1. health and fitness
2. disease
3. heart disease

C
A R D I A C
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E R I E S
#15
The Basics of
Neonatal EKG Interpretation
Lyn Vargo, RNC, MSN, NNP
T
HE ELECTROCARDIOGRAM (EKG) CAN PROVIDE THE
measurements found in a normal neonate would be considneonatal nurse with information about an infant’s
ered abnormal in an adults For this reason, it is imperative
heart rate, the conduction system of the neonatal heart, and
that the appropriate age-adjusted tables be used to interpret
the formation of normal and abnormal electrical impulses.’
EKG measurements.
Clinicallv, the EKG is used to make deductions about the
This article reviews the basic physiologic principles of the
cardiac impulse and the EKG. It
electrid’ hctivity of the heart and
then relates these principles to
inferences about cardiac pathology.2 The EKG is easily obtained
the unique findings of the
This article reviews the basic physiologic principles of the
and is noninvasive. A 12-lead
neonate and premature infant.
cardiac impulse and the EKG. It then relates these findings
EKG is most often used in evaluto the unique findings of the neonate and premature infant.
ating cardiac arrhythmias, atrial
EXAMINING
Emphasis is placed on familiarizing nurses with the tktors
or ventricular hypertrophy, eiecEKG PAPER
afkting the basic neonatal EKG and on the usetirlness of
An actual tracing of the
trolyte abnormalities, myocardial
cardiac rhythm strips and 12-lead EKGs. Topics addressed
include evaluation of neonatal heart rate, examination of
heart’s electrical activity can be
or pericardial infections, myocarcomponents of the cardiac cycle, identification of possible
made by a recording machine on
dial ischemia and infarction, and
cardiac dystimction, recognition of electrolyte imbalances,
heat-sensitive EKG paper. EKG
congenital heart disease.s
and effects of digoxin administration on cardiac rhythm.
paper is graph paper composed
The normal EKG of the
of small and large squares. Each
neonate is very different from
small square measures 1 mm by
that of the older infant, child, or
1 mm, and each large square measures 5 mm by 5 mm. One
adult (Figure 1). The EKG of the full-term neonate is slightly
large square contains 25 small squares (Figure 2).
different from that of the premature infant (Table 1).
EKG paper measures two elements: time and voltage.’ In
Changes occur in the normal EKG during the first minutes,
routine EKG interpretation, the recording speed of the paper
hours, days, weeks, and months of life.4 The major changes
is 25 mm (about I inch) per second. (If the speed is any slowtake place during the first year of life. Thereafter, changes are
er or faster, this must be noted because it will change the
relatively minor. The differences between a neonate’s EKG
EKG pattern and alter measurements.) Time is measured on
and the EKG of an older patient are caused by the unique
hemodynamics of fetal and transitional circulation, by overall , the horizontal axis, reading left to right. Each small square
equals 0.04 second, and each large square equals 0.2 second
changes in physiology, by changes in the size and position of
(Figure 2). In the top border of the EKG paper, every 7.5 cm
the heart chambers relative to one another, and by changes in
is marked by a heavy black vertical line. The distance between
the size and position of the heart relative to the rest of the
one line and the next equals 3 seconds (Figure 3).6 By meabody. It is especially important to understand these differsuring along the horizontal asis of the EKG paper, you can
ences when evaluating a neonate’s EKG because most of the
Accepted for publication April 199% Revised June 1998.
NEONAT~~L
VOL. 17, NO. 8, DECEMBER 1998
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~
FIGURE 1 m Comparison of neonatal 124ead EKG to adult 12-lead EKG. Not reproduced to scale.
N E 0 N A T A L N E T 8’ 0 R Ii
8
DECEMREK 1998. VOL. I - . r\;O. 8
TABLE 1
n
FIGURE 2 m Standard EKG paper.
Findings of Premature Infant’s EKG
Compared to EKG of Full-Term Infant
Small squares measure 1 mm by 1 mm.
Large squares measure 5 mm by 5 mm.
Less right ventricular dominance (or more left ventricular
dominance) than the full-term infant
Lower voltages of the QRS complex and T wave in the
standard leads
Relatively shorter PR, QRS, and QT intervals than the fullterm infant
More variability in the EKG overall
Adapted from: Park MK, and Guntheroth WC. 1992. How
to Read Pediutric ECGs, 3rd ed. St. Louis: Mosby-Year
Book, 33-34.
