This is because of lengthening of the ST segment. Lengthening of the ST segment in turn represents prolongation of Phase 2 of the action potential in the working myocardium. This happens as the calcium gradient driving calcium influx into cardiac myocytes in the plateau phase is reduced in hypocalcemia. This also explains why QT interval is shortened in hypercalcemia.
Reference: Basil M. RuDusky. ECG Abnormalities Associated With Hypocalcemia.
http://chestjournal.chestpubs.org/content/119/2/668.2.full [accessed 13 Jan 2011]
The intent of the question is merely to provoke reflection. Sympathetic preganglionic neurons emerge from the thoracolumbar (T1-L2) segments of the spinal cord; [http://commons.wikimedia.org/wiki/File:Gray839.png] most sympathetic preganglionic neurons terminate in sympathetic ganglia in the sympathetic trunk located adjacent to the vertebral column. This is an organizational structure more conducive to mass discharge of the sympathetic nervous system; in contrast, the parasympathetic preganglionic neurons are much longer than sympathetic preganglionic neurons and terminate in postganglionic cholinergic neurons located close to or in the wall of the viscus innervated. Locating the efferent parasympathetic ganglia more peripherally appears conducive to eliciting discrete responses in target organs. This is just a thought. It is important to note, however, that sympathetic nerve traffic to different viscera and vascular districts could also be differentially regulated (see Morrison, 1991 http://ajpregu.physiology.org/content/281/3/R683