FOR THE HEART TO contract and pump blood throughout the body, it needs an electrical stimulus. Generation and transmission of electrical impulses depend on four characteristics of cardiac cells:
- automaticity—the cell's ability to spontaneously initiate an electrical impulse
- excitability—the cell's ability to respond to an electrical stimulus
- conductivity—the cell's ability to transmit an electrical impulse
- contractility—the cell's ability to contract after receiving an electrical stimulus.
As the electrical impulses are transmitted, the cardiac cells undergo cycles of depolarization and repolarization.1 The electrical activity of depolarization and repolarization results in the mechanical activity of contraction and relaxation. This electrical activity can be seen on a 12-lead ECG or on a continuous cardiac monitor.
The heart has four chambers. The two upper chambers are called the atria and the two lower chambers are called the ventricles. The right atrium receives unoxygenated (venous) blood from the body through the superior and inferior venae cavae and from the coronary sinus, which drains blood from the heart. The left atrium receives oxygenated (arterial) blood from the lungs through the four pulmonary veins. From the atria, the blood flows to the ventricles. About 70% of the blood from the atria passively enters the ventricles before atrial contraction. When the atria contract, an additional 30% of its blood enters the ventricles. This is referred to as the “atrial kick.”2
The right ventricle receives unoxygenated blood from the right atrium and pumps it through the pulmonary artery to the lungs, where oxygenation takes place. The left ventricle receives oxygenated blood from the left atrium and pumps it to the body through the aorta (See Normal heart structures).
The body's cells depend on the heart pumping enough oxygenated blood to meet their energy needs.2 To pump efficiently, the heart needs electricity. This is where the cardiac conduction system comes into play.
Current: It's electric
When cardiac cells are at rest, they're electrically polarized, that is, no electrical activity is taking place. Once the cell is stimulated, ions (potassium, sodium, calcium, and magnesium) are exchanged across the cell membrane and cause an action potential. This stimulus passes from cell to cell and results in depolarization (an electrical event), and ultimately causes the myocardial filaments to shorten, which causes a contraction (a mechanical event). After depolarization is complete, the electrical charges in the cell reverse, and it returns to its resting state. This process is called repolarization.1
The electrical conduction system lets electricity pass through the heart to ultimately cause a myocardial contraction. This is possible because the heart is made of two types of cells: myocardial cells and pacemaker cells.3 When a wave of depolarization reaches a myocardial cell, ions are released within the cell, causing it to contract. Pacemaker cells can spontaneously generate an impulse. Pacemaker cells are the specialized cells of the sinoatrial (SA) node, atrioventricular (AV) node, and Purkinje fibers; however, pacemaker cells are present all along the heart's electrical conduction system. Any one of these pacemaker cells can spontaneously generate an impulse at a faster rate than the SA node. This enhanced automaticity of a pacemaker cell other than those located in the SA node may result in a dysrhythmia.
The SA node is considered the heart's normal pacemaker and spontaneously generates an impulse between 60 and 100 beats per minute. The impulse then travels through the atria along the interatrial tracts and along the internodal tracts to the AV node. Once the impulse reaches the AV node, the AV node instantaneously delays the impulse to let the ventricles fill with blood. The AV node also acts as a gatekeeper for impulses getting through to the ventricles, and it doesn't always let every impulse get through. This gatekeeper function is especially important in atrial dysrhythmias, such as atrial fibrillation and atrial flutter, because the ventricles would otherwise contract extremely fast. Once the impulse passes through the AV node, it travels down a common path called the bundle of His. From here, the impulse passes through the ventricles via the right and left bundle branches to the Purkinje fibers. Any deviation from this pathway results in cardiac dysrhythmias.
The conduction system has some built-in compensatory mechanisms. If the SA node fails to fire, the AV junction (made up of the AV node and bundle of His) will generate an impulse a little less efficiently at a rate of 40 to 60 beats per minute. If the SA node and the AV node fail to fire, an impulse will be generated somewhere in the ventricles. If the ventricles pace the heart, the heart rate will be 20 to 40 beats per minute. These compensatory mechanisms also come into play when electrical impulses are blocked along the normal conduction pathways.
