ECG Rhythm Strip Interpretation, Basic-Lesson 1

Cardiac anatomy
 The heart lies behind the sternum in the mediastinal cavity, with two-thirds of the heart extending to the left of the
body's midline.
 The heart is surrounded by a fluid-filled sac called the pericardium, which consists of a fibrous layer and a serous layer.
 The heart's wall is made up of three layers of tissue: the epicardium, myocardium, and endocardium.
 The inside of the heart consists of four hollow chambers: two atria, separated by the interatrial septum, and two
ventricles, separated by the interventricular septum.
 The heart contains four valves: the atrioventricular valves (tricuspid and mitral valves) and the semilunar valves (aortic
and pulmonic valves).
 Three methods of circulation carry blood throughout the body: pulmonary, systemic, and coronary.

Cardiac physiology
 The cardiac cycle includes cardiac events that occur from the beginning of one heartbeat to the beginning of the next; it
consists of systole and diastole.
 The phases of the cardiac cycle include isovolumetric ventricular contraction, ventricular ejection, isovolumetric
ventricular relaxation, ventricular filling, and atrial systole.
 The generation and transmission of electrical impulses start at the cellular level and depend on four characteristics of
cardiac cells: automaticity, excitability, conductivity, and contractility.
 The depolarization-repolarization cycle consists of five phases: rapid depolarization, early repolarization, plateau phase,
rapid repolarization, and the resting phase.
 After depolarization and repolarization, an electrical impulse travels through the heart along a pathway called the
conduction system.
 Abnormal impulse conduction, such as automaticity, retrograde conduction, reentry, and ectopy, can cause heart rate
changes and other arrhythmias.

Cardiac Cycle

Characteristics of the cardiac cycle:

• it is defined as the cardiac events that occur during one

heartbeat
• it includes systole and diastole
Isovolumetric ventricular contraction:

• occurs as a response to ventricular depolarization

• causes increased tension and rising pressure within the
ventricles
• Results in closure of the mitral and tricuspid valves. (The
pulmonic and aortic valves remain closed throughout this
phase.)

Ventricular ejection:

• begins when ventricular pressure exceeds the pressures in the

aorta and pulmonary artery
• causes aortic and pulmonic valves to open
• Results in ejection of blood from the ventricles.

Isovolumetric relaxation:

• occurs when ventricular pressure falls below the pressures in the aorta and pulmonary artery
• causes the aortic and pulmonic valves to close (all valves are closed during this phase)
• Results in atrial diastole as blood fills the atria.

Ventricular filling:

• occurs when atrial pressure exceeds ventricular

pressure
• causes the mitral and tricuspid valves to open
• Allows blood to flow passively into the ventricles.
• About 75% of ventricular filling occurs at this time.

Atrial systole:

• coincides with late ventricular diastole

• fills the ventricles with the remaining 25% of blood for
each heartbeat
• May be referred to as the atrial kick.

Cardiac Impulses

Heart pumping:
 • requires an electrical stimulus
• Starts at the cellular level.

Four characteristics of cardiac cells:

• automaticity
• excitability
• conductivity
• Contractility.

In transmission of electrical impulses:

• a negative charge is maintained inside the cell (resting

potential)
• an electrical stimulus produces an ion shift, causing action
potential (depolarization)
• the cell attempts to return to its resting state (repolarization).

Five phases of the depolarization-repolarization cycle:

• Phase 0—Rapid depolarization

• Phase 1—Early repolarization
• Phase 2—Plateau phase
• Phase 3—Rapid repolarization
• Phase 4—Resting phase

The pathway of the cardiac electrical pulse is called the conduction

system. The cardiac impulse:

Begins at the sinoatrial (SA) node travels through three internodal tracts
of the right atrium (anterior, middle [Wenckebach's], and posterior
[Thorel's]) and through Bachmann's bundle in the left atrium reaches
the AV node, where it's momentarily delayed before entering the
ventricles (continued)

The pathway of the cardiac electrical pulse is called the conduction

system. The cardiac impulse:

• continues along the bundle of His

• travels down the right or left bundle branch
• Terminates at the Purkinje fibers.

Abnormal impulse conduction

Automaticity:

• Cells generate electrical impulses without stimulation.

• Retrograde conduction:
• Electrical impulses begin below the AV node and are transmitted backward toward the atria.
• Abnormal impulse conduction

Reentry:

• Impulses cause depolarization twice in a row at a faster-than-normal rate.

• An impulse reenters the same area and produces another impulse.

Ectopy:

• Injured cells partially depolarize; Spontaneous or secondary depolarization results.

ECG Rhythm Strip Interpretation, Basic-Lesson 2

Obtaining a rhythm strip

What an electrocardiogram (ECG) does:

• Monitors electrical currents created by impulses in the heart through electrodes attached to the skin
• Shows the sequence of electrical events (wave forms, interval, and segments)
• Doesn't show the heart's mechanical activity or pumping ability

Steps to interpret an ECG:

