FAR EASTERN UNIVERSITY

INSTITUTE OF NURSING
1ST SEMESTER – AY 2021 – 2022
NUR 1219 - NCM 118 NURSING CARE OF CLIENTS WITH LIFE THREATENING
CONDITIONS / ACUTE ILL / MULTI ORGANPROBLEMS / HIGH ACUITY
AND EMERGENCY SITUATIONS

MODULE 1:
ELECTROCARDIOGRAPHY (ECG)

OVERVIEW TYPES OF ECG RECORDINGS:

The module provides an overview of the
electrocardiogram (ECG) which is one of the most
useful diagnostic tests in emergency medicine. It is an
easy and inexpensive test that is used routinely in the
assessment of patients with chest pain. The ECG is the
cornerstone for making the diagnosis of cardiac
ischemia and is used for making decisions about
eligibility for thrombolytic therapy. The 12-lead ECG is
an important diagnostic tool that pro- vides information
about myocardial ischemia, injury, cell necrosis,
electrolyte disturbances, increased cardiac muscle mass
(hypertrophy), conduction abnormalities, and abnormal
heart rhythms.
To avoid misinterpreting the ECG, the clinician
and nurse must have a systematic approach. This
module is designed to guide the learner through a
stepwise approach to ECG interpretation.
TOPIC OUTLINE
ELECTROCARDIOGRAM
A. Obtaining an Electrocardiogram
B. Interpreting the Electrocardiogram
1. Waves, Complexes and Intervals
2. Determining Heart Rate from the
Electrocardiogram
3. Determining heart Rhythm from the
Electrocardiogram
C. Analyzing the Electrocardiogram Rhythm
Strip
1. Normal Sinus Rhythm
2. Dysrhythmias
ELECTROCARDIOGRAM
• An ECG is a series of waves and deflections
recording the heart’s electrical activity from a
certain “view.”
• Many views, each called a lead, monitor
voltage changes between electrodes placed in
different positions on the body.
• 12 Leads (Standard) ECG.
• Electrodes are placed on the patient’s limb to
create Limb Leads & at specific points on his
chest to create the Precordial Leads.
• 6 LIMB LEADS - reflects electrical activity in
the heart’s frontal plane & this consist of :
Leads I,II,III, AVR( Augmented Vector Right),
AVL (Augmented Vector Left) & AVF
(Augmented Vector Foot).
• 6 Precordial Leads - provide information on
the heart’s horizontal plane & consist of:
V1,V2,V3,V4,V5,V6
• Single Lead ECG commonly referred to as the
Rhythm Strip, commonly monitored lead in
Rhythm Strip Leads I,II,III.
• Electrodes are applied in patient’s chest to pick
up heart’s electrical activity
• This strip attached to monitor display
measurements such as heart rate & provides
print outs of cardiac rhythm
SKIN PREPARATION:
• Shave hair away from electrode placement site.
• Rub site briskly with alcohol pad.
• Rub site with 2x2 gauze.
• Place electrode. Be sure that the electrode has
adequate gel and is not dry
CHEST LEAD PLACEMENT
• V1-4th Intercostal space to right of sternum
• V2-4th Intercostal space to left of sternum
• V3-Directly between V2 and V4
• V4-5th Intercostal space at left midclavicular
line
• V5-Level with V4 at left anterior axillary line
• V6-Level with V5 at left midaxillary line

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 P – R INTERVAL
• Represents the activity from the beginning of
atrial depolarization to the beginning of
ventricular depolarization; or it is the time it
takes an impulse to travel from the SA node
through the atria & to AV node down to the
bundle branches.
• Time duration – about 0.12 to 0.20 seconds ( 3-
5 small squares)

