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| Year : 2014 | Volume
: 25
| Issue : 3 | Page : 386-389 |
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| The ECG made easy for the dental practitioner |
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UR Anoop1, Ramesh2, Kavita Verma3, Narayanan4
1 Department of Oral Pathology, KMCT Dental College, Kerala, India
2 Mahatma Gandhi Postgraduate Institute of Dental Sciences, Pondicherry, India
3 Consultant Oral Implantologist, K.K.Uthaman Dental Care and Implant Center, AUM Hospitals Pvt Ltd, Pondicherry, India
4 Senior Consutant Nephrologist and Founder, Pondicherry Kidney Foundation, Pondicherry, India
Click here for correspondence address and email
| Date of Submission | 22-Mar-2010 |
| Date of Decision | 20-May-2014 |
| Date of Acceptance | 16-Jun-2010 |
| Date of Web Publication | 7-Aug-2014 |
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 Abstract | | |
ECG is not taught to dental students formally in the dental curriculum. The general assumption is that dental surgeons do not handle any ECG related cases in clinical practice. But with an increase in medically compromised patients, the need for an interdisciplinary approach among dental and medical practitioners in the treatment of critically ill patients is becoming more relevant. Hence, we have to be aware of the basics of common medical investigations to be competent to assess and comprehend the medical conditions. So, this paper focuses on orienting the beginner to the basic concepts of ECG from the clinical perspective. The paper also discusses the ECG changes of myocardial infarction to familiarize the dental surgeon to read the ECG. Keywords: Dental practice, ECG, rate, rhythm, myocardial infarction
How to cite this article:
Anoop U R, Ramesh, Verma K, Narayanan. The ECG made easy for the dental practitioner. Indian J Dent Res 2014;25:386-9 |
The ECG is a record of the electrical activity of the heart. The electrical activity precedes the mechanical contraction of the heart muscle. This activity when recorded by electrodes produces waves and segments as shown in [Figure 1]. The waves have been called by Einthoven as P, Q, R, S, and T. The segments are PR segment and ST segment. They do not contain any waves. The segments are isoelectric which means they are at the same level. The intervals include waves and are called PR interval and QT interval. PR interval is from the beginning of the P wave to the beginning of the QRS complex. Ideally, it should be called as PQ interval. But as some leads do not show any Q waves, it is conventionally called as PR interval. QT interval is from the beginning of the QRS complex to the end of the T wave. [1]
| The basics of electrophysiology | |  |
In a resting cardiac cell, the outside of the cardiac cell is positively charged and the inside is negatively charged. The cardiac muscle has the property of automatic rhythmic contraction. When an impulse is generated, the inside becomes positive and the outside becomes negative. This is called depolarization. During recovery, the inside of the cell becomes negative by pumping out the positive ions and the outside becomes positive. This is called repolarization. These electrical charges are recorded in the ECG as waves. [2]
[Figure 2] shows that the direction of the impulse flow determines the type of deflection produced in the respective lead. A positive deflection is produced when the impulse flows toward the lead, whereas if the flow is away from the lead, it results in a negative deflection. However, an equiphasic deflection is recorded if the impulse flows past the lead. [3]
[Figure 3] shows that in the heart, excitation or depolarization usually begins in the sinoatrial node. It spreads as a wave through the atrial muscle. The depolarization wave cannot spread directly to the ventricles as the atria are insulated from the ventricles. The only normal connection between the two is the atrioventricular (AV) node. From the AV node, the depolarization spreads through the bundle of His and its branches and the Purkinje fibers. The interventricular septum gets depolarized from the left to the right. This is followed by the depolarization of the ventricular muscle from the endocardial surface toward the outside. [4]
Each heart beat begins with the depolarization of the sinoatrial node. This does not produce any noticeable wave on ECG. When the impulse spreads from the SA node resulting in depolarization of the atria, the P wave is produced. [3] No wave is produced when the impulse reaches the AV node. But there is a delay in conduction as this node conducts impulses slowly. This is a protective mechanism to prevent rapid atrial impulses from spreading into the ventricle. Thus, the time taken for the depolarization wave to move from the SA node, across the atria through the AV node to the ventricular muscle is the PR interval as shown in [Figure 1]. This is measured from the beginning of the P wave to the beginning of the R wave. [3]
From the AV node, the impulse spreads through the bundle of His into the interventricular septum and depolarizes it from left to right. This produces the first deflection in the QRS complex. Thus, depolarization of the interventricular septum produces the Q wave depending on the leads. Then, the impulse spreads through the right bundle branch and the left bundle branch to the right and left ventricles, respectively. This produces the R and the S waves. Thus, the QRS complex represents the depolarization of the ventricles. [3]
By convention, as shown in [Figure 1], the first downward deflection of the QRS complex is called Q wave. The first upward deflection is called an R wave irrespective of whether a Q wave is present or not. A downward deflection after the R wave is called an S wave. The waves present in a lead will depend on the location of the lead. [3]
The ST segment is the transient period when no further electrical current passes through the muscle. It is measured from the end of the S wave to the beginning of the T wave. [3]
The T wave represents the repolarization of the ventricular myocardium to the resting electrical state. The QT interval is the total time taken for the activation of the ventricles and its recovery to the normal resting state. [3]
| The ecg paper | | |
The ECG paper is a graph paper that moves through the machine at a constant rate of 25 mm/second. The paper has 5 mm squares which contain 1 mm squares as shown in [Figure 4]. The lines of 5 mm squares are bolder. Each 1 mm square represents 0.04 second and each 5 mm square represents 0.04 × 5 = 0.2 second. By correlating the height and width of the waves with the squares, the ECG is interpreted. [1] The normal values of the waves, segments and intervals are shown in [Table 1].
