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26Electrocardiograms/ Basic Rhythm Interpretation

June 23, 2024

Electrocardiograms/ Basic Rhythm Interpretation

Cardiovascular System

ANATOMY AND PHYSIOLOGY REVIEW

Heart

Structure. The human heart is a cone-shaped, hollow, muscular organ located in the mediastinum between the lungs. It is approximately the size of an adult fist. The heart rests on the diaphragm, tilting forward and to the left in the client’s chest. This small organ must pump continuously. Each beat of the heart pumps approximately 60 mL of blood, or approximately 5 L/min. During strenuous physical activity, the heart can double the amount of blood pumped to meet the increased oxygeeeds of the peripheral tissues.

Surface anatomy of the heart.

The heart is encapsulated by a protective covering called the pericardium. Cardiac muscle tissue is composed of three layers: epicardium, myocardium, and endocardium. The epicardium, the outer surface, is a thin, transparent tissue. The myocardium, the middle layer, is composed of striated muscle fibers interlaced into bundles. This layer is responsible for the contractile force of the heart. The innermost layer, the endocardium, is composed of endothelial tissue. This tissue lines the inside of the chambers of the heart and covers the four heart valves.

CHAMBERS OF THE HEART

A muscular wall (septum), separates the heart into two halves: right and left. Each half has an upper chamber (atrium) and a lower chamber (ventricle).

RIGHT SIDE. The right atrium is a thin-walled structure that receives deoxygenated venous blood (venous return) from all peripheral tissues by way of the superior and inferior venae cavae and from the heart muscle by way of the coronary sinus.

Most of this venous return flows passively from the right atrium, through the opened tricuspid valve, and to the right ventricle during ventricular diastole, or filling. The remaining venous return is actively propelled by the right atrium into the right ventricle during atrial systole, or contraction.

The right ventricle is a flat muscular pump located behind the sternum. The right ventricle generates enough pressure (approximately 25 mm Hg) to close the tricuspid valve, open the pulmonic valve, and propel blood into the pulmonary artery and the lungs. The workload of the right ventricle is light compared with that of the left ventricle because the pulmonary system is a low-pressure system, which imposes less resistance to flow.

LEFT SIDE. After blood is reoxygenated in the lungs, it flows freely from the four pulmonary veins into the left atrium. Blood then flows through an opened mitral valve into the left ventricle during ventricular diastole. When the left ventricle is almost full, the left atrium contracts, pumping the remaining blood volume into the left ventricle. With systolic contraction, the left ventricle generates enough pressure (approximately 120 mm Hg) to close the mitral valve and open the aortic valve. Blood is propelled into the aorta and into thesystemic arterial circulation.

The left ventricle is ellipsoid in shape and is the largest and most muscular chamber of the heart. Its wall is two to three times the thickness of the right ventricular wall. The left ventricle must generate a higher pressure than the right ventricle because it must contract against a high-pressure systemic circulation, which imposes a greater resistance to flow.

Blood is propelled from the aorta throughout the systemic circulation to the various tissues of the body; blood returns to the right atrium because of pressure differences. The pressure of blood in the aorta of a young adult averages approximately 100 to 120 mm Hg, whereas the pressure of blood in the right atrium averages about 0 to 5 mm Hg. These differences in pressure produce a pressure gradient, with blood flowing from an area of higher pressure to an area of lower pressure. The heart and vascular structures are responsible for maintaining these pressures.

HEART VALVES

The four cardiac valves are responsible for maintaining the forward flow of blood through the chambers of the heart. These valves open and close passively in response to pressure and volume changes within the cardiac chambers. The cardiac valves are classified into two types: atrioventricular (AV) valves and semilunar valves. Both AV valves are supported by chordae tendineae, which keep them from everting into the atria during systole.

ATRIOVENTRICULAR VALVES. The AV valves separate the atria from the ventricles. The tricuspid valve is composed of three leaflets and separates the right atrium from the right ventricle. The mitral (bicuspid) valve is composed of two leaflets and separates the left atrium from the left ventricle.

During ventricular diastole, the valves act as funnels and facilitate the flow of blood from the atria to the ventricles. During systole, the valves close to prevent the backflow (re-gurgitation) of blood into the atria.

SEMILUNAR VALVES. There are two semilunar valves: the pulmonic valve and the aortic valve. The pulmonic valve separates the right ventricle from the pulmonary artery. The aortic valve separates the left ventricle from the aorta. Each semilunar valve consists of three cuplike cusps, or pockets, around the inside wall of the artery. These cusps prevent blood from flowing back into the ventricles during ventricular diastole. During ventricular systole, these valves are open to permit blood flow into the pulmonary artery and the aorta.

