Electrocardiography

ELECTROCARDIOGRAPHY
DR. ANAND PATEL
M.P.T. CARDIO-RESPIRATORY
ASSISTANT PROFESSOR

CORONARY CIRCULATION
 Figure 1

CORONARY CIRCULATION
Superior & Inferior Vena Cava
Right Atrium
Tricuspid Valve
Right Ventricle
Pulmonary Semi-lunar Valve

Pulmonary Trunk
Right & Left Pulmonary
Arteries
Lungs
Left Atrium
Pulmonary Veins

Mitral Valve
Left Ventricle
Aortic Semi-lunar Valve
Aorta
Body

RIGHT CORONARY ARTERY
 Supplies blood to:
 Right Atrium
 Right Ventricle
 The SA Node and in 55% of population the LV inferior wall
 The LV posterior wall and ⅓ of the posterior interventricular septum in 90% of the population

LEFT CIRCUMFLEX ARTERY
 the Left Atrium
 the LV lateral wall
 the SA Node in 45% of the population and to the LV posterior wall
 ⅓ of the interventricular septum
 AV Node and Bundle of His in 10% of the population

LEFT ANTERIOR DESCENDING ARTERY
 the LV anterior and lateral walls
 the Left and Right Bundle Branches
 the anterior ⅔ of the interventricular septum

2
ELECTRICAL CONDUCTION
OF THE HEART

CARDIAC CONDUCTION
 The Conduction System of the Heart

CARDIAC CONDUCTION
 The SA Node is the primary pacemaker for the heart at 60-100 beats/minute
 The AV Node is the “back-up” pacemaker of the heart at 40-60 beats/ minute.
 The Ventricles (bundle branches & Purkinje fibers) are the last resort and maintain an intrinsic rate of
only 20-40 beats/minute

CARDIAC CONDUCTION
 The normal conduction pathway:
SA Node AV Node
Bundle of
His
Right & Left
Bundle
Branches
Purkinje
Fibers
Myocardial
Contraction

WHAT IS AN ECG?
 An electrocardiogram (ECG) is a graphic recording of the electrical activity of the heart.
 The machine is called Electrocardiograph while the recording is called Electocardiogram & is used as a
diagnostic tool to assess cardiac function.

ECG PAPER
 ECG paper comes in a roll of graph paper consisting of horizontal and vertical light and dark lines.
 The horizontal axis measures time
 The vertical axis measures voltage.

ECG PAPER
 One small square = 0.04 seconds
 One large square = 0.2 seconds Or [One small square(0.04)] x 5

ECG PAPER
 The light lines circumscribe small squares of 1 x 1 mm.
 One small square = 0.1 mV
 The dark lines delineate large squares of 5 x 5 mm
 One large square = 0.5 mV

ELECTROCARDIOGRAM – 12 LEADS
 6 limb leads
 6 precordial leads
 Positioning measures 12 perspectives or views of the heart
 The 12 perspectives are arranged in vertical columns
 Limb leads are I, II, III, AVR, AVL, AVF
 Precordial leads are V1, V2, V3, V4, V5, V6
 Horizontal marks time
 Vertical marks amplitude

ELECTROCARDIOGRAM - 12-LEADS
 Each limb lead I, II, III, AVR, AVL, AVF records from a different angle
 All 6 limb leads intersect and visualize a frontal plane
 The 6 chest leads (precordial) V1, V2, V3, V4, V5, V6 view the body in the horizontal plane to the AV node
 The 12 lead ECG forms a camera view from 12 angles

ELECTROCARDIOGRAM LEAD PLACEMENT
 Each positive electrode acts as a camera looking
at the heart
 10 leads attached for 12 lead diagnostics. The
monitor combines 2 leads.
 Mnemonic for limb leads
 White on right
 Black on left
 Smoke(black) over fire(red)
 Snow(white) on grass(green)

UNIPOLAR AND BIPOLAR LEADS
 Limb leads I, II, III are bipolar and have a negative and positive pole
 Electrical potential differences are measured between the poles
 AVR, AVL and AVF are unipolar
 No negative lead
 The heart is the negative pole
 Electrical potential difference is measured betweeen the lead and the heart
 Chest leads are unipolar
 The heart also is the negative pole

PRECORDIAL LEADS
 Anteroseptal: V1, V2, V3, V4
 Anterior: V1–V4
 Anterolateral: V4–V6, I, aVL
 Lateral: I and aVL
 Inferior: II, III, and aVF
 Inferolateral: II, III, aVF, and
V5 and V6

NORMAL WAVEFORM
 The waveforms that represent depolarization of the myocardium are labeled P, QRS, T, and U.
 The P wave is normally rounded, symmetric, and upright, representing atrial depolarization.
 A P wave should occur before every QRS complex.
 The PR interval is the interval that starts at the beginning of the P wave and ends at the beginning of the
QRS complex; the portion following the P wave is also defined as the isoelectric line.
 The PR interval is normally 0.12 to 0.20 second (or up to five small squares on the ECG paper). This
period of time represents the atrial depolarization and the slowing of electrical conduction through the
AV node.

