Capnography: Riding the Wave!

In the conclusion of my last post – “Capnography: The Intro” – I stated that “today’s technology provides a numerical value and a waveform that is important in the diagnostic process of your patient.” Some people make the analogy of capnography to electrocardiograms (ECG), although, in my opinion, first of all, capnography can be used for many different body system analyses – remember, it provides us with feedback on ventilation, metabolism, and circulation – and second and best of all, the waveform components are easier to learn than the PQRST structure of the ECG.


So with no further ado, here is the “normal” graphic display of capnography, also known as a waveform:

Point A to B represents the inspiratory phase of ventilation and is referred to as the respiratory baseline. In other words, the patient is breathing in. Easy enough!


The almost vertical line from point B to C denotes the sudden increase in CO2 that occurs as alveolar gas enters the capnograph.  This rise in CO2 from B to C occurs when the expired gas from the anatomical deadspace has been washed out and the capnograph senses the arrival of alveolar gas. It is commonly referred to as the expiratory upslope.


The horizontal plateau from point C to D represents the CO2 concentration in the alveolar gas, and is called the expiratory plateau. This plateau should be fairly horizontal.  Any significant upslope of the expiratory plateau signifies an obstruction in the emptying of the alveoli – most often caused by bronchospasm.  This steep upslope is modestly enough called a “shark-fin” waveform, which adequately describes its morphology.  More on that in another post!


However, here is a picture of the "shark-fin" waveform:

The concentration at point D is termed the end-tidal partial pressure of CO2, or simply the EtCO2.  This point represents the peak concentration of CO2 at the end of exhalation.  The EtCO2 is a numerical value provided to you in millimeters of Mercury (mmHg) and is very important in our clinical assessment and treatment of the patient. For now, just remember that under “normal” physiology, the capnography should display an EtCO2 of 35 to 45 mmHg. Higher values indicate hypercarpnia or CO2 retention, and lower levels, well, that’s called low CO2.  Either way, there are a number of reasons for each, stemming from problems in either ventilation, circulation, or (you guessed it) metabolism.


How about that!!!

Capnography: The Intro

One of my favorite tools in the field is capnography.  This technology has been around since the 1970s and has been used in operating rooms by anesthesiologists as a standard of care since 1991.  EMS has taken this technology and incorporated it into the prehospital setting with more uses than just endotracheal tube (ETT) placement confirmation - although, initially, that was its primary purpose for paramedics.  What is so amazing about this tool is that it not only gives you feedback on the ventilatory status of your patient, if you understand the physiology of the body, you can interpret their circulatory and metabolic processes as well.


In short, capnography gives you feedback on ventilation, circulation AND the metabolic status of your patient.  And it does so, continuously, immediately, basically… breath for breath!

This picture shows the "normal" waveform of a capnograph.

We know the basic concept of respiratory physiology.  We breath in oxygen, which gets circulated to the end tissue and used by cells to create energy.  One of the waste products the cell expels is carbon dioxide (CO2).  CO2 is returned to the lungs via the venous system and then diffused into the alveoli, to be blown off during expiration.


With capnography, you can recognize if either metabolism, circulation, or ventilation changes - and you will note it before blood pressure or oxygen saturation variations occur.  Heck, we can even tell when return of spontaneous circulation (ROSC) occurs during a cardiac arrest with this tool. And now, research is suggesting it can be used as a noninvasive diagnostic tool for metabolic emergencies such as gastroenteritis, diabetic ketoacidosis and more.


To sum up this “new topic” that I will dedicate a few posts to, start by knowing that capnography is simply the measurement of exhaled carbon dioxide.  Today’s technology provides a numerical value and a waveform that is important in the diagnostic process of your patient. And the key to using capnography to its fullest potential is recognizing that it provides us with feedback on ventilation, metabolism, and circulation.


How about that!

No Oxygen, Please!

If you have been in EMS for a while, you may have been told, at some point, that there is no contraindication to oxygen in the emergency setting. Well, let me burst your bubble. I use this little known fact in many of my classes - as a fun fact of a sort.


"Oxygen is contraindicated in Paraquat poisoning!"


Paraquat is the trade name for one of the most widely used herbicides in the world. Paraquat is a quick-acting and non-selective killer of green plant tissue. It is also toxic to human beings. To touch on an earlier post related to neurology, research has shown that it is linked to development of Parkinson's disease, too.


