Chapter 25 - Fluid and Electrolytes
Briefly discuss how the kidneys regulate fixed acids to help maintain blood pH in response to INCREASED blood H+ concentration.
he input of acid into the blood, except that produced from CO2, occurs from two major sources: nutrients absorbed by the gastrointestinal (GI) tract and body cells (figure 25.12a). Typically, more acid is absorbed from the GI tract because most individuals, at least in the United States, consume a diet rich in animal protein and wheat. These various ingested items contribute H+ to the blood. Cells also contribute acid as waste products from metabolic processes. These products include lactic acid, phosphoric acid, and ketoacids. Acidic conditions may also result from the excessive loss of HCO3- (a weak base) as a consequence of diarrhea. (HCO3- is normally lost in the feces, but excess amounts can be lost when an individual has diarrhea. The additional H+ must be eliminated to maintain acid-base balance. Recall from section 24.6d that kidney tubules respond to increased blood H+ concentration, as follows: Reabsorb all filtered HCO3− along the length of the nephron tubule Synthesize and absorb new HCO3− while excreting H+ into the filtrate through type A intercalated cells in the distal convoluted tubule and collecting tubules Thus, under conditions when blood H+ concentration is increasing, kidneys help to maintain a normal blood pH by both eliminating excess H+ and synthesizing and reabsorbing HCO3-.
Briefly describe the role of bicarbonate and carbonic acid in the bicarbonate buffer system.
The bicarbonate buffering system in the blood is the most important buffering system in the ECF. Bicarbonate ion and carbonic acid are the key components of this buffering system. Bicarbonate (HCO3-) serves as a weak base, whereas carbonic acid (H2CO3) acts as a weak acid.
Briefly explain the relationship between breathing rate and blood pH.
An abnormal increase or decrease in the respiratory rate, however, that occurs independently of changes in the Pco2 may affect acid-base balance because it drives the reversible reaction involving carbonic anhydrase either to the left or to the right (see section 3.2b). The following changes occur within several minutes (figure 25.13): An abnormal increase of the respiratory rate causes elevated levels of CO2 to be expired, resulting in a decrease in blood CO2 concentration (blood Pco2 decreases). The decreased level of blood CO2 drives the chemical reaction to the left (figure 25.13a). Blood H+ concentration decreases, and blood pH increases (becomes more alkaline). An abnormal decrease of the respiratory rate (or exchange of respiratory gases) results in an increase in the amount of CO2 retained, thus elevating blood CO2 (blood Pco2 increases). The increased levels of blood CO2 drive the equation to the right (figure 25.13b). Blood H+ concentration increases, and blood pH decreases (becomes more acidic).
Name a hormone that increases urine output and briefly explain its mechanism of action.
Atrial Natriuretic Peptide (ANP) increases urine output to decrease both blood volume and blood pressure.
Intracellular Fluid (ICF)
Intracellular fluid (ICF) is the fluid within our cells
Distinguish between electrolytes and non-electrolytes.
Molecules that do not dissociate (or come apart) in solution are called nonelectrolytes. Most of these substances are covalently bonded organic molecules (e.g., glucose, urea, and creatinine). In contrast, an electrolyte is any substance that dissociates in solution to form cations and anions. The term electrolyte refers directly to the ability of these substances, when dissolved and dissociated in solution, to conduct an electric current. Electrolytes include salts, acids, bases, and some negatively charged proteins.
List the six major electrolytes in body fluids besides H+ and HCO3-.
The human body fluids contain common electrolytes. The common electrolytes include Na+, K+, Cl−, Ca2+, PO43-, Mg2+ (as well as H+ and HCO3-).
Name two buffering systems that regulate each category of acid.
The level of each acid is regulated by separate physiologic buffering systems: 1. Fixed acid is regulated by the kidney through the reabsorption and elimination of HCO3- and H+. 2. Volatile acid is regulated by the respiratory system through the regulation of the respiratory rate.
Describe the conditions that lead to the release of, and the actions of the following hormones, c. Aldosterone.
Aldosterone (ALDO) is normally released from the adrenal cortex in response to angiotensin II, decreased blood plasma Na+ levels, or most importantly, increased blood plasma K+ levels (figure 25.10) Aldosterone is a steroid hormone that is transported within the blood plasma and eventually binds to receptors within principal cells of the kidney, as described in sections 17.8c and 24.6d. The binding of aldosterone to these cells causes increased reabsorption and retention of both Na+ and water, and increased secretion and then excretion of K+. Aldosterone increases the number of Na+/K+ pumps and Na+ channels, so more Na+ is reabsorbed from the filtrate back into the blood. Water follows the Na+ movement by osmosis. Fluid retention results in decreased urine output. Because equal amounts of Na+ and water are reabsorbed, blood osmolarity remains constant. Both low blood pressure and changes in Na+ and K+ blood plasma levels cause aldosterone release. Blood volume and blood pressure are maintained through the reabsorption of both Na+ and water in the kidneys, with no change to osmolarity. K+ secretion is increased (unless there is an increase in H+). As blood volume, blood pressure, and both Na+ and K+ blood plasma levels return to normal ranges, aldosterone release is decreased. Thus, as with angiotensin II and ADH, aldosterone release and its effects are regulated by negative feedback.
