain portions of the sinus node.

Clinical Implications

·   Sinus tachycardia is a physiologic mechanism occurring appropriately in response to known stimuli. This includes hypotension, fever, anemia, thyrotoxicosis, and pain, among other things.

·   Sinus tachycardia is appropriate when it is due to a secondary cause. Sinus tachycardia however may be difficult to differentiate from SVT, especially if the P waves are obscured by the T waves of the preceding complex. The clinical significance and therapy of sinus tachycardia are different from that of SVT, and every attempt should be made to differentiate one from the other.

·   Although sinus tachycardia is usually physiologic and appropriate in response to a variety of clinical conditions, sinus tachycardia may result in unnecessary increase in heart rate without a definite secondary cause. When this occurs, the sinus tachycardia is abnormal and could be due to inappropriate sinus tachycardia, postural orthostatic tachycardia syndrome, or sinoatrial reentrant tachycardia.

o    Inappropriate sinus tachycardia: Sinus tachycardia is inappropriate when there is no known cause for the sinus tachycardia. Inappropriate sinus tachycardia occurs usually in young females in their 30s. Most are health care workers. Inappropriate sinus tachycardia is important to differentiate from appropriate sinus tachycardia because the abnormality may reside in the sinus node itself due to inappropriate enhancement in automaticity of the sinus node cells rather than due to secondary causes.

o    POTS: This type of sinus tachycardia is similar to inappropriate sinus tachycardia except that the tachycardia is triggered by the upright posture and is relieved by recumbency. The tilt table test may result in increase in heart rate ≥30 bpm from baseline or increase in heart rate ≥120 bpm without significant drop in blood pressure. The drop in blood pressure should not be ≥30 mm Hg systolic or ≥20 mm Hg mean blood pressure within 3 minutes of standing or tilt. The cause of POTS is multifactorial and approximately half of patients have antecedent viral infection. It may be due to the presence of a limited autonomic neuropathy associated with postganglionic sympathetic denervation of the legs, resulting in abnormality in vasomotor tone and blood pooling. It may also be due to a primary abnormality of the sinus node cells similar to inappropriate sinus tachycardia. Other secondary causes such as venous pooling in the splanchnic bed, hypovolemia, or failure to vasoconstrict have also been implicated. Because the abnormality in POTS may be in the sinus node itself (primary), but could also be due to abnormalities outside the sinus node (secondary causes), response to therapy may be difficult to predict. Thus, therapy to suppress sinus node automaticity with the use of pharmacologic agents or radiofrequency modification of the sinus node may be appropriate if the abnormality is in the sinus node itself, but may not be effective if the abnormality is due to secondary causes.

o    Sinoatrial reentrant tachycardia: This is further discussed in Chapter 17, Supraventricular Tachycardia due to Reentry. The tachycardia can be precipitated or terminated by a premature ectopic atrial impulse. Unlike the other types of sinus tachycardia, sinoatrial reentrant tachycardia is usually associated with structural cardiac disease.

Treatment

·   Sinus tachycardia: Appropriate sinus tachycardia does not need any pharmacologic therapy to suppress the arrhythmia. The underlying cause of the tachycardia should be recognized and corrected.

o    Occasionally, sinus tachycardia may occur in a setting that is not advantageous to the patient. For example, sinus tachycardia may be related to pericarditis, acute myocardial infarction, congestive heart failure, or thyrotoxicosis. In these patients, it may be appropriate to slow down the heart rate with beta blockers and identify other causes of sinus tachycardia that can be corrected. Beta blockers are standard drugs for congestive heart failure resulting from systolic dysfunction as well as for patients with acute myocardial infarction, whether or not sinus tachycardia is present. It is also commonly used to control sinus tachycardia associated with thyrotoxicosis.

