Pulseless Rhythms Pulseless Ventricular Tachycardia

Ventricular Fibrillation
Pulseless Electrical Activity
Asystole
Bradyarrhythmias First Degree AV Block
Second Degree AV Block (Type 1)
Second Degree AV Block (Type 2)
Complete Heart Block
Tachyarrhythmias Supraventricular Tachycardia
Atrial Fibrillation
Atrial Flutter
Other Tachycardias

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 pulse.
Pulselessness with a tachyarrhythmia occurs because the ventricles are not effectively moving blood out of the heart and there is therefor
no cardiac output. Many tachyarrhythmias of a rate >150 will deteriorate into pulselessness if timely treatment is not given.

Pulseless ventricular tachycardia is treated using the left branch of the puslesless arrest arrest algorithm.
VENTRICULAR FIBRILLATION

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.
Ventricular fibrillation is always pulseless and must be confirmed by EKG or defibrillator monitor. Defibrillation is the treatment of choice
and should occur as soon as possible.

Ventricular fibrillation is treated using the left branch of the puslesless arrest arrest algorithm.

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 situation.
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.
HS AND TS OF ACLS
Knowing the Hs and Ts of ACLS will help prepare you for any ACLS scenario. Dont forget your Hs and Ts when using the ACLS
Megacode Simulator. The Hs and Ts of ACLS is a mnemonic used to help recall the major contributing factors to pulseless arrest
including PEA, Asystole, Ventricular Fibrillation, and Ventricular Tachycardia. These Hs and Ts will most commonly be associated with
PEA, but they will help direct your search for underlying causes to any of arrhythmias associated with ACLS. Each is discussed more
thoroughly below.

The Hs include:
Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hyper-/hypokalemia, Hypoglycemia, Hypothermia.
The Ts include:
Toxins, Tamponade(cardiac),Tension pneumothorax, Thrombosis (coronary and pulmonary), and Trauma.

Hypovolemia
Hypovolemia or the loss of fluid volume in the circulatory system can be a major contributing cause to cardiac arrest. Looking for
obvious blood loss in the patient with pusleless arrest is the first step in determining if the arrest is related to hypovolemia. After CPR,
the most import intervention is obtaining intravenous access/IO access. A fluid challenge or fluid bolus may also help determine if the
arrest is related to hypovolemia.

Hypoxia
Hypoxia or deprivation of adequate oxygen supply can be a significant contributing cause to cardiac arrest. You must ensure that the
patients airway is open, and that the patient has chest rise and fall and bilateral breath sounds with ventilation. Also ensure that your
oxygen source is connected properly.

Hydrogen ion (acidosis)

To determine if the patient is in respiratory acidosis, an arterial blood gas evaluation must be performed. Prevent respiratory acidosis by
providing adequate ventilation. Prevent metabolic acidosis by giving the patient sodium bicarbonate.

Hyper-/hypokalemia
Both a high potassium level and a low potassium level can contribute to cardiac arrest. The major sign of hyperkalemia or high
serum potassium is taller and peaked T-waves. Also, a widening of the QRS-wave may be seen. This can be treated in a number of
ways which include sodium bicarbonate (IV), glucose+insulin, calcium chloride (IV), Kayexalate, dialysis, and possibly albuterol. All
of these will help reduce serum potassium levels.
The major signs of hypokalemia or low serum potassium are flattened T-waves, prominent U-waves, and possibly a widened QRS
complex. Treatment of hypokalemia involves rapid but controlled infusion of potassium. Giving IV potassium has risks. Always
follow the appropriate infusion standards. Never give undiluted intravenous potassium.
 Hypoglycemia
Hypoglycemia or low serum blood glucose can have many negative effects on the body, and it can be associated with cardiac arrest.
Treat hypoglycemia with IV dextrose to reverse a low blood glucose. Hypoglycemia was removed from the Hs but is still to be
considered important during the assessment of any person in cardiac arrest.

Hypothermia
If a patient has been exposed to the cold, warming measures should be taken. The hypothermic patient may be unresponsive to drug
therapy and electrical therapy (defibrillation or pacing). Core temperature should be raised above 86 F (30 C) as soon as possible.

Toxins
Accidental overdose of a number of different kinds of medications can cause pulseless arrest. Some of the most common include:
tricyclics, digoxin, betablockers, and calcium channel blockers). Street drugs and other chemicals can precipitate pulseless arrest.
Cocaine is the most common street drug that increases incidence of pulseless arrest. ECG signs of toxicity include prolongation of the QT
interval. Physical signs include bradycardia, pupil symptoms, and other neurological changes. Support of circulation while an antidote or
reversing agent is obtained is of primary importance. Poison control can be utilized to obtain information about toxins and reversing
agents.

