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Have you ever had trouble identifying a rhythm or just wished you could recognize an EKG quickly and easily? After completing this course you will be able to rapidly identify most rhythms.
When we were initially trained in school to identify rhythms, we had to memorize what the rhythm
looked like to identify it. But the trick is to understand what is happening to the heart, more specifically the Electrophysiology of the heart. It is important to understand what's going on with the heart to interpret any rhythm. Understanding is the key to knowledge. Today we are going to learn how to understand and read EKG's. It's simple and easy. You just have to follow the 5 basic steps of rhythm recognition. If you apply these steps you will be able to identify most rhythms with no tools or calipers, just your eyes and head.
The electrocardiogram (EKG) will be our main area of study today. We will cover several topics in this course including cardiac anatomy and physiology, electrodes, lead placement, measuring heart rates, and identifying EKG wave forms.
Note: Although we freely use the term EKG as an abbreviation for electrocardiogram, the abbreviation ECG is the proper term but is easily confused with electroencephalograph (EEC).
Anatomy and Physiology
The heart is a four chambered structure made up of two receiving chambers
and two pumping chambers called ventricles. The right atrium receives oxygen poor
blood returning from the body through the superior and inferior vena cava. The right
ventricle pushes the oxygen poor blood to the lungs through the pulmonary arteries.
The left atrium receives oxygen rich blood returning from the lungs through pulmonary veins.
The left ventricle pushes the oxygen rich blood out through the aorta, which directs the
blood to all parts of the body. The right and left atria are separated by the
interatrial septum while the right and left ventricles are separated by the interventricular septum.
When blood flows through the heart it follows a unidirectional pattern. It
first enters both atria
and then fills both ventricles before leaving the heart. In order to prevent backflow
against this pattern there are four valves in the heart that serve this function.
Found between the atria and ventricles are two atrioventricular (A-V) valves
that prevent blood from reentering the atria. The valve that guards the right
atrium is called the tricuspid valve while the valve guarding the left atrium
is called the bicuspid or mitral valve.
The two remaining valves are called semilunar valves. The valve located where
pulmonary trunk meets the right ventricle is called the pulmonary semilunar valve.
The valve found where the aorta and left ventricle meet is called the aortic semilunar
valve. Both semilunar valves prevent backflow of blood into the ventricles.
The heart is a specialized structure, which is made of muscle that has unique
The cell membranes of myocardial cells form very close connections to each other.
These connections are called intercalated disks and allow groups of muscle
cells to function as one. This unique contractile ability of myocardium is known
as a syncytium. The muscle cells that make up the atria and ventricles act as two separate
syncytia, therefore contracting as two single units.
Cardiac muscle has the ability to adapt to the amount of blood being
delivered to it. There is
a direct proportion between the amount of blood returning to the heart and the force of
cardiac muscle contraction. The more blood returning through the veins, the stronger
the muscular contraction ejecting blood out of the heart into the arteries. This occurs
due to the heart muscle responding to a stretch in the chamber walls as a result of an
increased amount of blood volume entering the heart. The ability of the heart to be able
to equalize the amount of blood entering and exiting it is called Frank-Starlings law of the heart.
Compared to skeletal muscle, heart muscle cells have a longer rest or
This allows the myocardium to relax after each contraction preventing a tetanic contraction
of the heart. It also gives the heart chambers time to fill with blood before the next
Unlike skeletal muscle, which needs nerve innervation for stimulation,
needs no outside stimulus. This is what is known as automaticity. Heart muscle also
possesses inherent rhythm, which means it will contract at a regular rate.
The conduction system of the heart explains how heart muscle has
and is able to contract without the help of outside nervous or hormonal innervation.
It is made up of specialized cardiac cells that initiate and guide myocardial
contraction. The conduction system consists of the sinoatrial node (S-A node),
atrioventricular node (A-V node), atrioventricular bundle (A-V bundle or A-V bundle of His),
Purkinje fibers and bundle branches.
The S-A node is located in the posterior wall of the right atrium. It
sets off impulses
that trigger atrial contraction. It discharges impulses quicker than any other part of
the heart and establishes the rate and rhythm for the entire
heart. Because of this it is more commonly known as the pacemaker.
Note: A node is the same thing as a pacer or pacemaker.
The contracted atrial cells then send the impulse to the A-V node,
which is located in the
atrial wall near the interatrial septum. Once the A-V node picks up the signal, the speed
of impulse transmission is slowed down to allow the atria
time to complete contraction before ventricular contraction occurs.
From the A-V node the impulse then travels to the A-V bundle (bundle of
which is made up of special fibers called Purkinje fibers. The A-V bundle begins
at the right side of the interatrial septum and runs down to the beginning of the
interventricular septum. It then branches into right and left bundle branches
that run down the length of the interventricular septum. The bundle branches further
divide into Purkinje fibers that cover the inner surface of the ventricles. The impulses
relayed from the Purkinje fibers initiates ventricular contraction.
The EKG is a recording of the electrical impulses produced by the
The body acts as a giant conductor of electrical currents. Any two points on the body may be
connected by electrical leads (electrodes) to register an EKG or to monitor the rhythm of the heart.
The tracing recorded from the electrical activity of the heart forms a series of waves and
complexes that have been arbitrarily labeled (in alphabetical order) the P, Q, R, S, T waves,
and sometimes the U wave. The waves or deflections are separated in most patients by regularly occurring intervals.
Depolarization (electrical firing) of the atria produces the P wave.
Depolarization of the ventricles produces the QRS complex
Repolarization (electrical recharging) of the ventricles causes the T wave. The significance of the U wave is uncertain, but it may be
due to repolarization of the Purkinje system.
The key to rhythm interpretation is the analysis of the form and
interrelations of the P wave, the PR interval,
and the QRS complex. The EKG should be analyzed with respect to its rate, its rhythm, the site of the
dominant pacemaker, and the configuration of the P and QRS waves.
The P wave is generated by the Sinoatrial(SA) Node or sinus node. Once the SA node fires the electricity goes though both atria and a P wave is then
present on the monitor. That's why we call it a sinus rhythm. OK let me put it like this; if the rhythm has one P wave for every QRS complex
and is under 150 BPM, then we call it a sinus rhythm because it is generated by the Sinus node (SA node).