This abstract from the National Center for Biotechnology Information (NCBI) gives a little more specific information on the subject:

High concentrations of oxygen are known to enhance the toxic effects of paraquat in the lung. We have examined the effects of paraquat (2.5 mg/kg or 20 mg/kg subcutaneously) and diquat (10 mg/kg or 20 mg/kg subcutaneously) on mortality and lung pathology in rats exposed to air or to an atmosphere of 85% oxygen. Our results show a 10-fold increase in mortality when paraquat is given to rats placed in 85% oxygen rather than air, but only a 2-fold increase in the lethality of diquat. Lung damage typical of early paraquat intoxication is seen following 20 mg/kg paraquat in air or oxygen, with damage to type I and type II alveolar cells. Selective damage to the type II cell is produced by lower levels of paraquat (2.5 mg/kg) and by 20 mg/kg diquat, both in 85% oxygen, other cell types showed little change. Lung damage is minimal following 2.5 mg/kg paraquat or 20 mg/kg diquat in air, or exposure to 85% oxygen alone. It is suggested that the type II cell may be the primary target cell for paraquat and diquat in the lung. (http://www.ncbi.nlm.nih.gov/pubmed/6933951)

How about that!

D'oh!-PAMINE

In the prehospital setting, they do not provide us with many tools to treat hypotension, but they do provide us with some effective ones.  I always like to stick to basic interventions first - oxygen and trendelenburg - identifying the cause and rapid transport to definitive care; but, what if that is not enough?  The large bore IV with fluid challenge and then dopamine administration comes next.  By this point, I should be getting close to the emergency room.  Easy, right?


I love the drug Dopamine! Effective and interesting to administer in the field.  Weight based drugs that require a drip administration are fun.  We do not have pumps on our trucks, so calculating the drip rate required from the concentration on hand, for the patient’s weight in kilograms, to the desired dose over a certain time period - all in your head - is one of those skills that can quickly impress the FNG (Friendly New Guy).  But you have to know what you are doing!  Each patient must be individually titrated to the desired hemodynamic response.  At the wrong dosage, Dopamine will either be ineffective or dangerous to the patient.


Dopamine, a simple organic chemical in the catecholamine family, plays a number of important physiological roles in the body. As an intravenous medication acting on the sympathetic nervous system, Dopamine produces effects such as increased heart rate and blood pressure. But you know that! However, because dopamine cannot cross the blood–brain barrier, dopamine given as a drug does not directly affect the central nervous system.  On the other hand, I like to joke around that the increased cerebral perfusion pressure will have an effect on the brain. You never know, the patient might even wake up and thank you before you arrive at the ER.  This could be a good time to ask him an important question I have come to contemplate.


"Are you on any MAOIs?"


Why is that important?  Well, once again, I am happy you ask!


Dopamine's onset of action occurs within five minutes of intravenous administration, and with dopamine's plasma half-life of about two minutes, the duration of action is less than ten minutes. If monoamine oxidase (MAO) inhibitors are present, however, the duration may increase to one hour. "D'oh!!!"


I think this means we can inadvertently overdose a patient on dopamine. Maybe that is why my last patient started those runs of VT after the administration?!? The more you know!!!


How about that!


(For my two faithful followers:  If you can recall, I have written about manoamine oxidase inhibitors before - in my post "Do you want some cheese with that MAOI?" In that post, I mentioned a little about the function of manoamine oxidase. MAO inhibitors act by impeding the activity of monoamine oxidase, thus preventing the breakdown of neurotransmitters and endogenous catecholamines, such as dopamine. It is one of my favorite posts.  Check it out. Hope you enjoy it, too.)

P.Y.F.M.O.!!!

Over the years, I have taught a number of continuing education classes on respiratory and airway problems to fire departments in the area.  One of the objectives I like to cover during these classes is prevention of smoke inhalation during structural firefighting.  I am most successful in conveying some medical knowledge to firefighters during this portion, since everyone actually becomes interested.


Understanding the chemical composition of smoke in modern fires is vitally important.  Nasty, deadly chemicals are ubiquitous in all structure fires.  Just understanding how carbon monoxide (CO) and cyanide will sicken a human body is often enough to get the recruits and especially the “old timers” to put their S.C.B.A. masks on - and keeps them on - all the way through the overhaul phase of the operation.


