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What is the primary focus of ACLS?

CPR and defibrillation. CAB’s are followed and then D, which is defibrillation.


What are the concepts of ACLS?

  1. Resuscitate the heart, restore the brain. Need to start resuscitation early.
  2. Treat the patient, not the arrhythmia. Don’t wait! If pt has no pulse, do chest compressions.
  3. Value of the unbroken chain of survival: BLS-Defibrillation-ACLS.
  4. Time is critical. The quicker you defibrillate someone in pulseless v tach or v fib, the higher the chances of survival.
  5. Seek and Treat the Cause.
  6. Restart the Heart and Keep It Restarted.
  7. Know the Phases of Resuscitation.
  8. Expect Deaths and Futile Resuscitations.
  9. Chain of Survival Can Be Applied in the Community.
  10. Strengthen the Chain of Survival.

What are the characteristics of an oropharyngeal airway?

Oral airway (Oropharyngeal airway) a J-shaped plastic device; distal tip lies between the base of the tongue and the back of the throat

Proper size is important. Could possibly slide down and obstruct the airway, but don’t see them used very often.

The oral airway is just the little plastic piece that you use to compress the tongue so it doesn’t get in the way.


What are the characteristics of a nasopharyngeal airway?

Nasal airway is soft uncuffed rubber or plastic tube

Many sizes

Used when we need to suction the patient. Allows suction without much trauma to the airway.


What are the characteristics of endotracheal intubation?

Endotracheal intubation provides definitive airway management and should be performed by properly trained personnel.

Tube is placed directly into the trachea

Laryngoscope handle and blade are used to place the tube

Indications for endotracheal intubation include: cardiac arrest with ongoing chest compression, inability of a conscious patient in respiratory compromise to breathe adequately, inability of the patient to protect the airway (coma, cardiac arrest), inability of the qualified rescuer to ventilate the unresponsive patient with conventional methods, trauma and deeply comatose.

Not a sterile procedure to intubate someone.

After intubation, listen for breath sounds in all lobes. Common problem is that the tube goes into the right side. If breath sounds are uneven, deflate the bulb on the end of the tube and have it replaced. Listen for BS again. If in place, call for CXR to confirm placement. After placement, secure the tube.

Certain drugs maybe administered via ETT double the dose of IV route. NAVEL - Narcan, Atropine, Valium/Vasopressin, Epinephrine, Lidocaine


What is the nurse's responsibility in endotracheal intubation?

Checking for correct placement

Securing with tape

Administering 100% oxygen

Requesting x-ray


What is cricoid pressure and when is it used?

Cricoid pressure- To protect against regurgitation and help ensure tube placement in the tracheal orifice. During intubation a second rescuer applies pressure to the cricoid area.

Pushes the tracheal orifice backward and more into the visual field of the person performing the intubation.

Release pressure only when proper tube placement is confirmed and the cuff is inflated.


What are some other advanced airway tools used in emergency situations?

Bag valve mask – Ensure adequate seal. Hard to obtain a seal. Many clinicians recommend that 2 rescuers work together.

End tidal CO2 detectors – Indicates CO2 exhaled from the lungs. Color change - Yellow is yes, purple is no.

Laryngeal Mask Airway (LMA)– Provides an airway adjunct with a cuffed masklike projection at the distal end that is introduced into the pharynx and advanced until resistance is felt. Resistance indicates the distal end has reached the hypopharynx.

Combitube –Is a tracheal tube bonded side by side with an esophageal oburator. Ventilation can be given through either lumen depending on where the end inserted in the patient rests.


What are the characteristics of dysrhythmias?

Any disorder of the heartbeat.

Results from the following:

–A disturbance in the relationship between electrical conductivity and the mechanical response of the myocardium.

–A disturbance in impulse formation (either from an abnormal rate or ectopic focus).

–A disturbance in impulse conduction( delays and blocks).

–Or a combination of the above.


What are the characteristics of bradydysrhythmias?