• Recognize the key components. (recognize key components, know how they appear on a normal ecg, know the
deviation)
• Analyze the key components separately.
• Correlate findings to reach a conclusion.
Two types of ECGs:
• 12-lead ECG
• Rhythm strip
12-lead ECG:
• Records 12 different views of the heart: 6 limb leads and 6 precordial leads
• Is used as a diagnostic tool (cardiac abnormalities)
• Is obtained using 10 electrodes (4 limb, 6 chest)
Rhythm strip:
• Records electrical activity during a 6-second period
• Is used to monitor cardiac status
• Easily identifies rate, rhythm, and abnormal
patterns
Electrodes
• Detect electrical currents from the heart that
radiate to the skin
• Are placed at different locations to obtain a
total picture of the heart's electrical activity
Leads
• Provide a view of the heart's electrical activity
between two points, or poles (has an
imaginary line as an axis)
• Consist of one positive pole and one negative
pole
• Produce either positive or negative
deflections on the ECG (upward or downward from the baseline)
• Are bipolar (+ and – and ground electrode) or unipolar (+ electrode)
Lead I
• Positive electrode on left arm or left side of the chest
• Negative electrode on right arm
• Deflection: positive (negative to positive flow of the current)
Lead II
• Positive electrode on left leg (+ electrode continuous monitoring= torso lowest palpable rib at the mid clavicular
line)
• Negative electrode on right arm (- electrode continuous monitoring= torso below the right clavicle)
• Deflection: positive (tall PRT waves)
Lead III
• Positive electrode on left leg
• Negative electrode on left arm
• Deflection: positive
aVR
• Positive electrode on right arm (augmented leads)
• Deflection: negative
aVL
• Positive electrode on left arm (augmented leads)
• Deflection: positive
aVF
• Positive electrode on left leg (augmented leads)
• Deflection: positive
Lead V1
• Right side of sternum at fourth intercostal rib space (corresponds with the placement of the SA node)
• Deflection: biphasic
Lead V2
• Left of sternum at fourth intercostal space
• Deflection: biphasic
Lead V3
• Between V2 and V4 at fifth intercostal space
• Deflection: biphasic
Lead V4
• Fifth intercostal space at midclavicular line
• Deflection: positive
Lead V5
• Fifth intercostal space, anterior to axillary line, between V4 and V6
• Deflection: positive
Lead V6
• Fifth intercostal space, midaxillary line
• Deflection: positive
MCL1
• Equivalent of V1
• Negative electrode: left upper chest
• Positive electrode: right side of the heart
• Ground electrode: right upper chest
• Deflection: negative; ectopic beats deflect in positive direction
MCL6
• Equivalent of V6
 • Negative electrode: below left shoulder
• Positive electrode: midaxillary line of left fifth intercostal space
• Ground electrode: below right shoulder
Continuous monitoring setup:
• Electrodes are placed on the chest instead of the limbs.
• Electrodes may be hardwired directly to cardiac monitor to continuously display cardiac cycles and print rhythm
strip recordings.
Common monitoring systems:
• Three- or five-electrode system is typically used.
• Electrode positions for one lead may be identical to those for other leads.
• Leads II, MCL1, and MCL6 are the most commonly used leads.
• Monitored leads can be varied by changing a selector switch or moving an electrode.
• Simultaneous dual monitoring may be possible. (lead 2 and v1)
Three-electrode system: (v1, v2, v3)
• One positive electrode (below the lowest palpable rib at the mid clavicular line)
• One negative electrode (below the right clavicle)
• A ground electrode (below the left clavicle)
Five-electrode system:
• Two additional electrodes—a permanent ground for all leads and a chest lead that can be repositioned to monitor
other leads (lowest palpable line)
• Color-coded lead wires to aid correct placement
Electrode site preparation:
• Choose a site over soft tissue or close to bone. 9 not over a (boney prominence, thick muscle, skin folds)
• Prepare the skin. (brisk rubbing not to damage the skin, clip hair)
• Dry moistened areas.
When to attach the lead wire to the electrode:
• If using Snap-On type, attach electrode to lead wire first.
• If using clip-on type, attach lead wire after electrode is secured to skin.
To apply electrodes:
• Remove electrode backing. (make sure it is still moist)
• Press one side of electrode against patient's skin, pull gently, and then press the opposite side against the skin.
• Press adhesive edge around outside of electrode to the patient's chest.
• Repeat for each electrode.
After positioning electrodes:
• View waveform on screen.
• Adjust waveform size and position on screen as necessary.
ECG paper:
• Consists of horizontal and vertical lines • Each small block equals 0.04 second.
forming a grid • Five small blocks form one large block equaling
• Is also called an ECG strip or tracing 0.2 second.
• Horizontal axis represents time: • Five large blocks equal 1 second.

Vertical axis measures amplitude—number of small blocks from the

baseline to the highest or lowest point:
• Each small block equals 1 mm or 0.1 mV.
• Each large block equals 5 mm or 0.5 mV.
(To determine amplitude, count the number of small block from
the base line to the highest point of the wave segment or interval)

ECG stylus reflects directional flow of the heart's electrical impulse

by upward and downward movement:
• Upward deflection: formed as current travels toward
positive pole
• Downward deflection: formed as current travels
toward negative pole
• Biphasic (both directions): current flows perpendicular to lead

Understanding the ECG complex

ECG complex: conduction of electrical impulses from the

atria to the ventricles in one cardiac cycle (depolarization
and repolarization cycle)

Basic waveforms:

• P wave
• QRS complex
• T wave

Additional components:

• PR interval
 • ST segment
• QT interval
• U wave (may not be present)

Isoelectric line: baseline reading between cardiac cycles, when no electrical activity occurs (records a straight line)

P wave

• Represents atrial depolarization—conduction

of an electrical impulse from sinoatrial (SA)
node through atria (check location,
configuration and deflection)
• Location: precedes QRS complex
• Amplitude: 2 to 3 mm high
• Duration: 0.06 to 0.12 second
• Configuration: usually rounded and smooth
• Deflection: positive in leads I, II, aVF, and V2 to
V6; usually positive but may vary in leads III
and aVL; negative or inverted in lead aVR;
biphasic or variable in lead V1

PR interval

• Tracks atrial impulse from atria through the atrioventricular (AV) node, bundle of His, and right and left bundle
branches (check amplitude, configuration and deflection)
• Location: measured from the beginning of the P wave to the beginning of the QRS complex
• Duration: 0.12 to 0.20 second

QRS complex

• Represents depolarization of and impulse conduction through the blood ventricles (contract and eject =pulse)
• Location: measured from the beginning of the Q wave to the end of the S wave, or from the beginning of the R wave
if the Q wave is absent
• Amplitude: 5 to 30 mm high; differs in each lead
• Duration: 0.06 to 0.10 second, or one-half of PR interval
• Deflection: positive (most of the complex above the baseline) in leads I, II, III, aVL, aVF, and V4 to V6; negative in
leads aVR and V1 to V2; biphasic in lead V3

ST segment

• Represents end of ventricular conduction (depolarization) and beginning of ventricular recovery (repolarization)
• Location: extends from the S wave to the beginning of the T wave
• J point= end of a QRS complex and the beginning of an ST segment
• Deflection: usually isoelectric (on the baseline); may vary from –0.5 to +1 mm in some precordial leads

T wave

• Represents relative refractory period of repolarization (ventricular recovery)

• Location: follows the ST segment
• Amplitude: 0.5 mm in leads I, II, and III and up to 10 mm in the precordial leads
• Configuration: typically rounded and smooth
• Deflection: usually positive or upright in leads I, II, and V2 to V6; inverted in lead aVR; variable in leads III and V1

QT interval

• Measures time needed for ventricular depolarization and repolarization

• Varies with heart rate; faster rate, shorter QT interval
• Location: extends from the beginning of the QRS complex to the end of the T wave
• Duration: 0.36 to 0.44 second; varies according to age, gender, and heart rate; with regular rhythm, shouldn't be
greater than one-half the distance between the two consecutive R waves

The 8-step method

Step 1: Determine the atrial and ventricular rhythms

• Use the paper-and-pencil method or caliper method.

• To evaluate ventricular rhythms, use R-R intervals.
• To evaluate atrial rhythms, use P-P intervals.
• Analyze findings for irregularities and patterns. (Slightly irregular of 0.04 is normal)

Step 2: Calculate the atrial and ventricular rates (ALWAYS CHECK PULSE TO CORRELATE THE HEART RATE ON THE STRIP)

1. Times-10 method (IRREGULAR HEART RATE)

Obtain a 6-second strip and count the number of P waves for atrial rate and the number of R waves for ventricular rate. 2.
Multiply each by 10. (3 SECONDS OR 15 LARGE BOXES, COUNT NUMBER OF P WAVES X 10, USE THE SAME WAY FOR THE R WAVE)

1,500 method (NORMAL HEART RATE)

 • Count the number of small squares between identical points on two consecutive P waves for atrial rate; then count
the number of small squares between identical points on two consecutive R waves for ventricular rate.
• Divide 1,500 by the number of small squares to get each rate.

