The pharyngeotracheal lumen airway (continuing report of a new airway for emergency ventilation)

AMERICANJOURNAL OF EMERGENCY MEDICINE n Volume 2, Number 4 n July 1984

of additional unknown factors were minimized by the use of concurrent controls and randomization. Brain damage was quantitated in terms of cerebral performance categories (CPC no. l-5), neurological deficit scoring (ND 0% = normal, 100% = brain death), cerebrospinal fluid or brain enzyme activity, and histopathological damage (HD) scoring. Results obtained in the 1970s and published by these authors or by others indicated that the following are promising in ameliorating brain damage: post-arrest intensive care by protocol (compared with usual care), reflow promotion by intracarotid hemodilution plus hypertension, barbiturates, phenytoin, and a multifaceted therapeutic approach. Beneficial results, however, were not always evident and reproducible. Results obtained by these authors in the 198Os, still unpublished, indicate that methyl prednisolone (in a rat asphyxial model), dextran plus free radical scavangers (in a dog asphyxial model) and the calcium entry blocker lidoflazine (in a dog ventricular fibrillation model) are promising. In our calcium entry blocker study, lidoflazine, 1 mg/kg in three doses over 24 hours, was administered to dogs after 10 minutes of VE Compared with standard therapy, this resulted in lower ND and CPC scores at 96 h (P < 0.05). Five of 11 lidoflazine treated dogs achieved CPC no. 1 (normal), versus O/l 1 control dogs; 6111 control dogs showed secondary neurological deterioration, versus O/l 1 lidoflazine dogs; all lidoflazine dogs but only 7/11 control dogs awakened (P < 0.05). Cerebrospinal fluid, CPK, and HD scores correlated with ND scores and CPC. Post-arrest cardiovascular parameters were improved with lidoflazine. This study is one of four animal outcome studies of calcium blockers post cardiac arrest. All four studies in four different groups showed amelioration of neurological deficit. The testing in our animal models of IV hemodilution alone, heparinization alone, prolonged severe hypertension, THAM, and certain drugs to combat intracellular necrotizing cascades all revealed no improvement in outcome. In our laboratory, semi-empirical selection of treatment protocols to be evaluated is now being replaced with a systematic multi-organ system study of the post-resuscitation syndrome, to allow the development of “tailored” pathophysiology-specific therapeutic protocols. Expired Pcq as an Index of the Coronary Perfusion Pressure. Arther B. Sanders, Matthew Atlas, Gordon A. Ewy, Karl B. Kern, Steven Bragg. University of Arizona, Tucson, AZ 85724. At present there is no reliable noninvasive method of assessing the adequacy of cardiopulmonary resuscitation (CPR). Animal studies have shown that during prolonged arrest the coronary perfusion pressure (CPP) is correlated with successful resuscitation. During previous studies it appeared that expired Pcoz correlated with CPP. Accordingly, a study was done to investigate this relationship. Eight mongrel dogs with a mean weight of 22.7 ~fr 5.8 kg were anesthetized with pentobarbitol. Catheters were placed in the thoracic aorta and right atrium. The animals were electrically fibrillated, and CPR was started by means of a mechanical resuscitator. The Pco2 was determined at end expiration using a Hewlett Packard 47210A Capnometer with 360