SIGNIFICANCE:
• The PR interval can provide some evidence of
TROUBLE SHOOTING
an impulse formation or conduction delay
When no signal or a poor signal is observed the
disturbance such as AV Blocks.
following should be considered:
• The PR interval varies with the HR shortens
1. Have the cables been correctly connected?
with Tachycardia & lengthen with Bradycardia.
2. Is the equipment functioning correctly?
VARIANCE:
3. Could external electrical equipment
• Short PR interval- indicates that the impulse
interference be a problem? Was skin
originated in other areas like the AV junction
preparation adequate?
but not the SA Node.
a. Could the electrodes suffer from gel
dry out? • Prolonged PR interval- indicates impulse is
b. Poor adhesion? delayed as it passes through the AV node but
there are blocks such as 1st degree heart block.
WAVES, COMPLEX, AND INTERVALS Or cardiac toxicity.
P - WAVE
QRS COMPLEX
• First component of a normal ECG ; & always
precedes the QRS waves. • Represents ventricular depolarization that
follows the PR interval.
• Represents that Atrial Depolarization
(stimulation) has occurred & the impulse • Configuration differs in all 12 leads
originated in the SA node at the atria. • Time duration: 0.06 to 0.10 seconds adult.
• Time duration- between 0.6 to 0.11 seconds. • Q - having negative deflection; R-positive
• Configuration- usually rounded & upright. deflection & S-negative deflection

Variance of P Wave: VARIANCE:

• Peaked P-wave- signify right atrial • If QRS longer than 0.10 sec & P-wave not
hypertrophy apparent- signify the impulse probably
originated in the ventricle indicating a
• Broad or Notched P wave- associated with left
Ventricular Arrhythmia
atrial hypertrophy.
• If QRS longer than 0.10 second but P wave
• Inverted P wave- indicate impulse not coming
apparent- signify impulse most likely is of
from SA node meaning not from the pacemaker
supra ventricular in origin & is delayed in the
but from AV or junctional areas.
ventricle due to a conduction defect such as
• Varying P waves- if the shapes & sizes of P
BBB. And with BBB - QRS configuration show
wave vary, the impulse may be originating at
an extra notch in RS wave.
various sites, at times caused by irritability in
• QRS complex does not appear or is missing
the atrial tissue or damage near the SA node.
after each P wave- we suspect a condition in
• Missing P wave- if a P wave doesn’t precede
which the impulse conduction to the ventricle is
each QRS complex, a third degree AV block is
being interrupted such as AVB or Ventricular
suspected.
Standstill.

