Tuesday, November 17, 2009

Sudden Death in the Young

EMS providers should be aware of a variety of conditions that can cause fatal cardiac arrest in the young.

By James Davis, RN, MA, EMT-P
James Davis, RN, MA, EMT-P, has been in EMS for 25 years and is currently a fire captain/paramedic with the Columbus (OH) Division of Fire and a flight RN for Medflight of Ohio. He is an adjunct faculty member at Columbus State Community College and sits on the State EMS Board in Ohio. Contact him at jdavis@medflight.com

Your EMS crew is dispatched to the local neigborhood park for an injured person. Upon arrival, you see kids frantically waving from the basketball court. On arrival, you find a male patient in his late teens who is unresponsive and pulseless, and CPR is in progress.

As you start resuscitation, you ask the friends to tell you what happened. They explain they had been playing basketball for about 30 minutes when the patient was running down the court and collapsed. You ask about medications, medical history and allergies as friends try frantically to reach the boy's parents. The friends say they don't know his medical history, and they absolutely deny any drugs or alcohol.

CPR is ongoing, the patient is defibrillated and ALS care is continued en route. Despite your aggressive treatment and the hospital's efforts, he's pronounced dead by the emergency department physician. As you clean up the truck and write your report, you tell yourself, "We deal with older patients in cardiac arrest frequently, but not a young, healthy appearing kid like this. His friends have to be lying. There has to be more to this story."

In the United States, it is estimated that 200–300 young people die each year from cardiovascular events during physical exercise.1 [http://] While this number is relatively low compared with other causes of death in similar age groups and considering how many athletic events take place annually, several times a year, television media report an athlete's death. These deaths are always high profile and generate community attention. But what causes a healthy appearing child, teen or young adult to suffer fatal cardiac arrest?

The generally accepted definition of sudden death is a sudden loss of consciousness from a cardiovascular event within an hour of the onset of symptoms. Sadly, diagnosis is often made upon autopsy.2 [http://] In the U.S., 90% of deaths occur during competitive sports like basketball or football. Soccer has the highest death rate in Europe. Males are nine times more likely to die than females.3 [http://]

Many paramedics have responded to a child with chest pain. While the majority are non-cardiac, a 2007 study in the Journal of Pediatrics should raise awareness that it is possible for coronary artery disease to be present even in the young. Over an 11-year period, nine children ages 12 to 20 were diagnosed with myocardial infarction after arriving at an Ohio hospital with chest pain radiating to the left arm and jaw. Interestingly, there was no drug use involved and no other risk factors.4 [http://] In 2002, 33-year-old St. Louis Cardinals pitcher Darryl Kile was found dead in his hotel room after complaining of left shoulder pain during dinner with his brother the previous evening. Upon autopsy, he was found to have 90% occlusion of three heart vessels. San Francisco 49ers offensive lineman Thomas Herrion, age 23, died of coronary artery disease after suffering cardiac arrest following a preseason game in Denver.5 [http://]


There are structural changes in the heart that are considered normal in athletes. Because the heart is a muscle, it functions as any other muscle. When it is worked, it grows. This increases the size and mass of the muscle to allow for increased stroke volume and cardiac output. The question is, what are normal physiologic changes compared to changes in a diseased heart? The typical answer is rest. When the athlete is noncompetitive for a period upwards of three months, the nondiseased "athletic heart" will remold and reshape itself, whereas the diseased heart will remain enlarged.6 [http://]

The normal heart has a ventricular wall measurement of 12 millimeters. Hypertrophic cardiomyopathy (HCM) is diagnosed in patients with a myocardial wall thickness of greater than 15 millimeters. In general, the thicker the wall the less effective the heart is and the harder it has to work. A study of 387 U.S. deaths found that HCM was the most common cause of death in the young. Twenty-six percent, equating to 102 deaths, were diagnosed post-mortem with HCM. Although it can be caused by drug use, it is primarily an inherited disease that develops during conception when an overgrowth in the muscle interferes with the heart's ability to contract.7 [http://] In 1998, Italian researchers examined 49 competitive athletes who died from HCM and found that 44 were males with an average age of 23. Many times the first symptom a patient experiences is cardiac arrest. Studies have found that only 21% of patients had symptoms prior to their event. These symptoms include shortness of breath, chest pain, syncope or an abnormal blood pressure response during exercise. While shortness of breath is the most commonly seen symptom, syncope identifies patients who are at greater risk of sudden death and is a huge red flag for EMS providers.8 [http://] Palpitations are encountered in up to 70% of athletes, depending upon their age and the sport. These palpitations are described in different ways and are most commonly benign.9 [http://]

