MEDICAL SURGICAL NURSING 3

ELECTROCARDIOGRAM
ECG READING AND INTERPRETATION
• The electrical activities of the heart can be precisely measured and monitored via electrocardiography (ECG)
• Any disturbances of the heart electricity result in various types of arrhythmias which can lead to serious
consequences including death.

Major components of the electrical activities of the heart:

• SA Node
o Atrium
• AV Node
• Bundle of HIS
o Right Bundle Branch
o Left Bundle Branch
• Ventricles

ECG
• is a recording of the electrical activity of the heart via external electrodes (a conductive pads attached to the
patient's chest and limbs) and transcribed onto graph paper.
• ECG paper is marked with a grid of small and large squares.
o Each small square represents 40 milliseconds (ms) in
time along the horizontal axis.
o Each larger square contains 5 small squares, thus
representing 200 milliseconds.
o Standard paper speeds and square markings allow easy
measurement of cardiac timing intervals. This enables
calculation of heart rates and identification of abnormal
electrical conduction within the heart.

ECG PAPER
• ECG machine runes at a standard rate of 25 mm/s and use paper with standard-sized squares
• Horizontally, one large box = 0.2 sec and one small box = 0.04 sec.
• Vertically, one large box = 0.5 mV
• scale of voltage, measured on the vertical axis; time on the horizontal axis

ECG LEADS
• ECG leads are the graphical representation of the depolarization of the heart.
• Precordial leads (V1 – V6) captures the electrical activity of the
heart in a horizontal plane.
• I, II, III, aVL, aVF, aVR – captures the electrical activity of the heart
in a vertical plane.

Electrode Placement
• Limb Electrodes
o Left arm
o Right arm
o Left leg
o Right leg (neutral electrode)
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ELECTROCARDIOGRAM
6 Chest (Precordial) Electrode
• V1 – 4th ICS, Right parasternal region
• V2 – 4th ICS, Left parasternal region
• V3 – midway between V2 and V3
• V4 – 5th ICS, left midclavicular line
• V5 – 5th ICS, left anterior axillary line
• V6 – 5th ICS, left mid axillary line

Anatomical Relationship of Leads

Limbs leads Precordial leads Corresponding heart structure
Inferior leads II, III, aVF Inferior surface of the heart
Lateral leads I, aVL V5, V6 Left ventricle, lateral wall
Anteroseptal leads V1-V4 Anterior wall of both ventricles
Posterior wall of the left ventricles

ECG COMPONENTS
1. Wave - a deflection of the ECG line resulting from change of the electrical activity of the heart.
• Positive deflection (upward) – the electrical impulse is
moving toward the electrodes.
• Negative deflection (downward) – the electrical
impulse is moving away from the electrode.
• Equiphasic (equally upward and downward) – the
electrical impulse is moving perpendicular to the
electrode.
• Other waves – forms complexes e.g. QRS complex

P wave
• The P wave represents atrial depolarization.
• It occurs when the sinus node, also known as the sinoatrial node, creates an action potential that depolarizes the
atria.
• It appears upright in lead II if the action potential is originating from the SA node
• Each P wave should be followed by a QRS complex.

QRS complex
• The Q wave, R wave and S wave, the “QRS complex” represents ventricular depolarization.
• The normal duration (interval) of the QRS complex is between 0.08 and 0.10 seconds — that is, 80 and 100
milliseconds.
• When the duration is between 0.10 and 0.12 seconds, it is intermediate or slightly prolonged.
• A QRS duration of greater than 0.12 seconds is considered abnormal.
• QRS duration lengthens when electrical activity takes a long time to travel throughout the ventricular myocardium.
• The normal conduction system in the ventricles is called the HIS - Purkinje system and consists of cells that can
conduct electricity quite rapidly.
o Thus, normal conduction of an electrical impulse through the atrioventricular, or AV, node, then to the
ventricles via the HIS - Purkinje system, is fast and results in a normal QRS duration.
o When electrical activity does not conduct through the His-Purkinje system, but instead travels from
myocyte to myocyte, a longer time is necessary, and the QRS duration is widened.

T wave
• T waves occurs after the QRS complex and is a result of ventricular repolarization.
• T waves should be upright in most leads; the exceptions are aVR and V1.
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• T waves should be asymmetric in nature. The second portion of the T wave should have a steeper decline when
compared with the incline of the first portion.
o If the T wave appears symmetric, cardiac pathology such as ischemia may be present.

T-P segment
• The TP segment is the portion of the ECG from the
end of the T wave to the beginning of the P wave.
• This segment should always be at baseline and is
used as a reference to determine whether the ST
segment is elevated or depressed, as there are no
specific disease conditions that elevate or depress
the TP segment.
• During states of tachycardia, the TP segment is
shortened and may be difficult to visualize
altogether. It is good to examine the TP segment
closely for the presence of U waves or atrial activity
that could indicate pathology.

QT Interval
• The QT interval is the time from the beginning of the QRS complex, representing ventricular depolarization,
to the end of the T wave, resulting from ventricular repolarization.
• To distinguish a prolonged QT interval is to examine if the T wave ends beyond the halfway point between
the RR interval.
o If the T wave ends past the halfway point of the RR interval, it is prolonged.

