nursCE.com presents Basics of ECG Reading: Part I

The heart sits in the middle of the chest at a slight angle pointing downward, to the left, and slightly anterior (Figure 1). The right ventricle (RV) dominates the anterior view (Figure 2). Most of the anterior surface of the ventricles consists of the RV surface. A key point to remember is that, though the RV dominates this visual view, the left ventricle (LV) dominates the electrical view.


Figure 1 - Anatomical position of the heart	Figure 2 - Anterior heart surface

The heart consists of four main chambers: the two atria and the two ventricles. The atria empty into their corresponding ventricles. The left ventricle empties into the peripheral circulatory system, and the right ventricle empties into the pulmonary system. Veins bring blood to the heart, while arteries take blood away from the heart. The circulatory system is a closed system. Blood circulates inside this closed system over and over, taking up oxygen in the lungs and giving it up to the peripheral tissues (Figure 3).

Figure 3 - Overview of circulatory system

Electrical Conduction System

In the heart there is a special conducting system, which provides the automatic formation and propagation of the excitatory process in such a way that the heart can perform its pumping function (Figure 4). The conduction system of the heart differs functionally and histologically from the working myocardium.

Figure 4 - Heart conduction system

The electrical conduction system of the heart is made up of specialized cells. Some of these are specialized for pacemaking functions and some for the transmission of the impulses that travel through them. The main function of the conduction system is to create an electrical impulse and transmit it in an organized manner to the rest of the myocardium. This is an electrochemical process that creates electrical energy. The electrocardiogram (ECG) can record this energy.

The specialized conduction system is interwoven with the myocardial tissue itself, and is only distinguishable with certain stains under a microscope. The conduction system is actually in the heart walls. The atrial myocytes are innervated by direct contact from one cell to another. The internodal pathways transmit the impulse from the sino-atrial (SA) node to the AV node (Figure 5). The Purkinje system encircles the entire ventricles, just under the endocardium, and is the final component of the conduction system (Figure 6). The Purkinje cells innervate the myocardial cells themselves.


Figure 5 - Internodal pathways	Figure 6 - Purkinje system

Sino-atrial node

The SA node develops during the embryonal period together with the compact AV node in the region where the right superior cardinal vein is united with the sinus venosus. The AV node migrates internally to its definitive position whereas the SA node remains in its original position. It is situated in the vicinity of the entrance of superior vena cava to the right atrium, along the crista terminalis (figure 7). Its internal end lies subendocardially. The SA node is 1-2 mm in width, l0-20 mm in length and it is pyramidal in shape, and the cross section is triangular with the base directed towards the entrance of the right atrium. There is a small artery in the center of the triangle. This artery gives off many small branches to provide the SA node with nutrition.

Figure 7 Sinoatrial (SA) node

Besides the pacemaker function, the SA node monitors the central aortic pressure and the pulse. The SA node artery is the first branch of the right coronary artery. The substances that increase the SA node activity cause dilatation of the SA node artery and vise versa, the substances which depress the SA node activity cause constriction of the SA node artery. This feedback mechanism provides stabilization of the SA rhythm.

The fundamental basis of the SA node is thick collagenous connective tissue, which surrounds the central artery. This connective tissue is composed of an irregularly distributed collagen fibers that form a layer that encircles the central artery. On the edges of the node the cells join to form the efferent pathways. The amount of collagen in SA node increases with age. The center of the SA node contains large number of nerve endings, and cholinergic ganglia are found on the peripheries. The afferent nerve fibers to the node join the nodal cells. The parasympathetic supply originates from the right vagal nerve and the adrenergic supply comes from the postganglionic sympathetic nerves.

There are at least 2 types of specialized cells in the SA node. The first type is the P cells (pole cells) that preserve the ability to generate impulses endogenously from embryonal period. The main characteristic of the P cells is their automaticity, which is the ability to depolarize the cellular membrane till reaching the threshold level without any external stimulation. This characteristic is unique for the P cells, which are among the fastest among the conductive system cells that have the ability to spontaneously depolarize the cellular membrane. As a result they are known as the pacemaker cells. Apart from P cells in the SA node there are transitional cells that form a network of fibers and are mainly found on the SA node periphery. They are attached to the P cells on one side and to the myocardial cells in the atria on the other side. This makes it is possible to transmit activation from the SA node to the atrial myocardium.

The Internodal Pathways

The mechanism by which the SA activation spreads through the atria to the atrioventricular node (AV node) is not yet certain. There are three internodal pathways: anterior, middle, and posterior (figure 8). Their main purpose is to transmit the pacing impulse from the SA node to the AV node. In addition, there is a small tract of specialized cells known as the Bachmann’s Bundle that transmits the impulses through the inter-atrial septum. All of these pathways are found in the walls of the right atrium and the inter-atrial septum.

Figure 8- Internodal pathways

These pathways possess specialized cells and are not continuous with each other (in other words they are interrupted). It is possible that these tracts or pathways conduct activation during pathological conditions and it was found that the posterior pathway has an important task during the shortening of P-Q interval. Those pathways do not exist as defined structures. They could be composed of groups of cells having different electrophysiological characteristics. These pathways can sometimes be the basis for the reentry circles that occur during the cardiac arrhythmias.

The activation of the atria reaches the atrioventricular junction, which is a more complicated structure and can be anatomically divided into 4 parts:

The atrionodal region (junction) , which is a transitional zone
The compact AV node
The penetrating bundle (the proximal part of bundle of His)
The branching bundle (the distal part of bundle of His)

The parts mentioned in 1, 2 and 3 are referred to as the junctional area. The branching bundle together with the bundle branches is referred to as the subjunctional area.

The atrionodal region or junction or what is known as the transitional zone is composed of groups of cells which are found between the atrial myocardium and the AV node. These cells (the transitional cells) are smaller than the active myocardial cells. They form tiny clusters that are separated by a connective tissue septi. These transitional cells enter the superficial and the deep part of the compact AV node.

Atrioventricular Node (AV node)

The compact AV node is located in the wall of the right atrium just next to the opening of the coronary sinus, the largest vein of the heart, and the septal leaflet of the tricuspid valve (figure 9). Its area is nearly 10 x 6 mm. It is responsible for slowing down conduction from the atria to the ventricles just long enough for atrial contraction to occur. This slowing allows the atria to "overfill" the ventricles and helps maintain the output of the heart at a maximum level. The AV node is supplied by the right coronary artery.

Figure 9- Atrioventricular (AV) node

Autonomic nerve fibers are found in the compact AV node in the vicinity of the node arteries and veins. The parasympathetic fibers come from the left vagus and the sympathetic fibers come from the postganglionic neurons. The area where the AV junction crosses to the fibrous ring is considered to be the beginning of the bundle of His.

