Dear EMS Family, 



I think it is fair to say that everyone is getting excited about Push Dose Epinephrine. As a paramedic, when is the last time you started an Epinephrine drip or Dopamine drip? After completing numerous lectures in January for our protocol update, I did an unofficial survey and found out the Epinephrine drip and Dopamine drips are extremely rare in the field.  

When is the last time you had a hypotensive patient who did not respond to an appropriate fluid challenge? This seems to occur much more commonly. Over the last 2 months, our CEs covered the AHA update-and the protocol update.  Perhaps the biggest concern was to ensure providers maintain a MAP of greater than 65 or a systolic greater than 90.  

We have all dealt with an ROSC patient who, we later find out, suffered an anoxic brain injury, only to have their life-support removed and the patient expired. AHA has identified three areas in which this can be reduced: bystander CPR, access to more AEDs rapidly, and maintaining CNS perfusion once ROSC is obtained, with a MAP of at least 65.    

Acknowledging that our use of Epinephrine drips and Dopamine drips are nearly nonexistent, leaves IV fluids as our only response to post ROSC hypotension. The reasons for not using drips vary from, no pumps, complicated math in the field, and simply low-frequency exposure to their use. We needed a serious solution, which did away with math and was simple to use in the field, with a strong safety profile. 

This was presented by Dr. Chris Myers at the regional level, and then all medical directors at the meeting tweaked it to ensure it is used safely, while maintaining concentrations of Epinephrine for other Epinephrine use emergencies. The 1mg ampule of Epinephrine remains the correct concentration for IM Epinephrine utilized for anaphylactic reactions and severe respiratory emergencies. The 1mg in 10cc (cardiac Epinephrine) will still be the concentration for cardiac arrest in a non-shockable rhythm and anaphylactic shock. Remember with anaphylactic shock, the 1mg in 10cc concentration is given at 1cc/minute until there is a return of the radial pulse with a range of .3-.5mg. 

What about all the other shock states not responding to appropriate fluid boluses? The following events warrant the use of push dose epinephrine: 

1. Septic Shock 

2. Neurogenic Shock 

3. Cardiogenic shock 

4. Post ROSC shock 

5. Symptomatic bradycardia 

If you as a provider have started the fluid challenge and the patient is not responding, it would be time to prepare the push dose of Epinephrine, with an incredibly safe concentration of 10ug/cc.  Simply take the ampule of 1mg Epinephrine, draw it out with a filter needle, change the needle and place it into the 100cc bag of D5W, shake the bag and draw out 5-10cc.  Then administer 1cc every 2-5 minutes, until a MAP greater than 65 or a systolic greater than 90. It’s that simple, and here is the beautiful part, providers can now respond to shock safely, accurately, and simply. Even with pediatric shock of the above types of shock, with medical control authorization, it is safe in pediatrics too. The dose is 1ug/Kg, so any child more than 10 Kg gets and adult 1cc.  This means any child older than a year should be at least 10 Kg. In other words, if the child is not responding to fluids, has the above shock states, and is over a year, contact medical control and give the adult dose of 1 cc every 2-5 minutes until you get a systolic greater than (2x age + 70). 

Let’s help our perfusion compromised patients and start utilizing this incredible change to our current protocol. The entire region is behind this and most importantly our patient outcomes will improve. Thanks very much for your time and consideration in this matter. 

Sincerely, 

Don Spaner, MD 

UH EMSI President 

Shock - February 8, 2021

 Shock is the “final common pathway to death.” This month’s director message focuses on various topics related to this lethal condition. Today we will focus on introductory concepts necessary for establishing a foundation to understand clinical manifestations of various shock types and approaches to treatment. The four main classifications of shock are:  

• Hypovolemic 

• Distributive (the overall most common type of shock) 

• Obstructive 

• Cardiogenic 

To best understand shock, we must comprehend normal perfusion at the cellular level. Perfusion involves the transfer of oxygen (from the lungs) and glucose (eaten daily or broken down from glycogen stores in the liver during times of fasting or starvation) via the bloodstream to all our body cells. Cells take in oxygen and glucose and through three complex processes, (glycolysis, Kreb’s Cycle, and Electron Transport Chain) convert oxygen and glucose to carbon dioxide and energy in the form of ATP. Energy is necessary for our cells to function (cellular reproduction, protein synthesis, immunity, repair damages, etc.).  Without energy, cells die and eventually the entire organism dies.   

Notice that carbon dioxide (CO2) is a byproduct of normal metabolism. Oxygen goes into the cell, metabolism occurs, and carbon dioxide is released from the cell. It is transported via the bloodstream to the lungs to be released during exhalation. It can be seen WHY and HOW carbon dioxide production is an index of perfusion. No perfusion means no oxygen to the cells. No oxygen into the cells means no carbon dioxide out of the cells. This is one reason why we measure and monitor carbon dioxide levels in low perfusion states such as cardiac arrest. 

