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Ecg Preparation
Ecg Preparation
OVERVIEW
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.
Skin preparation
Trouble Shooting
• 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
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
S-T SEGMENT
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.
• 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
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.