Chapter Thirteen: Mayo post U.S. Army – Neuroanesthesia, Research

Chapter 13 Sub-sections

In September 1969, I returned to Mayo neuroanesthesia and a quest for research time to investigate succinylcholine-induced hyperkalemia. Additional reports now documented similar hyperkalemia in patients with direct muscle trauma (Birch et al, 1969), upper motor neuron lesions such as cord section (Cooperman et al, 1970) or stroke, and lower motor neuron lesions such as peripheral motor nerve dysfunction, poliomyelitis, or Guillain-Barré syndrome (Case History, 1971).

One report suggested that pre-treatment with curare prior to use of succinylcholine prevented dangerous potassium efflux (Birch et al, 1969), but the response of one of our burn patients contradicted this interpretation (Gronert, 1970). Later reports confirmed its ineffectiveness.

Neuroanesthesia Publications

My role in neuroanesthesia involved both clinical care and clinical research. We had multiple projects, with fine leadership from Michenfelder.

Cucchiara documented 3827 sitting position cases at Mayo from 1966 through 1983 (average number of sitting cases per year was 240), with no intra-operative deaths, and just 2 major complications, incidence 0.05% (Cucchiara, 1984). The only death due to air embolism occurred during a prone position patient of mine, in the 15-20º head up position (Gronert, Messick et al, 1979). This case occurred prior to use of the Doppler. The neurosurgeon, Colin McCarty, was removing a meningioma from the posterior dura mater. He tented up the dura to clip a bleeding vessel. The dura mater at that point overlay the trigone, and the hole in the dura permitted massive entry of air into the venous channels.

In that position, with the head close to being level with the body, we did not suspect the possibility of air embolism. The heart sounds abruptly disappeared and the arterial monitoring trace went flat. The EKG appeared normal for about two minutes. Resuscitation was unsuccessful. I attended the autopsy that afternoon; there were several hundred ml of air in the patient's superior vena cava and right heart, with air in the coronary arteries via a patent foramen ovale.

In our experience, air embolism of greater danger was more likely to occur in posterior fossa cases, rather than cervical spine cases. For the latter, the sitting position provides superior advantages: less venous pooling, less tissue swelling, less blood loss, and easier visibility than the prone position. I have worked with enough neurosurgeons - some preferring the prone position, some preferring sitting - to be convinced that the sitting position is preferred for cervical spine surgery if the anesthesia-surgical team is experienced in that approach.

Vascular neurosurgery was prominent at Mayo, with cooperative operating room contributions of neurosurgeons, neurologists, and anesthesiologists. There were several areas of interest. One continuous ongoing project involved multi-monitoring of patients undergoing carotid endarterectomy. Inherent in carotid surgery is the threat of inadequate regional cerebral blood flow with carotid occlusion, as this affects flow in the middle cerebral artery. The surgery is a serious risk and success depends in large part on a long-term well-functioning operating team that routinely works together, and is aware of the problems that can need immediate attention.

One approach utilizes regional anesthesia, e.g., deep cervical block; the anesthesiologist monitors the patient's level of consciousness, and ability to move the contralateral arm and leg. While in private practice in Denver, I performed deep cervical block for a number of awake carotid endarterectomies with one of the vascular surgeons, and it worked well. However, several demands must be satisfied for this risky procedure in an awake patient: for the patient, the proper personality and disposition during stress; for the nurses, everyday routine experience in the demands of carotids; for the anesthesiologist, skill in the nerve block and ease in communicating with the patient; for the surgeon, one who will not panic when something goes wrong. We did not use regional anesthesia in carotid surgery at Mayo, and this was not due to surgeons' factors.

The surgeon Thor Sundt and the neurologist Frank Sharbrough monitored regional cerebral blood flow with a collimator outside the skull, aimed at the area perfused by the middle cerebral artery. To measure regional cerebral blood flow in the middle cerebral distribution, Sundt injected small amounts of 133Xenon prior to carotid occlusion, at the moment of occlusion, and during surgery on the occluded carotid. Sharbrough used a 16 lead EEG to monitor electrical activity over the entire brain surface. Sundt measured internal carotid artery shunt pressure during occlusion. These extraordinary approaches evaluated effects with varied monitoring and various anesthetic agents in carotid endarterectomy (McKay et al, 1976). Measurements of regional cerebral blood flow and the multi-lead EEG were of value in determining ischemia during occlusion and indications for an internal shunt. Stump pressure was of value only with critical value adjustments related to arterial PaCO2, and with the type of anesthetic, e.g., volatile vs. narcotic based. The latter increased the critical value for stump pressure compared to that associated with halothane.

