​

By Kelly Grayson

Drowning is a significant public health issue in the United States and worldwide, and represents a frequent need for resuscitation from EMS and emergency department providers. While the frequency of unintentional drowning has decreased over the last generation, roughly 10 people still die of drowning every day in the United States, 20 percent of which are ages 14 and under [1].

Drowning is the leading cause of unintentional traumatic death in children ages 1-4, the second-ranked cause of unintentional trauma death in children ages 5-9 years old, and the 5th ranked cause of death in children ages 10-14. Drowning ranks 10th among causes of accidental trauma deaths for all ages in the United States [2].

For every child that dies from accidental drowning, another five are treated in the ED for non-fatal injuries. Roughly one-third of survivors suffer moderate to severe neurologic sequelae.

Terminology
The root cause of death by drowning is fatal asphyxia, but due to a historically wide variance in terminology and definitions, environment (water temperature, cleanliness of the water, salt versus fresh water, submersion interval, and other comorbidities), the pathophysiology of the drowning process has been somewhat muddled.

At the 2002 World Congress on Drowning, a consensus definition was reached, defining drowning as "primary respiratory impairment from submersion in a liquid medium [3]." It was further resolved that other terminology adhere to Utstein reporting criteria to ensure conformity in pooled data. Outcomes reporting for drowning was classified as death, morbidity or no morbidity; other non-standard terminology such as dry drowning, wet drowning, near drowning, active or passive drowning or delayed drowning are discarded. The World Congress on Drowning met again in November 2015, but findings from that meeting have yet to be promulgated.

Drowning can further be classified as warm-water (>20 C) or cold-water (<20 C). While sequelae and the management of each may vary somewhat depending on the salinity of the drowning medium, salt versus fresh water makes little difference in the prehospital management of the drowning patient.

Drowning pathophysiology
The drowning process begins with the victim’s airway submerged beneath the surface of the water. While victims initially attempt to hold their breath and may reflexively swallow substantial quantities of water, relatively little aspiration of water occurs in the initial phase of a drowning.

The body’s natural response is, "OK, if I can drink the lake first, then I’ll be able to breathe." When that unobstructed breath does not occur, the first water to enter the oropharynx or larynx during an attempted breath may trigger a brief laryngospasm.

It was long believed that a significant percentage of drowning victims suffered prolonged laryngospasm, resulting in the proverbial "dry drowning," but a number of studies have disproven that notion [3, 4]. In one study of 598 autopsied drowning victims, 98.6 percent had water in their lungs [3]. The study authors noted that active ventilation is required to aspirate water into the lungs; water does not flow passively into the lungs of drowning victims. Those few victims found without significant amounts of water in their lungs were believed to be dead, and thus without respiratory effort, when they went into the water.

As time submerged increases, hypoxia and hypercarbia set in, the brainstem triggers involuntary breathing, and water enters the lungs whether there was a brief interval of laryngospasm or not.

Water — regardless of type — entering the lungs disrupts surfactant, resulting in atelectasis, pulmonary shunting and significant ventilation/perfusion (V/Q) mismatch. Water is also toxic to pneumocytes, the cells that make up alveoli. Contact with fresh water, relatively hypotonic to plasma, results in disruption of alveolar surfactant, while hypertonic salt water creates an osmotic gradient that draws fluid into alveoli, diluting and washing out surfactant.

The end result is disruption of alveolar capillary membranes, damage to the alveolar basement membrane and inflammation of pneumocytes. In addition, aspirated fluid produces vagally-mediated vasoconstriction and pulmonary hypertension. Bronchoconstriction, edema and varying degrees of atelectasis and pulmonary shunting usually follow.

In the past, it was common to differentiate salt versus fresh water drownings based upon the premise that aspiration of hypertonic sea water could cause fluid shifts, electrolyte imbalances, and lysis of red blood cells. However, this premise was based upon canine studies in which the test animals typically aspirated a great deal of water, roughly 20 mL/kg. Human drowning subjects typically aspirate far less (2-4 mL/kg), and this amount is not believed to significantly alter body chemistry, at least in the resuscitation phase of management [5].

Drowning patient with adequate perfusion management and resuscitation
The primary goal in the management and resuscitation of the drowning victim is to reverse the hypoxic insult. In the patient with respiratory compromise or arrest, but with adequate perfusion, oxygenation should be provided with 100 percent oxygen, and artificial ventilation should be performed if necessary.

Advanced airway management, if it can be performed quickly by expert rescuers, should be performed if indicated. Keep in mind that supraglottic airways, while convenient and effective short-term alternatives to endotracheal intubation, offer limited protection against further aspiration. The victim will likely have swallowed a good deal of water in addition to whatever amount may have entered the lungs.

Use waveform capnography to guide patient ventilation. The goal is a physiologically normal ETCO2 of 35-45 mm Hg, with normal waveform morphology.

Because of the amount of water aspirated by most drowning patients, pulmonary secretions may be a concern, and frequent suctioning may be required. These pulmonary secretions also necessitate vigilant monitoring of capnograph waveforms, and frequent replacement of sidestream capnograph adapter and tubing if it becomes occluded.

Remember that the inflammatory cascade triggered by aspirated water contacting pneumocytes may require positive-end expiratory pressure to recruit and retain patent alveoli. Most BVM devices include a PEEP adapter that attaches to the exhalation valve, and a PEEP setting of 7.5 – 10.0 cm H20 may be beneficial.

For the adequately perfusing drowning patient with spontaneous breathing, CPAP may accomplish the same thing.

Be alert for the characteristic shark fin waveform of acute bronchospasm and administer bronchodilators and corticosteroids as appropriate. While some sources note that analyzing the slope of the alveolar plateau (Phase III) can be useful for detecting significant ventilation/perfusion (VQ) mismatch from increased dead space ventilation or intrapulmonary shunt — both of which may be present in drowning patients — this is only true of volumetric capnography, a technology not commonly found in prehospital monitor/defibrillators [6].

Drowning patient in low perfusion states management and resuscitation
Waveform capnography is also an excellent indirect measure of perfusion. In drowning victims in cardiac arrest, waveform capnography can reliably confirm tube placement, gauge effectiveness of chest compressions, detect migration or displacement of advanced airway devices and detect return of spontaneous circulation [7].

Diminishing ETCO2 during cardiopulmonary resuscitation can indicate compressor fatigue, or if there is a significant disparity in ETCO2 readings between rescuers, a flaw in one rescuer’s compression technique. A sudden increase in ETCO2 during cardiopulmonary resuscitation is a strong indicator of ROSC and may precede a palpable pulse [8, 9, 10].

Remember that the root cause of the arrest is hypoxia. As such, conventional CPR techniques with artificial ventilation should be performed, rather than cardiocerebral resuscitation techniques utilizing passive oxygenation.

One caveat applies in using capnography in drowning patients. While ETCO2 readings consistently below 10 mm Hg despite effective chest compressions and artificial ventilation have been considered a criterion for terminating resuscitation efforts, ETCO2 readings may be significantly decreased in hypothermic states. Do not terminate resuscitation prematurely.

However, although the mantra has long been, "You don’t have a dead body until you have a warm dead body," it should be noted that even with hypothermic arrest patients, the prognosis for patients who have undergone resuscitation longer than 30 minutes is dismal [11]. The majority of patients are not resuscitated and those who survive usually suffer profound neurological impairment.

Conclusion
Since the common pathophysiology in all types of drowning death is profound hypoxic insult, oxygenation and ventilation are the most effective tools in managing the drowning patient. Knowing the benefits and limitations of waveform capnography in these patients and how to troubleshoot equipment will help guide the provision of oxygenation and ventilation.

References

1. Laosee OC, Gilchrist J, Rudd R. Drowning 2005-2009. Morbidity and Mortality Weekly Report 2012; 61(19):344-347. 
2. Centers for Disease Control and Prevention. (2013). 10 Leading Causes of Injury Death by Age Group Highlight Unintentional Injury Deaths, United States 2009. In Centers for Disease Control and Prevention. Retrieved February 16, 2016, from http://www.cdc.gov/injury/images/lc-charts/leading_causes_of_injury_deaths_highlighting_unintentional_injury_2013-a.gif
3. Lunetta P, Modell JH, Sajantila A. What is the Incidence and Significance of "Dry-Lungs" in Bodies Found in Water? American Journal of Forensic Medical Pathology. 2004 Dec. 25(4):291-301.
4. Orlowski JP, Szpilman D. Drowning, Rescue, Resuscitation, and Reanimation. Pediatric Clinics of North America. 2001;48(3):627–646.
5. Oehmichen M, Hennig R, Meissner C. Near-Drowning and Clinical Laboratory Changes. Legal Medicine (Tokyo). 2008;10(1):1–5.
6. Blanch L, Romero PV, Lucangelo U. Volumetric Capnography in the Mechanically Ventilated Patient. Minerva Anestesiologica. 2006 Jun;72(6):577-85.
7. Morisaki H, Takino Y, Kobayashi H, Ando Y, Ichikizaki K. End-tidal Carbon Dioxide Concentration During Cardiopulmonary Resuscitation in Patients with Pre-hospital Cardiac Arrest. Masui. 1991 Jul;40(7):1048-51.
8. Berg RA, Henry C, Otto CW, Sanders AB, Kern KB, Hilwig RW, Ewy GA. Initial End-tidal CO2 Is Markedly Elevated During Cardiopulmonary Resuscitation After Asphyxial Cardiac Arrest. Pediatric Emergency Care. 1996 Aug;12(4):245-8.
9. Steedman DJ, Robertson CE. Measurement of End-tidal Carbon Dioxide Concentration During Cardiopulmonary Resuscitation. Archives of Emergency Medicine. 1990 Sep;7(3):129-34.
10. Falk JL, Rackow EC, Weil MH. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. New England Journal of Medicine. 1988 Mar 10;318(10):607-11.
11. Kieboom JK, Verkade HJ, Burgerhof JG, Bierens JJ, van Rheenen PF, Kneyber MC, Albers MJ. Outcome After Resuscitation Beyond 30 Minutes in Drowned Children with Cardiac Arrest and Hypothermia: Dutch Nationwide Retrospective Cohort Study. British Medical Journal. 2015;350:h418.

By Robert L. Dickson, Guy R. Gleisberg, and John E. Hancock

The Montgomery County Hospital District initiated a ketamine use clinical guideline in 2010 and has been collecting quality assurance data on the drug’s use for sedation, pain Management and rapid sequence intubation. 

The Montgomery County Hospital District is located within a suburban and rural community that provides non-fire based EMS and north of Houston. The district covers 1,100 square miles and responds to approximately 59,000 calls for service per year and is staffed by 190 paramedics, 900 EMTs among 15 local agencies. 

Excited delirium is an acute and potentially life threatening medical condition for a patient. EMS providers and police officers are challenging to accurately identify the syndrome and restrain the patient before the patient can harm others or cause further self-harm.

"The dilemma confronting paramedics is they can’t provide medical care until they can restrain the individual and they can’t restrain the individual until they provide sedation"
- West J Emerg Med. 2014;15(7):742-743.

Features evident at scene include:

• Call for disturbance / psychomotor agitation / excitation
• Violent / combative / belligerent / assault call
• Non responding to authorities / verbal commands
• Psychosis / delusional / paranoid / fearful
• Yelling / shouting / guttural sounds
• Disrobing / inappropriate clothing
• Violence toward / destruction of inanimate objects
• Walking / running in traffic
• Subject obese

- American College of Physicians Excited Delirium Task Force.

Background on ketamine
Ketamine's mechanism of action is as an N-Methyl-D-Aspartate NMDA receptor antagonist with both a dissociative and anesthetic properties [1].  Ketamine is a versatile medication and can be given intravenous, intraosseous, intramuscular, intranasal, or per oral with recommended intravenous doses of 1-2 mg/kg and 3-4 mg/kg IM for dissociation [2].

Potential side effects of ketamine (estimates are for children, no information available yet for adults):

• Airway misalignment requiring repositioning of head (occasional)
• Transient laryngospasm (0.3%)
• Transient apnea or respiratory depression (0.8%)
• Hypersalivation (rare)
• Emesis usually well into recovery (8.4%)
• Recovery agitation (mild 6.3%, clinically 1.4%)
• Muscular hypertonicity and random, purposeless moves (common)
• Clonus, hiccupping, or short non-allergic rash face / neck

Ann Emerg Med. 2011;57:449-61.

Ketamine is a yes or no medication regarding dissociation and once achieved there is no benefit in additional medication to enhance effect [2]. Ketamine given at dissociative doses has no respiratory depression or loss of airway reflexes [3-5]. There is literature to suggest no increase in these complications even with doses of 7-15mg/kg intramuscular [6].

Previous studies suggest intranasal ketamine 0.5-.75mg/kg is effective for pain control, but scant data on this route of administration in the excited delirium patient [7].

In a pediatric study oral ketamine at a dose of 6mg/kg provided successful dissociation without an increase in adverse effects [6]. A longer onset of action with the oral and intranasal routes may limit their use in the agitated excited delirium patient [7].

From previous reviews we know that the patient population who receives this therapy is quite ill, with diagnosis ranging from drug and alcohol intoxication to seizures and intracerebral hemorrhage [11]. In a series of prehospital patients with excited delirium treated with ketamine 61 percent were ultimately hospitalized and 15percent admitted to intensive care [11].

"A trancelike cataleptic state characterized by profound analgesia and amnesia, with retention of protected airway reflexes, spontaneous respirations, and cardiopulmonary stability" i.e., Dissociative Sedation
- American College of Emergency Physicians

Case review methods
We conducted a retrospective quality review of consecutive patients receiving prehospital ketamine administration by paramedics from our ePCR database from October 2012 through March 2016.  

Ketamine administration indications were for rapid control of the violent or agitated patient requiring medical intervention and transport. 

Conversely, Ketamine contraindications included the control of patient parameters by other less invasive means. Those cases where combativeness, aggressive/violent behavior was identified within the ePCR were abstracted.  

Data collected included NEMSIS response to medication, demographic information, dosages, route of administration, need for additional dosages and unexpected adverse events for a sub population of ketamine administration specifically for excited delirium. Descriptive statistics were utilized to describe and calculate standard study data characteristics.

Ketamine administration results
During the study period we had a total of 902 ketamine interventions, 338 for aggressive violent behavior/excited delirium, 119 for pain management, 250 for rapid sequence intubation, 186 for post intubation management and 9 other indications.  

Of the 338 ketamine administrations for violent behavior/excited delirium 67 percent were male, mean age of 36 years (range 11-81) with a mean weight of 81kg.  

Eighty-three percent of administrations were intramuscular, 17 percent intravenous with a mean dose of 291mg (3.6mg/kg).  

We recorded improvements in 317/338 (94 percent) of patients after ketamine, 17/338 (5 percent) were unchanged and 4/338 (1 percent) had a worsening of their clinical condition. Additional doses of medication were required in 77/338 (23 percent) of cases.

Ketamine effectiveness for excited delirium syndrome
In this patient population, our data indicates the use of prehospital ketamine by paramedics was effective in improving agitation for the majority of patients. 