S wave
• The S wave is the first downward deflection of the QRS complex that occurs after the R wave. However, a S wave
may not be present in all ECG leads in a given patient.
• In the normal ECG, there is a large S wave in V1 that progressively becomes smaller, to the point that almost no
S wave is present in V6. A large slurred S wave is seen in leads I and V6 in the setting of a right bundle
branch block.

S-T Segment
• represents the interval between depolarization & repolarization
• A horizontal isoelectric line, but may slope upward slightly before the T wave.
• Extends from the J point to the start of the T wave.

S-T Etiology:
• Normal findings: small concave elevation in young healthy adults due to early depolarization.
• STEMI – significant S-T elevation in MI.
• LBBB – left bundle branch block
• Pericarditis: widespread S-T elevations
• Pulmonary embolism
• Brugada Pattern
• Left ventricular aneurysm
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S-T depression etiology:
1. Down sloping S-T depression or horizontal ST depression
• Subendocardial myocardial ischemia
• Stress-induced myocardial Ischemia
• Reciprocal change from myocardial Infarction

2. Upsloping of S-T depression

• Normal during tachycardia
• May indicate myocardial ischemia if the clinical feature suggests acute coronary syndrome

3. Sagging of S-T segment depression

• Digoxin

4. Secondary repolarization abnormalities

• Ventricular hypertrophy
• LBBB

5. Non-specific S-T segment depression

• Hypokalemia

J wave
• A positive deflection occurring between the QRS
complex and the ST segment
• The point where it marks the end of depolarization and
start of repolarization.
• J waves appears on the following conditions:
o Brugada syndrome
o Idiopathic ventricular fibrillation
o Hypercalcemia
o Hypothermia

U wave
• Small deflection after the T wave
• Polarity is the same as the T wave
• Best seen in leads V2 to V4, but not always visible
• Normal finding in athletes
• Etiology of its occurrence is unknown , thought to be due to delayed
• repolarization of the myocardial cells, and the His-Purkinje system
• Most prominent in patients with:
o Hypokalemia
o Hypercalcemia
o Bradycardia

COUNTING THE HEART RATE

Heart rate
Regular heart rhythm: R-R Interval
• The standard paper speed is 25 mm (5 large squares)/sec. This means that if the interval between two beats
(R-R) is 5 large squares, the HR is 60 beat/min.
• The HR may be counted by simply dividing 300 by the number of the large squares between two heart beats
(R-R).
• If the interval between two beats is one large square, the HR is 300 beat/min, 2 squares →150, 3 squares →100,
4 squares → 75, 5 squares → 60, 6 squares → 50 beat/min.
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ELECTROCARDIOGRAM

Irregular heart rhythm: QRS complex

• If a patient’s heart rhythm is irregular the first method of heart rate calculation doesn’t work (as the R-R interval
differs significantly throughout the ECG).
• As a result, apply a different method:
o Count the number of complexes on the rhythm strip.
o Irregular QRS rhythm: HR = 6 x total number of QRS complexes
o Multiply the number of complexes by 6 (giving you the average number of complexes in 1 minute).

DETERMINING THE HEART RHYTHM

• The cardiac muscle cells (myocytes) have an inherent automaticity and can generate an electric impulse.
• The SA nodal cells have the fastest automaticity (pacemaker) and hence control the heart rate and rhythm.
• 4 levels of conductions and potential pacemakers in the heart from fastest to slowest: SA node → atria →
AV node → ventricles.
• If the rhythm is not sinus, we have to determine the origin of the pacemaker and where the impulse is
initiated.

Potential pacemakers from fastest to slowest

1. SA nodal rhythm
2. Atrial rhythm
3. AV nodal or junctional rhythm
4. Ventricular rhythm

SA nodal rhythm (Normal Sinus Rhythm)

1. The sinus node is located at the
Superior Vena Cava or Right Atrial
Junction.
• Sinus rhythm requires ALL of the
following 3 criteria:
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o One P wave preceding each QRS complex
o All P waves should be uniform in shape
o Normal P wave axis is in the left lower quadrant (0-
90 degrees), i.e. upright in both lead I and aVF
(unless there is dextrocardia)

2. The R-R interval in NSR does not have to be identical as it

may change with breathing (sinus arrhythmia)The sinus
arrhythmia is easier to appreciate with slower heart rates.
• HR increases during inspiration due to:
o Increased venous return
o Increased sympathetic tone
• HR decreases during expiration due to:
o Decreased venous return
o Increased parasympathetic tone

Atrial rhythm
1. Characterized by narrow QRS complexes preceded by P waves that do not fulfill one or more of the
normal sinus rhythm (NSR) criteria mentioned earlier.
2. If the P wave morphology changes, this may indicate a multifocal origin which is called "wandering
pacemaker".

AV nodal or junction rhythm

1. Characterized by narrow QRS complexes that are not preceded by P waves.
2. An inverted P wave may be seen following the QRS due to retrograde conduction.

