Conduction System

Four properties of cardiac cells enable the conduction system to start an electrical impulse, send it through the cardiac tissue, and stimulate muscle contraction (Table 36-1). The heart’s conduction system consists of specialized neuromuscular tissue located throughout the heart (Fig. 32-4, A). A normal cardiac impulse begins in the sinoatrial (SA) node in the upper right atrium. It spreads over the atrial myocardium via interatrial and internodal pathways, causing atrial contraction. The impulse then travels to the atrioventricular (AV) node, through the bundle of His, and down the left and right bundle branches. It ends in the Purkinje fibers, which transmit the impulse to the ventricles.

Nervous Control of the Heart

The autonomic nervous system plays an important role in the rate of impulse formation, the speed of conduction, and the strength of cardiac contraction. The components of the autonomic nervous system that affect the heart are the vagus nerve fibers of the parasympathetic nervous system and nerve fibers of the sympathetic nervous system.

Stimulation of the vagus nerve causes a decreased rate of firing of the SA node and slowed impulse conduction of the AV node. Stimulation of the sympathetic nerves increases SA node firing, AV node impulse conduction, and cardiac contractility.²

Electrocardiographic Monitoring

The electrocardiogram (ECG) is a graphic tracing of the electrical impulses produced in the heart. The waveforms on the ECG represent electrical activity produced by the movement of ions across the membranes of myocardial cells, representing depolarization and repolarization.

The membrane of a cardiac cell is semipermeable. This allows it to maintain a high concentration of potassium and a low concentration of sodium inside the cell. Outside the cell a high concentration of sodium and a low concentration of potassium exist. The inside of the cell, when at rest, or in the polarized state, is negative compared with the outside. When a cell or groups of cells are stimulated, the cell membrane changes its permeability. This allows sodium to move rapidly into the cell, making the inside of the cell positive compared with the outside (depolarization). A slower movement of ions across the membrane restores the cell to the polarized state, called repolarization. Fig. 36-1 describes the phases of the cardiac action potential.

The ECG has 12 recording leads. Six of the leads measure electrical forces in the frontal plane. These are bipolar (positive or negative) leads I, II, and III; and unipolar (positive) leads aVr, aVl, and aVf (Fig. 36-2, A and B). The remaining six unipolar leads (V₁ through V₆) measure the electrical forces in the horizontal plane (precordial leads) (Fig. 36-2, C). The 12-lead ECG may show changes suggesting structural changes, conduction disturbances, damage (e.g., ischemia, infarction), electrolyte imbalance, or drug toxicity. Obtaining 12 ECG views of the heart is also helpful in the assessment of dysrhythmias. Fig. 36-3 is an example of a normal 12-lead ECG.

One or more ECG leads can be used to continuously monitor a patient. The most common leads selected are leads II and V₁ (Fig. 36-4). A modified chest lead (MCL₁) is used when only three leads are available for monitoring (eFig. 36-1, showing MCL₁ lead placement, is available on the website for this chapter). MCL₁ is similar to V₁. Accurate interpretation of an ECG depends on the correct placement of the leads on the patient. The monitoring leads used are determined by the patient’s clinical status.^3,4

The monitor continuously displays the heart rhythm. ECG paper attached to the monitor records the ECG (i.e., rhythm strip). This provides a record of the patient’s rhythm. It also allows for measurement of complexes and intervals and for assessment of dysrhythmias.

To correctly interpret an ECG, you measure time and voltage on the ECG paper. ECG paper consists of large (heavy lines) and small (light lines) squares (Fig. 36-5). Each large square consists of 25 smaller squares (five horizontal and five vertical). Horizontally, each small square (1 mm) represents 0.04 second. This means that one large square equals 0.20 second and that 300 large squares equal 1 minute. Vertically, each small square (1 mm) represents 0.1 millivolt (mV). This means that one large square equals 0.5 mV. Use these squares to calculate the heart rate (HR) and measure time intervals for the different ECG complexes.