Some intra-cranial aneurysms are difficult to treat because they are deep within brain tissue and there can be substantial blood loss. This obstructs the surgeon's vision, particularly when using a mounted microscope for closer views of the deep, tiny field. A combined approach with Mayo cardiac surgeons was the application of profound hypothermia, utilizing surface hypothermia supplemented by a cardiac pump-oxygenator-heat exchanger. In patients with normal heart function, temporary cardiac arrest at a diminished body temperature (12? C, 53.6? F) permitted bloodless access for some 30-40 minutes while the neurosurgeon clipped the aneurysm. Bypass cannulas were inserted into major vessels in the groin in readiness for bypass. The chest was not opened. Bypass was not started until the head was open, the surgeon had dissected the aneurysm, and s/he was ready to clip it (Sundt et al, 1972). Once the aneurysm had been clipped, the heat exchanger in line with the bypass pump rapidly warmed the patient. Circulating water blankets with warm water continued to supply heat to the external body after the bypass pump was discontinued. Review of a large group of Mayo's profound hypothermia patients revealed that results were no better than a parallel group of patients having surgery at normal body temperature. After that, profound hypothermia was used only in very difficult-to-expose aneurysms.

Figure 11
Fig. 11. See text

An early neurosurgeon, Temple Fay (1959) of Philadelphia, applied hypothermia beginning in the 1930s in treatment of brain tumors, since the lowered temperature slowed tumor growth. He used two approaches: hypothermia via cooling the entire body, and localized hypothermia. Fay noted that whole body hypothermia, prolonged for several days, had an associated mortality rate. For localized hypothermia, he placed catheters within the brain, and cooled just that portion. At least one patient did not seem particularly bothered. Fig. 11. (Fig. 8, in: Fay T, Early experiences with local and generalized refrigeration of the human brain, Journal of Neurosurgery, May, 1959, number 3; 16:239-260, used with permission.

In one complex case, June, 1981, Mayo neurosurgeons, anesthesiologists, obstetricians, and pediatricians combined Caesarean section delivery with clipping of an intracranial aneurysm (Lennon et al, 1984). The patient's family and I have remained in contact ever since. In spring 2007, the patient's husband surprised me by providing for the first time his specific recollections and impressions about his interactions with me prior to surgery. The reader needs to interpret this story in terms of the stresses this family suffered, their terrible expectations – beginning as soon as someone told them about the ruptured aneurysm – and the realization that, while the risks were considerable, the procedure went well. The family graciously permitted me to include their story here, based on how they recall it:

The patient, a 35-year-old nursing school teacher, and her husband had been anticipating an August delivery of their second child and were on vacation near Brownsville, Texas, about 200 miles from home. Her aneurysm ruptured early on a Sunday morning and she was admitted to a local hospital. Her condition, especially in light of the pregnancy, was critical and called for intervention beyond the resources available. Based on the recommendation of the attending neurosurgeon, she was transferred by air ambulance on Tuesday afternoon to Mayo, about a 1300 mile flight. Her husband and a friend flew commercially, and had departed Houston before his wife had arrived in Rochester. He couldn't find out whether his wife or child had survived the flight until after he landed. On arrival in Chicago, he anxiously phoned St. Mary's hospital in Rochester. Without identifying himself or his wife, he told the operator that he was seeking information on an emergency patient from Texas. The operator immediately said, “I'll connect you to her room.” Which she did.

The husband and his friend were trial lawyers and long time acquaintances, both knowledgeable about medicine. The husband had once been a surgical technician. In Texas, they had been advised that the patient could die at any moment, and that the baby gave every indication of being healthy and viable. They had been in a strange place for less than 18 hours when the aneurysm had ruptured and he had authorized transfer of his wife to Mayo without having ever talked to anyone at Mayo. Furthermore, he had no idea how his wife was doing, nor the future plans for her care. He knew nothing about Dr. Sundt or me, except that the Mayo staff said that Dr. Sundt and I had worked there a number of years.