 The QRS complex follows the PR interval and has multiple deflections and may have numerous
variations, depending on the lead that is being monitored.
 The QRS complex begins at the end of the PR interval and appears as a thin line recording from the ECG
stylus, ending normally with a return to the baseline.
 The QRS duration reflects the time it takes for conduction to proceed to the Purkinje fibers and for the
ventricles to depolarize.
 The normal duration is 0.06 to 0.10 second

 The ST segment follows the QRS complex, beginning where the ECG tracing transforms from a thin line
to a thicker line and terminating at the beginning of the T wave.
 The ST segment should be represented as an isoelectric line along the same line (if measured with a
ruler) as the PR interval or the baseline.
 The T wave follows the ST segment and should be rounded, symmetric, and upright. The T wave
represents ventricular repolarization.

 The QT interval (from the beginning of the QRS complex until the end of the T wave) normally measures
between 0.32 and 0.40 second if a normal sinus rhythm is present.
 Finally, the RR interval is reviewed throughout the rhythm strip to assess regularity of rhythm.
 Normal rhythm requires a regular RR interval throughout; however, a discrepancy of up to 0.12 second
between the shortest and the longest RR interval is acceptable for normal respiratory variation.

ECG ANALYSIS
 Four elements are specifically assessed on a 12-lead ECG tracing:
▪ Heart rate
▪ Heart rhythm
▪ Hypertrophy
▪ Infarction

HEART RATE
 Six second tracing
 R wave measurement
 Counting box

SIX SECOND TRACING
 The investigator obtains an ECG recording that is 6 seconds in length.
 The number of QRS complexes found in the 6-second recording is then multiplied by 10 to determine
the heart rate per minute:
 number of QRS complexes in a 6-second recording × 10 = heart rate per minute.

R WAVE MEASUREMENT
 An alternative method of measuring heart rate is by identifying a specific R wave that falls on a heavy
black line.
 For each heavy black line that follows this R wave until the next R wave occurs, the therapist counts 300,
150, 100, 75, 60, 50.
 Where the next R wave falls in this counting method gives the actual heart rate.
 The one problem with R wave measurement for determining heart rate is that it cannot be used with
irregular heart rhythms.

COUNTING BOXES
 The third method of obtaining the heart rate from the graph paper is to count the number of large
boxes (5 mm or 0.2 second in length) between the first QRS complex and the next QRS complex.
 The number of large boxes is then divided into 300 to obtain an estimate of the heart rate: 300 ÷
number of large boxes between the next QRS complex and the next QRS complex = heart rate per
minute.
 A more accurate measurement of the heart rate can be made by counting the number of small boxes (1
mm or 0.04 second in length) between the QRS complexes and then dividing this number into 1500.

 The 12-lead ECG is used primarily for determining ischemia or infarction, as well as for comparing
previous ECG recordings for an individual.
 However, for simple detection of rate or rhythm disturbances, single-lead monitoring is the appropriate
choice.
 Single-lead monitoring is limited to detection of rate and rhythm disturbances; it cannot detect
ischemia.
 Twelve-lead ECG monitoring is used when ischemia is suspected or when a change in condition is noted

THE PHYSIOLOGY UNDERLYING THE NORMAL WAVEFORMS
 The cardiac cycle from diastole through systole can be explained by discussing the physiology during
each of the waveforms of the ECG.
 Starting with the end of the QRS at the point where the S wave ends and the beginning of the T wave
occurs is the actual end of systole and the beginning of diastole.
 It is here where the semilunar valves (aortic and pulmonic) close and the mitral and tricuspid open with
the beginning of diastole.
 The ventricles start filling passively with blood from the atrium throughout the entire T wave.

 The T wave ends and the beginning of the P wave begins, atrial depolarization begins, which involves the
atria contracting and forcing the last bit of volume into the ventricles.
 This actually comprises approximately 15% to 20% of the effective stroke volume.
 At the end of the P wave and PR interval, the mitral and tricuspid valves now close signaling the end of
diastole.

 Instantaneously all four valves are closed, which creates an isometric contraction until enough force is
developed and the semilunar valves are forced open, ejecting blood out into the pulmonary artery and
the aorta with the initiation of systole.
 The cardiac cycle begins again with the end of systole occurring, semilunar valves closing, and mitral and
tricuspid opening to initiate ventricular filling and diastole.

CLINICAL TIP
 Because the P wave represents the atrial contraction, which forces approximately 15% to 20% of the
stroke volume into the ventricles, if an individual does not have a P wave, then he or she also has
approximately 15% to 20% lower stroke volume with every beat.

