Chapter - 007 Student

Chapter 7
Dysrhythmia Interpretation and

Management
Copyright © 2017 Elsevier Inc. All rights reserved.

Introduction
 Dysrhythmia interpretation is a fundamental skill
of critical care nurses
 Crucial for early nursing and medical
intervention
Copyright © 2017 Elsevier Inc. All rights reserved. 2

Cardiac Physiology Review
 Pacemaker cells and automaticity
 Electrical signals generated by pacemaker cells
 Cells can generate stimulus without outside
stimulation
 Automaticity
 Cardiac cycle

Cardiac Cycle
 Composed of two activities
 Electrical (caused by automaticity)
 Mechanical (muscular), known as a contraction

Cardiac Cycle
(Cont.)
 Two phases of electrical activity
 Depolarization = active
 Repolarization = resting
 Two mechanical responses
 Systole
 Diastole

Cardiac Cycle
(Cont.)
 Depolarization = systole = contraction
 Repolarization = diastole = resting or filling
phase
 Electrical activity precedes mechanical activity
 Electrical + mechanical = cardiac contraction

Cardiac Electrophysiology
 Cardiac muscle cells generate an electrical
current = cardiac action potential
 Sinoatrial node (SA node)
 Exchange of electrolytes

Cardiac Action Potential
(Cont.)
 Depolarization
 Na outside cell; K inside the cell
 Change cell permeability
 Na enters cells; K leaves cells
 Ca slowly enters cells
 ATP needed to move electrolytes back to resting state
 Repolarization begins

Muscular Contraction
 Depolarization leads to contraction
 Repolarization leads to resting and filling of
ventricles from atria
 ECG is evidence of electrical activity, not
contraction

Cardiac Conduction Pathway
Figure 7-1. The electrical conduction system of the heart.

(Cont.)
 SA node (inherent rate of 60 – 100 beats per
minute)
 Depolarization begins
 Atrial contraction or atrial kick
 Intraatrial and internodal pathways to AV node

(Cont.)
 AV node (inherent rate of 40-60 beats per
minute)
 Delays impulse to ventricles; allows for filling
 Backup pacemaker
 Bundle of His (inherent rate of 20-40 beats per
minute)
 Left and right bundle branches; fascicles
 Purkinje fibers

Cardiac Physiology Review
Figure 7-2. The cardiac cycle. (Modified from Wesley K. Huszar’s Basic Dysrhythmias
and Acute Coronary Syndromes: Interpretation and Management. 4th ed. St. Louis:
Mosby JEMS; 2010.)

Cardiac Electrophysiology

Cardiac Electrophysiology (Cont.)
Figure 7-4. Cardiac action potential with the electrocardiogram and movement of electrolytes. ATP,
Adenosine triphosphate; Ca, calcium; K, potassium; Na, sodium. (From American Heart Association.
Advanced Cardiac Life Support Textbook. Dallas: Author; 1997.)

Autonomic Nervous System
Figure 7-5. Autonomic nervous system.

Inherent Rates
 SA node = 60 to 100 beats/min
 AV node = 40 to 60 beats/min
 Ventricles (Purkinje fibers) = 20 to 40 beats/min

The 12-Lead Electrocardiogram
Figure 7-6. A. A positive complex is seen in any lead if the wave of depolarization spreads toward the positive pole of the
lead. B. A negative complex is seen if the depolarization wave spreads toward the negative pole (away from the positive pole)
of the lead. C. A biphasic (partly positive, partly negative) complex is seen if the mean direction of the wave is at right angles.
These apply to the P wave, QRS complex, and T wave. (From Goldberger AL. Clinical Electrocardiography: A Simplified
Approach. 7th ed., St. Louis: Mosby; 2006.)

The 12-Lead Electrocardiogram
(Cont.)
Figure 7-7. Direction of normal current flow through the ventricles.

12-Lead ECG (Cont.)
 Leads
 3 standard limb leads
 3 augmented limb leads
 6 precordial leads
 Impulses toward electrode
 Positive QRS complex
 Impulses away from electrode
 Negative QRS complex

12-Lead ECG (Cont.)
Figure 7-9. A. Einthoven’s triangle.