Although clinical appearance and electrocardiogram can raise suspicion for HCM, the main diagnostic test is echocardiography, which allows visualization and measurement of the heart walls. Over 200 genes have been associated with HCM. Genetic testing is available for about $4,500. There is no specific cure. Treatment includes medication, automatic pacemaker/defibrillator, and, in some cases, surgical remodeling. Patients with this disease are generally restricted from participating in competitive sports, and the court system has upheld schools' decisions to deny student participation in athletic events if they have HCM.10 [http://]


As the second leading cause of sudden death in athletes, commotio cordis is Latin for commotion of the heart. It is caused from blunt, non-penetrating trauma to the chest in the immediate area of the heart during the period of vulnerability (T wave). While 62% suffered sudden death during competitive sports, 32% died during daily activities like falls from a jungle gym. Deaths have occurred during hockey, karate and lacrosse, but baseball is the sport attributed to the most deaths. A study of 63 deaths found that all but one occurred during baseball: 35 playing in the field and 14 while at bat. It appears that a strike to the chest with a hard object is to blame. Athletes died less frequently in sports using air-filled balls, such as basketball.11 [http://] Of the deaths studied, males were involved 95% of the time; 87% were Caucasian. The mean age was 13, and 80% of deaths occurred in athletes younger than age 18. Patients are most commonly found in ventricular fibrillation; sadly, fewer than 15% are successfully resuscitated.12 [http://] It is often the case that after the blow to the chest, the athlete has a period of several seconds where they continue playing before becoming unconscious. There are commercial chest protectors on the market to protect the sternum from inadvertent chest blows; however, it should be noted that a 2006 study found 28% of kids suffering commotio cordis were wearing protective devices, questioning their effectiveness and potentially giving a false sense of security.13 [http://]

Electrophysiological studies conducted in a controlled setting using swine found that a 30 mph impact during a 20 ms window of ventricular repolarization (t wave) will generate ventricular fibrillation 30% of the time. It is estimated that the ball in Little League pitching travels at approximately 50 mph. As velocity of the impact increases, so does the rate of ventricular fibrillation. Compare that to chest strikes outside that 20 ms window where no incidents of ventricular fibrillation were noted. Again, strikes outside the immediate silhouette of the heart generated no case of ventricular fibrillation. There is no documented evidence that these events are caused by ischemia of the myocardium. Rather, it is believed that this is an electrical conduction event.14 [http://]


"Pistol" Pete Maravich is the leading scorer in NCAA history with an average 44 points a game. He played in the NBA for 10 years and retired in 1980. Eight years later, at age 41, he was playing in a pick-up game when he suffered sudden cardiac arrest and died. Upon autopsy, it was determined that only one coronary artery was supplying blood flow to his heart.15 [http://]

Cardiac anomalies like these pose challenges to both athletes and EMS providers. For example, John, a healthy 20-year-old, grew up playing competitive sports. After high school he continued working out, but became frustrated at his fatigue and some occasional chest pain during exertional activity. While playing soccer with friends, he dropped to one knee when he became lightheaded and dizzy, and woke up in a cardiac care unit hearing how his heart had stopped. A nurse watching the game started CPR, and there was return of spontaneous circulation after three shocks by EMS. He was transported to the local hospital, where hypothermia was initiated, and then transferred to a tertiary care facility. He told his mom that he had been having these spells of pain and dizziness for several months. While his initial EKG was suspicious for LVH, his echocardiogram was negative for an enlarged myocardium, effectively ruling it out. Further examination determined that a coronary artery anomaly was present and was caused by his right coronary artery tunneling under the pulmonary artery. Upon exertion, his pulmonary artery dilated to accommodate the increased demand for oxygen, compressing his coronary artery and restricting blood flow to the inferior wall of his heart at a time when demand was greatest. This caused a myocardial infarction, which led to cardiac arrest. After stabilization, he was taken to the operating room, where the coronary artery was re-routed to prevent future complications.


