Saturday Night, Homemade Pizza, Pistachio Ice Cream, and a Little Trip Back to the 1990s

Hello, friends. It is Saturday evening, just about 7:00, and there is something wonderfully satisfying about reaching this particular hour on the last weekend of August and realizing that, for once, there is absolutely nowhere we need to be. No hospital corridor waiting for me, no patients to round on, no pager demanding attention, no meeting, no obligation, no reason to put on anything more sophisticated than whatever happens to be comfortable. The day has been long enough to feel earned, but the evening is still young enough to feel full of possibilities. Outside, it is about 73 degrees, the humidity has finally surrendered, and the air has that unmistakable late-August character that tells you summer is beginning its slow retreat. The leaves haven’t turned, the gardens are still green, and the days are still reasonably long, but there is a subtle change in the atmosphere, as though New England itself is quietly clearing its throat before autumn arrives. It is one of those evenings that makes you want to leave the doors open, turn off every machine in the house that doesn’t absolutely need to be running, and spend the night doing things that have no practical purpose whatsoever.

Which, naturally, is exactly what Sadie and I are doing.

Our Saturday began in the usual fashion for us, with work of a sort, although it is work that we willingly volunteer to do. We spent the day at the local Fire/EMS department, because apparently being physicians isn’t enough of a commitment to public service for either of us. We both maintain our paramedic licenses and continue to volunteer, and there is something deeply satisfying about putting those skills to use in the community where we live. Medicine has a funny way of becoming a very different thing when you take it out of the hospital and put yourself in a station house, an ambulance, or standing beside a patient on somebody’s front lawn. In the hospital, everything is structured around an enormous infrastructure of technology, personnel, laboratory medicine, imaging, operating rooms, intensive care units, and all the other machinery of modern medicine. Out here, medicine is distilled down to the patient, the examination, the physiology, the equipment you have with you, and the judgment you have accumulated over the years. We enjoy that immensely, although I suspect neither of us would admit that to anyone who thinks volunteering should be relaxing. It isn’t always relaxing. It is simply rewarding in a way that is difficult to explain unless you’ve done it.

Eventually, though, the day wound down, and we went our separate ways for a few hours. Sadie headed out to do the grocery shopping, which is one of those mundane domestic responsibilities that somehow becomes considerably more important when you know what the groceries are going to become later in the evening. I, meanwhile, did what any reasonable surgeon-paramedic with a few free hours on a beautiful Saturday afternoon would do: I went to the country club and played golf. I managed to get a pretty good deal on the course, and naturally, when a man is presented with the opportunity to save money while simultaneously spending nearly four hours chasing a little white ball around several acres of grass, there is really only one intellectually defensible decision to make. I took the deal and played the round.

Four hours later, I came home smelling faintly of golf course, sun, and the sort of peculiar combination of exertion and satisfaction that accompanies a round that has been just good enough to make you forget the shots that weren’t. There is something about golf that I have always found amusingly masochistic. You can hit one beautiful shot that makes you briefly believe you have finally figured the game out, followed three minutes later by a shot that makes you question whether you have ever actually held a golf club before. Yet somehow you keep going. By the time I pulled back into the driveway, however, I wasn’t particularly interested in analyzing my score. I was interested in being home.

And home was looking pretty good.

The first thing we did was turn off the central air conditioning, which may sound like an insignificant event to anyone who doesn’t live in a large old house, but those of you who have ever received an electric bill after running two four-ton units through the summer understand the emotional significance of that particular switch. There are moments in life when you don’t need a financial adviser, a spreadsheet, or an economist to explain the situation. You simply look at the thermostat, look at the outdoor temperature, and say, “We’re turning this damn thing off.” Tonight was one of those nights. With the temperature hovering around 73 degrees and virtually no humidity, there was no reason to seal ourselves inside a mechanically conditioned environment when nature had finally decided to provide us with better air for free. We opened things up, let the house breathe, and immediately the entire evening seemed to change character.

The dogs, naturally, interpreted this as an invitation to begin an entirely separate Saturday-night celebration.

We let Bentley and Davey out onto the property, and within seconds they were gone, charging off across our 65 acres with the sort of enthusiasm that suggests they had been personally imprisoned for the preceding several decades rather than spending the day at home with two adults who had been working and golfing. Watching dogs run on that much land is one of the great pleasures of living where we do. They don’t merely walk outside. They disappear into the landscape. One moment you can see them, and the next they are somewhere beyond the trees, racing after some scent that only a dog could possibly consider worthy of immediate investigation. Every so often one of them reappears, usually moving considerably faster than seems physiologically necessary, looking for all the world like he has just returned from an important expedition and expects us to be impressed.

While the dogs conducted their wilderness operations, Sadie and I went swimming in our pond. There is something particularly pleasant about swimming outside on a cool late-August evening, especially after a long day. The water felt wonderful, and for a little while there was nothing particularly complicated about life. We weren’t doctors, paramedics, volunteers, administrators, golfers, or anything else. We were simply two people floating around in a pond on a beautiful Saturday evening, enjoying the fact that the calendar had given us permission to slow down for a few hours.

Afterward, we dried off and settled into the evening. We had a hookah, spent some time outside, and played with the dogs whenever they happened to come barreling back into civilization. There was also an ulterior motive behind all of this interaction with the dogs: we were trying to wear them out. Anyone who owns large, energetic dogs understands the strategy. You don’t simply hope they’ll become tired. You actively work toward the desired physiologic endpoint. You run them, play with them, let them explore, throw things, chase things, encourage them to expend every available reserve of enthusiasm, and then you pray that when you eventually bring them inside, they will collapse somewhere comfortable and remain there. We had ambitions for a peaceful movie night, and Bentley and Davey were therefore being subjected to what amounted to an informal endurance-training program.

Meanwhile, the most important culinary project of the evening had already been underway.

We have an outdoor wood-fired pizza oven, and Sadie had wisely started preparing everything while I was off playing golf and she was doing the grocery shopping. She had already made the dough, and she had put wood into the oven and gotten the fire going so that by the time I returned home, the oven would be approaching the proper temperature. There is something wonderfully old-fashioned about a wood-fired pizza oven. We have refrigerators, convection ovens, microwaves, induction cooktops, sophisticated kitchen appliances, and all the other conveniences of modern life, yet somehow we still find ourselves standing outside feeding pieces of wood into a fire because apparently pizza tastes better when you’ve made the process unnecessarily complicated.

And, of course, it does.

There is a particular smell that comes from a wood-fired oven heating up, a mixture of smoke, burning hardwood, and the anticipation of food that is about to be spectacularly unhealthy in exactly the right way. By the time we start making the pizzas, the oven will be roaring, the interior will be radiating heat, and the dough will go from a pale, innocent-looking circle to a blistered, browned, bubbling piece of edible happiness in a matter of minutes. We are going to make several pizzas tonight, because there is no such thing as making “a pizza” when you have an outdoor pizza oven. You make several. You experiment. You put different things on them. You eat slices standing around outside. You tell yourself you’re finished, then look at the remaining pizza and decide that throwing it away would be wasteful. Eventually you realize you’ve eaten enough pizza to require its own gravitational field.

After that comes the real event: 1990s movie night.

We currently have three movies sitting out and ready to go: Reservoir Dogs, Pulp Fiction, and Cruel Intentions. There are also two additional contenders waiting in reserve, The Usual Suspects and Ronin. Whether we actually make it through all five remains questionable, although we have made the rookie mistake of drinking quite a lot of coffee. That means the evening could theoretically become considerably longer than originally intended. There is always something slightly dangerous about saying, “We’ll just watch one movie,” when you have coffee, snacks, comfortable furniture, a wife who also appreciates 1990s cinema, and an assortment of movies that you haven’t seen in a while. One movie becomes two, two becomes three, and suddenly you are looking at the clock wondering why birds are beginning to make noises outside.

The snacks, naturally, are already lined up.

We have powdered donuts, glazed donuts, and pistachio nut ice cream, because apparently tonight’s nutritional philosophy is that if something contains sugar and makes you happy, it qualifies. The pistachio ice cream is particularly important to me because it has become one of those small traditions that connects adulthood with childhood in a way that is almost embarrassingly simple. I inherited my affection for pistachio nut ice cream from my father, Roger, and whenever I eat it, I am reminded of Saturday nights growing up in the 1980s and 1990s.

Back then, Saturday night movies were a different experience. There was no streaming service presenting an infinite grid of thumbnails. There wasn’t a television in every room, and you certainly didn’t have a little glowing rectangle in your pocket containing essentially every piece of entertainment humanity has ever produced. We watched what was on television, rented movies, or eventually bought them, and when a movie was playing that everybody wanted to see, you sat down and watched it. My father and I had a particular Saturday-night routine, and my mother and brother would sometimes join us and sometimes disappear to do their own thing. But my father almost always had two things with him: milk with ice and pistachio nut ice cream.

The milk with ice became its own little ritual. My father would pour the milk, put ice into it, and say, with the satisfaction of a man who had discovered one of life’s great secrets, “Milk with ice, nice.” It was one of those little sayings that probably seemed completely ordinary at the time but somehow survives decades later, preserved not because it was profound, but precisely because it wasn’t. Childhood memories rarely announce themselves as important while you’re living them. You don’t realize that sitting on a couch with your father, eating pistachio ice cream and watching a movie on a Saturday night, is something you’ll remember when you’re 44 years old. You simply live it.

Then one day, years later, you find yourself sitting in your own house on a Saturday night, eating pistachio ice cream while a 1990s movie is waiting to be played, and you realize that some things have followed you all the way through life.

Tonight, I have the pistachio ice cream.

And I have the milk with ice.

Nice.

There is something comforting about those little continuities. Life changes enormously between childhood and adulthood. Careers happen. People move. Houses change. Responsibilities accumulate. Parents grow older, friends come and go, and eventually you find yourself looking backward at decades that once seemed impossibly far away. Yet every now and then, something as insignificant as a bowl of pistachio ice cream manages to collapse the distance between then and now. For a moment, you’re not a grown man sitting in his house at the end of August. You’re just a kid watching a movie with his father on a Saturday night, waiting to see what happens next.

Meanwhile, there is another member of the household who seems less than thrilled about this evening’s arrangement, and that would be Schnitzel.

Our orange tabby cat has developed certain expectations regarding Saturday nights, and apparently those expectations involve having the house to himself. Ordinarily, Sadie and I might go out to dinner, attend an event, meet people, or otherwise leave the premises for several hours. Schnitzel, in his mind, presumably considers this a perfectly reasonable arrangement. He gets the house, the furniture, the quiet, and the opportunity to move through the property without two humans constantly appearing in the same rooms as him. Tonight, however, we have committed the unforgivable offense of staying home.

I suspect he is not pleased.

Cats are remarkable creatures in this regard. You can provide them with food, water, warmth, shelter, toys, affection, medical care, and an objectively excellent life, and they will still occasionally look at you as though you have personally violated an international treaty by sitting in the wrong chair. Schnitzel has spent part of the evening observing us with the unmistakable expression of a cat who would prefer that his tenants leave the premises. I suppose he will have to endure the indignity of having his people home tonight. Perhaps he’ll eventually discover that 1990s movies are culturally enriching.

The dogs, on the other hand, are still somewhere outside.

At some point we’ll call them in, and the hope is that the combination of running across 65 acres, swimming, playing, and whatever other adventures they have invented will finally have exhausted them. Ideally, they will wander inside, drink approximately the volume of Lake Erie in water, collapse on the floor, and remain unconscious for the duration of the first movie. This is the dream. Whether reality cooperates is another question entirely.

As I write this, Sadie has just finished her shower, which means the evening is officially moving into its next phase. I still need to take mine, and then the sequence of events is pretty well established: pizza, snacks, more gummies, ice cream, coffee we probably shouldn’t have consumed, and a long parade of 1990s movies. We started taking gummies about an hour ago, and we’re probably going to take a few more later, which means the combination of wood-fired pizza, pistachio ice cream, nostalgic movies, and a chemically enhanced appreciation for cinema could make for a rather entertaining evening. I have no idea whether Reservoir Dogs will be followed by Pulp Fiction or whether we’ll wander into Cruel Intentions and then somehow end up watching Ronin at an hour when sensible people have long since gone to bed. That is tomorrow’s problem.

Tonight belongs to Saturday.

And honestly, this is exactly the sort of Saturday evening I love. There is no grand adventure planned, no expensive reservation, no elaborate itinerary, and no particular reason to make the night into anything more than what it naturally wants to be. We worked. We volunteered. We helped our town. I played a round of golf. Sadie did the shopping. We swam in our pond. The dogs ran across the property. The house is cool because we finally gave the air conditioners a rest. There is a fire burning in the pizza oven, the dough is ready, the movies are stacked up, and there is pistachio ice cream waiting in the freezer.

Outside, the last weekend of August is quietly slipping toward September. The evenings are beginning to cool, the summer light is fading a little earlier, and somewhere beyond the trees the dogs are probably conducting one final inspection of the property before we summon them back inside. Soon the pizza oven will be glowing, we’ll be sitting down with plates in our laps, and some movie made thirty years ago will be playing on the television while we eat enough junk food to make tomorrow’s breakfast almost irrelevant.

And perhaps that is what makes these evenings so good. They aren’t trying to become memories. They simply are, while you’re living them.

So, friends, I’m going to take my shower, because apparently even a Saturday night requires a certain minimum standard of hygiene, and then we’re lighting up the pizza oven, calling in the dogs, annoying Schnitzel by continuing to exist in his house, opening the ice cream, and starting our little journey back to the 1990s.

Pizza, pistachio ice cream, milk with ice, gummies, dogs, a grumpy cat, and Tarantino.

Honestly, I can’t think of a better way to spend the last Saturday night of August.

Happy Saturday, friends.

Saturday Afternoon Golf: A Surgeon Finally Gets to Operate on Something That Doesn’t Move

There are certain late-August afternoons in New England when the weather seems to apologize for everything it put us through earlier in the summer. Today was one of those afternoons. It was 77 degrees, the humidity had apparently decided to take the day off, the sky was completely clear, and there was just enough breeze to keep the air moving without turning the golf course into a meteorological problem. It was the sort of afternoon that makes you look at the clock, look at the golf clubs sitting in the corner, and realize that there are only so many Saturdays in a year. I had a free afternoon, so I did what any surgeon with a pulse, a set of clubs, and a country-club membership would reasonably do: I loaded the clubs into the BMW M8 and went golfing. If I am going to continue paying dues, assessments, cart fees, and all the other small financial reminders that country-club membership entails, I might as well occasionally extract some actual value from the arrangement. Besides, there are worse ways to spend an August afternoon than walking onto a manicured golf course with a driver in your hands and absolutely nothing requiring a differential diagnosis.

I arrived with no grand competitive agenda and no intention of turning the afternoon into some sort of heroic examination of my golfing abilities. I was there to play 18 holes, enjoy the course, and see what kind of golf showed up. There is something I genuinely enjoy about the preparation before a round because golf begins long before the first tee shot. Clubs come out of the trunk, gloves and balls get sorted, rangefinder gets checked, and the familiar ritual of figuring out whether today is going to be a driver day or a “let’s keep the ball in the same county as the hole” day begins. I hit a few balls to get loose, working progressively through wedges, short irons, mid-irons, and finally the longer clubs. The swing felt reasonably synchronized, which is always encouraging because golf has a remarkable ability to expose even the smallest disconnect between what your brain thinks your body is doing and what your body is actually doing. The irons were carrying with a nice trajectory, the wedges had some bite, and the driver felt particularly comfortable. That was enough information. I headed for the first tee.

The opening holes were a useful reminder that scoring well in golf is less about producing spectacular shots than it is about avoiding unnecessary mistakes. My ball striking was solid from the outset. The driver was producing a relatively penetrating flight with enough height to carry the fairway hazards while still giving me useful rollout. I was finding the center or just off-center portion of the clubface often enough that the ball speed remained respectable and, more importantly, the dispersion pattern was manageable. That distinction matters. Golfers sometimes become obsessed with how far a particular shot traveled, but distance without dispersion control is merely a more efficient way to reach the trees. A 275-yard drive in the middle of the fairway is tremendously more useful than a 300-yard drive buried behind a cluster of hardwoods with a six-foot opening through which you are now contemplating a punch-out.

My first several tee shots gave me exactly what I wanted: playable angles into the greens. From there, the round became largely an exercise in approach-shot execution, and this was probably the strongest part of my game today. I was making reasonably good decisions about club selection, taking the pin position into account rather than simply firing at the flag as though it were a surgical target that absolutely had to be hit. Golf rewards conservative aggression. If the flag is tucked behind a bunker on the right, there is very little virtue in attacking it from 175 yards with a marginal lie when the center of the green gives you a much larger landing area and leaves a relatively straightforward two-putt. I found myself choosing targets based on where I wanted the ball to finish rather than merely where I wanted it to start. That subtle distinction improved the quality of the round.

The irons were particularly pleasing. There is a very specific sensation when you catch a mid-iron properly, when the clubface meets the ball slightly ahead of the low point and the strike produces that compressed, penetrating flight that golfers spend years trying to reproduce consistently. Several of my approach shots had exactly that character. The ball came off the face with a clean trajectory, climbed into the blue sky, and then descended onto the greens with enough spin to hold rather than bounding twenty feet over the back. I was not trying to manufacture elaborate shot shapes. There was no reason to draw a seven-iron around a tree simply because I could theoretically do it. Straight or slight-draw stock shots were the order of the day, and the objective was to put the ball on the correct portion of the green and give myself realistic birdie opportunities while protecting against the big number.

The greens themselves were in very good condition, and that changed the complexion of the round considerably. Putting is one of those peculiar aspects of golf in which the physical movement is relatively simple while the cognitive component can become absurdly complicated. A putt is not simply a matter of judging distance. You are reading grain, slope, speed, the relationship between the ball and the hole, and the amount of break that will actually manifest at the reduced velocity of the ball as it approaches the cup. I spent a little more time than usual reading longer putts, particularly those from outside twenty feet, because lag putting is where a respectable round can quietly become a good one. The objective on those putts was not to make them. The objective was to get the ball inside a three-foot radius of the hole and eliminate the dreaded three-putt.

That strategy paid dividends. I was rolling the ball with a fairly consistent pace and, importantly, avoiding the first putt that leaves you with a six-footer coming back. There were birdie attempts that never had a chance of dropping, but they finished close enough that the subsequent par putt was largely procedural. That’s good golf. A birdie is wonderful, but a stress-free par is often the more valuable currency over 18 holes. The best rounds usually contain fewer moments of recovery than people realize. You don’t necessarily remember the six pars that required nothing more than a straightforward approach and two putts; you remember the one hole where you drove it into the trees, clipped a branch trying to escape, pitched out again, and then spent ten minutes negotiating with yourself over whether a triple bogey would somehow be philosophically meaningful.

The middle portion of the round was where the course began asking more interesting questions. Longer par fours required proper tee-shot positioning because simply hitting the ball as far as possible was not always the best strategy. On several holes, the fairway narrowed substantially around the typical driver landing zone, creating a decision between taking the driver and accepting a greater dispersion pattern or laying back with a three-wood or hybrid and accepting a longer approach. I generally favored the driver when the hole gave me sufficient margin because my ball striking was good enough to make the additional distance useful. A shorter approach shot means a shorter club, and a shorter club generally means tighter dispersion. That’s one of the fundamental strategic advantages of distance that gets lost in the endless “how far do you hit it?” conversations at the clubhouse. It isn’t merely about bragging rights. Twenty yards gained off the tee can turn a demanding five-iron approach into a comfortable seven-iron, and the difference in expected proximity is substantial.

The par threes were particularly enjoyable because they stripped the game down to its essentials. There is something wonderfully honest about standing on a tee box with nothing between you and the flag except a prescribed distance, a club selection, and the contents of your own head. There is no fairway to bail out into and no opportunity to convince yourself that you can recover from a poor drive. The target is right there. Club selection becomes everything. A slightly elevated green with a breeze moving across the hole can make a seemingly ordinary 165-yard shot play considerably differently from the number on the sprinkler head. I was generally choosing enough club to carry the front edge comfortably rather than trying to hit a perfect number. That may sound mundane, but avoiding short-sided misses is one of those boring decisions that separates sensible golf from recreational self-sabotage.

My wedge game was also cooperative today, which helped enormously. Inside roughly 120 yards, I was able to control trajectory and distance reasonably well, and I had several opportunities where the approach left me inside fifteen feet. The goal with those shots was not simply proximity but leaving the ball on the correct side of the hole. Golfers know exactly what this means. A ten-foot putt uphill with four inches of break is a completely different proposition from a ten-foot downhill slider. When the pin position allows it, I want the ball below the hole, because uphill putts are generally more forgiving. I was thinking about that throughout the round, particularly on approach shots where a slightly less aggressive line left a much more favorable putt.