12-Lead ECG (Cont.)
 Lead I
 Records flow from
right arm to left arm
 Lead II
 Records flow from
right arm to left leg
 Lead III
 Records flow from left
arm to left leg
Figure 7-8. Standard bipolar limb leads. A. Lead I. B.
Lead II. C. Lead III.
12-Lead ECG
(Cont.)
 Augmented limb leads; unipolar center of heart
to lead
 aVR = from heart to right arm
 aVL = from heart to left arm
 aVF = from heart to left foot

12-Lead ECG (Cont.)
Figure 7-9. A. Einthoven’s triangle. B. The triangle is converted to a triaxial diagram by

shifting leads I, II, and III so that they intersect at a common point. C. Triaxial lead diagram
showing the relationship of the three augmented (unipolar) leads, aV R, aVL, and aVF.
Notice that each lead is represented by an axis with a positive and negative pole. D. The
hexaxial reference figure.
12-Lead ECG (Cont.)
Figure 7-10. Precordial chest leads.

12-Lead ECG (Cont.)
Figure 7-11. Lead placement for a 15-lead ECG. A. Anterior leads. B. Posterior
leads.

Cardiac Monitoring
 Continuous monitoring via three-lead or five-lead
systems

Cardiac Monitoring
(Cont.)
 Record and interpret 6-second strip every 4
hours
 Monitor ST segment
 Monitor dysrhythmias
 Daily 12-lead ECG for cardiac patients

ECG Graph Paper
 Graph paper
 Used to
standardize
tracings
 Vertical boxes
measure
voltage/amplitude
 Horizontal boxes
measure time
Figure 7-14. ECG paper records time horizontally in seconds or milliseconds.

Each large box contains 25 smaller boxes with five on the horizontal axis and
five on the vertical axis. Each small horizontal box is 0.04 seconds while each
large box is 0.20 seconds in duration. Vertically, the graph depicts size or voltage
in millivolts and in millimeters. 15 large boxes equals 3 seconds and 30 large
boxes equals 6 seconds used in calculating heart rate. (From Wesley K.
Huszar’s Basic Dysrhythmias and Acute Coronary Syndromes: Interpretation
and Management. 4th ed. St. Louis: Mosby JEMS; 2010.)

Normal ECG Tracing
Figure 7-15. ECG waveforms.

P Wave
 Atrial depolarization
 Normally indicates firing of the sinoatrial node
 Not to exceed three boxes high

QRS Complex
 Ventricular depolarization
 Q wave first negative deflection after P wave
 R wave first positive deflection after P wave
 S wave negative waveform after R wave
 Not everyone has a traditional QRS

Variations in QRS Complexes
Figure 7-17. Nomenclature for QRS complexes of various shapes. Different types of QRS complexes. An R wave is a
positive waveform. A negative deflection before the R wave is a Q wave. The S wave is a negative deflection after the
R wave. If the waveform is tall or deep, the letter naming the waveform is a capital letter. If the waveform is small in
either direction, the waveform is labeled with a lowercase letter.

R-Wave Progression
Figure 7-16. The normal 12-lead precordial R wave progression.

Pathological Q waves
 0.04 seconds in
width
 More than one
fourth of the R-wave
amplitude
 Indication of a
myocardial
infarction
Figure 7-18. Pathological Q wave is greater than one fourth

the height of the R wave.