Name three hormones that decrease urine output and briefly explain their mechanism of action.
Angiotensin II, Antidiuretic Hormone (ADH), and Aldosterone help decrease urine output. These three hormones function to maintain both blood volume and blood pressure. The specific mechanisms employed by each of these hormones in regulating fluid output in the kidneys also function in regulating some electrolytes (e.g., Na+).
List the causes and explain how the fluid movement among the three fluid compartments of the body is altered under the following fluid imbalances, a. dehydration.
Certain types of fluid imbalance involve fluid loss or gain that is not isotonic. Dehydration can result from profuse sweating, diabetes mellitus, intake of alcohol, hyposecretion of antidiuretic hormone (ADH—a hormone that stimulates water reabsorption in the kidney; see section 24.6d), insufficient water intake, or overexposure to cold weather. In each case, the water loss is greater than the loss of solutes, and the blood plasma becomes hypertonic. Consequently, water shifts between fluid compartments with a net movement of water from the cells into the interstitial fluid and then into blood plasma. Body cells may become dehydrated as a result (figure 25.3b).
List various sources of fixed acids.
Examples of fixed acids include lactic acid from glycolysis, phosphoric acid from nucleic acid metabolism, and ketoacids from metabolism of fat.
Define fluid balance.
Fluid balance exists when fluid intake is equal to fluid output, and a normal distribution of water and solutes is present in the two major fluid compartments.
Differentiate between the intracellular fluid (ICF) and the extracellular fluid (ECF) compartments of the body. Briefly explain how fluid moves between these two compartments.
Fluid movement between compartments occurs continuously in response to changes in relative osmolarity (concentration). This happens when the fluid concentration in one fluid compartment becomes either hypotonic or hypertonic (see section 4.3b), with respect to another compartment; water immediately moves by osmosis between the two compartments until the water concentration is once again equal (figure 25.3). You may recall from section 4.3b that water always moves by osmosis from the hypotonic solution to the hypertonic solution. This movement of water between the compartments is possible because the plasma membranes and the capillary wall are both permeable to water.
Fluid intake is controlled by various stimuli that either activate or inhibit the thirst center located within the?
Hypothalamus
List the causes and explain how the fluid movement among the three fluid compartments of the body is altered under the following fluid imbalances, b. hypotonic hydration.
Hypotonic hydration is also called water intoxication, or positive water balance. It can result from ADH hypersecretion, but it is generally caused from drinking a large amount of plain water following excessive sweating. An example would be an amateur athlete who runs a marathon, and drinks excessive amounts of plain water instead of using an electrolyte-enhanced solution. Both Na+ and water are lost during sweating, and drinking water replaces only the water, but not the solutes. The blood plasma then becomes hypotonic to the other fluid compartments. Fluid moves from blood plasma into the interstitial fluid, and then into the cells (figure 25.3a). Cells may become swollen with fluid. One of the consequences of extreme hypotonic hydration is cerebral edema. Brain cells become impaired as they swell with excess fluid. The person may experience headaches, nausea, or both. Convulsions, coma, or death may result in severe cases. In addition, some individuals have died after having been forced or enticed to drink excessive amounts of water (e.g., fraternity hazings and water-drinking contests).
Name two physiological buffering systems that bring blood pH back to normal.
In response to a transient acid-base disturbance, the physiologic buffering system of the kidneys, the respiratory system, or both function to offset the disturbance. The response of physiologic buffering systems to acid-base disturbances that results in the return of blood pH to normal is called compensation.
Differentiate between the intracellular fluid (ICF) and the extracellular fluid (ECF) compartments of the body. State the major distinctions in the chemical composition of solutes in interstitial fluid and blood plasma.
Interstitial fluid and blood plasma exhibit one significant difference—namely, that protein is present in blood plasma—but very little protein is within the interstitial fluid. The similarity in ionic composition and the difference in protein composition reflect the relative permeability of the capillary wall: Proteins are generally too large to move out of the blood through the openings in the capillary wall to enter the interstitial fluid, whereas fluids and ions move freely. Therefore, during capillary exchange, blood plasma and all of its dissolved substances—except for most proteins—are filtered to become part of the interstitial fluid.
Differentiate between the intracellular fluid (ICF) and the extracellular fluid (ECF) compartments of the body. List the solutes of the intracellular fluid (ICF) and extracellular fluid (ECF).
Intracellular fluid is the most distinct compartment; it contains more potassium (K+) and magnesium (Mg2+) cations, phosphate anion (PO43-), and negatively charged proteins than the extracellular fluid. The two fluids composing the extracellular fluid—interstitial fluid and blood plasma—are, in comparison, both distinct chemically from intracellular fluid and similar in chemical composition to one another. Both interstitial fluid and blood plasma have a high concentration of these ions: sodium (Na+) and calcium (Ca2+) cations, and chloride (Cl−) and bicarbonate (HCO3-) anions.
