ABSTRACTS FROM PERDUE CONFERENCE ON CPR

Philip Troiano, Harlan Stveren, David Olson, Denis Tons- feldt, Eugene Kasterson, Dennis Birchall, Edward Barthell. Medical College of Wisconsin, Milwaukee, WI 53226.

Recent reports in the literature have begun to question the efficacy of CPR. The major criticism that has been directed towards these studies, which have critically analyzed CPR versus no CPR save rates, is that neurological outcomes have not been considered. To answer the question as to whether bystander CPR effects neurological outcome, a ret- rospective study of pre-hospital cardiac arrests was per- formed.

Between January 1983 and March 1985, 138 patients from six major participating hospitals were dischared alive fol- lowing pre-hospital cardiac arrests. For 531138 (38.4%) pa- tients, either the patient or a direct family member was con- tacted for information concerning neurological outcome. For 69/138 (50.0%) patients, contact with patient or family was unsuccessful; consequently, neurological outcome at time of discharge was obtained from the medical record. For 161138 (11.6%) patients, no data on neurlogical outcome were ob- tainable.

Neurological outcome was rated by a S-point Cerebral Performance Categories Scale (CPC) developed by the Re- suscitation Research Center, University of Pittsburgh. The five parameters of measurement were as follows: 1) minimal disability; 2) moderate; 3) severe; 4) vegetative; and 5) brain dead.

The CPR group had 53% (CPC = l), 25% (CPC = 2), 18% (CPC = 3), and 4% (CPC = 4). The no CPR group had 58% (CPC = l), 17% (CPC = 2), 17% (CPC = 3), and 8% (CPC = 4). There is no significant difference at any CPC level (P = NS). Furthermore, there is no statistically significant dif- ference between either group when compared for age, resus- citation time, witnessing of arrest, or distribution of rhythms.

The results indicate that there is no statistically significant difference in neurological outcome whether or not bystander CPR is administered to cardiac arrest victims.

Drown-retardant Swimming Pool Water. James P. Orlowski, Cleveland Clinic Foundation, Cleveland, OH.

Drowning is the second leading cause of accidental death in children and approximately 50% of the deaths occur in swimming pools. The author studied the pulmonary injury and ability to resuscitate dogs drowned in six different solu- tions of varying tonicities.

Six different solutions were studied: sterile water (0% NaCl), % normal saline (0.225% NaCl), % normal saline (0.45% NaCl), normal saline (0.9% NaCl), 2% NaCl, and 3% NaCl. Five dogs were studied in each of the six drowning fluids-two solutions without chlorine in the water and three solutions with chlorine added at a final concentration of 1 to 2 parts per million. The dogs were anesthetized with sodium thiopental, intubated, and mechanically ventilated. Arterial and pulmonary artery catheters were placed, and hemodynamic and pulmonary parameters including arterial and mixed venous blood gases were obtained prior to and at 1, 2, 3, and 4 hours after 20 ml/kg of the drowning fluid was

instilled down the endotracheal tube. A control study was also conducted where the animal was made anoxic but no fluid was introduced into the lungs.

For the pulmonary variables of Aa-DO,, QslQt, and Pa& FiOz, the 0.225% NaCl solution was least injurious to the lung, followed closely by the 0.45% NaCl solution, and these values at all time periods were similar to the control study where no fluid was introduced into the lung. The pres- ence of chlorine in the solution did not influence the data. The 0.225% and 0.45% NaCl solutions were significantly better than the other solutions studied, especially the sterile water (0% NaCl) with or without chlorine. The 0.9% NaCl (isotonic, normal saline), 2% NaCl, and 3% NaCl were not significantly different from each other and were better than the sterile water (0% NaCl) in terms of pulmonary injury, but were significantly worse than the 0.225% and 0.45% NaCl solutions (P s 0.05). The 0% solution (sterile water) was clearly the worst whether chlorinated or unchlorinated (P G 0.001).

Hemodynamic Effects of Rapid CPR Compression Rate in Humans. Joseph P. Omato, Edgar R. Gonzalez, A. Ran- dolph Garnett, Ronald L. Levine, Barbara K. McClung. Medical College of Virginia, Richmond, VA 23298.

Studies in animals have yielded different results over whether systemic blood pressure (BP) and cardiac output can be improved by performing CPR at a higher rate (up to 150 bpm). The authors prospectively studied 13 pre-hospital arrest patients (8 men 5 women, age 50 + 4 years) to deter- mine the effect of faster CPR compression rate on radial ar- terial pressure and end tidal carbon dioxide concentration (ETCO&. All patients were in ventricular fibrillation (VF) on arrival of the paramedic unit and had failed standard ACLS therapy. Radial artery pressure was monitored through a #20 angiocath inserted by cutdown within 10 minutes after emergency department (ED) arrival. Compression rate was increased from 60 to 140 bpm in 20-bmp increments using a microprocessor-controlled CPR Thumper with a constant 50:50 downstroke:upstroke ratio. Ventilation rate was held constant at lumin; inspiratory pressure was 45 cm water.

Systolic pressure declined progressively with minimal change in mean and diastolic pressure as the rate was in- creased from 60 bpm (BP 49 + 6/27 ? 5 mm Hg) to 140 (BP 33 ? 5/20 5 4 mm Hg). The ETCOz remained low (1.7-2.0%) despite increases in the rate.

Systemic arterial BP in adult humans falls slightly but is relatively rate-insensitive between 60 and 140 bpm using a constant 50:50 CPR downstroke:upstroke ratio. The ETCOt (as an index of pulmonary blood flow) is also relatively rate- insensitive. The findings support the theory that change in intrathoracic pressure (not direct cardiac compression) is the major mechanism of blood flow during CPR in adult humans and indicate that a faster CPR compression rate offers no significant hemodynamic advantage if all other variables are kept constant.

Aortic and Right Atria1 Systolic Pressures an Indicators of the Mechanism of Blood Flow during Cardiopulmonary Resus- citation. Kenneth L. Raessler, Karl B. Kern, Arthur B.

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