If the rhythm has more than one P wave for each QRS we call it an Atrial rhythm. If for some reason the sinus (SA) node fails to act as the normal cardiac pacemaker, other atrial foci may take over, and the P wave may have a different configuration. Alternatively, a secondary pacemaker (eg, the AV junction)
may provide an "escape rhythm."
PR Interval: When conduction through the atria, the AV node, or bundle
of His is slowed, the PR interval
becomes longer. Changes in conduction through the AV node are the most common cause of changes in the PR interval.
The P to R interval is important in identification of heart blocks. We'll cover some of that later on.
The PR interval extends from the beginning of the P wave (the beginning of atrial depolarization) to the onset of the
QRS complex (the beginning of ventricular depolarization). It should not exceed 0.20 seconds as measured on
EKG graph paper, where each small square represents 0.04 seconds.
QRS Complex. The QRS complex represents the
depolarization of the ventricles. The upper limit of normal duration of the QRS complex is less than 0.12 seconds. A QRS
complex duration of less than 0.12 seconds means that the impulse was initiated from the AV node or above (supraventricular).
A wide QRS complex (more than 0.12 seconds) may signify conduction that either arises from the ventricle or comes from
supraventricular tissue. Prolonged conduction through the ventricles produces a widened QRS complex.
If there is a delay or interruption in conduction in either bundle branch, the QRS will widen in a
manner typical for either right or left bundle branch block. An ectopic focus that initiates an impulse from the
ventricle also can alter the shape of the QRS. When an ectopic beat arises above the bundle branches, the
ventricles are activated in a normal fashion and the QRS complex will remain the same, assuming that there is no
conduction delay in either bundle branch. If the depolarization occurs below the bundle branches, the QRS complex
will be widened and notched or slurred because a different sequence of conduction will ensue.
A wide QRS complex with no P waves is usually a ventricular rhythm.
There are many types of cardiac monitoring systems, but they generally consist of a monitor screen
(cathode ray oscilloscope) on which the EKG is displayed and a write-out system that directly transcribes the rhythm strip onto paper. The write-out may be automatic or controlled by a switch, and a ratemeter may be set to write out a rhythm strip if the rate goes below a preset figure (eg, 50 beats per minute) or above a certain rate (eg, 120 beats per minute) for at least 6 seconds, and sometimes for as long as 30 seconds.
A ratemeter triggered by the QRS complex of the EKG is usually part of the system. Lights and beepers may provide visual and audible signals of the heart rate.
Monitor leads or electrodes may be attached to the patient's chest or extremities. The chest leads must be placed to show clearly the waves and complexes of the EKG strip.
Conventional locations for the chest electrodes are illustrated below. The arrow indicates the direction of polarity from negative to positive. In lead I the positive electrode is below the left clavicle and the negative below the right.
In lead II the positive
electrode is below the left pectoral muscle and the negative below the right clavicle .
Lead III is displayed by attaching the positive electrode beneath
the left pectoral muscle and the negative below the left clavicle. Although these simulate or approximate the I, II, and III leads
of the standard EKG, they are not identical.
Another popular monitoring lead is the MCL1 lead. To connect this lead, the negative electrode is placed near the left shoulder,
usually under the outer third of the left clavicle, and the positive is placed to the right of the sternum in the fourth intercostal space.
The ground electrode in all four leads can usually be placed almost anywhere but is commonly located below the right pectoral muscle or under the left clavicle. The electrodes are often color-coded for ease of application, lessening confusion in location.
The negative lead is usually white, the positive lead is red, and the ground lead is black, green, or brown. The popular phrase "white-to-right, red-to-ribs, and black left over" helps to recall where the leads for lead II should be placed.
Remember the following points when monitoring patients:
1. A prominent P wave should be displayed if organized atrial activity is present. Leads that show the P wave clearly should be chosen.
2. The QRS amplitude should be sufficient to properly trigger the ratemeter.
3. The patient's pericardium must be kept exposed so that defibrillation paddles can be readily used if necessary.
4. Monitoring is for rhythm interpretation only. One should not try to read ST abnormalities or attempt more elaborate EKG interpretation.
5. Artifacts should be noted: a straight line will show if the electrode is loose, or a bizarre, wavy baseline resembling ventricular fibrillation (VF) may appear if an electrode is loose or the patient moves. Sixty-cycle interference also may be present.
Always remember that any EKG findings should be correlated with clinical observations of the patient.
Different electrode placements may be used for telemetry or other special purposes. The positive electrode should be to the left or below the negative electrode. Otherwise the deflections will all be reversed and the rhythm strips can be confusing.
How To Identify an EKG
Alright, lets get down to it. In order to identify rhythms, we
need to follow the 5 basic steps
of rhythm recognition.
1. Rate (Calculate the heart rate)
2. Rhythm (Measure the regularity or rhythm of the R waves)
3. P-wave (Examine the P-wave)
4. P to R interval ( Measure the P to R interval)
5. QRS (Measure the duration of the QRS complex)
Step 1 - Rate
Ok, first thing is rate. In order to identify a rhythm we need to know the heart rate. The patient's heart rate reveals a great deal of information. If the rate is slow (under 60 beats per minute), we call it bradycardia.
If the heart rate is fast (over 100 beats per minute) then it is called tachy or tachycardia.
There are several ways to determine a heart rate.
You can actually take a radial pulse.
The second way to obtain a rate is to look at a strip from the monitor. We call this strip of paper graph paper.
EKG paper is a grid where time is measured along the horizontal axis.
Each small square is 1 mm in length and represents 0.04 seconds.
Each larger square is 5 mm in length and represents 0.2 seconds.
Voltage is measured along the vertical axis.10 mm is equal to 1mV in voltage.
The diagram below illustrates the configuration of EKG graph paper and where to measure the components of the EKG wave form.
Heart rate can be easily calculated from the EKG strip:
The graph paper that the EKG records on is standardized to run at 25mm/second, and is marked at 1 second intervals on the top and bottom. The horizontal axis correlates the length of each electrical event with its duration in time. Each small block (defined by lighter lines) on the horizontal axis represents 0.04 seconds. Five small blocks (shown by heavy lines) is a large block, and represents 0.20 seconds. Duration of a waveform, segment, or interval is determined by counting the blocks from the beginning to the end of the wave, segment, or interval.
