Tachycardia

Gehan Devendra

Tachycardia is commonly found in both hospitalized and ambulatory patients. It can be either physiologic or pathologic and is defined as a heart rate greater than 100 beats/ minute. Tachycardia can initiate in two main areas, either supraventricular or ventricular, and can be divided into wide complex or narrow complex tachycardia.

Approach

In the evaluation of tachycardia, the important tasks are to determine if an underlying cause exists and to determine precisely the specific dysrhythmia producing tachycardia (1).

History

 A. Determining the cause. The clinical history is directed toward determining the underlying cardiac disease. Symptoms associated with tachycardia are palpitations, lightheadedness or presyncope, syncope, or congestive heart failure (CHF) (Chapters 2.12, 7.5, and 7.9). Some patients will also complain of irregular heartbeat, whereas others can be asymptomatic even with a profoundly abnormal rhythm. Prior history of myocardial infarction, cardiomyopathy (both ischemic and nonischemic heart disease), arrhythmias, pulmonary hypertension, cardiac surgery, rheumatic heart disease, valvular disease, and family history of cardiac arrythmias are all important. Medications such as any of the class IA or III antiarrythmic agents or over-the-counter cold preparations can cause tachyarrhythmias. Even a combination of medicines (e.g., certain antibiotics and newer nonsedating antihistamines) can contribute to tachyarrythmias.

Physical examination

The physical examination should include vital signs; pulse rate and blood pressure are the most important. Decreased blood pressure suggests a need for immediate treatment. A general assessment of mental status and skin perfusion also provides clues to the stability of the patient. A good cardiovascular and pulmonary examination is essential. Palpation of the heart (point of maximal impulse, PMI) can discern left ventricular enlargement. Auscultate systematically. The rhythm should be assessed to whether it is regular or irregular. Determine the specific heart rate. Next, determine if an associated murmur, rub, or gallop exists. Include in the examination an assessment for evidence of ventricular failure (e.g., pulmonary crackles, jugular venous distension, and lower extremity edema). In the respiratory assessment, include respiratory rate and evidence of labored breathing.

Testing

A. Electrocardiogram (ECG). The main diagnostic test is the 12-lead ECG: a rhythm strip during a tachycardia event is ideal. The Holter or event monitor can also be used in diagnosis in an outpatient setting. Rhythm and the QRS width are important in distinguishing the major types of tachycardia.

 B. Laboratory tests. Electrolyte abnormalities, especially hypomagnasemia and hypokalemia, can precipitate tachycardia. Digitalis toxicity can be another cause and, therefore, levels should be monitored. Also consider tests for common problems such as anemia, hyperthyroidism, and hypoxemia.

Diagnostic assessment

A. Narrow complex tachycardia (QRS < 120 msec)

 1. Sinus tachycardia. Sinus tachycardia is normal in infants and children aged less than 2 years. In adults, it is often secondary to physiologic factors (anxiety, fever), pharmacologic factors (β-agonist therapy), and pathologic factors (anemia, thyrotoxicosis, hypoxemia, hypotension, pulmonary embolism). ECG findings reveal a normal P wave and PR interval. Management of sinus tachycardia is directed at correcting the underlying cause; specific therapy is rarely indicated.

 2. Atrial fibrillation. Atrial fibrillation (AF) occurs in approximately 10% of patients aged more than 70 years. The hallmark on ECG is an irregularly irregular rhythm and rate with the absence of P waves. The rate in AF can vary from normal to fast (> 200 beats/min). The QRS morphology can vary a great deal as well. Usually, the impulse originates from the atrium and travels down the His or Purkinje system with depolarization of the ventricle. Occasionally, the impulse from the atrium travels down to the ventricle abnormally, resulting in aberrant conduction, and it can mimic ventricular tachycardia (VT). The key to distinguishing the two is recognizing a regular rhythm for VT and irregular rhythm for AF with aberrant conduction. In addition, patients with a prior bundle branch block who go into rapid AF can also mimic VT (see below). AF can result from cardiac [coronary artery disease, Wolff-Parkinson-White (WPW) syndrome, congestive heart failure, valvular abnormalities] or noncardiac (thyrotoxicosis, pulmonary embolism) sources. The underlying cause of the AF must be elucidated.