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 T - WAVE
• Represent ventricular repolarization; where the
heart cells can regain (-) charge; here the cells
are readying to be depolarized again; cells here
are vulnerable to another strong stimuli
• Configuration- round & symmetrical.
VARIANCE:
• Inverted T-wave to some lead is normal;
however, but for L1,L2,L3 & V6– indicative of
myocardial ischemia.
• Peaked T wave- indicative of Hyperkalemia (
Tented P wave)
• Notched T wave- indicative of Pericarditis in
adult but is normal for children.
• Varied T wave- indicative of electrolyte
imbalance (may be large & small ).
Q – T INTERVAL
• Represent ventricular depolarization &
repolarization ; this extends from the beginning
of the QRS complex to the end of the T wave.
• Time duration- between 0.36 to 0.44 seconds
• RULE OF THUMB: QT interval should not be
greater than ½ the distance between
consecutive R wave ( called the R-R interval)
within a regular rhythm.
VARIANCE:
1. Shortened QT interval indicative of
Hypercalcemia
2. Prolonged QT interval indicative of:
a. Congenital anomaly
b. Due to some medication (anti-
arrhythmias)
c. Normal for some trained adult athletes
d. Lead to other life-threatening
condition
S – T SEGMENT
• Represent the end of ventricular depolarization
& beginning of ventricular repolarization.
SIGNIFICANCE:
Any changes in ST segment such as an
elevation may indicate Myocardial infarction.
VARIANCE:
1. ST segment elevation - indicative
myocardial injury
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2. ST depression- indicative of Ischemia
3. ST changes- indicative of inflammatory heart
conditions, LVH, PE, Electrolyte imbalance.
HEART RATE COMPUTATION USING ECG
• Formula 1: HR = 300 / no. of big square
between R-R
• Formula 2: HR = 1,500 / no. of small squares
between R-R
NORMAL SINUS RHYTHM
SINUS RHYTHM
Sinus Rhythm - is a term which is applied when ALL
the following criteria are met. This rhythm is consistent
with an intact conduction pathway from the SINUS
NODE to the VENTRICULAR CONDUCTION
SYSTEM.
• P wave - present, configuration normal, before
the QRS
• Rhythm – regular / ( irregular)
• Rate - 60 – 100 / minute
• PR INTERVAL - 0.12-0.20 seconds
• QRS width - 0.06-0.10 seconds
• QT INTERVAL - 0.35-0.44
• ST Segment - Normal
TYPES OF DYSRYTHMIAS
SINUS TACHYCARDIA
• Occurs when sinus node creates an impulse at a
faster than normal rate around 100-160
beats/min
• Rate ↑ 160/min - indicate Ectopic Focus)
• QRS shape/configuration normal
• ST is almost same as NSR except for the rate
ETIOLOGY:
• ST occurs sometimes in a healthy person
without seriousness ; but when ST persist or is
prolonged – needs medical attention.
• ST persist too long
• Acute blood loss
• Anemia
• Shock
• Hypovolemia
• Congestive heart failure
• Extreme pain
• Hypermetabolic states
of • High fever, too strenuous exercise, too much
anxiety.
CLINICAL MANIFESTATION CLINICAL MANIFESTATION
1. Patient will have a peripheral pulse rate greater • The Pt. will have a peripheral rate of 60/min and
than 100 beats/min, but with a regular rhythm. below but have regular rhythm.
2. Usually, Pt. will be asymptomatic. • If Pt. unable to compensate for the decrease in
3. However, if Pt.’s cardiac output falls & cardiac output - S/S:
compensatory mechanisms fall, Pt. may o Hypotension
experience hypotension, syncope & blurring of o Syncope
vision. o Blurring of vision
o Palpitation
INTERVENTION
1. Unless Pt. shows signs & symptoms of decrease INTERVENTION
cardiac output or hemodynamic instability, • If Pt. asymptomatic, treatment isn’t necessary,
treatment usually isn’t required. but if symptomatic, treatment should be aimed
2. A symptomatic Pt. may be given drugs such as to identify & correct the underlying cause.
Propranolol to regulate the HR. But treatment • Atropine may be given by IV push to regulate
would focus on finding the cause of Sinus the HR.
Tachycardia. • If medical management not effective may have
to start Temporary Pacemaker.
SINUS BRADYCARDIA
o Sinus node creates an impulse at a slower than PREMATURE VENTRICULAR CONTRACTION
normal rate below 60/min. (PVC)
o ECG tracing shows the PQRST complexes to • In PVC, ventricles are stimulated by an ectopic
be normal in size & configuration, except for focus in their walls. They contract too early
