Finding the root of depression starts with empathy!

The recent event involving Robin Williams has spawned a lot of comments and discussion on the subject of depression and suicide, a topic that has also had a lot of attention in the emergency services world recently. We know that depression is an illness and we should treat it as such; however, we have to recognize that there is so much we don't know, understand, nor are able to appreciate about it. Henry Thoreau once wrote “There are a thousand hacking at the branches of evil to one who is striking at the root." Some people work in a positive force toward helping those afflicted with depression; unfortunately, there are many that provide no positive recourse toward healing, intentionally or not, by belittling and criticizing the actions of severely afflicted individuals without scientific or clinical backing. They judge with no credibility!

Giant, Goya (Francisco de Goya y Lucientes)

Take a second and imagine having no vitality. In a recent article I read, the author asked “What if you are unable to see the worth in anything, or the beauty, or the reason, or the point, or the hope. Could you imagine the complete, total, absolute rejection of life?” This reminded me of a quote in which Laurell K. Hamilton so eloquently describe the pain of depression. She said, “There are wounds that never show on the body that are deeper and more hurtful than anything that bleeds.”

As an example, take the life of David Foster Wallace, an American novelist, short story writer, and professor. He lived an extraordinary life filled with success and external happiness. He published novels, received the only award you get in the nation for being a genius, wrote some of the most feel good essays in the contemporary world, was married, and hanged himself at the age of 46.

Now, listen to these words by Mr. Wallace, and just for a minute, put aside your preconceived notions:

“The so-called ‘psychotically depressed’ person who tries to kill herself doesn’t do so out of quote ‘hopelessness’ or any abstract conviction that life’s assets and debits do not square. And surely not because death seems suddenly appealing. The person in whom its invisible agony reaches a certain unendurable level will kill herself the same way a trapped person will eventually jump from the window of a burning high-rise. Make no mistake about people who leap from burning windows. Their terror of falling from a great height is still just as great as it would be for you or me standing speculatively at the same window just checking out the view; i.e. the fear of falling remains a constant. The variable here is the other terror, the fire’s flames: when the flames get close enough, falling to death becomes the slightly less terrible of two terrors. It’s not desiring the fall; it’s terror of the flames. And yet nobody down on the sidewalk, looking up and yelling ‘Don’t!’ and ‘Hang on!’, can understand the jump. Not really. You’d have to have personally been trapped and felt flames to really understand a terror beyond falling.” 

Did this change your understanding? Can we consider approaching the problem differently?

Clinical depression is an unimaginable suffering. A pain that many people choose to battle, often times for years and decades. They hold on and burn until the heat becomes too much, which should be applauded - the strength and endurance of people that hold on. This is the time they give us to help. When someone ultimately commits suicide, it is the failure of all mankind. It is our failure for hacking at the branches of the problem and not working toward finding the root.

A good friend and colleague told me that when we see depression as a true medical condition instead of a weakness or crutch, then the way we talk, interact, and ultimately treat our patients will change.  We have to change our perspective, not only personally, but clinically and scientifically. This will take more research, more money, and more time; however, right now, we need to provide, to our best ability, every ounce of empathy that we can muster. If not for the sake of our patients, please start for the sake of our brothers and sisters in uniform.

FTM-PTB-DTRT-KTF-EGH … EGH

The Goldilocks Rule for Ventilation

A successful resuscitation requires a well-executed bundle of interventions that are interdependent. To borrow from Dr. Snyder in Wake County, North Carolina, “there is no silver bullet, but there is a silver chain!”

High quality chest compressions are the foundation of the resuscitation – this includes proper rate of compressions, proper depth, and limiting “no-flow” times. Technological advances in real-time CPR feedback have improved the quality of CPR, and novel approaches to keep the compression fraction above 90 percent are implemented in many systems. Two of the biggest improvements to increase the compression fraction are to limit the peri-shock pause and to de-emphasize airway management. As an example, intubation should be performed without interrupting compressions, or the provider can utilize a blind insertion airway device. The execution of the resuscitation bundle can vary; however, the key is to limit any interruption in compressions. Although compressions precede airway management in a cardiac arrest, we have to remember that ventilation plays a very important role to compliment these compressions and other interventions.