Sequence method (MEMORIZE A SEQUANCE OF NUMBERS)

• Find a P wave that peaks on a heavy line.

• Assign 300, 150, 100, 75, 60, and 50 to the next six heavy lines.
• Find peak of the next P wave.
• Estimate the atrial rate based on the number assigned to nearest heavy line.
• Repeat with R waves for ventricular rate.

Step 3: Evaluate the P wave

• Determine if P waves are present for every QRS complex.

• Check for normal configuration and similar size and shape.

Step 4: Calculate the PR interval

• Count the number of small squares between the start of a P wave and the start of a QRS complex.
• Multiply the number of small squares by 0.04 second.
• Determine whether the duration is within normal limits (0.12 to 0.20 second, or 3 to 5 small squares).
• Determine whether the PR interval is constant.

Step 5: Calculate the QRS-complex duration

• Count the number of small squares between the end of the PR interval and the end of the S wave.
• Multiply the number of small squares by 0.04 second.
• Determine whether the duration of the QRS complex falls within normal limits (0.06 to 0.10 second).
• Check for consistent size and shape of all QRS complexes; measure and describe each as necessary.
• Check for a QRS complex after every P wave.

Step 6: Evaluate the T wave

• Determine whether T waves are present for every QRS complex.

• Check for normal configuration and similar size and shape. (CHECK FOR SAME DEFLECTION AS IN THE QRS COMPLEX)
• Check for hidden P waves.

Step 7: Calculate the duration of the QT interval

• Count the number of small squares between the beginning of the QRS complex and the end of the T wave, where
the T wave returns to baseline.
• Multiply the number of small squares by 0.04 second.
• Determine whether the duration of the QT interval falls within normal limits (0.36 to 0.44 second, or 9 to 11 small
squares). 9-11 SMALL SQUARES
• Determine whether the QT interval is constant.

Step 8: Evaluate other components

Check for:

• ectopic beats or other abnormalities

• abnormal ST segments
• presence of U wave.

Classify the rhythm strip by one or all of the following:

• origin of the rhythm

• rate
• rhythm interpretation.

Normal sinus rhythm:

• Has an impulse conduction that travels from the SA node to atria and AV node, through the bundle of His, to bundle
branches, and on to Purkinje fibers
• Is the standard against which all other rhythms are compared

ECG rhythm and rate characteristics:

• Rhythm: atrial and ventricular rhythms are normal and regular

• Rate: atrial and ventricular rates are regular; 60 to 100 beats/minute

Other ECG characteristics:

• P wave: round, smooth, and upright in lead II;
amplitude of 2 to 3 mm; duration of 0.06 to
0.12 second; one P wave for every QRS
complex
• PR interval: 0.12 to 0.20 second
• QRS complex: duration of 0.06 to 0.10 second;
amplitude of 5 to 30 mm; upright in lead II
• T wave: rounded, smooth, and upright in lead
II; amplitude in lead II of 0.5 mm
• QT interval: 0.36 to 0.44 second
 • Other: no ectopic or aberrant beats present

ECG Rhythm Strip Interpretation, Basic-Lesson3

Sinoatrial (SA) node: heart's primary pacemaker
Firing rate (in adult at rest): 60 to 100 times per minute

Arrhythmias can be caused by:

 changes in SA node's automaticity

 alterations in SA node's blood supply
 structural abnormalities
 sinus node diseases
 genetics
 autonomic nervous system influences.

Blood supply to SA node comes from:

 right coronary artery

 left circumflex artery.

Innervation of SA node is through autonomic nervous system via:

 the vagus nerve

 a parasympathetic nerve
 several sympathetic nerves.

Factors affecting SA node firing rate include:

 vagus nerve stimulation decreases firing rate

 sympathetic system stimulation increases firing rate.

Sinus arrhythmia is characterized by irregular firing of SA node's pacemaker cells.

Usually corresponds with the respiratory cycle (inhibition of reflex vagal ton)

 Inspiration increases heart rate (reduce vagal tone increases heart rate)
 Expiration decreases heart rate (increases
vagal tone and increases heart rate)

Can occur normally in:

 athletes-
 children (rare in infants)
 older adults.

Causes unrelated to respiration include:

 advanced age  carotid sinus pressure

 myocardial infarction  drugs (digoxin, morphine).
 increased intracranial pressure

Clinical significance

 Usually not significant

 Typically produces no symptoms
 If accompanied by bradycardia and hemodynamic compromise, atropine IV may be indicated
 May indicate a more serious condition in an older adult (sick sinus syndrome)

Rhythm

Irregular

 P-P and R-R intervals: shortened during

inspiration, lengthened during expiration
 Difference between shortest and longest
P-P intervals: exceeds 0.12 second

Rate

 Atrial and ventricular rates: 60 to 100 beats/minute

 Varies with respirations (increases during inspiration; decreases during expiration)

P wave

 Normal size and configuration

 Precedes each QRS complex

PR interval: Within normal limits; may vary slightly

QRS complex

 Normal duration and configuration

 Preceded by P wave

T wave: Normal size and configuration

QT interval: May vary slightly; usually within normal limits

Other: None

SINUS BRADYCARDIA

Sinus bradycardia is characterized by:

 heart rate less than 60 beats/minute

 impulses originating in the SA node.

Possibly occurs as a normal response to reduced

demand for blood flow.

May occur normally:

 during sleep
 in person with a well-conditioned heart.

Can occur from:

 cardiac disorders  obstructive sleep apnea

 noncardiac disorders  increased intrancranial pressure
 conditions producing excess vagal stimulation  some infectious diseases
or decreased sympathetic stimulation  severe prolonged hypoxia.
 use of certain drugs

Clinical significance depends on:

 the underlying cause

 how slow the rate is
 whether the patient can compensate for decreased cardiac output
 whether the patient is symptomatic.

May predispose some patients to:

 more serious arrhythmias

 palpitations and pulse irregularities.

Hemodynamic instability may require:

 atropine IV
 cardiac pacing.

Rhythm: Regular

Rate: Less than 60 beats/minute

P wave

 Normal size and configuration

 Precedes each QRS complex

PR interval: Within normal limits and constant

QRS complex: Normal duration and configuration

T wave: Normal size and configuration

QT interval: Within normal limits; may be prolonged

Other: None

SINUS TACHYCARDIA

Sinus tachycardia is characterized by:

 accelerated firing of the SA node

 rate greater than 100 beats/minute.

Sinus tachycardia is characterized by:

 accelerated firing of the SA node

 rate greater than 100 beats/minute.
May be clinically insignificant if caused by:

 exercise
 pain
 stress
 fever
 strong emotions.

Clinically significant causes include:

 cardiac conditions
 use of certain drugs
 other conditions in which increased heart rate serves as a compensatory mechanism.

