There are five specialized tissues which are called conductive system of the heart. These are:
- Sinoatrial (SA) node
- Atrioventricular (AV) node
- Bundle of His
- Right bundle branch (RBB) and left bundle branch (LBB)
- Purkinje fibers
These specialized conductive pathways allow the heart to be electrically activated in a predictable manner (see the sequence below).
The electrical activity or the impulse of the heart starts in the SA node (which is called primary pacemaker), then spreads across the atria (by three internodal pathways and Bachmann's bundle), causing depolarization of both atria. From the atria, the impulse reaches the AV node, where there is some delay, which allows atria to contract and pump blood into the ventricles. The impulse then spreads along the bundle of His, then along the LBB and RBB, finally into the ventricular muscles through Purkinje fibers, causing ventricular depolarization.
Initially, the ventricular septum is depolarized and moves from left to right, then depolarization is of body of the left ventricle, and finally the right ventricle.
This is the normal sequence of stimulation of the specialized tissue. Normal rhythm is called sinus rhythm. The way electrical impulse flows through the heart is called conduction. If abnormalities of electrical activity of the heart or if any disturbance of this sequence occur, there is rhythm disturbance, which is called arrhythmia, or if there is any abnormality of conduction, it is called heart block. Any changes of normal flow of electricity through the heart can be detected by electrocardiogram (ECG) tracing and may indicate damaged cardiac muscle or any abnormality.
Sinoatrial node is the dominant pacemaker. Other pacemaker sites in the heart are atria, AV node, and ventricles. All these are dormant, but can initiate impulse at a slow rate when SA node fails.
- SA node: It is located in the superior and right side of right atrium, near the root of superior vena cava. Normally, the impulse arises in the SA node, called sinus rhythm. From the SA node, the impulse spreads along three internodal pathways (anterior, middle, and posterior) into both right and left atria. Finally, these three internodal pathways enter into the AV node. There is an additional internodal pathway, called Bachmann's bundle, which transmits impulse to the left atrium.Normal rate in SA node is 60–100/min.
- AV node: The AV node is smaller than the SA node. It is located in the subendocardial surface of right side of right atrium, at the posterior part of interatrial septum, near the opening of coronary sinus, just above the tricuspid valve.If the SA node is blocked or fails, the AV node can initiate cardiac impulse and perform as a pacemaker. Normal rate of the AV node is 40–60/min. According to the electrical response, the AV node is divided into three parts:
- High nodal (AN region)
- Mid nodal (N region)
- Low nodal (NH region)
In ECG, these three regions can be detected by looking at the configuration of “P” wave (see details on page no. 17). - Bundle of His: It is the extension of the tail of the AV node that extends downward and to the left, then enter into the interventricular septum, near the junction of muscles and fibrous part of ventricular septum. Then, it is divided into two branches: Right and left bundle branches.When there is AV block, bundle of His can initiate cardiac impulse and perform as a pacemaker. Normal rate of bundle of His is 20–40/min.
- Right bundle branch: It extends on the right side of interventricular septum and spreads into the right ventricle through Purkinje fibers.
- Left bundle branch: It divides into anterior and posterior fascicles. Anterior fascicle spreads into the anterosuperior part of the left ventricle. Posterior fascicle spreads into the posteroinferior part of the left ventricle, through Purkinje fibers.
- Purkinje fibers: These are the terminal network of fibers, diffusely spread into the ventricular muscles in subendocardial and subepicardial myocardium. Normal intrinsic rate of Purkinje fibers is 15–40/min.
NB: Most specialized cardiac fibers contain large number of automatic cells. But atrial and ventricular muscles fibers, under normal condition, have no automatic activity.
There are two major coronary arteries: (1) Right and (2) left.
1. Right Coronary Artery
It arises from the right coronary sinus of Valsalva, runs along the right AV groove, and gives marginal branch that supplies right atrium and right ventricle. It continues as posterior descending artery, which runs in the posterior interventricular groove and spreads into the posterior part of interventricular septum and inferoposterior aspect of the left ventricular wall.
Right coronary artery supplies the following parts:
- SA node: 60% cases
- AV node: 90% cases
- Right atrium and right ventricle
- Inferoposterior aspect of left ventricle
So, the occlusion of right coronary artery results in sinus bradycardia, AV block, infarction of inferior part of left ventricle, and occasionally of right ventricle.
2. Left Coronary Artery
It arises from the left coronary sinus of valsalva. Within 2.5 cm of its origin, left main coronary artery divides into two branches: (1) Left anterior descending artery and (2) Circumflex artery.
- Left anterior descending artery: It runs in the anterior interventricular groove and gives branches to supply the anterior part of interventricular septum, anterior wall, and apex of the left ventricle.
- Circumflex artery: It runs posteriorly in the left AV groove and supplies the marginal branch to the left atrium, also lateral and posteroinferior part of the left ventricle.
Left coronary artery also supplies:
- SA node in 40% cases
- AV node in 10% cases
- Bundle of His
- Right and left bundle branches
Occlusion of the left anterior descending artery and the circumflex artery causes infarction of the corresponding territories of left ventricle. Occlusion of the left main coronary artery causes extensive damage and is usually fatal.
Venous system mainly follows coronary arteries, but drains to the coronary sinus in the AV groove, then to the right atrium.
Coronary vessels receive sympathetic and parasympathetic innervations. Stimulation of α-receptor causes vasoconstriction and β2 causes vasodilatation. Sympathetic stimulation of coronary artery causes dilatation and parasympathetic stimulation also causes mild dilatation of normal coronary artery. Healthy coronary endothelium releases nitric oxide, which promotes vasodilatation. Systemic hormones, neuropeptides, and endothelin also influence arterial tone and coronary flow.
Cardiac muscles have some special properties:
- Automaticity: Without external stimulus, heart muscle can initiate normal cardiac impulse by the SA node.
