Why Did I Write a Book?

“We read to find out what we think. We write to find out who we are” -Rick Kreinbring

Writing is a way we gain a 3rd person perspective of our own human experiences. The two themes common across all literature are love and death. Writing describes how we transcend these two limits of our biology: the basic drive to benefit ourselves at the expense of others and what happens to us after we die.

Love is the illogical emotion that binds us together. It seems to run in opposition to our evolution as biological organisms. Biologically, it shouldn’t exist. Humans would be more successful as individuals without love. We would probably be more efficient, reproduce more often, and make more money. Yet pure selfish people tend to not exist. People are almost always a mix of both selfish and selfless actions. They have illogical emotions, preferences, and habits that seem to be at odds with natural selection. Why is that? Writing about the things we love is a way for humans to understand the discrepancy between what makes logical sense and what we actually choose.

Death is the fundamental limit of the human experience. Because no one can come back to life after they are medically brain dead humans cannot know what happens after death. Instead they wrote myths and invented stories about how and why we die! The stories of Greek mythology and the Holy Bible have permeated almost every aspect of our moderns society. For every theme in modern literature involving death (especially Western Literature) there is a corresponding story from Greek Mythology and/or the Bible. Stories such as David and Goliath, Narcissus and the Reflecting Pool, and Cain & Abel are all as relevant today as they were thousands of years ago.

Writing, unlike people, can live forever as long as it is passed down from one generation to another. That means the most important ideas can be learned early by the next generation, giving them a head start in life. Anyone who sits down and writes unconsciously believes they have an accomplishment important enough to pass down to the next generation.

I want my knowledge and experience about anesthesiology to be available to the next generation of physicians. Anesthesiologists have found a way to successfully preserve human life against all odds! And we have the data to prove it. Anesthesia-related deaths in the United States—primarily from Black Swan events– have decreased from 640 per million anesthetics between 1948-1952, to 8.2 per million anesthetics between 1999-2005. This represents a >98% absolute reduction over 50 years. My book is the story of how that happened!

For perspective that means on average one patient dies every 120,481 cases. If I did 3 cases per day every day without taking any days off I would encounter a single death in 111 years. In 2020 that number is probably even lower than 8.2 per million cases. Furthermore, over the last 70 years patients became exponentially more complex, yet anesthesia became exponentially safer. It seems counterintuitive, yet our results speak for themselves.

I wrote my book to find out who I was an a doctor, an intensivist, and an anesthesiologist. Just as a physician is part historian, part practical scientist, and part craftsman my book contains historical anecdotes, explanations of scientific principles, statistical models, and philosophical questions. It combines both art and science to tell the story of modern anesthesiology and more importantly why that story can be used to manage and prevent the never-ending disasters that characterize our modern world.

Intubating COVID Patients in the ICU

What it is like intubating a COVID patient?

Successful COVID intubations require preparation, intelligence, and meticulous attention to detail. These situations have A LOT of synergy: the patients quickly decompensate, are highly infectious, and only the minimum number of people should be in the room.

The SARS-CoV-2 viral pneumonia (infection of the lungs) can cause acute respiratory distress syndrome (ARDS), a constellation of symptoms related to severe lung inflammation. ARDS is also seen in severe pancreatitis, bacterial pneumonia, and rarely influenza. These patients have very little physiologic reserve- meaning they quickly decompensate without aggressive oxygen and ventilatory support.

When I intubate a COVID patient I have to remove their respiratory support devices, such as oxygen masks or high flow nasal cannula, in order to place a breathing tube. The amount of oxygen in their blood falls precipitously. If I don’t get the tube in quickly I will create a very dangerous situation for the patient, myself, and everyone around me.

In emergencies people often lose their cool then make poor decisions. I protect everyone when I can keep the situation calm, linear, and simple. I bring everything I could possibly need into the room because I don’t want additional physicians, nurses, or respiratory therapists exposing themselves to a highly infectious possibly lethal disease. In highly complex situations simplicity and planning are your only hope.