You can use a variety of methods to calculate the HR from an ECG. The most accurate way is to count the number of QRS complexes in 1 minute. However, because this method is time consuming, a simpler process is used. Note that every 3 seconds a marker appears on the ECG paper (see Fig. 36-5). Count the number of R-R intervals in 6 seconds and multiply that number by 10. (An R wave is the first upward [or positive] wave of the QRS complex.) This is the estimated number of beats per minute (Fig. 36-6).

Another method is to count the number of small squares between one R-R interval. Divide this number into 1500 to get the HR. Last, you can count the number of large squares between one R-R interval and divide this number into 300 to get the HR (see Fig. 36-6). All these methods are most accurate when the rhythm is regular.¹

An additional way to measure distances on the ECG strip is to use calipers. Many times a P or an R wave will not fall directly on a light or heavy line. Place the fine points of the calipers exactly on the parts you need to measure and then move to another part of the strip for a more precise time measurement.

ECG leads consist of an electrode pad fixed with electrical conductive gel. Before placing these on the patient, you must properly prepare the skin. Clip excessive hair on the chest wall with scissors. Gently rub the skin with dry gauze until slightly pink. If the skin is oily, wipe with alcohol first. If the patient is diaphoretic, apply a skin protectant before placing the electrode.

You will see artifact on the monitor when leads and electrodes are not secure, or when there is muscle activity (e.g., shivering) or electrical interference. Artifact is a distortion of the baseline and waveforms seen on the ECG (Fig. 36-7). Accurate interpretation of heart rhythm is difficult when artifact is present. If artifact occurs, check the connections in the equipment. You may need to replace the electrodes if the conductive gel has dried out.

Assessment of Cardiac Rhythm

When assessing the cardiac rhythm, make an accurate interpretation and immediately evaluate the patient’s clinical status. Assess the patient’s hemodynamic response to any change in rhythm. This information will guide the selection of your interventions. Determination of the cause of dysrhythmias is a priority. For example, tachycardias may be the result of fever and may cause a decrease in cardiac output (CO) and hypotension. Electrolyte disturbances can cause dysrhythmias and, if not treated, can lead to life-threatening dysrhythmias. At all times, the patient, not the “monitor,” must be assessed and treated.

Normal sinus rhythm refers to a rhythm that starts in the SA node at a rate of 60 to 100 times per minute and follows the normal conduction pathway (Fig. 36-8). Fig. 36-9 shows the components of a normal ECG tracing. Table 36-2 describes ECG waveforms and intervals, normal durations, and possible sources of disturbances in these features.

Electrophysiologic Mechanisms of Dysrhythmias

Dysrhythmias result from disorders of impulse formation, conduction of impulses, or both. The heart has specialized cells in the SA node, atria, AV node, and bundle of His and Purkinje fibers (His-Purkinje system), which can fire (discharge) spontaneously. This is termed automaticity. Normally, the SA node is the pacemaker of the heart. It spontaneously fires 60 to 100 times per minute (Table 36-3). A secondary pacemaker from another site may fire in two ways. If the SA node fires more slowly than a secondary pacemaker, the electrical signals from the secondary pacemaker may “escape.” The secondary pacemaker will then fire automatically at its intrinsic rate. These secondary pacemakers may start from the AV node at a rate of 40 to 60 times per minute or the His-Purkinje system at a rate of 20 to 40 times per minute.

Another way that secondary pacemakers can start is when they fire more rapidly than the normal pacemaker of the SA node. Triggered beats (early or late) may come from an ectopic focus or accessory pathway (area outside the normal conduction pathway) in the atria, AV node, or ventricles. This results in a dysrhythmia, which replaces the normal sinus rhythm.

The impulse started by the SA node or an ectopic focus must be conducted to the entire heart. The property of myocardial tissue that allows it to be depolarized by a stimulus is called excitability. This is an important part of the transmission of the impulse from one cell to another. The level of excitability is determined by the length of time after depolarization that the tissues can be restimulated. The recovery period after stimulation is the refractory phase or period. The absolute refractory phase or period occurs when excitability is zero and the heart cannot be stimulated. The relative refractory period occurs slightly later in the cycle, and excitability is more likely. In states of full excitability, the heart is completely recovered. Fig. 36-10 shows the relationship between the refractory period and the ECG.

