Cardiology: Back to Basics

This segment is brought to you via guest contributor, Jayson McConnell. 

AN EYE-OPENING EDUCATION

It was a quiet May afternoon working in an a high-volume EMS service. As I was finishing one chart, the tones drop yet again. “Medic 13, we have a priority one run for you on chest pain and shortness of breath.” Just like every other run in my career, I responded to the call without hesitation. Our unit arrived on scene with the local fire department and the patient who had made his way out to the end of the driveway. As I approached the patient, I introduced myself and my partner and I started our assessment. The patient was awake, alert, and oriented. He appeared to be in good health. His skin was pink, warm, and dry. The patient had no problem speaking in long winded sentences and did not have any signs of shortness of breath or difficulty breathing for that mater. I questioned the patient about his chest pain and any other related symptoms. At this time the patient was essentially pain free and looked be back to his normal pre-incident status. The local fire department was dismissed and the patient was assisted to the ambulance for further assessment and in my mind, a possible refusal of transport. At this time the patient was laughing and joking with us, “I think it’s just stress or it’s my way out of my honey do list for the day”. After a brief interview and with some additional encouragement the patient agreed to allow me to apply the heart monitor and check some baseline vitals. The patient’s vital signs were nearly the same as a world class athlete: BP 118/68, RR 12, lung sounds clear and equal bilaterally both anterior and posterior auscultation.  The monitor display showed a heart rate of 68 normal sinus and the 12-lead revealed a left bundle branch block (LBBB) with some slight ST-segment abnormalities.

sgarbossa1

I began to explore his medical history and any possible contributing factors. The patient denied any medical history, didn’t take any prescribed medications, and had no family or lifestyle risk factors for acute coronary syndrome (ACS). At this point, I was running out of ideas. I asked the patient to repeat his story one more time to make sure I had everything correct before allowing him to sign a refusal form. During the third and final question and answer session, the patient decided to mention the near syncope incident that preceded this entire episode. “Oh, I didn’t hear you mention the feeling of almost passing out” I said. With the near syncope, chest pain, and acute shortness of breath, the patient finally agreed to be treated and transported to the hospital. We ran through the standard treatment: aspirin, nitro, and oxygen. The patient continued to be pain free with no other symptoms present through transport. A repeat 12-lead was done en route, strictly due to my own curiosity. LBBB was noted with no additional changes from the first. “I told you, it’s just the stress.” said the patient. As we continued to joke back and forth, the patient appeared to be back to his normal. I told this patient its probably nothing serious. “I don’t believe you are having a heart attack from the 12-leads we have performed.” Pairing my assessment with the patients nonexistence for previous medical history, I truly believed this would be a simple in-and-out for the patient. We pulled in to the hospital and transferred the patient  to the ER cot with a bedside report to the receiving RN and attending ER physician. The ED staff started with all of the normal treatments: lab draws, monitor applied, and a 12-lead.

As I finished up with my signatures and shaking the hand of my patient, the ER physician requested a copy of my 12-leads for comparison. Crap. Did I miss something obvious? Returning to the ER with 12-leads in hand, I began to converse with the physician again. He interrupted our conversation to contact the cath lab and activate the system for emergent cath procedure. As the Physician hung up the phone, I hoped and prayed he would not walk into my patients room and tell him the bad news. I could feel the anxiety set in followed by the palpitations and nausea. The physician returned to the patient’s room with the news, “Sir, you’re having a heart attack”. I hung my head low and departed the emergency room and returned to the ambulance where my paramedic partner was restocking the ambulance. “What’s wrong with you?” he asked. “I somehow just missed a MI on that guy” I replied. A few minutes of silence went by and just as the nausea was letting up, someone tapped me on my shoulder. I turn around to see the ER physician. “Do you know why you missed that one” asked the physician. Before I could produce any response the physician said “it’s because you were never taught to look for those kinds of heart attacks”. The look of confusion and anger must have been plastered all over my face because just moments later the physician smiled, laughed, and said “Follow me, I’ll explain it to the both of you”.

After a brief field education and a new term I had never heard before, I returned to my ambulance more determined than ever.  Sgarbossa? WTF, I thought to myself.  As I look back, I can now answer that questions that I must have asked myself over a hundred times that day.  What just happened was that I had received an incredible education that I didn’t know I needed.  Along with that education, the physician ignited the desire for me to learn cardiology.  Over the next few years I would dive deep into cardiology books, attend multiple cardiology in-services, interview local cardiologists, and download, print, and review any online documents I could find.  What I discovered is that the subject of cardiology is much more complex than what was presented to me in paramedic class.  The purpose of this blog, and the next few blogs that follow, is to explain and expand on some of the information and education I have been able to gather over the past few years.  I want to provide the hard to find and even harder to interpret information along with some addition education of cardiology topics to you the reader.  The plan for this series of blogs is to start at the beginning with heart anatomy including the electrical pathways and the coronary arteries and progress all the way through each type of myocardial infarction (MI) and anything in between.  Along with the breakdown of each category of MI, case studies, actual 12-leads, and video imaging will be presented to help explain the topics from multiple angles.

Back to the Basics

Heart Anatomy

The heart is made up of four chambers, with each chamber completing a specific task each time the heart contracts.  The right side of the heart operates on a low pressure scale and contains the right atrium and right ventricle.  The primary function of the right side of the heart is to receive blood from the body and pump it to the lungs for oxygen and carbon dioxide exchange.  The left side of the heart operates on a high pressure scale and contains the right atrium and right ventricle.  The primary function of the left side of the heart is to receive oxygenated blood from the lungs and pump it throughout the body.