When the rhythm is regular, the heart rate is 300 divided by the number of large squares between the QRS complexes. For example, if there are 4 large squares between regular QRS complexes, the heart rate is 75 (300/4=75).
Another sequence method gives an approximate heart rate
through simple waveform observation.
To calculate the atrial rate, find a P wave that peaks on a heavy black line. Count off the following heavy black lines as 300, 150, 100, 75, 60, and 50, respectively until you reach the next heavy black line on which the next P wave peaks. The number assigned to this line is the estimated atrial rate. Calculate the ventricular rate by repeating the above calculation, using the R wave instead of the P wave.
The second and easier method can be used with a regular or irregular rhythm to estimate the rate.
Count the number of R waves in a 6 second strip and multiply by 10.
For example, if there are 7 R waves in a 6 second strip, the heart rate is 70 (7x10=70).
Lets give it a try. Look at the rhythm above and count all the R waves.
There are 8 R waves, so our patient's rate is 8 X 10 or 80.
Then there's the1500 Method. You can only use this method if the cardiac rhythm is regular. To calculate the atrial rate, identify two consecutive P waves. Select identical points in each wave. Count the number of small blocks between these two points. Divide 1500 by the number of small blocks counted. The resulting number is the atrial rate. Calculate the ventricular rate by repeating the above calculation, but count the number of small blocks between the R waves. Another way to calculate your patient's heart rate is to look in the upper right hand corner of the monitor, if they're on a monitor. The heart rate should be displayed there. So remember step 1 is the heart rate.
Step 2 - Rhythm
Step 2 is rhythm. Is the rhythm regular or is it irregular? Very few rhythms are irregular. For example, atrial fibrillation is always irregular. So if your rhythm is regular it's not a-fib.
|This is a regular rhythm.||This is an irregular rhythm.|
Step 3 - P Wave
Step 3 is the P wave. Does the rhythm have a P wave? If it does, and you know
that the P wave is generated by the SA node, then we would usually call it a
sinus rhythm since it comes from the Sinus node or SA node. However, it's a
sinus rhythm only if there's one P wave for every QRS, and the rate is under
150 bpm. This will be come clearer in the next chapter when we do some
The P wave represents atrial depolarization - the time necessary for an electrical impulse from the sinoatrial (SA) node to spread throughout the atrial musculature.
Look at the rhythm and ask yourself?
Are P waves present?
Do P waves have a normal shape - usually upright and rounded on the rhythm strip?
Are all the P waves similar in size and shape?
Do all the P waves point in the same direction?
Do you see a 1:1 relationship between P waves and QRS complexes?
Is each P wave the same distance from it's QRS complex?
Step 4 - P to R Interval
The P to R interval represents the time it takes an impulse to travel from the atria through the AV node, bundle of His, and bundle branches to the Purkinje's fibers.
Location: The P to R interval extends from the beginning of the P wave to the beginning of the QRS complex.
Duration: 0.12 to 0.20 seconds.
The P to R interval is important in order to determine if there's a heart block or conduction system disease.
Now the P to R interval should take about .20 seconds or one box on the graph paper.
I'll give you examples of the P to R interval in a few chapters from now.
Look at the P to R interval and ask yourself?
What is the duration of the P to R interval? (Normal 0.12 to 0.20 seconds)
Is the P to R interval constant?
Step 5 - QRS Complex
The QRS complex represents ventricular depolarization. The QRS complex consists of 3 waves: the Q wave, the R wave, and the S wave. The Q wave is always located at the beginning of the QRS complex. It may or may not always be present. The R wave is always the first positive deflection.
The S wave, the negative deflection, follows the R wave.
Location: Follows the P-R interval.
Duration: No longer than 0.10 seconds.
Look at the QRS and ask yourself?
Are all the complexes the same size and shape?
What is the duration of the QRS complex? (Normal duration is no more than 0.10 seconds; if greater, it indicates a Bundle Branch Block (BBB))
Are all the QRS complexes the same distance from the T waves that follow them?
Do all the QRS complexes point in the same direction?
Are any QRS complexes present that appear different from the other QRS complexes on the strip? If so, measure and describe each one individually.
Note: The S-T segment represents the end of the ventricular depolarization and the beginning of ventricular repolarization. The Q-T interval represents the time necessary for ventricular depolarization and repolarization. The T wave represents the repolarization of the ventricles. On rare occasions, a U wave can be seen following the T wave. The U wave reflects the repolarization of the His-Purkinje's fibers.
In the next chapter we'll put these 5 steps together and see how it works.
This is a 6 second strip.
The first step is calculating the heart rate. Count the R's and multiply by 10.
There are 8 R waves, so the rate is 80. Is 80 beats per minute fast (tachy), slow (brady), or
or normal. ( 60 to 99bpm is normal for most people)
Step 1 rate is normal.
Step 2, is this a regular or irregular rhythm? Look at the rhythm. Are the R
to R intervals regular?
Does this rhythm seem to have a regular beat? It does. If a rhythm is regular it's not a-fib. Step 2 rhythm is regular.
Step 3, are P waves present? Yes, look up there! You should easily be
able to see that P waves
precede each QRS complex. If there's a P wave present and only one P wave for each QRS complex, and the rate is under 150 then it's a sinus rhythm. We call it a sinus rhythm because the Sinus node or SA node generates to P wave.
Note: In a Sinus rhythm the P wave is upright.
Step 3 it's a sinus rhythm.
Step 4 is the P to R interval. A normal P to R interval is quick, less than
.20 seconds, or about one big box on the graph paper.
If the P to R interval is delayed or longer than .20 seconds (one big box on the graph paper) then there may be conductive system disease or what we call a heart block. We'll do the blocks later.
Step 4 is the P to R interval normal (within .20 seconds) or is there a delay or a heart block? It looks normal to me.
Step 5 is the QRS complex. Is it there and if so, is it wide or narrow? The
QRS complex indicates ventricular depolarization, or contraction of the
ventricles. Analyze the QRS complex. Are all the complexes the same
size and shape? What is the duration of the QRS complex?
(Normal duration is no more than 0.10 seconds or about half a box on the graph paper; if greater, it indicates a Bundle Branch Block (BBB).)
