We report the neurologically intact survival of a 28-year-old male marathon cardiac arrest victim.
In 2000, a 28-year-old man collapsed immediately upon finishing, with an initial presenting rhythm of ventricular fibrillation (VF). He was defibrillated 3 min later with a return of spontaneous circulation (ROSC) and was intubated endotracheally. His rhythm deteriorated, and seven precordial blows and seven additional defibrillations were performed on scene. He received five more precordial blows en route to the hospital. The prehospital medications used during the resuscitation included 25 g of dextrose 50% in water, a single 5-mg dose of epinephrine, 1 mg of atropine, and 100 mg of lidocaine.
The patient was pulseless and apneic on arrival to the emergency department and was given 1 mg of epinephrine, 2 mg of magnesium sulfate, 50 mEq of sodium bicarbonate, an initial dose of 300-mg amiodarone followed by a second dose of 150 mg and an intravenous (IV) drip set at 1 mg·min−1, and a lidocaine IV drip at 2 mg·min−1. A repeat high dose of epinephrine (5 mg) was administered, two additional doses of atropine (1 mg each) were given, and the patient was defibrillated an additional seven times. A sustained ROSC occurred approximately 47 min after onset of cardiac arrest.
His initial laboratory values are seen in the Table. He received 5 L of normal saline IV during the resuscitation, as the treating physicians suspected a right ventricular infarction based on the initial electrocardiogram. The initial coronary angiogram showed an anomalous, nondominant right coronary artery (RCA) arising from the left coronary cusp. The repeat angiogram was interpreted as normal, with no mention of an anomalous RCA.
Four hours postarrest, he experienced another episode of VF that responded to defibrillation. He continued to require significant fluid administration to support his blood pressure (a total of 16 L of normal saline in the first 8 h postadmission). Approximately 14 h after the patient’s initial cardiac arrest, he was diagnosed with bilateral lower extremity compartment syndrome and underwent emergent lower extremity fasciotomies. Pressor support with norepinephrine was added at 16 h postarrest.
His creatine kinase (CK) on day 1 was 78,275, and it peaked on day 2 at 285,933. His troponin I peaked on day 1 at 135.8. A sodium bicarbonate drip of 1 mg·min−1 was started to alkalinize his urine. Hemodialysis was initiated on day 1 for acute renal failure and continued until discharge. He sustained significant muscle damage from the elevated compartment pressures and required five additional lower extremity debridement procedures. On day 8, he had a slight memory deficit but no significant focal neurological deficits. Due to extensive muscle necrosis, the patient underwent a through-the-knee amputation of his right lower leg on day 14.
He was transferred to the rehabilitation unit on day 30. A muscle biopsy demonstrated a mitochondria enzyme variant defect that has been suspected of playing a role in his initial event and recovery (7). At the end of 1 year, he had returned to full-time employment with no apparent cognitive deficits.
The 2000 American Heart Association’s Advanced Cardiac Life Support (ACLS) cardiac arrest guidelines primarily focused on treating the diseased or atherosclerotic heart. There was some flexibility for varying the treatment under special circumstances for target populations who may benefit from nonstandard treatment (2). The risk of sudden cardiac death in an older marathon runner (>35 years old) usually is related to unrecognized atherosclerotic cardiovascular disease (6,9). Sudden arrest and death of a young athlete is usually a result of VF due to a congenitally anomalous coronary vessel, hypertrophic cardiomyopathy, or long QT syndrome (8). Due to etiology, sudden cardiac arrest in a young long-distance runner may require a different set of ACLS needs than a cardiac arrest in an older patient.
It is well known that glycogen stores are decreased following long-distance running (4). It was assumed this marathon runner was substrate depleted, and treatment was altered to include 50% dextrose in water early in the resuscitation. Since these patients tend to be substrate depleted, the authors also believe that the addition of empiric glucose to the ACLS algorithm might be a consideration. Even though it has been shown that marathon finishers tend to have high normal blood glucose, insulin, cortisol, and epinephrine (3), these studies have included only healthy marathon runners and not cardiac arrest victims.
Previous literature has reported that >50% of cardiac arrests in marathon runners occurred either at or near the finish line (9). While this may be an anomaly, it may indicate a catecholamine- or steroid-mediated event or some other yet unknown biochemical explanation. Healthy runners’ blood glucose levels may be supported by catecholamine and steroid secretion. In the cardiac arrest victim, one or both of these supports becomes interrupted, leading to low blood glucose in patients who already are substrate depleted due to low glycogen stores.
The acidosis seen in this case likely is related to the lactic acidosis of long-distance running in addition to the prolonged resuscitation. Earlier use of bicarbonate in larger doses should be considered in these situations.
Elevated troponin I and T levels have been documented in marathon runners without cardiac arrest or myocardial infarction, which presents an additional clinical challenge in interpretation of these patients’ laboratory values (10). Elevated CK total and myocardial band values also have been documented in marathon runners, presenting the same interpretation challenge for physicians (5). In the troponin studies, examination of the heart via echocardiogram showed a reduction in the peak early or late end-diastolic filling ratio but no long-term damage to the myocardium (10).
A postmarathon cardiac arrest survivor presents a unique set of problems in the intensive care unit setting. Capillary fluid leak following muscle damage from exertion has been demonstrated in rats (1). This patient had similar leaking of fluid in the primary muscle groups used during running. This case demonstrates the need for on-going pressure testing of leg muscle compartments in marathon runners who have prolonged, high-volume fluid resuscitation.
The physiological alterations in long-distance runners may introduce different variables for physicians to consider when treating cardiac arrest in this population.
The authors declare no conflicts of interest and do not have any financial disclosures.
1. Amelink GJ, Bar PR. Exercise-induced muscle protein leakage in the rat: effects of hormonal manipulation. J. Neurol. Sci. 1986; 76: 61–8.
2. American Heart Association. Part 1: Introduction to the International Guidelines 2000 for CPR and ECC: a consensus on science. Circulation. 2000; 102: I1–11.
3. Anderson RA, Polansky MM, Bryden NA, et al. Effect of exercise (running) on serum glucose, insulin, glucagon, and chromium excretion. Diabetes. 1982; 31: 212–6.
4. Koivisto VA, Harkonen M, Karonen SL, et al. Glycogen depletion during prolonged exercise: influence of glucose, fructose, or placebo. J. Appl. Physiol. 1985; 58: 731–7.
5. Kratz A, Lewandrowski KB, Siegel AJ, et al. Effect of marathon running on hematologic and biochemical laboratory parameters, including cardiac markers. Am. J. Clin. Pathol. 2002; 118: 856–63.
6. Maron BJ, Poliac LC, Roberts WO. Risk for sudden cardiac death associated with marathon running. J. Am. Coll. Cardiol. 1996; 28: 428–31.
7. Ratliff NB, Harris KM, Smith SA, et al. Cardiac arrest in a young marathon runner. Lancet. 2002; 360: 542.
8. Reisdorff EJ, Prodinger RJ. Sudden cardiac death in the athlete. Emerg. Med. Clin. North Am. 1998; 16: 281–94.
9. Roberts WO, Maron BJ. Evidence for decreasing occurrence of sudden cardiac death associated with the marathon. J. Am. Coll. Cardiol. 2005; 46: 1373–4.
10. Scharhag J, Herrmann M, Urhausen A, et al. Independent elevations of N-terminal pro-brain natriuretic peptide and cardiac troponins in endurance athletes after prolonged strenuous exercise. Am. Heart J. 2005; 150: 1128–34.