Right Side of the heart

Blood enters the heart through two large veins, the inferior and superior vena cava, emptying oxygen-poor blood from the body into the right atrium. As the atrium contracts, blood flows from your right atrium into your right ventricle through the open tricuspid valve. When the ventricle is full, the tricuspid valve shuts. This prevents blood from flowing backward into the right atrium while the ventricle contracts. As the ventricle contracts, blood leaves the heart through the pulmonic valve, into the pulmonary artery and to the lungs, where it is oxygenated. The oxygenated blood then returns to the heart through the pulmonary veins.

Left Side of the Heart

The pulmonary veins empty oxygen-rich blood fromheart the lungs into the left atrium.  As the atrium contracts, blood flows from your left atrium into your left ventricle through the open mitral valve.  When the ventricle is full, the mitral valve shuts. This prevents blood from flowing backward into the atrium while the ventricle contracts.  As the ventricle contracts, blood leaves the heart through the aortic valve, into the aorta and to the body.  During relaxation, blood flows into the right coronary artery (RCA) and left coronary artery (LCA) to provide blood flow to the heart.

Tracing the Hearts Electrical Pathways

The contraction of the muscle fibers in the heart is very organized and pathwayscontrolled. Rhythmic electrical impulses flow through the heart in a precise manner along distinct pathways and at a controlled speed. The sinoatrial node (1) initiates an electrical impulse that flows through the right and left atria (2), making them contract. When the electrical impulse reaches the atrioventricular node (3), it is delayed slightly. The impulse then travels down the bundle of His (4), which divides into the right bundle branch for the right ventricle (5) and the left bundle branch for the left ventricle (5). The impulse then spreads through the ventricles, making them contract.

The rate at which the pacemaker sends out its impulses, and thus governs the heart rate, is determined by two opposing systems—one to speed the heart rate up (the sympathetic division of the nervous system) and one to slow it down (the parasympathetic division). The sympathetic division works through a network of nerves called the sympathetic plexus and through the hormones epinephrine(adrenaline) and norepinephrine (noradrenaline), which are released by the adrenal glands and the nerve endings. The parasympathetic division works through a single nerve—the vagus nerve—which releases the neurotransmitter acetylcholine.

Coronary Artery Anatomy

Coronary arteries supply blood to the heart muscle and like all other tissues in the body, the heart muscle needs oxygen-rich blood to function.  The coronary arteries consist of two main arteries: the RCA and LCA.  The left coronary artery then splits into two additional main branches: the left anterior descending (LAD) and the circumflex artery (Cx).  To try and simplify the coronary anatomy lets isolate each artery and take an in-depth look.  For this blog we are going to assume normal cardiac anatomy and leave out any of the abnormal cardiac anatomy presentations.

Right Coronary Artery

The right coronary artery emerges from the aorta just a short distance from the heart.  The artery travels in the AV grove giving way to multiple branches until turning posteriorly to supply blood flow to the back side of the heart.  For purposes of simplicity this blog will focus on RCA and the two main branches:  the right marginal branch and the posterior descending artery.  Near the start of the RCA a small artery knows as the sinoatrial nodal artery to supply blood flow to the SA node.  Studies very slightly, but this appears true for approximatly 60% of the population.  In the remaining 40% the sinoatrial nodal branch comes from the LCA.   Continuing down the RCA the right marginal branches off and travels toward the apex and continues to supply blood flow to the right ventriclerca1 and inferior portion of the right and left ventricles.  Next the posterior descending artery wraps around to the back of the heart just after the marginal branch to provide blood supply to the posterior wall of the right ventricle and the posterior and inferior portion of the left ventricle along with the posterior septum wall.  This artery and its main branches will be shown in more detail in a following blog along with video imaging.

Left Coronary Artery

The left coronary artery is tasked with providing blood flow to a slightly larger area.  The left coronary artery emerges from the aorta, and passes between the pulmonary trunk and the left atrial appendage. Under the appendage, the artery divides into the anterior interventricular descending artery (LAD) and the left circumflex arteryreaper-heart-5-300x295-jpg1(LCx).  This division happens fairly anterior and results in a very small LCA compared to the RCA.  The short length of the LCA is actually beneficial in some ways because there is less room for occlusions to happen  resulting in the well known field term “the widow maker”.  The branches of the LCA are more complexed and will require some detailed explanations in an attempt to paint a clear picture.  The first branch of the left coronary artery is the LAD and it travels along the anterior portion of the heart through the anterior interventricular sulcus (AIVS), an anterior groove in between the right and left ventricles and toward the apex.  The branches off the LAD include: the diagonal artery branches and septal artery branches.  The diagonal branches course diagonally on the anterolateral portion of the left ventricle and provide blood flow to large portions of the anterior wall. The first diagonal branch is designated as D1; the second diagonal branch is designated as D2; and so on.  Again for simplicity the focus will be D1 and D2 only.  For anatomy purposes the portion of the LAD between D1 and the LCA split is refereed to as the proximal LAD.  The last 1/3 of the LAD is refereed to as the distal LAD.  The portion of the LAD that is between the proximal and distal LAD is refered to as?  Yep you guessed it, the mid-LAD.  As the LAD courses through the anterior interventricular sulcus it gives off several branches called septal perforators (SP), which supply blood to the interventricular septum.

The left circumflex artery(LCx) originates at the bifurcation of the LCA and passes down the left atrioventricular groove. The LCx branches into smaller branches called Obtuse marginal (OM) as it paslca1ses down the groove. It also gives rise to one or two left atrial circumflex branches that supply the lateral and posterior aspects of left atrium.  Finally the artery wraps around the lateral wall and travels down the posterior interventricular groove giving the posterior descending artery blood supply.

Wrapping it Up

Its obvious that there is a lot of information thrown at you in this blog. For most paramedics, this is probably just review, but we felt this was a great place to start.  The section on coronary arteries was a bit lengthy and detailed and it was planned that way.  To truly understand some of the cardiology topics and myocardial infarcts in the future blogs, a solid understanding of this anatomy will be crucial. We hope this blog was helpful, enjoyable, and beneficial for you, and we hope you stay tuned for our next cardiology blog on STEMI imitators.  As always, comments, questions, and academic feedback are welcome!

