elsevier

how continuous cardiac, co & etco2 monitoring are reshaping prehospital care

Trend Setterselsevier MArch 2009A supplement to JEMS sponsored by Physio-Control, Inc.

trend setters

4 introduction Exciting changes in patient monitoring I By A.J. Heightman, MPA, EMT-P

5 Where there’s co, there’s not AlWAys Fire How Pulse CO-Oximetry serves as an important assessment & triage tool I By Bryan E. Bledsoe, DO, FACEP, & Mike McEvoy, PhD, RN, EMT-P

9 WhAt is MetheMoglobineMiA? What this level means in your patients & why you should monitor it I By Bryan E. Bledsoe, DO, FACEP, & Mike McEvoy, PhD, RN, EMT-P

14 universAl cApnogrAphy A vital asset that improves patient care on almost any call I By Patricia A. Brandt, RN, BSN, MHR

18 getting the trend Maximizing the potential of the prehospital 12-lead ECG I By Tim Phalen

disclosure of Author relationships: Contributing authors have been asked to disclose any relation-ships they may have with commercial supporters of this supplement or with companies that may have relevance to the content of the supplement. Such disclosure at the end of each article is intended to provide readers with sufficient information to evaluate whether any material in the supplement has been influenced by the writer’s relationship(s) or financial interests with said companies.

LIFEPAK 15 is a registered trademark of Physio-Control, Inc. Masimo, the Radical logo, Rainbow, SET, SpCO, SpMet, Pulse CO-Oximeter and Pulse CO-Oximetry are trademarks or registered trademarks of Masimo Corp.

MArch 2009 Trend Setters 3

Vice President/Publisher Jeff Berendeditorial director A.J. HeigHtmAn, mPA, emt-Pmanaging editor LisA BeLL, emt-BAdvertising director Judi LeidigerCover Photo Courtesy PHysio-ControL, inC.

trend setters is a supplement sponsored by Physio-Control, inc., with support from masimo and oridion, and published by elsevier Public safety, 525 B street, ste. 1900, san diego, CA 92101-4495; 800/266-5367 (fed id # 13-1958712). Copyright 2009 elsevier inc. no material may be reproduced or uploaded on computer network services without the expressed permission of the publisher. subscription information: to subscribe to an elsevier publication, visit www.jems.com. Advertising information: rates are available on request. Contact elsevier Public safety, Advertising department, 525 B street, ste. 1900, san diego, CA 92101-4495; 800/266-536.

tAble oF contents

JOURNAL OF EMERGENCY MEDICAL SERVICES

TheConscience

of EMS

4 Trend Setters Journal of emergency Medical services (JeMs)

This editorial supplement discusses important enhance-ments in prehospital monitoring being presented by Physio-Control’s new monitor/defibrillator—the LIFEPAK 15. These monitor enhancements illustrate how new technology will enable you to do your job easier, recognize dangerous trends occurring in your patient’s condition, bet-ter document those trends (and the care you rendered), and present that documentation and trending data to receiving emergency department staff.

Physio-Control’s LIFEPAK 15 monitor/defibrillator (510(k) pending) offers Masimo’s breakthrough Rainbow SET Pulse CO-Oximetry technology as an option to allow crews to non-invasively and continuously monitor carboxy-hemoglobin, methemoglobin and oxygen levels in the blood. Through use of a revolutionary sensor that employs 7+ wavelengths of light to collect and analyze an extraordinarily rich stream of physiological data, crews can now accurately measure carbon monoxide and methemoglobin levels in the blood in addition to oxygen saturation and pulse rates.

To illustrate the importance of this new technology, this supplement explains the basics of carbon monoxide and methemoglobin and monitoring for both. Being able to monitor oxygen and carbon monoxide concentrations in a patient’s blood eliminates the risk of misdiagnosing unsus-pected CO poisoning as flu or fatigue, and will enable crews to detect and treat potentially life-threatening conditions.

Dr. Bledsoe’s article describes the utility of the met-hemoglobin detection. Similar to CO, the symptoms of methemoglobinemia can be misdiagnosed but have dire consequences. This new technology uses the same finger probe used in pulse oximetry and will enable crews to non-invasively detect carbon monoxide and methemoglobin lev-els in a patient’s blood and better understand their patient’s medical status in the field and render treatments sooner.

As with most changes introduced in EMS, particu-larly the introduction of new technology, there are often questions and some degree of skepticism, with naysayers asking, “Why do we need it now when we’ve done just fine without it in the past?”

The reality is that in the short 40-year history of modern EMS, we’ve experienced numerous changes in the educa-tion of our personnel and the refinement of the equipment deployed in the field. Let’s look back at our evolution.

In the 1970s, EMS crews were using bouncing-ball ECG scopes, three-lead cable/electrode sets, defibrillation paddles and monophasic energy to render care to patients. And, for a while, the only way to externally pace a patient’s heart was to hook up a separate pacing device that then had to be linked into our monitor/defibrillators.

exciting chAnges in pAtient Monitoring By A.J. Heightman, mPA, emt-P

introduction

Battery life was also a major issue, with non-replaceable batteries that weighed almost as much as the inner work-ings of the monitor/defibrillators.

In the late ’70s, pulse oximetry arrived as an important assessment tool for our crews. But it also added another device that had to be carried into, and accounted for, at each emergency scene.

Hospitals had monitor/defibrillators that could assess multiple patient parameters and 12-lead ECGs, but they were too large to take out in the field. But in the ’80s and ’90s, technological advances and better engineering enabled us to reduce the weight of our monitor/defibrillators and integrate more capabilities into compact cases.

Having internal pacing capabilities and replaceable, rechargeable batteries were major advancements for prehospital systems, but that was only the beginning. Soon, longer-lasting batteries and biphasic defibrillation were added and we thought we had really taken our monitoring and defibrillation capabilities to the highest level.

Then, because it was difficult to hear blood pressures us-ing stethoscopes in moving ambulances (still is), engineers designed electronic BP capabilities into prehospital moni-tors. And integral pulse oximetry was introduced in cardiac monitors, with EMS systems quickly adopting it as a useful feature that could be immediately available to crews, assist them in determining the severity of patient illnesses and reduce the amount of equipment that needed to be carried.

However, when 12-lead ECG capabilities were offered, many EMS agencies were ambivalent, scoffing at the extra training (and wires/electrodes) it required. But cardiologists and EMS medical directors soon convinced progressive ALS systems that if they truly wanted to assess and provide the earliest treatment, they should use 12-lead ECGs.

Thus, we have embraced the prehospital monitoring enhancements that have been presented to us over the past 40 years and need to understand the impact that cardiac trending and the measurement of methemoglobin, carboxy-hemoglobin and oxyhemoglobin in the blood will have on the assessment and care of our patients. Being able to monitor multiple vital signs and patient parameters, and generate comprehensive reports that show your care and patient trending, truly brings critical care technology to the field. These changes will be good for you and your patients.

A.J. heightman, MPA, EMT-P, is the editor-in-chief of JEMS and the editorial director of Elsevier Public Safety. He has served as director of operations for Cetronia Ambulance in Allentown, Pa., and as executive director of the Eastern Pennsylvania Emergency Medical Services Council. Contact him at [email protected].

T


The paramedics quickly formulated a differential diagnosis that included food poisoning and carbon monoxide (CO) poisoning. A Pulse CO-Oximeter was applied to each family member, and all were found to have elevated car-boxyhemoglobin (SpCO) levels. Additional ambulances were summoned, and the family was transported to the hospital.

During assessment, the paramedics had also learned the family was staying in a local hotel. The Raleigh Fire Department was notified, and an engine was sent to the hotel. Dangerously high environmental CO levels were detected within the hotel, and 50 people were safely evacuated. Three hotel guests had elevated SpCO levels and were transported to the hospital. Through the use of Pulse CO-Oximetry, only those patients with elevated SpCO levels were

transported while those without elevated levels remained at the scene—averting a significant mul-tiple casualty incident and excess use of EMS and hospital resources.

introductionCO poisoning remains the most com-mon cause of poisoning in industrial-ized countries.1 CO is an odorless, tasteless and colorless gas that results from the incomplete combustion of carbon-containing substances, such as wood and petroleum products. The incidence of CO poisoning tends to peak following disasters and cold weather and is related to the use of heaters and gasoline-powered devices, such as portable generators.2

Hemoglobin, the chemical in the blood responsible for transport-ing oxygen, is highly susceptible to the effects of CO. Hemoglobin will preferentially bind CO over oxygen until the molecule contains nothing but CO (see Figure 1). In addition, CO will actually displace the oxy-gen already bound to hemoglobin. The resultant combination of CO and hemoglobin is a compound called carboxyhemoglobin (COHb), which cannot transport oxygen to body tissues. This binding is fairly irreversible.