I have to identify all possible emergencies then be able to rescue myself if anything bad happens. Some COVID patients are quite old and sick- one of mine last week had a non-functioning left lung and heart failure! I think of this as buying insurance for myself. I want to be covered in every circumstance I can think of. Sometimes this means I will place an arterial line or additional IVs before intubation. In the world of anesthesia preparation is everything. Once a dangerous situation occurs you have already lost. The greatest victory is that which requires no battle.

Intubating these patients is quite unnerving. After medications are given I use a laryngoscope to visualize the vocal cords. Only my PAPR shield, a few millimeters of plastic, separates me from the virus. It feels like I’m looking down the barrel of a gun. Additionally it is very hard to communicate outside of the room- if something goes wrong it is highly unlikely I will get the help I need before the patient decompensates.

The process starts with me learning everything about the patient, choosing my drugs, and rescue strategies; then donning proper PPE, making sure the nurse and respiratory therapist understand the plan. In the room the ventilator is prepared, drugs are prepared, additional lines are placed if appropriate, then it’s go time! The actual intubation, when all goes well, takes about 15 seconds. Overall it takes about 45 minutes from start to finish, longer if lines are placed.

After the intubation I take off my PPE in a specific manner, clean my equipment with anti-viral disinfectant, then change my scrubs. If i’m in the room for an extended period of time I will also shower. I don’t want to spread COVID in the hospital.

Anesthesiology can be a cruel teacher- there are no participation trophies, only a small margin between life and death. So far I have not caused any emergencies during my COVID intubations…but I can’t help but feel like a turkey awaiting Thanksgiving. Statistics affect everyone. Anesthesiologists say better lucky than good.

Anesthesiology is high-stakes, open-ended chess game: we can’t fully know our opponent, don’t have defined rules, and losing is not an option. We play every day in operating rooms and ICUs. Our profession is more of an art than a science- there is no “correct” way to intubate a COVID patient or do an OR case because every patient is unique. We don’t think in terms of populations because in our world only unique situations exist. Additionally our actions are not reversible- once a drug is pushed it can’t be taken back, once a dangerous situation occurs we have to deal with it, and if we are unable to deal with the complications of our decisions our patients can die within minutes.

My 45 minute COVID intubation was a chess match against uncertainty, fate, and Death itself. The 15 seconds of routine were my game-ending move. Checkmate.

Why I Chose to Self Publish With Help From Scribe Media

After I decided to write a book I set out to learn about the publishing process. I learned there were two primary options: traditional publishing and self-publishing.

Traditional publishing consists of the author sending a book proposal to a large publishing company such as Norton, HarperCollins, or Simon & Schuster. If the company thinks the book will sell it will send the author a contract containing the following:

  1. Lump sum (usually called an advance) for the author to complete the book
  2. Publishing company ultimately controls editing, cover design, marketing, and distribution
  3. Author retains a small percentage of book sales royalties
  4. Publishing company retains majority of book sales royalties

The traditional contract places the liability on the publishing company. They provide the capital for the book. They benefit from high book sales…but also suffer from low book sales. The primary way publishing companies make money is through book sales so their financial and legal priorities are making sure they sell as many books as possible to make as much money as possible.

The other option is self-publishing. In this model the author is responsible for everything, including writing the manuscript, editing, cover design, marketing, and distribution. He or she may hire creative professionals to do all or part of the publishing work for him or her. The author is ultimately responsible for the entire process. He or she bears full financial and legal responsibility: if the book sells well he or she makes money…if it doesn’t he or she loses money.

I chose the self-publishing option because my first priority was creating a high-quality book. Selling copies was a secondary goal. Furthermore author benefits for writing a book go beyond profits from book sales: they include increasing visibility in his or her field, speaking engagements, and other ancillary opportunities. For an author the primary benefits of writing a book are not the volume of book sales. This is why I chose the self-publishing option. I wanted to focus on the quality of my book not pump out safe, processed, mediocre content to sell books.