CORONARY ARTERIES

The heart muscle receives blood to meet its metabolic needs through the coronary arterial system . The coronary arteries originate from an area on the aorta just beyond the aortic valve. There are two main coronary arteries: the left coronary artery (LCA) and the right coronary artery (RCA). Coronary artery blood flow to the myocardium occurs primarily during diastole, when coronary vascular resistance is minimized. To maintain adequate blood flow through the coronary arteries, diastolic blood pressure must be at least 60 mm Hg.

LEFT CORONARY ARTERY. The LCA divides into two branches: the left anterior descending (LAD) and the circumflex coronary artery (LCX). The LAD branch descends toward the anterior wall and the apex of the left ventricle. It supplies blood to portions of the left ventricle, ventricular septum, chordae tendineae, papillary muscle, and right ventricle.

The LCX descends toward the lateral wall of the left ventricle and apex. It supplies blood to the left atrium, the lateral and posterior surfaces of the left ventricle, and sometimes portions of the interventricular septum. In 45% of people, the LCX supplies the sinoatrial (SA) node, and in 10% of people it supplies the AV node. Peripheral branches (diagonal and obtuse marginal) arise from the LAD and LCX and form an abundant network of vessels throughout the entire myocardium.

RIGHT CORONARY ARTERY. The RCA originates from the right sinus of Valsalva, encircles the heart, and descends toward the apex of the right ventricle.

The RCA supplies the right atrium, right ventricle, and inferior portion of the left ventricle. In most people (more than 50%), the RCA supplies the SA node and the AV node. Considerable variation in the branching pattern of the coronary arteries exists among individuals.

■ Function

■ ELECTROPHYSIOLOGIC PROPERTIES OF THE HEART

The electrophysiologic properties of heart muscle are responsible for regulating heart rate and rhythm. Cardiac muscle cells are unique and possess the special characteristics of automaticity, excitability, conductivity, contractility, and refractoriness.

Automaticity refers to the ability of all cardiac cells to initiate an impulse spontaneously and repetitively. Excitability is the ability of the cells to respond to a stimulus by initiating an impulse (depolarization). Conductivity means that cardiac cells transmit the electrical impulses they receive.

Because the cells possess the property of contractility, they also contract in response to an impulse. Refractoriness means that cardiac cells are unable to respond to a stimulus until they have recovered (repolarized) from the previous stimulus. .

CONDUCTION SYSTEM OF THE HEART

The cardiac conduction system is composed of specialized tissue capable of rhythmic electrical impulse formation . It can conduct impulses much more rapidly than other cells located in the myocardium. The SA node, located at the junction of the right atrium and the superior vena cava, is considered the main regulator of heart rate. The SA node is composed of pacemaker cells, which spontaneously initiate impulses at a rate of 60 to 100 times per minute and myocardial working cells, which transmit the impulses to the surrounding atrial muscle. An impulse from the SA node initiates the process of depolarization and hence the activation of all myocardial cells. The impulse travels through both atria to the atrioventricular (AV) node located in the junctional area. After the impulse reaches the AV node, conduction of the impulse is delayed briefly. This delay allows the atria to contract completely before the ventricles are stimulated to contract. The intrinsic rate of the AV node is 40 to 60 beats/min.

The Bundle of His is a continuation of the AV node and is located in the interventricular septum. It divides into the right and left bundle branches. The bundle branches extend downward through the ventricular septum and fuse with the Pur-kinje fiber system. The Purkinje fibers are the terminal branches of the conduction system and are responsible for carrying the wave of depolarization to both ventricular walls. Purkinje fibers can act as an intrinsic pacemaker, but their discharge rate is only 20 to 40 beats/min. Thus these intrinsic pacemakers seldom initiate an electrical impulse.

SEQUENCE OF EVENTS DURING THE CARDIAC CYCLE

The phases of the cardiac cycle are generally described in relation to changes in pressure and volume in the left ventricle during filling (diastole) and ventricular contraction (systole). Diastole, normally about two thirds of the cardiac cycle, consists of relaxation and filling of the atria and ventricles, whereas systole consists of the contraction and emptying of the atria and ventricles.

