Electrocardiography - Clinical Methods - NCBI Bookshelf
Nevertheless, as the result of careful correlation of electrocardiographic patterns The V1 electrode position is located in the fourth right intercostal space adjacent to . Reentry Unidirectional block and slowed conduction in reentry pathway. The recording of the conduction system is physically represented as an ECG. You can record a clinical lead ECG using just 4 electrodes and an app on the propagation and regression of electrical excitation in the heart in relation to the. The American Dental Association recently revised its monitoring guidelines to Abnormalities within this conduction system will compromise cardiac output and are for surface electrodes to record and produce a tracing known as an ECG.
Conversely, with hypercalcemia, the QT interval is foreshortened as a result of an abbreviation of phase 2 and the isoelectric ST interval. Derivation of Cardiac Rhythm from Cellular Action Potential Recall that in order for the cell to propagate a transmembrane action potential, or depolarize, its resting potential must be brought to threshold. There are two mechanisms by which this may be accomplished. The first, and simplest, is electrically to stimulate the cell from an outside source.
If the stimulus is too weak, the resting potential will be reduced but not to threshold, so no depolarization will occur. If the stimulus is sufficiently strong to reduce the resting potential to threshold, then a transmembrane action potential is propagated. Nearly all the cells in the heart are depolarized in this fashion; each cell is stimulated externally by its neighboring cell. The second mechanism by which the resting potential is reduced to threshold is termed automaticity.
An automatic cell is one that displays a gradual, spontaneous loss of negativity during diastole, a phenomenon termed diastolic depolarization and numbered phase 4 of the transmembrane action potential Figure In the heart there are two kinds of cells, electrically automatic and electrically nonautomatic.
The muscle cells are generally nonautomatic. Their resting potential remains constant until the cell is stimulated to reach threshold. The automatic cell, on the other hand, demonstrates phase 4 diastolic depolarization see Figure Specialized cells in the sinus node, AV node, and the remainder of the His and Purkinje conducting system demonstrate automaticity. The cells with the most rapid slope of diastolic depolarization reach threshold first, so these are the cells, generally located in the sinus node, which control the rate of the heart.
Clinical electrocardiography and ECG interpretation
In other words, heart rate depends on the rapidity or slope of diastolic depolarization of the most automatic cells. The more rapid the slope, the earlier the cell reaches threshold and the faster the heart rate. Altered automaticity would be one cause of rhythm abnormalities.
A second common mechanism of rhythm disturbances is reentry. Considering the box in Figure Reentry refers to the phenomenon of an impulse depolarizing this segment or cell, to produce an action potential or, on the surface ECG, a QRS complex, then traversing around another portion of the heart in a circuitous movement to reenter the first segment at a later time, eliciting a second response a second QRS, for instance, on the surface ECGsuch as a coupled premature ventricular complex.
Ladder diagram illustrating supraventricular tachycardia due to AV nodal reentry: Two conditions must prevail for reentry to occur. First, the impulse must leave the selected segment to conduct through other cardiac muscle.
Cardiovascular Lab: Electrocardiogram: Basics
If the impulse that depolarized the first cell had conducted through the remainder of the heart, then the neighboring cells would be refractory; conduction into the circus pathway would not be possible. In other words, for the circus pathway to be excitable, the initial wave of depolarization must not have reached that pathway—that is, there must be unidirectional block block forward into the reentry pathway, but not retrograde into this portion of the pathway.
Without unidirectional block, reentry would not have been possible.
Second, there must be a slowing in conduction. Of course, the heart is not that large. So the only alternative explanation is that conduction must have been remarkably slowed. Slowing in conduction is easily recognized at the level of the AV node by measuring the PR segment on the surface electrocardiogram. Thus, reentry can often be diagnosed or inferred from the surface electrocardiogram when reentry develops in the AV junction.
On the other hand, slowing in conduction and reentry may not be so easily recognized in other portions of the heart. With the help of a ladder diagram, which denotes electrical activation of the atrium, AV junction, and ventricle, consider the mechanism of a supraventricular tachycardia resulting from reentry at the level of the AV node Figure The first two diagrammed complexes originate in the sinus node, with atrial activation conducting normally through the AV junction, with the appropriate AV and resultant PR delay, before depolarizing the ventricle.
Note the prolongation in the AV interval, and in the PR interval on the surface tracing. Recall that this slowing in conduction is a prerequisite for reentry so that this impulse may "turn around" in the junction to conduct retrograde back through the junction via a second pathway, to excite the atrium a second time—that is, the atrium has now been depolarized twice as a result of a single stimulus which is the definition of reentry.
This impulse, in turn, can conduct antegrade, though slowly, through the AV junction into the ventricle, and then reciprocate back and forth between the two chambers, resulting in a supraventricular tachycardia.
Clinically, the mechanism of reentrant supraventricular tachycardia can often be differentiated from a supraventricular tachycardia resulting from augmented automaticity, such as that resulting from digitalis excess. The latter is diagrammed in Figure Then, rather than a regular tachycardia ensuing, the automatic focus generally "warms up" — that is, there is a gradual acceleration in the rate to the ultimate rate of the tachycardia.
Finally, the automatic rate of the tachycardia is often not terminated by a premature atrial complex, but gradually slows before stopping.
