An electrocardiogram (ECG) complex represents the electrical events occurring in one cardiac cycle. A complex consists of five waveforms labeled with the letters P, Q, R, S, and T. The letters Q, R, and S are referred to as a unit known as the QRS complex. The ECG tracing represents the conduction of electrical impulses from the atria to the ventricles. (See Components of an ECG waveform.)

♦ The P wave is the first component of the normal ECG waveform. It represents atrial depolarization.

♦ The PR interval tracks the atrial impulse from the atria through the atrioventricular (AV) node, the bundle of His, and the right and left bundle branches. It begins with atrial depolarization and ends with the beginning of ventricular depolarization.

♦ The QRS complex follows the P wave and represents ventricular depolarization.

♦ The ST segment represents the end of ventricular depolarization and the beginning of ventricular repolarization. The J point marks the end of the QRS complex and the beginning of the ST segment.

♦ The T wave represents ventricular repolarization.

♦ The QT interval measures the time needed for ventricular depolarization and repolarization.

♦ The U wave represents His-Purkinje repolarization.

Analyzing a rhythm strip is a skill that’s developed through practice. You can use several methods, as long as you’re consistent. (See The 8-step method of rhythm strip analysis, pages 150 and 151.)

When the heart functions normally, the sinoatrial (SA) node acts as the


primary pacemaker, initiating the electrical impulses. The SA node assumes this role because its automatic firing rate exceeds that of the heart’s other pacemakers, allowing cells to depolarize spontaneously.

Normal sinus rhythm records an impulse that starts with the sinus node and progresses to the ventricles through a normal conduction pathway —from the sinus node to the atria and AV node, through the bundle of His, to the bundle branches, and onto the Purkinje fibers. Normal sinus rhythm is the standard against which all other rhythms are compared; you must be able to recognize normal sinus rhythm before you can recognize an arrhythmia.

Based on the location of the electrical disturbance, arrhythmias can be classified as sinus, atrial, junctional, or ventricular arrhythmias, or as AV blocks. Functional disturbances in the SA node produce sinus arrhythmias. Enhanced automaticity of atrial tissue or reentry may produce atrial arrhythmias, the most common arrhythmias.

Junctional arrhythmias originate in the area around the AV node and bundle of His. These arrhythmias usually result from a suppressed higher pacemaker or from blocked impulses at the AV node.

Ventricular arrhythmias originate in ventricular tissue below the bifurcation of the bundle of His. These rhythms may result from reentry or enhanced automaticity or may occur after depolarization.

An AV block results from an abnormal
interruption or delay of atrial impulse conduction to the ventricles. It may be partial or total and may occur in the AV node, bundle of His, or Purkinje system.

In sinus arrhythmia, the heart rate stays within normal limits, but the rhythm is irregular and corresponds to the respiratory cycle and to variations in vagal tone. During inspiration, an increased volume of blood returns to the heart, reducing vagal tone and increasing sinus rate. During expiration, venous return decreases, vagal tone increases, and sinus rate slows.

Conditions unrelated to respiration may also produce sinus arrhythmia. These conditions include inferior wall myocardial infarction (MI) and digoxin toxicity.

Sinus arrhythmia is easily recognized in elderly, pediatric, and sedated patients. The patient’s pulse rate increases with inspiration and decreases with expiration. Usually, the patient is asymptomatic.

Characterized by a sinus rate of less than 60 beats/minute, sinus bradycardia usually occurs as the normal response to a reduced demand for blood flow. It’s common among athletes, whose well-conditioned hearts can maintain stroke volume with reduced effort. It may also be caused by drugs, such as cardiac glycosides, calcium channel blockers, and beta-adrenergic blockers. Sinus bradycardia may occur after an inferior wall MI involving the right coronary artery, which supplies the blood to the SA node. This rhythm may develop during sleep and in patients with increased intracranial pressure. It may also result from vagal stimulation caused by vomiting or defecating. Pathologic sinus bradycardia may occur with sick sinus syndrome.

The patient with sinus bradycardia is asymptomatic if he can compensate for the decrease in heart rate by increasing stroke volume. If he cannot, he may have signs and symptoms of decreased cardiac output, such as hypotension, syncope, confusion, and blurred vision.

Sinus tachycardia is an acceleration of firing of the SA node beyond its normal discharge rate. In an adult, it’s characterized by a sinus rate of more than 100 beats/minute. The rate rarely exceeds 180 beats/minute except during strenuous exercise. The maximum rate achieved with exercise decreases with age.

A normal response to cellular demands for increased oxygen delivery and blood flow commonly produces sinus tachycardia. Conditions that cause such a demand include heart failure, shock, anemia, exercise, fever, hypoxia, pain, and anxiety. Drugs that stimulate the beta receptors in the heart also cause sinus tachycardia. They include aminophylline, epinephrine, dobutamine, and dopamine. Alcohol, caffeine, and nicotine may also produce sinus tachycardia.

An elevated heart rate increases myocardial oxygen demands. If the patient can’t meet these demands (for example, because of coronary artery disease), ischemia and further myocardial damage may occur.

In sinus arrest, the normal sinus rhythm is interrupted by an occasional, prolonged failure of the SA node to initiate an impulse. Therefore, sinus arrest is caused by episodes of failure in the automaticity of impulse formation of the SA node. The atria aren’t stimulated, and an entire PQRST complex is missing from the ECG strip. Except for the missing complex, or pause, the ECG usually remains normal.

During a sinus arrest, the sinus node resets itself so that when the impulse is initiated, the complex that occurs after the pause will be out of the cycle and the rate will usually be different from the rate before the pause.

Sinus arrest may result from an acute inferior wall MI, increased vagal tone, or the use of certain drugs, such as cardiac glycosides, calcium channel blockers, and beta-adrenergic blockers. The arrhythmia may also be linked to sick sinus syndrome. The patient has an irregular pulse rate associated with the pauses in sinus rhythm. If the pauses are infrequent, the patient is asymptomatic. If they occur frequently and last for several seconds, however, the patient may have signs of decreased cardiac output.