Close the Eyes

As a first responder, I hope you have heard of the Subway Sarin Incident in Tokyo on March 20, 1995.  There are many lessons to be learned in a case review of this terrorism incident perpetrated by members of a Japanese religious cult called Aum Shinrikyo.  If you have not, look it up… it will be worth your time.

A really interesting fact from this incident is that the most common complaint of victims and first responders alike was the sensation that "everything was going black, like they are entering a tunnel."  In a medical assessment, when we inspect the pupils in this event, we would find miosis.

Miosis is a term derived from the ancient Greek that means "to close the eyes".  It is a medical term that denotes a constriction of the pupils to an abnormal or excessive degree, caused, in this case, by exposures to an organophosphate based chemical weapon known as Sarin Nerve Gas (GB).

Nerve agents attack the nervous system by inactivating acetylcholinesterase (AChE), producing a toxic accumulation of acetylcholine (ACh) at the muscarinic, nicotinic, and CNS synapses. This causes an end organ overstimulation, which is often referred to as a cholinergic crisis. Vapor exposure of these nerve agents provides the most rapid onset of symptoms, and since the most exposed muscarinic receptors are found in the eyes, nerve agent vapor easily crosses the cornea and produces miosis.

So if you are ever responding to such an attack or another organophosphate based toxicological event, and you start to get literal “tunnel vision”, you know why!

How about that!

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!