L
00.4
second
of
%
I
determine the duration of any part
the cardiac
cycle and the actual heart rate.
Voltage (or nmplitztde) is measured on the
vertical axis of the EKG paper. Voltage measures
the height and depth of a cardiac impulse or its
upward or downward deflection. It also measures the depression or elevation of baseline segments of the cardiac impulse.’ Each small square
equals 1 mm of amplitude. Ten millimeters of
amplitude (two large squares) equal 1 millivolt
(mV) (Figure 2).
With a single-lead rhythm strip, the voltage
measurement is not as important as the time
measurement. This is because the amplitude of
the impulse is usually adjusted so that the
impulses can be clearly visualized and measured.
With a 12-lead EKG, the amplitude of deflections is used for diagnostic purposes.
CARDIAC RHYTHM STRIP (LEAD II)
V E R S U S 12-LEAD EKG
Two categories of EKGs are commonly used
in the care of neonates: single-lead cardiac
rhythm strips and 12-lead EKGs. Both are
important tools in the cardiac evaluation of the
neonate and provide valuabIe information about
the heart and conduction system. At the infant’s
bedside, single-lead EKG rhythm strip provides
one view (or angle) of cardiac activity. It can give
general information about heart rate and identify deviations in normal cardiac rhythm instantaneously. The ability to accurately assess the single-lead rhythm strip for identification of possiFIGURE 3
n
ble cardiac dysmnction is critical for the bedside
nurse and is the focus of this article.
There are limitations to the singIe-lead EKG
rhythm strip, though, and it is imperative that
the neonatal nurse be aware of these. As stated,
the single-lead EKG rhythm strip provides only
one view of cardiac activity. For a more complete
view of the heart, a 12-lead EKG is required. A
12-lead EKG provides an examination of the
entire heart because it assesses the heart from
several different angles. Each of the leads presents a different pattern or a slightly different
view of the same cardiac activity.’ This gives us a
more complete picture of the electrical activity of
the heart than is possible with a cardiac rhythm
strip. Because of the difference between
rhythm strips and a 12-lead EKG, rhythm strips
(although invaluable as a screening tool for rate
and rhythm) should not be used to diagnose
cardiac conditions. A 12-lead EKG is necessary
for accurate diagnosis of cardiac conditions.
The 12-lead EKG is one important tool used
in the complete cardiac evaluation of the newborn. The electrical record that it provides gives
valuable information about the heart’s structure
and its function.’ However, the 12-lead EKG
does not provide a complete assessment of
mechanical function. For example, it will not
show how well the heart is contracting in an
infant with acute pulmonary edema. Nor does it
always directly depict structural abnormalities.8
.
EKG paper showing black vertical markings above gridlines.
The distance between two of these marks measures 7.5 cm and is equal to 3 seconds.
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VOL. 17, NO. 8, DECElMBER 1 9 9 8
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FIGURE 4
n
Cardiac depolarization and reoolarization.
POLARIZED RESTING CELL
DEPOLARIZING CELL
DEPOLARIZED CELL
REPOLARIZING CELL
c
+
-
lular ion, potassium, which exerts only a relatively weak positive charge inside the cell.’ This difference benveen the inner and outer cell membranes is actively maintained by a pump mechanism called the sodium-potassium pump.
At some point, the sodium-potassium pump
is no longer able to maintain the separation of
charges between the cell membranes, and the
process of depolarization and myocardial contraction occurs.7 In depolarization, the sodium
and calcium ions enter the cell. The influx of
sodium and calcium ions pushes the potassium
ions out of the cell. This causes a reversal of the
charges between the cell membranes. The outside of the cell is now negatively charged and the
inside of the cell is positively charged, and the
cardiac stimulation occurs in a wavelike fashion
throughout the heart (Figure 4)’
Repolarization is an electrical phenomenon
that occurs after stimulation, when the mvocytes
regain their resting negatively charged interior
(Figure 4).’ Repolarization must occur before
depolarization can occur again. In repolarization, the sodium-potassium pump actively
pumps the sodium and calcium ions out of the
cell and the potassium ions into the cell to reestablish the electrical charge across the cell
membrane.’ For individual mvocytes, depolarization and repolarization occur in the same
direction. For the entire myocardium, depolarization occurs from the endocardium (innermost
layer) to the epicardium (outermost layer), and
repolarization occurs in the opposite direction.R
D
Depolarization and repolarization. The resting heart muscle cell, A, is polarized; that is, it
carries an electrical charge, with the outside of the cell positively charged and the inside
negatively charged. When the cell is stimulated (I), as in 6, it begins to depolarize
(stippled area). The fully depolarized cell, C, is positively charged on the inside and
negatively charged on the outside. Repolarization, D, occurs when the stimulated cell
returns to the resting state. The direction of depolarization and repolarization is
represented by orrows. Depolarization (stimulation) of the atria produces the P wave on
the ECG, whereas depolarization of the ventricles produces the QRS complex.