BASIC INTERPRETATION OF HEART RHYTHM
 key to the basic interpretation of heart rhythm in the clinical setting involves using the systematic
approach as presented earlier, correlating the interpretation with the history and the signs and
symptoms of the patient and then deciding if the rhythm is benign or life threatening.
 If the decision is that the rhythm is truly benign, then the patient does not require ECG monitoring.
 If the rhythm is relatively benign, then occasional ECG monitoring may be necessary, or at least
physiologic monitoring of the heart rate and blood pressure should be employed.
 If the arrhythmia is determined to be life threatening, ECG monitoring and physiologic monitoring
should be carried out. In some cases, the patient may not be a candidate for any activity or procedure
until the arrhythmia is controlled.

NORMAL SINUS RYTHM
 The characteristics of NSR include the following:
▪ All P waves are upright, normal in appearance, and identical in configuration; a P wave exists before every
QRS complex.
▪ The PR interval is between 0.12 and 0.20 second.
▪ The QRS complexes are identical.
▪ The QRS duration is between 0.06 and 0.10 second.
▪ The RR interval is regular (or, if irregular, the difference between shortest and longest intervals is less than
0.12 second).
▪ The heart rate is between 60 and 100 beats per minute.

SINUS BRADYCARDIA
 Sinus bradycardia differs from NSR only in the rate, which is less than 60 beats per minute. The
characteristics of sinus bradycardia include the following:
 ▪ All P waves are upright, normal in appearance, and identical in configuration; a P wave exists before every QRS
complex.
 ▪ The PR interval is between 0.12 and 0.20 second.
 ▪ The QRS complexes are identical.
 ▪ The QRS duration is between 0.06 and 0.10 second.
 ▪ The RR interval is regular throughout.
 ▪ The heart rate is less than 60 beats per minute.

SIGNS, SYMPTOMS, AND CAUSES
 Sinus bradycardia is normal in well-trained athletes because of their enhanced stroke volume.
 It is also common in individuals taking β-blocking medications.
 Sinus bradycardia may occur because of a decrease in the automaticity of the SA node or in a condition
of increased vagal stimulation, such as suctioning or vomiting.
 Sinus bradycardia has been seen in patients who have traumatic brain injuries with increased intracranial
pressures and in patients with brain tumors.
 Sinus bradycardia may also occur in the presence of second- or third-degree heart block; therefore close
evaluation of the PR interval and the P-to-QRS ratio is necessary to rule out heart block.

SINUS TACHYCARDIA
 Sinus tachycardia differs from NSR in rate only, which is greater than 100 beats per minute . The
characteristics of sinus tachycardia include:
 ▪ All P waves are upright, normal in appearance, and identical in configuration; a P wave exists before
every QRS complex.
 ▪ The RR interval is regular.
 ▪ The heart rate is greater than 100 beats per minute.

 Sinus tachycardia is typically benign and is present usually in conditions in which the SA node
automaticity is increased (increased sympathetic stimulation).
 Examples of conditions that induce sinus tachycardia include pain; fear; emotion; exertion (exercise); or
any artificial stimulants such as caffeine, nicotine, amphetamines, and atropine.
 Sinus tachycardia is also found in situations in which the demands for oxygen are increased, including
fever, congestive heart failure, infection, anemia, hemorrhage, myocardial injury, and hyperthyroidism.
 Usually individuals with sinus tachycardia are asymptomatic.

SINUS ARRHYTHMIA
 Sinus arrhythmia is classified as an irregularity in rhythm in which the impulse is initiated by the SA node
but with a phasic quickening and slowing of the impulse formation.
 The irregularity is usually caused by an alternation in vagal stimulation . The characteristics of sinus
arrhythmia include the following:

every QRS complex.
 ▪ The RR interval varies throughout.
 ▪ The heart rate is between 40 and 100 beats per minute.

 The most common type of sinus arrhythmia is related to the respiratory cycle, with the rate increasing
with inspiration and decreasing with expiration.
 This type of arrhythmia is usually found in the young or elderly at rest, and it disappears with activity.
 The other type of sinus arrhythmia is nonrespiratory and therefore is not affected by the breathing cycle.
 Nonrespiratory sinus arrhythmia may occur in conditions of infection, medication administration
(particularly toxicity associated with digoxin or morphine), and fever.

SINUS PAUSE OR BLOCK
 Sinus pause or sinus block occurs when the SA node fails to initiate an impulse, usually for only one
cycle.
 The characteristics of sinus pause and block include the following:
every QRS complex.
 ▪ The PR interval of the underlying rhythm is 0.12 to 0.20 second.
 ▪ The RR interval is regular for the underlying rhythm, but occasional pauses are noted.
 ▪ The heart rate is usually 60 to 100 beats per minute.

 Sinus pause or block can occur for a number of reasons, including a sudden increase of parasympathetic
activity, an organic disease of the SA node (sometimes referred to as sick sinus syndrome), an infection, a
rheumatic disease, severe ischemia or infarction to the SA node, or a case of digoxin toxicity.
 If the pause or block is prolonged or occurs frequently, the cardiac output is compromised, and the
individual may complain of dizziness or syncope episodes.