Bundle of HIS

The bundle of His starts at the AV node and eventually gives rise to both the right and left bundle branches (figures 10 & 11). It is found partially in the walls of the right atrium, and in the interventricular septum. The His bundle is the only route of communication between the atria and the ventricles.


Figure 10 - Left bundle branch	Figure 11 - Right bundle branch

The penetrating part and the remaining part of the branching bundle will pass through the annulus fibrosus after giving off it's branches, as the continuity of the compact node. Then it passes through the membranous part of the interventricular septum. It starts to branch at the lower part of the membranous septum. The bundle of His is formed by parallel muscle fibers, which are separated by connective tissue into a number of stripes. Its diameter can reach 3 mm and length 12 to 40 mm where its penetrating part forms about 8-10 mm.

Branching of bundle of His starts at the lower edge of the membranous part of the interventricular septum. The anatomical division of the bundle of His into right and left bundle branches is referred to as pseudobifurcation. The reason for this is that the bundle of His fibers are divided before the anatomical bifurcation, so they differ in function yet they still pass alongside together for a small distance. An analogous situation is present in the anterior (superior) and the posterior (inferior) branches of the left bundle. Their division already occurred in the bundle of His. They run in the left bundle branch but they differ in their function. In some cases a third (branch) fasciculus is described to be present in the left bundle branch. The division or the bundle branches is extremely variable. There are some junctions between the branches. The bundle branches pass to the Purkinje fibers (figure 12) at the apical part of the heart.

Figure 12 - Purkinje fibers

Hierarchy of conduction/pacemaker sites

The pacemaker dictates the rate at which the heart will cycle through its pumping action to circulate the blood. The pacemaker creates an organized beating of all of the cardiac cells, in a specialized sequence, to produce effective pumping action. It sets the pace that all of the other cells will follow.

In the heart there are specialized cells whose function is to create an electrical impulse and act as the heart's pacemaker. The main structure that fulfills this important function is the SA node, found in the muscle of the right atrium. This area responds to the needs of the body, controlling the beat based on information it receives from the nervous, circulatory, and endocrine systems. The main pacemaker paces at a rate of 60 to 100 beats per minute (BPM), with an average of 70.

Every cell in the conduction system is capable of being a pacemaker. However, the intrinsic rate of each type of cell is slower than the cells that precede it. This means that the fastest pacemaker is the SA node, the next fastest is the AV node, and so on (figure13). The fastest pacemaker sets the pace because it causes all the ones that come after it to reset after each beat. In this way, the slower pacemakers will never fire. If the faster pacemaker does not fire for some reason, the next fastest will be there as a backup to ensure that the heart functions as close to normal as possible.

Figure 13 - Intrinsic pacemaker hierarchy & rates

RBB and LBB and Left Fascicles

The Right Bundle Branch (RBB)

The right bundle branch is the continuity of the bundle of His, and is (histologically) similar to it (figure 14). The proximal part of the right bundle branch is situated in the vicinity of the aortic and tricuspid valve. The distal part is situated subendocardially near the septal papillary muscle, and it continues its pathway till reaching the apex of the right ventricle.

Figure 14- Right bundle branch

The Left Bundle Branch (LBB)

The left bundle begins at the end of the His bundle and travels through the interventricular septum (figure 15). The left bundle gives rise to the fibers that will innervate the LV and the left face of the interventricular septum. It first connects to a small set of fibers that innervate the upper segment of the interventricular septum. This will be the first area to depolarize. The left bundle ends at the beginning of the left anterior (LAF) and left posterior fascicles (LPF).

Figure 15 - Left bundle branch

The Left Anterior Fascicle (LAF)

The LAF, also known as the left anterior superior fascicle, travels through the left ventricle to the Purkinje cells that innervate the anterior and superior aspects of the left ventricle (figure 16). It is a single-stranded fascicle, in contrast to the LPF.

Figure 16 - Left anterior fascicle

The Left Posterior Fascicle (LPF)

The LPF is a fan-like structure leading to the Purkinje cells that will innervate the posterior and inferior aspects of the left ventricle (figure 17). It is very difficult to block this fascicle because it is so widely distributed, rather than being just one strand.

Figure 17 - Left posterior fascicle

The Purkinje System

The Purkinje system is made up of individual cells just beneath the endocardium (figure 18). They represent the peripheral branching of the bundle branches. They form a subendocardially situated network and they are the cells that directly innervate the myocardial cells and initiate the ventricular depolarization cycle. Purkinje fibers contain myofibrils and are divided by collagen fibers that prevent the sideways or lateral spread of activation. The Purkinje fibers spread among the fibers of the ventricular muscle fibers.

Figure 18 - Purkinje system

Electrophysiology

It is necessary to understand a lot about the generation of electrical activity in a cell and the effect of electrolytes on the electrocardiogram (ECG). Electrolytes are the means by which the cell develops "electricity" and its imbalances can cause life-threatening problems. For example, if one knew that peaked, sharp T waves were a sign of hyperkalemia (elevated potassium), or that a prolonged QT interval could be a sign of hypocalcemia or hypomagnesaemia, one could avert a serious arrhythmia.

The heart is made up of a series of cells. Each of these cells is made up of two halves that slide over each other and are held together by actin and myosin proteins. The actin molecules are attached to the outside edges of the cell wall, and the myosin molecules are interspersed between the actin molecules (figure 19). The outsides of the cells are fused together to form tang bands, or myofibrils. These bands, in turn, are held together side-to-side by connective tissue to form sheets, which are covered with extracellular fluid (figure 20). The main function of the bands is to contract and expand. When one of the cells contracts, the whole sheet shortens by a small amount. When all of the cells contract, the whole sheet shortens significantly. The sheet returns to its starting size as all of the cells relax. The sheets are arranged to form the four sacs that constitute the heart: two small, thin ones on top (the atria) and two large, thick ones on bottom (the ventricles).


Figure 19 - Myofibrils	Figure 20 - Myofibril sheets

Ion Movement Across Cell Membranes

The fluid inside and outside of the cell contains water, salts, and proteins. The fluids are not the same, however; the concentrations of salt molecules and proteins are different in each area. In liquids, salts break down into positively and negatively charged particles known as ions (figure 21). In the body, the main positively charged ions are sodium (Na+), potassium (K+), and calcium (Ca++). Chloride (CI-) is the main negatively charged ion.


Figure 21 - Ions in solution	Figure 22 - Cellular electrical potential

If the cell were not alive, the concentrations of all of the ions and charges would be the same on both sides of the cell membrane. However, a live cell maintains differences in these concentrations across the cell membrane. The inside of the cell has a higher potassium concentration, whereas the outside has a higher concentration of sodium (figure 22). The higher positive charge outside the cell thus causes relatively more negative charge inside the cell. The outside of the cell wall also has more calcium, which adds to the greater positive charge outside the cell. This difference between the charges outside, and inside of the cell wall is known as its electrical potential.