Repolarization of the ventricles produces the ST-T complex.
From: Goldberger AL, and Coldberger E. 1994. Clinical flectrocardiogrophy, 5th ed.
St. Louis: Mosby-Year Book, 8. Reprinted by permission.
To be most effective, the 12-lead EKG must be
used in conjunction with other tools for assessing structure and function.
THE ELECTRICAL IMPULSE AND
THE EKG
The heart acts much like an electrical generator. Currents flowing from the heart travel within the entire body and create a cardiac electrical
field that forms repetitive patterns. The basic
EKG complex is a representation of these currents in the body.4
In general, an upward deflection of a wave on
an EKG complex is called a positive deflection
and a downaard deflection is called a nefiative
deflection. ,4 deflection that is partly positive and
partI!. negative is called hipbasic. A segment that
is flat on the baseline is isoelectC8
There are three phases to the cardiac cycle.
They are i 1) polarization, 12 ) depolarization,
and (3) repolarization. During the polarization
(or resting) phase of the cardiac qrcle, the
heart’s mvocytes (muscle cells) have a negativel!
charged interior and a positively charged exterior
(Figure 4). This is due to the differential
between the primary extracellular ions, sodium
and calcium, i\Thich esert a strong positi1.e
charge outside the cell, and the primary intracel-
NEONATAL
I (1
THE CARDIAC CYCLE
One cardiac cycle consists of a P wave, followed by the QRS complex, followed by the T
wave. These cardiac cycles occur successively on
an EKG tracing. These waves and complexes
also produce the PR interval, the QT interval
(which are discussed later), and the ST segment
(Figure 5).6 Evaluating and measuring the various components of the cardiac qcle in a systematic fashion vield, information about the heart
rate, the regularity of the heartbeat, and the
general state of the conduction system.
The ceils in the cardiac conduction system differ from the other cells in the heart in that the!
can depolarize spontaneously. This abilitv is
called azrtornaticiq. In the health!. heart, the cells
of the atria and ventricles \vill not depolarize
spontaneousl!y thev will an.ait a stimulus from
the sinoatrial (SA) node.9 The S_i node, located
NETWORK
DECFh4HF.K 1998. \ OL. I - . Ii<). 8
FIGURE 5
n
FIGURE 6
intervals and segments of the cardiac
cycle.
l
Diagram of heart conduction system.
SA node
AV node
Bundle of His
Left bundle branch
Right bundle branch
Purkinje Fibers
Adapted from: Park MK. 1996. Pediatric Curdiology for
Practitioners, 3rd ed. St. Louis: Mosby-Year Book, 41.
Reprinted by permission.
From: Park MK, and Cuntheroth WC. 1992. How to Read
Pediatric KCs, 3rd ed. St. Louis: Mosby-Year Book, 1.
Reprinted by permission.
in the posterior wall of the right atrium, is the
normal heart’s dominant pacemaker (Figure 6).
It generally initiates the impulse wave ofdepolarization. This wave proceeds outward from the SA
node, and both atria are stimulated to contract.’
The normal P wave of the cardiac impulse represents the depokuization and contraction of the
atria (Figure 5). The first half of the P wave represents depolarization of the right atrium, and
the second half represents depolarization of the
left atrium. When atriai depolarization is stimulated by other pacemakers, the shape and direction of the P wave will be altered.2
Following depolarization of the atria, the cardiac impulse travels to the atrioventricular (AV)
node (Figure 6). The AV node is located in the
lower part of the right atrium very close to the
interatrial septum.’ The AV node is the only
pathway that allows the cardiac impulse to travel
from the atria to the ventricles through the
fibrous AV valves (mitral and tricuspid).’ The
AV node also serves as a backup pacemaker if SA
node firing or atria1 depolarization should fail to
0ccur.l The stimulus of depolarization is delayed
slightly through the AV node as blood flows
through the AV valves into the ventricles. Once
the impulse has reached the ventricular conduction system, it proceeds very rapidly through the
His-Purkinje system. This system consists of the
bundle of His, the right and left bundle branches, their terminal ramifications, and the Purkinje
fibers (Figure 6).9 The bundle of His is located
in the top left corner of the right ventricle and at
the top of the interventricular septum.’ It carries
the cardiac impulse horn the AV junction to the
lower conduction system of the ventricles. The
VOL.