In this large series of EMS patients with violent behavior/excited delirium ketamine was quite effective in improving their symptoms and appears to be a safe and effective therapy in this very difficult patient population.  

There have been several previous reported case series of ketamine use for prehospital agitation/excited delirium which all found similar efficacy to ours, however to our knowledge this is the largest data set for ketamine use in EMS for this indication [8-11].

While it is clear that there seem to be few unexpected adverse events with EMS administration of ketamine for sedation of violent behavioral/excited delirium patients, further prospective studies with patient hospital diagnosis and outcomes are needed.

Take home points
Keep in mind these important points about ketamine administration to patients with excited delirium syndrome:

• Excited delirium is a medical emergency in the prehospital setting
• Ketamine appears to be a safe and effective way to chemically restrain violent behavioral/excited delirium patients
• The preferred method is intramuscular injection with a dose of 4mg/kg
• Full monitoring including end tidal CO2 is recommended after control is established with vigilance for laryngospasm, airway compromise or hypoventilation

References:

1. Craven R. Ketamine. Anesthesia. 2007;62:S48-S53.
2. Green SM, Roback MG, Kennedy RM, Baruch K. Clinical Practice Guideline for Emergency Department Ketamine Dissociative Sedation: 2011 Update. Annals of Emergency Medicine. 2011;57(5):449-461.
3. Green SM, Roback MG, Krauss B, et al. Predictors of airway and respiratory adverse events with ketamine sedation in the emergency department: an individual-patient data meta-analysis of 8,282 children. Ann Emerg Med. 2009;54:158-168.
4. Green SM, Roback MG, Krauss B, et al. Predictors of emesis and recovery agitation with emergency department ketamine sedation: an individual-patient data meta-analysis of 8,282 children. Ann Emerg Med. 2009;54:171-180.
5. Green SM, Johnson NE. Ketamine sedation for pediatric procedures: part 2, review and implications. Ann Emerg Med. 1990;19:1033-1046.
6. Gutstein, HB. Oral ketamine preanesthetic medication in children. Anesthesiology 1992;76(1):28-33
7. Andolfatto,G. Intranasal ketamine for analgesia in the emergency department: a prospective observational series. Acad Emerg Med. 2013 Oct;20(10):1050-4
8. Scheppke KA, Prehospital use of i.m. ketamine for sedation of violent and agitated patients. West J Emerg Med. 2014 Nov;15(7):736-41
9. Keseg, D. The Use of Prehospital Ketamine for Control of Agitation in a Metropolitan Firefighter-based EMS System. Prehosp Emerg Care. 2015 January-March;19(1):110-115.
10. Ho, JD. Successful management of excited delirium syndrome with prehospital ketamine: two case examples. Prehosp Emerg Care. 2013 Apr-Jun;17(2):274-9
11. Burnett, AM. The emergency department experience with prehospital ketamine: a case series of 13 patients. Prehosp Emerg Care. 2012 Oct-Dec;16(4):553-9.

​

By Bob Sullivan

Pediatric anaphylaxis, which is a systemic allergic reaction that can cause respiratory and circulatory compromise, is a high-risk situation that requires prompt recognition and treatment with epinephrine. Atypical presentations of anaphylaxis, combined with children's physiology, can make decisions about when to administer epinephrine challenging. Waveform capnography is a tool that can help providers of all levels assess, treat and monitor patients of all ages with suspected anaphylaxis.

Anaphylaxis starts with an exaggerated immune response to an allergen. The most common triggers in children are food — usually nuts, seafood, milk, soy, medications and insect envenomation [1]. After exposure to the allergen, histamine and other chemical mediators cause inflammation in an attempt to neutralize the foreign substance.

With a simple allergic reaction, the inflammatory response is localized and only affects the area exposed. In anaphylaxis, this response is systemic and life-threatening. Anaphylaxis usually begins shortly after exposure to the allergen, but can occur minutes or hours later, and can also recur, which is a biphasic reaction, hours after successful treatment.

Anaphylaxis typically, but not always, affects two or more body systems, and usually begins with the skin. Eighty percent of patients present with itching, hives and flushed skin color across a large surface area [1].

Pediatric anaphylaxis overview
Anaphylaxis can cause respiratory and circulatory compromise through:

• Swelling of the larynx, tongue, and lips compromise the upper airway, which can cause stridor, difficulty swallowing, and a hoarse voice. Because children have a relatively large tongue and small upper airway, which is lined with more soft tissue than adults, this creates a greater risk of compromise from upper airway edema.
• Bronchoconstriction and mucus secretion compromise the lower airways, which can cause a cough, wheezing, rhonchi, or diminished breath sounds. Children can tire from increased work of breathing from bronchospasm and go into respiratory failure.
• Systemic vasodilation and increased capillary permeability can cause a 30 percent decrease in circulating blood volume, leading to hypotension. Children also have relatively less circulating blood volume than adults, which makes them less able to compensate for distributive shock.
• Nausea, vomiting, and diarrhea can cause hypovolemia. Children can compensate for hypovolemic shock for long periods with increased heart rate before their blood pressure drops, but shock in children is often irreversible after hypotension occurs.

Diagnosing anaphylaxis, and differentiating anaphylaxis from a simple allergic reaction, can be difficult in pediatric patients. Normal vital sign ranges and behavior vary with age, and many EMS providers get little experience caring for children. Young children may not be able to report their symptoms or what they were exposed to, and may cry during assessment. Also, atypical presentations of anaphylaxis do not affect the skin; some children in anaphylaxis will only have gastrointestinal syndromes or hypotension from vasodilation, which can make the diagnosis even more challenging.

Hives and flushed skin on a pediatric patient after multiple bee stings. (Photo courtesy of Greg Friese)

When in doubt, treat for anaphylaxis.

Treat with epinephrine
Epinephrine is the main treatment for all causes and symptoms of anaphylaxis. Mortality rates increase with any delay to epinephrine administration in anaphylaxis. Early recognition and treatment is critical [2].

Epinephrine causes vasoconstriction and bronchodilation, which reduces edema in the upper airway, opens constricted lower airways and improves systemic circulation.

The dose for anaphylaxis is 0.01 mg/kg of the 1 mg/mL concentration. Pediatric epinephrine auto-injectors (EpiPens) are also available and carried by many BLS units. The EpiPen Jr. auto-injector has a standard 0.15 mg dose of epinephrine, and should be given to children who weigh 10-30 kg. Children who weigh more than 30 kg should be given the adult EpiPen, which has 0.3 mg of epinephrine.

Use an adult EpiPen on a child heavier than 30 kg. (Photo courtesy of Greg Friese)

Administer epinephrine intramuscularly in the anterolateral thigh and repeat every five minutes if symptoms persist. Whether using an EpiPen or drawing epinephrine from a vial with a syringe, use a reference card and medication cross-check to ensure that epinephrine is given at the correct dose, concentration, and route.  

After epinephrine, administer intravenous or intraosseous fluid to patients with hypotension and administer albuterol to patients with bronchospasm. Other treatment includes administration of antihistamines, such as diphenhydramine (Benadryl) and ranitidine (Zantac), and a steroid to inhibit inflammation, such as methylprednisolone (Solu-Medrol) or prednisone. 

The role of capnography in pediatric anaphylaxis
Waveform capnography provides real-time, breath-to-breath feedback on ventilation and perfusion. Through a sample of exhaled air captured from nasal prongs or an adaptor connected to a bag-valve mask or advanced airway device, each exhalation generates a rectangular-shaped waveform on the capnograph.

Capnography also measures respiratory rate and the amount of carbon dioxide exhaled with each breath. Normal ETCO2 is 35-45 mm Hg, which is consistent across all age groups. When incorporated into a physical exam, waveform capnography can help identify respiratory and circulatory symptoms of anaphylaxis in children, and determine if treatment is working.

Capnography and respiratory compromise in anaphylaxis
In patients with edema of the upper airway, waveform capnography can be used to monitor upper airway patency and help determine when ventilation needs to be assisted with a bag-valve mask. If a capnography waveform appears with each breath, at least for the moment, the upper airway is patent.

When assisted ventilation is needed, capnography can be used with the BVM to provide feedback on whether ventilation is effective and to guide respiratory rate. If no waveform appears with each squeeze of the BVM, check for proper airway positioned, mask seal and tidal volume.

Bronchospasm from anaphylaxis can also be diagnosed with capnography. A slurred, shark fin capnogram is diagnostic of bronchospasm, even when wheezing cannot be heard. This identifies which anaphylaxis patients should receive albuterol, after epinephrine administration.

The more severe the bronchospasm, the more pronounced the shark fin. As air exchange worsens in the lower airways worsens, CO2 is not be eliminated effectively and it builds up in the lungs. This causes an increase in ETCO2, which suggests respiratory failure and the need for assisted ventilation.

Capnography and circulatory compromise in anaphylaxis
Waveform capnography can also be used to assess perfusion. ETCO2 depends on adequate blood flow to the lungs to excrete carbon dioxide. In shock there is less blood flow to the lungs, and less CO2 gets excreted with each breath. A study of children with vomiting and diarrhea from gastroenteritis found that ETCO2 less than 31 mm Hg identified metabolic acidosis from shock and the need for intravenous fluid [3].

Capnography can help detect atypical presentations of anaphylaxis and identify children who in shock, but still compensating. Look for low ETCO2 along with delayed capillary refill and low blood pressure to identify the need for epinephrine.  

Capnography and response to treatment for anaphylaxis
After administering epinephrine and initiating treatment for breathing and circulation, the next decision is whether repeated doses of epinephrine are needed. For patients with respiratory symptoms, look for the slurred waveform to shift to a rectangular shape and for ETCO2 to shift to the 35-45 mm Hg range.

For patients in shock, look for ETCO2 to increase as perfusion improves. If there is no improvement after five minutes, administer a second dose of epinephrine.

Pediatric anaphylaxis is a can't miss diagnosis. When used with history, physical exam findings and vital signs, waveform capnography can help make the diagnosis and determine when anaphylaxis treatment is working. Remember though to treat anaphylaxis as soon as you recognize it, which may be before or after applying capnography.

References
1. Linzer J, Bechtel K. Pediatric anaphylaxis. Medscape 2014, Nov 7. Retrieved from: http://emedicine.medscape.com/article/799744-overview

2. Jacobsen R, Millin M. PEC The use of epinephrine for out-of-hospital treatment of anaphylaxis: resource document for the National Association of EMS Physicians position statement. Prehospital Emergency Care 2011;15:570–576.

3. Becker H, Langhan M. Capnography in the pediatric emergency department: clinical applications. Pediatric Emergency Medicine Practice 2013;10(6):1-24.

By Bradley Dean

Following the release of two pivotal landmark reports by the Institute of Medicine Committee on Quality of Health Care in America in 1999 and 2001, patient safety has become a priority issue and area of focus, but only recently has EMS joined the movement [1,2].

While some demonstrated improvement has occurred, there is still much room for improvement in delivering safe, high-quality health care within the realm of EMS. In late 2015 another report, "Free from Harm: Accelerating Patient Safety Improvement Fifteen Years after 'To Err Is Human" called for the establishment of a total systems approach and a culture of safety [3].

In EMS, we are forced to make critical decisions during tough clinical moments, which is difficult when there are different people and personalities involved in the care of a seriously ill or injured patient. As providers, we make decisions based on clinical judgement, personal experience and the immediate information available.

In the early stages of patient care, accurate information is limited and to some extent our decisions are educated guesses. Better quality background information reduces the degree of guesswork and increases the quality of care through open communication among all providers involved.

Error reduction strategies
We all make mistakes and we must recognize that human error is inevitable. We must also realize what we can do to reduce those errors in critical situations.

1. Recognize predictable human factors
James Reason, a psychologist human performance expert, describes numerous human factors that predictably lead to errors in complex systems [4]. When people are fatigued or stressed, memory, vigilance and attention to detail often decrease, leading to increased possibility for errors.

Providers who are required to perform multiple complex cognitive tasks simultaneously are likely to experience errors in techniques or skill performance, such as calculation of pediatric medication dosages and maintaining an airway.

2. Designate a team leader
The emphasis in ACLS and PALS on the identification of a team leader is crucial to optimizing chances for survival of critically ill patients. The team leader distributes the cognitive load as reasonable assignments to responsible providers.

A dedicated team leader who briefs the team and allows the members to introduce themselves to each other opens communication streams and allows input to decision making. The team leader then should stand back, maintain situational awareness, observe the team, watch and listen, remain conscious of the ticking clock, allow the team members to perform their individual specialty roles while ensuring that care is swift and targeted.

3. Team familiarity
Crew familiarity is another aspect that causes hesitation in communication and impairs appropriate resource management. EMS is a high-risk setting because of the unpredictable patient needs, and the wide range of skills required to manage individual patients.

With critically ill or injured patients, whether field response, or critical care transport, team familiarity is important to improve communication and clinical care. Field care of patients should not be comparable to a pick-up basketball game or a flag football game where individual teammates have a shared understanding of the goals of the game, they know their individual roles and responsibilities, but they may not be acquainted or familiar with each other [5].

Crew resource management for critical interventions
In the case of an improperly placed endotracheal tube that goes unrecognized, the rapid deterioration of the patient should direct at least one provider to recheck the tube, but let’s take a moment to look at the management of the situation.

During the process of rapid sequence induction, there are generally multiple providers involved in managing the patient. Someone must clearly be in charge of the overall management of the patient, while others are in charge of their respective tasks: ventilation and pre-oxygenation; medication preparation and administration; preparation of intubation equipment; patient monitoring and recording. While all of these tasks are being performed simultaneously, yet independently to reduce the cognitive load, the crew must work together to communicate and make informed decisions so each person is aware of the entire clinical picture.

The death of a patient from an improperly placed endotracheal tube occurs when provider attention is diverted and inadvertently skips steps and priorities. This can occur because of a piece of equipment is not working as expected, medication calculations, different medication packaging, such as calling a medication by brand name, though it is packaged under a generic name. Perhaps you are suddenly working on an ambulance that is not situated the same as the one you are normally working on, changing your environmental awareness. 

Do it for Drew
Drew Hughes died of an anoxic brain injury as the result of an unrecognized improperly placed endotracheal tube after being re-intubated during a hospital-to-hospital transfer. There were likely some crew resource management and patient safety issues.

The on-duty EMS crew at the transferring facility was in the process of completing another transfer and not immediately available. The crew assembled to initiate the transport by the transferring facility was not familiar with one another and did not normally work together.

The respiratory therapist assigned to the transfer was the least experienced one available and not the one who initially intubated Drew who was familiar with his case. Both the respiratory therapist and nurse assigned to the transfer were unfamiliar with the ambulance and specifics of EMS operations.

During transport, the paramedics did a crew change, introducing additional personnel unfamiliar with the nurse and respiratory therapist, to complete the transport. The new paramedic in charge of Drew's care did not have any communication with the paramedic she was replacing and did not receive a full patient report, from the remaining crew, prior to continuation of the transport.

This unfortunate chain of events created opportunities rather than reducing the risk for predictable human errors, lacked a clear team leader to see the big picture to distribute the load and formed teams with unfamiliar crew configurations, as well as normal operations.

