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Anatomy and Physiology

Lets firstly revisit some basic Anatomy and Physiology about the heart...The
heart is made up of four chambers: the right atria, the left atria, the right ven-
Page 1 tricle, and the left ventricle. The atria receive the blood. The ventricles pump
the blood.

The heart is a specialized muscular structure made up of myocardial cells.

These cells are grouped closely together forming intercalated disks which al-
low the groups of muscle cells to function together as one. This allows the atria
and the ventricles to contract independently of each other.

Cardiac muscle also adapts to the amount of blood that it needs to pump.
There is a direct proportion between the amount of blood returning to the
heart and the force of contraction which empties the ventricle. The greater the
amount of blood entering the heart the stronger the contraction. This is caused
by the heart muscle stretching to accommodate the amount of blood. This abil-
ity is called Frank-Starling’s Law of the Heart.

The heart muscle cells (the myocardium) have a long rest period which is
called the refractory period between contractions. This allows the heart cham-
bers enough time to fill with blood before the next contraction.
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Cardiac muscle cells have four properties:

1. Cardiac muscle cells provide their own stimulation. They do not have
nerve innervation like skeletal muscle cells do. This is called
Page 2 automaticity.
2. Cardiac muscle cells are able to respond to an electrical impulse.
This is called excitability.
3. Cardiac muscles also have conductivity, the ability to transmit an
impulse to another cardiac cell.
4. Cardiac muscle cells also have contractility, the ability to contract
after receiving an impulse.

Three ions are necessary for muscle cell contraction:

1. Na+ (Sodium)
2. K+ (Potassium)
3. Ca+ (Calcium)

The sympathetic and parasympathetic nervous systems affect the heart.

The stimulation of the sympathetic nervous system:

• causes release of epinephrine
• this causes the heart rate, cadiac output, and blood pressure to in-
crease

The stimulation of the parasympathetic nervous system:

• causes release of acetylcholine`
• this slows heart rate and decreases cardiac output and blood pressure

Electrical Conduction through the Heart

The conduction system of the heart is made up of specialized cardiac cells

that initiate impulses for contraction. This explains the automaticity property
of the heart. The conduction system consists of the sinoatrial node (S-A node),
the atrioventricular node (A-V node), the atrioventricular bundle (A-V bundle or
A-V bundle of HIS), the Purkinje fibers and the bundle branches.
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Electrical Conduction through the Heart cont...

Page 3

The S-A node is located in the posterior wall of the right atrium. It is commonly
known as the pacemaker as it normally starts the rate and rhythm for the
entire heart. The S-A node sends impulses that trigger atrial contraction. If the
S-A node doesn’t fire other sites in the heart will respond. If higher sites don’t
respond the lower ones will. The lower the site, the slower the speed. This will
make more sense as you learn the different rhythms.
The stimulated atrial cells then send the impulse down the internodal path-
ways to the A-V node. The A-V node is located near the interatrial septum. The
A-V node slows the impulses allowing the atria to finish contracting before the
ventricles start to contract.
From the A-V node the impulse then travels to the A-V bundle. The A-V bundle
goes from the right side of the intra-atrial septum to the beginning of the inter-
ventricular septum where it branches into the right and left bundle branches.
These branches divide further into Purkinje fibers that cover the inner surface
of the ventricles. Impulses relayed from the Purkinje fibers initiate ventricular
contraction.
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The EKG (ECG)

The EKG is a recording of the electrical impulses produced by the heart. Each
cardiac cycle should correlate with a pulse. Please Note—this is not proof of
muscular contraction—just the electoral impulse!
Page 4

The cardiac cycle consists of:

