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Learn to recognize bundle-branch blocks, myocardial infarction, and common dysrhythmias
LAST MONTH, I described the components of the 12-lead electrocardiogram (ECG) and how to recognize a normal ECG. In this article, I'll explain some advanced techniques that you can use to interpret common ECG abnormalities: bundle-branch blocks, myocardial infarction (MI), and common dysrhythmias.
Probably the most common ECG abnormality you'll encounter is a bundle-branch block, which appears on the ECG as a wider-than-normal QRS complex (more than 0.12 second in duration). As you know, the cardiac impulse, originating in the sinoatrial (SA) node, normally travels through the bundle of His into the right and left bundle branches in the septum. The two bundle branches terminate in the Purkinje fibers. When the impulse reaches them, ventricular depolarization begins.
Normally the impulse is delivered to myocardial cells on both sides of the heart simultaneously, so depolarization begins at the same time on both sides of the heart. The result is a very fast, synchronous contraction of the ventricles. On ECG, the normal QRS complex duration from two intact bundle branches is 0.12 second or less (three or fewer small squares of the ECG paper).
A bundle-branch block occurs when one of the two bundle branches can't conduct the cardiac impulse to the myocardial cells. The most common cause of chronic bundle-branch block is ischemic heart disease. When an artery supplying the bundle branch narrows, the flow of oxygenated blood is reduced and the bundle branch can't conduct impulses normally.
A common cause of acute bundle-branch block is acute MI. If the MI involves the ventricular septum, one of the bundle branches may become infarcted, leading to a loss of conduction. Although uncommon, physical injury of a bundle branch during an invasive procedure such as cardiac cathe terization or heart surgery also may produce a bundle-branch block.1
* In a right bundle-branch block (RBBB), impulse conduction to the right ventricle is blocked. The cardiac impulse is conducted only to the left side of the heart where left ventricular depolarization begins. The right side of the heart depolarizes only in response to the cell-to-cell wave of depolarization that travels from the left side of the heart. This cell-to-cell depolarization is much slower than the normal synchronous depolarization; that's why the QRS complex is significantly wider than normal.
Examine lead V1 to identify an RBBB. In lead V1, the normal QRS complex consists of a small R wave, then a large S wave. As you recall, lead V1 looks at the right side of the heart. A small vector originating in the septum toward V1 creates a small upward R wave, then the predominant mean QRS vector creates the large S wave as the mean QRS vector flows away from lead V1.
In RBBB, the path of the mean QRS vector is changed due to left-to-right slow conduction; lead V1 now records a delayed R wave approaching it, resulting in a positive R wave. So the key identifier of RBBB in lead V1 is a QRS complex wider than 0.12 second with a delayed (longer than 0.07 second) positive main R wave. Some RBBBs may display a triphasic waveform ("rabbit ears") consisting of a small r wave, downward S wave, and a second, larger R wave.2
* In a left bundle-branch block (LBBB), electrical impulses don't reach the left side of the heart normally, so once again, synchronous depolarization of the ventricles doesn't occur. Depolarization begins in the right side of the heart and travels in a right-to-left direction via slow cell-to-cell depolarization. Lead V1 records the mean QRS vector directed away from its positive lead, resulting in a wide downward complex. Because the mean vector takes a relatively longer time to cross to the left side of the heart, the QRS complex is wider than 0.12 second. The key to recognizing an LBBB is a wide, downward S wave or rS wave in leads V1 and V2.
One of the most critical functions of the 12-lead ECG is to determine whether a patient is experiencing an acute MI. A series of predictable ECG changes that occur during an MI help you identify it quickly and initiate appropriate treatment.
Among one of the earliest changes in the ECG tracing is an elevation of the ST segment, indicating reversible myocardial injury (see Understanding ST-segment elevation). In a normal ECG, the ST segment is level with the tracing's baseline. When myocardial cells sustain injury from MI, depolarization is impaired, resulting in ST-segment elevation in the leads monitoring the affected areas of the heart. An ST-segment-elevation MI (STEMI), the most serious type of MI, is associated with more complications and a higher risk of death.3
The leads with ST-segment elevations identify the area of myocardial injury, so you can determine the region of the heart affected by knowing which area is monitored by which ECG lead. Let's look at some examples.
* Because leads II, III, and aVF all monitor the inferior (or bottom) wall of the heart from slightly different directions, they're usually described as the inferior leads. This area of the heart is perfused by the right coronary artery. A patient with a STEMI involving the inferior wall of the heart will have elevated ST segments in leads II, III, and aVF (see Inferior-wall STEMI).