| The leads | | |
The electrodes are the wires that connect the patient to the ECG machine. These electrodes provide us with 12 different views or "leads" of the heart. The standard ECG has a record of 12 leads. Hence, the normal ECG is a record of the electrical activity of the heart from 12 different views. [3]
The 12 leads of the ECG, as shown in [Figure 5], include six limb leads and six chest leads. [3] The six limb leads are I, II, III, aVR, aVL, and aVF. Leads I, II, and III look at the heart from the sides or the coronal plane. Lead aVR looks from the patient's right shoulder. Lead aVL looks from the patient's left shoulder. Lead aVF looks upward from the feet. Hence, leads I, II, and aVL look at the left lateral surface of the heart. [5] Leads III and aVF look at the inferior surface of the heart. [5]
The six chest leads are V 1 , V 2 , V 3 , V 4 , V 5 , and V 6 , as shown in [Figure 5]. The chest leads look at the heart from the front and around the side. [3] V 1 and V 2 look at the right ventricle, whereas V 3 and V 4 look at the interventricular septum and the anterior wall of the left ventricle. V 5 and V 6 look at the anterior and lateral walls of the left ventricle.
As depicted in [Figure 6], the direction of depolarization of the heart is downward and leftward from the 11'o clock position to the 5'0 clock position. [5] Hence, the ECG recordings are positive in all the leads except aVR. As the depolarization wave moves away from this lead, the recordings in this lead are negative. [5]
The Q wave is a downward deflection seen only in left-sided leads V 4-6 . It is produced by the activation of the interventricular septum from left to right. The R wave represents the ventricle a lead is looking at, while the S wave represents the other ventricle. Hence, in leads V 1-2 , the R wave represents the right ventricle and the S wave represents the left ventricle. In leads V 5-6 , the R wave represents the left ventricle and the S wave represents the right ventricle. [1]
If two muscle masses of markedly different sizes are stimulated at the center, the impulse spreads from the inner surface to the outer surface. But the activity in the larger mass dominates and is recorded as positive or negative depending on the leads. In the heart, the right ventricle has less muscle mass while the left ventricle is more muscular. Hence, the electrical activity in the left ventricle leads dominates. As depolarization of the ventricles is from the endocardial surface to the outside, the right-sided leads V 1 -V 2 see a weak wave in the right ventricle moving toward them and a stronger wave in the left ventricle moving away from them. Hence, as shown in [Figure 7], they record a short R wave and a tall S wave. [1]
The left-sided leads V 5 -V 6 see a strong wave in the left ventricle moving toward them and a weak wave in the right ventricle moving away from them. Hence, they record a tall R wave and a short S wave as in [Figure 7]. The leads V 3 -V 4 which look at the interventricular septum thereby see waves of similar magnitude move past the leads and hence record R and S waves which are almost equal in magnitude. Hence, the R wave increases in size from right to left leads and the S wave decreases in size from right to left leads. The transition occurs in V 3 -V 4 . [1]
| Rate | | |
Heart rate refers to the ventricular rate which correlates with the pulse rate. As depolarization of the ventricles produce the QRS complex, the rate of QRS complexes gives us the heart rate. [5] The ECG paper moves at the rate of 25 mm/second. Hence, five large squares are covered per second. So, in a minute, 60 × 5 = 300 large squares are covered.
