Saladin/Anatomy and Physiology

Lecture Outline

Lecture Outline - Chapter 24

Chapter Twenty-Four - Water, Electrolyte, and Acid-Base Balance

I. Water Balance (p. 865)

A. Fluid Compartments (p. 865; Fig. 24.1; Transp. 432)

1. An average-sized young male has about 40 L of total body water (TBW). This is distributed among fluid compartments.

a. Intracellular fluid (ICF) makes up 65% of TBW.

b. Extracellular fluid (ECF) makes up 35% of TBW and can be divided among the following: 25% tissue fluid, 8% blood plasma and lymph, and 2% transcellular fluid (a catch-all category).

2. Fluid is continually exchanged between compartments. Water moves by osmosis to the bloodstream and by capillary filtration from the blood to tissue fluid. From there, it may be reabsorbed by capillaries, osmotically taken into cells, or taken up by the lymphatic system and returned to the blood.

3. Osmotic gradients are rather transient by nature.

4. Osmosis from one fluid compartment to another is determined by the relative concentration of solutes in each compartment.

5. Electrolytes are the more abundant solute molecules and thereby play a principal role in governing the body's water distribution and content.

B. Water Gain and Loss (p. 866; Fig. 24.2)

1. A person is in a state of fluid balance when daily gains and losses are equal. Water gained is from two sources.

a. Metabolic water is produced as a byproduct of aerobic respiration.

b. Preformed water is ingested in food and drink.

2. Routes of water loss include water in urine, feces, expired breath, sweat at rest, and cutaneous transpiration. Water losses vary greatly with physical activity and environmental conditions.

3. Output through the breath and cutaneous transpiration is called insensible water loss because we are not usually conscious of it.

4. Obligatory water loss, that occurs even in those who are dehydrated, is the unavoidable loss of water through expired air, cutaneous transpiration, fecal moisture, and urine output.

C. Regulation of Intake (p. 867; Fig. 24.3; Transp. 433)

1. Fluid intake is governed mainly by thirst.

a. Dehydration reduces blood volume and pressure and raises its osmolarity. This results in a smaller volume and greater viscosity of saliva.

b. Also during dehydration, salivation is inhibited by sympathetic output from the thirst center. Reduced salivation is not the primary motivation to drink.

c. Long-term satiation of thirst depends on absorbing water from the small intestine and lowering the osmolarity of the blood. This makes the saliva more abundant and watery by promoting capillary filtration and stopping the osmoreceptor response.

D. Regulation of Output (p. 868; Fig. 24.4; Transp. 434)

1. The only way to control water output significantly is through variations in urine volume.

a. The kidneys cannot restore fluid volume or osmolarity, but in dehydration they can support existing fluid levels and slow down the rate of loss until water and electrolytes are ingested.

2. Changes in urine volume are usually linked to adjustments in sodium reabsorption. As sodium is reabsorbed or excreted, proportionate amounts of water accompany it.

3. Antidiuretic hormone (ADH) provides a means of controlling water output independently of sodium.

a. In true dehydration, blood volume declines and sodium concentration rises. The increased osmolarity of the blood stimulates the hypothalamic receptors, which stimulate the posterior pituitary to release ADH.

b. ADH targets the collecting tubules of the nephrons, and the kidneys reabsorb more water and produce less urine.

c. Sodium continues to be excreted, so the ratio of sodium to water in the urine increases.

4. If blood volume and pressure are too high or blood osmolarity too low, ADH release is inhibited. The renal tubules absorb less water, urine output increases, and total body water declines.