Carbon monoxide will displace oxygen in the blood because it has a high affinity for heme-containing proteins such as hemoglobin, myoglobin and cytochromes. Its affinity for hemoglobin is actually more than 200 times that of oxygen. And then, hydrogen cyanide directly impacts the cells by disabling their ability to convert oxygen into usable energy. Carbon monoxide and cyanide combined are referred to as the “toxic twins.”   That should be enough to make you stay clear from smelling the smoke of a burning building, not to mention the hundreds of other chemicals found in the fine particles that rise up from the incomplete combustion of a home on fire. 

"Putt-Your-*Freaking-Mask-On!!!"

But why are homes today so toxic?  Well, I am happy you ask!


One of the funny side effects of fire prevention efforts of the 1970s are laws that require the utilization of chemicals to prevent fires in homes.  As an example, if you ever look at your furniture, you may find a tag that states:

“This article meets the flammability requirements of the California Bureau of Home Furnishings Technical Bulletin 117."

This should indicate to you that it is the most chemically treated piece of wood and fabric you can find - to protect your family, of course.  You can rest assured; the foam inside your upholstered furniture will be able to resist a flame from a cigarette lighter for 12 seconds without catching fire. However, the fabric it is covered in … not so. WTF!  Once the fabric catches on fire, the flame that the foam is exposed to is much larger than the flame requirement in TB 117.  And now we have all the flame retardant chemicals off gassing during that residential structure fire.


How about that!

May I have some radiation, please?

Glaucoma is one of those diseases we encounter often in the prehospital setting, but don’t do anything about.  The reason is that glaucoma has a slow and gradual onset, and although detrimental to the patient, it is a condition that does not affect airway, breathing, or circulation, and therefore, does not become of much concern to prehospital providers.  We are actually only concerned with knowing which medications we administer that has glaucoma as a relative contraindication.  Since glaucoma is a disease that affects more than 4 million Americans, and is the leading cause of blindness, it is an important possible contraindication to keep in mind.

However, this blog is not about basic facts. It is about interesting concepts!  So let me tell you about some new discoveries concerning glaucoma.

First, researchers have figured out that in response to early stresses on ocular tissue, endothelial cells that line the blood vessels of the eye allow the entry of immune cells known as monocytes into the optic nerve and retina, which end up expressing molecules that damag the nerves—causing glaucoma. The good news is that other researches have figured out a way to prevent this from occurring.

The first hint came from Hiroshima survivors, who, although experiencing countless other health problems from the radiation exposure, tended to not develop glaucoma.  And a decade ago, researchers discovered that a single dose of whole-body irradiation seemed to provide protection against glaucoma.  Now, scientists have discovered that localized and targeted radiation exposures to the eyes of mice that tend to develop glaucoma, provides lifelong protection against this disease. The idea is that radiation changes how those endothelial cells respond to those early tissue stresses and reduces the entry of monocytes into the optic nerve and retina. No monocytes, no glaucoma!

How about that!!!

Where have you been?

My back injury has improved enough for me to return to light duty.  This means I had to tackle a number of projects and rearrange my schedule to accommodate "regular" work hours.  Not an easy task when you are used to shift work, and have a family life  build around the fireman schedule.


I will be back to "normal" full time status soon (I hope), and then I should have time to resume my blogging endeavor.  I have missed it ... almost as much as I have missed working these streets.  Until then!


... How about that!

Alzheimer's disease

Do you want a quick lesson on Alzheimer’s disease?  Just understand this, Alzheimer’s is characterized by loss of neurons in the cerebral cortex and certain subcortical regions, resulting in gross atrophy of the brain.  A part of your brain, called the hippocampus is involved in memory.  Specifically, the left hippocampus is involved in forming stories of your life from bits and pieces of your experiences.  It will form the neuronal impulses describing how you view yourself.  Basically, it forms the internal autobiography of who you are.  Alzheimer’s takes this away.

Combination of two brain diagrams in one for comparison. In the left normal brain, in the right brain of a person with Alzheimer's disease.

Source: http://en.wikipedia.org/wiki/File:COMPARISONSLICE_HIGH.JPG

Unlike other neurological disorders like schizophrenia or hallucinations where your interactions should be focused on bringing the patient into reality, when treating an Alzheimer’s patient, you have to enter “their world” and interact with them “there.”

Preach Heaven...

This past month we celebrated Saint Valentine’s Day.  A little known fact about Saint Valentine is that he is not only the patron saint of love, he is also the patron saint of epilepsy.  Legend has it that St Valentine miraculously cured a young woman afflicted with what is now thought of as epilepsy.  Another interesting correlation of religion and epilepsy is a seizure disorder originating in the temporal lobe that causes hyper-religiosity.