* Another common infarct lead pattern occurs when an MI involves the intraventricular septum, which is perfused by the left anterior descending (LAD) coronary artery. In a septal MI, the leads monitoring the septum's electrical activity will display elevated ST segments. Precordial (or chest) leads V1 and V2, which are located on the anterior chest wall directly over the septum, most accurately monitor the septum's electrical activity. (These leads also are known as the septal leads.) The patient experiencing a septal MI will have ST-segment elevations in leads V1 and V2.
* Directly to the left of the septal area of the heart is the large frontal or anterior wall of the heart, which is also perfused by the LAD coronary artery. As the most muscular and powerful pumping wall of the heart, the anterior wall is responsible for a large proportion of cardiac output. Anatomically, leads V3 and V4 are located directly above the anterior wall of the heart and monitor its electrical activity. An anterior-wall STEMI will cause the ST segments in these leads to be elevated (see Anterior-wall STEMI).
* The lateral wall of the heart, perfused by the left circumflex artery, is located to the left of the anterior wall and follows the curve of the left lateral chest wall. Relatively muscular, it also contributes significantly to the heart's pumping ability. The ECG lead pattern that monitors the lateral wall's electrical activity is more complex because the lateral wall is monitored by a combination of precordial (chest) leads and frontal (limb) leads.
Chest leads V5 and V6 are located on the left lateral chest wall and monitor electrical activity by looking down at the lateral heart wall. Leads I and aVL also monitor the lateral wall's electrical activity. A patient with a lateral-wall STEMI will have ST-segment elevations in leads I, aVL, V5, and V6.
Although patients can have MIs affecting a single heart wall, such as a discrete septal MI or anterior-wall MI, the area of infarction may involve more than one area of the heart. In such a case, ST-segment elevations appear in the leads monitoring all of the involved areas. For example, if the infarction extends into both the septum and the anterior wall, the ST-segment elevations would appear in leads V1, V2, V3, and V4. The areas involved in the MI are reflected by the descriptive name; in this case, an anterioseptal MI. For information on how MI affects heart muscle, see Tissue damage after MI.
Now let's examine some common ECG rhythm abnormalities you may encounter in your practice, keeping in mind that you always treat the patient, not the rhythm. When you find an abnormal rhythm or a rhythm change, assess your patient and document level of consciousness, vital signs, chest pain, shortness of breath, and other signs and symptoms associated with the dysrhythmia. By using your assessment skills, nursing judgment, and knowledge of ECGs, you can determine the level of urgency of the situation.
* Sinus bradycardia is a sinus rhythm slower than the lower normal sinus rate of 60 beats/minute. The P waves, QRS complexes, and T waves are all normal. Sinus bradycardia is commonly caused by ischemic heart disease that causes the SA node to malfunction. Sinus bradycardia can also be caused by acute MI and some types of medications, such as beta-blockers. Well-conditioned athletes may have normal resting heart rates slower than 60 beats/minute. Assess your patient for hemodynamic stability if he has a new or profound sinus bradycardia. Contact the health care provider if your patient is symptomatic. Signs and symptoms that may accompany sinus bradycardia include hypotension, lethargy, fatigue, chest pain, and difficulty breathing. Be prepared to transfer your patient to the intensive care unit (ICU) for a temporary pacemaker.
* Sinus tachycardia is a sinus rhythm that's faster than the upper normal sinus rate of 100 beats/minute. Sinus tachycardia can produce heart rates of 100 to 150 beats/minute. At faster rates, the heart's myocardial oxygen demand increases, and a patient with preexisting heart disease may experience chest pain or other cardiac symptoms. Sinus tachycardia usually is related to a physiologic cause, such as fever, infection, pain, physical exertion, anxiety, hypoxia, or shock. If you can identify and treat the cause, the heart rate will usually decrease. To manage sinus tachycardia with an unknown cause, the health care provider may order a beta-blocker such as metoprolol or atenolol.4
* Atrial fibrillation (AF), one of the most common dysrhythmias you'll see in practice, has two predominant characteristics: an irregularly irregular heart rhythm and no meaningful P waves. Normally, after passive ventricular filling, the atria contract regularly and eject their load of blood into the ventricles (atrial kick). In AF, atrial kick is lost. Instead of contracting normally, the atria quiver due to random and chaotic depolarization of atrial cells. The random atrial depolarization is also responsible for the irregular ventricular rate, which can vary from 40 to 180 beats/minute. Atrial fibrillation has many causes, including atrial enlargement from chronic obstructive pulmonary disease or other lung disease, thyroid disease, ischemic heart disease, acute MI, stress or fatigue, and excessive use of caffeine, alcohol, or cigarettes.