• P wave - atrial depolarization, normally generated by the S-A node
• PR interval - includes the P wave and the PR segment. Changes in the con-
duction through the AV node are the most common cause of changes in
the PR interval. The PR interval is important in identifying heart blocks.
• PR segment - isoelectric line (area of inactivity) between the P wave and
the QRS complex
• QRS complex – ventricular depolarization. A wide QRS may indicate that
the conduction originated from the ventricle. A delay in conduction through
either bundle branch will also widen the QRS. A wide QRS with no P waves
is usually a ventricular rhythm.
• ST segment – area of electrical inactivity between the QRS and T wave)
• T wave – ventricular repolarization
• QT interval – includes QRS and T wave (normal measurement is ½ the pre-
vious R-R interval).
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How to count the Heart Rate from a Strip

Time is measured across the paper horizontally. The standard rate at which the paper moves
is 25 mm per second. The small boxes represent .04 seconds (or 40 ms). The large boxes
represent 0.20 seconds (or 200 ms). Every 3 seconds there is a vertical mark at the top of
Page 5 the paper.
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Page 6

The Four Methods for rate calculation

1. Count the number of R waves in the six second strip, and multiply by 10.
2. Count the number of large boxes between the two R waves in a regular
rhythm and divide into 300.
3. Count the number of small boxes between two R waves in a regular
rhythm and divide into 1500.
4. Another quick and easy
way to determine the
ventricular rate is to examine
the R to R interval and use a
standard scale to find the
rate. If two consecutive R
waves are separated by only
one large box, then the rate
is 300 beats per minute. If
the R waves are separated
by two large blocks, then the
ventricular rate is 150 beats
per minute. The scale contin-
ues down to show that if two
consecutive R waves are
separated by 8 large boxes,
then the rate is 37 beats per
minute.
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How to interpret an EKG strip

The first thing you do when you look at an EKG strip, is to ask yourself the
following Six Questions:
Page 7
1. What is the rate? (60-100 beats per minute is normal)

2. Is there a P-wave for every QRS complex and do they look alike?

3. What is the P-R interval? (Long, short , all the same?)

4. Is there a normal QRS complex and do they all look alike?

Are they regular, or evenly spaced?

5. Is there a pattern to any abnormalities?

6. What do I need to do about it?

This is regular

This is irregular
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RATE
Determine the heart rate. If the heart rate is over 100 beats per minute it is
called tachycardia. If the rate is under 60 beats per minute it is called brady-
cardia.
Page 8
P-WAVE
Is there a P-wave before each QRS? Is there a one to one relationship between
P waves and the QRS? Do the P waves look the same? Do they point in the
same direction? Is each P wave the same distance from the QRS?

PR INTERVAL
The PR interval represents the time it takes for the impulse to travel from the
atria to the AV node. It should measure 0.12 to 0.20 seconds. The PR interval
is important to determine if there is a heart block or
some other conduction prob- lem.

The QRS
The QRS represents ventricular depolarization. The first downward deflection is
called a Q wave. It is not always present. The first upward deflection is called
an R wave. The downward wave following is the S wave. The QRS should be no
longer than 0.10 seconds.
Look at the QRS. Are they all the same size and shape? Do they all point in
the same direction? Are they the same distance from the T wave?
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Normal Sinus Rhythm

Page 9

The R-R intervals are constant, the rhythm is regular.

Sinus Bradycardia

HR is < 60. Sinus bradycardia may be normal in athletes although more often
it is the result of a conduction abnormality or a drug effect.

Sinus Tachycardia

HR > 100 ( usually 100 to 160bpm) If your patient has this arrhythmia, try to
identify the cause.
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Sinus Arrhythmia

Page 10

The R – R intervals vary; the rate changes with the patient’s respirations.
Treatment is not usually required unless symptomatic bradycardia is present.
Sinus arrhythmia can be confused with sinus arrest (also called sinus pause).

Premature Atrial Contractions

This indicates the early contraction of the atria

Atrial Fibrillation

The atrial rhythm is not able to be measured as all atrial activity is chaotic. This
is the “jelly on the plate” scenario—wobble, wobble, but NO contractions in the
atria. The ventricular rhythm is irregular with no pattern to its irregularity.
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Atrial Flutter

Page 11

Atrial flutter has a “saw tooth” appearance similar to Atrial Fibrillation, but in
the flutter the “R” to “R” complexes are regular.