Symptoms

 Usually produces no symptoms

 May cause symptoms if cardiac output falls and compensatory mechanisms fail

Adverse effects

 May occur without serious adverse effects

 Can cause or worsen myocardial ischemia and lead to heart muscle injury

Rhythm: Regular

Rate: Greater than 100 beats/minute (usually between 100 and 160 beats/minute)

P wave

 Normal size and configuration; may increase in amplitude

 Precedes each QRS complex; as heart rate increases, it may be superimposed on the preceding T wave

PR interval: Within normal limits and constant

QRS complex: Normal duration and configuration

T wave: Normal size and configuration

QT interval: Within normal limits; commonly shortened

Other: None

SINUS ARREST

Sinus arrest characteristics

 Results when SA node fails to initiate impulse

 Missing an entire PQRST complex
 Length of pause not a multiple of underlying
P-P or R-R intervals
 When the next beat falls "on time" (when
expected), it is a pause; if not, it is an arrest
 Pause may end with resumption of sinus
rhythm or often with a junctional escape beat

SA exit block characteristics

 Results when SA node discharges at regular intervals but impulses are delayed or blocked from reaching the atria
 Sinus rhythm interrupts the pause
 Pause is a multiple of underlying P-P interval

Common causes include:

 hypoxia
 cardiac disorders
 sinus node diseases
 increased vagal tone
 use of certain drugs
 acute infection.

Clinical significance

 May be asymptomatic with short and infrequent pauses

 May have signs and symptoms of decreased cardiac output including dizziness, pre-syncope, or syncope with recurrent
or prolonged pauses
 May include arrhythmias precipitated by extremely long pauses
 Frequent pauses may require atropine IV or a temporary or permanent pacemaker
Rhythm: Atrial and ventricular rhythms: usually regular, except during arrest or exit block

Rate

 Atrial and ventricular rates: usually within normal limits before arrest or exit block
 Length or frequency of pause: often results in bradycardia

P wave

 Absent during pause; entire PQRST complex missing

 Normal in size and configuration when present
 Precedes each QRS complex when present

PR interval: Within normal limits and constant when P wave is present

QRS complex: Normal duration and configuration; absent during pause

T wave: Normal size and configuration; absent during pause

QT interval: When present, usually within normal limits; absent during pause

Other: Sinus arrest may end with sinus rhythm or with a junctional escape beat

ECG Rhythm Strip Interpretation, Basic-Lesson 4

Introduction
Atrial arrhythmias:

 are the most common cardiac rhythm disturbances

 are caused by impulses originating in atrial tissue outside the sinoatrial (SA) node
 result from three mechanisms: altered automaticity, reentry, and triggered
activity.

Premature atrial contractions (PACs):

 are produced by an irritable focus in the atrium that fires before the SA node and
takes over as the heart's pacemaker for one or more beats.
 originate outside SA node from enhanced automaticity in atrial tissue

Conducted PAC

 Ventricular conduction is usually normal

 Early P wave followed by QRS complex

Nonconducted PAC

 No QRS complex
 P wave buried in preceding T wave

Causes can include:

 cardiac conditions
 respiratory conditions
 use of drugs (quinidine, procainamide, epinephrine, theophylline, digoxin)
 Non-cardiac and non-pulmonary causes (hyperthyroidism, electrolyte imbalances,
anxiety, fatigue, fever, infection, alcohol, cocaine, caffeine, or nicotine use).

Clinical significance

 With heart disease: can lead to atrial fibrillation, atrial

flutter, or decreased cardiac output
 Without heart disease: rarely of clinical significance
 Treat the cause in patient's with frequent premature atrial
contractions

Rhythm

 Underlying rhythm: may be regular

 Frequent PACs: often create an irregular rhythm
 Atrial and ventricular rhythms: irregular

Rate

Atrial and ventricular rates: vary with underlying rhythm

Premature P wave
  Abnormal configuration
 Varying configurations indicate more than one ectopic site
 May be hidden in preceding T wave

PR interval

 Usually within normal limits

 May be shortened or slightly prolonged

QRS complex

 Usually of a normal duration and configuration with

conducted PAC
 No QRS with nonconducted PAC

T wave

 Usually normal
 May appear distorted with a hidden P wave

QT interval

 Usually within normal limits

Other

 May occur as a single beat, in a bigeminal or trigeminal pattern, or in couplets

 Commonly followed by a pause as the SA node resets

ATRIAL TACHYCARDIA

Characterized by:

 impulses originating above the ventricles

 three or more successive ectopic atrial beats at a
rate of 150 to 250 beats/minute
 the rapid rate that shortens diastole, resulting in a
loss of atrial kick.

Three types include:

 atrial tachycardia with block

 multifocal atrial tachycardia
 paroxysmal atrial tachycardia.

Most atrial tachycardias are paroxysmal and self-limiting but in some patients may be present almost consistently.

Causes include:

 digoxin toxicity
 primary or secondary cardiac disorders
 other conditions (pulmonary embolism, cor pulmonale, hyperthyroidism, systemic hypertension, electrolyte imbalance,
hypoxia, physical or psychological stress)
 marijuana or cocaine use
 excessive stimulant use.

Clinical significance

 May be a forerunner of ventricular arrhythmias

 Results in decreased ventricular filling time, reduced cardiac output, increased myocardial oxygen consumption, and
decreased oxygen supply to the myocardium
 May produce rapid apical and peripheral pulse rates, palpitations, and signs and symptoms of reduced cardiac output
and hypotension

Atrial tachycardia with block

Rhythm

 Atrial: regular
 Ventricular: regular if the block is constant;
irregular if the block is variable

Rate
  Atrial: 150 to 250 beats/minute and multiple of ventricular rate
 Ventricular: varies with block

P wave

 Slightly abnormal
 More than one P wave for each QRS complex

PR interval: Usually normal; may be hidden

QRS complex: Usually normal

T and QT wave: Indiscernible

Other: None

Multifocal atrial tachycardia

Rhythm: Irregular

Rate

 Atrial: typically 100 to 250 beats/minute, but usually

under 160 beats/minute
 Ventricular: usually 100 to 250 beats/minute

P wave: Configuration varies with at least three different P-

wave shapes appearing

PR interval: Varies

QRS complex: Usually normal; may become aberrant

T wave: Usually distorted

QT interval: May be indiscernible

Other: None

Paroxysmal atrial tachycardia

Rhythm: Brief periods of tachycardia, alternating with

periods of normal sinus rhythm

Rate: 140 to 250 beats/minute

P wave

 Abnormal
 Precedes each QRS complex
 May be hidden in previous T wave

PR interval: Identical for each cycle

QRS complex: May be aberrantly conducted

T wave: Indistinguishable

QT interval: Indistinguishable

Other

 Has a sudden onset and end

 Typically initiated by a premature atrial contraction

Atrial Flutter

Characterized by:

 an atrial rate of about 300 beats/minute

 flutter, or F, waves on ECG (hallmark of
atrial flutter).

Results from:
  circus reentry
 possibly increased automaticity.

