41 notecards = 11 pages (4 cards per page)
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?
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
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
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.
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.
What are the characteristics of dopamine and epinephrine infusions?
What are the characteristics of asystole?
A cardiac arrest rhythm associated with no discernable electrical activity on the monitor.
Sometimes called ventricular standstill.
Is rarely associated with a positive outcome, usually a negative outcome.
Large percentage do not survive.
Represents the total absence of any electrical activity.
No ventricular contraction occurs because depolarization does not occur.
You may see a P wave but no QRS complex.
The sinoatrial node may continue to fire and depolarize the atria.
Requires immediate attention.
Check asystole in TWO LEADS before acting on it.
Ventricular fibrillation may masquerade as asystole.
The nurse must assess the rhythm in another lead for accurate interpretation, check monitor display for sensitivity or gain.
Treatment of these two rhythms (VF,Asystole) differs greatly, the nurse must be familiar with the specific treatment.
Clinical associations: Advanced cardiac disease, severe cardiac conduction system, advanced heart failure, severe hyperkalemia, acidosis.
Physical 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
Vasopressin 40 U IV to replace the first or second dose of epinephrine. Can be given only once!
May give sodium bicarbonate equal to 1 mEq/kg. This is helpful if known to have hyperkalemia or a known drug overdose with tricyclic antidepressants.
If asystole persists, ask these questions
DO NOT SHOCK
What are the differential diagnoses and common causes for asystole?
3.Hydrogen ion (acidosis)
1.Tablets (drug overdose)
4.Thrombosis (heart, AMI)
5.Thrombosis (lungs, pulmonary embolus)
What are the characteristics of the 6 H's of frequent causes of asystole?
Hydrogen ion (acidosis):
Hyperkalemia or hypokalemia:
What are the specific characteristics for the 5 T's of common causes of asystole?
Thrombosis (coronary, MI):
What is pulseless electrical activity?
Refers to any semiorganized or organized electrical activity that can be seen on the monitor although the patient lacks a palpable pulse.
Excludes VF, ventricular tachycardia (VT) and asystole.
Prognosis is poor unless the underlying cause can be identified and corrected.
Focus on assessing and treating patients.
Search for the reversible cause, which is the key to treating these patients.
Many conditions may cause PEA.
PEA displays electrical activity but produces no clinically detectable pulse.
Pathophysiology – cardiac conduction impulses occur in organized pattern, but this fails to produce myocardial contraction; or insufficient ventricular filling during diastole; or ineffective contractions.
Key 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.
Rapid assessment and aggressive management offer the best chance of success.
PEA is often associated with a reversible clinical state.
Need to search for a reversible cause.
Remember the 6 H’s and 5 T’s.
DO NOT SHOCK!
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
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
If does not convert:
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:
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.
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.
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:
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