By: Bong, Tess & Albert

Pulseless Arrest (Cardiac Arrest)

Algorithm

The Pulseless Arrest Algorithm which is

now known as the Cardiac Arrest Algorithm

takes its place as the most important

algorithm in the ACLS Protocol. There are 4

rhythms that are seen with pulseless

cardiac arrest. These four rhythms are

pulseless ventricular tachycardia (VT),

ventricular fibrillation (VF), asystole, and

pulseless electrical activity (PEA).

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.

Understanding the importance of diagnosing

and treating the underlying cause is

fundamental to management of all cardiac

arrest rhythms.

Treating Potentially Reversible

Causes of PEA/Asystole

PEA

reversible conditions

treated successfully if those conditions are identified

and corrected

Hypoxemia: advanced airway

severe volume loss or sepsis: administration of

empirical IV/IO crystalloid.

severe blood loss: blood transfusion

pulmonary embolism: empirical fibrinolytic

therapy (Class IIa, LOE B)

tension pneumothorax: needle decompression

Medications used in PEA

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.

Atropine is no

longer

recommended for

the treatment of

PEA per the 2010

ACLS guidelines.

ASYSTOLE

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.”

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.

Asystole for many patients is the result

of a prolonged illness or cardiac arrest, and

prognosis is very poor.

The H’s and T’s 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:

• DNR status

• Threat to the safety of rescuers

• Family or personal information such as a living

will or advanced directive

• Rigor mortis

Asystole is treated using the right branch of the

pulseless arrest algorithm.

Ventricular Fibrillation

Ventricular fibrillation is a heart rhythm

problem that occurs when the heart beats

with rapid, erratic electrical impulses. This

causes pumping chambers in your heart

(the ventricles) to quiver uselessly, instead

of pumping blood. VF is the rhythm most

commonly seen in adults who have sudden

cardiac arrest.

Ventricular Tachycardia

Pulseless VT is associated with no

effective cardiac output, hence, no

effective pulse, and is a cause of

cardiac arrest.

Chain of Survival

Immediate recognition of cardiac arrest

and activation of the emergency response

system

Early cardiopulmonary resuscitation (CPR) with

an emphasis on chest compressions

Rapid defibrillation

Effective advanced life support

Integrated post-cardiac arrest care

Survival from these cardiac arrest rhythms

requires

basic life support (BLS)

system of advanced cardiovascular life support

(ACLS)

integrated post– cardiac arrest care

Periodic pauses in CPR

brief as possible

assess rhythm, shock VF/VT, perform a pulse check

when an organized rhythm is detected, or place an

advanced airway

absence of an advanced airway

synchronized compression–ventilation ratio of 30:2

compression rate of at least 100 per minute.

After placement of a supraglottic airway or an

endotracheal tube

chest compressions should deliver at least 100

compressions per minute continuously without

pauses for ventilation

delivering ventilations should give 1 breath every 6-8

seconds (8-10 breaths per minute)

avoid delivering an excessive number of ventilations

Pulseless Arrest

(Cardiac Arrest)

Algorithm

resume CPR while charges the defibrillator

chest compressions should switch at every 2-

minute cycle to minimize fatigue

CPR Before Defibrillation

Performing CPR while a defibrillator is readied

for use is strongly recommended for all patients

in cardiac arrest.

Defibrillation after minimally interrupted CPR

gives the best chance of success.

If ventricular fibrillation recurs, reinitiate

defibrillation at the energy level that previously

resulted in successful defibrillation.

Drug Therapy in VF/Pulseless

VT

Amiodarone: first-line antiarrhythmic agent

Magnesium sulfate

torsades de pointes associated with a long QT

interval

Class IIb, LOE B

Physiologic Parameters

Pulse

End-Tidal CO2

Coronary Perfusion Pressure and Arterial

Relaxation Pressure

Central Venous Oxygen Saturation

Pulse Oximetry

Arterial Blood Gases

Echocardiography

Pulse

No studies have shown the validity or clinical

utility of checking pulses during ongoing CPR.

Because there are no valves in the inferior vena

cava, retrograde blood flow into the venous

system may produce femoral vein pulsations.