PR Interval
 Atrial depolarization/delay in AV node
 Beginning of P wave to beginning of QRS
complex
 0.12 to 0.20 seconds
 Shorter interval = impulse from AV junction
 Longer interval = first-degree AV block

QRS Interval
 Ventricular depolarization
 Various configurations
 Wide: slowed conduction
 Bundle branch block (BBB)
 Ventricular rhythm

ST Segment
 Look for depression or elevation
 ST elevation: myocardial injury
 ST depression: reciprocal changes, digoxin, and
ischemia

T Wave
 Ventricular repolarization
 Follows a QRS complex
 Bigger than a P wave
 No greater than five small boxes high
 Inversion indicates ischemia to myocardium

QT Interval
 Beginning of QRS complex to end of T wave
 Varies with heart rate

U Wave
 Sometimes seen after T wave
 Unknown origin
 May be normal
 May indicate hypokalemia

Interpretation of Rhythms
 Develop a systematic approach
 Atrial and ventricular rates
 Regularity of rhythm
 Measurement of PR, QRS, and QT/QTc intervals
 Shape of waveforms and their consistency
 Identification of underlying rhythm and
dysrhythmias
 Patient tolerance of rhythm
 Clinical implication of the rhythm

Rhythmicity
 Regularity or pattern of heartbeats
 PP intervals (atrial)
 Is regular when distance between PP intervals is
equal
 RR intervals (ventricles)
 Is regular when distance between RR intervals is
equal

Measuring
Establishing ventricular rhythmicity with calipers. Establishing ventricular rhythmicity with paper and
pencil.

Calculating Heart Rate
 Regular
 Small blocks into 1500
 Large blocks into 300
 Irregular = 6-second strip
 Calculate atrial (PP) and ventricular rates (RR)
Figure 7-19. Six-second method of rate calculation.

Waveform Configuration and
Location
 Check P, Q, R, S, and T waveforms
 Each waveform has unique shape
 Comparison of waveform on 6-second strip
 Check for correct sequence of each waveform

Interval
 Measure PR interval
 Measure QRS interval
 Measure QT interval

Basic Dysrhythmias
 Grouped by anatomical areas
 SA node
 Atria
 AV node
 Ventricles
 AV blocks

Normal Sinus Rhythm
 Regular rhythm
 Rate 60 to 100 beats/min
 Normal P wave in lead II
 P wave before each QRS
 Normal PR, QRS, and QT intervals
Figure 7-24. Normal sinus rhythm.

Sinus Tachycardia
 Sinus rhythm with a rate of 100 to 150 beats/min
 Causes: Hyperthyroidism, hypovolemia, heart failure,
anemia, exercise, use of stimulants, fever, and
sympathetic response to fear or pain and anxiety may
cause sinus tachycardia.
 Assess for symptoms of low cardiac output
Figure 7-25. Sinus tachycardia.

Sinus Bradycardia
 Sinus rhythm with rate less than 60 beats/min
 Causes: vagal, drugs, ischemia, disease of the
nodes, ICP, hypoxemia, and athletes (normal)
 Produces various hemodynamic responses
Figure 7-26. Sinus bradycardia.

Sinus Arrhythmia
 Sinus rhythm
 Rate varies with respirations
 Inspire = increase
 Expire = decrease
 Rarely affects hemodynamic status
Figure 7-27. Sinus arrhythmia. The heart rate increases slightly with inspiration and decreases
slightly with expiration.
Sinus Arrest or Exit Block
 Sinoatrial node fails to initiate impulse
 Causes: vagal, heart disease, and drugs that
slow heart rate
 Heart rate can be normal or slow
 Irregular rhythm
 Can decrease cardiac output

Sinus Arrest or Exit Block (Cont.)
Figure 7-28. A. Sinus arrest. B. Sinus exit block.

Atrial Dysrhythmias
 Increased automaticity in the atrium
 Generally have P-wave changes

Atrial Dysrhythmias
(Cont.)
 Causes  Digitalis toxicity
 Stress  Hypothermia
 Electrolyte imbalances  Hyperthyroidism
 Hypoxia  Alcohol
 Atrial injury  Pericarditis

Premature Atrial Contractions
 Early beats initiated by atrium
 P waves and PR interval may vary
 Noncompensatory pause
 P wave may be found in T wave

Premature Atrial Contractions
(Cont.)
Figure 7-29. A, Premature atrial contractions (PAC) shown in the third beat. B, A nonconducted
PAC. (Modified from Association of Critical-Care Nurses: Essentials of Critical Care Orientation.)

