What Happened?!?

Well, quite frankly, I took a blogger break.

It happens from time to time.  One minute you're bustling with ideas, and the next you've got a writer's block the size of Rhode Island.  Then, before you know it, its been 6 months.

Suffice to say, I'm back.  Hopefully we should be getting back to normal here in a bit...

GCP

There Has Got to be a Better Way...

This isn't really a post.  It's not really even a fully formed thought.  It's more of a proto-thought, or a half-formed idea.  You might even call it a gut feeling.  You would be justified in taking this with a grain of salt

With regards to calls for psychiatric issues, I've begun wondering if EMS is perhaps not best suited to respond.  Some would say "Well, GCP, you just don't like going on psych calls."  I won't deny that they aren't my favorite, but that's not the reason.

Last night, my partner and I responded to a psych call.  This by itself is not out of the ordinary in Gotham City.  However, the circumstances of the call were a bit different.  Without going into too much detail, one party requested EMS, stating that the second party (who happened to be an ex) was threatening to hurt himself/herself, as well as the child that the two parties had parented together (are you following me so far?).  We responded, along with several representitives of the Gotham City Police Department.  On arrival, we found the second party who vehemently denied suicidal and homicidal ideations or plans, stated that the first party was lying and that they had been involved in an extended argument recently, and denied any and all physical complaints.  After consultation with the GCPD officers, we all agreed that the second party did not pose a danger to him/herself or others, and we cleared.

As I sat on post in a 7-11 parking lot and wrote the call report a few minutes later, it occurred to me that maybe we're going about this the wrong way.  As a paramedic, my speciality is in treating patients with physical issues, be they of medical or traumatic origin.  While I understand that many psychological issues stem from biological issues of altered brain chemistry or past trauma, the typical psych patient does not actually need emergent medical care, because they are not experiencing a physical issue.  All I do on most psych calls is monitor vitals to insure that the the patient is in no physical danger, and provide an empathetic listening ear on the way to the hospital.

I would also suggest that paramedic school left many of us woefully underprepared for dealing with patients having psychological issues.  We spent a lot of time talking about what the different disorders are, and why they occur, but we did not spend much time learning how to actually help the person experiencing them.  Mostly, we were just told "be sympathetic, caring, try to listen."  However, we were not trained in counseling techniques.

To be fair, there are some patients with psych issues who are also having medical issues.  Or, due to suicidal ideations and gestures, have given themselves traumatic injuries or medical injuries.  These patients absolutly need paramedics, EMTs, and ambulances.  But I'm not really talking about those patients.  Right now, I'm talking about the medically stable patient with depression, suicidal or homicidal ideations, or hallucinations.

My patient last night was not having psycological issues.  But let's pretend, for a mement, that my call was for real suicidal ideations, rather than simply the product of a nasty custody battle.  My call report was full of "medical speak;" I wrote about my physical exam, vitals, past medical history, allergies, and prescribed medications.  All were normal.  I used the tools and training that I, as a paramedic, have.  However, my assessment was not the assessment needed, and did nothing towards diagnosing what the patients problem was.  The problem was not "medical."

And that's why I'm starting to think we're doing patients with psycological issues but no medical problems a disservice by sending paramedics, EMTs, and ambulances to them.  We are not giving them the care they need, despite doing excellent patient assessment and collecting pristine vital signs.  Are we hurting them?  Probably not.  We are, after all, getting them to definative care.  But should we be satisfied with that level of treatment?  Would we be satisfied with that level of treatment for STEMI patients?  Or diabetics?  Or trauma?  I say no.

So what's the answer?  I'm not really sure.  I don't really have an alternative.  My partner and I bounced some ideas around, and I think the best one we came up with consisted of a two-person team in a mini-van; a psychological ambulance, if you will.  Make one of them an EMT so you have some basic medical training on board.  If something requiring a medical response happens on the mini-van, Gotham City EMS is just around the corner (probably literally; we at Gotham City EMS are known for haunting every 7-11 parking lot in the city).  The other crew member on the van should be a counselor.  Someone who can do psych assesments in the field, and maybe start untangling the true issue the patient is dealing with.

