Therapeutic Hypothermia in the Field

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On March 18, thousands of participants lined up for the Quintiles Wrightsville Beach Marathon in North Carolina. The race seemed to be going smoothly when 38-year-old James Glasgow collapsed just a few hundred yards from the finish line.¹ Paramedics from New Hanover Regional EMS arrived at his side within moments and found him in ventricular fibrillation. After several minutes of CPR and defibrillation, they restored his pulse. During transport the paramedics performed their routine return-of-spontaneous-circulation care, which included ensuring a patent airway, making sure two IVs were in place and initiating 30 ml/kg of iced normal saline. Upon arrival at New Hanover Regional Medical Center, Glasgow’s core body temperature had been reduced to 32°C. Less than 10 days later, he was released from the hospital neurologically intact, though with no recollection of the marathon.

Introduction

Knowledge of the potential benefits of therapeutic hypothermia (TH) is actually quite ancient. Hippocrates was the first physician known to have documented them when he noted that soldiers with severe head injuries had better survival rates when their injuries occurred in the winter compared to the summer.² Unfortunately, this knowledge was then neglected until 1938, when deep hypothermia was first tested and used to slow cancer cell metabolism and division.² Since then, TH has been used during many thoracic and neurological surgical procedures,³ and since the 1950s has been used to protect the brain during cardiothoracic and neurosurgery.⁴

TH began gaining attention in cardiac arrest care during the first years of this century. Two landmark studies published in the New England Journal of Medicine in 2002—the first led by Australian physician Stephen Bernard, MD,⁵ the second known as the Hypothermia After Cardiac Arrest (HACA) study⁶—prompted the International Liaison Committee on Resuscitation (ILCOR) to first recommend therapeutic hypothermia for out-of-hospital cardiac arrest due to VF and pulseless ventricular tachycardia in 2003.⁴ These studies observed that cardiac arrest survival with good neurologic outcome increased from 26% to 49% and 39% to 55%, respectively, for out-of-hospital cardiac arrest survivors who were cooled. In 2010, the American Heart Association updated its recommendations and identified therapeutic hypothermia as a Class I recommendation for VF cardiac arrest and a Class IIb recommendation for cardiac arrest with asystole/PEA as the initial presenting rhythm.

Post-Cardiac Arrest Syndrome

It is difficult to understand how TH benefits cardiac arrest patients without understanding what happens within the body when medical providers halt the dying process (i.e., successfully resuscitate a patient). Pre-resuscitation, several organs were exposed to some period of hypoxia. As a result, a constellation of simultaneous events began occurring throughout the body, collectively termed post-cardiac arrest syndrome. These events include post-arrest brain injury, myocardial dysfunction, systemic inflammatory response, and persistence of the precipitating pathology.⁴

Brain injury following cardiac arrest can be either immediate or reperfusion-related. Immediate injury occurs as a result of brain ischemia and neuron, or brain cell, infarction that develops during the initial cardiac arrest as energy stores are consumed. During this time cell swelling develops as a result of the loss of intracellular sodium and potassium ion gradients. The cell’s sodium and potassium pump ceases to function during cardiac arrest, and when ROSC occurs this pump is slow to restart, causing fluid shifts as a result of an osmotic gradient.

If return of spontaneous circulation (ROSC) occurs, blood flow returns to the ischemic neurons, and the brain is exposed to a natural inflammatory response and free oxygen radicals that were released systemically during the arrest.⁴ Both swelling and free oxygen radicals damage lipids, proteins and the DNA of neuron cells. All of this causes irreversible cell damage. Free oxygen radicals irreparably damage neuron membranes.² This triggers a cascade of events that promotes injury to nearby cells, worsening the injury size. Additionally, ischemia causes a weakening of the cellular blood-brain barrier, which allows for additional fluid shifts from the bloodstream into intracellular and interstitial spaces. This worsens cerebral edema.⁴

While this occurs, cardiac tissues are also stressed and consuming oxygen at an accelerated rate as they, too, try to compensate for an extended period of ischemia. During this time ischemic cardiac cells are prone to triggering atrial and ventricular dysrhythmias. Transient post-cardiac arrest tachycardias are common and in general should not be treated, as they are typically benign. Sustained life-threatening tachydysrhythmias such as ventricular tachycardia or SVT require treatment.

