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Education, Tips & Tricks...

This part of our site is dedicated to something I truly believe in: education. I love teaching and passing the things that I have learned on to a newer generation and will do it all day long. I'm a firm believer that everyone can learn something from everyone they come into contact with.... whether that is what TO do or what NOT to do, you should strive to learn from everyone you encounter.

Which one are are you?

1) I'm a paramedic because I enjoy practicing medicine in the streets and learning. I pursue knowledge on my own by reading journal articles, going to conferences, getting more CE hours than are required, and researching on my own, and I try to take something away from every call I run.

2) I'm a paramedic because I had to go to paramedic school in order to get hired by/keep my job with Anytown Fire Department. I want to be a firefighter and ride the big red truck and I don't care about riding an ambulance at all.

If you are Paramedic #2, and you really don't give a hoot about being a paramedic, please do your patients, your coworkers, and yourself a favor and either go work for a department that doesn't have an ambulance or change careers. Unless you truly love being a paramedic and embrace it wholeheartedly, please get out before you hurt someone.

The graphics and principles that you will see in this part of the page are things that I have developed over the years either to teach myself a concept or to teach it to someone else. They are all pretty much standard information (I just put them into an easier to understand form), so feel free to use them as you see fit, BUT please give us credit by linking to our site. My overall goal in this page is to give you another tool to put in your toolbox to help you take care of patients. If you are able to take something you see on our page away and use it to help a patient at some point in your career, I have done my job.

 

12-Lead Map
ABG Interpretation
A-Fib with RVR
Circulatory System Overview

Right Ventricular MI/Inferior Wall MI
Use of pressors in the Inferior Wall MI
Acid-Base Balance
Metabolic Acidosis

 

Omni's ABG's:

ABG interpreation

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Omnimedic's 12-Leads:

12-Lead interpretation

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Atrial Fibrillation with RVR
Atrial Fibrillation: Atrial = the source (the atria), Fibrillation = quivering. As you know, the physical contractions in the heart are as a result of electrical impulses which are generated in the atria, passed down to the AV junction, which usually passes the signal on to the bundle of His, purkinje fibers, etc. Imagine if you were to take Jello, and smack it with a spoon... it will quiver in a disorganized manner. THIS is atrial fibrillation… each movement in the quivering is generated by an electrical impulse.

The atrial rate in A-Fib can be upwards of 300 beats (or quivers) per minute; if all of these were passed through conduction system to trigger a ventricular contraction, the ventricles wouldn’t have time to refill before the next beat, resulting in inefficient pumping. To prevent this, the AV junction blocks out most of the impulses coming from the atrial, resulting in a ventricular rate in the relatively normal range, so, by definition, Atrial Fibrillation is a type of second degree heart block.

When the patient is in A-Fib, the AV junction is doing its best to block out most of those impulses, but sometimes it gets overwhelmed, and sends too many of those impulses on down the line. This results in an elevated ventricular rate – THIS is RVR, or “Rapid Ventricular Response”. Depending on who you ask, the exact number which differentiates “A-Fib” from “A-Fib with RVR” will usually be somewhere between 120-160. The absolute value of the number isn’t as significant as the clinical presentation and if signs of hypoperfusion as present. Treatment in the stable patient is with calcium channel blockers, and is directed at helping the heart block more impulses from reaching the ventricles to trigger a beat. Treatment in the unstable patient is synchronized cardioversion, although it must be used cautiously – prolonged A-Fib increases the risk of blood pooling and clot formation. If you convert the patient out of A-Fib and they begin pumping more efficiently, it increases the chance of them throwing a clot, and creating an embolic stroke, a PE, or a STEMI.
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Circulatory system

I created this diagram when I was studying for the FP-C exam... thought someone else might benefit from it. Keep scrolling for a detailed explanation.

circulatory sytem diagram

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Right Ventricular (Inferior Wall) MI and the use of vasodilators

This assumes that you know the pathophysiology of a myocardial infarction in the first place (i.e. blockage of a coronary artery, ischemia/injury/death of myocardial tissue, what to look for in a 12-Lead, etc). If you’re not clear on those concepts, review them… if you need a 12-lead review, see above. This picks up with the pathophysiology of a Right Ventricular MI (RVMI, also known as an Inferior Wall MI) and the danger of using vasodilators such as nitroglycerine in those patients.