WANDERING ATRIAL PACEMAKER
 The pacemaking activity in wandering pacemaker shifts from focus to focus, resulting in a rhythm that is
very irregular and without a consistent pattern.
 Some of the impulses may arise from the AV node.
 The characteristics of wandering pacemaker include the following:

 ▪ P waves are present but vary in configuration; each P wave may look different.
 ▪ A P wave exists before every QRS complex.
 ▪ The PR intervals may vary but are usually within the normal width.
 ▪ The QRS complexes are identical in configuration.
 ▪ The RR intervals vary.
 ▪ The heart rate is usually less than 100 beats per minute.

SIGNS AND SYMPTOMS
 The cause is usually an irritable focus; however, the discharge of the impulse and the speed of discharge
vary within the normal range.
 This type of arrhythmia is seen in the young and in the elderly and may be caused by ischemia or injury
to the SA node, congestive heart failure, or an increase in vagal firing.
 Usually this arrhythmia does not cause symptoms.

PREMATURE ATRIAL COMPLEXES
 A premature atrial complex is defined as an ectopic focus in either atria that initiates an impulse before
the next impulse is initiated by the SA node.
 The characteristics of premature atrial complexes include the following:

 ▪ The underlying rhythm is sinus rhythm.
 ▪ Normal complexes have one P wave and one QRS wave configuration.
 ▪ The P wave of the early beat is noticeably different from the normal P waves.
 ▪ Depending on the heart rate, the P wave of the early beat may be buried in the previous T wave.
 ▪ The QRS complex involved in the early beat should look similar to the other QRS complexes.
 ▪ All PR intervals are 0.12 to 0.20 second.
 ▪ All QRS durations are between 0.06 and 0.10 second.
 ▪ Often a pause follows the premature atrial complex, but it may not be compensatory.

 Causes of premature atrial complexes include emotional stress, nicotine, caffeine, alcohol, hypoxemia,
infection, myocardial ischemia, rheumatic disease, and atrial damage.
 There may be no signs or symptoms associated with premature atrial complexes unless the pulse is
palpated and the irregularity noticed

ATRIAL TACHYCARDIA
 The definition of atrial tachycardia is three or more premature atrial complexes in a row. Usually the
heart rate is greater than 100 and may be as fast as 200 beats per minute.
 The characteristics of atrial tachycardia include the following: ▪
 P waves may be the same or may look different.

 ▪ P waves may not be present before every QRS complex.
 ▪ The PR intervals vary but should be no greater than 0.20 second.
 ▪ The QRS complexes should be the same as the others that originate from the SA node.
 ▪ The QRS duration is generally between 0.06 and 0.10 second.
 ▪ The RR intervals vary.
 ▪ The heart rate is rapid, being greater than 100 and possibly up to 200 beats per minute.

 The causes of atrial tachycardia include the causes of premature atrial complexes as well as those of
severe pulmonary disease with hypoxemia, pulmonary hypertension, and altered pH.
 Atrial tachycardia is often found in patients with chronic obstructive pulmonary disease.
 Symptoms may develop due to a compromised cardiac output if prolonged, thereby causing dizziness,
fatigue, and shortness of breath.

PAROXYSMAL ATRIAL TACHYCARDIA
 Paroxysmal atrial tachycardia (PAT) or paroxysmal supraventricular tachycardia (PSVT) is the sudden
onset of atrial tachycardia or repetitive firing from an atrial focus.
 The underlying rhythm is usually NSR, followed by an episodic burst of atrial tachycardia that eventually
returns to sinus rhythm.
 The episode may be extremely brief but can last for hours.
 The rhythm starts and stops abruptly.
 The characteristics of PAT include the following:

 ▪ P waves may be present but may be merged with the previous T wave.
 ▪ The PR intervals may be difficult to determine but are less than 0.20 second.
 ▪ The QRS complexes are identical unless there is aberration.
 ▪ The RR intervals are usually regular and may show starting and stopping of the PAT.
 ▪ The ST segment may be elevated or depressed, yet the magnitude of change is not diagnostically
reliable.
 ▪ The heart rate is very rapid, often greater than 160 beats per minute.

 The causes of PAT can include emotional factors; overexertion; hyperventilation; potassium depletion;
caffeine, nicotine, and aspirin sensitivity; rheumatic heart disease; mitral valve dysfunction, particularly
mitral valve prolapse; digitalis toxicity; and pulmonary embolus.
 The clinical description of paroxysmal atrial tachycardia is a sudden racing or fluttering of the heartbeat.
 If PAT continues beyond 24 hours, it is considered sustained atrial tachycardia.
 If the rapid rate continues for a period of time, other symptoms may include dizziness, weakness, and
shortness of breath (possibly even due to hyperventilation).