E. Disorders of Water Balance (p. 868)

1. Fluid Deficiency (p. 868; Fig. 24.5)

a. Fluid deficiency arises when output exceeds input over a prolonged period. There are two kinds of deficiency (volume depletion and dehydration) which differ with respect to the relative loss of water and electrolytes and the resulting osmolarity of the ECF.

b. Volume depletion occurs when proportionate amounts of water and sodium are lost without replacement. Total fluid volume declines but osmolarity remains normal. Volume depletion occurs during hemorrhage, severe burns, and chronic vomiting or diarrhea. The most serious effects of volume depletion are circulatory shock due to loss of blood volume, and neurological dysfunction due to dehydration of brain cells.

c. Dehydration (negative water balance) occurs when the body eliminates significantly more water than sodium and the ECF osmolarity rises. The simplest cause of dehydration is a lack of drinking water. Dehydration from diarrhea is a major cause of infant mortality, and can be a serious problem for elderly or bedridden people who depend on others to provide them with water.

d. Dehydration affects all fluid compartments. As the blood loses water its osmolarity rises and water from the tissue fluid enters the bloodstream to balance the loss. This raises the osmolarity of the tissue fluid, and water moves out of the cells to balance that.

2. Fluid Excess (p. 870; Fig. 24.6)

a. Fluid excess is less common than fluid deficiency because the kidneys are highly effective at compensating for excessive intake by excreting more urine.

b. Fluid excesses are of two types, called volume excess and hypotonic hydration. In volume excess, both sodium and water are retained and the ECF remains isotonic. This condition can result from aldosterone hypersecretion or renal failure.

c. In hypotonic hydration (water intoxication), more water than sodium is retained or ingested, and the ECF becomes hypotonic. This can occur if you lose a large amount of water and salt through urine and sweat and you replace it by drinking plain water.

d. Among the most serious effects of either type of fluid excess are pulmonary and cerebral edema.

3. Fluid Sequestration (p. 870)

a. Fluid sequestration is a condition in which excess fluid accumulates in a particular location. Total body water may be normal, but the volume of circulating blood may drop to the point of causing circulatory shock.

b. The most common form of sequestration is edema, the accumulation of tissue fluid in the interstitial spaces. Edema is typically marked by swelling of the face, fingers, abdomen, or ankles.

c. The three fundamental causes of edema are increased capillary filtration due to poor venous return, reduced capillary absorption due to albumin deficiency, and obstructed lymphatic drainage.

d. Whatever the cause, edema can result in a loss of blood volume and pressure, which creates the potential for circulatory shock. Pulmonary edema presents a threat of suffocation. Cerebral edema produces headaches, nausea, and sometimes seizures and coma.

II. Electrolyte Balance (p. 871; Table 24.1)

A. Electrolytes are physiologically important for two reasons: they are chemically reactive and participate in all metabolism, and they strongly affect the osmolarity of the body fluids and the body's water content and distribution.

1. Major cations of the body are sodium, potassium, calcium, and hydrogen.

2. Major anions of the body are chloride, bicarbonate, and phosphate.

3. The typical electrolyte concentrations and the terms for their imbalances are listed in Table 24.1, p. 871.

B. Sodium (p. 871; Fig. 24.7; Transp. 435)

1. Sodium is one of the principal ions responsible for the resting membrane potential of cells, and is the principal cation of the ECF, and is therefore the most significant solute in determining total body water and its concentration among fluid compartments.

2. Dietary deficiency of sodium is rare, and the primary concern is adequate renal excretion of the excess.

a. Aldosterone plays the primary role in adjustment of sodium excretion. The primary effects of aldosterone are that the urine contains less NaCl and more K⁺ and has a lower pH.

b. Hypertension inhibits the renin-angiotensin-aldosterone mechanism.

c. Antidiuretic hormone modifies water excretion independently of sodium excretion. A drop in sodium concentration inhibits ADH release.

d. Atrial natriuretic factor (ANF) is secreted by the atrial myocardium in response to hypertension. It inhibits sodium and water reabsorption and the excretion of renin and ADH. The kidneys thus eliminate more sodium and water and lower blood pressure.

e. Several other hormones affect sodium homeostasis. These include estrogen, progesterone, and glucocorticoids.