A reentrant supraventricular tachycardia can be initiated in the laboratory by an appropriately timed atrial stimulus, and terminated similarly. In contrast, automatic tachycardia can generally not be initiated and terminated by atrial pacing.
Compare these complexes with those in the middle of the second trace. Note that the PR interval is shorter. It is likely that each P wave has nothing to do with the ensuing QRS complex. Instead, as the sinus rate gradually slows, a hitherto unrecognized ventricular rhythm at a rate of about cpm becomes manifest, and usurps control of the ventricle. The broad complexes are ventricular in origin, resulting from augmented automaticity of that focus.
Toward the end of the middle trace, and in the bottom trace, as the sinus rate accelerates, as a result of increasing automaticity at the level of the sinus node, the atrium again captures and controls the ventricle.
Accelerated idioventricular rhythm due to augmented automaticy. Sequence of Activation; The Vector Concept The surface ECG tracing is the result of summing the electricity generated from the multitude of cardiac cells. As the segment of myocardium diagrammed in Figure The force is termed a vector, and it is characterized by a given magnitude and direction.
By convention, the positive pole of the vector is represented by an arrowhead; also, by convention, when the positive pole is directed toward an electrode the ECG stylus is deflected upward, whereas if the vector is directed away from an electrode, a negative deflection is recorded. The amplitude of the deflection depends on the magnitude of the vector. Thus, in Figure Like all medical tests, what constitutes "normal" is based on population studies.
The heartrate range of between 60 and beats per minute bpm is considered normal since data shows this to be the usual resting heart rate. In order to understand the patterns found, it is helpful to understand the theory of what ECGs represent. The theory is rooted in electromagnetics and boils down to the four following points: For example, depolarizing from right to left would produce a positive deflection in lead I because the two vectors point in the same direction.
In contrast, that same depolarization would produce minimal deflection in V1 and V2 because the vectors are perpendicular and this phenomenon is called isoelectric. Normal rhythm produces four entities — a P wave, a QRS complex, a T wave, and a U wave — that each have a fairly unique pattern. The P wave represents atrial depolarization. The QRS complex represents ventricular depolarization. The T wave represents ventricular repolarization. The U wave represents papillary muscle repolarization.
However, the U wave is not typically seen and its absence is generally ignored. Changes in the structure of the heart and its surroundings including blood composition change the patterns of these four entities. Electrocardiogram grid[ edit ] ECGs are normally printed on a grid. The horizontal axis represents time and the vertical axis represents voltage.
The standard values on this grid are shown in the adjacent image: The "large" box is represented by a heavier line weight than the small boxes. The exploring electrode is placed anteriorly on the chest wall.
This will be discussed in greater detail in the next chapter but for the current discussion it is sufficient to note that the exploring electrode is located anteriorly on the chest and the reference point is located inside the chest Figure 7. We shall now examine the main electrical vectors of the heart and how they are reflected in V1 and V5.
The main electrical vectors in the horizontal plane. Note how the electrical vectors that travel in the horizontal plane yield the P-wave and the QRS complex. The depolarization starts in the sinoatrial node, from where it spreads through the right atrium and subsequently to the left atrium.
During activation of the right atrium, the vector is directed anteriorly and to the left and downwards. The vector turns left and somewhat backwards as the depolarization heads towards the left atrium.
Thus, the atrial vector is slightly curved Figure 7.Electrocardiography (ECG/EKG) - simplified
Lead V1 detects the initial vector heading towards it and displays a positive deflection, the P-wave. The vector is directed forward and to the right. The ventricular septum is relatively small, which is why V1 displays a small positive wave r-wave and V5 displays a small negative wave q-wave. The explanation for this is as follows: The vector resulting from activation of the right ventricle does not come to expression, because it is drowned by the many times larger vector generated by the left ventricle.
Thus, the vector during activation of the ventricular free walls is actually the vector generated by the left ventricle.
Activation of the ventricular free wall proceeds from the endocadrium to the epicardium. This is because the Purkinje fibers run through the endocardium, where they deliver the action potential to contractile cells.
The subsequent spread of the action potential occur from one contractile cell to another, starting in the endocardium and heading towards the epicardium. As evident from Figure 7, the vector of the ventricular free wall is directed to the left and downwards. Lead V5 detects a very large vector heading towards it and therefore displays a large R-wave. Lead V1 records the opposite, and therefore displays a large negative wave called S-wave. The vector is directed backwards and upwards. It heads away from V5 which records a negative wave s-wave.
Lead V1 does not detect this vector. The vector of the T-wave The T-wave represents the rapid repolarization phase phase 2. A QRS complex which is net negative should be followed by a negative T-wave, whereas a QRS complex which is net positive should be followed by a positive T-wave. Concordant and discordant T-waves.
It may seem illogical that the QRS complex and the T-wave should have the same direction, given that the ion flows during de- and repolarization are opposite.
It seems more logical that de- and repolarization should have opposite direction. Evidently, this is not the case because not only are the ion flows opposite, but so is the direction of the electrical vector. Recall that depolarization of the ventricular free wall proceeds from endocardium to epicardium. Repolarization, on the other hand, starts in the epicardium and is directed towards the endocardium Figure 9. This is explained by the fact that epicardial cells have shorter action potentials and therefore begin repolarizing earlier than endocardial cells.