Why Your Patient Isn’t Just Drunk

Beer BottlesLet’s start off with a scenario that I am sure all of us are familiar with. You and your partner are dispatched to a reported fall outside of a bar at 0100. As you arrive to the scene, you see an approximate 35 year old staggering around with blood noted on his forehead. The patient tells you that he “only had a couple of beers” and “just lost [his] footing”. He denies any loss of consciousness or neck/back pain. The only visible trauma is a 2” laceration on the right-side of the forehead and you have controlled the bleeding. As you begin to assess the patient’s mentation, he is answering all of your questions appropriately, his vital signs are stable, and he denies any medical hx, current medications, or allergies. You and your partner attempt to coax the patient into moving into the back of the ambulance for further examination. The patient repeatedly tells you “I’m fine” and is refusing further examination and transport to the hospital. Do you allow this patient to refuse?

SOBRIETY V. INTOXICATION

BreathalyzerSo is merely drinking “a few beers” grounds for calling someone intoxicated? At what point can we call someone intoxicated and use the rules of implied consent in treating patients even against their expressed wishes? After scanning several different definitions of intoxication, there are a few disparities. Definitions like this: “a state in which a person’s normal capacity to act or reason is inhibited by alcohol or drugs” (Encyclopedia of American Law) are widely accepted, but where does that leave us? Obviously, these situations are handled differently depending on your medical direction, but here are some things to consider. Sure, your patient may be able to answer all of your questions appropriately, but what is their environment like? What are the chances that if you leave this patient exactly where you found them, that the patient or someone around them will be harmed? What is your patient’s speech like? Are they slurring or able to speak without difficulty? What is their motor function? Are they able to walk with steady gait? Are they aware of their surroundings, or are they going to wander off into traffic without intervention? Is there a chance that maybe their alcohol consumption could be masking other problems?

ALCOHOL, BLOOD, AND HYPOVOLEMIA

Alcohol does two different things to the cardiovascular system. It inhibits platelet aggregation as well promotes platelet aggregation. Yes, you just read that correctly. Alcohol accomplishes two polar opposite things within the blood stream. A way of looking at it is that platelets stick together in the bloodstream from consistent alcohol consumption leaving the chronic alcohol drinker with a higher risk of stroke, MI, PE, etc. The problem from platelet aggregation inhibition comes when there is a source of bleeding within the body whether due to a traumatic or a medical cause. A study linked here, shows that alcohol can actually “inhibits platelet adhesion to fibrinogen-coated surface under flow”. symptoms-blood-clot-knee_d9b3c4b45c84d7f1

So once your chronic alcohol drinker starts to bleed, it is very difficult to get said bleeding under control, BUT that’s assuming that you have discovered the bleeding to begin with. Anyone that has been in the field for any length of time should have a healthy fear and reverence for the intoxicated patient that has fallen and struck their heads. Even if not recently, immediate signs of brain hemorrhage can lie dormant, and for the patient that is potentially already altered, the subtle changes could easily be masked. Due to the corrosive nature of alcohol, chronic drinkers are much more likely to develop intestinal bleeding. There is a communal eyeroll anytime someone complains of hematemesis or melena, but for alcoholics, this is a potentially life-threatening problem that is often blown off in the emergency department and in the prehospital world. Hypovolemia whether due to blood loss or sheer volume depletion because of vomiting from conditions like pancreatitis or being on diuretics like lactulose (commonly prescribed for patients with cirrhosis to assist in filtering out toxins within the body) is a common problem that needs to be addressed. Was that a long enough run-on sentence for you? I promise I can do better. subarach ct

ALCOHOL: THE GREAT DECEIVER

Let’s roll with another scenario here. You and your partner are dispatched to a report of an unconscious party at a private residence. A landlord went over to check in on a tenant and found him “unresponsive” on the ground. The patient is bradypneic and is unable to awake with painful stimuli. The patient wreaks of ETOH, but can you definitely say that this patient is just intoxicated? Can you as a prehospital provider state that the patient did not suffer a cardiac, neurologic, or diabetic event? Can you definitively say that there are no other intoxicating agents onboard; i.e. barbiturates, opiates, etc? Obviously, being unable to prove a life-threatening problem is not a reason to suspect that every intoxicated patient is suffering from one, but as critical thinkers prehospital providers have to be on the lookout for deterioration. We are not advocating for cookbook medicine or performing innumerable diagnostic tests for the sake of doing them, but when clinical and vital signs are not adding up, maybe it’s time to stop assuming that our patient is just intoxicated.

Pediatric Tachyarrhythmias

You are dispatched to a residence on a report of a child with an altered mental status. Upon arrival, you find an 8 year old boy lying on the couch responsive to verbal stimuli. His mother states he had been playing outside today when he came inside and complained of extreme weakness. He laid on the couch to rest and the mother was unable to rouse him.

HISTORY

  • WPW syndrome

MEDICATIONS

  • None

ALLERGIES

  • Penicillin

VITALS

  • BP -90/58
  • HR -190
  • BSL- 98
  • O2 sats – 95% with clear lung sounds

BROSELOW

  • 50 inches tall, 57 lbs (25.9kg)

INTERVENTIONS

  • Monitor applied showing a rapid, narrow complex tachycardia.
  • Oxygen via NC at 2lpm
  • Vagal maneuvers

Attempts to slow heart rate by vagal maneuvers prove inadequate. The pt is seemingly becoming more lethargic. IV 22g is established in the right AC.

  • Adenosine
    • 0.1 mg/kg = 2.6 mg
      • IV
      • Rapid flush with 20 ml saline
    • repeat double the original dose x1 = 5.2 mg

Adenosine proves ineffective in reducing heart rate and child continues to deteriorate in condition.