ATRIAL FLUTTER
 Atrial flutter is defined as a rapid succession of atrial depolarization caused by an ectopic focus in the
atria that depolarizes at a rate of 250 to 350 times per minute.
 Because only one ectopic focus is firing repetitively, the P waves are called flutter waves and look
identical to one another, with a characteristic “sawtooth” pattern.
 The characteristics of atrial flutter include the following:

 ▪ P waves are present as flutter waves with a characteristic “sawtooth” pattern.
 ▪ There is more than one P wave before every QRS complex.
 ▪ The atrial depolarization rate is 250 to 350 times per minute.
 ▪ The QRS configuration is usually normal and identical in configuration, but usually there is more than
one P wave for every QRS complex.
 ▪ The QRS duration is 0.06 to 0.10 second.
 ▪ The RR intervals may vary depending on the atrial firing and number of P waves before each QRS
complex. The conduction ratios may vary from 2:1 up to 8:1.
 ▪ The heart rate varies.

 Atrial flutter can be caused by numerous pathologic conditions, including rheumatic heart disease, mitral
valve disease, coronary artery disease or infarction, stress, drugs, renal failure, hypoxemia, and
pericarditis, to name the most common causes.
 Because the rate of discharge from the ectopic focus is rapid, the critical role is played by the AV node,
which blocks all the impulses from being conducted.
 Consequently, there may be an irregular rhythm associated with atrial flutter.
 This rhythm is usually not considered life threatening and may even lead to atrial fibrillation.
 Usually no symptoms are present, and the cardiac output is not compromised unless the ventricular rate
is too fast or too slow.

ATRIAL FIBRILLATION
 Atrial fibrillation is defined as an erratic quivering or twitching of the atrial muscle caused by multiple
ectopic foci in the atria that emit electrical impulses constantly.
 None of the ectopic foci actually depolarizes the atria, so no true P waves are found in atrial fibrillation.
 The AV node acts to control the impulses that initiate a QRS complex; therefore a totally irregular rhythm
exists.
 Thus the AV node determines the ventricular response by blocking impulses or allowing them to
progress forward.
 This ventricular response may be normal, slow, or too rapid.
 The characteristics of atrial fibrillation include the following:

 ▪ P waves are absent, thus leaving a flat or wavy baseline.
 ▪ The RR interval is characteristically defined as irregularly irregular.
 ▪ The rate varies but is called ventricular response.

 Numerous factors may play a part in causing atrial fibrillation, including advanced age, congestive heart
failure, ischemia or infarction, cardiomyopathy, digoxin toxicity, drug use, stress or pain, rheumatic heart
disease, and renal failure.
 Atrial fibrillation presents problems for two reasons.
 Without atrial depolarization, the atria do not contract.
 The contraction of the atria is also referred to as the atrial kick.
 This atrial kick forces the last amount of volume to flow into the ventricles during diastole.
 The amount of volume that is forced into the ventricles because of atrial contraction provides up to 30%
of the cardiac output. Therefore without atrial contraction, the cardiac output is decreased up to 30%.

 Atrial fibrillation (irregularly–irregular heart rhythm) is very common in the older population and is not
considered life threatening unless the heart rate is elevated at rest (above 100 is considered to be
uncontrolled).
 Due to a lack of “atrial kick,” cardiac output is lower than normal (by 15% to 20%).

NODAL OR JUNCTIONAL ARRHYTHMIAS

PREMATURE JUNCTIONAL OR NODAL COMPLEXES
 Premature junctional complexes are premature impulses that arise from the AV node or junctional tissue.
 For reasons that are not understood, the AV node becomes irritated and initiates an impulse that causes
an early beat.
 Premature junctional complexes are similar to premature atrial complexes except for the fact that an
inverted, an absent, or a retrograde (wave that follows the QRS) P wave is present.
 The characteristics of premature junctional complexes include the following:

 ▪ Inverted, absent, or retrograde P waves are present.
 ▪ The QRS configurations are usually identical.
 ▪ The RR interval is regular throughout except when the premature beats arise.
 ▪ The heart rate is usually normal (between 60 and 100 beats per minute).

 Some of the causes of premature junctional complexes include decreased automaticity and conductivity
of the SA node or some irritability of the junctional tissue.
 Pathologic conditions that can cause premature junctional complexes include cardiac disease and mitral
valve disease.
 Usually no symptoms or signs are present.

JUNCTIONAL (OR NODAL) RHYTHM
 Junctional rhythm occurs when the AV junction takes over as the pacemaker of the heart. Junctional
rhythm may be considered an escape rhythm.
 The characteristics of junctional rhythm include the following:
 ▪ Absence of P waves before the QRS complex, but a retrograde P wave may be identified.
 ▪ The QRS complex has a normal configuration.
 ▪ The RR intervals are regular.
 ▪ The ventricular rate is between 40 and 60 beats per minute.

 Causes of junctional rhythm include a failure of the SA node to act as the pacemaker in conditions such
as sinus node disease or increase in vagal tone, digoxin toxicity, and infarction or severe ischemia to the
conduction system (typically right coronary artery disease).