- Autorhythmicity: Cardiac muscle can contract after a regular interval called autorhythmicity.
- Excitability: Cardiac muscle can be excited by adequate external stimulus.
- Conductivity: Cardiac muscle has the ability to conduct impulse from one muscle cell to another cell.
- Contractility: Ability to contract after depolarization.
- Refractory period: It is a period during which activated muscle fibers do not respond to further stimulus. It is of two types: (1) Absolute refractory period and (2) Relative refractory period.
- Absolute refractory period: During this period, muscle fibers do not respond to any stimulus.
- Relative refractory period: With very strong stimulus, muscle fibers may respond.
- All-or-none law: If external stimulus is too little, no cardiac impulse is initiated. But with adequate stimulus, all muscle fibers contract with its best ability.
- Functional syncytium: Cardiac muscle fibers are electrically connected with one another by a gap junction. When one muscle fiber is excited, the action potential spreads to whole cardiac muscle fibers, because of the presence of intercalated disc. It is called syncytium.
NB: Remember the following points:
NERVE SUPPLY OF THE HEART
The heart is supplied by both sympathetic and parasympathetic (in cardiac plexus).
- Sympathetic (adrenergic) supplies both atria and ventricular muscle, and also conductive specialized tissue.
- Parasympathetic preganglionic fibers and sensory fibers reach the heart through vagus nerves. Cholinergic nerves supply the SA node and the AV node via muscarinic (M2) receptors.
Nerve supply is mainly through β1 and β2 receptors.
- β1 receptor is predominant in heart, having both inotropic and chronotropic effect.
- β2 receptor is predominant in vascular muscles and causes vasodilatation.
Under basal condition, predominant effect is parasympathetic through vagus nerve over sympathetic, resulting in slow heart rate. So during sleep, the heart rate is slow. Also in athlete, there is predominant vagal effect (so heart rate may show bradycardia).
Heart consists of three types of cells:
- Pacemaker cells: They generate the impulse.
- Electricity conducting cells: They transmit the impulse.
- Myocardial cells: They maintain the contractile functions of the heart.
Definition
It is the graphical representation of electrical potentials produced when the electric current passes through the heart. Electrical activity is the basic characteristic of heart and is the stimulus for cardiac contraction.
Electrical activity is detected by electrodes attached to the skin. Normal electrical conduction of the heart allows the impulse that is generated by the SA node, to be propagated to and stimulate the cardiac muscle, which contracts after stimulation. It is the ordered, rhythmic stimulation of the myocardium during the cardiac cycle that allows efficient contraction of the heart, thereby allowing blood to be pumped throughout the body. Disturbance of electrical function is common in heart disease.
Electrocardiogram records the electrical impulse on ECG paper by electrodes placed on the body surface, called waves or deflections. Waves that appear on ECG paper represent the electrical activities of the myocardial cells. The following points of waves are observed recorded on ECG paper:
- Duration: It is measured in horizontal direction.
- Height or amplitude: It is measured in vertical direction.
- Configuration: It indicates the shape and appearance of particular wave.
One heartbeat is recorded as a grouping of waves which are designed by P-QRS-T and U.
| — It represents atrial depolarization |
| — It represents the time taken for the cardiac impulse to spread over the atrium |
| — It represents ventricular depolarization |
| — It represents ventricular repolarization |
| — It represents repolarization of interventricular septum |
In a normal ECG recording, there are 12 leads, which are different view parts of heart's electrical activity.
- Three bipolar limb leads
- Three unipolar limb leads
- Six chest leads
Bipolar Limb Leads
These are also called limb leads, which are designated as LI, LII, and LIII.
Unipolar Limb Leads
These are also called augmented limb leads, which are designated as aVR, aVL, and aVF (which means augmented vector right, augmented vector left, and augmented vector foot, respectively). Three unipolar leads have very low voltage, which cannot be recorded satisfactorily. For this reason, recordings of these leads are increased in amplitude. For this reason, they are called augmented unipolar leads, which are represented as aVR, aVL, and aVF.
Chest Leads (Unipolar)
Designated by “V”.
Electrodes are placed in the following places on the chest wall (See figure on page 2).
- V1—4th intercostal space at right sternal border.
- V2—4th intercostal space at left sternal border.
- V3—midway between V2 and V4 on left side.
- V4—5th intercostal space in left midclavicular line.
- V5—5th intercostal space in left anterior axillary line.
- V6—5th intercostal space in left midaxillary line.
NB: Before application of the electrode, skin preparation by a special jelly should be ensured which improves the quality of ECG. Limb lead electrodes are attached at the wrists and ankle, with the patient in a supine position and a pillow under the head.
By looking the following leads, the site and surface of heart lesion are identified.
NB: Remember the following points:
Before interpreting an ECG, one must know the details about the ECG paper, standardization, and different waves in ECG. It is a matter of good exposure, experience, and understanding of the pattern interpretation, which requires a method of systematic ECG analysis.
So, everyone must have some basic knowledge about the ECG paper, normal ECG tracing, different waves, limits of normal value, duration and rhythm, etc.
During interpretation: Look at the following points carefully:
- Standardization (see in the beginning)—like this ∏, which is 10 mm (1 mV), normally.
- Paper speed—25 mm/s.
- Rhythm—by looking at RR interval (LII is usually called rhythm lead), see whether it is regular or irregular.
- Count the heart rate (per minute).
- Different waves and segments: Important points to be seen are as follows:
- P—Whether normal, small or tall, inverted, wide, notched, bifid, variable configuration
- PR—Normal or prolonged or short
- Q—Normal or pathological
- R—Normal or tall or short, notched or M pattern
- QRS—Normal or wide, high or low voltage, variable or change of shape
- ST segment—Normal or elevated or depressed
- T—Normal or tall or small or inverted
- U wave—Normal or small
- QT—Short or prolonged
- Axis—whether normal or right or left axis deviation (LAD).