right and left bundle branches are the major
bifurcations of the bundle of His. These branches subdivide further to become the Purkinje
fibers. These fibers carry the cardiac impulse to
the myoqites of the ventricles via their terminal
filaments.’ Right and left ventricular depoiarizadon occur virtually simultaneously.2 Any part of
the ventricles, as well as the Purkinje fibers, may
serve as a backup pacemaker should the higher
pacemakers fail to function. Ventricular or
Purkinje pacemaker sites tend to be less regular,
slower, and more unreIiabIe than higher pacemaker sites, however.’ The depolarization of the
ventricles is represented as the QRS complex on
the EKG (Figure 5).
The first downward deflection of the QRS
complex is called the Q wave. It is produced primarily by depolarization of the ventricular septum.6 On a 12-lead EKG, the presence or
absence of Q waves in certain leads can be
abnormal. Thus, for example, the absence of Q
waves in V6 may indicate L-transposition of the
great arteries (congenitally corrected transposition), single ventricle, mirror image dextrocardia, or left bundle branch block. The presence of
Q waves in V, may indicate severe right ventricular hypertrophy, L-transposition of the great
arteries, or single ventricle; it may occasionally
be normal in newborns.6 The first upward
deflection of the QRS complex is cahed the R
wave. Following any upward deflection of the
QRS complex, the next downward deflection is
called the S wave.’
Ventricular repolarization is represented on
the basic EKG complex as the ST segment and
.
N EONATAL N ETWORK
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11
I
FIGURE 7
n
Quick method for determining heart rate (1).
Use the first R wave that falls on a heavy black line as a starting point. The line that the
next R wave falls on determines the rate.
FIGURE 9 H Quick method for determining heart rate (3).
Count the number of RR cycles in six large squares (I .2
seconds) and multiply by 50. In this example, there are
3 R-R cycles. Therefore, the heart rate is 3 x 50 = 150
bpm (enlarged in size).
. Six large squares = 1.2 seconds
I
. _ __..
:
1
_
2
From: Dubin D. 1996. Ropid lnterpretotion of EKG, 8th ed. Tampa, Florida: Cover, 77.
Reprinted by permission.
the T wave. The ST segment, which occurs after
the QRS and just before the T wave (Figure 5),
is usually referred to as the plateau phase of ventricular repolarizatiom8 The normal ST segment
is flat and level with the basic EKG complex.
Elevation or depression of this segment can be
pathologically significant (see “Examining the
ST Segment” later in this article). The T wave
represents that period of time when the repolarization of the ventricles is occurring rapidly and
efficiently.s Occasionall!; a U wave may be present on a normal basic EKG complex tracing.
The U Leave should folio\\; and be in the same
direction as, the T uvave. Its mechanism is not
k n o w n , b u t i t may b e c o m e t a l l e r i n
h!Fokalemia.9
EVALUATING THE HEART RATE
There are several quick and easy methods for
determining the heart rate using the single-lead
rhythm strip or a 12-lead ERG. In the first
method, the first R \vave that falls directly on a
FIGURE 8 m Quick method for determining heart rate (2).
Count the number of RR cycles between hhro vertical marks and multiply by 20. In this
example, there are 6 RR cycles between two vertical marks. Therefore, the heart rate is
6 x 20= 120 bpm.
4
......
5
_
6 I
:
j . .
.:
.._
.:
3
__..
.j
.,
,_.
heavy black line is used as a starting point. The
subsequent hea\? black lines are numbered 300,
150, 100, and 75, respectivellr. The line that the
next R wave falls upon determines-the approximate rate (Figure 7).7
A second method for determining the heart
rate uses the vertical marks in the upper border
of the single-lead EKG rhythm strip paper.