Are all the QRS complexes the same distance from the T waves that follow them?
Do all the QRS complexes point in the same direction?
Are any QRS complexes present that appear different from the other QRS complexes on the strip? If so, measure and describe each one individually.
Step 5 the QRS looks ok to me.
Now lets put it all together and see what we get!
Step1 rate 80 bpm, Normal.
Step 2 rhythm, regular.
Step 3 P wave, the P wave is there so its a sinus rhythm.
Step 4 P to R interval is normal, no blocks.
Step 5 The QRS complex is within normal limits (WNL).
So, from the steps above we get a Normal (rate), Sinus (there's
a P wave), Rhythm.
Very good, the above rhythm is Normal Sinus Rhythm or NSR.
Normal Sinus Rhythm
NSR is the normal rhythm produced when the cardiac electrical impulse is initiated by the SA node.
Rate: 60 - 99.
P waves: Upright and normal.
P to R Interval: WNL .12 - .20 seconds, less than one big box on the graph paper.
QRS Complexes: WNL .10 seconds, about half a box on the graph paper.
Significance: We should all be this lucky.
OK, let's try another one.
1.What's the rate? Count the R waves. The rate is 120. There are 12 R waves and we multiply 12
times 10 and the answer is 120bpm. Is that fast, slow, or normal. It's fast so we call it a tachy rhythm
2. Is it regular?
3. Are there P waves?
Yes, there is one P wave for every QRS and they are upright. P waves are from the SA node, so it's a sinus rhythm.
4. If there are P waves present, then what is the P to R interval?
The P to R is WNL less then .20 seconds or one box on the graph paper. It's not a block.
5. Examine the QRS complex, Is it wide or narrow or normal?
It looks normal.
What is this rhythm?
It is Sinus( P wave) Tachycardia( rate over 100 tachy).
Sinus tachycardia is characterized by an increase in the rate of discharge of the sinus node. Perhaps secondary to multiple factors
(eg, exercise, fever, anxiety, hypovolemia), it is a physiological response to a demand for a higher cardiac output.
Never "treat" sinus tachycardia; treat the cause of sinus tachycardia.
Rate: Greater than 100 bpm.
P wave: Upright and normal (Sinus Rhythm).
P to R interval: WNL .12 - .20 seconds, one box on the graph paper.
QRS Complex: WNL <.10 seconds, half a box on the graph paper.
Ok this looks easy!
1. Rate is 50 bpm which is slow so we'll call it brady or bradycardia.
2. Rhythm is regular, that's good.
3. P waves are upright and normal (sinus rhythm).
4. P to R interval is WNL.
5. QRS is WNL.
So we have Sinus (P wave) Bradycardia (under 60 bpm).
Sinus Bradycardia is characterized by a decrease in the rate of atrial depolarization due to slowing
of the sinus node. It may be secondary to sinus node disease, increased parasympathetic tone, or
drug effects (eg, digitalis, propranolol, or verapamil).
Rate: Sinus bradycardia is a sinus rhythm of less than 60 bpm.
P wave: Normal in size and configuration. The P wave precedes each QRS complex.
P to R interval: WNL.
This looks different.
Start with the 5 basic steps.
What is the rate? 190bpm (Count the R waves). This is tachy or
The rhythm is regular. Are there P waves present? Don't see any. Just looks like a lot of QRS complexes. If there is no P wave, then it can't be a sinus rhythm. And if there are no P waves, then forget about the P to R interval. But there are a lot of QRS complexes. Where do they come from? The QRS complex comes from the AV Node.
So since the QRS complex comes from the Atrio Ventricular node then we'll call it a Ventricular rhythm. We call it a ventricular rhythm because it's generated by the atrio VENTRICULAR node (AV Node). The QRS complex is wider than normal, that also tells you that its a ventricular rhythm.
Rate: Greater than 100 beats per minute and usually not faster than 220 beats per minute
Rhythm: Usually regular but may be irregular.
P waves: In rapid VT the P waves are usually not recognizable. At slower ventricular rates, P waves may be recognized and may represent normal atrial depolarization from the sinus node at a rate slower than VT, but the electrical activities do not affect one another.
QRS, ST segment, T wave: The PVC is premature; ie, it must occur before the next expected sinus beat unless atrial fibrillation is present since preactivity cannot be assessed. The width of the QRS is 0.12 second or greater. The QRS morphology is often bizarre, with notching. The ST segment and T wave are usually opposite in polarity to the QRS. When multiformed (or multifocal),
the coupling interval and morphology of the QRS vary.
Ventricular Tachycardia (VT) is defined as three or more beats of ventricular origin in succession at a rate greater than 100 beats per minute. There are no normal-looking QRS complexes. The rhythm is usually regular, but on occasion it may be modestly irregular. This arrhythmia may be either well tolerated or associated with grave, life-threatening hemodynamic compromise. The hemodynamic consequences of VT depend largely on the presence or absence of myocardial dysfunction (such as might result from ischemia or infarction) and on the rate of VT. Atrioventricular dissociation usually is present. This means that the sinus node is depolarizing the atria in a normal manner at a rate either equal to or slower than the ventricular rate. Thus sinus P waves sometimes can be recognized between QRS complexes. They bear no fixed relation to the QRS complexes unless the atrial and ventricular rates happen to be equal. Conduction from atria to ventricles is usually prevented because the AV node or ventricular conduction system is refractory due to ventricular depolarizations. Sometimes retrograde conduction from ventricles to atria occurs. In this instance there will be a relation between the QRS complex and the retrograde P wave.
Occasionally an atrial impulse arrives when the AV node and His-Purkinje system are not refractory and AV conduction can occur. This results in a capture beat, in which ventricular conduction occurs over the normal pathways, resulting in a normal-appearing (narrow) QRS complex. A capture beat occurs at a shorter RR interval than the RR interval of the VT. AV conduction also may occur simultaneously with depolarization of the ventricular focus. In this instance the ventricle will be depolarized in part over the normal pathway and in part from the ventricular focus. The resulting QRS complex will be intermediate in morphology between a normal QRS and a QRS of ventricular origin. In this instance the RR interval will not change. This is called a fusion beat. Ventricular tachycardia may be monomorphic (all QRSs with the same shape) or polymorphic (varying QRS shapes during the tachycardia).