the lowered rate. giving an extra heart beat & because the focus
of stimulation is outside the normal pathway,
SIGNIFICANCE the impulse will travel around the ventricle at a
o Many athletes develops sinus bradycardia slower rate, resulting in wide & bizarre QRS
because their heart are well- conditioned & thus complex.
maintain stroke volume with reduced effort.
ETIOLOGY
ETIOLOGY • Ventricular Dysrhythmia can cause a decrease
1. SB may be seen when Pt. may be in a slower
in cardiac output which in turn will make the
metabolic needs
heart work harder to eject the additional blood
o sleep
on the next sinus beat.
o hypothermia
• Exercise, ingestion of caffeine, tobacco &
o hypothyroidism
alcohol can trigger PVC’s
o vagal stimulation activities such as
• A PVC may be caused by certain drugs
o vomiting
o Cardiac glycosides
o suctioning
o Sympathomimetic drugs
o severe pain
o Epinephrine
o extreme emotion
• Conditions
2. In MI Pt. involving the Inferior wall, has a
o Electrolyte imbalance
tendency to increase vagal tone & may
o Hypokalemia
eventually cause SB.
o Hypocalcemia
3. Certain drugs such as
o Anti-cholinesterase
CLINICAL MANIFESTATION
o Beta blockers
• PR may be normal 60-100/min but it is the
o Digitalis
rhythm that may be irregular.. When palpating
o Morphine
the peripheral pulse, one may feel a longer than
normal pause immediately after the PVC.
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 • Palpitation
• Signs of decrease cardiac output -
o Hypotension,
o Syncope
o Blurring of vision.
INTERVENTION
• Treatment will depend on the cause of the
problem.
• If PVC results from a cardiac problem- DOC is
Lidocaine ( Xylocaine) 50-100mg given by IV
Bolus followed by a constant infusion of 1-
4mg/min IV drip.
• If PVC is caused by SB where myocardial
irritation triggers its manifestation – DOC is
Atropine to increase the HR - treating the SB
you eliminate the PVC.
VENTRICULAR TACHYCARDIA
• When 3 or more PVC’s occurs in a row & the
rate exceeds 100/min this is called VT
• It may be Paroxysmal ( lasting for a few beats)
or sustained (longer time).
PATHOLOGY
• There is no association between the atrial
rhythm & ventricular rhythm ; hence, VT
develops & ends suddenly.
• It is a major Arrhythmia, which can reduce
cardiac output & lower BP.
• Here the Pt. may not be able to withstand the
increase Myocardial irritability &
consequently, V Fib will develop.
• The rapid ventricular rate of PVC’s will lower
down the effective ventricular filling time®
Atrial & vent. Activity are dissociated®
decrease cardiac output abruptly® increase
risk for CV collapse lead to V. Fibrillation
(Fatal)
ECG INTERPRETATION
• ECG show series of wide, slightly irregular
QRS complexes.
• Rate: Atrial ( P wave) cannot be determined or
looks absent; but is actually obscured by QRS.
• Ventricular ( QRS complex) rapid 100-200/min
& are very wide.
• PR Interval & Q - not measurable
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ETIOLOGY
• VT usually results from Myocardial irritability.
• Some cardiac condition can bring about VT
such as : AMI, CAD, RHD, Mitral Valve
prolapse, Heart Failure & Cardiomyopathy.
• Non-cardiac conditions
• Pulmonary Embolism
• Electrolyte imbalance
• Drug toxicity – Digitalis
o Quinidine
o Epinephrine
CLINICAL MANIFESTATION
o Pt’s peripheral pulses is not palpable anymore
because rate is too fast- due to low perfusion.
o S/S of low cardiac output and eventually
became unresponsive.
INTERVENTION
o When you detect VT, immediately check your
pt for responsiveness & LOC.
o Give immediate treatment. If pt. alert - give
lidocaine bolus ; if after medication still not
effective may recommend to proceed to
Synchronized cardioversion.
o If patient suffers CV collapse - loss of
consciousness, prepare instead to defibrillate. If
you are at patient’s bedside immediately deliver
a single precordial thump, while CPR team are
preparing the paddles & awaiting for electrical
charge.
VENTRICULAR FIBRILLATION
• Rapid disorganized & quivering of the
ventricles developed because of rapid impulse
formation & irregular impulse transmission.
The focus of impulse is in the Ventricles but all
fire together so there is no organized
conduction & no organized contraction.
• The Ventricles displays those quivering motion
& are unable to fill or expel blood with any
rhythmic pattern
SIGNIFICANCE