I think you could send an ambulance on these calls as well, just as some extra insurence to assess the patient and make sure that this isn't actually a medical problem in disguise.  But I think having a resource which responds with psychological care in the field, as well as the capability for transport to definitive care would be far more effective than sending an ambulance staffed with two medical techniticians who have been given a minimum of training in psycological emergencies.  Let's face it; that's kind of like sending a carpenter with some basic knowlege of pipes to an overflowing bathtub, rather than a fully trained and equipped plumber.

My whole goal in this is the same as for every other patient I treat; to provide them with the best, most effective, and most appropriate care.  Again, this is a proto-thought, and isn't fully thought out yet.  If you have uestions or comments, or would just like to help me refine my thinking, feel free to comment or email me.

Let's Shine the Bat Signal on Sickle Cell Anemia

I’m starting a series of posts on medical and traumatic conditions which the paramedic or EMT will frequently encounter.  One could say that we are going to shine the spotlight on one lucky condition each week.  However, this is Gotham City.  And in Gotham City, a simple spotlight will not do.  Oh no.  We have the “Bat Signal.”  So, each week we will shine the Bat Signal on a different condition and discuss what causes it, what its signs and symptoms are, and how we as pre-hospital providers should begin to treat it.  So, without further ado, let’s shine the Bat Signal on…

Sickle Cell Anemia

Sickle Cell Anemia sounds complicated, but it is actually very simple.  Red blood cells are responsible for carrying oxygen to all the tissues of the body.  They do this by bonding oxygen molecules to a protein called hemoglobin, which also gives blood its distinctive red color.  Normal red blood cells are disk-shaped, with a sunken center.  They look a bit like donuts.  Red blood cells (from here on, I’m going to refer to them as “RBC’s,” mostly so I don’t have to keep writing out the term) do not have a cell nucleus, which gives them their distinct donut shape.  

In this picture, you can graphically see the difference.

In patients with sickle cell anemia, a tiny change in the DNA which contains the instructions for building hemoglobin causes the whole hemoglobin protein to change shape.  This change causes the whole RBC to collapse and become dehydrated.  The end result is that the RBC’s with the different hemoglobin become shaped like crescents, or “sickles.”  

When RBCs sickle, they cannot carry oxygen to the tissues of the body.  This causes anemia and the feeling of shortness of breath.  Anemia is simply a condition caused by not having enough red blood cells to carry the oxygen required by your body’s tissues.  Sickle RBCs also become stiff and sticky, which causes them to stick together.  These cells can block blood flow in the blood vessels which perfuse the patient’s limbs and internal organs.  These blockages cause pain, organ damage, and increased risk of infection.  

How is Sickle Cell Anemia Transmitted?

Sickle Cell Anemia is a genetic disorder, passed from parents to children.  

Before we go much further, we should take a moment and differentiate between “Sickle Cell Disease” and “Sickle Cell Trait.”  In your DNA, you have genes.  Each gene is a chunk of DNA which contains the instructions for one protein.  You have two copies of each gene; one from your father, and one from your mother.  Only one of those copies is used; we call that gene the dominant trait.  The other gene, the recessive trait, is not used.  

Patients with Sickle Cell Trait have two genes which contain instructions for building hemoglobin.  One has the the change that causes blood cells to become sickle shaped.  The other gene is normal and usually dominant, and does not cause sickle shaped RBCs.  Patients with Sickle Cell Trait typically make both normal RBCs and some sickle-shaped RBCs.  Many do not have any complications from sickle cell trait; some, however, do experience pain and other symptoms.  

On the other hand, patients with Sickle Cell Disease have two copies of the gene that causes RBCs to sickle, one from each parent.  Because the gene which causes RBCs to sickle is the only gene available, these patients are far more likely to have problems associated with sickled RBCs.  

Who Gets Sickle Cell Anemia?  And How is it Diagnosed?

All states require every newborn to be screened for sickle cell anemia and for sickle cell trait.  All that is required is a simple blood test at birth.