Treatment: Ventricular tachycardia when sustained but hemodynamically stable is initially treated with lidocaine, procainamide, or bretylium. The tachycardia algorithm presents the recommended pharmacologic agents and sequence of interventions. Ventricular tachycardia that is hemodynamically unstable should be treated the same as VF.
Occasionally a narrow QRS complex may occur with a slightly shorter RR interval (capture beat), or a QRS complex may be seen with morphological features intermediate between a beat of ventricular origin and one of supraventricular origin but with a constant RR interval (fusion beat).
Rate: Rate is
very rapid and usually too disorganized to count.
Ventricular Fibrillation (VF)
Ventricular fibrillation is the single most important rhythm for the health care provider to recognize. It is a rhythm in which multiple areas within the ventricles display marked variation in depolarization and repolarization. Since there is no organized ventricular depolarization, the ventricles do not contract as a unit. When observed directly, the ventricular myocardium appears to be quivering.
There is no cardiac output. This is the most common mechanism of cardiac
arrest resulting from myocardial ischemia or infarction. The terms coarse
and fine have been used to describe the amplitude of the waveforms in VF.
Coarse VF usually indicates the recent onset of VF, which can be readily
corrected by prompt defibrillation. The presence of fine VF that approaches
asystole often means there has been a considerable delay since collapse, and
successful resuscitation is more difficult.
Treatment: Initial treatment is always defibrillation. Only defibrillation provides definitive therapy. The exact benefit of antifibrillatory agents administered to persistent VF independent of defibrillation is unknown. Because their contribution (if any) remains doubtful, never delay defibrillation while waiting for pharmacologic agents to have an effect.
P wave: None
P to R interval: None
QRS complex: None
Asystole represents the total absence of electrical activity. Since depolarization does not occur, there is no ventricular contraction. This may occur as a primary event in cardiac arrest, or it may follow VF or pulseless electrical activity.
Asystole can occur also in patients with complete heart block in whom there is no escape pacemaker. VF may masquerade as asystole; it is best always to check two leads perpendicular to each other to make sure that asystole is not VF. In addition, the distinction between very fine VF and asystole without any escape beats (agonal QRS complexes) may be very difficult. If it might be VF, it should be treated, like VF, with defibrillation. However, shocks to asystole are potentially harmful. Sometimes, however, P waves may occur, or rare, erratically occurring ventricular escape beats (agonal beats) may be seen. Patients with these beats will not have a pulse and must be treated immediately if they are to be saved. If no organized QRS complex is seen and the patient has a pulse, then the EKG is improperly connected, turned off, or improperly calibrated.
Treatment: Use CPR, external pacer, epinephrine, atropine and actively search for reversible causes.
atrial rate as a rule cannot be counted. In the untreated patient, the
ventricular rate is usually 160 to 180 beats per minute.
Atrial fibrillation may result from multiple areas of reentry within the atria or from multiple ectopic foci. Atrial fibrillation may be associated with sick sinus syndrome, hypoxia, increased atrial pressure, pericarditis, and many other conditions. In the setting of acute ischemic heart disease, increased left atrial pressure secondary to congestive heart failure is the most common cause. The atrial electrical activity is very rapid (approximately 400 to 700 per minute), but each electrical impulse results in the depolarization of only a small islet of atrial myocardium rather than the whole atrium.
As a result, there is no contraction of the atria as a whole. Since there is no uniform atrial depolarization, there is no P wave. The chaotic electrical activity does produce a deflection on the ECG, referred to as a fibrillatory wave. Fibrillatory waves vary in size and shape and are irregular in rhythm. Transmission of these multiple atrial impulses into the AV node is thought to occur at random, resulting in an irregular rhythm. Some impulses are conducted into but not through the AV node; ie, they are blocked within the AV node. This is a form of "concealed conduction" and is important since such nonconducted impulses contribute to the overall refractoriness of the AV node. For this reason the ventricular rate of atrial fibrillation is often slower (averaging 160 to 180 per minute) than that seen in atrial tachycardia or atrial flutter. Atrial fibrillation is usually the result of some underlying form of heart disease (usually with congestive heart failure) and may occur intermittently or as a chronic rhythm. It may, however, be seen in a paroxysmal form in which there is no other evidence of heart disease.
Treatment: Rate control is the initial treatment goal, using agents such as diltiazem, verapamil, ß blockers, or digoxin. Chemical cardioversion, usually after a period of anticoagulation, can then be attempted with procain-amide or quinidine. Electrical cardioversion is the third therapeutic option, after rate control and chemical cardioversion. Place a higher priority on electrical cardioversion in symptomatic patients if the atrial fibrillation is of new onset and is known to be of short duration, eg, 1 to 3 days.
If the patient with atrial fibrillation and a rapid ventricular response is in clinical distress, synchronized cardioversion is the treatment of choice. Hypotension induced by atrial fibrillation is usually seen only in patients with acute myocardial infarction or abnormalities of ventricular filling, eg, idiopathic hypertrophic subaortic stenosis or mitral stenosis. These patients should be immediately cardioverted. The vast majority of patients with atrial fibrillation will have ventricular rates of 120 to 200 beats per minute. If acute ischemic heart disease is present, cardioversion is recommended. Other asymptomatic patients, even those with a modest response (less than 120 beats per minute), can be treated conservatively by controlling their rate initially with digitalis, verapamil, or ß-adrenergic blocking agents. In the undigitalized patient, ß-adrenergic blocking agents and verapamil may not cause sufficient slowing and may lead to congestive heart failure.
Once the heart rate is controlled or if symptoms occur, a decision about cardioversion should be made. Success in cardioverting and preventing recurrence of atrial fibrillation depends on atrial size and the length of time the patient has been in atrial fibrillation. The larger the atrial size and the longer the patient has been in atrial fibrillation, the lower the likelihood of successful maintenance of sinus rhythm. Before cardioversion is attempted either electrically or pharmacologically with an agent such as quinidine or procainamide, anticoagulation should be considered. Patients with mitral stenosis, cardiomyopathy, and large atria are more likely to have thrombus in the atrium and are thus at higher risk for emboli and stroke. Anticoagulation must be considered.