Cardiac muscle contraction results from the release of large numbers of calcium ions from the sarcoplasmic reticulum. These ions diffuse into the myofibril sarcomere (the basic contractile unit of the myocardial cell). Calcium ions promote the interaction of actin and myosin protein filaments, causing these filaments to link and overlap. Cross-bridges, or linkages, are formed as the protein filaments slide over or overlap each other. These cross-bridges act as force-generating sites. The sliding of these protein filaments of multiple myofibril sarcomeres shortens the sarcomeres, producing myocardial contraction. Cardiac muscle relaxes when calcium ions are pumped back into the sarcoplasmic reticulum, causing a decrease in the number of calcium ions around the myofibrils. This reduced number of ions causes the protein filaments to disengage or dissociate, the sarcomere to lengthen, and the muscle to relax.

MECHANICAL PROPERTIES OF THE HEART

The electrical and mechanical properties of cardiac muscle determine the function of the cardiovascular system. The heart is able to adapt to various pathophysiologic conditions (e.g., stress, infections, and hemorrhage) to maintain adequate blood flow to the various body tissues.

Blood flow from the heart into the systemic arterial circulation is measured clinically as cardiac output (CO), the amount of blood pumped from the left ventricle each minute. CO depends on the relationship between heart rate (HR) and stroke volume (SV); it is the product of these two variables:

Cardiac output = Heart rate x Stroke volume

CARDIAC OUTPUT AND CARDIAC INDEX. Cardiac output (CO) is the volume of blood (in liters) ejected by the heart each minute. In adults, the CO ranges from 4 to 7 L/min. Because cardiac output requirements vary according to body size, the cardiac index is calculated to adjust for differences in body size.

The cardiac index can be determined by dividing the CO by the body surface area. The normal range is 2.7 to 3.2 L/min/m² of body surface area.

HEART RATE. Heart rate refers to the number of times the ventricles contract each minute. The normal resting heart rate for an adult is between 60 and 100 beats/min.

Increases in heart rate increase myocardial oxygen demand. Heart rate is extrinsically controlled by the autonomic nervous system, which adjusts rapidly wheecessary to regulate cardiac output. The parasympathetic system slows the heart rate, whereas sympathetic stimulation has an excitatory effect. An increase in circulating endogenous catecholamine (e.g., epinephrine and norepinephrine) usually causes an increase in heart rate, and vice versa.

Other factors, such as the central nervous system (CNS) and baroreceptor (pressoreceptor) reflexes, influence the effects of the autonomic nervous system on heart rate. Pain, fear, and anxiety can increase heart rate. The baroreceptor reflex acts as a negative-feedback system. If a client experiences hypotension, the baroreceptors in the aortic arch sense a lessened pressure in the blood vessels. A signal is relayed to the parasympathetic system to have less of an inhibitory effect on the sinoatrial (SA) node; this results in a reflex increase in heart rate.

STROKE VOLUME. Stroke volume is the amount of blood ejected by the left ventricle during each systole. Severalvariables influence stroke volume and, ultimately, CO. These variables include heart rate, preload, afterload, and contractility.

PRELOAD. Preload refers to the degree of myocardial fiber stretch at the end of diastole and just before contraction. The stretch imposed on the muscle fibers results from the volume contained within the ventricle at the end of diastole. Preload is determined by left ventricular end-diastolic (LVED) volume.

An increase in ventricular volume increases muscle fiber length and tension, thereby enhancing contraction and improving stroke volume. This statement is derived from Starling’s law of the heart: the more the heart is filled during diastole (within limits), the more forcefully it contracts. However, excessive filling of the ventricles results in excessive LVED volume and pressure and a decreased cardiac output

AFTERLOAD. Another determinant of stroke volume is afterload. Afterload is the pressure or resistance that the ventricles must overcome to eject blood through the semilunar valves and into the peripheral blood vessels. The amount of resistance is directly related to arterial blood pressure and the diameter of the blood vessels.

Impedance, the peripheral component of afterload, is the pressure that the heart must overcome to open the aortic valve. The amount of impedance depends on aortic compliance and total systemic vascular resistance, a combination of blood viscosity and arteriolar constriction. A decrease in stroke volume can result from an increase in afterload without the benefit of compensatory mechanisms.

CONTRACTILITY. Contractility also affects stroke volume and CO. Myocardial contractility is the force of cardiac contraction independent of preload. Contractility is increased by factors such as sympathetic stimulation and calcium release. Factors such as hypoxia and acidemia decrease contractility.