OK, so we all know the heart sits at an angle in the chest just a little to the left of the sternum, with the apex (the narrow end) pointed towards the left hip. With the angle that it sits in the chest, the “right” side of the heart is kinda oriented on the lower, or inferior, side of the heart. There’s the “inferior” part… right side = inferior.

If your 12-lead shows ischemia/injury/infarct in the inferior leads (II, III, aVF), it indicates that the right side of the heart has a problem. Some people say “now you need a V4R or a 15-lead”. But do you, really?? If it makes you feel better, and you have plenty of time during transport, OK, but think about this: it’s probably going to tell you the same thing. Even if, for some reason, it doesn’t, is it really going to matter what it says? Don't get me wrong, V4R and a 15-Lead are great tools. But they are better used to rule out something that you aren't sure of than to confirm something that you already know. Before your crucify me for that statement, think about this: If the clinical presentation and the 12-lead show inferior wall STEMI but the V4R or 15-lead doesn’t, are you going to NOT transport them to a cath lab because of it?

The right side of the heart is the side that receives blood back from the systemic circulation, via the vena cava; blood enters through the right atrium, and exits via the right ventricle into the pulmonary artery where it goes to the lungs to be re-oxygenated. Whenever the muscle tissue that makes up the a ventricle is damaged, it doesn’t pump as effectively, meaning that the amount of blood coming out of that side of the heart is reduced. In this case, the right ventricle is damaged, and output from the heart going into the pulmonary system is reduced. Since this is a closed system, a reduction of right ventricular output means that everything else in the system will be reduced, including the amount of fluid that comes back to the heart, which is known as “preload”. THIS is the key for this concept… read on:

We all know the phrase “MONA greets all chest pain patients”…. except in this case, nitroglycerine and/or morphine will hurt our patient. Why? Nitroglycerine is a vasodilator, which reduces the blood pressure by dilating all the vessels in the body. By doing this, all the blood is hanging out in the now larger-capacity systemic circulation you created with the nitroglycerine, which means that you reduced the amount of blood that is coming back to the heart in the vena cava… again, the “preload”.

Now, if the heart is already having problems getting blood out of the right ventricle due to an RVMI, and you reduce the amount of blood coming into the heart, you have just compounded the matter by further reducing cardiac output. Or, stated another way, the heart can’t maintain a cardiac output at a rate of 3-5 liters per minute if it’s not getting blood IN at least the same rate.

So if less input means less output, and it’s a closed system, why do we intentionally dilate the vessels and drop the blood pressure in other types of MIs? How is that safe?

The key lies in the fact that the systemic circulation is MUCH larger than the pulmonary circulation, and the majority of the body’s blood (90% or so) is hanging out in the systemic circulation at any given time. This means that giving a patient nitro will have a MUCH greater effect (about 9:1) on right-sided input (“preload”) than left-side input, which is coming into the heart from the much smaller pulmonary circulation.

Back to our inferior wall MI:

The end goal here to maintain the patient’s BP and cardiac output (CO) to ensure that all the organs have enough blood & oxygen going to them.  Blood pressure and cardiac output are directly related, so when you increase the CO, the BP goes up with it, so let’s look at ways to boost them:

Given formula for cardiac output:  CO = SV x HR, the two ways to increase CO directly are to either increase the stroke volume or increase the heart rate; you don’t carry a drug that can increase your patient’s SV (at least not without another set of side effects), and increasing the HR increases myocardial oxygen demand, and in the MI patient, that’s a bad idea.

So we can’t increase the cardiac output directly, but since BP and CO are directly related, when you increase one, it increased the other, so how about increasing CO by increasing the BP? The circulatory system is a closed system composed of pump, pipes, and fluid, and the blood pressure is simply the measurement of the pressure that the fluid exerts on the walls of the pipes.

