Foundations of arrhythmia interpretation

Foundations of arrhythmia interpretation

Delma A. Scrima

Cardiac monitoring, once a skill isolated to critical care units, is being used with increasing frequency in a variety of clinical settings. Staff in oncology units, medical/surgical units, progressive care units, labor and delivery units, outpatient surgical units, and ambulatory care areas provide patient support that incorporates cardiac rhythm recognition. Critical thinking skills represent a second aspect of practice that is related to cardiac rhythm interpretation and are important to providing effective patient care. Understanding the cardiac anatomy and physiology and the parameters for arrhythmia definition allow the nurse at the bedside to correlate the significance of an arrhythmia with a patient’s’s clinical state.


A first step in arrhythmia identification and interpretation of the clinical significance of that rhythm is an understanding of cardiac structure and function. The heart contains two important but separate muscle masses: the atrial muscle and the ventricular muscle. These structures attach to the fibrous skeleton of the heart called the annuli fibrosi or valve rings (Basmajian & Slonecker, 1989). A key point to remember is that atrial and ventricular fibers are entirely separate muscle masses that are expected to work in a coordinated effort to provide nutrients and oxygen to cells and remove carbon dioxide and end products of metabolism from cells. The heart’s conduction system provides the coordination tool for cardiac muscle electrical stimulation, mechanical contraction, and cardiac output.

The atria are thin walled chambers with a fiber structure that is horizontal in configuration (Basmajian & Slonecker, 1989). The atria have similar work demands under normal conditions and are similar in thickness. The horizontal fiber structure influences atrial response to an increased workload, and patients with an excess in volume may develop stretching, thinning, and dilatation. Stretched fibers become irritable; and clinical factors, such as congestive heart failure or mitral stenosis, that increase atrial stretch, are associated with atrial dysrhythmias (Kastor, 1994). Atrial contraction in late diastole contributes to ventricular filling volume. The loss of atrial contraction can decrease ventricular filling by 15% to 25% and limits cardiac output (Ganong, 1991).

The ventricles vary in thickness because the workload of the ventricles is unequal. The right ventricle pumps blood to a low resistance pulmonary circuit with an average systolic pressure of 25 to 30 mmHg. The left ventricle pumps to a systemic circuit with an average systolic pressure of 120 mmHg (Schlant & Sonnenblick, 1990). Under normal conditions, the left ventricle has a work demand that is about six times greater than the demand on the right. Both ventricles have a figure-eight fiber configuration, making ventricular fibers more difficult to dilate and irritate (Basmajian & Slonecker, 1989). Clinical factors such as acute myocardial infarction and cardiomyopathy that contribute to ventricular remodeling and dilatation increase the frequency of ventricular dysrhythmias (Effat, 1995).

Cardiac function comprises two phases — systole and diastole. Systole is a brief period that lasts about 10 milliseconds and results in ejection of the contents of the ventricles. Several features of systole are important to normal cardiac function. Systole remains a relatively fixed period regardless of heart rate. During systole, the coronary perforator vessels that arise from the coronary arteries on the epicardial or outer surface of the heart are squeezed by the myocardial muscle layer contraction. Systole provides blood and oxygen to systemic sites but limits the available oxygen supply to the endocardium and the working myocardial muscle.

Diastole, the second phase of the cardiac cycle, provides a period for ventricular relaxation. Early passive filling is the expected physiologic response. Late in diastole, the atria contract to complete ventricular filling. During diastole, while the cardiac wall is relaxed, perforator vessels of the coronary arteries supply the endocardium and myocardium with oxygen. As heart rates increase, the portion of each cardiac cycle devoted to diastole shortens. A decrease in the duration of the diastolic interval reduces myocardial oxygenation and is a factor in generating arrhythmias.


There are five primary features of cardiac function that, when altered, contribute to the incidence of cardiac rhythm disturbances. These features are automaticity, conductivity, contractility, rhythmicity, and excitability. Each of these features influences normal anticipated function of cardiac tissue and alterations in one or all of these features can be related to cardiac rhythm disturbances.


