ECGsInterpreting them with ease and accuracy

Interpreting them with ease and accuracy

Normal ECG

Analyzing the ECG waveform

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.

How to read an ECG rhythm strip: The 8-step method

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 105 and 106.)

Normal sinus rhythm

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.


Sinus arrhythmia

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.


Treatment isn’t necessary unless the patient is symptomatic or the sinus arrhythmia stems from an underlying cause. If symptoms are associated with symptomatic bradycardia, atropine may be administered.

Sinus bradycardia

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.


If the patient is asymptomatic, treatment isn’t necessary. If he has signs and symptoms, the goal of treatment is to identify and correct the underlying cause. The heart rate may be increased with drugs such as atropine. A temporary (transcutaneous or transvenous) or permanent pacemaker may be necessary if bradycardia persists.

Sinus tachycardia

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 stress. 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.


Treatment focuses on finding the primary cause. If it’s high catecholamine levels, a beta-adrenergic blocker may slow the heart rate. After MI, persistent sinus tachycardia may precede heart failure or cardiogenic shock.

Sinus arrest

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.


For a symptomatic patient, treatment focuses on maintaining cardiac output and discovering the cause of sinus arrest. If indicated, atropine may be given or a temporary (transcutaneous or transvenous) or permanent pacemaker may be inserted.

Premature atrial contractions

Premature atrial contractions (PACs) usually result from an irritable focus in the atrium that supersedes the SA node as the pacemaker for one or more beats.

Although PACs commonly occur in normal hearts, they’re also associated with coronary and valvular heart disease. In an inferior wall MI, PACs may indicate a concomitant right atrial infarct. In an anterior wall MI, PACs are an early sign of left-sided heart failure. They may also warn of more severe atrial arrhythmia, such as atrial flutter or atrial fibrillation.

Possible causes include digoxin toxicity, hyperthyroidism, elevated catecholamine levels, acute respiratory failure, and chronic obstructive pulmonary disease. Alcohol, caffeine, or tobacco use can also trigger PACs. Patients who eliminate or control these factors can usually correct the arrhythmia.


Symptomatic patients may be treated with beta-adrenergic blockers or calcium channel blockers.

Atrial tachycardia

Atrial tachycardia is a supraventricular tachycardia, which means that the impulse originates above the ventricles. In this rhythm, the impulse originates in the atria. The rapid atrial rate shortens diastole, resulting in a loss of atrial kick, reduced cardiac output, reduced coronary perfusion, and ischemic myocardial changes.

Although atrial tachycardia can occur in healthy patients, it’s usually associated with high catecholamine levels, digoxin toxicity, MI, cardiomyopathy, hyperthyroidism, hypertension, and valvular heart disease. Three types of atrial tachycardia exist: atrial tachycardia with block, multifocal atrial tachycardia, and paroxysmal atrial tachycardia.


If the patient has atrial tachycardia or paroxysmal atrial tachycardia and is symptomatic, prepare for immediate cardioversion. If the patient is stable, the physician may perform carotid sinus massage (if no bruits are present) or order drug therapy, such as adenosine (Adenocard), a calcium channel blocker, a beta-adrenergic blocker, or digoxin (Lanoxin). If these treatments are ineffective in rhythm conversion, then procainamide or amiodarone may be needed. If these measures fail, cardioversion may be necessary.

Atrial flutter

Characterized by an atrial rate of 250 beats/minute or more, atrial flutter is caused by multiple reentry circuits within the atrial tissue. On the ECG, the P waves lose their normal appearance as a result of rapid atrial rate and blend together in a sawtooth configuration known as flutter waves. These waves are the hallmark of atrial flutter.

Causes of atrial flutter include conditions that enlarge atrial tissue and elevate atrial pressures. Atrial flutter is associated with MI, increased catecholamine levels, hyperthyroidism, and digoxin toxicity.