If conduction is depressed and some areas of the heart are blocked (e.g., by infarction), the unblocked areas are activated earlier than the blocked areas. When the block is unidirectional, this uneven conduction may allow the initial impulse to reenter areas that were previously not excitable but have recovered. The reentering impulse may be able to depolarize the atria and ventricles, causing a premature beat. If the reentrant excitation continues, tachycardia occurs.

Evaluation of Dysrhythmias

Dysrhythmias occur as the result of various abnormalities and disease states. The cause of a dysrhythmia influences the patient’s treatment. Table 36-4 presents common causes of dysrhythmias. Table 36-5 presents a systematic approach to assessing a heart rhythm.

Dysrhythmias occurring in nonmonitored settings present management challenges. If the patient becomes symptomatic (e.g., chest pain), determination of the rhythm by cardiac monitoring is a high priority. Activate the emergency medical services (EMS) system. Table 36-6 outlines emergency care of the patient with a dysrhythmia.

In addition to continuous ECG monitoring during hospitalization, several other tests can assess dysrhythmias and the effectiveness of antidysrhythmia drug therapy. An electrophysiologic study, Holter monitoring, event monitoring (or loop recorder), exercise treadmill testing, and signal-averaged ECG can be performed on an inpatient or outpatient basis (see Table 32-6 for nursing care related to these tests).

An electrophysiologic study (EPS) can identify the causes of heart blocks, tachydysrhythmias (dysrhythmias with rates greater than 100 beats/minute), bradydysrhythmias (dysrhythmias with rates less than 60 beats/minute), and syncope. An EPS study can also locate accessory pathways and determine the effectiveness of antidysrhythmia drugs.

The Holter monitor continuously records the ECG while the patient is ambulatory and performing daily activities. The patient keeps a diary and records activities and any symptoms. Events in the diary are correlated with any dysrhythmias seen on the ECG. Use of event monitors has improved the evaluation of dysrhythmias in outpatients. Event monitors are recorders that the patient activates only when he or she experiences symptoms. New technology using smart phones can obtain and save ECG recordings and even detect atrial fibrillation.

Exercise treadmill testing evaluates the patient’s heart rhythm during exercise. If exercise-induced dysrhythmias or ECG changes occur, they are analyzed and drug therapy evaluated.

The signal-averaged ECG identifies late potentials strongly suggesting that the patient may be at risk for developing serious ventricular dysrhythmias. Chapter 32 discusses the diagnostic procedures for assessment of the cardiovascular system and related nursing care.

Types of Dysrhythmias

Figs. 36-11 to 36-19 provide examples of the ECG tracings of common dysrhythmias. Table 36-7 presents the descriptive characteristics.

Sinus Bradycardia.

In sinus bradycardia the conduction pathway is the same as that in sinus rhythm but the SA node fires at a rate less than 60 beats/minute (Fig. 36-11, A). Symptomatic bradycardia refers to an HR that is less than 60 beats/minute and is inadequate for the patient’s condition, causing the patient to experience symptoms (e.g., chest pain, syncope).

Clinical Associations.

Sinus bradycardia may be a normal sinus rhythm in aerobically trained athletes and in some people during sleep. It also occurs in response to carotid sinus massage, Valsalva maneuver, hypothermia, increased intraocular pressure, vagal stimulation, and administration of certain drugs (e.g., β-adrenergic blockers, calcium channel blockers). Common disease states associated with sinus bradycardia are hypothyroidism, increased intracranial pressure, hypoglycemia, and inferior myocardial infarction (MI).

ECG Characteristics.

In sinus bradycardia, HR is less than 60 beats/minute and the rhythm is regular. The P wave precedes each QRS complex and has a normal shape and duration. The PR interval is normal, and the QRS complex has a normal shape and duration.

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