Individuals most at risk are: 

1. Those of African or African-American heritage.
2. Those from Central and South America, especially natives of Panama.
3. Individuals from the Caribbean Islands.
4. Individuals from Turkey, Greece, Italy, India, and Saudi Arabia.  

Some facts and figures:

1. Sickle cell anemia effects 70.000 to 100.000 individuals in the USA.  Most of these are African-American.
2. 2,000 children are born every year in the USA with sickle cell anemia.
3. Sickle cell anemia is present in 1 of every 500 African-American babies.
4. Sickle cell anemia is present in 1 of every 36,000 Hispanic babies.
5. Sickle cell trait is present in 1 out of every 12 African-Americans.  

Based on these numbers, the chance of you getting someone with either sickle cell anemia or sickle cell trait in the back of your ambulance is extraordinarily high.  

Let’s Talk About Some Signs and Symptoms

Sickle cell anemia may be present at birth.  However, most patients don’t show symptoms until they are at least four months old.  

Symptoms to pay attention to:

1. Shortness of breath.
2. Dizziness.
3. Headaches.
4. Cold hands and feet.
5. Paler than normal skin or mucosa (in the mouth or nose, and around the eyes).
6. Jaundice (yellowing of the skin or sclera of the eyes).
7. Sudden pain throughout the body.

A sickle cell crisis is an acute episode of sudden pain through the body, which often affects the bones, lungs, abdomen, and joints.  Sickle cell crises are caused by sickled RBCs blood blood flow to the limbs and organs, and are the most frequent cause of EMS calls related to sickle cell anemia.  Patients who are dehydrated are at increased risk of experiencing sickle cell crises, as loss of fluid volume increases the chances of blood cells clumping up and causing blockages.

EMS providers should bear in mind that patients with sickle cell disease are at increased risk for a variety of associated conditions.  Big ones are:

1. Hand-Foot Syndrome:  This is mostly found in young children, especially younger than four, and is caused by sickle cells blocking capillaries in the extremities.  This causes pain, swelling in the extremities, and fever. 
2. Splenic Crisis:  The spleen is responsible for filtering dead cells and other “junk” out of the blood.  Sometimes, the spleen traps RBCs that should be in circulation, which causes the spleen to swell.  If too many RBCs are trapped by the spleen, the body can become anemic due to lack of RBCs carrying oxygen to the body’s tissues.  This can require blood transfusions to correct the anemia until the body can make more blood cells.
3. Chronic Infections:  Due to spleen disfunction, patients with sickle cell anemia are more prone to infection.  When infections do occur, these patients have a harder time fighting them off.
4. Acute Chest Syndrome:  Acute chest syndrome is caused by either an infection in the chest, or by sickled RBCs trapped in the lungs.  It can be similar to pneumonia, and typically presents with chest pain, shortness of breath, and fever.  These patients may also have low SPO2 values, and will have chest abnormalities visible on chest x-rays.
5. Pulmonary Hypertension:  When RBCs sickle, they cause damage to the blood vessels in the lungs.  This damage makes it harder to pump blood through the lungs and increases cardiac workload.  This causes increased blood pressure in the lungs, which in turn causes shortness of breath and fatigue.
6. Stroke:  Patients with sickle cell disease are at increased risk of ischemic stroke (due to blockages which prevent oxygenated blood from reaching portions of the brain) and hemorrhagic stroke (caused by sickled RBCs causing damage to blood vessels, which eventually bleed into the brain).
7. Eye Problems:  Sickle cells can damage the blood vessels which perfuse the retina, causing vision problems and blindness. 
8. Priapism:  Sickle cells can also block blood flow out of the penis, which causes prolonged and painful erections.  Persistent erections can lead to vascular damage, which can lead to impotence.
9. Gallstones:  The body breaks hemoglobin down into a protein called bilirubin.  Elevated bilirubin levels lead to the formation of gallstones.
10. Sickle Cell Ulcers:  Not much is known about what causes ulcers to form in patients with sickle cell anemia.  They typically occur in males rather than in females, and are typically found in patients older than 10.
11. Multiple Organ Failure:  Multiple organ failure occurs when at least two major organs fail at the same time due to damage caused by sickled RBCs.  Sighs that this has occurred are fever, rapid heart rate, shortness of breath or other breathing problems, and altered mental status.