A systemic inflammatory response is the body’s natural response to a major body insult and can be described as generalized inflammation and swelling. It is diagnosed by the presence of any two of the following:

• Temperature less than 96.8°F or greater than 100.4°F;

• Heart rate greater than 90 bpm;

• Respiratory rate greater than 20 or PaCO₂ less than 32 mmHg;

• White blood cell count less than 4,500 µl/mm³ or greater than 10,000 µl/mm³.

This inflammatory response leads to a shifting of fluids into interstitial spaces and vasodilation, both of which may exacerbate hypotension. Additionally these fluid shifts increase the amount of fluid between cells and capillaries, which makes it more difficult for cells to receive oxygen and offload waste products, including carbon dioxide and lactic acid (Figure 1). As a result, already irritable organs are stressed even further and may show signs of dysfunction. Organs that are particularly sensitive to dysfunction include the liver, kidneys and brain.⁷

Finally, think of the cardiac arrest as a sign of an underlying issue that caused it. This could be a myocardial infarction, primary respiratory arrest, myocardial trauma, etc. As long as this trigger remains uncorrected, the patient is likely to go back into cardiac arrest. Thus, in addition to managing the cardiac arrest itself, the underlying cause must also be managed.

Actions and Effects

The goal of TH is to halt the physiologic events occurring during post-cardiac arrest syndrome and thereby minimize damage to the body’s organs, particularly the brain. This works because cooling tissues is believed to reduce metabolic demands, the production of free radicals and the volume of inflammatory cytokines.³ Cytokines are messenger chemicals responsible for the inflammation and fluid shifts that occur during an inflammatory response.

When the body is cooled from its baseline of 37°C (98.6°F) to 31°–34°C, the following occurs:^2,4

• Neuronal metabolic rate decreases;

• Neuron membranes are stabilized;

• Minimal buildup of glutamine and dopamine;

• Reduced production of free oxygen radicals;

• Chemical pathways responsible for cellular apoptosis (cell death process) halt;

• Pro-inflammatory cytokines are reduced;

• The blood-brain barrier is preserved and enhanced;

• The function of mitochondria, the cell’s energy powerhouse, improves;

• Cellular survival pathways improve;

• Microthrombi formation is limited.

While the physiology limiting some of these events is understood, how cooling positively influences many of these cascades is not. While the mechanisms enhancing the cellular survival pathways are not known, it is well known that microthrombi develop in the arterioles during and following the hypotension and stagnant blood flow that occur during and following cardiac arrest. These impair circulation and cause tissues to become hypoxic. Hypothermia is known to impair the clotting cascade, and as a result fewer of these microthrombi develop.

Some of these actions are understood. With cooling there is a measurable decrease in cerebral edema because fewer cytokines are available to trigger swelling.² Normally ischemic neurons work in overdrive to compensate for becoming ischemic. The result is a local increase in formation of free oxygen radicals. However, intracellular metabolism slows during TH, leading to a decreased oxygen demand and decreased neuron workload, which results in fewer free oxygen radicals being released. This allows ischemic and injured neurons time to heal and reduces overall damage. The result is limited central nervous system injury following cardiac arrest.⁴

Neurons also benefit during TH by a stabilization of the cellular membranes. Exactly how this happens is not well understood, but the resulting benefit is that there is a limited calcium influx. An influx of calcium normally excites the cell-speeding metabolism. With less calcium, metabolism remains reduced, enhancing healing.⁴

Determining Cooling Candidates

Like any procedure, it is important to understand who can and cannot receive therapeutic hypothermia. Most studies of TH for post-cardiac arrest patients have excluded children, and some have excluded women of childbearing years.³ This does not mean these patients cannot be cooled, just that these patient groups haven’t been studied for TH following cardiac arrest.

General inclusion criteria for patient cooling following prehospital cardiac arrest are as follows:⁴

• At least 18 years old;

• Time from arrest to ROSC less than 60 mins.;

• At least 5 minutes of CPR performed;

• SBP greater than 90 mmHg (MAP greater than 60) with only one vasopressor;

• GCS less than 9;

• Less than 6 hours since ROSC.

