ACLS and Epinephrine

Epinephrine is the primary drug used in the pulseless arrest algorithm. It is used for its potent vasoconstrictive effects and also for its ability to increase cardiac output. Epinephrine is considered a vasopressor. Indications for ACLS 1. Vasoconstriction effects: epinephrine binds directly to alpha-1 adrenergic receptors of the blood vessels (arteries and veins) causing direct vasoconstriction, thus, improving perfusion pressure to the brain and heart. 2. Cardiac Output: epinephrine also binds to beta-1adrenergic receptors of the heart. This indirectly improves cardiac output by: o Increasing heart rate o Increasing heart muscle contractility o Increasing conductivity through the AV node Epinephrine is used in the pulseless arrest algorithm as a direct IV push and also in the bradycardia algorithm as an infusion. See the respective algorithm pages for more information about their use in each.

Routes
During ACLS, epinephrine can be given 3 ways: intravenous; intraosseous, and endotracheal tube

Dosing
y y

Intravenous Push/IO: 1mg epinephrine IV is given every 3-5 minutes. IV infusion for bradycardia: 1mg epinephrine is mixed with 500ml of NS or D5W. The infusion should run at 2-10 micrograms/min (titrated to effect). Endotracheal Tube: 2-2.5mg epinephrine is diluted in 10cc NS and given directly into the ET tube. Epinephrine should be used with caution in patients suffering from myocardial infarction since epinephrine increases heart rate and raises blood pressure. This increase in HR and BP can increase myocardial oxygen demand and worsen ischemia.

Note: There is no clinical evidence that the use of epinephrine, when used during cardiac arrest, increases rates of survival to discharge from the hospital. However, studies have shown that epinephrine and vasopressin improve rates of ROSC (return of spontaneous circulation).

ACLS and Vasopressin

Vasopressin is a primary drug used in the pulseless arrest algorithm. In high concentrations, it raises blood pressure by inducing moderate vasoconstriction, and it has been shown to be more effective than epinephrine in asystolic cardiac arrest One major indication for vasopressin over epinephrine is its lower risk for adverse side effects when compared with epinephrine. With epinephrine, some studies have shown a risk of increased myocardial oxygen consumption and post arrest arrhythmias because of an increase in heart rate and contractility (beta 1 effects). Vasopressin also is thought too cause cerebral vessel dilation and theoretically increase cerebral perfusion. Trivia: Another name for vasopressin is antidiuretic hormone (ADH).

Routes
Vasopressin may be given IV/IO or by endotracheal tube.

Dosing
40 units of vasopressin IV/IO push may be given to replace the first or second dose of epinephrine, and at this time, there is insufficient evidence for recommendation of a specific dose per the endotracheal tube. In the ACLS pulseless arrest algorithm, vasopressin may replace the first or second dose of epinephrine.

Amiodarone and ACLS

Amiodarone is considered a class III antiarrhythmic agent and is used for various types tachyarrhythmias. Because of its associated toxicity and serious side-effects it should be used cautiously and care should be taken to ensure that cumulative doses are not exceeded.

Indications for ACLS

Amiodarone is an antiarrhythmic that is used to treat both supraventricular arrhythmias and ventricular arrhythmias. The mechanism of action of amiodarone remains unknown, but within the framework of ACLS, amiodarone is used primarily to treat ventricular fibrillation and ventricular tachycardia that occurs during cardiac arrest and is unresponsive to shock delivery, CPR, and vasopressors.

Amiodarone should not be used in individuals with polymorphic VT as it associated with a prolonged QT interval which is made worse with antiarrhythmic drugs.

Amiodarone should only be used after defibrillation/cardioversion and first line drugs such as epinephrine and vasopressin have failed to convert VT/VF.

Route
Amiodarone can be administered by intravenous or intraosseous route.

Dosing
The maximum cumulative dose in a 24 hour period should not exceed 2.2 grams.