3. Imbalances in sodium homeostasis include hypernatremia, characterized by a plasma sodium concentration in excess of 145 mEq/L, and hyponatremia (less than 130 mEq/L).

a. Hypernatremia is usually the result of administration of intravenous saline. Its major consequences are water retention, hypertension, and edema.

b. Hyponatremia is usually the result of excess body water rather than due to sodium excretion.

C. Potassium (p. 873; Fig. 24.8; Transp. 436)

1. Potassium is the most abundant cation in the ICF and is the greatest contributor to intracellular osmosis and cell volume. Along with sodium, it produces the resting membrane potentials and action potentials of nerve and muscle cells. Potassium is also an essential cofactor for protein synthesis and some other metabolic processes.

2. Potassium homeostasis is closely linked to that of sodium. Normally about 90% of the potassium ions filtered by the glomerulus are reabsorbed by the PCT and the rest is excreted in the urine.

a. Variations in potassium excretion are controlled later in the nephron by changing the amount of potassium secreted into the tubular fluid by the DCT and cortical portion of the CD.

b. Aldosterone regulates potassium excretion and reabsorption along with sodium.

3. Sodium imbalances include hyperkalemia (> 5.5 mEq/L) and hypokalemia (< 3.5 mEq/L).

a. Hyperkalemia can result from aldosterone deficiency, renal failure, or acidosis, and sometimes follows blood transfusions. Potassium tends to leak from erythrocytes into the plasma of donated blood during storage. Hyperkalemia is a very dangerous condition that can quickly produce cardiac arrest.

b. Hypokalemia seldom results from dietary deficiency. It more often results from heavy sweating, chronic vomiting or diarrhea, excessive use of laxatives, aldosterone hypersecretion, or alkalosis. Hypokalemia is reflected in muscle weakness, loss of muscle tone, depressed reflexes, and irregular electrical activity of the heart.

D. Chloride (p. 873)

1. Chloride ions are the most abundant anions of the ECF and thus make a major contribution to its osmolarity. Chloride ions are required for the formation of stomach acid (HCl), and they are involved in the chloride shift mechanism that accompanies carbon dioxide loading and unloading.

2. Cl^- is strongly attracted to Na⁺, K⁺, and Ca²⁺, so Cl^- homeostasis is achieved primarily as an effect of Na⁺ homeostasis. As sodium is retained or excreted, Cl^- passively follows.

3. Imbalances of chloride include hyperchloremia (> 105 mEq/L) and hypochloremia (< 95 mEq/L).

a. Hyperchloremia is usually the result of dietary excess or administration of intravenous saline.

b. Hypochloremia is usually a side effect of hyponatremia.

E. Calcium (p. 874)

1. Calcium lends strength to the skeleton, activates the sliding filament mechanism of muscle contraction, serves as a second messenger for some hormones and neurotransmitters, activates exocytosis of neurotransmitters and other cellular secretions, and is essential factor in blood clotting. Cells maintain a very low intracellular concentration because they require a high concentration of phosphate ions.

2. Homeostasis of calcium is regulated chiefly by parathyroid hormone and, in children, by calcitonin.

3. Calcium imbalances include hypocalcemia (< 4.5 mEq/L) and hypercalcemia (> 5.8 mEq/L).

a. Hypocalcemia can result from vitamin D deficiency, diarrhea, pregnancy, lactation, acidosis, and certain thyroid conditions. It increases the sodium ion permeability of plasma membranes, causing the nervous and muscular systems to be overly excitable. If calcium levels drop too low, laryngospasm and suffocation may follow.

b. Hypercalcemia can result from alkalosis, hyperparathyroidism, or hypoparathyroidism. At concentrations above 12 mg/dL, hypercalcemia causes muscular weakness, depressed reflexes, and cardiac arrhythmia.

F. Phosphates (p. 875)

1. Phosphates are relatively concentrated in the ICF. They are needed for the synthesis of ATP, other nucleotide phosphates, nucleic acids, and phospholipids. Every process that depends on ATP depends on phosphate ions.