How is Sickle Cell Disease Treated?

The long-term goal of treatment in patients with sickle cell disease is to relieve pain, prevent infections, organ damage, and strokes, and to control complications and associated disorders.  Patients are encouraged to remain hydrated, as this helps prevent blockages.  Patients are also typically prescribed antibiotics, especially when an infection has occurred.  Some patients are prescribed antibiotics to prevent infection.  Patients with sickle cell disease are typically prescribed medication for pain management; these can range from over the counter options like tylenol and NSAIDs to strong opioid analgesics such as dilauded.  Many patients also take a drug called hydroxyurea.  Hydroxyurea causes the body to make a version of hemoglobin found in infants, called fetal hemoglobin.  Fetal hemoglobin helps keep RBCs from sickling.  Patients with sickle cell disease should also get routine head ultrasounds, to detect strokes.  Finally, blood transfusions may be necessary to correct anemia.

Prehospital Treatment 

When EMS is called for a patient with sickle cell disease, its typically because the patient is experiencing a sickle cell crisis.  Remember, sickle cell crises are caused by sickled RBCs causing blockages in organs and limbs, which then causes lack of perfusion to tissues.  

You should take a good set of vitals, and take several more during transport to an appropriate facility so that you can establish a trend.  This is a no-brainer.  

If the patient is experiencing chest pain or shortness of breath, put them on a cardiac monitor and a 12 Lead EKG.  This is also a no-brainer; most agencies require a 12 lead for any mention of chest pain.  This will allow you to see any cardiac ischemia, or at very least to rule out a STEMI.  I always take at least two EKG’s; one at the beginning of transport, and one at the end.  This allows me to see if there has been any changes.

If you can, establish an IV.  We have lots of folks with sickle cell anemia and sickle cell trait in Gotham City, and many have crappy veins.  Do your best.  If you are able to get an IV, start running normal saline.  Dehydration makes sickle cell crises worse.  Keep in mind that you don’t want to give too much fluid to patients with renal or heart failure.

If the patient is hypoxic, or says that oxygen therapy is helpful for pain, give the patient supplemental oxygen.  Oxygen administration also maximizes the amount of oxygen in the patient’s blood stream; remember, they’re anemic, which means they don’t have enough blood cells to carry the oxygen their body requires.  By giving them oxygen, we’re trying to do an end-run around the anemia and beat it using quality rather than quantity.  Typically, I give my patients four liters/minute by nasal cannula.

You can consider pain meds.  Bear in mind, most patients who have been diagnosed with sickle cell disease are already on pain meds, and require much larger doses of analgesic than we can give pre-hospital.   Most EMS systems carry either fentanyl or morphine; hypothetically, some might carry diluted.  If you decide that you should give some medication to take the edge off, the doses are:

1. Fentanyl:  1-3 mcg/kg slow IV push, every 20-30 minutes as needed; pediatric dose is 1 mcg/kg slow IV push, also every 20-30 minutes as needed.
2. Morphine:  2.5-5 mg slow IV push, every 5-10 minutes as needed; pediatric dose is 0.1-0.2 mg/kg slow IV push, every 5-10 minutes as needed.  
3. Dilauded:  1-4 mg slow IV push every 3-6 hours; pediatric dose is 1-2 mg slow IV push every 3-6 hours.

Provide symptomatic relief as needed.  Put the patient in a position of comfort.  If your patient is nauseous, consider giving them some Zofran (its better then cleaning vomit out of the back of the truck); dosage is 4 mg slow IV push.  

Transport your patient to an appropriate facility; typically, patients with sickle cell disease know what sorts of treatments work best for them, and have history with one particular facility.

As always, if you have any questions or comments, feel free to share them in the comments or email me.  Enjoy your weekend!  I’ll be out on the streets of Gotham City for the next two days.