Automaticity means that a cell is able to spontaneously depolarize and respond electrically. All cardiac conduction fibers have an intrinsic rate of automaticity. Table 1 includes the rate ranges for automaticity normally attributed to cardiac conduction fibers. The ranges provide guidelines for arrhythmia interpretation. All cardiac rhythms have recognized rate ranges that are important to interpretation. A rule of cardiac function is that the cell with the greatest automaticity will control myocardial response. Since the sinus node is normally the portion of the conduction system with the most automaticity, the sinus node is the genesis of normal cardiac rhythm. If sinus node automatically fails, subsidiary pacers are available to protect cardiac output. The intrinsic rate of perinodal fibers of the atrioventricular (AV) junction are the first line of protection, and when they fail, the Purkinje fibers of the ventricular system provide the last option for ensuring tissue perfusion. When sinus node automaticity is depressed or fails, the rhythms that occur to protect cardiac output are called escape rhythms. Escape rhythms are considered protective for cardiac output. Patients who experience stimulation of the vagus nerve, a parasympathetic fiber that is responsible for slowing of heart rate, can develop depression of the sinus rate and subsequent escape rhythms.

Table 1.

Adult Intrinsic Rate Ranges

Structure Anticipated Rate Parameters

Sinus (SA) node 60 to 100 beats per minute

Atrioventricular (AV) node 40 to 60 beats per minute

Purkinje or ventricular fibers 20 to 40 beats per minute

When cells are ischemic or subject to electrolyte abnormalities they can become ectopic, abnormal, pacing sites. Ischemic tissues may be interspersed in areas of normal tissue and generate individual ectopic beats or sustained cardiac rhythms. Ischemic tissues have rates of recovery that are different from normal tissues. When tissues with variable rates of electrical activity have bordering cell membranes, cardiac irritability is enhanced. When myocardial tissues have variable rates of recovery, an impulse may not be able to depolarize the entire myocardium with one pass through the muscle and re-entrant rhythms occur. The phenomenon of re-entry results from these alterations in conductivity and is associated with rhythm disorders.

Re-entry can also occur within the AV node. The AV node is a structure with two conduction pathways and has the capability of supporting either brief or sustained episodes of re-entrant conduction. Because the two pathways within the AV node have different rates of recovery, an early impulse can first travel down the pathway that has recovered and then return to the atria via the pathway that was slower to recover. The returning, retrograde, impulse initiates a second myocardial response. The mechanism of re-entry at the level of the AV node can be the source of rapid heart rates.


Contractility is the property of cardiac muscle that allows sustained contraction and ejection of ventricular contents in response to electrical stimulation. Contractility of cardiac tissues can be influenced by many clinical factors. The Frank-Starling law states that to a point, cardiac tissue will respond to increased stretch by increasing contractility (Schlant & Sonnenblick 1990). Patients require adequate circulating volume to stretch cardiac fibers in diastole and support cardiac output in systole. Patients with dehydration or hemorrhage have an inadequate diastolic stretch and the volume ejected with each contraction falls. Patients with an excess, vascular volume limit cardiac output as diastolic stretch exceeds the systolic ability of the muscle to contract and shorten.

Poor contractility due to inadequate or excess vascular volume results in a decrease in cardiac output. This decrease in cardiac output activates the sympathetic nervous system and heart rates increase. A second problem related to overstretching fibers is the increased workload or demand on the myocardium as it attempts to shorten for contraction. Myocardial fibers may become ischemic and irritable as the work of contraction exceeds the available oxygen supply. Since cardiac output is the product of stroke volume multiplied by heart rate, decreased contractility due to poor filling or overstretching and dilatation contributes to increased heart rates. Increased rates decrease the cardiac diastolic interval, reduce myocardial muscle perfusion, and contribute to myocardial ischemia and arrhythmias.