As an example, Idris et al shows that ventilating in cardiac arrest favorably affects hypoxia, hypercarbic acidosis, and acidemia. This has a direct influence on the efficacy of drugs and defibrillation. Lurie et al also showed “that periodic lung inflation maintains the structural integrity of the lungs and lowers pulmonary vascular resistance,” thereby improving blood flow through the lungs.

On the other hand, hypoventilating during cardiac arrest causes detrimental consequences. Lurie et al showed that giving only 2 breaths per minute versus 10 breaths per minute causes the lungs become more atelectatic. The atelectasis is believed to cause a “reduction in the transmission of the energy from the elastic chest-wall recoil during CPR” which decreases blood flow. In addition, pulmonary vascular resistance increases causing trans-pulmonary blood flow to decrease.

Not ventilating also affects medication administration. Idris et al showed that CPP responded better to epinephrine in ventilated animals versus non-ventilated animals. This would suggests that “ventilation may play an important role in regulating CPP and ROSC through the vascular response to catecholamines,” making it more likely to achieve ROSC in a ventilated patient.

Another consequence of improper ventilation in cardiac arrest is hypercarbic acidosis, which causes peripheral vasodilation and “blunts the vasoconstriction response to exogenous epinephrine.” Higher PACO2 also effects cerebral blood flow by increasing cerebral vasodilation secondary to cerebral autoregulatory mechanisms. In addition, if ROSC is achieved, the hypoxia and hypercarbia “profoundly decreases the myocardial force of contraction.” This would make a re-arrest more likely.

In summary, not ventilating has profound and potentially harmful effect on the resuscitation process. When deploying the “silver chain” of resuscitation, we should also follow the “goldilocks rule” of performing interventions correctly. Whether we perform compressions or ventilate the patient, rates that are too fast or too slow are detrimental. We have to do things “just right!”

How about that!

The Goldilocks Rule: Rate Matters

A lot of positive progress has been made in the process of resuscitating cardiac arrest victims. Our understanding of the physiology has improved, the tools at our disposal to successfully intervene in a code are phenomenal, and a cultural philosophy that “it actually works” is sweeping our profession. One of the biggest changes in the process has been a revival on focusing on the basics – and nothing is more basic in a resuscitation than chest compressions.

Chest compressions are the foundation on which a resuscitation is built. And like any foundation, we need it to be of high quality or the entire process will crumble.  I do not care if you have the best drugs, the greatest defibrillator, or the smartest clinician at a code. Without high quality chest compressions, the ultimate outcome will be less than desirable.

In the last few years, there have been some great PSA about performing CPR. My favorite is “Vinnie Jones' hard and fast Hands-only CPR.” Check it out!

Although this PSA is for lay-person CPR, Vinnie hinted at some important aspects of high quality CPR that professional providers need to remember - push hard and fast. However, the actual rate matters.

Think about the baseline in a healthy person. There is a small range in all of our vitals, but a deviation to one extreme or another is a bad thing. A heart rate of 30 or a rate of 240 is a bad thing in a living person. Those rates must be really bad in a person whom we are resuscitating with compressions. Right?

So we do not want a rate that is too slow, nor too fast. We want a rate that is just right! Call it the Goldilocks rule! 100 compressions per minute. That’s the rate! And while we are on the subject of rates, do not breathe too fast for them either! The AHA recommends a rate no faster than 10 breaths per minute.

Build that foundation and watch a real life fairy-tale unfold!

How about it?

Chest Compressions As An Art Form

Over the last few weeks, I have been reading a lot of medical research on resuscitation. This has made me ponder about the realistic ability to perform “randomized, controlled trials” in the pre-hospital setting on such a dynamic and complicated issue as cardiac arrest.  Now, do not get me wrong,  I fully understand the need, purpose, and benefit of  clinical trials and the scientific method as a whole; however, how realistic is it to perform a large enough study on cardiac arrests in which you can account and control for all variables of patients and clinical care?