Luckily for me one of my mentors in residency, Dr. Kaveh Navab, introduced me to a company called Scribe Media. Scribe is a publishing company that specializes in the “back-end” publishing tasks: essentially all of the things first-time book writers like me don’t know how to do including editing, copy editing, proofreading, cover design, copywriting, marketing, printing, and distribution. More importantly they will do all of these tasks for an up-front cost. In the process the author retains full creative and legal control of the process. They will only work with authors who have a tangible target audience, reasonable expectations, and the motivation to survive the arduous process of writing a book.

I chose to work with Scribe because I thought our goal is the same: to create the highest quality book possible. My primary benefits are from writing a high quality book that creates ancillary benefits for my myself. Their primary benefit is me writing a high quality book because it raises the profile of their company, incentives me to recommend them to others, and creates a constructive, profitable business relationship. They get paid the same whether my book sells well or poorly. Our priority is book quality. Book sales are still important, just not the primary goal.

The shift in priorities reflects the changing publishing market of the 21st century. Book sales are conducted primarily online instead of in book stores. Therefore a book that sells only 500 copies but results in millions of dollars in ancillary opportunities for the author is much more valuable than one that sells 10,000 copies without those opportunities. Non-fiction books written by professionals are the most valuable when they are targeted at a specific audience or solves a specific problem. When drilling for oil you don’t pick 20 sites and drill shallow, you pick the best spot and drill deep.

Like the publishing industry the rest of our world is also changing. I decided to write a book because my experiences in anesthesiology give me a unique perspective into the management of those changes- especially synergy, Black Swans, and complex systems. The reality is I may not make any money from this book. I may not even gain additional opportunities. Regardless of the outcome I will be happy as long as my book remains true to my observations, education, and values. Readers can decide the rest. Results are temporary, the process is eternal.

More information about Scribe can be found at https://scribemedia.com/

Book Update Dec 2, 2020

After finishing my first draft (10 chapters and 50K words) I realized I needed to make major structural changes: I deleted the last 3 chapters and added 5 new chapters. The current manuscript is 12 chapter and 47K words. I also changed the title to “Vigilance: An Anesthesiologist’s Notes on Thriving in Uncertainty”.

Now we wait for my publishing company to give feedback then another round of structural editing. Overall I’m happy with the result. I want to write the highest quality book possible- sometimes that means I have to step back and rewrite entire chapters.

Also the cover is being designed as we speak! I’m both anxious and excited to see how the ideas of the book will be communicated in images!

The Birth of Critical Care

Bjorn Ibsen, a Danish Anesthesiologist, had a problem. In the 1900s polio, once a quiet endemic pathogen, evolved into epidemics in Europe and North America. During the 1940s and 1950s the disease paralyzed or killed over 500,000 people every year. Lockdowns, similar to the COVID-19 lockdown in 2020, frequently occurred to stop the spread of the virus. The modern polio vaccine did not exist yet. In early 1952 Copenhagen was preparing for an unusually large polio epidemic. The problem was they didn’t have enough staff, money, or equipment. They were desperate for a solution.

Polio is a neurological disease. Its scientific name, poliomyelitis, is a combination of the Greek words “polio” meaning grey, “myelo” referring to the inside of the spinal cord, and “itis” meaning inflammation. Literally the virus causes inflammation of grey neurons located in the anterior (front) of the spinal cord. The virus is transmitted via fecal-oral route. It replicates in the gastrointestinal (GI) tract of its human host, then spreads to its next victim when the host touches other people or objects without proper hand hygiene. When inside its host it replicates in the GI tract then moves to the spinal cord, where it causes inflammation of motor neurons responsible for voluntary movement of the extremities.