Junctional Rhythm

Represents retrograde conduction, that is if the SA node is damaged, then the

AV node may take over

Supraventricular Tachycardia

SVT is generally defined as an fast arrhythmia which originates at or above the

AV node. This is a narrow complex tachycardia of 140 – 220 bpm.
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HEART BLOCKS

These are atrioventricular blocks. This arrhythmia is a delay or interruption in

conduction between the atria and the ventricles
Page 12
Type of Block PRI R–R Conduction

1st Degree Greater than 0.20 seconds Usually regular One P for every
(depending on the QRS

2nd Degree Type 1 Increasing longer until one P Irregular More P’s than
(Wenkebach) is blocked/dropped QRS’s
2nd Degree Constant on conducted Usually regular (can More P’s than
Type 2 beats (can be greater than be irregular if con- QRS’s
0.20 seconds duction varies)
3rd Degree No relation of P’s to QRS’s. Regular More P’s than
Complete Heart Block Not constant. P’s march QRS’s
through
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First Degree A—V Block

This is the most common conduction disturbance. It occurs in healthy and dis-
eased hearts. It can be caused by an inferior MI, Digitalis Toxicity, myocarditis,
and hyperkalemia. Treat the underlying cause and observe for any progression
Page 13
to a more advanced AV block.

Second Degree A—V Block—Type 1 (Wenkebach)

This represents ischemia and is reversible. The HR tends to be slower, as
some beats are missed. The PRI elongates until a QRS complex is missed,
then shortens again as the cycle repeats.

Second Degree A—V Block—Type 2 (Mobitz II)

Represents injury and is NOT reversible. This may progress rapidly and without
warning to third degree heart block (complete heart block) or asystole.

Above is an example of a constant Second Degree Heart Block Type II. It is con-
stant because every other p wave is conducted. Below is periodic Second De-
gree Heart block. There is no pattern or consistency to the dropping of the p
wave.
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Third Degree Heart Block or Complete Heart Block (CHB)

This can progress rapidly to asystole without warning, so you need to have an
external pacemaker nearby. Both the atria and the ventricles are firing regular-
ly, but they are not “in sync”. They do not relate to each other!
Page 14

Premature Ventricular Contractions (PVC’s)

PVC’s interrupt the regular rhythm of the heart. The PVC’s rarely create a
pulse, so are not counted in the rate.

Ventricular Tachycardia
Check your patient!!! This is a lethal rhythm. They may or may not have a
pulse. This rate can be counted on a rhythm strip.

Ventricular Fibrillation
This is a lethal arrhythmia. If this is real and not artifact your patient has no
pulse!!! This cannot be counted on a rhythm strip.
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Asystole
This indicates no electrical activity. Increase the gain on the monitor, check an-
other lead. If this is truly asystole there will be no pulse. Start CPR!!!
Page 15

Pacemaker Rhythms
The type of pacemaker determines the appearance of the strip. The pacemak-
er will generate a spike on the strip. There should be a response from the heart
for each spike. If the pacer lead is in the atria you will see a P wave after the
spike. If the pacer lead is in the ventricle there will be a QRS after the spike.
This QRS will be wide because the impulse is generated in the ventricle. If
there is a lead in both the atria and the ventricle then it is “dual chambered” or
A-V paced.

This is an example of ventricular pacing.

This is an example of ventricular pacing.

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ST Segment Elevation
This means there has been myocardial injury. This is usually a reliable sign
that a true infarction has occurred.
Page 16

This could be caused by angina or a non-Q wave infarction. With angina the ST
segment will return to baseline shortly after the pain is relieved. With a non-Q
wave infarction the ST segment remain down for at least 48 hours. The only
EKG changes seen with non-Q wave infarctions are T wave inversion and ST
segment depression.