- Abnormalities—any arrhythmia, infarction, hypertrophy, etc.
Ques. What is rhythm?
Ans. It is the interval between two successive RR waves.
Ques. What are the diseases diagnosed by looking at an ECG?
Ans.
- Tachycardia or bradycardia
- Chamber enlargement (right or left atrial or both and right or left ventricular or both)
- Myocardial infarction (acute or old)
- Myocardial ischemia
- Arrhythmias (such as atrial fibrillation or flutter, ventricular tachycardia or fibrillation or ectopics, etc.)
- Pericardial disease such as acute pericarditis and pericardial effusion.
- Block (first degree block, SA block, AV block, and bundle branch block)
- Drug effect (such as digoxin)
- Extracardiac abnormalities—electrolyte imbalance (such as hypokalemia or hyperkalemia), hypocalcemia or hypercalcemia, low-voltage tracing (in myxedema, hypothermia, and emphysema). Pulmonary disease such as pulmonary embolism and cor pulmonale.
- Exercise ECG to see coronary artery disease.
- Also, Holter monitoring ECG to detect arrhythmia and conduction defect.
Systematic approach in ECG interpretation: Look at the following points chronologically–
- Rate—what is the rate?
- Rhythm—regular or irregular, regularly followed by occasional irregular.
- Characters of individual waves (P, PR, Q, R, QRS, ST, T, and U).
- Specific pathological changes.
Electrocardiogram paper shows small and large squares. In each small square, thin horizontal and vertical lines are present in 1 mm interval. A heavier thick line is present in every 5 mm interval (five small squares). Time is measured horizontally and voltage height is measured vertically.
- One small square:
- Height = 1 mm
- Horizontal (in time) = 0.04 second
- One big square (five small squares):
- Height = 5 mm
- Horizontal (in time) = 0.04 × 5 second = 0.2 second
So, 0.2 second = 5 mm1 second = 5/0.2 = 25 mmSo, recording speed is 25 mm/s (i.e., 1,500 mm/min).A faster recording speed (50 mm/s) is occasionally used to visualize wave deflection. - Isoelectric line: It is the baseline in ECG paper.
- Different waves or deflections in ECG tracings are measured. If the wave is above the baseline, it is called positive deflection and if it is below the baseline, it is called negative deflection.
- Positive deflection means the stimulus spreads toward the electrode, and negative deflection means stimulus spreads away from the electrode.
NB: Remember the following points:
- Before telling low voltage or high voltage, always see whether the normal standardization is correct or not (i.e., it should be 10 mm in height).
- Arm leads are properly placed or not.
- Be careful about artifact.
Criteria of Low-voltage Tracing
- In standard limb leads—QRS <5 mm (mainly R wave in LI, LII, and LIII)
- In chest leads—QRS <10 mm (mainly R wave in V1 to V6)
Causes of Low-voltage ECG Tracing
- Incorrect standardization (i.e., if <10 mm)
- Obesity
- Pericardial effusion
- Chronic constrictive pericarditis
- Myxedema
- Emphysema
- Hypothermia
- Pneumothorax
- Plural effusion
- Previous massive myocardial infarction
- Dilated cardiomyopathy
Causes of High-voltage ECG Tracing
- Incorrect standardization (i.e., if >10 mm)
- Hypertrophy of left or right ventricle
Summary of ECG Conventions and Intervals
Ans.
- Depolarization: It means initial spread of stimulus through the muscle, causing activation or contraction.
- Repolarization: It means the return of stimulated muscle to the resting state (recovery from activation or contraction).
Artifact in ECG
Sometimes in an ECG tracing, there may be unexplained abnormal waves which are due to electrical current interference or muscle tremor or spasm. These are actually artifacts.
Characters of Normal ECG
- Normal ECG recording consists of P wave (atrial beat), followed by QRS, ST, and T waves (ventricular beat).
- Capital letters P, Q, R, S, and T indicates large wave (>5 mm).
- Small letters p, q, r, s, and t indicates small wave (<5 mm).
Types of Waves in ECG
| — | It is the deflection produced by atrial depolarization |
| — | It is the deflection produced by ventricular depolarization |
| — | It is the first negative deflection produced by ventricular depolarization. It precedes the R wave |
| — | It is the first positive deflection produced by ventricular depolarization |
| — | It is the negative deflection after R wave produced by ventricular depolarization |
| — | It indicates ventricular repolarization |
- J point—seen at the beginning of ST segment. J point is the junction between the termination of QRS complex and beginning of ST segment. J (junction) point indicates the end of QRS complex. It is often situated above the baseline, particularly in healthy young males.
- U wave—not always seen. When present, it follows the T wave, preceding the next P wave. It indicates the repolarization of interventricular septum or slow repolarization of the ventricles.
Electrocardiogram of Reversed Arm Leads
If the limb electrodes are wrongly attached (right one on the left and left one on the right), there will be inverted P in LI.
Also, abnormal QRS complex and T wave in LI. It is called “technical dextrocardia.” QRS is normal in chest leads.
In any ECG, there are different waves and intervals described as follows:
- PR interval: It is the distance between the beginning of P to beginning of QRS (or Q). Ideally, it is called PQ interval.
- PP interval: It is the distance between two successive P waves. In sinus rhythm, P-P interval is regular.
- RR interval: It is the distance between two successive R waves. In sinus rhythm, R-R interval is regular.
- QT interval: It is the distance between the beginning of Q wave and the end of T wave.
Segment in ECG
The portion of the baseline is called the isoelectric line.
- ST segment: It is the distance from the end of QRS complex to the beginning of T wave. It indicates the beginning of ventricular repolarization. Normally, it is in isoelectric line, but may vary from −0.5 to +2 mm in chest leads.
- PR segment: It is the distance between the termination of P wave and the onset of QRS complex. Normally, it is at the isoelectric line.