Ventricular rhythm
1. Characterized by wide QRS complexes that are not preceded by P waves.
• If the sinus node fails to initiate the impulse, an atrial
focus will take over as the pacemaker, which is usually
slower than the NSR.
• When the atrial focus fails, the AV node will take over.
• If the AV node fails, the ventricular focus, which is the
slowest, will take over as a pacemaker.
• Each time the focus is downgraded, the heart rate
becomes slower based on the inherent automaticity of
the pacemaker.
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ELECTROCARDIOGRAM
HEART BLOCKS
First-Degree Heart Block
• Sinus rhythm with 1st degree heart block is a sinus
rhythm with a prolonged PR interval > 0.20
seconds due to a delay in transmission from the
atria to the ventricles.

Second-Degree AV Heart Block

• A 2nd degree AV block is usually classified as Mobitz Type I (Wenckebach) or Mobitz Type II.
• A Mobitz Type I heart block is characterized by progressive lengthening of the PR interval until a QRS
complex is dropped.
• A Mobitz Type II heart block is characterized by an intermittent dropped QRS that is not in a Mobitz Type I
pattern. The Mobitz Type II block must be evaluated since it is one that can rapidly progress to a complete
heart block.

Third-Degree Heart Block

• A 3rd degree heart block (sometimes called a complete
heart block) is a rhythm in which there is no
relationship between the P and QRS waves. In this
case, the P to P intervals are regular but have no
relationship to the QRS complexes on the ECG.

CARDIAC AXIS
• The electrical axis of the heart represents the mean direction of ventricular depolarization in a frontal plane.
• The normal cardiac axis in an adult is between -30° and +90° (11:00 0’clock to 5:00 0’clock).
• To determine the cardiac axis, look at leads I,II and III.
• The overall direction of electrical activity is towards leads I, II and III, resulting to a positive deflection in all of
these leads, with lead II showing the most positive deflection as it is the most closely aligned to the overall
direction of electrical spread.
• The most negative deflection is aVR. This is due to aVR looking at the heart in the opposite direction.

METHODS OF DETERMINING CARDIAC AXIS

1. Isoelectric (equiphasic) QRS method
• Determine the lead in which the QRS complex are
isoelectric.
• Assess the 2 leads perpendicular to the Cabrera circle
• The cardiac axis corresponds to the perpendicular lead
• This method is more accurate than the leads 1 and aVF
method.
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ELECTROCARDIOGRAM
2. Lead 1 and aVF method
• Determine the QRS complex polarity in leads 1 and aVF.
o Positive QRS complex: the area above the
isoelectric line and under the curve is larger than
the area under the isoelectric line above the
curve.
o Negative QRS complex: the area under the
isoelectric line and above the curve is larger than
the area above the isoelectric line and under the
curve.

• The cardiac axis can be approximated by evaluating the

combinations of QRS complex polarities in leads 1 and
aVF.
o Positive in both leads 1 and aVF = normal axis
o Positive lead in 1 and negative in aVF = left
axis deviation
o Negative in lead 1 & positive in aVF = right
axis deviation
o Negative in both leads 1 & aVF = extreme right
axis deviation

• Lead II can be used for more accurate determination of

the cardiac axis if the QRS complex is positive in leads 1
and negative in aVF.
o Negative QRS complex in lead II = left axis
deviation
o Positive or isoelectric QRS complex in lead II
= normal axis

CARDIAC RHYTHMS
Normal Sinus Rhythm
• Electrical conduction that begins in the SA
node generates a sinus rhythm. Normal sinus
rhythm occurs when the electrical impulse
starts at a regular rate and rhythm in the SA
node and travels through the normal
conduction pathway.
• Normal sinus rhythm is generally indicative of
good cardiovascular health. However, an
increase of 10 bpm or more in the resting heart rate increases the risk for sudden cardiac death, atrial
fibrillation, heart failure, coronary artery disease, stroke, and cardiovascular disease
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Characteristics:
• Ventricular and atrial rate: 60 to 100 bpm in
the adult
• Ventricular and atrial rhythm: Regular
• QRS shape and duration: Usually normal, but
may be regularly abnormal P wave: Normal and
consistent shape; always in front of the QRS
• PR interval: Consistent interval between 0.12
and 0.20 seconds
• P:QRS ratio: 1:1

SINUS NODES ARRHYTHMIAS

Sinus Bradycardia
• Sinus bradycardia occurs when the SA node
creates an impulse at a slower- than-normal rate.
• All characteristics of sinus bradycardia are the
same as those of normal sinus rhythm, except for
the rate.