Wandering Atrial Pacemaker
 Varying configurations of P waves
 At least three different P-wave shapes must be seen
 Heart rate not greater than 100
 PR interval varies
 Irregular rhythm
Figure 7-31. Wandering atrial pacemaker. Arrows indicate different shapes of P waves.

Atrial Tachycardia
 Rapid rhythm
 Ectopic focus in atria
 1:1 conduction (ventricle responds to every atrial
impulse)
 2:1 conduction (ventricle responds to every two
atrial impulses)

Multifocal Atrial Tachycardia
 Almost identical to wandering atrial pacemaker
 Heart rate exceeds 100 beats/min
 Common in COPD patients
Figure 7-32. Multifocal atrial tachycardia. Arrows indicate different shapes of P waves.

Paroxysmal Atrial Tachycardia
 Heart rate 150 to 250 beats/min
 Regular rhythm
 P waves (if present) may merge in T waves
 QRS complex width is normal
 Hemodynamic effects vary
Figure 7-30. Atrial tachycardia with 1:1 conduction.

Atrial Flutter
 Ectopic foci in atria, heart disease
 Classic “sawtooth” pattern in leads II, III, and aVF
 Atrial rate fast and regular (250 to 350 beats/min)
with AV block
 Description of atrial flutter might be constant at 2:1,
3:1, 4:1, 5:1, and so forth, or it may be variable
 Causes: Lung disease, ischemic heart disease,
hyperthyroidism, hypoxemia, heart failure, and
alcoholism can cause atrial flutter.

Atrial Flutter (Cont.)
Figure 7-33. Atrial flutter. A, Flutter waves show sawtooth pattern. B, Enlarged view
shows one large box between flutter waves.

Atrial Fibrillation
 Erratic impulse formation in atria
 No discernible P wave
 Irregular ventricular rate
 Aberrant (abnormal) ventricular conduction can occur
 Results in loss of atrial kick
 High risk for pulmonary or systemic emboli
Figure 7-34. Atrial fibrillation.

Junctional Rhythms
 Dysrhythmias from the AV junction
 Junctional escape rhythm
 Premature junctional contractions
 Accelerated junctional rhythms
 Junctional tachycardia
 Paroxysmal supraventricular tachycardia
 P-wave changes
 Shorter PR intervals
 No P wave
 Retrograde P waves

Examples of P Waves in Junctional
Rhythms
Figure 7-36. P waves in junctional dysrhythmias. A, Backward conduction with

inverted P wave. B, Forward and backward conduction with retrograde P wave. C,
Forward conduction with absent P wave.
Junctional Escape Rhythm
 Regular rhythm
 PR interval low end of normal
 P-wave changes
 Rate usually 40 to 60 beats/min
 Possible decreased cardiac output
Figure 7-37. A, Junctional escape rhythm.

B, Junctional escape beat.
Accelerated Junctional Rhythm
and
Junctional Tachycardia
 Rhythm initiated from the AV junction
 Rate is 60 to 100 beats/min for accelerated
junctional tachycardia
 Rate is greater than 100 beats/min for junctional
tachycardia

Junctional Tachycardia (Cont.)
Figure 7-38. A, Accelerated junctional rhythm. B, Junctional tachycardia.

Premature Junctional Contractions
 Early beats initiated by AV junction
 P-wave changes
 PR interval is shorter than normal
 Usually a noncompensatory pause
Figure 7-39. Sinus rhythm with premature junctional contraction (PJC).

Paroxysmal Supraventricular
Tachycardia
Figure 7-40. Paroxysmal supraventricular tachycardia (PSVT). A, The abrupt onset

initiated by a PJC. B, The abrupt cessation of the PSVT.
Ventricular Dysrhythmias
 Impulses initiated from lower portion of the heart
 Depolarization occurs, leading to abnormally
wide QRS complex
 Ectopic and escape beats

Ventricular Dysrhythmias
(Cont.)
 Common causes
 Myocardial ischemia, injury, and infarction
 Low potassium or magnesium
 Hypoxia
 Acid-base imbalances