The cell is a structural unit in all living organisms. The cellular membrane has an important role in all the electric events that precede the contraction. Cellular membranes are complicated structures that protect the intracellular environment. Membranes are lipid structures or layers that are interrupted by protein molecules. Soluble substances in the extra cellular space can pass intracellularly by simple diffusion or active transport where the protein receptors in the cell membrane take part. Phospholipids are the building units apart from them are the neutral fat and glycolipids. The lipids form polar hydrophilic heads and non-polar hydrophobic ends. The membrane proteins are arranged asymmetrically. Sometimes they surround lipid rings and hence form some non-specific hydrophilic configurations that act as channels through which electrolytes can pass. Some membrane protein are mobile, they can rotate or change their position in the membrane.

The transmembrane transport can be active or passive. Influx means the in-flow of solutes and the outflow is know as efflux. The active transport (or cellular "pumps") needs energy supply, which is mainly from the ATP. Most probably the active transport is the result of no equilibrium of ions and electric charges on both sides of the membrane. The ATP-ase enzyme is unequally distributed in the cell membrane and it can change its position. When the ATP-ase is directed intracellularly (to the inside) it has a high affinity to Na+. When it is directed to the outside it has a higher affinity to K+.

The pumps actively move ions around to maintain the resting concentration and charge of the cell (figure 23). The pump uses one ATP, the body's fuel, to push out three sodium ions (three positive charges) and bring in two potassium ion (two positive charges). The result is a greater number of positive charges outside the cell than inside. In other words, the outside solution has a positive charge, while the inner solution has a more negative charge. Because of this pumping action, the electrical potential of the resting myocyte is approximately -70 to -90 mV.

Figure 23 - ATP pump

Action potential

Upon stimulating the myocardial cell, a characteristic change takes place, this change is known as the action potential (figure 24). The resting potential in these cells ranges around –90mV. Upon adequate stimulation the resting potential starts to change. This adequate stimulation may be an electrical stimulation from the outside or an activation which is transmitted from a neighboring cell. A mechanical or a chemical stimulation can be an adequate impulse. This stimulus is followed by a change in the membrane permeability and a change in the state of the gates in the membrane channels.

Figure 24 - Action potential

The membrane activation increases the membrane permeability for Na+ by opening the gates in the fast Na+ channels allowing Na+ ions to flow freely along their electrochemical gradient. The Na+ influx causes the extinction of the Na+ gradient between the intra and extracellular spaces. The Na+ influx cancels the potential difference of the membrane. This process is very fast, lasting only 2-4 ms and hence its name, the fast depolarizing influx. On the transmembrane action potential curve this change (the fast depolarization) is shown as phase 0 (figure 24). The Na+ influx changes the membrane potential, which further leads to opening of the Na+ channel. So there is a positive connection in which an increasing Na+ influx will facilitate even more Na+ influx. The potential changes its values and becomes near 0. Usually there is an overshooting of the potential value reaching +20mV. This overshoot will cause the Na+ influx inactivation. The sharp change in the potential in 0 phase is known as the steep edge of the action potential. So the steepness of the curve decides the quality of spread of the action potential to the neighboring cells.

When the membrane fast depolarization by the Na+ influx membrane potential reaches -40 mV the Ca2channels open. This will facilitate the Ca2+ ions to influx along their electrochemical gradient. Thus the influx of the Ca2+ ions join the influx of Na+ ions in the process of membrane depolarization. The calcium channels open and begin to allow calcium to enter the cell. Calcium is a double positive ion. It has two positive charges instead of one. The influx of calcium and the slow influx of sodium help to maintain the cell in the depolarized state. Calcium is needed for the cells to contract. Calcium acts like a key, activating a clamp composed of the proteins troponin and tropomyosin. The clamp brings together the two ratcheting proteins, actin and myosin, and allows them to move along each other and to cause the cell to contract. Without calcium, the right key is not present to unlock and free the clamping proteins, and the actin and myosin do not come close enough together to engage with each other. The more calcium, the faster the clamping action, and the longer the contraction is maintained.

The K+ ion escape from the cell occurs simultaneously with the continuation of the membrane depolarization and the process of repolarization actually begins. The fast K+ ion efflux starts with the overshoot to +20 mV. This is known as phase 1. In this phase the Na+ influx slows down whereas the Ca2+ influx continues. Here the membrane potential does not change because the Ca2+ influx equalizes the K+ efflux. This equilibrium represents a process of remedy, or rectification. Because the K+ ion efflux is opposed by a high resistance, the Ca2+ flow stops at the end of phase 2.

In phase 3 only the K+ flow remains. The membrane potential gradually returns to the original value at the end of phase 4. Yet the ion balance is markedly different from the original state. There is a surplus of Na+ and Ca2+ ions with a depletion of K+ ion. The correction of the ion levels starts after reaching the original potential. Ca2+ ions are exchanged by Na+ ions (the action of Na-Ca pump) and the Na+ ions surplus is then corrected by the Na-K pump. So during phase 4 there is an intensive exchange of ions with no change in the membrane potential (figure 24).

In automatic or rhythmogenic cells phase 4 does not represent the previously described isoelectric interval. In the sinoatrial cells and other cells in the conducting system, when the maximal diastolic potential is reached its negativity starts to decrease gradually (i.e. if -70 was its maximal diastolic potential it gradually reaches –60). This change is marked as the spontaneous diastolic depolarization, which is caused by Na+ ion influx. This is due to inadequate pumping out of the Na+, which is caused by a low Na-K pump performance.

The SA node cells have the steepest (fastest) diastolic depolarization. After reaching the threshold potential (-40 to -30m V) phase 0 takes place (fast depolarization). The following phase (phase 1) is not as steep as in the myocardial cells. In the SA node cells the depolarization (phase O) results from the Ca2+ ion influx and only partially due to the Na+ ion influx. The overshooting usually does not occur and the plateau usually does not exist. The SA node cells do not need Ca2+ for contraction (an obvious plateau is present in the contractile cells). Thus in the action potential curve phase 1 is directly followed by phase 3. The diastolic potential can only reach (-50 m V)- (-70mV). The potassium potential is low. The spontaneous diastolic depolarization takes place in phase 4. The in-flowing Na+ ions cause the membrane potential to reach the threshold levels upon which phase 0 takes place. The whole process is repeated approximately 70 times per minute. A similar process can occur in other pacemaker cells in the conductive system of the heart. In this case phase 4 takes longer.