Within the VT/VF pulseless arrest algorithm, the dosing is as follows: 300mg IV/IO push (if no conversion) 150 mg IV/IO push (after conversion) Infusion #1 360 mg IV over 6 hours (1mg/min) Infusion #2 540 mg IV over 18 hours (0.5mg/min) For tachyarrhythmias other than life threatening, expert consultation should be considered before use. For Tachycardia other than pulseless VT/VF, Amiodarone dosing is as follows: (see above note) 150 mg over 10 minutes repeat as needed if VT recurs maintenance infusion of 1mg/min for 6 hours

ACLS Drugs for Bradycardia

When bradycardia is being treated in ACLS, if an underlying cause cannot be identified and corrected, medications are indicated. There are three medications used in the bradycardia algorithm: atropine, epinephrine, and dopamine. Each drug and its use within the bradycardia algorithm is explained below.

Atropine
Atropine is the first drug used to treat bradycardia in the bradycardia algorithm. It is classified as an anticholinergic drug and increases firing of the SA Node by blocking the action of the vagas nerve on the heart resulting in an increased heart rate.

Atropine should be used cautiously in the presence of myocardial ischemia and hypoxia since it increases oxygen demand of heart and can worsen ischemia.

The dosing for Atropine is 0.5 mg IV every 3-5 minutes as needed, and the maximum total dosage that can be give is 3 mg. Atropine should be avoided in hypothermic bradycardia and it will not be effective for Mobitz type II/Second Degree Block Type 2.

Epinephrine and Dopamine

Epinephrine and dopamine are second-line drugs for symptomatic bradycardia. They are both used as infusions in the bradycardia algorithm if atropine is ineffective. New 2010 ACLS guidelines state that if bradycardia is unresponsive to atropine, an equally effective alternative to transcutaneous pacing is the use of an IV infusion of the beta-adrenergic agonists (dopamine or epinephrine).

Dosing:
Begin the epinephrine infusion at 2 to 10 mcg/min and titrate to patients response. The goal of therapy is to improve the patients clinical status rather than target an exact heart rate.

Begin the dopamine infusion at 2 to 10 mcg/kg/min and titrate to the patients response.

Precautions
Prior to use of ACLS drugs in the treatment of symptomatic bradycardia, contributing factors of the bradycardia should be explored then ruled out or corrected.

ACLS and Adenosine:

Adenosine should be used within the tachycardia algorithm when vagal maneuvers fail to terminate stable narrow-complex SVT.

Adenosine is the primary drug used in the treatment of stable narrow-complex SVT (supraventricular Tachycardia). It can now also be used for regular monomorphic wide-complex tachycardia. When given as a rapid IV bolus, adenosine slows cardiac conduction particularly effecting conduction through the AV node. The rapid bolus of adenosine also interrupts reentry (SVT causing) pathways through the AV node and restores sinus rhythm in patients with SVT. When injected into the body, adenosine is rapidly absorbed by red blood cells and blood vessel endothelial cells and metabolized for natural uses throughout the body. In light of this adenosine should be administered by RAPID intravenous bolus so that a significant bolus of adenosine reaches the heart before it is metabolized.

A change from the 2010 guidelines now has adenosine given up to two times rather than three.

Dosing
The first dose of adenosine should be 6 mg administered rapidly over 1-3 seconds followed by a 20 ml NS bolus. If the patients rhythm does not convert out of SVT within 1 to 2 minutes, a second 12 mg dose may be given in similar fashion. All efforts should be made to administer adenosine as quickly as possible.

Precautions

Some side effects of adenosine administration incude flushing, chest pain/tightness, brief asystole or bradycardia. Make sure that adenosine is not used for irregular, polymorphic wide-complex tachycardia or VT. Use in these cases may cause clinical deterioration.

CLS 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.

ACLS Algorithms and Their Primary Drugs 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 Aspirin

VF/Pulseless VT
Treatment of Ventricular Fibrillation (VF) and Pulseless Ventricular Tachycardia (VT) is included in the Pulseless Arrest Algorithm. VF and pulseless VT are shockable rhythms and treated in similar fashion. Asystole and PEA are also included in the pulseless arrest algorithm but are nonshockable rhythms. Watch this short video about the 2010 revised and simplified pulseless arrest algorithm. Many of the patients that experience sudden cardiac arrest demonstrate VF at some point in their arrest, therefore, training emphasis is placed on the pulseless arrest algorithm.