Premature Ventricular Contractions
 Wide and bizarre  QRS complex greater
beats than 0.10 seconds
 Compensatory pause  Irregular rhythm
 Patterns  Compensatory pause
 Bigeminy and  Absent P waves
trigeminy
 Couplets and triplets
 Unifocal vs. multifocal

(Cont.)
 Assess and treat cause
 Hypoxia
 Ischemia
 Electrolyte imbalance
 May need antidysrhythmic agents

(Cont.)
Figure 7-41. Premature ventricular contractions (PVCs). A, Sinus rhythm with unifocal PVCs. 1 is the
sinus beat; 2 points to the presence of an inverted T wave. B, Sinus rhythm with multifocal PVCs; note
the different configuration of the PVCs, indicating generation from more than one focus. C, The PVCs
are in pairs and look the same, indicating that they are from the same foci.
(Cont.)
Figure 7-42. R-on-T. A, Single PVC on T wave. B, PVC causing

ventricular fibrillation.
Ventricular Tachycardia
 Rapid, life-threatening dysrhythmia
 Three or more PVCs in a row
 Fast rate (>100 beats/min)
 Initiated by ventricles

Ventricular Tachycardia
(Cont.)
 Wide QRS complex; greater than 0.10 seconds
 Usually regular
 May or may not have pulse
 Treat pulseless same as ventricular fibrillation
 Significant loss of cardiac output
 Hypotension

Ventricular Tachycardia (Cont.)
Figure 7-43. Ventricular tachycardia.

Torsades de pointes
Figure 7-44. Torsades de pointes.

Ventricular Fibrillation
 Chaotic pattern
 No discernible P, Q, R, S, or T waves
 Coarse versus fine
 No cardiac output; life-threatening
 Emergent defibrillation

Ventricular Fibrillation (Cont.)
Figure 7-45. Ventricular fibrillation. A, Course. B, Fine.

Idioventricular Rhythm
 Escape ventricular rhythm from Purkinje fibers
 Rate 15 to 40 beats/min
 Regular rhythm
 Wide QRS interval
 No P waves
 Do not give lidocaine!

Idioventricular Rhythm (Cont.)
Figure 7-46. A, Ventricular escape rhythm or idioventricular rhythm. B, Two ventricular escape
beats followed by sinus rhythm.

Accelerated Idioventricular Rhythm
 Same as idioventricular rhythm
 Rate more than 40 beats/min
 Hemodynamic effects correspond to heart rate

Accelerated Idioventricular Rhythm
(Cont.)
Figure 7-47. Accelerated idioventricular rhythm (AIVR).

Asystole
 No P, Q, R, S, or T waveforms
 Assess in two leads
 Why?
 No cardiac output
 Death

Asystole/Ventricular Standstill
(Cont.)
Figure 7-48. A, Asystole. B, Ventricular standstill

Pulseless Electrical Activity
 How can it be assessed?
 What are its causes?
 Must treat the cause

Pulseless Electrical Activity (Cont.)
 Hypoxia  Tablets (overdose)
 Hypovolemia  Tamponade (cardiac)
 Hypothermia  Tension
 H+ ions (acidosis) pneumothorax
 Hypokalemia or
 Thrombosis
hyperkalemia (coronary)
 Thrombosis
(pulmonary)

Atrioventricular Blocks
 Block of conduction from atria to ventricles
 Coronary artery disease
 Myocardial infarction (e.g., inferior wall)
 Infections
 Enhanced vagal tone
 Drug effects (e.g., digoxin toxicity)

Atrioventricular Blocks
(Cont.)
 Always assess for decreased cardiac output and
treat cause
 Four types
 First-degree block
 Second-degree block, Mobitz type I Wenckebach
 Second-degree block, Mobitz type II
 Third-degree block (complete)

First-Degree Block
 Delayed conduction from SA node to AV node
 Prolonged PR interval
 Greater than 0.20 seconds
 Same PR interval for each beat
Figure 7-49. First-degree AV block.

