ELECTROCARDIOGRAM

BASIC PRINCIPLES
1. Despite its limited sensitivity and specificity, the 12-lead ECG is still the standard for the
evaluation of myocardial
ischemia.
2. Electrical activity is generated by the cells of the heart as ions are exchanged across cell
membranes.
3. Electrodes that are capable of conducting electrical activity from the heart to the ECG
machine are placed at strategic positions on the extremities and chest precordium
4. The electrical energy sensed is then converted to a graphic display by the ECG machine.
This display is referred to as the ECG.
5. Each ECG lead consists of a positive and negative pole; each lead also has an axis that
represents the direction in which current flows.
6. Each lead takes a different view of the heart; therefore, the tracing will be different with each
view obtained.
7. The direction in which electrical current flows determines how the waveform will appear.
8. There are three sets of leads:
a. Standard limb or bipolar leads (I, II, III) utilize three electrodes; these leads form a
triangle known as Einthoven's Triangle.
b. Augmented unipolar leads (aVR, aVL, aVF).
c. Precordial unipolar leads (V1 , V2 , V3 , V4 , V5 , V6 ).
9. A heart contraction is represented on the ECG graph paper by the designated P wave, QRS
complex, and T waves.
a. The P wave is the first positive deflection and represents atrial depolarization or atrial
contraction.
b. The PR interval represents the time it takes for the electrical impulse to travel from the
sinoatrial node to the AV node and down the bundle of His to the right and left bundle
branches.
c. The Q wave is the first negative deflection after the P wave; the R wave is the first
positive deflection after the P wave.
d. The S wave is the negative deflection after the R wave.
e. The QRS wave form is generally regarded as a unit and represents ventricular
depolarization. Atrial repolarization (relaxation) occurs during the QRS complex, but
cannot be seen.
f. The T wave follows the S wave and is joined to the QRS complex by the ST segment.
The ST segment represents ventricular repolarization or relaxation. The point that
represents the end of the QRS complex and the beginning of the ST segment is known
as the J point.
g. The T wave represents the return of ions to the appropriate side of the cell
membrane. This signifies relaxation of the muscle fibers and is referred to as
repolarization of the ventricles.

h. The QT interval is the time between the Q wave and the T wave; it represents
ventricular depolarization (contraction) and repolarization (relaxation).

ECG ELECTRODE PLACEMENT. The standard left precordial leads are V1fourth intercostal
space, right sternal border; V2fourth intercostal space, left sternal border; V3diagonally
between V2 and V4; V4fifth intercostal space, left midclavicular line; V5same level as V4,
anterior axillary line; V6 (not illustrated)same level as V4 and V5, midaxillary line. The right
precordial leads, placed across the right side of the chest, are the mirror opposite of the left
leads. RA, right arm; LA, left arm; RL, right leg; LL, left leg.

PROCEDURES
Equipments
ECG Machine
Recording Paper
Electrodes
Conduction gel Optional
Clippers
Alcohol swab or pad
1. Procedure Preparation Of Equipment
Place the ECG machine close to the client's bed and plug the cord into the wall outlet
or, batteryoperated, ensure that it is functioning.
Turn on the machine and input required client information.
Check that machine settings are standard.
2. Step by step standard ECG settings;
Steps:
Enter menu button by pressing the knob: EKG PRINT SETUP EXIT
Rotate knob and highlight menu blue light then enter by press knob
3. When you select ECG in menu
ECG LEAD SPEED GAIN FILTER MUSLE BASELINE NOTCH RETURN
4. Contd LEAD 3 1 3 2 61 62 RETURN
5. Contd Speed 12.5 mm/sec 25.0 mm/sec 50.0 mm/sec RETURN
6. Contd GAIN 5 mm/mV 10 mm/ mV 15 mm/ mV RETURN
7. Contd PRINT MODE MONITOR DIAGNOSIS FREEZE RETURN WAVE SIZE 29 BRIGHTNESS RECORDS RETURN
8. Verify the Physician order.
Indentify the patient according to FH policy.
Provide privacy and explain the procedure to the client. Explain that the test records the
heart's electrical activity and that it may be repeated at certain intervals. Emphasize that
no electrical current will enter the body. Tell the client that the test typically takes about 5
minutes.
9. Perform hand hygiene. Advice the client lie supine position in the center of the bed with
arms at his sides. You may raise the head of the bed to promote comfort. Expose the
arms and legs and cover the client appropriately. The arms and legs should be relaxed
to minimize muscle trembling, which can cause electrical interference. Make sure the
feet are not touching the bed board.
10. Select flat, fleshy areas to place the limb lead electrodes, Avoid muscular and bony
areas. If the client has an amputated limb, choose a site on the stump.
If an area is excessively hairy, clip it. Clean excess oil or other substances from the skin
with alcohol pad to enhance electrode contact
Apply disposable electrodes to the client's wrists and to the medial aspects of the
ankles.

Expose the client's chest. Put a pre-gelled electrode at each electrode position. If your
client is a woman, be sure to place the chest electrodes below the breast tissue. In a
large-breasted woman, you may need to displace the breast tissue laterally.
11. Limb Lead Placement
12. Connect the lead wires to the electrodes. The tip of each lead wire is lettered and
colorcoded for easy identification.
The red or RA lead wire goes to the right arm
The yellow or LA lead wire goes to left arm
The black or N/ RL lead wire goes to right leg The green or LL lead wire goes to left
leg
13. Chest lead placement
V1 ---- Red lead 4th Intercostal space to the right of the sternum
V2 ----- Yellow Lead4th Intercostal space to the left of the sternum
V3 ---- Green Lead Midway between V2 and V4
V4 ----- Brown lead 5th Intercostal space at the midclavicular line
V5 ----- Black lead Anterior axillary line at the same level as V4
V6 ---- Violet lead Midaxillary line at the same level as V4 and V5
14. Now you ready to begin the recording
Ask the patient to lie still and not to talk , breath normally and relax when recording
ECG
machines have a display screen so that you can preview waveforms before the
machine records them on paper.
Press the PRINT button. Observe the tracing quality. The machine will record all 12
leads automatically, recording three consecutive leads simultaneously.
15. When the machine finishes recording the 12-lead ECG, remove the electrodes and
clean the client's skin
After disconnecting the lead wires from the electrodes, CLEAN & DRY the electrodes as
per manufacture instruction. Assist the client to a comfortable position.
Ensure the bed is in a low position.
Remove any remaining equipment and wash your hands. Label ECG recording with
Patients name Medical record no Date Time Signature
Document the procedure in Nurses notes .