The body rids itself of CO through both the breakdown of carboxyhemoglobin and the slow off-loading of CO from the heme portions of the hemoglobin molecule. When CO is released from the hemoglobin, it’s removed from the body through the respiratory system. The removal of CO from car-boxyhemoglobin takes four to six hours in room air conditions. The CO removal rate can be decreased to ap-proximately 80 minutes with the administration of 100% oxygen. Hyperbaric oxygen (HBO) therapy, and possibly

How Pulse CO-Oximetry serves as an important assessment & triage tool

Where there’s co, there’s not AlWAys Fire

OOn March 5, 2008, paramedics from Wake County EMS in Raleigh, N.C., re-sponded to a 10-year-old child with a headache. The family called EMS from their vehicle because they couldn’t locate a hospital. On arrival at the vehicle, paramed-ics Junith Peterson and Beth Staley found and assessed the child. They learned the family had eaten together at a local restaurant earlier in the evening and then went to sleep shortly after that. Around 10 p.m., several family members had awakened with headaches, including the child.

By Bryan e. Bledsoe, do, fACeP, & mike mcevoy, Phd, rn, emt-P

Figure 1: oxygen vs. co

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emitting diodes (LEDs), pass through a finger vascular bed and are detected by photoreceptors on the other side (see Figure 2). The amount of light received by these photoreceptors is fed into a processor, which then determines the percent-age of carboxyhemoglobin present. Because Pulse CO-Oximetry is an indirect measure of carboxyhemoglobin levels, it reports these levels as SpCO, which cor-responds to actual carboxyhemoglobin levels in the patient.6 Therefore, you’re able to get a continuous reading and can monitor the effects of treatment.

Generally speaking, when a patient with CO poisoning receives 100% oxy-gen in the prehospital setting, you’ll see a steady decline in SpCO levels. With Physio-Control’s LIFEPAK 15, historical patient trending data is recorded for up to eight hours and available to print out as a summary for emergency department (ED) and documentation purposes.

indicAtions For pulse co-oxiMetryWith the advent of any new technology, it’s important to define the role of the technology in the prehospital and emergency setting. The detection and monitoring of SpCO levels have several applications and advantages for prehospital professionals. These include detection and diagnosis of CO poisoning, differential diagnosis of CO and cyanide poisoning, monitoring and rehabilitation of firefighters and other emergency personnel, historical

trending of CO levels during prehospital care, and epidemiological monitor-ing and detection.

Detection & diagnosis of CO poisoning: In the past, the diagnosis of CO poisoning in the prehospital setting has been virtually impossible. Thus, many patients have been transported who did not have CO poisoning. Likewise, some

patients with CO poisoning may not have been transported. It’s clear from the medical literature that the earlier CO poisoning is diagnosed and treated, the better the ultimate outcome for the patient. Thus, obtaining a fairly definitive diagnosis in the prehospital setting is of paramount importance.

It’s important to point out that exclusion of CO poisoning in the pre-hospital setting can be almost as important as detection. CO emergencies

continuous positive airway pressure (CPAP), can speed CO elimination even more.

Recently, it has been shown that CO also affects other iron-containing proteins, such as myoglobin, neuro-globin and cytochrome oxidase. In fact, much of the adverse effects seen in CO poisoning are more related to CO binding to non-hemoglobin iron-containing proteins rather than hemoglobin itself.3 We’ve always known that the signs and symp-toms of CO poisoning are strikingly similar to cyanide poisoning. Now, we know this is due to the fact that both CO and cyanide bind to the enzyme cytochrome oxidase and in-hibit the normal processing of oxy-gen and the subsequent formation of energy within the cells. With the advent of Pulse CO-Oximetry, pre-hospital personnel can now rule in or rule out CO exposure in patients who have had possible exposure to products of combustion.4

signs & syMptoMs oF co poisoningThe signs and symptoms of CO expo-sure can be extremely vague, making prehospital diagnosis difficult (see Table 1, p. 7). In addition, because the pathophysiological effects of CO poisoning are extremely complex, there’s often no identifiable relation-ship between carboxyhemoglobin levels and the signs and symptoms found.5 Thus, diagnosis and detec-tion of CO poisoning requires the use of technology. Although common environmental (four-gas) detectors used by fire departments can detect CO in the surrounding environment, they cannot determine specific levels in a given patient. Patient CO levels can be detected only through exhaled carbon monoxide gas monitoring or through Pulse CO-Oximetry.

pulse co-oxiMetryPulse CO-Oximetry is a monitor-ing technology that uses multiple wavelengths of light to measure levels of carboxyhemoglobin in the blood. Light waves are emitted from light-

As more is learned about the effects of CO, there’s a growing body of scientific evidence that shows that both acute and chronic CO exposure can lead to such problems as early cardiovascular death.

High-concentration oxygen should be provided early in cases of suspected cyanide poisoning because CO is often also present.

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often involve numerous people and can severely tax prehospital and hos-pital resources. Thus, the ability to exclude CO poisoning as a diagnosis can help to avoid un-necessary transport and the associated expenses to the EMS system and the patients.

Calls involving CO detector alarm activa-tions are a common fire service response. Traditionally, firefighters have utilized atmospheric monitors to assess for en-vironmental CO poisoning, often missing toxic levels of CO when a structure was ventilated prior to their arrival. With the availability of technology to screen people for CO poisoning, firefighters are now able to accurately and safely determine whether CO detector alarms are indicative of real danger to building occupants.

Differential diagnosis of CO & cyanide poisoning: Now that a safe antidote (hydroxocobalamin) is available for cyanide poisoning, it’s important to try to determine whether a patient may be suffering from cyanide poisoning.7 In the past, this was extremely difficult in both the prehospital and hospital settings. When confronted by a poisoned patient, especially one who came from an environment where they were exposed to products of combustion, prehospi-tal personnel should attempt to distinguish the etiology. As discussed earlier, the effects of CO poisoning and cyanide poisoning are extremely similar. For example, in a patient who presents with chest pain, altered mental status, dys-rhythmias or shock, it’s often unclear whether the cause is cyanide or a large dose of CO. Thus, the determination of a SpCO can help direct the best course of treatment. If the patient has a relatively high SpCO, then CO is more likely the cause (although this does not necessarily exclude concomitant cyanide poisoning). Likewise, if the patient has a relatively low SpCO but has signifi-cant signs and symptoms, cyanide may be more likely and hydroxocobalamin administration should be considered. In addition, high-concentration oxygen should also be provided, because both toxins are often present.

Firefighter monitoring & rehabilitation: It has always been thought that CO exposure is an occupational risk for firefighters. As more is learned about the effects of CO, there’s a growing body of scientific evidence that shows that

both acute and chronic CO exposure can lead to such problems as early cardiovascular death and even neurological diseases. Because of this risk, the National Fire Protection Association (NFPA) has published a standard (NFPA 1584) that calls for medical monitoring of firefighters on the fire ground and in certain training situations. NFPA 1584 recommends both

the use of pulse oximetry and CO detection.8 This can be accomplished with Pulse CO-Oximetry (as a stand-alone device) or through the patient monitoring capabilities of a cardiac monitor, such as the LIFEPAK 15 (with the CO and pulse oximetry modules). With the guidance of medi-cal directors, fire departments must develop policies and procedures for CO monitoring and subsequent treat-ment if elevated CO levels are found.

Historical trending of CO levels during prehospital care: High- concentration oxygen therapy signifi-cantly increases the rate of carboxy-hemoglobin elimination. Thus, it’s not uncommon for an EMS crew to detect an elevated SpCO in a patient, provide high-concentration oxygen therapy during assessment and trans-port, and subsequently deliver the patient to the ED with near normal SpCO readings.