Causes
• Lower metabolic needs (e.g., sleep, athletic
training, hypothyroidism)
• Vagal stimulation (e.g., from vomiting, suctioning, severe pain)
• Medications (e.g., calcium channel blockers [e.g., nifedipine, amiodarone], beta-blockers [e.g., metoprolol])
• Idiopathic sinus node dysfunction
• Increased intracranial pressure
• Coronary artery disease, especially myocardial infarction (MI) of the inferior wall.
• Unstable and symptomatic bradycardia is frequently due to hypoxemia.
• Other possible causes include acute altered mental status (e.g., delirium) and acute decompensated heart failure

Characteristics:
• Ventricular and atrial rate: Less than 60 bpm in
the adult
Ventricular and atrial rhythm: Regular
QRS shape and duration: Usually normal, but
may be regularly abnormal P wave: Normal and
consistent shape; always in front of the QRS
PR interval: Consistent interval between 0.12
and 0.20 seconds
P:QRS ratio: 1:1

Management:
• If the decrease in heart rate results from stimulation of the vagus nerve, such as with bearing down during
defecation or vomiting, attempts are made to prevent further vagal stimulation.
• If the bradycardia is caused by a medication such as a beta- blocker, the medication may be withheld.
• If the bradycardia is caused by a medication such as a beta- blocker, the medication may be withheld.
• If the slow heart rate causes significant hemodynamic changes resulting in shortness of breath, acute alteration of
mental status, angina, hypotension, ST-segment changes, or premature ventricular complexes (PVCs), treatment
is directed toward increasing the heart rate.
• Slow heart rate may be due to sinus node dysfunction (previously known as sick sinus syndrome), which has a
number of risk factors including increased body mass index, presence of right and left bundle branch block,
history of a major cardiovascular event, increased age, and hypertension
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ELECTROCARDIOGRAM
Medical Management:
• Treatment may be necessary if the client is symptomatic (signs of decreased cardiac output).
• Management depends on the cause and symptoms. Resolving the causative factors may be the only treatment
needed.
• If the bradycardia produces signs and symptoms of clinical instability (e.g., acute alteration in mental status, chest
discomfort, or hypotension), 0.5 mg of atropine may be given rapidly as an intravenous (IV) bolus and
repeated every 3 to 5 minutes until a maximum dosage of 3 mg is given.
• Rarely, if the bradycardia is unresponsive to atropine, emergency transcutaneous pacing can be instituted, or
medications, such as dopamine, isoproterenol, or epinephrine, are given

Sinus Tachycardia
• Sinus tachycardia occurs when the sinus
node creates an impulse at a faster- than-
normal rate.
• Sinus tachycardia does not start or end
suddenly (i.e., it is nonparoxysmal). As the
heart rate increases, the diastolic filling time
decreases, possibly resulting in reduced
cardiac output and subsequent symptoms of
syncope (fainting) and low blood pressure. If
the rapid rate persists and the heart cannot compensate for the decreased ventricular filling, the patient may
develop acute pulmonary edema.

Causes
• Physiologic or psychological stress
o e.g., acute blood loss, anemia, shock, hypervolemia, hypovolemia, heart failure, pain, hypermetabolic
states, fever, exercise, anxiety
• Medications that stimulate the sympathetic response
o e.g., catecholamines, aminophylline, atropine, stimulants [e.g., caffeine, nicotine], and illicit drugs [e.g.,
amphetamines, cocaine, ecstasy]
• Enhanced automaticity of the SA node and/or excessive sympathetic tone with reduced parasympathetic tone that
is out of proportion to physiologic demands, a condition called inappropriate sinus tachycardia
• Autonomic dysfunction, which results in a type of sinus tachycardia referred to as postural orthostatic tachycardia
syndrome (POTS). POTS is characterized by tachycardia without hypotension, and by presyncopal symptoms
such as palpitations, lightheadedness, weakness, and blurred vision, which occur with sudden posture changes

Characteristics
• Ventricular and atrial rate: Greater than
100 bpm in the adult, but usually less than
120 bpm
• Ventricular and atrial rhythm: Regular
• QRS shape and duration: Usually
normal, but may be regularly abnormal
• P wave: Normal and consistent shape;
always in front of the QRS, but may be
buried in the preceding T wave
• PR interval: Consistent interval between
0.12 and 0.20 seconds
• P:QRS ratio: 1:1

Medical Management
• Vagal maneuvers, such as carotid sinus massage, gagging, bearing down against a closed glottis (as if having a
bowel movement), forceful and sustained coughing, and applying a cold stimulus to the face (such as applying an
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ELECTROCARDIOGRAM
ice- cold wet towel to the face), or administration of adenosine should be considered to interrupt the
tachycardia.
• If the tachycardia is persistent and causing hemodynamic instability (e.g., acute alteration in mental status,
chest discomfort, hypotension), synchronized cardioversion (i.e., electrical current given in synchrony with the
patient’s own QRS complex to stop an arrhythmia) is the treatment of choice, if vagal maneuvers and adenosine
are unsuccessful or not feasible.
• IV beta-blockers (Class II antiarrhythmic) and calcium channel blockers (Class IV antiarrhythmic) may also be
considered in treating hemodynamically stable sinus tachycardia, although synchronized cardioversion may be
used if medications are ineffective or contradicted

Sinus Arrythmia
• Sinus arrhythmia occurs when the sinus node creates an impulse at an irregular rhythm; the rate usually
increases with inspiration and decreases with expiration.