NB: Remember the following points:
P Wave
Characters of Normal P Wave
- P wave results from spread of electrical activity through the atria.
- Width or duration (in time, horizontally): 0.10 second (2.5 small squares).
- Height: 2.5 mm (2.5 small squares). Height × Duration = 2.5 × 2.5 small squares.
- P wave is better seen in LII, as atrial depolarization is toward LII (also seen in V1), because the impulse spreads from the right atrium to the left atrium.
- P wave is upright in all leads, mainly LI, LII, and aVF (except aVR). P is inverted in aVR and occasionally in aVL.
- P wave in V1 may be biphasic: Equal upward and downward deflection, notched, and wide. Activation of the right atrium produces positive component and activation of the left atrium produces negative component.
- Normal P is rounded, neither peaked nor notched.
Abnormalities of P Wave
P wave may be:
- Absent, or fibrillary or saw-toothed
- Tall or small
- Wide, notched, and biphasic
- Inverted
- Variable and multiple
Causes of absent P wave:
- Atrial fibrillation (P is absent or replaced by fibrillary f wave)
- Atrial flutter (P is replaced by flutter wave, which shows saw-tooth appearance)
- SA block or sinus arrest
- Nodal rhythm (usually absent in mid nodal)
- Ventricular ectopic and ventricular tachycardia
- Supraventricular tachycardia (SVT) (P is hidden within QRS, due to tachycardia)
- Hyperkalemia (may be small or absent)
- Idioventricular rhythm
Causes of tall P wave:
- Tall P is called P pulmonale (height >2.5 mm, i.e., >2.5 small squares).
- It is due to right atrial hypertrophy or enlargement [due to cor pulmonale and chronic obstructive pulmonary disease (COPD)].
- Atrial tachycardia
- Atrial ectopic
- Nodal rhythm (high nodal)
- Nodal ectopic (high nodal)
- Hyperkalemia
Causes of wide P wave:
- It is broad and notched P is called P mitrale (duration >0.11 second, or >2.5 small squares). It is found in mitral stenosis.
- It is due to left atrial hypertrophy or enlargement.
- In V1, P wave may be biphasic with a small positive wave preceding a deep and broad negative wave (indicates left atrial enlargement or hypertrophy).
Causes of inverted P wave (negative in LI, LII, and aVF):
- Incorrectly placed leads (reversed arm electrodes)
- Dextrocardia
- Nodal rhythm with retrograde conduction
- Low atrial and high nodal ectopic beats
Causes of variable P wave:
- Presence of variable P waves indicates wandering pacemaker (P may be inverted, some small, and some upright).
Causes of multiple P waves (consecutive two or more):
- AV block (either partial or complete heart block)
- SVT with AV block
Characters of Normal P-R Interval
- It is the distance between the onset of P wave to the beginning of Q wave (if Q wave is absent, then measure up to the onset of R wave).
- It is the time required for the impulse to travel from the SA node to the ventricular muscle. The impulse is transmitted to the ventricle via the AV node.
- P-R interval varies with age and heart rate.
- P-R interval is short, if the heart rate is increased, and long, if the heart rate is decreased.
- Normal PR interval—0.12–0.20 second (maximum five small squares):
- In children, upper limit is 0.16 second.
- In adolescent, upper limit is 0.18 second.
- In adult, upper limit is 0.20 second.
- P-R is short, if it is <0.10 second and long, if it is >0.20 second.
Abnormalities of P-R Interval
PR interval may be:
- Prolonged
- Short
- Variable
Prolonged P-R interval (>0.2 second)
It is due to first degree heart block. Causes are as follows:
- Ischemic heart disease (occasionally, inferior myocardial infarction)
- Acute rheumatic carditis
- Myocarditis (due to any cause)
- Atrial dilatation or hypertrophy
- Hypokalemia
- Hypomagnesemia
- Drugs—digitalis toxicity, quinidine, occasionally β-blocker, and calcium channel blocker (e.g., verapamil)
Short P-R interval (<0.12 second)
Causes are as follows:
- Normal variant
- Wolff–Parkinson–White (WPW) syndrome. In this case, there is delta wave.
- Lown–Ganong–Levine (LGL) syndrome. In this case, there is no delta wave.
- Nodal rhythm
- Nodal ectopic (high nodal)
- Occasionally, if dissociated beat is present and also in infant, steroid therapy
Variable P-R interval
Causes are as follows:
- Wenckebach phenomenon (Mobitz type I): In such case, there is progressive lengthening of P-R interval followed by a drop beat.
- Partial heart block (Mobitz type II): P-R interval is fixed and normal, but sometimes P is not followed by QRS.
- 2:1 AV block: In which, alternate P wave is not followed by QRS.
- Complete AV block: There is no relation between P and QRS.
- Wandering pacemaker: There is variable configuration of P.
Characters of Normal QRS Complex
- QRS complex represents the depolarization of ventricular muscles.
- It consist of three waves: Q, R, and S.
- First downward deflection is called Q wave.
- Upward deflection after Q is R wave.
- Downward deflection after R is S wave.
- Depolarization of the left ventricle contributes to main QRS (as the mass of the left ventricle is two to three times more than the mass of right ventricle).
- QRS is predominantly positive in leads that look at the heart from the left side—L1, aVL, V5, and V6.
- It is negative in leads that look at the heart from the right side—aVR, V1, and V2.
- In V1, S is greater than R.
- In V5 and V6, R is tall.
- QRS appears biphasic (part above and part below the base line) in V3 and V4.
- Normal duration of QRS is 0.08–0.11 second (<3 small squares) and height <25 mm.
Various Forms and Components of QRS Complex
- Q wave: Initial downward deflection.
- R wave: Initial upward deflection.
- S wave: Downward deflection after R wave.
- rS complex: Small initial r wave, followed by large S wave.
- RS complex: A complex with R and S waves of equal amplitude.
