N240 Olol - (Final Exam) Test 3 - Ekg Workbook / Interpretation

Front 1

Electrocardiogram (EKG)

Back 1

recording of the electrical activity of the heart.

Front 2

NORMAL SINUS RHYTHM

Back 2

CHARACTERISTICS of NSR

Rate:
60-100 BPM

Rhythm:
Regular

P waves:
Present before every QRS
Upright and rounded
Consistent in size and shape.

PR interval:
0.12-0.2 seconds

Clinical significance:
Normal rhythm that originates in SA node, conducted normally to AV node, and ventricles

Front 3

SINUS BRADYCARDIA

Back 3

CHARACTERISTICS SINUS BRADYCARDIA

Rate:
Less than 60 BPM

Rhythm:
Regular

P wave:
Present before every QRS
Upright and rounded
Consistent in size and shape

PR interval:
0.12-0.2 seconds

Clinical significance:
Normal in athletes

Front 4

SINUS TACHYCARDIA

Back 4

CHARACTRISTICS SINUS TACHYCARDIA

Rate:
Greater than 100

Rhythm:
Regular

P wave:
Present before every QRS
Upright and rounded
Consistent in size and shape

PR interval:
0.12-0.2

Clinical significance:
Normal after activity
Dangerous after acute MI

Front 5

More information about SINUS TACHYCARDIA

Back 5

Sinus tachycardia is normal in response to increased metabolic demands such as exercise.
It is also a compensatory mechanism for decreases in blood pressure and cardiac output. CO = SV X HR.
When baroreceptors sense a decrease in cardiac output the sympathetic nervous system stimulates the heart to beat faster and harder to increase production of oxygenated blood.

This becomes a problem for the patient with an acute MI.

Increases in heart rate (tachycardia) increase oxygen demand and decrease oxygen supply.

Front 6

SINUS ARRHYTHMIA

Back 6

CHARACTERISTICS SINUS ARRHYTHMIA

Rate:
60-100 BPM

Rhythm:
Irregular

P wave:
Present before ever QRS
Upright and rounded
Consistent in size and shape

PR interval:
0.12-0.2 seconds

Clinical significance:
Normal in children and young adults.
Abnormal in older adults.

Front 7

More information about SINUS ARRHYTHMIA

Back 7

Sinus arrhythmia is normal is young people because the autonomic nervous system will vary the heart rate with respiration.
During inspiration negative intrathoracic pressure causes more blood to enter the right atrium.
The heart rate increases slightly to compensate.
During expiration intrathoracic pressure is positive.
Flow of blood through the heart is normal and the heart rate slows down.
In sinus arrhythmia heart rate increases and decreases slightly with respiration in a cyclic pattern.

Front 8

ATRIAL FLUTTER

Back 8

CHARACTERISTICS ATRIAL FLUTTER

Rate:
Atrial rate 250-400 BPM
Ventricular rate varies with degree of block. Usually from 60-100

Rhythm:
May be regular or irregular

P wave:
Sawtooth wave pattern.

PR interval:
Not true P wave so the PR interval is not measured

Clinical significance:
Can cause the patient to progress to atrial fibrillation

Front 9

More information about ATRIAL FLUTTER

Back 9

In atria flutter an ectopic focus has become irritable and taken over from the sinus node as the pacemaker of the heart.
This irritable cell is discharging very rapidly so the SA node doesn’t have a chance to regain control.
The atria are contracting at 250-400 BPM.
Impulses are bombarding the AV node and the ventricles while they are still in the absolute refractory period so not all of the impulses will create a QRS.
Therefore the conduction is irregular.
Some will have two P waves for every QRS (2:1), some will have three or more (3:1), and some patients in atrial flutter vary in their degree of block.
The impulses are traveling down an abnormal pathway so the PR interval will not be within normal limits.

