Diagnosis. The absence of a palpable pulse in a major peripheral artery (carotid, radial, or femoral) for >10 seconds in an unconscious, unmonitored patient, is diagnostic. Within the OR, monitoring equipment might
show a precipitous drop in end-tidal CO2 (ETCO2), loss of pulse oximetry waveform, a low or nondetectable noninvasive blood pressure, or a flattening and drop in the arterial pressure waveform. Nonperfusing cardiac rhythms on EKG include tachyarrhythmias such as VF and VT as well as nontachyarrhythmias such as asystole, pulseless electrical activity (PEA), or severe bradycardia.Etiologies. Commonly recognized causes of cardiac arrest, the five Hs and Ts, are:
Hypovolemia.
Hypoxemia.
Hydrogen ion/acid-base disturbances.
Hyper/hypokalemia/electrolyte derangements (K, Ca, Mg).
Hypothermia.
Toxins (drug toxicity).
Tamponade (cardiac).
Tension pneumothorax.
Thrombosis (pulmonary embolus).
Thrombosis (cardiac/myocardial infarction).
Hypoglycemia (not in the 5 Hs and Ts, but a critical assessment).
Within the OR, additional etiologies to consider are:
Local anesthetic systemic toxicity.
Neuraxial anesthesia causing severe sympathectomy.
Anaphylaxis (eg, paralytics, antibiotics).
Malignant hyperthermia.
Excessive vagal tone during surgical manipulation or laparoscopy.
Embolism of air, fat, amniotic fluid, or procedural cement.
Excessive anesthetic.
Coronary stent thrombosis (in setting of holding antiplatelet medication).
Postreperfusion syndrome in liver transplantation.
Pathophysiology. If CPR is not immediately started after cardiac arrest, the cessation of blood flow causes tissue hypoxia, anaerobic metabolism, accumulation of cellular wastes, depletion of ATP, and ion-gradient breakdown (eg, uncontrolled calcium flow into cells that is excitotoxic and may trigger apoptosis). Widespread anaerobic metabolism leads to a sudden, severe acidemia with effects including systemic vasodilation, pulmonary vasoconstriction, and decreased response to catecholamines. Neurologic injury can become irreversible in as little as 4 to 6 minutes of absent circulation. After restoration of cardiac output, patients can have ischemia reperfusion injury with the generation of reactive oxygen species, mitochondrial dysfunction, and an immune/inflammatory cascade for which targeted temperature management (formerly therapeutic hypothermia) may be beneficial. The cumulative effects of absent flow and reperfusion injury result in variable multiorgan damage and neurologic disability.
Epidemiology. There are roughly 350,000 yearly out-of-hospital arrests in the United States, of which half are witnessed and only 1 in 10 survive to hospital discharge. Even fewer (~8.4%) survive with good functional status. Shockable rhythms (pulseless VT/VF) represent around 20% of the initial observed rhythms.