- Rs complex: A large R wave followed by a small s wave.
- qRS complex: Small initial downward deflection, followed by a tall R, which is followed by a large S.
- Qr complex: Large Q, followed by a small r.
- QS complex: Complex with complete negative deflection (no separate Q and S).
- rSr complex: Small r, then deep S, followed by small r.
- RSR complex: Tall R, then deep S, followed by tall R.
- RR complex: When deflection is completely positive and notched (M pattern).
Abnormalities of QRS Complex
QRS may be:
- High voltage
- Low voltage
- Wide
- Change in shape
- Variable
Causes of high-voltage QRS
- Incorrect calibration
- Thin chest wall
- Ventricular hypertrophy (right or left or both)
- WPW syndrome
- True posterior myocardial infarction (in V1 and V2)
- Incorrect calibration
- Thick chest wall or obesity
- Hypothyroidism
- Pericardial effusion
- Emphysema
- Chronic constrictive pericarditis
- Hypothermia
Causes of wide QRS (>0.12 second, three small squares)
If it is >0.12 second, it is called wide QRS.
- Bundle branch block [left bundle branch block (LBBB) or right bundle branch block (RBBB)]
- Ventricular ectopics
- Ventricular tachycardia
- Idioventricular rhythm
- Ventricular hypertrophy
- Hyperkalemia
- WPW syndrome
- Pacemaker (looks like LBBB with spike)
- Drugs (quinidine, procainamide, phenothiazine, and tricyclic antidepressants)
Causes of changes in shape of QRS
- Right or left bundle branch block (slurred or M pattern)
- Ventricular tachycardia
- Ventricular fibrillation
- Hyperkalemia
- WPW syndrome
Causes of variable QRS
- Multifocal ventricular ectopics
- Torsades de pointes
- Ventricular fibrillation
Alternative QRS voltage (alternate large and small QRS complex)
Normally, voltage of all QRS complex is same. But, if the voltage of QRS complex alternates between high and low in successive beats, it is called electrical alternans. Causes are as follows:
- Moderate-to-severe pericardial effusion (due to malignant, tubercular, or postsurgical). It may indicate cardiac tamponade or impending tamponade.
- Organic heart disease such as ischemic cardiomyopathy and diffuse myocarditis.
NB: Electrical alternans of QRS may be clinically associated with cardiomegaly, gallop rhythm, and signs of left ventricular failure.
Q Wave
Characters of Normal Q Wave
- Q wave is usually absent in most of the leads. However, small q wave may be present in I, II, aVL, V5, and V6. This is due to septal depolarization.
- Small q may be present in LIII (which disappears with inspiration).
- Depth—<2 mm (two small squares).
- Width—one small square.
- It is 25% or less in amplitude of the following R wave in the same lead (one-fourth of the R wave).
- Deep >2 mm (two small squares)
- Wide >0.04 second or more (>1 mm or one small square)
- Should be present in more than one lead (if present in one lead, it is not pathological).
- Associated with loss of height of R wave.
- Q wave should be >25% of the following R wave of the same lead.
Causes of Pathological Q Wave
- Myocardial infarction (the most common cause)
- Ventricular hypertrophy (left or right)
- Cardiomyopathy
- LBBB
- Emphysema (due to axis change or cardiac rotation)
- Q only in LIII is associated with pulmonary embolism (SI, QIII, and TIII pattern).
NB: Remember the following points:
R Wave
Characters of Normal R Wave
- It is the first positive (upward) deflection, due to ventricular depolarization.
- Duration <0.01 second.
- R wave usually small (<1 mm) in V1 and V2. It increases progressively in height in V3 to V6 (tall in V5 and V6), i.e., R is small in V1 and V2, tall in V5 and V6.
Normal Height of R Wave
- In aVL <13 mm
- In aVF <20 mm
- In V5 and V6 <25 mm
(If R wave is >25 mm, it is always pathological).
Abnormalities of R Wave
R wave may be:
- Tall
- Small
- Poor progression
Causes of tall R wave
- Left ventricular hypertrophy (in V5 or V6 >25 mm, aVL >13 mm, aVF >20 mm).
Causes of small R wave
Looks like low-voltage tracing.
- Incorrect ECG calibration (standardization)
- Obesity
- Emphysema
- Pericardial effusion
- Hypothyroidism
- Hypothermia
R wave progression
The height of R wave gradually increases from V1 to V6. This phenomenon is called R wave progression.
Poor progression of R wave:
Normally, amplitude of R wave is tall in V5 and V6. In poor R wave progression, amplitude of R wave is progressively reduced in V5 and V6. Causes are as follows:
- Anterior or anteroseptal myocardial infarction
- Left bundle branch block
- Left ventricular hypertrophy (though R is tall in most cases)
- Dextrocardia
- Cardiomyopathy
- COPD
- Left-sided pneumothorax
- Left-sided pleural effusion (massive)
- Marked clockwise rotation
- Chest electrodes placed incorrectly
- Deformity of the chest wall
S Wave
Characters of Normal S Wave
- It is the negative deflection after R wave (normally one-third of R wave).
- Normally, deep in V1 and V2, as the impulse is going to the muscles of the left ventricle and then to the right ventricle.
- It is progressively diminished from V1 to V6 (small S wave may be present in V5 and V6).
- In V3, R and S waves are almost equal (corresponds with interventricular septum).
Characters of Normal ST Segment
- Measured from the end of S to the beginning of T wave. It represents beginning of ventricular repolarization.
- Normally, it is in isoelectric line (lies at same level of ECG baseline).
- ST elevation is normal up to 1 mm in limb leads and 2 mm in chest leads (mainly V1 to V3).
- In Negroes, ST elevation of 4 mm may be normal, which disappears on exercise.
- Normally, ST segment may be depressed, <1 mm.