In severe cases the virus can move up the spinal cord into the brainstem, called “bulbar polio”. Bulbar refers to the cerebellum, pons, and medulla; structures at the base of the brain. This disables the nerves responsible for moving the diaphragm and the victim suffocates. The paralysis usually improves over the course of 2 weeks;  however victims may have residual paralysis of their lower extremities. Since 1928 the iron lung, a rudimentary ventilator, was used to breathe for bulbar polio patients until their paralysis improved. Unfortunately for Dr. Ibsen the iron lung had several practical limitations: it was expensive, difficult to maintain, required a dedicated experienced operator, and patients’ secretions were difficult to manage; they sometimes aspirated into the lungs causing a severe chemical pneumonia. And there was only 1 iron lung in the whole city of Copenhagen. Every day 50 patients were admitted to Blegdam hospital and 6-12 of them developed bulbar polio. In the first three weeks of the Copenhagen epidemic 27 of 31 patients with bulbar polio died, an 87% mortality rate. Half of them were children.

Luckily Dr. Ibsen had a plan. First, polio patients who developed the severe bulbar form would be given tracheostomies. Tracheostomies are literally a “stoma”, Greek for “hole” in your trachea. Through the hole a plastic tube, called an endotracheal tube (endo means inside) would be inserted. The plastic tube was connected to a bag mask valve, a rubber bag that could be squeezed to force air through the endotracheal tube into the patient’s lungs. Ventilation could be achieved with easy management of secretions reducing the incidence of aspiration pneumonia close to zero. The bulbar polio patients were organized into a new ward: medical students squeezed the rubber bags for 24 hours a day in 6-8 hour shifts under supervision of doctors and nurses. At the height of the epidemic it had 105 beds. Furthermore he used recent advances in respiratory physiology to measure blood pH (indirect measure of carbon dioxide in the blood) in order in order to optimize their ventilation. From August to December 1952 about 3000 patients were admitted to Blegdam hospital for polio and 345 developed bulbar polio. The mortality rate decreased from 90% to 25% due to Dr. Ibsen’s innovative polio treatment. His use of positive pressure ventilation, organization of patients based on severity of disease, and efficient distribution of labor is considered the world’s first intensive care unit. Dr. Ibsen was the world’s first intensive care physician.

The first US polio epidemic occurred in 1894. 14 years later, in 1908, the cause of these epidemics was identified as poliovirus. The iron lung was invented in 1929 to prevent death from bulbar polio. For the first 42 years of polio outbreaks scientists did not have a way to study the virus; then in 1936 Dr. Peter Olitsky and Albert Sabin grew the virus in human embryonic brain tissue. This was the first time the virus was cultured. Later in 1949 Drs. John Enders, Thomas Weller, and Frederick Robbins grew poliovirus in embryonic skin and muscles cells. Finally in 1952 Dr. Jonas Salk and his team at the University of Pittsburgh invented the inactivated polio vaccine. By 1961, after 9 years of vaccination campaigns, only 161 cases were reported in the United States. 67 years had passed between the first polio outbreak and an effective vaccine.

Many people do not realize the March of Dimes, a charitable organization devoted to improving the health of mothers and babies, was founded by President Franklin Delano Roosevelt in 1938 as “The National Foundation for Infantile Paralysis” to raise money for polio treatment and research. He was afflicted by a paralytic illness at age 39, presumed to be polio, rendering him paraplegic. The name “March of Dimes” was coined by Eddie Cantor, an American entertainer. He popularized a fundraising campaign where anyone could buy a pin for a dime the week before FDR’s 56th birthday in January 1938. Within a week the White House received 40-50,000 letters and about $85,000 in dimes; $1.5 million in 2020 dollars. Over the next 20 years the foundation spent $233 million on polio patient care. About 80% of American polio patients received medical care because of the foundation alone. Because of his leadership in polio treatment and research, in 1946 the US mint placed FDR’s face on the dime, a design still present today. Go find a dime in your pants pocket! See for yourself!

Chapter 8: Beginner’s Luck

“Better lucky than good”

-Physician saying


I will never forget my first day of intern year. My first rotation was hepatobiliary surgery plus I was on general surgery trauma call.

