Advanced Cardiovascular Life Support (ACLS) EXAM 2 Flashcards by o e

What does C A B stand for?

Compression
Airway
Breathing

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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

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When is a patient considered to be in cardiac arrest?

No palpable Pulse

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What are the shockable rhythms?

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-Ventricular fibrillation (V. fib)
-Pulseless Ventricular tachycardia (V. tach)

there is some electrical activity, but disorganized

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What are the Non-shockable rhythms?

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-Asystole (flat line, no electricity)
-Pulseless Electrical Activity (PEA) - something is preventing the blood from flowing through the heart (like PE)

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What are the components of an ECG/EKG?

P-wave: atrial depolarization
QRS-complex: ventricular depolarization
T-wave: ventricular repolarization

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What is the role of Magnesium in QT prolongation?

Mg helps to pump out K+ during repolarization (T-wave) -> thereby decreasing the QT interval

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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

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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)

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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

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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)

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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)

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How many minutes of CPR are recommended between the steps in ACLS?

2 min of CPR

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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)

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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)

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What dose of Amiodarone is used in ACLS?

First dose: 300 mg bolus
Second dose: 150 mg

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What dose of Lidocaine is used in ACLS?

First dose: 1-1.5 mg/kg

Second dose: 0.5 - 7.5 mg/kg

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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

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What should be given after every medication that was administered?

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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?

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1-2 g of Magnesium diluted in 10 ml of NS/D5 over 5 minutes

Which drugs may given via the Endotracheal tube (ET)?

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NAVEL
Narcan
Atropine
Vasopressin
Epinephrine
Lidocaine

for systemic absorption

What are common reversible causes of cardiac arrest? (H’s and T’s)

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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?

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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)?

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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)

Advanced Cardiovascular Life Support (ACLS) EXAM 2 Flashcards

(47 cards)