Advanced Cardiovascular Life Support (ACLS) EXAM 2 Flashcards
What does C A B stand for?
Compression
Airway
Breathing
Which component of ACLS has proven to improve outcomes for patients witch cardiac arrest?
high-quality CPR
early defibrillation
NO meds have been proven to improve outcomes but have not shown any harm either
When is a patient considered to be in cardiac arrest?
No palpable Pulse
What are the shockable rhythms?
!!!
-Ventricular fibrillation (V. fib)
-Pulseless Ventricular tachycardia (V. tach)
there is some electrical activity, but disorganized
What are the Non-shockable rhythms?
!!!
-Asystole (flat line, no electricity)
-Pulseless Electrical Activity (PEA) - something is preventing the blood from flowing through the heart (like PE)
What are the components of an ECG/EKG?
P-wave: atrial depolarization
QRS-complex: ventricular depolarization
T-wave: ventricular repolarization
What is the role of Magnesium in QT prolongation?
Mg helps to pump out K+ during repolarization (T-wave) -> thereby decreasing the QT interval
Identify Ventricular Fibrillation (V. Fib) on a picture
What is V. Fib?
Is it shockable? What is the treatment of choice?
Do patients with V. Fib have a pulse?
-unorganized electrical activity
-shockable -> Defribillation
-No pulse
Identify Pulseless Ventricular Tachycardia (V. tach) on a picture.
What is V. tach?
Is it shockable? What is the treatment of choice?
Do patients with V. tach have a pulse?
Tombstone pattern
rapid ventricualr rate (200 bpm)
it is shockable -> Defibrillation
sometimes, if no pulse its bc the heart beats so fast it can’t fill with blood between beats
if they have a pulse - SHOCK (defibrillation)
Identify Torsade de Pointes on a picture.
What is a Torsade de Pointes?
Does it have a pulse?
What are the potential causes of Torsade de Pointes?
What is the treatment of choice?
A special form of polymorphic Ventricular Tachycardia, it can result from QT prolongation
No pulse (it is a polymorphic V. tach)
It is shockable -> give Mg right after
Causes: drugs and electrolyte abnormalities
Treatment: Magnesium
Identify Asystole on a picture.
What is Asystole?
Is it shockable? What is the treatment of choice?
No electrical activity (Flatline)
Not shockable
Must be confirmed in 2 leads (in case wire became disconnected)
Treatment: Compression, drugs (epinephrine)
Identify Pulseless Electrical Activity (PEA) on a picture.
What is PEA?
Is it shockable? What is the treatment of choice?
organized electrical activity without a Pulse (due to large PE, cardiac tamponade (fluid compression))
Not shockable
Treatment: Compression, drugs (epinephrine)
How many minutes of CPR are recommended between the steps in ACLS?
2 min of CPR
Which drug is recommended after the second episode of shock and CPR?
1 mg Epinephrine every 3-5 min
after another episode of Defibrillation (shock) and CPR -> try Amiodarone or lidocaine (class Ib antiarrhythmic)
What needs to be checked before giving Amiodarone or Lidocaine?
pulse
do not administer if they have a pulse (it will disrupt their pulse if they have one, since it is a anti-arrhythmic)
What dose of Amiodarone is used in ACLS?
First dose: 300 mg bolus
Second dose: 150 mg
What dose of Lidocaine is used in ACLS?
First dose: 1-1.5 mg/kg
Second dose: 0.5 - 7.5 mg/kg
Which drug is used if the patient has no shockable rhythm (Asystole or PEA)?
1 mg Epinephrine every 3-5 minutes
continue with CPR for 2 min
if they have a shockable rhythm -> SHOCK
What should be given after every medication that was administered?
10 ml NS flush
-if sodium bicarbonate and calcium were administered close together use 20 ml of NS
to ensure proper circulation bc blood flow is impaired
Which drug is used for Torsade de Pointes?
1-2 g of Magnesium diluted in 10 ml of NS/D5 over 5 minutes
Which drugs may given via the Endotracheal tube (ET)?
NAVEL
Narcan
Atropine
Vasopressin
Epinephrine
Lidocaine
for systemic absorption
What are common reversible causes of cardiac arrest? (H’s and T’s)
Hypovolemia -> use IV fluids
Hypoxia -> use O2 ventilation
Hydrogen ion (acidosis) -> sodium bicarboante
Hypo or Hyperkalemia
Hypothermia
Tension pneumothorax
Tamponade, cardiac
Toxins -> use antidotes
Thrombosis, coronary or pulmonary -> Fibrinolytic therapy
Which drugs are used to correct Hyperkalemia?