I arrived at the hospital at 530am, then spent the morning rounding on 25 sick hepatobiliary surgery patients while answering pages about newly admitted trauma patients from the night before. I somehow managed to write 25 notes as my pagers continued ringing for the next 16 hours. At 8pm I was in the middle of breakfast when the trauma pager went off. I rushed to the emergency department.

By the time I got there the senior surgical resident had already intubated the patient and my attending was examining the abdomen. He looked up, turned to the senior surgical resident and said: “let’s go to the OR”. I learned later the patient was a young woman with several gunshot wounds to her abdomen. She needed emergent surgery to explore her abdomen then repair the damage. After my attending and senior resident went to the operating room I answered the 10 pages that accumulated over the last 45 minutes. When my pages were finally taken care of, and I ate lunch at 11pm, the trauma pager went off yet again.

Before my senior resident and attending could arrive my junior resident and I met at the trauma bay. Suddenly 6 people burst though the glass receiving doors leaving a trail of blood behind them. The patient was ghost white. Blood was slowly oozing out of 4 stab wounds in her abdomen. Tonight was not a good night to be an abdomen. I looked with wide eyes at my junior resident- I really hoped she knew what to do! With a slight tremor in her voice she asked for the thoracotomy tray.

A thoracotomy is an incision between the ribs to access the chest cavity in order to perform surgery on the heart and lungs. In the context of a trauma it is used to clamp the aorta to prevent catastrophic bleeding , especially if a large abdominal branch of the aorta is injured. The aorta is clamped just distal to the take-off of the carotid and brachiocephalic arteries, the large blood vessels that supply oxygenated blood to the head and arms. When done correctly all blood is shunted to the arms and brain, buying time to repair the damage to the blood vessel and before the patient loses all of their blood volume or sustains irreversible brain damage.

Branches of the Aorta

I saw a few emergency room thoracotomies in medical school in Detroit- they are brutal, bloody, and have a 99% failure rate. Most of the time patients already have irreversible hypoxic brain injury by they get to the emergency department. My junior resident decided to do a thoracotomy because someone witnessed the stabbing and called 911 immediately; EMS, who happened to be nearby, arrived within 10 minutes, performed high quality CPR, then brought her immediately to the emergency department. If there was anyone who could benefit from an ER thoracotomy it was this patient.

The junior resident and I donned sterile gloves. She made an incision between two ribs, retracted so she could visualize the left thorax, then bluntly dissected until she visualized the heart and aorta. Then she clamped the aorta! Now all blood flow would be redirected ONLY to the head and upper extremities. Furthermore the patient could no longer bleed from her wounds because there was no blood going to her abdomen or legs. I carefully inserted my hand into our patient’s chest and manually pumped her heart as nurses gave blood products. She wasn’t conscious, but she did have a blood pressure. And my hand was pumping blood to her brain. Hopefully we could get to the OR in time.

ED Thoracotomy

After what seemed like an eternity our attending arrived from the operating room- he asked for a scalpel and made a large midline incision in the emergency department! He pulled out the patient’s bowel, examining it for any injury. Then he looked at the major arteries and veins of the abdomen. He carefully returned her bowel to her abdomen, taped gauze over the incision, and helped transport her to another operating room, which apparently was ready. My junior resident and I locked eyes. I knew this was a once in a lifetime case for her. I also knew I had no idea what I was doing in the operating room. Without her asking I offered to take her pager so she could scrub in. Now I was holding 5 pagers and 2 phones!

For the rest of the night I managed half of all the surgical patients in the hospital and saw 5 more consults. Luckily nothing was serious enough to warrant the operating room. I wrote all the notes, ate dinner at 430am, then met my attending and junior resident in the surgical ICU at 5am. I presented my consults with their history of present illness, medical history, and plan. Then I met my fellow intern at 0530, signed out my patients and stumbled home. As I collapsed on the couch, my last thought before falling asleep was: “what in the world did I sign up for?!?!”.

The patient walked out of the hospital 2 months later.