References
1. Institute of Medicine, Committee on Quality of Health Care in America. To Err Is Human: Building a safer Health System. Kohn LT, Corrigan JM, Donaldson MS, eds. Washington, DC: National Academies Press; 2000.

2. Institute of Medicine, Committee on Quality of Health Care in America. Crossing the Quality Chasm: A New Health System for the 21^st Century. Washington, DC: National Academies Press; 2001.

3. National Patient Safety Foundation. Free from Harm: Accelerating Patient Safety Improvement Fifteen Years after To Err Is Human. National Patient Safety Foundation, Boston, MA; 2015.

4. Reason JT. Human Error. New York, NY: Cambridge University Press; 1990.

5. Paterson, PD, et al. How familiar are clinician teammates in the emergency department? Emerg Med J 2015;32:258-262.

By Rom Duckworth

It's more common than a heart attack. It takes more lives than any cancer. It causes the deaths of over 4,400 children per year in the United States. Yet if you asked most health care providers to rate their top five medically preventable causes of death, sepsis probably wouldn't even make the list [1, 2].

With sepsis responsible for more than 1 million hospital admissions per year in the United States, at a cost of over $20 billion and increasing at almost 12 percent per year, it is no wonder that there is an enormous effort to get this challenging but preventable problem under control [3, 4].

The term sepsis was first coined by Hippocrates in the fourth century, but at the time it referred simply to the breakdown of living tissues [5]. Now, known more commonly as blood poisoning, scientists and clinicians have been trying to come up with better definitions and criteria for sepsis for more than 25 years in an effort to advance the fight against this deadly disorder [5].

"Sepsis is caused when the body’s immune system becomes overactive in response to an infection, causing inflammation which can affect how well other tissues and organs work. When sepsis is recognized early, people can be quickly given the right treatment. However, the signs and symptoms of sepsis can vary and may be subtle which can lead to it being missed if it is not considered early on."
- National Institute for Health and Care Excellence (NICE) Guidelines [6]

Sepsis has a high mortality rate, variable clinical presentations and few unifying features technically making it a syndrome, a group of body dysfunctions that are commonly found together and that typically progress together, often in a predictable way, but the cause remains a mystery, not a disease where the underlying cause or causes are known.

How EMS can make a difference
EMS providers familiar with anaphylaxis can think of sepsis as progressing in a somewhat similar way. There is an initial injury (say, a bee sting for anaphylaxis or a bacterial infection for sepsis).

While the initial injury is bad, what’s worse is that it triggers an overreaction of the body's normal immune system (different pathways for sepsis and anaphylaxis, but both are inappropriate over-responses) ultimately resulting in organ dysfunction and cardiovascular collapse (again, the pathways are different but the end results are similar).

Perhaps the biggest difference an EMS provider will notice is that anaphylaxis occurs very quickly and can often be unavoidably obvious. Sepsis tends to progress more slowly, with signs and symptoms that are much more subtle right up to the point of complete cardiovascular collapse.

Fortunately, early recognition of sepsis by sharp EMS providers has been shown to improve time to treatment and early treatment of patients has been shown to greatly improve outcomes [7-13]. However, the challenge is not just that the signs and symptoms can be subtle and easily missed; many physicians disagree as to exactly what clinical indicators to look for. That's where the shared definition and agreed-upon clinical criteria are helpful.

Sepsis 1.0
The 1991 Chicago Consensus Conference was the first to formally define sepsis, simply calling it, "the systemic response to infection [14]." The clinical criteria were also relatively simple with a diagnosis of sepsis based only on the presence of known or suspected infection and presentation of Systemic Inflammatory Response Syndrome (SIRS) [14], which is defined by the presence of these exam findings.

• Temp >100.4F or <96.8F
• Heart Rate > 90
• Respiratory Rate >20 or requires Ventilation
• White Blood Cell Count > 12,000/mm3, <4,000/mm3, or >10% bands

This provided a framework for clinical health care providers and researchers to both raise awareness of and begin the fight against sepsis.

The 1991 conference went on to classify the severity of sepsis, categorizing it in order of increasing severity as sepsis, severe sepsis and septic shock. While this was a step forward in formally codifying sepsis so that it could be studied and treatment improved, many health care providers were still left confused.

Sepsis 2.0
In 2001, The Washington Consensus Conference attempted to clarify things with new diagnostic criteria for sepsis. In addition to the SIRS and other criteria, the Sepsis-related Organ Failure Assessment score (SOFA) was proposed to better identify the presence and degree of sepsis the patient may have [15, 16].

Unfortunately, these broad definitions and complex criteria still fell short when it came to the identification and treatment of patients with sepsis, especially in the emergency department and the prehospital arena. They simply weren't designed to be used to rapidly identify and begin treatment of patients with sepsis in the field. In addition, they were criticized for still falsely identifying some patients who did not have sepsis while missing some patients who actually did. Calls for the redefinition of sepsis with more user-friendly bedside criteria began as early as 2013 [17, 18].

Sepsis 3.0
The Washington Consensus Conference has now attempted to clarify things with a new 2016 definition of sepsis and new diagnostic criteria to improve clinical care, research and reporting of sepsis [19].

"Considerable advances have since been made into the pathobiology (changes in organ function, morphology, cell biology, biochemistry, immunology, and circulation), management, and epidemiology of sepsis, suggesting the need for reexamination."
- The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)

In 2014, the Society for Critical Care Medicine and the European Society for Intensive Care Medicine convened a task force to revise the current definition and criteria for sepsis. Noticeably absent was any involvement or representation from the American College of Emergency Physicians, the Society for Academic Emergency Medicine, The American College of Chest Physicians who developed the first definitions or any prehospital emergency care representation.

The recommended definition and clinical criteria of sepsis from this conference is "Life-threatening organ dysfunction caused by a dysregulated host response to infection [19]." While "suspected infection" is left undefined, the clinical criteria for organ dysfunction are "a Sequential Organ Failure Assessment (SOFA) score of 2 points or more [19].

Since this criteria was developed by critical care physicians typically working in academic hospitals, it is not surprising that the clinical criteria rely on a SOFA score that includes factors such as PaO2, bilirubin and creatinine levels and coagulation labs. Recognizing the need for some type of quick bedside assessment that did not rely on such labs they also developed the quick SOFA or qSOFA score, more suitable for EMS. The qSOFA score consists of:

• Respiratory Rate => 22/min
• Altered Mental Status (GCS <13), and / or
• Systolic BP =< 100 mm/Hg.

Thus, suspected infection plus two or more of these should be enough to begin sepsis care and coordination with specialty staff.

This definition and clinical criteria were based on systematic reviews, surveys and cohort studies as well as a great deal of discussion of those directly involved in the task force [19]. While the SOFA score has existed for some time, the qSOFA score is new and was developed and validated only retrospectively. Although it is intended for use outside of the intensive care unit, there has been no prospective analysis of its use in the emergency department, in EMS, or anywhere else as of yet.

Pros, cons and room for improvement
This update is intended to replace previous definitions, offer greater consistency for studies and clinical trials and ultimately assist in early recognition and timely treatment of patients with sepsis. However, it has come under scrutiny by a great number of individuals and organization evaluating its relative pros and cons [20, 21]. While the Sepsis 3.0 definition and criteria have been peer-reviewed and endorsed by 31 international professional societies, it has notably not been endorsed by ACEP, SAEM and has even been criticized by the ACCP and the UK Sepsis Trust [22, 23].

Pros of Sepsis 3.0

• Definition and the qSOFA criteria are simple, straightforward and easy to teach and understand especially compared to previous criteria.
• qSOFA remains focused on signs and symptoms indicative of problems in key organ systems.
• qSOFA has been retrospectively validated.
• qSOFA sensitivity/specificity appears to be improved over previous criteria when used outside of the ICU environment.
• The release of Sepsis 3.0 and the ensuing discussion may raise awareness of the sepsis problem among EMS providers and help initiate EMS Sepsis Alert systems where none currently exist.

Cons of Sepsis 3.0

• The simplicity and broad applicability of the Sepsis 3.0 definition and criteria have acknowledged limitations in the treatment of individual sepsis patients.
• The Sepsis 3.0 definition and criteria hinge on "known or suspected infection" and yet the statement acknowledges that infection cannot always be positively identified, even with in-hospital blood cultures [19].
• The UK Sepsis Trust says that qSOFA "may prove excessively sensitive in the out of hospital setting."
• The Sepsis 3.0 definitions and criteria have not been adopted by the Center for Medicare and Medicaid Services (CMS) who still use Sepsis 2.0.

Sepsis 3.0 room for improvement

• Sepsis remains an overly broad term being applied to an incompletely understood syndrome.
• Several members of the task force agreed that serum lactate should be measured as an important supplement to the qSOFA score, if available.
• The Sepsis 3.0 definition and criteria are not specific for key sepsis subcategories including children, the elderly and people at high risk of infection.
• qSOFA has yet to be prospectively validated.
• qSOFA may be misinterpreted as a sepsis screen leading some providers to focus solely on the possibility of sepsis when other identifiable severe illnesses (cardiogenic shock, anaphylaxis, pulmonary embolism, etc.) may remain uninvestigated on untreated.

Sepsis 3.0 implications for EMS providers
EMS systems may not need to jump to replace existing sepsis alert criteria with Sepsis 3.0. Likewise, simply because the qSOFA criteria focus on blood pressure, altered mental status and tachypnea does not mean that other clinical criteria such as ETCO2, urine output, serum lactate and more are no longer valid assessment criteria associated with sepsis.

Sepsis assessment is based on multiple clinical criteria (Photo courtesy of Rom Duckworth)

None of these criteria, including the qSOFA test, serum lactate, or ETCO2, produce a definitive diagnosis of sepsis. What they do is help EMS providers begin early treatment based on local capabilities, resources and protocols as well as alert and coordinate with in-hospital specialty resources to provide sepsis emergency care.

The Mervyn Singer, MD, co-chair of the Sepsis Definition Task Force, says that qSOFA was devised to give, "the ability to rapidly differentiate/distinguish the risk patient [24]."

For EMS providers working in systems with no current sepsis alert, this would be a great time to begin one without having to reinvent the wheel. EMS providers with existing sepsis alert systems must carefully consider the return on investment they will get in changing their system and retraining their providers.

Change or no change, this is a perfect time to refresh providers on what is known about sepsis, especially that extra care is needed in assessing the very young, the very old and those particularly susceptible to infections due to impaired immune systems from chemotherapy, chronic steroid use, splenectomy, or sickle cell disease, placement of indwelling devices and catheters, recent trauma or surgery, breach of skin integrity from wounds and burns, IV drug abusers and women who have recently given birth or had a termination of pregnancy or miscarriage.

Looking forward to Sepsis 4.0
Sepsis 3.0 will continue to generate a good deal of commentary and discussion in critical care and emergency medicine for some time. The consensus statement itself identifies that this is only one step in an iterative process, yet hopefully we will not have to wait another fifteen years for Sepsis 4.0.

Guidance remains desperately needed for sepsis recognition and treatment in specific sepsis subcategories, most notably pediatrics which has not been updated in over ten years [25]. Meanwhile, the next big step for sepsis appears to be the National Institute for Health and Care Excellence (NICE) clinical guideline on sepsis due out in July, 2016 [6]

While no field usable, sepsis specific tests are on the horizon, new procalcitonin tests are currently in the works. Procalcitonin is released into the bloodstream when there is a bacterial infection in the body. High levels of procalcitonin may show that a patient has a significant infection.

Finally, while advances in treatment for the syndrome of sepsis may seem slow, it was not that long ago that treatment for cancer, a syndrome as it was then known, was also less than desirable. Eventually, underlying causes were identified raising cancer to the category of disease. Biomarkers and tests were developed, ultimately leading to targeted cancer treatment geared to the physiological dysfunction specific to the individual patient resulting in more lives saved.

While some argue that Sepsis 3.0 is more of a stumble than a solid step, there is no doubt that for EMS and for medicine in general, sepsis care continues to move in the right direction.

About the author:
Rom Duckworth is a dedicated emergency responder and award-winning educator with more than twenty-five years of experience working in career and volunteer fire departments, hospital healthcare systems, and public and private emergency services. Currently a career fire Captain and paramedic EMS Coordinator, Rom is an emergency services advocate, and contributor to research, magazines and textbooks on topics of leadership, emergency operations, and educational methodology. Rom is a frequent speaker at conferences and symposia around the world and can be reached via RescueDigest.com.

References

1. Yeh, R. W. et al. Population Trends in the Incidence and Outcomes of Acute Myocardial Infarction. N Engl J Med 362, 2155–2165 (2010).

2.  Watson, R. S. & Carcillo, J. A. Scope and epidemiology of pediatric sepsis. Pediatric Critical Care Medicine 6, S3–S5 (2005).

3. Hall, M. J., Williams, S. N., DeFrances, C. J. & Golosinskiy, A. Inpatient care for septicemia or sepsis: a challenge for patients and hospitals. NCHS Data Brief 1–8 (2011).

4. Torio, C. M. & Andrews, R. M. National Inpatient Hospital Costs. Healthcare Cost and Utilization Project (2011).

5. Marshall, J. C. Sepsis: rethinking the approach to clinical research. J Leukoc Biol 83, 471–482 (2008).

6. National Institute for Health and Care Excellence. NICE consults on guideline to speed up recognition and treatment of sepsis. NICE (2016).

7. Kumar, A. et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock*. Critical Care Medicine 34, 1589–1596 (2006).

8. Wang, H. E., Weaver, M. D., Shapiro, N. I. & Yealy, D. M. Opportunities for Emergency Medical Services care of sepsis. Resuscitation 81, 193–197 (2010).

9. Whitehead, S. Prehospital Sepsis Alert Protocols | EMSWorld.com. EMS World (2010).

10. Seymour, C. W. et al. Prediction of critical illness during out-of-hospital emergency care. JAMA 304, 747–754 (2010).

11. Marik, P. E. Surviving sepsis: going beyond the guidelines. Ann Intensive Care (2011).

12. Halimi, K. et al. Prehospital identification of sepsis patients and alerting of receiving hospitals: impact on early goal-directed therapy. Crit Care 15, P26 (2011).

13. 4 steps to prepare for prehospital antibiotic administration. (2015).

14. Bone, R. C. et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. in 101, 1644–1655 (1992).

15. Vincent, J. L. et al. The SOFA (Sepsis-related Organ Failure Assessment) score to describe organ dysfunction/failure. On behalf of the Working Group on Sepsis-Related Problems of the European Society of Intensive Care Medicine. in 22, 707–710 (1996).

16. For the International Sepsis Definitions Conference et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Intensive Care Medicine 29, 530–538 (2003).

17. Vincent, J.-L., Opal, S. M., Marshall, J. C. & Tracey, K. J. Sepsis definitions: time for change. The Lancet 381, 774–775 (2013).