Myocardial oxygen demand is reduced from the slow heart rate.

Coronary perfusion time may be adequate

Coronary perfusion pressure may decrease if the rate is too slow to provide adequate cardiac output and blood pressure.

If you notice a client with a bradydysrhythmia, check the BP and LOC first. Is the pt stable or unstable? Is their condition changing?


What are the characteristics of sinus bradycardia?

Sinus = a P wave before every QRS and a PR interval that is .12-.20

Impulses originate at SA node at a slow rate.

This slows the heart rate and decreases the speed of conduction through the AV node and conduction system.

When the sinus node discharge is less than 60 beats/min in adults, the rhythm is called sinus bradycardia.

Coronary perfusion time may be adequate.

Myocardial oxygen demand maybe decreased.

Only clinical manifestation is sinus node discharges at a rate of less than 60 bpm


What is the significance of sinus bradycardia?

Depends on how each patient tolerates the rate.

Is the patient being effected hemodynamically? Check BP!

Hypotension with decreased cardiac output may occur in some cases.

Note that a slow heart rate may be normal for some individuals.


What are the types of AV blocks from least dangerous to most dangerous?

First degree AV Block (least dangerous)

Second degree - Mobitz Type I AV Block or Wencheback

Second degree - Mobitz Type II AV Block

Third degree block AV Block (most dangerous)

With any of these, no matter how stable the pt, watch for progression and worsening.

They are most often caused by occlusion of the left anterior descending artery.

Transcutaneous pacing can be used as a bridge until a transvenous pacer becomes available.


What are the characteristics of a first-degree AV block?

Pt's PR interval is longer than .20

Caused by degenerative changes in the heart or myocardial infarction

Drugs: Beta blockers, calcium blockers, digoxin

Usually will just watch for progression and worsening.


What are the characteristics of Type I second-degree AV block?

The PR intervals get progressively longer until a QRS is eventually dropped.

Caused by CAD, drug use (like amphetamines or cocaine), increased parasympathetic tone, or inferior-wall MI.


What are the characteristics of a Type II second-degree block?

QRS complexes are dropped at a more significant and more consistent rate. Can drop multiple QRS complexes in a row before finally having one.

Caused by anterior wall MI, degenerative changes in the conduction system, organic heart disease, and severe CAD.

Can convert to complete third degree without warning.


What are the characteristics of third-degree AV block?

P waves and QRS complexes are completely independent of one another. They fire at a completely different rhythm than one another.

Caused by AV node damage, increased parasympathetic tone, inferior-wall MI, and toxic effects of drugs like digoxin and propanolol.


What are the key clinical questions to ask for all bradydysrhythmias?

1.Does the slow rate make the patient ill?

2.Are there “serious” signs or symptoms?

3.Are the signs and symptoms related to the slow heart rate (hypotension, decreased LOC, lethargy, etc.)?


What would a physical assessment of a patient who is experiencing symptoms related to bradycardia most likely include?

Pulse rate less than 60 bpm.

Dizziness, Shortness of breath

Weakness, fatigue, lightheadness


Confusion, decreased LOC


Serious symptoms – chest pain, shortness of breath, decreased level of consciousness, weakness, fatigue, lightheadness, dizziness, and syncope.

Signs – hypotension, pulmonary congestion, pulmonary edema, congestive heart failure and ventricular tachycardia.


What are some interventions available for bradydysrhythmias?

Atropine 0.5mg IV (q5min, 3 mg max)


TCP (transcutaneous pacing): For pacing, place the pads on the pt. Set the BPM on the machine. Then manipulate the milliamps until the heart captures the pacemaker’s impulse. You’ll have a spike or electricity followed by a QRS. After you have capture, check a pulse and a BP to see if they’re becoming hemodynamically stable.

Dopamine infusion

Epinephrine infusion


What are the characteristics of atropine as an intervention for bradydysrhythmias?