Chapter 7: Fool Me Once

“You don’t get another chance, life is no Nintendo game!”

-Eminem, “Love the Way You Lie”


I once had a patient with polycystic kidney disease. The autosomal dominant disease is caused by mutations in cell signaling genes PKD1, PKD2, and PKD3 genes- named for the disease in which the mutations occur (PKD=polycystic kidney disease). When the genes are defective it causes widespread cyst formation in organs such as the kidneys, liver, and pancreas. It also causes aneurysms in blood vessels. The most recognized sign is enlarged, cystic, non-functional kidneys. If the kidneys become large enough they can cause abdominal pain, acid reflux, and shortness of breath. My patient was a young guy in his 30s with these exact problems. He was scheduled for robotic resection.

Robotic urologic procedures are ominous for anesthesiologists. Most of the time they have no complications and the patients do well. Once in a while a major blood vessel is injured, the bleeding cannot be controlled with the robotic arms, and the patient can bleed out before the robot can be removed from the surgical field for an open surgical exploration. Large blood vessels like the renal artery, renal vein, inferior vena cava, and abdominal aorta can hemorrhage 1L of blood per minute. For perspective the blood volume of a 70kg person is about 5.5L. Sometimes the difference between a successful surgery and massive hemorrhage is measured in millimeters. I’m always impressed my surgical colleagues don’t injure MORE blood vessels. Their results are a testament to their precision.

On the morning of surgery anesthesia was induced and the patient intubated uneventfully. The robot was docked then the urologists carefully dissected the fascial planes around the massive, cystic kidneys. Considering two patients died the previous year from vascular injuries during robotic urological surgery my eyes were glued to the video screen of the surgery. Hundreds of these procedures are done every year- the overall mortality rate is very low. I hoped this case would be in the uneventful 99%. Then I saw pulsating red liquid.

In the next 5 minutes I gave him a liter of IV fluids. The surgeons quickly ligated the bleeding artery. I breathed a sigh of relief as my sphincters relaxed. The rest of the surgery proceeded uneventfully. I extubated him in the OR then transported him to the post-anesthesia care unit (PACU), one floor below. At that time he was breathing spontaneously without support. Upon arrival the PACU about 3 minutes later a nurse plugged in his pulse oximeter- his oxygen saturation was 10%. I immediately ran to the bedside. He wasn’t breathing. I quickly asked for an ambu-bag. As I watched his lips turn blue I bagged oxygen into his lungs. His saturation slowly rose to 100% as the oxygen diffused from his lungs into his blood and circulated around his body.

The next 30 minutes were the scariest of my life. Even though he was breathing on his own and only 3 minutes had passed since traveling from the OR to the PACU I was still nervous. Hypoxic brain injury also only takes minutes. The only thing left to do was wait- as the anesthesia wore off we would know if he had brain damage or not. After what seemed like an eternity he woke up neurologically intact. I went into the hallway and paradoxically laughed with my head in my hands. I almost gave my patient brain damage.

As I talked with my attending (and several other attendings) we reviewed everything I did so I could learn from the adverse event. I confirmed my patient was breathing before leaving the operating room, but looking back I did a few things differently. The operating nurse had a trainee so I let her drive the bed to the PACU- I usually drive to watch my patient’s breathing. I asked the OR nurse if there was oxygen in the tank, she said yes- I should have verified it for myself.

Perhaps he obstructed- the soft tissue of the mouth and pharynx loses its tone under anesthesia- sometimes it can prevent proper adequate ventilation. But my patient was breathing appropriately when he left the OR! Perhaps there was no oxygen in the O2 tank? Perhaps it wasn’t turned on? Perhaps he simply obstructed and I did not catch it because I didn’t drive the bed? I have taken thousands of patients to the PACU without this complication. Some I watched, some I didn’t. Some I checked the O2 tank myself, some I didn’t. Most I drove, some I let my medical student or a nursing student drive. What is the lesson?