The ability to provide historical trending data (and patient docu-mentation) will demonstrate to the ED staff the degree of CO exposure and the response to treatment. It’s important to point out that this goes beyond documentation issues. Early high-concentration oxygen administration can prevent many of the serious effects (both short-term and long-term) of CO poisoning. On the other hand, there’s growing evidence that indicates late admin-istration of oxygen can induce the formation of dangerous chemicals called “oxygen free-radicals.” These harmful chemicals are thought to


table 1: signs & symptoms of co poisoningMalaise Confabulation Visual disturbancesFlu-like symptoms Agitation SyncopeFatigue Nausea SeizuresDyspnea on exertion Vomiting Fecal incontinenceChest pain Diarrhea urinary incontinencePalpitations Abdominal pain Memory disturbancesLethargy Headache Gait disturbancesConfusion Drowsiness Bizarre neurologic symptomsDepression Dizziness ComaImpulsiveness Weakness DeathHallucination Confusion

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Light waves are processed to determine the percentage of carboxyhemoglobin present in the blood.


about the deleterious effects of CO, it is becoming increasingly clear that early diagnosis and treatment makes a difference. This concept not only applies to EMS patients, but also has significant applications in monitoring and main-taining the health and safety of emergency personnel in dangerous fire and industrial situations.

bryan bledsoe, DO, FACEP, is a board-certified emergency physician and clinical professor of emergency medicine at the university of Nevada School of Medicine and the university Medical Center of Southern Nevada. He’s a frequent contributor to JEMS and regular speaker at EMS conferences worldwide. Contact him at [email protected].

Mike Mcevoy, PhD, RN, EMT-P, is the EMS coordinator for Saratoga County. N.y., as well as a criti-cal care nurse and an instructor in critical care medicine at Albany Medical College. He’s active in firefighter health and safety research and a regular speaker at fire and EMS conferences. Contact him at [email protected].

disclosure: Dr. Bledsoe serves as a consultant and speaker for Masimo and has reported receiving honoraria from Masimo. Dr. McEvoy serves as a consultant and speaker for Masimo and has reported receiv-ing honoraria from Masimo and Physio-Control, Inc.

reFerences1. Kao LW, Nañagas KA: “Carbon monoxide poisoning.” Emergency Medicine Clinics of North America.

89:1161–1194, 2005.2. Hampson NB, Stock AL: “Storm-related carbon monoxide poisoning: Lessons learned from recent

epidemics.” undersea and Hyperbaric Medicine. 33:257–263, 2006.3. Iheagwara KN, Thom SR, Deutschman CS, et al: “Myocardial cytochrome oxidase activity is decreased

following carbon monoxide exposure.” Biochimica et Biophysica Acta. 1772:1112–1116, 2007. 4. Alarie y: “Toxicity of fire smoke.” Critical Reviews in Toxicology. 32:259–289, 2002.5. Chee KJ, Nilson D, Partridge R, et al: “Finding needles in a haystack: Case series of carbon monoxide

poisoning detected using new technology in the emergency department.” Toxicology Review. 46:461–469, 2008.

6. Barker SJ, Curry J, Redford D, et al: “Measurement of carboxyhemoglobin and methemoglobin by pulse oximetry: A human volunteer study.” Anesthesiology. 105:892–897, 2006.

7. Shepherd G, Velez LT: “Role of hydroxocobalamin in acute cyanide poisoning.” Annals of Pharmaco-therapy. 42:661–669, 2008.

8. National Fire Protection Association: “NFPA 1584: Standard on the Rehabilitation Process for Members During Emergency Operations and Training Exercises (2008 Edition).” NFPA: Quincy, Mass., 2008.

be associated with many of the del-eterious, and sometimes permanent, effects of CO poisoning.

Epidemiological monitoring & detection: As an example of how important CO monitoring capa-bilities are, we’ll look at a 2008 case involving firefighters in Walker County, Ga., who were called to a local brake factory after an employee went home sick. On closer evalua-tion, several workers exhibited signs and symptoms of CO exposure. The fire agency’s four-gas meter showed markedly elevated levels of CO in the factory. However, the source of the CO was unclear.

The firefighters measured the SpCO levels of the affected workers. They then obtained a floor plan (pre-plan) for the building and marked where each worker had been and the SpCO level found in that worker. Through this method, they deter-mined that workers in a certain area of the building had a higher SpCO than those in other areas. Once the firefighters were able to localize the area with high CO levels, they investigated and determined that a recently installed furnace was the CO source. In addition, through Pulse CO-Oximetry, they were able to triage exposed patients and send those with low SpCO levels home while routing those with elevated levels to the hospital for treatment.

This process and use of field tech-nology allowed for a more appropriate use of resources and reduced un-necessary hospital costs and worker’s compensation costs for the employer. Thus, the informed use of Pulse CO-Oximetry can, in certain situations, be used to identify the source of a CO exposure when the results of environ-mental monitoring devices are unclear.

suMMAryNew and evolving technologies are revolutionizing the practice of pre-hospital care. The ability to monitor beat-to-beat changes in a patient’s condition allows EMTs and para-medics to provide rapid and de-finitive treatment. As we learn more

Because high-concentration oxygen therapy helps the body eliminate carboxyhemoglobin, it’s not uncommon to deliver a CO-exposed patient to the ED with near normal SpCO readings.

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The patient was asymptomatic at the start of the procedures and later began to complain of palpitations and shortness of breath. The dentist’s office staff placed the patient on a pulse oximeter, which showed an oxygen saturation (SpO2) of 89% and a pulse rate of 140 beats per minute. On arrival, the EMS crew found she was receiving oxygen at 2 L per minute via a nasal cannula.

The crew examines the patient and finds marked cyanosis, anxiousness and some chest discomfort. They replace the nasal cannula with a non-rebreather mask and increase the delivered oxygen concentration to near 100%.

Despite these actions, the patient’s cyanosis persists, as do her other signs and symptoms. ECG leads are placed, and patient monitoring probes are applied. The carbon monoxide screen (SpCO) is moderately high at 14%. However, the methemoglobin level (SpMet) is detected at 43%. The patient is questioned about prior problems with local anesthetics and denies any history of problems or reactions. She is a non-smoker, has a carbon monoxide (CO) detector in her home, and reports no recent activities that might be associated with CO exposure.

The crew moves the patient to the ambulance and notifies the local emergency department (ED) of the high SpMet level. An IV line is placed, and she’s rap-idly transported to the hospital. There, she’s promptly evaluated by ED staff, who confirm the likely diagnosis of methemoglobinemia. A 1% solution of methylene blue is administered intravenously at a dose of 1 mg

per kilogram. Following administra-tion, the patient significantly im-proves over the next 30 minutes. Her cyanosis clears, and other signs and symptoms of methemoglobinemia abate. She is monitored for 12 hours and discharged home.

introductionHemoglobin, an iron-containing protein that transports oxygen, is essential for life. It’s produced and contained within the red blood cells (erythrocytes), which constantly circulate throughout the circulatory system, delivering oxygen to all body tissues. The typical lifespan of a red blood cell is approximately 120 days.

Hemoglobin is made up of four protein chains—normally two alpha (α) and two beta (β) chains. Each of the four chains contains an iron-based structure called a “heme.” The heme structure is where oxygen binds to hemoglobin. Thus, each molecule of hemoglobin can bind four mol-

What this level means in your patients & why you should monitor it

WhAt is MetheMoglobin?

AAn ambulance is dispatched to a local oral surgery clinic for a patient with difficulty breathing. The paramedic crew arrives promptly and is brought back to a surgical room. The patient is a middle-aged female in respira-tory distress and exhibiting marked cyanosis. The paramedics question the dentist and the dental assistant about the procedure. The patient was being prepped to have a dental implant placed and some mucosal lesions removed with a laser. She had not yet been sedated, but the staff had washed her mouth with 30 mL of a 20% benzocaine solution for mucosal anesthesia. In addition, the dentist had also administered a mandibular nerve block with 2% lidocaine.

By Bryan e. Bledsoe, do, fACeP, & mike mcevoy, Phd, rn, emt-P

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Increased levels of methemoglobin reduce the blood’s ability to transport oxygen, leading to hypoxia.


causes an increase in methemoglobin production. The other is a problem or deficiency in the enzyme systems that convert (reduce) methemoglobin back to deoxyhemoglobin. This deficiency subsequently decreases the rate of methemoglobin elimination. Typically, methemoglobinemia is the result of both of these factors.

