Calcium and Potassium: Effects on Cardiac Function

Calcium Regulation

The normal level of calcium in the body is 9.4 mg/dl. Calcium is needed for muscle contraction and is regulated by hormonal secretion. Hypocalcemia is seen when levels are less than 8 mg/100 ml, and below 7 mg/100 ml, tetany occurs, causing muscle contraction and contracture, including major cardiac systole. Hypercalcemia is diagnosed when levels are over 12 mg/100 ml; this delays body functions, and the heart does not contract properly. Certain hormones are responsible for maintaining calcium levels; if there is no calcium in the diet, it is taken indiscriminately from the bones.

  • During growth, out of 200 mg, 100 mg remains; there is a positive balance.
  • In adulthood, the balance is 0.
  • In old age, the balance is negative; at menopause, calcium fixation decreases in women.

The calcium-regulating hormones are PTH, calcitonin, and active vitamin D3. They are active in the digestive tract, bone, and kidney. PTH has 84 amino acids (aa), but the active fragments are 34 aa. It has a direct action on bone and kidney. In bone, it increases the resorption of exchangeable or stable calcium in extreme situations. In the renal tubules, it increases calcium reabsorption. Osteoclastic resorption occurs because of RANK, which binds to its ligand.

Calcitonin is 32 aa, and its action is to fix calcium to bone, thus lowering calcium levels. It is produced in thyroid parafollicular cells. It also decreases bone pain. If there is high calcium, the thyroid increases calcitonin, but this effect is unimportant because the decrease performed by vitamin D and PTH is more significant.

Vitamin D3 exerts a powerful facilitating effect on calcium absorption in the gastrointestinal tract and bone. It must first be converted by successive reactions in the liver and kidney into the final active product, 1,25-dihydroxycholecalciferol. This active form of vitamin D has effects on the intestine, kidney, and bone, increasing the absorption of calcium and phosphate into the extracellular fluid. It acts as a hormone to promote intestinal calcium absorption, mostly by increasing (over 2 days) the formation of a calcium-binding protein in intestinal epithelial cells.

Hormonal control of calcium ion concentration: after 3 to 5 minutes of an acute increase in the concentration of ionic calcium, PTH secretion declines, and calcitonin rises. In cases of excessive or prolonged calcium deficiency, only the PTH mechanism has real efficacy in maintaining a normal concentration of calcium ions.

Effects of Potassium Ions on Cardiac Function

  • Potassium (K): Excess K causes the heart to become dilated and flaccid, and it also reduces heart rate. Large amounts can block the conduction of the cardiac impulse from the atria to the ventricles through the AV bundle. Beta-blockers can affect this.
  • Calcium (Ca): Excess Ca ions produce the opposite effect, causing the heart to progress to a spastic contraction. In contrast, a calcium ion deficit produces cardiac flaccidity. Digitalis affects this.

Intrinsic Regulation of the Pumping Mechanism: Frank-Starling

The amount of blood pumped by the heart each minute is determined almost entirely by the rate of blood flow to the heart from the veins (venous return). All of the body’s peripheral tissues control their own local blood flow, and all of these local flows combine and return through the veins to the right atrium. The heart’s intrinsic ability to adapt to increasing volumes of inflowing blood is called the Frank-Starling mechanism of the heart. The more the heart muscle is stretched during filling, the greater the force of contraction and the greater the amount of blood pumped into the aorta.

  • Preload: Ventricular end-diastolic volume (before systole) equals the length of the fibers at rest. Produces volume overload and eccentric hypertrophy.
  • Afterload: Pressure to be overcome at the start of ejection. Pressure overload produces concentric hypertrophy.

Lower preload is better than higher afterload.

Lymphatic System Functions

  • Drain excess fluid from the interstitial space.
  • Recover proteins from the interstitial space.
  • Remove remains of pathogenic microorganisms in the interstitial space.
  • Transport lipids absorbed into the systemic circulation.
  • Fluid reabsorption of virtual spaces (pleural, peritoneal).