When ROSC occurs carbon dioxide levels rise, often even before the blood pressure rises. Therefore, we monitor CO2 capnography. Metabolism under normal conditions is known as Aerobic metabolism – meaning that oxygen is required. Aerobic metabolism is very efficient AND very productive, yielding 36 molecules of ATP for every molecule of glucose burned.  When oxygen is insufficient in quantity, the body switches to ANAEROBIC metabolism which only produces 2 molecules of ATP per molecule of glucose burned and produces lactic acid.   

Normal perfusion requires a functioning heart to pump the blood to the cells.  The heart must be able to contract effectively and therefore pump the blood with enough vigor; the heart rate must not be too fast or too slow.   Heart valves must be intact to allow the one-way flow of blood into and out of the heart chambers.  When the pump fails, this causes cardiogenic shock. 

Normal perfusion requires healthy blood vessels – the containers of the blood supply. Both arteries and veins are important in the normal perfusion cycle. Arteries carry blood from the heart to all cells, and veins return blood to the heart from the cells. Arteries are thick-walled vessels which can constrict when necessary as a compensatory mechanism to increase the blood pressure to ensure perfusion during times of illness or trauma.  Veins are essential to the perfusion process –if blood is not returned to the heart in adequate amounts, the heart cannot fill. If the heart cannot fill, the heart cannot expel or eject appropriate amounts of blood. Damaged veins remain dilated, therefore causing blood to pool in the lower extremities. Damaged veins also become ‘leaky” thereby resulting in peripheral edema. Damaged or dysfunctional blood vessels (so-called container problem) is the mechanism involved in distributive shock, which includes Anaphylactic, Septic, and Neurogenic shock subcategories. Next week we will discuss distributive shock, which is the most common type among the 4 main shock categories.   

Andrew P. Garlisi MD, MPH, MBA, VAQSF 

Distributive Shock - February 15, 2021

This week, as part of our shock discussion for the month, we will focus on the distributive shock category, which includes septic, neurogenic, and anaphylactic shock sub-classifications.  

Simply put, distributive shock is a problem with the container of the body’s blood supply –the blood vessels.  When the arteries (supply lines TO the cells) are dysfunctional, the cells cannot receive the glucose and oxygen necessary for normal metabolism to occur. ENERGY production is disrupted and CO2 production declines. Cells deprived of oxygen convert to anaerobic metabolism, which is inefficient and produces lactic acid.  

Blood vessel problems include:  

• Inability to constrict (persistent vasodilation)

• Disruption of the vascular endothelial lining resulting in leakage of plasma fluids into the surrounding tissues 

• Multiple uncontrolled intravascular clotting (in the case of sepsis) 

In distributive shock, the central problem involves dilated vessels, leaky vessels, clotted vessels.

Septic shock, in my opinion, is the “STEMI of infectious disease.”  It carries an extremely high mortality rate approaching 50%.  It is the most common cause of admissions into the intensive care unit. It is the most commonly missed type of shock among EMS providers and emergency physicians. Septic shock is the extreme end of the spectrum which initiates as “Sepsis,” defined as a systemic infection resulting in end-organ damage.  

What causes the end-organ damage?  Organ damage is most commonly caused by the consequence of an overwhelming immune-inflammatory reaction to an infection.  In essence, the body’s own inflammatory reaction which intends to contain and destroy the pathogens also causes damage to blood vessels and organs. During the inflammatory (or immune) response, a cascade of complicated cellular and chemical reactions occur. These cells include antibodies, lymphocytes (both T and B lymphocytes), and macrophages (which ingest or engulf damaged cells and pathogens). A variety of chemicals, generally referred to as cytokines, are also released. With sepsis and septic shock, the inflammatory reaction is often “exaggerated” or “out-of-control” resulting in harm to blood vessels and organs.  The clinician recognizes sepsis when SIRS criteria are present AND when there is suspicion of an infectious process.  

SIRS criteria: 

• Temperature > 38 or < 36 C° 

• Heart rate > 90; RR > 20 or PCO2 < 32 

• White blood count > 12,000 

Treatment involves early recognition, O2monitoring (including capnography) as well as IV or IO fluid boluses. If repeat fluid bolus fails, we now have the option in the field to use push dose epinephrine. The dose is 10 micrograms IV/IO.  The dose can be repeated every 2 minutes as needed to generate a mean arterial pressure at least 65 mm Hg. Early antibiotic administration within one hour of diagnosis reduces mortality. Research is currently ongoing for EMS providers to obtain point-of-care lactate levels and provide first-dose antibiotics!