INTERPRETATION OF A RHYTHM STRIP

Develop a systematic approach to assist in accurate interpretation.
1.

Determine the rhythmis it regular, irregular, regularly irregular, or irregularly irregular?

Use calipers, count blocks between QRS complexes, or measure the distance between
R waves to determine regularity.

2.

Determine the rateis it fast, slow, or normal?

A.) A gross determination of rate can be accomplished by counting the number of QRS
complexes within a 6-second time interval (use the superior margin of ECG paper) and
multiplying the complexes by a factor of 10.
Note: This method is accurate only for rhythms that are occurring at normal intervals and should
not be used for determining rate in irregular rhythms. Irregular rhythms are always counted for 1
full minute for accuracy.
B.) Another means of obtaining rate is to divide the number of large 5-square blocks
between each two QRS complexes into 300. Three hundred large blocks represent 1 minute on
the ECG paper.
Example: In
Figure 12-3, the number of large square blocks between complexes #5 and #6 equals 5, and
300 5 = 60, or a rate of 60.
C.) Evaluate the P waveare P waves present? Is there a P for every QRS complex? If
there is not a P for every QRS, do the P waves have a normal configuration?
D.) Measure and evaluate the PR interval.

E.) Evaluate the QRS complexMeasure the QRS complex and examine its
configuration.
F.) Evaluate the ST segmentAn elevated ST segment heralds a pattern of injury and
usually occurs as an initial change in acute MI. ST depression occurs in ischemic states.
Calcium and potassium changes also affect the ST segment.
G.) Evaluate the T waveare T waves present? Do all T waves have a normal shape?
Could a P wave be hidden in the T wave, indicating a junctional rhythm or third degree
heart block? Is it positively or negatively deflected (inverted T waves indicate ischemia)
or peaked (indicative of hyperkalemia)?
H.) Evaluate the QT intervalshould be less than one half the R-R interval. Prolonged
QT interval may indicate digoxin toxicity, long-term quinidine (Quinaglute) or
procainamide (Pronestyl) therapy, or hypomagnesemia.

TYPES OF DYSRHYTHMIAS
Dysrhythmias include sinus, atrial, junctional, and ventricular dysrhythmias and their various
subcategories.

SINUS NODE DYSRHYTHMIAS

NORMAL SINUS RHYTHM
Normal sinus rhythm occurs when the electrical impulse starts at a regular rate and rhythm in
the sinus node and travels through the normal conduction pathway. Normal sinus rhythm has
the following characteristics (Fig. 27-5):

Ventricular and atrial rate: 60 to 100 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 BRADYCARDIA.
Sinus bradycardia occurs when the sinus node creates an impulse at a slower-than-normal rate.
Causes
include lower metabolic needs (eg, sleep, athletic training, hypothyroidism),
vagal stimulation (eg, from vomiting, suctioning, severe pain, extreme emotions),
medications (eg, calcium channel blockers, amiodarone, beta-blockers),
idiopathic sinus node dysfunction,
increased intracranial pressure (ICP),
myocardial infarction (MI), especially of the inferior wall.
Other possible contributing factors in clinically significant bradycardia
hypovolemia
hypoxia
hydrogen ion (acidosis)
hypokalemia or hyperkalemia,
hypoglycemia, and hypothermia;
toxins, tamponade (cardiac)
tension pneumothorax,
thrombosis (coronary or pulmonary)
trauma (hypovolemia, increased ICP)

Sinus bradycardia has the following characteristics (Fig. 27-6):

Ventricular and atrial rate: Less than 60 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

NURSING INTERVENTION
The patient is assessed to determine the hemodynamic effect and the possible cause of the
dysrhythmia. 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
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,
treatment is directed toward increasing the heart rate. If the slow heart rate is due to sinus node
dysfunction, which most often occurs in people older than 50 years of age, decreased exercise capacity,

fatigue, unexplained confusion, or memory loss may result (Fuster, Walsh & ORourke, 2008). Atropine,
0.5 mg given rapidly as an intravenous (IV) bolus every 3 to 5 minutes to a maximum total dose of 3 mg,
is the medication of choice in treating symptomatic sinus bradycardia. It blocks vagal stimulation, thus
allowing a normal rate to occur. Rarely, catecholamines and emergency transcutaneous pacing also are
implemented.

SINUS TACHYCARDIA
Sinus tachycardia occurs when the sinus node creates an impulse at a faster-than-normal rate.
Causes may include the following:
Physiologic or psychological stress (eg, acute blood loss, anemia, shock, hypervolemia, hypovolemia,
heart failure, pain, hypermetabolic states, fever, exercise, anxiety)
Medications that stimulate the sympathetic response (eg, catecholamines, aminophylline, atropine),
stimulants (eg, caffeine, alcohol, nicotine), and illicit drugs (eg, amphetamines, cocaine, Ecstasy)
Enhanced automaticity of the SA node and/or excessive sympathetic tone with reduced
parasympathetic tone, a condition called inappropriate sinus tachycardia
Autonomic dysfunction, which results in a type of sinus tachycardia called postural orthostatic
tachycardia syndrome (POTS). Patients with POTS have tachycardia without hypotension within 5 to 10
minutes of standing or with head-upright tilt testing. Sinus tachycardia has the following characteristics
(Fig. 27-7):

Ventricular and atrial rate: Greater than 100 in the adult, but usually less than 120
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
All aspects of sinus tachycardia are the same as those of normal sinus rhythm, except for the
rate. Sinus tachycardia does not start or end suddenly (nonparoxysmal). As the heart rate increases, the
diastolic filling time decreases, possibly resulting in reduced cardiac output and subsequent symptoms of
syncope 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. Treatment of sinus
tachycardia is usually determined by the severity of symptoms and directed at identifying and abolishing
its cause. Beta-blockers and calcium channel blockers, although rarely used, may be administered to
reduce the heart rate quickly. Catheter ablation (discussed later in this chapter) of the SA node may be
used in cases of persistent inappropriate sinus tachycardia unresponsive to other treatments. Treatment
for POTS may include increased fluid and sodium intake and use of anti-embolism stockings to prevent
pooling of blood in the lower extremities.

SINUS ARRHYTHMIA.
Sinus arrhythmia occurs when the sinus node creates an impulse at an irregular rhythm; the rate
usually increases with inspiration and decreases with expiration. Nonrespiratory causes include heart
disease and valvular disease, but these are rare. Sinus arrhythmia has the following characteristics (Fig.
27-8):

Ventricular and atrial rate: 60 to 100 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
Sinus arrhythmia does not cause any significant hemodynamic effect and usually is not treated.