  • Medical control contacted for Synchronized cardioversion
    • 1 J/kg = 26 j
    • Repeat to 2 J/kg = 52 j

Patient is successfully converted to a normal sinus rhythm. He becomes alert and is able to answer questions appropriately,  though he complains of some weakness and tiredness.

  • Causes of SVT in children

    • Wolff-Parkinson-White syndrome
      • Most common type of SVT in children
      • Extra pathway within the heart’s electrical system that connects the atria to the ventricles
        • Typically only AV node is the connection (causing a short circuit)
      • Most of the time this doesn’t affect the rhythm
        • Early beat (PAC,PVC) will cause the impulse to travel through AV node and back through extra circuit
            • “Dog chasing its tail”
      • Be conscientious of using AV blocking medications (i.e. Adenosine, diltiazem, verapamil, etc.) in A-fib with accompanying WPW; can result in V-Fib; cardioversion is the gold standard for unstable A-Fib with WPW patients

A-Fib wWPW

Atrial Fibrillation with WPW

    • Atrioventricular Reentrant tachycardia
      • 10% of cases of SVT in children
      • “Pacemaker” or extra focus that is located above the SA node and beats faster.
      • Diagnosis and treatment of both are similar to all forms of SVT

pediatric svt

Pediatric SVT

    • Almost all SVT cases have excellent outcomes and quality of life
      • Avoid caffeine
      • Certain medications
    • Generally, no restrictions are necessary unless extenuating circumstances. Activities involving climbing or heights are discouraged due to dizziness/fainting associated with episodes, resulting in a fall.

Anxiety as a Clinical Finding

Anxiety JPEGIt’s 0200. Your shift is dragging on, and all you want to do is go home. You and your partner get called for a complaint of difficulty breathing in an apartment complex. As you roll up to the scene, you see a mid-20s female walking out to your ambulance. You disregard the engine coming to assist you and walk the girl to your truck. She’s hyperventilating and appears markedly anxious. You attempt to coach her through her breathing, assess her lung sounds and hear clear and equal breaths throughout, and note an SpO2 of 98% on room air. She’s just anxious, right? You secure the patient for transport, and transport her to the emergency department with no other interventions. How many of us have done this? Why are we so quick to dismiss anxiety as a non-issue?If you listened to Episode 14: The Suspected Pulmonary Embolism Patient, you can probably see where we are going with this… We are wrong most of the time when we blow off the anxious patient, but we keep doing it…

WHY DON’T WE ASSESS ANXIOUS PATIENTS?

It’s time to cut the bravado bullshit… I remember the first time I did a 12-lead on a 20 year old complaining of chest pain. I would have bet my paycheck that this patient wasn’t experiencing a STEMI, but I did one anyway knowing that there are other things to look out for. dirty harry jpegNone of my co-workers took me seriously. I was called a cookbook medic.  I could have easily documented that my patient that was hyperventilating and experiencing musculoskeletal chest pain and would have gotten away with it. 99 times out of 100, you might be right, but is it really worth it to be wrong that one time? Even if the patient is just experiencing an exacerbation of an underlying psychological problem, when did a mental health crisis stop being classified as a medical problem? Our job is to help figure out any additional causes of these situations, and not to write them off and make them someone else’s problem. 

WHAT MAKES A PATIENT ANXIOUS?

  • COMPENSATED SHOCK
    • One of the most overlooked causes of anxiety especially after a traumatic incident (i.e. MVC, assault, etc.) is the early stage of compensated shock.
    • We tend to brush off patient complaints of anxiety if the evidence of obvious injuries or abnormal vital signs aren’t present immediately.
    • Restlessness is one of the first signs that patients are starting to trend downwards; if we aren’t trending vital signs in the anxious patient, we aren’t doing our due diligence.
  • RESPIRATORY DISTRESS AND HYPOXIA
    • A 2013 study in the journal of Respiratory Care found that patients with COPD and severe nocturnal hypoxemia have been found to experience significantly higher levels of anxiety to the helpless feeling of “suffocation”.
      • As a result of this, it’s not uncommon to see COPD patients on antidepressants and mood stabilizers; don’t ignore their growing restlessness, though. Plan ahead and be ready for the worst.
      • Patients that have experienced medical emergencies know when they are declining, and as a result can start to panic.
    • PE patients frequently don’t show any clinical signs in the prehospital setting beyond anxiety, hyperventilation, and tachycardia before rapidly declining and even arresting. Remember that these patient will continue to have clear lung sounds and even decent Spo2 saturations for awhile.
  • ANXIETY DISORDER
    • For someone who already struggles with an anxiety disorder, how else would you expect them to react when they are encountered with a new stressor, let alone a legitimate medical emergency.
    • The simple fact that someone has a mental illness history is not a reason in and of itself to disregard a detailed assessment; while it is a piece to the puzzle, it is not the entire picture.
  • ARRHYTHMIAS AND HEART FAILURE
    • A little while ago, a friend of the show donated a set of 12-leads from a mid-60s female experiencing PSVT… the only symptom she was experiencing? Anxiety. Yes, I’m being a bit patronizing, but I think we’ve made our point that anxiety is a clinical sign of bad things going on in the body.
    • American Heart Association classifies some of the most common symptoms of arrhythmias as:
      • Dizziness
      • Shortness of breath (often manifesting in hyperventilation)
      • Palpitations
      • Fast heart rates
    • All of these are symptoms that can be caused by just the sheer sympathetic surge from a purely anxiety-driven episodes, but due to the gravity of what else could be causing them, we need to be better investigators.
    • Patient’s that have experienced heart failure leading to pulmonary edema often present with… anxiety, tachycardia, and dyspnea in the form of hyperventilation.
      • We need to be vigilant in our heart failure patients that are experiencing anxiety; prepare for the worst case scenario up to and including EKG monitoring, IV access, nitro therapy, high flow 02/PPV, and possible airway management.
  • HYPER/HYPOGLYCEMIA AND SEIZURES
    • Whether someone is postictal or is experiencing mild AMS due to a glucose related event, having multiple strangers enter your home while you feel out of control of your own body is a scary event.
    • Be calm, be concise, be firm, be respectful.
    • The American Diabetes Association released a study in 2004 that revealed acute hyperglycemic spikes in Type II diabetic patients that can reduce cognitive function and lead to extreme agitation and anxiety.
    • Anybody try to reason with an anxious and agitated hypoglycemic patient? How did that work for you? What were they like once you corrected the hypoglycemia? Night and day difference. 
  • PAIN
    • Have you broken your ankle? Have you had an appendectomy? Talk to someone who has… It’s a horrible experience that makes you feel out of control and miserable. It sounds simple, but sometimes we forget. Controlling pain can help reduce anxiety.
    • A 2001 study in the Journal of Neuroscience even suggests that anxiety amplifies underlying pain.