Atropine should be used with caution, especially if you suspect that the patient has AMI.

Atropine may exacerbate ischemia or induce VT or VF or both when used to treat bradycardia associated with AMI.

Atropine is ineffective in many patients with a higher-level block or serious conduction system failure

Dose: Symptomatic bradycardia, give atropine 0.5 mg IV, repeated every 3 to 5 minutes, to a total of 3 mg.


What are the characteristics of transcutaneous pacing?

Can be started quickly and conveniently at the bedside.

TCP requires no special equipment.

Accomplished through the application of two large external electrodes.

Used to stimulate ventricular depolarization when the patient’s heart rate is slower than the rate set on the pacer.


  • If the bradycardia is very slow with urgent symptoms and the patients clinical condition is unstable, perform TCP immediately.
  • Start TCP for patients who do not respond to atropine or who are severely symptomatic.
  • Mobitz type II second degree AV block, Third degree AV block.


  • Place pads on chest and turn pacer ON.
  • Electrical capture is usually characterized by a widening of the QRS complex (looks like a PVC) by a broad T wave.
  • Activate the device usually at a rate of 60 bpm or the physician’s orders.
  • Tell the patient what to expect if awake. Uncomfortable muscle contractions that the pacemaker creates.
  • Mild analgesia may be given.

What are the characteristics of dopamine and epinephrine infusions?


  • Used after the maximum dose of atropine is reached.
  • Dopamine infusion start at 2 to 10 micrograms/kg per minute and titrate to patient response.
  • Dopamine has an alpha-adrenergic and beta 1 effect, causing enhanced myocardial contractility, increased heart rate, and increased blood pressure.


  • If the patient has severe bradycardia with hypotension, the drug of choice is epinephrine.
  • Epinephrine infusion is also indicated when higher doses of dopamine is ineffective.
  • Begin the infusion at a dose of 2 to 10 micrograms/min and titrate to patient response.

What are the characteristics of asystole?

žA cardiac arrest rhythm associated with no discernable electrical activity on the monitor.

žSometimes called ventricular standstill.

žIs rarely associated with a positive outcome, usually a negative outcome.

žLarge percentage do not survive.

žRepresents the total absence of any electrical activity.

žNo ventricular contraction occurs because depolarization does not occur.

žYou may see a P wave but no QRS complex.

žThe sinoatrial node may continue to fire and depolarize the atria.

žRequires immediate attention.

Check asystole in TWO LEADS before acting on it.

žVentricular fibrillation may masquerade as asystole.

žThe nurse must assess the rhythm in another lead for accurate interpretation, check monitor display for sensitivity or gain.

žTreatment of these two rhythms (VF,Asystole) differs greatly, the nurse must be familiar with the specific treatment.

žClinical associations: Advanced cardiac disease, severe cardiac conduction system, advanced heart failure, severe hyperkalemia, acidosis.

žPhysical assessment: patients are in full arrest with a loss of conscious, absence of pulse, respirations, and blood pressure.


How is asystole treated?

CPR for 2 min each cycle

Epinephrine 1mg IV repeat every 3 to 5 minutes

  • žEpinephrine produces vasoconstriction and increases diastolic blood pressure, blood flow to the brain, and some blood flow to the heart, specifically the coronary arteries.


žVasopressin 40 U IV to replace the first or second dose of epinephrine. Can be given only once!

žMay give sodium bicarbonate equal to 1 mEq/kg. This is helpful if known to have hyperkalemia or a known drug overdose with tricyclic antidepressants.

žIf asystole persists, ask these questions

  • ž Withhold or cease resuscitative efforts?
  • žConsider quality of resuscitation?
  • žSupport for cease-efforts protocols in place?



What are the differential diagnoses and common causes for asystole?



3.Hydrogen ion (acidosis)




1.Tablets (drug overdose)


3.Tension pneumothorax

4.Thrombosis (heart, AMI)

5.Thrombosis (lungs, pulmonary embolus)


What are the characteristics of the 6 H's of frequent causes of asystole?