A 13-year-old female playing softball for her school team was rounding first base on her way to second when she collapsed. Those rushing to her side found her without pulses or respiration. When EMS arrived, CPR was in progress and she was in ventricular fibrillation. After being successfully resuscitated by EMS, she was transported to the local pediatric medical facility. Her only significant history was an upper respiratory infection approximately two weeks earlier. She was eventually diagnosed with myocarditis.

Myocarditis is an infectious disease that causes inflammation of the myocardium, which affects the heart's ability to pump and makes it irritable. Myocarditis is generally caused by the coxsackievirus, although it can also be from drug use. Frequently, patients are initially misdiagnosed. Symptoms such as fatigue, chest pain, fever, EKG changes and exertional shortness of breath mimic other conditions and make diagnosis challenging. Treatment includes rest, pain medication, antibiotics and steroids as needed. These patients will receive an echocardiogram to look at the structures of the heart. Seventy-five percent of patients will respond to treatment within two weeks, although approximately 10% will continue to have long-term difficulties; some will require transplant.16 [http://]


Long QT syndrome is a disorder that affects the sodium-potassium and calcium pump and places people at risk for sudden death. Although generally inherited, there are currently more than 70 medications that have been known to cause prolongation of the QT interval (QTI). QTI greater than 450 ms in females and 440 ms in males is diagnostic for long QT syndrome, which is estimated to be present in one in every 5,000 people. When long QT syndrome is suspected, the entire immediate family is screened. The most common arrhythmia causing death is torsade de pointes.17 [http://]

The Brugada brothers are three electrophysiologists who first described a genetically inherited problem with the sodium pump. When the sodium pump closes early, it pushes potassium out, causing early repolarization. First described in 1986, Brugada syndrome is characterized by EKG changes that include a prolonged PR interval, a right bundle branch block EKG pattern and ST segment elevation in V1-V3. Initial symptoms generally include syncope. It is interesting to note that fever can unmask Brugada. Experts speculate that the increase in heart rate caused by fever causes the sodium channel to work faster. An estimated 50% of sudden cardiac death patients with structurally normal hearts suffer from Brugada syndrome.18 [http://] It is unknown why Asian men are at highest risk.


There have been 61 reported deaths over a seven-year period from exercise-induced bronchospasm (EIB). Eighty-one percent of these deaths occurred in kids younger than 21 years of age and 57% in athletes at college level. While most had a history of asthma, 10% had no known medical history. This prompted Ohio State University researchers to look within their own athletic department. They initially tested 100 student athletes and found 39% with EIB; 88% had no known history of wheezing.19 [http://]

In April 2007, the FDA approved Singulair for use in prevention of EIB after three studies looked at 160 patients age 15 or older with EIB and found a statistically significant protective benefit when used two hours prior to exercise.20 [http://] While most physicians recommend this practice, others contend that premedication was found to be effective only 50% of the time and more important is an adequate warm up period. Thirty minutes into exercise, epinephrine and norepinephrine release is highest. During this refractory period, epinephrine kicks in and functions as a bronchodilator.21 [http://] It should be noted that premedication does not substitute the need for a rescue device, such as an albuterol inhaler.

Another situation that can cause wheezing in the athlete is vocal cord dysfunction. Most common in females in their early 20s, the vocal cords actually have been found to narrow during exertion, which decreases airflow to the lungs at a time when increased flow is in demand. This causes anxiety, shortness of breath and wheezing. Upon rest, the symptoms generally resolve. By the time EMS arrives, the patient may appear asymptomatic and is oftentimes not transported due to normal assessment findings.


