Page 263 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 25: Cardiopulmonary Resuscitation 167

TABLE 25-1 Etiologies of Cardiac Arrest TABLE 25-2 Contact Information for BLS and ACLS Training and Resources
Myocardial ischemia/infarction American Heart Association (AHA)
Primary cardiac arrhythmia Web site: www.heart.org
Hypothermia Telephone: (800) 242-8721
Septic shock American Red Cross (ARC)
Trauma Web site: www.redcross.org
Systemic inflammatory response syndrome Telephone: (800) 733-2767
Tension pneumothorax European Resuscitation Council (ERC)
Myocardial pump failure Web site: www.erc.edu
Pulmonary embolism Telephone: +32 3 826 9321
Cardiac tamponade
Ventricular wall rupture
Demographic data from multiple studies demonstrate that the mean
Severe valvular disease
age of patients who suffer out-of-hospital cardiac arrest is approximately
Infiltrative cardiomyopathy 68 to 70 years, with a slightly higher incidence in men than in women. 1,2,11
Inflammatory cardiomyopathy Over 70% of these patients experience arrest in the home or other
Massive hemorrhage residential location. 12,13 In-hospital cardiac arrest patients exhibit similar
demographics, with one survey showing a mean age of 71 years and
Postoperative also somewhat higher incidence in males. There do not appear to be
14
Trauma significant survival differences between men and women. 2
To standardize treatment during cardiac arrest, a number of treat-
Gastrointestinal bleeding ment algorithms have been developed based on laboratory and clinical
Hypoxemia/respiratory failure
evidence. These have been compiled into the Basic Life Support (BLS) and
Pneumonia Advanced Cardiopulmonary Life Support (ACLS) guidelines published
Pulmonary embolism and updated regularly by the American Heart Association’s Emergency
Cardiac Care Committee, as well as other international resusci tation
15
Status asthmaticus organizations (International Liaison Committee on Resuscitation). For
15
Suffocation, eg, foreign-body aspiration additional information about ACLS guidelines and their revisions, see
Electrolyte derangement the contact information listed in Table 25-2.
Hyperkalemia
Hypocalcemia PEDIATRIC CARDIAC ARREST
Drug toxicity/overdose The majority of discussion in this chapter pertains to adult cardiac arrest
because cardiac arrest in children, fortunately, is much less common. When
Digoxin
it occurs, pediatric cardiac arrest more often is secondary to trauma or
β-Blockers pulmonary derangements, such as drowning, status asthmaticus, or for-
16
Calcium channel blockers eign-body obstruction, rather than due to a primary cardiac arrhythmia.
17
Tricyclic antidepressants However, ventricular fibrillation does occur in the pediatric population.
Guidelines for pediatric resuscitation have been established and are com-
Note: This list is by no means exhaustive; a number of etiologies are grouped by mechanism, although piled in the Pediatric Advanced Life Support (PALS) manual. For neonates,
some likely involve multiple mechanisms (eg, pulmonary embolism causing hypoxemia and right in whom cardiac arrest is yet another specialized problem, the manual
ventricular pump failure). Myocardial ischemia and primary cardiac arrhythmia are the most common Neonatal Advanced Life Support (NALS) has been developed. While many
underlying pathophysiologic mechanisms in cardiac arrest, especially in out-of-hospital arrest.
of the general principles of this chapter also apply to children, readers
should refer to these additional texts for more detailed information. 15
underlying etiology of arrest. Conversely, cardiac arrest is the initial PREVENTION OF CARDIAC ARREST
presentation of myocardial ischemia in approximately 20% of patients.
2
A wide variety of other processes can lead to cardiac arrest, including Given the poor prognosis of cardiac arrest, prevention remains the best
septic shock, electrolyte abnormalities, hypothermia, pulmonary embo- hope to save lives. To this end, out-of-hospital and in-hospital cardiac
lism, and massive trauma (Table 25-1). arrests require different prevention strategies.
Survival from cardiac arrest remains dismal, even after the intro- In the outpatient setting, careful attention to coronary artery disease
duction of electrical defibrillation and cardiopulmonary resuscitation risk factors such as smoking, hypertension, and hypercholesterolemia,
(CPR) over 50 years ago. In the best cases (witnessed ventricular fibril- and aggressive treatment for these conditions can lower the risk of myo-
lation arrest with rapid defibrillation), survival to hospital discharge cardial ischemia and therefore the risk of cardiac arrest. In consultation
ranges from 30% to 46%, although overall out-of-hospital arrest with their physicians, most patients with multiple cardiac risk factors
3,4
survival is usually much lower, ranging from 2% to 26%. In large should be treated with aspirin to lower the probability and severity
5
American cities, out-of-hospital arrest survival may be even worse— of myocardial infarction. Patients otherwise at risk for sudden death,
survival rates of 1.4% and 1.8% have been reported for New York such as patients with bouts of ischemic ventricular tachycardia and/or
and Chicago, respectively. Even after successful resuscitation from a history of myocardial infarction with subsequently depressed ejection
6-8
cardiac arrest, most patients die within 24 to 48 hours despite aggres- fraction, should be considered for implantable cardioverter defibrillator
sive intensive care treatment. Reperfusion injury, a subject of much (ICD) placement (reviewed in refs. 18 and 19). The use of ICD devices
basic science investigation, is thought to be involved in this postarrest remains an area of active investigation and likely will expand as smaller
deterioration. 9,10 and less expensive devices are developed.

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