Electrocardiogram Identification

Christian Evans and Gary Brooks

Key Terms

Artifact

Electrical signaling is a primary method of communication, control, and regulation in the human body, and nowhere is this method employed with greater precision and elegance than in the heart. The rate, rhythm, and conduction of electrical signals are critical to cardiac function; these are the rhythmic electrical impulses that cause the mechanical contraction, or pumping, of the heart muscle. This electrical current is detectable by electrodes that are placed on the surface of the skin. The flow of current during the cardiac cycle is then recorded as the characteristic waveforms of the electrocardiogram (ECG; sometimes also called EKG). Mechanical events such as the contraction and relaxation of the myocardium are inferred from the waveforms produced by the ECG.

The ECG is an essential tool for the diagnosis and medical management of patients with cardiac disease. Information provided by the ECG may also assist the physical therapist in the assessment of a patient’s readiness for and response to physical activity. Physical therapists in many different practice environments have access to information afforded by the ECG. For example, in the intensive care unit or acute care setting or during cardiac rehabilitation, a patient’s ECG may be continuously monitored via telemetry (a remote monitoring system in which ECG signals are sent via radio waves to a distant receiver) or by a bedside unit. In both the acute and outpatient settings, past significant ECG recordings, as well as an interpretation, may be available in the medical record. Documentation accompanying a referral for outpatient physical therapy may also include a reference to the patient’s ECG. It is therefore crucial that all physical therapists have a basic understanding of the uses and limitations of the ECG in their practices.

As an example of how an understanding of ECG interpretation may be useful for physical therapists, consider the following scenario. A physical therapist in a cardiac intensive care unit (CCU) initiates exercise for a patient recovering from open-heart surgery. The patient’s ECG has been stable throughout the postoperative recovery phase, but the patient has not yet been challenged with moderate intensity activity or exercise. The therapist gets the patient up and begins an appropriate level of exercise; however, with this greater demand on the heart, the patient develops an exercise-induced dysrhythmia. This abnormal rhythm may be mild and fairly benign, or it could be malignant or life-threatening. If the physical therapist is able to interpret the ECG accurately in this situation, this dysrhythmia may be caught and then referred to and treated by the physician. If the dysrhythmia is not recognized, a less favorable outcome may occur.

This chapter briefly reviews the basic anatomy and physiology of the myocardial conduction system as it relates to the ECG. The configuration of the normal ECG is presented and discussed, along with several methods of quickly determining heart rate and rhythm from an electrocardiographic record, or ECG “strip.” Some of the more common dysrhythmias are examined, as are some other pathological features. Throughout the chapter, the uses and limitations of the ECG in physical therapy practice are highlighted.

Physiology and Anatomy of the Conduction System

Cardiac Action Potential

The cardiac action potential is generated by the flow of ions across myocardial cell membranes; it has a distinctive shape and five phases (phases 0 to 4).¹ In the cell’s resting state, a negative membrane potential exists, based on the selective permeability of the cardiac cell membrane and the relative concentrations of sodium (Na⁺), calcium (Ca²⁺), and potassium (K⁺) ions in the internal and external cellular environments. The relative time-sensitive ionic currents for each species are color-coded and labeled in Figure 12-1, and the cardiac action potential is superimposed over the individual currents that compose it. At rest, a typical ventricular cardiomyocyte membrane is primarily permeable only to K⁺ ions, allowing the movement of K⁺ out of the cell until the charge inside is approximately −90 mV, relative to the charge outside. This is the resting membrane potential of the cardiomyocyte and is close to the equilibrium potential for K⁺. The membrane potential changes rapidly at the onset of depolarization, with the opening of Na⁺ and Ca²⁺ channels, allowing these ions to cross the membrane and enter the cell. Calcium then becomes available for contraction of cardiac muscle myofibrils.

Fig. 12-1 Relationship of an individual ventricular cardiomyocyte action potential to the ECG. A, The time-dependent ionic currents (I_K, I_Na, and I_Ca,) of an individual ventricular cardiac cell that determine the shape, amplitude, and duration of the cell’s action potential (shown in red). The action potential can be broken down into five distinct phases (0-4). B, The QRS complex and T wave of the ECG are temporally related to the cardiac action potential and the phases. However, the ECG also reflects the anatomical orientation of the wave of depolarization through the heart and the location of the recording electrodes.