Her husband was apprehensive about meeting the physicians; the consultation took place at 11 a.m., adjacent to the ICU, in a large room reserved for family meetings or physician conferences. All that her husband knew was that they would meet with “the doctor.” I had been chosen to discuss the surgery with them, as I was the only involved physician who had direct and active experience with the combination of neurosurgery, obstetrics, and newborn resuscitation. I arrived in my scrub suit, and we huddled in a corner of the room, speaking in hushed tones since another family was being counseled at the other end of the room. Although not mentioned, they were concerned why, in a crisis of this magnitude, the initial contact doctor was the anesthesiologist and not the surgeon.

As he wrote in his letter, “it is very difficult to describe Dr. Gronert as he appeared to us. It is even more difficult to describe the conversation.” He didn't specifically remember much of what was said, but what he does recall is that he received “a powerful lesson in communication.” What I said in words was one thing. What he heard by way of communication was different and so important.

After short pleasantries and a brief summary of the backgrounds of Dr. Sundt and me, I began with the obvious facts and risks: his wife was gravely ill, and her not-yet-born baby was doing fine. Her angiogram showed two aneurysms, one of which was leaking or had leaked. Surgery would be the next day, and I explained that Dr. Sundt would operate on the aneurysm after the obstetrical surgeon performed a Caesarean Section and delivered the baby. I would provide anesthesia. The surgery was urgent, and required a team approach. I described how important it was for this dual surgical team to function cooperatively. I stated that the anesthetic would need to be balanced. For example, his wife's blood pressure could not increase during the C section, or it could force the clot off the aneurysmal opening and a re-bleed was potentially disastrous. Yet her blood pressure needed to be high enough to supply the uterine artery, or the baby would lack oxygen. I described a litany of risks and the percent likelihood of disability or death in mother and child.

I explained that I would control her blood pressure at the start and make certain before surgery commenced that I had enough control of her blood pressure to make it go up and down as needed during the C section and the craniotomy. I told them that the baby would be a bit depressed from medication his mother would receive that would cross the placenta into the baby, but that there would be doctors present to ventilate him to remove anesthetic gases and to reverse depressants.

These were the objective realities that I knew were true and which had to be covered. Her husband and friend with whom I was sharing this information received and processed these same facts. From their perspective, however, I was, with my own presence and personality, conveying another and probably far more important message on a different level. What occurred with this family is a profound lesson about doctor patient communications on life and death issues and proof that a physician's words may sometimes be only part, and perhaps a less important part, of the ultimate message that is conveyed.

The conversation, viewed as a whole, was, according to the husband, “… absurd from an intellectual perspective.” He recalls it this way:

“Here my friend and I were, in a room speaking with you, someone we had never heard of and never met, a long way from home, and in a very few minutes and with minimal preliminaries you just rolled out one after another of several possible fatal scenarios. As you were speaking, I was doing calculations in my head. The totals for these percentages meant that the probability of my wife being dead the next day were substantially above 50%. My mind was reeling as I tried to contemplate in just seconds these awful possibilities. Then, in a somewhat rapid fire fashion, you told us that you, Dr. Sundt, and the other physicians would be ready for whatever might happen. Then Dr. G said the most incredible thing, “Don't worry, I think that she'll do as well as we can ever expect.” In what seemed like just a few minutes more, you were gone.

My friend and I were then alone in the big silent room, the other family having left while we were talking with you. Any rational view of what just had transpired would conclude that now we would be ever more fearful than we were before we met you since now we had replaced anxious speculation with medical fact as to what might happen to my wife and baby.

But, the minute you left the room, my friend and I looked at one another in dumbfounded amazement. We were not despairing. On the contrary, we felt relief and a kind of paradoxical euphoria in that we now felt, after being in your presence, that we had done the best we could ever have done for my wife and baby in getting them to you and Dr. Sundt.”

In these few moments together, and in the face of their quite rational apprehension and fear, as her husband put it, my words alone were about risk and matters of practice and technique. But, as her husband reported, the deeper message I communicated was something else: “What we really felt in that brief visit, was your persona, your spirit and humanity, and, above all, your optimism. The real message was that you and Dr. Sundt and the entire team would do as much as humanly could be done for my wife and baby, and that we could trust you for that. Your spirit allowed us to let go of the elephant of fear on our back. Nothing objectively had changed. The risks were the same. But because of you everything was different due to our decision made then and there to simply have faith in you and Dr. Sundt.”