Blood pressure is a function of the heart rate (the pump), stroke volume (also the pump), systemic vascular resistance (the pipes) and fluid volume (the fluid) in the system. Increasing any of them increases the pressure in the system, and since these are directly related to blood pressure, and blood pressure is directly related to cardiac output, we can link them all by the magic phrase “increasing heart rate, stroke volume, SVR or fluid volume will increase CO.”

Now, we have already decided that increasing the HR is a bad idea in the MI patient because of the increased workload on the heart; likewise, increasing the SVR also increases the workload on the heart, so that’s out as well. We can’t affect stroke volume, as stated two paragraphs ago, which leaves adding fluid to the system as the only way we can boost cardiac output.

The only other option is to increase the cardiac output is to boost the blood pressure by adding fluid to the system…. and THAT is why you give a huge fluid bolus to inferior wall MI patients.

So back to the point of vasodilators: If their pressure is high enough, can you give them nitrates? Yes, but it requires very careful clinical judgment and evaluation of the overall situation. I would say that not having an IV in place would be an absolute contraindication, based on the fact that if you bottom them out, you are really screwed if you don’t already have an IV in place (preferable a BIG one) that you can crank up.

So if their BP is in the toilet, can/should you give pressors to get their pressure up? Keep reading...

This is the third in the series of our inferior wall/RVMI patient. The first was the scenario, the second was the pathophysiology of an RVMI and what makes it different from other MIs with regards to use of vasodilators.

So, if their pressure is in the toilet, should you use pressors to bring it up? Just like with the use of vasodilators, that is a double-edged sword, and there’s not a single straight answer. As always, my official answer is “Follow local protocols and medical control guidelines.” Unofficially? Read on.

 So you have a patient who is having an inferior wall MI as evidenced by clinical presentation and 12-lead findings. If you don’t know what “clinical presentation” is, review “Cardiology 101.” You give them a 1000mL fluid bolus and their pressure is still 80/40 (or some such other low number) and wonder if you should hang a dopamine drip.

 Keep in mind that when the patient is having an MI, it is because their heart isn’t getting enough blood, meaning it’s not getting enough oxygen. Any time you increase the workload on the heart, it increases the oxygen demand – whether it is by increasing heart rate or increasing peripheral vascular resistance.

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 Pressors in the RVMI

So you have a patient who is having an inferior wall MI as evidenced by clinical presentation and 12-lead findings. If you don’t know what “clinical presentation” is, review “Cardiology 101.” You give them a 1000mL fluid bolus and their pressure is still 80/40 (or some such other low number) and wonder if you should hang a dopamine drip.

 Keep in mind that when the patient is having an MI, it is because their heart isn’t getting enough blood, meaning it’s not getting enough oxygen. Any time you increase the workload on the heart, it increases the oxygen demand – whether it is by increasing heart rate or increasing peripheral vascular resistance.

 First of all, the case against:
Your goal is to get the patient to the cath lab as quickly as possible. This includes calling a “STEMI Alert” or whatever your local region uses to alert the receiving facility that they need to get the cath lab ready to go, preferably in the form of bypassing the ED and unloading on the cath table. By hanging a pressor, you are increasing the workload on the heart, and potentially worsening the infarct. If you have a relatively short transport time (say, less than 20 minutes) and the patient doesn’t appear to be deteriorating (still conscious, talking, respiratory distress is under control), I would say hold off on the pressor. Have it handy, have your calculations done if you have time, but don’t start it up yet.

Now, the case in favor:
The brain is selfish, and doesn’t like it when it doesn’t get enough blood. In fact, if it doesn’t get enough blood, it throws down the “ace of spades” and causes the body to lose consciousness, which results in the patient getting horizontal and reducing the heart having to work against gravity to pump, all in hopes of getting blood to itself. If the patient is showing signs of neurological effect from the hypoperfusion (i.e. altered mental status) the brain is saying “OK, you guys gotta do something, I’m not getting enough blood”. If that lasts too long, you get a hypoxic brain injury.