One critical point to understand about phase 4 is that different myocytes reach the threshold potential at different rates. The ones that maintain the pacemaking function of the heart, the sinoatrial (SA) nodal cells, reach the threshold potential first. In sequence, the next ones are the atrial cells, the atrioventricular (AV) nodal cells, the bundle cells, the Purkinje cells, and finally the ventricular myocytes (figure 25). It is interesting that the independent rates for each of these systems is slower than the ones before. This is the body' s protective mechanism, rather than having just one set of cells responsible for the pacing function. If the cells in the SA node cease to function, then the next fastest phase 4 belongs to the atrial myocytes. They will fire before the other cells, and will set the pace. This continues down the line, as needed.

Figure 25 - Intrinsic pacemaker hierarchy & rates

The time taken by the diastolic depolarization to reach the threshold potential is determined by three factors.

The ascending speed of diastolic transmembrane potential (phase 4). A quickly reached threshold potential causes a high automaticity.
Level of the threshold potential. When a more negative level of the threshold potential with the same ascending speed of the diastolic transmembrane potential the threshold potential is reached sooner. The final result is a faster automaticity with a more negative threshold potential that will increase the heart rate.
Level of the diastolic transmembrane action potential. As this level is more negative at the beginning of phase 4, more time is needed for the spontaneous diastolic depolarization to reach the threshold potential. The speed of the impulse formation is hence decreased. Otherwise, when the starting AP is not very negative the threshold potential is reached very soon and the speed of impulse generation is faster.

An impulse wave coming from the activated part of the conduction system of the heart reaches the myocardial cells before they reach the threshold potential and here phase 0 starts. The refractory phase lasts for the whole action potential. This fact prevents the SA node from an immature activation as a consequence of activated atria. The spontaneous depolarization of the SA nodal cells is not dependent on the Na+ and K+ concentration in the extracellular fluid. The speed of the diastolic depolarization determines the heart rate. Many substances achieve their action on the heart through changing the SA cellular membrane permeability and hence the length of phase 4.

From the electrophysiological point of view we can divide the heart cells into those which have the ability to spontaneously depolarize, and those which need activation from the nearby cells to depolarize. The action potential of one cell shifts the resting potential of the neighboring cell to the level of the threshold potential and then the process of depolarization takes place as previously described. The action potential of an activated cell is the impulse that causes depolarization of the neighboring cell, and its effect increases with increasing speed. That is why it is very easy for the steep 0 phase of the action potential to spread. It is very important to realize that after reaching the threshold potential through activating the cell by an action potential of another cell, the continuity of the event does not depend on the action potential but on electrophysiological properties of the activated cell.

The spread of the local current waves is affected by the characteristics of the conducting system as well as the characteristics of the myocardium, which can be described as cable characters. Local depolarization can spread over a distance of few millimeters.

Vectors

Each cell gives rise to its own electrical impulse. These impulses vary in intensity and direction. The term vector can be used to describe these electrical impulses. A vector is a diagrammatic way to show the strength and the direction of the electrical impulse.

Vectors represent the amount of energy and its direction. They add up when they are going in the same direction, and cancel each other out if they point in opposite directions. If they are at an angle to each other, they add or subtract energy and change directions when they meet (figure 26).

Figure 26 - Electrical axis

The final vector, after all of the addition, subtraction, and direction changes, is known as the electrical axis of the ventricle. Each wave and segment has its own respective vector. There is a P-wave vector, a T-wave vector, a ST segment vector, and a QRS vector. The ECG is a measurement of these vectors as they pass under an electrode. That is an electronic representation of the electrical movement of the main vectors passing under an electrode, or a lead (figure 27).

Figure 27 - Electrical Axis

Lead Formation Of The Limb Leads

The electrodes are sensing devices that pick up the electrical activity occurring beneath them. When a positive electrical impulse is moving away from the electrode, the ECG machine converts it into a negative (downward) wave (figure 28). When a positive wave moves toward an electrode, the ECG records a positive (upward) wave. When the electrode is somewhere in the middle, the ECG shows a positive deflection for the amount of energy that is coming toward it and a negative wave for the amount going away from it.

Figure 28 - ECG wave deflection

So, the electrodes (leads) pick up the electrical activity of the vectors, and the ECG machine converts them to waves. Each set of waves should be thought of as a picture. It can be concluded that ECG gives a three-dimensional picture of the heart's electrical axes (figure 29). From this picture, all sorts of information can be obtained about where pathologic processes - such as infarcts, hypertrophy, and blocks - are occurring.

Figure 29 - Electrical axis overview

Lead placement is very important to receive complete and true information. The limb leads (extremity leads) should be positioned as follows- the right arm (RA), left arm (LA), right leg (RL), and left leg (LL) and should be at least 10 cm from the heart (figure 30). It doesn't matter if the arm leads are placed on the shoulders or the arms, as long as they are 10 cm from the heart. The limb electrodes can be attached to the shoulders, the arms, or the wrists without altering the size of the ECG or the complexes. Once the electrodes are more than 10 cm away from the heart, the effect on ECG size is negligible.

The ECG machine reads the positive and negative poles of the limb electrodes to produce leads I, II, and III on the ECG.

Figure 30 - ECG lead placement

Einthoven’s Triangle

Using the same principle as before - that leads can be moved as long as the resultant lead is parallel and of the same polarity - the hexaxial (Einthoven) system can be produced. This as a system of analyzing vectors that cuts the center of the heart along a plane, creating a front half and a back half.

The Eithowen triangle system gives rise to the six limb leads: I, II, m, a VR, aVL, and aVF (figure 31). Traditionally, the side of the lead that has the positive electrode, or pole, is the one that has the lead name at its end. Hence, the positive pole of lead I is at the right side of the circle, the positive pole of aVF is down. Also, note that the leads are 30 degrees apart (figure 32). This will be very useful when axis is discussed.


Figure 31 - Einthoven's triangle	Figure 32 - Axis summary

The Precordial System

The precordial leads (chest leads) must be placed exactly. Position VI and V2 on each side of the sternum at the fourth intercostal space. V 4 is at the fifth intercostal space in the mid-clavicular line, V5 in anterior axillary line and V6 in mid-axillary line (figure 33).

Figure 33 - V lead placements

Axis Determination

The axis is an electrocardiographic summation of all the activity of the heart. Hypertrophy, blocks, infarcts, and the direction of the heart can all influence the axis. If there is hypertrophy of one of the ventricles, that ventricle would alter the ventricular axis in such a way as to assist in diagnosing the problem. Also in patients with a myocardial infarction or heart attack the ventricular axis would definitely be altered by the lack of electrical activity from the infarcted zone. When faced with an abnormal axis, remember the possible causes -- the differential diagnoses. When all the possible causes are considered it can be assured that one of these is the right one.