Abnormalities of ST Segment
ST segment may be:
- Elevated
- Depressed
Causes of ST elevation (>2 mm)
- Acute myocardial infarction (ST elevation with convexity upward)
- Acute pericarditis (ST elevation with concavity upward, chair-shaped or saddle-shaped)
- Prinzmetal's angina, also called vasospasm angina (ST elevation with tall T).
- Ventricular aneurysm (persistent ST elevation)
- Early repolarization (high take-off)
- Normal variant in Africans and Asians.
- May be in hyperkalemia.
- Acute myocardial ischemia (horizontal or down slope ST depression with sharp angle ST-T junction)
- Ventricular hypertrophy with strain (ST depression with convexity upward and asymmetric T inversion).
- Digoxin toxicity (sagging of ST depression—like thumb impression, also called reverse tick).
- Acute true posterior myocardial infarction (in V1 and V2), associated with dominant R and tall upright T wave.
- Reciprocal change in STEMI (ST-elevation myocardial infarction).
Early repolarization (high take-off)
- It is a benign, normal finding in young healthy person, more in black males.
- It is seen in chest leads, commonly V4 to V6 (rarely, in other chest lead).
- ST elevation is usually associated with J point elevation.
- It is not associated with inversion of T wave or abnormal Q wave.
NB: Remember the following points:
T Wave
Characters of Normal T Wave
- It indicates ventricular repolarization.
- It follows S wave and ST segment.
- It is upright in all leads, except aVR.
- Usually, it is >2 mm in height. It may be normally inverted in V1 and V2.
- Normally, it is not >5 mm in standard leads and 10 mm in chest leads.
- It is minimum one-fourth of R wave of the same lead.
- The tip of T is smooth (rounded).
Abnormalities of T Wave
T wave may be:
- Inverted
- Tall peaked and tented
- Small
- Biphasic
Causes of T inversion
- Myocardial ischemia and infarction
- Subendocardial myocardial infarction (non-Q wave myocardial infarction)
- Ventricular ectopics
- Ventricular hypertrophy with strain
- Cardiomyopathy
- Myxedema
- Bundle branch block
- Drugs (digoxin and phenothiazine)
- Physiological: Nonspecific (smoking, anxiety, anorexia, exercise, after heavy meal, or glucose)
Causes of tall peaked T wave
- Hyperkalemia (tall, tented, or peaked)
- Hyperacute myocardial infarction (tall T wave)
- Acute true posterior myocardial infarction (tall T in V1 to V2)
- Prinzmetal's angina
- It may be normal in some Africans and Asians.
Ques. How to differentiate between tall T due to hyperkalemia from hyperacute myocardial infarction?
Ans. As follows:
- In hyperkalemia: T is tall, tented, narrow-based, and symmetrically peaked. QT interval is short.
- In hyperacute myocardial infarction: T is broad, not tented, and asymmetrical. QT interval is prolonged.
Ques. What is the other causes of tall, peaked T?
Ans. Prinzmetal's angina (also called vasospasm angina).
Ques. How to differentiate between hyperacute myocardial infarction and Prinzmetal's angina?
Ans. Tall-peaked T wave may also be found in Prinzmetal's angina, confused with hyperacute myocardial infarction. To differentiate it from myocardial infarction, in Prinzmetal's angina, serial ECG shows fall down of T wave, Q wave never appears and enzymes are not raised.
Causes of small T wave:
- Hypokalemia
- Hypothyroidism
- Pericardial effusion
Biphasic T wave:
It means part of T is above isoelectric line and part below the isoelectric line. Causes are as follows:
- Myocardial ischemia
- Hypokalemia
To differentiate between these two, morphology of T is as follows:
- In myocardial ischemia: T wave goes up and then down (Fig. A).
- In hypokalemia: T wave goes down then up (Fig. B).
Ans. It is a disorder in which T is inverted in V1 to V3 (rarely V4 to V6). T inversion is neither symmetrical nor deep. It is common in children and young adults, more in female <40 years. Frequently, it is associated with sinus arrhythmia and high left ventricular voltage.
Camel hump T waves:
Camel hump T waves have a double peak. Causes are as follows:
- Prominent U waves fused to the end of the T wave (as seen in severe hypokalemia).
- Hidden P waves embedded in the T wave, as seen in sinus tachycardia and various types of heart block.
Flattened T waves:
Flattened T waves are usually considered as a nonspecific finding. However, flattened T wave may be due to the following causes:
- Ischemia
- Hypocalcemia
U Wave
Characters of Normal U Wave
- U wave is seen after T wave.
- It may be present in normal ECG, usually smaller and in the same direction of the preceding T wave.
- It represents slow repolarization of interventricular Purkinje fibers and also papillary muscles (but actual genesis of U wave is still controversial).
- Better seen in chest leads (V2 to V4).
- Normal amplitude is 1 mm (2 mm in athlete).
- U wave is easily visible when QT interval is short and heart rate is slow.
Abnormalities of U Wave
U wave may be:
- Inverted
- Prominent
Causes of inverted U wave
- Ischemic heart disease
- Left ventricular hypertrophy with strain (hypertensive heart disease).
Causes of prominent U wave
- May be normally present in young athlete (usually small).
- Hypokalemia (the most common)
- Bradycardia
- Ventricular hypertrophy
- Hyperthyroidism
- Drugs (phenothiazine, quinidine, and digoxin)
- Congenital long QT syndrome
Ques. What is the significance of large U wave?
Ans. The patient is prone to develop torsades de pointes tachycardia.
QT Interval
Characters of Normal QT Interval
- It is the distance from the beginning of Q wave (or R wave, if there is no Q wave) to the end of T wave.
- It represents the total time required for both depolarization and repolarization of the ventricles.
- Normal QT interval is 0.35–0.43 seconds. It is better seen in aVL (because there is no U wave).
- Its duration varies with heart rate, becoming shorter as the heart rate increases and longer as the heart rate decreases. In general, QT interval at heart rate between 60 and 90/min does not exceed in duration, half the preceding RR interval.