Because the distance between bvo of these marks
equals three seconds, the heart rate can be calculated by counting the number of RR c!~cles
between two vertical marks and multiplying by
20 (Figure S).h
A third method for determining the heart
rate is counting the number of RR c\lcles in six
large squares (1.2 seconds) and multiplying this
figure by 50 (Figure 9).6
The normal range for neonatal heart rate is 80
to 160 beats per minute (bpm), although some
healthy term neonates n-ill ha\-e a heart rate as
low as 70 bpm when in deep sleep. Neonates
cannot tolerate a heart rate consistently higher
than 200 bpm for an extended period of time.
This condition, which is called s?~~p~nnenb-icula;
tacl~cardia, represents a medical emergency and
requires immediate ilitervention.‘”
E\‘ALI’ATING THE CARDIAC CYCLE
Once the heart rate has been determined b!
the single-lead EKG rhythm strip or the l2-lead
EKG, several other areas on the EKG rh!rthm
strip can be used to help evaluate the cardiac
cycle. Definiti\re diagnosis should be made onI>.
from a 12.lead EKG, but the rhythm strip can
used to idcntic potential problems requiring
more definitive e\.aluation. Components of the
.
rhythm strip that should be examined systematically are the basic cardiac rhythm; the presence
or absence of the P wave and basic P wave configuration; the PR, QRS, and QT intervals; the
ST segment; and the T wave configuration. I
address each of these areas separately. QRS
amplitude, QRS axis, T axis, and QRS-T angle
are routinely evaluated on a 12-lead EKG, but
these factors cannot be evaluated on a basic
rhythm strip.
Cardiac monitors used in neonatal nurseries
generally offer a choice of leads I, II, and III.
Lead II is the one that reads from the right arm
to the left foot, assuming that the leads have
been placed correctly. Lead II is closest to the
normal heart’s vector following the pattern of
normal conduction. This is because the SA node
is near the top righthand comer
the heart and
the direction of impulse is from the right shoulder toward the left leg. For this reason, lead II is
generally thought to be the most appropriate
lead for standard monitoring. 1 1
of
Examining the Cardiac Rhythm
Rhythm refers to the regularity of the EKG
pattern. Is the pattern consistent or inconsistent?
The P-to-P intervals and the R-to-R intervals
should be the same over a six-second period. If
the intervals are inconsistent, the pattern is
irregular.’ Sinus rhythm is the normal cardiac
rhythm at any given age.t2 In sinus rhythm,
there is only one P wave, which occurs consistently before each QRS complex. The QRS
complex is consistently followed by a T wave
(Figure 10). The pattern should repeat itself at
regular intervals. This is because the SA node
generates impulses at a generally constant rate
within physiologic limits.7
A discussion of irregular cardiac rhythm patterns is beyond the scope of this article. In general, there are irregular rhythms, escape rhythms,
premature beats, tachyarrhythmias, and heart
blocks7
Examining the P Wave Configuration
The P wave, which represents depolarization
of the atria, should be upright (positive) in lead
II. The P wave should be rounded and consistent in shape and direction within each cardiac
cycle (Figure S). l A P wave that looks like a
steeple can indicate right atrial enlargement; a P
wave that is broad and notched can indicate left
atria1 enlargement.” The maximum duration of
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VOL. 17, NO. 8, D E C E M B E R 1 9 9 8
FIGURE 10 n Example of sinus rhythm.
Note the P wave, which occurs consistently oefore each QRS complex. The QRS is
consistently followed by a T wave. The pattern repeats itself at regular intervals.
the P Wave in infants less than 12 months of age
is 0.08 seconds. A prolonged P wave is an indication of let? atrial hypertrophv.h
Examining the PR Interval
The PR interval represents the time necessary
for atria1 depolarization and the delay of the
impulse at the AV node.6 The PR interval starts
at the beginning of the P wave and extends to
the beginning of the QRS comples (Figure 5).l
The PR interval varies with heart rate and age;
Table 2 gives normal values for neonates. A prolonged PR interval (first-degree AV block) indicates an abnormally long delay in the conduction of the impulse through the AV node. It may
be seen in myocarditis, atriai septal defect, endocardial cushion defect, Ebstein’s anomaly, digitalis toxicity, hyperkalemia, ischemia, or profound hypoxia; it may also be seen in an otherwise normal heart.6 A shortened PR interval
indicates that an abnormal accessory conduction
pathway is being used to excite the ventricles3
This may be seen with Wolff-Parkinson-White
(WPW) syndrome or in a normal heart with a
low right atria1 pacemaker.5 Variable PR intervals
.