ATRIAL DYSRHYTHMIAS
PREMATURE ATRIAL COMPLEX.
A premature atrial complex (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.
The PAC may be caused by caffeine, alcohol, nicotine, stretched atrial myocardium (eg, as in
hypervolemia), anxiety, hypokalemia (low potassium level), hypermetabolic states (eg, with pregnancy),
or atrial ischemia, injury, or infarction. PACs are often seen with sinus tachycardia. PACs have the
following characteristics (Fig. 27-9):

Ventricular and atrial rate: Depends on the underlying rhythm (eg, 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-thannormal PP interval, but one that is less than twice the

normal PP interval. This type of interval is called a noncompensatory 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.
P:QRS ratio: usually 1:1
PACs are common in normal hearts. The patient may say, My heart skipped a beat. A pulse
deficit (a difference between the apical and radial pulse rate) may exist. 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 dysrhythmias, such as atrial fibrillation. Treatment is directed
toward the cause.

ATRIAL FLUTTER.
Atrial flutter occurs because of a conduction defect in the atrium and causes a rapid, regular atrial rate,
usually between 250 and 400 times per minute. Because the atrial rate is faster than the AV node can
conduct, not all atrial impulses are conducted into the ventricle, causing a therapeutic block at the AV
node. This is an important feature of this dysrhythmia. If all atrial impulses were conducted to the
ventricle, the ventricular rate would also be 250 to 400, which could result in ventricular fibrillation, a lifethreatening dysrhythmia. Atrial flutter often occurs in patients with chronic obstructive pulmonary disease,
valvular disease, and thyrotoxicosis, as well as following open heart surgery and repair of congenital
cardiac defects (Fuster, et al., 2008). Atrial flutter has the following characteristics (Fig. 27-10):

Ventricular and atrial rate: Atrial rate ranges between 250 and 400; ventricular rate usually ranges
between 75 and 150
Ventricular and atrial rhythm: The atrial rhythm is regular; the ventricular rhythm is usually regular but may
be irregular because of a change in the AV conduction
QRS shape and duration: Usually normal, but may be abnormal or may be absent
P wave: Saw-toothed shape; these waves are referred to as F waves
PR interval: Multiple F waves may make it difficult to determine the PR interval
P:QRS ratio: 2:1, 3:1, or 4:1
Vagal maneuvers or administration of adenosine (Adenocard, Adenoscan), which causes
sympathetic block and slowing of conduction in the AV node, may allow better visualization of flutter
waves. Adenosine should be rapidly administered intravenously, followed by a 20-mL saline flush and
elevation of the arm with the IV line to promote rapid circulation of the medication. Atrial flutter can cause
serious signs and symptoms, such as chest pain, shortness of breath, and low blood pressure. Electrical
cardioversion (discussed later) is often successful in converting the rhythm to sinus rhythm. If the
dysrhythmia has lasted longer than 48 hours and a transesophageal echocardiogram has not confirmed
the absence of atrial clots, then adequate anticoagulation, using the same criteria as for atrial fibrillation,
may be indicated before cardioversion or ablation. Medications used to slow the ventricular response

rate include beta-blockers, nondihydropyridine calcium channel blockers, and digitalis, alone or in
combination (Fuster, et al., 2008).

ATRIAL FIBRILLATION.
Atrial fibrillation is an uncoordinated atrial electrical activation that causes a rapid, disorganized, and
uncoordinated twitching of atrial musculature. The ventricular rate response is dependent on the ability of
the AV node to conduct the atrial impulses, the level of sympathetic and parasympathetic tone, presence
of accessory pathways, and effects of any medications.For example, regular RR intervals in atrial
fibrillation may indicate the presence of complete AV block, junctional tachycardia, or ventricular
tachycardia. Atrial fibrillation may be transient, starting and stopping suddenly and occurring for a very
short time (paroxysmal dysrhythmia), or it may be persistent, requiring treatment to terminate the
rhythm or to control the ventricular rate. The lack of consistency in describing the pattern of atrial
fibrillation has led to use of numerous labels (eg, acute, chronic, paroxysmal, persistent, permanent) and
difficulty in comparative assessment of treatments (Fuster, et al., 2006).
Atrial fibrillation usually occurs in people of advanced age with structural heart disease, such as
valvular heart disease (most often mitral or tricuspid), inflammatory or infiltrative disease (pericarditis,
myocarditis, amyloidosis), coronary artery disease, hypertension, congenital disorder (especially atrial
septal defect), and heart failure (diastolic or systolic) (Fuster, et al., 2008). The dysrhythmia also may
be found in people with diabetes, obesity, hyperthyroidism, pheochromocytoma, pulmonary hypertension
and embolism, obstructive sleep apnea, and acute moderate to heavy ingestion of alcohol (holiday heart
syndrome), as well as following pulmonary or open heart surgery (Fuster, et al., 2006; Mehra, Benjamin,
Shahar, et al., 2006). Atrial fibrillation has been linked to increased risk of stroke and premature death,
and it is considered a growing health problem in developed countries (Fuster, et al., 2008). Neurogenic
atrial fibrillation that occurs with subarachnoid hemorrhage and nonhemorrhagic stroke is caused by
increased vagal or sympathetic stimulation. Sometimes atrial fibrillation occurs in people with no
underlying pathophysiology (called lone atrial fibrillation). Occurrence of atrial fibrillation after coronary
artery bypass, valvular replacements, and heart transplantation may prolong the duration and cost of the
hospitalization (Fuster, et al., 2008). Hospital admissions for atrial fibrillation increased by 66% over the
past 20 years, and occurrence of the dysrhythmia increases the length and cost of the hospital stay
(Fuster, et al., 2006). Atrial fibrillation has the following characteristics (Fig. 27-11):