Other less common causes involve Marfan's syndrome, which is an autosomal disorder that predisposes people for aortic dissection. In Marfan's, athletes are generally tall and slim with an arm span wider than their height. Weightlifters have been found to be prone to aneurysm due to the excessive pressure that is applied to the vessels during lifting. Systolic blood pressure may get as high as 400mmHg. It appears that a valsalva occurs, which increases blood pressure during lifts that exceed 80% of maximum voluntary contraction.22 [http://]

Certain drugs like ephedrine, a weight loss supplement, have been banned from many professional sports. When Baltimore Orioles pitcher Steve Bechler died during spring training, his death was attributed to ephedrine use. Cocaine took the life of basketball star Len Bias of Maryland in 1986.23 [http://]

Heat illness has been linked to multiple deaths. Minnesota Viking all pro lineman Corey Stringer became sick in excessive heat during training camp. At 300 pounds, his body had difficulty shedding heat, and his core temperature rose to 108.8°. He died August 1, 2001, at age 27 from multiple organ failure related to heat stroke. Ironically, four high school athletes died the same week from heat-related illness. Despite media attention to heat illness and changes in dealing with athletes and heat, five athletes ages 11 to 17 died in 2006, and a high school coach in Kentucky was recently indicted in the death of a student athlete who died from heat illness. Prevention involves proper hydration, adequate rest periods and limiting exposure to the heat. Temperatures of 90° with 70% humidity have been identified as increasing heat risks. Immediate cooling and hydration is the priority treatment.24 [http://]


In the United States, athletes must go through a medical screening process prior to playing competitive sports. The American Heart Association encourages routine pre-screening physicals based on assessment questions filled out by parents and a physical examination, but stop short of recommending electrocardiograms. The questionnaire asks about previous medical conditions, medical history of family members, other risk factors and symptoms. These documents are generally poor at catching disease and have only a 2.5% chance of finding a problem.25 [http://] In order for them to screen appropriately, both athletes and parents have to be honest when filling them out and appreciate how minor complaints can be linked to serious issues. Any suspicion during the pre-participation physical leads to further evaluation and testing.

Routine use of a 12-lead EKG as part of the physical exam has been debated. Knowing that 90% of hypertrophic cardiomyopathy can be picked up on EKG and conditions like long QT or Brugada syndrome are typically found on EKG, it seems reasonable to consider. Italian researchers found that a simple 12-lead EKG can help prevent episodes of cardiac arrest. They believed the research was conclusive enough that law changes in parts of Italy now require a 12-lead EKG for all athletes prior to competitive sports.26 [http://] The United States has not embraced this concept. A study in the New England Journal of Medicine reviewed 12,550 electrocardiograms and found t wave abnormalities in 81 athletes. Further assessment revealed 6% with HCM.27 [http://] The medical community believes that with 10 million kids playing sports, the concept would add $2 billion annually to the cost of healthcare and that there are not enough physicians to review all the test results. There is also the concern that a high false-positive EKG could add additional costs for unnecessary additional screening tests, as well as liability in the event of misinterpretation.28 [http://]

Understanding that sudden death can occur in even the healthiest appearing athletes, it is important to educate schools, coaches, parents, sports clubs and athletes themselves about appropriate screening, having an AED at sporting events, good bystander CPR and early access to advanced care. Athletes experiencing symptoms like fatigue, shortness of breath and syncope during activity need further assessment to determine their risk for serious problems. Athletes should be encouraged to report problems without fear of penalty from coaches and parents. EMS providers need to appreciate that syncope in athletes is a true concern that can be an ominous sign prior to sudden cardiac death.


1. 36th Bethesda Conference. Eligibility recommendations for competitive athletes with cardiovascular abnormalities. J Am Coll Cardiol Vol. 45, 2005

2. Maron BJ, Roberts WC. Sudden Death in Young Athletes. Circulation 62:218–229, 1980.

3. 36th Bethesda Conference. Eligibility recommendations for competitive athletes with cardiovascular abnormalities. J Amer Coll Cardiol Vol. 45, 2005

4. Lane JR, Ben-Shacher G. Myocardial infarction in healthy adolescents. Pediatrics 120(4):938–943, Oct 2007.

5. 49ers Offensive Lineman Herrion Dies at 23. ESPN. August 22, 2005.

6. Pelliccia A, Maron BJ, et al. Clinical significance of abnormal electrocardiographic patterns in trained athletes. Circulation 102:278, 2000.

7. 36th Bethesda Conference. Eligibility recommendations for competitive athletes with cardiovascular abnormalities. J Amer Coll Cardiol, Vol. 45, 2005.

8. ibid.

