I hypothesise that two  mechanisms can explain the cardiovascular changes associated with BH. Breath holding increases the arterial CO2 concentration, CO2 being a mediator of metabolic vasodilation, may induce a fall in BP by decreasing peripheral resistance. On the other hand, central chemoreceptors, located principally in the ventrolateral medulla respond to changes in H+ concentration, thus they are sensitive to changes in PCO2 . Rise in PCO2 associated with BH can directly stimulate the chemoreceptors in the vasomotor center in the medulla, thus enhancing the vasoconstrictor response of the peripheral vessels and consequently rise in BP.

 Fall in BP definitely would occur due to increased PCO2 during BH as CO2 is a potent vasodilator.Taking into consideration the crosssectional  area of all arterioles which is  enormous the peripheral effect would be masking the medullary effect.

Good question though.

I thing the typical intrathorax pressure -4mmHg dissapears if there is no gases exchange (typical respiratory quotient 0.8 says that there is lack of molecules during gases exchange in lungs, because for each 10 absorbed oxygen molecules are released 8 molecules of carbon dioxide). The change of intrathorax pressure in first seconds of breath holding (even because of these 4 mmHg) causes the Valsalva maneuver, which can be described as the spilover of blood from pulmonary to systemic circulation. Here I see the very short-time rise of blood pressure in the begining of BH, but I expect the lower blood pressure after this very short period. Of course many of regulation can be connected with this process reacting to pressure, gases and pH changes (aortic or carotid sinus receptors to autonomic nerves conneted with heart rate, contractility, vasoconstriction/vasodilation, venoconstriction, inspiration reflexes) and of course after a while the local receptors of CO2 (in brain vasodilation, in lungs weak vasoconstriction), and the local receptors of O2 (in lungs vasoconstriction, in other tissues vasodilation) can also react to the current state of the blood. 

If by breath holding, you mean slower or less deep breathing that increases pCO2 by about 4 mmHg, it increases blood pressure by a small amount.  This phenomenon was published in an article by Bagrov AY, et al. in an article in Hypertension in 1995.  The exact mechanism remains to be clarified.

Thanks David for your reply.  I had worked on similar project  and observed increase in BP and no change in HR, with increase in PCO2.  The possible mechanism was postulated to be increased sympathetic activity as observed by HRV studies.

One pathway could be a structure in the brain-stem (locus coeruleus) which is a CNS repository of norepinephrine and is sensitive to changes in CO2. Hypercapnic breathing would increase central sympathetic outflow. At any rate, it is a mistake to depend on dated Physiology textbooks based on experiments with anesthetized animals to infer the physiology of conscious, behaving individuals. An example is extrapolation of CO2 effects on blood pressure from experiments with vascular tissue in organ baths.