Cardiopulmonary Arrest






Katheri ne M. Hil ler, MD

Key Points

• Cardiac disease is the most common cause of nontraumatic death in the Un ited States.

• There are more than 300,000 sudden cardiac deaths

(SCD) each year in the United States. The survival rate of

INTRODUCTION

Cardiopulmonary arrest is defined by unconsciousness,

apnea, and pulselessness. Sudden cardiac death (SCD) is

associated with an underlying history of coronary artery

disease (CAD), but an acute thrombotic event is causal in

only 20-40% of cardiac arrests. Twenty-five percent of

cardiac arrests may have a non cardiac origin ( eg, pulmo -

nary embolus, respiratory arrest, drowning, overdose). The

most common initial rhythm is ventricular fibrillation

(VF), found in approximately 30% of patients. Asystole

and pulseless electrical activity (PEA) are the next most

common presenting rhythms.

The risk of SCD is 4 times higher in patients with

coronary artery disease risk factors and 6-10 times higher

in patients with known heart disease. Structural heart

disease ( eg, cardiomyopathy, heart failure, left ventricular

hypertrophy, myocarditis) accounts for 1 0% of cases of

SCD. Another 1 0% of SCD cases occur in patients with

no structural heart disease or CAD. These cases are

thought to originate from Brugada syndrome, commotio

cordis, prolonged QT syndrome, and familial ventricular

tachycardia (VT), which all cause dysrhythmias leading

to SCD.

Other risk factors associated with an increased risk of

SCD include smoking, diabetes mellitus, hypertension,

33

sco is dependent on the length of time without a pulse,

the underlying cardiac rhythm, and comorbidities.

• Early and uni nterrupted chest compressions and early

defi brillation are the keys to successful resuscitation.

dyslipidernia, and a family history of cardiac disease.

Moderate alcohol consumption ( 1-2 drinks per day) is

considered protective, whereas heavy alcohol consumption

(>6 drinks per day) is a risk factor for SCD.

Despite advances in the field of cardiac resuscitation,

the survival rate of out-of-hospital SCD is estimated to be

3-8%. Survival to discharge in out-of-hospital SCD is

largely determined by the presenting rhythm. Patients with

VF are 15 times more likely to survive to discharge than

patients in asystole (34% vs 0-2%).

CLINICAL PRESENTATION

� History

Obtain history from paramedics, bystanders, or any available family members. Inquire about medications, past

medical history, allergies, trauma, and events leading up to

SCD.

� Physical Examination

Do not halt treatment (including chest compressions and

bag-valve-mask ventilation) to perform a complete physical exam. If the patient has an endotracheal tube in place,

verify position by using end-tidal C02 capnography or

capnometry.

DIAGNOSTIC STUDIES

� Laboratory

CHAPTER 10

If the patient has a return of spontaneous circulation

(ROSC), order a complete blood count, electrolytes, renal

function, and myocardial markers (ie, troponin).

Coagulation studies, an arterial blood gas, and a lactate

may also be useful.

� Imaging

If the patient has a ROSC, obtain a chest x-ray to evaluate

endotracheal tube placement and an electrocardiogram to

evaluate for cardiac ischemia.

PROCEDURES

Pericardiocentesis is indicated if there is a suspicion of

cardiac tamponade in the setting of PEA. Bedside ultra ­

sound can be useful if tamponade is suspected. A long

spinal needle is inserted s ubxiphoid into the pericardia! sac

aimed toward the left shoulder. Pull back on a 60-mL

syringe while advancing the needle until blood is obtained.

A needle thoracostomy is indicated if there is a s uspicion of tension pneumothorax in the setting of PEA. I nsert

an 1 8-gauge needle into the second intercostals space in

the midclavicular line. A needle thoracostomy must always

be followed by a tube thoracostomy in patients with

ROSC.

MEDICAL DECISION MAKING

The differential diagnosis for SCD is broad. Management

of SCD depends on the presenting rhythm; however, every

patient should receive continuous high-quality uninterrupted chest compressions. Defibrillate VF/pulseless VT.

Administer epinephrine for asystole and PEA. Attempt to

correct reversible causes of PEA, the H's, and T's

(Table 10-1). Once ROSC occurs, initiate postresuscitative

care, including therapeutic hypothermia, which improves

neurologic outcome.

Table 1 0-1. The H's and T's of PEA.