If the patient’s pulse rate is normal, he usually has no symptoms. If his pulse rate is high, however, he’ll probably have signs and symptoms of decreased cardiac output, such as hypotension and syncope.


If the patient is symptomatic, prepare for immediate cardioversion. The focus of treatment for stable patients with atrial flutter includes controlling the rate and converting the rhythm. Specific interventions depend on the patient’s cardiac function, the presence of preexcitation syndromes, and the duration (less than or greater than 48 hours) of arrhythmia. For example, in patients with atrial flutter, normal cardiac function, and duration of rhythm less than 48 hours, cardioversion may be considered. When duration is greater than 48 hours, avoid nonemergent cardioversion unless adequate anticoagulation has been achieved.

Drugs that may be ordered to control atrial rate include amiodarone, ibutilide, procainamide, calcium channel blockers, and beta-adrenergic blockers.

Atrial fibrillation

Atrial fibrillation is chaotic, asynchronous electrical activity in the atrial tissue. It results from impulses in many reentry pathways. These multiple and multidirectional impulses cause the atria to quiver instead of contracting regularly.

With this type of arrhythmia, blood may pool in the left atrial appendage and form thrombi that can be ejected into the systemic circulation. An associated rapid ventricular rate can decrease cardiac output.

Possible causes include valvular disorders, hypertension, coronary artery disease, MI, chronic lung disease, ischemia, thyroid disorders, and Wolff-Parkinson-White syndrome. The disorder may also result from high adrenergic tone as a result of physical exertion, sepsis, alcohol withdrawal, or the use of drugs, such as aminophylline (theophylline ethylenediamine) and cardiac glycosides.


If the patient is symptomatic, synchronized cardioversion should be used immediately. Vagal stimulation may be used to slow the ventricular response, but it won’t convert the arrhythmia. Drugs that may be ordered to slow AV conduction include calcium channel blockers and beta-adrenergic blockers. Digoxin may be ordered if the patient is stable. After the rate slows, if conversion to a normal sinus rhythm hasn’t occurred, amiodarone (Cordarone), flecainide, or sotalol may be ordered. If atrial fibrillation is of several days’ duration, anticoagulant therapy is recommended before pharmacologic or electrical conversion. If atrial fibrillation is of recent onset, ibutilide (Corvert) may be used to convert the rhythm.

Junctional rhythm

Junctional rhythm, also known as junctional escape rhythm, occurs in the AV junctional tissue. It causes retrograde depolarization of the atrial tissue and antegrade depolarization of the ventricular tissue. It results from conditions that depress SA node function, such as an inferior wall MI, digoxin toxicity, and vagal stimulation. The arrhythmia may also stem from increased automaticity of the junctional tissue, which can be caused by digoxin toxicity or ischemia associated with an inferior wall MI.

Junctional rhythm is a regular rhythm with a ventricular rate of 40 to 60 beats/minute. A junctional rhythm with a ventricular rate of 60 to 100 beats/minute is known as an accelerated junctional rhythm. If the ventricular rate exceeds 100 beats/minute, the arrhythmia is called junctional tachycardia.


Treatment aims to identify and manage the primary cause of arrhythmia. If the patient is symptomatic, treatment may include atropine to increase the sinus or junctional rate. Alternately, the physician may insert a pacemaker or use transcutaneous pacing to maintain an effective heart rate.

Accelerated junctional rhythm

An accelerated junctional rhythm is an arrhythmia that originates in the AV junction and is usually caused by enhanced automaticity of the AV junctional tissue. It’s called “accelerated” because it occurs at a rate of 60 to 100 beats/minute, exceeding the inherent junctional rate of 40 to 60 beats/minute.

Digoxin toxicity is a common cause of accelerated junctional rhythm. Other causes include electrolyte disturbances, ventricular heart disease, heart failure, and inferior or posterior MI.

Aug 18, 2016 | Posted by in NURSING | Comments Off on ECGsInterpreting them with ease and accuracy

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