Methemoglobin results most frequently from toxic exposure. Several drugs and toxins induce methemoglobin production, including drugs used for local anesthesia (e.g., benzocaine, lidocaine), drugs used to treat cyanide poisoning (e.g., amyl nitrite and sodium nitrite), certain antibiotics, nitroglycerin and others (see Table 1). These are typically oxidizing agents and will induce a change in the charge state of the iron, thus forming methemoglobin.2

Some people are born with deficiencies in the enzyme systems that reduce methemoglobin to deoxyhemoglobin. Typically, these people are identified at

birth because of persistent cyanosis. However, not all infants who develop methemoglobinemia have enzyme deficiencies. In infants, methemoglobin-emia can result from systemic acidosis related to an infection, diarrhea or de-hydration. Infants may also be suscepti-ble to oxidizing toxins. This appears to be more common in rural areas where well water may contain a high level of nitrates, usually from fertilizer runoff and seepage into an aquifer.

signs & syMptoMsAs methemoglobin levels increase, the amount of normal hemoglobin available for oxygen transport falls. Eventually, signs and symptoms of hypoxia will develop. Thus, the signs and symptoms of methemoglobin-emia depend on the percentage of methemoglobin (SpMet) present. Methemoglobinemia results in a functional anemia. This means that although total hemoglobin stores are normal, the amount of hemo globin available to transport oxygen is decreased (see Table 2, p. 12). Body systems that are highly dependent on oxygen, such as the nervous and cardiovascular systems, are usually the first and most profoundly affected as methemo globinemia develops.

The signs and symptoms of methemoglobinemia are quite similar to the signs and symptoms of CO poisoning. The similarity in patient presentation is due to the fact that both conditions decrease the oxygen-carrying capacity of the blood by increases in abnormal hemoglobin types. When methemoglo-binemia and carbon monoxide poisoning occur concomitantly, the signs and symptoms of hypoxemia increase markedly.

non-invAsive technologyMethemoglobin levels can be measured through a multi-function Pulse CO-Oximetry finger probe, if the methemoglobin module is installed in your

ecules of oxygen (O2). When oxygen is bound to hemoglobin, the resultant molecule is called “oxyhemoglobin.” When oxygen is not bound, the mol-ecule is called “deoxyhemoglobin.”

Because heme is a metal (iron), it contains an electrical charge. When oxygen is not bound to the iron molecule, the iron molecule is in the ferrous (Fe2+) charge state. When oxy-gen binds to the iron, a process called “oxidation” changes the charge to the ferric (Fe3+) charge state. Iron in the ferric state cannot bind oxy-gen until it’s reduced back to the ferrous state. This reaction process is necessary to under-stand in order to understand methemoglobin (MetHb).

Methemoglobin is a form of hemoglobin in which the iron molecules are in the ferric (Fe3+) state. Thus, methemoglo-bin can neither bind nor trans-port oxygen. Methemoglobin has a bluish-brown color. Normally, there are enzyme systems (e.g., methemoglobin reductase) that can restore methemoglobin to the ferrous (Fe2+) state, forming deoxy-hemoglobin, so it can again transport oxygen. Typically, less than 2% of the hemoglobin in the body is in the form of methemoglobin and cannot bind or transport oxygen. However, several conditions and drugs can cause abnormal elevations of methemoglobin.1

pAthophysiologyNormally, methemoglo-bin forms and disappears without significantly af-fecting the body. However, because methemoglobin cannot transport oxygen, hypoxemia will steadily develop as methemoglobin levels rise—a phenomenon called “methemoglobinemia.” Two factors can lead to elevated methemoglo-bin levels. The first is the presence of drugs that oxidize the iron on hemoglobin (changing it from a ferrous to a ferric state). This

table 1: Agents implicated in Acquired MethemoglobinemiaAmyl nitrite (cyanide antidote) Aniline derivatives (dyes)Benzocaine (local anesthetic)Bismuth subnitrite (antiseptic)Butyl nitrite (antianginal, recreational drug “poppers”)Chloroquine (anti-malarial)Dapsone (anti-tubercular agent)Lidocaine (local anesthetic)Menthol (local anesthetic)Naphthalene (mothball agent)Phenytoin (anticonvulsant)Nitric oxide (vasodilator)Nitroglycerin (antianginal)Nitrophenol (hydrocarbon, irritant)Nitrates (antianginals)Nitrites (antianginals)Paraquat (herbicide)Phenacetin (older analgesic)Phenols (aromatic hydrocarbons)Propellants (for room deodorizers)Pyridium (urinary tract anesthetic)Quinones (oxidizing agents)Silver nitrate (cauterizing agent)Smoke inhalationSodium nitroprusside (antihypertensive)Sulfonamides (antibiotics)

monitor (see Figures 1 and 2). Pulse CO-Oximeters use multiple wavelengths of light to measure and distinguish the various types of hemoglobin present (de-oxyhemoglobin, oxyhemoglobin, carboxyhemoglobin and methemoglobin). The Pulse CO-Oximeter processes the data and reports oxygen saturation (SpO2), carboxy hemoglobin percentage (SpCO) and methemoglobin percentage (SpMet). These findings allow personnel to exclude methemoglobinemia as a diagnosis. If methemoglobinemia is present, it will allow for ongoing measurement.

Additionally, as seen in the case example, the presence of methemoglo-binemia falsely elevates reported Pulse CO-Oximeter SpCO values. The LIFEPAK 15 can record SpMet trends for intervals up to eight hours. There-fore, these data can be printed out in a prehospital patient summary to show ED staff any trends and changes in the patient’s condition that occurred in the field setting. This capability is especially valuable when the prehospital treatment improves or eradicates a patient’s methemoglobinemia.

pAtients to MonitorAlthough methemoglobinemia is relatively uncommon, prehospital personnel will be increasingly likely to encounter it. First, the development of freestand-ing surgical centers has resulted in more patients receiving local and general

anesthesia outside of the traditional hospital setting. Second, because of hospital specialization, critically ill or injured patients are often transported between facilities, and some of these patients are receiving medications (e.g., sodium nitroprusside, nitric oxide, nitroglycerin) that can induce methemo-globinemia.3 Methemoglobin monitoring of these patients provides an added margin of safety during critical care transport.

Third, the use of older cyanide antidotes (amyl nitrite and sodium nitrite), which purposely induce methemoglobin formation, can be more safely admin-

istered if SpMet levels are measured. The nitrites can cause dangerous elevations in selected individuals, particularly children and women, and can now be monitored (see Figure 3).

Thus, prehospital methemoglobin monitoring is valuable in cases involv-ing persistent cyanosis, nitric oxide and nitrate therapy, administration of a cyanide antidote kit, elevated SpCO readings and risk of inflammation.

Persistent cyanosis: Most cyanotic patients will respond favorably to supplemental oxygen administration. However, in those that do not, elevated methemoglobin levels should be considered a cause, because elevated methemoglobin levels can be treated with a relatively safe antidote.

Most cases of methemoglobine-mia encountered in the prehospital setting will be due to the effects of drugs and toxins. Elevated methemoglobin levels have been detected following the administra-tion of benzocaine, lidocaine and other local anesthetics. In one study,


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Figure 1: liFepAK 15 Monitor/defibrillator* trend summary of spMet

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of hemoglobin to methemoglobin (changes the heme groups from the ferrous [Fe2+] to the ferric [Fe3+] state). Cyanide then pref-erentially binds to methemoglobin in-stead of cytochrome oxidase, thus freeing

up cytochrome oxidase for energy production by the cells. The third step in the cyanide antidote kit, sodium thiosulfate, converts cyano-methemoglobin to normal hemoglobin and thiocyanate. Thiocyanate is subsequently excreted.

However, because methemoglobin cannot transport oxygen, the oxygen-carrying capacity of the blood falls as methemoglobin levels rise. This is especially important in patients who are small (e.g., children and women) or have pre-existing disease. In addition, concomitant poisoning with carbon monoxide will further decrease the oxygen carrying capacity of the blood as carboxyhemoglobin levels (SpCO) rise. Because of these factors, it’s prudent to measure both SpMet and SpCO levels when administering the nitrite compo-nents of the cyanide kit. Of note, the cyanide antidote hydroxocobalamin does not induce methemoglobinemia.6

Elevated SpCO readings: A phenomenon seen with Pulse CO-Oximetry technology is a tendency to report falsely elevated CO readings in the presence of significant methemoglobinemia. SpCO readings are not considered reliable when SpMet levels exceed 5%. A valuable benefit of Pulse CO-Oximetry then is that low SpMet readings can be used to confirm the accuracy of significant-ly elevated SpCO measurements.