Another factor that influences contractility is an adequate supply of the electrolyte calcium. Calcium enters cardiac muscle shortly after the peak of electrical depolarization and contributes to sustained mechanical contraction and ventricular emptying. Patients with deficiencies in calcium or receiving drugs that block calcium channels can develop alterations in cardiac contractility. Since drugs given to treat cardiac rhythm disturbances can block normal calcium influx, therapies for cardiac rhythms can alter cardiac output.


The property of rhythmicity means that the sequence of depolarization and repolarizations occur at regular and predictable intervals. Each of the normal cardiac pacing sites has an intrinsic rhythmicity. When the sinus node, AV junction, or ventricular Purkinje fibers escape to protect cardiac output, they have different intrinsic rates; but each site exhibits rhythmicity, a regular and predictable interval between beats. Changes in the predictable regularity of beats contributes to the identification of cardiac rhythm disturbances. Single premature beats may occur earlier than expected; brief and abrupt, paroxysmal rhythms may interrupt normal rhythmicity; or gradual phasic changes may vary the rate slowly over several beats.


The final property of cardiac tissue that aids in interpreting rhythm disturbances is the property of excitability. Cells rest in a polarized state, respond to stimulation with depolarization, and return to a resting state through repolarization. Excitability occurs as a result of ionic exchange; and the ions important to cardiac response are sodium, potassium, and magnesium.

The myocardial cell in a resting or polarized state is relatively negative on the inside with a high intracellular potassium level and a low intracellular sodium level. The environment outside of the cell has a high sodium content and a low potassium content. Since ions like to move from areas of high concentration to areas of low concentration. The natural direction for ionic diffusion is for potassium to leak out of the cell and sodium to enter the cell. Cell membranes are permeable to potassium, and leak of potassium from the cell contributes to the normal resting membrane ionic level. The cell wall is impermeable under resting conditions to sodium, and the large gradient of sodium cannot force ionic flow into a cell. When a resting cell is depolarized electrically, sodium gates open and the sodium ions enter the cell. This rapid influx of sodium depolarizes the cell and elicits a myocardial fiber response.

Once a cell has responded to one stimulation, it enters a period when it is refractory and cannot recognize or respond to another stimulus. A cell will remain refractory until it is able to repolarize, recognize, and respond to another depolarizing force. The natural leak of potassium from the high intracellular concentration to the low extracellular concentration contributes to the return of the cell to a resting, repolarized state. The natural leak of potassium is not sufficient, however, to return the cell to normal resting intracellular negativity, and a portion of the sodium that entered to depolarize the cell must also be removed from the intracellular content. Since sodium levels remain higher outside the cell, a pump is used to remove sodium from the intracellular content. Use of the pump requires energy that is supplied by adenosine triphosphate (ATP), the body’s usual energy source. Just as a car engine requires not only gasoline for fuel but oil to reduce friction, the sodium-potassium pump requires not only ATP for fuel but magnesium to make the pump run smoothly. Clinical states that decrease the availability of magnesium limit the effectiveness of the pump and contribute to the occurrence of rhythm disturbances. Patients with nutritional deficits are examples of patients at risk for magnesium deficits.

When the pump cannot return a cell to a normal resting electrical potential, or the integrity of the cell wall is altered by ischemia or potassium disorders, the cell cannot be returned to its usual level of intracellular negativity. This abnormal cell is described as resting closer to threshold, the point at which sodium channels will open and allow depolarization. Cells that rest closer to response levels require less stimulation to respond and become irritable. Hypokalemia is an electrolyte disorder associated with increased myocardial irritability. Measurement of potassium and magnesium are important to the clinical evaluation of irritable cardiac rhythms.

A high serum potassium level increases the extracellular level of potassium making it more difficult for cells to leak the ion and return to a resting level. High potassium levels depress myocardial excitability, increase the duration of normal electrical waveforms, and decrease heart rates.

Developing an understanding of the normal cardiac properties of automaticity, conductivity, contractility, rhythmicity, and excitability provides a foundation for critically interpreting the significance of cardiac rhythm disturbances in a clinical setting.