Second-Degree Block:
Mobitz Type I
 Steadily lengthening PR interval
 Nonconducted P waves
 PP interval regular
 RR interval irregular
 QRS normal
 Self-limiting; rarely progresses
 May decrease cardiac output

Mobitz Type I (Cont.)
Figure 7-50. Second-degree AV block type I (Mobitz I, Wenckebach).

Mobitz Type II
 More severe AV block
 Often associated with bundle branch block
 PR interval is fixed
 PP interval is regular
 Occasional P wave not followed by QRS
 What is the danger of this block?

Mobitz Type II (Cont.)
Figure 7-51. Second-degree AV block type II (Mobitz II). A. The PR interval is

constant; at the 3rd and 9th P waves, there is no QRS following the P wave. B. No
QRS follows the 4th and 7th P waves.

Third-Degree Block (Complete)
 Atria and ventricles beat independently of each
other
 P waves not associated with QRS complex
 PP intervals regular
 RR intervals regular

Third-Degree Block (Cont.)
 Complete heart block
 Junctional or ventricular escape rhythms
 May need pacemaker
 Hemodynamic status based on ventricular rate

Third-Degree Block
(Cont.)
Figure 7-52. Third-degree AV block (complete heart block). A, P waves regular and
present throughout at an atrial rate of 94 beats per minute and ventricular rhythm of
30 beats per minute. The P waves are not associated with the QRS complexes. B,
Similar tracing; atrial rate 100 and ventricular rate of 30.
Cardiac Pacemakers
 Deliver an electrical current to stimulate
depolarization
 Temporary versus permanent

Electrical Pacemakers
(Cont.)
 Method of pacing
 Transcutaneous: emergency
 Transvenous
 Epicardial
 Can pace:
 Atrium
 Ventricle
 Both chambers

Transvenous
Figure 7-54. Single-chamber temporary pulse generator. (Courtesy Medtronic USA, Inc.
Minneapolis, Minnesota).
Permanent
Figure 7-57. Permanent dual chamber (A-V) pacemaker. (From Wesley K. Huszar’s
Basic Dysrhythmias and Acute Coronary Syndromes: Interpretation and Management.
4th ed. St. Louis: Mosby JEMS; 2010.)
Atrial Pacing
Figure 7-58. Atrial paced rhythm.

Ventricular Pacing
Figure 7-59. Ventricular paced rhythm.

Biventricular (Dual-Chamber)
Pacing
Figure 7-60. Dual-chamber (AV) paced rhythm. A, Atrial pacer spike; AV, AV pacer spike interval;
V, ventricular pacer spike.

(Cont.)
 Terms
 Rate
 Mode
 Electrical output: milliamperes (mA)
 Sensitivity
 Sense-pace indicator
 AV interval

 Complications
 Failure to pace
 Failure to capture
 Failure to sense

Failure to Pace
Figure 7-61. Failure to pace/fire.

Failure to Capture
Figure 7-62. Failure to capture: ventricular pacemaker.

Failure to Sense
Figure 7-63. Failure to sense.

Implantable Cardioverter-
Defibrillator (ICD)
 Pacemaker
 Biventricular pacemaker and ICD

Rhythm Interpretation
 Practice makes perfect!

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Chapter 7

Dysrhythmia Interpretation and

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Figure 7-1. The electrical conduction system of the heart.

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Figure 7-5. Autonomic nervous system.

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Figure 7-7. Direction of normal current flow through the ventricles.

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Figure 7-9. A. Einthoven’s triangle.

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Figure 7-9. A. Einthoven’s triangle. B. The triangle is converted to a triaxial diagram by

Figure 7-10. Precordial chest leads.

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Figure 7-14. ECG paper records time horizontally in seconds or milliseconds.

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Figure 7-15. ECG waveforms.

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Figure 7-16. The normal 12-lead precordial R wave progression.

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Figure 7-18. Pathological Q wave is greater than one fourth

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Figure 7-19. Six-second method of rate calculation.

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Figure 7-24. Normal sinus rhythm.

Figure 7-25. Sinus tachycardia.

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Figure 7-26. Sinus bradycardia.

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