Electrocardiography (ECG, or EKG [from the German Elektrokardiogramm]) is a transthoracic interpretation of the electrical activity of the heart over time captured and externally recorded by skin electrodes.[1] It is a noninvasive recording produced by an electrocardiographic device. The etymology of the word is derived from the Greek electro, because it is related to electrical activity, cardio, Greek for heart, and graph, a Greek root meaning “to write”. In English speaking countries, medical professionals often write EKG (the abbreviation for the German word elektrokardiogramm) in order to avoid confusion with EEG.[citatioeeded]

The ECG works mostly by detecting and amplifying the tiny electrical changes on the skin that are caused when the heart muscle “depolarises” during each heart beat. At rest, each heart muscle cell has a charge across its outer wall, or cell membrane. Reducing this charge towards zero is called de-polarisation, which activates the mechanisms in the cell that cause it to contract. During each heartbeat a healthy heart will have an orderly progression of a wave of depolarisation that is triggered by the cells in the sinoatrial node, spreads out through the atrium, passes through “intrinsic conduction pathways” and then spreads all over the ventricles. This is detected as tiny rises and falls in the voltage between two electrodes placed either side of the heart which is displayed as a wavy line either on a screen or on paper. This display indicates the overall rhythm of the heart and weaknesses in different parts of the heart muscle.

Usually more than 2 electrodes are used and they can be combined into a number of pairs. (For example: Left arm (LA),right arm (RA) and left leg (LL) electrodes form the pairs: LA+RA, LA+LL, RA+LL) The output from each pair is known as a lead. Each lead is said to look at the heart from a different angle. Different types of ECGs can be referred to by the number of leads that are recorded, for example 3-lead, 5-lead or 12-lead ECGs (sometimes simply “a 12-lead”). A 12-lead ECG is one in which 12 different electrical signals are recorded at approximately the same time and will often be used as a one-off recording of an ECG, typically printed out as a paper copy. 3- and 5-lead ECGs tend to be monitored continuously and viewed only on the screen of an appropriate monitoring device, for example during an operation or whilst being transported in an ambulance. There may, or may not be any permanent record of a 3- or 5-lead ECG depending on the equipment used.

It is the best way to measure and diagnose abnormal rhythms of the heart,[2] particularly abnormal rhythms caused by damage to the conductive tissue that carries electrical signals, or abnormal rhythms caused by electrolyte imbalances.[3] In a myocardial infarction (MI), the ECG can identify if the heart muscle has been damaged in specific areas, though not all areas of the heart are covered.[4] The ECG cannot reliably measure the pumping ability of the heart, for which ultrasound-based (echocardiography) or nuclear medicine tests are used. It is possible to be in cardiac arrest with a normal ECG signal (a condition known as pulseless electrical activity).

Image showing a patient connected to the 10 electrodes necessary for a 12-lead ECG

History

Alexander Muirhead is reported to have attached wires to a feverish patient’s wrist to obtain a record of the patient’s heartbeat while studying for his Doctor of Science (in electricity) in 1872 at St Bartholomew’s Hospital.[5] This activity was directly recorded and visualized using a Lippmann capillary electrometer by the British physiologist John Burdon Sanderson.[6] The first to systematically approach the heart from an electrical point-of-view was Augustus Waller, working in St Mary’s Hospital in Paddington, London.[7] His electrocardiograph machine consisted of a Lippmann capillary electrometer fixed to a projector. The trace from the heartbeat was projected onto a photographic plate which was itself fixed to a toy train. This allowed a heartbeat to be recorded in real time. In 1911 he still saw little clinical application for his work.

Einthoven’s ECG device

An initial breakthrough came when Willem Einthoven, working in Leiden, Netherlands, used the string galvanometer that he invented in 1903.[8] This device was much more sensitive than both the capillary electrometer that Waller used and the string galvanometer that had been invented separately in 1897 by the French engineer Clément Ader. Rather than using today’s self-adhesive electrodes Einthoven’s subjects would immerse each of their limbs into containers of salt solutions from which the ECG was recorded.

Einthoven assigned the letters P, Q, R, S and T to the various deflections, and described the electrocardiographic features of a number of cardiovascular disorders. In 1924, he was awarded the Nobel Prize in Medicine for his discovery.[10]

Though the basic principles of that era are still in use today, there have been many advances in electrocardiography over the years. The instrumentation, for example, has evolved from a cumbersome laboratory apparatus to compact electronic systems that often include computerized interpretation of the electrocardiogram.