the electrode attached to the endotracheal tube. After 10 or 25 minutes of ventricular fibrillation and closed chest massage, the chest was opened and internal massage was performed. The CPP was calculated at least each minute and correlated with the P,,, values. A correlation coefficient of 0.78 was calculated based on 368 data points for eight dogs. This was significant at the P < .Ol level. The results of this study indicate that expired P,,, is positively correlated with CPP in the canine model of CPR. Since CPP correlates with survival in prolonged CPR, the noninvasive measurement of P co2 may be useful as a method of assessing the adequacy of CPR. The Pharyngeotracheal Lumen Airway (Continuing Report of a New Airway for Emergency Ventilation). Eugene N. Searberry, James T. Niemann, Penelope J. Hooks. University of Texas, Houston, TX 77043. The ABCs of cardiac life support dictate that adequate ventilation, by artificial means if necessary, be provided to the patient in cardiopulmonary emergency. However, this is easier said than done, since the mechanics of providing emergency airway management for the patient in respiratory or cardiopulmonary arrest remain a significant problem. The pharyngeotracheal lumen (PTL) airway employs a two-tube, two-cuff system, which is inserted into the airway in a “blind” fashion. The airway’s design allows it to function as an endotracheal tube if the treachea is entered, or as an esophageal obturator if the esophagus is intubated. At the last Purdue conference these authors presented early results of animal data with the PTL airway. In that paper, blood gas results were compared between the PTL airway and the endotracheal tube, and similar performance was shown. The efficiency of the PTL airway was also measured (efficiency-volume delivered to airway divided by volume exhaled by patient). The airway produced efficiencies of 80% to 100%. In both studies the PTL airway was used in the esophageal position. This paper presents early human data from three separate studies done at the University of Texas Medical School Department of Anesthesiology; the Royal Air Force hospital in Ely, Cambridgeshire; and the Emergency Department of Harbor-UCLA Medical Center. At the University of Texas ten healthy patients signed an informed consent (approved by the institutional committee for the protection of human subjects) to have the airway passed and evaluated while they were anesthetized and paralyzed prior to surgery (6 males, 4 females average age 26 years). They were ventilated with a standard endotracheal tube (ETT) and then through a PTL. The inspired and expired volumes were measured with two back-to-back Wright respirometers attached to the airway. Blood gases were measured after 5 minutes of stable ventilation. All patients were successfully and correctly intubated: Vi ml Ve ml Efficiency % Pao2mm Hg Paco2 mm Hg

933 707 77 194 39.3

PTL k 207 2 301 2 26 2 38 f 5.8

ETT 925 918 99% 153 ? 36 36.4 2 7.5

ABSTRACTS

At the Royal Air Force Hospital in Ely, Cambridgeshire, the assessment of ventilation through the PTL was carried out in 21 adult volunteers during anesthesia using IPPV. An integrated flow signal from a Fleisch pneumotachograph head was used to record tidal volumes, and end-expired carbon dioxide concentrations were measured with a solidstate infra-red analyzer. Readings were taken using a conventional endotracheal tube as a control (ETT), with the airway in the esophageal position (AE), and with the airway in the trachea (AT): Tidal Volumes (ml) ElT 751.6

End-tidal CO2 (%) 4.37 4.63 4.64

AE 662.6 AT 736.2

The Emergency Department at Harbor-UCLA reported the results of six patients undergoing standard CPR at two hospitals. Blood gases were measured during prolonged support with both the PTL airway and the ET tube: Pa0, ETT PTL

PH

pac0,

162 f 124

34 f 10

176 +- 105

36 f

12

7.40 7.28

t 0.23 ” 0.20

Endotracheal intubation is the optimum method of airway management. In the emergency setting its use has been limited by the technical expertise it requires. The PTL airway may offer substantial advantages over existing prehospital airway adjuncts, where competent ETT skills are not feasible or the patient is difficult to intubate. Clearly, further controlled studies are needed. Iron Delocalization into the Cerebrospinal Fluid during Cardiac Resuscitation in Dogs. Robert Walker, Blaine C. White, Thomas Hoehner, Marilyn Probst, John E Hildebrandt. Michigan State University, East Lansing, MI 48824. Reperfusion brain injury after prolonged cardiac arrest has been observed in several laboratories. One of the mechanisms proposed for this phenomenon is tissue injury by oxygen radical species. The presence of a transitional metal, such as iron, is essential for oxygen radical reactions in in vitro systems. The brain contains significant amounts of protein-bound and mitochondrial iron. The occurrence of acidosis in a medium rich in reducing equivalents can release Fe + + from ferritin. Particularly severe inhibition injury of brain mitochondria has occurred during 30 minutes of IAC-CPR following a 15 minute cardiac arrest in the authors’ laboratories. This injury is similar to that seen with in vitro injury of mitochondria by Fe+ +-oxygen radical systems. Therefore this study was conducted to determine if iron was delocalized into the CSF in the cisterna magna after a 15-minute cardiac arrest followed by 30 minutes of IAC-CPR. Six large dogs were anesthetized with ketamine and halothane. Central venous lines were placed in all six animals. Three nonischemic controls underwent cisternal puncture for withdrawal of about 2 ml of cerebrospinal fluid (CSF). The other three animals underwent cardiac arrest induced by KC1 (0.5 mEq/kg IV) and confirmed by ECG monitor.