Rate: Atrial usually 300 beats per minute, ranging between 220 and 350 beats per minute
If there are P waves but they occur rapidly with a characteristic "sawtooth" appearance, then the rhythm is atrial flutter.
This arrhythmia is the result of a reentry circuit within the atria . Atrial depolarization occurs in a caudad-to-cephalad direction and hence is best observed in leads II, III. It is often described as resembling a sawtooth or picket fence. Such a wave is called a flutter wave.
While it is possible to have 1:1 AV conduction, more commonly there is a physiological block at AV nodal level because the refractory period of the AV node results in 2:1 AV conduction or even higher grades of block.
Since the atrial rate is most commonly about 300 per minute, 2:1 AV block usually is present, and the ventricular rate is usually 150 per minute. The AV conduction ratio may be altered by AV nodal disease, increased vagal tone, and certain drugs (eg, digitalis, propranolol, verapamil) that will induce a higher degree of AV block (eg, 3:1, 4:1) or at times a variable block. Atrial flutter seldom occurs in the absence of organic heart disease. It is seen in association with mitral or tricuspid valvular heart disease, acute or chronic cor pulmonale, and coronary heart disease. It is rarely a manifestation of digitalis intoxication.
Treatment: If the patient is hypotensive, having ischemic pain, or in severe congestive heart failure, synchronized cardioversion is the treatment of choice. If the patient is only mildly symptomatic, pharmacologic therapy can be tried first. However, many experts recommend that cardioversion should always be the initial therapy. The ventricular rate can be slowed with diltiazem, verapamil, digitalis, or ß-blocking agents. Verapamil and ß blockers may exacerbate bradycardia and congestive heart failure. If digitalis is used to control the rate, care must be taken to avoid digitalis intoxication. Once the rate is controlled, the patient can be placed on a type I antiarrhythmic agent, such as quinidine or procainamide, to convert flutter. After a reasonable trial of pharmacologic conversion, the patient should be electrically cardioverted.
First-degree AV Block
First-degree AV block is simply a delay in passage of the impulse from atria to ventricles. This delay usually occurs at the level of the AV node but may be infranodal.
Remember that in the normal ECG every QRS complex is preceded by a P wave, and the time between the two forms is less than 0.20 second. Heart blocks are rhythms that are caused by altered conduction through the AV node. As conduction in the AV node slows, the interval between the P wave and the QRS complex lengthens. If slowing in the node becomes pronounced, some P waves will be blocked in the AV node. In the worst case no P waves will pass through the AV node to excite the ventricles.
The heart blocks are divided into three degrees. First-degree heart blocks are characterized by P to R intervals longer than 0.20 second and all of the P waves are followed by QRS complexes. Second-degree heart blocks are characterized by some P waves being blocked at the AV node. This results in some P waves occurring without following QRS complexes. Third-degree heart block is characterized by a complete dissociation between P waves and QRS complexes. A hint for separating the heart blocks into degrees is that first- and third-degree blocks usually have regular QRS rates.
Atrioventricular block is defined as a delay or interruption in conduction between atria and ventricles. It may be due to (1) lesions along the conduction pathway (eg, calcium, fibrosis, necrosis), (2) increases in the refractory period of a portion of the conduction pathway (such as may occur in the AV node when digitalis is administered), or (3) shortening of the supraventricular cycle length, ie, rapid atrial rates, with encroachment on the normal refractory period (as with atrial flutter, in which 2:1 AV block at the level of the AV node occurs because the normal AV node refractory period will not allow conduction at a rate of 300 beats per minute but will allow it at 150 beats per minute).
AV block may be classified in two ways:
1. According to the degree of block:
2. According to the site of block:
Each degree of block (first, second, third) may occur either at the level of
the AV node or below it. This distinction is not academic since pathogenesis,
treatment, and prognosis differ.
Treatment: Treatment for first-degree heart block is usually unnecessary when it occurs without symptoms.
Rate: The atrial rate is unaffected, but the ventricular rate will be
less than the atrial rate because of the nonconducted beats.
Rhythm: The atrial rhythm is usually regular. The ventricular rhythm is usually irregular with progressive shortening of the RR interval before the blocked impulse. The RR interval that brackets the nonconducted P wave is less than twice the normal cycle length.
P waves: The P waves will appear normal, and each P wave will be followed by a QRS complex except for the blocked P wave.
P to R interval: There is a progressive increase in PR interval until one P wave is blocked.
QRS complex: WNL.
In second-degree AV block, some impulses are conducted and others are blocked. This type of block is subdivided into two additional types.
This form of block almost always occurs at the level of the AV node (rarely at His bundle or bundle branch level) and is often due to increased parasympathetic tone or to drug effect (eg, digitalis, propranolol, or verapamil). It is usually transient and prognosis is good. Second-degree type I AV block is characterized by a progressive prolongation of the PR interval. Decreasing conduction velocity through the AV node occurs until an impulse is completely blocked. Usually only a single impulse is blocked, and the pattern is repeated.
The repetition of this pattern results in "group beating," eg, three conducted sinus beats with progressively lengthening PR intervals and a fourth sinus beat that is not followed by a QRS. Such a "group" is referred to as 4:3 conduction. Although the conduction ratio may remain constant, it is usual for it to change, eg, 4:3, 3:2, 2:1. The ventricular rhythm is irregular except in the presence of 2:1 block.
Treatment: Specific treatment is rarely needed unless severe signs and symptoms are present. Clinicians should place a high priority on identifying underlying causes.
Rate: The atrial rate is unaffected, but the ventricular rate will be
less than the atrial rate.
Rhythm: The atrial rhythm is usually regular, whereas the ventricular rhythm is most often irregular, with pauses corresponding to the nonconducted beats.
P waves: The P waves will appear normal, and each will be followed by a QRS except for the blocked P wave.
P to R interval: This interval may be normal or prolonged, but it will remain constant. There may be shortening of the PR interval after a pause.
QRS complex: The QRS will be normal when the block is at the bundle of His. However, the QRS will be widened with the features of bundle-branch block if the block is at the bundle branches.