ASSISTING THE HYPERVENTILATING PATIENT

  • THE PAPER BAG
    • For the few of you that still think that using a paper bag is a good idea to help a hyperventilating patient…please stop. Here’s why. Hyperventilating patients are experiencing respiratory alkalosis. By placing the bag in front of the patient, you remove the ability of the patient to receive oxygen, and they begin to breathe in CO2.
    • IF the underlying etiology is anything beyond purely hyperventilation, the chances of you causing hypoxia and hypercarbia is enormously high! There are several documented cases of patients that have experienced underlying MIs and hypoxemia that have had fatalities linked to this…
  • HYPERVENTILATION SYNDROME
    • We don’t have the technology to diagnose hyperventilation syndrome.
    • We don’t have the technology to diagnose hyperventilation syndrome.
    • We don’t have the technology to diagnose hyperventilation syndrome.
    • Any questions?
    • Hyperventilation syndrome is now starting to be referred to as psychogenic dyspnea.

DIAGNOSTICS

  • EKG MONITORING
    • Placing continuous EKG monitoring on your patient helps you do a couple of things:
    • Discover possible arrhythmias; especially PSVT, bouts of atrial fibrillation/flutter, and WPW.
    • Underlying cardiac strain, ischemia, or MI.
    • S1Q3T3 suggesting pulmonary embolism; even if this phenomenon isn’t present remember that it only appears in approximately 20% of all PE patients.  Sinus tachycardia is the most common presentation of PE.
  • GLUCOSE MEASUREMENT
    • Any patient that is acting anxious or altered needs to have their glucose evaluated. There is enough literature in circulation that supports loss of cognitive function and coping mechanisms due to hyper/hypoglycemia. It takes five seconds, just do it.
  • EtCO2
    • Someone that is experiencing hyperventilation syndrome (pschogenic dyspnea) will more than likely experience a lower EtCO2. Where this comes into play is that patients experiencing lower cardiac output or other signs of obstructive shock and have a lower EtCO2 should be suspected to have a PE.
    • Continuous waveform capnography can show the beginning stages of bronchoconstriction when audible wheeze may not be present.
  • SPO2
    • I’m not going to go into great detail about this now because we will eventually be doing a show about this, but don’t always trust your SpO2. There are delays in readings and hyperventilation may give an overly optimistic view of your patient’s needs.

SUMMARY

  • We do not have the capability to diagnose that someone is just anxious.
  • There are too many other serious conditions that have similar symptoms to panic disorders or psychogenic dyspnea for us to be cavalier about how we treat patients.
  • Are you going to get in trouble for overtreating (within reason) your patients, or for neglecting to do enough?

Why Social Media is Killing EMS

Mike Nerd EMSHumor was never the problem. Anyone who knows me on a personal level knows that I love to laugh. I love pranks. I am kind of a huge nerd. I love the fact that Young Frankenstein has so many applicable quotes at work while talking to my partner. One of my favorite movies is Nacho Libre. My humor isn’t always refined or well thought out. I tell jokes that fall flat, but I keep telling the same ones because they amuse me. Yet, there is a side of me that knows when to turn off the gag reel. Humor is not the problem. 

I have been mulling over how to approach this subject for some time, never finding the right words to say or the right ideas to put together. Today, I feel like I finally have a little clarity. Before I start to write my main body of thought, I want to make an important statement that I want there to be no confusion on. I am a hypocrite. I am not an idealistic person that is sitting in my glass house while throwing stones at everyone else’s. For the last four years I have worked in a high-volume EMS service and have felt the scorching effect of compassion fatigue and burnout. I have said things to my friends, family, and myself that make me cringe to this day. This is a personal topic for me, so allow me to editorialize instead of bringing you a clinical blog.

Social media is perhaps the greatest gift that has been introduced to modern day education, but it is a double-edged sword. If you remember in Episode 6: Social Media and EMS, Stephen and I raved about a lot of the applications that are available to EMS providers now, as well as some of our favorite blogs, chat rooms, and podcasts that we follow. When used in this manner, social media strengthens the medic’s knowledge base by allowing a platform for them to exchange ideas with other providers. So what’s the downside?

BULLYING

Look through any popular blog on Facebook that has anything to do with prehospital care… Not only will you see many unfounded personal opinions, but then you begin to notice the grade school name calling and playground antics. I observed a post in one of these forums. A newer EMT student was questioning the decision making process of the medics that were treating his brother for chest pain. The student provided a list of information for the crew, and was genuinely asking why the crew didn’t listen to him. Some responses were thoughtful, and tried to explain that the majority of providers just want to get a good baseline for themselves before taking bystander reports at face value. Others resorted to this… “Sounds like little girl got her feelings hurt because her first call didn’t go as planned and they weren’t hanging on her every word as an expert“. All of us started somewhere, and I can guarantee you weren’t a rockstar on your first day. There have been entire social media accounts dedicated strictly to mocking newer or inexperienced medics. This helps no one. It shames emerging providers for asking questions, and at the end of the day, the patient is the one who suffers.