The short game did not produce any disasters, which is perhaps the highest compliment one can give it. There were a few greens missed, as there inevitably are, but the misses were generally in manageable locations. I was able to use relatively conventional bump-and-run shots where appropriate rather than constantly trying to loft a 60-degree wedge into the air and land it next to the pin. Around the green, simplicity is usually your friend. A lower trajectory reduces the variables, and when there is plenty of green to work with, there is little reason to introduce additional risk. Several chips released exactly as anticipated, allowing me to get the ball within a comfortable putting distance and salvage par or, at worst, walk away with bogey without having turned a missed green into an avoidable catastrophe.

There was one stretch where the driver became slightly less cooperative, and this is where I was reminded that the golf swing is not a machine operating under sterile conditions. Fatigue creeps in. Tempo changes. You start trying to steer the club instead of swinging through the ball. The grip gets a little tighter, the backswing gets a fraction shorter, and suddenly the clubface is arriving at impact a few degrees differently. My solution was not to start rebuilding the swing in the middle of the round, because that is how golfers turn a minor technical fluctuation into a full-scale institutional collapse. I simply slowed the tempo down, focused on a balanced finish, and went back to the stock swing. The next tee shot was much better.

That is probably one of the more important lessons from the round. Golf is an extraordinarily poor environment for perfectionism. The ball is going to do things you didn’t intend, and your job is to respond appropriately rather than become emotionally attached to the previous shot. A poor drive doesn’t require a heroic recovery. A missed green doesn’t require a miracle pitch. A three-putt doesn’t mean the next hole needs to become a referendum on your putting stroke. You simply reset and play the next shot. In that respect, golf has some surprisingly useful parallels with medicine, although fortunately the consequences of a poor seven-iron are considerably less consequential than those of a poor clinical decision.

As the afternoon progressed, the course became even more beautiful. The late-August sun had that slightly lower, warmer quality that makes the fairways look almost impossibly green against the deeper colors beginning to emerge around the edges of the course. The rough moved gently in the breeze, the trees were full but beginning to show the first subtle signs that summer is already on borrowed time, and the shadows gradually lengthened across the fairways. There were birds moving through the tree line, the occasional distant sound of another group calling out after a particularly optimistic shot, and the familiar rhythmic sounds of golf all around: the click of a ball against a putter, the sharp crack of a driver, the whisper of a wedge through closely mown turf. It is difficult to spend four hours outside in surroundings like that and not appreciate how absurdly civilized the game can be.

The back nine became increasingly strategic as the round went on. By then I had a reasonably good sense of how the ball was behaving, which made club selection easier. I knew my driver was producing a predictable flight, my irons were carrying well, and the greens were accepting properly struck approaches. That allowed me to become more aggressive selectively. When the fairway presented enough room, I took advantage of it. When the pin was accessible, I attacked. When the risk outweighed the potential reward, I played toward the fat part of the green and accepted the par opportunity. This is the part of golf I find most interesting because strategy becomes more important as your technical understanding improves. You are no longer simply trying to hit good shots. You are trying to construct a sequence of good shots that makes the next shot easier.

There were several holes where that sequence worked beautifully. A well-positioned drive left a comfortable iron. The iron found the correct tier of the green. The resulting putt was uphill and relatively straight. Two strokes later I was walking toward the next tee without having needed to manufacture anything. Those are the holes that make golf feel almost effortless, even though they are actually the product of a series of small decisions made correctly. Conversely, there were a couple of holes where I left myself unnecessarily difficult second shots because the tee shot had been too ambitious or the approach had been aimed at the wrong portion of the green. Those holes reinforced the same lesson from the opposite direction: golf punishes poor planning with astonishing efficiency.

By the closing holes, I was still striking the ball well enough that I never felt as though I was simply trying to survive the round. That matters. Eighteen holes is a long enough sample size for almost every weakness in your game to eventually introduce itself, and maintaining reasonable mechanics late in the round is often more meaningful than what happens on the first three holes when everything feels fresh. My tempo remained controlled, the irons continued to produce good contact, and the putting stroke never completely abandoned me. There were missed birdie opportunities, certainly, but there were also very few holes where I felt I had given away strokes through careless decision-making.

The final score reflected that. It wasn’t some absurd, career-defining round that requires immediate submission to the World Golf Handicap Authority, but it was good to very good golf by any reasonable recreational standard: strong all-around performance that exceeded basic expectations, particularly for the price category I occupy, which is to say the category of someone who pays country-club dues and therefore feels morally obligated to occasionally justify them. More importantly, it was a complete round. The driver was reliable, the irons were probably the best part of the game, the wedges were controlled, the short game was dependable, and the putting was steady enough to prevent the scorecard from developing unnecessary hemorrhage.

And that is ultimately what made the afternoon so satisfying. Golf rarely gives you the feeling that you’ve solved the game, because the game is specifically designed to ensure that you haven’t. You can stripe your driver all afternoon and then miss a three-foot putt. You can stick an iron to six feet and somehow leave the birdie putt three inches short. You can make a magnificent recovery from behind a tree and then immediately hit your next approach into a bunker. The scorecard is an unforgiving little document, but it is also honest. Today, mine told the story of a round in which most of the important pieces were working together, and when they weren’t, I generally managed the damage rather than compounding it.

By the time I walked off the 18th green, the afternoon had begun giving way to early evening, and the temperature remained perfect. I had spent several hours doing something that has very little practical relationship to surgery, trauma, critical care, or any of the other things that normally occupy my brain. There were no ventilators, no trauma activations, no operating rooms, no consultants, no alarms, and no pager demanding an immediate decision. Instead, there had been fairways, greens, bunkers, rough, trees, wind, yardages, club selection, ball flight, putting lines, and the wonderfully ridiculous obsession golfers have with trying to make a little white ball behave according to their wishes.

It was exactly what a Saturday afternoon in late August ought to be. I got some value out of those country-club dues, the golf was genuinely good, the weather was nearly perfect, and the BMW M8 was waiting in the parking lot with eighteen holes’ worth of golf clubs back in the trunk. For once, the only thing I had to diagnose was why I didn’t make more birdie putts.

Three Arrests, Three ROSCs: The Day Statistics Surrendered

The late August sun cast long shadows across the apparatus floor as I leaned against the bay doors at Station 1, trying to savor what remained of the afternoon. Kevin had his trademark cigar going, that foul-smelling thing I pretended not to see as part of our unspoken arrangement. Mike and Sadie were in the middle of what had become an increasingly heated debate about tool brands.

“A Milwaukee drill has the torque, but the battery life is garbage,” Mike insisted, his voice rising with the passion of a man who takes his power tools seriously. “DeWalt’s the only way to go for reliability.”

Sadie scoffed, crossing her arms. “You say that because you’ve never had to field-repair a ventilator at 3 AM. I’ll take a Makita any day—better ergonomics for precision work.”

I tried to tune them out, my mind still processing the extraordinary events of the day. Two cardiac arrests in one shift was already unprecedented for our rural department. Two ROSCs was nothing short of miraculous. But as I looked at my wife, exchanging a knowing glance, neither of us could have imagined what the universe had in store for us next.

At 4:16 PM, the tones dropped with their familiar electronic urgency, shattering our moment of reflection.

“Attention Station 1: Special Signal Fly Car Request. Please respond to a 40 year old male, cardiac arrest.”

We moved as one unit, the practiced choreography of countless calls. Kevin stubbed out his cigar, Mike’s tool debate forgotten, and Sadie and I headed for the Fly Car.

“Station 2 district again,” I said, already calculating the route. “Same area as our last call.”

Our town is geographically large despite its small population, which means we maintain three stations strategically placed throughout our coverage area. This call came from our Station 2 or “Center” district—the same area where we had achieved our second ROSC of the day just hours earlier.

“The call originally came in as feeling faint,” Sadie noted as I drove. “Medics must have seen something concerning on his EKG.”

The Fly Car responded eagerly to my touch, its engine humming as we navigated the rural roads with lights and sirens. Hidden beneath the familiar Chevrolet bodywork was a climate-controlled mobile critical care platform that many emergency departments would envy. Custom-molded slide-out trays held a rolling blood bank of low-titer O-positive whole blood and liquid plasma kept at precise temperatures, alongside rapid fluid-warming devices to heat cold blood to body temperature in seconds during a massive hemorrhage. Dual-probe wireless ultrasound devices synced directly to rugged tablets for immediate point-of-care internal bleeding checks and lung evaluations, while handheld lab-quality blood analyzers delivered critical electrolyte and lactate readings in under two minutes. The vehicle’s climate-controlled drug vaults held broad-spectrum antibiotics for early sepsis intervention, continuous nerve-block and sedative infusions like propofol, pre-hospital clot-busting thrombolytics for acute strokes, and ultra-expensive blood-thinning reversal agents completely unavailable on standard ambulances. For advanced respiratory life support, the car was equipped with video laryngoscopes backed by turbine-driven transport ventilators capable of ICU-level lung protection and automated chest compression devices. Most imposing of all were the sterile surgical blocks, packed with specialized catheters to perform a REBOA—effectively inflating a balloon inside the aorta to clamp a ruptured vessel from the inside out—as well as field escharotomy kits, scalpel-access surgical airway gear, and manual skull drills to create emergency burr holes for patients dying of intracranial pressure while trapped in deep wreckage.

The scene was, unfortunately, familiar when we arrived. Medic 2 with Engine 2 were already working the code. EMTs were performing high-quality CPR, but the patient wasn’t intubated yet.

“What’s the story?” I asked, already pulling on gloves.

One of the medics answered between breaths. “Called in feeling faint. When we arrived, he was alert but diaphoretic. We put him on the monitor and saw ST-elevation in multiple leads. As we were calling for the special signal, he went into VF. We’ve been working him for about 6 minutes total.”

Sadie was already setting up the LUCAS device. “Let’s get him on the autopulse, free up some hands.”

As we applied the LUCAS, I began working through the Hs and Ts that form the framework of cardiac arrest management.

“Let’s consider our differentials,” I said aloud for the team. “Hypoxia—unlikely given his initial presentation. Hypovolemia—no signs of hemorrhage. Hydrogen ion—acidosis possible but unlikely primary cause. Hypo/Hyperkalemia—we’ll check with i-STAT. Hypothermia—he feels warm. Tension pneumothorax—no obvious clinical signs. Tamponade—we’ll check with ultrasound. Toxins—possible but no history. Thrombosis—MI or PE most likely given his presentation.”

We worked systematically through our differential, using the Fly Car’s advanced diagnostic capabilities. POCUS showed no pericardial effusion or pneumothorax. The i-STAT revealed normal electrolytes. The ultrasound showed severe hypokinesia of multiple coronary territories, consistent with extensive coronary artery disease.

About 4 minutes after we arrived, the monitor showed a shockable rhythm—coarse VF.

“Charging!” I called out. “Clear!”

200 joules delivered. The rhythm converted briefly to asystole, then back to VF.

“Resume CPR,” Sadie directed. “Let’s try another shock.”

200 joules delivered again. The rhythm remained VF.

“Continue CPR,” I said. “Let’s try something different. Amiodarone 300mg IV push.”

After another cycle of CPR, we checked the rhythm again—now showing a fine VF.

“One more shock,” I called out. “200 joules. Clear!”

This time, the rhythm converted to a sinus tachycardia at approximately 95 beats per minute.

We had a pulse. Carotid, femoral—weak but palpable. ROSC.

Three arrests in one day. Three ROSCs. The statistical improbability wasn’t lost on any of us.

This is where Sadie and I really went to work. While the EMTs continued their excellent care, we shifted into post-cardiac arrest protocol.

“I’ll intubate,” I said, already preparing the video laryngoscope. “Sadie, get pressors ready. Let’s start with norepinephrine.”

The intubation went smoothly—a 7.5 endotracheal tube passed without difficulty, confirmed immediately with colorimetric capnography and bilateral breath sounds.

“ETCO2 is 30 mmHg,” Sadie announced, already hanging the norepinephrine drip. “Perfusion improving but still compromised.”

While I managed the airway, Sadie was already working on the rest. “I’m starting a norepinephrine drip at 5 mcg/min. Let’s get a 12-lead EKG, arterial line, and another set of vitals. I want to see the extent of coronary involvement.”

The medics from Station 2 knew us well and immediately adapted to our pace. They didn’t need reassurance—they knew we were here to help, not take over.

“We’ll be transporting with you,” I said, securing the ET tube. “Sean, you’ll ride with us.”

Sean nodded, already gathering additional equipment. “Absolutely. Third time’s the charm, right?”

Despite the gravity of the situation, a small smile touched my lips. “Something like that.”

It was Sadie, I, and Sean in the back of the ambulance. Another firefighter took our Fly Car and followed us to the hospital. Three cardiac arrests in one day—a highly unusual occurrence in our rural department, where we might go months without a single code. That we had achieved ROSC on all three was nothing short of miraculous.

Primary Survey

• Airway: 7.5 endotracheal tube in place, secured with tape. Bilateral breath sounds present and equal with mechanical ventilations. No visible blood in the airway. Proper tube depth confirmed at 23 cm at the teeth.

• Breathing: Mechanically ventilated via turbine-driven transport ventilator. Tidal volume set at 450ml (6ml/kg based on estimated ideal body weight of 75kg), respiratory rate 12, PEEP 5 cmH2O, FiO2 100%. Chest wall rising equally with ventilations. No obvious chest wall deformities.

• Circulation: Weak carotid and femoral pulses palpable. Skin cool, clammy. Capillary refill approximately 4 seconds. Blood pressure 88/52 mmHg via cuff.

• Disability: Pupils 4mm bilaterally, sluggish but reactive to light. No corneal reflexes. No gag reflex. GCS = 3T (intubated).

• Exposure: Patient fully exposed. No obvious signs of trauma. Skin mottled on extremities.

Initial Rhythm Assessment

• Initial rhythm per medics: Ventricular fibrillation.

• Current rhythm: Sinus tachycardia at 95 bpm with ST-segment elevation in leads I, aVL, V1-V6.

• Quality of chest compressions: LUCAS device providing optimal compressions until ROSC achieved.

• Airway status: Securely intubated with confirmed placement via colorimetric capnography and bilateral auscultation.

Vital Signs

• HR: 95 bpm (sinus tachycardia)
• BP: 88/52 mmHg

• RR: 12 breaths/minute via mechanical ventilator
• SpO2: 98% on 100% FiO2
• Temp: 36.5°C (97.7°F) axillary
• Glucose: 132 mg/dL via fingerstick
• ETCO2: 30 mmHg (improving but still indicating compromised perfusion)

Interventions

• CPR with LUCAS device until ROSC achieved.

• Defibrillation: 200 joules biphasic delivered x3, resulting in ROSC after third shock.

• Advanced airway secured with 7.5 endotracheal tube.

• IV access: Two 18-gauge IVs in antecubital fossae, confirmed patent with flush.

• Intraosseous line: Right humeral IO established for additional access.

Medications

• Epinephrine 1mg IV administered x2 during arrest phase per ACLS protocol.

• Amiodarone 300mg IV administered during arrest phase for refractory VF.

• Norepinephrine drip started at 5 mcg/min for post-cardiac arrest hypotension.

Secondary Assessment

• HEENT: No signs of trauma. Pupils equal and reactive, though sluggish.

• Neck: Tracheal midline after intubation. No jugular venous distension.

• Cardiovascular: Weak peripheral pulses. No precordial thrills or heaves. Irregularly irregular rhythm noted.

• Pulmonary: Bilateral breath sounds equal but diminished with mechanical ventilations. No adventitious sounds noted.

• Abdomen: Soft, non-distended. No guarding or rigidity.

• Pelvis: Stable to palpation. No instability noted.

• Extremities: No obvious deformities. Cool to touch with delayed capillary refill. No edema noted.

• Back: No obvious step-offs or deformities. No signs of trauma.

• Neuro: GCS remains 3T. Pupils sluggish but reactive. No purposeful movement.

Diagnostics

• 12-Lead EKG: Sinus tachycardia at 95 bpm with ST-segment elevation in leads I, aVL, V1-V6 (extensive anterior and lateral leads), consistent with an acute extensive anterior-lateral wall myocardial infarction. Reciprocal changes noted in leads II, III, and aVF.

• POCUS: Subxiphoid view performed during rhythm check. No pericardial effusion noted. Severe hypokinesia of the anterior wall, lateral wall, and septum. Apical ballooning consistent with large territory infarction. Left ventricular function severely depressed with estimated ejection fraction of 20-25%.

• i-STAT analysis: pH 7.22, pCO2 45 mmHg, pO2 88 mmHg, lactate 5.2 mmol/L, potassium 4.1 mEq/L, ionized calcium 1.12 mmol/L, troponin I 12.6 ng/mL.

• ETCO2: 30 mmHg post-ROSC (indicating improving but still compromised perfusion).

Differential Diagnosis

  1. Acute extensive anterior-lateral wall myocardial infarction leading to cardiac arrest (most likely given EKG findings and troponin level)
  2. Cardiogenic shock secondary to MI (consistent with hypotension and poor perfusion)
  3. Post-cardiac arrest syndrome (contributing to metabolic acidosis and organ dysfunction)
  4. Pulmonary embolism (less likely without RV strain on ultrasound)
  5. Sepsis with underlying cardiac ischemia (possible but no obvious source)
  6. Electrolyte abnormality (no significant abnormalities noted)

Interventions Continued

• Dual sequential defibrillation considered but not required after successful ROSC with third shock.

• Mechanical CPR: LUCAS device continued until stable ROSC achieved, then discontinued.

• Targeted temperature management initiated: Patient cooled to 36°C using cooling blankets and cold saline IV bolus.

• Antiplatelet therapy: Aspirin 325 mg administered via NG tube.

• Anticoagulation: Heparin bolus 60 units/kg administered, followed by infusion to maintain target ACT.

• STEMI protocol activated: Notified receiving hospital of incoming post-cardiac arrest STEMI patient for potential cardiac catheterization.

Advanced Interventions During Transport

As we headed toward the hospital, Sean from Medic 2 assisted while Sadie and I performed advanced interventions that would typically be reserved for the emergency department.

“Given the extensive MI with severely depressed LV function, let’s consider mechanical circulatory support,” I said to Sean while preparing the equipment. “Sadie, can you place a right internal jugular central line for better medication administration and hemodynamic monitoring?”

Sadie nodded, already preparing the central line kit under the ambulance’s working lights. “I’ll use ultrasound guidance. Shouldn’t be a problem even in this moving environment.”

While Sadie placed the central line, I prepared the intra-aortic balloon pump (IABP) console that we carry in the Fly Car for just such circumstances.

“This patient would benefit from IABP counterpulsation,” I explained to Sean. “With an ejection fraction this low, he’ll need all the support we can give him, especially during catheterization.”

Sean’s eyes widened slightly. “You’re kidding me. You guys have an IABP in here?”

“We do,” Sadie confirmed, successfully placing the central line without complications. “And we’re not afraid to use it.”

The transport was a flurry of activity as we worked seamlessly as a team. Despite the confined space and movement of the ambulance, we were able to provide ICU-level care that likely made the difference between life and death.

Medications Continued

• Norepinephrine titrated to 10 mcg/min to maintain MAP >65 mmHg.

• Dobutamine infusion started at 5 mcg/kg/min for additional inotropic support given severely depressed LV function.

• Amiodarone infusion started at 1 mg/min for 6 hours, then 0.5 mg/min for 18 hours.

• Sodium bicarbonate 50 mEq administered for persistent metabolic acidosis (pH 7.22).

• Fentanyl 100 mcg IV administered for sedation.

Reassessment

• Rhythm remained sinus tachycardia with persistent extensive ST-segment elevation.

• Blood pressure improved to 92/54 mmHg with dual pressor and inotrope support.

• ETCO2 improved to 35 mmHg, indicating improving perfusion.

• POCUS showed no improvement in wall motion abnormalities with severely depressed LV function.

• Laboratory values showed improving acidosis but elevated lactate indicating ongoing tissue hypoperfusion.

Transport Decision

Given the patient’s age, downtime of approximately 6 minutes, and post-cardiac arrest presentation with confirmed extensive MI with severely depressed LV function, we knew the prognosis was guarded. However, the return of spontaneous circulation with a perfusing rhythm, combined with the clear STEMI on EKG, made him a potential candidate for emergent cardiac catheterization with possible mechanical circulatory support.

“We need to move quickly,” I said to the team. “The cath lab needs to be ready for extensive MI with possible need for mechanical support devices including IABP or even Impella.”

When we arrived at the hospital, the cardiac catheterization team was waiting. We provided a concise handoff, highlighting the key points: 40-year-old male, 6-minute downtime, ROSC after defibrillation, extensive anterior-lateral MI with severely depressed LV function, current hemodynamics on dual pressor and inotrope support, and all interventions performed including central line placement and preparation for IABP insertion.

As we transferred care to the hospital team, I caught Sadie’s eye. We both knew the significance of what we had accomplished. Three cardiac arrests in one day was extraordinary for our rural department. Achieving ROSC on all three was nothing short of miraculous. But we also knew that the real work was just beginning for the hospital team.

The ride back to Station 1 was filled with a quiet sense of accomplishment unlike anything we had experienced before. Mike and Kevin were waiting for us when we arrived.

“Well?” Mike asked, his usual sarcasm replaced by genuine curiosity.