This form of second-degree AV block occurs below the level of the AV node either at the bundle of His (uncommon) or the bundle branches (common). It is usually associated with an organic lesion in the conduction pathway, and unlike type I second-degree AV block, it is rarely the result of increased parasympathetic tone or drug effect. It is thus associated with a poorer prognosis, and complete heart block may develop. A hallmark of this type of second-degree AV block is that the PR interval does not lengthen before a dropped beat. More than one nonconducted beat may occur in succession. This type of block most often occurs at the level of the bundle branches.
For a dropped beat to occur, there must be complete block in one bundle
branch (ie, right or left bundle-branch block) with intermittent interruption in
conduction in the contralateral bundle as well. Thus, type II second-degree AV
block is often associated with a wide QRS complex.
When block occurs at the His bundle, the QRS may be narrow since ventricular conduction is not disturbed in beats that are not blocked. The rhythm may be irregular when block is intermittent or when the conduction ratio is variable. With a constant conduction ratio (eg, 2:1) the ventricular rhythm is regular
Rate: The atrial rate will be unaffected by third-degree AV block. The
ventricular rate will be slower than the atrial rate. With intranodal
third-degree AV block, the ventricular rate is usually 40 to 60 beats per
minute; with infranodal third-degree AV block, the ventricular rate is usually
less than 40 beats per minute.
Rhythm: The atrial rhythm is usually regular, although sinus arrhythmia may be present. The ventricular rhythm will be regular.
P waves: Normal.
P to R interval: Since the atria and ventricles are depolarized from different pacemakers, they are independent of each other, and the PR interval will vary.
QRS complex: Generally normal looking. When block occurs at the AV node or bundle of His, the QRS complex will appear normal. When block occurs at bundle branch level, the QRS complex will be widened.
Third-degree AV block indicates complete absence of conduction between atria and ventricles. The atrial rate is always equal to or faster than the ventricular rate in complete heart block. It may occur at the level of the AV node, the bundle of His, or the bundle branches. As in second-degree AV block, this distinction is not merely academic since pathogenesis, treatment, and prognosis may vary considerably, depending on the anatomic level of block. When third-degree AV block occurs at the AV node, a junctional escape pacemaker frequently will initiate ventricular depolarization. This is usually a stable pacemaker with a rate of 40 to 60 beats per minute. Since it is located above the bifurcation of the bundle of His, the sequence of ventricular depolarization usually is normal, resulting in a normal QRS. This type of third-degree AV block can result from increased parasympathetic tone associated with inferior infarction, from toxic drug effects (eg, digitalis, propranolol), or from damage to the AV node.
When third-degree AV block occurs at the infranodal level, it is most often due to block involving both bundle branches. This indicates the presence of extensive infranodal conduction system disease. When it results from coronary atherosclerosis, it is usually associated with extensive anterior myocardial infarction. It usually does not result from increases in parasympathetic tone or from drug effects. The only escape mechanism available is in the ventricle distal to the site of block. Such a ventricular escape pacemaker has an intrinsic rate that is slow, less than 40 beats per minute. Like any depolarization originating in a ventricle, the QRS complex will be wide. It is not a stable pacemaker, and episodes of ventricular asystole are common.
Treatment: The major interventions are atropine, transcutaneous pacing, catecholamine infusions (dopamine or epinephrine), and transvenous pacemaker. Isoproterenol is rarely indicated.
P waves: The sinus P wave is usually obscured by the QRS, ST segment, or T wave of the PVC. It may, however, sometimes be recognized as a notching during the ST segment or T wave. Retrograde P waves may occur. The presence of a sinus P wave (when it cannot be seen) may be inferred by the presence of a fully compensatory pause.
P to R interval: WNL
QRS: Not normal looking. Usually broadened to more than 0.12 second.
Some patients will have regular QRS complexes interspersed with occasional unusual-looking complexes. These unusual conformations are called PVCs. This aberrant activity can cause more serious ventricular arrhythmias. Clinical deterioration depends on the frequency of the PVCs.
A PVC is a depolarization that arises in either ventricle before the next expected sinus beat, ie, prematurely. It may result from the firing of an automatic focus or reentry.
Since PVCs originate in the ventricle, the normal sequence of ventricular depolarization is altered; ie, instead of the two ventricles depolarizing simultaneously, they depolarize sequentially. In addition, conduction occurs more slowly through the myocardium than through specialized conduction pathways. This results in a wide (0.12 second or greater) and bizarre-appearing QRS. The sequence of repolarization is also altered, usually resulting in an ST segment and T wave in a direction opposite to the QRS complex.
The interval between the previous normal beat and the PVC (the coupling interval) usually remains constant when PVCs are due to reentry from the same focus (uniform PVCs). When the coupling interval and the QRS morphology vary, the PVCs may be arising from different areas within the ventricles, or if the PVCs are arising from a single focus, ventricular conduction may vary. Such PVCs are referred to as multifocal or, more appropriately, multiformed.
A PVC may occur nearly simultaneously with the firing of the sinus node. The antegrade impulse originating in the sinus node (resulting in normal atrial depolarization) and the retrograde impulse traveling toward the atria from the ventricles may meet in the AV node. Then neither can spread further because of the other's refractory period. Since the rhythm of the sinus node is undisturbed, a fully compensatory pause usually results (ie, the next P wave should occur at the proper time). However, on occasion retrograde conduction can spread to the atria and reset the SA node.
PVCs may occur as isolated complexes, or they may occur repetitively in pairs (two PVCs in a row). When three or more PVCs occur in a row, VT is present. When VT lasts for more than 30 seconds, it is arbitrarily defined as sustained ventricular tachycardia.
If every other beat is a PVC, ventricular bigeminy is present. If every third beat is a PVC, the term ventricular trigeminy is used; if every fourth beat is a PVC, ventricular quadrigeminy is present; and so forth.
A PVC that falls on the T wave (during the so-called vulnerable period of ventricular repolarization) may precipitate VT or VF. However, PVCs occurring after the T wave may also initiate such VT.
Treatment: Isolated or nonVT PVCs are rarely treated except for needed symptomatic relief. In the setting of an acute myocardial infarction, PVCs indicate the need to aggressively treat the ischemia/infarction with oxygen, nitroglycerin, morphine, and thrombolytic therapy. Simply making the PVCs diminish with lidocaine does little to the underlying pathology and can lure physicians into an invalid clinical security that the problem has been resolved.