Characteristics
• Ventricular and atrial rate: 60 to 100 bpm in the adult
• Ventricular and atrial rhythm: Irregular
• QRS shape and duration: Usually normal, but may
be regularly abnormal P wave: Normal and consistent
shape; always in front of the QRS
• PR interval: Consistent interval between 0.12 and
0.20 seconds
• P:QRS ratio: 1:1

ATRIAL ARRHYTHMIAS
• Atrial arrhythmias originate from foci within the atria and not the SA node.

Premature Atrial Complex

• A PAC is a single ECG complex that occurs when an electrical impulse starts in the atrium before the next normal
impulse of the sinus node.

Causes
• Caffeine
• Alcohol
• Nicotine
• Stretched atrial myocardium (e.g., as in
hypervolemia)
• Anxiety
• Hypokalemia (low potassium level)
• Hypermetabolic states (e.g., with pregnancy)
• Atrial ischemia, injury, or infarction.
• PACs are often seen with sinus tachycardia.

Characteristics
• Ventricular and atrial rate: Depends on the underlying rhythm (e.g., sinus tachycardia)
• Ventricular and atrial rhythm: Irregular due to early P waves, creating a PP interval that is shorter than the
others. This is sometimes followed by a longer-than-normal PP interval, but one that is less than twice the normal
PP interval. This type of interval is called a non-compensatory pause
• QRS shape and duration: The QRS that follows the early P wave is usually normal, but it may be abnormal
(aberrantly conducted PAC). It may even be absent (blocked PAC)
• P wave: An early and different P wave may be seen or may be hidden in the T wave; other P waves in the strip
are consistent
• PR interval: The early P wave has a shorter-than-normal PR interval, but still between 0.12 and 0.20 seconds
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ELECTROCARDIOGRAM
• P:QRS ratio: Usually 1:1

Medical Management
• If PACs are infrequent; no treatment is necessary.
• If they are frequent (more than six per minute), this may herald a worsening disease state or the onset of more
serious arrhythmias, such as atrial fibrillation.
o Medical management is directed toward treating the underlying cause (e.g., reduction of caffeine intake,
correction of hypokalemia).

Atrial Fibrillation
• Atrial Fibrillation (Afib or AF) is a very
common arrhythmia. This rhythm is
characterized by no waves before the QRS
complex and a very irregular heart rate.
• Uncoordinated electrical activity in the atria
that causes rapid and disorganized “fibbing”
of the muscles in the atrium.

Characteristics:
• Rate: Usually over 100 bpm
• Rhythm: Irregular
• P wave: None. They are irregular (fibrillary waves)
• PR interval: Visible
• QRS complex: Normal
• Note: ATRIA IS QUIVERING!
o The atria quiver, which can lead to the formation of thrombi.

Causes:
• Open heart surgery
• Heart failure
• COPD
• Hypertension
• Ischemic heart disease

Manifestations (ALL DUE TO LOW OXYGEN)

• Most commonly asymptomatic
• Fatigue
• Malaise
• Dizziness
• Shortness of breath
• Tachycardia
• Anxiety
• Palpations

Management:
For stable patients:
• Oxygen
• Drug therapy
o Beta-blockers
o Calcium channel blockers
o Digoxin
o Amiodarone
o Anticoagulant therapy to prevent clot
§ Risk for clots: the atria quiver causes the pooling of blood in the heart which increases the risk for
clots = increased risk for MI, PE, CVA’s, and DVTs
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For unstable patients:
• Oxygen
• Cardioversion
o Synchronized administration of shock (delivery in sync with the QRS wave)
o Cardioversion is NOT defibrillation

Atrial Flutter
• Similar to A-fib, but the heart’s electrical signals
spread through the atria. The heart’s upper
chambers (atria) beat too quickly but at a
regular rhythm.

Characteristics:
• Rate: 75-150 bpm
• Rhythm: usually regular
• P wave: “sawtooth” P wave configuration shaped flutter waves
• PR interval: unable to measure
• QRS complex: usually normal and upright

Causes:
• Coronary Artery Disease
• Hypertension
• Heart failure
• Valvular disease
• Hyperthyroidism
• Chronic lung disease
• Pulmonary embolism
• Cardiomyopathy

Manifestations
• May be asymptomatic
• Fatigue / syncope
• Chest pain
• Shortness of breath
• Low blood pressure

Treatment
Stable patients:
• Drug therapy
o Calcium channel blockers
o Antiarrhythmics
o Anticoagulants
§ Atrial flutter causes pooling of blood in the atria = risk for clots

Unstable patients:
• Synchronized administration of shock (delivery in sync with QRS wave)
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ELECTROCARDIOGRAM
VENTRICULAR ARRHYTHMIAS
Premature Ventricular Contractions (PVCs)
• A PVC is an impulse that starts in a
ventricle and is conducted through the
ventricles before the next normal sinus
impulse.