“Third ROSC of the day,” Sadie said, stretching as she got out of the ambulance. “Extensive MI with severe LV dysfunction. 40 years old, 6 minutes down.”

Mike whistled softly. “Three arrests, three ROSCs in one shift. That’s not just a record, that’s statistically impossible.”

Kevin nodded, his expression thoughtful. “The universe decided to test you two today. And you passed with flying colors.”

I looked at my wife, at the team that had come together to save a life, and felt that familiar mixture of pride and humility that defines our work. In rural EMS, we don’t have the luxury of specializing in just one aspect of care. We are the first responders, the critical care transport team, the decision-makers, and sometimes, the bearers of difficult news.

Today was a remarkable day—not just because we saved lives, but because we demonstrated what’s possible when you bring advanced medical care to the prehospital setting, when you empower your team with knowledge and resources, and when you refuse to accept that geography should determine outcomes.

Three saves in one day. Excuse me while Sadie and I are riding a high that only comes from defying statistics and giving three people another chance at life. This is why we do what we do—this is why we volunteer, why we train, why we equip ourselves with everything we need to bring ICU-level care to the roadside. Because sometimes,

The Physician-Paramedic, a Glucose of 560, and When Hyperglycemia Becomes a Resuscitation

There is a particular kind of late-summer afternoon at our rural Fire/EMS station when absolutely nothing seems to be happening, which, in EMS, is usually the universe’s way of preparing you for the exact opposite. The bay doors were open, the apparatus was sitting ready, and the warm August sun was spilling across the concrete while an unusually pleasant breeze moved through the station. Sadie and I were volunteering as physician-paramedics, as we regularly do, with me serving as both Medical Director for EMS and Commander of EMS and Sadie serving as Assistant Commander and Assistant Medical Director. We both have our physician careers outside the station, but there is something about spending a shift with the town’s Fire/EMS department that brings medicine back to its most elemental form. You have a patient, you have a problem, you have whatever equipment you can carry through the front door, and you have to figure out what is happening before physiology makes the decision for you.

Medic 1 was staffed by Kevin and Mike. Kevin, our old-school Newark medic, was enjoying his trademark cigar, which I was once again doing my very best impression of not seeing. Mike, a master plumber who became a paramedic later in life because he wanted to serve the community, was smoking a cigarette nearby and apparently had no intention of pretending otherwise. I chose diplomacy and selective blindness. Sadie and I were sitting outside talking about what we were going to do later that evening, enjoying the sort of weather that makes you grateful to live in New England in August. It was one of those rare afternoons where the air was warm without being oppressive, the breeze had just enough movement to make sitting outside comfortable, and the station felt almost peaceful. The trucks were ready, the Fly Car was stocked, and everyone was enjoying that peculiar quiet period between calls when you can briefly convince yourself that you might actually finish a cup of coffee while it is still hot.

At 3:08 p.m., the tones dropped.

“Attention Station 1: Medic 1, Engine 1 and Fly Car. Please respond to a fifty-six-year-old female, diabetic emergency. Blood glucose five-sixty. Vomiting. Rapid heart rate. Caller is visiting nurse, still on scene.”

The phrase that caught my attention was not actually “blood glucose 560.” It was the combination of 560, vomiting, and tachycardia.

A glucose of 560 mg/dL is unquestionably severe hyperglycemia, but hyperglycemia by itself is not synonymous with diabetic ketoacidosis. The number tells you that glucose is markedly elevated; it does not tell you whether the patient is acidotic, whether she is profoundly dehydrated, whether ketones are present, whether she is hyperosmolar, or whether some entirely different process has precipitated the metabolic derangement. Vomiting, on the other hand, suggests that the metabolic disturbance may already be clinically significant. Tachycardia raises the possibility of substantial volume depletion. Together, those findings made this a metabolic resuscitation until proven otherwise.

Sadie and I headed for the Fly Car while Kevin and Mike moved toward Medic 1, with Mike driving. Engine 1 pulled out behind us, lights flashing, siren, horn, and the Q producing the familiar mechanical symphony of a rural emergency response. The drive was short, but the clinical discussion had already begun. We were considering diabetic ketoacidosis, hyperosmolar hyperglycemic state, mixed DKA/HHS physiology, sepsis with stress hyperglycemia, acute coronary syndrome as a precipitating event, occult infection, medication nonadherence, insulin pump failure if applicable, pancreatitis, gastrointestinal illness, and less common endocrine or toxicologic causes. A glucose of 560 can be the disease, but it can also be the laboratory footprint of another disease.

When we arrived, the visiting nurse was waiting for us at the door. She immediately provided the sort of history that makes a prehospital clinician’s job considerably easier: she knew the patient’s baseline, medications, recent food and fluid intake, insulin regimen, urine output, and mental status. The patient had reportedly been feeling progressively ill since the previous evening. She had been increasingly thirsty, urinating frequently, and complaining of profound weakness. That morning she had developed nausea followed by several episodes of vomiting. The visiting nurse had checked the glucose and obtained a reading of 560 mg/dL. A repeat measurement was similarly elevated.

The patient was lying semi-reclined on a couch, awake but exhausted. She looked dehydrated. Her lips and oral mucosa were dry, her skin had poor turgor, and her eyes had the slightly sunken appearance that is often seen in significant volume depletion. She was tachycardic and breathing faster than normal. The respiratory pattern was immediately interesting. She was not wheezing, there was no obvious pulmonary edema, and she was not struggling mechanically to move air. Instead, her breathing was somewhat deep and deliberate. It was not the classic textbook image of spectacular Kussmaul respirations, but there was enough increase in depth and respiratory effort to make metabolic acidosis part of the working diagnosis.

She was not confused, but she was slower than the visiting nurse said was normal for her. That distinction mattered. She could tell us her name, where she was, and what had happened, but she had the appearance of someone whose brain was beginning to feel the effects of systemic illness. Her blood pressure was still preserved, which was reassuring only to a point. A patient can lose a remarkable amount of intravascular volume before hypotension appears, particularly if the sympathetic nervous system is maintaining vascular tone.

Primary Survey

  • Airway: Patent; patient speaking spontaneously and protecting her airway.
  • Breathing: Tachypneic with mildly increased depth of respiration; no wheezing or focal respiratory distress.
  • Circulation: Sinus tachycardia with weakly palpable peripheral pulses and delayed capillary refill.
  • Disability: Awake and oriented but fatigued and mildly slowed compared with baseline.
  • Exposure: No obvious trauma, rash, peripheral edema, or external source of infection.

Vital Signs

  • HR: 126/min
  • BP: 104/68 mmHg
  • RR: 28/min
  • SpO₂: 98% on room air
  • Temperature: 100.4°F
  • Blood glucose: 560 mg/dL
  • ETCO₂: 24 mmHg

The vital signs made the physiology more concerning. The combination of tachycardia, borderline blood pressure, tachypnea, low ETCO₂, dry mucous membranes, and severe hyperglycemia strongly suggested a significant metabolic process. The low ETCO₂ was particularly useful as a physiologic clue. End-tidal carbon dioxide does not directly measure serum bicarbonate or arterial pH, and it should never be treated as a substitute for a blood gas. However, in the appropriate clinical context, a reduced ETCO₂ can correlate with metabolic acidosis because the patient is increasing alveolar ventilation in an attempt to eliminate carbon dioxide and partially compensate for the metabolic acid load.

We obtained vascular access while Kevin and Mike placed the patient on continuous monitoring. The first question was whether this was simply severe hyperglycemia or whether she had developed DKA, HHS, or some combination of the two. The distinction matters because the danger in these patients is not merely the glucose concentration. Hyperglycemia produces osmotic diuresis, and glucose in the renal filtrate pulls water and electrolytes with it. The patient loses water, sodium, potassium, chloride, phosphate, and other solutes through the kidneys. As intravascular volume contracts, renal perfusion decreases, which can further impair glucose clearance and worsen the metabolic disturbance.

In DKA, insulin deficiency also promotes lipolysis and hepatic ketogenesis, generating beta-hydroxybutyrate and acetoacetate. Those acids consume bicarbonate and produce metabolic acidosis. The respiratory system compensates by increasing minute ventilation. Meanwhile, total-body potassium is generally depleted even when serum potassium initially appears normal or elevated because acidosis and insulin deficiency shift potassium out of cells while osmotic diuresis causes substantial urinary potassium losses. This is one of the reasons that simply looking at a potassium number without understanding the underlying physiology can be misleading.

HHS produces a somewhat different metabolic picture. There is usually enough residual insulin activity to suppress substantial ketogenesis, but not enough to prevent extreme hyperglycemia. Serum osmolality rises, intracellular water shifts into the extracellular compartment, and eventually neurologic dysfunction can develop. The two syndromes can overlap, and our patient had enough vomiting, tachypnea, and altered energy level that we could not simply assume this was uncomplicated hyperosmolar hyperglycemia.

Secondary Assessment

  • HEENT: Dry oral mucosa; no facial swelling; pupils equal and reactive.
  • Neck: Supple; no jugular venous distention.
  • Cardiovascular: Tachycardic and regular; peripheral pulses diminished but present.
  • Pulmonary: Clear bilateral breath sounds; mildly deep respirations without wheezing or focal crackles.
  • Abdomen: Mild diffuse discomfort and nausea without guarding, rigidity, or focal peritoneal signs.
  • Pelvis: Stable and nontender.
  • Extremities: Cool distal extremities with delayed capillary refill; no significant edema.
  • Back: No acute findings.
  • Neuro: Awake, oriented, mildly slowed but without focal neurologic deficit.

The abdominal examination did not suggest an acute surgical abdomen, although pancreatitis remained on the differential because vomiting and metabolic decompensation can occur together. There was no focal neurologic deficit to suggest a large stroke, and her oxygenation was normal. There was no obvious respiratory infection on examination, but her temperature was slightly elevated, and infection remained one of the most important possible precipitants.

The point-of-care analyzer gave us more useful information. Her venous blood gas showed a pH of 7.24, with a bicarbonate of approximately 13 mEq/L. Lactate was elevated at 3.4 mmol/L, and the point-of-care electrolyte panel showed sodium 132 mEq/L and potassium 5.3 mEq/L. Her creatinine was elevated at 1.8 mg/dL, consistent with at least some degree of acute kidney injury or previously unrecognized chronic renal dysfunction.

The numbers were beginning to tell a coherent story.

She had significant hyperglycemia, metabolic acidosis, volume depletion, and renal hypoperfusion. The elevated measured sodium did not represent the entire sodium story because severe hyperglycemia lowers measured serum sodium through osmotic water shifts. Corrected sodium would therefore be higher than the measured value, reinforcing rather than reducing our concern about free-water loss. Her potassium was mildly elevated, but we knew that this did not mean she had an adequate total-body potassium store. If this was DKA, she could be profoundly potassium depleted despite the serum concentration being high.

Diagnostics

  • Point-of-care glucose: 560 mg/dL.
  • Venous blood gas: pH 7.24 with bicarbonate approximately 13 mEq/L, consistent with significant metabolic acidosis.
  • Lactate: 3.4 mmol/L, suggesting impaired perfusion and metabolic stress.
  • Sodium: 132 mEq/L, with corrected sodium expected to be higher because of severe hyperglycemia.
  • Potassium: 5.3 mEq/L, requiring cautious interpretation because serum potassium may be elevated despite substantial total-body potassium depletion in DKA.
  • Creatinine: 1.8 mg/dL, concerning for acute kidney injury or reduced baseline renal function.
  • ETCO₂: 24 mmHg, supporting increased ventilatory compensation for metabolic acidosis.
  • ECG: Sinus tachycardia without acute ST-segment elevation; no immediately dangerous potassium-associated conduction abnormality.
  • POCUS: Small, highly respiratory-variable IVC consistent with significant intravascular volume depletion; no obvious pulmonary edema.

The ultrasound findings were particularly useful as a piece of corroborating evidence rather than as a standalone diagnostic test. The IVC was small and markedly respiratory-variable, which fit the rest of the examination. Her heart appeared hyperdynamic rather than failing, and the lungs were free of diffuse B-lines. In other words, there was no sonographic suggestion that the tachycardia and dyspnea were being driven by cardiogenic pulmonary edema. The physiology looked much more like a patient who had lost a substantial amount of circulating water through osmotic diuresis.

Differential Diagnosis

  1. Diabetic ketoacidosis: Most likely given severe hyperglycemia, vomiting, metabolic acidosis, tachypnea, volume depletion, and low ETCO₂.
  2. Mixed DKA/HHS physiology: Highly plausible given the extreme hyperglycemia and significant dehydration; definitive serum osmolality and beta-hydroxybutyrate testing would help characterize the overlap.
  3. Hyperosmolar hyperglycemic state without substantial ketoacidosis: Considered, but the degree of metabolic acidosis and respiratory compensation made pure HHS less likely.
  4. Sepsis with stress hyperglycemia: Important possible precipitant, particularly given the low-grade fever; occult urinary, pulmonary, or other infection required hospital evaluation.
  5. Acute pancreatitis: Considered because of nausea and vomiting, although the abdominal examination was not strongly suggestive.
  6. Acute coronary syndrome: Considered because myocardial ischemia can precipitate metabolic decompensation and may present atypically in diabetic patients; ECG was reassuring but did not completely exclude ACS.
  7. Medication or insulin-delivery failure: Possible based on history and required medication reconciliation.
  8. Other causes of metabolic acidosis: Less likely but included lactic acidosis from dehydration/hypoperfusion and renal dysfunction.

At this point, there was no question that she needed transport. The question was how aggressively we needed to treat her before and during that transport.

We began with what the physiology was asking for: volume.

A patient in DKA has lost water long before the blood pressure necessarily collapses. Restoring intravascular volume improves renal perfusion, increases glucose clearance, improves tissue perfusion, and can reduce counter-regulatory hormone activation. We initiated 0.9% sodium chloride, 1 liter IV, using a controlled but relatively rapid infusion because she had clear clinical evidence of volume depletion, no history suggesting acute decompensated heart failure, and no ultrasound evidence of pulmonary congestion.

We deliberately did not begin with insulin in the field. This was not because insulin was unimportant. It was because insulin therapy in DKA is a carefully balanced intervention that requires attention to potassium, renal function, acid-base status, serial glucose measurements, and the patient’s overall trajectory. Insulin drives glucose and potassium intracellularly. If total-body potassium is substantially depleted, insulin can precipitate dangerous hypokalemia. In a patient whose definitive diagnosis and electrolyte profile still require hospital confirmation, initiating an insulin infusion without the ability to perform serial electrolyte monitoring would potentially create a new problem while attempting to solve the original one. The hospital could begin the definitive DKA protocol with laboratory surveillance, potassium replacement when indicated, and dextrose administration later in the course as glucose falls while ketosis continues to clear.

The prehospital priorities were therefore perfusion, monitoring, identification of the precipitating cause, and rapid transport.

Interventions

  • Two large-bore peripheral IVs established.
  • Continuous ECG, pulse oximetry, blood pressure, and waveform capnography.
  • Point-of-care glucose, electrolytes, venous blood gas, lactate, and renal-function assessment.
  • POCUS cardiac, pulmonary, and IVC evaluation.
  • 1 liter 0.9% sodium chloride IV initiated for clinically significant volume depletion.
  • Serial neurologic and respiratory examinations.
  • Repeat glucose and hemodynamic assessment during treatment.
  • Twelve-lead ECG obtained to assess for ischemia and potassium-associated electrical abnormalities.
  • Insulin infusion deferred to definitive hospital management because of the need for serial electrolyte monitoring and potassium-guided therapy.

Medications

  • 0.9% sodium chloride, 1,000 mL IV, administered for intravascular volume depletion associated with osmotic diuresis.
  • Ondansetron 4 mg IV, administered for persistent nausea and vomiting to reduce further gastrointestinal fluid loss and improve patient comfort.
  • No prehospital insulin was administered because definitive insulin therapy for suspected DKA requires careful assessment of potassium, renal function, acid-base status, and serial laboratory monitoring.
  • No sodium bicarbonate was administered because the patient’s pH of 7.24 did not meet the usual threshold for bicarbonate therapy in DKA and routine bicarbonate administration in less severe acidosis offers little benefit while carrying potential risks.

The response to the first liter of fluid was clinically meaningful. Her heart rate began to fall, first into the teens above 100 and eventually toward 105/min. Her blood pressure improved to 116/72 mmHg. Her capillary refill shortened, her extremities became warmer, and the patient reported that she felt somewhat less dizzy and less profoundly weak. The respiratory rate remained elevated, which was not unexpected. If she was acidotic, the increased ventilation was compensatory and should not be suppressed merely because the respiratory rate looked abnormal. In fact, the respiratory pattern was one of the most important clues that her body was actively trying to correct the metabolic disturbance.

This is another situation where the temptation to “normalize” a number can be dangerous. A respiratory rate of 28 in a patient with metabolic acidosis is not necessarily a problem to be treated. It may be the treatment. If you sedate such a patient because she looks tachypneic, you may remove the respiratory compensation that is keeping her pH from falling further.

Sadie and I continued to watch her closely. Her mental status remained stable, and there was no evidence of impending airway failure. She was nauseated but no longer actively vomiting. Her ETCO₂ increased modestly as perfusion improved, but the waveform remained compatible with ongoing metabolic compensation.

Reassessment

  • HR: Improved from 126/min to 104/min.
  • BP: Improved from 104/68 mmHg to 116/72 mmHg.
  • RR: 26/min, with persistent deep respirations.
  • SpO₂: 98% on room air.
  • ETCO₂: 26 mmHg.
  • Blood glucose: 528 mg/dL on repeat measurement.
  • Mental status: Awake, oriented, less fatigued.
  • Peripheral perfusion: Improved after fluid administration.
  • Nausea/vomiting: Improved following ondansetron.
  • POCUS: No development of pulmonary congestion following initial fluid administration.

The patient was clearly improving, but she was not fixed. That distinction mattered. A glucose dropping from 560 to 528 after initial fluid resuscitation was not a failure. The purpose of the first intervention was restoration of perfusion, not an immediate normalization of glucose. In DKA, fluids alone can produce a substantial fall in serum glucose because improved renal perfusion increases urinary glucose clearance. The definitive treatment, however, is suppression of ketogenesis through insulin along with careful fluid and electrolyte management.

Kevin and Mike had the patient completely under control from a transport standpoint. They had established the IVs, managed the monitoring, administered the medications, assisted with the point-of-care testing, and understood exactly what we were seeing. There was nothing happening in that ambulance that required physician-level intervention.

That was the important decision of the call.

Sadie and I did not go on the transport.

There is a tendency in medicine to equate the presence of a physician with improved care, but that is not how a mature EMS system should function. The question is not whether a physician is available. The question is whether the patient’s physiology demands physician-level intervention that exceeds what the paramedic crew can safely provide. This patient did not require an advanced airway, invasive ventilation, cardioversion, pacing, vasoactive medication, blood products, procedural sedation, or any other intervention that would require us to remain in the ambulance.

Kevin and Mike had this.

More importantly, they had it well.

We gave the receiving crew a detailed handoff emphasizing the likely DKA physiology, severe volume depletion, initial laboratory abnormalities, elevated lactate, acidemia, potassium level, response to fluids, and the possibility of an infectious or other precipitating process. We specifically highlighted that the patient’s potassium of 5.3 mEq/L should not be interpreted as evidence of adequate total-body potassium because DKA commonly produces profound intracellular and total-body potassium depletion. We also emphasized that she would need serial electrolytes before and during insulin therapy.

The receiving emergency department would have considerably more information available to complete the metabolic picture: formal serum beta-hydroxybutyrate, repeat chemistry panels, measured serum osmolality, venous or arterial blood gas analysis, CBC, urinalysis and culture, chest imaging if indicated, lipase, renal function, and investigation for the precipitating cause. The patient would likely require continued intravenous fluid replacement, insulin therapy, potassium surveillance and replacement, and treatment directed toward whatever had triggered the metabolic decompensation.

Once Medic 1 departed, Sadie and I cleared with Engine 1 and remained available with the Fly Car.

And that enormous vehicle sat there in the afternoon sunlight carrying an arsenal of equipment that we had not needed.

We did not need the whole blood. We did not need the ventilator. We did not need the surgical airway kit, REBOA equipment, automated compression device, thrombolytic therapy, or any of the other extraordinary resources contained within the vehicle. We needed two paramedics, two physicians who happened to be paramedics, a glucose meter, an ECG, a point-of-care analyzer, ultrasound, intravenous fluids, ondansetron, and an understanding of acid-base physiology.

That is one of the things I enjoy most about working EMS. The equipment is impressive, but equipment does not diagnose the patient. A monitor can display a heart rate of 126, but it cannot tell you whether the tachycardia represents pain, hypovolemia, sepsis, hemorrhage, arrhythmia, or compensation for metabolic disease. An ultrasound can show you a small IVC, but it cannot independently announce that the patient has DKA. A glucose meter can tell you that the blood sugar is 560 mg/dL, but it cannot tell you whether the patient has DKA, HHS, or stress hyperglycemia from another catastrophic illness.