Pharmacology Phridays: The "Dope" on Dopamine

Happy Pharmacology Phriday!  We’ve been talking about sympathomimetics, which are drugs which either imitate the actions of the sympathetic nervous system or cause effects in the sympathetic nervous system.  Earlier we took a moment to get a “down and dirty” intro to the sympathetic nervous system and sympathomimetics in general.  Now, we’re going to go into more detail with one of the most widely used sympathomimetic drugs in EMS, dopamine.

The “Dope” on Dopamine (Get It?  Yes?)

So how does it work?  Dopamine is a sympathetic agonist.  In plain speech, this means that it affects the sympathetic nervous system.  Agonist is just a big word for a chemical which binds to a receptor, and causes the receptor to cause a biological response.  Dopamine occurs naturally in the body, and is turned into norepinephrine.  If you want to get technical, it’s the norepinephrine which then binds to receptors, and causes a biological response.  

One of the many cool things about dopamine is that depending on dose, it can cause alpha, beta1, or dopaminergic effects.  Does that sound complicated?  Let’s break that down.  

Alpha 1 receptors cause peripheral vasoconstriction.  In other words, when dopamine binds with an alpha 1 receptor, the blood vessels in the extremities will get smaller.  When Beta 1 receptors are stimulated, they cause the heart to beat with increased force, without causing the rate to increase too much.  If you want to put that in medical terms, you could say that beta 1 receptors cause an increased inotropic effect, without causing an increased chronotropic effect.  Finally, dopaminergic receptors, when stimulated, cause dilation of the renal, coronary, and cerebral arteries.  So in high doses, dopamine increases blood flow to the kidneys, the heart, and the brain.  

What Does Dopamine Treat?

One of the most common uses of dopamine is treating cardiogenic shock.  Recall that cardiogenic shock is hypoperfusion caused by an underperforming heart.  Dopamine can be used to treat cardiogenic shock by causing vasoconstriction in peripheral blood vessels via alpha 1 receptors, which subsequently raises blood pressure.  Dopamine can also work directly on the heart by acting on beta 1 receptors, which causes the heart to squeeze harder.  In my system, one of the times we break out dopamine post-cardiac arrest/post-ROSC if we need to increase a patient’s blood pressure.  

We can also use dopamine to treat septic shock.  Septic shock is also hypoperfusion.  However, instead of being caused by a balky heart, septic shock is caused by toxic bacterial byproducts making the blood vessels become dilated.   We can use those beta 1 properties to make the heart beat stronger, and therefore compensate for the larger container size.  Or, we can use the alpha 1 properties to make the peripheral veins shrink.  

Dopamine is also used to treat prolonged anaphylactic reactions.  An anaphylactic reaction is a massive, overblown immune response which results in distributive and hypovolemic shock.  Recall that hypovolemic shock is hypoperfusion caused by lack of blood or fluid volume, and that distributive shock is hypoperfusion caused by abnormal distribution of blood.  Anaphylaxis causes capillaries to become “leaky,” which allows fluid to move out of the capillaries (which causes hypovolemia and low blood pressure) into the third space (which is “abnormal distribution”).  Again, just like in septic and cardiogenic shock, dopamine’s beta 1 properties to make the heart beat stronger, and therefore compensate for the loss of volume.  Or, we can use the alpha 1 properties to make the peripheral veins shrink, which also compensates for the loss of volume.

Dopamine as several other “odd-ball” uses.  Dopimine can be used as a second method of treatment in patients with symptomatic bradycardia who do not respond to atropine.  Dopamine can also be used to treat hypotension associated with calcium channel overdoses.  Calcium channel overdose causes distributive shock by causing vasodilation, which then causes hypoperfusion.  

Some Basics

The dosing for dopamine is 2-10 mcg/kg/minute, increased for effect to maximum of 20 mcg/kg/minute.  The effect you’re looking for is increased blood pressure.  Dopamine is given as an IV drip.  Lower doses (in the 5-10 mcg/kg/minute range) cause beta 1 effects/positive inotropic effects.  Higher doses (10-20 mcg/kg/minute range) cause alpha 1 effects/peripheral vasoconstriction.