 3. Atrial flutter. As with AF, atrial flutter can also be caused by both cardiac and noncardiac sources. The ECG is classically a “sawtooth” pattern in leads II, III, and aVF. The rate of the flutter waves is usually between 280 and 320 beats/minute. Ventricular conduction varies and usually demonstrates blocked conduction. The usual block is 2;1 or 4;1, with a ventricular rate of 150 to 75 beats/minute, respectively. Occasionally, the rate is too fast to discern any flutter waves. Carotid massage slows the ventricular rate, allowing for diagnosis. If carotid massage fails, pharmacologic treatment with adenosine or digitalis can slow the ventricular rate.

 4. Paroxysmal supraventricular tachycardia (PSVT). PSVT is precipitated by reentry of the atrial impulse at the level of the atrioventricular (AV) node. This is the most common mechanism in the initiation of PSVT. PSVT is characterized by sudden onset of a narrow, regular QRS complex without discernible P waves. The rate varies from 160 to 190 beats/minute but can be as slow as 120 to 130 beats/minute. If the patient has a prior bundle branch block, a wide QRS complex will also be seen with PSVT. A specific subset of PSVT caused by reentry is the WPW syndrome. Conduction in WPW can occur via an accessory pathway. In the resting ECG, this is usually manifested by an upsloping tracing on the ECG prior to the QRS complex, known as the “delta wave.” PR interval is also shortened. The accessory tract can predispose to PSVT, atrial flutter, or AF.

 5. Multifocal atrial tachycardia (MAT). This arrhythmia is usually seen in the setting of pulmonary disease, metabolic or electrolyte abnormalities, or, rarely, digitalis toxicity. ECG findings in MAT consists of an irregular rhythm combined with three different morphologies of P waves. The rate of this arrhythmia usually does not exceed 140 beats/minute. Removal of the inciting event can relieve the tachycardia, but patients may frequently have to tolerate a low-grade tachycardia (1,2).

 B. Wide complex tachycardia (QRS > 120 msec)

1. Ventricular tachycardia versus SVT with aberrant conduction. This is probably the hardest to diagnose of the tachycardias. Brudaga (3) put forth a schema to diagnose VT from SVT with aberrant conduction. The criteria are as follows:

a. Initially rule out right or left bundle branch block.

b. Is there an absence of an RS complex in all precordial leads? If yes then VT, if no then proceed to c.

c. Is the RS interval more than 100 msec in any one precordial lead? If yes then VT, if no then proceed to d.

 d. Is there AV dissociation? If yes then VT. If no is answered to all the above then the specificity or sensitivity that this is a SVT with aberrant conduction is 98% and 99%, respectively. Inexact features of VT are QRS more than 0.14 second, QRS concordance in all precordial leads, fusion or capture beats, and QRS negative in leads I and II.

 2. Ventricular fibrillation (VF). VF is not really a tachycardia but represents abnormal ventricular depolarization. The ventricle has numerous areas of depolarization and, therefore, cannot have organized contraction. This type of unorganized contraction produces no cardiac output. On ECG, it often appears as a “bag of worms” with coarse or fine waves varying in amplitude and duration. Coarse VF indicates the recent onset of VF and is usually correctable with defibrillation, whereas fine VF is indicative of prolonged VF that approaches asystole.

References

1. Scheinman M. Tachyarrythmias in primary cardiology. In: Goldman L, Braunwald E, ed. Heart disease: a textbook of cardiovascular medcicine. Philadelphia: WB Saunders, 1998:330–352.

2. Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med 1995; 332:162–173.

3. Brugada P. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991;83:1649–1659. >

Book Source Details

• Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
• Author(s): Robert B. Taylor (editor)
• Year of Publication: 2000
• Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.

Other Book Chapters Related to Arrhythmia

Read excerpts from these other book chapters related to Arrhythmia:

Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2008 Williams & Wilkins.

More About Causes of Arrhythmia

• Back to symptom: Arrhythmia: Introduction (review 234 causes)
• Next Book Extract About Arrhythmia: Heart Murmur, Diastolic (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
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More About This Book: Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter Authors: Robert B. Taylor (editor) Publisher: Lippincott Williams & Wilkins Copyright: 2000 ISBN: 0-78172-094-X

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