In the 2010 AHA guidelines, therapeutic hypothermia is described as a helpful therapeutic approach for patients who remain without meaningful response to verbal commands following ROSC.⁸ With these guidelines, TH between 32°–34°C for 12–24 hours was listed as a Class I, LOE B recommendation for patients presenting in VF, and a Class IIb, LOE B for patients presenting in PEA and asystole. This last recommendation was further supported in 2011 with a study demonstrating that TH does not reduce mortality for patients with asystole/PEA.⁹

Currently TH is recommended to be administered within 6 hours of ROSC, with a preference for the earliest possible initiation. There is clear data showing that the earlier TH is initiated, the better outcomes become.¹⁰

Known pregnancies and repetitive cardiac arrests are considered relative contraindications for therapeutic hypothermia. The benefits of TH for the mother may exceed the known risks (demise) for the fetus, but this remains controversial. Also, initiating TH while performing CPR during cardiac arrest is currently being studied. Intra-arrest TH initiation seems to be improving patient outcomes, which could suggest the need to initiate cooling during repeat arrests down the road. Currently, though, this research remains unpublished.

The generally accepted list of TH exclusion criteria includes:⁴

• Initial temperature less than 32°C;

• Patient responding to commands following ROSC;

• Cardiac arrest due to trauma/head injury;

• Major surgery within past 2 weeks;

• Known systemic infection;

• Comatose prior to cardiac arrest;

• Persistent hypotension (MAP less than 60 mmHg) despite vasoactive drugs for 30 mins.;

• Persistent hypoxemia (SaO₂ less than 85%).

Cooling Methods

There is no single cooling method shown to be superior to others in regards to patient outcomes.^2,8 Regardless of what method is selected, the goal is to obtain the target temperature within 300 minutes.³ Prior to initiating cooling, it is essential to carefully document a neurological examination.⁴ This baseline examination is essential for neurologists who later evaluate the patients so they can look for improvements from the baseline.

There are many cooling techniques, including ice packs along the axilla, groin and sides of the neck; ice baths; cooling blankets with circulating water; iced normal saline and other fluids; gel-coated cooling pads along the torso; cooling helmets and caps; and invasive lines. Once cooling is initiated, the goal is to achieve the temperature, most commonly 32°C, as rapidly as possible. This is important because slow cooling can exacerbate hypovolemia and electrolyte disorders, including hypokalemia, hypomagnesemia and hyperglycemia.⁴

For prehospital providers, the use of normal saline and lactated Ringer’s chilled to 4°C has become a standard for cooling. Administering 30 ml/kg over 30 minutes has been shown to cool patients 1.4°C.⁴ Additionally, a feasibility study administering 30 ml/kg of 4°C saline at 100 ml/min reduced temperatures by an average of 1.9°C.¹¹ In theory, administering 30 ml/kg of saline to any patient could push them into heart failure, but multiple case studies have demonstrated that saline can be used to induce hypothermia safely, effectively and without significant complications, including pulmonary edema.⁸ Preliminary data from New York City EMS has found that 7.7% of patients receiving prehospital intra-arrest iced saline develop some symptoms of pulmonary edema, but that these patients actually have better outcomes that those who don’t.¹²

There are several devices currently available that target cerebral cooling following cardiac arrest. The benefit of cerebral cooling for brain injuries is discussed later, but isolated cerebral cooling has not been well researched in cardiac arrest patients. All research is on systemic cooling. One study that reviewed targeted cranial cooling found no significant systemic cooling was achieved.¹¹

Temperatures and Length of Cooling

While the ideal target temperature has not been determined, nearly all studies cool patients to 33°–34°C.³ Cooling patients to 27°C has been shown to cause adverse effects and complications.² Currently most protocols aim for 32°–33°C.