Neurogenic shock is the least understood of all the shocks. It is not the same condition as "spinal shock" which is actually a misnomer. "Spinal shock" is perhaps more accurately termed "spinal stun" or spinal contusion. spinal shock is not a hemodynamic phenomenon. Spinal shock is an injury or stunning of the spinal cord resulting in weakness, paralysis, and/or numbness which eventually resolves. Neurogenic shock often occurs in association with spinal shock. Neurogenic shock is a true hemodynamic shock. It occurs when there is damage to the sympathetic nervous system which usually occurs in conjunction with spinal cord injuries. With damage to the sympathetic "fight or flight" nervous system, the body is unable to increase the vascular tone (unable to promote vasoconstriction) and unable to increase the heart rate and cardiac contractility.  This is because of reduction in output of the sympathetic nervous system neurotransmitters epinephrine and norepinephrine-which is a result of damage to the sympathetic system.    

Patients with neurogenic shock exhibit hypotension and relative bradycardia due to loss of neurotransmitter effect. Neurogenic shock is another example of a shock type for which push dose epinephrine is indicated when fluid bolus fails.  

Andrew P. Garlisi MD, MPH, MBA, VAQSF 

Cardiogenic Shock - February 22, 2021

Today’s discussion will be the final one in the shock series. Cardiogenic Shock is one of the 4 main categories of shock (Cardiogenic, Hypovolemic, Distributive, and Obstructive). Cardiogenic Shock, as the name suggests, is a result of the heart’s inability (the pump) to sustain perfusion and meet the metabolic demands of all cells. There are several reasons how and why the heart can fail to provide adequate perfusion. It will be useful to remember the formula that cardiac output = stroke volume X heart rate.

If the right side of the heart (right atrium and ventricle) cannot adequately fill, then blood cannot be pushed into the lungs via the pulmonary artery for oxygenation. Decreased blood to the lungs means decreased blood returning to the left side of the heart, and decreased blood to the left ventricle means decreased stroke volume, decreased cardiac output, therefore decreased perfusion.  

Anything which interferes with the “filling” process of the right side of the heart also interferes with perfusion. These conditions include valvular heart diseases (tricuspid valve stenosis/regurgitation). Pulmonic stenosis prevents blood from the right ventricle from accessing the lungs, and pulmonic insufficiency causes blood to regurgitate back into the right ventricle from the pulmonary artery. Furthermore, tachyarrhythmias (uncontrolled atrial fibrillation for example) severely shorten the duration of diastole (the relaxation or filling phase of the cardiac cycle). If the heart has a severely reduced relaxation phase, it cannot adequately fill with blood. If the heart cannot fill, it cannot eject an adequate volume to the systemic circulation, and perfusion is impaired. Remember that cardiac output is determined by stroke volume X heart rate. If the heart rate becomes profoundly reduced (severe bradycardia), cardiac output and perfusion suffer.  

STEMI is a common cause of Cardiogenic Shock. Extensive myocardial injury results in dysfunction of the heart muscle. The left ventricle in particular which is larger than the right ventricle and responsible for ejecting blood into the systemic circulation is the main target of acute coronary artery obstruction. With left ventricular injury or infarct (dead cardiac muscle), the left ventricular pumping mechanism can be severely impaired resulting in decreased cardiac output.  Pressure and blood build-up within the heart chambers and eventually the pulmonary veins become over-pressurized, forcing fluids and blood to fill the lungs.  This condition is referred to as Acute Congestive Heart failure with Acute Pulmonary Edema--due to Left Ventricular Failure.  

There are also several conditions which result in Chronic Congestive Heart Failure, which occurs over an extended period. The heart muscle becomes overly stiff and/or thickened due to chronic hypertension and other chronic conditions. Left heart failure produces signs and symptoms referable to the lungs: shortness of breath, cough, orthopnea, paroxysmal nocturnal dyspnea. Signs of right heart failure include jugular venous distention, ascites, and peripheral edema.

Treatment of cardiogenic shock depends upon the underlying cause. STEMI treatment may require anti-platelet medications: Heparin, Nitroglycerin, Balloon Angioplasty, or Coronary Bypass Surgery. Valvular Dysfunction might require valve repair or replacement. Profound Bradycardia may require a pacemaker. Uncontrolled Atrial Fibrillation in a patient in crisis (chest pain, dyspnea, shock) may require acute synchronized cardioversion.  

Hypotension due to cardiogenic Shock is best managed by vasopressors. Push dose Epinephrine 10 micrograms IV/IO has recently been added to our EMS protocols and is indicated for Cardiogenic, Neurogenic, and Septic shock. It is also approved for profound bradycardia with hypotension and for post-cardiac arrest hypotension.

Andrew P. Garlisi MD, MPH, MBA, VAQSF