Something in my spirit and optimism and in the equivalence of trust that arose in that brief moment together led to his willingness to let go of morbid fear. In retrospect, I don't know how I did it.

The next morning, the husband recalled, I came ‘flying' down the hall with a surgical stretcher to take his wife to surgery. There was no time for any conversation that morning. But he reported that he felt complete confidence in me and gratification that I had personally come to reassure his wife and be with her from start to finish on what would be a momentous and life-changing journey. Only after I had taken his wife to surgery did he meet Dr. Sundt for the first time and only for a brief moment. But it didn't matter --- he now had seen the Master, Dr. Sundt, and that was enough. Even to this day, he and his family remain in touch with Dr. Sundt's family. (Dr. Sundt was perhaps shy with families; on another occasion, he told this same family that he had stopped doing pediatric surgery because he could not take the emotions of dealing with kids, kids who put 100% faith in him at times when he knew that the outcome would be fatal.)

The New Yorker: Report on a New Anesthetic Agent

Because of concerns about volatile anesthetic agents, e.g., halothane and isoflurane, in increasing intracranial pressure, we measured spinal fluid pressure in craniotomy patients who did not have direct or indirect evidence of increased intracranial pressure (Adams et al, 1972, 1981). We noted that prior hyperventilation was needed to minimize ICP changes with halothane, but was not necessary with isoflurane. We postponed submission for publication of the isoflurane report – it was published 9 years later, because its introduction into clinical use was delayed due to the need for rebuttal of a scare concerning potential carcinogenic effects of isoflurane (Eger et al, 1978). The story is fascinating.

Thomas Corbett, in Michigan, had preliminary research results suggesting that isoflurane could cause cancer in rodents. He presented his data, in part, at the May 1975 meeting in Atlanta of the Association of University Anesthesiologists, but there was considerable criticism of his research. Because of problems in acceptance for publication in an anesthesia journal and Corbett's frustration that the pharmaceutical company would release isoflurane to the market by fall 1975 anyway (to coincide with the annual meeting of the American Society of Anesthesiologists), he contacted the FDA (Brodeur, 1975).

Because the data seemed sufficiently suspicious, the FDA withheld approval and delayed the introduction of isoflurane. In time, Corbett's findings were not substantiated (he is a co-author of the rebuttal study, Eger et al, 1978) and the FDA approved isoflurane.

Brodeur's article in The New Yorker described the turmoil. Corbett had been understandably concerned with potential long term toxic effects of anesthetic agents and that some of these might involve carcinogenesis. He and his wife had noted that the odors of whatever agent he had used during the day were obvious upon his return home, even on his breath. What long term effects might accrue from this?

Corbett's fascinating distractions occurred during our investigation of the puzzles of hyperkalemia after use of succinylcholine.

Hyperkalemia Research – a Blank Beginning

Non-clinical time for laboratory research was finally mine. Theye and I planned further study of the hyperkalemic response to succinylcholine in patients with thermal trauma. The main question now was: why did hyperkalemia after administration of succinylcholine occur in burn patients who had no evidence of muscle damage? Why should burned tissue be involved with this?

After evaluating the literature and various animal models, I proposed a swine model. A deep thermal burn that did not affect muscle would eliminate damaged muscle as a potential potassium source. Also, a full thickness burn would be painless if its border had minimal second degree burn. That's because the skin's nerve endings in a third degree burn are destroyed. We could produce this by briefly dipping anesthetized swine into boiling water. There would be a sharp demarcation between burned and normal skin, thus no pain.

A major problem was to convince the Mayo animal care committee to permit this sort of destructive, disturbing, and, to some, alarming study. Here Theye was invaluable; the protocol had been approved, but on the first day of study, several investigators assembled outside the laboratory to protest and hopefully block this new inexperienced investigator from starting. Theye profanely raged like a wounded bull out there in the corridor and that ended any and all protests.

The study went fine. The pigs were anesthetized with halothane by mask, their tracheas intubated, and thermal trauma produced by holding them upside down and dipping their backs into a trough of 95º C, 203º F, water for 20 secs (Fox et al, 1947). I personally cared for these swine, much as we had for the U.S. Army burn patients: individual pens, supplemental feedings, twice daily baths followed by Sulfamylon (mafenide) ointment, and close attention for signs of superficial or systemic infection (there were none). The pigs were healthy and maintained their weight. Sulfamylon had been used in thermal trauma for only a few years, and it was a virtual miracle drug in its efficiency in controlling infection.