The clinician has to assemble the pieces.

And in this case, the pieces fit together rather nicely: severe hyperglycemia had produced osmotic diuresis, osmotic diuresis had produced profound water and electrolyte loss, volume depletion had compromised perfusion, and metabolic derangement had produced acidosis and compensatory hyperventilation. The patient’s tachycardia was not simply a fast heart rate to be treated. Her respiratory rate was not simply an abnormal vital sign to be suppressed. They were manifestations of an organism attempting, quite intelligently, to maintain homeostasis while losing the battle.

By the time Sadie and I returned to our seats outside the station, the sun was still warm, the breeze was still moving through the open bay doors, and the afternoon had resumed its strange approximation of normality. Somewhere down the road, Kevin and Mike were delivering a patient with a serious metabolic disorder to a hospital capable of definitive treatment. We had contributed what we could, and then we got out of the way.

That last part is sometimes harder than the medicine.

Knowing when to step forward is important. Knowing when to step back is equally important. A good physician-paramedic should not be measured by how many advanced procedures they perform. Sometimes the most appropriate physician-level decision is recognizing that an experienced paramedic crew has already done exactly what needs to be done.

And knowing Kevin and Mike, I suspect they were probably more concerned about getting the patient to the hospital than they were about whether they were receiving adequate recognition for their heroic management of a glucose meter that had apparently decided to display the number 560.

They had the patient.

And they had it handled.

Two Arrests, Two ROSCs: When Statistics Defy Reality

The late August air hung thick with warmth as I leaned against the bay doors at Station 1, watching the afternoon light filter through the trees. Kevin had his trademark cigar going, that foul-smelling thing I pretended not to see as part of our unspoken arrangement. Mike and Sadie were in the middle of what had become an increasingly heated debate about tool brands.

“A Milwaukee drill has the torque, but the battery life is garbage,” Mike insisted, his voice rising with the passion of a man who takes his power tools seriously. “DeWalt’s the only way to go for reliability.”

Sadie scoffed, crossing her arms. “You say that because you’ve never had to field-repair a ventilator at 3 AM. I’ll take a Makita any day—better ergonomics for precision work.”

I tried to tune them out, savoring the rare moment of downtime. In our rural Fire/EMS department, these moments of peace are precious commodities. My wife Sadie and I serve as the department’s physician-paramedic team—she as Assistant Commander and Assistant Medical Director, me as Commander and Medical Director. The other volunteers appreciate our presence not because we hover over their shoulders, but because we bring a different level of knowledge while still respecting their autonomy to practice and make decisions.

At 1:58 PM, the tones dropped with their familiar electronic urgency, shattering the afternoon tranquility.

“Attention Station 1: Special Signal Fly Car Request. Please respond to a 47 year old male, cardiac arrest.”

We moved as one unit, the practiced choreography of countless calls. Kevin stubbed out his cigar, Mike’s tool debate forgotten, and Sadie and I headed for the Fly Car.

“Station 2 district,” I said, already calculating the route. “Originally came in as disoriented before he went down.”

Our town is geographically large despite its small population, which means we maintain three stations strategically placed throughout our coverage area. This call came from our Station 2 or “Center” district, putting us about 8 minutes out even with lights and sirens.

The Fly Car is more than just an SUV. Hidden beneath the familiar Chevrolet bodywork was a climate-controlled mobile critical care platform that many emergency departments would envy. Custom-molded slide-out trays held a rolling blood bank of low-titer O-positive whole blood and liquid plasma kept at precise temperatures, alongside rapid fluid-warming devices to heat cold blood to body temperature in seconds during a massive hemorrhage. Dual-probe wireless ultrasound devices synced directly to rugged tablets for immediate point-of-care internal bleeding checks and lung evaluations, while handheld lab-quality blood analyzers delivered critical electrolyte and lactate readings in under two minutes. The vehicle’s climate-controlled drug vaults held broad-spectrum antibiotics for early sepsis intervention, continuous nerve-block and sedative infusions like propofol, pre-hospital clot-busting thrombolytics for acute strokes, and ultra-expensive blood-thinner reversal agents completely unavailable on standard ambulances. For advanced respiratory life support, the car was equipped with video laryngoscopes backed by turbine-driven transport ventilators capable of ICU-level lung protection and automated chest compression devices. Most imposing of all were the sterile surgical blocks, packed with specialized catheters to perform a REBOA—effectively inflating a balloon inside the aorta to clamp a ruptured vessel from the inside out—as well as field escharotomy kits, scalpel-access surgical airway gear, and manual skull drills to create emergency burr holes for patients dying of intracranial pressure while trapped in deep wreckage.

The scene was controlled chaos when we arrived. Medic 2 with Engine 2 were already working the code. EMTs were performing high-quality CPR, but the patient wasn’t intubated yet.

“What’s the story?” I asked, already pulling on gloves.

One of the medics answered between breaths. “Wife called 911 for disorientation. He was conscious when she called but collapsed while she was on the phone with dispatch. We arrived 4 minutes after the call. Down time approximately 10 minutes total. Initial rhythm was VF, shocked once, no change.”

Sadie was already setting up the LUCAS device. “Let’s get him on the autopulse, free up some hands.”

Two minutes after we arrived, as we were applying the LUCAS, the monitor showed a shockable rhythm—coarse VF.

“Charging!” I called out. “Clear!”

200 joules delivered. The rhythm converted to a sinus tachycardia at approximately 105 beats per minute.

We had a pulse. Carotid, femoral—weak but palpable. ROSC.

This is where Sadie and I really went to work. While the EMTs continued their excellent care, we shifted into post-cardiac arrest protocol.

“I’ll intubate,” I said, already preparing the video laryngoscope. “Sadie, get pressors ready. Let’s start with norepinephrine.”

The intubation went smoothly—a 7.5 endotracheal tube passed without difficulty, confirmed immediately with colorimetric capnography and bilateral breath sounds.

“ETCO2 is 28 mmHg,” Sadie announced, already hanging the norepinephrine drip. “Perfusion improving but still compromised.”

While I managed the airway, Sadie was already working on the rest. “I’m starting a norepinephrine drip at 5 mcg/min. Let’s get a 12-lead EKG, arterial line, and another set of vitals. I want to know if this was an MI that led to the arrest.”

The medics from Station 2 knew us well and immediately adapted to our pace. They didn’t need reassurance—they knew we were here to help, not take over.

“We’ll be transporting with you,” I said, securing the ET tube. “Sean, you’ll ride with us.”

Sean nodded, already gathering additional equipment. “Absolutely. Good to have you both here.”

It was Sadie, I, and Sean in the back of the ambulance. Another firefighter took our Fly Car and followed us to the hospital. This was our second cardiac arrest of the day—a highly unusual occurrence in our rural department, where we might go months without a single code. That we had achieved ROSC on both was nothing short of miraculous.

Primary Survey

• Airway: 7.5 endotracheal tube in place, secured with tape. Bilateral breath sounds present and equal with mechanical ventilations. No visible blood in the airway. Proper tube depth confirmed at 24 cm at the teeth.

• Breathing: Mechanically ventilated via turbine-driven transport ventilator. Tidal volume set at 450ml (6ml/kg based on estimated ideal body weight of 75kg), respiratory rate 12, PEEP 5 cmH2O, FiO2 100%. Chest wall rising equally with ventilations. No obvious chest wall deformities.

• Circulation: Weak carotid and femoral pulses palpable. Skin cool, clammy. Capillary refill approximately 4 seconds. Blood pressure 82/48 mmHg via cuff.

• Disability: Pupils 4mm bilaterally, sluggish but reactive to light. No corneal reflexes. No gag reflex. GCS = 3T (intubated).

• Exposure: Patient fully exposed. No obvious signs of trauma. Skin mottled on extremities.

Initial Rhythm Assessment

• Initial rhythm per medics: Ventricular fibrillation.

• Current rhythm: Sinus tachycardia at 105 bpm with ST-segment elevation in leads II, III, and aVF.

• Quality of chest compressions: LUCAS device providing optimal compressions until ROSC achieved.

• Airway status: Securely intubated with confirmed placement via colorimetric capnography and bilateral auscultation.

Vital Signs

• HR: 105 bpm (sinus tachycardia)
• BP: 82/48 mmHg
• RR: 12 breaths/minute via mechanical ventilator
• SpO2: 97% on 100% FiO2
• Temp: 36.3°C (97.3°F) axillary
• Glucose: 128 mg/dL via fingerstick
• ETCO2: 28 mmHg (improving but still indicating compromised perfusion)

Interventions

• CPR with LUCAS device until ROSC achieved.

• Defibrillation: 200 joules biphasic delivered, resulting in ROSC.

• Advanced airway secured with 7.5 endotracheal tube.

• IV access: Two 18-gauge IVs in antecubital fossae, confirmed patent with flush.

• Intraosseous line: Right humeral IO established for additional access.

Medications

• Epinephrine 1mg IV administered x3 during arrest phase per ACLS protocol.

• Amiodarone 300mg IV administered during arrest phase for recurrent VF.

• Norepinephrine drip started at 5 mcg/min for post-cardiac arrest hypotension.

Secondary Assessment

• HEENT: No signs of trauma. Pupils equal and reactive, though sluggish.

• Neck: Tracheal midline after intubation. No jugular venous distension.

• Cardiovascular: Weak peripheral pulses. No precordial thrills or heaves. Irregularly irregular rhythm noted.

• Pulmonary: Bilateral breath sounds equal but diminished with mechanical ventilations. No adventitious sounds noted.

• Abdomen: Soft, non-distended. No guarding or rigidity.

• Pelvis: Stable to palpation. No instability noted.

Extremities: No obvious deformities. Cool to touch with delayed capillary refill. No edema noted.

• Back: No obvious step-offs or deformities. No signs of trauma.

• Neuro: GCS remains 3T. Pupils sluggish but reactive. No purposeful movement.

Diagnostics

• 12-Lead EKG: Sinus tachycardia at 105 bpm with ST-segment elevation in leads II, III, and aVF (inferior leads), consistent with an acute inferior wall myocardial infarction. Reciprocal changes noted in leads I and aVL.

• POCUS: Subxiphoid view performed during rhythm check. No pericardial effusion noted. Severe hypokinesia of the inferior wall and posterior wall. Right ventricle appears mildly dilated with reduced function, concerning for right ventricular involvement.

• i-STAT analysis: pH 7.18, pCO2 52 mmHg, pO2 82 mmHg, lactate 6.4 mmol/L, potassium 4.8 mEq/L, ionized calcium 1.08 mmol/L, troponin I 8.9 ng/mL.

• ETCO2: 28 mmHg post-ROSC (indicating improving but still compromised perfusion).

Differential Diagnosis

  1. Acute inferior wall myocardial infarction with right ventricular involvement leading to cardiac arrest (most likely given EKG findings and troponin level)
  2. Cardiogenic shock secondary to MI (consistent with hypotension and poor perfusion)
  3. Post-cardiac arrest syndrome (contributing to metabolic acidosis and organ dysfunction)
  4. Pulmonary embolism (possible contributor but RV strain could be from MI)
  5. Sepsis with underlying cardiac ischemia (possible but no obvious source)
  6. Electrolyte abnormality (mild hyperkalemia but not severe enough to explain arrest)

Interventions Continued

• Dual sequential defibrillation considered but not required after successful ROSC with first shock.

• Mechanical CPR: LUCAS device continued until stable ROSC achieved, then discontinued.

• Targeted temperature management initiated: Patient cooled to 36°C using cooling blankets and cold saline IV bolus.

• Antiplatelet therapy: Aspirin 325 mg administered via NG tube.

• Anticoagulation: Heparin bolus 60 units/kg administered, followed by infusion to maintain target ACT.

• STEMI protocol activated: Notified receiving hospital of incoming post-cardiac arrest STEMI patient for potential cardiac catheterization.

Advanced Interventions During Transport

As we headed toward the hospital, Sean from Medic 2 assisted while Sadie and I performed advanced interventions that would typically be reserved for the emergency department.

“Given the inferior MI with possible RV involvement, let’s get a right-sided EKG,” I said to Sean while preparing the equipment. “Sadie, can you place a right internal jugular central line for better medication administration and hemodynamic monitoring?”

Sadie nodded, already preparing the central line kit under the ambulance’s working lights. “I’ll use ultrasound guidance. Shouldn’t be a problem even in this moving environment.”

While Sadie placed the central line, I applied precordial electrodes for a right-sided EKG, which confirmed ST-segment elevation in leads V4R through V6R, confirming right ventricular infarction.

“Right-sided MI confirmed,” I announced. “Let’s start a dopamine infusion in addition to the norepinephrine. We need to support the right ventricle and maintain preload.”

Sean prepared the dopamine infusion while Sadie successfully placed the central line without complications.

“Central line in,” Sadie announced. “I’m drawing labs for blood gas, repeat troponin, and lactate. Let’s also get a portable chest X-ray when we arrive to confirm tube placement and check for pulmonary edema.”

The transport was a flurry of activity as we worked seamlessly as a team. Despite the confined space and movement of the ambulance, we were able to provide ICU-level care that likely made the difference between life and death.

Medications Continued

• Norepinephrine titrated to 8 mcg/min to maintain MAP >65 mmHg.

• Dopamine infusion started at 5 mcg/kg/min for RV support and additional inotropic support.

• Amiodarone infusion started at 1 mg/min for 6 hours, then 0.5 mg/min for 18 hours.

• Sodium bicarbonate 50 mEq administered for persistent metabolic acidosis (pH 7.18).

• Calcium gluconate 1g administered for borderline hyperkalemia and cardiac membrane stabilization.

Reassessment

• Rhythm remained sinus tachycardia with persistent inferior ST-segment elevation.

• Blood pressure improved to 92/58 mmHg with dual pressor support.

• ETCO2 improved to 34 mmHg, indicating improving perfusion.

• POCUS showed no improvement in wall motion abnormalities but confirmed RV involvement.

• Laboratory values showed improving acidosis but elevated lactate indicating ongoing tissue hypoperfusion.

Transport Decision

Given the patient’s age, downtime of approximately 10 minutes, and post-cardiac arrest presentation with confirmed inferior MI with RV involvement, we knew the prognosis was guarded. However, the return of spontaneous circulation with a perfusing rhythm, combined with the clear STEMI on EKG, made him a potential candidate for emergent cardiac catheterization.

“We need to move quickly,” I said to the team. “The cath lab needs to be ready for right-sided MI with possible need for RV support device.”

When we arrived at the hospital, the cardiac catheterization team was waiting. We provided a concise handoff, highlighting the key points: 47-year-old male, 10-minute downtime, ROSC after defibrillation, inferior MI with RV involvement confirmed by right-sided EKG, current hemodynamics on dual pressors, and all interventions performed including central line placement.

As we transferred care to the hospital team, I caught Sadie’s eye. We both knew the significance of what we had accomplished. Two cardiac arrests in one day was extraordinary for our rural department. Achieving ROSC on both was nearly miraculous. But we also knew that the real work was just beginning for the hospital team.

The ride back to Station 1 was filled with a quiet sense of accomplishment. Mike and Kevin were waiting for us when we arrived.

“Well?” Mike asked, his usual sarcasm replaced by genuine curiosity.

“Second ROSC of the day,” Sadie said, stretching as she got out of the ambulance. “Inferior MI with RV involvement. 47 years old, 10 minutes down.”

Mike whistled softly. “Two arrests, two ROSCs in one shift. That’s gotta be some kind of record for this department.”

Kevin nodded, his expression thoughtful. “The man upstairs was looking out for those folks today. And you two brought your A-game.”

I looked at my wife, at the team that had come together to save a life, and felt that familiar mixture of pride and humility that defines our work. In rural EMS, we don’t have the luxury of specializing in just one aspect of care. We are the first responders, the critical care transport team, the decision-makers, and sometimes, the bearers of difficult news.

Today was a remarkable day—not just because we saved lives, but because we demonstrated what’s possible when you bring advanced medical care to the prehospital setting, when you empower your team with knowledge and resources, and when you refuse to accept that geography should determine outcomes.

The Physician-Paramedic, the Ninety-Year-Old Combatant, and the Difference Between Agitation and Illness

There is a particular rhythm to a Saturday shift at our rural Fire/EMS station that I have come to appreciate more with every passing year. The apparatus is checked, the radios are charged, the medications are accounted for, the bay doors are open, and if the weather cooperates, everyone gradually migrates outside where the station becomes less of an emergency-services facility and more of a small-town porch. That was where Sadie and I found ourselves this afternoon, volunteering as physician-paramedics with our town’s Fire/EMS department. I serve as both Medical Director for EMS and Commander of EMS, while Sadie serves as Assistant Commander and Assistant Medical Director. We are both physicians by profession and licensed paramedics by choice, which makes for a slightly unusual combination but one that works remarkably well in our department. The other volunteers appreciate having us around not because we feel compelled to take over every call, but because we can contribute another layer of clinical reasoning when the situation genuinely requires it while allowing experienced paramedics to do what they were trained to do. There is a considerable difference between providing physician-level support and behaving like the world’s most annoying clinical backseat driver.

The crew on Medic 1 consisted of Kevin and Mike, which meant the ambulance was in very capable hands. Kevin is our old-school medic from Newark, a man who accumulated a lifetime of prehospital experience before eventually moving out to our quieter piece of New England to retire. He apparently considers retirement to be a condition in which one no longer has to work for money but continues volunteering indefinitely because the idea of staying away from an ambulance for too long is intolerable. Mike is a master plumber by trade and a paramedic because he decided, later in life, that serving the town was something worth doing. He is one of the strongest practical clinicians I know, partly because he understands systems and partly because he has an almost supernatural capacity for recognizing when someone is not telling the whole truth. His humor is extraordinarily dry, his sarcasm is legendary, and his threshold for being impressed by anything is roughly equivalent to the threshold for water flowing uphill through a properly installed drain.

The afternoon had been uneventful. The bay doors were open and sunlight was spilling across the apparatus floor. Kevin was sitting nearby with his trademark cigar, Mike was smoking a cigarette, and I was practicing the time-honored tradition of pretending that neither activity was occurring directly in front of me. Sadie and I were talking about what we were going to do that evening, which was considerably more pleasant than discussing staffing, protocols, or hospital politics. There is something wonderfully normal about those conversations. Two physicians who spend most of their working lives dealing with critically ill patients were sitting outside a fire station discussing dinner and evening plans like everyone else, surrounded by people whose professional lives could not be more different and yet somehow fit together perfectly when the radio tones sounded.

At 12:47 p.m., the station abruptly ceased being a porch.

“Attention Station 1: Medic 1, Engine 1 and Fly Car. Please respond to a ninety-year-old female. History of dementia. Combative.”

Mike looked toward Kevin, and Kevin looked toward Mike. There was a brief exchange of the sort that requires no elaborate explanation.

They were going to need hazard pay.

The humor continued as everyone moved toward the apparatus, with Kevin and Mike joking that they were apparently going to go twelve rounds with a ninety-year-old woman and should therefore be entitled to some form of combat compensation. It was funny, but underneath the joke was something important. A ninety-year-old described as “combative” is not necessarily an unruly patient. In fact, the word itself is often a clinical warning sign. Acute behavioral change in an elderly patient, particularly one with dementia, should be presumed to have a medical cause until demonstrated otherwise. Dementia may provide the substrate for confusion, but it does not explain why a patient suddenly becomes substantially more agitated than her baseline.

We headed toward the Fly Car while Kevin and Mike climbed into Medic 1, with Mike driving. Engine 1 followed behind us, lights flashing, sirens and the Q producing the unmistakable soundtrack of a rural EMS response. As we drove, Sadie and I were already discussing the differential. Delirium from infection was high on the list, but so were hypoglycemia, hyperglycemia, hypoxia, hypercapnia, stroke, intracranial hemorrhage, medication toxicity, withdrawal, urinary retention, constipation, dehydration, electrolyte abnormalities, occult trauma, pain, myocardial ischemia, and environmental causes. In an elderly patient with dementia, behavioral disturbance is frequently the final common pathway of a physiologic problem rather than the primary diagnosis.

When we arrived, the patient’s daughter met us at the door and immediately apologized for the condition of the house, which was unnecessary but entirely typical. She explained that her mother had been increasingly confused since that morning. Initially she had been restless and repetitive, then became verbally aggressive, and finally attempted to strike her daughter when she tried to help her into a chair. The family had described her to dispatch as “combative,” but the daughter emphasized something more important: this was not her mother’s baseline.

That single piece of information changed the call.

The patient was sitting in a recliner but was repeatedly attempting to stand. She was pulling at her clothing and trying to push away anyone who came within arm’s reach. Her speech was disorganized. She recognized her daughter intermittently but could not reliably answer questions. She was not simply angry. She was profoundly inattentive, unable to sustain a conversation, and fluctuating between periods of agitation and brief episodes of staring. Those features were much more consistent with delirium superimposed on dementia than with a primary psychiatric disorder.

We did not immediately restrain her or sedate her.