Calcium chloride (protects the cardiac membrane)
Sodium bicarbonate (push K+ into the cells)
Glucose + Insulin IV (push K+ into the cells)
Kayexalate, Locelma (removes K+, binds K+ and eliminates it in the stool)
Dialysis (removes K+)
for Hypokalemia:
-Potassium IV (add magnesium if cardiac arrest)
What do we consider in a patient post-cardiac arrest having a return of spontaneous circulation (ROSC)?
Targeted Temperature Management (cooling, therapeutic hypothermia)
What might happen after reperfusion of deoxygenated tissue?
How does decreasing the temperature help?
-reperfusion leads to injury of the tissue caused by inflammatory mediatros, metabolic changes, or superoxides
-cooling slows the metabolic processes and helps preserve neurological function
What is the goal of therapeutic hypothermia?
What are the tools used to decrease body temperature?
36°C (96.8°F) for 24h
tools used
-cold saline infusion
-ice packs (placed in armpits, neck, groin)
-cooling blankets
-cooling helmets
-cooling catheters
How fast do we restore body temperature after therapeutic hypothermia?
< 0.5°C per hour
usually takes 8h to complete
Which drugs may be used in therapeutic hypothermia to prevent shivering?
-Buspirone 20 mg q8h
-Meperidine 25-50 mg IV prn
-NMB: PRN or continous infusion
also need:
-sedation (cooling down is uncomfortable)
-maintain CPP (MAP > 80 mmHg)
-watch for bradycardia and hypokalemia
continuous shivering increases the risk of rhabdomyolysis
What should be considered when warming patients after therapeutic hypothermia?
-Fever (the body thinks the increased temperature is a fever) -> treat with acetaminophen
-Hypotension: IV fluids 6-8h before rewarming
-d/c NMB
-watch for Hyperkalemia (check every 4-6h)
When is a patient considered tachycardic?
HR over 90 bpm
What are common causes of Sinus tachycardia?
Tachycardia with Pulse
fever, dehydration, stress
elevated HR but usually not greater than 150 bpm
What is a Supraventricular Tachycardia?
Tachycardia with Pulse
-happens in the atria
-impulses repeatedly cycle through the heart -> rapid heart rate, the heart can’t refill with blood with each beat
HR is usually greater than 150 bpm
When is the QRS complex considered wide and when is it considered narrow?
Wide complex: QRS >0.12 seconds
Narrow complex: QRS <0.12 seconds
Where do most wide-complex tachycardias originate?
Ventricle
(adenosine (DOC for tachycardia) doesn’t work for this)
tachycardia with pulse
Where do most narrow-complex tachycardias originate?
above the ventricles, in the atria or around the AV node -> Supraventricular
Adenosine is effective for which type of Tachycardia?
Supraventricular Tachycardia (narrow-QRS complex)
it helps if the problem stems from the atria or AV node
What other drugs work for Supraventricular Tachycardia?
Beta-Blocker
Calcium Channel Blocker
they slow conduction through the AV node
What is the treatment approach in a stable tachycardic patient with a pulse?
Tachycardia with Pulses
Medicine before Edison
-Adenosine 6 mg IV push, then 20 ml NS flush (may repeat with 12 mg dose if needed)
-Antiarrhythmic: Amiodarone, Sotalol
What is the treatment approach in an unstable tachycardic patient with a pulse?
Tachycardia with Pulses
Edison before Medicine
-Synchronized Cardioversion (the defibrillator determines the best time to shock, sync with QRS complex)
-sedate the patient if possible
When is a patient considered stable?
No signs of decompensating (tachycardia, low BP)
No signs of failure or shock
may try vagal maneuver to stimulate the parasympathetic nerve system to reduce the HR
What is considered Bradycardia?
a HR <50 bpm (<60 bpm for children)
How do we treat bradycardia in stable patients?
Medicine before Edison
-Atropine 0.5 mg IV every 3-5 minutes until HR is high enough to perfuse tissues
(Atropine blocks M2 receptors in the SA node - increases HR)
-may use dopamine or epinephrine gtt (since those have ß-activity -> increases HR and contraction)
How do we treat bradycardia in unstable patients?
use the defibrillator as an external pacemaker
-> set it to Transcutaneous pacing
-provide sedation
-may also use dopamine or epinephrine in addition
What is a heart block?
What is a first-degree heart block?
slowing (delay) of conduction from the atrium to the ventricles
First degree: the QRS complex is delayed after the P-wave (consistently for every beat)
What is a 2nd-degree Type 1 heart block?
P to R interval gets longer with each beat until it skips a beat (no QRS) - then the pattern begins again
What is a 2nd-degree Type 2 heart block?
the QRS is delayed behind the P-wave, but some QRS are dropped in a predictable fashion
What is 3rd-degree heart block?
no communication between the atria and the ventricle
-the QRS is not right after the P-wave
-but both are there and stimulated with their own pacemaker (the ventricle pacemaker is not very strong)
-the patient’s HR is overly low (~30 bpm)