My answer would be this: if the patient is showing signs of cerebral hypoperfusion from the hypotension, and you’re a little ways from the cath lab (say, >10 minutes from the patient actually being ON the cath table… not 10 mins from the hospital), I would say to hang the pressor because in the end, if you save the heart and they have the brain of a carrot, did you really do them any good? There are other effects of extended hypoperfusion (renal failure, for one), but the brain is the big one. You can get a kidney transplant or go on dialysis… it’s awfully hard to replace a brain, although there are plenty of people who need it.


I’m not going to go into specifics of WHICH pressor to hang, as that is something that’s definitely going to be agency specific, and not everyone has a choice. Just be sure you are proficient with the calculations for the one you use (or visit out our homepage and check out our driprate calculator “Omnimedix”)

If your protocols aren’t specific and you’re not sure, don’t hesitate pick up the phone or radio and bounce it off Medical Control. Calling medical control is a great resource; you don’t always have to view it as a “mother may I”… it’s called a “consult”. In other words “I want to bounce an idea off of you, Doc.” Physicians do it EVERY DAY to other physicians, so don’t be shy. After all, that’s what the doc paid the big bucks for… put that monkey on their back.

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Acid-Base Balance

The concept of acid-base balance is important to grasp as either a nurse or a medic for a couple of reasons: First, the body’s metabolic processes require the body to be at an optimal pH of 7.35 - 7.45 that we all learned, and secondly, because many of the patient's signs and symptoms are the result of the body trying to get back to that range. Now, the same sign or symptom can be either a cause OR effect of an acid-base imbalance, and it takes a good understanding of the concept to be able to determine which you are looking at. So, let’s dive into it:

Remember the exploding volcano science fair project that made lava by dumping vinegar into the volcano filled with baking soda? That is the principle of acid-base balance… vinegar is an acid and baking soda is a base. When you mix the two, you get bubbling, which is the vinegar and baking soda is bartering to exchange hydrogen ions and come to an agreement on how much hydrogen each of them will get to keep. In the process they release carbon dioxide gas, and at the end, you are left with pure water and salt. 

Acids and bases are measured on the pH scale from 0 to 14. Lower numbers represent acids, and higher numbers represent bases, with 7 being perfectly balanced and neutral. Common examples are vinegar (pH of 2), water (pH of 7) and ammonia (pH of 11). An “acid” means that the substance, whatever it is, releases Hydrogen ions whenever it mixes with water and is written as H3O+; a “base” means that it accepts hydrogen ions in water and is written as OH-. The take-away point here: HYDROGEN = ACID. A “base” can be referred to as a base, or alkaline, (or... alkalosis)… same thing. You’ll see that later.

In the body, this occurs through a series of steps with carbon dioxide and some other compounds as an intermediate step in what is called the “bicarbonate buffer system”, shown below.

                                      CO2 + H2O  <-> H2CO3 <-> H+ + HCO3-

 You probably know what CO2 and H2O are, but H2CO3 is “carbonic acid”, HCO3- is “bicarbonate” (a base, the same compound that Johnny and Roy made famous in flipping the lids of the prefilled syringes and that we still give in the form of Sodium Bicarbonate) and H+ is the generic way to write “some acid”. The <-> means that the stuff on the left and right of it are in equilibrium with each other, meaning that they are in a constant tug-of-war, so that when one increases, the other decreases, and vice versa. This is a key point: increase one compound, something else has to decrease to maintain homeostasis.

The metabolic processes of the body operate within the range of 7.35 – 7.45, with the optimal at 7.40. Whenever the body senses that it is out of that 7.35 to 7.45 range, it starts compensating by turning on and off various processes to try to get back to the normal range. The two primary organ systems that maintain the body’s pH are the respiratory system and the renal system.

Here’s how they work:

The renal system compensates by directly retaining or excreting bicarbonate (HCO3-), which is a base. So, when the body senses that the body is too acidic, it tells the kidneys “hey, we’re getting acidic… until we tell you otherwise, hold on to more of that bicarbonate stuff to balance us out.” Likewise, if the body becomes too basic, the kidneys kick into high gear and dump more bicarbonate. Since you don’t pee every minute of every day, it takes somewhere in the range of a few hours to a few days for this mechanism to work, which is how you maintains your long-term pH balance. The problem? If you stay acidic for several days, you’ll die, so something has to be done quicker than that, which is where the respiratory system kicks in:

The respiratory system serves to maintain the body’s pH by adjusting the amount of hydrogen present in the in the blood, and works in a matter of minutes. Remember that the double-headed arrow <-> that indicates the tug of war? When the body retains carbon dioxide, it mixes with water to form “carbonic acid” (H2CO3), like this:

CO2 + H2O <-> H2CO3

Important point here: CO2 = Acid.

