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Pulseless Ventricular Tachycardia
The pulseless ventricular tachycardia rhythm is primarily identified by several criteria. First, the rate is
usually greater than 180 beats per minute and the rhythm generally has a very wide QRS complex.
Second, the patient will be pulseless and third, the rhythm originates in the ventricles. This is in contrast
to other types of tachycardias which have origination above the ventricular tissue (in the atria).
Not all ventricular tachycardias are pulseless and therefore, pulselessness must be established
prior to beginning an algorithm. This is accomplished simply by checking a carotid or femoral
Pulselessness with a tachyarrhythmia occurs because the ventricles are not effectively moving blood out
of the heart and there is therefore no cardiac output. Many tachyarrhythmias of a rate >150 will
deteriorate into pulselessness if timely treatment is not given.
Pulseless Electrical Activity (PEA) Rhythm
PEA rhythm occurs when any heart rhythm that is observed on the electrocardiogram (ECG) does not
produce a pulse. PEA can come in many different forms. Sinus Rhythm, tachycardia, and bradycardia can
all be seen with PEA.
Performing a pulse check after a rhythm/monitor check will ensure that you identify PEA in every
Pulseless electrical activity usually has an underlying treatable cause. The most common cause in
emergency situations is hypovolemia.
PEA is treated by assessing and correcting the underlying cause. These causes can be summed up in the 6
Hs and 6 Ts of ACLS. Use the link to review the Hs and Ts.
When an underlying cause for pulseless electrical activity cannot be determined, PEA should be treated in
the same fashion as asystole
Ventricular fibrillation or VF occurs when there are uncoordinated contractions within the ventricles of
the heart. The primary cause of VF is hypoxia (lack of oxygen) to the heart muscle which causes
hyperirritability in the cardiac muscle tissue.
As a result, multiple muscles cells within the ventricles simultaneously fire as pacemakers causing a
quivering or fibrillation that is ineffective for adequate cardiac output.
The two images above show what ventricular fibrillation will look like on a EKG rhythm strip.
VF can rapidly lead to heart muscle ischemia and there is a high likelihood that it will deteriorate into
Asystole or flatline
Asystole is not actually a true rhythm but rather is a state of no cardiac electrical activity. The main
treatment of choice for asystole is the use of epinephrine and CPR.
First-Degree Heart Block
Also called first-degree AV block is a disease of the electrical conduction system of the heart in which the
PR interval is lengthened beyond 0.20 seconds.
This lengthening of the PR interval is caused by a delay in the electrical impulse from the atria to the
ventricles through the AV node
Normally and in the case of ACLS, first-degree heart block is of no consequence unless it involves
myocardial infarction or an electrolyte imbalance.
Although first-degree heart block is not clinically significant for ACLS, recognition of the major AV
blocks is important because treatment decisions are based on the type of block present.
Second-Degree Heart Block (Type 1)
Also called Mobitz 1 or Wenckebach is a disease of the electrical conduction system of the heart in which
the PR interval has progressive prolongation until finally the atrial impulse is completely blocked and
does not produce a QRS electrical impulse.
Once the p-wave is blocked and no QRS is generated, the cycle begins again with the prolongation of the
One of the main identifying characteristics of second degree heart block type 1 is that the atrial rhythm
will be regular.
Second-Degree (AV) Heart Block (Type 2)
Also called Mobitz II or Hay is a disease of the electrical conduction system of the heart. Second-degree
AV block (Type 2) is almost always a disease of the distal conduction system located in the ventricular
portion of the myocardium.
This rhythm can be recognized by the following characteristics:
1. non-conducted p-waves (electrical impulse conducts through the AV node but complete conduction
through the ventricles is blocked, thus no QRS)
2. P-waves are not preceded by PR prolongation as with second-degree AV block (Type 1)
3. fixed PR interval
4. The QRS complex will likely be wide
1. The QRS on an ECG will most likely be wide because the block occurs in the His bundle
or bundle branches and conduction through the ventricles is slowed.