• Down sloping is more significant than

horizontal

• Upsloping is less significant than

horizontal

• Horizontal—1mm of horizontal or
down sloping depression of ST
segment = criterion for + exercise
test indicating myocardial ischemia

• Upsloping depression is positive

when it exceeds 1.5 mm
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How can I tell the difference?

Page 17

… this may help!

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Cardiac Medications to remember

Drugs to increase blood pressure

Epinephrine – This drug is often used in cardiac arrest. During CPR epineph-
Page 18
rine can help increase blood flow to the heart and brain. It increases peripher-
al vasoconstriction, increases heart rate, and makes ventricular arrhythmias
more responsive to electrical shock. Epinephrine is used for cardiac arrest,
symptomatic bradycardia, severe hypotension, and severe allergic reactions.

Dopamine – Increases heart rate and the force of contraction plus causes vas-
oconstriction. It is not as forceful as epinephrine. In higher doses it also in-
creases oxygen demand and decreases perfusion. Dopamine is used for he-
modynamically significant hypotension and bradycardia not responsive to atro-
pine.

Norepinephrine – This drug is similar to epinephrine. It is a potent vasocon-

strictor. This increases vascular resistance which increases myocardial oxygen
demand and may exacerbate myocardial ischemia (chest pain). It is used for
severe hypotension. Levophed is considered a drug of last resort for the man-
agement of cardiogenic shock.

Neosynephrine – This drug increases blood pressure and is used often after
cardiac arrest. It increases blood pressure without increasing heart rate.
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Drugs to decrease blood pressure

Nitroglycerine – Causes vasodilation in arterial and peripheral blood vessels

including coronary arteries. It decreases myocardial oxygen consumption. In-
Page 19 creases oxygen delivery. Nitroglycerine has a short half life. It is used for chest
pain and ischemia. It can lower blood pressure. Nitroglycerine is used for angi-
na pectoris, acute pulmonary edema, congestive heart failure, and acute myo-
cardial infarction (AMI). Standard protocols in the USA (unless otherwise stat-
ed) it to administer 3x doses of Nitroglycerine 5 mins apart. If this does not
help, then seek further medical advice.

Nitroprusside – This drug is a rapid acting vasodilator affecting venous and

arterial smooth muscle. Onset of action is immediate with the effects stopping
minutes after stopping infusion. It is used in patients with severe heart failure
and hypertensive emergencies and acute pulmonary edema

Drugs to stop Arrhythmias

Amiodarone —This drug decreases electrical conduction and the force of con-
traction. Amiodarone is ACLS’s favorite drug for controlling any rapid rate/
rhythm. It can cause hypotension which will cause decreased perfusion and
less oxygen delivery. Amiodarone is used for ventricular fibrillation, pulseless
VT, atrial fibrillation, atrial flutter, stable narrow-complex tachycardias, cardiac
arrest, and stable monomorphic VT.

Lidocaine – Lidocaine is not as effective as amiodarone. It suppresses ventric-

ular arrhythmias, contractility, and can help prevent ventricular fibrillation. It is
used for Ventricular fibrillation, pulseless VT, wide-complex tachycardia's, car-
diac arrest, and stable VT.
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Drugs to help heart rate

Beta Blockers – works by decreasing heart rate and the force of contraction.
Beta Blockers increase the survival rate after a heart attack (30%). Beta block-
Page 20 ers slow the heart rate, reduce myocardial oxygen consumption, and lower the
blood pressure. They are used for acute coronary syndrome and tachyarrhyth-
mia's (atrial fibrillation/flutter). This class of drugs ends in “lol”. Examples are
Metoprolol, Atenolol, and Labetalol.

Calcium Channel Blockers – decrease sinoatrial node automaticity and slow

AV node conduction. They are used to control the ventricular response in pa-
tients with rapid atrial fibrillation/flutter and narrow complex tachycardia's. Ex-
amples are Verapamil and Cardizem.

Atropine – enhances sinus node automaticity and AV conduction. Used to treat

symptomatic bradycardia.