If the body senses that the pH gets above 7.45 (or, it’s too basic) it tells the respiratory system “Hey… we need a little acid. Slow down a little and hold on to more of that carbon dioxide stuff.” The respiratory rate slows down, less carbon dioxide is blown off, and thus, more carbonic acid is created. More acid = lowering the pH, and the pH comes back to normal range. So, ↓RR = ↑ CO2 = ↓pH.

If the body senses that the pH gets below 7.35 (or, it’s too acidic), the opposite happens. It tells the respiratory system to kick into high gear; by breathing faster, the body blows off carbon dioxide. Since carbon dioxide = acid, blowing off more CO2 means less carbonic acid is created, and the pH goes up. So, ↑RR = ↓ CO2 = ↑pH.

This is the principle behind diabetic ketoacidosis and Kussmaul respirations. The body is producing “ketones” which are acidic… the body’s response to the increased acid is to increase respirations and blow off more CO2 to decrease the amount of acid in the body.

Now, the clinical link:

I would imagine that everyone’s protocols have bicarb in them somewhere in the CPR protocol, probably pretty far down the line now. Giving bicarb is a double edged sword: when you dump bicarb in the system, it neutralizes the acid… the problem is that without labwork, we don’t know EXACLTY how much acid is there, meaning we don’t know exactly how much bicarb they need. The result is that once the acid is neutralized, the excess is still hanging out in the circulation, and shifts the patient from being acidotic to being alkalotic. Hemoglobin does a little better at carrying oxygen in a slightly acidic state than it does in a slightly basic state. Personally, I would prefer keeping them a bit acidic for that reason. An alternative is to adjust your ventilation rate… if you increase your patient’s respiratory rate by bagging them faster or adjust your vent settings for a slower, deeper ventilation, it gives greater time for gas exchange, resulting in the same effect as Kussmaul respiratirions. It’s just something to think about….  As always, follow your local protocols and medical control orders. 

 I like to use the “first name/last name” method of understanding the acid-base derangements. The first name (respiratory or metabolic) is the CAUSE of the derangement and the last name is the type of imbalance. i.e. “Metabolic Acidosis” which is an acidosis caused by a metabolic process. (I’m not going to go over lab values that are the definitive diagnosis of each of these – that’s in the “ABG Interpretation” post, and you can find it on our Education page.) Now, keep in mind that the “other” system (in this case, the respiratory system) may also appear to be out of whack, as it tries to compensate for the metabolic processes going on. If that is the case, and the pH is still within normal range (7.35-7.45) it’s called “compensated”… if that’s the case and the pH is out of the normal range, it’s “uncompensated”.

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Metabolic Acidosis

Now, we all learned about the big four: metabolic acidosis, metabolic alkalosis, respiratory acidosis and respiratory alkalosis, but what are they and how do you know which is which? Well, for starters, you need an ABG to actually diagnose any of them. If you’re fuzzy on interpreting ABGs (which most of us are unless you do them on a regular basis), Omni’s method for interpreting ABGs is above. Even if you don’t have an ABG available to you, certain clinical signs and symptoms, a good patient history, and a thorough assessment with a few standard assessment tools can point you towards a fairly accurate diagnosis without an ABG. So, let’s go.