Second-degree AV block (Type 2) is clinically significant for ACLS because this rhythm can rapidly
progress to complete heart block
Second-degree AV block (Type 2) should be treated with immediate transcutaneous pacing or
transvenous pacing because there is risk that electrical impulses will not be able to reach the ventricles
and produce ventricular contraction.
Atropine may be attempted if immediate TCP is not available or time is needed to initiate TCP. Atropine
should not be relied upon and in the case of myocardial ischemia it should be avoided.
Complete Heart Block
Third-degree AV block or complete heart block is the most clinically significant AV block associated
with ACLS. Complete heart block occurs when the electrical impulse generated in the SA node in the
atrium is not conducted to the ventricles.
When the atrial impulse is blocked, an accessory pacemaker in the ventricles will typically activate a
ventricular contraction. This accessory pacemaker impulse is called an escape rhythm.
Because two independent electrical impulses occur (SA node impulse & accessory pacemaker impulse),
there is no apparent relationship between the P waves and QRS complexes on an ECG.
Characteristics that can be seen on an ECG include:
1. P waves with a regular P to P interval
2. QRS complexes with a regular R to R interval
3. The PR interval will appear variable because there is no relationship between the P waves and the
In the image above note that the p-waves are independent of the QRS complexes. Also note the 4th QRS
complex (impulse) looks different from the others. This is because it is from a different accessory
pacemaker in the ventricle than the other QRS complexes.
The most common cause of complete block is coronary ischemia and myocardial infarction. Reduced
blood flow or complete loss of blood flow to the myocardium damages the conduction system of the
heart, and this results in an inability to conduct impulses from the atrium to the ventricles.
Those with third-degree AV block typically experience bradycardia, hypotension, and in some cases
The treatment for unstable third-degree AV block in ACLS is transcutaneous pacing.
Supraventricular Tachycardia (SVT)
SVT is a broad term for a number of tachyarrhythmias that originate above the ventricular electrical
conduction system (purkinje fibers).
Classic Paroxysmal SVT has a narrow QRS complex & has a very regular rhythm. Inverted P waves are
sometimes seen after the QRS complex. These are called retrograde p waves
The heart fills during diastole, and diastole is normally 2/3 the cardiac cycle. A rapid heart rate will
significantly reduce the time which the ventricles have to fill. The reduced filling time results in a smaller
amount of blood ejected from the heart during systole. The end result is a drop in cardiac output &
With the drop in cardiac output, a patient may experience the following symptoms. These symptoms
occur more frequently with a heart rate >150 beats per minute:
Shortness of air (S)
Palpitation feeling in chest (S)
Ongoing chest pain (U)
Rapid breathing (S)
Loss of consciousness (U)
Numbness of body parts (S)
The pathway of choice for SVT in the tachycardia algorithm is based on whether the patient is stable or
unstable. The symptoms listed above that would indicate the patient is unstable are noted with the letter
(U). Stable but serious symptoms are indicated with the letter (S).
Unstable patients with SVT and a pulse are always treated with cardioversion
The most common cardiac arrhythmia, atrial fibrillation, occurs when the normal electrical impulses that
are generated by the SA node are overwhelmed by disorganized electrical impulses in the atria.
These disorganized impulses cause the muscles of the upper chambers of the heart to quiver (fibrillate)
and this leads to the conduction of irregular impulses to the ventricles.
For ACLS, atrial fibrillation becomes a problem when the fibrillation produces a rapid heart rate which
reduces cardiac output and causes symptoms or an unstable condition.
When atrial fibrillation occurs with a (RVR) rapid ventricular rate (rate > 100 beats/min), this is called a
tachyarrhythmia. This tachyarrhythmia may or may not produce symptoms. Significant symptoms that
occur are due to a reduction in cardiac output.
The following is a list of the most common symptoms.
palpitations or chest discomfort
shortness of air and possibly respiratory distress
hypotension, light-headedness and possibly loss of consciousness
peripheral edema, jugular vein distention, and possibly pulmonary edema
For the purpose of ACLS, it is important to be able to recognize atrial fibrillation when the patient is
symptomatic. On an ECG monitor, there are two major characteristics that will help you identify atrial
1. No p-waves before the QRS on the ECG. This is because there are no coordinated atrial contractions.
2. The heart rate will be irregular. Irregular impulses that the ventricles are receiving cause the
irregular heart rate.