2. The average diet provides ample phosphate ions, which are readily absorbed by the small intestine.

a. Parathyroid hormone increases the excretion of phosphate as part of the mechanism for increasing the concentration of free calcium ions in the ECF.

3. There are no real imbalances with respect to phosphates because phosphate homeostasis is not as critical as that of other electrolytes.

III. Acid-Base Balance (p. 875)

A. Acids, Bases, and Buffers (p. 876)

1. Enzymes are very sensitive to changes in pH, and can be denatured by even slight changes. Consequently, acid-base balance is one of the most important aspects of homeostasis. The blood and tissue fluid normally have a pH of 7.35-7.45.

2. Only free hydrogen ions (H⁺) determine the pH of a solution.

a. An acid is any chemical that releases H⁺ in solution; a strong acid ionizes freely. A weak acid ionizes only slightly.

b. A base is any chemical that accepts H⁺. A strong base has a strong tendency to bind H⁺ and raise the pH, whereas a weak base binds only a small portion of the available H⁺ and has less effect on pH.

3. A buffer is any mechanism that resists changes in pH by converting a strong acid or base to a weak one. The body has both physiological and chemical buffers.

a. A physiological buffer is a system (respiratory or urinary) that stabilizes pH by controlling the body's output of acids, bases, or carbon dioxide.

b. A chemical buffer is a substance that binds H⁺ and removes it from solution as its concentration begins to rise, or releases H⁺ into solution as its concentration falls. Chemical buffers can restore normal pH within a fraction of a second.

c. There are three major chemical buffer systems of the body: the bicarbonate, phosphate, and protein systems.

4. The Bicarbonate Buffer System (p. 876)

a. The bicarbonate buffer system is a solution of carbonic acid and bicarbonate ions. Carbonic acid (H₂CO₃) forms by the hydration of carbon dioxide and then dissociates into bicarbonate (HCO₃^-) and H⁺. This is a reversible reaction.

b. The bicarbonate system does not have a particularly strong buffering capacity. It does, however, work well in the body because the bicarbonate buffers are concentrated extracellular buffers and because the lungs and kidneys constantly remove CO² and prevent an equilibrium from being reached.

5. The Phosphate Buffer System (p. 876)

a. The phosphate buffer system is a solution of HPO₄^2- and H₂PO₄^-. It works in much the same way as the bicarbonate system.

b. The phosphate buffering system has a stronger buffering effect than an equal amount of bicarbonate buffer. However, phosphates are much less concentrated in the ECF than bicarbonate, so they are less important in buffering the ECF.

6. The Protein Buffer System (p. 876)

a. Proteins are more concentrated than either bicarbonate or phosphate buffers, especially in the ICF and blood plasma.

b. The protein buffer system accounts for about three-quarters of all chemical buffering ability of the body fluids.

c. The buffering capacity of proteins is due to the carboxyl groups that release H⁺ when pH begins to rise and thus lower pH, or to amino side groups, which bind H⁺ when pH falls too low, thus raising pH toward normal.

B. Respiratory Control of pH (p. 877)

1. Addition of carbon dioxide to body fluids raises H⁺ and lowers pH, while removal of CO₂ has the opposite effects. This is the basis for the strong buffering capacity of the respiratory system.

a. Rising CO₂ concentration and falling pH stimulate peripheral and central chemoreceptors, which stimulate an increase in pulmonary ventilation. This expels excess CO₂ and thus reduces H⁺ concentration.

b. Conversely, a drop in H⁺ concentration raises pH and reduces pulmonary ventilation.

c. These are classic negative feedback mechanisms that result in acid-base homeostasis.

C. Renal Control of pH (p. 877; Figs. 24.9, 24.10; Transps. 437, 438)

1. The kidneys can neutralize more acid or base than either the respiratory system or chemical buffers.

a. Renal tubules secrete hydrogen ions into the tubular fluid, where most of it combines with bicarbonate, ammonia, and phosphate buffers.

b. Bound and free H⁺ are then excreted in urine.