NODAL (JUNCTIONAL) TACHYCARDIA
 Junctional tachycardia develops because the AV junctional tissue is acting as the pacemaker (as in
junctional rhythm), but the rate of discharge is accelerated.
 The onset of increase in rate of discharge may be sudden, or it may be of long standing.
 The characteristics of junctional tachycardia include the following:

 ▪ P waves are absent, but retrograde P wave may be present.
 ▪ The QRS configurations are identical.
 ▪ The RR interval is regular.
 ▪ The rate is usually greater than 100 beats per minute.

 Causes of junctional tachycardia include hyperventilation, coronary artery disease or infarction,
postcardiac surgery, digoxin toxicity, myocarditis, caffeine or nicotine sensitivity, overexertion, and
emotional factors.
 When the rate is extremely rapid, the individual may experience symptoms of cardiac output
decompensation. Symptoms include dizziness, shortness of breath, and fatigue

FIRST-DEGREE ATRIOVENTRICULAR HEART BLOCK
 First-degree AV block occurs when the impulse is initiated in the SA node but is delayed on the way to
the AV node; or it may be initiated in the AV node itself, and the AV conduction time is prolonged.
 This results in a lengthening of the PR interval only

 The characteristics associated with first-degree AV block include the following:
 ▪ A P wave is present and with normal configuration before every QRS complex.
 ▪ The PR interval is prolonged (greater than 0.20 second).
 ▪ The QRS has a normal configuration.
 ▪ The RR intervals are regular.
 ▪ The heart rate is usually within normal limits (60 to 100 beats per minute) but may be lower than 60
beats per minute.

 Causes of first-degree AV block include coronary artery disease, rheumatic heart disease, infarction, and
reactions to medication (digoxin or β-blockers).
 Firstdegree AV block is a relatively benign arrhythmia as it exists without symptoms (unless severe
bradycardia exists in conjunction with first-degree AV block); however, it should be monitored over time
because it may progress to higher forms of AV block.

SECOND-DEGREE ATRIOVENTRICULAR BLOCK, TYPE I
 Second-degree AV block, type I (Wenckebach or Mobitz I heart block) is a relatively benign, transient
disturbance that occurs high in the AV junction and prevents conduction of some of the impulses
through the AV node.
 The typical appearance of type I (Wenckebach) second-degree block is a progressive prolongation of the
PR interval until finally one impulse is not conducted through to the ventricles (no QRS complex
following a P wave).
 The cycle then repeats itself

 ▪ Initially a P wave precedes each QRS complex, but eventually a P wave may stand alone (conduction is
blocked).
 ▪ Progressive lengthening of the PR interval occurs in progressive order.
 ▪ As the PR interval increases, a QRS complex will be dropped.
 ▪ This progressive lengthening of the PR interval followed by a dropped QRS complex occurs in a
repetitive cycle.
 ▪ The QRS configuration is normal, and the duration is between 0.06 and 0.10 second.
 ▪ Because of the dropping of the QRS complex, the RR interval is irregular (regularly irregular).
 ▪ The heart rate varies.

 Causes of Wenckebach heart block include right coronary artery disease or infarction, digoxin toxicity,
and excessive β-adrenergic blockade—a side effect of the medication.
 Usually the individual with type I second-degree AV block is asymptomatic.

SECOND-DEGREE ATRIOVENTRICULAR BLOCK, TYPE II
 Second-degree AV block, type II (Mobitz II), is defined as nonconduction of an impulse to the ventricles
without a change in the PR interval.
 The site of the block is usually below the bundle of His and may be a bilateral bundle branch block

 ▪ A ratio of P waves to QRS complexes that is greater than 1:1 and may vary from 2 to 4 P waves for
every QRS complex.
 ▪ The QRS configuration is normal.
 ▪ The RR intervals may vary depending on the amount of blocking that is occurring.
 ▪ The heart rate is usually below 100 and may be below 60 beats per minute.

 Second-degree AV block type II occurs with myocardial infarction (especially when the left anterior
descending coronary artery is involved), with ischemia or infarction of the AV node, or with digoxin
toxicity.
 Patients may be symptomatic when the heart rate is low and when cardiac output compromise is
present.

THIRD-DEGREE ATRIOVENTRICULAR BLOCK
 In third-degree (complete) AV block, all impulses that are initiated above the ventricle are not conducted
to the ventricle.
 In complete heart block, the atria fire at their own inherent rate (SA node firing or ectopic foci in the
atria), and a separate pacemaker in the ventricles initiates all impulses.
 However, there is no communication between the atria and the ventricles and thus no coordination
between the firing of the atria and the firing of the ventricles, creating complete independence of the
two systems

 ▪ P waves are present, regular, and of identical configuration.
 ▪ The P waves have no relationship to the QRS complex because the atria are firing at their own inherent
rate.
 ▪ The QRS complexes are regular in that the RR intervals are regular.
 ▪ The QRS duration may be wider than 0.10 second if the latent pacemaker is in the ventricles.
 ▪ The heart rate depends on the latent ventricular pacemaker and may range from 30 to 50 beats per
minute.