Ventricular and atrial rate: Atrial rate is 300 to 600; ventricular rate is usually 120 to 200 in untreated atrial
Fibrillation
Ventricular and atrial rhythm: Highly irregular
QRS shape and duration: Usually normal, but may be abnormal
P wave: No discernible P waves; irregular undulating waves that vary in amplitude and shape are seen
and are referred to as fibrillatory or f waves
PR interval: Cannot be measured
P:QRS ratio: Many:1
A rapid and irregular ventricular response reduces then time for ventricular filling, resulting in a
smaller stroke volume. Because atrial fibrillation causes a loss in AV synchrony (the atria and ventricles
contract at different times), the atrial kick (the last part of diastole and ventricular filling, which accounts
for 25% to 30% of the cardiac output) is also lost. This may lead to irregular palpitations and symptoms of

heart failure such as shortness of breath, fatigue, exercise intolerance, and malaise. Patients may be
asymptomatic or experience significant hemodynamic collapse (hypotension, chest pain, pulmonary
edema, and altered level of consciousness), especially if they also have hypertension, mitral stenosis,
hypertrophic cardiomyopathy, or some form of restrictive heart failure. There is usually a pulse deficit, a
numeric difference between apical and radial pulse rates. The shorter time in diastole reduces the time
available for coronary artery perfusion, thereby increasing the risk of myocardial ischemia with the onset
of chest discomfort. The erratic atrial contraction and the atrial myocardial dysfunction promote the
formation of thrombi, especially within the atria, increasing the risk of an embolic event.
In addition, a high ventricular rate response during atrial fibrillation can lead to dilated ventricular
cardiomyopathy.The rapid ventricular rate can also lead to mitral valve dysfunction, mitral regurgitation,
and intraventricular conduction delay. Controlling the ventricular rate may prevent and correct these
effects.
The clinical evaluation of atrial fibrillation should include a history and physical examination (to
identify pattern of atrial fibrillation, associated symptoms, and any underlying conditions); 12-lead ECG (to
identify presence of ventricular hypertrophy, preexcitation from accessory pathways, intraventricular
conduction defects, and history of MI); echocardiogram (to assess cardiac chamber size, thickness, and
function; to identify potential causes, such as cardiomyopathy or valvular dysfunction; and to identify the
presence of a thrombus); and blood tests to assess thyroid, renal, and hepatic function (Fuster, et al.,
2008). Additional tests may include a chest x-ray (to evaluate pulmonary vasculature), exercise test (to
assess rate control as well as myocardial ischemia), Holter or event monitoring, and an EP study. The
physical examination may reveal an irregular pulse, irregular jugular venous pulsations, and irregular S 1
heart sounds.
Treatment of atrial fibrillation depends on the cause, pattern, and duration of the dysrhythmia; the
ventricular response rate; and the patients symptoms, age, and comorbidities. In many patients, atrial
fibrillation converts to sinus rhythm within 24 hours and without treatment. Hospitalization may not be
necessary. Electrical cardioversion is indicated for patients with atrial fibrillation that is hemodynamically
unstable unless they have digitalis toxicity or hypokalemia. Because of the high risk of embolization of
atrial thrombi, cardioversion of atrial fibrillation that has lasted longer than 48 hours should be avoided
unless the patient has received warfarin (Coumadin) for at least 3 to 4 weeks prior to cardioversion.
Alternatively, the absence of a mural thrombus can be confirmed by transesophageal echocardiogram
and heparin can be administered immediately prior to cardioversion. Because atrial
function may be impaired for several weeks after cardioversion, warfarin is indicated for at least 4 weeks
after the procedure. Patients may be given amiodarone (Cordarone), flecainide (Tambocor), ibutilide
(Corvert), propafenone (Rythmol), or sotalol (Betapace) prior to cardioversion to prevent relapse of the
atrial fibrillation.
Medications that may be administered to achieve cardioversion to sinus rhythm include flecainide,
propafenone, or sotalol (Fuster, et al., 2008). Other choices include dofetilide (Tikosyn), amiodarone, and
ibutilide. Because of the incidence of torsade de pointes, a ventricular tachycardia, the use of ibutilide
warrants ECG monitoring for at least 4 hours after its administration.
If the QRS is wide and the ventricular rhythm is very fast and irregular, atrial fibrillation with an
accessory pathway should be suspected. An accessory pathway is congenital tissue between the atria,
His bundle, AV node, Purkinje fibers, or ventricular myocardium. This anomaly is known as WolffParkinson-White or WPW syndrome. Electrical cardioversion is the treatment of choice for atrial fibrillation
in the presence of WPW syndrome. Medications that block AV conduction (eg, digoxin [Digitek], diltiazem
[Cardizem], and verapamil [Calan]) should be avoided. If the patient is hemodynamically stable,
procainamide (Pronestyl), propafenone, flecainide, or ibutilide is recommended to restore sinus rhythm
(Fuster, et al., 2008). Other medications that may be used include sotalol, quinidine (Quinaglute),
disopyramide (Norpace), or amiodarone. Catheter ablation is performed for long-term management.
To control the heart rate in persistent atrial fibrillation, an IV beta-blocker or a nondihydropyridine
calcium channel blocker (diltiazem and verapamil) is recommended (Fuster, et al., 2006). However,
people with impaired ventricular function should not receive verapamil, those with bronchospasm should
not receive a beta-blocker, and those with AV block should not receive any of these medications. IV
digoxin or amiodarone may be used for rate control in patients with heart failure or left ventricular
dysfunction but without an accessory pathway. IV procainamide or ibutilide is an alternative for rate
control in patients with an accessory pathway. In pregnant women, digoxin, a betablocker, or a
nondihydropyridine calcium channel blocker may be used for rate control. If medications fail to control the
heart rate or cause significant side effects, catheter ablation may be indicated.
Persistent atrial fibrillation can cause sinus node dysfunction and alteration in the atrial
musculature and contractile function (atrial remodeling), which may persist for days or weeks following

conversion to sinus rhythm (Fuster, et al., 2006). This has implications for the length of recovery time and
the duration of anticoagulation therapy needed after conversion.
If maintenance of sinus rhythm is necessary to maintain quality of life, flecainide, propafenone, or
sotalol may be prescribed (Fuster, et al., 2006). Patients who have been observed in the hospital while
being given a dose of either propafenone or flecainide to convert atrial fibrillation may be given the
medication to self-administer outside the hospital if they have a recurrence, an approach called pill in the
pocket (Fuster, et al., 2008). Several approaches are used to prevent the occurrence of postoperative
atrial fibrillation; preoperative administration of a beta-blocker or amiodarone is the most successful
(Fuster, et al., 2006). Pacemaker implantation, ablation, or surgery may be indicated for patients who do
not respond to medications.
Although control of the rhythm had been the initial treatment of choice, recent studies have found
that controlling the heart rate (resting heart rate less than 80) is equal to controlling the rhythm in terms of
quality of life, frequency of hospitalization for heart failure, and incidence of stroke (AFFIRM Investigators,
2002; Fuster, et al., 2006). Antithrombotic therapy is indicated for all patients with atrial fibrillation. The
type of therapy should be based on the risks of stroke and bleeding versus its benefits in a particular
patient. Warfarin is indicated if the patient with atrial fibrillation is at high risk for stroke (ie, older than 75
years of age or has hypertension, diabetes, heart failure, or history of stroke) (Fuster, et al., 2008). If
immediate anticoagulation is necessary, the patient may be placed on heparin until the warfarin level is
therapeutic, usually defined as an international normalized ratio (INR) between 2 and 3. If a patient
sustains an ischemic stroke or develops a systemic embolization during treatment, the antithrombotic
therapy may be increased with the goal of increasing the INR to between 3.0 and 3.5 (Fuster, et al.,
2006). Although aspirin may be substituted for warfarin in patients with contraindications to warfarin or
those who are at a high risk of bleeding, warfarin is generally preferred (Fuster, et al., 2008). If a patient
will be undergoing a procedure that carries a risk of bleeding, anticoagulation therapy may be withheld for
up to a week. If more than a week is needed, heparin may be given, although its efficiency is unknown.
Patients with atrial fibrillation who have a coronary artery stent implanted should receive clopidogrel
(Plavix), an antiplatelet agent, plus warfarin for 1 to 12 months following the procedure.