  • —Features of electrical activity – narrow QRS complex and rapid rate.
  • —Physical assessment – patient’s history, narrow neck veins.
  • —Treatment – volume infusion, 500 mL normal saline as quickly as possible.
  • —Common cause of asystole and PEA.


  • —Features of electrical activity: slow rate.
  • —Physical assessment: cyanosis, blood gases, airway problems.
  • —Treatment: oxygenation, ventilation.
  • —Common cause.

žHydrogen ion (acidosis):

  • —Features of electrical activity: smaller QRS complexes.
  • —Physical assessment: history of diabetes, renal failure.
  • —Treatment: sodium bicarbonate, insulin, hyperventilation.

Hyperkalemia or hypokalemia:

  • —Features of electrical activity:
  • —Hyperkalemia will have higher T waves and peaked.
  • —Hypokalemia will have flat T waves with prominent U waves.
  • —Physical assessment of hyperkalemia: history of renal failure, diabetes, dialysis, medications
  • —Physical assessment of hypokalemia: abnormal loss of potassium, diuretic use.
  • Treatment: Hyperkalemia – sodium bicarbonate, glucose plus insulin, calcium chloride, Kayexalate, dialysis (long term). Hypokalemia- rapid but controlled infusion of potassium.


  • Physical assessment: History of exposure to cold, central body temperature.
  • Treatment: Bear Hugger, warm blankets
  • Don’t want to get temp up too fast though


  • Check blood glucose, administer Dextrose 50 if necessary.
  • žCheck history of patient.

What are the specific characteristics for the 5 T's of common causes of asystole?


  • —Features of electrical activity: various effects on EKG.
  • —Physical assessment: bradycardia, history of ingestion, pupils, neurologic exam
  • —Treatment: drug screens, lavage, activated charcoal, specific antidotes, lactulose.


  • —Features of electrical activity –narrow complex, rapid rate.
  • —Physical assessment – history, neck vein distention
  • —Treatment - pericardiocentesis

žTension Pneumothorax:

  • žFeatures of electrical activity – narrow complex slow rate.
  • žPhysical assessment – history, no pulse, neck vein distention, tracheal deviation, unequal breath sounds.
  • žTreatment – needle decompression.

žThrombosis (coronary, MI):

  • —Features of electrical activity – Abnormal EKG, Q wave, ST changes.
  • —Physical assessment – history, EKG, enzymes.
  • Treatment – Fibrinolytic agents


  • —Features of electrical activity – narrow complex, rapid rate.
  • —Physical assessment – history, distended neck veins.
  • —Treatment – surgical embolectomy, fibrinolytics.

What is pulseless electrical activity?

žRefers to any semiorganized or organized electrical activity that can be seen on the monitor although the patient lacks a palpable pulse.

žExcludes VF, ventricular tachycardia (VT) and asystole.

žPrognosis is poor unless the underlying cause can be identified and corrected.

žFocus on assessing and treating patients.

žSearch for the reversible cause, which is the key to treating these patients.

žMany conditions may cause PEA.

žPEA displays electrical activity but produces no clinically detectable pulse.

žPathophysiology – cardiac conduction impulses occur in organized pattern, but this fails to produce myocardial contraction; or insufficient ventricular filling during diastole; or ineffective contractions.

žKey treatment for this rhythm is to identify and treat reversible causes and to provide effective CPR.


How is PEA treated?

Same as asystole for the drugs.

žRapid assessment and aggressive management offer the best chance of success.

žPEA is often associated with a reversible clinical state.

žNeed to search for a reversible cause.

žRemember the 6 H’s and 5 T’s.



What are the characteristics of stable tachycardia?