That decision was deliberate. Physical resistance in an elderly patient is often interpreted as evidence that the patient needs chemical restraint, but restraint is a treatment of last resort, not a diagnostic shortcut. Before administering a sedating medication, we needed to determine whether we could safely evaluate her, whether she was actually dangerous to herself or others, and whether the behavior represented an immediately reversible medical problem.

Primary Survey

  • Airway: Patent; patient vocalizing spontaneously without upper-airway obstruction.
  • Breathing: Spontaneous respirations without obvious increased work of breathing.
  • Circulation: Peripheral pulses present; skin warm with mildly delayed capillary refill.
  • Disability: Marked acute confusion and agitation with inability to reliably follow commands; no obvious focal neurologic deficit on initial observation.
  • Exposure: No obvious external trauma; no major bleeding; temperature assessment performed because infection and environmental causes remained possible.

Vital Signs

  • HR: 104/min
  • BP: 168/86 mmHg
  • RR: 22/min
  • SpO₂: 94% on room air
  • Temperature: 100.8°F
  • Blood glucose: 118 mg/dL
  • ETCO₂: 39 mmHg

Her vital signs immediately provided several useful pieces of information. She was not profoundly hypoxic, her glucose was normal, and there was no obvious evidence of respiratory failure. Her mildly elevated temperature, however, mattered. A temperature of 100.8°F in a ninety-year-old is not diagnostic of infection, but in the context of acute delirium it increases the likelihood that an underlying infectious or inflammatory process is contributing to the change in mental status.

We began with a relatively quiet examination, because there was no advantage to surrounding a frightened elderly patient with four people talking simultaneously. Sadie and I approached from the front, spoke slowly, and allowed her daughter to remain within her field of vision. Kevin and Mike established the equipment and monitoring while keeping the environment as nonthreatening as possible. The patient repeatedly attempted to remove the blood-pressure cuff, which produced an irritated response from Mike that was sufficiently deadpan to make me laugh despite the circumstances.

The physical examination was more informative than the dispatch complaint.

Secondary Assessment

  • HEENT: Pupils equal and reactive; oral mucosa dry; no obvious facial trauma; no focal cranial abnormality.
  • Neck: Supple; no obvious meningismus; trachea midline.
  • Cardiovascular: Mild sinus tachycardia with regular rhythm; no obvious new murmur.
  • Pulmonary: Clear bilateral breath sounds without focal crackles or significant wheezing.
  • Abdomen: Soft with mild suprapubic fullness and apparent discomfort with palpation.
  • Pelvis: Stable without apparent tenderness.
  • Extremities: No obvious deformity; no unilateral swelling; mildly cool distal extremities.
  • Back: No obvious trauma or pressure-related injury identified during limited examination.
  • Neuro: Awake but severely inattentive; disoriented; fluctuating level of cooperation; no obvious unilateral weakness, facial asymmetry, or gross speech deficit beyond baseline confusion.

The suprapubic finding caught our attention. It was subtle, but the lower abdomen appeared somewhat full, and the patient reacted when we palpated that region. In an elderly patient who suddenly becomes agitated, urinary retention is one of those diagnoses that can be overlooked because it does not sound dramatic enough. Yet bladder distention can produce significant discomfort, agitation, autonomic activation, and delirium, particularly in patients who cannot articulate what hurts.

We performed point-of-care ultrasound of the lower abdomen, and the bladder was substantially distended. That did not prove that urinary retention was the sole cause of her delirium, but it provided an objective explanation for at least part of her behavior. The patient was uncomfortable, unable to communicate effectively, and reacting to that discomfort in the only way available to her.

We continued the evaluation because finding one abnormality in an elderly patient is not permission to stop thinking.

Diagnostics

  • POCUS bladder: Markedly distended urinary bladder consistent with significant urinary retention.
  • POCUS cardiac: Grossly preserved systolic function without obvious pericardial effusion.
  • POCUS lung: No diffuse B-line pattern or obvious focal finding suggesting acute pulmonary edema.
  • Point-of-care glucose: 118 mg/dL, excluding hypoglycemia as an immediate explanation.
  • ETCO₂: 39 mmHg without evidence of significant hypoventilation.
  • 12-lead ECG: Sinus tachycardia without acute ST-segment elevation or immediately apparent malignant dysrhythmia.
  • Temperature: 100.8°F, increasing concern for infection as a contributor to delirium.

The differential remained broad, but the probability distribution was beginning to change.

Differential Diagnosis

  1. Acute delirium secondary to urinary retention and discomfort: Strongly supported by acute behavioral change, suprapubic fullness, POCUS evidence of bladder distention, and apparent discomfort.
  2. Urinary tract infection with delirium: Remained a significant concern given age, low-grade fever, and acute mental-status change; definitive urinalysis and culture would be required.
  3. Dehydration/metabolic delirium: Possible given dry mucous membranes and mild tachycardia; electrolytes and renal function required hospital evaluation.
  4. Medication effect or toxicity: Important in an elderly patient, particularly with polypharmacy; medication reconciliation was requested from the family.
  5. Acute cerebrovascular event: Considered because of abrupt mental-status change, although the absence of focal findings made a large hemispheric stroke less likely.
  6. Intracranial hemorrhage: Remained possible in any unexplained acute change in an elderly patient, particularly if there was an unwitnessed fall or anticoagulant use.
  7. Hypoxia/hypercapnia: Considered but not supported by current oxygenation and capnography.
  8. Pain from occult trauma or another abdominal process: Possible, particularly given the patient’s inability to communicate reliably.
  9. Primary behavioral disturbance: Low on the list because the change was acute and clearly different from baseline.

At this point, Sadie and I began discussing the most important question: what did we actually need to do in the field?

The answer was not “sedate the patient.”

We needed to reduce the stimulus, maintain safety, identify immediately reversible causes, provide supportive care, and get her to definitive evaluation. Kevin and Mike were already managing the practical aspects beautifully. There was no reason to turn a cooperative paramedic-level call into a physician-paramedic transport merely because Sadie and I were standing there.

The patient’s agitation began to diminish somewhat once we stopped trying to force her to sit still and allowed her daughter to speak with her. We repositioned her comfortably, maintained a calm environment, and avoided unnecessary physical confrontation. We established IV access because of her age, altered mental status, and potential for deterioration, but we did not start an indiscriminate fluid bolus. Her blood pressure was adequate, her examination did not suggest profound shock, and there was no reason to flood a ninety-year-old with fluid simply because her mucous membranes were dry.

We did administer acetaminophen 650 mg orally, once she was sufficiently cooperative to safely swallow, because she had a low-grade fever and apparent discomfort. This was not intended as a treatment for delirium itself; it was supportive treatment for a possible infectious or inflammatory process and discomfort while awaiting definitive evaluation.

We did not administer benzodiazepines. In an elderly patient with delirium, particularly one with possible underlying infection or metabolic disturbance, benzodiazepines can worsen confusion and produce respiratory depression. They are useful in specific situations, including alcohol or benzodiazepine withdrawal and certain severe agitation scenarios, but they are not a reflexive answer to an elderly patient who is behaving badly.

We similarly did not reach immediately for an antipsychotic. Medications such as haloperidol or olanzapine can have a role in severe agitation when a patient poses an immediate danger and nonpharmacologic strategies fail, but they carry meaningful risks in older adults, including extrapyramidal effects, QT prolongation, hypotension, sedation, and aspiration. In this case, the patient was becoming manageable with environmental modification and reassurance, so medication-induced restraint would have solved a problem we no longer had.

Interventions

  • Continuous ECG, pulse oximetry, blood pressure, and mental-status monitoring.
  • IV access established.
  • Environmental stimulation reduced.
  • Family member used as a familiar calming presence.
  • Patient repositioned for comfort and fall prevention.
  • POCUS performed to evaluate suspected urinary retention.
  • Serial neurologic examinations performed because of acute delirium.
  • ECG obtained to evaluate occult cardiac contributors.
  • Oral acetaminophen administered for fever and discomfort.
  • No chemical restraint required.
  • No advanced airway intervention indicated.
  • No aggressive fluid resuscitation indicated based on current hemodynamics.

Medications

  • Acetaminophen 650 mg PO, administered for mild fever and suspected discomfort.
  • No benzodiazepine administered because there was no indication for chemical restraint and benzodiazepines could worsen delirium and respiratory status.
  • No antipsychotic administered because the patient’s agitation was controllable without pharmacologic sedation and the potential adverse effects outweighed any immediate benefit.

By this point, the patient was considerably calmer. She remained confused, but her behavior had changed from striking out and attempting to climb out of the chair to intermittently answering questions and allowing her daughter to hold her hand. Her heart rate decreased toward the mid-90s, her respiratory rate normalized, and she became less visibly distressed.

Reassessment

  • HR: 94/min
  • BP: 154/82 mmHg
  • RR: 19/min
  • SpO₂: 95% on room air
  • Temperature: 100.6°F
  • Blood glucose: 118 mg/dL
  • Mental status: Remained delirious but substantially less agitated.
  • Work of breathing: Normal.
  • Peripheral perfusion: Stable.
  • POCUS: Persistent bladder distention consistent with urinary retention.

The destination remained the emergency department because the underlying cause of her delirium had not been completely established. POCUS had identified significant urinary retention, but that was not the end of the medical evaluation. She needed urinalysis and culture, CBC, metabolic panel, renal function assessment, medication review, and potentially neuroimaging depending upon the history obtained at the hospital. If the family reported anticoagulant use or an unwitnessed fall, the threshold for CT imaging would be appropriately lower. The emergency department could also address the urinary retention definitively and determine whether catheterization was indicated based upon the complete clinical picture.

But there was no reason for Sadie or me to accompany her.

The entire clinical course had remained within standard paramedic practice. Kevin and Mike had established the IV, obtained the ECG, managed monitoring, assisted with the POCUS assessment, supported the patient and family, and were fully capable of continuing the transport. There was no airway intervention, no ACLS, no hemodynamic instability, no advanced medication strategy, and no procedure that required physician-level intervention. The patient’s condition had improved rather than deteriorated, and the most important intervention had been careful assessment rather than aggressive treatment.

That distinction is something I value enormously about our department. Being physician-paramedics does not mean that Sadie and I need to be physically present in the back of every ambulance. In fact, knowing when not to go is just as important as knowing when to go. We are fortunate to work with paramedics who are not waiting for a physician to tell them what to do. Kevin and Mike had the knowledge, experience, and judgment to manage this patient independently, and there was no clinical reason to deprive them of that responsibility.

Before Medic 1 departed, Kevin looked at the patient, then looked at Mike, and reminded him that he was still waiting for his hazard pay.

Mike, naturally, had several comments about the matter that I will politely omit from the medical record.

We cleared with the engine company after Medic 1 left for the hospital, and the station slowly returned to its earlier quiet. The Q stopped, the lights disappeared down the road, and the open bay once again became simply an open bay. The Fly Car remained ready, its remarkable collection of equipment sitting untouched in its climate-controlled compartments. There had been no need for whole blood, mechanical ventilation, advanced airway equipment, thrombolytics, REBOA, or any of the other extraordinary capabilities carried for the rare patient who truly needs them.

Instead, the call had required something much older and considerably less glamorous: observation.

A ninety-year-old woman had been labeled “combative,” but the patient herself was not the problem. Her brain was responding to something her body was experiencing. The job was to figure out what that something might be. In elderly patients, delirium is physiology expressed through behavior. Infection, urinary retention, hypoxia, hypercapnia, metabolic disturbances, medication effects, pain, dehydration, stroke, intracranial hemorrhage, and countless other insults can all manifest as agitation because the patient may no longer possess the cognitive or communicative reserve to tell you, in conventional terms, what is wrong.

That is why I have always been wary of the word “combative” when it appears on a dispatch screen. It describes what the patient is doing, not why she is doing it. If you treat the behavior without understanding the physiology underneath it, you may simply sedate the warning signal while the disease continues unchecked.

In this case, the ninety-year-old lady who was supposedly going to require twelve rounds of combat had ultimately required something much less dramatic: a careful examination, a little patience, a bit of ultrasound, supportive treatment, and a crew willing to look past the label.

Kevin and Mike could handle the transport.

They had this one.

And as Sadie and I walked back toward the Fly Car, I could already hear Mike complaining about how he was apparently going to have to finish his shift and go grocery shopping without receiving the hazard pay he had been promised.

Two Physicians, One Mission: A Mutual Aid Cardiac Arrest

The late August morning was perfect in a way that only rural towns can manufacture. The bay doors at Station 1 were thrown open, allowing the divine breeze to cut through the lingering warmth of summer. Kevin had his trademark cigar going, a foul-smelling thing I pretended not to notice as part of our unspoken arrangement. Mike, Sadie, and I were lounging in the sun-drenched entryway, debating our movie choices for the night.

“Pulp Fiction,” Sadie insisted, a playful glint in her eye. “It’s a classic. Plus, I want to see if you can still quote every line.”

Mike snorted. “Nothing like watching a movie about heroin addicts and gangsters to relax after a day of saving lives. I’m voting for something with fewer overdoses and car explosions.”

I laughed. “Sadie’s vote trumps yours, Mike. You know that.”

This is our rhythm. My wife Sadie and I, both physicians and paramedics, serving our community as Medical Director/Commander and Assistant Medical Director/Assistant Commander respectively. The other volunteers appreciate our presence not because we hover over their shoulders, but because we bring a different level of knowledge while still respecting their autonomy to practice and make decisions. We’re a resource, not a restriction.

At 11:27 AM, the tones dropped with their familiar electronic urgency, shattering the morning tranquility.

“Attention Station 1: Special Signal Fly Car Request. Please respond mutual aid to the next town over for an 89 year old male, cardiac arrest. Local town Engine 2 and Rescue 3 on scene.”

We moved as one unit, the practiced choreography of countless calls. Kevin stubbed out his cigar, Mike was already checking the equipment, and Sadie and I headed for the Fly Car.

“I’ll drive,” I said, sliding behind the wheel. “Sadie, you’re on medical direction.”

The Fly Car is more than just an SUV. Hidden beneath the familiar Chevrolet bodywork was a climate-controlled mobile critical care platform that many emergency departments would envy. Custom-molded slide-out trays held a rolling blood bank of low-titer O-positive whole blood and liquid plasma kept at precise temperatures, alongside rapid fluid-warming devices to heat cold blood to body temperature in seconds during a massive hemorrhage. Dual-probe wireless ultrasound devices synced directly to rugged tablets for immediate point-of-care internal bleeding checks and lung evaluations, while handheld lab-quality blood analyzers delivered critical electrolyte and lactate readings in under two minutes. The vehicle’s climate-controlled drug vaults held broad-spectrum antibiotics for early sepsis intervention, continuous nerve-block and sedative infusions like propofol, pre-hospital clot-busting thrombolytics for acute strokes, and ultra-expensive blood-thinner reversal agents completely unavailable on standard ambulances. For advanced respiratory life support, the car was equipped with video laryngoscopes backed by turbine-driven transport ventilators capable of ICU-level lung protection and automated chest compression devices. Most imposing of all were the sterile surgical blocks, packed with specialized catheters to perform a REBOA—effectively inflating a balloon inside the aorta to clamp a ruptured vessel from the inside out—as well as field escharotomy kits, scalpel-access surgical airway gear, and manual skull drills to create emergency burr holes for patients dying of intracranial pressure while trapped in deep wreckage.

As I drove, I used everything the car had—every siren, the rumbler, the air horn. Surrounding towns know we have a physician-paramedic unit, and they always call for larger cases if we’re on. We don’t mind; we encourage it. Mutual aid isn’t just about equipment—it’s about bringing the right expertise to the right place at the right time.

The scene was controlled chaos when we arrived. EMTs were performing high-quality CPR, but the patient wasn’t intubated yet. They had been working him for approximately 11 minutes before our arrival.

“What’s the story?” I asked, already pulling on gloves.

One of the EMTs answered between breaths. “Family called 911 for chest pain, then he collapsed. We arrived 6 minutes after the call. Down time approximately 11 minutes total. Initial rhythm was VF, shocked once, converted to asystole.”

Sadie was already setting up the LUCAS device. “Let’s get him on the autopulse, free up some hands.”

Two minutes after we arrived, as we were applying the LUCAS, the monitor showed a shockable rhythm—coarse VF.

“Charging!” I called out. “Clear!”

200 joules delivered. The rhythm converted to a sinus tachycardia at approximately 110 beats per minute.

We had a pulse. Carotid, femoral—weak but palpable. ROSC.

This is where Sadie and I really went to work. While the EMTs continued their excellent care, we shifted into post-cardiac arrest protocol.

“I’ll intubate,” I said, already preparing the video laryngoscope. “Sadie, get pressors ready. Let’s start with norepinephrine.”

The intubation went smoothly—a 7.5 endotracheal tube passed without difficulty, confirmed immediately with colorimetric capnography and bilateral breath sounds.

“ETCO2 is 32 mmHg,” Sadie announced, already hanging the norepinephrine drip. “Good perfusion.”

While I managed the airway, Sadie was already working on the rest. “I’m starting a norepinephrine drip at 5 mcg/min. Let’s get a 12-lead EKG, arterial line, and another set of vitals. I want to know if this was an MI that led to the arrest.”

The EMTs watched, initially hesitant but quickly adapting to our pace. They didn’t really know us, but they could see we were here to help, not take over.

“We’ll be transporting with you,” I said, securing the ET tube. “If that’s alright with your crew.”

The paramedic in charge nodded gratefully. “Absolutely. We’re glad you’re here.”

It was Sadie, I, and an EMT named Richard in the back of the ambulance. Another firefighter took our Fly Car and followed us to the hospital.

Primary Survey

• Airway: 7.5 endotracheal tube in place, secured with tape. Bilateral breath sounds present and equal with mechanical ventilations. No visible blood in the airway. Proper tube depth confirmed at 24 cm at the teeth.

• Breathing: Mechanically ventilated via turbine-driven transport ventilator. Tidal volume set at 450ml (6ml/kg based on estimated ideal body weight of 70kg), respiratory rate 12, PEEP 5 cmH2O, FiO2 100%. Chest wall rising equally with ventilations. No obvious chest wall deformities.

• Circulation: Weak carotid and femoral pulses palpable. Skin cool, clammy. Capillary refill approximately 4 seconds. Blood pressure 85/40 mmHg via cuff.

• Disability: Pupils 3mm bilaterally, sluggish but reactive to light. No corneal reflexes. No gag reflex. GCS = 3T (intubated).

• Exposure: Patient fully exposed. No obvious signs of trauma. Skin mottled on extremities.

Initial Rhythm Assessment

• Initial rhythm per EMTs: Ventricular fibrillation.

• Current rhythm: Sinus tachycardia at 110 bpm with ST-segment elevation in leads V1-V4.

• Quality of chest compressions: LUCAS device providing optimal compressions until ROSC achieved.

• Airway status: Securely intubated with confirmed placement via colorimetric capnography and bilateral auscultation.

Vital Signs

• HR: 110 bpm (sinus tachycardia)
• BP: 85/40 mmHg
• RR: 12 breaths/minute via mechanical ventilator
• SpO2: 98% on 100% FiO2
• Temp: 36.1°C (97.0°F) axillary
• Glucose: 142 mg/dL via fingerstick
• ETCO2: 32 mmHg (indicating good perfusion post-ROSC)

Interventions

• CPR with LUCAS device until ROSC achieved.

• Defibrillation: 200 joules biphasic delivered, resulting in ROSC.

• Advanced airway secured with 7.5 endotracheal tube.

• IV access: Two 18-gauge IVs in antecubital fossae, confirmed patent with flush.

• Intraosseous line: Right humeral IO established for additional access.

Medications

• Epinephrine 1mg IV administered x3 during arrest phase per ACLS protocol.

• Amiodarone 300mg IV administered during arrest phase for recurrent VF.

• Norepinephrine drip started at 5 mcg/min for post-cardiac arrest hypotension.

Secondary Assessment

• HEENT: No signs of trauma. Pupils equal and reactive, though sluggish.

• Neck: Tracheal midline after intubation. No jugular venous distension.

• Cardiovascular: Weak peripheral pulses. No precordial thrills or heaves. Irregularly irregular rhythm noted.

• Pulmonary: Bilateral breath sounds equal but diminished with mechanical ventilations. No adventitious sounds noted.

• Abdomen: Soft, non-distended. No guarding or rigidity.

• Pelvis: Stable to palpation. No instability noted.

• Extremities: No obvious deformities. Cool to touch with delayed capillary refill. No edema noted.

• Back: No obvious step-offs or deformities. No signs of trauma.

• Neuro: GCS remains 3T. Pupils sluggish but reactive. No purposeful movement.

Diagnostics

• 12-Lead EKG: Sinus tachycardia at 110 bpm with ST-segment elevation in leads V1-V4 (anterior leads), consistent with an acute anterior wall myocardial infarction. Reciprocal changes noted in leads II, III, and aVF.

• POCUS: Subxiphoid view performed during rhythm check. No pericardial effusion noted. Severe hypokinesia of the anterior wall and septum. Apical ballooning consistent with large territory infarction. Right ventricle appears normal size and function.

