Thyroid hormone T3 boosts heart performance by increasing the heart’s responsiveness to catecholamines through the adrenergic signaling and cAMP pathway. It does this mainly by upregulating beta-1 adrenergic receptors and components of the cAMP-PKA cascade inside cardiac cells. When catecholamines bind these receptors, Gs activates adenylate cyclase, raising cAMP, which then activates PKA. PKA phosphorylates targets that enhance calcium handling (like L-type calcium channels and phospholamban/SERCA), leading to stronger contractions and faster heart rate. Because these effects depend on receptor signaling and the cAMP pathway, they are not independent of adrenergic receptors and cAMP.

Alkalosis raises blood pH, which increases albumin’s affinity for calcium. Since most calcium is bound to albumin, tighter binding leaves less calcium in the free, ionized form. Ionized calcium is the physiologically active fraction, so alkalosis leads to a decrease in ionized calcium even if total calcium stays the same. (For contrast, acidosis tends to increase ionized calcium by reducing binding.)

The main idea here is to restore mom’s blood pressure in a way that also preserves or increases cardiac output so uteroplacental blood flow stays good. Ephedrine acts on both alpha and beta receptors, so it raises blood pressure (via some vasoconstriction) and, importantly, boosts heart rate and myocardial contractility (beta effects). That combination increases overall cardiac output, which helps maintain placental perfusion and fetal oxygen delivery during neuraxial anesthesia when venous pooling has reduced venous return. Pure vasopressors that mainly constrict blood vessels can raise pressure but may lower cardiac output and placental blood flow, which is less favorable for the fetus. Ephedrine historically offered advantages in this setting by supporting maternal perfusion and fetal status, making it the preferred choice in this scenario.

Ionized calcium is the active form of calcium in the blood, and its free concentration can be reduced either by chelation or by shifting calcium to the protein-bound pool depending on pH. Citrate used as an anticoagulant in stored blood products binds calcium to form calcium–citrate complexes, pulling calcium out of the ionized pool. This directly lowers the amount of free calcium available in circulation, which is why transfusion with citrate-containing products can cause hypocalcemia in the recipient. In contrast, acidosis tends to increase ionized calcium because hydrogen ions compete with calcium for albumin binding, displacing calcium into the free form, while alkalosis promotes more calcium binding to albumin and decreases the ionized fraction. Albumin binding itself means calcium is not ionized, so greater albumin-bound calcium reduces the ionized portion, but the clearest, most immediate decrease from a clinical standpoint during transfusion is citrate chelation.