Being young and healthy ... can suck!

From time to time, viruses evolve that seem to kill a disproportionate number of the young and healthy. In certain cases  like the “Spanish Flu of 1918”, the SARS outbreak in Hong Kong, and the recent bird flu pandemics, a healthy immune system may have been a liability rather than an asset. Intuitively, this does not make sense.  Why would a healthy person be at greater risk? Well, I am glad you asked!

Have you ever heard of a cytokine storm?

When the body identifies a pathogen, an immune response ensues. Part of the immune system communication is a small cell-signaling protein molecule called cytokine, which tells immune cells like macrophages and T-cells to travel to the site of the infection. Cytokines also activates other immune cells, stimulating them to produce more cytokines in a process called a positive feedback loop.  Normally, this feedback loop is kept under control by some processes I do not understand; however, sometimes, the reaction becomes uncontrolled. This is known as a cytokine storm.

In other words, a cytokine storm causes an exaggerated immune response that can kill a person. The precise reason for this is not entirely understood but it is believed that this is the reason why a new and highly pathogenic invader causes higher fatality rates among young, healthy people with good immune systems.

How about … never mind, that sucks!

Dystonia - not a polish travel destination!

A recent case posted on an EMS related Facebook page asked providers if they can and would treat dystonic reactions in the field. Dystonia is a reversible extrapyramidal effect that can occur after administration of certain drugs, characterized by sustained involuntary contractions of muscles throughout the body. It is not a polish destination spot! With treatment, these symptoms can be alleviated quickly and safely - even in the prehospital setting.  So the answer to the question is: yes, a prehospital provider should treat dystonic reactions in the field!

However, I understand that many providers may not be familiar with this condition and how to treat it.  I am not certain if dystonia is listed in the teaching objectives of initial EMS classes, and therefore, continuous education may need to focus on more abstract conditions like dystonia and other disorders, especially if they are a potential side effect of medications we give in the field. As an example, dystonic reactions can be induced by a potent dopamine D2 receptor antagonist like haloperidol, and even by commonly given antiemetic medications like promethazine. A quick search on Medscape showed that “although dystonic reactions are occasionally dose related these reactions are more often idiosyncratic and unpredictable.” They reportedly arise from a drug-induced dopaminergic-cholinergic imbalance “which leads to an excess of striatal cholinergic output.”

The treatment is simple, and well within the scope of EMS providers – although medical control contact may be required for orders since this is not commonly mentioned in protocols. If you encounter a suspected dystonic reaction, IV administration of diphenhydramine 25-50 mg is repeatedly recommended by literature. The reason is that diphenhydramine, although an antihistamine also possesses significant anticholinergic properties. These properties may help by blocking striatal cholinergic receptors, therefore rebalancing cholinergic and dopaminergic activity.

How about that!!!

This effect or that!!!

Dr. Bryan E. Bledsoe, D.O., one of the foremost authors of EMT Text books stated: “The EMT of today must be knowledgeable in all aspects of prehospital emergency medicine. Nowhere is this more important than when administering medications.”  Every medication that we give to treat a disease exerts a biochemical effect on cells, tissues, or organs.  And we need to understand these effects to help us anticipate not only the local reaction, but the systemic responses from our drug administration.

Another reason to be deliberate at learning the mechanism of action of drugs, and learn to understand them at a cellular level, is to allow us to consider certain medications for “uncommon usages”.  But first, we need to understand that the medications we administer do not confer any new properties on cells or tissues; they only modify or exploit existing conditions.  To understand this fact and to learn the different pharmacodynamics of drugs can help us use certain medications for unusual circumstances.

Take Glucagon as an example. Besides the use of this medication in the hypoglycemia protocol, Glucagon can also be used for symptomatic bradycardia secondary to β-blocker overdose and Ca-channel blocker overdose, Steakhouse syndrome, and refractory anaphylaxis.

How? Well, I'm so glad you asked! The effects of Glucagon causes a “cascade of activations resulting in an increase of cyclic-AMP (cAMP). cAMP is an important intracellular messenger, responsible for carrying the signals of epinephrine and glucagon across the cell membrane. cAMP also regulates the flux of Ca2+ through ion channels independent of β-adrenergic receptors. This quality of Glucagon is what is thought to explain the various changes to the cardiovascular system seen after its administration.”

Want some more details on this, then check out my good buddies blog at “My Variables Only Have 6 Letters” and read his Glucagon 2.0 section.

How about that!!!

To the right, or to the left?

The art of ECG interpretation has become a mystery to me.  I know the basics.  I can pass the National Registry exam with flying colors. But since I have met some real masters of ECG interpretation, I realized that there is so much more to know – so much more to understand.  A good friend, and ECG wiz kid, told me: “You need to read things with some meat to it.”  This is so true!  ECG interpretation is so much more than just pattern recognition. You have to have a deeper understanding of what actually happens in the heart.

For an example, let us talk about ventricular ectopies for a minute.  We are all familiar with a premature ventricular contraction, more commonly referred to as simply a “PVC”.  A PVC is a relatively common event where the electrical complex of the heart is initiated by Purkinje fibers in the ventricles rather than by the sinoatrial node.  To recognize it on an ECG is easy – look for the “funny looking beat” (FLB) that is wide and ugly.

From Wikipedia, the free encyclopedia

However, if you want to determine if a PVC originated from the right or the left ventricle, then head on over to ems12lead.com and learn from real masters of ECG interpretation. Not only will you learn that “… ventricular complexes that originate in the left ventricle show RBBB morphology in lead V1. Conversely, ventricular complexes that originate in the right ventricle show LBBB morphology in lead V1.”  You can also bite into some of that proverbial “meat” of ECG knowledge.

How about that!

Can you smell the "bitter almonds"???

As long as there are legitimate uses of chemicals in our society, there is a high potential for first responders to encounter situations where chemicals will provide a life threat to the public and themselves.  A recent situation in my neighboring town forced paramedics to withdraw from a residence following the detection and identification of potassium cyanide, a highly lethal substance that an individual used to commit suicide with. 

Potassium cyanide is a solid compound that when moistened emits hydrogen cyanide due to hydrolysis - which smells like bitter almonds. Unfortunately, the ability to detect the “bitter almond” smell is limited to people with a certain genetic trait.  Thank goodness, from the reports I received, one of the lead medics on the scene detected an obnoxious smell which lead to the rapid evacuation from the residence and subsequent decontamination of the crew.

Cyanide is a potent inhibitor of cellular respiration, which prevents the body from oxidizing food to produce useful energy. This is what presents initially in acute cyanide poisoning as the classic red complexion in the victim because the tissues are not able to use the oxygen in the blood. The person loses consciousness, and death by hypoxia of neural tissue follows quickly.

Let’s hope that if you do not possess this genetic trait of being able to detect that smell of“bitter almond”, one of your partners does ….

How about that!

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.)