When cooling patients it is essential to monitor temperatures continuously.³ This can be done with esophageal, rectal or Foley thermometers. The AHA says temperature monitoring is best done via esophageal or bladder catheter, and that axillary and oral thermometers are inadequate for ongoing monitoring.⁸ However, a study that compared tympanic to bladder and esophageal temperatures during management of therapeutic hypothermia found that an accurately obtained tympanic temperature reliably reflects esophageal and core body temperature.¹³

Once cooling is initiated it is essential to prevent premature rewarming. Maintain cooling until physicians can control the rewarming process. While the optimal cooling period has not been determined, most protocols maintain it for at least 24 hours.⁴ Some studies keep patients cool for as long as 48 hours.³ Additionally, cerebral edema can persist for up to 72 hours, so it is reasonable to suspect that down the road, the cooling time period may be extended.⁴

Shivering

Shivering, the rhythmic tremoring of skeletal muscle, is the most frequent side effect of therapeutic hypothermia. It is activated when a certain temperature is reached in the hypothalamus, most often between 36°–37°C.¹⁴ Effective shivering increases basal metabolic rate to 2–5 times normal, and is also associated with an increase in energy and oxygen consumption, as well as carbon dioxide elimination. Subclinical shivering may be as subtle as increased muscle tone and will also slow cooling.⁴ Shivering also increases blood pressure, heart rate, respiratory rate and intracranial pressure.

It is essential to control shivering as soon as it is recognized during the cooling process. Shivering is the body’s only warming mechanism, and it needs to be controlled to blunt the body’s thermoregulatory defenses.¹⁴ A variety of pharmacologic strategies are available, and for EMS the most practical are either fentanyl or benzodiazepine boluses that can be followed by infusions as necessary. If these methods fail, propofol (10–50 mcg/kg/min) provides both vasodilation and an active lowering of the shivering threshold; it is used by some EMS and many specialty-care transport systems. Should these methods fail to suppress shivering, consider paralytics, depending on availability.⁴

Skin temperature is suspected to influence an increase in shivering by as much as 20%. Thus, applying transient skin warming methods (e.g., a blanket) can warm the skin and blunt shivering while allowing the core to remain cool.¹⁴ Interestingly, this raises question over the true benefit of direct cooling on the axilla, groin and neck, as these cooling methods may be blunted by the shivering they produce as the skin first cools.

Pharmacology

Often lost in the excitement of implementing therapeutic hypothermia is consideration of its effects on pharmacokinetics and pharmacodynamics. All the sedatives, analgesics and neuromuscular blocking agents given during TH will have altered pharmacodynamics. Therapeutic hypothermia is expected to cause a delay in drug metabolism and elimination and may also modify drug response, potency and efficacy.⁷

Additionally, the length of cardiac arrest and pre-arrest health of the patient both impact hepatic and renal function. The functional level of the liver and kidneys directly impacts drug metabolism and elimination. As a result it is very difficult to anticipate how drugs will impact post-cardiac arrest patients, particularly once cooling is initiated.⁷

Using this knowledge, pharmacology is important during TH, as patients must be kept sedated. The goal is to keep a patient deeply sedated, which means unarousable and unresponsive to any tactile or verbal stimuli.⁴ Sedatives also provide amnesic effects so that patients ideally have no recollection of the cooling period. In addition to sedation, pain management following cardiac arrest is important, as CPR may result in rib fractures or other injuries.

Analgesia—A review of 68 intensive care units found that 26% did not administer analgesics to patients receiving therapeutic hypothermia.⁷ Current standards, however, stress the importance of administering analgesics prior to sedatives and especially prior to any neuromuscular blocking agents.

Fentanyl is a commonly administered and effective analgesic during TH. However, keep in mind that fentanyl clearance decreases by up to 3.7 times from normal when core body temperatures are decreased.⁷ Morphine metabolism results in many metabolites that are prone to accumulation during hypothermia, renal dysfunction and hepatic dysfunction. This makes the effects of morphine difficult to predict, which means it’s a poor analgesic for hypothermic patients.

Sedatives—Midazolam infusions are administered between 5 mg/hr and 0.3 mg/kg/hr. Midazolam metabolism is likely altered, as hepatic dysfunction is common.⁷ In addition, the metabolites—byproducts of metabolized midazolam—can build up when renal dysfunction exists. Another disadvantage to midazolam is that its ability to consistently sedate the patient becomes lost if it is not administered at regular intervals. Thus, when utilizing midazolam, ensure a constant dosing regimen (e.g., every 20 minutes).

Diprivan (propofol) is a better choice because its metabolites do not accumulate with hepatic or renal dysfunction.⁷ However, it does have a low therapeutic window, and its potential for toxicity increases during hypothermia. Diprivan also has the additional benefit of lowering the shivering threshold. While not typically used in prehospital care, it is often used during critical care interfacility transport, and EMS systems implementing TH protocols may want to discuss the use of Diprivan with their medical director.