TABLE 2 I Normal Values for Neonates for PR
Interval and QRS Duration
Age
Group
Less than 1 day
1 to 2 days
3 to 6 days
1 to 3 weeks
1 to 2 months
PR interval
(seconds)
0.08-O. 16
C-1’)
0.08-0.14
C.77)
0.07-0.14
Cl 0)
0.07-0.14
Cl 0)
0.07-O. 13
Cl 0)
QRS Duration
Vl
0.03-0.07
CO%
0.03-0.07
CO51
0.03-0.07
CO%
0.03-0.08
CO51
0.03-0.08
CO%
Adapted from: Carson A. 1998. Electrocardiography. In
The Science and Practice of Pediatric Cardiol~, 2nd ed.,
Carson A, et al., eds. Baltimore: Williams & Wilkins, 736.
Reprinted by permission.
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IFIGURE 11
n
Wenckebach phenomenon.
_ _ __.__._; ._ .- ._- _-.--;.-.--.. / ._..~.__~.~_ __._ ___._.; . _ __ ._L...,. ._ -___. _ _. _ . . . . _ __.__._ _ . . .._....__.__._...... _ _..-.
./
.
.
b
are seen with the irregular rhythms of wandering
atrial pacemaker and Wenckebach phenomenon
(Figure 11).6
Examining QRS Duration
The QBS duration represents the amount of
time necessary for ventricular depolarization to
take place.6 It is measured from the beginning
to the end of ventricular depolarization and
should be measured in a lead with a Q wave
(Figure 5). QRS duration will increase with
age.5 Table 2 gives normal values for neonates.
The initial EKG of a premature infant will have
a shorter QRS duration than the initial EKG of a
term infant.2 Most ventricular conduction disturbances result in prolonged QRS duration.
These disturbances include right and left bundle
branch blocks, WI%’ syndrome, hyperkalemia,
premature ventricular contractions, dysfunction
of the myocardium related to metabolic or
ischemic problems, ventricular tachycardia, and
implanted ventricular pacemaker.‘”
Examining the QT Interval
The QT interval starts at the onset of the
QRS complex and ends at the termination of the
T wave (Figure 5). It measures the amount of
time required for both ventricular depolarization
(QRS duration) and ventricular repolarization to
take place. When measuring the QT interval, use
the longest interval in any lead.” The QT interval varies with the heart rate, and this must be
corrected for using Bazett’s formula, lvhich nil1
vield a corrected QT (QTc) interval:
QTc interval =
QT
JXCZZ
A QTc interval of greater than 0.44 seconds
is considered abnormal at most ages, but some
newborns may have a normal QTc of 0.47 seconds.5 A prolonged QT interval may be seen in
hypocalcemia, viral myocarditis, head injury, or
cerebrovascular accident.6 QT prolongation ma)
also indicate the therapeutic effect of an antiarrhythmic drug such as procainamide.2 A shortened QT interval may be seen in hypercalcemia
and digitalis effect.12
Examining the ST Segment
The ST segment is the portion of the EKG
between the termination of the S wave (after
ventricular depolarization) and the beginning of
the T wave (before ventricular repolarization)
(F&m-e 5).s The ST segment should be isoelectric, although it may be depressed or elevated on
a 12-lead EKG up to 1 mm in infants in the
limb leads and up to 2 mm in the left precordial
leads. Abnormal shift of the ST segment will
occur in pericarditis, severe ventricular hypertrophv with strain (abnormal ventricular repolarization), digitalis effect, myocardial ischemia and
infarction, hyperkalemia or hypokalemia, and
intracranial injur!.,x+12 T wrave changes are often
associated with ST segment shifts.12
Examining the T Wave
The T wave represents ventricular repolarizanon. It should have a smooth, curved form, but it
.
r
FIGURE 12 R EKG findinqs
FIGURE 13 n S-T segment in hypercalcemia and hypocaicemia.
of hypokalemia and hyperkalemia.