The output of an ECG recorder is a graph (or sometimes several graphs, representing each of the leads) with time represented on the x-axis and voltage represented on the y-axis. A dedicated ECG machine would usually print onto graph paper which has a background pattern of 1mm squares (often in red or green), with bold divisions every 5mm in both vertical and horizontal directions. It is possible to change the output of most ECG devices but it is standard to represent each mV on the y axis as 1 cm and each second as 25mm on the x-axis (that is a paper speed of 25mm/s). Faster paper speeds can be used – for example to resolve finer detail in the ECG. At a paper speed of 25 mm/s, one small block of ECG paper translates into 40 ms. Five small blocks make up one large block, which translates into 200 ms. Hence, there are five large blocks per second. A calibration signal may be included with a record. A standard signal of 1 mV must move the stylus vertically 1 cm, that is two large squares on ECG paper.

Layout

By definition a 12-lead ECG will show a short segment of the recording of each of the 12-leads. This is often arranged in a grid of 4 columns by three rows, the first columns being the limb leads (I,II and III), the second column the augmented limb leads (aVR, aVL and aVF) and the last two columns being the chest leads (V1-V6). It is usually possible to change this layout so it is vital to check the labels to see which lead is represented. Each column will usually record the same moment in time for the three leads and then the recording will switch to the next column which will record the heart beats after that point. It is possible for the heart rhythm to change between the columns of leads. Each of these segments is short, perhaps 1-3 heart beats only, depending on the heart rate and it can be difficult to analyse any heart rhythm that shows changes between heart beats. To help with the analysis it is common to print one or two “rhythm strips” as well. This will usually be lead II (which shows the electrical signal from the atrium, the P-wave, well) and shows the rhythm for the whole time the ECG was recorded (usually 5–6 seconds). The term “rhythm strip” may also refer to the whole printout from a continuous monitoring system which may show only one lead and is either initiated by a clinician or in response to an alarm or event.

Leads

The term “lead” in electrocardiography causes much confusion because it is used to refer to two different things. In accordance with common parlance the word lead may be used to refer to the electrical cable attaching the electrodes to the ECG recorder. As such it may be acceptable to refer to the “left arm lead” as the electrode (and its cable) that should be attached at or near the left arm. There are usually ten of these electrodes in a standard “12-lead” ECG.

Alternatively (and some would say properly, in the context of electrocardiography) the word lead may refer to the tracing of the voltage difference between two of the electrodes and is what is actually produced by the ECG recorder. Each will have a specific name. For example “Lead I” (lead one) is the voltage between the right arm electrode and the left arm electrode, whereas “Lead II” (lead two) is the voltage between the right limb and the feet. (This rapidly becomes more complex as one of the “electrodes” may in fact be a composite of the electrical signal from a combination of the other electrodes. (See later.) Twelve of this type of lead form a “12-lead” ECG

To cause additional confusion the term “limb leads” usually refers to the tracings from leads I, II and III rather than the electrodes attached to the limbs.

Placement of electrodes

Ten electrodes are used for a 12-lead ECG. The electrodes usually consist of a conducting gel, embedded in the middle of a self-adhesive pad onto which cables clip. Sometimes the gel also forms the adhesive.

Electrode label (in the USA) Electrode placement

RA On the right arm, avoiding bony prominences.

LA In the same location that RA was placed, but on the left arm this time.

RL On the right leg, avoiding bony prominences.

LL In the same location that RL was placed, but on the left leg this time.

V1 In the fourth intercostal space (between ribs 4 & 5) just to the right of the sternum (breastbone).

V2 In the fourth intercostal space (between ribs 4 & 5) just to the left of the sternum.

V3 Between leads V2 and V4.

V4 In the fifth intercostal space (between ribs 5 & 6) in the mid-clavicular line (the imaginary line that extends down from the midpoint of the clavicle (collarbone)).

V5 Horizontally even with V4, but in the anterior axillary line. (The anterior axillary line is the imaginary line that runs down from the point midway between the middle of the clavicle and the lateral end of the clavicle; the lateral end of the collarbone is the end closer to the arm.)

V6 Horizontally even with V4 and V5 in the midaxillary line. (The midaxillary line is the imaginary line that extends down from the middle of the patient’s armpit.)

Limb leads

In both the 5- and 12-lead configuration, leads I, II and III are called limb leads. The electrodes that form these signals are located on the limbs—one on each arm and one on the left leg.The limb leads form the points of what is known as Einthoven’s triangle.

Lead I is the voltage between the (positive) left arm (LA) electrode and right arm (RA) electrode:

I = LA − RA.

Lead II is the voltage between the (positive) left leg (LL) electrode and the right arm (RA) electrode:

II = LL − RA.

Lead III is the voltage between the (positive) left leg (LL) electrode and the left arm (LA) electrode:

III = LL − LA.