 The causes of complete heart block usually involve acute myocardial infarction, digoxin toxicity, or
degeneration of the conduction system.
 If a slow ventricular rate is present, then the cardiac output often is diminished, and the patient may
complain of dizziness, shortness of breath, and possibly chest pain.

PREMATURE VENTRICULAR COMPLEXES
 Premature ventricular complexes (PVCs) occur when an ectopic focus originates an impulse from
somewhere in one of the ventricles.
 The ventricular ectopic depolarization occurs early in the cycle before the SA node actually fires.
 A PVC is easily recognized on the ECG because the impulse originates in the muscle of the heart, and
these myocardial cells conduct impulses very slowly compared with specialized conductive tissue.
 Therefore the QRS complex is classically described as a wide and bizarre-looking QRS without a P wave
and followed by a complete compensatory pause.

 An absence of P waves in the premature beat, with all other beats usually of sinus rhythm.
 ▪ The QRS complex of the premature beat is wide and bizarre and occurs earlier than the normal sinus beat
would have occurred.
 ▪ The QRS duration of the early beat is greater than 0.10 second.
 ▪ The ST segment and the T wave often slope in the opposite direction from the normal complexes.
 ▪ The PVC is generally followed by a compensatory pause.
 ▪ The PVC is called bigeminy when every other beat is a PVC, trigeminy when every third beat is a PVC, and so
on.
 ▪ The PVC is called unifocal if all PVCs appear identical in configuration.
 ▪ The PVCs are called multifocal if more than one PVC is present and no two appear similar in configuration.
 ▪ The PVC is paired or a couplet PVC if two are together in a row, a triplet or ventricular tachycardia (VTACH) if
three are together in a row.

VENTRICULAR TACHYCARDIA
 Ventricular tachycardia is defined as a series of three or more PVCs in a row. Ventricular tachycardia
occurs because of a rapid firing by a single ventricular focus with increased automaticity
 P waves are absent.
 ▪ Three or more PVCs occur in a row.
 ▪ QRS complexes of the ventricular tachycardia are wide and bizarre.
 ▪ Ventricular rate of ventricular tachycardia is between 100 and 250 beats per minute.
 ▪ Ventricular tachycardia can be the precursor to ventricular fibrillation.

SIGN,SYMPTOMS AND CAUSES
 Causes of ventricular tachycardia include ischemia or acute infarction, coronary artery disease,
hypertensive heart disease, and reaction to medications (digoxin or quinidine toxicity).
 Occasionally ventricular tachycardia occurs in athletes during exercise (possibly as a result of electrolyte
imbalance).
 Ventricular tachycardia indicates increased irritability and is an emergency situation because cardiac
output is greatly diminished, as is the blood pressure.
 Symptoms usually involve lightheadedness and sometimes syncope.

VENTRICULAR FIBRILLATION
 Ventricular fibrillation is defined as an erratic quivering of the ventricular muscle resulting in no cardiac
output.
 As in atrial fibrillation, multiple ectopic foci fire, creating asynchrony.
 The ECG results in a picture of grossly irregular up and down fluctuations of the baseline in an irregular
zigzag pattern

 The causes of ventricular fibrillation are the same as those of ventricular tachycardia because ventricular
fibrillation is usually the sequel to ventricular tachycardia.

OTHER FINDINGS ON A 12-LEAD
ELECTROCARDIOGRAM

HYPERTROPHY
 Hypertrophy refers to an increase in thickness of cardiac muscle or chamber size.
 Signs of atrial hypertrophy can be noted by examining the P waves of the ECG for a diphasic P wave in
the chest lead V1, or a voltage in excess of 3 mV.
 Signs of right ventricular hypertrophy are noted by changes found in lead V1 that include a large R wave
and an S wave smaller than the R wave.

 The R wave becomes progressively smaller in the successive chest leads (V2, V3, V4, V5).
 Hypertrophy of the left ventricle creates enlarged QRS complexes in the chest leads in both height of the
QRS (R wave) and depth of the QRS (S wave).
 In left ventricular hypertrophy a deep S wave occurs in V1 and a large R wave in V5.
 If, when the depth of the S wave in V1 (in mm) is added to the height of the R wave in V5 (in mm) the
resulting number is greater than 35, then left ventricular hypertrophy is present

ISCHEMIA, INFARCTION, OR INJURY
 A review of a 12-lead ECG to detect ischemia, infarction, or injury is performed in a variety of situations,
including after any episode of chest pain that brings a patient to the physician’s office or to the hospital,
during hospitalization, during a follow-up examination after a cardiac event, or before conducting an
exercise test.
 In simplistic terms, ischemia literally means reduced blood and refers to a diminished blood supply to
the myocardium.
 This can occur because of occlusion of the coronary arteries from vasospasm, atherosclerotic occlusion,
thrombus, or a combination of the three.
 Infarction means cell death and results from a complete occlusion of a coronary artery.
 Injury indicates the acuteness of the infarction.