A. If the rhythm is regular, count the number of large squares between the two QRS complexes. Then, divide 300 by the number of large squares between the QRS complexes. [3]
[Figure 6] shows the ECG of a 61-year-old female patient, who reported at our hospital. The rhythm was regular. As there are three large squares between the R waves, the heart rate is calculated as 300/3 = 100 beats/minute.
B. If the rhythm is irregular, then count the number of QRS complexes in 30 squares. This is the rate in 6 seconds. Multiply by 10 to get the rate in 60 seconds. [3]
| Rhythm | | |
Rhythm refers to the part of the heart which controls the activation sequence. [5] Most parts of the heart can depolarize spontaneously and rhythmically. But the part which depolarizes more frequently controls the rate of ventricular contraction. The SA node has the highest frequency and hence it usually controls the heart rate. [3] When depolarization begins in the SA node, the heart is said to be in sinus rhythm. [5]
The features of sinus rhytmn are the following. [5]
- Heart rate is 60-100 beats/minute.
- P wave is positive in Lead II and inverted in lead aVR.
- Every P wave is followed by a QRS complex.
If the rate of depolarization of the SA node slows down, depolarization begins in the other parts of the heart like the atrial muscle, AV node or the ventricular muscle. These rhythms are abnormal. When a focus in atrial muscle takes control, this rhythm is called atrial escape. [5] The atrial depolarization produces the following:
- an abnormal P wave and
- normal QRS complexes.
When depolarization starts in AV node, the rhythm is called a junctional rhythm. [5] It is characterized by these features:
- absent P waves and
- normal QRS complexes.
When depolarization starts in the ventricle, the rhythm is ventricular rhythm. [5] It is characterized by the following:
- P waves are absent,
- broad QRS complexes and
- abnormal T waves are present.
| Myocardial infarction | | |
To make the understanding of ECG easier for beginners, we discuss the ECG changes in myocardial infarction (MI) in different leads and correlate it with changes in the heart. MI causes permanent damage to the heart muscle. MI changes can be classified as
- Q wave infarcts or ST segment elevation myocardial Infarction (STEMI) and
- Non-Q wave infarcts or non-ST segment elevation myocardial infarction (NSTEMI).
In Q wave infarction, there is a sequence for the ECG changes. The sequence is: [3]
- Tall hyperacute T waves,
- ST segment elevation,
- Q wave formation and
- T wave inversion
As the leads are different views of the heart, the changes in the respective leads show the affected areas. [3] [Table 2] shows the ECG changes in the respective leads, which help in locating the infarct in the heart. When infarction occurs in the posterior wall of the left ventricle, a different situation arises. The right ventricle is in the front of the heart normally. Depolarization of the right ventricle moves toward V 1. Depolarization of the left ventricle moves away from V 1 . As left ventricle dominates, the S wave is dominant and R wave is smaller in V 1 . But when an infraction of the posterior wall of the left ventricle takes place, then the depolarization wave of the right ventricle is unopposed. Hence, a dominant R wave is seen in V1. [5] | Table 2: Leads showing ECG changes and location of infarct in the heart
Click here to view |
| Conclusion | | |
Thus, this paper orients the beginner to the ECG. Advanced books can provide further insight into the details of the ECG.
| References | | |
| 1. | Misra KP. A Primer of ECG: A Simple and Deductive Approach. 2 nd ed. India: University Press Private Limited; 2010. 
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| 2. | Tapas KK. Bedside Interpretation of ECG. Delhi: Lordson publishers; 1999.
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| 3. | Houghton AR, David G. Making Sense of The ECG. 2 nd ed. New York: Oxford University Press; 2003.
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| 4. | Hampton JR. The ECG in Practice. 4 th ed. London: Churchill Livingstone Elsevier; 2003.
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| 5. | Hampton JR. The ECG Made Easy. 7 th ed. London: Churchill Livingstone Elsevier; 2008.
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Correspondence Address:
U R Anoop
Department of Oral Pathology, KMCT Dental College, Kerala
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0970-9290.138349
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]
[Table 1], [Table 2] |
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| This article has been cited by | | 1 |
Functional cardiovascular assessment in dentists performing local anesthesia in out-patient settings |
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| S. A. Rabinovich,S. N. Razumova,Yu. L. Vasiliev | | Stomatologiya. 2017; 96(1): 20 | | [Pubmed] | [DOI] | | | 2 |
Functional cardiovascular assessment in dentists performing local anesthesia in out-patient settings |
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| S. A. Rabinovich,S. N. Razumova,Yu. L. Vasiliev | | Stomatologiya. 2017; 96(1): 20 | | [Pubmed] | [DOI] | |
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