• With Ventricular Fibrillation, the ventricles
quiver rather than contract. As a result, they fail
to pump blood & cardiac output falls to zero.
• If fibrillation continues, it eventually leads to
ventricular asystole or standstill.
CLINICAL MANIFESTATIONS
• There are no audible heart sounds, no palpable
pulses, no response – THIS IS A MAJOR
ARRYTHMIA may be fatal.
• This is a MEDICAL EMERGENCY-
immediate intervention is necessary or death
could occur within minutes.
TYPES OF VENTRICULAR FIBRILLATION
• Coarse Fibrillation - indicates more electrical
activity in the ventricles than the fine
fibrillation.
• Fine Fibrillation - fibrillatory waves become
finer as acidosis & hypoxemia develop.
ECG INTERPRETATION
• Atrial rate & rhythm cannot be determined.
• Ventricular rate & rhythm cannot be
determined.
• P wave is indiscernible ; PR interval is also
indiscernible.
• QRS complex duration is indiscernible.
• T- wave is indiscernible.
ETIOLOGY
• AMI
• Cardiomyopathy
• Drug induced – digitalis, quinidine toxicity
• Irritation from pacemaker electrode
• Acidosis and Electrolyte Imbalance
• During Cardiac Cath/ cardiac surgery
• Immediately following electrocution
CLINICAL MANIFESTATION
• The pt. will be in cardiopulmonary arrest, so pt
will be unresponsive & have no palpable pulse.
• To verify the absence of a pulse, try to palpate
the carotid or femoral pulse.
• If pt. is responsive & pulse is palpable, check to
see if pt is shivering. Because in some cases,
excessive muscle movement can create an ECG
pattern like that of ventricular fibrillation.
• Sometimes also, electrical interference such as
one coming from the most common electric
razor – so Nurses always evaluate the pt. first
when you see this ECG pattern.
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INTERVENTION
• The only effective treatment for ventricular
fibrillation is Defibrillation.
• To increase its effectiveness at the same time
give epinephrine & anti-arrhythmic drugs such
as lidocaine or procainamide give IV push
because time is critical.
• CPR & other life-support measures should be
started while you are waiting for the
defibrillator
VENTRICULAR ASYSTOLE- CARDIAC
STANDSTILL
• With VS, electrical activity in the ventricles
stops. What will be seen on an ECG Strip is
almost flat line.
• Some activity may be evident in the atria, but
the atrial impulse isn’t conducted to the
ventricles.
• P waves may continue for a time, but the QRS
complexes have disappeared.
SIGNIFICANCE
• Asystole is life threatening. Without ventricular
activity, ventricular contraction does not occur.
Consequently, there is no cardiac output or
perfusion.
ECG INTERPRETATION
• Atrial rate & rhythm is indiscernible
• Ventricular rate & rhythm doesn't even exist.
• P wave is absent.
• PR interval not measurable; QRS complex is
absent; T wave absent.
• Because of these findings, one would interpret
the ECG as showing Asystole.
ETIOLOGY
1. Any condition that causes inadequate blood
flow can lead to Asystole.
2. Non-cardiac causes include
• Pulmonary embolism
• Air embolism
• Hemorrhage
3. Cardiac causes include ineffective cardiac
contractility stemming from
• Heart failure
• Heart rupture
• MI
• Cardiac tamponade
 • Insufficient conduction
• AVB
• Cocaine overdose

CLINICAL MANIFESTATION
• The pt. will be in CP arrest; so pt will be
unresponsive & will not be able to palpate a
pulse.
• Nurse, please verify the absence the absence of
a pulse, try to palpate the carotid or femoral
pulse.
• Same ECG pattern may appear if the pt’s
electrodes fall off or the monitor probably is not
turned ON.
• Nurses evaluate the patient before you try to
perform any emergency measures.

INTERVENTION
• A pt. with Asystole needs immediate treatment
including CPT & other life-support measures.
• If pt. has a temporary demand pacemaker, turn
it on & check the electrodes as well.

LEARNING RESOURCES:
https://www.youtube.com/watch?v=Rt4kjD4z8vM
https://www.youtube.com/watch?v=EMmjwgwHkO0

REFERENCES:
Smeltzer, S. C., Bare, B. G., Hinkle, J. L., & Cheever,
K. H. (2010). Brunner and Suddarth’s textbook of
medical-surgical nursing (12th ed.). Philadelphia:
Lippincott Williams & Wilkins.
Sole, M. L., Klein, D. G., & Moseley, M. J.
(2013). Introduction to critical care nursing. St.
Louis, Mo: Elsevier/Saunders.

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