·   Inappropriate sinus tachycardia: If secondary causes have been excluded and the sinus tachycardia is deemed inappropriate, therapy includes beta blockers and nondihydropyridine calcium channel blockers such as diltiazem and verapamil. Beta blockers may be used as first-line therapy unless these agents are contraindicated. In patients who are resistant to pharmacologic therapy or patients who are unable to take oral therapy, sinus node modification using radiofrequency ablation has been used successfully. This carries a risk of causing sinus node dysfunction and permanent pacing and should be considered only as a last resort.

·   POTS: Because the cause of POTS may be a primary sinus node abnormality but could also be due to secondary causes, response to therapy is unpredictable.

o    Nonpharmacologic therapy: Volume expansion may be required with proper regular oral hydration combined with high-sodium intake of up to 10 to 15 g daily, use of compressive stockings, sleeping with the head of the bed tilted up, and resistance training such as weight lifting.

o    Pharmacologic therapy: Pharmacologic therapy has been shown to provide short-term, partial relief of symptoms in approximately half of patients, regardless of the agent used.

§  Beta blockers: If nonpharmacologic therapy is not effective, low-dose beta blockers such as propranolol 20 to 30 mg three to four times daily may be tried because the abnormality may be in the sinus node cells or the result of hypersensitivity to endogenous beta agonists.

§  Calcium channel blockers: If beta blockers are not effective or are contraindicated because of bronchospastic pulmonary disease, calcium channel blockers such as diltiazem or verapamil may be given. These drugs are contraindicated when there is left ventricular systolic dysfunction.

§  Mineralocorticoids: Mineralocorticoids, such as fludrocortisone 0.1 to 0.3 mg orally once daily, may be useful when there is hypovolemia, which is often seen in POTS. This should be considered only after nonpharmacologic therapy has been tried. These agents are usually combined with hydration and high sodium intake.

§  Adrenoceptor agonists: Adrenoceptor agonist such as midodrine 2.5 to 10 mg three times daily orally has been shown to improve symptoms during tilt table testing, although its efficacy during long-term therapy is not known.

§  Serotonin reuptake inhibitors: Response to selective serotonin reuptake inhibitors is similar to that of other pharmacologic agents.

o    Catheter ablation:Although catheter ablation or catheter modification has been performed in some patients with POTS, response to this type of therapy may be difficult to predict because the abnormality may be primarily in the sinus node but could also be due to secondary causes.

Prognosis

·   Appropriate sinus tachycardia: Sinus tachycardia is physiologic and is an expected normal response to a variety of clinical situations. The overall prognosis of a patient with sinus tachycardia depends on the underlying cause of the sinus tachycardia and not the sinus tachycardia itself.

·   Pathologic sinus tachycardia: Therapy for pathologic sinus tachycardia is given primarily to improve the quality of life rather than to prolong survival. In supraventricular tachycardia from sinoatrial reentry, the tachycardia may be associated with structural cardiac disease. The prognosis will depend on the nature of the underlying cause. Pathologic sinus tachycardia has not been shown to cause tachycardia mediated cardiomyopathy.

·   POTS: Up to 80% of patients with POTS improve with most returning to normal functional capacity. Those with antecedent viral infection seem to have a better outcome.

Suggested Readings

Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). J Am Coll Cardiol. 2003;42:1493-531.

Freeman R, Kaufman H. Postural tachycardia syndrome. 2007 UptoDate. www.utdol.com.

Sandroni P, Opfer-Gehrking TL, McPhee BR, et al. Postural tachycardia syndrome: clinical features and follow-up study. Mayo Clin Proc. 1999;74:1106-1110.

Singer W, Shen WK, Opfer-Gehrking TL, et al. Evidence of an intrinsic sinus node abnormality in patients with postural tachycardia syndrome. Mayo Clin Proc. 2002;77:246-252.

Thieben MJ, Sandroni P, Sletten DM, et al. Postural orthostatic tachycardia syndrome: the Mayo Clinic experience. Mayo Clin Proc. 2007;82:308-313.

Yussuf S, Camm J. Deciphering the sinus tachycardias. Clin Cardiol. 2005;28:267-276.