During depolarization, the membrane’s potential becomes positive and the cell contracts. As in skeletal muscle, the Na+ channels are fast-opening and fast-closing mechanisms, allowing Na+ to rapidly enter the myocardial cell on depolarization (referred to as phase 0 of the cardiac action potential in Figure 12-1). Unlike skeletal muscle, however, cardiac muscle has a prolonged action potential as a result of the slower and extended opening of the Ca²⁺ channels. After initial depolarization, some K⁺ channels remain open while others close, and repolarization begins (phase 1) as a result of outward K⁺ current flowing through the open K⁺ channels. A plateau phase (phase 2) of the action potential exists, during which the outward flow of K⁺ ions is balanced by an inward flow of Ca²⁺ ions. This prolongs depolarization and delays return to the resting membrane potential. Closure of the slow Ca²⁺ channels at onset of repolarization is accompanied by the opening of additional K⁺ channels, causing a rapid outflow of K⁺, which completes repolarization (phase 3 in Figure 12-1), restoring resting negative membrane potential. During the cell’s resting phase (phase 4 of Figure 12-1), Na⁺ and Ca²⁺ are actively pumped out of the cell, and K⁺ is pumped into the cell, restoring the ionic gradients needed for repolarization.^1,2,3

Each cell has an absolute refractory period during depolarization, meaning that an additional stimulus will not cause an additional depolarization. A brief but important relative refractory period follows depolarization, during which a stimulus of greater than normal intensity is necessary to depolarize the cell again. The refractory period of atrial cells is significantly shorter than that of ventricular cells, allowing a more rapid intrinsic atrial rhythm than intrinsic ventricular rhythm. Therefore atrial rhythms pace the heart, including the ventricles, given intact atrioventricular (AV) conduction.

From Figure 12-1 it can be seen that certain ionic currents contribute to particular phases of the cardiac action potential. The Na⁺ current is the predominant factor in the initial depolarization, whereas the Ca²⁺ current is important in the plateau phase, and the K⁺ currents are important in the duration of the action potential and in repolarization. Many of the drugs used to treat dysrhythmias work on the channels for one or more of these three ions and affect their permeability. Furthermore, the electrical current produced by these ionic currents is transmitted through the conductive tissues surrounding the heart. The “wave” of depolarization that is propagated through the conduction system and contractile tissue of the heart, as well as repolarization, which takes place in a particular spatial manner, are detectable by the surface electrodes of the ECG.

Conduction System

It is the conduction system that initiates and rapidly transmits impulses to specific locations within the myocardium (the atria, apex, septum, and lateral wall), allowing for effective, coordinated myocardial contraction and pumping. The conduction system is composed of specialized cardiac muscle that contracts minimally because it contains few contractile myofibrils. Any portion of the conduction system is capable of self-excitation and may act as a pacemaker, generating action potentials. However, because of the intrinsically more rapid rate of spontaneous depolarization of the sinoatrial (SA) node, it normally acts as the heart’s pacemaker. The rate of depolarization of the SA node determines the heart rate. In the absence of an impulse from the SA node, the AV node depolarizes spontaneously, taking over as pacemaker, with the important difference that the rate of depolarization is lower than that of the SA node.

Figure 12-2 displays the anatomical association of the cardiac electrical conduction system with its components on the ECG. Atrial depolarization is initiated by a spontaneously generated impulse that originates in the SA node. The impulse is then transmitted throughout the atrial muscle, resulting in atrial contraction. The event is recorded as the P wave of the ECG. The impulse is also transmitted, via rapidly conducting internodal pathways, to the AV node. Atrial repolarization is not recorded by the ECG because it occurs during ventricular depolarization.

Fig. 12-2 Relationship of ECG complex to conduction pathway. A, The sequence of events in depolarization: the wave of depolarization spreads from the SA node through the atria to the AV node. After a delay in the AV node, it travels through the bundle of His to the Purkinje fibers to the ventricular myocardium. The delay at the AV node accounts for the duration of the P-R interval. QRS duration is dependent on normal propagation from the atria and an intact ventricular conduction system. B, Ventricular repolarization.