With an abnormal axis, there is always other associated abnormalities on an ECG that will lead to the correct diagnosis. For example, if left axis deviation is found, start with the QRS complexes. If the QRS complexes are not wide, ectopic beats can be ruled out. If the ECG does not meet criteria for LVH, rule out LVH. Inferior myocardial infarction is associated with Q waves or ST - T wave abnormalities in the inferior leads. If these are not seen another diagnosis can be excluded. This leaves an anterior block hemiblock. If the additional criteria can be matched, then this is the correct diagnosis.

Axis determination also helps if there is a shift in the axis between a new ECG and an old one in the medical records. It can be a new block, a new infarct that caused some muscle tissue to die, or it could be that the leads are not placed correctly.

The electrical axis is the sum total of all the vectors generated by the action potentials of the individual ventricular myocytes. The ventricular axis cannot be evaluated directly. Instead, the way the vector is measured by the way it looks as it travels under each of the various electrodes. The "pictures" generated by each of the leads give a different view of this axis as it relates to the three-dimensional state (figure 34).

Figure 34 - Electrical axis

There are many ways to calculate the direction and intensity of the ventricular axis. The Einthoven hexaxial system is represented by a circle with all of the leads endorsed (figure 35). The entire circle is composed of six leads superimposed on each other. Each lead has a positive half and a negative half. Notice that the dividing line between each positive and negative half of a lead happens to fall on a lead that is at an exact 90° angle from it. This lead is referred to as the isoelectric lead, meaning that it is neither positive nor negative along that line. In other words, each lead has a corresponding isoelectric lead, lead I is isoelectric to aVF, II is isoelectric to aVL, III is isoelectric to a VR, etc.

Figure 35 - Einthoven hexaxial system

On the ECG, any positive vector will be represented as taller or more positive. Any negative vector will appear as a deeper or more negative complex. A lead is considered positive if it is even more positive than negative. Likewise, it is considered negative if it is even more negative than positive. A lead is isoelectric when it is exactly the same distance positive as it is negative (figure 36). Normally, there is only one isoelectric limb lead on the ECG because there is only one ventricular axis. All the other leads are either positive or negative.

Figure 36 - Hexaxial system vector summary

When the vector is plotted on the hexaxial system, a vector that is even slightly positive will be found on the positive half of the circle. By the same token, any negative complex has to be on the negative half of the circle. If it is exactly isoelectric, then it will fall directly along the isoelectric lead.

Because the vector cannot be seen, the complexes are used, and their relative positivity or negativity in each lead, to calculate the exact direction of the ventricular axis. When a 12-lead ECG is looked at it is not known where the axis is pointing. To start isolating that direction, we look first at leads I and aVF. First, look at lead I and figure out whether it is positive or negative. If it is positive, it would have to be on the positive side of the lead, if negative, it will fall in the negative half of the lead. Next, look at lead aVF. Repeat the same thought process. Suppose a 12-lead has a positive lead I and a positive lead aVF. The only quadrant that matches this pattern is the normal quadrant (figures 37 & 38).


Figure 37 - Axis ECG summary	Figure 38 - Normal ECG quadrant

There are four quadrants in the hexaxial system: normal, left, right, and extreme right. Any axis that falls outside the normal quadrant should be considered abnormal. In reality, the normal range extends from -20 to +100°, not 0 to +90°. If the axis falls into the left quadrant, it is considered to have a left axis deviation (figure 39). If it falls into either the right or extreme right, it has a right axis deviation. Normal axis extends all the way to -20°, and the area from - 21 to - 29° is neither pathological nor normal. This tiny area is an electrical "no man's land." To simplify things, the area from -1 to - 29° have been labeled as the physiologic left axis. This term helps to distinguish that area from the area that is the true pathologic left axis - from -30 to -90°.

Figure 39 - Axis summary

The axis can be isolated to the left quadrant by seeing if the QRS is positive in lead I and negative in aVF. Now to isolate the area a bit further, from - 30 to -90°. Lead II has aVL as its isoelectric lead. Lead II separates the hexaxial system at exactly -30°. If the complex is positive, it will lie on pathological half of the diagram. If the complex is negative, it will lie on the normal clear half of the diagram from - 30 to + 150°.

So in conclusion, if the positive complexes are identified in lead I and negative complex in aVF, this is in the left quadrant (figures 40 & 41). If lead II is negative then the axis is in the area between -30 and -90°, which defines the axis as a left axis deviation. On an ECG, look at leads I, II, and aVF. If there are positive complexes in lead I and negative complexes in a VF, look at lead II. If the complexes are negative in this lead, there is a left axis deviation and the axis is pathologic.


Figure 40 - Axis isolation	Figure 41 - Axis summary

The first and most common cause of left axis deviation is a left anterior hemiblock. This means that the left anterior-superior fascicle (LAF) of the left bundle branch is blocked for some reason (usually MI or ischemia). The result of this block is that innervation of the left ventricle starts at the bottom and travels upward. This produces an upwardly deflecting axis, and hence, an left axis deviation. Another common cause is left ventricular hypertrophy (LVH). Left ventricular hypertrophy means that the muscle wall of the left ventricle is enlarged, or hypertrophied. The heart becomes hypertrophied, most commonly because it has to pump against a greater amount of pressure in a hypertensive patient. LVH can sometimes, but not always, shift the axis and cause left axis deviation. An inferior wall myocardial infarction destroys the muscle in the bottom part of the heart. This also kills off any downward-going vector, leaving the upward vector unopposed. The net result is left axis deviation. Finally, ectopic beats can start anywhere. If they start at the bottom of the heart, they cause an upward spread of the impulse, which in turn creates an upward vector and left axis deviation

Right axis deviation is similarly based on events that direct the vector to the right. Children have bigger right ventricles than adults, and therefore, the vector points more to the right. Right ventricular hypertrophy pulls the vector to the right because of the increased mass of the hypertrophied RV. A block of the left posterior-inferior fascicle (LPF) of the LBB causes a vector that points rightward and upward. Dextrocardia is a heart that faces in the opposite direction of normal, that is, toward the right. Hence, the axis is toward the right.

Paper and Measurement

Boxes and Time

Currently most electrocardiographs record ECG rhythms on paper. The ECG paper passes under a stylus or pen at a rate of 12.5, 25, 50 or 100 millimeters per second (mm/s). At a standard speed of 25 mm/s, each little box is 1/25^th of a second, or 0.04 seconds. Because a big box is made up of five little boxes, it represents 5 x 0.04 sec = 0.20 sec, so five big boxes make 1 second (figure 42). Thus the full ECG on standard ECG paper is 12 seconds long. Almost all ECG machines label each individual lead for easy identification. Often, there is a recording at the bottom of each 12 lead ECG. This is known as a rhythm strip and usually prints in a default lead II.

The vertical height of a ECG wave or segment can be measured on in millimeters. On ECG paper one little box is one millimeter high. Likewise, a darker big box is five millimeters high. Everything on the ECG can be measured in millimeters or milliseconds.