NOT EVERYONE DEALS WITH TRAUMA THE SAME WAY

Nobody cares memeBefore I continue my tirade, let me stop and point out the positive strides that are being made in this arena. I can’t stop applauding the efforts of the Code Green Campaign for very publicly opening up the dialogue of PTSD and first responder suicide. It is a problem. In a study conducted in 2012, 4,022 medics in the United States were polled asking if they had ever contemplated suicide or had ever attempted it. 1,383 (37%) pollers stated that they contemplated suicide, while 225 (6.6%) stated that they had attempted suicide in the past. Both of these rates are exponentially higher than the national average… Before telling someone to “get over it” or “it’s part of the job”,1510JEMS_stress_fig1 take a moment and think about your worst day and the help you wished you would have had. Don’t be so quick to invalidate someone else’s experiences. We don’t know what triggers other have. We are all just “one bad day” away from making a life-altering choice without the proper support group. There is no way to tell where on this spectrum someone is.

PUBLIC PERCEPTION

720x405-inline_blurred_paramedic_1afsl9o-1afsl9u

In the spring of 2015, a Russian paramedic took to social media posting some horrendous selfies of her flipping off deceased patients, as well as referring to MVC victims as a reason for hating her job. Granted, this is one isolated incident. The public doesn’t care. The minute the seed is planted that we don’t care about our patients, we lose credibility in the public’s eye. As animosity grows, it is my genuine opinion that we will continue to see violence towards first responders as a whole rise. We are not responsible for others’ actions, but we can quit throwing fuel on the already out of control fire that is violence on prehospital professionals by openly condemning and separating ourselves from these actions.Nurse Twitter Post

Yes, the location was intentionally blurred out as to not to continue to affiliate this hospital with this nurse’s bad choices. What message are we sending by doing this? We don’t care about our patients. This job is about what makes me feel good. Social media has added significant complexity to our jobs, but responding to it like this is killing our profession’s integrity.

PUNITIVE MEDICINE

Narcan PostSince I have entered the field, I have never once been able to select who calls 911 and who doesn’t. I will admit that I have experienced great frustration witnessing a patient that has just woken up from an opiate overdose decide to go back home and shoot up again. My job is not to judge this patient’s life choices, but to treat their condition, regardless of what they do fifteen minutes after I leave. Opiate addiction and overdose in the region I work in is a gigantic problem, but our response should still be one of patient advocacy. Refusing  to give a medication because of a punitive reason is despicable, and it happens. It is a breach of duty. Addiction for many is not a choice. Take a second to stop reading this post, and read this article that highlights what happens to your body throughout the cycle of addiction. Education about these issues is the only way we can move beyond this mindset. Drunk IV memeConversely, providing interventions that are invasive and not necessary isn’t just being an asshole to your patient. It’s abuse. We have all heard the stories about medics cramming an NPA in someone’s nare because they were “faking it”, or starting a 14g IV on a belligerent intoxicated patient for no other reason other than they were being annoying. The more we glorify these posts, the more we desensitize ourselves to what is really happening here. We are betraying the oath we took when we became medics. It is time to stop acting like this humor is cute, amusing, or worst of all acceptable practice. It’s time to start encouraging our brothers and sisters in the field to vent in ways that are therapeutic and constructive, instead of spewing out hateful blanket statements. So, as I am ending my day-consuming rant about the state of personal conduct and social media, I will implore my friends and colleagues (including myself) to take a step back and ask yourselves three questions. 61dcb7a312872a5ad1efee8f77695cc61. Is what I am about to post in line with my core beliefs? 2. Is what I am about to post going to help someone else or hinder them? 3. Is what I am about to post in line with the oath I took when I became an EMT? “The fault, dear Brutus, is not in our stars, but in ourselves, that we are underlings.” – Shakespeare, Julius Caesar

 1e63d561c022e8578bd94ab1b663471a.jpg

Every once in a while, when I feel burned out and cynical, I like to stop and take a look back at what I enlisted to do, and the reason I did it. Here’s a copy of that reminder. I’ll find something else to get on my soapbox  about next week, but I promise, it will at least be something clinical. If you have any gripes, concerns, or comments about this post, you know where to find me.

-Mike

Urban vs. Rural: Can We Just Stop the Pissing Match?

Urban Vs. Rural

The age old debate. Who does it better? From which service can you glean the most information and become the best version of the medic you strive to be? After much research and discussion, it appears we’ve been going about this debate the wrong way. In fact, most would concede that it’s much like comparing apples to oranges.

While there are pros and cons to each type of service, most discussions on the subject appear to be borne out of personal preference.  We’ve compiled a list of considerations for each type of service. Bear in mind, this list is not exhaustive and was accumulated after much dialogue with many providers of each type of service.

Pros for Urban EMS

  • Shorter response times
  • Resources (fire, police, specialized teams) more readily available
  • Familiarization with plethora of patient presentations that could aid in the recognition and treatment of other patients
  • Further opportunity for career advancement due to tiered leadership
  • Familiarity and use of majority of protocols as a whole in respect to frequency of diverse patient presentation

Pros for Rural EMS

  • Typically, a larger scope of practice is made available thanks to longer transport times
  • Because of increase in transport time, more interventions may be initiated and the provider may be able to actually see the interventions work for the patient while still in their care
  • Smaller services may be able to make capital purchases more quickly because fewer physical items are needed
  • Fewer employees with more down time results in closer relationships with coworkers and family-like atmosphere
  • Prolonged periods of time spent with patients requires great critical thinking skills and some creativity to optimize patient care

Each system has so many components, it’s impossible to list the many attributes of those respective providers. Along with that, negative perceptions aren’t always accurate. Lower call volume doesn’t necessarily mean less knowledge. Just as more patient contacts don’t equal a burnt out medic.