Front 10

ATRIAL FIBRILLATION

Back 10

CHARACTERISTICS ATRIAL FIBRILLATION

Rate:
Atrial rate 400-600
Vary by extent of block.
Rate does not determine A fib

Rhythm:
Irregularly irregular

P waves:
No discernable P wave

PR interval:
None

Clinical significance:
Slow the ventricular response.
Prolonged afib can produce embolism and CVA

Front 11

More information about ATRIAL FIBRILLATION

Back 11

In atrial fibrillation the atria are depolarizing so rapidly that the atria are actually only quivering instead of contracting.
You may be able to see this quivering on the EKG in an erratic quivering baseline.
Not every impulse makes it through the AV node to stimulate the ventricle to depolarize so the rhythm is always irregular.
A rapid ventricular rate with atrial fibrillation produces hypotension, lightheadedness, palpitations, shortness of breath, or chest pains.
If the patient has these symptoms and ventricular rate is rapid the physician will order medications to slow the ventricular response.
Examples of medications that slow ventricular response in atrial fibrillation are: digoxin, calcium channel blockers, beta blockers, diltiazam, and amiodarone.
If the patient is unstable cardioversion may be used.
Patients with chronic atrial fibrillation are susceptible to atrial thrombus formation.
Patients are at risk for CVA from thrombi in the left atrium that embolize to the brain.
It is believed that 15-20% of CVAs are the result of atrial fibrillation.

Front 12

Occurance of PVCs

Back 12

can occur in:

Pairs = couplet

Every other beat = bigeminy

Every third beat = trigeminy

Runs of three or more in a row = ventricular tachycardia

PVCs can be configured the same = unifocal,
or different = multifocal

Front 13

VENTRICULAR TACHYCARDIA

Back 13

CHARACTERISTICS VT

Rate:
150-250 BPM

Rhythm:
Regular

P wave:
None

PR interval:
None

QRS interval:
Greater than 0.1

Clinical significance:
Poor cardiac output, requires immediate defibrillation

Front 14

More information about VENTRICULAR TACHYCARDIA

Back 14

When three or more PVCs occur consecutively a diagnosis of ventricular tachycardia is made.
This rhythm originated from an ectopic focus in the ventricles.
There are no P waves because the rhythm originates in the ventricle.
QRS complexes are wide and bizarre.
Ventricular tachycardia may be regular or slightly irregular.
Patients may have a pulse and blood pressue with ventricular tachycardia but will suffer decreased cardiac output.
Other symptoms frequently observed with ventricular tachycardia are syncope, chest pain, palpitations, deterioration to unconsciousness, pulselessness.
Common causes are heart disease, anterior myocardial infarction, hypokalemia, and cardiomyopathy.
For patients with stable ventricular tachycardia, apply oxygen and administer antiarrhythmics as prescribed.
Patients who have an unstable ventricular tachycardia should be defibrillated.
If the patient is alert, sedate before applying electrical shock.

Front 15

TORSADES DE POINTES

Back 15

CHARACTERISTICS TORSADES DE POINTS

Rate:
150-250 BPM

Rhythm:
Irregular

P wave:
None

PR interval:
None

QRS:
Wider than 0.1 bizarre spiral appearance

Clinical significance:
More difficult to treat than ventricular tachycardia

Front 16

More information about TORSADES DE POINTES

Back 16

A variant of ventricular tachycardia that is related to prolonged QT interval.
The phrase Torsades de Points means twisting of the points in French.
In Torsades de Points, the EKG tracing gives the appearance of twisting or spiraling around the isoelectric line.
This arrhythmia is caused by medications that can increase the QT interval like pronestyl, quinidine, norpace, or cardarone.
This variant of ventricular tachycardia is more persistent and difficult to convert than regular ventricular tachycardia.

Front 17

VENTRICULAR FIBRILLATION

Back 17

CHARACTERISTICS V FIB

Rate:
Unable to count

Rhythm:
Chaotic no pattern

P waves:
None

PR interval:
None

QRS interval:
No QRS

Clinical significance:
Patient has no pulse or blood pressure.

Treatment is immediate defibrillation

Front 18

More information about VENTRICULAR FIBRILLATION

Back 18

Ventricular fibrillation is a chaotic rhythm that originates in the ventricle.
There is no ventricular depolarization or muscle contraction, resulting in a pulseless patient.
Can be defined as fine V fib or coarse V fib according to the amplitude of the fibrillation waves.
Many patients with sudden death in the community have been found to be in V fibrillation.
Treatment for witnessed ventricular fibrillation is immediate defibrillation followed by CPR.
The emphasis is on CPR with minimal interruptions.
Defibrillation continues until the patient’s rhythm and pulse is restored.
Most common causes are ischemic heart disease, anterior myocardial infarction, V tachycardia that deteriorates into ventricular fibrillation, and hypokalemia.

