Circulatory Arrest: Manual and Mechanical Means for Emergency Management

Abstract

During the year since Kouwenhoven, Jude, and Knickerbocker (1) introduced closed chest compression as a means for artificial circulation, many lives have been saved, including at least 3 at the institution from which this report comes. All such resuscitations have been in the relatively small group of patients whose primary defects eventually permitted an effective heartbeat, however paced. While proportionately small, the annual number of our countrymen dying of potentially reversible causes is approximately 100,000 (based upon the estimated number of sudden “mechanism” deaths from coronary disease). It follows that all should become familiar with the emergency management of circulatory arrest. General principles are well covered in Stephenson's monograph (2), and details of the closed chest technic have been published recently (3). A brief description follows. Manual Closed-Chest Artificial Circulation Where resuscitation is indicated, circulatory arrest may be countered by posterior displacement and release of the precardiac chest wall, 60 to 100 times a minute. This is done with the patient supine, the heel of the operator's hand being used to push the lower sternum inward about 2 inches. Recoil is passive. The maneuver compresses the heart against the spine, with resulting ejection of blood, thus making use of the heart's valves in converting it to a passive pump powered by the operator. Effectiveness should be gauged by palpation of the peripheral pulses produced. Mouth-to-mouth artificial respiration is instituted immediately (intermittently if necessary; not at all if adequate spontaneous respiration is present). Drug therapy and electrocardiographic diagnosis can be deferred until means for definitive therapeutic attempts are available. To the radiologist in private practice, this will generally entail emergency transfer of the patient to a hospital. The foregoing method was used in a recent instance where death was delayed for two and one-half hours following total loss of left ventricular function due to massive myocardial infarction. Case I: A 38-year-old male was examined by contrast cardiovascular visualization prior to planned surgery for aortic valvular stenosis (Fig. 1). Two or three minutes following an injection of Hypaque into the proximal aorta, chest pain and the characteristic electrocardiographic changes of myocardial infarction heralded the onset of left heart failure and acute pulmonary edema. Ventricular tachycardia soon led to ventricular fibrillation. Closed chest artificial circulation and mouth-to-mouth artificial respiration were begun; electrical defibrillation was accomplished less than a minute following the onset of fibrillation. The patient was intubated and thereafter pulmonary ventilation was maintained by an anesthesiologist (who had been sought at the onset of chest pain).