- Corrected formula for real QT is:
QT interval may be:
- Short
- Long
Causes of short QT interval
- Digoxin effect
- Hypercalcemia
- Hyperthermia
- Tachycardia
- Hyperkalemia
- Acidosis
Causes of long QT interval
- Hypocalcemia
- Hypokalemia
- Hypomagnesemia
- Bradycardia
- Acute myocarditis
- Acute myocardial infarction
- Hypothermia
- Drug (quinidine, procainamide, flecainide, amiodarone, tricyclic antidepressant, disopyramide, and pentamidine)
- Cerebral injury (head injury and intracerebral hemorrhage)
- Hypertrophic cardiomyopathy
- During sleep
- Congenital long QT syndrome
- Hereditary syndrome:
- Jervell and Lange-Nielsen syndrome (congenital deafness, syncope and sudden death)
- Romano–Ward syndrome (same as above except deafness)
Ques. What are the clinical importance of prolongation of QT interval?
Ans. Prolonged QT interval may be detected in an asymptomatic individual. It may be associated with ventricular arrhythmia. Rarely, it can cause torsades de pointes tachycardia and sudden death.
To see the rhythm—successive RR interval should be seen.
- If the RR interval is equal, it is called regular rhythm.
- If the RR interval is irregular, then it is called irregular rhythm.
NB: Remember the following points:
Causes of Irregular Rhythm
- Physiological: Usually found in sinus arrhythmia
- Pathological:
- Atrial fibrillation
- Atrial flutter
- SA block or sinus arrest
- Atrial tachycardia with block
- Second-degree heart block
- Ventricular fibrillation
Ques. What are the causes of regularly irregular rhythm?
Ans. Causes of regularly irregular rhythm are:
- Physiological: Common in sinus arrhythmia
- Pathological: Ectopic beat, second-degree heart block (e.g., 2:1 or 3:1 block), SA block or sinus arrest
Ques. What are the causes of irregularly irregular rhythm?
Ans. Causes of irregularly irregular rhythm are:
- Atrial fibrillation
- Atrial flutter
- Multiple ectopics
- Atrial tachycardia with block
- Ventricular fibrillation
Characters of Sinus Rhythm
Sinus rhythm shows the following five characters:
- P wave is of sinus origin (means characters of normal P wave).
- P waves and QRS complexes are regular (that means P-P and R-R interval should be constant and identical).
- Constant P wave configuration in a given lead.
- P-R interval and QRS interval should be within normal limit.
- Rate should be between 60 beats/min and 100 beats/min (atrial and ventricular rates are identical).
NB: Remember the following points:
Ques. What is arrhythmia?
Ans. It is the abnormality in initiation or propagation of cardiac impulse.
In any ECG, heart rate should be calculated. Methods vary according to the cardiac rhythm, whether regular or irregular. Standard speed in ECG paper is 25 mm/s. Heart rate is the number of beats per minute. It is calculated by looking at the ECG tracing in the following way:
In the ECG paper:
| = | 1 small square |
| = | 5 small squares or 1 large square |
| = | 25 small squares or 5 large squares |
| = | 25 × 60 = 1,500 small squares or 5 × 60 = 300 large squares |
Heart rate is determined in the following way:
Examples:
- Suppose, the number of small squares between R-R and P-P is 15.
- Suppose, the number of large squares between R-R is 5.
- When the rhythm is irregular:
In irregular rhythm, the above method is not valid. In such case, QRS complex is counted in 6 seconds (30 small square) in rhythm strip, multliplied by 10.
Proceed in the following way:
- Count the number of R in 30 large squares (it is equivalent to 6 seconds).
- Then, simply multiply this by 10 (it becomes rate in 1 minute).
Example:
- Suppose, the number of R in 30 large squares is 12.
- So, the heart rate is 12 × 10 = 120 beats/min.
NB: In ECG, PP interval indicates atrial rate and RR interval indicates ventricular rate. Normally, PP and RR intervals are same. But in some arrhythmia, atrial and ventricular rates are different. These should be counted separately. Examples are atrial fibrillation, atrial flutter, complete heart block, ventricular fibrillation, etc.
Definition
It is the sum of all the depolarization waves as they spread through the ventricles as seen from the front. Axis is the direction of the ECG waveform in frontal plane measured in degrees. The axis of ECG is the major deflection of the overall electrical activity of the heart. It may be normal, LAD, right axis deviation (RAD), or indeterminate. QRS complex is the most important to determine the axis, usually limb leads are examined (not precordial leads).
Axis Determination
- Axis can be derived most easily from the amplitude of QRS complex in LI, LII, and aVF.
- The greatest amplitude of R wave in LI or LII or aVF indicates the proximity of cardiac axis to that lead.
- The axis lies at 90° to the isoelectric complex, i.e., positive and negative deflections are equal in any of the lead LI, LII, LIII, aVL, aVR, and aVF.
Normal axis is between −30° and +90°.
Type of axis deviation:
- Left axis deviation
- Right axis deviation
- Indeterminate axis deviation
- Positive QRS in both LI and aVF means axis is normal.
- Positive QRS in LI and negative in aVF (tall R in LI and deep S in aVF) means LAD. However, in such case, look at LII. If negative in LII, it is more likely to be LAD. But, if positive in LII, axis may be normal.
- Negative QRS in LI and positive in aVF (deep S in LI and tall R in aVF) means RAD.
- If negative QRS in LI and also aVF, the axis is indeterminate.