Impulse conduction slows within the AV node considerably, resulting in a delaying of the impulse before it reaches the ventricular conduction system. The pause in impulse propagation allows the atria to contract and fill the ventricles with blood. The P-R interval of the ECG represents this period between the onset of atrial depolarization and the onset of ventricular depolarization. Normally the P-R interval lasts between 0.12 and 0.20 second.⁴

Following passage through the AV node, the impulse continues to the AV bundle (bundle of His) and then to Purkinje fibers, which transmit the impulse rapidly to the ventricular endocardium. Ventricular depolarization corresponds to phase 0 of the cardiac action potential (see Figure 12-1) and is represented in the ECG by the QRS complex. The depolarization wave propagates relatively slowly throughout the ventricular myocardium. The span of time elapsing during ventricular depolarization is reflected by the QRS interval, which normally ranges between 0.06 and 0.1 seconds. Ventricular depolarization originates in the interventricular septum, creating the Q wave, which is normally small or absent, depending on the lead. The depolarization wave next spreads to the apex and then to the right and left ventricles, causing the R and S waves. Depolarization also propagates in an endocardial to epicardial direction within the ventricles.^2,3 A normal QRS duration indicates that the impulse originated in the SA node or a region above the AV node (supraventricular). A long QRS interval (≥0.1 second) suggests that the impulse arose from the ventricle or originated abnormally in supraventricular tissue. The normal sequence of depolarization is as follows: SA node to AV node to bundle of His to Purkinje fibers to the ventricular myocardium. When this sequence is followed, the ECG correlates with the mechanical events of the cardiac cycle as shown in Figure 4-13.

After ventricular depolarization, the ECG deflection returns to baseline, and this pause in electrical activity corresponds with the plateau phase (phase 2) of the cardiac action potential. Ventricular repolarization is represented by the T wave and corresponds to phase 3 of the cardiac action potential. The configuration of the S-T segment is an important marker of myocardial ischemia or infarction. Following the T wave, a U wave may also be present. The source of the U wave is not well understood.⁵ Although U wave inversion may indicate ischemia involving the left ventricular wall,⁶ it is not a unique marker and is not as sensitive as S-T segment changes in predicting ischemia; therefore it is not a useful clinical marker.⁷

Within the ventricle, individual cardiomyocytes are in direct communication with each other via gap junctions. This facilitates rapid spread of the wave of depolarization from cell to cell, allowing the right and left ventricular heart muscle to function as a syncytium, or a single pumping unit.⁸ Note that the ventricles remain in a state of contraction until slightly after repolarization. This period of contraction corresponds to the Q-T interval on the ECG. Diastole, therefore, begins subsequent to the end of the T wave and continues until the next ventricular depolarization. Note also that atrial depolarization and contraction occur during diastole.

Electrocardiogram

Recording the Electrocardiogram

Before examining the timing of the wave forms and the rhythms of the ECG, a basic understanding of the principles of electrocardiography is needed. A standard 12-lead configuration is used for the diagnosis and medical management of cardiac conditions (Figure 12-3): six leads record the electrical signals in the frontal plane, and six leads record signals in the transverse plane. The placements of the 10 electrodes for a 12-lead ECG are shown in Figure 12-4 (note that 12 electrodes are not necessary because some leads serve a dual purpose).

The frontal-plane leads include three standard bipolar limb leads, referred to as leads I, II, and III, and three augmented unipolar limb leads, referred to as aVR (right arm), aVL (left arm), and aVF (left leg). These two sets of leads share the same electrodes but view the electrical activity of the heart from different perspectives. The bipolar leads have a single positive and a single negative electrode and record the difference in electrical potential between them. The augmented limb leads have a single positive electrode and derive the negative electrode from the combination of the other electrodes. The standard limb leads form a triangle, known as the Einthoven’s triangle, around the heart that allows for advanced calculations related to the net vector of depolarization, or the axis of the heart (an index of the cardiac mass and position). If only a single lead is recorded, standard limb lead II is often chosen because all of the deflections are typically upright.⁴

The transverse-plane leads are referred to as the precordial, or chest, leads. These six leads form a semicircle around the anterior aspect of the heart; their placement is described in Figure 12-4. In addition to the three electrodes for the limb leads and the six electrodes for the chest leads, a 10th electrode that serves as a neutral ground must be used to reduce artifacts and stabilize the baseline. Imagine that each of the 12 leads “views” the heart from a different angle, therefore recording events in different locations of the heart in different ways. By convention, the waveform on the ECG is positive (upward) as current travels toward a positive electrode or lead and is negative (downward) when current travels away from a lead. Other lead configurations may be used for exercise testing.⁹ Single-lead monitoring is commonly used during exercise training or in the acute care settings.