Figure 42 - ECG paper grid

ECG Rulers and Calipers

ECG represents a complicated recording of various waves and intervals. To simplify the ECG interpretation ECG calipers and rulers were designed (figure 43). They are used for measurements of intervals and waves, evaluating the rhythm and its disturbances.

Figure 43 - Examples of calipers and ECG rulers

It is quite simple to use the caliper. Place one of the pins at the beginning of the object being measured, and move the other pin to the end (figure 44). Then transfer that distance to a clear part of the ECG paper to evaluate the height or the time of the measured object. Once the distance has been measured, it is easier to calculate the actual time frame. Using the calipers see if the distance between consecutive complexes is the same (figure 45). Walk the calipers back and forth across an ECG to check the regularity of the complexes. Take that distance and move it anywhere on the paper you want. This technique is useful in determining third-degree heart blocks and many other ECG abnormalities.


Figure 44 - Caliper basics	Figure 45 - Caliper use

Use your ca1ipers to measure the heights of waves to see if there is net positivity or negativity. This will be useful when determining the axis of the heart. When evaluating e.g. amplitudes of QRS complexes, use calipers to add the negative depth of one wave to the positive height of another in a different lead and calculate different indexes (figures 46 & 47). With calipers also compare widths, which is especially useful for comparisons in looking for atrioventricular blocks, aberrant beats, atrial premature contractions, ventricular premature contractions and so on.


Figure 46 - Positive deflection	Figure 47 - Negative deflection

Another helpful tool for ECG interpretation is axis-wheel ruler that is especially very useful in calculating the true axis of waves and segments (ruler1). It shows a representation of the hexaxial, Einthoven´s system on the back part of the ruler. Other most used rulers have one side that measures the rate, and a metric ruler on the other. A set of calipers and the ECG paper can give the same thing. Finally straight edges are useful in eva1uating the baseline and determining whether there is any elevation or depression present.

Calibration Markers

At one end of each ECG strip there is usually a step-like structure called a calibration box (figure 48). The standard box is 10 mm high and 0.20 seconds wide. The calibration box is there to confirm that the ECG conforms to the standard format. Occasionally, a ECG has been formatted in half-standard calibration. This is usually done when the complexes are so tall that they run into each other. Half-standard is indicated by an additional step halfway up the box that lasts for half the width of the standard box. This stair-like configuration indicates half-standard. The only other calibration seen is one in which the paper speed is set to 50 mm/sec, instead of the traditional 25 mm/sec. In this case, the calibration box will be 0.40 seconds wide, instead of 0.20.

Figure 48 - Calibration boxes

Rate 300, 150, 100, 75, 60, 50

The easiest way to calculate the rate is to use the method of separated boxes. Find a QRS complex that starts on a thick line. The best is to use the tip of the tallest wave on the QRS complex- R wave. This will be a starting point. As a second step, find the next QRS complex or any other spot- your end point. Then just count the thick lines in between the two spots, and calculate the rate from memorized numbers 300, 150, 100, 75, 60, 50, where each number represents one of the previous rates (figure 49). So if between two consecutive QRS complexes are two thick lines, it means that the heart rate is 150 bpm.

Figure 49 - ECG rate summary

Another way to calculate the rate is to use calipers to measure from the top of one complex to the top of the next. Then move the calipers - maintaining the measured distance - so that the left tip rests on a thick line, and calculate the rate as above for the distance between the two tips. The advantage is not having to hunt for a QRS that lands on a thick line to use as a starting point. An ECG ruler can also be used to find the rate.

The measurements using this simplified technique are very good for a fast estimate, but the exact rate should be measured using precise methods.

ECG complex: PQRSTU

A wave is a deflection from the baseline that represents an electrical event in the heart, such as atrial depolarization, atrial repolarization, ventricular depolarization, ventricular repolarization, or transmission through the His bundles, and so on. For instance, the P wave represents atrial depolarization (figure 50). Waves can be single, isolated, positive, or negative deflections, biphasic deflections with both positive and negative components, or combinations that have multiple positive and negative components. Waves are deflections from the baseline, line from one TP segment to the next.

Figure 50 - ECG complex summary

A segment is a specific portion of the complex as it is represented on the ECG. For example, the segment between the end of the P wave and the beginning of the Q wave is known as the PR segment (figure 51).

Figure 51 - PR segment

An interval is the distance, measured as time, occurring between two cardiac events. The time interval between the beginning of the P wave and the beginning of the QRS complex is known as the PR interval (figure 52). Note that there is a PR interval, as well as a PR segment.

Figure 52 - PR interval

In addition to the waves mentioned below, there are a few others not mentioned, such as the R' (R prime) wave and the U wave (figure 53).

Figure 53 - U wave

Components

The P wave represents the atrial activation (depolarization) (figure 54). The QRS complex represents the ventricular activation.

Figure 54 - P wave

The Q wave is a negative wave representing the initial stage of the QRS complex. The R wave is the initial positive wave that immediately follows the Q wave. The S wave is a negative wave following the R wave. If instead of the QRS complex there is only negative wave, which is followed by a positive wave it is then known as the S wave. Other waves of R or S are known as R' and S' waves (figures 55 & 56).


Figure 55 - QRS complex	Figure 56 - R & S wave primes

T wave represents the ventricular repolarization and sometimes is followed by a U wave (figures 57 & 58).


Figure 57 - T wave	Figure 58 - U wave

The atrial repolarization is represented by Tp wave, this wave can occur in the PR interval (figure 59). The section from the end of the QRS complex till the beginning of T wave is known as the ST segment (figure 60).


Figure 59 - Tp wave	Figure 60 - ST segment

It is the segment between the ventricular depolarization and its fast repolarization. The PR or (PQ) interval is the interval between the beginning of the P wave and the beginning of the QRS complex (figure 61), normal duration is 0.12-0.20 sec (figure 62).


Figure 61 - PR interval	Figure 62 - Normal PR interval

The QRS complex takes about 0.04-0.10 sec. The QT represents the approximate refractory period of the ventricles (figure 63).

Figure 63 - Normal QRS interval

The P Wave

Atrial excitatory process begins in the SA node and from the SA node the activation spreads radially and continuously across the atrial myocardium. In the beginning and after the rising of activation from the SA node, the right atrium is the first to be activated. Shortly afterwards the activation proceeds to the atrial septum and the left atrium respectively.

The P wave is usually the first wave and it represents the electrical depolarization of both atria (figure 64).


Figure 64 - P wave	Figure 65 - Atrial depolarization

The wave starts when the SA node fires. It begins when the wave leaves the baseline and ending on its return to baseline before the PR interval (figure 66). It also includes transmission of the impulse through the three internodal pathways, the Bachman Bundle, and the atrial myocytes themselves. The duration of the wave itself can vary between 0.08 and 0.11 seconds in normal adults. The axis of the P wave is usually directed downward and to the left, the direction the electrical impulse travels on its journey to the atrioventricular node and the atrial appendages.