 As a result of ischemia, injury, or infarction, conduction of electrical impulses is altered, and therefore
depolarization of the muscle changes.
 As the ECG records the depolarization of the cardiac muscle, changes occur on the ECG in the presence
of ischemia, infarction, or injury.
 The location of the ischemia, infarction, or injury is determined according to the specific leads of the ECG
that demonstrate an alteration in depolarization.

 Ischemia is classically demonstrated on the 12-lead ECG with T-wave inversion or ST-segment
depression.
 The T wave may vary from a flat configuration to a depressed inverted wave.
 The T wave is an extremely sensitive indication of changes in repolarization activity within the ventricles.

 The location of the ST segment (that portion of the ECG tracing beginning with the end of the S wave
and ending with the beginning of the T wave) is another indication of ischemia or injury.
 Elevation of the ST segment above the baseline when following part of an R wave indicates acute injury

 Elevation of the ST segment above the baseline when following part of an R wave indicates acute injury.
 In the presence of acute infarction, the ST segment elevates and then later returns to the level of the
baseline (within 24 to 48 hours)

 The ECG may demonstrate ST-segment depression while the patient is at rest in the presence of chest
pain or of suspected coronary ischemia.
 The ST-segment depression in this situation represents subendocardial infarction and also requires
immediate treatment.
 A subendocardial infarct (also called a nontransmural, non–Q-wave infarct, or non–ST-segment elevation
myocardial infarction [STEMI] infarct) is an acute injury to the myocardial wall, but it does not extend
through the full thickness of the ventricular wall. Instead, the injury is only to the subendocardium.

 ST-segment depression in the absence of suspected ischemia or angina may be caused by digitalis
toxicity.
 ST-segment depression that develops during exercise, as seen during exercise testing, is defined as an
ischemic response to exercise, and following rest it should return to the isoelectric line.
 This is an abnormal response to exercise that indicates an impaired coronary arterial supply during the
exercise.
 This type of ischemic response should be further evaluated to determine the extent of the coronary
artery involvement

 During myocardial injury, the affected area of muscle loses its ability to generate electrical impulses, and
therefore alterations in the initial portion of the QRS complex occur.
 The cells are dead and cannot depolarize normally, which results in an inability to conduct impulses.
Therefore because ST-segment elevation or depression is diagnostic for acute infarction, the presence of
a significant Q wave is also diagnostic for infarction.

 The leads that demonstrate the presence of T-wave inversion, ST-segment changes, or Q waves identify
the location of the ischemia, injury, or infarction.
 The presence of significant Q waves in the chest leads, particularly in V1, V2, V3, and V4, indicates an
infarction in the anterior portion of the left ventricle.
 When only V1 and V2 are involved, these infarctions are often called septal infarctions because they
primarily affect the interventricular septum

 An inferior infarction is identified by significant Q waves in leads II, III, and aVF .
 Inferior infarctions are also referred to as diaphragmatic infarctions because the inferior wall of the heart
rests on the diaphragm.
 Given that the right coronary artery primarily supplies the inferior aspect of the myocardium, an inferior
infarction implies an occlusion somewhere in the right coronary artery.

 A lateral infarction demonstrates Q waves in leads I and aVL.
 Because the circumflex artery supplies primarily the lateral and posterior aspects of the myocardium, an
occlusion of the circumflex artery is suspected in a lateral infarction.

 Probably the most difficult infarction to detect is the posterior infarction because none of the 12 leads is
directly measuring the posterior aspect of the heart.
 Only two leads detect posterior infarcts—V1 and V2—as they measure the direct opposite wall (anterior).
 Therefore the direct opposite ECG tracing of an anterior infarction in V1 and V2 should be the ECG
tracing of the posterior infarction.
 An anterior infarction demonstrates a significant Q wave in V1 and V2 with ST-segment elevation.
 The mirror image of this is seen , which demonstrates a large R wave in V1 or V2 and ST-segment
depression.
 Given that the posterior aspect of the myocardium may be supplied by either the right coronary artery
or the circumflex artery, a posterior infarction may indicate a problem in either one of these arteries.

A SYSTEMATIC APPROACH INCLUDES THE FOLLOWING:
 ▪ Identify and separate the 12 leads by applying vertical lines between leads I and avR, avR and V1, and
V1 and V4.
 ▪ Scan all leads to identify if there are any significant Q waves. If so, note which leads demonstrate a
significant Q wave.
 ▪ Scan all leads to identify if there is any ST elevation or ST depression. If so, note which leads
demonstrate ST changes.
 ▪ Scan leads V1, V5, and V6 to look for ventricular hypertrophy. A large R in V1 indicates R ventricular
hypertrophy, and a deep S in V1 with a large R in V5 indicates left ventricular hypertrophy.

Electrocardiography

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