Rapid treatment of VF using the pulseless arrest algorithm has been established as the best scientific approach to restoring spontaneous circulation.

There are several important points that should be considered when initiating the pulseless arrest algorithm:

y y y y

High-quality CPR should be performed until the defibrillator is attached the patient. Interruptions in chest compressions should be kept to a minimum. Rapid use of the defibrillator should be emphasized. If possible, use a manual defibrillator over an AED since the use of the AED can result in prolonged interruptions in chest compressions for rhythm analysis and shock administration. No longer are stacked shocks used. CPR is resumed for 5 cycles between each shock.

Defibrillation and the Shock

Most defibrillators used today are biphasic. Biphasic means that the electrical current travels from one paddle to the other paddle and then back in the other direction. The biphasic shock also requires less energy to restore normal heart rhythm and is believed reduce skin burns and cellular damage to the heart. When using a biphasic defibrillator in VF and/or pulseless VT, you will use a dose of 120-200 Joules to shock. To ensure safety during the shock, providers should always announce the following statement, I am going to shock on three. One, Im clearTwo, youre clearThree, everybody is clear.

Do you know the difference between defibrillation, synchronized cardioversion, and unsynchronized cardioversion? Find out here.

Vasopressors
A vasopressor is a medicaton that produces vasoconstriction and a rise in blood pressure. The vasopressors that can be used in the treatment of VF/Pulseless VT are epinephrine and/or vasopressin.Epinephrine is is primarily used for is vasoconstrictive effects. Vasoconstriction is important during CPR because it will help increase blood flow to the brain and heart. Vasopressin is also used for its vasoconstrictive effects and has been shown to have effects similar to those of epinephrine. Rhythm checks should be performed after 5 cycles of CPR. Limit rhythm checks to less than 10 seconds to minimize interruptions in CPR

Antiarrhythmic Drugs
Amiodarone, lidocaine, and magnesium are antiarrhythmic medications that are used in the pulseless arrest algorithm. To learn more detailed information about go here. Learn how to recognize ventricular fibrillation and other rhythms on a defibrillator monitor.

Asystole and Its Treatment in ACLS

Asystole is defined as a cardiac arrest rhythm in which there is no discernible electrical activity on the ECG monitor. Asystole is sometimes referred to as a flat line. Confirmation that a flat line is truly asystole is an important step in the ACLS protocol. Ensure that asystole is not another rhythm that looks like a flat line. Fine VF can appear to be asystole, and a flat line on a monitor can be due to operator error or equipment failure

The following are common causes of an isoelectric line that is not asystole: 1. loose or disconnected leads; 2. loss of power to the ECG monitor; 3. low signal gain on the ECG monitor.

Asystole for many patients is the result of a prolonged illness or cardiac arrest, and prognosis is very poor. Few patients will likely have a positive outcome and successful treatment of cardiac arrest with asystole will usually involve identification and correction of an underlying cause of the asystole. The Hs and Ts of ACLS should be reviewed to identify any underlying cause that could have precipitated the asystole. Some of the most common reasons to stop or withhold resuscitative efforts are:
y y y

DNR status Threat to the safety of rescuers

Family or personal information such as a living will or advanced directive y Rigor mortis To learn more about asystole and watch a short video showing asystole and fine VF on a monitor:

PEA (Pulseless Electrical Activity)

PEA is defined as any organized rhythm without a palpable pulse and is the most common rhythm present after defibrillation. PEA along with asystole make up half of the Pulseless Arrest Algorithm with VF and VT consisting of the other half. Patients with PEA usually have poor outcomes.

Positive outcome of an attempted resuscitation depends primarily on two actions: 1. Providing effective CPR; and 2. Identification and correction of the cause of PEA.

Medications used in PEA

Atropine is no longer recommended for the treatment of PEA per the 2010 ACLS guidelines.