When should you reach for the dopamine?  Indications are: 1)  Hypotension, with a systolic blood pressure between 70 and 100 mmHg not resulting from hypovolemia.  2)  Cardiogenic shock.  3)  Symptomatic bradycardia that does not respond to atropine.  

Perhaps more importantly, when should you NOT reach for the dopamine?  1)  Dopamine should not be used by its self to manage patients in hypovolemic shock without fluids running.  2)  Don’t use dopamine if the patient is allergic to it (duh).  3)  Dopamine should not be given to patients with tumors of the adrenal gland, which is called pheochromocytoma.  

Some things to keep in mind: dopamine can increase heart rate.  It can also induce or make supraventricular and ventricular arrhythmias worse, so it should not be given to patients in SVT, or to patients in ventricular fibrillation.  When dopamine is given in doses over 20 mcg/kg/minute, alpha 1 effects dominate and  its effects become very much like norepinephrine (also called levophed).  Common side effects are nervousness, headache, arrhythmias, palpitations, chest pain, shortness of breath, nausea, and vomitting.  

Dopamine can be deactivated by alkalotic compounds, such as sodium bicarbonate.  If a patient is taking MAOI’s (monoamine-oxidase inhibitors; a type of antidepressant), they should get a reduced dose of dopamine.  Dopamine can cause hypotension if given with dilantin (used to treat seizures).  

As always, if you have edits or questions please don't hesitate to share.  I write this blog for its educational value, both for those who may be able to use the information, as well as for the re-education I get when i research.  As always, follow your local protocols and directives from your medical director.

Pharmacology Phridays: A "Quick and Dirty" Guide to Sympathomimetics

Congratulations folks, it’s Friday!  Granted, for those of us in EMS, weekends do not really mean that much.  However, it’s an important milestone none-the-less, if for no other reason than trying to keep up with the rest of society.  If you’re a reader here, you have another reason to be happy, because today marks the start of “Pharmacology Phridays.”  I’ve decided that I’ll try to profile a different medication you’re likely to encounter in the field every Friday.  These drugs will probably be the ones you’re likely to be using, but I’ll also throw in the odd prescription or OTC medication for giggles once in awhile as well.

Our first Pharmacology Phriday will be a bit of a twofor; you have my partner at work to thank for that.  As we were waiting to pick up a patient from one of our local ICU’s the other day, he began quizzing me on how dopamine works, and why we would find ourselves giving it.  I wasn’t able to answer him with the level of confidence I wanted, so decided it was probably time to hit the books (again) myself.  The more I studied, the more I realized that I should first do a “quick and dirty” look at the sympathetic nervous system and sympathomimetics in general, and then hit dopamine, specifically.  So you’re welcome.

Gotham’s “Quick and Dirty” to the Sympathetic Nervous System

Batman vs. Joker, Parasympathetic vs. Sympathetic...seems about right.

The nervous system is made up of two major parts, the Sympathetic and the Parasympathetic nervous systems.  The parasympathetic nervous system controls most of the things that happen when your body is relaxed, such as digestion, excretion, etc.  You could call it the “feed and breed” system.  On the other hand, the sympathetic nervous system controls all the things that happen when your body is stressed, like increasing your heart rate, increasing respiratory rate, etc; its the "fight or flight" side of the nervous system.  The parasympathetic and sympathetic systems oppose each other, like Batman and the Joker.  If one is being stimulated, the other is being repressed.  We're not going to worry about the parasympathetic system right now, just know that it's there.

The sympathetic nervous system is also called the adrenergic system.  The adrenergic system passes information from the brain to target organs (such as the heart, lungs, and muscles) using cells called neurons, and chemicals called neurotransmitters.  Neurotransmitters pass information from neuron to neuron, and from neuron to target organ by bonding to, or interacting with, small structures in cells called receptors.  When a neurotransmitter binds to a receptor, it causes a biological effect to take place.  So, for example, if the body wants to increase its heart rate due to being pursued by the Joker’s minions, an impulse would be sent from the brain to the heart via the sympathetic nervous system’s neurons.  Neurotransmitters would be released from the neurons which would bind to receptors in the heart muscle myocardium.  That interaction would cause a series of changes which would cause the heart to beat faster.  