FROM

PURDUE

CONFERENCE

ON CPR

After 15 minutes of cardiac arrest, resuscitation was carried out with IAC-CPR. Epinephrine (16 mcg/kg) and NaHCO, (3 mEq/kg) were given IV, and epinephrine drip was maintained at 3 mcg/kg/min throughout 30 minutes of artificial perfusion and ventilation. Blood gas determinations at 10 minutes of resuscitation were near normal. After the 30minute resuscitation, cisternal punctures for CSF were performed, all within 90 seconds. The iron content of the CSF was determined on a JarrellAsh #99.5 Inductively Coupled Plasma Atomic Emission Spectrometer, which is sensitive to 1 part per 108. All nonischemic CSF iron levels were zero. Post-resuscitation CSF iron levels were 4.3 mcM 2 2.3 (P < 0.05 against controls). This small study is the first direct demonstration of iron delocalization into the CSF during a resuscitation technique. Other techniques should be similarly studied, and the valence and chelation states of the delocalized iron must be determined.

Flunarizine in the Treatment of Experimental Canine Cardiac Arrest. A. Wauquier, H. L. Edmonds, Jr., W. Melis, J. Van Loon. Janssen Pharmaceutics, Beerse, Belgium. The calcium entry blocker flunarizine improves cerebral cortical blood flow and vascular resistance after cardiac arrest in the dog (White MC, et al. Ann Emerg Med 1982;11:119-126). The purpose of this study was to extend the evaluation to the degree of early neurological recovery by using a similar protocol. After determination of arrest neurological status before arrest, dogs were anesthetized with alfentanil, immobilized with succinylcholine, intubated, and mechanically ventilated. Epidural screw electrodes were used for EEG recording. Continuous quantification of the EEG was achieved by power spectral analysis using APDP 1I-23 (Wauquier A et al. Drug Dev Res 1981;1:167-179) and by an anesthesia and brain activity (ABM) monitor (Datex Instrumentarium OY, Helsinki). The product of mean integrated amplitude and mean zero-cross frequency (PAF) was used as a single univariate descriptor of ischemic changes in the EEG. Ventricular fibrillation and cardiac arrest were produced by an electrode catheter placed in the right ventricle. Resuscitation began 10 minutes after the onset of arrest. It consisted of closed chest cardiac massage, artificial ventilation, sodium bicarbonate 2 mEq/kg, epinephrine 0.1 mg/ kg, and DC countershock (20 J/kg). The ten dogs were randomly assigned to control or treatment groups. Coded syringes containing flunarizine (0.1 mg/kg) or solvent were infused (1 ml/min x 10 min) at the beginning of resuscitation. Neurological status was determined six hours later by two independent raters with no knowledge of the drug code. The mean PAF in the flunarizine group (41 * 13% of pre-arrest value) was significantly higher (P < 0.03) than in controls (33 + 12%). Furthermore, the neurological status of flunarizine-treated dogs (55 * 14) was significantly better (P < 0.001) than that of the control group (82 * 16). Thus, flunarizine had a beneficial effect on early neurological recovery as determined by two independent measures. Preliminary studies in the authors’ laboratory suggest this effect is due in part to both vascular and neuronal actions. 361