SERUM K
Depressed ST Segment
(2.5 mEq/L
Hypercalcemia
Normal
Hypocalcemia
Normal
From: Park MK, and Cuntheroth WC. 1992. How to Reod Pediatric EC&,
> 6.0 mEq/L
&
>9.0 mEq/L
Absent P Wave
Sinusoidal Wave
From: Park MK, and Cuntheroth WC. 1992. How to Read Pediatric ECGs,
3rd ed. St. Louis: Mosby-Year Book, 108. Reprinted by permission.
may be notched or slightly asymmetric (Figure 5). The amplitude of the T wave varies widely with many physiologic processes. On a 12-lead EKG, in ‘any infant over 48 hours of age, it
should be greater than 2 mm in leads I, II, and V6.s Tall,
peaked T waves may be seen in hyperkalemia, lef‘t ventricular
hypertrophy, cerebrovascular accident, and posterior myocardial
infarction. Flat or low T waves may be seen in normal newborns. They may also be seen in hypokalemia, hypothyroidism,
hyper- or hypoglycemia, pericarditis, myocarditis, myocardial
ischemia, shock, anemia, and digitalis effect.6
EXAMINING THE EKG FOR ELECTROLYTE
EFFECTS IN NEONATES
Various electrolyte imbalances will affect the cardiac
impulse. The most common electrolyte imbalances that cause
EKG changes are hypo- and hyperkalemia and hypo- and
hypercalcemia.
Hypokalemia will produce the least specific EKG changes.
When the serum potassium level falls below 2.5 milliequivalents (mEq)/liter, a prominent U wave may be present. In
addition, there may be prolongation of the QTc interval, flat
or biphasic T waves, and ST segment depression (Figure
12).12 Arrhythmias are not usuallv seen with hypokalemia
unless the infant is receiving digitalis, in which case tachycardia arrhythmias are the most comrnon.5 Hypokalemia may be
seen, for esample, in a neonate with congestive heart failure
on chronic diuretics.
With hyperkalemia, the potassium IeveI is easily predicted
by the EKG (Figure 12).5 With levels greater than 6
mEq/liter, tall, peaked T waves will become apparent. At Ievels greater than 7.5 mEq/liter, the PR interval will become
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3rd ed. St. Louis: Mosby-Year Book, 107. Reprinted by permission.
Tall T Wave
EONATAL
prolonged, the QRS duration will lengthen, and the T waves
will be peaked. At levels greater than 9 mEq/liter, the P
waves will disappear and wide, bizarre QRS complexes will be
present. Eventually, ventricular fibrillation or asystole will
occur.6’12 Hvperkalemia mav be seen in an extremely dehydrated 24-week gestational infant in the first few days of life.
Hypocalcemia will cause prolongation of the ST segment,
and this will lengthen the QT interval (Figure 13).s The T
wave is delayed, but not widened.8 Hypocalcemia may be
seen in an alkalotic intant being hyperventilated for persistent
pulmonary hypertension of the newborn.
Hypercalcemia will shorten the ST segment, and this will
shorten the QT interval (Figure 13). Hypercalcemia mav also
slow the sinus rate or cause SA block or sinus arrest. Digitalisinduced arrhythmias may be potentiated by hypercalcemia.”
Hypercalcemia may be seen in the neonate with rapid infusion
of calcium gluconate.
EXAMINING THE EKG FOR DIGITALIS
EFFECTS AND TOXICITY
Digitalis toxicity in the neonate is more readily detected
by monitoring the EKG than by evaluating serum digoxin
levels, especially in the first three to five days after digitalization. A baseline EKG should be obtained before loading
with digitalis. In addition, a rhythm strip should be assessed
before starting maintenance digitalis and at regular intervals
for three to five days thereafter. A pharmacokinetic steady
state should be achieved within three to five days. In general, digitalis effects will be confined to ventricular repolarizanon, and digitalis toxicity will cause disturbances in the formation and conduction of the impulse.‘z The earliest sign of
digitalis effect is shortening of the QTc. Sagging of the ST
segment, diminished T wave amplitude, and slowing of the
heart rate may then follow. ProIongation of the PR interval
(which could progress to second-degree AV block) is a very
reliable sign of early digitalis toxicity. Profound sinus
bradycardia or SA block and supraventricular arrhythmias
are also signs of digitalis toxicity.13 Although isolated premature ventricular contractions may be seen with digitalis
toxicity in the neonate, ventricular bigeminy or trigeminy is
uncommon.12
N
E T W O R K
15
.
I
FIGURE 14 m Example of artifact.