Characteristics:
• Rate: depends on the underlying rhythm
• Rhythm: regular but interrupted due to early P waves
• P wave: visible but depends on timing of PVC
o May be absent (hidden in the QRS or T wave) or in front of the QRS. If the P wave follows the QRS, the
shape of the P wave may be different.
• PR interval: slower than normal but still 0.12-0.20 seconds
• QRS complex: sharp, bizarre, and abnormal during the PVC

Causes:
• Heart failure
• Myocardial infarction or ischemia
• Drug toxicity
• Caffeine, tobacco, alcohol
• Stress or pain
• Increased workload on the heart
o Exercise
o Fever
o Hypervolemia
o Heart failure
o Tachycardia

Treatment
• Treatment is based on the underlying cause
• May not be harmful if the client has a healthy heart
• Oxygen
• Decrease caffeine intake
• Correct the electrolyte imbalances
• D/C or adjust the drug causing toxicity
• Decrease stress or pain

Manifestations
• May be asymptomatic
• Feels like your heart…
o Skipped a beat
o Heart is pounding
• Chest pain
o Notify the HCP if the patient complains of chest pain, if the PVC’s increase in frequency or if the PVC’s
occur on the T-wave (R-on-T phenomenon)
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ELECTROCARDIOGRAM
Ventricular Tachycardia
• VT occurs because of a repetitive firing
of an irritable ventricular ectopic focus at
a rate of 140 to 250 beats per minute or
more.
• VT may present as a paroxysm of three
self- limiting beats or more, or may be a
sustained rhythm.
• VT can lead to cardiac arrest.
• Irregular, coarse waveforms of different
shapes. The ventricles are quivering and there is no contractions or cardiac output which may be fatal!
• LOOKS LIKE TOMBSTONES

Characteristics:
• Rate: 100-250 bpm
• Rhythm: regular
• P wave: not visible
• PR interval: none
• QRS complex: wide (like tombstone) > 0.12 seconds

Causes:
• Myocardial ischemia / infarction
• Electrolyte imbalances
• Digoxin toxicity
• Stimulants: caffeine and methamphetamines

Manifestations
• Patient is usually awake
• Chest pain
• Lethargy
• Anxiety
• Syncope
• Palpations
• No cardiac output = LOW OXYGEN

Treatment
Stable patient with pulse
• Oxygen
• Antidysrhythmic
o Amiodarone – stabilizes the rhythm
• Synchronized cardioversion

Unstable patient without a pulse (pulseless V-Tach)

• CPR
• Follow ACLS protocol for defibrillation = shock
• Possible intubation
• Drug therapy
o Epinephrine, vasopressin, amiodarone
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ELECTROCARDIOGRAM
Ventricular Fibrillation (V-Fib)
• Rapid, disorganized pattern of electrical activity
in the ventricle in which electrical impulses arise
from many different foci!
• VF is a chaotic rapid rhythm in which the
ventricles quiver and there is no cardiac output.
• VF is fatal if not successfully resolved within 3
to 5 minutes.
• Client is unconscious with no pulse, BP,
respirations, or heart sounds.

Characteristics
• Rate: unknown
• Rhythm: chaotic and irregular
• P wave: not visible
• PR interval: not visible
• QRS complex: not visible

Causes:
• Cardiac injury
• Medication toxicity
• Electrolyte imbalance
• Untreated ventricular tachycardia

Manifestations
• Loss of consciousness
• May not have a pulse or blood pressure
• Respirations have stopped
• Cardiac arrest and death
o NO CARDIAC OUTPUT = NO OXYGEN TO THE BODY
Treatment
• CPR
o The client is defibrillated immediately with
120 to 200 joules (biphasic defibrillator) or
360 joules (monophasic defibrillator);
check the entire length of the client 3 times
to make sure no one is touching the client
or the bed; when clear, proceed with
defibrillation.
o CPR is continued for 2 minutes, and the
cardiac rhythm is reassessed to determine
the need for further countershock.
• Oxygen
• Defibrillation (DEFIB THE VFIB)
• Possible intubation
• Drug therapy
o Vasoconstriction: epinephrine
o Antiarrhythmic: amiodarone, lidocaine
o Possible magnesium
MEDICAL SURGICAL NURSING 3

ELECTROCARDIOGRAM
MANAGEMENT ON CARDIAC RHYTHMS
ATRIAL FLUTTER AND ATRIAL FIBRILLATION
Pharmacologic Heart Rate Control During Atrial Fibrillation
• Control of heart rate using either a beta-blocker or nondihydropyridine CCB (in most cases) for patients with
persistent or permanent AF (Level B).
• Administration of AV nodal blocking agents is recommended to achieve heart rate control in patients who develop
postoperative AF (Level B).
• In the absence of preexcitation, I administration of beta-blockers (esmolol, metoprolol, or propranolol) or
nondihydropyridine CCBs (verapamil, ditiazem) to slow ventricular response to AF in the acute setting, exercising
caution in patients with hypotension or HF (Level B).
• IV administration of digoxin or amiodarone to control heart rate in patients with AF and HF who do not have an
accessory pathway (Level B).
• Oral digoxin is effective to control heart rate at rest and is indicated for patients with HF, LV dysfunction, or for
sedentary individuals (Level C).
• In IV amiodarone is recommended to slow a rapid ventricular response to AF and improve LV function in patients
with acute MI (Level C).
• IV beta-blockers and nondihydropyridine CBs are recommended to slow a rapid ventricular response to AF in
patients with acute MI who do not have clinical LV dysfunction, bronchospasm, or AV block (Level C).