Conduction System

The conduction system of the myocardium is responsible for initiating a cardiac impulse, rapid delivery of the depolarizing electrical impulse to all cardiac cells, and facilitating the coordination of atrial and ventricular muscle contraction. The conduction system comprises the sinus (SA) node, atrioventricular (AV) node, bundle of His (common bundle), right bundle branch (RBB), left bundle branch (LBB), and Purkinje fibers.

The sinus node is located in the right atrium near the entry of the superior vena cave The sinus node, with an intrinsic automaticity range of 60 to 100 beats per minute, is the source of normal cardiac rhythm. The sinus node depends on calcium for the ability to respond electrically. Calcium channel blocking agents decrease the rate of sinus output. The normal rhythmicity of the sinus node is predictable and regular. Impulses released from the sinus node travel through the atria, resulting in depolarization and the subsequent contraction of atrial fibers. This depolarization is recognized by the graphic recording of a “P” wave on an electrocardiograph recording (ECG).

The impulse next enters the AV node, a maze structure with multiple pathways that slow the cardiac impulse The maze configuration of the AV node protects the ventricles from potentially high atrial rates. Irritable atrial fibers that develop fibrillation can generate rapid electrical impulses that exceed rates of 600 each minute (Sorenson, Vulich, McErlean, & McCarthy, 1992). Delay of the impulse by the AV node also allows time for the mechanical contraction of the atria that follows electrical stimulation and contributes to ventricular filling.

The impulse leaves the AV node and travels into the bundle of His. Within this common bundle, the fibers resume a longitudinal configuration and the impulse proceeds rapidly through the fibers of the ventricle. The bundle of His is a short segment that bifurcates into two distinct branches on the right and left side of the septum. The right bundle branch supplies the right side of the septum and the right ventricle. The fiber is long and thin and is slower to recover than the fibers of the left bundle branch (Petrie, 1988). At normal heart rates, the slower recovery is not significant to conduction intervals. At rapid heart rates, aberration, the term used to describe bundle branch block conduction, can alter the shape of the ECG waveform. Since the RBB has a longer recovery period, rate-related conduction deficits are more commonly seen as right bundle branch block configurations, but both right and left bundle branch conduction deficits occur with rate changes (Akhtar, Shensa, Jazayeri, Caceres, & Tchou, 1988). The LBB divides into two distinct fiber groups called fascicles. Each fascicle supplies a different portion of the left ventricle. Patients who develop disease in only one fascicle of the left bundle are said to have a hemiblock. Patients may exhibit hemiblock or LBBB, a total loss of conduction in the left main branch bundle. Blocks in conduction are recognized by evaluation of select lead patterns on the ECG. Table 2 summarizes the characteristic ECG changes associated with conduction blocks in the bundle branches.


Impulses leaving the bundle branches on either side of the heart travel over Purkinje fibers to the endocardial or innermost surface of the heart. Impulses delivered to the endocardium are conducted through the myocardium and epicardium until all cells of the structure depolarize. This activity is transcribed by the ECC as a “QRS.” The heart contracts and ejects blood in response to the electrical depolarization. When the impulse is rapidly conducted through the ventricles, a QRS of normal duration is transcribed. If the bundle branches are blocked or conduction originates outside of the normal ventricular conduction fibers, the slower depolarization over alternative pathways results in a wide QRS waveform. The duration or width of the QRS reflects the amount of time that it took the impulse to travel through the myocardium.

Waveforms and Intervals

Waveforms are seen on the ECG when differences in electrical potential are present. As the sinus impulse travels through the atrial and ventricular cells, the depolarization and repolarization of the myocardial cells create characteristic waveforms. The first waveform evaluated is the P wave of atrial depolarization. The PR segment represents the bridge between atrial and ventricular activity, and occurs as impulse conduction is delayed in the maze structure of the AV node. As the impulse enters the bundle of His, bundle branches, and Purkinje fibers, the electrocardiograph records the QRS of ventricular electrical activity. Mechanical events follow electrical events, and the relatively flat or isoelectric ST segment that follows the QRS correlates with an electrical plateau as the heart empties. Electrical recovery of the ventricles corresponds to the T wave of an ECG. In addition to the usual waveforms, a small positive wave may follow the T wave and is designated the U wave of a complex.