Simplified electrocardiograph sensors designed for teaching purposes at e.g. high school level are generally limited to three arm electrodes serving similar purposes.

Unipolar vs. bipolar leads

There are two types of leads: unipolar and bipolar. Bipolar leads have one positive and one negative pole.[21] In a 12-lead ECG, the limb leads (I, II and III) are bipolar leads. Unipolar leads also have two poles, as a voltage is measured; however, the negative pole is a composite pole (Wilson’s central terminal) made up of signals from lots of other electrodes In a 12-lead ECG, all leads besides the limb leads are unipolar (aVR, aVL, aVF, V1, V2, V3, V4, V5, and V6).

Wilson‘s central terminal VW is produced by connecting the electrodes, RA; LA; and LL, together, via a simple resistive network, to give an average potential across the body, which approximates the potential at infinity (i.e. zero):

Augmented limb leads

Leads aVR, aVL, and aVF are augmented limb leads (after their inventor Dr. Emanuel Goldberger known collectively as the Goldberger’s leads). They are derived from the same three electrodes as leads I, II, and III. However, they view the heart from different angles (or vectors) because the negative electrode for these leads is a modification of Wilson‘s central terminal. This zeroes out the negative electrode and allows the positive electrode to become the “exploring electrode”. This is possible because Einthoven’s Law states that I + (−II) + III = 0. The equation can also be written I + III = II. It is written this way (instead of I − II + III = 0) because Einthoven reversed the polarity of lead II in Einthoven’s triangle, possibly because he liked to view upright QRS complexes. Wilson‘s central terminal paved the way for the development of the augmented limb leads aVR, aVL, aVF and the precordial leads V1, V2, V3, V4, V5 and V6.

Lead augmented vector right (aVR) has the positive electrode (white) on the right arm. The negative electrode is a combination of the left arm (black) electrode and the left leg (red) electrode, which “augments” the signal strength of the positive electrode on the right arm:

Lead augmented vector left (aVL) has the positive (black) electrode on the left arm. The negative electrode is a combination of the right arm (white) electrode and the left leg (red) electrode, which “augments” the signal strength of the positive electrode on the left arm:

Lead augmented vector foot (aVF) has the positive (red) electrode on the left leg. The negative electrode is a combination of the right arm (white) electrode and the left arm (black) electrode, which “augments” the signal of the positive electrode on the left leg:

The augmented limb leads aVR, aVL, and aVF are amplified in this way because the signal is too small to be useful when the negative electrode is Wilson‘s central terminal. Together with leads I, II, and III, augmented limb leads aVR, aVL, and aVF form the basis of the hexaxial reference system, which is used to calculate the heart’s electrical axis in the frontal plane. The aVR, aVL, and aVF leads can also be represented using the I and II limb leads:

Precordial leads

The electrodes for the precordial leads (V1, V2, V3, V4, V5 and V6) are placed directly on the chest. Because of their close proximity to the heart, they do not require augmentation. Wilson‘s central terminal is used for the negative electrode, and these leads are considered to be unipolar (recall that Wilson‘s central terminal is the average of the three limb leads. This approximates common, or average, potential over the body). The precordial leads view the heart’s electrical activity in the so-called horizontal plane. The heart’s electrical axis in the horizontal plane is referred to as the Z axis.

Vectors and views

Graphic showing the relationship between positive electrodes, depolarization wavefronts (or mean electrical vectors), and complexes displayed on the ECG.

Interpretation of the ECG relies on the idea that different leads (by which we mean the ECG leads I,II,III, aVR, aVL, aVF and the chest leads) “view” the heart from different angles. This has two benefits. Firstly, leads which are showing problems (for example ST segment elevation) can be used to infer which region of the heart is affected. Secondly, the overall direction of travel of the wave of depolarisation can also be inferred which can reveal other problems. This is termed the cardiac axis . Determination of the cardiac axis relies on the concept of a vector which describes the motion of the depolarisation wave. This vector can then be described in terms of its components in relation to the direction of the lead considered. One component will be in the direction of the lead and this will be revealed in the behaviour of the QRS complex and one component will be at 90 degrees to this (which will not). Any net positive deflection of the QRS complex (i.e. height of the R-wave minus depth of the S-wave) suggests that the wave of depolarisation is spreading through the heart in a direction that has some component (of the vector) in the same direction as the lead in question.

Axis

Diagram showing how the polarity of the QRS complex in leads I, II, and III can be used to estimate the heart’s electrical axis in the frontal plane.

The heart’s electrical axis refers to the general direction of the heart’s depolarization wave front (or mean electrical vector) in the frontal plane. With a healthy conducting system the cardiac axis is related to where the major muscle bulk of the heart lies. Normally this is the left ventricle with some contribution from the right ventricle. It is usually oriented in a right shoulder to left leg direction, which corresponds to the left inferior quadrant of the hexaxial reference system, although −30° to +90° is considered to be normal. If the left ventricle increases its activity or bulk then there is said to be “left axis deviation” as the axis swings round to the left beyond -30°, alternatively in conditions where the right ventricle is strained or hypertrophied then the axis swings round beyond +90° and “right axis deviation” is said to exist. Disorders of the conduction system of the heart can disturb the electrical axis without necessarily reflecting changes in muscle bulk.

Waves and intervals

P wave

The P wave represents the wave of depolarization that spreads from the SA node throughout the atria, and is usually 0.08 to 0.1 seconds (80-100 ms) in duration. The brief isoelectric (zero voltage) period after the P wave represents the time in which the impulse is traveling within the AV node (where the conduction velocity is greatly retarded) and the bundle of His. Atrial rate can be calculated by determining the time interval between P waves. Click here to see how atrial rate is calculated.

The period of time from the onset of the P wave to the beginning of the QRS complex is termed the P-R interval, which normally ranges from 0.12 to 0.20 seconds in duration. This interval represents the time between the onset of atrial depolarization and the onset of ventricular depolarization. If the P-R interval is >0.2 sec, there is an AV conduction block, which is also termed a first-degree heart block if the impulse is still able to be conducted into the ventricles.

QRS complex

The QRS complex represents ventricular depolarization. Ventricular rate can be calculated by determining the time interval between QRS complexes. Click here to see how ventricular rate is calculated.

The duration of the QRS complex is normally 0.06 to 0.1 seconds. This relatively short duration indicates that ventricular depolarizatioormally occurs very rapidly. If the QRS complex is prolonged (> 0.1 sec), conduction is impaired within the ventricles. This can occur with bundle branch blocks or whenever a ventricular foci (abnormal pacemaker site) becomes the pacemaker driving the ventricle. Such an ectopic foci nearly always results in impulses being conducted over slower pathways within the heart, thereby increasing the time for depolarization and the duration of the QRS complex.

The shape of the QRS complex in the above figure is idealized. In fact, the shape changes depending on which recording electrodes are being used. The shape will also change when there is abnormal conduction of electrical impulses within the ventricles. The figure to the right summarizes the nomenclature used to define the different components of the QRS complex.

ST segment

The isoelectric period (ST segment) following the QRS is the time at which the entire ventricle is depolarized and roughly corresponds to the plateau phase of the ventricular action potential. The ST segment is important in the diagnosis of ventricular ischemia or hypoxia because under those conditions, the ST segment can become either depressed or elevated.

T wave

The T wave represents ventricular repolarization and is longer in duration than depolarization (i.e., conduction of the repolarization wave is slower than the wave of depolarization). Sometimes a small positive U wave may be seen following the T wave (not shown in figure at top of page). This wave represents the last remnants of ventricular repolarization. Inverted or prominent U waves indicates underlying pathology or conditions affecting repolarization.

Q-T interval

The Q-T interval represents the time for both ventricular depolarization and repolarization to occur, and therefore roughly estimates the duration of an average ventricular action potential. This interval can range from 0.2 to 0.4 seconds depending upon heart rate. At high heart rates, ventricular action potentials shorten in duration, which decreases the Q-T interval. Because prolonged Q-T intervals can be diagnostic for susceptibility to certain types of tachyarrhythmias, it is important to determine if a given Q-T interval is excessively long. In practice, the Q-T interval is expressed as a “corrected Q-T (QTc)” by taking the Q-T interval and dividing it by the square root of the R-R interval (interval between ventricular depolarizations). This allows an assessment of the Q-T interval that is independent of heart rate. Normal corrected Q-Tc intervals are less than 0.44 seconds.

There is no distinctly visible wave representing atrial repolarization in the ECG because it occurs during ventricular depolarization. Because the wave of atrial repolarization is relatively small in amplitude (i.e., has low voltage), it is masked by the much larger ventricular-generated QRS complex.

A 12-lead electrocardiogram (ECG) is the standard form of electrocardiogram used to diagnose cardiac rhythm disturbances and many types of cardiac problems

such as myocardial ischemia or infarction. The ECG may reveal other cardiac structural or functional abnormalities such as hypertrophy, certain drug effects,

and electrolyte abnormalities; however, other modalities exist for diagnosis of these types of abnormalities and the ECG offers only initial or screening information for these conditions.