Preventing Thromboembolism
• Antithrombotic therapy is recommended for all patients with AF except those with lone AF or contraindications
(Level A).
• For patients without mechanical heart valves at high risk of stroke (prior stroke, TIA, or systemic embolism;
rheumatic mitral stenosis), chronic oral anticoagulant therapy with a vitamin K antagonist is recommended in a
dose to achieve the target IN of 2.0 to 3.0 unless contraindicated (Level A).
• Anticoagulation with a vitamin K antagonist is recommended for patients with more than one moderate risk factor
(age = 75, hypertension, HF, LVEF<35%, diabetes) (Level A).
• IN should be determined at least weekly during initiation of therapy and monthly when anticoagulation is stable
(Level A).
• Aspirin 325 mg daily is an alternative to vitamin K antagonists in low risk patients or those with contraindications
to anticoagulation (Level A).
• For patients with mechanical heart valves, the target intensity of anticoagulation should be based on the type of
prosthesis, maintaining an IN of at least2.5 (Level B).
• For patients with AF of = 48 hours duration, or when the duration is unknown, anticoagulation (INR: 2.0-3.0) is
recommended for at least 3 weeks priorto and 4 weeks after cardioversion (electrical or pharmacologic) (Level B).
• For patients with AF of 48 hours duration requiring immediate cardioversion, heparin should be administered
concurrently (unless contraindicated) by an initial IV bolus followed by a continuous infusion in a dose adjusted to
prolong the aPTT to 1.5 to 2 times the reference control value. Oral anticoagulation (INR: 2.0-3.0) should be given
for at least 4 weeks after cardioversion. Limited data support SQ administration of LMWH in this category of
patient condition (Level C).
• For patients with AF of <48 hours duration and hemodynamic instability (angina, MI, shock, or pulmonary edema),
cardioversion should be performed immediately without delay for prior anticoagulation (Level C).

Cardioversion of Atrial Fibrillation

• Administration of flecainide, dofetilide, propafenone, or ibutilide is recommended for pharmacologic cardioversion
(Level A).
• Immediate electrical (direct-current) cardioversion is recommended for patients with AF involving preexcitation
when very rapid tachycardia or hemodynamic instability occurs (Level B).When a rapid ventricular response does
not respond promptly to pharmacologic measures in patients with myocardial ischemia, symptomatic hypotension,
angina, or HF, immediate R-wave-synchronized cardioversion is recommended (Level C).
• Electrical cardioversion is recommended in patients without hemodynamic instability when symptoms of AF are
unacceptable to the patient. In case of early relapse of AF after cardioversion, repeated electrical cardioversion
attempts may be made following administration of antiarrhythmic medication (Level C).
• Electrical cardioversion is recommended for patients with acute MI and severe hemodynamic compromise,
intractable ischemia, or inadequate rate control with drugs (Level C).
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ELECTROCARDIOGRAM
• There are no Class I recommendations for pharmacologic conversion of atrial fibrillation.

Maintenance of Sinus Rhythm

• An oral beta-blocker to prevent postoperative AF is recommended for patients undergoing cardiac surgery (unless
contraindicated) (Level A).
• Before initiating antiarrhythmic drug therapy, treatment of precipitating or reversible causes of AF is
recommended (Level C).
• Level of Evidence Definitions:
• Level A: Data derived from multiple randomized clinical trials or meta-analyses.
• Level B: Data derived from a single randomized trial or nonrandomized studies.
• Level C: Only consensus opinion of experts, case studies, or standard of care.

VENTRICULAR ARRHYTHMIAS
Sustained Monomorphic Ventricular Tachycardia
• Wide ORS tachycardia should be presumed to be VT if the diagnosis is unclear. (Level C)
• Electrical cardioversion with sedation is recommended with hemodynamically unstable sustained monomorphic
VT (Level C).
• Contraindicated. Calcium channel blockers (verapamil, diltiazem) should not be used to terminate wide ORS
tachycardia of unknown origin, especially with history of myocardial dysfunction.

Polymorphic Ventricular Tachycardia

• Electrical cardioversion with sedation is recommended for sustained PVT with hemodynamic compromise (Level
B).
• IV beta-blockers are useful if ischemia is suspected or cannot be excluded (Level B).
• Iv amiodarone is useful for recurrent PVT in the absence of OT prolongation (congenital or acquired) (Level C).
• Urgent angiography and revascularization skould be considered with PVT when myocardial ischemia cannot be
excluded (Level C).

Torsades de Pointes
• Withdrawal of any offending drugs and correction of electrolyte abnormalities are recommended for TdP (Level
A).
• Acute and long-term pacing is recommended for TdP due to heart block and symptomatic bradycardia (Level A).