• i-STAT analysis: pH 7.21, pCO2 48 mmHg, pO2 89 mmHg, lactate 5.8 mmol/L, potassium 4.2 mEq/L, ionized calcium 1.15 mmol/L, troponin I 15.2 ng/mL.

• ETCO2: 32 mmHg post-ROSC (indicating good perfusion but decreased cardiac output).

Differential Diagnosis

  1. Acute anterior wall myocardial infarction leading to cardiac arrest (most likely given EKG findings and troponin level)
  2. Cardiogenic shock secondary to MI (consistent with hypotension and poor perfusion)
  3. Post-cardiac arrest syndrome (contributing to metabolic acidosis and organ dysfunction)
  4. Pulmonary embolism (less likely without RV strain on ultrasound)
  5. Sepsis (possible contributing factor but no obvious source)
  6. Electrolyte abnormality (no significant abnormalities noted)

Interventions Continued

• Dual sequential defibrillation considered but not required after successful ROSC with first shock.

• Mechanical CPR: LUCAS device continued until stable ROSC achieved, then discontinued.

• Targeted temperature management initiated: Patient cooled to 36°C using cooling blankets and cold saline IV bolus.

• Antiplatelet therapy: Aspirin 325 mg administered via NG tube.

• Anticoagulation: Heparin bolus 60 units/kg administered, followed by infusion to maintain target ACT.

• STEMI protocol activated: Notified receiving hospital of incoming post-cardiac arrest STEMI patient for potential cardiac catheterization.

Medications Continued

• Norepinephrine titrated to 10 mcg/min to maintain MAP >65 mmHg.

• Amiodarone infusion started at 1 mg/min for 6 hours, then 0.5 mg/min for 18 hours.

• Lidocaine infusion considered for arrhythmia prophylaxis but held due to stable rhythm.

• Sodium bicarbonate 50 mEq administered for persistent metabolic acidosis (pH 7.21).

Reassessment

• Rhythm remained sinus tachycardia with persistent ST-segment elevation.

• Blood pressure improved to 95/55 mmHg with norepinephrine at 10 mcg/min.

• ETCO2 improved to 38 mmHg, indicating improving perfusion.

• POCUS showed no improvement in wall motion abnormalities.

• Laboratory values showed improving acidosis but elevated lactate indicating ongoing tissue hypoperfusion.

Transport Decision

Given the patient’s age, downtime of approximately 11 minutes, and post-cardiac arrest presentation, we knew the prognosis was guarded at best. However, the return of spontaneous circulation with a perfusing rhythm, combined with the clear STEMI on EKG, made him a potential candidate for emergent cardiac catheterization.

“We need to move,” I said to the EMTs. “Let’s package and transport. Sadie, you’ll manage the pressors and ventilation. I’ll handle the monitoring and documentation. Richard, you’re our extra set of hands.”

They nodded, already moving in coordinated fashion. The transfer from the living room floor to the stretcher was smooth, with minimal interruptions in care. As we loaded the patient into the ambulance, I took a moment to update the receiving hospital.

“We’re en route with your 89-year-old male, cardiac arrest, now with ROSC. He’s intubated, sedated, on norepinephrine drip, and showing an anterior STEMI on 12-lead. We’ve initiated post-cardiac arrest and STEMI protocols. ETA 13 minutes.”

“Copy that. Cath lab is being notified. They’ll be ready for you.”

The ride to the hospital was a flurry of activity. Sadie managed the ventilator settings, titrated the norepinephrine, and administered additional medications as needed. I monitored the EKG, documented our interventions, and performed repeat POCUS examinations to reassess cardiac function. Richard assisted with equipment management and medication preparation, proving himself invaluable despite being “just an EMT.”

“You know,” Sadie said quietly during a brief moment of stability, “for an 89-year-old with 11 minutes of downtime, this is actually a remarkable outcome so far.”

I nodded, my eyes still on the monitor. “The question is whether we got there soon enough to prevent irreversible brain injury. The lactate is still concerning, and his blood pressure is tenuous despite the pressors.”

This is the reality of pre-hospital medicine—small victories in the face of overwhelming odds. We had brought this man back from death’s door, but the journey was far from over. The next critical hours would determine whether our efforts would result in a meaningful recovery or merely prolonged dying.

When we arrived at the hospital, the cardiac catheterization team was waiting. We provided a concise handoff, highlighting the key points: 89-year-old male, 11-minute downtime, ROSC after defibrillation, anterior STEMI, current hemodynamics, and all interventions performed.

As we transferred care to the hospital team, I caught Sadie’s eye. We both knew the statistics. An 89-year-old with that much downtime, even with ROSC and STEMI identification, faced an uphill battle. But we also knew that without our mutual aid response, without the advanced interventions we were able to provide in the field, he wouldn’t have had any chance at all.

The ride back to Station 1 was quieter than the ride out. The adrenaline had faded, replaced by the familiar exhaustion that follows a critical call. Kevin and Mike were waiting for us when we arrived.

“Well?” Mike asked, his usual sarcasm replaced by genuine curiosity.

“ROSC in the field,” Sadie said, stretching as she got out of the ambulance. “Anterior STEMI. 89 years old, 11 minutes down.”

Mike whistled softly. “That’s either a miracle or a long-term vent patient in the making.”

Kevin nodded, his expression thoughtful. “You gave him a chance. That’s all we can do sometimes.”

I looked at my wife, at the team that had come together to save a life, and felt that familiar mixture of pride and humility that defines our work. In rural EMS, we don’t have the luxury of specializing in just one aspect of care. We are the first responders, the critical care transport team, the decision-makers, and sometimes, the bearers of difficult news.

Today was a good day—not because we saved a life, but because we gave a life a chance. In our world, sometimes that’s everything.

The Physician-Paramedic, the COPD Exacerbation, and a Saturday Morning Lesson in Breathing

There is a certain tranquility to a late-August Saturday at our rural Fire/EMS station that makes the eventual interruption by the radio tones feel almost unfair. The bay doors were rolled open, the apparatus was sitting ready inside, and the weather had settled into one of those beautiful late-summer mornings that New England occasionally gives us as an apology for all the humidity we endured earlier in the season. Sadie and I were volunteering as physician-paramedics, as we routinely do, with me serving as both Medical Director for EMS and Commander of EMS and Sadie serving as Assistant Commander and Assistant Medical Director. Although both of us spend our professional lives practicing medicine at a considerably different level of intensity in the hospital, there is something about coming back to a rural Fire/EMS station that remains wonderfully grounding. Here, nobody particularly cares what operating room you were in yesterday or how many credentials happen to follow your name. You are another member of the crew until the patient requires something different, and that is precisely the way I prefer it.

The crew that morning was Kevin and Mike on Medic 1, which is about as reassuring a combination as you can have when you are sitting around waiting for the radio to ruin your plans. Kevin is an old-school medic who spent years working in Newark before moving out to our quieter corner of New England to retire. Retirement, apparently, was interpreted as “move somewhere rural and continue volunteering indefinitely.” He has the experience of someone who has encountered nearly every variation of human illness that can occur between a front door and an emergency department, and he has developed the particular clinical temperament that comes from having seen enough bad outcomes to understand which details actually matter. Mike is a master plumber by trade who became a paramedic later in life because he wanted to serve the community. He has an extraordinary clinical instinct, a spectacularly dry sense of humor, and an ability to identify bullshit with the efficiency of a laboratory assay. His personality is somewhere between a paramedic, a philosopher, and a man who has been waiting twenty years for someone to give him a legitimate reason to make a sarcastic comment.

Kevin had his trademark cigar, which I was very carefully pretending not to notice. There are certain traditions in EMS that are apparently more durable than protocol revisions, and Kevin’s cigar is one of them. We were sitting outside enjoying the breeze, talking about the evening ahead, and the conversation had migrated toward movies. Sadie suggested Pulp Fiction, which immediately produced the usual debate about whether we were going to watch the entire film or somehow get distracted halfway through and start discussing something else. It was a perfectly ordinary Saturday morning conversation, the sort that makes you forget that you are sitting beside an ambulance carrying enough medical equipment to manage a critically ill patient.

At 10:13 a.m., the tones dropped.

“Attention Station 1: Medic 1, Engine 1 and Fly Car. Please respond to a seventy-four-year-old female, difficulty breathing, on oxygen. History of COPD.”

The transition from casual conversation to clinical thinking is almost automatic after enough years in EMS. Before we had even left the station, I was already considering the broad differential. A seventy-four-year-old with COPD and dyspnea certainly could be experiencing an acute exacerbation, but “COPD” is a diagnosis that can become an intellectual trap if you allow it to explain every respiratory complaint. Pneumonia, pulmonary edema, acute coronary syndrome, pulmonary embolism, pneumothorax, mucus plugging, aspiration, arrhythmia, medication nonadherence, hypercapnic respiratory failure, metabolic acidosis, and even anemia all remain possible. The dispatch diagnosis is merely the opening hypothesis, not the conclusion.

We headed toward the Fly Car while Kevin drove Medic 1 and Mike rode with him. Engine 1 pulled ahead, lights flashing, siren and air horn working in concert with the unmistakable mechanical bellow of the Q. The Fly Car followed, carrying the more advanced diagnostic and resuscitation equipment, but we had no preconceived notion that any of it would necessarily be required. One of the advantages of having a sophisticated response vehicle is not that you have to use everything on every patient. Quite the opposite. The real advantage is having the capability available when physiology dictates that you need it.

We arrived to find the patient sitting upright in a chair near an open window, leaning forward with her forearms braced against her thighs. That posture immediately caught my attention. Patients with significant obstructive lung disease will often instinctively assume the tripod position because it optimizes the mechanics of the accessory muscles of respiration. Her daughter was nearby and explained that her mother had become increasingly short of breath since the previous evening, initially with exertion and then at rest. She had used her rescue inhaler several times overnight without achieving her usual relief. She normally wore supplemental oxygen at home and had increased it somewhat that morning because she felt that she “couldn’t get enough air.”

The patient was awake, frightened, and working hard to breathe. She could speak, but only in short phrases. Her respiratory rate was elevated, and her expiratory phase was noticeably prolonged. There was diffuse wheezing, but the important finding was not simply that she was wheezing. The more concerning feature was the reduction in air movement throughout both lungs. Severe bronchospasm can paradoxically produce less wheezing as airflow becomes so restricted that there is insufficient movement of air to generate the sound. The phrase “silent chest” is often used for the extreme version of this phenomenon, and although this patient had not reached that point, her breath sounds were considerably less impressive than one might expect from the degree of respiratory distress.

Primary Survey

  • Airway: Patent; patient speaking in short phrases without upper-airway obstruction.
  • Breathing: Significant tachypnea, prolonged expiratory phase, diffuse expiratory wheezing, diminished bilateral air movement, and visible accessory-muscle recruitment.
  • Circulation: Tachycardic with palpable peripheral pulses; no evidence of active hemorrhage.
  • Disability: Awake, anxious, oriented, and initially able to follow commands; no focal neurologic deficit.
  • Exposure: No obvious trauma; no cyanosis or peripheral edema; no urticaria or other findings suggesting anaphylaxis.

Vital Signs

  • HR: 112/min
  • BP: 156/84 mmHg
  • RR: 32/min
  • SpO₂: 89% on her baseline supplemental oxygen
  • Temperature: 99.1°F
  • Blood glucose: 124 mg/dL
  • ETCO₂: 51 mmHg initially, with a prolonged, obstructive capnogram

The combination of hypoxemia, tachypnea, increased work of breathing, and elevated end-tidal carbon dioxide immediately changed the level of concern. The ETCO₂ was not being interpreted as an arterial PCO₂ measurement, because it is not equivalent to one, particularly in severe obstructive lung disease. What mattered was the trend and the waveform. The prolonged upsloping expiratory phase was consistent with significant airflow obstruction, and the elevated value suggested that alveolar ventilation was becoming inadequate. In a patient with COPD, carbon dioxide retention may be chronic, acute, or acute-on-chronic, so a single elevated number does not establish the diagnosis of acute hypercapnic respiratory failure. The patient’s clinical trajectory and subsequent response to therapy would be far more informative.

I started the initial assessment while Kevin and Mike began the standard paramedic interventions. One of the things I appreciate most about working with experienced paramedics is that they do not require a physician standing over them to tell them how to treat a textbook COPD exacerbation. They recognized the respiratory pattern immediately, established monitoring, confirmed the oxygen delivery system, and began preparing bronchodilator therapy. My role at that point was not to seize control of the patient but to make sure that we were not overlooking something more dangerous hiding underneath the COPD label.

Her history provided several useful clues. She had no chest pain, no sudden onset of dyspnea, no hemoptysis, no unilateral leg swelling, and no recent immobilization. There had been no aspiration event. She had not developed urticaria, facial swelling, or hypotension. She had experienced several days of increasing cough and sputum production, although she denied a dramatic change in sputum color. She had no known history of congestive heart failure. There was also no obvious infectious syndrome, although her age and COPD made pneumonia entirely plausible even without a high fever.

Secondary Assessment

  • HEENT: Airway patent; mucous membranes mildly dry; no facial edema or angioedema.
  • Neck: No significant jugular venous distention; trachea midline.
  • Cardiovascular: Tachycardic, regular rhythm; no obvious new murmur; peripheral pulses symmetric.
  • Pulmonary: Diffuse expiratory wheezing with prolonged expiration and globally diminished air movement; no focal unilateral absence of breath sounds.
  • Abdomen: Soft and nontender without distention.
  • Pelvis: Stable and nontender.
  • Extremities: No significant peripheral edema; no unilateral calf swelling or tenderness.
  • Back: No acute findings.
  • Neuro: Alert and oriented, anxious but appropriate; no focal neurologic deficit.

The physical examination did not support pneumothorax, pulmonary edema, or overt cardiogenic shock, although none could be excluded solely on examination. We therefore supplemented the assessment with POCUS. The lungs showed the expected hyperinflation-related limitations, but there was no obvious lung point to suggest pneumothorax and no diffuse bilateral B-line pattern suggestive of pulmonary edema. Cardiac imaging showed preserved gross left ventricular systolic function without an obvious large pericardial effusion. The IVC was not particularly useful as a standalone volume assessment in this patient, and we did not pretend otherwise. In a spontaneously breathing patient with obstructive lung disease, intrathoracic pressure changes can complicate interpretation, and there was no clinical reason to make volume status the centerpiece of the evaluation.

Diagnostics

  • POCUS cardiac: Grossly preserved LV systolic function; no large pericardial effusion.
  • POCUS lung: No obvious pneumothorax; no diffuse B-line pattern suggesting acute pulmonary edema.
  • ETCO₂ waveform: Prolonged obstructive expiratory upstroke consistent with significant airflow limitation.
  • Point-of-care glucose: 124 mg/dL.
  • ECG: Sinus tachycardia without acute ST-segment elevation or other immediately diagnostic ischemic pattern.
  • Clinical interpretation: Findings favored acute obstructive airway exacerbation with emerging hypercapnic ventilatory impairment rather than primary cardiogenic pulmonary edema, pneumothorax, or acute coronary occlusion.

Differential Diagnosis

  1. Acute COPD exacerbation with significant bronchospasm: Most likely, given the progressive dyspnea, increased rescue-inhaler use, prolonged expiration, diffuse wheezing, and diminished airflow.
  2. Acute-on-chronic hypercapnic respiratory failure: Concerning because of the elevated ETCO₂ and increasing work of breathing, although definitive arterial or venous blood gas analysis would be required to characterize the degree of hypercapnia and acidemia.
  3. Lower respiratory tract infection/pneumonia: Considered because of increased cough and sputum, although the absence of high fever, focal lung findings, or significant systemic toxicity made severe pneumonia less likely.
  4. Acute cardiogenic pulmonary edema: Less likely given the examination and ultrasound findings, particularly the absence of diffuse B-lines and obvious LV dysfunction.
  5. Pulmonary embolism: Considered but lower on the differential because of the gradual onset, prominent obstructive physiology, absence of pleuritic pain or hemoptysis, and lack of obvious thromboembolic risk factors.
  6. Pneumothorax: Important to exclude in a COPD patient because bullous disease can predispose to spontaneous pneumothorax, but bilateral air movement and POCUS findings made it unlikely.
  7. Acute coronary syndrome or arrhythmia: Considered because elderly patients can present with dyspnea rather than chest pain, but the ECG and clinical presentation did not support this as the primary process.

Treatment began with aggressive inhaled bronchodilation. We administered albuterol 2.5 mg by nebulizer combined with ipratropium bromide 0.5 mg, with repeated bronchodilator therapy according to protocol. The objective was not simply to make the wheezing disappear. The pharmacologic target was airway smooth-muscle relaxation and reduction of airflow resistance. In severe obstruction, small changes in airway radius can have disproportionately large effects on resistance because of the relationship between airway radius and laminar flow. Clinically, that translates into a patient who may suddenly move air considerably better after bronchodilation even though the underlying disease has not disappeared.

We also administered methylprednisolone 125 mg IV, recognizing that corticosteroids do not provide an immediate bronchodilator effect. Their value is downstream: reducing airway inflammation, decreasing the duration and severity of the exacerbation, and reducing the risk of relapse. This is one of those areas where emergency medicine requires patience. A medication does not have to produce an immediate physiological change to be important.

Oxygen was titrated rather than simply maximized. The goal was adequate oxygenation without reflexively driving the saturation toward 100 percent. Patients with COPD who retain carbon dioxide can develop worsening hypercapnia through several mechanisms when exposed to excessive supplemental oxygen, including worsening ventilation-perfusion mismatch and alterations in the relationship between oxygenated and deoxygenated hemoglobin. The simplistic notion that oxygen is universally beneficial at the highest possible concentration does not survive contact with pulmonary physiology. We targeted an SpO₂ generally in the 88–92% range, adjusting to her clinical condition and response.

As the nebulized therapy took effect, the change was gradual but unmistakable. Her respiratory rate decreased from the low 30s toward the mid-20s, the accessory-muscle recruitment became less pronounced, and air movement improved. The wheezing actually became somewhat louder initially, which was not concerning; in a patient who was previously moving very little air, louder wheezing can represent improved airflow rather than deterioration. Her ETCO₂ also began trending downward, and more importantly, the waveform became less severely obstructive.

At that point, Sadie stepped forward.

Pulmonology is one of her major specialties, and this patient was almost perfectly constructed to become an impromptu pulmonary physiology lecture. Sadie did not simply announce the diagnosis. She walked the crew through the reasoning. She explained why the patient’s posture mattered, why the prolonged expiratory phase mattered, why diminished air movement could be more concerning than loud wheezing, and why oxygen should be titrated rather than indiscriminately increased. She discussed the significance of the capnography waveform and, importantly, why we could not simply look at the ETCO₂ number and declare the patient hypercapnic. She explained dynamic hyperinflation and auto-PEEP, the mechanism by which incomplete exhalation causes progressively increasing end-expiratory lung volume, placing the respiratory muscles at a mechanical disadvantage and potentially producing severe ventilatory failure.

It was not a lecture for the sake of a lecture. Every point related directly to what we were seeing in front of us.

Sadie also discussed why noninvasive positive-pressure ventilation would become appropriate if the patient’s work of breathing remained excessive or her ventilatory failure progressed. The purpose of BiPAP in this setting is not merely to “give oxygen.” Inspiratory positive pressure augments ventilation and reduces the work required to generate adequate tidal volumes, while expiratory pressure can splint open collapsible airways and counterbalance intrinsic PEEP. The trick is that positive pressure must be used intelligently in severe obstructive disease. Excessive pressures or inappropriate timing can worsen dynamic hyperinflation and impair venous return.

Fortunately, we did not need to escalate that far.

Interventions

  • Continuous ECG, pulse oximetry, blood pressure, and waveform capnography.
  • Supplemental oxygen titrated to an appropriate COPD target rather than maximal oxygenation.
  • Nebulized albuterol and ipratropium.
  • IV corticosteroid administration.
  • POCUS cardiac and lung assessment.
  • Serial respiratory examinations focusing on work of breathing, air movement, respiratory rate, mental status, and capnography.
  • Preparation for noninvasive ventilation if respiratory fatigue or worsening hypercapnia developed.
  • Continuous reassessment for pneumothorax, pulmonary edema, arrhythmia, or other alternate causes of deterioration.

Medications

  • Albuterol 2.5 mg nebulized, administered for acute bronchospasm and airflow obstruction.
  • Ipratropium bromide 0.5 mg nebulized, administered with albuterol to provide additional bronchodilation through anticholinergic blockade.
  • Methylprednisolone 125 mg IV, administered to reduce airway inflammation and decrease the duration and recurrence of the exacerbation.

There was no indication for epinephrine, antibiotics in the field based solely on the available presentation, diuretics, nitrates, or a prehospital advanced airway. Most importantly, there was no indication for intubation. In fact, intubating a patient with severe obstructive lung disease is something you should approach with considerable respect because positive-pressure ventilation can convert severe obstruction into catastrophic dynamic hyperinflation. If an obstructed patient cannot adequately exhale before the next ventilator breath arrives, pressure accumulates within the thorax. That intrinsic PEEP increases intrathoracic pressure, impairs venous return, reduces cardiac output, and can ultimately produce profound hypotension or cardiovascular arrest. Sometimes the most sophisticated airway intervention is knowing that the airway does not yet need to be taken away from the patient.