18. Beesley, S. J. & Lanspa, M. J. Why we need a new definition of sepsis. Annals of Translational Medicine (2015). doi:10.3978/j.issn.2305-5839.2015.11.02

19. Singer, M. et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 315, 801–810 (2016).

20. Rezaie, S. Sepsis 3.0 - R.E.B.E.L. EM - Emergency Medicine Blog. (2016).

21. Farkas, J. Top ten problems with the new sepsis definition. (2016).

22. The UK Sepsis Trust. Interim Statement regarding the New International Consensus Definitions of Sepsis. (2016).

23. Simpson, S. Q. New Sepsis Criteria: A Change We Should Not Make. Chest (2016). doi:10.1016/j.chest.2016.02.653

24. European Society of Intensive Care Medicine. icTV interview with Mervyn Singer. (2016). at <http://www.esicm.org/news-article/icTV-sepsis-3-the-new-definitions-clinical-criteria-Singer-final>

25. Goldstein, B., Giroir, B. & Randolph, A. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics. Pediatric Critical Care Medicine 6, 2–8 (2005).

By Kelly Grayson

Traumatic brain injury, hemorrhagic stroke and spinal cord injury are three pathologies that can result in devastating neurological injury. While we can do little in the prehospital environment to treat them, careful assessment of the patient, including waveform capnography, can alert us to potential life-threatening sequelae and help us make sure our interventions do not inadvertently make the patient worse.

Traumatic brain injury accounts for nearly 40 percent of all trauma deaths in the United States, approximately 52,000 deaths per year. Roughly 200,000 TBI victims yearly require hospitalization, at a cost of nearly $4 billion per year in medical expenses, lost wages and productivity. The mortality rate for severe TBI — Glasgow Coma Score < 8 — is roughly 33 percent [1].

Hemorrhagic stroke accounts for nearly 13 percent of the 795,000 strokes yearly in the United States, of which 3 percent are subarachnoid hemorrhage and 10 percent are intracerebral hemorrhage [2, 3]. Prognosis in these patients is based upon location, size and severity of hemorrhage as defined by Glasgow Coma Scale.

The presence of a large volume of blood at presentation and growth of hematoma size are associated with higher mortality. The Intracerebral Hemorrhage score is the most commonly used prognostic indicator for hemorrhagic stroke, and is calculated thusly:

Each increase in the patient's ICH score is associated with an increase in 30-day mortality; those patients with an ICH score of 3 had 72 percent mortality, those scoring 4 had 97 percent mortality. All patients with an ICH score of 5 died [4].

Approximately 12,500 people in the United States suffer spinal cord injuries every year, and it is estimated that there are as many as 276,000 SCI survivors in the United States as of 2014 [5]. Patients with incomplete and complete tetraplegia represent 30.1 percent and 20.4 percent of SCI victims, respectively. These two categories represent over half of SCI patients, and are at highest risk of respiratory dysfunction.

While these three pathologies — traumatic brain injury, spinal cord injury and hemorrhagic stroke — may represent a broad constellation of clinical syndromes ranging from minor to potentially devastating neurological sequelae, we will limit our focus to the most severe of each, which may pose high risk of severe respiratory and vascular dysfunction. Proper care of these patients can be guided with the use of quantitative waveform capnography.

Primary and secondary neurological injury
Injury resulting from severe neurological trauma can be classified into two broad categories: primary and secondary.

Primary injury occurs at the time of and in the area of the original insult, while secondary injury may occur hours to days or weeks afterward the initial insult. While little can be done in the prehospital realm to limit or reverse primary injury, careful assessment and monitoring, including quantitative waveform capnography, can provide clues to the caregiver of the impending neurological sequelae of secondary injury.

Although hemorrhagic stroke — or other causes of intracranial bleeding — has not been typically classified into primary and secondary syndromes, one might consider the mass effect of an expanding intracranial hemorrhage to be a secondary injury.

Traumatic brain injury and hemorrhagic stroke
Primary injury in TBI can be classified into two broad categories: focal and diffuse.

Focal injuries affect one discrete part of the brain and include skull fractures, penetrating wounds, intracranial hematomas and the like, while diffuse injuries are more widespread, such as diffuse axonal injury.

Diffuse axonal injury is present in nearly half of severe TBI and its primary symptom is prolonged unconsciousness. DAI may be difficult to identify with neuroimaging, as most of the changes are microscopic.

While focal TBI is primarily caused by direct impact, DAI is caused by indirect force, typically the acceleration-deceleration phenomenon common in automobile accidents, sports impacts, and blast injuries. Cerebral axons bridging different brain regions are stretched and damaged by rapid acceleration or deceleration.

While it was long thought that the axonal tracts are sheared as a result of primary injury, we now know that these axons are merely damaged, and the biochemical cascade that results in secondary injury is responsible for most of the neuron death. Excitatory amino acids such as glutamate and aspartate are released in large quantities after primary injury, and these biochemical transmitters are largely responsible for cellular edema.

The axonal tracts commonly damaged in DAI are concentrated in the corpus callosum, cerebral hemispheres and the brain stem. It is the damage to the brain stem that is most likely to cause severe derangements in vascular and respiratory function.

Monro-Kellie doctrine
Whether the insult to brain tissue results from focal impact, diffuse axonal injury, intracranial hemorrhage or the mass effect resulting from it, the syndrome we wish to avoid is increased intracranial pressure.

The Monro-Kellie doctrine holds that the cranial vault is a non-expandable chamber, and as a result, the volume of that chamber remains constant. Consequently, the three elements occupying that chamber — blood, cerebrospinal fluid and brain tissue — must remain in constant equilibrium.

If the volume of one of the elements increases, the volume of one or both of the other elements must correspondingly decrease to maintain that equilibrium. An increase in intracranial pressure from cerebral edema or an expanding hematoma can compress and damage surrounding brain tissue, impair cerebral blood flow, cause brainstem herniation and result in profound neurological damage or death.

Normally, cerebral perfusion pressure remains constant due to autoregulation and may vary from 70-85 mm Hg. For patients with abnormal mean arterial pressure or abnormal intracranial pressure, the cerebral perfusion pressure is calculated by subtracting the intracranial pressure from the mean arterial pressure:

CPP = MAP − ICP

One of the main dangers of increased ICP is that it can cause ischemia by decreasing CPP. As ICP approaches mean arterial pressure, cerebral perfusion falls. The body responds to this fall in CPP by raising blood pressure and dilating cerebral blood vessels. This increases cerebral blood volume, further worsening ICP and starting a vicious cycle that lowers CPP even further.

Recognition of low-perfusion states
Quantitative waveform capnography can help us recognize hypoperfusion states early — remember, MAP is essential in maintaining CPP — and recognizing the signs of increased ICP. While volume resuscitation does not significantly increase CPP in patients with intact autoregulation, patients with TBI may have severely impaired autoregulation. A number of studies have demonstrated that hypotension — systolic blood pressure < 90 mm Hg — is one of the biggest predictors of mortality and the generally accepted recommendation is to maintain a physiologically normal MAP of 65 mm Hg [6,7,8].

Since quantitative waveform capnography is an excellent indirect measure of perfusion, the astute clinician may be alert to falling ETCO2 levels as a precursor to frank hypotension and titrate fluid therapy accordingly.

While an ETCO2 of < 25 mm Hg was strongly associated with serum lactate > 4 mmol/L in sepsis patients [9], the relationship between serum lactate and cerebral perfusion in TBI has not been firmly established.

Rather than focus on a specific ETCO2 threshold at which to initiate fluid therapy, simply correlate trends in ETCO2 readings with mean arterial pressure. If the trend of both is downward, it may be reasonable to initiate judicious fluid boluses before the patient’s systolic blood pressure falls.

For instance, a patient with a systolic blood pressure of 100 mm Hg may have a MAP of only 50 mm Hg and a downward-trending ETCO2. This patient needs fluid boluses to maintain a MAP of ≥ 65 mmHg.

Avoidance of inappropriate hyperventilation
Where waveform capnography really shines is in avoiding inappropriate patient hyperventilation. While traditionally, induced hypocapnea at 25-28 mm Hg was considered a prophylactic therapy for traumatic brain injury, it also significantly limits cerebral blood flow and may worsen cerebral ischemia and is associated with worse outcomes [10].

In the TBI patient, cerebral vascular response to CO2 levels may be significantly increased, and thus hypocapnea is likely to significantly decrease cerebral blood flow regionally in the damaged area [11,12,13]. Therefore, hyperventilation, if done, must be carefully controlled, even in patients with increased ICP.

Ventilations should be titrated to maintain the patient at the lower limit of eucapnia, which means an optimal or normal level presence of arterial carbon dioxide which is 35 mm Hg, and quantitative waveform capnography is essential to accurate titrate volume and rate of ventilations.

Recognition of abnormal respiratory patterns
Abnormal respiratory patterns such as Biot’s respirations, Cheyne-Stokes respirations and central neurogenic hyperventilation are sometimes present in TBI patients, and may signify lesions to the brain stem or impending brain herniation. Biot’s and Cheyne-Stokes are similar in that the patient exhibits periodic breathing, but differ in that Biot’s respirations typically involve breaths at similar volumes alternating with periods of apnea, while Cheyne-Stokes respirations exhibit a crescendo-decrescendo pattern alternating with periods of apnea.

Central neurogenic hyperventilation occurs as a response to reduced carbon dioxide levels in the brain resulting from the constriction of cranial arteries associated with brainstem lesions.

While these patterns may not be readily apparent in the TBI patient who is being mechanically ventilated, they may be recognized in the spontaneously breathing patient. While your TBI or hemorrhagic stroke patient may not initially exhibit these abnormal respiratory patterns, they may occur as secondary injury begins to occur from edema.

A trend capnograph is useful in identifying these abnormal patterns.

Recognition of ventilatory dysfunction in patients with SCI
Patients with cervical spinal cord injury may exhibit some degree of respiratory dysfunction. Typically, patients with injury at the C1-C2 level retain only 5-10 percent of vital respiratory capacity and have no cough reflex, and those with C3-C6 injury only retain 20 percent of vital respiratory capacity, and cough reflex is weak and ineffective [14].

While a primary spinal cord lesion in these areas should be immediately obvious to caregivers, secondary injury from cord edema may be more insidious, particularly if the caregiver’s attention is directed elsewhere. Pay particular attention to rising ETCO2 levels indicative of hypoventilation, and provide ventilatory support as indicated. A trend capnogram may help providers recognize subtle changes in ventilatory efficiency over time.

Vascular dysfunction in patients with SCI
Patients with SCI above the level of T5-T6 may present with some degree of vascular dysfunction, resulting in hypotension, bradycardia, and hypothermia. While the effects of spinal shock are usually transient, true neurogenic shock must be managed with adequate temperature management and treatment of hypotension, either with judicious fluid boluses or pressors. Decreased ETCO2 levels, both from hypoperfusion and hypothermia, may alert you to impending neurogenic shock and allow timely intervention.

Summary
Severe traumatic brain injury, severe hemorrhagic stroke and high spinal cord injury all pose significant risk to vascular and respiratory function. Thorough assessment, including the use of quantitative waveform capnography, will help you identify lethal derangements in perfusion and ventilation, and guide your management of these dysfunctions.

References
1. Segun TD. Traumatic Brain Injury (TBI): Definition and Pathology. Emedicine, Medscape. September 2015.
2. Murray CJ, Lopez AD. Mortality by cause for eight regions of the world: Global Burden of Disease Study. Lancet. 1997; 349(9061):1269-76
3. Roger VL, Go AS, Lloyd-Jones DM, Benjamin EJ, Berry JD, Borden WB, et al. Heart disease and stroke statistics--2012 update: a report from the American Heart Association. Circulation. 2012 Jan 3. 125(1):e2-e220.
4. Hemphill JC 3rd, Bonovich DC, Besmertis L, Manley GT, Johnston SC. The ICH score: a simple, reliable grading scale for intracerebral hemorrhage. Stroke. 2001 Apr. 32(4):891-7.
5. National Spinal Cord Injury Statistical Center (NSCIS). Spinal Cord Injury Facts and Figures at a Glance. February 2015.
6. Marmarou A, Anderson RL, Ward JD, Choi SC, Young HF. Impact of ICP instability and hypotension on outcome in patients with severe head trauma. Journal of Neurosurgery, Supplemental. November 1991 / Vol. 75 / No. 1s / Pages S59-S66.
7. Chesnut RM, Marshall SB, Piek J, Blunt BA, Klauber MR, Marshall LF. Early and late systemic hypotension as a frequent and fundamental source of cerebral ischemia following severe brain injury in the Traumatic Coma Data Bank. Acta Neurochirurgica, Supplementum. 1993;59:121-5.
8. Trauma.org: Cerebral Perfusion Pressure
9. Hunter CL, Silvestri S, Dean M, Falk JL, Papa L. End-tidal carbon dioxide is associated with mortality and lactate in patients with suspected sepsis. American Journal of Emergency Medicine. 2013 Jan; 31(1):64-71.
10. Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: A randomized controlled trial. Journal of Neurosurgery. 1991;75:731-9.
11. Marion DW1, Firlik A, McLaughlin MR. Hyperventilation therapy for severe traumatic brain injury. New Horizons. 1995 Aug;3(3):439-47.
12. Ausina A, Báguena M, Nadal M, Manrique S, Ferrer A, Sahuquillo J, Garnacho A. Cerebral hemodynamic changes during sustained hypocapnia in severe head injury: can hyperventilation cause cerebral ischemia? Acta Neurochirurgica, Supplement. 1998;71:1-4.
13. Soustiel JF1, Mahamid E, Chistyakov A, Shik V, Benenson R, Zaaroor M. Comparison of moderate hyperventilation and mannitol for control of intracranial pressure control in patients with severe traumatic brain injury--a study of cerebral blood flow and metabolism. Acta Neurochirurgica. 2006 Aug;148(8):845-51.
14. Chin LS. Spinal Cord Injuries. Emedicine, Medscape. July 2015.

By Caitlyn Armistead

No other tool is more closely associated with the practice of medicine than the stethoscope, but choosing the right one and using it well is not an easy task. A stethoscope is also crucial diagnostic tool for assessing any patient in respiratory compromise and the patient's response to treatments. A stethoscope, along with capnography, is essential for confirming placement of an endotracheal tube or a supraglottic airway.

Here are 10 things to consider when choosing and using your stethoscope.

1. Choose the right stethoscope
Make sure you have the right tool for the job. Disposable and cheap stethoscopes are often recommended for students, but many of these stethoscopes have poor sound profiles. If you have young ears, a cheap scope may be good enough, but if you have less-than-perfect hearing or need a full range of sounds for diagnostics, then you will need a good scope.

Double-lumen, Sprague scopes, can cause artifact when the tubes rub against each other. Shorter tubes, in theory, will have better volume, but longer tubes are nice when the patient starts coughing.

Diaphragms — the side of the head with a solid disc — are great for listening to relatively higher-frequency breath sounds and bowel sounds, but for low-frequency heart tones and murmurs you will want a bell — the side that's hollow.

Whichever brand or model you choose, remember, you generally get what you pay for. And never buy what you cannot afford to lose.

2. Know your stethoscope
Is that a pediatric diaphragm or is it a bell? Is the bell pressure activated? Which of the provided ear pieces work best for you?

