ECG PREPARATION, 12 LEAD PLACEMENTS

OVERVIEW

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.

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.

TYPES OF ECG RECORDINGS

 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

Trouble Shooting

When no signal or a poor signal is observed the following should be considered:

1. Have the cables been correctly connected?

2. Is the equipment functioning correctly?
3. Could external electrical equipment interference be a problem?
4. Was skin preparation adequate?
5. Could the electrodes suffer from
a. gel dry out?
b. Poor adhesion?
P-WAVE

 First component of a normal ECG; & always precedes the QRS waves.
 Represents that Atrial Depolarization (stimulation) has occurred & the impulse
originated in the SA node at the atria.
 Time duration- between 0.6 to 0.11 seconds.
 Configuration- usually rounded & upright.
 VARIANCE:
 Peaked P-wave- signify right atrial hypertrophy.
 Broad or Notched P wave- associated with left atrial hypertrophy.
 Inverted P wave- indicate impulse not coming from SA node meaning not
from the pacemaker but from AV or junctional areas.
 Varying P waves- if the shapes & sizes of P wave vary, the impulse may
be originating at various sites, at times caused by irritability in the atrial
tissue or damage near the SA node.
 Missing P wave- if a P wave doesn’t precede each QRS complex, a third-
degree AV block is suspected.

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 an impulse formation or
conduction delay disturbance such as AV Blocks.
 The PR interval varies with the HR shortens with Tachycardia & lengthen
with Bradycardia.
 VARIANCE:
  Short PR interval- indicates that the impulse originated in other areas like
the AV junction but not the SA Node. (Junctional arrythmia)
 Prolonged PR interval- indicates impulse is delayed as it passes through
the AV node but there are blocks such as 1st degree heart block or
cardiac toxicity. (Heart block, ischemia)

QRS COMPLEX

 Represents ventricular depolarization that follows the PR interval.

 Configuration differs in all 12 leads
 Time duration: 0.06 to 0.10 seconds adult.
 Q- having negative deflection; R-positive deflection & S-negative deflection
 VARIANCE:
 If QRS longer than 0.10 sec & P-wave not apparent- signify the impulse
probably originated in the ventricle indicating a Ventricular Arrhythmia.
 If QRS longer than 0.10 second but P wave apparent- signify impulse
most likely is of supra ventricular in origin & is delayed in the ventricle due
to a conduction defect such as BBB. And with BBB - QRS configuration
show an extra notch in RS wave.
 QRS complex does not appear or is missing after each P wave- we
suspect a condition in which the impulse conduction to the ventricle is
being interrupted such as AVB or Ventricular Standstill.

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:
 Shortened QT interval indicative of Hypercalcemia.
 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:
a. ST segment elevation - indicative of myocardial injury
b. ST depression - indicative of Ischemia
c. 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

SINUS RHYTHM

 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

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
 High fever, too strenuous exercise, too much anxiety.
 CLINICAL MANIFESTATION
a. Patient will have a peripheral pulse rate greater than 100 beats/min, but
with a regular rhythm.
b. Usually, Pt. will be asymptomatic.
c. However, if Pt.’s cardiac output falls & compensatory mechanisms fall, Pt.
may experience hypotension, syncope & blurring of vision.
 INTERVENTION
a. Unless Pt. shows signs & symptoms of decrease cardiac output or
hemodynamic instability, treatment usually isn’t required.
b. A symptomatic Pt. may be given drugs such as Propranolol to regulate the
HR. But treatment would focus on finding the cause of Sinus Tachycardia.

SINUS BRADYCARDIA

 Sinus node creates an impulse at a slower than normal rate below 60/min.
 ECG tracing shows the PQRST complexes to be normal in size & configuration,
except for the lowered rate.
 SIGNIFICANCE
 Many athletes develop sinus bradycardia because their heart are well-
conditioned & thus maintain stroke volume with reduced effort.
 ETIOLOGY
a. SB may be seen when Pt. may be in a slower metabolic need
 sleep,
 hypothermia,
 hypothyroidism,
 vagal stimulation activities such as
 vomiting,
 suctioning,
  severe pain,
 extreme emotion.
b. In MI Pt. involving the Inferior wall, has a tendency to increase vagal tone
& may eventually cause SB.
c. Certain drugs such as
 Anti-cholinesterase
 Beta blockers
 Digitalis
 Morphine
 CLINICAL MANIFESTATION
 The Pt. will have a peripheral rate of 60/min and below but have regular
rhythm.
 If Pt. unable to compensate for the decrease in cardiac output - S/S:
 Hypotension
 Syncope
 Blurring of vision
 Palpitation
 INTERVENTION
 If Pt. asymptomatic, treatment isn’t necessary, but if symptomatic,
treatment should be aimed to identify & correct the underlying cause.
 Atropine may be given by IV push to regulate the HR.
 If medical management not effective may have to start Temporary
Pacemaker.

PREMATURE VENTRICULAR CONTRACTION – PVC

 In PVC, ventricles are stimulated by an ectopic focus in their walls. They contract
too early giving an extra heart beat & because the focus of stimulation is outside
the normal pathway, the impulse will travel around the ventricle at a slower rate,
resulting in wide & bizarre QRS complex.
 ETIOLOGY
  Ventricular Dysrhythmia can cause a decrease in cardiac output which in
turn will make the heart work harder to eject the additional blood on the
next sinus beat.
 Exercise, ingestion of caffeine, tobacco & alcohol can trigger PVC’s
 A PVC may be caused by certain drugs
 Cardiac glycosides
 Sympathomimetic drugs
 Epinephrine
 Conditions
 Electrolyte imbalance
 Hypokalemia
 Hypocalcemia
 CLINICAL MANIFESTATION
 PR may be normal 60-100/min but it is the rhythm that may be irregular.
When palpating the peripheral pulse, one may feel a longer than normal
pause immediately after the PVC.
 Palpitation
 Signs of decrease cardiac output –
 Hypotension,
 Syncope
 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
 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
 Quinidine
 Epinephrine
  CLINICAL MANIFESTATION
 Pt’s peripheral pulses is not palpable anymore because rate is too fast-
due to low perfusion.
 S/S of low cardiac output and eventually became unresponsive.
 INTERVENTION
 When you detect VT, immediately check your pt for responsiveness &
LOC.
 Give immediate treatment. If pt. alert - give lidocaine bolus ; if after
medication still not effective may recommend to proceed to Synchronized
cardioversion.
 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 Inbalance
 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.
 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
a. Any condition that causes inadequate blood flow can lead to Asystole.
 b. Non-cardiac causes include
c. Pulmonary embolism
d. Air embolism
e. Hemorrhage
f. Cardiac causes include ineffective cardiac contractility stemming from
g. Heart failure
h. Heart rupture
i. MI
j. Cardiac tamponade
k. Insufficient conduction
l. AVB
m. 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.

Video References:

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.