Without exception, these types of providers deserve commendation for the unique way they provide care to their patients. Though we all do the same job, it’s unfair to make comparisons when considering the exclusive points that make each type of service its own.

Keep in mind we are all responsible for our own knowledge and continuing education. Training varies from job to job. Some may be more stringent in certain areas or skills while others are lax. We should all push ourselves to maintain and continue building our proficiencies whether it’s a job requirement or not. When we focus on our own enlightenment, the other concerns seem less substantial.

At the end of the day, our focus cannot be on our own personal identity as providers, but on what we can do for our patients…

Levophed Infusion in the Presence of Septic Shock and SIRS

B89ECB67-657F-4570-A5C2-3206FCB56ED5Though dopamine has long been the vasopressor of choice in EMS, recent studies have shown support for the use of Levophed (norepinephrine) in SIRS and septic shock. SIRS, or Systemic Inflammatory Response Syndrome, is an inflammatory state affecting the entire body that oftentimes is a response to infection. SIRS is related to sepsis in that patients with sepsis generally meet the criteria for SIRS in addition to having an infection.

Levophed is classified as an endogenous catecholamine. It is a direct alpha and beta adrenergic receptor agonist. Its alpha effects tend to be stronger than its beta. In addition to its vasoconstrictive properties, it also shows an increase in venous return as well as increased preload. For patients with suspected infection it is important to document findings such as fever, tachypnea, tachycardia, and hypotension. These signs can indicate SIRS.

Patients that are experiencing profound hypotension in relation to these other signs and symptoms should receive fluid boluses immediately. If hypotension is refractory to this, Levophed should be considered. Typically if you have administered a liter of fluid, and you aren’t seeing any type of improvement, more aggressive means should be contemplated.

Septic shock has a mortality rate of 40-70%. We are frequently the patient’s first contact with a medical provider and early recognition is key in timely treatment. There are many protocols in place that may differ from facility to facility in caring for the patient with septic shock. These vary from multiple antibiotics to lab tests and time spent in the hospital.

As EMS providers, we generally provide care that is needed immediately in the prehospital setting to insure the patient is delivered safely and (hopefully) in better condition to the hospital. So, it’s no stretch of the imagination to predict that most providers that may have a short transport time would prefer to leave the Levophed infusion to the hospital. There are many factors in considering this: being uncomfortable with drip rates and/or medical math, or a critical patient that would benefit from immediate transport, among other things. Though each case will be different, it is judicious to consider using Levophed if a patient meets the above criteria. Transport need not be delayed to start the infusion. Many services provide detailed directions because it is a lesser used infusion. There are also many apps and drug calculators available to EMS providers to safeguard a proper administration. Below, we have attached a simple calculation chart with the most common setup regionally. Keep in mind that it will differ from service to service.

DRUG CALCULATION FOR MCG/MIN

______ mcg/min   X   60   ÷   _____ mcg/mL   =   ______mL/h

 Dosage                                     concentration                    pump setting

IF YOU RECEIVE A PATIENT ON A PUMP ALREADY

______ mcg/mL   X   ______ mL/h   ÷   60   =   ______ mcg/min

Concentration                    pump setting                                   dosage

COMMON CONCENTRATION DRIP CHARTS

This chart is strictly for a 4mg (4,000mcg) vial that is mixed in a 250ml bag of D5W.

2mcg

8gtts/min

4mcg

15gtts/min

6mcg

23gtts/min

8mcg

30gtts/min

10mcg

38gtts/min

12mcg

45gtts/min

This chart is strictly for an 8mg (8,000mcg) vial that is mixed in a 250ml bag of D5W.

2mcg

4gtts/min

4mcg

8gtts/min

6mcg

11gtts/min

8mcg

15gtts/min

10mcg

19gtts/min

12mcg

23gtts/min

We hope that this was helpful, but also understand that eyeballing 23gtts/min without a pump can be difficult! Let us know what you think in the comments section; also if your department carries a different concentration we’d love to hear about it so we can get it up here for other providers.

ADDITIONAL READING

Right-Sided 12 Lead and 15 Lead EKGs

We would like to offer a special thanks to the Clinical Department of the Three Rivers Ambulance Authority in Fort Wayne, IN for the use of their training center and equipment in the making of this blog. 

WHEN TO CONSIDER A RIGHT-SIDED 12 LEAD

  • All patients with inferior STEMI (Elevation in II, III, AvF)
  • ST elevation in V1
  • ST elevation in lead III is greater than lead II
  • If no inferior STEMI is detected, but ST elevation in V1 with depression in V2

If a right sided EKG is warranted, simply place leads V1-V6 as you would on the pt’s left side, except place on the right side. V1 and V2 can be left in place as they are already a mirror image. Pay close attention to lead V4R as its placement is most likely to capture evidence of right ventricular infarction. Make sure to label right sided EKG appropriately. For example: V3R, V4R, V5R, V6R.

HOW TO SET UP A RIGHT-SIDED 12 LEAD

IMG_3731

HOW TO LABEL A RIGHT-SIDED 12 LEAD

R-side EKG 001

SPECIAL CONSIDERATIONS OF RIGHT VENTRICULAR INVOLVEMENT

Due to damage done to the right ventricle in this type of infarction, patients may be very susceptible to adverse effects with nitroglycerin administration. If the right ventricle is not working at full capacity, preload is already reduced. Nitroglycerin will further reduce preload by vasodilation. However, it is encouraged that you follow your standing orders and/or contact medical control. Pre-treating the patient with a fluid bonus may be a viable option for potential hypotension.