After you've bought your scope, read the owner’s manual. Visit the company's website. Check out YouTube for training videos. There are lots of great resources out there on how to get the most from your particular scope.

3. Keep things clean
Make sure your ears are clean. Ear wax blockages are one of the most common causes of hearing loss. If you keep your stethoscope in your pants pocket, make sure that lint and dirt hasn't clogged the ear pieces. Also bear in mind that stethoscopes are a potential vector disease transmission — disinfect it after every patient.

4. Check your scope's condition
If you suddenly can't hear through your scope, make certain the head is turned the correct way. Check to make sure that the diaphragm isn't cracked and the rings aren't loose. Also, make sure the cord is intact; oils from your neck can damage the material over time.

5. Use good auscultation technique
Move the ear pieces into position. They should be angled slightly so that they point toward your nose. This way the ear pieces are aligned with your ear canals.

Turn the stethoscope's head to the correct side. If you are using a double-sided scope, the head will turn on a pivot that will allow the sound to travel from the operating side to the cord or tube. Check your owner’s manual to learn how to determine which side is activated. Usually, the flat side of the attachment — or the side with the hole — indicates which side is active.

When taking a patient's blood pressure, make certain the stethoscope is directly over the brachial artery. You can find it by palpating the medial aspect of the antecubital fossa. Once you have the stethoscope in place, do not place your thumb on top to hold it — it can add artifact. Instead, secure it in place your fingers or cradle it between finger and thumb at the base with the cord draped over the back of your hand.

6. Skin contact is important
Sound loses quality when it travels through the patient's clothing. You can buy the best stethoscope in the world, but if you use it over clothing, you are blocking sound from ever reaching it. Place the stethoscope directly on the patient's skin, exposing the patient's skin when necessary to auscultate a blood pressure, lung sounds or heart sounds.

7. Learn the tricks of the trade
When taking a patient's blood pressure, don't rest the patient's arm on the stretcher rail; vibrations will travel through the person and add to the artifact. Place your feet on the stretcher instead of the floor so fewer vibrations will pass through your boots. Sometimes simply lifting your heels is sufficient. If you need to, shut the whole truck down so you don't have to listen over the engine rumble.

For hard to hear breath sounds, listen in the axillary region and press the patient's arm down over the stethoscope to block ambient noise.

8. Do not adjust your ear pressure
Do not attempt to change the pressure in your ears to improve your earpiece positioning. Changes in pressure remain in the eustachian tubes unless you have a perforated tympanic membrane. It may feel different, but it has no real effect on ear piece placement. That pressure change is much more likely to affect sound conduction through your ear and make hearing more difficult.

9. Be honest
NEVER lie about the patient's blood pressure.

NEVER be afraid to say you couldn't hear what you were attempting auscultate.

NEVER be afraid to ask your partner to listen in and confirm.

If you can't hear the patient's blood pressure, try palpating. It is better to have a palpated systolic BP than a wildly inaccurate systolic/diastolic. In the end, we are here for good patient care, not our own egos.

10. Get your hearing checked
If hearing through your stethoscope is a consistent problem or you are considering an electronic scope, get your hearing checked. There are many options for hearing support available, and many of them interface well with stethoscopes and radios. Your audiologist can help find the right stethoscope for you.

About the author
Caitlyn is a teacher, AEMT, and lifeguard. She has worked for large hospitals, several EMS services, and as a research librarian for a state Bureau of Emergency Medical Services.

Overexertion is a result of exercising too intensely, continuously being thrown into situations where your adrenaline spikes, or being overworked and stretched too thin. Whether your muscles are stressed or your mind is stressed, it’s important to spot your overexertion, and deal with it.

The Department of Labor took a look into EMS personnel to understand their risk of injury. The DOL was trying to solve why work-related injury and fatality rates among US paramedics and EMTs are higher than the national average for all occupations. The results yielded some startling information: the most common source of injury and fatality was overexertion (56 percent of all reported cases). Overexertion is a very real issue.

This image, with attribution to EMS1.com, can be shared and reprinted without alteration. For any other uses contact the editor. Click to see a larger image. 

Print this graphic and tape it somewhere visible. Make it a constant reminder to take care of yourself. The longer your body experiences unhealed overexertion, the more damage you’re doing to yourself. 

By Christopher Kroboth

Asthma is a condition in which lower airways narrow and swell and produce extra mucus. This can make breathing difficult and trigger coughing, wheezing and shortness of breath [1].

The CDC reports that 8.3 percent of the pediatric population has asthma and of those 57.9 percent reported a history of having an asthma attack [2].

When treating asthma, remember that it is an airway geometry problem. Imagine the bronchioles are large milkshake straws, nice and large for low resistance airflow to move in and out.

During an asthma attack, that milkshake straw narrows to the diameter of a coffee stir straw. Now visualize a light coat of petroleum jelly on the inside of the coffee straw representing the excess mucus production. See the problem?

Inhalation is an active process, while exhalation is a passive process. It is much easier to inhale past the resistance of bronchoconstriction than passively exhale through resistance of bronchoconstriction.

Exhaling and inhale through a milkshake and coffee stirrer straw to understand. You will feel the increased ventilatory resistance of the smaller straw. For this reason asthma is traditionally a ventilatory problem first. As the inability to ventilate increases and retention occurs this in turn inhibits good end alveolar gas exchange later causing the oxygen saturation to decrease.

Asthma signs and symptoms
Watch this short video of a pediatric patient experiencing an asthma attack.

Here is what to look for during patient assessment:

• Tachypnea to increase oxygen uptake
• Patient self-positions for optimal chest expansion and maximum tidal volume
• Tachycardia from stress response as well as increased respiratory effort
• Hypo- or Hypercapnia depends on the severity of air retention or trapping

Hypercapnia is a worrisome sign of patient severity. Carbon dioxide retention is a sign of inhibited ability to exhale.

Hypoxia is also a late sign in many asthma cases and should be a concern to the provider to determine why the patient's oxygen saturation is decreasing in a patient experiencing a bronchiole lumen — airway narrowing — problem.

Asthma treatments
Typical treatments for asthma patients include:

• Nebulized beta-agonist, like albuterol, for bronchodialation and some mucus inhibition.
• Nebulized anti-parasympathetic, like Atrovent, to help inhibit the continued production of mucus and augment the Beta-agonist.
• Epinephrine, intramuscular or subcutaneous, especially when nebulizer medication delivery may be inhibited or ineffective. Epinephrine provides bronchodilation effects. Consider strongly the early usage of epinephrine in the patient who shows signs of severe asthma, such as hypercapnia, decreasing oxygen saturation and impending respiratory failure or arrest.
• Magnesium sulfate, a smooth muscle relaxant, works on the bronchiole smooth muscle to decrease constriction and inflammation. Magnesium sulfate is another systemic medication that can help in those patients that are not responding to nebulizer medications.
• Long-lasting corticosteroid to help maintain the anti-inflammatory effects of the quick acting medications. Since most steroids have a longer onset administration is lower on the priority list.

Asthma patient monitoring
Watch this short video showing how vital signs might change as a pediatric patient receives asthma attack treatment.

Here are important signs to measure and monitor during patient assessment and treatment:

• Capnography to help initial bronchoconstriction assessment. Watch for the waveform to transition from shark fin to normal after intervention. If the waveform continues to shark fin, additional intervention is needed.
• Pulse oximetry guides decisions to correlate medication delivery and titration of oxygen.
• Cardiac monitoring of heart rate and rhythm is critical in any patient receiving medications. Tachycardia in a stress state is normal and many asthma medications increase the heart rate to some degree because of their effect on the sympathetic system.
• Blood pressure monitoring because as a patient hypoventilates and isn't able to exhale their normal volume they begin to retain. This increased volume within the lungs also increases the intrathoracic pressure in turn compressing the vena cava and heart which causes a drop in blood pressure. This is especially seen in children who have smaller trunks than adults.

During the asthma patient assessment always consider the patient's positioning, work of breathing and appearance. Take into account the environment as well. Is the patient in an environment that is causing the asthma exacerbation? Is there a chemical, mold or other allergen triggering this response? Are you in a school chemistry lab, attic, basement or outside a building? Investigate when and where the patient's symptoms started in relation to where you are now. What current medications does the patient take for asthma? Are they on oral steroids or do they use an inhaler only as needed? Has the patient ever been hospitalized for asthma and if so to what degree? Have they ever been intubated?

These questions will help understand how severe or potentially severe the patient may become. Remember a child can rapidly transition from "not yet sick" to "sick" in the span of minutes.

References

1. Asthma. (2015, October 17). Retrieved March 01, 2016, from http://www.mayoclinic.org/diseases-conditions/asthma/basics/definition/con-20026992

2. Most Recent Asthma Data. (2015, October 02). Retrieved March 01, 2016, from http://www.cdc.gov/asthma/most_recent_data.htm

About the author
Chris works for Fairfax County Fire and Rescue. He is a Lieutenant currently assigned to the EMS Training Section and serves as the lead instructor for their Paramedic Program in conjunction with Virginia Commonwealth University. Chris also is the U.S. Clinical Education Manager for iSimulate and travels throughout the country teaching simulation and various EMS topics.

By Bob Sullivan

Tension pneumothorax is a condition that can quickly cause death from respiratory and circulatory compromise [1]. Prompt recognition of tension pneumothorax and treatment with needle decompression can be lifesaving [1,2,3].

However, it is also important to differentiate tension pneumothorax from conditions with similar symptoms, and to avoid performing inappropriate needle decompression. Waveform capnography and ultrasound are two tools that EMS providers can use to help identify tension pneumothorax and determine if treatment is effective.

Tension pneumothorax overview
A pneumothorax is a condition where damage to lung tissue causes air to leak into the pleural space. The pleural space is normally a potential space with a small amount of fluid lining the lungs and chest wall. With a pneumothorax, pressure changes in the chest can cause more air to enter the pleural space during inhalation, which creates a one-way valve that traps air in the pleural space on exhalation. This progressive increase in pressure can cause the lung to collapse leading to respiratory compromise.

A tension pneumothorax occurs when pressure in the pleural space is so high that it compresses the heart and great vessels, in addition to the lungs [1]. Pressure on the vena cava reduces blood flow to the heart and impairs cardiac output, leading to respiratory and circulatory compromise. A pneumothorax can evolve into a tension pneumothorax rapidly, or develop during the course of care.

A pneumothorax can be caused by blunt or penetrating chest trauma, positive pressure ventilation, or can occur spontaneously. Signs and symptoms of a pneumothorax include difficulty breathing, chest pain that is usually sharp and increases with inhalation, decreased or absent breath sounds on the affected side, and subcutaneous emphysema. 

A tension pneumothorax also has signs of poor perfusion, such as agitation, altered mental status, tachycardia, hypotension. Jugular venous distention and tracheal deviation are late and unreliable findings of tension pneumothorax [1,2].

For patients receiving positive pressure ventilation, consider a pneumothorax if there is a high pressure alarm on the ventilator or if it is difficult to squeeze a bag-valve mask.

Administer high flow oxygen for any pneumothorax. Perform needle chest decompression for a tension pneumothorax.
A pneumothorax of any size can affect oxygenation and ventilation. Pulse oximetry and capnography should be monitored in any patient with a suspected pneumothorax, and high-flow oxygen should be administered via non-rebreather mask. Avoid assisted ventilation with a bag-valve mask if at all possible — unless respiratory arrest is imminent, because positive pressure can worsen a pneumothorax [1,2].

Definitive treatment for a pneumothorax is a chest tube, though a small pneumothorax may resolve on its own. In most trauma systems chest tubes are placed in the hospital and not by EMS.

For a tension pneumothorax, where there are signs of respiratory failure and hypoperfusion, a needle chest decompression is a temporizing measure to relieve pressure in the chest until a chest tube can be placed. PHTLS recommends needle chest decompression should be done for patients with:

• Worsening shortness of breath or difficulty with assisted ventilation
• Decreased or absent breath sounds on one side
• Blood pressure less than 90 systolic with narrow pulse pressure [2]

This paramedic-level skill involves placing a large bore needle and a 16-gauge or larger catheter, in the second intercostal space at the midclavicular line, just above the third rib. Chest wall thickness can vary, and there is a significant rate of failure from needles not penetrating the chest wall [1].

PHTLS recommends using a needle that is at least 8 cm (3.5 inches) long; using the standard 5 cm needle and intravenous catheter will not penetrate the chest wall up to 42 percent of the time [2]. Insert the needle until a rush of air is felt, remove the needle, and leave the catheter in place. Vital signs and ventilation should rapidly improve if successful.

Only a tension pneumothorax should receive needle decompression, and the procedure carries a number of complications when performed when it is not indicated [4]. In addition to causing significant pain, it will cause a small pneumothorax if the needle penetrates the lungs. There is also risk of damage to nerves and blood vessels that are under the ribs. Even when pneumothorax is indicated and an 8 cm needle/catheter is used, there is a chance that the needle will not penetrate the chest wall.

The role of capnography in tension pneumothorax
It is important to be judicious with patient selection for needle decompression, and to determine whether or not it worked. Here is how waveform capnography and ultrasound can help.

Waveform capnography provides continuous feedback on ventilation and perfusion. Through a sample of exhaled air captured from nasal prongs, or an adaptor connected to a bag-valve mask or advanced airway device, each exhalation generates a rectangular-shaped waveform on the capnograph. Capnography also measures the amount of carbon dioxide exhaled with each breath (ETCO2), which is normally 35-45 mm Hg.

When ventilation is compromised, such as with a pneumothorax, CO2 cannot be eliminated effectively and it builds up in the lungs. This causes a higher concentration of CO2 to be exhaled with each breath, and for ETCO2 to rise. In the setting of a suspected pneumothorax, a high or increasing ETCO2 (above 45 mm Hg) suggests that it is getting worse.

ETCO2 is also affected by perfusion to the lungs. With a tension pneumothorax, decreased cardiac output causes less CO2 to be delivered to the lungs for exhalation. This would cause ETCO2 to be low — below 35 mm Hg. Thus, as a pneumothorax evolves, ETCO2 would first increase due to inadequate ventilation, and then decrease when circulation is impaired from a tension pneumothorax. A normal to high ETCO2 effectively rules out a tension pneumothorax and the need for needle decompression, and a decrease in ETCO2 may be the first sign of a tension pneumothorax.

When needle chest decompression is performed, ETCO2 is one of the first vital signs to change if it is successful. As air is released from the pleural space, ETCO2 will rapidly increase. If there is no change in ETCO2 after decompression, assess whether the needle penetrated the chest wall, and reassess whether a tension pneumothorax was present in the first place.

In patients with chest injuries or receiving assisted ventilation, however, changes in ETCO2 are not specific to a pneumothorax. Pain from rib fractures on inhalation may cause patients to hypoventilate and for ETCO2 to increase. Hypovolemic shock and traumatic arrest also cause low ETCO2 from decreased perfusion.

Waveform capnography is the gold standard to confirm airway placement in intubated patients. In addition to pneumothorax, ET tube dislodgement, obstruction, and equipment failure are other possible causes of ETCO2 loss. A right mainstem intubation will also cause a decrease in ETCO2, along with decreased breath sounds on the left side. Reassess tube placement, patency, and depth in intubated patients before treating for a tension pneumothorax.