Left Axis Deviation
When the cardiac axis is between −30° and −90°. Causes are as follows:
- Normal variant (with increased age)
- Left ventricular hypertrophy
- Left anterior hemiblock
- Left bundle branch block
- Inferior myocardial infarction
- WPW syndrome (some)
- Ventricular ectopic
- Pacing from the apex of the right or left ventricle (endocardial pacing)
When the cardiac axis is between +90° and +180°. Causes are as follows:
- Normal variant (common in children and young adult)
- RVH (due to any cause such as chronic cor pulmonale, pulmonary embolism, and congenital heart diseases, i.e., tetralogy of Fallot)
- Anterolateral myocardial infarction (high lateral myocardial infarction)
- Left posterior hemiblock
- Dextrocardia
- WPW syndrome (type A)
- Right bundle branch block
- Epicardial pacing
- Ventricular ectopic
Indeterminate Axis
Occurs when QRS lies between +180° and −90°. This term is used when exact axis can not be determined (all six limb leads are biphasic). It may be found in:
- Severe right ventricular hypertrophy.
- Aneurysm of left ventricular apex.
NB: Remember the following points:
In an ECG, occasionally, there are certain findings detected, which are the normal variants, may be observed in healthy individuals. These are commonly found in young adults and children. Some examples are:
- Sinus arrhythmia
- Early repolarization syndrome (in young black males)
- Inverted P (in inferior leads)
- Short P-R interval
- QRS in V1 (not >0.12 second) and RBBB pattern
- Q wave in LIII (disappears with deep inspiration)
- Tall R in V1 (R/S ratio ≥1)
- T inversion in LIII, aVR, and V1
- Left ventricular hypertrophy (in children and young adults)
- RAD (in children and young adults)
- Mild LAD or left anterior hemiblock, in the absence of cardiac disease
- Wandering pacemaker
- Low voltage in obese people
- First-degree heart block
- Wenckebach phenomenon
- Juvenile T wave pattern in children and young adults.
Careful interpretation is essential for the diagnosis. This should not be confused with underlying pathology. Detailed history and physical findings should be correlated with the ECG findings.
Ques. What are the possible ECG features of healthy athletes?
Ans. There may be change in normal rhythm and ECG pattern in healthy athletes, which are usually normal findings. The following may be the variations in rhythm and variations in ECG pattern.
- Variations in rhythm:
- Sinus bradycardia
- Marked sinus arrhythmia
- Junctional rhythm
- Wandering atrial pacemaker
- First-degree heart block
- Second-degree heart block (Wenckebach phenomenon)
- Variations in ECG pattern:
- Tall P waves
- Prominent septal Q waves
- Tall R and deep S waves
- Counterclockwise rotation
- Slight ST segment elevation
- Tall symmetrical T waves
- T wave inversion, especially in lateral leads
- Biphasic T waves
- Prominent U waves
Exercise ECG is a technique used to assess the cardiac response during exercise. The 12-lead ECG is recorded, while the patient walks or runs on a motorized treadmill. The traditional Bruce protocol is followed. The limb leads are placed on the shoulders and hips, rather than on the wrists and ankles. Blood pressure is recorded, symptoms such as anginal pain are assessed, and ST depression or elevation is noted.
The test is positive, if there is:
- Anginal pain
- Blood pressure falls or fails to rise
- ST depression >1 mm (planar or downsloping depression is more important rather than upsloping ST depression which is nonspecific)
- ST elevation may occur, which indicates transmural ischemia due to coronary spasm or critical stenosis.
The patient who can perform exercise <6 minutes, generally have poor prognosis. Sustained fall of blood pressure indicates severe coronary artery disease.
Exercise tolerance test (ETT) may be false positive (20%), or false negative. It has a specificity of 80% and sensitivity of 70%.
Indications of Exercise Testing
Contraindications of Exercise Testing
Causes of false positive exercise test:
- Digoxin toxicity
- Hypokalemia
- Ventricular hypertrophy
- Bundle branch block
- WPW syndrome
- Mitral valve prolapse
- Significant aortic or mitral valve insufficiency
- Significant aortic valve stenosis
- Female sex
39False negative ETT may occur if the patient is on: β-blocker, verapamil, diltiazem, and nitrate group of drugs.
Reasons for stopping of ETT: During ETT, if any of the following is detected, the procedure should be stopped.
- Sign and symptoms:
- If the patient request stopping, because of severe fatigue
- Severe chest pain, dyspnea, or dizziness or syncope
- Fall in systolic blood pressure (>20 mm Hg).
- Hypertensive response (SBP >260 mm Hg and DBP >130 mm Hg)
- Ataxia
- ECG criteria:
- Severe ST-segment depression (>3 mm)
- ST-segment elevation >1 mm in non-Q wave lead
- Frequent ventricular extrasystoles (unless the test is to assess ventricular arrhythmia)
- Onset of ventricular tachycardia
- New atrial fibrillation or supraventricular tachycardia
- Development of new bundle branch block
- New second- or third-degree heart block
- Cardiac arrest
Holter monitor is a battery-operated portable ECG. It records the electrical activity of the heart continuously over 24–48 hours or longer depending on the type of monitoring used. The patient is provided with a pocket-sized device, which can record and store a short segment of ECG. Electrodes, which are small, plastic patches that stick to the skin, are placed at certain points on the chest and abdomen. The electrodes are connected to an ECG machine by wires, which is kept at the belt of waist. It does not interfere with patient's physical activity. The electrical activity of the heart can be measured, recorded, and printed. No electricity is sent into the body.
Indications:
- To detect suspected arrhythmia in patient with symptoms such as palpitation, dizziness, or syncope.
- To determine the risk or type of arrhythmia or conduction defect.
- To assess the rate control in patient with atrial fibrillation.
- To detect transient myocardial ischemia using ST segment analysis.
- To monitor the efficacy of antiarrhythmic drug therapy.
Patients with the following disease that may require documentation of an arrhythmia:
- Structural heart diseases such as postmyocardial infarction, dilated or hypertrophic cardiomyopathy, and valvular heart disease.
- Primary electrical heart disease such as sick sinus syndrome, WPW syndrome, and high grade AV block.
- Family history of sudden death or arrhythmia.