ECG waveforms are recorded graphically, and the grid pattern behind the printed waveform provides a method for measuring the height or amplitude, duration or width, and rate of electrical activity. Nursing staff use the known duration and amplitude of the printed grid to measure selected waveforms.

The grid is made up of small squares that are divided by heavier lines into blocks of 25 squares. Each larger square is five blocks long and five blocks high. Time or duration of the waveform is measured on the horizontal axis of the grid. Each tiny square of the grid equates with 40 milliseconds or 0.4 seconds of time. Each larger block of the grid is equal to 200 milliseconds or 0.20 seconds. Amplitude is measured on the vertical axis. Each tiny square is 1 mm in height and equal electrically to 0.1 millivolt (mV). Each larger block is 5 mm in height. Two larger blocks, 10 mm, equates with 1.0 mV and is considered the standard height against which electrical output can be evaluated. ECG recorders compare patient waveforms against that known standard in evaluating patients for normal amplitude. Figure 1 illustrates the grid used for ECG recording and evaluation.


Delays in conduction due to disease or medications can cause the waveforms to increase in duration. Digoxin is given to reduce the rate of conduction of rapid atrial impulses by the AV node and changes in the PR interval may be noted. Some antiarrhythmic therapies may decrease intraventricular conduction and result in widening of the QRS waveform. Bundle branch block conduction or ectopic beats that do not use the normal pathways may increase the duration of a waveform. Each waveform has a given duration for normal conduction. These standards are used to evaluate normally of measured complexes.

The amplitude or height of the waveform can be influenced by disease states or patient characteristics. Patients with prior myocardial infarction have lost a portion of the normal electrically active tissue. If scar tissue is present, the electrical waveform will be reduced in amplitude. Patients with hypertrophy have an increase in tissue mass, and electrical complexes are increased in height. The amount of tissue between the electrode and the heart, the origin of the electrical activity, also influences amplitude. Aesthetically thin patients may have an increase in amplitude and patients with morbid obesity may have smaller complexes as their respective chest wall sizes influence the distance between the heart, the source of electrical activity, and the electrode on the outer surface of the chest wall that senses electrical activity. The waveforms noted and characteristics that influence the normal appearance of waveforms are included in Table 3.

Table 3. Waveforms and Intervals

Waveform Characteristics

P waves * In adults the normal P wave is

[is less than]0.12 seconds in

duration and

less than 2.5 mm in amplitude. P

waves are measured from the

point that they leave the isoelectric

line to the point where they return to

the isoelectric line. P waves are

usually rounded and symmetrical

in appearance.

PR interval * The PR interval includes the P

wave and the flat segment that

bridges the P wave to the QRS

of ventricular depolarization.

* Normal adult PR duration is 0.12

to 0.20 seconds.

* PR interval is measured

from the beginning of

the P wave to the point where the

QRS leaves the isoelectric line.

QRS * The QRS contains the Q, R, and S

waves of ventricular depolarization.

* Normal adult QRS duration is 0.06

to 0.10 seconds.

Normal Q wave * A normal Q wave is [is less than] 0.04

seconds in duration and

[is less than] 25% of

the amplitude of the QRS.

* Q waves may or may not be seen.

* Q waves are only seen if the

waveform leaves the isoelectric PR

segment in a negative direction.

Abnormal Q wave * An abnormal Q wave is

[is greater than] 0.04

seconds in duration and is

[is greater than] 25% of

the amplitude of the QRS.

R wave * An R wave is the first positive

deflection of the QRS. Patients may

have a more than one positive

deflection for a single beat. The

second positive deflection is

considered an R’ (prime).

S wave * S waves are negative waves that

follow R waves.

* S waves may or may not be present.

* S waves end when the ST segment begins.

ST segment * The ST segment follows the S wave

and bridges the QRS to the T wave.

* The duration of the ST is not

measured, but the position of the

ST is important to clinical states.

T wave * Normal T waves are asymmetric

in appearance.

