(This is an another article directed more to people who are interested in a medical career than to those already involved. Feel free to read along but I again offer my usual warning that there is nothing profound or exciting to follow and I cannot be held responsible for your boredom. I’m going to try to write this without jargon and I will clearly explain everything which is where the boredom is going to come in for those of you who are in the know. -PB)
Because I am a second year Emergency Medicine Resident, at my program I carry the trauma pager which alerts us whenever a trauma or a seriously sick patient is on the way. As part of my training I get “first crack” at all these difficult patients, those for whom a delay of immediate interventions or decisions could result in serious long-term disability or death.Â Our attendings supervise us but they generally stand back and only correct us if we are doing something either completely wrong or not the way they want to handle things. It is the attending’s patient, not mine,Â even if she just stands in the back with her hands folded across her chest looking bored.Â As we gain proficiency our attendings stand around looking bored more but to start out we are supervised fairly closely.
We really don’t get as many of this kind of difficult patient as you might imagine. We get plenty of really, really sick and injured people but in most cases, they are stable enough where a delay of five minutes or even a half hour might not have too many serious consequences. Most trauma patients that we receive for example, even Level One traumas for which the entire trauma team is mobilized, are stable enough to be taken to the CT scanner before the decision is made by the trauma surgeons whether to operate.Â (On the other hand sometimes the patient is so badly injured, particularly in the case of penetrating abdominal injuries, that they go straight to the operating room with barely a how-do-you-do in the trauma bay).
The trauma pager usually but not always alerts us that a critical patient is on the way and gives us time to prepare.Â In this case, the terse message on the pager screen said “57 M SVT Chest Pain” which meant that the paramedics were bringing in a 57-year-old man with chest pain who the paramedics believed to be in Supraventricular Tachycardia. Supraventricular tachycardia, as the name implies, is a fast heart rate with the pacemaker, a focus of electrically active cells in the heart, located above the ventricles in either the atria (the top chambers of the heart) or the atrioventricular node (the specialized cells between the top and bottom chambers of the heart that allows the transmission of electrical signals). A rapidly firing pacemaker in the atrioventricular node is more correctly called an accelerated junctional escape rythm but it looks somewhat like SVT on an EKG. The heart has a normal physiological pacemaker in the right atrium called the sinoatrial (SA) node but this is not what is usuall driving the heart in SVT.
The heart itself is an electrically active muscle. Unlike skeletal muscle, and with the exception of the SA node, it is not innervated but instead receives its signals to contract via a wave of electrical current generated by the flow of ions into and out of individual heart muscle cells. The SA node is not directly innervated (attached to nerves) but is modulated with neurotransmitters like acetylcholine released from nerve endings of the parasympathetic nervous system (of rest and digest fame) located close to the SA node. The wave of electrical current produces a progressive cascade of electrical depolarization and repolarization of individual muscle cells, sequentially opening and closing voltage-gated ion channels on the cell surface, that allows the flow of sodium, potassium, and calcium to power the cellular machinary that causes contraction and relaxation. Usually, this process is initiated in the sinoatrial node which has a natural automaticity and, absent any external influences from the autonomic nervous system, paces the heart at anywhere from 60 to 100 beats per minute. Every heart cell can pace on its own but since the SA node paces faster, its signals interrupt the pacing potential of the rest through something called overdrive suppression.
I am simplifying things considerably and once in medical school you will learn about the heart in great detail. Like many things in nature, the mechanism of cardiac activity is wonderfully elegant and simple to understand but frightfully complex once you get into the details. The important thing to remember is that measurable electric current flows in the heart. An EKG is a representation of this current as it flows towards an electrode (also called a lead) and is more specifically the magnitude of the vector component of the current (well, actually the electrical potential which is a voltage) coming towards or moving away from the electrode. The EKG, either on a monitor or printed on paper, is a graph of time and voltage with time represented on the horizontal axis and voltage on the vertical axis. By convention, a printed EKG uses twelve leads, looking at the heart from twelve different electrical points-of-view. A cardiac monitor like you see over hospital beds or on a portable defibrillator of the kind carried by paramedics is just an EKG with two or three leads instead of twelve.
A normally functioning heart has a distinctive EKG pattern representing the flow of current in the heart. Abnormalities of the heart cause their own distinctive pattern on the EKG. A Q-wave, for example, is an abnormal downward deflection on the EKG caused by the lead “looking” through dead (and therefore electrically silent) heart tissue to the opposite side of the heart and is something that develops after a heart attack in many patients.