Refers to a condition in which the patient has:

1. Heart rate more than 100 bpm

2. No significant signs or symptoms caused by the increased rate.

3. Or it could be an underlying cardiac abnormality that generates the rhythm.

These stable tachycardias include:

1. Narrow-complex tachycardias with a pulse

2. Wide-complex tachycardias with a pulse

3. Atrial fibrillation/flutter

Treatment focus:

1. Control the rate

2. Convert the rhythm

3. Provide anticoagulation if needed


What are the key questions to ask when evaluating a patient with stable tachycardia?

1.Are symptoms present or absent?

2.Are symptoms due to the tachycardia?

3.Is the patient stable or unstable?

4.Is the QRS complex narrow or wide?

5.Is the rhythm regular or irregular?

6.Is the rhythm sinus tachycardia?

The answers guide treatment and diagnosis.

If at any point the patient starts to become unstable, begin to prepare for synchronized cardioversion for narrow complex tachycardia.


What are some treatment methods for stable tachycardia that is narrow complex and is regular?

Vagal maneuvers increase vagal nerve stimulation and can slow an SVT. In addition to a therapeutic value, these maneuvers can have a diagnostic value. If the vagal maneuvers appear to change the rate, it is much more likely to be of the supraventricular origin.

Carotid sinus massage is contraidicated in those who are known to have carotid artherosclerosis. (check for bruit)

Other techniques include Valsalva maneuver.


Cold water to face


  • First drug for most forms of narrow tachycardia.
  • Does not convert atrial fibrillation, flutter, or VT.
  • Initial dose is 6 mg IV rapidly over 1 to 3 seconds. (half life is 10-13 seconds)
  • Repeat dose of 12mg in 1 to 2 minutes if needed.
  • May repeat dose of 12 mg dose once
  • Should be administered using filter
  • May shortly go into asystole after dose of adenosine. Don’t be alarmed, it’s temporary.
  • Side effects could include flushing, chest pain, or tightness.
  • May cause bronchospasm; avoid using it in patients with airway disease.

If converts:

  • Observe for recurrence
  • Treat recurrence with Adenosine or longeracting AV nodal blocking agents such as diltiazem, beta blockers

If does not convert:

  • May use diltiazem, beta blockers to control rate, treat underlying cause
  • Could be atrial flutter or a junctional tachycardia.
  • Try to control rate with diltiazem, beta blockers
  • Treat underlying cause
  • Consider expert consultation

How is stable tachycardia that's regular with a wide complex (greater than .12) treated?

Consider adenosine only if regular and monomorphic (looks consistent)

Consider antiarrhythmic infusion:

  • Procainamide IV Dose:
    • 20-50 mg/min via IV drip until arrhythmia suppressed, hypotension ensues, QRS duration increases > 50%, or maximum dose 17 mg/kg given.
    • Maintenance infusion: 1-4 mg/min. Avoid if prolonged QT or CHF.
    • Constantly monitor BP on this drip
  • Amiodarone 150 mg IV over 10 minutes
    • Repeat as needed if VT recurrs.
    • Follow by maintenance infusion of 1 mg/min for first 6 hours.
  • Sotalol IV Dose:
    • 100 mg (1.5 mg/kg) over 5 minutes
  • Prepare for elective synchronized cardioversion if regular.
    • Cardioversion – is a countershock that depolarizes a critical mass of myocardium.
    • It is intended to stop the re-entry circuit and allow the sinus node to regain control of the heart.
    • The machine synchs with the heart beat and delivers the shock on the R wave in order to try to establish a new rhythm.

Consider expert consultation


What are the characteristics of unstable tachycardia?

Exists when the heart beats too fast for the patients cardiovascular condition.

Two keys to management of these type:

1. Rapid recognition that the patient is unstable.

2. Rapid recognition that the signs and symptoms are caused by the tachycardia.

3. Remember the patient has a pulse!


How is unstable tachycardia treated?

Establish IV access and give sedation.

Prepare for immediate cardioversion.

If time, premedicate.

Synchronized cardioversion:

  • 50-100 J for narrow regular
  • 120-200 J for narrow irregular
  • 100 J for wide regular

What is the difference between cardioversion and defibrillation?

