Sunday, March 3, 2013

ACLS EKG Rhythms and Interpretation

ACLS EKG Rhythms and Interpretation
Each link below will take you to a page for the Respective ACLS EKG. These pages cover all of the basic ACLS EKG’s from Ventricular Fibrillation to Complete Heart Block. After each article is a short video that simulates the ACLS EKG on a defibrillator monitor.

Pulseless Rhythms

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 or AV node. 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
Play the video below to see what a Pulseless Ventricular Tachycardia will generally look like on a defibrillator monitor.

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.
VF should be treated per the pulseless arrest algorithm which is also used for pulseless ventricular tachycardia.
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 H’s and 6 T’s of ACLS. Use the link to review the H’s and T’s.
When an underlying cause for pulseless electrical activity cannot be determined, PEA should be treated in the same fashion as asystole
Question #1: If you saw the rhythm below after defibrillation, how would you determine if it is pulseless electrical activity?

click here for answer» You should check for a carotid or femoral pulsePowered by Hackadelic Sliding Notes 1.6.5

Question #2: What is the most common cause of PEA?
click here for answer» HypovolemiaPowered by Hackadelic Sliding Notes 1.6.5
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.
Below is a short video which will help you quickly identify first-degree AV block
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» The PR interval is the electrical firing of the atria and conduction of that electrical impulse through the AV node to the ventricles.Powered by Hackadelic Sliding Notes 1.6.5 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 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.
Below is a short video which will help you quickly identify second-degree AV bloc
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. no 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 click here to see why» 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 slowedPowered by Hackadelic Sliding Notes 1.6.5
Second-degree AV block (Type 2) is clinically significant for ACLS because this rhythm can rapidly progress to complete heart block
Secocnd-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.

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 tissue and pass through the AV node causing a ventricular contraction for every atrial impulse.
Supraventricular tachycardia is sometimes referred to as atrial tachycardia since the the impulse originates in the atria.
Most SVT’s have a narrow QRS complex. P-waves will be present unless the rate is so rapid that the p-waves are buried in the QRS complexes.
The rapid beating of the heart will often times make the heart have a less-effective pump, which can decrease cardiac output and blood pressure.
A patient may experience the following symptoms which are typical with a rapid pulse of 150–251 or more 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 wheter 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.
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 ventricular 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
  • 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)
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.
Atrial Flutter which produces rapid ventricular rates can degenerate into ventricular fibrillation, causing hemodynamic collapse and death.

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 rhythm.
ACLS Drugs
Each of the ACLS Algorithms utilizes a number of drugs which we will classify as “primary drugs”. The “primary drugs” are the medications that are used directly in an ACLS Algorithm. Here are the Primary ACLS drugs broken down by ACLS Algorithm.
Each is a link to its respective page which covers, in detail, all aspects of the medication and it use in each ACLS algorithm and in post resuscitation efforts.
Vent. Fib./Tach.: Epinephrine,Vasopressin, Amiodarone, Lidocaine, Magnesium
Asystole/PEA  ;Epinephrine, Vasopressin,Atropine (removed from algorithm per 2010 ACLS Guidelines)
Bradycardia ; Atropine, Epinephrine, Dopamine
Tachycardia : adenosine, diltiazem, beta-blockers, amiodarone, digoxin, verapamil, magnesium
Acute Coronary Syndromes: Oxygen, Aspirin, Nitroglycerin, Morphine, Fibrinolytic therapy
Heparin, Beta-Blockers
Acute Stroke
tPA-tissue plasminogen activator, Glucose (D50), Labetalol, Nitroprusside, Nicardipine

Review of Respiratory Arrest
Respiratory Arrest simply means cessation of breathing. In ACLS, respiratory arrest typically means that a patient’s respirations are completely absent or inadequate to maintain oxygenation, but a pulse is present.
Management of respiratory arrest includes the following interventions:
Give oxygen
Open the airway
Provide basic ventilation
Provide respiratory support with the use of artificial airways (OPA and NPA)
Suction to maintain a clear airway
Maintain airway with advanced airways
During respiratory arrest, the ACLS provider should avoid hyperventilation of the patient. Hyperventilation is providing too many breaths per minute or too large of a volume per breath during ventilation. Hyperventilation may lead to increased intrathoracic
pressure, decreased venous return to the heart, diminished cardiac output, and increased gastric inflation, all of which can decrease the likelihood of positive outcomes.
For patients with a perfusing rhythm deliver 1 breath every 5 to 6 seconds
Opening Airway
The most common cause of airway obstruction in a patient that is unresponsive is the loss of tone in the throat muscles. When loss of throat muscle tone occurs the tongue can fall back and obstruct the airway. This type of obstruction is easily prevented
with a basic airway opening technique called the head tilt-chin lift. In the case that spinal injury is suspected, the jaw thrust maneuver can be utilized. This jaw thrust maneuver allows the BLS/ACLS provider to maintain a stable cervical spine.
ACLS Ventilation
There are 5 basic airway skills used to ventilate a patient. Basic ventilation skills are discussed in the BLS course and will not be
discussed in detail here. The following is a list of the 5 basic airway skills: 1.) Head tilt-chin lift; 2.) Jaw thrust without head
extension for possible cervical spine injury; 3.) Mouth-to-Mouth ventilation; 4.) Mouth-to-Barrier device (using a pocket mask); and 5.) Bag-mask ventilation.
Bag-Mask ventilation
Bag-Mask ventilation is the most common method of providing positive-pressure ventilation. Both the oropharyngeal airway and the nasopharyngeal airway may be used as adjuncts to improve effectiveness of patient ventilation. The oropharyngeal airway may only be used on the unconscious patient because it can stimulate gagging and vomiting in a conscious patient. The nasopharyngeal airway may be used on the unconscious patient or on the semiconscious patient and is also indicated if a patient has massive trauma around the mouth or wiring of the jaws.
If the airway is being maintained with the basic airway skills listed above, blood, secretions, and vomit become the primary causes of an obstructed airway in the unconscious patient. Suctioning should be used to clear the airway if it becomes occluded with these body fluids.
Limit suctioning to 10 seconds or less to reduce the risks of hypoxemia. Monitor for changes in heart rate as oropharyngeal suctioning can cause vagal stimulation resulting in bradycardia.
Advanced Airways
Advanced Airways used during ACLS include Combitube, LMA (Laryngeal mask airway), and ET tube (endotracheal tube).
Once an advanced airway is in place, chest compressions are no longer interrupted for ventilations.
1 breath should be given every 6-8 seconds (10-12 breaths per minute).
You should be given adequate time to practice with these devices during your ACLS training before ACLS megacode testing.

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