I learned about this disorder from a book I have mentioned many times – Incognito.  In it the author describes epilepsy as such: “…the long list of influences on your mental life stretches far beyond chemicals – it includes the details of circuitry, as well…. If an epileptic seizure is focused in a particular sweet spot in the temporal lobe, a person won’t have motor seizures, but instead something more subtle.  The effect is something like a cognitive seizure, marked by changes of personality…”


Any provider knows to use caution with patients in the postictal state.  I cannot recount the number of violent outburst I have personally had to deal with from combative postictal patients.  In conclusion:  I rather have someone preach heaven to me, instead of beat hell out of me.


How about that!

That smells like ...

Have you ever noticed that Parmesan cheese smells like vomit?  Why you ask? Because Parmesan cheese and vomit is full of butyric acid.  Scientist will say that we traded our olfactory acuity for better color vision a long time ago, and therefore, smell has become a subjective experience.

This does not make our noses simple. Actually, three percent of our genome is dedicated to the evolution of 350 separate receptor types.  We have 10 million odor receptors lined in our nasal passage in an area the size of a thumb print.  Yet, we are comparatively less efficient in the sense of smell than other animals.  The point is this, when you smell something, the context in which you experience the odor is important.

So the next time your partner piles a mountain of Parmesan cheese on his plate of spaghetti, tell him to take a deep breath as you remind him of the last vomiting call you guys ran …


I know; that’s mean …but, how about it?

Let no man's ghost return to say ...

Most first responders are familiar with the “fight and flight” principle - our sympathetic reaction to a stressful stimulus, like fear.  Anatomically speaking, the amygdala, an almond shaped mass of nuclei located in the temporal lobe, is the structure at the very center of this fear response.  Its function includes arousal, memory, hormone secretion and emotional regulation, especially autonomic responses to fear.  It has been indicated in disorders like Post Traumatic Stress Disorders and panic attacks, to name a few.

The amygdala and our fear response are vital.  It prepares us to avoid or ward off danger; however, it can easily overcome our rational senses and ability to perform critical thinking.  After all, the amygdala is an “emotional” system.  The good news is that the amygdala’s complex circuitry is directly connected to our higher regions of the brain, like the prefrontal cortex, where decision making takes place.  The constant feedback loop embedded in our system allows for us to control our emotions - if we have practiced to do so.

As an example, pilots use a technique called “deliberate calm.”  When everyone else is panicking from fear of crashing, the well trained pilot remains calm and performs the necessary actions to avoid or reduce casualties.  Remember Captain Chesley "Sully" Sullenberger, the US Airway Pilot that successfully crash landed flight 1549 in the Hudson River? This is a perfect example of “deliberate calm.”

An interesting case study that more emergency services persons can relate to is the Mann Gulch Fire of 1949.  On August 5^th that year, smoke jumpers where dispatched to Helena National Forest in Montana for a small wild land fire. Of the 19 man crew, only three survived that day.  View this link to the Forest Service report written by Richard C. Rothermel in 1993. A must read for all firefighters.

The long story short, the fire conditions changed rapidly and pursued the smoke jumper crew up a hill.  The crew could not out run the advancing fire and 16 of the men perished. This tragedy was a severe blow to the Forest Service, which had not experienced a fatality during a decade of smoke jumping.  One of the survivors was the foreman, Wag Dodge. This excerpt from the fore mentioned report explains Wag Dodge’s actions:

“Dodge must have realized they could not reach safety and conceived the idea of burning away a small clearing. This escape fire, as it has come to be called, would quickly clear an area where the crew could go, after the fine fuels burned away, giving them a chance to escape the flames of the main fire. … Dodge sized up the situation better than most of his crew … No one stayed with Dodge.”

This ingenious idea of Wag Dodge to burn the fuel away from around him, giving him an island of safety, saved his life.  In more modern times, this technique is used by Wildland firefighters.  The escape fire technique was used by 73 firefighters who avoided injury and death after being trapped on the Butte Fire in 1985.  “The crews were well disciplined; no one attempted to run from the fire. They stayed together and followed orders even though they were badly frightened” (Rothermel).

The point of this post is this: Fear is a natural and vital emotion build into our neural circuitry. It can be helpful and detrimental.  As first responders, we walk into situations other people run away from; therefore, we have to train to control our response to the amygdala’s emotional input.

