Abstract
Calder and Till 1 provide an interesting theory about the cause of Shackleton’s apparent heart problems. However, the facts do not support the hypothesis of an atrial septal defect.
Shackleton was the son of a doctor. 1 At the age of 16, Shackleton went to sea as a naval apprentice, sailing around Cape Horn on a square rigger in 1890. 2 It would seem highly unlikely his father would send his son on such a hazardous journey had he harboured any suspicion of a congenital heart defect.
Shackleton developed acute symptoms during two attempted marches to the South Pole in 1902 and 1908.1,2 If his symptoms were triggered primarily from the haemodynamic effects of an atrial septal defect, these might be expected to have been most prominent during the vigorous exertion of man-hauling a heavily laden sled at the hypoxic altitude of over 9000 feet on the Polar Plateau, not pulling a lightened sled near sea level.
Rather, on both expeditions, severe symptoms developed after more than three months of a diet deficient in vitamin C and thiamine. The connective tissue damage of scurvy can variously produce ventricular dilation, heart valve incompetence, tachycardia and other arrhythmias, pericarditis, dyspnoea and sudden death.3–5 Some of these problems persist long after treatment with anti-scorbutics, and may even be irreversible.4,5
Shackleton’s acute signs and symptoms of tachycardia, breathlessness and right-sided murmur are all consistent with the well-described cardiac consequences of scurvy and beriberi. The persistence of a cardiac murmur after Shackleton’s first voyage, as well as possible paroxysmal dysrhythmias, would be consistent with long-term structural damage.
While there are holes in the hypothesis of a congenital atrial septal defect, nutritional deficiencies may provide food for thought. The only definitive answer would come from a postmortem, but it is surely best to let sleeping sea dogs lie in peace.