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!