This EKG demonstrates a wandering baseline caused by movement.
ARTIFACT
A@?act is defined as anv type of activity on the
EKG that is noncardiac in origin. It can be caused
by loose elecnodes, broken wires, hiccups, muscle
tremors, patient movements, or elecuical interference.’ Artifact can appear on the EKG as a
wandering or jagged baseline, as spikes in the cardiac cycle, as a masking of the entire cycle, or as a
flat line if the electrodes have become loose
(Figure 14). Knowing how to identi+ and correct
art&act can be challenging. This is an important
skill for the neonatal bedside nurse.
CONCLUSIONS
The EKG rhythm strip can provide valuable
information about the general status of the neonatal heart and conduction system. NeonataI
nurses who are familiar with the normal cardiac
impulse and the factors affecting it are better
able to use the EKG as a screening tool for identifying possible cardiac dysfunction, electrolyte
imbalance, and drug effects in their patients.
Understanding EKG basics, and the usefulness
and limitations of the EKG, is essential in the
care of neonates. ;z
REFEREKCES
Catalan0 JT. 1993. Guide to ECG Ana&i?ris.
Philadelphia: JB Lippincort, l-47.
Benson DW, and Duf$ CE. 1990. Electrocardiography. In Fetal and hieonatal Cnrdiolog?: Long
W, ed. Philadelphia: WB Saunders, 236-248.
Stromberg D. 1996. Electrocardiography In
Pediatric nnd Neonatal Tests ami Procedures,
Taeusch my, Christiansen RO, and Buescher ES,
eds. Philadelphia: WB Saunders, 207-23 1.
Liebman J, and Rudy Y. 1990. Electrocardiography. In Fetal, ,Xco~iamI. aud Ir!fnut Cardiac
Disease, hioiler JH, and Seal K.-i, eds. Norwalk,
Connecticut: Appleton & Lange, 179-238.
Garson _I. 199s. Electrocardiograph!.. In T h e
Sciemc ami APnice of Pediatric Cardiohgy, 2nd
ed., Garson A, et al., eds. Baltimore: W’illiams &
Wilkins, 735-783.
6. Park MK, and Guntheroth WG. 1992. How to
Read Pediatric ECGs, 3rd ed. St. Louis: MosbyYear Book, l-130.
7. Dubin D. 1996. Rapid Interpretation of EKG’s,
8th ed. Tampa, Florida: Cover, 1-189.
8. Goldberger AL, and Goldberger E. 1994.
Clinicai Electrocardiography, 5th cd. St. Louis:
Mosbp-Year Book, 7-20.
9. Conover MB. 1992. Understanding Electrocaudiograpby, 6th ed. St. Louis: Mosby-Year
Book, 1-51.
10. Vargo L. 1996. Cardiovascular assessment of the
newborn. In Physical Assessment of the Newborn,
2nd ed., Tapper0 EP, and Honeyfield ME, eds.
Petaluma, California: NICU Lw 77-91.
11. Woodrow l? 1998. An introduction to the reading of electrocardiograms. British Journal o f
Nursing 7( 3): 135-142.
12. Park MK. 1997. The Pediatric Cardiology
Handbook, 2nd ed. St. Louis: Mosby-Year Book,
25-58.
13. Park MK. 1996. Pediatric Cardiologgl for
Practitioners, 3rd ed. St. Louis: Mosby-Year
Book, 34-5 1.
About the Author
Lyn Va,;go is a neonatal muse practitioner in the
NICU at St. John’s Mercy Medical Center in St. Louis,
Missouri, and has worked in neonatal nursivg for the
past 20 ?ears. She was co-coordiuator of the neonatal
nurse practitioner program at St. John’s Mercy Medical
Center porn 1989 to 1997. She zs presentIy a regional faculty member of the neonatal nurse pspctitionw program
at the State liniversity of ,Xew York-Stan? Brook. She
obtained her BSN and her MSA’ fT*om St. Louis
Linirersir?; St. Louis. She is presentrjl~ working on her PhD
i?i nursiq at l?nivcrsi~ of Missouri, St. Louis. She is a
Ynevuber of NANN
For further information, please contact:
Lyn Vargo, RNC, MSN, SSP
St. John’s Merq hlcdical Center
Department of Seonatolo,?
621 South New Ballas 2009-B
St. Louis, lM0 63141
LEVGDF@ir.netcom.com
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