Risk of inflammation: The free-radical compound nitric oxide (NO) is produced when hemoglobin is converted to methemoglobin. Methemoglobin releases free heme and iron, which activate the cells that line blood vessels (endothelial cells). These cells release NO, causing an inflammatory response. This inflammatory response, initiated by NO and other free radicals, is a cas-cade of events called “oxidative stress.” Oxidative stress has been linked to the development of numerous conditions, including atherosclerosis, heart disease, Alzheimer’s disease, Parkinson’s disease and other chronic conditions. Measure-ment of SpMet levels, especially over time, may help identify those at increased risk of oxidative stress and the subsequent problems associated with it.

treAtMentPatients found to have elevated methemoglobin levels but who are as-ymptomatic should be treated conservatively with supplemental oxygen and monitoring. However, patients with elevated SpMet levels (generally > 20–30%) who are symptomatic may benefit from antidotal treatment. The antidote for methemoglobinemia is the dye methylene blue. Methylene blue reduces methemoglobin to deoxyhemoglobin. Thereafter, the dye is recycled. The typical dose of methylene blue is 1–2 mg per kilogram body weight in-fused intravenously over three to five minutes. It’s supplied in a 1% solution (10 mg/mL).

The decision to administer methylene blue in the prehospital setting is one of local medical directors and should consider patient acuity mix and transport times. It’s important to point out that methylene blue is a dye and following administration, pulse oximeters and laboratory instruments will register erroneous readings for a short period of time (usually less than

signs and symptoms typically developed within 20 minutes. SpMet concentra-tions ranged from 19–75%. Deaths were reported.4 Other drugs, such as certain antibiot-ics, can also induce methemoglobinemia.

Nitric oxide & nitrate therapy: Nitric oxide (NO) therapy is often used to treat newborns with hy-poxic respiratory failure (HRF). NO is administered as a gas and causes pulmonary vasodilation through smooth muscle relaxation. This serves to increase the partial pressure of oxygen in arterial blood (PaO2). Some centers are starting to use NO in adults with adult respira-tory distress syndrome (ARDS). NO induces the oxidation of hemoglobin to methemoglobin. Thus, it’s impor-tant to monitor methemoglobin lev-els during NO therapy—especially in neonates in whom levels of fetal hemoglobin (HgF) are elevated. Ide-ally, SpMet levels should be kept at less than 5%.5

Several other drugs used in the critical care setting can induce methemoglobin formation. The most commonly encountered of these are sodium nitroprusside and nitroglycerin. Sodium nitroprus-side is used to lower blood pressure. Nitroglycerin is used for angina and is a vasodilator and subse-quently decreases cardiac work. When administered at doses often encountered in the critical care setting, both of these drugs can lead to methemoglobin formation. As methemoglobin levels rise, the amount of hemoglobin available for oxygen transport falls. This can be problematic in patients with severe cardiac or respiratory disease and who are otherwise highly dependent on adequate oxygen delivery.

Cyanide antidote: The first two components of the cyanide anti-dote kit (amyl nitrite and sodium nitrite) induce the conversion

table 2: signs & symptoms of Methemoglobinemia

spMet signs and symptoms1–3% Normal, asymptomatic3–15% Slight grayish-blue discoloration15–20% Cyanotic, but asymptomatic25–50% Headache, dyspnea, confusion, weakness, chest pain50–70% Altered mental status, delirium>70% Fatal

20 minutes). Using a Pulse CO-Oximeter can help avoid drawing repeated blood samples by providing continuous monitoring of SpO2 and SpMet levels once the effects of the dye subside.

suMMAryMethemoglobinemia, although uncommon, is a concern for EMS providers— especially during critical care transport. The ability to measure and monitor SpMet levels in the prehospital setting allows for more definitive care, an improved safety margin for the patient, and better documentation for the providers and medical staff. As with all monitoring technologies, it’s wise to consider these findings with the overall patient condition and physical exam findings.

bryan bledsoe, DO, FACEP, is a board-certified emergency physician and clinical professor of emergency medicine at the university of Nevada School of Medicine and the university Medical Center of Southern Nevada. He’s a frequent contributor to JEMS and regular speaker at EMS conferences worldwide. Contact him at [email protected].

Mike Mcevoy, PhD, RN, EMT-P, is the EMS coordinator for Saratoga County. N.y., as well as a critical care nurse and an instructor in critical care medicine at Albany Medical College. He’s active in firefighter health and safety research and a regular speaker at fire and EMS conferences. Contact him at [email protected].

disclosure: Dr. Bledsoe serves as a consultant and speaker for Masimo has reported receiving honoraria from Masimo. Dr. McEvoy serves as a consultant and speaker for Masimo has reported receiving honoraria from Masimo and Physio-Control, Inc.

reFerences 1. Wright RO, Lewander WJ, Woolf AD: “Methemo-

globinemia: Etiology, pharmacology, and clinical management.” Annals of Emergency Medicine. 34:646–656, 1993.

2. umbreit J: “Methemoglobin—It’s not just blue: A concise review.” American Journal of Hematology. 82:134–144, 2007.

3. Alapat PM, zimmerman JL: “Toxicology in the Critical Care unit.” Chest. 133:1006–1013, 2008.

4. Abu Laban RB, zed J, Purssell RA, et al: “Severe methemoglobinemia from topical anesthetic spray: Case report, discussion and qualita-tive systematic review.” Canadian Journal of Emergency Medicine. 3:51–56, 2001.

5. Ware LE: “Inhaled nitric oxide in infants and children.” Critical Care Nursing Clinics of North America. 14:1–6, 2002.

6. Geller RJ, Barthold C, Sairs JA, et al: “Pediatric cyanide poisoning: Causes, manifestations, management, and unmet needs.” Pediatrics. 118:2146–2158, 2006.


Figure 3: Methemoglobinemia diagnosis strategy

OTHER DIAGNOSIS OTHER DIAGNOSIS

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As your partner tries to get ad-ditional medical history from the mother, you approach the teen, who’s leaning forward in the classic tripod position, gasping for breath and clutching her inhaler. When you ask how many times she has used the inhaler, she manages to force out a single word —“lots.”

While you offer reassuring words, you simultaneously attach the leads to the monitor, place the pulse oxi-metry probe on her finger and begin oxygen administration. You also apply a nasal filterline, which you attach to the capnography outlet of your monitor.

The monitor shows sinus tachycardia at a rate of 140 and an oxygen saturation reading of 98%, which at one time would have been a reassuring sign. However, your newly acquired knowledge of capnography, along with the very sharp shark-fin waveform on the monitor’s capnography display and an end-tidal CO2 (EtCO2) reading of 70, give you reason to think oth-erwise. Your partner has already set up an updraft treatment, and you begin to administer the broncho-dilator immediately. After several minutes, although your patient’s respiratory rate has decreased, the ominous shark-fin waveform and elevated EtCO2 reading—now 78—remain.

You recognize the decreased respi-ratory rate is not a sign of improve-ment from the updraft but instead a warning that your patient is becom-ing extremely tired from trying to maintain adequate oxygenation. Although your protocols allow for a second updraft, you know you’re running out of time and choose to contact medical control to obtain orders for the administration of magnesium sulfate IV. Upon receiv-ing the required order, you admin-ister it, and the patient’s breathing eases within minutes. You’re also relieved to see the more normal box-like capnography waveform and


A vital asset that can improve patient care on almost any call

universAl cApnogrAphy

You’re on a 24, and as the end of your shift approaches, you marvel at how quiet it has been. Then, you mentally kick yourself for eliciting the “quiet jinx,” because moments later, you’re dispatched to a severe difficulty breath-ing call. On arrival, you’re met by the patient’s mother, who frantically tells you her 15-year-old daughter can’t breathe. The mother, nearly hysterical, says the girl has recently been evaluated by the doctor for asthma.

By Patricia A. Brandt, rn, Bsn, mHr

Because it provides real-time assessment of respiratory, circulatory and metabolic status, capnography is an incredibly important assessment tool in a multitude of emergency conditions.

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an EtCO2 reading of 45, which confirm a significant resolution of the severe bronchospasm.

poWerFul cApAbilitiesCapnography is the monitoring of CO2 concentration in respiratory gases. Because capnography provides a real-time assessment of respiratory, circula-tory and metabolic status, it can be an incredibly important and powerful assessment tool for determining patient status, appropriate treatment and treatment effectiveness for a multitude of emergency conditions.1 The vast majority of patients with emergent conditions will benefit from capnography.

Initially, capnography was primarily used by anesthesiologists to monitor the respiratory status of mechanically ventilated patients in the operating room. But eventually, for this same purpose, it was adopted in the field.