We anesthetized these swine each week while they were recuperating and injected succinylcholine. None developed hyperkalemia. We either had too small a burn, or the wrong species. To confirm that swine did develop this problem, we additionally examined succinylcholine-related potassium changes after sciatic nerve section, thus denervating the muscle. This confirmed that swine were an appropriate species (Gronert, Theye, 1971).

While the model was inadequate for study of burns and hyperkalemia, it did provide departmental barbecues at our farm home. These barbecues used pork that had not been damaged in a study. The National Institutes of Health banned this approach a few years later. On one occasion, I used our horse trailer to bring home the last pig from a study. When our eight-year-old Mary asked about it, I said that this was Esmeralda. She thought that it was neat to have a pig, until the next morning, when I took Esmeralda to the Pine Island Meat Market for slaughter.

Our First Porcine MH Episode, Death Due to an Open Oxygen Valve

One pig was unique in our burn/hyperkalemia study: after receiving succinylcholine, it developed MH (malignant hyperthermia), with acidosis, rigidity, and pronounced fever. We routinely measured esophageal temperature and serial arterial and mixed venous blood gases in these animals, valuable aids when MH started. With rigorous symptomatic treatment, we saved this pig. When we could finally relax our efforts, we took him off the ventilator for spontaneous breathing and attached a plastic tube to the endotracheal tube for added oxygen. When we opened the high pressure valve on the G tank of oxygen, the flowmeter had unfortunately been left full on. There was a large poof as the high pressure (2000 lb/in2) oxygen ruptured the lungs, stomach, and diaphragm, and the pig turned into a true pigskin, or American shaped football.

We regretfully lost our first MH research pig, but we now knew that we could study MH, as Theye had already designed the methodology for studying specific organ metabolism during anesthesia (Theye et al, 1975). This was perfect for investigation of MH, but that was postponed until later.

Hyperkalemia Research Is First

We examined the release of potassium after succinylcholine, and quantitified canine potassium efflux from gastrocnemius muscle during four states that reflect varying muscle abnormalities. Its blood supply is simple, and we could totally isolate the venous drainage that enters the general circulation. We collected and measured total blood flow of the muscle and its venous potassium and oxygen contents for comparison to the blood arterial content. General anesthesia was used in all investigations.

Our four conditions were: 1) normal muscle in active healthy dogs; 2) denervated muscle, a lower motor neuron lesion due to section of the sciatic nerve (Gronert, Lambert et al, 1973); 3) disuse atrophy related to cast immobilization of the pelvis and one hind limb (Gronert, Theye, 1974); 4) an upper motor neuron lesion produced by section of the spinal cord at the level of the sixth thoracic vertebra (Gronert, Theye, 1975). Thirty-four years later, the American Society of Anesthesiologists via its journal Anesthesiology honored this as a classic paper (Gronert, 2009). The last three conditions were studied in the laboratory one month after onset.

Denervation of the sciatic nerve eliminates muscle stimulation by halting release of acetylcholine from the motor nerve ending to its site of action at the muscle endplate receptor sites. Extra acetylcholine receptor sites now develop all across the muscle membrane. Succinylcholine, composed of two acetylcholine molecules connected by an ester linkage, acts as a long-duration acetylcholine. Succinylcholine, like acetylcholine, stimulates individual receptor sites to release small amounts of potassium. The circulation carries succinylcholine to the entire muscle membrane, and thus stimulates potassium release at the added receptors, with cumulative greater amounts.

We measured several effects of succinylcholine in the denervated state, condition 2 (see above): Ed Lambert, the pioneer in electromyography, brought electromyographic equipment to our laboratory and demonstrated in canine denervated muscle the silent muscle uncoordinated stiffening (contracture) concomitant with depolarization and exaggerated potassium efflux. This is a supersensitivity response. We were excited about these supposedly new and unique experimental findings until we found Brown's 1937 paper with similar findings in denervated muscle exposed to acetylcholine. Brown injected minute quantities of acetylcholine to examine the response in the laboratory. That exposed the entire muscle membrane to the acetylcholine. So, almost 40 years before, he had accomplished exactly what we had, and we no longer thought that we were wonderful. We again learned that few findings are new.