* Abnormal T waves are symmetric

and arrowhead in appearance.

* If a QRS is abnormal

(depolarization), the T

wave will be abnormal


* Abnormal T waves

after a normal QRS are

associated with ischemia.

U wave * U waves are small positive

deflections that may follow T


QT interval * Measured from the beginning of the

QRS to the end of the T wave.

* Normal QT range is 0.32 to 0.40

seconds or 320 to 400 milliseconds.

* QT varies with rate. The slower the

rate of depolarization, the slower the

rate of repolarization.

* The faster the rate of depolarization,

the faster the rate of repolarization.

Waveform Clinical Factors

P waves * Represents atrial depolarization.

* Atrial repolarization is not normally seen

as the depolarization of the larger

ventricular muscle mass masks atrial


* P wave size and shape will be altered by

clinical conditions that cause changes in

atrial size.

* Pulmonary hypertension that increases

the work of the right atria or mitral

stenosis that increases the work of the

left atria are examples of disease that

increase the size and alter the shape of

P waves.

PR interval * The PR interval represents that

depolarization of the atria and the delay of

the impulse in the maze of the AV node.

* Drug therapies that decrease the velocity

of AV node conduction can cause

prolongation of this interval.

* Patients with ischemic coronary

artery disease (CAD)

may have slowed conduction at the AV

node and a lengthening of the PR


QRS * Impulses travel through the bundle of His,

the bundle branches, and the Purkinje

fibers make up the QRS.

* A QRS [is greater than]0.10 to 0.11 is seen

in hemiblocks of conduction

or hypertrophy.

* A QRS [is greater than]0.12 in duration is

associated with bundle branch blocks,

ectopic beats from the ventricles,

hyperkalemia, or some antiarrhythmic


* A QRS that is wide but does not

follow a specific bundle branch block

pattern is termed an intraventricular

conduction delay (IVCD).

Normal Q wave * Normal Q waves are seen in

selected leads as a part of normal

impulse conduction.

Abnormal Q wave * Abnormal Q waves are seen in necrosis

of myocardial tissue as in acute

myocardial infarction.

* Q waves take hours to develop

in an acute injury. New

Q waves are always significant

regardless of diagnostic size.

R wave * Size of the R wave varies as the amount

of cardiac muscle mass increases or


* The distance between the

electrode and the heart muscle alters

the size of waveforms.

* R wave size is influenced by

the lead selected for


S wave * In normal conduction, the S wave ends

with a return to the isoelectric line.

* S waves are a portion of the QRS and must

be included in measurement when

determining for normal or abnormal


ST segment * The ST segment corresponds

to the plateau phase of

cardiac conduction.

* In this phase, the heart

has depolarized but is not

actively repolarizing.

* In the plateau phase the heart

is contracting to provide cardiac


* Because the heart is

electrically in a relative silence,

the ST segment should be seen as


* When the ST segment is

depressed below or elevated

above the isoelectric line it

correlates with abnormal

electrical rates of myocardial

ischemic and injured tissue.

T wave * T waves represent recovery or

repolarization of the ventricles.

* Abnormal T waves following a

normal QRS should be

evaluated clinically

for the etiology

* Abnormal T waves following

an abnormal QRS are an

electrical phenomenon.

* Abnormal T waves following

an abnormal QRS may mimic or

mask cardiac disorders and

require clinical evaluation

when symptoms of cardiac disease

are noted.

U wave * The significance of a U

wave is not determined.

* Large U waves are associated

with hypokalemia and may

fuse with T waves and alter

the T wave shape.

QT interval * QT may be clinically

corrected to correlate

with the patient rate

that is observed.

* Any QT that is greater than

0.50 seconds or 500 milliseconds

increases the risk of lethal rhythms.

* Large U waves make QT

appear prolonged as they

fuse with and obscure the

end of the T wave.

* QT may be difficult to

measure accurately in all leads

or in all rhythms.

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Delma A. Scrima, MSN, RN, is an Instructor, Education Department, Forbes Regional Hospital, Monroeville, PA.

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