Gas exchange is under precise control in terms of the rate and depth of inspiration and expiration mediated by the hypothalamus and the respiratory centre in the medulla oblongata. The chemoreceptors in the carotid body (near the bifurcation of the carotid artery) can detect the level of CO2 and therefore the pH of the blood passing over it. Insufficient oxygen delivery to the metabolizing tissues e.g. the muscles during exertion, leads to hypercapnia (high level of CO2 in the blood), and when this is detected by the carotid body, the latter sends messages to the hypothalamus, which responds by neural output to the diaphragm via the phrenic nerve and to the intercostal muscles to "put themselves into overdrive mode".
Also, look up the effect of stimulation of beta-2 receptors in the bronchioles.
The opposite occurs if blood CO2 levels drop.
This is controlled by the balance between sympathetic (mediated by adrenaline and noradrenaline) and parasympathetic (mediated by ACh [acetylcholine]) activity and hence their actions on the SA node (sino-atrial node near the entry point of the venae cavae in the right atrium of the heart), which is in normality the pacemaker of the heart i.e. it has the fastest intrinsic rate of depolarization ["firing"] so determines the heart rate).
Increased sympathetic activity e.g. due to release of adrenaline from the adrenal gland during the "fight, [fright], or flight reaction" [which would occur if a lion jumps in through your window - extremely unlikely here in UK, but I have heard of it happening in Kenya where I was brought up! [don't let that put you off from going on a safari holiday! - increases the slope of the spontaneous depolarization of the neuromyocytes of the SA node [which gives the heart its intrinsity = ability to beat spontaneously] so that the resting potential reaches the threshold earlier, and therefore an increase in heart rate occurs.
ACh has the opposite effect via the vagus nerve.
If there is a drop in blood pressure due to any reason e. g. when standing up from a sitting position [due to gravity pulling blood towards the feet which reduces venous return to the heart thus reducing the force of contraction of the heart by the Frank-Starling Law), baroreceptors in the carotid sinus detect this fall in bp, and send impulses to the cardiac centre in the brain, which responds by increasing sympathetic input to the heart. The action of the noradrenaline thus released acting on beta-1 adrenoceptors in the heart increases the heart rate in an attempt to rectify the fall in blood pressure. The opposite effect is produced by any increase in bp.
Several other mechanisms modulate the heart rate and force of contraction of the heart i.e. (positive and negative) chronotropic and inotropic effects, respectively, and the calibre of the resistance vessels (medium-sized arterioles) e.g. the alpha-1 agonist effect of adrenaline causes vasoconstriction by stimulating contraction of the smooth muscle layer [in the tunica media] of the arterial wall - this narrowing of arterioles leads to an increase in blood pressure to compensate for the initial drop.
Google ALL the words in bold, and read up all about the topic - if stuck on any point please feel free to PM me.