Management of Cardiac ArrestPaleerat Jariyakanjana, MD

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

Chain of Survival

OVERVIEW

Cause ventricular fibrillation (VF) pulseless ventricular tachycardia (VT) pulseless electric activity (PEA) asystole

Ventricular Fibrillation

Ventricular Tachycardia

Asystole

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

Understanding the importance of diagnosing and treating the underlying cause is fundamental to management of all cardiac arrest rhythms.

RHYTHM-BASED MANAGEMENT OF CARDIAC ARREST

Paddles and electrode pads: anterior-lateral position

Iany doubt about the presence of a pulse chest compressions

rhythm can be diagnosed before CPR is initiated

VF/PULSELESS VT

resume CPR while charges the defibrillator chest compressions should switch at every 2-

minute cycle to minimize fatigue

Defibrillation Strategies

Waveform and Energy biphasic defibrillator: manufacturer’s

recommended energy dose (120-200 J) (Class I, LOE B)

unaware of the effective dose range: maximal dose (Class IIb, LOE C)

Defibrillation Strategies

Waveform and Energy Second and subsequent energy levels should

be at least equivalent, and higher energy levels may be considered if available (Class IIb, LOE B).

monophasic defibrillator: 360 J subsequent shocks at the previously successful

energy level

CPR Before Defibrillation

Performing CPR while a defibrillator is readied for use is strongly recommended for all patients in cardiac arrest (Class I, LOE B).

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

Treating Potentially Reversible Causes of VF/Pulseless VT

refractory VF/pulseless VT: AMI

PEA/ASYSTOLE

Drug Therapy for PEA/Asystole

vasopressor can be given as soon as feasible Available evidence suggests that the routine

use of atropine during PEA or asystole is unlikely to have a therapeutic benefit (Class IIb, LOE B).

For this reason atropine has been removed from the cardiac arrest algorithm.

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

Treating Potentially Reversible Causes of PEA/Asystole

Asystole end-stage rhythm that follows prolonged VF or PEA,

and for this reason the prognosis is generally much worse

MONITORING DURING CPR

Mechanical Parameters

rate of compression: ≥ 100/min depth of compression: ≥2 inches (5 cm) rate of ventilation: 1 breath every 6-8 s (8-10

breath/min)

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 ArterialRelaxation 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 DURINGCARDIAC 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?