By the time we had completed the second respiratory assessment, the patient looked considerably better. She was still sick, but she was no longer fighting for every breath. Her speech had lengthened from short phrases to complete sentences. Her respiratory rate was down to 22/min, her heart rate had decreased to 98/min, and her oxygen saturation was 91% on appropriately titrated supplemental oxygen. Her capnographic waveform had improved, and her expiratory phase, although still prolonged, was less labored.

Reassessment

  • HR: 98/min
  • BP: 148/80 mmHg
  • RR: 22/min
  • SpO₂: 91% with titrated supplemental oxygen
  • ETCO₂: 44 mmHg with improved obstructive waveform
  • Work of breathing: Substantially improved.
  • Air movement: Improved bilaterally.
  • Mental status: Remained alert, oriented, and appropriate.
  • Clinical trajectory: Significant response to standard paramedic-level bronchodilator and corticosteroid therapy without need for advanced airway intervention.

At that point the decision about transport became straightforward, but it was also an important distinction for Sadie and me. This patient absolutely needed to go to the hospital. She had experienced a significant COPD exacerbation with hypoxemia and increased work of breathing, and her response to initial therapy did not eliminate the possibility of recurrent bronchospasm or delayed deterioration. The appropriate destination was an emergency department capable of obtaining formal blood-gas analysis, chest imaging, laboratory testing, and additional respiratory therapy while evaluating for an infectious or cardiac trigger.

What she did not require was physician-level intervention during transport.

That distinction mattered to us. I had performed the initial assessment and worked alongside Kevin and Mike, and Sadie had contributed substantially to the pulmonary assessment and treatment plan, but every intervention actually required for stabilization had remained comfortably within experienced paramedic practice. There was no need for RSI, invasive ventilation, advanced hemodynamic support, blood products, cardioversion, transcutaneous pacing, or another intervention that would make physician-paramedic presence essential during the transport. Kevin and Mike had this patient. More importantly, they had this patient well.

We therefore cleared with the engine company once Medic 1 departed for the hospital. Kevin and Mike continued the transport while Sadie and I remained with the Fly Car and Engine 1 returned to service. There was no ego involved in the decision, and there shouldn’t be. One of the most important forms of clinical judgment is recognizing when your additional skill set is genuinely necessary and when the people standing beside you are already completely capable of managing the problem. A physician-paramedic who feels compelled to remain on every call because of the letters after their name is not demonstrating leadership; they are demonstrating insecurity.

This was a paramedic call, and it was handled beautifully by paramedics.

What made it memorable was the opportunity to watch an experienced crew recognize a familiar disease, treat it appropriately, and then use the physiology behind the treatment to understand the patient’s response. Sadie simply took that opportunity and turned the back of an ambulance into a short pulmonary critical-care conference, which is very much in keeping with her personality. The crew did not need a physician to rescue them from the call. They needed experienced clinicians working together, each bringing something different to the assessment.

There is also a lesson here that extends well beyond COPD. Medicine becomes dangerous when labels replace thinking. “She has COPD” is not a diagnosis of the current episode. It is a piece of medical history. The actual diagnosis comes from the history, examination, physiology, response to treatment, and exclusion of competing pathology. A seventy-four-year-old with dyspnea can have COPD, pneumonia, pulmonary edema, pulmonary embolism, pneumothorax, myocardial ischemia, anemia, or several of those problems simultaneously. The fact that one diagnosis is printed on her medical record does not grant it exclusive jurisdiction over the differential.

By the time Sadie and I were back outside the station, the late-August sun was still shining through the open bay doors. The breeze had picked up again, and the station had returned to its normal Saturday rhythm. Somewhere down the road, Medic 1 was carrying our patient toward definitive evaluation, and Kevin and Mike were doing exactly what they have done countless times before: treating the patient, watching the physiology, and getting her safely to the hospital.

The Fly Car sat ready beside us, carrying enough equipment to manage some of the most catastrophic emergencies imaginable, but none of it had been necessary that morning. We had not needed whole blood, REBOA, surgical airway equipment, advanced mechanical ventilation, thrombolytics, or any of the other extraordinary capabilities packed into that vehicle. We needed oxygen, bronchodilators, steroids, a monitor, capnography, clinical judgment, and a crew that knew what it was doing.

Sometimes the most sophisticated EMS medicine is knowing exactly how much medicine you actually need.

And somewhere in the back of my mind, I was still wondering whether we were actually going to watch Pulp Fiction tonight.

The Physician-Paramedic and the Coffee-Ground Call

There is a particular kind of Saturday morning that exists only in a rural Fire/EMS station, when the bay doors are rolled open, the weather is cooperative, the trucks are washed, the coffee is tolerable, and nobody has yet heard the tones. That was where Sadie and I found ourselves this morning, sitting outside the station with the apparatus bays open to the late-August sunshine, enjoying one of those extraordinary New England breezes that makes you temporarily forget that summer will eventually surrender to autumn. We were volunteering as physician-paramedics with our town’s Fire/EMS department, something that has become an important part of our lives despite the fact that both of us already have demanding physician careers. I serve as Medical Director for EMS and Commander of EMS, while Sadie serves as Assistant Commander and Assistant Medical Director. The arrangement sounds rather official when written down, but around the station it mostly means that we are two physicians who are perfectly comfortable sitting on a folding chair outside the bay drinking coffee, listening to the crew complain about the weather, and waiting for the radio to ruin everyone’s morning.

The crew today was a particularly good one. Kevin was on Medic 1, the old-school medic from Newark who came to our quiet corner of New England to retire but apparently forgot to retire from EMS. He has the accumulated experience of someone who has been doing this long enough to remember when certain things that younger clinicians consider standard practice were still experimental ideas. He has seen the ugly side of prehospital medicine, and consequently he does not scare easily. His humor is dry, his clinical judgment is grounded in experience, and his tolerance for nonsense is approximately zero. His trademark cigar was smoldering nearby, technically in a location where I could not see it, which meant that I was doing the traditional physician thing of pretending not to notice. Mike was also there, a master plumber by trade who became a paramedic later in life because he wanted to contribute to the community. He is an exceptionally good clinician, partly because he understands systems intuitively and partly because he has an almost pathological ability to recognize when somebody is giving him a story rather than an accurate history. His sense of humor is crude enough to require no further documentation, and his sarcasm is sufficiently dry that you sometimes need to check whether he is joking before laughing.

Sadie and I were talking with them about the weekend, including Mike’s ambitious plans to go grocery shopping after his shift, which seemed to be occupying more of his attention than any hypothetical emergency. The discussion was entirely ordinary, which is generally how these things begin. We had no reason to believe that a patient was about to turn our pleasant Saturday morning into a high-acuity resuscitation.

Then, at 8:45 a.m., the tones dropped.

“Attention Station 1: Medic 1, Engine 1 and Fly Car. Please respond. Thirty-nine-year-old female, vomiting, looks like coffee grounds. Patient is on blood thinners.”

The nature of the dispatch immediately changed the clinical picture. “Coffee-ground emesis” is one of those descriptions that sounds relatively benign to someone unfamiliar with gastrointestinal hemorrhage, but clinically it is often the visual consequence of blood sitting in the stomach long enough for gastric acid to alter hemoglobin. Fresh hematemesis suggests more brisk proximal bleeding, whereas coffee-ground material indicates that at least some blood has remained in the stomach long enough to undergo chemical alteration. Neither description tells you how much blood the patient has lost. A patient can have relatively modest bleeding and produce dramatic emesis, while another can have a substantial upper gastrointestinal hemorrhage with little witnessed vomiting at all. The addition of anticoagulant therapy changed the stakes further because whatever lesion was bleeding might be producing hemorrhage that the normal hemostatic system could no longer adequately contain.

Sadie and I headed for the Fly Car while Kevin and Mike moved toward Medic 1, with Mike driving. Engine 1 followed behind us, lights and siren activated, the Q roaring through the morning as we moved through town. The Fly Car was not simply a department-issued SUV carrying a jump bag and a cardiac monitor. It was, for practical purposes, a climate-controlled resuscitation bay on four wheels, designed around the concept that the interval between the patient’s front door and definitive hospital care is not dead time. It is part of the treatment. The vehicle carried low-titer O-positive whole blood and liquid plasma, rapid fluid warming capability, point-of-care ultrasound, handheld laboratory analysis, advanced airway equipment, transport ventilation, sophisticated medication storage, and the invasive equipment necessary for extremely unusual surgical emergencies. Most of that inventory would remain untouched on an ordinary call. That is precisely the point. You do not carry advanced capability because you expect to use every item; you carry it because occasionally a patient arrives at the worst possible moment with the worst possible physiology, and the treatment that matters is the one you already have.

Sadie and I were quiet during the short drive, going through the differential rather than assuming that “coffee grounds plus anticoagulant” automatically meant a peptic ulcer. Upper gastrointestinal hemorrhage has a broad differential: peptic ulcer disease, erosive gastritis or duodenitis, esophageal or gastric varices, Mallory-Weiss injury, malignancy, vascular lesions, and less common causes such as Dieulafoy lesions. Anticoagulation does not necessarily create the lesion; it can transform a relatively contained lesion into a clinically significant hemorrhage. At thirty-nine, certain diagnoses would be less statistically dominant than they would be in an older patient, but age does not exclude serious pathology. We needed to know what anticoagulant she was taking, why she was taking it, whether she had liver disease, alcohol-related disease, prior ulcers, previous gastrointestinal bleeding, recent vomiting or retching, NSAID exposure, pregnancy possibility, abdominal pain, syncope, melena, and, most importantly, how much physiologic reserve she had left.

The answer became apparent before we even entered the house.

There was a smell associated with the scene that I have learned to recognize immediately. Blood has a particular metallic, organic odor, and in a confined environment mixed with gastric contents it becomes unmistakable. The house smelled like gastrointestinal bleeding. The patient was on a couch near the kitchen, pale enough that the difference between her skin and the surrounding room was immediately obvious. She was awake but profoundly ill appearing. There was no meaningful drive in her movements. She was not sitting upright and complaining loudly about feeling terrible; she looked exhausted in the way patients do when their physiology has already consumed most of the energy available to them. A basin beside her contained dark granular material consistent with coffee-ground emesis, with a small amount of darker red blood mixed through it.

We approached with the assumption that this was a potentially significant upper GI hemorrhage until proven otherwise.

Our first priority was determining whether she was currently protecting her airway and whether she was maintaining adequate ventilation and perfusion. She could answer questions, but her responses were delayed, her voice weak, and she had the exhausted appearance of someone who had been vomiting repeatedly. Her airway was technically patent, but that did not mean it was safe. The distinction became increasingly important as we continued the examination because an actively bleeding patient with a stomach full of blood has a very different airway risk profile from a patient who simply feels nauseated. If she lost consciousness, vomited again, or became unable to coordinate swallowing, the airway could rapidly become contaminated with blood and gastric contents. Aspiration of blood is not merely a nuisance; substantial aspiration can produce airway obstruction, chemical pneumonitis, impaired gas exchange, and severe hypoxemia, while hypoxemia superimposed upon hemorrhagic shock is a particularly unforgiving physiologic combination.

Primary Survey

  • Airway: Initially patent with spontaneous phonation; airway protection was judged tenuous because of active/recent hematemesis and progressive fatigue.
  • Breathing: Spontaneous respirations with initially preserved oxygen saturation but increasing respiratory effort and poor physiologic reserve.
  • Circulation: Marked pallor and cool extremities with weak peripheral pulses and delayed capillary refill, concerning for clinically significant blood loss and impaired oxygen delivery.
  • Disability: Awake but lethargic, with slowed responses; no focal neurologic deficit apparent on initial examination.
  • Exposure: No obvious external hemorrhage, significant abdominal distention, or traumatic injury.

Vital Signs

  • HR: 128/min
  • BP: 88/54 mmHg
  • RR: 26/min
  • SpO₂: 96% on room air initially
  • Temperature: 98.1°F
  • Blood glucose: 108 mg/dL
  • ETCO₂: 31 mmHg when monitored, consistent with increased minute ventilation in the setting of physiologic stress

The blood pressure was concerning, but the blood pressure alone did not tell the entire story. Her tachycardia, cool peripheral skin, pallor, delayed capillary refill, altered energy level, and narrow pulse pressure collectively suggested impaired effective circulating volume. Hemorrhagic shock is fundamentally a problem of oxygen delivery. Losing blood reduces circulating volume, but it also removes hemoglobin, which is the principal carrier of oxygen in the blood. Early in hemorrhage, the body attempts to compensate through sympathetic activation, increasing heart rate and systemic vascular resistance while redistributing blood flow toward the heart and brain. Peripheral vasoconstriction explains why these patients become cold and pale. As blood loss progresses, compensation begins to fail, and the patient can transition from compensated shock to hypotension, altered mental status, metabolic acidosis, and ultimately cardiovascular collapse.

Secondary Assessment

  • HEENT: Marked conjunctival and facial pallor; oral mucosa dry; no facial trauma.
  • Neck: No jugular venous distention; trachea midline.
  • Cardiovascular: Tachycardic, regular rhythm; weak peripheral pulses; cool extremities.
  • Pulmonary: Initially clear bilateral breath sounds without wheezing or focal crackles; no obvious aspiration at initial assessment.
  • Abdomen: Soft with mild epigastric discomfort but no guarding, rigidity, or peritoneal signs.
  • Pelvis: Stable without tenderness.
  • Extremities: Cool and pale with delayed capillary refill; no peripheral edema.
  • Back: No obvious trauma or external bleeding.
  • Neuro: Awake and oriented but lethargic; speech appropriate; no focal motor deficit identified.

The absence of peritonitis was reassuring only in a very narrow sense. We were not dealing with an obviously perforated viscus, but a benign abdominal examination does not make gastrointestinal hemorrhage benign. The abdomen can be remarkably unimpressive in a patient losing substantial blood into the gastrointestinal tract. Likewise, the fact that she was still awake did not reassure us sufficiently. Cerebral perfusion can be maintained surprisingly late in some patients, particularly younger patients with strong compensatory mechanisms, and then deteriorate rapidly once those mechanisms are exhausted.

We established large-bore intravenous access while the second line was obtained, placed her on continuous ECG and pulse oximetry, and began preparing the blood warmer. At the same time, the point-of-care analyzer provided the first objective evidence of what her clinical appearance was already telling us. Her hemoglobin was profoundly reduced, and although the exact value had to be interpreted in the context of acute hemorrhage, it was low enough to support the concern for substantial blood loss or significant pre-existing anemia compounded by active bleeding. The laboratory picture was accompanied by an elevated lactate, consistent with impaired tissue oxygen delivery. Importantly, hemoglobin is not a perfect real-time marker of acute blood loss because early hemorrhage can occur before equilibration of plasma and red-cell compartments. In this patient, however, the severely abnormal value combined with her clinical appearance and hemodynamics made the transfusion decision considerably easier.

We also used POCUS, not because ultrasound could tell us exactly where the gastrointestinal bleeding originated, but because it could provide additional information about her hemodynamic state and help exclude competing catastrophic processes. The inferior vena cava was small and demonstrated substantial respiratory variation, supporting low effective intravascular volume in the appropriate clinical context. POCUS is not a magic “volume status meter,” and I would never interpret IVC behavior in isolation; respiratory mechanics, right-heart function, intra-abdominal pressure, spontaneous versus positive-pressure ventilation, and many other variables influence IVC appearance. Here, however, the ultrasound findings aligned with the physical examination and laboratory data rather than contradicting them. The overall picture was one of significant volume depletion in a patient with suspected active upper GI hemorrhage.

Diagnostics

  • POCUS: Small, markedly respiratory-variable IVC, supporting significant intravascular volume depletion in conjunction with clinical findings.
  • Cardiac POCUS: Hyperdynamic left ventricular appearance without an obvious large pericardial effusion.
  • Lung POCUS: No significant bilateral B-lines or obvious pneumothorax; no sonographic evidence of pulmonary edema before transfusion.
  • Point-of-care hemoglobin: Severely decreased, consistent with significant anemia.
  • Point-of-care lactate: Elevated, supporting impaired systemic oxygen delivery.
  • Blood glucose: 108 mg/dL.
  • ECG: Sinus tachycardia without acute ischemic changes.

Differential Diagnosis

  1. Acute upper gastrointestinal hemorrhage from peptic ulcer disease: Most likely given the coffee-ground emesis and clinical presentation; anticoagulation could significantly worsen bleeding from an otherwise contained ulcer.
  2. Erosive gastritis or duodenitis: Plausible, particularly if there were NSAID, alcohol, or other mucosal-injury exposures.
  3. Esophageal or gastric variceal hemorrhage: Considered because variceal bleeding can be catastrophic and requires a different early treatment strategy, although there was no known history of cirrhosis or portal hypertension at the scene.
  4. Mallory-Weiss tear: Possible if repeated forceful vomiting preceded the bleeding, although the degree of physiologic compromise made a substantial hemorrhage more concerning than a minor mucosal tear.
  5. Less common vascular or structural upper-GI lesions: Remained possible but were less likely based on the limited history available in the field.

The anticoagulant became particularly important. We confirmed that she was taking a therapeutic anticoagulant, although the precise agent and last dose required clarification. Anticoagulation changes the risk-benefit calculation around hemorrhage because the problem is not merely replacing what has been lost; it is also determining whether the bleeding source is capable of achieving hemostasis while anticoagulant activity persists. Definitive management would require hospital-based endoscopy and potentially reversal therapy depending on the specific anticoagulant, timing, renal function, severity of bleeding, and institutional protocol.

At this point, Sadie and I agreed that this was no longer simply a patient who needed an ambulance ride to the emergency department. She needed a controlled resuscitation during transport, and her airway represented a second immediate threat. She was still conscious and initially oxygenating, but she had recently vomited blood, remained profoundly weak, and had evidence of significant anemia and hypoperfusion. The concern was not that intubation would somehow treat the hemorrhage. It would not. The concern was that deterioration could turn a manageable airway into a contaminated airway at precisely the moment when hypotension and hypoxemia would be least tolerated.

We therefore elected to proceed with rapid-sequence intubation, with the understanding that induction itself can worsen hypotension in a patient whose circulating volume is already critically reduced. This is where physician-level airway management becomes less about performing a procedure and more about understanding the physiology surrounding it. Positive-pressure ventilation reduces venous return, while induction agents can diminish sympathetic vascular tone. In a patient with hemorrhagic shock, either effect can precipitate cardiovascular collapse. We therefore prioritized blood resuscitation, preoxygenation, suction readiness, hemodynamic monitoring, and a carefully selected induction strategy rather than treating RSI as a generic medication sequence.

The airway was aggressively suctioned before and during laryngoscopy. Video laryngoscopy provided visualization while a second clinician maintained suction, and the endotracheal tube was placed successfully on the first attempt. Bilateral chest excursion, auscultation, continuous waveform capnography, and subsequent ventilator mechanics confirmed tracheal placement. We transitioned her to the transport ventilator using lung-protective settings appropriate for an intubated adult without established ARDS, while recognizing that excessive mean airway pressure could further compromise venous return in a profoundly volume-depleted patient.

Interventions

  • Two large-bore peripheral IV lines established.
  • Continuous ECG, pulse oximetry, noninvasive blood pressure, and waveform capnography monitoring.
  • Point-of-care laboratory testing and serial hemodynamic assessment.
  • POCUS assessment of cardiac function, lungs, and IVC.
  • Aggressive airway suctioning because of recent hematemesis.
  • Preoxygenation followed by physician-paramedic RSI because of inadequate airway reserve and high aspiration risk.
  • Video laryngoscopic endotracheal intubation with continuous suction.
  • Mechanical ventilation using lung-protective transport settings.
  • Rapid initiation of warmed low-titer O-positive whole blood because of clinically significant hemorrhagic shock and severe anemia.
  • Careful reassessment of blood pressure, peripheral perfusion, mental status, and respiratory mechanics throughout resuscitation.
  • Preparation for anticoagulant reversal at the receiving facility once the exact anticoagulant and relevant laboratory information could be confirmed.

Medications

Medication selection was deliberately conservative because this was a patient in hemorrhagic shock rather than a stable elective intubation. For RSI, we used ketamine 1.5 mg/kg IV as the induction agent, selected for its relative preservation of sympathetic tone compared with agents such as propofol in a profoundly volume-depleted patient. Neuromuscular blockade was achieved with rocuronium 1.2 mg/kg IV to facilitate rapid, reliable intubation and minimize the period during which airway contamination could occur.

Because the clinical presentation was consistent with significant nonvariceal upper GI hemorrhage, we administered pantoprazole 80 mg IV, followed by preparation for continued acid suppression according to receiving-hospital protocol. The purpose was to reduce gastric acidity and support clot stability while definitive endoscopic management was arranged, although medication therapy was understood to be adjunctive rather than definitive treatment for the hemorrhage.