9. Lawless CE, Briner W. Palpitations in athletes. Sports Medicine 38(8):687–702, 2008.

10. Competitive athletes with cardiovascular disease: The case of Nicholas Knapp. N Eng J Med 339:1632–1635.

11. Link MS, Maron BJ. Sudden death caused by innocent chest wall blows. Ital Heart J 6(4):281–283, 2005.

12. ibid.

13. Weinstock J, Maron BJ, et al. Failure of commercially available chest wall protectors to prevent sudden cardiac death induced by chest wall blows in an experimental model of commotio cordis. Pediatrics 117(4): April 2006.

14. Yabek SM. Commotio Cordis. EMedicine, July 17, 2007.

15. Reisdorff EJ, Prodinger RJ. Sudden cardiac death in the athlete. Emerg Med Clin 16(2):281–294, May 1998.

16. 36th Bethesda Conference. Eligibility recommendations for competitive athletes with cardiovascular abnormalities. J Amer Coll Cardiol, Vol. 45, 2005.

17. ibid.

18. Brugada J, Brugada P. Right bundle branch block, persistent ST segment elevation and sudden death. J Amer Cardiol 20:1391–1396, 1992.

19. Parsons J, Mastronarde J, Keading C, et al. Prevalence of exercise-induced bronchospasm in varsity college athletes. Journal Medicine and Science in Sports and Exercise 39(9):1487–1492, Sep 2007.

20. New indication for Singulair approved by the FDA to prevent exercised induced bronchospasm. Medical News Today, April 27, 2007.

21. Parsons J, Mastronarde J, Keading C, et al. Prevalence of exercise-induced bronchospasm in varsity college athletes. Journal Medicine and Science in Sports and Exercise 39(9):1487–1492, Sep 2007.

22. MacDougall JD, McKelvie RS, et al. Factors affecting blood pressure during heavy weightlifting and static contraction. J App Physiol 73:1590–1597, 1992.

23. Harriston K, Jenkins S. Maryland basketball star is dead at 22. Washington Post, June 20, 1986.

24. Heat-related deaths in middle, high school football players spike in 2006. Science Daily, August 7, 2007.

25. Chaitman BR. Should an electrocardiogram be included in the routine participation screening of young athletes. Circulation 116:2610–2615, 2007.

26. Corrado D, et al. Screening reduces sudden cardiac death in Italian athletes. JAMA, October 4, 2006.

27. Pelliccia A, DiPaola FM, et al. Outcomes in athletes with marked EKG repolarization abnormalities. N Engl J Med 358:152–161, Jan 10, 2008

28. 36th Bethesda Conference. Eligibility recommendations for competitive athletes with cardiovascular abnormalities. J Amer Coll Cardiol, Vol. 45, 2005.

James Davis, RN, MA, EMT-P, has been in EMS for 25 years and is currently a fire captain/paramedic with the Columbus (OH) Division of Fire and a flight RN for Medflight of Ohio. He is an adjunct faculty member at Columbus State Community College and sits on the State EMS Board in Ohio. Contact him at jdavis@medflight.com.

Thursday, September 10, 2009

Medical News: Lacrosse Players Have Excess Burden of Cardiac Arrest from Chest Blows

A recently released news reports states that commotio cordis accounts for a disproportionate number of sudden deaths in high school and college lacrosse players, compared with athletes in most major sports, researchers found.
»Click here to read article

Monday, July 27, 2009

New Study Finds AED Programs in Schools Beneficial

A recently released AHA study finds that school-based AED programs provide a high survival rate for both student athletes and older non-students who suffer sudden cardiac arrest (SCA) on school grounds. High schools are strongly encouraged to implement onsite AED programs as part of a comprehensive emergency response plan to SCA.

Wednesday, April 8, 2009

Nurses Save Life of Boy With Rare Sporting Injury

By Lela Garlington

Wednesday, April 8, 2009 - It was as if lightning had struck the baseball player in the chest and shorted his heart's electrical circuit, medical staff say.

Instead, a catcher throwing a ball to third base last weekend hit Kyle McCammon in the chest. The impact, which hit Kyle between the second and fourth rib, stopped his heart from beating.

Luckily for 12-year-old Kyle, who plays competitive baseball as a Southaven Panther, his mother is a nurse, and she and two other nurses ran to his aid.