JUNCTIONAL DYSRHYTHMIAS
Premature Junctional Complex. A premature junctional complex is an impulse that starts in the AV
nodal area before the next normal sinus impulse reaches the AV node. Premature junctional complexes
are less common than PACs. Causes include digitalis toxicity, heart failure, and coronary artery disease.
The ECG criteria for premature junctional complex are the same as for PACs, except for the P wave and
the PR interval. The P wave may be absent, may follow the QRS, or may occur before the QRS but with a
PR interval of less than 0.12 seconds. This dysrhythmia rarely produces significant symptoms. Treatment
for frequent premature junctional complexes is the same as for frequent PACs.

Junctional Rhythm. Junctional or idionodal rhythm occurs when the AV node, instead of the sinus node,
becomes the pacemaker of the heart. When the sinus node slows (eg, from increased vagal tone) or
when the impulse cannot be conducted through the AV node (eg, because of complete heart block), the
AV node automatically discharges an impulse. Junctional rhythm not caused by complete heart block has
the following characteristics (Fig. 27-12):

Ventricular and atrial rate: Ventricular rate 40 to 60; atrial rate also 40 to 60 if P waves are discernible
Ventricular and atrial rhythm: Regular
QRS shape and duration: Usually normal, but may be abnormal
P wave: May be absent, after the QRS complex, or before the QRS; may be inverted, especially in lead II
PR interval: If the P wave is in front of the QRS, the PR interval is less than 0.12 seconds
P:QRS ratio: 1:1 or 0:1
Junctional rhythm may produce signs and symptoms of reduced cardiac output. If this occurs, the
treatment is the same as for sinus bradycardia. Emergency pacing may be needed.
NONPAROXYSMAL JUNCTIONAL TACHYCARDIA.
Junctional tachycardia is caused by enhanced automaticity in the junctional area, resulting in a rhythm
similar to junctional rhythm, except at a rate of 70 to 120. Although this rhythm generally does not have
any detrimental hemodynamic effect, it may indicate a serious underlying condition, such as digitalis
toxicity, myocardial ischemia, hypokalemia, or chronic obstructive pulmonary disease. Because junctional
tachycardia is caused by increased automaticity, cardioversion is not an effective treatment; in fact, it
causes an increase in the ventricular rate (AHA, 2005).
ATRIOVENTRICULAR NODAL REENTRY TACHYCARDIA.
Atrioventricular nodal reentry tachycardia (AVNRT) is a common dysrhythmia that occurs when an
impulse is conducted to an area in the AV node that causes the impulse to be rerouted back into the
same area over and over again at a very fast rate. Each time the impulse is conducted through this area,
it is also conducted down into the ventricles,causing a fast ventricular rate. AVNRT that has an abrupt
onset and an abrupt cessation with a QRS of normal duration has been termed paroxysmal atrial
tachycardia (PAT). AVNRT also occurs when the duration of the QRS complex is 0.12 seconds or greater
and a block in the bundle branch is known to be present. This dysrhythmia may last for seconds or
several hours. Factors associated with the development of AVNRT include caffeine, nicotine, hypoxemia,
and stress. Underlying pathologies include coronary artery disease and cardiomyopathy; however, it
occurs more often in females and not in association with underlying structural heart disease (BlomstrmLundqvist, et al., 2003). AVNRT has the following characteristics (Fig. 27-13):

Ventricular and atrial rate: Atrial rate usually 150 to 250; ventricular rate usually 120 to 200
Ventricular and atrial rhythm: Regular; sudden onset and termination of the tachycardia
QRS shape and duration: Usually normal, but may be abnormal
P wave: Usually very difficult to discern
PR interval: If the P wave is in front of the QRS, the PR
interval is less than 0.12 seconds
P:QRS ratio: 1:1, 2:1
The clinical symptoms vary with the rate and duration of the tachycardia and the patients
underlying condition. Then tachycardia usually is of short duration, resulting only in palpitations. A fast
rate may also reduce cardiac output, resulting in significant signs and symptoms such as restlessness,
chest pain, shortness of breath, pallor, hypotension, and loss of consciousness.

Because AVNRT is generally a benign dysrhythmia, the goal of treatment is to alleviate

symptoms that affect quality of life. Patients who become significantly symptomatic and require
emergency department visits to terminate the rhythm may want to initiate therapy immediately. However,
those with minimum symptoms with an AVRNT that terminates spontaneously or with minimal treatment
may choose just to be monitored.
The aim of therapy is to break the reentry of the impulse. Catheter ablation is the initial treatment
of choice and is used to eliminate the area that permits the rerouting of the impulse that causes the
tachycardia. Vagal maneuvers, such as carotid sinus massage gagging, breath holding, and immersing
the face in ice water, may be used to interrupt AVNRT. These techniques increase parasympathetic
stimulation, causing slower conduction through the AV node and blocking the reentry of the rerouted
impulse. Some patients use some of these methods to terminate the episode on their own. Because of
the risk of a cerebral embolic event, carotid sinus massage is contraindicated in patients with carotid
bruits. If the vagal maneuvers are ineffective, the patient may then receive a bolus of adenosine to correct
the rhythm; this is nearly 100% effective in terminating AVNRT (Fuster, et al., 2008). Patients who are
also taking dipyridamole (Persantin) or who are cardiac transplant recipients are more sensitive to
adenosine, and they should receive a lower initial dose (Fuster, et al., 2008). Because the effect of
adenosine is so short, AVNRT may recur; the first dose may be followed with a larger dose or with a
calcium channel blocker, such as verapamil, followed by one or two additional boluses. Digoxin is not
indicated because of it slow onset. If the patient is unstable or does not respond to the medications,
cardioversion is the treatment of choice. The unstable patient may be given adenosine while preparations
for cardioversion are being made. For recurrent sustained AVNRT, treatment with calcium channel
blockers such as verapamil and diltiazem, class 1a antiarrhythmic agents such as procainamide and
disopyramide, class 1c antiarrhythmics such as flecainide and propafenone, and class 3 agents such as
sotalol and amiodarone may prevent a recurrence. If the rhythm is infrequent and there is no underlying
cardiac structural disorder, a single oral dose of flecainide or a combination of diltiazem and propranolol
during an episode of tachycardia may be effective.
If P waves cannot be identified, the rhythm may be called supraventricular tachycardia (SVT),
or paroxysmal supraventricular tachycardia (PSVT) if it has an abrupt onset, until the underlying rhythm
and resulting diagnosis is determined. SVT and PSVT indicate only that the rhythm is not ventricular
tachycardia (VT). SVT could be atrial fibrillation, atrial flutter, or AVNRT, among others. Vagal
maneuvers and adenosine may be used to convert the rhythm or at least slow conduction in the AV node
to allow visualization of the P waves. If the ECG does not assist in the differentiation of the dysrhythmia,
invasive electrophysiology testing may be necessary to make the diagnosis.