The role of ultrasound for tension pneumothorax
Ultrasound is emerging as a tool for EMS to identify a number of conditions, and is highly sensitive and specific to diagnose a pneumothorax. When examining a normal chest with ultrasound, movement of the lung along the chest wall can be seen with a characteristic sliding lung sign during the respiratory cycle. The sliding motion disappears from air in the pleural space from a pneumothorax [5].

Ultrasound has also been used in the military to triage patients with a suspected pneumothorax, and has helped prevent unnecessary needle chest decompression, chest tubes, and transfer to higher levels of care [6]. In another study of 57 patients who received needle decompression by paramedics, 26 percent were found to have no pneumothorax when assessed by ultrasound in the emergency department, and it was determined that no chest tube was needed [7].

There is also evidence suggesting a short learning curve for ultrasound. A study of 20 paramedics showed that after a two-hour training session on ultrasound, paramedics could correctly identify pneumothorax, pericardial effusion, and cardiac activity [8].

Ultrasound would be especially useful to detect pneumothorax in situations when a physical exam and lung sound assessment are difficult, such as a helicopter transport. Look for this technology to become more widely available in the near future.

Tension pneumothorax is a critical diagnosis for EMS providers to make, and to differentiate from conditions with similar signs and symptoms. Waveform capnography and ultrasound are two tools that can improve diagnostic accuracy of tension pneumothorax.   

References
1. Page D, Chu S, Bown M, Lyman K. Tension Pneumothorax. EMS Reference (2015) Retrieved from: https://emsreference.com/articles/article/tension-pneumothorax-0

2. Prehospital Trauma Life Support Committee of the National Association of Emergency Medical Technicians in cooperation with the Committee on Trauma of the American College of Surgeons. PHTLS: Prehospital Trauma Life Support. 8^th ed. Burlington, MA: Jones and Bartlett

3. Weichenthal L, Crane D, Rond L. (2016): Needle Thoracostomy in the Prehospital Setting: A Retrospective Observational Study, Prehospital Emergency Care [Epub ahead of print] DOI:10.3109/10903127.2015.1102992

4. Warner K, Copass M, Bulger E. (2008). Paramedic Use of Needle Thoracostomy in the Prehospital Environment. Prehospital Emergency Care, 12 (2): 162-168.

5. Sun J, Juang C, Huang Y, Sim S, Chong K, Wang H, Lein W. (2014). Prehospital Ultrasound. Journal of Medical Ultrasound; 22:71-77.

6. Roberts J, McManus J, Harrison B. (2006). Use of Ultrasonography to Avoid an Unnecessary Procedure in the Prehospital Combat Environment: a Case Report. Prehospital Emergency Care; 10:502-506

7. Blaivas M. (2010). Inadequate Needle Thoracostomy Rate in the Prehospital Setting for Presumed Pneumothorax. Journal of Ultrasound in Medicine; 29 (9): 1285-1289

8. Chin E, Chan C, Mortazavi R, Anderson C, Kahn C, Summers S, Fox J. (2013). A Pilot Study Examining the Viability of a Prehospital Assessment with UltraSound for Emergencies Protocol. Journal of Emergency Medicine; 44 (1): 142-149. 

A 56-year-old male collapsed at a restaurant and received several minutes of dispatcher-assisted CPR. A civilian responding to a mobile phone alerting system retrieved an AED from an adjacent business and administered one shock prior to arrival of EMS.

Initial assessment revealed the morbidly obese patient had a pulse and blood pressure but was unresponsive and apneic. Bag-valve-mask ventilations were difficult due to the patient’s size, so the ALS transport crew elected to intubate. After two unsuccessful oral endotracheal intubation attempts, a King LT-D supraglottic airway was inserted and manual ventilation was continued. 

Consistent with protocol, waveform capnography was attached; the following tracing was obtained.

The ALS providers believed the supraglottic airway was placed properly. They theorized that the zero value ETCO2 and absence of a discernable capnography waveform resulted from the use of monitoring equipment designed for endotracheal tubes with an alternative (supraglottic) airway.

In fact, the supraglottic airway was not in place; the patient shortly thereafter became bradycardic, rearrested and subsequently died.

Comparing waveforms from different airway adjuncts
There are some studies that compare ETCO2 waveforms and measurements obtained from endotracheally intubated patients to those using supraglottic or other alternative airways. In the mid 1990s, supraglottic airways began to gain popularity as an alternative to endotracheal intubation for short duration surgical procedures requiring general anesthesia.

In that era, multiple papers were published comparing capnography waveforms and values obtained from multiple types of airways and using a wide variety of ventilation modes. It was during that same period when comparisons were made using nasal cannula derived end-tidal values. 

Those studies established two findings unequivocally. First, ETCO2 values obtained from measurements made in-line with any airway device, including bag-valve-mask devices and nasal cannulas, are equivalent to those obtained from an endotracheal tube. Second, waveforms obtained from any airway device, including BVMs and nasal cannulas, are identical to those obtained from an endotracheal tube. 

The implications of these earlier and innumerable studies from the anesthesia world were significant. Capnography was a safe and reliable means of assessing the adequacy of ventilation in endotracheally intubated patients, of patients being ventilated with all types of airways and of patients being ventilated with no airway adjuncts at all. 

Research studies also demonstrated that capnographic waveforms could be used with alternative airways to evaluate a wide variety of conditions such as cuff leaks, ventilator dyssychrony, bronchospasm, air trapping and low cardiac output with equal efficacy regardless of the type of airway they were attached to. These findings should not be lost on EMS.

There are no differences
While there remain some questions about proper sampling and use of capnography in certain high-flow gas therapies such as jet ventilation in neonates and high-flow nasal cannula therapy for adults, neither of these therapies are currently used by EMS. 

Continuous waveform capnography is an EMS standard of care and must be used to monitor placement and adequacy of ventilation with any artificial airway. The voluminous anesthesia and prehospital literature tells us that the waveforms and values obtained from any alternative airway will be identical to those obtained from an endotracheal tube. 

There are no differences. If you place supraglottic airways and fail to see a four-phase capnographic waveform, the airway is not in place and ventilation is not occurring.

The incidence of misplaced supraglottic airways may not be low nor is the number of ALS providers who mistakenly attribute lack of a clearly observable capnography waveform to use of an alternative airway. An abstract presented in January by Vithalani et al, reported a 13.9 percent incidence of unrecognized misplaced King airways by paramedics in a large urban 911 EMS system. 

ETCO2 is irrefutable indication of airway placement and ventilation
There are many reasons why an alternative airway may not be properly placed, some related to operator error and some to variations in patient anatomy.

Regardless of why, the absence of a clearly discernable four-phase capnography waveform and the presence of measureable CO2 is a clear and irrefutable indication that the airway is not in place and ventilation is not occurring. 

Finally, EMS providers should use capnography waveforms obtained during ventilation — regardless of the type of airway in place — to assess the effectiveness of ventilation and troubleshoot airway and ventilatory issues such as cuff leaks, air trapping, airway resistance and dyssychrony. 

References reviewed:

1. Gottschalk A, Mirza N, Weinstein GS, Edwards MW.  Capnography during jet ventilation for laryngoscopy.  Anesth Analg. 1997;85:155-159.
2. Chhibber AK, Kolano JW, Roberts WA.  Relationship between end-tidal and arterial carbon dioxide with laryngeal mask airways and endotracheal tubes in children.  Anesth Analg.  1996;82:247-250.
3. Chhibber AK, Fickling K, Kolano JW, Roberts WA.  Comparison of end-tidal and arterial carbon dioxide in infants using laryngeal mask airway and endotracheal tube.  Anesth Analg.  1997;84:51-53.
4. Fukuda K, Ichinohe T, Kaneko Y.  Is measurement of end-tidal CO₂ through a nasal cannula reliable?  Anesth Prog.  1997;44:23-26. 
5. Lee JS, Nam SB, Chang CH, Han DW, Lee YW, Shin CS.  Relationship between arterial and end-tidal carbon dioxide pressures during anesthesia using a laryngeal tube.  Acta Anaesthesiologica Scandinavica.  2005;49: 759-762. 
6. Casati A, Fanelli G, Cappelleri G, Albertin A, Anelati D, Magistris L, Torri G. Arterial to end-tidal carbon dioxide tension difference in anaesthetized adults mechanically ventilated via a laryngeal mask or a cuffed oropharyngeal airway.  Eur J Anaesthesiol. 1999;16:534-538.
7. Freeman JF, Ciarallo C, Rappaport L, Mandt M, Bajaj L.  Use of capnographs to assess quality of pediatric ventilation with 3 different airway modalities.
8. Vithalani VD, Richmond N, Davis SQ, Hejl L, Howerton D,  Gleason W, Emergency Physicians Advisory Board, MedStar Mobile Healthcare.  Unrecognized failed airway management using a blind-insertion supraglottic device.  Abstracts for the 2016 NAEMSP Scientific Assembly.  Prehospital Emergency Care. 2016;20:144. 

This image was based on a call I did for a boy who was having an asthma attack. He was fine, but his father was distraught. His wife, the boys mother, had died a week prior from cancer. He said she used to deal with and handle these types of family matters. He told me he was really missing her and this just made it worse for him. The spirit is the boys mother still at her son's side.

Seizures are one of the most common conditions encountered by EMS providers and one where critical interventions can significantly affect patient outcomes [1]. Timely seizure management is a benchmark proposed by a group of metropolitan medical directors and is currently being studied as a performance measure by the EMS Compass initiative [2].

Oxygenation and ventilation can be compromised during prolonged the seizures, as well as during the postictal phase after seizures. Here are three things you should know about seizures and respiratory compromise.

1. Seizures can cause upper airway obstruction and respiratory depression
A seizure is an episode of abnormal electrical discharges from neurons in the brain that causes a change in behavior, sensory perception or motor activity [3]. Seizures can be generalized or partial, depending on how much of the brain is affected [4].

Generalized tonic-clonic seizure is the most common type of seizure EMS providers encountered. Generalized tonic-clonic seizures occur when both hemispheres of the brain are affected by abnormal neuronal discharges. They present with a loss of consciousness, body-wide muscle rigidity (tonic phase), and are followed by rhythmic convulsions (clonic phase) [4]. A deviated gaze and incontinence are also common signs of a tonic-clonic seizure.

Seizures can affect both respiration and upper airway protection. Patients may stop breathing at the beginning of a convulsive seizure as muscles contract [4]. Generalized seizures then cause a catecholamine surge and increased metabolic rate, which increases cerebral oxygen demand and strains the cardiovascular system [3,4].

The gag reflex is also suppressed during a seizure and the patient may aspirate if they vomit. The patient’s upper airway may also be obstructed by their relaxed tongue.

Generalized tonic-clonic seizures usually last a few seconds to a few minutes. Afterward, there is often a postictal phase, during which patients have an altered mental status before returning to a full alertness.

Since seizures are usually of short duration, patients are most often in the postictal phase when EMS arrives [4]. Patients may be unconscious or only respond to painful stimuli during the postictal phase. The patient is likely to have respiratory depression and diminished airway reflexes [4].

Postictal patients may also be confused or combative, especially as they transition from somnolent to awake. The postictal phase may last a few minutes to several hours, but patients usually fully recover after 20 minutes. If a patient remains confused for longer than 20 minutes after a seizure, consider another cause of altered mental status [4].

A seizure that lasts more than 20 minutes, or recurs before a patient regains consciousness, is a life-threatening condition known as status epilepticus [1]. This may lead to brain damage, hypoxia, hypercapnia, pulmonary edema, hypoglycemia, and metabolic acidosis [4].

It is important to determine the duration of seizures, how many seizures the patient had, what the patient was doing before the seizure and whether or not the patient regained consciousness after each seizure to identify status epilepticus.

Epilepsy is the most common cause of seizures, particularly when patients are not compliant with prescribed anticonvulsants. Seizures can also be caused by hypoxia, head injury, stroke, hypoglycemia, brain tumor, poisoning, meningitis and fever [4].

It is important to identify and treat the underlying cause of seizures and to never assume that one was caused by epilepsy. Ask bystanders and look for a medical identification bracelet to determine if the patient has a history of seizures.

Ask if the patient was complaining of anything before the seizure began, if they struck their head or if they may have overdosed. Check blood glucose on any suspected seizure patient to assess for hypoglycemia.

Two other types of seizures are absence and partial seizures. An absence seizure is a type of generalized seizure that usually occurs in children, which causes a temporary loss of awareness that may only last for a few seconds. Patients are unable to communicate during the episode and there is no postictal phase afterwards [4].

Partial seizures affect only part of the brain and patients usually remain conscious during the episode. They may report an odd feeling or you might see a shaking of one limb. Partial seizures can progress to a generalized tonic-clonic seizure, which are known as complex partial seizures [4].

2. Waveform capnography can help guide airway management during and after seizures
Airway management for a patient having a seizure involves protecting the upper airway, administering high-flow oxygen and assisting ventilation if needed [4]. Waveform capnography provides continuous feedback on upper airway patency and ventilation, which can help determine what treatment is needed to achieve those goals.

Capnography measures the amount of carbon dioxide exhaled (end-tidal CO2, or ETCO2) after each breath. Normal ETCO2 is 35 to 45 mm HG. Capnography also displays a waveform for each breath and continuously measures the patient’s respiratory rate. ETCO2 can be measured with nasal prongs or a circuit connected to a bag-valve mask.

Elevated ETCO2 with a normal respiratory rate may be caused by an increase in basal metabolic rate. Elevated ETCO2 with a slow respiratory rate indicates hypoventilation, as excess CO2 accumulates in the lungs and is not excreted effectively. Hypoventilation may also cause low ETCO2 if respirations are shallow and little exhaled air reaches the sensor or if the patient exhales excess CO2.

Pulse oximetry measures oxygenation through a probe attached to a finger, toe or earlobe. Pulse oximetry may be difficult to obtain during a tonic-clonic seizure, so look for cyanotic skin as another sign of hypoxia. Remember that patients may be adequately oxygenated and have a normal pulse oximetry reading, but still be hypoventilating and have an abnormal ETCO2.

Administer oxygen via non-rebreather mask at 12-15 liters per minute to any patient who is actively seizing or is postictal, regardless of their pulse-ox reading, to help with the increased metabolic demands of the brain for oxygen [4]. Patients who are hypoventilating during a seizure, remain hypoxic despite high-flow oxygen or have poor respiratory effort require assisted ventilation with a bag-valve mask connected to oxygen.

Waveform capnography is also useful to assess upper airway patency. A waveform will be absent if the airway is obstructed by the tongue or oral secretions. A waveform will reappear if interventions work at achieving patency.

Start by positioning the patient on their side, suction the oropharynx and insert a nasal airway to clear a path for oxygenation and ventilation. Do not place anything in a seizure patient’s mouth. 

3. Definitive airway management for seizures is stopping the seizure
As important as oxygenation and ventilation are during a seizure, it is equally important to stop the seizure. Depending on resources available, airway management may have to be temporarily deferred in order to administer anti-seizure medication.