The pharmacokinetic profiles of ketamine and lorazepam make both drugs inappropriate for the sedation of patients receiving therapeutic hypothermia.⁷

Neuromuscular blocking agents—When aggressive sedation fails to control shivering, the use of neuromuscular blocking agents is indicated. A serious downside to NMBAs is that they mask seizure activity, which can be present following cardiac arrest, particularly if there is an anoxic brain injury. Seizures exacerbate the brain injury and are associated with worsened outcomes.⁷

The selection of NMBAs varies widely and includes pancuronium, cisatracurium, rocuronium, vecuronium and atracurium. Nearly all NMBAs are free of major hemodynamic effects, which makes them safe for use during TH, but use caution with vecuronium and pancuronium, which both have active metabolites that accumulate in patients with renal dysfunction.⁷ Vecuronium and rocuronium are currently the most commonly administered NMBAs in prehospital care.

Coordination

Implementing a prehospital cardiac arrest protocol cannot be done alone. It must be coordinated with at least one hospital, because the in-hospital management of these cooled patients demands educated and prepared emergency department physicians, trained ICU nursing staff, pharmacologists, neurologists, cardiologists, pulmonologists and critical care intensivists.^3,4 Additional support may be needed from trauma surgeons, neurosurgeons, hepatologists and rehabilitation departments.⁴

Throughout the cooling period patients require ongoing monitoring and care. While at target temperature, glucose is closely controlled with sliding scale insulin, electrolytes are kept well within normal limits, shivering is prevented, and ventilator support is provided.³ This can only be done when a hospital has properly trained its ICU staff to manage these patients. This is why it is essential that prior to EMS implementation of prehospital cooling, a hospital capable of maintaining these patients is identified. It may be necessary to develop a plan for transfer to tertiary care. Continuity of care from the field through the ED and ICU to discharge and rehab is critical for success.

Future Uses

Since at least 2006, physicians have been researching the benefits of cooling for patients experiencing acute stroke.³ In one study awake stroke patients were cooled to 33.4°C within 1.7 hours and maintained cold for 24 hours. None of these patients experienced complications; this seems to support the feasibility of using TH for stroke care.¹⁵ A 2007 review of animal studies found cooling the brain during acute ischemic events within 3 hours reduced infarct size and nearly completely abolished the ischemic region.¹⁶ This review concluded there are true beneficial neuroprotective properties to therapeutic hypothermia during stroke, but that the ideal cooling method, rate and duration were unknown.¹⁶ Finally, a multicenter study published in 2010 by the same author demonstrated that endovascular TH of acute stroke patients following tPA administration was safe.¹⁷

Hypothermia has been demonstrated to reduce intracranial pressure following severe traumatic brain injuries, particularly in children. At this point, however, its benefit for improving neurological outcomes has not been proven.² The hope is that with more research, appropriately applied hypothermia can reduce the secondary effects from evolving injuries and inflammation that occur following TBI. It is theorized to reduce mortality and improve neurological outcomes (having the greatest benefits when used for at least 48 hours) but not be as helpful when ICP is initially high or when barbiturates are used at high doses.⁴

Therapeutic hypothermia is also being researched for benefits to patients receiving PCI for STEMI.³ One animal study found that rapid cooling during a simulated left ventricular myocardial infarction preserved LV function, reduced injury size and preserved mitochondrial function.¹⁸

Since May 2005 the National Institute of Child Health and Human Development has supported the use of therapeutic hypothermia for neonates suffering from hypoxic-ischemic encephalopathy, while acknowledging more research is needed.²

What’s in It for EMS?

It is not often that a drug, therapy or intervention can be clearly shown as more beneficial when administered during prehospital care than in the emergency department. Therapeutic hypothermia may be this intervention. All of the research presented to this point has shown that the earlier TH is applied, the better patient outcomes become. Further, current research seems to be showing that intra-arrest TH raises the rates for ROSC.

There many devices and strategies for initiating prehospital therapeutic hypothermia. Administering 30 ml/kg of iced 4°C normal saline continues to be the most rapid and effective strategy. Systems without ALS providers can initiate TH by applying ice packs to the groin, neck and axilla to patients who experience ROSC. A variety of systems are available for maintaining cooling devices and having them readily available. Currently EMS systems only utilize TH for post-cardiac arrest patients, but in the future it may be reasonable to initiate on patients suspected of acute strokes or with ST segment-elevation myocardial infarctions.