The ECG records amplified electrical activity of the heart only and offers little information regarding contractile or hemodynamic function. It is, however, the most frequently used test of cardiac function other than pulse and blood pressure determinations.

The 12-lead ECG provides “views” of cardiac electrical activity from 12 different vantage points on the body surface. It is noninvasive and painless and can be obtained within a few minutes by a person who does not require extensive training. Interpretation of the recorded data requires an advanced level of practice. Most ECGs are obtained with a machine that provides computer-derived interpretation simultaneous with the graphed wave tracing. Thus, preliminary and usually accurate information is available immediately and is later confirmed by a cardiologist or other trained provider who “overreads the tracing.

ASSESSMENT

1. Assess age, gender, and current medication history for any medications with possible cardiac or hemodynamic effects. Gather other data that may be

required by unit/institution protocol (height, weight, recent blood pressure, operator identification). Reference standards are tailored to age and gender. Some medications cause abnormalities in portions of the ECG complex that must be recognized as medication effect.

2. Determine that the client is able to tolerate a supine position and that adequate exposure of chest and limbs is possible for electrode placement.

Correct siting of electrodes is enhanced by comfortable, stable position.

3. Determine presence of neck, arm, jaw, or other pain with possible cardiac origin. Chest or other pain may provide additional information useful in serial comparison of ECGs.

4. Assess client need for information about the procedure purpose and requirements and ability to cooperate: that client should lie still and refrain from talking, electrode attachment, procedure lasts only a few minutes and is painless. Anxiety may be relieved by simple explanation of intent, duration, and purpose.

DIAGNOSIS

8.1.1 Knowledge Deficit regarding the ECG procedure

9.3.1 Anxiety related to the procedure or to the diagnosis and treatment

1.4.2.1 Decreased Cardiac Output

PLANNING

Expected Outcomes:

1. The client will be able to cooperate with procedure.

2. The client will not be anxious.

3. The client will be able to describe the reason for

the ECG.

Equipment Needed

• Twelve-lead ECG machine with charged battery, cables and leads, graph paper

• Disposable electrodes (12)

• Electrode paste or gel

• Alcohol wipes

• Pillows

• Sheet or drape

• Towel and washcloth

• Disposable razor

CLIENT EDUCATION NEEDED:

1. Assure the client that no electrical current goes through the body from the machine.

2. Explain to the client that he will feel nothing during the procedure.

3. Instruct the client to report chest pain or other symptoms to the nurse or physician.

4. Explain to the client that he will need to be in the supine position and will need to lie still during this test.

5. Explain to client that he will need to breathe normally and refrain from talking.

6. Explain to client that it may be necessary to shave body hair at some sites where electrodes are to be placed to provide good contact.

7. Tell the client that he will have to remove his clothes from the waist up and expose his lower arms and legs but that he will be covered as much as possible during the procedure.

8. Assure the client that his privacy will be guarded.

EVALUATION

• The client tolerated the ECG procedure.

• The client is able to state purpose of ECG.

• The client is free of chest pain or other cardiac complaints.

• An accurate tracing was obtained for analysis.

DOCUMENTATION

Nurses’Notes

• Note the date and time of the ECG.

• Describe the reason for the ECG and any significant findings.

• Record the time the tracing results were reported to the physician or qualified practitioner.

Medication Administration Record

• Note the date and time of any cardiac medication

> CRITICAL THINKING SKILL

Introduction

Quick response to any cardiac symptoms or complaints is essential in giving appropriate and timely treatment. Taking an ECG should be second nature to staff in

emergency rooms, medical units, and cardiac care units.

Possible Scenario

A woman being treated for recently diagnosed diabetes on the medical unit had just eaten her lunch when she mentioned to the nurse that she had heartburn. She

said she often got it after eating and it always went away when she reclined in her chair. The nurse noted that she looked comfortable and went to her next client.

Possible Outcome

An hour later, the client put on her call light and told the nurse that her heartburn had not disappeared as it usually did. The nurse then took her vital signs and

called the doctor. He ordered an ECG and the nurse called the ECG technician. The preliminary result showed possible cardiac ischemia. When the doctor was notified, he ordered the client to be transferred to the cardiac care unit for further evaluation.

Prevention

The nurse should have listened to the client’s complaint and acted immediately by calling the doctor or doing the ECG herself if the institution policy allowed it.