You may first encounter AF during a routine vital signs check. If your patient has a new irregular heart rate, or has an abnormally fast or slow heart rate, obtain an order for a 12-lead ECG. Look for an irregularly irregular rhythm and f waves, the two hallmarks of AF. Perform a thorough physical assessment because patients can rapidly become hemodynamically unstable or develop worsening heart failure. If your patient has unstable or symptomatic AF, administer supplemental oxygen and establish or maintain intravenous (I.V.) access before transferring him to the ICU or telemetry unit for treatment with I.V. diltiazem or a beta-blocker.
If the patient is stable, the health care provider may order various oral medications to control or convert AF, such as digoxin, diltiazem, amiodarone, or metoprolol.
All patients with AF lasting more than 48 hours are at high risk for thrombus formation because of irregular blood flow in the atria. If released into the circulation, these thrombi can cause arterial obstruction resulting in life-threatening complications such as stroke. As ordered, administer I.V. heparin and start the patient on oral warfarin to prevent thrombus formation.5
* Premature ventricular contractions (PVCs) are characterized by a wide, abnormal QRS complex because conduction is through the ventricular tissue and not the His-Purkinje system. Look for a QRS greater than 0.12 second that appears large, abnormal, and premature (occurring before the next sinus beat). Caused by irritable ventricular tissue that depolarizes early and unpredictably, PVCs can be triggered by heart failure, electrolyte imbalances, stimulants such as caffeine, hypoxia, acute MI, mitral valve prolapse, thyroid disease, and injury or infarct of the myocardial tissue. Rare or isolated PVCs seldom require aggressive treatment. However, if you notice that the frequency of PVCs is increasing, or if you see new groups or "runs" of PVCs, contact the health care provider for further evaluation.
* Ventricular tachycardia (VT) is a very rapid (100 to 250 beats/minute) series of wide-complex ventricular depolarizations. In this dysrhythmia, abnormal ventricular tissue rapidly depolarizes, taking rhythm control away from the sinus node. Along with the rapid rate, VT is characterized by wide, bizarre QRS complexes usually followed by large T waves in the opposite direction of the major QRS deflection.
If your patient is unconscious, apneic, and pulseless, call a code and start cardiopulmonary resuscitation. If your patient has a pulse and is awake, treat this situation as a medical emergency. Call for the physician stat (and the rapid response team, if your facility has one), bring a crash cart with a monitor/defibrillator to the bedside, and prepare to transfer the patient to the ICU.
Like any new skill, interpreting 12-lead ECGs takes practice and commitment. Make a habit of reviewing your patients' ECGs routinely. Seek guidance from colleagues experienced in ECG interpretation, such as senior staff nurses, clinical nurse specialists, and clinical nurse-educators. Many physicians will also be happy to review an ECG with you if they know you're interested in learning to spot problems early.
With practice and experience, ECG interpretation will become a valuable nursing tool, helping you to recognize problems promptly and provide even better patient care.
Guy Goldich is assistant nurse-manager of the cardiac intensive care unit at Abington (Pa.) Memorial Hospital and an adjunct faculty member at the hospital's Dixon School of Nursing.
The author has disclosed that he has no significant relationship with or financial interest in any commercial companies that pertain to this educational activity.
1. Kinney M, et al. (eds). AACN Clinical Reference Guide to Critical Care Nursing, 4th edition. St. Louis, Mo., Mosby, Inc., 1998. [Context Link]
2. Conover MB. Understanding Electrocardiography, 8th edition. St. Louis, Mo., Mosby, Inc., 2002. [Context Link]
3. Huszar RJ. Basic Dysrhythmias: Interpretation & Management, 3rd edition. St. Louis, Mo., Mosby, Inc., 2002. [Context Link]
4. Urden LD, et al. Thelan's Critical Care Nursing: Diagnosis and Management, 5th edition. St. Louis, Mo., Mosby, Inc., 2005. [Context Link]
5. American Heart Association. (2005). Atrial fibrillation. Retrieved August 21, 2005, from http://www.americanheart.org/presenter.jhtml?identifier=1596. [Context Link]
Dubin D. Rapid Interpretation of EKGs, 6th edition. Tampa, Fla., Cover Publishing, 2000.
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