Abstract
Participation in competitive sports is not completely free from risk. The death rate for marathon runners in London is approximately 1 in 80,000 finishers 1 and among high school athletes playing competitive sport in the USA, it is approximately 1 in 200,000. 2 Although rare, because they are so unexpected, these deaths hugely affect not only the family but the wider community as well. Kim et al. 3 reported a survival rate of just 29% following cardiac arrest in long distance runners and this dropped to only 7% in those younger than 40 years of age. One likely reason for this is the higher incidence of undiagnosed hypertrophic cardiomyopathy (HCMP) in younger athletes. 3 However, cardiac arrest during competitive sports is also complicated by several physiological factors, which we believe should be addressed during resuscitation.
Compared to the oxygen consumption of about 250 ml min−1 at rest, the oxygen consumption in a male marathon runner can reach 5100 ml min−1. 4
During heavy exercise, within a few minutes athletes develop oxygen debt, which has to be ‘repaid’ once the exercise is over. Hence, during the recovery period for about 30–40 min, the oxygen uptake remains considerably higher than normal. 4 The temperature of athletes also rises and may reach up to 40°C or even higher. 4 A cardiac arrest in such a case would worsen the metabolic acidosis much faster than in a resting person. Therefore, establishing adequate ventilation and oxygenation promptly could be a critical factor in athletes. Presently, Advanced Life Support (ALS) guidelines do not have any specific recommendations for doing cardiopulmonary resuscitation (CPR) in athletes. In a study on out of hospital cardiac arrests, Wang et al. 5 reported that endotracheal intubation (ETT) was associated with improved outcomes compared to supraglottic airways. It is conceivable that early use of ETT may be even more important in athletes.
During extreme exercise, athletes can lose up to 3–5 kg of their weight in an hour largely because of sweating. 4 Their skeletal muscle blood vessels are also maximally dilated. 4 This degree of dehydration and vasodilatation may create a relative deficit of circulatory volume and contribute to failure to resuscitate during CPR. In a situation such as this, a rapid intravenous infusion of 1–2 l of fluids such as Hartmann’s solution can improve circulatory volume, help in cooling and may improve the chances of a successful resuscitation.
Third, since HCMP could be a cause of cardiac arrest in young athletes, 3 use of magnesium may prove to be beneficial in these cases. In HCMP, sarcoplasmic mutations alter calcium balance by increasing the affinity of troponin C for calcium in sarcoplasm, resulting in increased calcium levels during diastole. Sarcomeric mutations also increase the energy requirements of myosin ATPase and reduce the activity of other ATP consuming processes such as ion pumps. 6 During cardiac arrest, presence of sustained hypoxia causes a failure to extrude calcium from cytosol which is a highly energy-dependent process. 7 It is easy to see how this process is likely to be amplified in presence of HCMP.
Magnesium is a physiological antagonist of calcium and drives calcium into the sarcoplasmic reticulum, reduces mitochondrial overload and competes with calcium for binding to troponin C. It also increases the threshold stimulus required to provoke ventricular arrhythmias. 8
Although magnesium has not been shown to improve outcome in the general population having cardiac arrest, perhaps in athletes, where the underlying cause may be undetected HCMP, early intravenous administration of 4–5 g magnesium could be beneficial and worth an investigation.
There is a need for further research to improve outcome in this group.
Present ALS guidelines do not have specific recommendations for athletes suffering cardiac arrest on the field. We believe that cardiac arrest in athletes should be given specific consideration in the ALS guidelines.
In summary, cardiac arrest during competitive sports in young athletes may have several contributing physiological (and likely underlying genetic) factors. If defibrillation and standard ALS are not immediately successful in restoring cardiac output, then early ETT and ventilation, intravenous fluid resuscitation and magnesium administration may improve the likelihood of a successful outcome.