A quote from my first department’s training philosophy: "Let no man's ghost return to say, ‘My training let me down’."

“How about it!”

Anosognosia

Anosognosia is a condition in which a patient has a total lack of awareness about an impairment. A famous example of this is Supreme Court Justice William O. Douglas, when a debilitating stroke in 1974 paralyzed his left side and confined him to a wheelchair.  However, Justice Douglas completely denied his very obvious disability - calling it a myth.

Once again, the elegant writing of David Eagleman explains this syndrome effortlessly.  In his book, Incognito, he explains that “it’s not that Justice Douglas was lying – his brain actually believed that he could move just fine….The point about anosognosia is that the patients are not lying, and are not motivated by neither mischievous nor by embarrassment; instead, their brains are fabricating explanations that provide a coherent explanation about what is going on with their damaged bodies.”

As I hope you can realize, this is not a defense mechanism like denial.  These patients have a true syndrome rooted in physiological damage.  Anosognosia is common following brain injuries like strokes, but can occur in combination with other neurological impairment, too. However, it is not related to global mental disabilities like dementia or Alzheimer’s.  “Anosognosia can be selective in that an affected person with multiple impairments may seem unaware of only one handicap, while appearing to be fully aware of any others*.”

*Re: Hirstein, William (2004). Brain fiction: self-deception and the riddle of confabulation. MIT Press.

The Camel Hump

If you are a paramedic and learned to read ECGs, you are an expert at locating the J-point.  It’s not hard to do; the J-point is the point in the ECG where the QRS complex joins the ST segment.  Simply put, it represents the end of the ventricular contraction.  When the J-point deviates from the baseline along with the ST-segment, we should become a little concerned.   We will quickly look for the infamous STEMI, or try to identify a STEMI imitators like early repolarization or a bundle branch block, to name a few.  But when the J-point itself forms a deflection, spike or dome, or like I like to call it a “bump”, we refer to this most commonly as an Osborn wave.

Pictures copyright J.A.M.B-ing

It is called an Osborn wave, as you may have guessed, because it was named after a doctor named Osborn - although he was neither the first to discover this deflection nor describe it.  A quick search on Wikipedia will present you with other names for this wave, such as late delta wave, prominent J wave, hathook junction, hypothermic wave, and my favorite, the camel-hump sign.

J-waves--or Osborn waves--appreciated in the lateral precordial leads

Picture courtesy of sixlettervariable.blogspot.com/. Reproduced with permission.

The causes for an Osborn wave are varied.  Hypothermia and hypercalcemia are some of the more common reasons, however - to keep with the current topic of this blog - brain injury, subarachnoid hemorrhage, and damage to sympathetic nerves in the neck have been reported to cause this wave, too.

How about that?

Do you want some Cheese with that MAOI?

In this past century, neuroscientist have discovered many details involved in psychiatric and neurological disorders. They have also worked hard at developing pharmacological options with mechanisms that effectively cause “antidepressive” feeling in patient suffering disorders like depression and anxiety.  We have all heard about these drugs: the selective serotonin reuptake inhibitors (SSRI), tricyclics (TCAs), and the designer drugs like Prozac.  One other drug, the monoamine oxidase inhibitors, or MAOIs, will be the topic of this post.

One of the interesting facts about MAOIs is that although they are generally as effective as SSRIs and TCAs, they are used less frequently because of adverse reactions when mixed with certain foods containing tyramine.  Tyramine is a naturally occurring monoamine compound that acts as a catecholamine. As you may have guessed from the title of this post, this amino acid is found in cheese.

MAOIs act by inhibiting the activity of monoamine oxidase, thus preventing the breakdown of monoamine neurotransmitters and thereby increasing their availability.  When you combine the endogenous levels of increased monoamines with amino acids found in certain foods, you can quickly cause an overload of dopamine, norepinephrine and serotonin known as the “Cheese Effect.”

This can cause a storm of problems resulting in migraines and high blood pressure, just to name a few.  In the worst case scenario, a hypertensive crisis occurs that results in a hemorrhagic stroke. Ouch!

So tell me, how about it ... Do you want some cheese with that?

A Matter of Terminology

If you have ever walked into a nursing home, the chances are you have seen someone affected by Parkinson’s disease. Parkinson’s is the second most common neurological syndrome in the U.S. characterized by tremor, hypokinesia, rigidity, and postural instability.  This disease was named for Dr. James Parkinson, after he was the first to describe this “Shaking Palsey” that is a result of damage to the “black substance” in the brain we call the substania nigra.