Cardioversion (synchronized) uses a sensor to deliver a shock that is synchronized with a peak of the QRS complex (highest point of the R wave). Avoids the shock delivery during cardiac repolarization.

Defibrillation (unsynchronized) is accomplished by the passage of a direct current (DC) electrical shock through the heart that is sufficient to depolarize the cells of the myocardium. The intent is to allow the SA node to resume the pacemaker role. The shock will be delivered as soon as the operator pushes the shock button.

  • Biphasic - A type of defibrillation waveform where a shock is delivered to the heart via two vectors. Biphasic waveforms were initially developed for use in implantable defibrillators and have since become the standard in external defibrillators. 120-200 J of energy
  • Monophasic - A type of defibrillation waveform where a shock is delivered to the heart from one vector. Max is 360 J of energy

What are the characteristics of pulseless ventricular tachycardia?

Sometimes referred to as “V tach”

Occurs with repetitive firing of an irritable ventricular ectopic focus.

Ventricular tachycardia may occur with/ without a pulse and may be stable or unstable. Make sure to feel for a pulse! Probably need to go for the femoral or the carotid.

Pathophysiology of VT: Ventricles consist of areas of normal myocardium alternation with areas of ischemic, injuried, or infarcted myocardium, leading to chaotic pattern of ventricular depolarization.

VT may occur in clients with ischemic heart disease, MI, cardiomyopathy, hypokalemia, hypomagnesmia, valvular heart disease, drug toxicity.

VT is commonly the initial rhythm before deterioration into ventricular fibrillation as the terminal rhythm.

Some signs/symptoms include: shock, chest pain, hypotension, shortness of breath, pulmonary congestion, congestive heart failure, and acute MI.


What are the characteristics of ventricular fibrillation?

Pathophysiology of VF: is the result of electrical chaos in the ventricles. Impulses from many irritable foci fire in a totally disorganized manner so that ventricular contraction cannot occur. The ventricles merely quiver, consuming a large amount of oxygen.There is no cardiac output or pulse and therefore no cerebral, myocardial, or systemic perfusion.

This rhythm is rapidly fatal if not terminated within 3 to 5 minutes.

VF may be the first manifestations of coronary artery disease. Patients with myocardial infarction are at great risk for VF.

VF may occur in patients with myocardial ischemia, hypokalemia, hypomagnesemia, electroculation.

Physical assessment: patient may become faint, immediately loses consciousness, and becomes pulseless and apneic. Seizures may occur, pupils become fixed and dilated, skin is cold and mottled.

Death ensues without treatment.


What are the treatments for both pulseless V. tach and V. fib?

Treatment: Shock !!! Monophasic @ 360 J; if biphasic 120 to 200 J. Resume CPR Immediately. Give 5 cycles of CPR

Early Defibrillation is essential.

Check rhythm; is it shockable or unshockable such as with PEA/Aystole

Shock @ 360 if monophasic, continue CPR while defibrillator is charging.

Defibrillation or unsynchonized is accomplished by the passage of a direct current (DC) electrical shock through the heart that is sufficient to depolarize the cells of the myocardium.

The intent is that the repolarization will allow the SA node to resume the role of the pacemaker.

Rhythm after shock? Examine the monitor to identify one of the following possibilities:

  • VT/VF
  • Potentially perfusing rhythm
  • Pulseless electrical activity
  • Asystole

What medications are used for treatment of V. tach and V. fib?

oEpinephrine 1 mg IV/IO push, repeat every 3 to 5 minutes or may give 1 dose of Vasopressin 40 U IV/IO (Does not have the negative, adverse effects of epinephrine on the heart such as increased ischemia and irritability)

Consider other antiarrhythmics such as:

Amiodarone 300 mg IV/IO once, then consider additional 150 mg once. Monitor for hypotension.

Magnesium is indicated for VF with torsades de pointes