Clinical significance

 Determined by the number of impulses conducted through the atrioventricular (AV) node; expressed as a conduction
ratio (2:1 or 4:1)
 May maintain normal peripheral and apical pulses since the pulse reflects the number of ventricular contractions (not
atrial impulses)

Rapid ventricular rate

 Faster the rate, the more dangerous the arrhythmia

 Produces symptoms due to reduced ventricular filling time and coronary perfusion
 Causes angina, heart failure, pulmonary edema, hypotension, and syncope

Normal ventricular rate: May be asymptomatic

Analyzing the ECG rhythm strip

Rhythm

 Atrial: regular
 Ventricular: typically regular, but
depends on AV conduction pattern

Rate

 Atrial: typically 250 to 400 beats/minute

 Ventricular: depends on degree of AV block; usually one-half to one-fourth of atrial rate; one of the most commonly
seen rates�a ventricular rate of 150
beats/minute with an atrial rate of 300
beats/minute�is known as a 2:1 block

P wave

 Abnormal
 Saw-toothed pattern

PR interval: Unmeasurable

QRS complex

 Usually within normal limits in duration

 May be widened if flutter waves are within
complex

T wave: Unidentifiable

QT interval: Unmeasurable

Other: Atrial rhythm: may vary between a fibrillatory

line and flutter waves, referred to as atrial fib-flutter

ATRIAL FIBRILATION

Characterized by:

 chaotic, asynchronous, electrical activity in the

atrial tissue
 the firing of 400 to 600 erratic impulses each
minute from numerous ectopic atrial
pacemakers
 the appearance of baseline fibrillatory waves, rather than P waves
 irregularly irregular ventricular response as the AV node blocks impulses
 a wide variation in R-R intervals.

Common causes include:

 cardiac surgery
 cardiac disorders
 respiratory disorders
 use of certain drugs (aminophylline or digoxin)
  other conditions (hyperthyroidism, electrolyte imbalances, endogenous catecholamine release during exercise).

In otherwise healthy persons, may be caused by:

 fatigue  coffee
 obesity  antihistamines
 stress  nonprescription cold remedies
 smoking  alcohol use.

Clinical significance

 Loss of approximately 20% of normal end-diastolic

volume due to the loss of atrial kick
 Decreased diastolic filling time
 Reductions in cardiac output
 High potential for thrombus formation
 Can lead to a thrombotic stroke, cardiovascular collapse, and systemic arterial or pulmonary embolism
 Evaluation for anticoagulation therapy may be
necessary

Rhythm

 Grossly irregular atrial and ventricular rhythms

 Typically described as "irregularly irregular"

Rate

 Atrial: exceeds 400 beats/minute; most impulses

aren't conducted through AV junction
 Ventricular: varies from 100 to 150 beats/minute;
can be less than 100 beats/minute

P wave: Appearance of erratic baseline fibrillatory waves

instead

PR interval: Indiscernible

QRS complex: Usually normal in duration and configuration

T wave: Indiscernible

QT interval: Unmeasurable

Other: May develop atrial fib-flutter

ECG Rhythm Strip Interpretation, Basic-Lesson 5

Junctional arrhythmias

 Originate in pacemaker cells in atrioventricular (AV) junction

 Usual firing rate: 40 to 60 beats/minute
 Inverted P wave; normal QRS complex

Differentiating junctional arrhythmias from atrial arrhythmias

 Atrial: inverted P wave before QRS complex; normal PR interval

 Junctional: inverted P wave before QRS complex; PR interval T 0.12 second

P wave positioning and depolarization

 If atria depolarize first: P wave occurs before QRS complex

 If ventricles depolarize first: P wave occurs after QRS
complex
 If simultaneous depolarization occurs: P wave is hidden in
QRS complex

Premature junctional contractions

Characterized by:

 ectopic beat that occurs before normal beat due

to an irritable focus
 premature or out-of-sequence firing
 irregular rhythm.

Causes include:
  toxic digoxin levels
 excessive caffeine intake
 cardiac disorders.

Clinical significance:

 usually isn't dangerous

 requires monitoring for other signs of intrinsic
pacemaker failure
 may be asymptomatic.

Rhythm

 Atrial: Irregular during premature junctional

contraction
 Ventricular: Irregular during premature junctional
contraction
 Atrial and ventricular: Underlying rhythm possibly regular

Rate: Atrial and ventricular: Reflect underlying rhythm

P wave

 Usually inverted
 May precede, follow, or be hidden in QRS complex

PR interval

 Shortened if P wave precedes QRS complex

 Not measurable if no P wave precedes QRS complex

QRS complex: Usually normal configuration and duration

T wave: Usually normal configuration

QT interval: Usually within normal limits

Other: Commonly accompanied by a compensatory pause, reflecting retrograde atrial conduction

Junctional escape rhythm

Characterized by:

 string of beats from AV junction after failure of

the sinus node or atria depolarization of atria by
retrograde conduction
 inverted P waves
 firing rate of 40 to 60 beats/minute.

Causes include:

 conditions that disturb normal sinoatrial (SA) node function or impulse conduction
 cardiac conditions
 certain drugs
 other conditions (increased vagal stimulation,
electrolyte imbalances, and hypoxia).

Clinical significance:

 depends on patient's tolerance of decreased

heart rate and cardiac output
 should never be suppressed because this type of
arrhythmia is protective and prevents ventricular
standstill
 may be asymptomatic or cause signs and
symptoms of decreased cardiac output.

Rhythm: Atrial and ventricular: Regular

Rate: Atrial and ventricular: 40 to 60 beats/minute

P wave

 Usually inverted
 May precede, follow, or be hidden in the QRS complex

PR Interval

 Shortened if P wave precedes QRS complex

  Unmeasurable if no P wave precedes QRS complex

QRS complex: Usually normal

T wave: Usually normal

QT interval: Usually normal

Other: None

Accelerated junctional rhythm

Characterized by:

 irritable focus in AV junction

 depolarization of atria by retrograde conduction
 firing rate of 60 to 100 beats/minute.

Causes include:

 digoxin toxicity
 cardiac surgery
 cardiac conditions
 hypokalemia.

Clinical significance:

 may cause decreased cardiac output

 may cause no symptoms because rate equals
sinus rhythm.

Rhythm: Atrial and ventricular: regular

Rate: Atrial and ventricular: range from 60 to 100

beats/minute

P wave

 If present, will be inverted

 May precede, follow, or be hidden in QRS complex

PR interval

 Shortened if P wave precedes QRS complex

 Unmeasurable if no P wave precedes QRS complex

QRS complex: Usually normal

T wave: Usually normal

QT interval: Usually normal

Other: None

Junctional tachycardia

Characterized by:

 three or more premature junctional

contractions occurring in a row
 irritable focus that overrides the SA node to
function as heart's pacemaker
 rate of usually 100 to 200 beats/minute.

Causes include:

 digoxin toxicity (most common cause; aggravated by hypokalemia)

 cardiac surgery
 cardiac conditions.

