Fragile Lives Read online

  But it was not all bad news. Far from it. I was really surprised by the change in Abel’s own heart. It had enjoyed months of rest following the insertion of the HeartMate, and this had reversed his heart failure and changed his heart’s globular shape back to normal. As we carefully dissected out the inflow cannula we found the bleeding point – a tear in the heart muscle itself. I peeled off the crescent of muscle attached to the metal inflow cannula and kept it for pathological examination, to compare it directly with the core of muscle excised to accommodate the inflow cannula in his first operation.

  This was better than rocket science. We’d shown that the enlarged heart muscle cells had reverted to normal size and structure, and that we could help sick hearts to recover. We called this the ‘Keep Your Own Heart’ strategy. But were the structural changes sustainable and would the hearts continue to function? We didn’t know. Only time would tell, but it was a monumental finding.

  The surgery had taken seven hours. We delivered Abel’s pump like a baby, as I wanted to keep it. The inflow cannula site was repaired with deep Teflon-buttressed stitches. His heart now looked like a dog’s dinner, but it still worked and was contracting well, boosting his circulation as we re-warmed the blood. We separated from cardiopulmonary bypass as if it had been a simple, straightforward operation. There was bleeding from every cut surface but his blood pressure was fine.

  Was this going to be the world’s first successful ‘bridge to recovery’ in a chronic dilated cardiomyopathy patient? The bleeding eventually abated, and we closed the chest and abdomen. This was a triumph in itself. Abel’s family were ecstatic, Ralph and Jean were relieved, and my staff were optimistic. But I was still unsettled. We were perched on a knife edge here.

  I had no choice but to leave the post-operative care to the intensive care team. I was buggered, at best. At worst? Psychopathic, I guess, juggling too many balls in the air, pushing my own life – and other people’s – to extremes. Surgery I find easy, politics less so. And taking risks with open-ended bills from the NHS was stressful. More than individual lives were at risk here. Many influential characters were claiming that mechanical hearts would never work and it was a battle to prove them wrong.

  Abel remained completely stable for the next thirty hours, everything normal. His kidneys were passing urine despite the prolonged shock. Yet I was still uneasy. The stakes were too high, and I was walking on water but waiting to sink. I didn’t have to wait long. Late at night Abel’s own heart flipped into uncontrolled atrial fibrillation with a rate so fast that the left ventricle was suffering, a straightforward problem that happens to almost half of heart surgery patients. It should have been easy to fix, but it wasn’t. None of the junior doctors on site dared shock him, so he deteriorated rapidly. I rushed into the hospital but by then he was beyond help.

  Abel died with his family around his bed. I could do one of two things – go ballistic and get sacked, or walk away. I did the right thing, passing Ralph’s bed on the way out. Jean was asleep, with her head on the sheets, oblivious to everything. Ralph stared straight forward, consumed with anxiety. His eyes followed me as I passed. He understood how I felt and there was nothing I could say to reassure him. He’d heard everything – ‘Shall we shock him? Should we call the consultant? What if …?’ Then the inevitable. Shit and derision.

  There’s such a narrow margin between life and death. Survival depends upon those present being able to treat the problem, upon whether the correct treatment is applied and if it’s done at the right time. Abel needed that electric shock to return his fast heart rhythm back to normal. For that he needed someone to take charge and rescue the situation, but it didn’t happen. It’s what we now call ‘failure to rescue’. I felt that he’d died needlessly, after all that effort.

  Thankfully Ralph went from strength to strength. He’d been transformed by technology and soon learned to live with the ‘alien’ inside pumping away noisily, hissing through the air vent, circulating six litres of blood each minute with a strong, bounding pulse. Within two weeks both he and his family had mastered the equipment. The most important thing was dealing with the stiff white power cable as it emerged from his side. It needed to be kept scrupulously clean and the bugs kept out as the surrounding skin had to bond with it, integrating with the Dacron covering. Ralph’s biggest risk was of driveline infection, very common with this device and much worse for a diabetic like him. Indeed patients suffering from diabetes had initially been excluded from consideration for a heart pump for this very reason.