In some patients conducting tissue near the AV node has taken over the pacemaker function of the heart. These patients will have slow heart rates (40 to 60 beats per minute) and inverted but narrow QRS complexes, and often one can see retrograde P waves in leads II and III.
A premature junctional complex is an electrical impulse that originates in the AV junction and occurs before the next expected sinus impulse. This often results in retrograde atrial depolarization (hence the P wave in leads II, III, and aVF will be negative). The retrograde P wave may precede, coincide with, or follow the QRS. The relation of a retrograde P wave to QRS complex depends on the relative conduction times from the site of origin within the junction to the atria and ventricles. It is therefore likely that an impulse arising in the higher portion of the junction, above the AV node, would result in a P wave occurring before or during the QRS complex, whereas one arising at a lower level would result in a P wave that occurs after the QRS complex. Conduction from the junction to the ventricles usually occurs along normal pathways. Thus the QRS complex is usually normal, although it can be wide owing to either a bundle-branch block or aberrant conduction. The pause following a premature junctional complex may be noncompensatory (if the sinus node is depolarized by the premature beat) or fully compensatory if the sinus node has discharged before it is reached by the premature beat.
Treatment: Specific suppressive treatment is rarely needed.
Rate: A junctional escape rhythm has a rate of 40 to 60
beats per minute.
Junctional Escape Rhythm
The AV junction can function as a pacemaker. It initiates impulses at a rate of 40 to 60 beats per minute, equivalent to an RR interval between 1.0 and 1.5 seconds. Under normal circumstances, the sinus node pacemaker, which is faster, predominates. If the AV node is not depolarized by the arrival of a sinus impulse within approximately 1.0 to 1.5 seconds, it will initiate an impulse. This is called a junctional escape complex. It occurs because of failure of the sinus node to initiate an appropriately timed impulse or because of a conduction problem between the sinus node and the AV junction. A repeated series of such impulses is referred to as a junctional escape rhythm.
Treatment: Most commonly, junctional escape complexes and rhythms are events of automaticity. They may also be due to digitalis intoxication. In nonparoxysmal junctional tachycardia due to digitalis intoxication, digitalis should be withheld. The serum potassium level should be checked, and if low, potassium should be given to raise the serum potassium to the normal range. If the patient is severely compromised, antibodies to digitalis may be used.
Glossary Of Terms
Arrhythmia: Irregularity or absence of a heartbeat. See dysrhythmia.
Asystole: (Cardiac Arrest, Ventricular Standstill): The absence of a heartbeat.
Atrioventricular Block: A cardiac impulse conduction disturbance in the atrioventricular (AV) node, bundle of His, or it's branches.
Automatic Beat: An impulse arising in an automatic focus, independent of the dominant rhythm.
AV Dissociation: The independent beating of the atria and ventricles.
Bigeminy: A normal beat alternating with a premature beat.
Block: A pathologic delay or interruption in impulse conduction.
Bradycardia: A heart rate slower than the normal for that pacemaker site; e.g., less than 60 beats/minute for the sinoatrial (SA) node.
Bradydysrhythmia: Any rhythm disturbance causing a slow heart rate (less than 60 beats/minute).
Bundle Branch Block: An abnormality in cardiac impulse conduction through the fibers of the bundle of His.
Compensatory Pause: The period following a premature contraction during which the heart regulates itself, allowing the SA node to resume normal conduction.
Conduction Time: The interval between the origination of an impulse at the SA node and the stimulation of ventricular contraction.
Coupling: The relationship of a premature beat and the preceding beat.
Dysrhythmia: Any disturbance in the normal rhythm of the heartbeat; irregularities may occur in discharge of impulses from the SA node, or in conduction of impulses through the cardiac tissue.
Ectopic Beat: A beat originating from a source of cardiac stimulus other than the SA node, usually caused by some irritation of the myocardium.
EKG (or ECG): Electrocardiogram; a graphic tracing of the electrical activity of the heart.
Electromechanical Dissociation: Electrical activity without evidence of myocardial contraction.
Escape Beat: An automatic beat that occurs after an interval longer than the dominant cycle.
Extrasystole: An ectopic beat, occurring before the next dominant beat, that depends on and couples with the preceding beat; contraction of
the heart that occurs prematurely and interrupts the normal cardiac cycle.
Fibrillation: Quivering or uncoordinated muscular contraction.
Fusion Beat: Simultaneous activation of one chamber of the heart by two foci.
Group Beating: A pattern of repetitive QRS complexes.
Heart Block: Impairment of cardiac conduction so that electrical impulses from the atria fail to pass through the AV node to the ventricles.
Idiojunctional Rhythm: A relatively slow, independent rhythm that arises in the AV junction and controls the ventricles.
Idioventricular Rhythm: A relatively slow rhythm that originates from and controls the ventricles.
Junctional Dysrhythmia: The irregular heartbeat that results when the AV node assumes the SA node's role as the heart's primary pacemaker.
Mobitz Type I (Wenckebach) Block: A second-degree or partial AV block in which the P-R interval increases progressively until the atrial impulse arrives during the absolute refractory period and the corresponding ventricular beat is not conducted.
Mobitz Type II Block: A second-degree or partial AV block characterized by the sudden nonconduction of an atrial impulse and a periodic nonconducted beat that occurs without warning - without previous lengthening of the P-R interval.
Pacemaker: The SA node, so called because it initiates the electrical impulse that sets the rhythm of cardiac contractions. An artificial pacemaker is an electrical device implanted to pace a cardiac rhythm, used particularly when a patient has symptomatic heart block.
Parasystole: An ectopic, independent rhythm that operates concurrently with the dominant rhythm, whose foci can't be discharged by the dominant pacemaker impulses.
Paroxysmal: Recurring suddenly and abruptly.
Sinus Arrhythmia: A slight variation or irregularity in sinus rhythm or normal heartbeats.
Systole: Contraction of the heart, which causes ejection of blood from the heart chambers into the circulatory system.
Tachycardia: A heart rate faster than the normal for that pacemaker site; e.g., greater than 100 beats/minute for the SA node.
Tachydysrhythmia: Any rhythm disturbance causing a fast heart rate (over 100 beats/minute).
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