The freakish incident happened at 5:35 p.m. Saturday during the Rumble on the River tournament between the Southaven Panthers and the Arkansas Rattlers at First Tennessee Fields in Cordova.

When his mother, Mary McCammon, rushed on the field, she saw that her son was still breathing, but it was shallow and labored. His eyes had glazed over and he couldn't respond.

Her husband, assistant coach David McCammon initially thought the breath had been knocked out of him -- a typical baseball injury. But Mary McCammon, a home health nurse, realized it was much more serious.

Taking her middle and index fingers she placed them against her son's neck: "I couldn't feel a pulse. It was like I was in a tunnel. It was just me and Kyle."

Another nurse and mom, Cyndi Herrington of Olive Branch tried the other side. She couldn't feel a pulse either.

Color was draining from Kyle's face. His lips were turning blue.

"I think we all said in unison, 'He's not breathing. We need to do CPR,'" the child's mother recalled.

That's when another nurse from the opposing team, Deanna Gilbert of Marked Tree, Ark., stepped in and offered to help. "I got this Mom," Gilbert told Mary McCammon.

Twenty compressions to the chest. A single breath. Twenty more compressions to the chest. Another breath.

For seven minutes, the two nurses did what they had been trained to do. Because of them, Kyle survived.

As tears streamed down her face that day, Herrington said all she could think about was, "I can't let this child die."

By the time the ambulance arrived, Kyle had regained consciousness. He stayed overnight at Le Bonheur Children's Medical Center, and Mary McCammon said doctors gave her son a clean bill of health.

Kyle was diagnosed with "commotio cordis," which means commotion or concussion of the heart.

"It's very rare," explained Dr. Barry Gilmore, Le Bonheur's medical director for Emergency Services. When it happens, it is often with boys playing sports -- particularly baseball. "We don't even see one a year. The overall survival rate is 15 percent," he said. "The ones who have immediate CPR or a defibrillator -- within the first one to three minutes -- survive."

From 1996 to 2007, just 188 cases have been reported to the U.S. Commotio Cordis Registry.

That is why the Southaven Panther coaches are now getting CPR training.

Kyle remembers being hit and trying to get up but nothing after that.

His mother is hoping her son's brush with death will convince others to get cardiopulmonary resuscitation or CPR training. Even better, she said, "These defibrillators are under $1,000. They should be really anywhere people are.

"Never in a million years would you think a ball would stop his heart. But it did," Mary McCammon said. "Those nurses saved his life."

© 2009 Scripps Newspaper Group - Online

Monday, March 16, 2009

Mastic Beach Man Stable After Softball Field Collapse


March 16, 2009 - A Mastic Beach man who collapsed on a Patchogue softball field was in stable condition yesterday after being revived by teammates, two Suffolk police officers and a Patchogue public safety officer.

The officers, Paul Schreiber and Edward Ryby, and a Patchogue Village public safety officer, Jim Mylett, responded to a 911 call Saturday night from Shore Front Park in Patchogue, where they found Christian Barton, 30, unconscious, police said.

Barton, who was fielding a ground ball at second base, collapsed as he was about to throw the ball, according to police.

Schreiber, who was only three blocks away when he received the call, arrived first. Barton's teammates were already performing CPR.

"As soon as I got there, his teammates were waiting for me," Schreiber said. "Nobody was panicking, which helped the situation tremendously."

They rolled Barton on his back and used a defibrillator from Schreiber's car to monitor his condition. Mylett and Ryby arrived shortly after and took over the CPR.

When Barton stopped breathing, the defibrillator signaled that shock was needed. After a second shock, Ryby noticed a pulse on Barton's neck.

A Patchogue ambulance arrived and took Barton to Brookhaven Memorial Hospital Medical Center, where he was treated in the emergency room. He was transferred to Stony Brook University Medical Center and was sedated overnight, said Barton's cousin, Brian Jenkins, 26, of Amityville.

Jenkins said that already yesterday evening, Barton, of Spar Drive was breathing on his own and laughing with his two young sons.

"I'm just so happy we were all able to help," Schreiber said. "That's why they call them teammates. It was a complete group effort."

Staff writer Patrick Whittle contributed to this story.

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