  Jean practised dealing with unexpected problems and how to troubleshoot if the alarms went off. At such moments life itself depended upon doing the right thing, so she learned how to pump the HeartMate manually should the electrics fail. Then off they went, happy and confident, anticipating a new life, the swiftest hospital discharge of any artificial heart patient to date. Although Ralph came back for check-ups every month, they resumed travelling in their caravan, making the most of his resurrection. He was happy.

  The winter brought predictable problems – a simple cold, coughs and sneezes. These caused shear stress at the stiff abdominal driveline exit site, the delicate seal between skin cells and Dacron broke down, and bacteria infiltrated the break in the skin’s defences. Jean tried hard to keep the area clean with normal driveline care, but then it started to discharge pus, becoming hot, red and sore. Ralph’s GP took a swab and put him on antibiotics. Infection made his diabetes more difficult to control, his higher blood sugar levels helping to feed the bacteria. After being on antibiotics for several weeks a fungus intervened, and we admitted Ralph to hospital for a few days to try to get on top of the problem. By now there was an infected and painful crater around the line, so we tried to revise it surgically. It certainly looked much better, and Ralph’s own heart had improved considerably as he spent hours on an exercise bike building muscle.

  Eventually the fungal infection reached the pump itself and I knew this was the writing on the wall. Over in Houston Bud was experiencing the same problem with his bridge in transplant patients, although none were diabetics, and I called him regularly for advice. We knew we could never sterilise it with antibiotics, but could we risk removing it as we’d done for Abel? I was seriously contemplating that when the infection gained entry to his bloodstream. Septicaemia, we call it. Now both the inside and outside of the pump were infected, the pig valves covered in masses of fungus and beginning to disintegrate. There was no way out of this. I had to explain to Jean that it was too late for heroics.

  The septic shock had caused kidney and liver failure, and Ralph was now yellow, his lungs filling with fluid as the valves in the pump started to leak torrentially. The HeartMate even sounded different, more like a washing machine as blood sploshed to and fro though the pumping chamber, its hiss now like a boiling kettle rather than a snake. For me it was finished, and Jean understood when I said it would be inappropriate to try ‘Abel type’ heroics. Ralph couldn’t survive these. We should help his breathing with the ventilator and see him off with the dignity he deserved.

  Ralph had helped to start something. ‘The man with two hearts’, as the Sunday Times called him, had done so well. He died eighteen months after the implant, surrounded by his family, and after all the suffering they remained grateful for this chance of life and time well spent.

  We learned a considerable amount from Abel and Ralph. They were pioneers, the very first patients to receive an artificial heart on a ‘lifetime basis’. We accepted that this ‘lifetime’ had been short, but all life is precious. Ask cancer patients about that. All we needed was better blood pumps – and we were working on that.

  7

  saving julie’s heart

  ‘Ah, Nothing is too late, till the tired heart shall cease to palpitate.’

  Henry Wadsworth Longfellow

  Why did patients die after heart surgery? Was it because the surgeon made a mistake, damaging the heart through a technical error, operating on the wrong valve or coronar
y artery, or letting the patient bleed to death? Very rarely was it any of these. Usually it was because the patient was so sick beforehand that their survival remained in the balance even when the operation went well. As in any other profession mistakes could and did happen, but the majority of patients died because their diseased heart gradually deteriorated during the operation.

  In conventional surgery at the time, the heart suffered during the period when it was deliberately stopped without its blood supply, irrespective of the protective solutions we infused, none of which were perfect. At the end of the operation it was simply too weak to sustain the circulation, tired yet potentially recoverable. When the bypass machine was turned down the heart just wouldn’t take over, and without help the patient died on the operating table. Quite frequently the heart limped off the machine but gradually failed over the next few hours, and however much we flogged it with drugs, the die had already been cast in the operating theatre. The longer the heart muscle was deprived of blood flow, the more likely this was to happen. Then off to the mortuary the body went, leaving a grieving family behind.