In the adrenergic system the primary neurotransmitter, also called a catecholamine, is a chemical called Norepinephrine.  As for receptors, we’ve classified six different types of receptors in the adrenergic system, each of which have different effects when stimulated.  The six kinds of adrenergic receptors are:

1. Alpha 1 Receptors:  When stimulated, cause the blood vessels in the extremities to constrict (the professional way to put this is “peripheral vasoconstriction”).
2. Alpha 2 Receptors:  When stimulated, cause the adrenal glands to stop producing norepinephrine.
3. Beta 1 Receptors:  When stimulated, cause the heart to beat more rapidly, with greater force, with more automaticity, and conduction.
4. Beta 2 Receptors:  When stimulated, cause the blood vessels in the extremities to get bigger (“peripheral vasodilation”).
5. Beta 3 Receptors:  When stimulated, causes body fat to be broken down, and body heat to be produced.
6. Dopaminergic Receptors:  When stimulated, cause dilation of the renal, coronary, and cerebral arteries.  

Weren't You Going to Talk about Sympathomimetics?

Right.  So how does this affect us in EMS?  First of all, its pronounced "sym-path-o-my-met-ics."  As medics, we are able to give a variety of drugs which either simulate the effects of of the sympathetic nervous system on target organs, or directly stimulate the sympathetic nervous system (or the adrenergic system, whichever works better for you) to signal to target organs.  Drugs which either directly cause an effect similar to a catecholamine like norepinephrine, or stimulate the production of catacholamines which then go on to cause the effect are called sympathomimetics (because they “mimic” the “sympathetic” system).  The most commonly used sympathomimetics are epinephrine, norepinephrine (Levophed), isoproterenol (Isuprel), dopamine (Intropine), and dobutamine (Dobutrex).  

We're going to get to know this one very well...

Sympathomimetics are usually used in EMS to treat shock by improving systemic blood pressure.  Recall that shock is hypoperfusion of tissues due to loss of blood volume (hypovolemic shock), problems with the heart, such as the heart not beating at all, not beating fast enough, or not beating with enough force (cariogenic shock), and problems with the vascular container, such as the blood vessels becoming leaky or too dilated either due to massive bacterial infection or nervous damage (distributive shock, with anaphylactic shock and septic shock).  

A quick glance at the various types of receptors will show you that if we stimulate the right receptor, we have our choice of how to raise a patient’s blood pressure because, luckily for us, some sympathomimetics target vein and artery size, while others target the heart itself.  Of those that target the heart, we say that some are positive Chronotropic Agents (which means they cause an increase in heart rate), others are positive Inotropic Agents (which means they cause an increase in the force of cardiac contraction), and others are positive Dromotropic Agents (which means they cause an increase in speed of conduction through the heart’s AV node, which in turn increases heart rate).  

So, to treat a patient who is experiencing shock (with the exception of hypovolemic shock—more on that later):  Option one is to increase systemic blood pressure by increasing peripheral vasoconstriction by stimulating alpha 1 receptors (making the blood’s container smaller).  Option two is we could increase systemic blood pressure by  increasing cardiac output using positive chronotropic/inotropic/dromotropic agents which stimulate beta one receptors (improving the pump).  

The various sympathomimetics (epinephrine, norepinephrine, isoproterenol, dopamine, and dobutamine) all have slightly different properties, which means that they all target a slightly different combination of adrenergic receptors.  So a doctor can fine-tune a patient’s drug therapy depending on a great number of factors.  For those of us who ride ambulances, the options are somewhat more limited.  In my system, we carry dopamine or norepinephrine (Levophed), which we use for all patients who need any kind of sympathomimetic drug therapy.  

Stay tuned—we will dig a little deeper into a specific sympathomimetic tomorrow.

Sources:

Bledsoe, BE and Clayden, DE.  Prehospital Emergency Pharmacology, 7th ed.  Pearson, New York New York, 2012.