Quantitation involved measurement of venous blood flow, to estimate total blood flow through the muscle, and of the amounts of venous and arterial potassium and oxygen. The Fick equation permitted calculation of gastrocnemius potassium efflux and oxygen consumption after administration of succinylcholine:

quantity of substance produced (potassium) or consumed (oxygen) =      
[blood flow X (difference between arterial content and venous content)]

Figure 12a Figure 12b
Fig. 12. The colored portion is a schematic of the upper portion

This equation is accurate only if there is a steady state as regards blood flow, metabolism or excretion, perfusion pressure, etc. Otherwise we estimate values; we know whether there has been an increase or decrease, but the precise magnitude is uncertain. Our 1975 Medical Intelligence article summarized the field of succinylcholine-induced hyperkalemia (Gronert, Theye). Fig. 12. Note that potassium changes following succinylcholine are miniscule in the normal dog, are modestly increased during disuse atrophy, and reach toxic levels during upper and lower neuron lesions. (Fig 1, in: Gronert GA, Theye RA: Pathophysiology of hyperkalemia induced by succinylcholine, Anesthesiology 1975, July, vol. 43, number 1, pp 89-99, copyright owner Lippincott, Williams & Wilkins,, used with permission.)

Human findings (Schaner et al, 1969; Gronert, Dotin et al, 1969; Viby-Mogensen et al, 1975) show that succinylcholine, because of the risk of cardiac arrest due to hyperkalemia, is contra-indicated in patients with serious burns between about one week post burn and about two months post burn, if healing is then complete as to skin coverage, and the patient is mobile and gaining weight. Canine results in conjunction with human findings demonstrated: 1) skeletal muscle disuse atrophy alone, unless marked over the entire body, does not contra-indicate use of succinylcholine, and 2) a denervation lesion involving more than one hind leg, e.g., Guillain Barré, paraplegia or worse (quadriplegia), or stroke contraindicates succinylcholine. Furthermore, direct muscle trauma acts similarly to denervation and succinylcholine is not safe.

Other Muscle Relaxants and Abnormal Muscle

In 1985, two new shorter acting non-depolarizing muscle relaxants were introduced, vecuronium and atracurium. They would not produce exaggerated potassium release, since they did not depolarize muscle membranes, and thus were candidates for replacement of succinylcholine in patients who were at risk for hyperkalemia. However, they required greater doses than usual for rapid intubation. We investigated these in normal humans; the drugs were useful for that purpose, although their usual prolonged duration was exaggerated, and histamine side effects were pronounced with atracurium (Lennon et al, 1986). These side effects could be modified (Hosking et al, 1988).

LBJ and Mayo Conservatives

It's interesting that LBJ became a Mayo trustee at this time, the 1970s. Mayo is conservative and had never served alcohol at its dinners or meetings. When LBJ was told that, he said that they'd be serving it if they wanted him at any meetings. And they did. One of our conservative plastic surgeons said that he planned to push LBJ hard when they got together, socially, that evening, at the Mayo Foundation House. The morning after, the surgeon told us that that was impossible. LBJ walked into the room and effortlessly dominated it the entire time he was there. He controlled every conversation he was involved with, and countered anyone even before they began to express ideas. Our conservative surgeon was astounded, for he was himself accustomed to pushing others.

Tragic Anaphylaxis

Until 1981, the Mayo neuroradiology suite at St. Mary's Hospital was located on the floor just above the four neurosurgical operating rooms, directly accessible by a stairway. As the associated anesthesia team, we also covered this area, via a call light for aid and an alarm system for acute emergencies. A woman about 30-years-old received dye for a diagnostic study and immediately went into shock. The nurse anesthetist who monitored her called for help while she and the radiologist began therapy. When we arrived upstairs, we noted that she had hives on her skin, was loudly wheezing, was unable to breathe effectively, and had both a low blood pressure and an irregular heart beat. We intubated her trachea, and tried to ventilate her with oxygen, but this was ineffective, as her airways had shut down so completely that effective ventilation was not possible. Next her pulses disappeared, and her heart sounds were gone. We performed external cardiac massage, but her bronchospasm was so tight that we couldn't force oxygen into her lungs. The entire process had been quick and nothing worked. This was no mystery but a terrible event. We had the proper drugs, experienced personnel, and appropriate equipment immediately available --- and we were helpless. How much frustration can one have?