  I felt that this pathway to death was preventable. The heart just needed an opportunity to recover, and staying longer on cardiopulmonary bypass was not the answer. In fact it made things worse. The more time that blood interacted with the foreign surfaces, the greater the likelihood of whole-body inflammation, which in turn meant worse organ function and more bleeding.

  So what about some other type of pump? A simple circuit without the oxygenator might work better, and this could be used for a few hours, perhaps days – or, in the worst cases, several weeks, until the heart’s own contractile function and the benefits of the surgical repair would allow the circulation to be free-standing again.

  A safe and reliable temporary blood pump would probably save half to two-thirds of those who might otherwise die. How did we know? Post-mortem examination showed us that the heart was structurally sound in most cases. It just got tired. Give it a rest and support the rest of the organs, then the patient might get better.

  Inevitably most pioneers working on blood pumps thought that they needed to generate a pulse to replicate the human circulation. Early pumps had to empty and fill, and be large enough to mimic the normal heart. Usually it was just the left ventricle that needed help; if necessary, separate systems could be used to support both left and right ventricles. But the early pulsatile devices with bellows and valves created turbulence, friction and heat, a perfect environment in which to promote blood clot formation and the disastrous complication of a stroke – always a dismal and feared end point in the battle to save life.

  At Allegheny General Hospital in Pittsburgh, George Magovern, the chief of surgery, was less convinced about the need for pulsatility. He argued that when blood reaches the tissues it’s through tiny capillaries one cell thick. There’s no pulse in this micro-environment as pulse pressure has already dissipated in the small arteries before reaching the capillaries. Should a pulse be unnecessary – as we’d suggested – then smaller, less traumatic pumps could be made, pumps that spin at high speed and deliver between five and ten litres of blood per minute. The pump just needed to be kind to the blood. So Magovern engaged his friend Professor Richard Clark, head of cardiac surgery research at the National Institutes of Health in Washington, DC, to work with him on the project.

  It took the team five years to produce a spinning blood pump. It was the size of a bicycle bell and weighed just half a pound, electromagnets driving one single moving part – a six-bladed turbine. First called the AB-180, it was intended to support the circulation for up to six months, long enough for bridge to transplant. The design was so simple that one of the technicians attached a prototype to his garden hose and used it to drain his fish pond. It performed well in the laboratory without damaging the red blood cells and it worked fine when used in sheep. As a result the US Food and Drugs Administration (FDA) sanctioned a human trial with the AB-180 in 1997 on the strict understanding that the pump was only used on a ‘last resort’ basis. A trial of pump versus certain death.

  In February 1998 I was invited to Washington by the FDA for a heart conference to discuss the recent operations I’d performed on Abel and Ralph. It was there that I met Richard Clark, who had been expected to retire but didn’t want to cut the umbilical cord. Cardiac surgery was his life. Over dinner he showed me the AB-180 and asked whether I’d take him on as a research fellow for a year. I was flattered and suggested that he should bring the pump with him, and on 7 August that year he and his wife arrived in Oxford. It made for some stark contrasts: from skyscrapers to the dreaming spires, from the world’s best-funded health care system to the National Health Service. Up until that point the AB-180 had still not been used successfully in a patient – three valiant attempts to rescue patients in shock all ending in death – and there was a distinct possibility that the clinical trial in the States would be stopped.

  Two o’clock in the morning, 9 August 1998, and my phone woke me. Strange, as I wasn’t on call that night. It was a cardiologist from the Middlesex Hospital in London. She was looking after Julie, a twenty-one-year-old student teacher who was home for the summer with her parents in Surrey and who’d initially complained of flu-like symptoms. Within days she’d become exhausted, listless and short of breath, sweating but cold, and not passing urine. Dying, in fact.

  The district general hospital recognised this and passed her rapidly on to the London teaching hospital, where an ultrasound scan showed a poorly contracting heart. She had viral myocarditis – a viral illness like a cold but, when it involves the heart, potentially fatal. Inflammation and fluid accumulation had destroyed Julie’s heart function, the cardiac output monitor confirming very poor blood flow throughout her body, less than a third of what it should have been. All in all it was a pretty desperate situation for a girl who’d been perfectly normal the previous week.