Anesthesiology has changed significantly since the 1940s. Before pulse oximetry and capnography anesthesiologists would literally watch their patients breath. Small barely perceptive changes in their chest excursion and breathing patterns were the only differences between adequate and inadequate ventilation. Modern anesthesia is safer than anesthesia in the 1940s due to better technology, monitors, and drugs- and anesthesiologists who know how to apply those complex tools to ambiguous clinical situations. Some days I feel like a modern anesthesiologist doing dangerous cases on complex patients without complications. And some days I feel like an anesthesiologist in the 1940s, watching my patient breathe, praying he will wake up without brain damage.

The next day I did a cardiac catheterization case on a pleasant man in his 80s. He was calm, kind, and grateful for the doctors and nurses- the ideal patient. The case was uneventful. He was extubated in the same manner as my polycystic kidney disease patient. He was also breathing on his own. The nurses and I moved him from the OR bed to the gurney before transport to the PACU. I checked the oxygen tank. It was empty.

Chapter 6: Code Blue

My 2nd month of my 3rd year of medical school was in the medical intensive care unit. During my first week I arrived promptly at 6:45am 7am to help the residents compile data such as vital signs, urine output, and labs from the last 24 hours. At 7:05 AM the overhead paging system announced: “Code Blue Karmanos Cancer Center 4th floor, Code Blue Karmanos Cancer Center 4th floor, Code Blue Karmanos Cancer Center 4th floor”. The residents immediately stopped what they were doing and walked quickly out of the room. Not wanting to be left out I followed them. I had no idea what I was doing or where I was going.

We arrived in the inpatient unit of the Karmanos Cancer Center, a cancer hospital affiliated with and connected to Wayne State University School of Medicine. Our patient was an 89 year old women with stage IV lung cancer metastatic to her brain. She was thin, pale, and frail; her vitality was consumed by the uncontrollable, rapidly-dividing cells in her lungs and brain. Her skin looked like white paper-mâché. The residents told me to “get in line for chest compressions”.

I had practiced chest compressions on a mannequin but this was my first time on a real person. When it was my turn I was shocked how little resistance I encountered. I felt several popping sensations for the next 90 seconds as I manually pumped blood around her body. Suddenly the residents pushed me away from the patient. I thought I did something wrong so I immediately apologized. The resident assertively said: “we have ROSC”, pronounced “rawsk”. I learned later ROSC means return of spontaneous circulation- her heart started beating again.

On rounds that morning the residents joked I “had the hands of God” and “I should be required to do chest compressions on all their patients”. I didn’t understand their joke, so our attending kindly explained it to me. Chest compressions are part of a larger strategy called cardiopulmonary resuscitation (CPR). It is the initial steps of chest compressions and ventilation after a cardiac arrest and before more advanced medical management. She also explained the popping sounds- those were broken ribs. There is a common phrase in residency training when teaching CPR: “if you’re not breaking ribs you’re not trying hard enough”. This phrase exists because high quality chest compressions are the most important factor for survival after cardiac arrest.

Advanced cardiac life support (ACLS) is the medical management of life-threatening cardiovascular emergencies like heart attack, stroke, and cardiac arrest occurring after CPR. It is taught to every resident physician in the hospital because when emergencies occur we are the ones who direct care. ACLS is a way for strangers to coordinate effective emergency medical care within seconds of arriving at the bedside. The success of ACLS is mixed. For in hospital cardiac arrests 25% survive to hospital discharge. That means in 75% of people it would not have made a difference. However it is impossible to tell who that 25% will be. I think of those residents snickering at me during rounds whenever one of my patients die despite high quality CPR and ACLS. The 25% success rate is consistent with my personal experience.

During my first call as an intern I had two patients code at the same time! One was a sick elderly man who recently had a partial lung resection. His oxygen saturation continued to fall despite non-invasive ventilatory support (BiPAP machine). He briefly lost pulses. As I arrived at that code another one was called across the hall. Multiple nurses asked questions at rapid fire speed as my pagers continued to go off. Drowning in pages with no idea what to do I called my junior resident for help. Despite her multiple consults in the emergency departments she came to help me, her pink shoes moving at 2x speed through the hallway.