Hypoxia

Hypovolemia

Hydrogen ion (acidosis)

Hypo-/hyperkalemia

Hypothermia

Toxins

Tamponade (cardiac)

Tension pneumothorax

Thrombosis (pulmonary, cardiac)

TREATMENT

If there is a clear, written, advanced directive signed by the

patient or medical power of attorney stating that resuscitative efforts should not be instituted, or if the resuscitation

would be futile because of clear signs of irreversible death

(decapitation, rigor mortis), resuscitative efforts should

not be initiated or continued.

The resuscitative team must orchestrate simultaneous

assessment and management of patients in cardiopulmo ­

nary arrest.

1. Defibrillation. Indicated for patients in VF or pulseless

VT. The rate of successful defibrillation when attempted

within 1 minute of VT is >90o/o, but falls lOo/o with each

subsequent minute.

2. Chest compressions. The carotid pulse is the most reliable in low-flow states. If no pulse is detected, chest

compressions should be initiated. Survival is greatly

increased when chest compressions are performed

properly (depth 1.5-2 inches, > 1 00/min) and greatly

decreased when there are delays or interruptions in

chest compressions. Chest compressions should be

performed continuously and should not be interrupted

for ventilation. A brief rhythm check should be undertaken after every 2 minutes of chest compressions.

When defibrillation is indicated, compressions should

be continued while the manual defibrillator or AED is

charging. Chest compressions should only be briefly

halted ( < 10 seconds) to deliver the shock and irnmediately resumed after delivery.

3. Airway. The most common airway obstruction in the

unconscious patient is the tongue falling back against

the posterior pharynx. This can be managed immediately with a jaw thrust or chin lift maneuver. Bag-valvemask ventilation should then be used until enough

providers are available to allow continued compressions and defibrillation while advanced airway adjuncts

are assembled. Endotracheal intubation is the definitive

airway management technique used for patients in cardiac arrest. Attempts at intubation should be brief so as

not to hinder delivery of high-quality continuous chest

compressions.

4. Pharmacologic therapy.

a. Vasopressors. The current recommended dose of

epinephrine is 1 mg initially, with repeated doses

every 3-5 minutes. "High-dose" epinephrine confers no benefit and may be harmful. When there is

no IV access, epinephrine can be given in the

endotracheal tube at a dose 2-2.5 times the IV

dose. Alternatively, vasopressin 40 units IV may be

given once.

b. Antidysrhythrnics. Amiodarone, 300 mg IV push,

repeated as a second dose of 150 mg IV push may be

useful for defibrillation refractory VT /VF. Magnesium,

2 g IV, may be useful in patients with torsade de

points.

CARDIOPULMONARY ARREST

Patient unresponsive

Assess airway, breath ing, circulation

No pulse

Initiate chest compressions, while

attaching monitor or defibri llator

Admit for hypothermia and postresuscitative care

Asystole/PEA

2 Minute cycles of CPR

intubate, IV access

epinephrine 1 mg IV every

3-5 minutes

Consider treating reversible

causes (H's and T's)

• Figure 1 0-1. Cardiac arrest algorithm. U, Un its; VT/VF, ventricular tachyca rd ia/ventricular fibri llation;

PEA, pulse less electrica l activity.

CHAPTER 10

5. Postresuscitation care. All patients who remain

comatose with an ROSC should receive therapeutic

hypothermia (33°C for 24 hours, then rewarm over

24 hours).

DISPOSITION

..... Admission

All patients with ROSC should be admitted to the intensive

care unit or cardiac care unit for postresuscitative care as

well as management of underlying conditions leading to

the arrest. If CAD/acute coronary syndrome is the pre ­

sumed cause of SCD, all therapies, especially percutaneous

coronary intervention, should be considered.

SUGGESTED READING

Field JM, Hazinski MF, Sayre MR, Chameides L, Schexnayder SM,

et al. Part 1: Executive Summary: 2010 American Heart

Association Guidelines for Cardiopulmonary Resuscitation

and Emergency Cardiovascular Care. Circulation. 20 1 0; 122:

S640-S656.

Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, et al .

Part 8: Adult Advanced Cardiovascular Life Support: 2010

American Heart Association Guidelines for Cardiopulmonary

Resuscitation and Emergency Cardiovascular Care.

Circulation. 2010;1 22:S729-S767.

Omato, JP. Sudden cardiac death. In: Tiutinalli JE, Stapczynski

JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD. Tintinalli's

Emergency Medicine: A Comprehensive Study Guide. 7th ed.

New York, NY: McGraw-Hill, 201 1, pp. 63--67.

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