Using capnography to ensure successful intubation has become the gold standard and is mandated in many EMS systems. The detection of CO2 on expiration is a completely objective confirmation of tracheal intubation.2 Also, because capnography directly correlates with cardiac output, it’s useful

in the cardiac arrest patient to help to determine the effectiveness of CPR compressions, recognize the return of spontaneous circulation and assist with decisions regarding the termination of resuscitation.3

In addition to being an essen-tial assessment tool in intubated patients, capnography has been shown to be an extremely valuable technology to use in non-intubated patients. It provides EtCO2 readings and exhibits the related waveform. The configuration of this waveform can be used in the intubated and non-intubated patient to assess the adequacy of ventilation, status of metabolic activity and effective-ness of circulation. The normal capnogram will consist of box-like waveforms directly related to the dif-ferent phases of the respiratory cycle (see Figure 1).

Patients who are hyperventilating will have a capnogram with a faster rate but lower amplitude of wave-forms, resulting from the decreased CO2 in each breath (see Figure 2).

Patients who are hypoventilating will have a lower rate but a higher amplitude of waveforms, resulting from the increased amount of CO2 being released with each breath (see Figure 3).

The final basic capnographic waveform results from the physi-ological effects of bronchospasm. Bronchospasm causes a slower and more erratic emptying of CO2 from the alveoli, which results in a slower rise in the expiratory upstroke. Instead of the normal box-like wave-form, the presence of bronchospasm results in the characteristic shark-fin shape of the bronchospastic wave-form (see Figure 4).

respirAtory eMergencies Patients with asthma and chronic obstructive pulmonary disease (COPD), as in the opening case study, can be monitored for the pres-ence and severity of bronchospasm and the choice and effectiveness of treatment. Patients who are sedated or receiving pain management can

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Figure 1: normal capnography Waveform

A–B: Respiratory baselineB–C: Expiratory upslope

C–D: Expiratory plateauD: End-tidal value


Capnography should be carefully monitored in the patient with acute myocardial infarction to evaluate the impact on cardiac output. It can be especially useful in the patient who may need pressor support or fluid chal-lenges in order to assess the effectiveness and need for increased or contin-ued administration. Patients with inferior wall myocardial infarction with right ventricular involvement may obtain enhanced benefit from this moni-toring, because they may often require large amounts of infused fluids to maintain adequate blood pressure. In this case, capnography would reflect changes in cardiac output even prior to blood pressure improvement.

Future usesResearch into expanded uses of capnography is ongoing and may reveal even more evidence-based uses. The EMS community has recognized the exciting potential for capnography to be used as a primary assessment tool in many emergency situations, such as detection of pulmonary emboli, sepsis, thyrotoxicosis and malignant hyperthermia.5 Other areas that appear promising include the use of capnography to regulate CO2 levels for patients with head injury and stroke.

Capnography is also being studied as a way to continually assess the re-spiratory status during seizures and in patients who have undergone neuro-

be monitored for hypoventilation, and capnography can assist in deci-sions regarding continued adminis-tration of sedatives or pain control.4 Decisions regarding the need for intubation or assisted ventilation for the overdose patient can also be guided by capnography.

Patients who are hyperventilat-ing and exhibiting anxiety can be particularly difficult diagnostic categories. Capnography can provide assistance in determining a working diagnosis, because hyperventilation with normal or high EtCO2 levels is much more likely to reflect pathol-ogy, whereas hyperventilation with low EtCO2 levels is more likely to reflect anxiety. The capnography waveforms can even be used as a biofeedback technique when coach-ing the anxious patient to decrease their respiratory rate.

MetAbolic eMergenciesCapnography can also be useful in evaluating diabetic ketoacidosis and helping to differentiate diabetic ketoacidosis and hyperglycemic hy-perosmolar non-ketotic coma. It can also aid in determining treatment for sympathomimetic overdoses, including the administration of ben-zodiazepines (which can be guided by increases in EtCO2).

The severity of hypothermia and hyperthermia can be determined by capnography and clinical decision making can be adjusted. Even the severity of metabolic acidosis associ-ated with gastroenteritis, especially in children, can be determined with the use of capnography.

circulAtory eMergenciesThe presence of bronchospasm in the congestive heart failure (CHF) patient can be assessed with cap-nography. It can be especially use-ful in the patient with co-existent CHF and COPD. If bronchospasm isn’t present, the unnecessary administration of bronchodila-tors can be avoided, and their potentially harmful cardiac effects prevented.

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muscular blockade. Its use has even been suggested in the triage of patients involved in a bioterrorism event. Its practical uses are almost limitless.

Another cAseLet’s take a look at another scenario, this one involving a trauma patient. As you arrive on scene at a single vehicle crash, you note an SUV had apparently lost control on the wet road and impacted a light pole with moderate force. The driver appears somewhat dazed but responsive and still restrained by his lap and shoulder belt.

His initial vital signs are a BP of 120/70, HR of 72 and RR of 16. Your head to toe assessment reveals the telltale red seatbelt marks across his chest and abdomen. There are no other obvious signs of injury.

As you maintain C-spine immobilization, you contemplate the transport destination. You’re about two miles from a community hospital and about 12 miles from the Level 1 trauma center. The patient doesn’t meet any of the criteria to mandate transport to the trauma center, so as you begin to attach the monitor leads and apply oxygen via nasal cannula per your EMS protocols, you suggest transporting to the closer hospital.

As the capnography from the nasal filterline initializes, you note a normal capnography waveform with a low EtCO2 reading of 30 mmHg. This imme-diately concerns you because the patient’s respiratory rate continues to be at an apparently normal rate of 16.

As you start en route, you note that the EtCO2 has dropped to 28. You recheck the BP and note a systolic blood pressure of 110, but due to the fur-ther decrease in EtCO2, you divert to the Level 1 trauma center because you know that blood loss and the resulting decrease in cardiac output transports less CO2 to the alveoli and causes an almost immediate drop in EtCO2.

On arrival, the patient is immediately triaged to the trauma room where an abdominal tap confirms intra-abdominal bleeding. The patient is emer-gently transferred to the OR. Once again capnography has helped you identify a significant vital sign variance and provide the highest level of care to your patient.

in conclusionHopefully this article has increased your interest in the use of capnography in not only the intubated but also the non-intubated patient. Watch for a

complete capnography learning program to be sponsored by Physio-Control, Inc. in the near future.

pat brandt has worked in EMS for more than 25 years as an EMS transport nurse, an emergency department nurse, a paramedic educator and as an EMS quality manager. Recently retired from Orange County (Fla.) Fire Rescue Department, she now leads her own medical education and consulting business in Dunlap, Tenn. Contact her at [email protected].

disclosure: The author has reported receiving honoraria and/or research support, either directly or indirectly, from Physio-Control, Inc.

reFerences1. Eipe N, Tarshis J: “A system of classification for

the clinical uses of capnography.” Canadian Journal of Anesthesia. www.cja-jca.org/cgi/content/full/54/suppl_1/44578

2. American Heart Association: Currents, Winter Edition 2005–2006.

3. Levine RL, Wayne MA, Miller CC: “End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest.” The New England Journal of Medicine. 337(5):301–306, 1997.

4. Krauss B, Hess D: “Capnography for procedural sedation and analgesia in the emergency department.” Annals of Emergency Medicine. 50(2):172–181, 2007.

5. Blonshine S: “Expanding the knowledge base: New applications of capnography.” AARC Times. February 1999. 51–53.


orAnge county Fire rescue depArtMent

the prototype Agency for universal capnography

Orange County (Fla.) Fire Rescue Department (OCFRD), with 1,200 firefighter/EMS personnel, is the 25th largest fire department in the nation. It was also one of the first departments to embrace universal capnography, having used it for intubated and non-intubated patients since 2002.

“Orange County Fire Rescue EMTs and paramedics rely on capnography as one of their most important assessment tools,” states EMS Battalion Chief Jose P. Gainza Jr. “They know that the real-time, objective information that they get from capnography regarding the patient’s respiratory, circulatory and metabolic status can have a big impact on their treatment decisions and ultimately impact the patient outcome in a very positive way.” That’s why the Fire Chief Carl Plaugher and their medical director, Dr. George Ralls, a former firefighter/para-medic himself, are so committed to its use.

Capnography is mandatory per protocol for all intubated and artificially ventilated patients and all patients who are chemically or physically restrained. It’s also a component of almost every other treatment protocol, including all patients with respiratory distress, chest pain, decreased level of consciousness and trauma, and any patient receiving sedation or pain management. OCFRD facilitates this with the use of 167 capnography-equipped LIFEPAK 12 monitors.