Front 19

FIRST DEGREE AV BLOCK

Back 19

CHARACTERISTICS FIRST DEGREE AV BLOCK

Rate:
Bradycardia

Rhythm:
Regular

P wave:
Rounded, upright, consistent

PR interval:
Greater than 0.2 seconds

QRS interval:
Less than 0.1 seconds

Clinical significance:
No treatment required

Front 20

More information about FIRST DEGREE AV BLOCK

Back 20

Prolonged PR interval means that conduction time was slowed through the AV node.
If patient is asymptomatic no treatment required.

Front 21

SECOND DEGREE AV BLOCK
MOBITZ TYPE I
WENCKEBACH

Back 21

CHARACTERISTICS WENCKEBACH

Rate:
Atrial rate is greater than ventricular rate (more P than QRS)

Rhythm:
Irregular

P wave:
Rounded upright consistent

PR interval:
Lengthens with each beat until one P wave is not conducted

QRS interval:
Less than 0.1 seconds

Clinical significance:
No treatment required

Front 22

More information about SECOND DEGREE AV BLOCK
MOBITZ TYPE I
WENCKEBACH

Back 22

Conduction delay in AV node causes conduction to take longer with each atrial depolarization.
This results in a lengthening of the PR interval with each beat.
Eventually a P wave occurs during the absolute refractory period of ventricular repolarization and no QRS occurs.
This appears as a dropped beat on the EKG.
Pattern is lengthening of the PR interval from beat to beat with a dropped QRS.
This results in more P waves than QRS on the EKG tracing.

Front 23

SECOND DEGREE AV BLOCK
MOBITZ TYPE II
2:1 BLOCK

Back 23

CHARACTERISTICS 2:1 BLOCK

Rate:
Bradycardia

Rhythm:
Atrial rhythm is regular
ventricular irregular

P wave:
More P waves than QRS.
Ps are rounded upright and consistent

PR interval:
Less than 0.2 seconds, constant

QRS:
Usually greater than 0.1 seconds

Clinical significance:
May progress to 3rd degree heart block

Front 24

More information about SECOND DEGREE AV BLOCK
MOBITZ TYPE II
2:1 BLOCK

Back 24

Conduction from the SA node is normal resulting in normal P waves that are regular, rounded, upright in lead II, with a consistent PR interval.
Conduction delay occurs below the AV node resulting in a slightly wider than normal QRS, and dropped beats when the impulse fails to conduct.
EKG will show more P waves than QRSs, but all PR intervals are the same because the problem is below the AV junction.
Danger is that this rhythm can deteriorate into third degree heart block.

Front 25

THIRD DEGREE HEART BLOCK
AV DISSOCIATION OR COMPLETE HEART BLOCK

Back 25

CHARACTERISTICS THIRD DEGREE HEART BLOCK

Rate:
Bradycardia

Rhythm:
Regular

P wave:
Rounded, upright, consistent
More p waves than QRS

PR interval:
Varies from beat to beat

QRS interval:
Wider than 0.1 seconds

Clinical significance:
Pacemaker required if high degree block with symptoms

Front 26

More information about THIRD DEGREE HEART BLOCK
AV DISSOCIATION OR COMPLETE HEART BLOCK

Back 26

Also called complete heart block because unlike the second degree blocks where some of the atrial impulses are conducted, none of the P waves in third degree heart block are conducted to the ventricles.
The atrium and ventricles are beating independent of each other.
The pacemaker in the atrium (SA node) is firing at regular intervals, however all impulses are blocked somewhere in the interventricular conduction system below the level of the AV node.
The ventricle develops a pacemaker of its own and the ventricle continues to beat at a regular rate.
Atrial and ventricle rates are regular but are not coordinated with each other.
Characteristic pattern on EKG is a normal P wave, and a regular QRS that may be wider than 0.1 depending on where the ectopic pacemaker originates from, and a variable PR interval.