VENTRICULAR DYSRHYTHMIAS
PREMATURE VENTRICULAR COMPLEX.
A premature ventricular complex (PVC) is an impulse that starts in a ventricle and is conducted through
the ventricles before the next normal sinus impulse. PVCs can occur in healthy people, especially with
intake of caffeine, nicotine, or alcohol. PVCs may be caused by cardiac ischemia or infarction, increased
workload on the heart (eg, heart failure, and tachycardia), digitalis toxicity, hypoxia, acidosis, or
electrolyte imbalances, especially hypokalemia. The Sleep Heart Health Study found that those people
with sleep disordered breathing (eg, obstructive sleep apnea) had a significantly higher prevalence of
complex ventricular ectopy and nonsustained ventricular tachycardia during sleep (Mehra, et al., 2006).
The implication of the presence of PVCs during and after exercise is not clear and remains controversial
(Fuster, et al., 2008). In a rhythm called bigeminy, every other complex is a PVC. In trigeminy, every third
complex is a PVC, and in quadrigeminy, every fourth complex is a PVC. PVCs have the following
characteristics (Fig. 27-15):

Ventricular and atrial rate: Depends on the underlying rhythm (eg, sinus rhythm)
Ventricular and atrial rhythm: Irregular due to early QRS, creating one RR interval that is shorter than the
others. PP interval may be regular, indicating that the PVC did not depolarize the sinus node.
QRS shape and duration: Duration is 0.12 seconds or longer; shape is bizarre and abnormal
P wave: Visibility of P wave depends on the timing of the
PVC; 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: If the P wave is in front of the QRS, the PR interval is less than 0.12 seconds
P:QRS ratio: 0:1; 1:1
The patient may feel nothing or may say that the heart skipped a beat. The effect of a PVC
depends on its timing in the cardiac cycle and how much blood was in the ventricles when they
contracted. Initial treatment is aimed at correcting the cause.
In the absence of disease, PVCs usually are not serious.n PVCs that are frequent and persistent
may be treated with amiodarone or sotalol. Long-term pharmacotherapy for only PVCs is not indicated. In
patients with acute MI, PVCs may warrant more aggressive therapy. Lidocaine (Xylocaine) may be used
in the patient with acute MI. Patients with acute MI who did not receive thrombolytics and had more than
10 PVCs per hour and those who did receive thrombolytics and had more than 25 PVCS per hour were
found to be at the greatest risk for sudden cardiac death (Fuster, et al., 2008). In the past, PVCs were
considered to be indicative of an increased risk for ensuing VT. However, PVCs that (1) are more
frequent than six per minute, (2) are multifocal or polymorphic (having different shapes and rhythms), (3)
occur two in a row (pair), and (4) occur on the T wave (the vulnerable period of ventricular depolarization)
have not been found to be precursors of VT in patients without structural heart disease (Cardiac
Arrhythmia Suppression Trial Investigators, 1989). These PVCs are no longer considered as warning or
complex PVCs.
VENTRICULAR TACHYCARDIA.
VT is defined as three or more PVCs in a row, occurring at a rate exceeding 100 bpm. The causes are
similar to those of PVC. Patients with larger MIs and lower ejection fractions are at higher risk of lethal
ventricular tachycardia. VT is an emergency because the patient is usually (although not always)
unresponsive and pulseless. VT has the following characteristics (Fig. 27-16):

Ventricular and atrial rate: Ventricular rate is 100 to 200 bpm; atrial rate depends on the underlying
rhythm (eg, sinus rhythm)
Ventricular and atrial rhythm: Usually regular; atrial rhythm may also be regular
QRS shape and duration: Duration is 0.12 seconds or more; bizarre, abnormal shape
P wave: Very difficult to detect, so atrial rate and rhythm may be indeterminable
PR interval: Very irregular, if P waves are seen
P:QRS ratio: Difficult to determine, but if P waves are apparent, there are usually more QRS complexes
than P waves
The patients tolerance or lack of tolerance for this rapid rhythm depends on the ventricular rate
and severity of ventricular dysfunction. However, hemodynamic stability does not predict mortality risk
(Fuster, et al., 2008). Several factors determine the initial treatment, including the following: identifying the
rhythm as monomorphic (having a consistent QRS shape and rate) or polymorphic (having varying QRS