It is commonly cited that we have more than 330,000 deaths annually from out-of-hospital cardiac arrests in the United States. The causes, however, are varied and often unknown or initially speculated. Other factors such as down time prior to EMS arrival, quality of bystander CPR, overall health of the patient, and so on, cannot be controlled. One article I read by Dr. Arthur B. Sanders, M.D., M.H.A, in a New England Journal of Medicine (NEJM) editorial from September 1st, 2011, suggested that “it may be more useful to consider out-of-hospital cardiac arrest as a public health problem rather than as a disease process. Randomized, controlled trials may not be the best strategy for making progress in the management of public health problems, such as cigarette smoking or motor vehicle deaths. The efficacy of closed-chest massage, mouth-to-mouth rescue breathing, layperson-administered CPR, and pre-hospital defibrillation by medics were major clinical advances in the field of resuscitation science that were not subjected to randomized clinical trials.”  He went as far as to suggest an alternative strategy to improve the science of resuscitation thru the use of a “continuous quality- improvement model.”

As an example, a big driving force in the higher survival rates over the last few years come from a fundamental focus in our performance of cardiopulmonary resuscitation (CPR). Observational analysis showed that the rate of survival improves as the chest compression fraction increases. It is therefore, that the clinical process of increased compression fraction at a proper rate and depth with full chest recoil became a practice that has tripled survival rates in systems. As another example, Dr. Sanders described how “in the ROC PRIMED trial, the baseline database analysis [of CPR performance in perspective sites]… resulted in improvements in the clinical process during the preparation phase of the clinical trial. Ironically, this analysis and the resulting improvements in process may have greater importance for clinical practice than the two randomized trials.”

The point I am trying to make is that we can study techniques that work in saving more lives thru other means. We need to stay open minded and willing to evaluate our own practice and understanding. Just like a cardiac arrest, healthcare is very dynamic and ever changing.  I know that medicine is therefore a practice; however, certain proven techniques and fundamental skills like chest compressions have to be practiced as an art.

So please, be an artist. Do the compressions like someones life depends on it! Get it?

How about that!

"Yeah, we got all kinds of traditions...like dying young."

Histotoxic hypoxia is the inability of cells to take up or utilize oxygen from the bloodstream, despite physiologically normal delivery of oxygen to such cells. This occurs in a few circumstances, but it is most concerning to me as a firefighter these days since so many synthetic materials found in structures off gas cyanide when burned. The cyanide ion halts cellular respiration by inhibiting an enzyme in the mitochondria called cytochrome c oxidase, the last enzyme in the respiratory electron transport chain.

And this is probably the cause of more firefighter deaths than we know about.  There is research out there that suggests that Line of Duty Deaths (LODD) attributed to heart attacks, medical emergencies, or worst of all, the firefighters that are though of as having  "panicked inside the fire", may have actually suffered from acute cyanide poisoning.

Acute cyanide poisoning can cause confusion and delirium that is mistaken for "panic", and lethal arrhythmias that are mistaken for heart attacks.  Definitive treatment is very specific to antidote kits, but most health care providers would not consider it as a differential.  Not their fault, the information is just not out there!

Thank God there are some good people doing important research in bringing this information to light. Until this information is more defined, and the rest of the community realizes this is a problem, we in the fire service need to look out for our selves, get informed, and share the information when needed.

We need to do better in understanding the "new beast" we fight. This is not the same fire as our forefathers fought. Everything is different. The construction, the material, the smoke... it is all different. Let's study it, understand it, and teach each other what to do about it. Enough of us have died!  It's our worst tradition... dying young.

How about it?

Dystextia: masked by autocorrect!

Recently, you could find many articles talking about doctors in Detroit that tested a man for a stroke because his text messages were "garbled"— even though he had no other symptoms.

His score of 2 on the NIHSS indicated the possibility of a minor stroke, which, in turn, prompted a brain scan that showed the man had indeed suffered a mild stroke. This is not a unique nor isolated case of what doctors are calling "dystextia". The Archives of Neurology lists other cases that spawned medical evaluation from signs of incoherent text messages.

This picture is for entertainment purpose only, and not a diagnostic example.

These case studies have let to a new hypothesize that the brain may treat text messaging entirely differently than other forms of language and writing. For instance, the man from Detroit couldn't accurately type a sentence on his phone that was given to him, although he could repeat the sentences correctly verbally.

Considering incoherent texts as a sign of stroke could prove useful to medical professionals. In addition to diagnosing a patient, we may be able to use the time stamps from texts to determine the precise timing of a stroke’s onset, unless, of course, autocorrect has masked the symptom of dystextia.

How about that!

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!