2. The kidneys are the only organs that actually expel H⁺ from the body. Other buffering systems only reduce its concentration by binding it to another chemical.

3. Figure 24.9, p. 878 (Transp. 437), shows the process of H⁺ secretion and neutralization. It is numbered to correspond to the step-by-step description given on page 877.

a. Tubular secretion of H⁺ continues only as long as there is a sufficient concentration gradient between a high H⁺ concentration in the tubule cells and a lower H⁺ concentration in the tubular fluid.

b. Note that for every bicarbonate ion that enters the peritubular capillaries, a sodium ion does too. Thus the reabsorption of Na⁺ by the renal tubules is part of the process of neutralizing acid.

D. Disorders of Acid-Base Balance (p. 879; Figs. 24.11, 24.12; Transp. 439; Table 24.2)

1. If the pH of the ECF falls below 7.35 a state of acidosis exists. If pH rises above 7.45, a state of alkalosis exists. Either of these imbalances has potentially fatal effects.

a. Acidosis depresses the central nervous system and causes such symptoms as confusion, disorientation, and coma.

b. In alkalosis, the net gain in positive intracellular charges shifts the membrane potential closer to firing level and makes the nervous system hyperexcitable. Nerves fire spontaneously and overstimulate skeletal muscles.

2. Acid-base imbalances are classified as respiratory or metabolic.

a. Respiratory acidosis occurs when the rate of alveolar ventilation fails to keep pace with the body's rate of carbon dioxide production.

b. Respiratory alkalosis results from excessive ventilation, in which carbon dioxide is eliminated faster than it is produced.

d. Metabolic acidosis can result from elevated production of organic acids. Dying people normally exhibit this condition.

e. Metabolic alkalosis is rare but can result from overuse of bicarbonates or from loss of stomach acid in chronic vomiting.

E. Compensation of Acid-Base Imbalances (p. 880)

1. Uncompensated acidosis or alkalosis is a pH imbalance that the body fails to correct. Compensated acidosis or alkalosis is a more temporary condition that the body corrects by means of its physiological and chemical buffers.

2. The respiratory system compensates for some states of acid-base imbalance by adjusting the partial pressure of carbon dioxide. This is effective in correcting pH due to carbon dioxide imbalances, but not in correcting other causes of acidosis or alkalosis.

3. The kidneys are slower to respond to pH imbalances, but better at restoring a fully normal pH. The kidneys cannot act quickly enough to compensate for short-term pH imbalances, such as the acidosis that might result from an asthmatic attack or alkalosis resulting from a brief episode of emotional hyperventilation. The kidneys are, however, effective at compensating for pH imbalances that last a few days or longer.

a. In acidosis, the renal tubules increase the rate of H⁺ secretion and must also secrete more ammonia to buffer this increase.

b. In alkalosis, the bicarbonate concentration and pH of the urine are elevated.

F. pH Imbalances in Relation to Electrolyte and Water Imbalances (p. 881; Table 24.3)

1. Imbalances of water, electrolyte, or acid-base equilibrium cannot be discussed in isolation from each other. If one of these is out of balance, it will affect the other two. A number of these interactions are explained in Table 24.3, p. 881.

CHAPTER ESSAY: Fluid Replacement Therapy (p. 882)

i. Fluid replacement therapy is one of the most important life-saving techniques for the ill or injured. Drinking water alone does not replace lost electrolytes.

ii. Parenteral routes are all those except via the digestive tract, and include I.V., subcutaneous, and intramuscular routes of fluid replacement therapy.

iii. Solutions used include normal saline, Ringer's lactate solution, and plasma volume expanders.

iv. For severely ill or injured patients, total parenteral nutrition or hyperalimentation provide complete nutritional needs.

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