shapes and rhythms); determining the existence of a prolonged QT interval before the initiation of VT; and
ascertaining the patients heart function (normal or decreased). If the patient is stable, continuing the
assessment, especially obtaining a 12-lead ECG, may be the only action necessary.
However, the patient may need antiarrhythmic medications, antitachycardia pacing, or direct
cardioversion. IV procainamide is the antiarrhythmic medication of choice for a patient with stable acute
MI with VT, whereas IV amiodarone is the medication of choice for a patient with unstable VT or impaired
cardiac function. Sotalol may also be used. Although lidocaine has been the medication most commonly
used for immediate, short-term therapy, especially for patients with impaired cardiac function, it has no
proven short-term or long-term efficacy in cardiac arrest (AHA, 2005). Cardioversion is the treatment of
choice for monophasic VT in a symptomatic patient. Defibrillation is the treatment of choice for pulseless
VT. Any type of VT in a patient who is unconscious and without a pulse is treated in the same manner as
ventricular fibrillation: immediate defibrillation is the action of choice. For long-term management,
patients with an ejection fraction less than 35% should be considered for an implantable cardioverter
defibrillator. Those with an ejection fraction greater than 35% may be managed with amiodarone. A small
percentage of patients with VT have structurally normal hearts and respond well to medications and
ablation, and they have an excellent prognosis (Fuster, et al., 2008). If the ventricular rate is above 200,
then presence of an accessory pathway should be suspected. If the ventricular rhythm is irregular, atrial
fibrillation should be suspected and treated appropriately (Fuster, et al., 2006).
Torsade de pointes is a polymorphic VT preceded by a prolonged QT interval. Common causes
include central nervous system disease; certain medications; or low levels of potassium, calcium, or
magnesium. Congenital QT prolongation is another cause. Because this rhythm is likely to cause the
patient to deteriorate and become pulseless, immediate treatment is required: correction of any
electrolyte imbalance, administration of isoproterenol (Isuprel) IV, or initiation of ventricular pacing.
Magnesium has frequently been used to treat torsades, but its use has not been proved effective (AHA,
2005).
Ventricular Fibrillation. The most common dysrhythmia in patients with cardiac arrest is ventricular
fibrillation, which is a rapid, disorganized ventricular rhythm that causes ineffective quivering of the
ventricles. No atrial activity is seen on the ECG. The most common cause of ventricular fibrillation is
coronary artery disease and resulting acute MI. Other causes include untreated or unsuccessfully treated
VT, cardiomyopathy, valvular heart disease, several proarrhythmic medications, acid-base and
electrolyte abnormalities, and electrical shock. Another cause is Brugada syndrome, in which the patient
(frequently of Asian descent) has a structurally normal heart, few or no risk factors for coronary artery
disease, and a family history of sudden cardiac death. Ventricular fibrillation has the following
characteristics (Fig. 27-17):

Ventricular rate: Greater than 300 per minute

Ventricular rhythm: Extremely irregular, without a specific pattern
QRS shape and duration: Irregular, undulating waves without recognizable QRS complexes
Ventricular fibrillation is always characterized by the absence of an audible heartbeat, a palpable
pulse, and respirations. Because there is no coordinated cardiac activity, cardiac arrest and death are
imminent if the dysrhythmia is not corrected. Early defibrillation is critical to survival, with administration of
immediate bystander cardiopulmonary resuscitation (CPR) until defibrillation is available. The chance of
survival decreases by 7% to 10% for every minute in delay of defibrillation (AHA, 2005). If the

arrest was not witnessed or there was more than a 4-minute delay in emergency services response, five
cycles of CPR may be given prior to defibrillation (AHA, 2005). After the initial defibrillation, five additional
cycles of CPR (about 2 minutes of continuous chest compressions in the intubated patient), beginning
with chest compression and alternating with a rhythm check and defibrillation, are used to convert
ventricular fibrillation to an electrical rhythm that produces a pulse. Cardiocerebral resuscitation for
cardiac arrest with continuous chest compressions, interrupted only with defibrillation, and its deemphasis on the use of positive-pressure ventilation continues to be explored as a better method for
improving survival (Fuster, et al., 2008). Epinephrine should be administered as soon as possible after
the second rhythm check (immediately before or after the second defibrillation) and then every 3 to 5
minutes. One dose of vasopressin (Pitressin) may be administered instead of epinephrine if the cardiac
arrest persists. Other antiarrhythmic medications (amiodarone, lidocaine, or possibly magnesium) should
be administered as soon as possible after the third rhythm check (immediately before or after the third
defibrillation).
For refractory ventricular fibrillation, amiodarone may be the medication of choice. However, once
the patient is intubated, CPR should be given continuously, not in cycles, and the rhythm check and
medication administration occur every 2 minutes. In addition, underlying and contributing factors are
identified and eliminated throughout the event (AHA, 2005).
Current AHA guidelines recommend inducing mild hypothermia in unconscious adults who
experience cardiac arrest (including cardiac arrest due to ventricular fibrillation) and who receive CPR
within 10 minutes. Hypothermia is defined as a core body temperature of 32_C to 34_C (89.6_F to
93.2_F). Induction should be started as soon as possible after circulation is restored, preferably within 60
minutes, and maintained for 12 to 24 hours. It is usually initiated by applying ice packs to the axilla and
groin as well as administering iced saline gastric lavage until a cooling machine is obtained. The nurse
caring for a patient with hypothermia (passive or induced) needs to monitor for appropriate level of
cooling, sedation, and neuromuscular paralysis to prevent seizures, myoclonus, and shivering.
The nurse also needs to monitor for complications of hypothermia, which include electrolyte
imbalance (especially due to the diuresis caused by hypothermia), hypotension, pneumonia, sepsis,
hyperglycemia, dysrhythmias, and coagulopathy, especially if the temperature drops below the intended
goal. Because of these numerous nursing interventions, patients receive care in intensive care units.
Each patient should be assigned three nurses during the induction process and two nurses during the
hypothermia state.
IDIOVENTRICULAR RHYTHM.
Idioventricular rhythm, also called ventricular escape rhythm, occurs when the impulse starts in the
conduction system below the AV node. When the sinus node fails to create an impulse (eg, from
increased vagal tone) or when the impulse is created but cannot be conducted through the AV node (eg,
due to complete AV block), the Purkinje fibers automatically discharge an impulse. When idioventricular
rhythm is not caused by AV block, it has the following characteristics (Fig. 27-18):

Ventricular rate: 20 and 40; if the rate exceeds 40, the rhythm is known as accelerated idioventricular
rhythm (AIVR)
Ventricular rhythm: Regular
QRS shape and duration: Bizarre, abnormal shape; duration is 0.12 seconds or more
Idioventricular rhythm commonly causes the patient to lose consciousness and experience other
signs and symptoms of reduced cardiac output. In such cases, the treatment is the same as for asystole

