Publications

OBJECTIVES

The purpose of this study was to test the hypothesis that active compression-decompression would improve resuscitation success in human subjects after cardiac arrest.

BACKGROUND

Active compression-decompression cardiopulmonary resuscitation is a new method that improves cardiopulmonary hemodynamic function in animal models and humans after cardiac arrest.

METHODS

We conducted a prospective randomized clinical trial in patients with in-hospital cardiac arrest. Patients were assigned to receive standard manual or active compression-decompression cardiopulmonary resuscitation. The primary study end points were spontaneous return of circulation, 24-h survival and survival to hospital discharge.

RESULTS

Fifty-three consecutive patients after cardiac arrest undergoing 64 resuscitation attempts were studied (30 women, 23 men; mean [+/- SD] age 71 +/- 13 years, range 38 to 96). Spontaneous return of circulation was observed in 24 (47%) of 53 patients and was increased in patients receiving active compression-decompression compared with those receiving standard manual cardiopulmonary resuscitation (15 [60%] of 25 vs. 9 [32%] of 28, respectively, p = 0.042); 24-h survival was increased (12 [48%] of 25 vs. 6 [21%] of 28, respectively, p = 0.041); and there was a trend toward improved survival to hospital discharge (6 [24%] of 25 vs. 3 [11%] of 28, respectively, p = 0.198) when active compression-decompression was compared with standard manual cardiopulmonary resuscitation.

CONCLUSIONS

Active compression-decompression cardiopulmonary resuscitation improves return of spontaneous circulation and 24-h survival after in-hospital cardiac arrest. Active compression-decompression cardiopulmonary resuscitation appears to be a beneficial adjunct to standard manual cardiopulmonary resuscitation.

Powerful new approaches for the identification and sequencing of novel cDNAs have produced a backlog of proteins seeking functions. Traditional approaches for characterizing protein function (e.g., blocking monoclonal antibodies and heterologous expression) have significant limitations, especially in identifying the roles specific proteins play in vivo. An alternative approach is to engineer mutations in the protein of interest that abolish its function and that also inhibit the function of simultaneously expressed wild-type protein (dominant negative mutations). This approach has wide application to the study of a number of different kinds of proteins but tends to be most effective for proteins that need to assemble into multimers to be functional. Dominant negative mutants have already provided insights into the molecular mechanisms of action of a number of protein families, including hormone receptors, oncogenes, and growth factor receptors, and have been identified as the cause of at least a few autosomal dominant diseases. Expression of dominant negative mutants under the control of highly active lung cell-specific promoters holds great promise for the study of the roles specific proteins and protein families play in lung development, health, and disease.