Pulse

Carotid pulsations during CPR do not indicate

the efficacy of myocardial or cerebral perfusion

during CPR.

no more than 10 seconds to check for a pulse

If it is not felt within that time period chest

compressions should be started

End-Tidal CO2

During untreated cardiac arrest CO2 continues

to be produced in the body, but there is no CO2

delivery to the lungs.

Under these conditions PETCO2 will approach

zero with continued ventilation. With initiation of

CPR, cardiac output is the major determinant of

CO2 delivery to the lungs.

If ventilation is relatively constant, PETCO2

correlates well with cardiac output during CPR.

End-Tidal CO2

If PETCO2 is <10 mm Hg, it is reasonable to

consider trying to improve CPR quality by

optimizing chest compression parameters

(Class IIb, LOE C).

If PETCO2 abruptly increases to a normal value

(35-40 mm Hg), it is reasonable to consider that

this is an indicator of ROSC (Class IIa, LOE B).

Coronary Perfusion Pressure and Arterial

Relaxation Pressure

Increased CPP correlates with improved 24-

hour survival rates and is associated with

improved myocardial blood flow and ROSC

If the arterial relaxation “diastolic” pressure is

<20 mm Hg, it is reasonable to consider trying

to improve quality of CPR by optimizing chest

compression parameters or giving a

vasopressor or both (Class IIb, LOE C).

Pulse Oximetry

typically does not provide a reliable signal

because pulsatile blood flow is inadequate in

peripheral tissue beds

Arterial Blood Gases

Arterial blood gas monitoring during CPR is not

a reliable indicator of the severity of tissue

hypoxemia, hypercarbia, or tissue acidosis.

Routine measurement of arterial blood gases

during CPR has uncertain value (Class IIb, LOE

C).

ACCESS FOR PARENTERAL

MEDICATIONS DURING

CARDIAC ARREST

worsened survival for every minute that

antiarrhythmic drug delivery was delayed

Time to drug administration was also a predictor

of ROSC

insufficient evidence to specify exact time

parameters or the precise sequence with which

drugs

Peripheral IV Drug Delivery

bolus injection and followed with a 20-mL bolus

of IV fluid

IO Drug Delivery

all age groups

Central IV Drug Delivery

peak drug concentrations are higher and drug

circulation times shorter

interrupt CPR

Endotracheal Drug Delivery

lidocaine, epinephrine, atropine, naloxone, and

vasopressin

2-21⁄2 times the recommended IV dose

dilute the recommended dose in 5-10 mL of

sterile water or normal saline and inject the drug

directly into the endotracheal tube

ADVANCED AIRWAY

delayed endotracheal intubation combined with

passive oxygen delivery and minimally

interrupted chest compressions was associated

with improved neurologically intact survival after

out-of-hospital cardiac arrest in patients with

witnessed VF/VT

When an advanced airway (eg, endotracheal

tube or supraglottic airway) is placed, 2

providers no longer deliver cycles of

compressions interrupted with pauses for

ventilation.

1 breath every 6-8 seconds (8-10 breaths per

minute)

MEDICATIONS FOR ARREST

RHYTHMS

Epinephrine

It is reasonable to consider administering a 1

mg dose of IV/IO epinephrine every 3-5 minutes

during adult cardiac arrest (Class IIb, LOE A).

If IV/IO access is delayed or cannot be

established, epinephrine may be given

endotracheally at a dose of 2-2.5 mg.

Vasopressin

nonadrenergic peripheral vasoconstrictor

1 dose of vasopressin 40 units IV/IO may

replace either the first or second dose of

epinephrine in the treatment of cardiac arrest

(Class IIb, LOE A)

Amiodarone

An initial dose of 300 mg IV/IO can be followed

by 1 dose of 150 mg IV/IO.

Lidocaine

considered if amiodarone is not available (Class

IIb, LOE B)

The initial dose is 1-1.5 mg/kg IV.

If VF/pulseless VT persists, additional doses of

0.5-0.75 mg/kg IV push may be administered at

5- to 10-minute intervals to a maximum dose of

3 mg/kg.

Magnesium Sulfate

torsades de pointes

IV/IO bolus of magnesium sulfate at a dose of 1-

2 g diluted in 10 mL D5W (Class IIb, LOE C)

ANY QUESTIONS?