Metabolic Acidosis is the result of some metabolic process that results in acidic products building up in the system faster than the kidneys can react to maintain the acid-base balance. Treatment for metabolic acidosis is centered around identifying and treating the underlying cause of the metabolic acidosis. The more common causes of metabolic acidosis are as follows:

Diabetic Ketoacidosis

The biggest one that we learn about is diabetic ketoacidosis; the primary fuel for the body’s metabolism is sugar (carbohydrates), but all the tissues in the body can use a variety of fuels for metabolism, including muscles, which are made of protein. If the body switches over to using proteins for fuel, a class of compound called “ketones” are produced. Ketones are acidic, so if the patient is producing too many ketones, the pH drops, resulting in ketoacidosis. In the field, this is diagnosed through history, obtaining a blood glucose (which will typically be through the roof), and the classic “fruity odor” breath. Treatment here is cautious administration of insulin and slowly lowering the blood sugar over a period of 24-48 hours.

Lactic Acidosis

Another of the more common causes of metabolic acidosis is lactic acidosis. Normal cellular metabolism requires both sugar and oxygen to perform at optimal levels, and produces CO2 and water as byproducts. When oxygen isn’t available in sufficient quantities, the body switches to “anaerobic metabolism” (which means metabolism without oxygen) and produces lactic acid as a byproduct – lactic acid buildup is the cause of muscle soreness after a hard workout. The muscles that you are working aren’t getting enough oxygen to meet the demand of the workout, and lactic acid builds up in those muscles. The quantities of lactic acid produced from working out are limited to an isolated muscle group for a short time, so soreness is typically the worst effect. The problem with lactic acidosis comes In the case of global hypoxia (whether it be hypoxic, stagnant, hypemic, or histotoxic hypoxia), where all of the tissues of the body aren’t getting enough oxygen and they ALL switch over to anaerobic metabolism to maintain some energy output. A common cause here is a severely septic patient, such as would be seen in a meningitis patient. This results in massive production of lactic acid, which gets dumped into the bloodstream to carry it away from the cells, and lowers the blood pH. Hospitals can run labs to determine the lactate level, but until recently, we haven’t been able to do lactate in the field. One of the newer technologies that is becoming more common is a lactate monitor, which works much like a glucometer to measure lactate levels, and will probably be mainstream in the next few years as sepsis therapy becomes more common in the prehospital setting. Definitive treatment here is identifying the specific bacteria or virus causing the illness, and killing it. Patients who progress this far typically have a high mortality rate, and in the preshospital setting, our main therapy is supportive, in the form of fluid boluses, pressors if indicated by the blood pressure, and high-flow diesel.

Kidney disease

As we discussed in the first post, the renal system is the main long-term regulator of the body’s pH. Without going into the cellular pathophysiology of it, suffice it to say this: when the kidneys aren’t functioning properly, they can’t properly regulate the amount of bicarbonate being retained. Too little bicarbonate = too much acid, resulting in acidosis. These patients are typically on dialysis, and there’s not much we can do other than supportive therapy.

Poisoning/Overdose

The classic patients here are aspirin overdoses, ethylene glycol poisoning and methanol poisoning. We all know that aspirin is abbreviated “ASA”, which is the shortened form of the chemical name: acetylsalicylic acid. It says right there in the name “acid”, so it stands to reason that if the patient takes a whole bottle of an acid, they will become acidotic. Ethelyne glycol is the active ingredient in antifreeze, and when the cells try to metabolize it, it breaks down into glycolic acid and oxalic acid, which are excreted from the cell into the bloodstream. Methanol poisoning is roughly the same mechanism; methanol is the cousin of everyone’s favorite off-duty recreational activity, ethanol. Methanol is sometimes referred to as “wood alcohol”, and is most commonly used as a racing fuel or solvent for cleaning (naptha, mineral spirits), and chemically, the difference between methanol and ethanol is that ethanol has one more carbon atom, which makes it safe to drink. When methanol is metabolized by the cells, it breaks down into formic acid. In all cases here, a type of acid is being added to the patient’s bloodstream, and it’s a pretty simple concept: if you add acid to the patient, they become acidic. Prehospital treatment is supportive therapy, as well as good detective work at the scene to determine what the patient might have ingested, so you can relay it to the hospital. Ironically, treatment for ethylene glycol or methanol poisoning is ethanol; the ethanol competes for binding sites in the cells and allows the ethylene glycol or methanol to be filtered by the kidneys. I don’t see us starting to carry booze to administer to these patients anytime in the near future, so prehospital treatment Is still supportive therapy.

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