She took one look at the patient, rapidly read his chart, gave direction to 2 nurses and 2 respiratory technicians, then made 3 phone calls- all in the span of 5 minutes. She told me what happened, what to do about it, and then gave me the phone number of the surgical ICU. She had already diagnosed the patient, ordered the relevant labs and imaging, and arranged for an ICU bed. After that she quickly dealt with the 2nd code before I cold process the first one! She then circled back, gave me an empathetic look and said: “one day you will be in my shoes, don’t worry”, then walked away at 2x speed back to the emergency department.

11 months later I was again on call with the same junior resident. I was paged by a nurse to see a colorectal surgery patient who had increased work of breathing. Her respiratory rate was 45 and heart rate 140. I arrived at the bedside took one look at her, directed 2 nurses, and rapidly absorbed her medical history from the electronic medical record. Then I managed her hemodynamics, ordered the initial laboratory tests and imaging, and arranged for her transfer to the surgical ICU. I presented the patient via phone to my junior resident. She said: “sounds good now come to the ED we have a trauma.”

I diagnosed the patient with a pulmonary embolism. Because she could not have a CT scan for definitive diagnosis, the SICU team preemptively treated her. She slowly improved over the next week. A subsequent imaging study confirmed my initial diagnosis! 2 weeks after my diagnosis I saw my junior resident in the resident lounge. I told her about my first call and most recent one. I had come so far since the beginning of intern year! I thanked her for her patience and guidance over the last year. Admittedly my random expression of appreciation was a little awkward; but I wanted her to know she made a difference in my training. She smiled for a brief second, her eyes softened. Then she told me about 2 recently admitted patients I needed to see on the floor.

I never did buy pink shoes but I did become better at managing cardiopulmonary emergencies. During my PGY-3 year, 4 years after I saw my first code blue, I was called to intubate an elderly man in the coronary care unit, an ICU managing heart failure patients. He had an extensive medical history including heart failure, kidney failure, sleep apnea, peripheral vascular disease, and pulmonary hypertension (pHTN). Any small changes in his physiology can be a disaster- this was bad news for me because anesthetic drugs and intubation cause large changes in cardiac and pulmonary physiology.

At first he was awake and talking. He could ventilate and protect his airway. Initially we decided not to intubate him because the intubation could cause more harm than benefit. For now he was struggling but still breathing on his own. 30 minutes later they called again. Now he was rendered unconscious by the high level of carbon dioxide in his blood.

I knew he was at very high risk of deterioration so I immediately directed the nurses to bring arterial and central line kits- I needed to place invasive lines to monitor his physiology. I quickly guided a needle into his femoral vein- at that point in my training I could feel the difference between the wall of an artery and vein. I threaded a flexible metal guidewire into the vein and removed the needle. I knew he was at very high risk of deterioration so I never took my hand off of his femoral pulse…then his pulse disappeared. With one hand holding a wire in his femoral vein I called a code blue.

I directed my junior resident to place a breathing tube while I led the nurses, respiratory therapists and pharmacists in the proper ACLS protocols. During his 9 minutes of CPR he received epinephrine to raise his blood pressure and stimulate his heart, bicarbonate to decrease the acid content of his blood, and multiple shocks for a deadly heart rhythm called ventricular fibrillation; the whole time receiving high quality chest compressions. While directing the code I managed to place a large central line in his femoral vein as nurses were doing chest compressions. After 9 minutes his heart started to beat again. We had ROSC.

After I talked to the patient’s family and debriefed with the ICU residents and nurses I thought of my first call sitting with my head in my hands while my pagers went off. Maybe my junior resident would be proud? More realistically she would tell me I should have intubated the patient earlier. In cardiovascular emergencies the difference between life and death can be seconds.

%d bloggers like this: