Oooh I know this.
Decreased pH = increased H+ in the ECF. To alleviate the low pH in the blood, the kidneys (DCT) exchange out H+ for K+ (H+/K+ antiport of the alpha intercalated cells) - this helps increase blood pH BUT makes you hyperkalaemic, because you're reabsorbing the K+.
So now: the ECF is rich in K+ (hyperkalaemia).
Now when there's hyperkalaemia you will find that K+ will be taken in by the myocardium in exchange for Na+ (Na+/K+ ATPase). This causes increased Na+ (hypernatraemia) in the ECF. And now the Na+/Ca2+ exchanger activates. This causes the heart to spit out calcium into the ECF and take in the sodium again.
So the net result is decreased Ca2+ inside the cell. It's all out in the ECF. Unfortunately to carry out the power stroke cycle troponin C needs Ca2+, so now that can't happen because the sarcoplasm is deficient in Ca2+. Thence the decreased contractility; and because SV is dependent on how much the muscle cells contract, that drops as well.
(I've also heard something about increased H+ inactivating Ca2+ in the power stroke cycle? Not sure tho.)
Hypoxia and hypercapnia are features seen in respiratory acidosis. Respiratory insufficiency (decreased gas exchange) leads to drop in O2 and buildup of CO2; CO2 forms H2CO3 via c.a. which dissociates to form H+ and HCO3-, leading to buildup of H+/decreased pH, leading to the above events.
EDIT: I had misconceived. Fixed now.