Every rescue and fire apparatus in the department carries a LIFEPAK 12 with capnography capabilities to ensure that those assess-ment tools are available to every patient in an expedient manner. In addition, all oxygen nasal cannulas have been replaced with Oridion combination filterlines that deliver oxygen and provide capnography through the same cannula. universal capnography is literally a way of life at OCFRD.


In terms of improving ST-elevation myocardial infarction (STEMI) care, two goals are primary: First, increase the number of identified STEMI pa-tients and, second, reduce the time to treatment. The answers to the follow-ing questions will shed light on strategies to improve EMS contribution to STEMI care. Although the questions may appear overly simplistic, they may yield some surprising answers.

Who gets A 12-leAd?EMS agencies have chest pain protocols. However, according to one study of more than 434,877 patients with a discharge diagnosis of acute myocardial infarction (AMI), 33% had no chest pain.1 By implication, if EMS uses chest pain exclusively to “suspect AMI” and run a 12-lead, then one-third of AMIs could be missed.

To maximize the likelihood of catching STEMI on the 12-lead, it’s necessary to go beyond chest pain as the only patient complaint that would prompt a 12-lead ECG. So what other complaints should raise suspicion of possible AMI? Table 1 lists some “pain equivalents,” or anginal equivalents, associated with AMI and STEMI.

Beyond the anginal equivalents, many AMI patients have pain that may not immediately seem cardiac in nature. Chest pain that’s inter-mittent, sharp, low intensity or not sub-sternal may be attributed to a variety of other conditions. However, although costracondritis, pleurisy and other conditions may indeed produce these types of complaints, they don’t preclude AMI. Aside from “non-cardiac sounding” chest pain, many AMI patients complain of pain to the abdomen, jaw, shoulder, teeth and elbow. All of these can be categorized as “atypical pain” presentations.

Certainly, not all atypical pain is from AMI; in fact, only a minor-ity of these complaints are due to myocardial infarction. When these complaints are encountered, however, we must seriously consider the possibility of AMI.

With the extensive list of anginal equivalents (pain-free but not com-plaint-free) and atypical pain presentations (some pain present but not “classic” cardiac pain), it may seem that everyone should be getting a 12-lead ECG. Obviously, not everyone needs a 12-lead, but we can’t wait for

classic chest pain to obtain an ECG. So the original question remains, “Who should get a 12-lead?”

One approach to consider is shown in Figure 1. This approach is offered not as a protocol recommen-dation, but rather as a starting point for discussion and critical thinking. In reviewing Figure 1, it’s obvious that all cardiac chest pain patients should have a 12-lead. However, not all anginal equivalents and atypi-cal pain presentations necessarily require a 12-lead.

When faced with an anginal equiv-alent or atypical pain presentation, it’s worthwhile to recall the three groups of patients most likely to present in a non-classic manner: the elderly, females and diabetics. Therefore, you should seriously consider obtain-ing a 12-lead when you encounter a non-classic presentation in an elderly female or diabetic patient.

As a final double-check before deciding against a 12-lead, use your own clinical instinct. If you have a gut feeling this patient might be experiencing AMI, run a 12-lead. No harm will result from obtaining it. Similarly, it may be fruitful to ask about obvious cardiac risk factors.

When using this or a similar approach, the number of 12-leads obtained will certainly increase, but hopefully so will the number of iden-tified STEMIs. Remember, finding STEMI is like panning for gold: You

Maximizing the potential of the prehospital 12-lead ECG

More thAn A trend

MMost EMS providers are aware of the increased attention hospitals are giv-ing the prehospital 12-lead ECG. Although they’ve been around for years, recent research, recommendations and reimbursement structures have led to the increased use and valuation of 12-lead ECGs within the hospital. With this renewed interest, it’s appropriate to examine strategies to maximize the benefits of prehospital 12-lead ECGs.

By tim Phalen

table 1: Anginal equivalents Associated with AMi & steMi

Respiratory distressSense that something is “wrong”“Weakness”“Fatigue”“Dizziness”“Malaise”“Syncope or near syncope”Alterations in blood sugarAlterations in level of consciousness (particularly in the elderly)

don’t expect to find a gold nugget in every pan, but when you do find one it’s worth all the effort. Likewise, it can be expected that most 12-leads will not identify STEMI; however, when STEMI is identified, and time to treat-ment is shortened, mortality and morbidity will decrease.

When do you obtAin the 12-leAd?Getting early and (preferably) sequential ECGs can help improve the rate of STEMI recognition. Examine the 12-lead ECGs in Figure 2. Both trac-ings were obtained at the scene of a suspected AMI. ST elevation is obvious in the first ECG, but it disappeared only 12 minutes later when the second ECG was taken. Obviously, if efforts had been limited to a single ECG in the field, STEMI recognition may have been delayed.

hoW MAny leAds?Although the 12-lead ECG is currently the best, most available, most economical, most informative screening tool for STEMI, it’s not perfect. The 12-lead ECG has two “blind spots.” The 12-lead ECG doesn’t directly “see” the right ventricle or the posterior wall of the left ventricle. Additional leads can be used to allow health-care providers to screen for STEMI in those areas.

For example, a patient may have an isolated posterior wall infarc-tion. In that case, the 12-lead ECG may show some depression in the range of V1 to V3 or even V4 but would not demonstrate ST elevation. If additional leads were obtained from the patient’s back, ST elevation might be found.

Figure 3 shows an example of when an initial 12-lead did not show ST-segment elevation. However, the paramedic on the call suspected AMI clinically and noted the ST depression in the range of V1–V4. This prompted the acquisi-tion of V4r (of the right ventricle) and V8–V9 (of the posterior wall). Because the additional leads were obtained, this STEMI was identified and directed for reperfusion.

hoW oFten do chAnges occur & Why?A clear answer is still emerging, but departments have reported a range of 7–34% of prehospital 12-lead ECGs capturing dynamic changes in STEMI. Although not necessarily


Figure 1: Who should get a 12-lead?

clAssic chest pAin AtypicAl pAin

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The first ECG was non-diagnostic, but the second ECG—taken only 12 minutes later—identified a STEMI with elevation in V1–V4.

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Figure 2: if at First it’s normal ... Keep your eye on it


transient changes can make a difference.

Better recognition of STEMI: The ECG changes associated with AMI and STEMI can be dynamic. Serial (consecutive) ECGs can increase the likeli-hood of catching those changes. Researchers have determined that, when compared with the initial 12-lead ECG at emergency depart-ment (ED) presentation, ST monitoring improves the sensitivity and specificity in recogniz-ing acute coronary syndrome (ACS) and AMI. In the case of AMI, one study has shown that diagnostic sensitivity improved

from 55.4% in the initial ECG to 68.1% with serial ECGs.4,5

Improved identification of reperfusion candidates: Not all infarct patients improve with immediate reperfusion. STEMI is the primary indi-cation that a patient would benefit from either fibrinolytics or percutane-ous intervention (PCI), such as angioplasty and stenting. Serial ECGs help better identify not only MI, but also the subset of infarct patients who are

representative of all response-area demograph-ics, the findings of one community are summa-rized on Figure 4. In this case, 34% of the STEMI patients had either ST elevation that was gone in later ECGs or had ST elevation present only in later ECGs.

Dynamic ischemic changes on an ECG can result from many potential causes. It may be impos-sible to tell exactly which is responsible in any given situation, but here are a few possibilities.

Infarct is dynamic in nature: An ongo-ing interplay of fac-tors contributes to ECG changes. Among them are variations in myocardial oxygen demand and chemical factors in the clotting process, which can induce coronary artery vasoconstriction. For these and other reasons, ST changes can occur simply as part of the infarct process.

EMS treatment: Oxygen has been shown to reduce or eliminate ST change.2 In addition, nitroglycerin can dilate the target coronary artery and also reduce or eliminate ST elevation.3

Vasospastic angina: Prinzmetal’s angina results from coronary artery vasospasm. During episodes of vasospasm, the ST segment typically elevates. Nitroglycerin often relieves the vasospasm and the ST eleva-tion along with it. Trending can help capture this (see sidebar, p. 22).

do ecg chAnges MAtter?Transient changes on the ECG are more than just interesting little quirks of electrocardiography. In some cases, they can completely alter the diagnosis and resulting treatment, and there are several specific ways that the presence of

The first ECG is an initial 12-lead that did not show ST-segment elevation. However, because the paramedic suspected AMI clinically and noted the ST depression in the range of V1–V4, additional leads were obtained (V4r and V8–V9), and this STEMI was identified and directed for reperfusion.