When the heart rate is extremely rapid, it may be difficult to determine if the rate is irregular, and the
absence of p-waves will be the best indicator of atrial fibrillation.
For the purposes of ACLS atrial fibrillation is treated when the arrhythmia/tachyarrhythmia produces
hemodynamic instability and serious signs and symptoms.
For the patient with unstable tachycardia due to a tachyarrhythmia, immediate cardioversion is
recommended. Drugs are not used to manage unstable tachycardia.
Cardioversion of stable atrial fibrillation should be performed with caution if the arrhythmia is more than
48 hours old and no anticoagulant therapy has been initiated due to the risk of emboli that can cause MI
This abnormal heart rhythm technically falls under the category of supra-ventricular tachycardias. Atrial
flutter is typically not a stable rhythm and will frequently degenerate into atrial fibrillation.
Atrial Flutter will usually present with atrial rates between 240-350 beats per minute. These rapid atrial
rates are caused by electrical activity that moves in a self-perpetuating loop within the atria.
The impact and symptoms of atrial flutter depend upon the ventricular rate of the patient (i.e. cardiac
output). Usually, with atrial flutter, not all of the atrial impulses will be conducted to the ventricles, and
the more atrial impulses that are conducted, the greater the negative effect.
Symptoms of atrial flutter are similar to those of atrial fibrillation and may include the following:
palpitations, chest pain or discomfort
shortness of air
lightheadedness or dizziness
nervousness and feelings of impending doom
symptoms of heart failure such as activity intolerance and swelling of the legs occur with prolonged
As with its symptoms, atrial flutter shares the same complications as atrial fibrillation. These
complications are usually due to ineffective atrial contractions and rapid ventricular rates. Ineffective
atrial contractions can lead to thrombus formation in the atria and rapid ventricular rates can cause
decompensation and heart failure.
Prevent complications from atrial flutter with early cardioversion.
For the purposes of ACLS, atrial flutter is treated the same as atrial fibrillation. When atrial flutter
produces hemodynamic instability and serious signs and symptoms, it is treated using ACLS protocol.
For the patient with unstable tachycardia due to this tachyarrhythmia (atrial flutter), immediate
cardioversion is recommended. Drugs are not used to manage unstable tachycardia.
Atrial flutter is considerably more sensitive to electrical direct-current cardioversion than atrial
fibrillation, and usually requires a lower energy shock. 20-50J is commonly enough to revert to sinus
Other Tachycardia Rhythms
There are several other tachycardia rhythms that can be seen with both stable and unstable tachycardia.
These rhythms include monomorphic ventricular tachycardia and polymorphic ventricular
tachycardiaboth of which are wide-complex tachycardias.
Wide complex tachycardias are defined as a QRS of 0.12 second. Expert consultation should be
considered with these rhythms.
These wide-complex tachycardias are the most common forms of tachycardia that will deteriorate to
Monomorphic Ventricular Tachycardia
With monomorphic VT all of the QRS waves will be symmetrical. Each ventricular impulse is being
generated from the same place in the ventricles thus all of the QRS waves look the same.
Treatment of monomorphic VT is dependent upon whether the patient is stable or unstable. Expert
consultation is always advised, and if unstable, the ACLS tachycardia algorithm should be followed.
Polymorphic Ventricular Tachycardia
With polymorphic ventricular tachycardia, the QRS waves will not be symmetrical. This is because each
ventricular impulse can be generated from a different location. On the rhythm strip, the QRS might be
somewhat taller or wider.
One commonly seen type of polymorphic ventricular tachycardia is torsades de pointes. Torsades and
other polymorphic VT are advanced rhythms which require additional expertise and expert consultation is
If polymorphic VT is stable the ACLS tachycardia algorithm should be used to treat the patient. Unstable
polymorphic ventricular tachycardia is treated with unsynchronized shocks (defibrillation). Defibrillation
is used because synchronization is not possible.
These wide complex tachycardias tend to originate in the ventricles rather than like a normal rhythm
which originates in the atria.