  The cardiologist had admitted Julie to the cardiac intensive care unit for what we call a balloon pump. This is a sausage-shaped latex balloon attached by a catheter to an external air compressor, the catheter being fed through the leg artery up into the aorta in the chest and the balloon inflating when the heart relaxes. This raises the blood pressure and marginally reduces the amount of energy the heart needs to expend, but you do require some pressure and flow for it to work. In Julie it was bloody useless and just obstructed the blood flow to her leg. This was already blue – pouring out lactic acid – and at the time of the call the highest blood pressure was 60 mm Hg, half what it should have been.

  I was considered the last chance saloon, and the Middlesex cardiologist wondered whether anything at all could be done. ‘Is there any technology you’ve got that could help?’ she asked, then reassured me that it was okay if I couldn’t do anything as the shocked parents and younger sister had already said their goodbyes. They felt Julie had gone when she was anaesthetised to be put on the ventilator. Conventionally the ventilator and balloon pump were the final option – but they’d made no difference, and, inevitably, her blood pressure had dropped even further after the anaesthetic drugs.

  Most patients with viral myocarditis get over it. As with influenza, the effects of the virus dissipate and the heart recovers – but this was not happening with Julie. The lethal blood chemistry and deteriorating organ function had gone too far, and she was bang in the middle of the vicious cycle of acute heart failure that invariably leads to death.

  In the small hours of the morning you sometimes feel like saying, ‘Sorry, I’m not on call. I’ve had a few beers and can’t help you.’ To be honest I don’t recall what I said in this case, but it was probably along the lines of, ‘Get her to Oxford as quickly as possible. I’ll get the team ready.’

  So Julie was brought by ambulance to Oxford in the middle of the night with doctors, nurses and masses of equipment. I called Richard Clark, who rushed straight in to unpack the kit, excited by the prospect of early action, and my earnest Japanese right-hand man Takahiro
Katsumata came in to assist.

  We met Julie and her helpers in the accident department following the harrowing sixty-mile dash from London. By then Julie’s liver and kidneys had failed and her blood pressure was negligible, so we’d no choice but to rush her straight into theatre. She was as good as dead. Her parents hadn’t arrived by then, still struggling to get out of London even at that time in the morning.

  One thing that subsequent media reports stated was incorrect. They said that I’d been given the green light from my hospital’s ethics committee to use the AB-180, but sadly this was wrong. Absolutely wrong. No one but me and Richard Clark had any idea that we had the device, and neither of us considered that we might need it so quickly. Up to this point it had a 100 per cent mortality rate, which is, to put it mildly, statistically significant. But I was not the kind of doctor who’d let a young patient die because of some bureaucratic detail.

  It was fortunate that Brian, the perfusionist, had the heart–lung machine primed and ready. The intensive care doctor accompanying Julie already thought that they were too late, and when I put a hand on Julie’s leg I too suspected she was dead. White and cold, her veins looked empty and her feet were blue. Even so it was difficult to move her quickly – although she didn’t weigh much – and the drips, ventilator and balloon pump had to be shifted carefully. Katsumata and I lifted her gently onto the operating table, and Sister Linda was scrubbed up, gowned and set to go.

  Dawn, the second nurse, stripped away Julie’s white hospital robe. Her urinary catheter was caught in part of the equipment, stretched like catapult elastic, the inflated balloon still inside her bladder. Dawn fixed it. I told Linda to paint up with skin prep and get the drapes on. Katsumata and I scrubbed with haste – what was more important now, survival or sterility? Mike, our anaesthetist, grappled with the multiple lines and drugs, trying to make sense of it all, helped by the visiting anaesthetist, who held the key to the puzzle. It didn’t really matter what went into the lines – nothing was helping. I asked Mike to focus the beam of the operating light on Julie’s chest, then grabbed the scalpel.