Figure 3: More leads is sometimes better

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candidates for immediate reperfusion.The 2004 ECC Guidelines make serial ECGs a Class I recommenda-

tion in the ED: “If the clinical ECG is not diagnostic of STEMI but the patient remains symptomatic and there is a high clinical suspicion for STEMI, serial ECGs at five- to 10-minute intervals or continuous 12-lead ST-segment monitoring should be performed to detect the potential development of ST elevation.”3

LBBB & other confounding patterns: Left bundle branch block (LBBB) frequently causes ST elevation when no infarct exists and, in that sense, is an imitator of infarct. However, AMI can also pro-duce a new onset LBBB, and in that setting immediate reperfusion is indicated.

Unfortunately, it can be difficult to determine if the presence of LBBB on the ECG of a suspected AMI patient is pre-existing or is a new onset. If the LBBB is infarct-induced, it has a high mortality rate—up to 60%. Therefore, the patients who may need reperfusion the most are the least likely to receive it. However, dynamic changes on serial ECGs shed light on the situation. A hallmark of infarct is change over time. If a patient has had an LBBB for the past 15 years, it’s not likely to change much during the next 15 minutes. But when changes occur in a short period of time, suspect AMI.

When AMI is suspected clinically, LBBB is present on the 12-lead and changes are observed in serial ECGs, then new onset LBBB is presumed to be infarct-induced. Such patients are potential candidates for immedi-ate reperfusion.

Better identification of high-risk unstable angina: AMI and STEMI are two points on the continuum of ACS. Another point on that continuum is unstable angina. In this condition, the coronary artery is often blocked by a blood clot but shows no evidence of tissue death. Hence, it can’t be called infarction. Treatment of unstable angina varies depending on certain find-ings. High-risk unstable angina patients, although not eligible for immediate reperfusion, may receive an urgent catheterization. Dynamic ECG changes are one criterion used to identify high-risk unstable angina patients.

To date, little work has been done to determine the number of patients whose diagnosis or treat-ment decision could be made from information exclusively present on the prehospital ECG. However, one recent study looked at how often the prehospital 12-lead contained information that would identify high-risk unstable angina patients. It found that 22% of patients with ACS (not necessarily AMI or STEMI) had evidence of ischemia that was not present on arrival at the hospital.6 This is an important finding.

hoW do you coMMunicAte your ecg Findings?Once specific ECG findings sug-gest STEMI has been identified, minutes matter. It’s imperative to communicate that the patient is a potential candidate for immediate reperfusion. Some possible commu-nication strategies include present-ing the 12-lead at arrival or using the radio to alert the receiving facility of your ECG findings and transmitting the ECG.

Several studies have looked at various strategies. One recent example of the importance of early notification demonstrated the results shown in Table 2.

When deciding which commu-nication strategy works best for a particular community, several fac-tors, such as terrain, cellular cover-age and budget, must be taken into consideration. Bear in mind, recent technological improvements make 12-lead transmission much more reliable and practical than even a few years ago.


Figure 4: prehospital serial ecgs & Final diagnoses

12-leAd obtAined on 9,087

eMs pAtients

8,796 PATIENTS =NO ECG EVIDENCE

OF STEMI

102 (31%) = STEMI DETECTED TO NO STEMI

8 (3%) = NO STEMI TO STEMI

91(27%) = BOTH ECGS NORMAL

130 (39%) = STEMI DETECTED ON BOTH ECGS

source: rowley J, mcginnis-Hainsworth d, megargel r, et al: “Value of serial Prehospital eCgs in the diagnosis of st-elevation myocardial infarction (stemi).” Paper Presenta-tion. Annual meeting of the national Association of ems Physicians, registry resort, naples, fla., 2008.

331 PATIENTS =ECG EVIDENCE

OF STEMI

table 2: patients with treatment time of 90 Minutes or less

Patients with no 12-lead ECG 37.5%Patients with 12-lead presented at arrival 51.0%Patients with STEMI Alert from field 85.7%


occur in every patient, or even every shift, routine acquisition of early and serial 12-lead ECGs increases the likelihood of recognizing STEMI, thus shortening the time to lifesaving treatment.

Increasing our level of suspicion as to who should get a 12-lead, striving to obtain the first 12-lead as early as possible and prioritizing the impor-tance of serial ECGs are three important steps to improve STEMI care. Considering that EMS is in the unique position to obtain early and repeat ECGs, the logical question to ask ourselves is, “Are we seizing this valuable opportunity?”

tim phalen has presented 12-lead education to more than 35,000 participants. He is the co-author of the textbook The 12-lead ECG in Acute Coronary Syndromes and developer of online 12-lead and STEMI educational programs. He can be reached through his Web site at ECGSolutions.com.

disclosure: Tim Phalen serves as a consultant to Physio-Control, Inc. He has also provided education sponsored by Physio-Control, Inc.

reFerences1. Canto JG, Shlipak MG, Rogers WJ, et al: “Prevalence, clinical characteristics and mortality without

chest pain among patients with myocardial infarction presenting.” JAMA. 283(24):3223–3229, 2000.2. Harvey RA, Fuller FP: “The dynamic nature of ST segment and T-wave changes during acute MI.”

Prehospital and Disaster Medicine. 12(4):313–317, 1997.3. Antman EM, Anbe DT, Armstrong PW, et al: “ACC/AHA guidelines for the management of patients with

ST-elevation myocardial infarction.” Circulation. 110(9):e82–292, 2004.4. Fesmire FM, Percy RF, Bardoner JB et al: “usefulness of automated serial 12-lead ECG monitoring

during the initial emergency department evaluation of patients with chest pain.” Annals of Emergency Medicine. 31(1):3–11, 1998.

5. Jernberg T, Lindhal B, Wallentin L: “ST-segment monitoring with continuous 12-lead ECG improves early risk stratification in patients with chest pain and ECG nondiagnostic of acute myocardial infarc-tion.” Journal of the American College of Cardiology. 34(5):1413–1419, 1999.

6. Drew BJ, Dempsey ED, Joo TH, et al: “Pre-hospital synthesized 12-lead ECG ischemia monitoring with trans-telephonic transmission in acute coronary syndromes: Pilot study results of the ST SMART trial.” Journal of Electrocardiology. 37(suppl.):214–221, 2004.

prActicAl considerAtions EMS has a logistical advantage when it comes to performing serial ECGs. In the ED, patients outnum-ber the staff, but in the field an entire team focuses on one cardiac patient. In the ED, patients aren’t typically assigned their own 12-lead machine, but in the field, that’s precisely the case.

In the ED, repeat ECGs are often done at 30-minute intervals; EMS can easily get a repeat ECG with every set of vitals, or if ST trending is available, automatically obtain a 12-lead every 30 seconds (see sidebar, p. 22).

With practice, 12-leads can be obtained on scene with little or no increase in scene time. In many situations, it’s possible to work the 12-lead into the call early on, even before nitroglycerin would be administered. When this is fea-sible, it provides an opportunity to establish a baseline ECG before medications are administered. As mentioned above, this process is worthwhile but should be done without delaying treatment.

conclusion When it comes to recognizing STEMI, EMS is in a privileged position. Who better to obtain early ECGs, serial ECGs as often as every 30 seconds and even get additional leads when indicated? No one. Although dynamic changes won’t

st-segMent trending capabilities

Because of the dynamic nature of acute coronary syndromes, when STEMI is suspected but the initial ECG is non-diagnostic, EDs are generally required to either manually obtain a 12-lead ECG every five to 10 minutes or use an ST-segment monitor to trend the ST segment (a Class I recommendation).

At least one prehospital monitor offers a feature known as “ST segment trending,” which emulates the function of an ST-segment monitor. In units with ST trending, once the “12-lead” button is pressed, the device not only samples and prints a 12-lead ECG but will then automatically re-sample a 12-lead every 30 seconds thereafter. This re-sampling is done internally, and the 12-lead is not

printed out or displayed on the screen.The monitor analyzes the re-sampled ECGs and identifies changes

of at least 1 mm in the ST segment, whether upward or downward. Such a change in one sample may be due to an ischemic event or may simply be the result of patient movement or artifact. Therefore, the ST-segment trending algorithm requires the change to persist for five samples, or about two and a half minutes, before meeting the threshold for an alert.

If the ST segment change meets that threshold, a new 12-lead is printed, alerting the care provider and documenting the event. The ECGs in Figure 1 captured the STEMI by use of this feature.

Finding STEMI is like panning for gold: you don’t expect to find a gold nugget in every pan, but when you do find one it’s worth all the effort.

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