If your system uses TH, keep using it as often as clinically indicated, and consider the application of intra-arrest iced saline. If your EMS system does not utilize TH, consider a conversation with your medical director and the closest tertiary care center. Initiating therapeutic hypothermia requires coordinated medical care, but its use is a prime example of how a healthcare system can work together to benefit patients.

References

1. WECT. Runner Collapses During Marathon, Released from Hospital, www.wect.com/story/17264996/runner-collapses-during-marathon-released-from-hospital.

2. Harrison E. Hypothermic Life Support, www.asfhm.com.

3. Lutes M, Larsen N. Focus On: Therapeutic Hypothermia, www.acep.org/content.aspx?id=26776.

4. Marshall PS, Siegel, MD. Therapeutic Hypothermia, www.chestnet.org/accp/pccsu/therapeutic-hypothermia?page=0,3.

5. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002; 346: 557–63.

6. Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002; 346: 549–56.

7. Chamorro C, Borrallo JM, Romera MA, et al. Anesthesia and analgesia protocol during therapeutic hypothermia after cardiac arrest: a systematic review. Anesth Analg 2010 May 1; 110(5): 1,328–35.

8. Peberdy MA, Callaway CW, et al. Part 9: Post Cardiac Arrest Care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010; 122: s768–s786.

9. Dumas F, Grimaldi D, Zuber B, et al. Is hypothermia after cardiac arrest effective in both shockable and nonshockable patients?: insights from a large registry. Circulation 2011 Mar 1; 123(8): 877–86.

10. Chiota NA, Freeman WD, Barrett K. Earlier hypothermia attainment is associated with improved outcomes after cardiac arrest. J Vasc Interv Neur 2011; 4(1): 14–17.

11. Kämäräinen A, Hoppu S, Silfvast T, Virkkunen I. Prehospital therapeutic hypothermia after cardiac arrest—from current concepts to a future standard. Scand J Trauma Resusc Emerg Med 2009 Oct 12; 17: 53.

12. Freese J. SmartCPR, QCPR, Project Hypothermia, Zofran & the QT Interval. Continuing Medical Education—News & Information 18(2–3): 5–13.

13. Hasper D, Nee J, et al. Tympanic temperature during therapeutic hypothermia. Emerg Med J 2011; 28: 483–85.

14. Presciutti M, Bader MK, Hepburn M. Shivering management during therapeutic temperature modulation: nurses’ perspective. Crit Care Nurse 2012 Feb; 32(1): 33–42.

15. Guluma KZ, Hemmen TM, Olsen SE, et al. A trial of therapeutic hypothermia via endovascular approach in awake patients with acute ischemic stroke: methodology. Acad Emerg Med 2006 Aug; 13(8): 820–7.

16. Hemmen TM, Lyden PD. Induced hypothermia for acute stroke. Stroke 2007 Feb; 38(2 Suppl): 794–99

17. Hemmen TM, Raman R, et al. Intravenous thrombolysis plus hypothermia for acute treatment of ischemic stroke (ICTuS-L): final results. Stroke 2010 Oct; 41(10): 2,265–70.

18. Tissier R, et al. Rapid cooling preserves the ischaemic myocardium against mitochondrial damage and left ventricular dysfunction. Cardiovascular Research 2009; 83: 345–353.                

Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, is an educator, e-learning content developer and author of numerous articles and textbook chapters. He is also the performance improvement coordinator for Vitalink/Airlink in Wilmington, NC, and a lead instructor for Wilderness Medical Associates. Contact him at kcollopy@colgatealumni.org.

Sean M. Kivlehan, MD, MPH, NREMT-P, is an emergency medicine resident at the University of California San Francisco and a former New York City paramedic for 10 years. Contact him at sean.kivlehan@gmail.com.

Scott R. Snyder, BS, NREMT-P, is the EMT program director for the San Francisco Paramedic Association in San Francisco, CA. Scott has worked on numerous publications as an editor, contributing author and author, and enjoys presenting on both clinical and EMS educator topics. Contact him at scottrsnyder@me.com.