Clinical significance:

 depends on rate, cause, and severity of accompanying cardiac disease

 may compromise cardiac output and hemodynamic instability
 typically causes signs and symptoms of decreased cardiac output
 may lead to heart failure, MI, and cardiogenic shock with acute coronary syndrome.
Rhythm

 Atrial and ventricular: usually regular

 Atrial: may be difficult to determine if P wave is
hidden in QRS complex or preceding T wave

Rate

 Atrial and ventricular: exceed 100 beats/minute

 Atrial and ventricular: usually between 100 and
200 beats/minute
 Atrial: may be difficult to determine

P wave

 Usually inverted
 May precede, follow, or be hidden in QRS
complex

PR interval

 Shortened if P wave precedes QRS complex

 Unmeasurable if no P wave precedes QRS
complex

QRS complex: Usually normal duration and configuration

T wave

 Usually normal except with hidden P wave

 May be indiscernible due to increased rate

QT interval: Usually within normal limits; may vary

Other: None

Wandering pacemaker

Characterized by:

 pacemaker site changing from sinoatrial node

to another area above ventricles
 origin of impulse (includes sinoatrial node, atrioventricular node, other atrial sites, and atrioventricular junction) possibly
wandering from beat to beat
 three different shapes of P waves on rhythm strip
 P wave and PR interval varying from beat to beat
 QRS morphology unchanged.

Causes include:

 increased vagal influences

 digoxin toxicity
 valvular heart disease
 organic heart disease such as rheumatic carditis.

Clinical significance

 Transient; rarely serious

 May be normal in young patients and athletes
 Generally asymptomatic unless heart rate is slow
 When chronic, should be monitored

Rhythm

 Atrial: varies slightly, with irregular P-P interval

 Ventricular: varies slightly, with irregular R-R
interval

Rate

 Atrial and ventricular vary

 Atrial and ventricular: usually within normal
limits
 Atrial and ventricular: may be slower than 60
beats/minute

P wave

 Varies in shape, size, and deflection

  May come before, during, or after QRS complex

PR interval

 Varies from beat to beat

 Always less than 0.20 second
 If impulse originates in AV junction: less than 0.12 second

QRS complex: Usually normal duration and configuration

T wave: Normal size and configuration

QT interval: Usually within normal limits; may vary

Other: None

ECG Rhythm Strip Interpretation, Basic-Lesson 6

Ventricular arrhythmias

Ventricular arrhythmias originate in ventricles below the bundle of His.

They may be benign or potentially deadly.

Characteristic appearance on ECG:

 wide QRS complex

 T wave and QRS complex deflections in opposite directions
 absent P wave.

Premature ventricular contractions

Characteristics of premature ventricular contractions (PVCs)

 Characterized as an ectopic beat originating in the

ventricles, usually caused by electrical irritability in
the ventricular conduction system or muscle tissue
 Described as uniform or multiform, and unifocal or
multifocal
 Commonly followed by a compensatory pause
 Occurring singly, in clusters of two or more, or in
repeating patterns

Dangerous PVCs

 Two or more in a row

 Multiform
 Bigeminy and trigeminy
 R-on-T phenomenon

Causes include:

 electrolyte imbalances
 drug intoxication
 cardiac conditions
 other conditions, such as metabolic acidosis, hypoxia, increased sympathetic stimulation
 use of caffeine, alcohol, or tobacco.

Clinical significance:

 depends on how well perfusion is maintained and how long abnormal rhythm lasts
 may be insignificant in healthy people
 can be lethal in patients with underlying heart disease.

Analyzing the ECG rhythm strip

Rhythm

 Atrial and ventricular: irregular during PVCs

 Atrial and ventricular: possibly regular underlying
rhythm

Rate: Atrial and ventricular: reflect underlying rhythm

P wave

 Usually absent in the ectopic beat

 May appear after QRS complex with retrograde
conduction
PR interval: Not measurable, except in the underlying rhythm

Analyzing the ECG rhythm strip

QRS complex

 Occurs earlier than expected

 Duration exceeds 0.12 second
 Has a wide, bizarre configuration

T wave: Deflects in opposite direction of QRS complex

QT interval: Usually isn't measured

Other: May be followed by a compensatory pause

Idioventricular rhythms

Safety mechanisms to prevent ventricular standstill

 Cells of His-Purkinje system act as heart's

pacemaker.
 Slow ventricular rate and loss of atrial kick
reduce cardiac output.

Characteristics of idioventricular rhythms

May be transient or continuous

 Ventricular escape beats: characterized by fewer than three QRS complexes

 Idioventricular rhythm: occurrence of consecutive ventricular beats (also called ventricular escape rhythm); usually has a
regular rhythm at 20 to 40 beats/minute

May occur as an accelerated idioventricular rhythm

 Rate of 40 to 100 beats/minute

 Characterized by enhanced automaticity of ventricular tissue

Causes include:

 third-degree heart block

 metabolic imbalances
 cardiac conditions
 use of certain drugs
 digoxin toxicity

Clinical significance:

 continuous idioventricular rhythms�produce symptoms associated with marked reduction in cardiac output; can result
in death if not treated promptly
 transient idioventricular rhythms�usually are not significant.

Analyzing the ECG rhythm strip

Rhythm

 Atrial: can't be determined

 Ventricular: regular

Rate

 Atrial: can't be determined

 Ventricular: 20 to 40 beats/minute

P wave: Absent

PR interval: Not measurable

Analyzing the ECG rhythm strip

QRS complex

 Duration longer than 0.12 second

 Wide, bizarre configuration

T wave: Deflection in direction opposite that of QRS complex

QT interval: Usually prolonged

Other: None
Ventricular tachycardia

Characteristics of ventricular tachycardia

Life-threatening arrhythmia resulting from increased myocardial irritability

Characterized by:

 occurrence of three or more PVCs in a row

 ventricular rate typically 100 to 250 beats/minute
 short, paroxysmal bursts or sustained unstable rhythm.

Causes include:

 electrolyte imbalances
 cardiac conditions
 drug intoxication.

Clinical significance:

 unpredictable course and outcome

 may result in various patient conditions: stable with few symptoms; unstable, with decreased level of consciousness;
unconscious, without respirations or pulse
 has potential for causing death.

Analyzing the ECG rhythm strip

Rhythm

 Atrial: can't be determined

 Ventricular: usually regular but may be slightly irregular

Rate

 Atrial: can't be determined

 Ventricular: usually 100 to 250 beats/minute

P wave

 Usually absent
 May be obscured by QRS complex
 Dissociated from QRS complexes
 May demonstrate retrograde P waves

PR interval: Not measurable

QRS complex

 Duration greater than 0.14 second

 Bizarre appearance with increased amplitude
 Monomorphic: uniform shape
 Polymorphic: constantly changing shape

T wave: If visible, in opposite direction of QRS complex

QT interval: Not measurable

Other: None

Torsades de pointes

Characteristics of torsades de pointes

Variation of polymorphic ventricular tachycardia

Characterized by:

 rate that varies between 150 and 300

beats/minute
 prolonged QT interval
 QRS polarity that spirals around isoelectric
line
 life-threatening condition.

Causes include:

 conditions that prolong QT interval

 use of certain drugs
 myocardial ischemia
 electrolyte abnormalities.
 Clinical significance:

 requires rapid intervention to prevent cardiovascular collapse

 causes severe symptoms in most patients.

Analyzing the ECG rhythm strip

Rhythm

 Atrial: can't be determined

 Ventricular: may be regular or irregular

Rate: Ventricular: between 150 and 300 beats/minute

P wave: Usually indiscernible

PR interval: Not measurable

QRS complex: Wide, with changing amplitude

T wave: Indiscernible

QT interval: Prolonged

Other: May start and stop suddenly

Ventricular fibrillation

Characteristics of ventricular fibrillation

Characterized by:

 chaotic pattern of electrical activity

 electrical impulses arising from multiple ectopic
pacemakers in the ventricles
 no effective muscular contraction and no cardiac
output
 life-threatening condition that leads to
ventricular standstill and death if untreated.

Causes include:

 cardiac conditions
 electrolyte imbalances
 drug toxicity
 other conditions (acid-base imbalance, electric shock, and severe hypothermia).

Clinical significance:

 patient is in full cardiac arrest, unresponsive, and without a detectable blood pressure or central pulses.
 chance of successful electrical defibrillation is greater with coarse fibrillatory waves than with fine fibrillatory waves.

Analyzing the ECG rhythm strip

Rhythm

 Atrial: can't be determined

 Ventricular: no pattern or regularity; just
fibrillatory waves

Rate: Atrial and ventricular: can't be determined

P wave: Can't be determined

PR interval: Can't be determined

QRS complex: Can't be determined

T wave: Can't be determined

QT interval: Not measurable

Ventricular asystole

Characteristics of ventricular asystole

Characterized by:

 ventricular standstill or asystole

 no discernible electrical activity in the ventricles
 no cardiac output
  need to rule out fine ventricular fibrillation, using more than one ECG lead.

Causes include:

 inadequate blood flow to the heart

 severe, uncorrected acid-base disturbances
 severe electrolyte imbalances
 drug intoxication
 cardiac conditions
 other conditions (massive pulmonary embolism, tension pneumothorax, prolonged hypoxemia, electric shock,
hypothermia, and hypovolemia).

Clinical significance:

 patient completely unresponsive, without

spontaneous respirations, blood pressure, or pulse
 typically considered confirmation of death.

Analyzing the ECG rhythm strip

ECG components

 Nearly a flat line

 No electrical activity evident
 Possibly P waves for a time
 No measurements possible

ECG Rhythm Strip Interpretation, Basic-Lesson 7

Atrioventricular (AV) block refers to an interruption or delay in the

conduction of electrical impulses between the atria and ventricles.

Can occur at:

 AV node
 bundle of His
 bundle branches.

Classified by severity:

first-degree AV block

 type 1 second-degree AV block (Wenckebach or Mobitz 1)

 type 2 second-degree AV block (Mobitz 2)
 third-degree (complete).

Causes of AV block include:

 congenital anomalies
 underlying heart conditions
 use of certain drugs
 conditions that disrupt the cardiac conduction system
 inadvertent damage to conduction pathways.

First-degree AV block

Characterized by:

 impulses traveling through the normal pathway

 delay occurring at AV node or bundle of His
 constant, prolonged PR interval.

Causes include:

 cardiac conditions
 use of certain drugs.

Clinical significance:

 usually produces no symptoms

 cardiac output not significantly affected
 pulse rate usually normal; rhythm regular
 may occur normally in healthy persons.

Rhythm: Atrial and ventricular: regular

Rate: Atrial and ventricular: equal and within normal limits

P wave
  Normal
 Followed by QRS complex The PR interval is 0.36 second. Each small
PR interval box on the rhythm strip is 0.04 seconds.
Measure from the beginning from the P wave
 Prolonged
to the beginning of the R wave which, in this
 Constant
example, equals 9 small boxes.
QRS complex

 Usually normal when delay is in AV node

 If more than 0.12 second, conduction delay possibly in His-Purkinje system

T wave: Normal in size and configuration unless QRS complex is prolonged

QT interval: Usually within normal limits

Other: None

Type 1 second-degree AV block

Second-degree AV block

 Some electrical impulses from the AV node are

blocked; some are conducted through normal
conduction pathways
 Subdivided into type 1 second-degree AV block
and type 2 second-degree AV block

Type 1 second-degree AV block, also called Wenckebach or Mobitz 1 block, is characterized by:

 repetitive sequence of two or more consecutive impulses, each delayed slightly longer than the previous one, followed
by an impulse that fails to be conducted
 impulse typically blocked at AV node.

Causes include:

 increased vagal stimulation

 cardiac conditions
 use of certain drugs.

Clinical significance:

 may occur normally in healthy persons

 usually asymptomatic; associated with a good prognosis
 may produce symptoms, especially with a slow ventricular rate
 can progress to a more serious form.

Rhythm

 Atrial: regular
 Ventricular: irregular; R-R interval shortens progressively until a P wave appears without a QRS complex

Rate

 Atrial rate exceeding ventricular rate

 Both usually within normal limits

P wave

 Normal in size and configuration

 Followed by QRS complex except for blocked P wave

PR interval

 Progressively longer with each cycle until a P wave appears without a QRS complex
 Repetitive pattern of "long, longer, dropped"

QRS complex

 Usually normal
 Periodically absent

T wave: Usually normal

QT interval: Usually normal

Other: Pattern of grouped beating

Type II second-degree AV block

Characterized by:

 impulses from sinoatrial (SA) node that occasionally fail to conduct to ventricles
 occurrence below level of AV node, commonly at bundle branches
 failure of PR interval to lengthen before a dropped beat
 successive nonconducted beats.

Causes include:

 anterior-wall myocardial infarction

 degenerative changes in the conduction system
 severe coronary artery disease.

Clinical significance:

 usually chronic
 may progress to complete heart block
 may produce symptoms if patient has a slow sinus rhythm, a slow ventricular rate, and decreased cardiac output
 commonly requires pacemaker placement.

Rhythm

 Atrial: regular
 Ventricular: regular or irregular

Rate

 Atrial: usually within normal limits

 Ventricular: may be within normal limits; slower than atrial rate

P wave

 Normal in size and configuration

 Some not followed by QRS complex

PR interval

 Within normal limits or prolonged

 Constant for conducted beats

QRS complex

 Periodically absent
 Within normal limits or narrow in bundle of His block
 Widened if block occurs at bundle branches

T wave: Usually normal

QT interval: Usually normal

Other

 PR and R-R intervals don't vary before a dropped beat.

 P-P interval is constant, including the extra P wave.
 R-R interval with nonconducted P wave equals two normal R-R intervals.

Third-degree AV block

Characterized by:

 complete absence of impulse conduction

between the atria and ventricles
 occurrence at the level of the AV node, bundle of
His, or bundle branches
 continuation of atrial impulses at SA node;
typically maintains normal atrial rate (60 to 100
beats/minute)
 ventricular impulse conduction originating in junctional tissue or Purkinje fibers; ventricular rate typically slower than
atrial rate.