and pulseless electrical activity (PEA) if the patient is in cardiac arrest or for bradycardia if the patient is
not in cardiac arrest. Interventions include identifying the underlying cause; administering IV epinephrine,
atropine, and vasopressor medications; and initiating emergency transcutaneous pacing. In some cases,
idioventricular rhythm may cause no symptoms of reduced cardiac output. However, bed rest is
prescribed so as not to increase the cardiac workload.
VENTRICULAR ASYSTOLE.
Commonly called flatline, ventricular Asystole is characterized by absent QRS complexes
confirmed in two different leads, although P waves may be apparent for a short duration. There is no
heartbeat, no palpable pulse, and no respiration. Without immediate treatment, ventricular asystole is
fatal.
Ventricular asystole is treated the same as PEA, focusing on high-quality CPR with minimal
interruptions and identifying underlying and contributing factors. The guidelines for advanced
cardiovascular life support (ACLS) (AHA, 2005) state that the key to successful treatment is rapid
assessment to identify a possible cause, which may be hypoxia, acidosis, severe electrolyte imbalance,
drug overdose, hypovolemia, cardiac tamponade, tension pneumothorax, coronary or pulmonary
thrombosis, trauma, or hypothermia. After the initiation of CPR, intubation and establishment of IV access
are the next recommended actions, with no or minimal interruptions in chest compressions. After 2
minutes or five cycles of CPR, a bolus of IV epinephrine is administered and repeated at 3- to 5-minute
intervals. One dose of vasopressin may be administered for the first or second dose of epinephrine. A
bolus of IV atropine may also be administered as soon as possible after the rhythm check (AHA, 2005).
Because of the poor prognosis associated with asystole, if the patient does not respond to these actions
and others aimed at correcting underlying causes, resuscitation efforts are usually ended (the code is
called) unless special circumstances (eg, hypothermia, transportation to a hospital is required) exist.
Conduction Abnormalities
When assessing the rhythm strip, the underlying rhythm is first identified (eg, sinus rhythm, sinus
arrhythmia). Then the PR interval is assessed for the possibility of an AV block. AV blocks occur when the
conduction of the impulse through the AV nodal or His bundle area is decreased or stopped. These
blocks can be caused by medications (eg, digitalis, calcium channel blockers, beta-blockers), Lyme
disease, myocardial ischemia and infarction, valvular disorders, cardiomyopathy, endocarditis, or
myocarditis. If the AV block is caused by increased vagal tone (eg, long-term athletic training, sleep,
coughing, suctioning, pressure above the eyes or on large vessels, anal stimulation), it is commonly
accompanied by sinus bradycardia. AV block may be temporary and resolve on its own, or it may be
permanent and require permanent pacing.
The clinical signs and symptoms of a heart block vary with the resulting ventricular rate and the
severity of any underlying disease processes. Whereas first-degree AV block rarely causes any
hemodynamic effect, the other blocks may result in decreased heart rate, causing a decrease in perfusion
to vital organs, such as the brain, heart, kidneys, lungs, and skin. A patient with third-degree AV block
caused by digitalis toxicity may be stable; another patient with the same rhythm caused by acute MI may
be unstable. Health care providers must always keep in mind the need to treat the patient, not the rhythm.
The treatment is based on the hemodynamic effect of the rhythm.
FIRST-DEGREE ATRIOVENTRICULAR BLOCK.
First-degree AV block occurs when all the atrial impulses are conducted through the AV node into
the ventricles at a rate slower than normal. This conduction disorder has the following characteristics (Fig.
27-20):

Ventricular and atrial rate: Depends on the underlying rhythm

Ventricular and atrial rhythm: Depends on the underlying rhythm
QRS shape and duration: Usually normal, but may be abnormal
P wave: In front of the QRS complex; shows sinus rhythm, regular shape
PR interval: Greater than 0.20 seconds; PR interval measurement is constant
P:QRS ratio: 1:1

SECOND-DEGREE ATRIOVENTRICULAR BLOCK, TYPE I (WENCKEBACH).

Second-degree AV block, type I, occurs when there is a repeating pattern in which all but one of a series
of atrial impulses are conducted through the AV node into the ventricles (eg, every four of five atrial
impulses are conducted). Each atrial impulse takes a longer time for conduction than the one before, until
one impulse is fully blocked. Because the AV node is not depolarized by the blocked atrial impulse, the
AV node has time to fully repolarize, so that the next atrial impulse can be conducted within the shortest
amount of time. Second-degree AV block, type I, has the following characteristics (Fig. 27-21):

Ventricular and atrial rate: Depends on the underlying rhythm

Ventricular and atrial rhythm: The PP interval is regular if the patient has an underlying normal sinus
rhythm; the RR interval characteristically reflects a pattern of change. Starting from the RR that is the
longest, the RR interval gradually shortens until there is another long RR interval.
QRS shape and duration: Usually normal but may be abnormal
P wave: In front of the QRS complex; shape depends on underlying rhythm
PR interval: PR interval becomes longer with each succeeding ECG complex until there is a P wave not
followed by a QRS. The changes in the PR interval are repeated between each dropped QRS, creating
a pattern in the irregular PR interval measurements.
P:QRS ratio: 3:2, 4:3, 5:4, and so forth

SECOND-DEGREE ATRIOVENTRICULAR BLOCK, TYPE II.

Second degree AV block, type II, occurs when only some of the atrial impulses are conducted through the
AV node into the ventricles. Second-degree AV block, type II, has the following
characteristics (Fig. 27-22):

Ventricular and atrial rate: Depends on the underlying rhythm

Ventricular and atrial rhythm: The PP interval is regular if the patient has an underlying normal sinus
rhythm. The RR interval is usually regular but may be irregular, depending on the P:QRS ratio.
QRS shape and duration: Usually abnormal but may be normal
P wave: In front of the QRS complex; shape depends on underlying rhythm
PR interval: PR interval is constant for those P waves just before QRS complexes
P:QRS ratio: 2:1, 3:1, 4:1, 5:1, and so forth
THIRD-DEGREE ATRIOVENTRICULAR BLOCK.
Third-degree AV block occurs when no atrial impulse is conducted through the AV node into the
ventricles. In third-degree AV block, two impulses stimulate the heart: one stimulates the ventricles (eg,
junctional or ventricular escape rhythm), represented by the QRS complex, and one stimulates the atria
(eg, sinus rhythm or atrial fibrillation), represented by the P wave. P waves may be seen, but the atrial
electrical activity is not conducted down into the ventricles to cause the QRS complex, the ventricular
electrical activity. Having two impulses stimulate the heart results in a condition called AV dissociation,
which may also occur during VT. Complete block (third-degree AV block) has the following characteristics
(Fig. 27-23):

Ventricular and atrial rate: Depends on the escape rhythm and underlying atrial rhythm
Ventricular and atrial rhythm: The PP interval is regular and the RR interval is regular, but the PP interval
is not equal to the RR interval
QRS shape and duration: Depends on the escape rhythm; with junctional rhythm, QRS shape and
duration are usually normal; with idioventricular rhythm, QRS shape and duration are usually abnormal
P wave: Depends on underlying rhythm
PR interval: Very irregular
P:QRS ratio: More P waves than QRS complexes

ASSIGNMENT

ELECTROCARDIOGRAM

SUBMITTED BY:
THINA C. TORRES
BSN III

SUBMITTED TO:
MRS. KAREEN SISON RN, MN
CLINICAL INSTRUCTOR

August 7, 2014