The patient finally arrived and was a reasonably fit-looking middle-aged man sitting up in the gurney who was awake, alert, and in no obvious distress except he was dripping with sweat. His chest pain and sweating had started about fifteen minutes before while working in his home shop sweeping sawdust into a dust pan. The nurses, who actually do most of the work of patient care, hooked the patient up to our monitor and established another intravenous line to complement the one placed by the paramedics as I listened to the rest of the report and looked at the “rhythm strip” printed from their defibrillator. It showed a wide-complex, monomorphic tachycardia with a rate of 280 beats-per-minute, also known as Ventricular Tachycardia or “V-tach,” not SVT as originally advertised (an earlier strip showed what could have been SVT however). A normal heart rate is, as we said, anywhere from 60 to 100 beats per minute with an EKG pattern showing that the beat originates in the SA node. This was a rhyhtm originating in the ventricle and pacing the heart at a rate three to four times normal. It was “wide complex” because the QRS complex, the pattern of electrical force from the ventricle as represented on the EKG, was of a longer duration than a normal QRS indicating that the normal conduction pathway of the left ventricle (which provides the power stroke of the cardiac pump that sends blood to the body) was being bypassed.
The patient’s medical history was unremarkable, at least from our point of view although I have no doubt that many of my physician friends in Europe would have considered him marvelously complex and lucky even to be alive as this kind of patient is a rarity over there. The usual COPD (from emphysema), the usual coronary artery disease with a history of two stents (expanded wire cages in the arteries of his heart to open them up and allow blood flow), and the usual non-insulin dependent diabetes. He was a very pleasant guy and despite his chest pain cracked a few jokes and expressed a little dismay at all the trouble he was causing. Not twenty feet away in another room was a patient a third his age with no medical problems whatsoever and complaining vociferously to everyone and anybody about the slow service in our department which is typical and shows how profound are the generational differences of our patients. Except for his sweating and fast heart rate, the rest of the physical exam was unremarkable. He was on the usual medications for a guy with his medical problems and had no allergies.
Ordinarily we shock (or cardiovert) V-tach immediately if it is unstable. Unstable arrhythmias are those producing symptoms; things like low blood pressure, altered mental status, obtundation (unconsciousness), chest pain, or sweating. In our patient’s case, as he was somewhat stable (talking and perfectly alert) we decided to get everything we needed set up before attempting cardioversion which would certainly be required. Nobody can maintain that kind of heart rate for long. If he became unconscious, for example, maintaining an airway would be important so I set up for a possible endotracheal intubation (insertion of a breating tube through the vocal chords into the trachea) while the nurses drew up a couple of milligrams of Midazolam (Versed) for sedation before we jolted him. I have had patients report that being cardioverted feels like being hit in the chest with a sledgehammer so sedation is the merciful thing to do for conscious patients.
No sooner had the Midazolam been injected into his intravenous line when he rolled his eyes and became limp and totally unresponsive. The monitor still showed V-tach so now it was definitely time to shock him. I set the defibrillator to 100 joules, was reminded by my attending to make sure the machine was set to synchronized cardioversion as shocking at the wrong place in the cardiac cycle can make the problem worse, pressed the charge button, and after checking that nobody was touching the patient, pressed the button with the lightning bolt on it and sent the charge into the pads that had been previously glued to his chest. very satisfying jump from the patient (just like on TV) as every single cell in his heart depolarized, looked around at its neighbors, said “What the fuck?,” and waited for the regular signal coming from the SA node to resume a normal heart beat.
Which is exactly what happened. After a brief period of asystole (or no electrical activity) the monitor showed a normal cardiac rhythm. I made sure that the patient was still breathing and that he had a pulse and not thirty seconds later he opened his eyes and asked how he was doing. In the meantime the cardiology fellow (an internist who is doing additional training to become a cardiologist) who we had previoulsy called arrived to evaluate the patient. V-tach has many causes from electrolyte abnormalities to a tension pneumothorax (a collapsed lung with increasing pressure in the chest cavity compressing the heart) but in this case, given the presentation the most likely cause was cardiac ischemia which was confirmed by a post-cardioversion EKG showing unmistakable signs of myocardial infarction (a heart attack). Ten minutes later and after starting an infusion of an antiarrhythmic agent the patient was on his way to the coronary catheterization lab for an emergent “heart cath.”
Total time in our department? Ten minutes, fifteen at the most which made him both my quickest and most satisfying patient of the week and an official “Perfect Emergency Medicine Patient.” By this I mean that he arrived with an unmistakable chief complaint, was able to give a good history, had solid physical exam findings, and responded to our intervention beautifully. Not only that but he had a quick disposition and was taken off our hands early for definitive treatment. We don’t get many of this kind of patient either.
My next patient was a 14-month-old with a fever, vomiting, and cough. This is the worst kind of patient because while the child probably has nothing more serious than a cold or some self-limiting viral syndrome, the differential diagnosis is long and sometimes we keep a patient like this for hours and hours, eventually obtaining a perfectly normal lumbar puncture (where we stick a needle through the back to obtain spinal fluid to check for potentially deadly infections) before sending them home.