Understanding the ECG
A cardiac cycle consists of one heartbeat or one PQRST sequence, which consists of a P wave, a QRS complex, and a T wave. The P wave represents atrial depolarization—the passing of electricity through the atria. This impulse results in atrial contraction. If the impulse is being generated from the SA node, a P wave should appear before every QRS complex, but it may look different depending on what lead is being viewed. The P wave on an ECG tracing usually is:
- round and upright in leads I, II, aVF, and V2 to V6
- usually positive, but may vary in leads III and aVL
- negative or inverted in lead aVR
- biphasic or variable in lead V1.1
If P waves are peaked, notched, or enlarged, the patient may have atrial hypertrophy as a result of chronic obstructive pulmonary disease or heart failure. If the P wave is inverted (in a lead where it's normally upright), hidden, or follows the QRS complex, the impulse was generated by the AV junction and not the SA node. If there are more P waves than QRS complexes, there's a problem getting the impulse through the AV node to the ventricles and the patient has some type of AV block. The QRS complex represents ventricular depolarization that results in ventricular contraction. Normally, the QRS complex, like the P wave, looks different depending on what lead is being viewed. QRS complex is:
- positive in leads I, II, III, aVL, aVF, and V4 to V6
- negative in leads aVR and V1 to V3.1
The QRS normally has a narrow configuration (0.06 to 0.10 second). If the QRS complex is wide (greater than 0.12 second), the impulse is likely to have been generated from the ventricles. In this case, the P wave usually is absent because atrial depolarization doesn't occur. If the QRS complex is wide and is preceded by a P wave, the impulse is likely to have been generated from an area above the ventricles, but it's delayed as it travels down the right and left bundle branches to the Purkinje fibers. This delay is due to some type of bundle branch block.
The T wave represents ventricular repolarization—the time in which the ventricles are getting ready to receive another impulse. The T wave should follow the QRS complex and be:
- round and upright in leads I, II, and V3 to V6
- inverted in lead aVR
- variable in all other leads.1
Tall, peaked, or notched T waves may be a sign of hyperkalemia or pericarditis. Flattened T waves may indicate hypokalemia.2 If the T wave flips and becomes inverted in a lead where it's normally upright, it's likely the patient is experiencing an ischemic event and part of his myocardium isn't receiving enough oxygen. If this isn't reversed, tissue death will occur, resulting in a myocardial infarction.
Segment by segment
Certain segments and intervals of the cardiac cycle are also evaluated. The PR interval is the time it takes the impulse to travel from the SA node down to the ventricles. It's measured from the beginning of the P wave to the beginning of the QRS complex, and should be from 0.12 to 0.20 second. If the PR interval is short (less than 0.12 second) and the ventricular rate is within normal limits, the AV node probably generated the impulse. If the PR interval is prolonged, there's a conduction delay through the atria or AV junction that can result from digoxin toxicity or heart block.
The ST segment is the part of the cardiac cycle that extends from the end of the QRS complex to the beginning of the T wave. This segment should lie on the baseline (isoelectric line). The isoelectric line can be determined by looking at the flat line after the P wave and before the QRS complex. A change in the ST segment may indicate myocardial injury or ischemia. If it's depressed below the baseline, there's probably myocardial ischemia. If the ST segment is elevated, there may be myocardial injury or pericarditis.1
The QT interval represents the time between ventricular depolarization and repolarization. It's the part of the cardiac cycle that extends from the beginning of the QRS complex to the end of the T wave. The QT interval typically measures between 0.36 and 0.44 second, but will naturally shorten as the heart rate increases. This interval is monitored frequently to detect any lengthening of this process. A prolonged QT interval puts the patient at risk for sudden death related to polymorphic ventricular tachycardia (torsades de pointes) or ventricular fibrillation.2 Often the QT interval can be measured more accurately if it's corrected for the patient's heart rate. The corrected QT interval is written as QTc.2
Path to good conduction
If the SA node generates an impulse between 60 and 100 beats per minute and it follows the normal conduction pathway, the rhythm is a normal sinus rhythm. (See Normal sinus rhythm.) Normal sinus rhythm is the standard against which all other rhythms are compared, so you need to understand the normal cardiac conduction system before trying to interpret abnormal rhythms. Such knowledge will also help you effectively care for patients with cardiac conditions.
1. ECG Interpretation Made Incredibly Easy!
3rd edition. Philadelphia, Pa.: Lippincott Williams & Wilkins; 2005.
2. Aehlert B. ECGs Made Easy
. 3rd edition. St. Louis, Mo.: Mosby; 2006.
3. Thaler MS. The Only EKG Book You'll Ever Need
. 5th edition. Philadelphia, Pa.: Lippincott Williams & Wilkins; 2007.