Assume that any patient who is actively seizing on EMS arrival is in status epilepticus, which can cause permanent brain damage even with adequate oxygenation and ventilation [3]. Seizures that last longer than 5 minutes are unlikely to stop without intervention and should be promptly treated with a benzodiazepine [3]. 

Benzodiazepines, such as Valium (diazepam), Ativan (lorazepam) or Versed (midazolam), are the first line treatment for seizures. The earlier a seizure is treated with a benzodiazepine, the more likely it is to terminate [3].

While intravenous administration of a benzodiazepine is ideal, obtaining intravenous access can be difficult in a seizing patient, as well as time consuming. Diazepam, lorazepam, and midazolam can all be administered intramuscularly.

A large trial showed that intramuscular midazolam terminated seizures faster than intravenous lorazepam [5]. Midazolam can also be administered intranasally, and diazepam can be administered rectally.

Depending on local protocols, it may be best to administer a benzodiazepine by intramuscular, intranasal or rectal route before attempting to obtain intravenous access. Whichever medication or route is used, use a reference or cross-check process to ensure that the correct dose is administered. The few extra seconds to perform a medication cross check is well worth the added layer of patient safety.

Repeated doses of benzodiazepines may be needed to terminate seizures, and they should be administered until all seizure activity has ceased. Seizure activity may still be taking place in the brain, even if generalized convulsions have stopped. A deviated gaze, irregular respiratory pattern and occasional muscle contractions are all signs that the patient is still seizing and requires more medication.

Respiratory depression is a side effect of benzodiazepines, which can be detected immediately when monitoring waveform capnography. Assist ventilation with a bag-valve mask if respiratory depression occurs, and titrate respiratory rate and tidal volume to maintain ETCO2 between 35 and 45 mm Hg.

Generalized seizures can cause many forms of respiratory compromise, including respiratory arrest, respiratory depression and loss of upper airway reflexes. Waveform capnography is a reliable tool to help detect respiratory compromise, make airway management decisions and provide feedback on how well airway interventions are working.

References:

1.    Michael G, O’Connor R. The diagnosis and management of seizures and status epilepticus in the prehospital setting. Emerg Med Clin N Am (2011) 29; 29-39.

2.    Myers JB, Slovis CM, Eckstein M, et al. Evidence based performance measures for emergency medical services systems: a model for expanded EMS benchmarking. Prehosp Emerg Care, 2008; 12: 141–51.

3.    Pillow M, Howes, D, O’connor, R et al. Seizure assessment in the emergency department. Medscape 2015, Jan 8. Retrieved from: http://emedicine.medscape.com/article/1609294-overview

4.    EMS Training: Epilepsy and Seizure Management. Epilepsy Foundation, 2011.

5.    Silbegleit R, Durkalski V, Lowenstein D, et al. Intramuscular versus intravenous therapy for prehospital status epilepticus. N Engl J Med. 2012; 366(7):591-600 

Medic 23 and Engine 16 respond to a private residence for shortness of breath. Both arrive to find a 59-year-old female who says she is having difficulty breathing, which she attributes to a bad cold. Although she has these episodes occasionally, she had a flu vaccination this year to try to keep it from happening again.

The patient is afebrile with a few scattered wheezes that seem to disappear after coughing. Her blood pressure is 136/88 mm Hg, heart rate is 109, respiratory rate is 30 and her room air pulse oximetry value is 91 percent. Her lead II ECG is sinus tachycardia.

The patient reports a history of asthma as a child that continued into adulthood but disappeared after her second child was born 26 years ago. Her mother died in her mid-60s from emphysema.

She says she does not take any regular medications. She once smoked about three packs of cigarettes a month, but quit two years ago.

Firefighters from Engine 16 begin oxygen therapy at 2 lpm via nasal cannula and the patient’s oxygen saturation value climbs to 95 percent. Paramedic Torres administers nebulized albuterol while they prepare for transport.

The patient responds well to treatment during the ride to the hospital. Once there, Torres transfers care to the emergency department staff without any complications.

Torres documents asthma as the primary diagnosis. However, his partner thinks it is early onset emphysema because of her family and smoking history.

Study review
Researchers in Australia sought to determine how accurately paramedics could diagnose acute episodes of asthma or COPD [1]. The researchers included all patients transported by St. John’s Ambulance – Western Australia (STA-WA) during a 12-month period and transported to one of eight hospitals in metropolitan Perth.

For the prehospital diagnosis, researchers searched the electronic patient care report for the appropriate asthma and COPD code, which was entered by the primary paramedic. The ED discharge diagnosis came from a mandatory field in the Emergency Department Information System, which was entered by a member of the ED clinical staff.

Examining the accuracy of paramedic diagnosis of asthma or COPD is a two-step process. First, the researchers had to compare the prehospital diagnosis to the ED discharge diagnoses.

The second step required the researchers to compare the ED discharge diagnosis of asthma or COPD to whatever diagnosis the paramedic made. The second step allowed researchers to find those patients with asthma or COPD that paramedics completely missed.

Results
During the study period, paramedics transported 2,252 patients who met the inclusion criteria. Paramedics diagnosed asthma in 1,117 of those patients, while the remaining 1,135 patients had a diagnosis of COPD.

As expected, the asthma patients were significantly younger (median age 51 vs. 74 years). Twenty percent of the asthma group was under the age of 16 years compared to 10 percent in the COPD group. There was also a significant difference in gender distribution with 57 percent of the asthma group being female compared to only 46 percent in the COPD group.

Patients with a prehospital diagnosis of asthma were more likely to be wheezing when compared to the COPD group (86 percent vs. 55 percent), although the presence of cough, accessory muscle use and the ability to speak were similar between the two groups.

Despite the fact that all patients reported some degree of respiratory distress, paramedics recorded pulse oximetry values for only 93 percent of the patients. Only 88 percent of the patients had a second (or more) pulse oximetry value recorded.

When the information was available, the mean initial pulse oximetry value for the asthma patients was 93 percent while the mean initial pulse oximetry value for the COPD patients was 88 percent. Both groups had significant improvements in pulse oximetry values after the prehospital administration of supplemental oxygen.

There was a significant difference in the use of bronchodilators between the two groups. Paramedics administered a bronchodilator to 89 percent of the asthma patients with a documented wheeze compared to 65 percent of the COPD patients with a documented wheeze.

Three patients with a prehospital diagnosis of asthma died in the emergency department compared to eight deaths in the COPD group.

Despite the fact that 2,252 transported patients met the inclusion criteria, complete emergency department records were available for only 2,115 patients, 1,067 of the group with a prehospital diagnosis of asthma and 1,048 of the group with a prehospital diagnosis of COPD.

To measure the accuracy of the prehospital diagnosis, researchers calculated the positive predictive value (PPV) for both the paramedic diagnosis of asthma and of COPD. The PPV is the probability that a patient with a prehospital diagnosis of asthma (or COPD) really does have asthma (or COPD).

For the 1,067 patients with a paramedic diagnosis of asthma, only 433 patients had an ED discharge diagnosis of asthma, thus giving it a positive PPV of 41 percent. In fact, 19 percent of the patients actually had COPD as the ED discharge diagnosis.

Paramedics were slightly more accurate when it came to diagnosing COPD. For the 1,048 patients with a paramedic diagnosis of COPD, 860 patients had an actual ED discharge diagnosis of COPD, giving it a PPV of 57 percent. Only 4 percent of the patients with a paramedic diagnosis of COPD actually had asthma.

For the second step of the study, researchers identified 2,204 patients with an ED discharge diagnosis of asthma or COPD who were transported by ambulance. Of the 653 patients with an ED discharge diagnosis of asthma, paramedics also diagnosed asthma in 66 percent of the cases.

This statistic is called sensitivity, which means the ability of paramedics to find asthma when it truly exists.

The sensitivity of paramedic diagnosis for COPD was much worse. For the patients with an ED discharge diagnosis of COPD, paramedics also diagnosed COPD in only 39 percent of the cases.

Combining the results from these two examination steps suggests that when paramedics make a diagnosis of asthma, they are correct about 41 percent of the time (PPV). However, in about one-third of the patients who really do have asthma, the paramedics attribute the signs and symptoms to some other condition.

When paramedics make a diagnosis of COPD, they are correct about 57 percent of the time (PPV). However, in about 39 percent of the patients who really do have COPD, the paramedics attribute the signs and symptoms to some other condition.

What this means for you
Respiratory distress is a common prehospital presentation. Asthma and COPD are two of the most common sources of lung disease in the United States [2]. Although both are considered separate diseases, the two conditions may coexist [3].

Some EMS treatment protocols require field personnel to differentiate between asthma and COPD in order to provide treatment [4,5]. Due to the limitations of providing medical care in the field, such as an inability to verify the patient medical’s medical history and limited diagnostic capabilities, this can be a very difficult task.

Other studies of prehospital management of respiratory-related complaints have produced conflicting results regarding diagnostic accuracy. Researchers studying oxygen use in the United Kingdom found prehospital diagnosis was accurate only 32 percent of the time for COPD and 29 percent of the time for asthma [6].

Researchers in Boston found paramedics and emergency department physicians agreed on the diagnosis of patients with dyspnea about 77 percent of the time [7]. However in this study, paramedics were only asked to determine whether the dyspnea was cardiac or non-cardiac related.

Similarly, researchers in New York City found paramedics and ED physicians agreed on the origin of difficulty breathing complaints about 81 percent of the time [8]. Again, the paramedics were only asked to determine whether the complaint had a cardiac, respiratory or other origin.

Researchers in Australia comparing the effects of prehospital administration of high-flow versus titrated oxygen administration to patients with acute exacerbations of COPD found the diagnostic accuracy of paramedics to be 53 percent [9].

Although the causal mechanisms that underlie these two respiratory conditions are different, field treatment for acute exacerbations are similar. Both conditions require oxygen administration if the patient is hypoxemic and both conditions require nebulized bronchodilators if bronchospasm is present.

Given the diagnostic limitations of the field and similarity in prehospital treatment, a single treatment protocol or guidelines for respiratory distress seems reasonable.

Study limitations
One limitation of the current study lies in using the ED discharge diagnosis as the gold standard for asthma and COPD. It assumes that ED physicians can reliably differentiate between these two conditions, an assumption that remains unproven.

ED misdiagnosis has been reported as high as 10 percent [10]. Additionally, the EDIS used here only allows one discharge diagnosis. In some cases, patients may have more than one problem and the asthma or COPD diagnosis was relegated to an unsearched field.

A similar restriction on data entry exists in the prehospital ePCR. The choice of what to enter into the prehospital diagnosis or impression field was left to the paramedic’s discretion, which could affect the accuracy measurement.

For example, if the patient was experiencing an acute exacerbation of COPD caused by a respiratory infection (which is common), the paramedic may have recorded COPD as the diagnosis. Alternatively, the paramedic may have entered respiratory infection, which could lower accuracy rates.

Finally, one threat to the ability to generalize these results lies in the difference in paramedic training in Australia, which generally far exceeds the training required in the United States. To be a paramedic at St. John’s Ambulance – Western Australia, candidates must complete of a three-year university-based training program that awards a baccalaureate degree in paramedicine [11].

It is reasonable to believe paramedics trained in less time might have lower accuracy rates than demonstrated here.

A number of limitations reduce the accuracy of prehospital diagnosis of asthma and COPD. Signs and symptoms associated with the two conditions overlap further impacting diagnostic accuracy. Because field treatment of the two problems is similar, EMS agencies should adopt treatment protocols that focus on symptom management rather than clinical diagnosis.

References

1. Williams, T. A., Finn, J., Fatovich, D., Perkins, G. D., Summers, Q., & Jacobs, I. (2015). Paramedic differentiation of asthma and COPD in the prehospital setting is difficult. Prehospital Emergency Care, 19(4), 535-543. doi:10.3109/10903127.2014.995841
2. U.S. Department of Health and Human Services. (2012). Disease statistics. Retrieved from www.nhlbi.nih.gov/about/documents/factbook/2012/chapter4#4_5
3. Kim, S. R., & Rhee, Y. K. (2010). Overlap between asthma and COPD: Where the two diseases converge. Allergy, Asthma, and Immunology Research, 2(4), 209–214. doi:10.4168/aair.2010.2.4.209
4. Georgia Department of Public Health. (2013). Emergency medical services prehospital clinical operating guidelines. Retrieved from https://dph.georgia.gov/sites/dph.georgia.gov/files/EMS%202013%20clinical%20guidelines_0.pdf
5. Oklahoma State Department of Health. (2014). State of Oklahoma emergency medical services protocols. Retrieved from https://www.ok.gov/health2/documents/2014%20State%20of%20Oklahoma%20Protocols%20Field%20Edition.pdf
6. Denniston, A. K., O’Brien, C., & Stableforth, D. (2002). The use of oxygen in acute exacerbations of chronic obstructive pulmonary disease: A prospective audit of pre-hospital and hospital emergency management. Clinical Medicine, 2(5), 449–451. doi:10.7861/clinmedicine.2-5-449
7. Pozner, C. N., Levine, M., Shapiro, N., & Hanrahan, J. P. (2003). Concordance of field and emergency department assessment in the prehospital management of patients with dyspnea. Prehospital Emergency Care, 7(4), 440–444. doi:10.1197/S1090-3127(03)00214-4
8. Ackerman, R., & Waldron, R. L. (2006). Difficulty breathing: Agreement of paramedic and emergency physician diagnoses. Prehospital Emergency Care, 10(1), 77–80. doi:10.1080/10903120500366888
9. Austin, M. A., Wills, K. E., Blizzard, L., Walters, E. H., & Wood-Baker, R. (2010). Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: Randomized controlled trial. BMJ (Clinical Research Edition), 341, c5462. doi:10.1136/bmj.c5462
10. O’Conner, P. M., Dowey, K. E., Bell, P. M., Irwin, S. T., & Dearden, C. H. (1995). Unnecessary delays in accident and emergency departments: Do medical and surgical senior house officers need to vet admissions? Journal of Accident and Emergency Medicine, 12(4), 251-254. doi:10.1136/emj.12.4.251
11. St. John’s Ambulance – Western Australia. (n.d.). Graduate student ambulance officer program. Retrieved from http://www.stjohnchangelives.com.au/assets/templates/main/documents/STJO0841B_web.pdf

There has been an increasing amount of attention placed on the rapid identification and treatment of patients experiencing sepsis. Recall that sepsis is a highly exaggerated response by the body’s immune system to an infection. As the reaction worsens, hypoperfusion can cause one or more of the patient's organ systems to fail.

Severe sepsis affects more than one million people in the United States annually [1]. Between 26 and 50 percent of those patients with sepsis die. Moreover, the rate of sepsis is rising.

It has been shown that early recognition and treatment of sepsis by EMS providers can reduce the mortality rate [2]. Early fluid therapy and early notification for antibiotic treatment may be the reasons for why sepsis patients do better when transported by EMS. Here are five key points to keep in mind when assessing a suspected sepsis patient.