Causes of blocks originating at the AV node level include:

 congenital conditions (most common)

 increased parasympathetic tone
 AV node damage
 toxic drug effects.

Causes of infranodal level blocks (blocks originating at the bundle of His or bundle branches) include:
extensive anterior myocardial infarction.

Clinical significance:

 potentially life-threatening situation

 can cause a dramatic drop in cardiac output
 AV node level—usually transient; generally favorable prognosis
 infranodal level—unstable pacemaker, commonly with episodes of ventricular asystole; less favorable prognosis
 severity of symptoms dependent on ventricular rate; most patients experience significant symptoms.

Rhythm: Atrial and ventricular rhythms: usually regular

Rate

 Atria and ventricles beat independently of each other

 Atrial: usually 60 to 100 beats/minute; exceeds ventricular rate
 Ventricular: varies with type of block (AV node: 40 to 60 beats/minute; infranodal: usually below 40 beats/minute)

P wave

 Normal in size and configuration

 Doesn't conduct QRS complex that follows it
 Some possibly buried in QRS complexes or T waves

PR interval: Not applicable or measurable

QRS complex

 Normal if block is at level of the AV node or bundle of His

 Widened if block is at level of bundle branches

T wave: Usually normal except when QRS complex originates in ventricle

QT interval: Usually within normal limits; may vary

Other: P waves occurring without QRS complexes

Complete AV dissociation

Characterized by:

 atria and ventricles always beating independently of

each other
 ventricular rate that's the same or faster than atrial rate

Caused by one of three underlying rhythm disturbances:

 slowed or impaired sinus impulse formation or SA conduction

 accelerated impulse formation in the AV junction or ventricle
 AV conduction disturbance.

Clinical significance:

 depends on underlying cause

 depends on the effect on cardiac output.

Rhythm: Atrial and ventricular: regular

Rate: Atrial and ventricular: nearly equal; ventricular can be faster

P wave: No relation to QRS complex

ECG Rhythm Strip Interpretation, Basic-Lesson 8

Pacemaker functions

 Electrically stimulates the myocardium

to depolarize
 Initiates mechanical contractions
 Used for arrhythmias or following
myocardial infarction or cardiac
surgery; may be temporary or
permanent

Pacemaker spike

 Represents transmission of electrical impulse to heart

 Appears on ECG as a vertical line; group of spikes is called
artifact
  May be found in various locations on waveform, depending on electrode positioning

Atrial pacing

 Spike is followed by a P wave, then patient's intrinsic QRS complex and a T wave.
 P wave appears different from patient's normal P wave.
Atrial & Ventricular
Ventricular pacing Atrial pacing Ventricular pacing pacing

 Spike is followed by a QRS complex and a T wave.

 QRS complex appears wider than patient's own QRS complex.

Atrial and ventricular pacing

 Initial spike is followed by a P wave, another spike, then a QRS complex.

 Pacemaker type and patient's condition may affect pacing.

Temporary pacemakers

Used in emergencies for:

 high-grade heart block

 bradycardia
 low cardiac output.

Types include:

 Transvenous
 Epicardial
 transcutaneous.

Transvenous

 Most commonly used

 Inserted through vein (typically the
subclavian or internal jugular)

Leadwires passed into right atrium or ventricle, then

connected to pulse generator

Epicardial

 Used in patients undergoing cardiac surgery

 Leadwires attached to heart's surface;
brought through chest wall to pulse generator

Transcutaneous

 Used as emergency treatment until placement of transvenous pacemaker or resolution of arrhythmia

 Electrode pads placed on anterior chest wall and back

Pulse generator settings

 Rate control
 Output control
 Sensitivity control

Permanent pacemakers

Characteristics

 Helps treat chronic heart conditions

 Leads placed transvenously and anchored to endocardium
 Generator implanted in a subcutaneous pocket

Biventricular pacing

 Treats patients with uncoordinated contraction of the right and left

ventricles
  Also called cardiac resynchronization therapy

Leads and electrodes

 Three leads
 Both ventricles paced at same time, causing simultaneous contraction
 Electrode for left ventricle not anchored, increasing risk of lead displacement

Pacemaker codes

Five-letter coding system

 First letter: identifies the

chambers paced
 Second letter: signifies the
chambers where the pacemaker
senses intrinsic activity
 Third letter: indicates mode of
response to intrinsic electrical
activity
 Fourth letter: describes degree of
programmability and presence or
absence of adaptive rate
response
 Fifth letter: denotes the
pacemaker's response to a tachyarrhythmia

Single-chamber pacemakers

Types of single-chamber pacemakers include:

 AAI (electrode placed in atrium)

o Senses and paces atria only
o Inhibits pacing and resets itself with intrinsic atrial activity
o Characterized by P wave following spike (signifies atrial
depolarization has occurred)
o Requires functioning atrioventricular (AV) node and intact
conduction system
 VVI (electrode placed in ventricle).
o Senses and paces ventricles only
o Inhibits pacing and resets itself with intrinsic ventricular
activity
o Doesn't synchronize ventricular activity with spontaneous
atrial activity
o Characterized by QRS complex following spike (signifying
ventricular depolarization)

Both types automatically fire if they don't sense intrinsic electrical activity.

Dual-chamber pacemakers

DDD pacemaker

 Mimics normal physiologic cardiac cycle, maintaining AV

synchrony
 Can sense and pace the atria and ventricles
 Won't fire if it doesn't need to

Rhythm strip evaluation

 Pacemaker spike follows the P wave: indicates adequate atrial impulses; ventricular response paced
 Pacemaker spike occurs only before the P wave, with an intrinsic QRS complex following: indicates low atrial rate with
normal conduction through ventricles
 Pacemaker spike occurs before P wave and
before QRS complex: indicates absence of
intrinsic activity in the atria or ventricles

Pacemaker malfunction

Pacemaker malfunction can lead to:

  arrhythmias
 low cardiac output
 loss of AV synchrony.

Common types of malfunction include:

 failure to capture
 failure to pace
 failure to sense intrinsic beats
 oversensing.

Failure to capture

 Pacemaker's inability to stimulate heart chamber

 Appears on ECG as a spike without a P wave or QRS
complex response
 Caused by increased pacing thresholds or lead
malfunction

Failure to pace

 Failure of pacemaker to initiate an impulse

 Absence of pacemaker spike on ECG when it's expected
 Caused by battery or circuit failure, electromagnetic interference, lead malfunction, or inappropriate programming of
sensing function

Failure to sense

 Pacemaker's initiation of an impulse when it doesn't need to

 Pacemaker spike when intrinsic cardiac activity is present, which may appear anywhere in the cardiac cycle
 Caused by electrolyte imbalances, displacement of electrode tip, increased sensing threshold, or a depleted pacemaker
battery

Oversensing

 Pacemaker doesn't initiate impulse when it needs to

 On an ECG, there are no spikes when intrinsic activity is absent
 Caused by misinterpretation of muscle movements or other
events as intrinsic activity