In medicine, the term Parkinson’s disease is attributed to the syndrome when it results from an unknown cause.  If someone develops “Parkinson’s” as a result of a known reason, like carbon monoxide poisoning or medication toxicity, then it should be referred to as Parkinsonian signs and symptoms.

“How about that…”

Just a little nice-to-know side for EMS workers, one of the most common causes of Parkinsonian signs and symptoms is the long term use of antipsychotics drugs such as Haldol.

Some of my Photographs

One of my job responsibilities at my department that falls under the "as the chief deems necessary" is photographer.  One of my more favorite alternative responsibilities as a firefighter/paramedic.

Save the Penumbra

“Save the Penumbra” will be the new mantra of paramedics all over the United States.  This phrase will replace “Time is Brain”, an off-shoot of “Time Is Muscle” that is most commonly applied to heart attack treatments.  The issue is that understanding the processes that occur during a cerebral vascular accident is a little more complex than a myocardial infarction.

To start, the etiologies of stroke are varied.   We can place strokes into two broad categories.  We know about the hemorrhagic stroke that results in a space occupying lesion.  These CVAs account for about 20 percent of strokes.  The other category is ischemic stroke, which will be the main focus of my next few posts.

Ischemic stroke refers to a stroke that is caused by thrombosis or embolism.  These thrombi, or clots, can be caused by a number of pathologies, but most of my patients suffering a CVA have had a number of the underlying risk factors such as cardiovascular disease, atrial fibrillation, diabetes and hypertension, just to name a few.

Now, let’s imagine that a small terminal artery supplying a cortical region of the brain is compromised by a thrombus.  The distal tissues supplied by that artery will quickly infarct.  That is because neural tissue is not capable of storing any oxygen and glucose.  In my previous post, I mentioned that the brain consumes twenty percent of our energy. To put this into perspective, it only takes 10 seconds of disruption of blood supply to the brain to cause syncope.  The region of the brain immediately affected will die irreversibly in just a few minutes.  Our job is to recognize the signs and symptoms of stroke and get our patients to definitive care quickly.  So we can “SAVE THE PENUMBRA!”

Think of the penumbra as an umbrella.  Just picture the area surrounding the immediate infarct forming a cone shape around the dead tissue like an umbrella covering a head in a rain storm.  That is the tissue that can be saved.  The penumbra, therefore, is the “zone of reversible ischemia around the core of irreversible infarction.”

I will get into more detail in the next few posts, but until then ...

"How about that?!"

Our amazing Brain

Our brain is so amazing. I first got interested in neurology when I discovered a book written by David Eagleman, called “Incognito: The Secret Lives of the Brain”.  In it, he refined a complex subject into a compelling read -- and made me realize that I knew very little about the mission control center of my body.  Just to introduce the subject of neurology, I like to sum up some of the basic facts about the brain.  I have always appreciated facts and statistics that relegate the importance of a subject. So here is my version to introduce the human brain.

This pink-ish three pound organ encapsulated in your skull accounts for only 2 percent of your mass but consumes 20 percent of your resting cardiac output. It is an intricate system of 100 billion neurons “connected to one another in a network of such complexity that it bankrupts human language and necessitates new strains of mathematics” (Eagleman).  One-hundred billion is the same number as stars found in our galaxy. Each one of these neurons can make a thousand individual connections with other neurons, which communicate with each other at speeds faster than a race car can drive.  At its slowest, impulses travel between neurons at 260 mph.  And finally, try to put this into perspective: more electrical impulses are generated in one day by a single human brain than by all the telephones in the world. 

"Now, how about that..."

So This Is Blogging?!?

Hello world of blogging? I am "Just Another Medic Blogg-er" trying my hand at filling the world with more information.


I'm doing this at the moment because I am out on injured leave from a job I love.  I am trying to use my down time productively and read as much as I can, listen to as much as I can, and learn as much as I can ....


I believe in the motto: "See One, Do One, Teach One!" ... well, this is my attempt at "doing" and "teaching" ... hope it works out.


Currently I am learning a lot about neurology and neuroscience as a whole.  This is a subject that is so under taught to folks in the EMS and the First-Responder world, (at  least in my opinion.)  I will attempt to provide some "nice-to-know" info into this blog that I have been learning, and then we will see where it takes me...