1. Sepsis is not always septic shock
EMS providers may mistakenly believe that a patient has to be hypotensive or in shock before being labeled septic. Much like other forms of hypoperfusion, the body will be in shock long before a drop in blood pressure. Suspect compensated shock if the patient is tachypneic (respiratory rate greater than 20 breaths per minute) and tachycardic (heart rate greater than 90 beats per minute).

2. Measure temperature accurately
Historically, a patient’s body temperature is not measured in the field as part of the patient assessment vital sign process. However, detecting either a fever (temperature greater than 36 C or 100.4 F) or a lower than normal temperature (less than 38 C or 96.8 F) can help drive a suspicion of sepsis. Technology such as temporal scan thermometers are accurate and noninvasive, making them well suited to field use.

3. Develop a strong history of the chief complaint
While many patients will describe a classic development of an infection — fever, chills, body aches —others may not. Geriatric patients are well known for not having a fever when having an infection, due to the aging process. Ask patients about recent procedures such as surgery or diagnostic testing that may have exposed the patient to the risk of infection. Changes in urinary frequency, color and consistency may point to a urinary tract infection. Diabetic patients and immunocompromised patients, such as those with cancer or HIV, are at greater risk for sepsis.

4. Assess lactate levels if possible
Lactate is a byproduct of anaerobic metabolism occurring in tissues where oxygen levels are low. A lactate level greater than 4 mmols, in conjunction with other vital sign findings, may be a strong indicator of sepsis. Several EMS systems have successfully used point of care meters to measure lactate levels in the field. However, these devices have been restricted for such use. Other systems are using more complex diagnostic equipment such as iSTATs to measure lactate in the field.

5. Measure exhaled carbon dioxide to strengthen a suspicion of sepsis
Carbon dioxide is a byproduct of metabolism and is excreted through the lungs during exhalation. A normal capnography reading ranges between 35 to 45 mm Hg. Patients in sepsis will have lower than normal end tidal carbon dioxide readings secondary to hypoperfusion and the formation of microclots along the capillary beds. An ETCO2 reading of less than 25 mm Hg, coupled with a suspicious history and the vital signs described earlier, may point to a patient who needs immediate intervention.

6. Treat sepsis early and aggressively
Finally, don’t be timid about initiating sepsis treatment. A patient who is showing significant signs of sepsis will require a large amount of fluid quickly. Up to two liters may be needed in the early phases of resuscitation. A vasopressor such as norepinephrine or dopamine may also be needed to maintain vascular tone while antibiotic therapy is initiated.

Reference
1. National Center for Health Statistics Data Brief No. 62 June 2011. Inpatient care for septicemia or sepsis: a challenge for patients and hospitals

2. Guerra, W. F., Mayfield, T. R., Meyers, M. S., Clouatre, A. E., & Riccio, J. C. (2013). Early detection and treatment of patients with severe sepsis by prehospital personnel. Journal of Emergency Medicine, 44(6), 1116–1125. doi:10.1016/j.jemermed.2012.11.003

Capnography, which is the monitoring of end tidal carbon dioxide, is a tool for EMS providers to monitor ventilation and perfusion in ill and injured patients. In this EMS1 poll call we want to know about your use and familiarity with capnography equipment, types of patients it is well suited for using, and training you have received on capnography and waveform interpretation.

Create your own user feedback survey

Read more about capnography in patient assessment and care at CapnoAcademy.com.

EMS tends to attract action-oriented people with short attention spans, which is a challenge when designing education programs. Whether for initial or continuing education, students are more likely to remember material if they are involved in lessons, and directed to analyze and apply what they learn. Active learning uses activities to engage learners in higher-order thinking tasks rather than passively receiving knowledge conferred by an instructor [1].

Capnography is a valuable assessment tool that many EMS providers do not utilize to its full potential. Here are three strategies that use active learning principles to teach about capnography use for respiratory compromise, sepsis and resuscitation:

1. Embrace mobile devices and media during lectures
Everyone has sat through torturous lectures driven by PowerPoint slides, and knowledge retention even from good lectures is notoriously poor. Students are more likely to remember material if they are involved in lessons and directed to analyze and apply what they learn, and lectures are more effective when students are given the opportunity to participate. Frequent recall of material, such as answering questions throughout chapters in a textbook, greatly improves knowledge retention [1].

Mobile devices allow review questions to be answered during a lecture, which keeps students thinking about the material and shows the instructor how well they are grasping it. Free polling programs such as Poll Everywhere and Kahoot allow you to insert multiple-choice questions into PowerPoint slides, and participants can see the poll results immediately. Polling can gamify a lecture.

Videos can also be embedded into slides that demonstrate content in action. Thousands of videos of real patient care on YouTube and Vimeo show abstract concepts being applied in practice. For example, in a lesson about respiratory compromise, present students with a case study about an 84-year-old female short of breath, with a history of CHF and COPD, speaking in two- or three-word phrases and with diminished breath sounds. Use an online polling program to give participants the choice to:

A.   Apply supplemental oxygen

B.   Administer albuterol

After the class sees their preferred treatment, follow up by asking why participants chose their answers. Both can be justified, and the real value is in the discussion about why they thought one choice was better.

Then show this video where paramedics apply capnography to a patient with that same presentation. After seeing the nearly-rectangular capnography waveform indicating no bronchospasm, ask the poll question again to see if the results are different. Show the rest of the video, which includes a lesson from well-known EMS educator Dave Page, about assessing respiratory patients and end with a discussion about how applying capnography early can affect critical treatment decisions.

Using mobile devices to answer questions and showing videos that demonstrate the concepts during a lecture will help students remember information and make the experience more meaningful.

2. Assign class work at home and homework in class
An alternative to a lecture is the flipped classroom model, in which learners watch a video, listen to a recorded lecture or podcast or complete a reading assignment before class. Students then do activities that apply material from those assignments in class. This allows class time to be used for higher-level thinking and problem solving.

For example, a service wants to use capnography to improve sepsis patient care. Instead of lecturing from slides in a classroom about how EMS recognition of severe sepsis, IV fluid administration and hospital notification can save lives, participants could watch a free online presentation from Mike McEvoy about capnography and sepsis before their face-to-face training meeting. After watching the video, ask participants to write an email or post on a discussion board completing the following sentences:

• Now I understand _____ about sepsis.
• I still don’t get _____ about sepsis.
• EMS sepsis recognition is or is not important because _____.

This pre-class activity allows the instructor to plan the lesson and focus on the less-understood areas of sepsis and capnography in class, as well as learn if there will be any resistance to the idea. It also encourages learners to reflect on and process what they watched in their own words, which improves knowledge retention [1].

After a review of the webinar in class, participants could work on cases in small groups that apply capnography for suspected sepsis. Some example cases:

• 80-year-old male with altered mental status and decreased urine output.
• 70-year-old female with difficulty breathing and isolated wheezing.
• 40-year old male with pain and redness around his knee three days after surgery.
• 12-year old with pain and red streaks up his arm three days after being bitten by a dog.

Assign vital signs for each patient, including ETCO2 and temperature, and have the groups of students report to their classmates' answers to these questions:

1. Is the patient in systemic inflammatory response syndrome, sepsis, severe sepsis or septic shock? How do you know?
2. How would monitoring ETCO2 help determine which patients need IV fluid? (ETCO2 below 25 mm HG with signs of infection is correlated with severe sepsis) [2].
3. How could reporting the patient’s ETCO2 and temperature affect the patient’s hospital course?

By recalling, analyzing and applying content while working out problems in class, learners have more tools to use that information in their practice.

3. Practice like you plan to play with simulation
Simulation allows learners to practice psychomotor skills, build pattern recognition and improve team dynamics in a safe environment. Simulators range from task trainers, such as an airway head or IV arm, to human actors and high-fidelity patient simulators that talk, generate cardiac rhythms and lung sounds and physiologically respond to medications.

Regardless of the tools used, applying a few active learning principles can make simulation a successful learning experience. Write learning objectives before the simulation. Make participants actually perform the steps of as many assessment and treatment tasks as possible. Finally, participants should reflect on the experience in a debriefing after the simulation.

For example, use a pit-crew resuscitation simulation focused on the use of capnography. An instructor with a CPR torso, airway head, IV arm and rhythm generator available will read vital signs and ETCO2 levels to the pit crew. The participants need to use ETCO2 levels to guide compression quality, change compressors, identify a spike and sustained ETCO2 after ROSC and recognize re-arrest after a loss of ETCO2.

Participants should carry gear the same way they would into someone’s home. Teams should practice performing chest compressions around other interventions (including placing an advanced airway, starting an IV, administering simulated medications, applying the capnography circuit and checking blood pressure before having one read to them by the facilitator) and rotating compressors every two minutes. The facilitator could read trends in the patient’s ETCO2 as feedback on the quality of compressions. Have participants work through problems together, even if mistakes are made, and discuss them during a debriefing.

The debriefing should likely last at least half as long as the scenario [3]. The facilitator should guide the discussion in a way that allows students to learn from each other. Instead of giving an American Idol-style critique of the simulation, the facilitator should ask what the participants thought went well and what could have gone better, and then ask how they feel about the learning points. For this scenario, the facilitator could ask what could cause a sudden drop in ETCO2 (hint: misplaced airway, secretions in the tube or a pneumothorax). Practice followed by reflection helps participants apply that experience later.

When developing an education program, think about ways to engage learners. Using mobile devices in lectures, flipping the classroom and simulation exercises are three ways to get students to analyze, apply and practice using capnography.

References:

1. Brown PC, Roediger HL, McDaniel MA. Making it stick: the science of successful learning. Belknap Press of Harvard University Press, Cambridge, MA: 2014.

2. Hunter CL, Silvestri S, Dean M, Falk JL, Papa L. End-tidal carbon dioxide is associated with mortality and lactate in patients with suspected sepsis. American Journal of Emergency Medicine. 2013 Jan; 31(1):64-71.

3. Kamerer J. Teaching healthcare professionals using simulation. Net CE; 2015.

Early adoption of new and emerging technologies is a trend for many EMS professionals. There are times when those technologies fit into the gap perfectly, such as WiFi and Bluetooth for EKG transmissions or tablets for documentation. There are other times when employing the latest technologies is about trying to appear cutting edge, about trying to fit the square peg into the round hole such as using Twitter as a substitute for a mobile data terminal messaging incident locations to responding crews.

Such is the case with virtual reality.

Virtual reality technology immerses the user in an environment other than their actual surroundings through sight and sound. The user's ability to interact and manipulate in this alternate environment is the key ingredient that defines virtual reality.

The concept of virtual reality has been around since the 1930s and emerged with concrete applications in the early 1980s. The technology remained limited to research labs though it was popularized through science fiction media and popular culture in the 1990s and 2000s.

Recently, virtual reality has experienced a resurgence as the technology has matured enough to become a consumer product. Hardware and software for virtual reality is  primarily geared for media consumption and use within the video gaming community.

Despite this progress, the prospect of paramedics utilizing virtual reality in their day-to-day functions remains bleak. There is no practicality to a paramedic visiting a patient through virtual reality. If you were to go to such lengths of deploying the technology, then it would likely be more efficient to utilize a physician with their larger scope of practice.

There are a number of programs around the country that utilize paramedics as the in-real-life physical provider of care before, during and after an assessment from a physician using telemedicine tools. These community paramedicine programs use sight and sound to provide the physician with the setting and general impression of a patient, while the on-scene provider relays tactile information gained from any directed physical assessment. Virtual reality technologies are extensions of these mobile integrated health programs, creating greater demand for paramedics to deliver the actual physical treatment on scene.

Virtual reality for EMS training
While deployment of virtual reality in the field is impractical, there are some places in EMS where it can help bridge a gap. The most effective area is likely simulation training. While many institutions utilize hands-on practical sessions to help students develop skills, the actual environments used are often idealized and not representative of the reality where patient assessment and treatment skills will be utilized.

Even absent smell, touch and taste, students using virtual reality for scene simulation could be exposed to more realistic environments in which they'll eventually find themselves outside the classroom. Darkened bedrooms infested with insects, overturned vehicles and industrial facilities are some of the environments that may be more easily created for student paramedics using virtual reality than those created physically in a school or training center.

Augmented reality for EMS training
Augmented reality has long been considered the halfway point on the road to virtual reality. Augmented reality blends the user’s actual environment with computer generated and interactive elements to allow added functionality like physical manipulation.

The technological requirements for augmented reality are considerably less than for virtual reality, allowing for quicker hardware and application development. Products for augmented reality, like Google Goggles and Yelp’s Monocle feature, have been available since 2011. The Monocle lets Yelp users view nearby businesses with the camera on their smartphone.

The summer of 2016 Pokemon Go gaming craze, which has resulted in additional ambulance runs, is another recent example of augmented reality already being used in the real world.

Wearable devices for augmented reality have been commercially available since 2013, allowing both further development and proof of concept in health care. Google’s Project Glass and Microsoft’s HoloLens are examples of commercially available augmented reality devices.

Augmented reality devices, specific to paramedic use, are likely to become available as wearable pieces of equipment, a heads-up-display (HUD) and a conductive swath or glove.

The HUD will most likely take a physical form similar to current eye-protection goggles or glasses. A paramedic would be able to see a variety of information including GPS directions, biometric readings from a patient and even treatment protocols that progress step by step as the paramedic completes them in the field. The HUD information would be overlaid upon the paramedic’s actual surroundings.

The HUD could help the paramedic with other tasks like walking through a dark or dimly lit room by providing digitally enhanced night-vision or acting as a conduit for translation services to overcome a language barrier. By tying into or connecting HUD devices worn by other members of the service, the HUD could also provide an operational overview at mass casualty incidents, transmit alarms when the user is in danger or has become injured and direct teammates to their side quickly. Ultimately, a HUD device might be capable of providing eyes and ears to a physician assessing a patient with a telemedicine system.

The conductive swath that the paramedic would wear on their forearm, upper leg or a glove on their hand would provide both an input link to the ePCR system and a second screen for the mobile data terminal. When viewing the swath, the augmented reality system would overlay patient or protocol information and virtual input buttons for navigating the operating system.

Diagrams, maps and a patient’s electronic medical record might be viewed through a conductive swath without causing disorientation for the user or completely eclipsing their surroundings from view. Overlaying a keyboard on the swath would provide a method for non-verbal communication with the command center, easy access to document findings or allow a medic to perform quick searches for relevant information regarding a patient's condition. Because it would be constructed of conductive materials, the swath could also be used to secure signatures from patients for refusals of care or acceptance of the patient by a nurse at a receiving facility.

Performing gestures with a glove, which includes a conductive swath, could provide similar access to system features. Additionally, the glove might contain tools that assess a patient’s biometric information by directly displaying it in the HUD and saving the information in the patient’s medical record. Oxygen saturation, pulse rate, skin temperature and carbon monoxide oximetry are some of the measurements that might be possible with integrated sensors.

As virtual reality and augmented reality continue to develop, we will undoubtedly see them gain traction in the consumer marketplace before being adapted to health care, specifically the type of mobile healthcare that EMS personnel provide.

It is vital we don't simply adopt expensive and impractical technologies of the moment for the sake of their novelty. Instead, we must integrate what we've learned from mistakes of the past with practical and proven applications of new technologies to provide positive patient outcomes and provider work experiences.