We did not automatically administer octreotide simply because the patient had an upper GI bleed. Octreotide is particularly useful when variceal hemorrhage is suspected, and there was insufficient evidence at the scene to make portal hypertensive bleeding the leading diagnosis. Had she demonstrated known cirrhosis, portal hypertension, prior varices, significant stigmata of chronic liver disease, or another compelling clinical reason to suspect variceal hemorrhage, an appropriate prehospital protocol could include octreotide 50 mcg IV, followed by 50 mcg/hour continuous infusion. In this case, however, indiscriminate treatment would have added complexity without a clear indication.

Most importantly, we did not attempt to dilute the problem with large volumes of crystalloid. In hemorrhagic shock, liters of saline may transiently increase the blood pressure while doing nothing to restore oxygen-carrying capacity and potentially contributing to dilutional coagulopathy, tissue edema, and worsening hypothermia. The patient needed blood, not an impressive-looking collection of IV fluid bags.

The first unit of low-titer O-positive whole blood was warmed and initiated under controlled conditions. Her response was not judged by a single blood-pressure number. We watched the entire physiologic picture: heart rate, pulse pressure, skin temperature, capillary refill, mental status, waveform capnography, respiratory mechanics, and subsequent blood pressure. Within minutes, her peripheral perfusion began to improve and her heart rate decreased modestly. The improvement did not mean that the bleeding had stopped. It meant that we had temporarily improved oxygen delivery and circulating volume enough to buy her time.

Reassessment

  • HR: Improved from 128/min to approximately 108/min after initial blood resuscitation.
  • BP: Improved from 88/54 mmHg to approximately 102/62 mmHg.
  • SpO₂: Maintained at 99–100% following intubation and controlled ventilation.
  • ETCO₂: Approximately 34–36 mmHg after stabilization on the transport ventilator.
  • Peripheral perfusion: Capillary refill and extremity temperature improved.
  • Mental status: No longer assessable after RSI, but pre-intubation lethargy did not progress to cardiovascular collapse.
  • POCUS: No new evidence of pulmonary edema during early transfusion.

The decision regarding destination was straightforward. This patient required a hospital capable of definitive upper gastrointestinal hemorrhage management, including emergency endoscopy, blood bank support, critical care, and anticoagulant reversal. She did not need the nearest small emergency department simply because it was geographically closer. She needed the facility capable of stopping the bleeding. That distinction is one of the most important functions of advanced EMS: the ambulance is not merely transportation, and the destination is not merely a postcode. The destination is part of the treatment plan.

Because Sadie and I had taken direct responsibility for the advanced airway, induction, transfusion strategy, and ongoing resuscitation, we went into the back of Medic 1 for transport. Kevin and Mike continued their respective roles in the resuscitation, with the rest of the apparatus crew supporting movement and logistics. A firefighter from Engine 1 took the Fly Car back toward the station. There was no reason for every resource to follow the ambulance to the hospital when the clinical need had already been concentrated into the transporting unit.

The transport itself was relatively uneventful, which in this context was exactly what we wanted. The patient remained mechanically ventilated, blood continued under controlled administration, and serial blood-pressure measurements demonstrated maintenance of the initial improvement. We continued to watch for the complications that could develop during transport: recurrent hypotension, worsening airway contamination, aspiration, pulmonary edema from transfusion, hypothermia, arrhythmia, or abrupt deterioration from continued hemorrhage. The fact that the patient had improved did not make us complacent. A bleeding patient can look better because you have temporarily increased circulating volume while the lesion continues to hemorrhage. Resuscitation buys time; it does not create hemostasis.

At the receiving hospital, the handoff was deliberately concise but comprehensive. We reported the witnessed hematemesis, anticoagulant use, initial hemodynamics, examination findings, point-of-care hemoglobin and lactate abnormalities, POCUS findings, airway status, RSI medications, transfusion, response to blood, and the concern for significant upper GI hemorrhage. We emphasized that her improvement represented response to resuscitation rather than resolution of the underlying problem. The receiving team would need to determine the exact anticoagulant exposure and whether specific reversal was indicated, obtain formal laboratory studies including coagulation testing and serial hemoglobin measurements, activate additional blood products if necessary, and proceed toward definitive hemorrhage control, most likely with urgent endoscopic evaluation.

Once the transfer of care was complete, Sadie and I stepped away from the resuscitation bay and let the hospital team take over. There is always a peculiar transition at that moment. For the preceding thirty or forty minutes, every physiological variable has mattered, every decision has had an immediate consequence, and the patient’s survival depends upon the coordination of a relatively small number of people working in a confined space. Then the stretcher crosses the threshold, another team assumes responsibility, and the prehospital portion of the story is finished. That transition is not an ending so much as a handoff in a much larger chain of care.

What stayed with me about this patient was not the sophistication of the equipment or even the fact that we performed an advanced airway procedure in a living room on a Saturday morning. It was the underlying physiology. Gastrointestinal hemorrhage can be deceptive because the source of the blood is hidden. There is no puddle on the floor, no obvious external wound, and no dramatic mechanism of injury to announce the severity of the problem. Instead, the body quietly tells you what is happening through tachycardia, vasoconstriction, pallor, weakness, altered mentation, falling blood pressure, rising lactate, and ultimately failure of compensation. The clinician’s job is to recognize those signals early enough to intervene before physiology becomes anatomy, and before compensation becomes collapse.

By the time we returned to the station, the late-August morning had become considerably more ordinary again. The bay doors were still open, the sunlight was still coming through, and the station somehow looked exactly as it had before the tones dropped. Kevin’s cigar had apparently survived the call. Mike was still talking about grocery shopping. Sadie and I went back to being two physicians sitting around a rural fire station rather than two clinicians managing a patient with hemorrhagic shock in someone’s living room.

That is the strange rhythm of volunteer EMS. One moment you are discussing what to buy at the supermarket, the next you are standing beside a critically ill patient deciding whether blood, airway control, medication, or transport destination will make the difference. Then, when the patient has been handed over, you return to the station, check the equipment, restock what was used, clean what needs cleaning, and wait for the next set of tones. Medicine is often described as a succession of dramatic moments, but most of the real work is quieter than that. It is recognizing physiology, respecting uncertainty, using the right resource at the right moment, and handing the patient to the next team in a condition better than the one in which you found them. For a physician-paramedic, that is the work, whether it happens in a trauma bay in Boston or on a Saturday morning in a quiet rural town.

Saturday Shift: Oochie Wally, The Fly Car, and a Day With the Real Boss

Good morning, indeed. It is Saturday, finally, and not merely Saturday but the last weekend of August, which always carries with it a peculiar little emotional undertow. Summer is still technically here, the gardens are still producing, the afternoons can still be hot and humid enough to make you question your life choices, and yet there is something unmistakable in the air that says the season is beginning to turn the page. The mornings are a little different, the light has begun to acquire that softer late-summer quality, and there is a subtle suggestion that September is waiting just around the corner with its cooler evenings, football, changing leaves, and the annual New England ritual of pretending that we are somehow surprised when winter eventually arrives. Today, however, is supposed to be beautiful, and I intend to enjoy every bit of it. At 4:00 this morning, Sadie and I were up for our usual morning jog, because apparently we have collectively decided that sleep is overrated and that voluntarily running around in the darkness before sunrise is a perfectly reasonable way for two physicians to begin their Saturday. It was actually a beautiful morning for it, and once we finished our run, we took the dogs out so they could stretch their legs and conduct whatever highly classified canine business apparently requires a thorough inspection of the property. There is something particularly peaceful about being outside that early, when the rest of the neighborhood is still quiet and the day has not yet accumulated its noise. No hospital phones, no pages, no EMS radio traffic, no consultants asking questions, no administrators sending emails that somehow require an answer immediately despite having apparently waited until Saturday morning to become urgent. Just the dogs, the cool morning air, and the two of us getting the day started.

Once I came back inside, showered, and regained something resembling human consciousness, I made the questionable decision to check a few emails from work. I know, I know. I can already hear the collective groan from anyone who works in medicine. You tell yourself that you are merely going to glance at the inbox, perhaps clear one or two insignificant things, and then suddenly you are mentally back in the hospital, thinking about patients, operative plans, staffing, documentation, and whatever administrative nonsense managed to crawl into your inbox overnight. Being a trauma and critical care surgeon has a funny way of following you home even when you are technically off. The difference today was that I eventually closed the laptop and reminded myself that I was not going to the hospital. Neither Sadie nor I had our usual physician jobs today, which meant that we were not heading into Boston to spend the day immersed in the controlled chaos of medicine. Instead, we were heading to our other medical workplace, the one where the pager is replaced by a radio, the operating room by a roadside, and the hospital bed by whatever piece of ground happens to be available when the patient needs it. Today was our volunteer day with the town Fire/EMS department, and both of us were scheduled to work as physician-paramedics.

That arrangement is still one of the things I find most satisfying about volunteering. I serve as both the Medical Director for EMS and Commander of EMS for the department, while Sadie serves as Assistant Commander and Assistant Medical Director, so when we are on duty together we occupy a slightly unusual niche. We are physicians, certainly, but we are also licensed paramedics who still actually get on the truck, take calls, perform assessments, establish access, manage airways, interpret physiology, and work alongside everyone else. The distinction matters because I have never wanted the department to become a place where the physician walks through the door and everyone else suddenly puts their brains in a locker. Quite the opposite. The paramedics and EMTs we work with are experienced clinicians in their own right, and our job is not to hover over their shoulders and second-guess every decision they make. The best EMS systems are not built around physician interference; they are built around competent people who understand their scope, know their protocols, recognize when something exceeds them, and have access to physician-level clinical reasoning when it is actually needed. Our volunteers know that Sadie and I are there to support them, not to perform some strange prehospital version of supervisory theater. They make decisions, they practice medicine, and they retain their autonomy. We simply bring another layer of experience to the table, particularly when a patient’s physiology becomes complicated enough that the usual algorithm begins to look suspiciously inadequate.

The guys at the station are always happy when the physician-paramedics are on duty, although I suspect some of that enthusiasm has less to do with our clinical qualifications and more to do with the fact that having two physicians around makes the station an excellent place to obtain unsolicited medical opinions about everything from someone’s blood pressure to whether the coffee is actually fit for human consumption. We also tend to bring a different perspective. A paramedic sees the patient from the prehospital side, a physician sees the patient from the hospital side, and being both means I am constantly thinking about the bridge between those two worlds. I know what the patient will encounter when the ambulance doors open at the trauma bay, what information the emergency physician and trauma team will need, what interventions actually change downstream management, and which pieces of prehospital data are going to matter when the patient is lying beneath the CT scanner or on an operating table. That perspective is useful, particularly when you are deciding whether something should be done now, whether it can wait, or whether doing something simply because you can do it is actually a terrible idea.

And then there is the Fly Car.

The Fly Car was originally conceived as a vehicle to get advanced clinical capability to a patient, but describing it as merely a department-issued Chevy Tahoe would be like describing an aircraft carrier as a large boat. This thing was effectively a million-dollar, climate-controlled resuscitation bay on four wheels, engineered with the sort of equipment that makes an emergency physician look at the inventory and wonder why their department does not have half of it. Custom-molded slide-out trays contained a rolling blood bank of low-titer O-positive whole blood and liquid plasma maintained at controlled temperatures, along with rapid fluid-warming devices capable of bringing cold blood toward physiologic temperature in seconds during catastrophic hemorrhage. Dual-probe wireless ultrasound units communicated directly with rugged tablets, allowing us to assess the lungs, heart, abdomen, and other structures when the mechanism and physiology suggested that an immediate answer might change management. Handheld laboratory-grade analyzers could provide critical electrolyte and lactate information in minutes, which is an entirely different world from the old EMS model of taking a blood pressure, checking a pulse, and hoping the patient looked better by the time you arrived at the hospital.

The medication systems were equally ridiculous by ordinary prehospital standards. Climate-controlled drug vaults contained broad-spectrum antibiotics for situations in which early treatment could matter, sedative and nerve-blocking infusions including agents such as propofol when advanced airway and sedation management required them, thrombolytic therapy for carefully selected acute stroke patients, and blood-thinner reversal agents that would be extraordinarily difficult to carry in a conventional ambulance. Advanced respiratory support included video laryngoscopy, turbine-driven transport ventilation capable of applying sophisticated lung-protective strategies, and automated chest-compression equipment for prolonged resuscitations when manual compressions became physiologically or operationally unsustainable. The surgical inventory was perhaps the most surreal component, with sterile equipment for advanced hemorrhage control, REBOA capability for selected patients with exsanguinating torso hemorrhage, escharotomy equipment for severe circumferential burns, surgical airway supplies, and specialized cranial equipment for extraordinary circumstances involving catastrophic intracranial pressure when a patient might otherwise die before reaching definitive surgical care. None of these tools exists simply because they are impressive. Every piece of equipment has to answer the same question: does having this capability in the field potentially change whether a patient reaches definitive care alive? If the answer is yes, then there is an argument for carrying it. If the answer is no, it becomes expensive decoration.

Of course, before any of that sophisticated equipment came into play, there was the much more immediate matter of getting to the station. The drive from our house to the station is only about three minutes, which is just long enough for a song, a few laughs, and perhaps one mildly questionable decision behind the wheel. I climbed into the BMW M8, fired it up, and almost immediately the station radio started playing “Oochie Wally” by Nas. Sadie turned the volume up as if we were suddenly teenagers rather than two physicians in our early forties heading to a Fire/EMS station before sunrise, and within approximately thirty seconds she was singing along and dancing in the passenger seat. This is one of those moments where I am reminded that marrying a Bavarian pulmonologist has many advantages, but predictability is not necessarily among them. Sadie has never been apologetic about enjoying a good raunchy song, and she has absolutely no problem dancing to music that would make a Victorian grandmother clutch her pearls. So there we were, driving through the quiet early-morning streets in an M8, with a song that probably has no business being the soundtrack to a physician-paramedic shift, while Sadie enthusiastically sang along. I would elaborate further on her performance, but this is a family-friendly blog and I would prefer not to have to explain certain lyrics to someone’s grandmother.

There was, however, something oddly appropriate about the song being our soundtrack as we headed toward the station. Medicine has its own soundtrack, although it is usually the hum of ventilators, the clatter of surgical instruments, the chirp of monitors, the radio traffic of an ambulance, and the peculiar acoustics of a trauma bay at 2:00 in the morning. Songs like “Oochie Wally” belong to a different world, one that reminds you that physicians and paramedics existed as human beings long before they put on scrubs or clipped a radio to their shoulder. The song carried with it that late-1990s and early-2000s energy that seems permanently associated with a particular generation, and there was something fitting about hearing it on a late-August Saturday morning as summer begins its slow retreat. We spend so much of our professional lives moving from season to season through hospital windows that sometimes the calendar becomes abstract. Then you drive through town before sunrise, hear an old song from your younger years, feel the humid August air through the open window for a moment, and suddenly you remember that time is actually moving. The hospital will still be there Monday morning, the trauma pager will still go off, and the ICU will still be full of physiology demanding our attention, but for this particular Saturday, the season was late summer, the road was nearly empty, and Sadie was happily dancing beside me like we had nowhere else to be.

When we pulled into the station, the crew was already there, and the reaction was immediate. Apparently my arrival meant that the “real boss” had shown up. Everyone laughed, and then Sadie, without missing a beat, confirmed that yes, the real boss had arrived and that there was going to be a lot of cleaning today. That announcement was received with approximately the same enthusiasm as a surprise tax audit. There were boos, groans, exaggerated expressions of suffering, and the sort of theatrical outrage that only a group of firefighters and paramedics can produce when someone suggests that their workplace should actually be cleaned. I reminded everyone that I had merely arrived and had not yet issued a single order. Sadie, meanwhile, looked entirely too pleased with herself. She has a particular talent for saying something completely reasonable in a tone that makes everyone else realize they are about to have a less comfortable day.

Medic 1 was staffed by Kevin and Mike, which is about as strong a crew as you could ask for. Kevin is the old guard, the kind of paramedic who seems to have been present at every major EMS evolution of the last several decades. He worked as a medic in Newark before I was even born, which means he accumulated an enormous amount of experience before I had learned to tie my shoes. He has seen the spectrum of prehospital medicine, from the days when EMS was much more limited to the modern era of advanced airway management, sophisticated cardiac care, hemorrhage control, and increasingly complex protocols. He is retired now and could easily spend his days doing something considerably more comfortable, but that would require him to stop being Kevin, and I am not convinced that is physiologically possible. He volunteers because the work is part of him. The tattoo on his arm reading Born to Raise Hell is probably the most concise professional biography I could write for him. He is tough as nails, blunt without being cruel, realistic without being cynical, and possesses the sort of deadpan humor that can make a sentence about a profoundly serious medical problem sound like a comment about the weather.

Mike is a completely different flavor of paramedic. He is a master plumber by trade, which means he spends his professional life solving problems that involve pressure, flow, leaks, obstruction, and systems that inevitably fail at the worst possible moment. Frankly, there is a certain poetic logic to a plumber becoming an excellent paramedic. Both professions involve understanding systems rather than merely memorizing isolated facts, and Mike has that ability in spades. He loves the town and the department enough that he went through the work of obtaining his paramedic license, and he has become one of the strongest clinical medics I have had the pleasure of working with. He has an uncanny ability to look at a patient and strip away all the extraneous noise. His favorite clinical skill may be identifying bullshit, and he is remarkably good at it. Mike can listen to a patient give a ten-minute explanation of why they are perfectly healthy while simultaneously observing their respiratory rate, skin perfusion, work of breathing, mental status, and the way they are sitting in the stretcher, and somehow arrive at the correct conclusion before the patient has finished their story. His humor is extraordinarily dry, his realism is almost surgical, and he has perfected the art of saying something hilarious without changing his facial expression by even one millimeter.

Then there was me, your usual trauma and critical care surgeon who happens to be a licensed paramedic, which is an occupational combination that makes perfect sense to me and almost nobody else. My professional life tends to exist at the intersection of catastrophe and physiology. In the hospital, I spend my time dealing with the consequences of trauma, hemorrhage, shock, respiratory failure, sepsis, and the myriad ways the human body can decide that maintaining homeostasis is no longer worth the effort. Out here, the challenge is different. We have fewer resources, less certainty, fewer diagnostic tools, and a moving target in terms of geography and time, yet the underlying physiology has not changed. Blood pressure still falls when circulating volume disappears. Oxygen delivery still depends upon cardiac output and arterial oxygen content. A patient with an occult hemorrhage does not care whether the blood loss occurred in a Level I trauma center or beside a rural road. The body obeys the same rules everywhere.

That is ultimately why I enjoy these days so much. The station is relaxed, the people are funny, the coffee is questionable, and somebody is always threatening to put somebody else on a cleaning assignment, but underneath the humor is a remarkably serious group of people who have chosen to spend their free time helping strangers. They do not have to do this. Nobody becomes a volunteer EMT or paramedic because they thought it would be an easy way to spend Saturday. They do it because somewhere along the way they discovered that being useful to other people matters. The fact that they can joke around, complain about cleaning, make fun of one another, and still switch immediately into clinical mode when the radio tones drop is one of the things I respect most about them.

And today, at least for a little while, we get to enjoy the quiet before the radio decides otherwise. There is something almost ritualistic about a Saturday EMS shift. You arrive, check the truck, check the medications, check the equipment, make sure the oxygen cylinders are where they are supposed to be, make sure the cardiac monitor is ready, verify the airway equipment, review the blood products, look over the Fly Car, and then settle into the peculiar rhythm of waiting. Sometimes the radio remains silent for hours. Sometimes the first call comes before the coffee is finished. Sometimes you spend the day responding to relatively straightforward medical complaints. Sometimes the call that comes across the radio sounds mundane and turns out to be anything but mundane. EMS teaches you very quickly that dispatch information is merely a hypothesis.

For now, though, it is Saturday morning, the last weekend of August, and I am exactly where I want to be. Sadie is here, Kevin is here, Mike is here, the Fly Car is ready, Medic 1 is ready, and the station has already been informed that there may be consequences for its cleanliness. The weather looks beautiful, summer is beginning its slow migration toward autumn, and there is something satisfying about spending a day doing medicine in a completely different environment from the hospital. There will be calls, undoubtedly. There will be patients who need us, problems to solve, decisions to make, and probably at least one situation in which somebody says something so dryly funny that the rest of us nearly lose it. That is part of the job.

Eventually, tonight, Sadie and I will leave the station and head home, trading radios and medical equipment for flour, tomatoes, mozzarella, and a bottle of wine. We are planning to make homemade pizza in the outdoor wood-fired pizza oven, which seems like exactly the right way to end a late-August Saturday. There is something wonderfully primitive about cooking dinner with fire after spending the day surrounded by sophisticated medical technology. One moment you are thinking about hemorrhagic shock, airway management, ventilation, perfusion, and advanced prehospital medicine, and a few hours later you are standing beside a glowing oven arguing about whether the crust needs another thirty seconds. After dinner, we will probably settle in and watch a couple of 1990s blockbusters, because apparently neither of us has any intention of allowing nostalgia to die quietly.

That sounds like a pretty damn good Saturday to me.