There are 2 medications used in the PEA algorithm, epinephrine and vasopressin. These medications should be given while maintaining high-quality CPR. 1 milligram of epinephrine is given IV or IO every 3-5 minutes. 40 Units of vasopressin can be given IV or IO to replace the first or second dose of epinephrine.

Vasopressors have not been shown to increase survival from PEA

Hs and Ts
The identification and correction of the causes of PEA should be a high priority as a cardiac emergency progresses. One easy way to remember the most common causes of PEA as well as other cardiac emergencies is the Hs and Ts of ACLS. See the Hs and Ts page for more information on the causes and treatment of PEA. Test your skills with the megacode simulator.

Bradycardia Algorithm Review

(includes 2010 AHA Guideline Update)
The major ECG rhythms classified as bradycardia include: Sinus Bradycardia First-degree AV block Second-degree AV block Type I Wenckenbach/Mobitz I Type II Mobitz II Third-degree AV block complete block (See the ECG Interpretation section for images and more detailed information on rhythms)

Bradycardia vs. Symptomatic Bradycardia

Bradycardia is defined as any rhythm disorder with a heart rate less than 60 beats per minute. (Typically it will be <50/min) This could also be called asymptomatic bradycardia. Bradycardia can be a normal non-emergent rhythm. For instance, well trained athletes may have a normal heart rate that is less than 60 bpm. Symptomatic bradycardia however is defined as a heart rate less than 60/min that elicits signs and symptoms, but the heart rate will usually be less than 50/min. Symptomatic bradycardia exists when the following 3 criteria

are present: 1.) The heart rate is slow; 2.) The patient has symptoms; and 3.) The symptoms are due to the slow heart rate.

Functional or relative bradycardia occurs when a patient may have a heart rate within normal sinus range, but the heart rate is insufficient for the patients condition. An example would be a patient with an heart rate of 80 bpm when they are experiencing septic shock.

Bradycardia Pharmacology
There are 3 medications that are used in the Bradycardia ACLS Algorithm. They are atropine, dopamine (infusion), and epinephrine (infusion). More detailed ACLS pharmacology information can be found here. 2010 AHA Update: For symptomatic bradycardia or unstable bradycardia IV infusion chronotropic agents (dopamine & epinephrine) is now recommended as an equally effective alternative to external pacing when atropine is ineffective. Atropine: The first drug of choice for symptomatic bradycardia. Dose in the Bradycardia ACLS algorithm is 0.5mg IV push and may repeat up to a total dose of 3mg. Dopamine: Second-line drug for symptomatic bradycardia when atropine is not effective. Dosage is 2-10 micrograms/kg/min infusion. Epinephrine: Can be used as an equal alternative to dopamine when atropine is not effective. Dosage is 2-10 micrograms/min.

Bradycardia Algorithm
The decision point for ACLS intervention in the bradycardia algorithm is determination of adequate perfusion. For the patient with adequate perfusion, you should observe and monitor. If the patient has poor perfusion, preparation for transcutaneous pacing should be initiated, and an assessment of contributing causes (Hs and Ts) should be carried out.

Transcutaneous pacing (TCP)

Preparation for TCP should be taking place as atropine is being given. If atropine fails to alleviate symptomatic bradycardia, TCP should be initiated. Ideally the patient should receive sedation prior to pacing, but if the patient is deteriorating rapidly, it may be necessary to start TCP prior to sedation.

For the patient with symptomatic bradycardia with signs of poor perfusion, transcutaneous pacing is the treatment of choice. Do not delay TCP for the patient with symptomatic bradycardia with signs of poor perfusion. TCP rate should use 60/min as a starting rate and adjust up or down based on the patients clinical response. The dose for pacing should be set at 2mA (milliamperes) above the dose that produces observed capture.

TCP is contraindicated for the patient with hypothermia and is not a recommended treatment for asystole. A carotid pulse should not be used for assessment of circulation as TCP can create muscular movements that may feel like a carotid pulse. Assess circulation using the femoral pulse. Identification of contributing factors for symptomatic bradycardia should be considered throughout the ACLS protocal since reversing of the cause will likely return the patient to a state of adequate perfusion.