Figure 66 - PR interval

The first half of the P wave is a picture of the right atrial activation whereas the second half of the P wave represents the activation of the left atrium. The P wave is normally positive in leads I, II, aVL, but is inverted in the AVR lead. It is usually the highest in lead II. The P wave is commonly biphasic in leads V1 and V2, being initially positive with a negative terminal part. The positive part represents the activation of the right atrium whereas the negative part represents the activation of the left atrium. In the chest leads that are close to the heart the P wave is usually larger. In the left precordial leads the P wave is positive.

The morphology of the P waves will vary in any one lead depending on the location of the area acting as the pacemaker. If the SA node acts as the pacemaker, the morphology of the P wave will look like the description above. If the impulse originates at any other pacemaker site in any of the atria, the P wave morphology and the PR interval will both be different (figure 67). Because many areas can act as secondary pacemakers, a wide variety of P wave morphologies are possible.

Figure 67 - Pacemaker morphology

The Tp wave

The repolarization of atrial muscle fibers is related to depolarization and it is represented as the Tp wave (figure 68). The Tp wave, which represents repolarization of the atria, deflects in the opposite direction of the P wave. It is usually not seen because it occurs at the same time as the QRS wave and is obscured by this more powerful complex. However, it can sometimes be seen when there is no QRS after the P wave. This occurs in AV dissociation or non-conducted beats. It may also be seen in PR depression (figure 69), or in the ST segment depression present in very fast sinus tachycardias. It appears as ST depression because the QRS comes sooner in the cycle, and the Tp wave, if it is negative, draws the ST segment downward.


Figure 68 - Tp wave	Figure 69 - PR depression

The atrial repolarization can cause pseudodepression of the ST segment in the J point (figure 70).

Figure 70 - Pseudodepression of ST

The PR Segment

The PR segment occupies the time frame between the end of the P wave and the beginning of the QRS complex. It is usually found along the baseline. It can be depressed by less than 0.8 mm under normal circumstances (figure 71). Anything greater than that is pathological. It is pathologically depressed in pericarditis, and when there is an atrial infarct.

Figure 71 - PR segment morphologies

The PR Interval

The PR interval represents the time period from the beginning of the P wave to the beginning of the QRS complex (figure 72). It includes the P wave and the PR segment. The PR interval covers all the events from the initiation of the electrical impulse in the sinoatrial (SA) node up to the moment of ventricular depolarization.

Figure 72 - PR interval

First, the atria begin to depolarize by the transmission of the electrical impulse through the specialized conduction pathway of the atria, the Bachman bundles, to the atrial myocytes. The impulse reaches the AV node before al1 of the atrial myocytes have depolarized because of the faster transmission down the Bachmann bundles (figure 73). The depolarization of all of the atrial myocytes represents a larger electrical force than depolarization of the AV node, so that the force seen on the ECG tracing is the P wave. In the AV node, the conduction slows momentarily. This physiologic slowing is needed to allow the mechanical emptying of atrial blood into the ventricles. Without this block, the atria and the ventricles would beat simultaneously and the ventricles would fill only by the passive inflow of blood during diastole. This would result in a decreased volume entering the ventricles and a smaller amount ejected from the ventricles. The His bundle is the next to be activated, and transmits the impulse down the left and right bundle branches (figure 74). Finally, the impulse reaches the individual Purkinje fibers, which will then innervate the ventricular myocytes. This is represented by the QRS complex on the ECG tracing.


Figure 73 - Atrial depolarization	Figure 74 - Myocardial depolarization summary

The normal duration is from 0.12 seconds to 0.20 seconds. If the PR interval is less than 0.11 seconds, it is considered to be shortened. A PR interval longer than 0.20 seconds is a first-degree AV block (figure 75). The PR interval can be quite long, sometimes 0.40 seconds even more. The term PQ interval is sometimes used interchangeably if there is a Q wave as the initial component of the QRS complex.

Figure 75 - First degree block

The interval should be measured in the lead with the widest P wave and the widest QRS complex in order to avoid the inadvertent omission of an isoelectric portion of a P wave. If the calculation does not take into account this isoelectric portion, it will give you a falsely shortened PR interval. Avoid the problems with isoelectric portions by using the lead with the longest PR interval to take your measurement. The PR interval should be the same throughout all of the leads. It is shortened in sinus tachycardia and in children and it is usually longer in the elderly.

When the PR segment is analyzed focus on possible PR depression (figure 76). The PR segment is usually on the baseline. However, it is sometimes found to be slightly depressed. In order to consider it as normal, it cannot be depressed more than 0.8 mm below the baseline. This normal variant is due to atrial repolarization, which pulls the PR segment downward. Whenever a pathological PR depression is present, check to see if it is found in multiple leads or in just one isolated lead. If it is found in only one lead, it is usually not clinically significant.

Figure 76 - PR segment

A true PR depression may occur in pericarditis and atrial infarction. Pericarditis is an inflammation of the pericardium, the fibrous sac that encases and protects the heart. It is a pathological process that may or may not have PR depression that is greater than or equal to 0.8 mm. Atrial infarction is very rare condition. It can be seen when there is significant PR depression in an ECG with signs of infarction and without any of the criteria for pericarditis.

The QRS Complex

The QRS complex represents ventricular depolarization. It is composed of two or more waves. Each wave has its own name or label and they can become quite complex. The main components are the Q, R, and S waves (figure 77). By convention, the Q wave is the first negative deflection after the P wave. The Q wave can be present or absent. The R wave is the first positive deflection after the P. This will be the initial wave of the QRS complex if there is no Q present. The first negative deflection after the R wave is the S wave. If there are additional components in the QRS complex, they will be named as prime waves (figure 78).


Figure 77 - QRS complex	Figure 78 - Prime waves

Normally, not every wave in every complex or lead is seen. The QRS complexes are just physical manifestations of the summation of the vectors generated by the heart's electrical potentials. The bigger the ventricle, the bigger the vector. The vector is represented on the ECG by its size and the direction in which it travels. A big myocardial infarction that infarcts the anterior wall and makes the heart incapable of producing an electrical force will lead to a dramatic change of vector identified on ECG as QS configuration in precordial leads. If there were fluid around the heart, a pericardial effusion, the directions of the vector would be the same, but would be represented on the ECG as small complexes because the amount of electrical force is dampened by the fluid (figure 79).

Figure 79 - ECG dampening due to an effusion

Depending on the angle and size of these vectors, some portions of the complex may be isoelectric, they are therefore invisible on the ECG. The events in cardiac depolarization and repolarization occur sequentially, not discrete events occurring separately. The events in the cycle flow from one to another in an organized pattern. Ventricular activation is one continuous event. Basically each deviation during the process of activation is shown immediately as a projection on the corresponding axis of the lead.