WHEN TO CONSIDER A 15 LEAD

  • A 12 lead EKG has confirmed an inferior STEMI (Leads II, III, AvF)
  • A 12 lead EKG has confirmed a lateral STEMI (Leads I, AvL, V5, V6)
  • Symptomatic ACS patient with ST depression in leads V1 and V2

Posterior myocardial infarction is associated with 15-20% of STEMI’s. Typically this is seen with inferior or lateral involvement. Posterior MI associated with either inferior or lateral STEMI is much more complicated and exponentially increases likelihood of left ventricular damage and debilitation.

Studies have shown acquiring a 15 lead after the initial 12 lead EKG provided better odds of detection of STEMI before more detrimental side effects were noted in patients. It was also determined a larger pool of patients were selected for thrombolytic therapy than with a 12 lead EKG alone.

At the very least, a 15 lead EKG can determine the extent of possible damage to the myocardium, and it involves simply relocating leads and acquiring another EKG.

HOW TO SET UP A 15-LEAD

IMG_3736

IMG_3733

HOW TO LABEL A 15-LEAD

15 EKG labeling 001

We hope that this was helpful, and as always, if you have any comments, tips, or suggestions, leave it in the comment section. Hope you guys have a safe and happy Friday!

Glucagon: Not Just for Diabetes

Glucagon

You are dispatched to a 911 call for difficulty breathing. Upon arrival, you find a 60YOM sitting in the tripod position. He states he was stung by a bee about 10 minutes ago and began experiencing shortness of breath. The patient is pale and diaphoretic and exhibiting signs and symptoms of shock. During your assessment, the patient states he takes a beta blocker.  You administer 0.3 mg epinephrine IM and 50 mg diphenhydramine with no relief. Additional epinephrine and albuterol show no improvement in patient condition.

What could be causing anaphylaxis refractory to first line medications?

Patients that are prescribed beta blockers are well known to be resistant to the therapeutic effects of epinephrine when treating anaphylaxis. Some of these patients may even be at risk for a hypertensive crisis after epinephrine administration due to largely uncontested vasoconstriction.

TREATMENT CONSIDERATIONS

Glucagon IV will likely be required for this patient. Typically 1-3 mg IV push can reverse the effects of the beta blocker and allow the epinephrine to provide relief. In some cases, patients may need a continuous infusion.

Most emergency services may not have the means nor permission to administer such treatment. If glucagon is available, a quick call to medical control may be advisable. It is prudent to provide the patient with timely transport to a hospital, as their condition will only deteriorate. Though you may have limited options in the field for treating this patient, your thorough assessment and patient report to the receiving facility can save precious time in getting him the help he needs.

GLUCAGON OVERVIEW

Glucagon is most commonly used in the prehospital setting for treatment of hypoglycemia. Usually this is our last-ditch effort to raise the patient’s blood glucose when all other treatment options have failed. As a rule, it is administered IM with a dosage of 1mg. Glucagon stimulates the liver to convert stored glycogen into glucose which, in turn, is released into the bloodstream resulting in an increase in blood glucose levels.

When used as an antidote to calcium channel blocker or beta blocker overdose, glucagon has been shown to have positive chronotropic and inotropic effects. This is in part to its ability to stimulate cAMP (cyclic adenosine monophosphate) synthesis independent of the beta adrenergic receptor that had been blocked by the overdose. In conjunction with supportive care such as IV fluid resuscitation, atropine, and possible external pacing, glucagon has been shown to assist in recovery of CCB or BB overdose.

It is important to keep in mind that routes of administration would likely vary in each circumstance. Glucagon is typically administered IM for the hypoglycemic patient, due to the inability to obtain intravenous access. However, it is most useful in the CCB or BB overdose patient if given IV. It is advisable to monitor the patient for adverse effects from glucagon administration. Most commonly are nausea and vomiting. In other cases, hypertension and tachycardia are noted. In the hospital setting, patients should be monitored and treated for possible hypokalemia. Remember that in all things, it is important to follow your departmental standing orders, but this could be something to address with online medical control. This is certainly not a first line drug that we encourage routine administration of, but on evaluation of your patient’s H/Ts a consideration.

ADDITIONAL READING

 

Nebulizing a Breathing Treatment Through a BVM

How many of us have attempted to pipe a nebulizer treatment through a BVM? I know the few times I have used them are when I have had a very sick pediatric patient that a CPAP mask doesn’t fit on or an asthma/COPD related arrest. Your stress level is through the roof, and one more fine motor task  just adds to it. It feels like you need twenty hands to get all of the pieces to fit properly, and then you always end up missing at least one connecting piece. This is one of those rarely used contraptions that is easy to forget, but when you need it, you typically need it fairly quickly. Here is a quick and pretty easy way to set up a nebulizer through a BVM.

WHAT YOU NEED

IMG_3699IMG_3700IMG_3701

  • BVM
  • Ventilator Elbow
  • “T” Piece
  • Reservoir tubing
  • Oxygen tubing
  • Medication Chamber

STEP ONE

IMG_3702

Connect the “T” piece into the BVM.

STEP TWO

IMG_3703

Connect the reservoir tubing onto the end of the “T” piece.

STEP THREE

IMG_3704

Connect the medication chamber to the bottom of the “T” piece.

STEP FOUR

IMG_3705

Hook up the oxygen tubing to the end of the medication chamber.

STEP FIVE

IMG_3706

Connect your ventilator elbow to the end of your reservoir tubing.

STEP SIX

IMG_3707

Make sure that your ventilator elbow gets capped, as to create a closed circuit.

STEP SEVEN

IMG_3709

Hook up your mask to the ventilator elbow.

STEP EIGHT

IMG_3711

Consider placing a PEEP valve for patients that you believe may need extra pressure support.

THE FINISHED PRODUCT

IMG_3710

When you’re completed with the assembly, your end product should look something like this. Every service carries their own distinct products, so you may have to tinker around with everything to get the perfect fit, but the majority of this stuff is pretty standard commission. We hope that this was a good review, or an idea starter for those of you that have never used anything like this before!