Tamponade
Cardiac tamponade is an emergency condition in which fluid accumulates in the pericardium (sac in which the heart is enclosed). The
buildup of fluid results in ineffective pumping of the blood which can lead to pulseless arrest. ECG symptoms include narrow QRS
complex and rapid heart rate. Physical signs include jugular vein distention (JVD), no pulse or difficulty palpating a pulse, and muffled
heart sounds due to fluid inside the pericardium. The recommended treatment for cardiac tamponade is pericardiocentesis.

Tension Pneumothorax
Tension pneumothorax occurs when air is allowed to enter the plural space and is prevented from escaping naturally. This leads to a
build up of tension that causes shifts in the intrathroacic structure that can rapidly lead to cardiovascular collapse and death. ECG signs
include narrow QRS complexes and slow heart rate. Physical signs include JVD, tracheal deviation, unequal breath sounds, difficulty with
ventilation, and no pulse felt with CPR. Treatment of tension pneumothorax is needle decompression.

Thrombosis (heart: acute, massive MI)

Coronary thrombosis is an occlusion or blockage of blood flow within a coronary artery caused by blood that has clotted within the
vessel. The clotted blood causes an acute myocardial infarction which destroys heart muscle and can lead to sudden death
depending on the location of the blockage.
ECG signs during PEA indicating coronary thrombosis include ST-segment changes, T-wave inversions, and/or Q waves. Physical
signs include: elevated cardiac markers on lab test.
For patients with cardiac arrest and without known pulmonary embolism (PE), routine fibrinolytic treatment given during CPR has
shown no benefit and is not recommended.
Treatments for coronary thrombosis before cardiac arrest include use of fibrinolytic therapy, PCI (percutaneous coronary
intervention). The most common PCI procedure is coronary angioplasty with or without stent placement.

Thrombosis (lungs: massive pulmonary embolism)

Pulmonary thrombus or pulmonary embolism (PE) is a blockage of the main artery of the lung which can rapidly lead to respiratory
collapse and sudden death. ECG signs of PE include narrow QRS Complex and rapid heart rate. Physical signs include no pulse felt with
CPR. distended neck veins, positive d-dimer test, prior positive test for DVT or PE. Treatment includes surgical intervention (pulmonary
thrombectomy) and fibrinolytic therapy.

Trauma
The final differential diagnosis of the Hs and Ts is trauma. Trauma can be a cause of pulseless arrest, and a proper evaluation of the
patients physical condition and history should reveal any traumatic injuries. Treat each traumatic injury as needed to correct any
reversible cause or contributing factor to the pulseless arrest. Trauma was removed from the Ts but is still to be considered important
during the assessment of any person in cardiac arrest.

When an underlying cause for pulseless electrical activity cannot be determined, PEA should be treated in the same fashion as asystole

Pulseless electrical activity is treated using the right branch of the puslesless arrest arrest algorithm.
Question #1: If you saw the rhythm below after defibrillation, how would you determine if it is pulseless electrical activity? You should check
for a carotid or femoral pulse.

Question #2: What is the most common cause of PEA? Hypovolemia.

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.

Asystole is treated using the right branch of the puslesless arrest arrest algorithm.

During asystole, there is no blood flow to the brain and other vital organs. This results in very poor outcomes if resuscitation is successful.
If asystole is visualized on the monitor, you should ensure that all leads are connected properly. If all leads are properly connected, you
should rapidly assess for any underlying causes for the asystole.
As with pulseless electrical activity (PEA), asystole can have possible underlying causes which can be remembered using the Hs and Ts
mnemonic.
Question: What can sometimes be mistaken for asystole during a code? Fine ventricular fibrillation.

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 PR interval.
One of the main identifying characteristics of second degree heart block type 1 is that the atrial rhythm will be regular.

In the above image, notice that the p-waves are regular, the PR-interval progressively gets longer until a QRS is dropped and only the p-
wave is present.
Although second degree heart block type-1 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 (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 (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 it
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 QRS Complexes

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.

Common Causes
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 hemodynamic instability.
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 & hypotension.
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)
Dizziness (S)
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

ATRIAL FIBRILLATION
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 fibrillation.
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.

ACLS Treatments
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 and stroke.

ATRIAL FLUTTER
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
palpitations, chest pain or discomfort
shortness of air
lightheadedness or dizziness
nausea
nervousness and feelings of impending doom
symptoms of heart failure such as activity intolerance and swelling of the legs occur with prolonged fast flutter)

Complications
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.

Treatment
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.

Cardioversion
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 rhythm.

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 tachycardia both 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 ventricular fibrillation.

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 advised.
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.