Tachycardia and its ACLS Algorithm

Tachycardia/tachyarrhythmia is defined as a rhythm with a heart rate greater than 100 bpm. An unstable tachycardia exists when cardiac output is reduced to the point of causing serious signs and symptoms. Serious signs and symptoms commonly seen with unstable tachycardia are: chest pain, signs of shock, SOA, altered mental status, weakness, fatigue, and syncope

One important question you may want to ask is: Are the symptoms being caused by the tachycardia? If the symptoms are being caused by the tachycardia treat the tachycardia.

There are many causes of both stable and unstable tachycardia and appropriate treatment within the ACLS framework requires identification of causative factors. Before initiating invasive interventions, reversible causes should be identified and treated.

Causes
The most common causes of tachycardia that should be treated outside of the ACLS tachycardia algorithm are dehydration, hypoxia, fever, and sepsis. There may be other contributing causes and review of the Hs and Ts of ACLS should take place as needed. Administration of OXYGEN and NORMAL SALINE are of primary importance for the treatment of causative factors of sinus tachycardia and should be considered prior to ACLS intervention.

Once these causative factors have been ruled out or treated, invasive treatment using the ACLS tachycardia algorithm should be implemented.

Associated Rhythms
There are several rhythms that are frequently associated with stable and unstable tachycardia these rhythms include:
y y y y y y

Atrial fibrillation Atrial flutter Supraventricular tachycardia (SVT) Monomorphic VT Polymorphic VT Wide-complex tachycardia of uncertain type

Visit the links above to learn about each specific rhythm.

ACLS Treatment for Tachycardia

The fist question that should be asked when initiating the ACLS tachycardia algorithm is: Is the patient stable or unstable? The answer to this question will determine which path of the tachycardia algorithm is executed.

Patients with unstable tachycardia should be treated immediately with synchronized cardioversion. If a pulseless tachycardia is present patients should be treated using the pulseless arrest algorithm. Patients with stable tachycardia are treated based upon whether they have a narrow or wide QRS complex. The following flow diagram shows the treatment regimen for stable tachycardia with narrow and wide QRS complex. y Stable (narrow QRS complex) vagal maneuvers adenosine (if regular) beta-blocker/calcium channel blocker get an expert
y

Stable (wide/regular/monomorphic)

adenosine

consider antiarrhythmic infusion

get an expert

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.
y y y y

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
Symptoms of atrial flutter are similar to those of atrial fibrillation and may include the following:
y y y y y y

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.

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:
y y y y y

Shortness of air (S) Palpitation feeling in chest (S) Ongoing chest pain (U) Dizziness (S)

Rapid breathing (S) y Loss of consciousness (U) y 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

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 pusleless 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), andTrauma. 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. The Ts include:

Toxins
Accidental overdose of a number of different kinds of medications can cause pulseless arrest. Some of the most common include: tricyclics, digoxin, betablockers, calcium channel blockers, and erythromycin). 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 drug 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 indicating coronary thrombosis are 12 lead ECG with ST-segment changes, T-wave inversions, and/or Q waves. Physical signs include: elevated cardiac markers on lab tests, and chest pain/pressure. Treatments for coronary thrombosis 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.

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

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 the6 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

Pop-Quiz:
Question #1: If you saw the rhythm below after defibrillation, how would you determine if it is pulseless electrical activity?

click here for answerYou 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 answerHypovolemiaPowered by Hackadelic Sliding Notes 1.6.5

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. 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.

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 in the pulseless arrest algorithm is the use of epinephrine and CPR. 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.

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. nonconducted 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 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 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:
y y y y y y

Shortness of air (S) Palpitation feeling in chest (S) Ongoing chest pain (U) Dizziness (S) Rapid breathing (S)

Loss of consciousness (U) y 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.

y y

palpitations or chest discomfort

shortness of air and possibly respiratory distress y hypotension, light-headedness and possibly loss of consciousness y 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
Symptoms of atrial flutter are similar to those of atrial fibrillation and may include the following:
y y y y y y

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.