The initial septal is activation (0.01s). The interventricular septum in the cavity of the left ventricle is the first to be activated during the activation of the ventricles. The interventricular septum is nearly parallel to the frontal plane of the human body. That is why the projection of initial vector that represents the septal activation on chest lead axis will form the positive (R wave) on the right chest leads (VI and V2 ) and a small negative wave (q wave) on the leads V5 and V6 (figure 80).

Figure 80 - Q wave morphology

The next is progression of activation to the septal and apicoanterior parts of the right and left ventricles (0.02). During this phase the interventricular septal activation continues from both sides. The electrical power is partially similar but a larger part of the septum is depolarized from the left side. The septal activation spreads from the apex to the heart base, and from the anterior to the posterior part simultaneously meanwhile the activation could spread fast to both ventricles. The apex of the heart, the lateral wall of the right ventricle, and the anterior apical part of the left ventricle are mainly activated during this phase.

The following is complete activation of the interventricular septum, the right ventricle, and the larger part of the left ventricle (0.04-0.06 s). In this phase the activation of the septum and the right ventricle except its posterobasal part is completed. Most of the left ventricle is activated as well. The projection of this activation on the chest leads will result in recording the shortest S wave in lead VI and highest R in left chest leads.

Activation of the basal part of the interventricular septum and the posterobasal part of the left ventricle (0.06-0.08 s) is the last in ventricular depolarization process.

In conclusion, during the ventricular activation the right precordial leads will record negative ventricular QRS complexes. On the other hand the complexes recorded by medial precordial leads will be equiphasic.

The Q wave can be benign, or it can be a sign of dead myocardial tissue. A Q wave is considered significant if it is 0.03 seconds or wider, or its height is equal to or greater than one-third the height of the R wave (figure 81).

Figure 81 - Q wave morphology

It is better to have both criteria, but the first one is more significant if a tracing meets either of these criteria, it indicates a myocardial infarction over the region involved. If it does not, it is not a significant Q wave. Insignificant Q waves are commonly found in I, aVL and V6, where they are due to septal innervation. These are therefore called septal Qs. They are small, thin Q waves that represent the first vector of ventricular depolarization. QS waves are so named because there is no intervening R wave to break up the two, so you do not know if it is a Q wave or an S wave. QS waves are found in lead VI in many cases, and if they are isolated only to that lead, they are benign. If the QS waves extend through to V2, or especially V3, then they are significant for an infarct of the anteroseptal areas of the heart at some time in the past or in the present. Another example of a benign Q wave is one that is isolated to lead III only. This is usually a thin Q wave. If a significant Q wave is found in II or aVF, it indicates an inferior wall myocardial infarction.

The intrinsicoid deflection is measured from the beginning of the QRS complex to the beginning of the negative down-slope of the R wave in leads that begin with an R wave and do not contain a Q wave (figure 82). It represents the amount of time it takes the electrical impulse to travel from the Purkinje system in the endocardium to the surface of the epicardium immediately under an electrode. It is shorter (up to 0.035 seconds) in the right precordial leads, because the right ventricle is thin in comparison with the left. It is longer (up to 0.045 seconds) in the left precordial leads, because the left ventricle has greater thickness. Therefore the intrinsicoid deflection will be prolonged in ventricular hypertrophy, or when it takes longer for the electrical system to conduct to that area, because of an intraventricular conduction delay such as in left bundle branch block.

Figure 82 - Intrinsicoid deflection

There are various things to look at when interpreting the QRS complex: height or amplitude, width or duration, morphology, the presence of pathological Q waves, the axis along the frontal plane, and the transition zone.

In general, men have a larger amplitude than women, young people have higher amplitudes than the elderly, and the precordial leads have higher voltages than the limb leads because the electrodes are close to the heart

Many factors alter the height of the QRS complex. The main components causing a change are the size and direction of the vectors. The size of the vector reflects the number of action potentials generated by the heart in a certain direction. This, in turn depends on the number of cells and the size of the ventricles. Another important aspect that will determine the size of the QRS complex is the direct opposition of various vectors. Infarcted areas and scar tissue are electrically inert. So, when we have a vector opposite an area of infarct, it will be unopposed. Because there is nothing to dampen its size, it will appear out of proportion to the normal ECG. A pericardial effusion and high body fat can affect the amplitude of the QRS complex. Obese patients, in general, will have smaller voltages due to excess adipose tissue. Amyloid deposits work in the same way in hypothyroid patients. Also pleural effusion can cause decreased voltage in V5 and V6, in the leads closest to the area where effusions usually accumulate.

Voltage in all of the limb leads of less than 5 mm is abnormal. Waves less than 10 mm high in all of the precordial leads are also highly abnormal. Very often an ECG criteria can meet limb-lead voltage without meeting precordial criteria. This occurs because the precordial leads are directly overlying the heart on the chest wall. A thin person with an effusion will have larger precordial leads than a more robust person with an effusion. In the heavier person, you have not only the effusion to contend with but also the size of body wall between the heart and the electrode. The damping effect is present not only with a pericardial effusion but with any body tissue or fluid that comes between the electrode and the heart. It can occur with pleural fluid, fat, lung tissue (in a patient with chronic obstructive pulmonary disease), and even breast tissue - which is why the electrodes have to be placed beneath the breasts of a female patient.

The ORS complex duration should be measured from the onset of the first deflection after the PR interval to the end of the complex. Normally, this measures between 0.06 and 0.11 seconds (figure 83). Always measure the widest QRS complex in the ECG or it will mislead as to the true duration of the complex. There are some sections of the complex that are isoelectric and graphically invisible on the ECG. If just any lead is chosen, a shorter duration may be obtained than what is really present. This can lead to serious mistakes in your interpretation. This is especially true in cases of bundle branch blocks. In addition, a U wave could be mistaken for a biphasic T wave. There are many instances in which the exact measurement of the interval is critical to the correct interpretation.

Figure 83 - QRS duration

When wide complexes are seen on an ECG, there are two possibilities. There may be a beat or rhythm of ventricular origin, when complexes that are triggered by a ventricular focus are wide and bizarre. This is because the conduction of the impulse takes place by cell-to-cell transmission and not through the normal conduction system. Ventricular premature beats and rhythms, idioventricular rhythms, and ventricular tachycardia and flutter are examples of these types of complexes.

A second possibility occurs if the normal conduction through the left or right bundle is blocked for any reason. Then the conduction of the impulse after that blocked point must occur by direct cell-to-cell transmission. This gives rise to abnormally wide and bizarre patterns, very similar in appearance to the ventricular beats.