Incessant Ventricular Tachycardia

• Revascularization and beta blockade followed by IV antiarrhythmic drugs such as procainamide or amiodarone
are recommended for recurrent or incessant PVT (Level B).

ACLS WITH PULSELESS ARREST ALGORITHM

• The treatment for ventricular fibrillation is rapid defibrillation.
Every minute that defibrillation is delayed, the chance of
survival is reduced by 10%.

The key steps to treating ventricular fibrillation are:

• Rapid assessment to confirm cardiac arrest
• Starting CPR
• Applying the defibrillator and delivering the first shock as
soon as possible
o High quality CPR needs to be performed with as few
interruptions as possible. Cycles of 30 compressions
at a depth of 2 to 2.4 inches deep and at a rate of
100 to 120 per minute should be given, followed by
two (2) breaths. The teammate performing
compressions needs to be changed every 2 minutes
to avoid fatigue.
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ELECTROCARDIOGRAM
After the initial shock, an IV or IO needs to be established to give medications.
• The first medication to give is epinephrine, 1 mg 1:10,000 IV or IO push every 3-5 minutes
• After the initial dose of epinephrine, a second shock should be given
• Placing an advanced airway with capnography should be considered. Once an advanced airway is in place, CPR
compressions become continuous at 100 to 120 compressions a minute, and one breath is given every 6 seconds
• If the patient remains in persistent ventricular fibrillation after the initial shocks and epinephrine administration, the
next medication to give is amiodarone at 300 mg via rapid IV or IO push
• A 150 mg dose of amiodarone may repeated one time in 3-5 minutes
• Successful treatment of ventricular fibrillation continues with high quality CPR, reassessing the patient’s cardiac
rhythm every 2 minutes, delivering a shock if ventricular fibrillation is present, and giving medications as indicated

ACLS WITH BRADYCARDIA ALGORITHM

Treatment for bradycardia should be based on controlling the
symptoms and identifying the cause using the Hs and Ts
1. Do not delay treatment but look for underlying causes of
the bradycardia using the Hs and Ts.
2. Maintain the airway and monitor cardiac rhythm, blood
pressure and oxygen saturation.
3. Insert an IV or IO for medications.
4. If the patient is stable, call for consults.
5. If the patient is symptomatic, administer atropine 1.0 mg
IV or IO bolus and repeat the atropine every 3 to 5
minutes to a total dose of 3 mg:
o If atropine does not relieve the bradycardia,
continue evaluating the patient to determine the
underlying cause and consider transcutaneous
pacing
o Consider an IV/IO dopamine infusion at 2-10
mcg/kg/minute
o Consider an IV/IO epinephrine infusion at 2-10 mcg/minute.
6. In the cases of Mobitz type II second-degree heart block, third-degree AV block, or third-degree AV block with
new widened QRS complex, atropine is unlikely to be effective. Consider transcutaneous pacing immediately or a
beta-adrenergic infusion to increase heart rate.

ACLS TACHYCARDIA ALGORITHM

1. The ACLS Tachycardia Algorithm is used for patients
who have marked tachycardia, usually greater than 150
beats per minute, and a palpable pulse.
2. Some patients may have cardiovascular instability with
tachycardia at heart rate less than 150 bpm. It is
important to consider the clinical context when treating
adult tachycardia.
3. If a pulse cannot be felt after palpating for up to 10
seconds, move immediately to the ACLS Cardiac Arrest
VTach and VFib Algorithm to provide treatment for
pulseless ventricular tachycardia.
4. The immediate response to an adult patient with
tachycardia and a palpable pulse is
o To maintain an open airway
o Assist breathing if necessary
o Apply monitors to assess cardiac rhythm, blood
pressure, blood oxygenation
5. Provide supplement oxygen to maintain O2 saturation
between 94% and 99%
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ELECTROCARDIOGRAM
6. The main assessment in adult patients with tachycardia is to determine whether the patient is stable or not. Signs
of cardiovascular instability are hypotension, signs of shock or acute heart failure (flash pulmonary edema, jugular
venous distention), altered mental status, or ischemic chest pain.
7. Unstable patients with tachycardia should be treated with synchronized cardioversion as soon as possible.

Cardioversion rules:
• QRS narrow and regular: 50-100 joules
• QRS narrow and irregular: 120-200 joules
• QRS wide and regular: 100 joules
• QRS wide and irregular: turn off the synchronized mode and defibrillate immediately

Stable patients with tachycardia with a palpable pulse can be treated with more conservative measures first.
• Attempt vagal maneuvers
• If unsuccessful, administer adenosine 6 mg IV bolus followed by a rapid normal saline flush
• If unsuccessful, administer adenosine 12 mg IV bolus followed by a rapid normal saline flush
• Beta-blockers and calcium channel blockers may be considered for narrow QRS tachycardia (QRS <0.12 sec)
• For stable, wide QRS complex tachycardia (QRS ≥0.12 sec)
• Strongly consider expert consultation
• Consider procainamide 20-50 mg/min IV, OR
• Amiodarone 150 mg IV over 10 minutes, OR
• Sotalol 100 mg (1.5 mg/kg) over 5 minutes