For the different acid-base imbalances METABOLIC ALKALOSIS do the following, a. define them. b. identify several causes. c. describe the change in pH, pCO2, and bicarbonate before compensation. d. briefly explain renal and/or respiratory compensation.
Metabolic alkalosis is defined as arterial blood levels of HCO3- that exceed 26 mEq/L. A loss of H+ or an increase in HCO3- can bring about this condition (see figure 25.12b). Causes include the following: Vomiting (the most common cause) or prolonged nasogastric suction Increased loss of acids by the kidneys with overuse of diuretics (medications that increase urine output) Increased alkaline input from consuming large amounts of antacids
Explain why electrolytes exert a greater osmotic pressure than non]electrolytes.
NaCl dissociates into two ions, Na+ and Cl−. Because osmotic pressure is dependent upon the number of solutes, NaCl exerts twice the osmotic pressure of the same concentration of a nonelectrolyte, such as glucose, which does not dissociate into ionic forms. Further, CaCl2 in solution dissociates into three components, Ca2+ and two Cl−, and exerts three times the osmotic pressure compared to that of glucose. To account for this difference in exerting osmotic pressure, the concentration of electrolytes in solution is commonly expressed in milliequivalents per liter (mEq/L), which reflects the amount or equivalent number of electrical charges in 1 liter of solution. (Milliequivalents is a measure of either the amount of H+ an anion can bind, or the amount of bicarbonate ion (HCO3-) a cation can bind, in 1 liter of solution.)
Explain the differences between obligatory loss and facultative loss of fluid.
Obligatory water loss is a loss of water that always occurs, regardless of the state of hydration of the body. It includes water lost through breathing and through the skin (insensible water loss), as well as fluid lost in the feces and in the minimal amount of urine produced to eliminate wastes from the body, approximately 0.5 L (500 mL) per day. Facultative (fak′ŭl-tā-tiv) water loss is controlled water loss through regulation of the amount of urine expelled from the body. It is dependent upon the degree of hydration of the body and is hormonally regulated in the distal convoluted tubule, collecting tubules, and collecting ducts in nephrons of the kidney (see sections 24.6d and 25.4).
Compare and contrast the electrolytes, sodium and POTASSIUM IONS, with regards to their, a. main location, b. functions, and c. regulation.
POTASSIUM IONS In contrast to Na+, approximately 98% of potassium is in the ICF and only 2% is in the ECF. Potassium is required for normal neuromuscular physiologic activities, and it has a significant role in controlling heart rhythm. Although the vast majority of the total body K+ is located within the ICF, it is only the 2% of the K+ in the ECF that is continually regulated. The normal plasma value for K+ in the ECF is between 3.5 mEq/L and 5.0 mEq/L (figure 25.7a). Small changes in blood plasma K+ levels can readily lead to a K+ imbalance—the most potentially lethal of the electrolyte imbalances. Neuromuscular changes (e.g., cardiac arrhythmia, muscle weakness) are the most significant effects of a K+ imbalance. These can lead to either cardiac or respiratory arrest. Both the total body K+ and the distribution of K+ must be regulated in order to maintain K+ balance in our body fluids. Total body potassium is regulated by K+ intake and output. The daily dietary requirement for K+ is 40 mEq/L, although it may vary from 40-150 mEq/L. Potassium is generally obtained from fruits and vegetables, but input is increased with salt substitutes that contain K+. Only small amounts of K+ are lost from the body through sweat and in feces. Most K+ (approximately 80-90%) is lost in urine. Some K+ is always being lost because the body has no means to conserve all of its K+. The amount of K+ lost in the urine fluctuates, and greater amounts are lost during conditions of high blood plasma K+, increased aldosterone secretion, and high blood pH.
Explain the differences between sensible and insensible perspiration.
Sensible and insensible fluid loss reflects whether the fluid loss is measurable. Sensible water loss is measurable, and it includes fluid lost through feces and urine. In contrast, insensible water loss is not measurable. It includes both fluid lost in expired air and fluid lost from the skin through sweat and cutaneous transpiration.
Briefly describe three conditions and stimuli that decrease fluid intake.
Stimuli for inhibiting the thirst center are produced when fluid intake is greater than fluid output. All of these stimuli (except distension of the stomach, described here) oppose stimuli that activate the thirst center. These include the following: Increased salivary secretions. When body fluid level is high, salivary secretions increase, and the mucous membranes of the mouth and throat become moist. Sensory input to the thirst center decreases. Distension of the stomach. Fluid entering the stomach causes it to stretch, and nerve signals are relayed to the hypothalamus to inhibit the thirst center. (Note that an empty stomach does not stimulate the thirst center; rather, only a stretched stomach wall will inhibit the thirst center.) Decreased blood osmolarity. Blood osmolarity decreases when additional fluid enters the blood. In response, the thirst center is no longer stimulated directly, and the hypothalamus decreases stimulation of ADH release from the posterior pituitary. Increased blood pressure. Blood volume and blood pressure increase with the addition of fluid. This rise in blood pressure inhibits the kidney from releasing renin, and the subsequent production of angiotensin II decreases. A decrease in angiotensin II results in a reduced stimulation of the thirst center.
Briefly describe three conditions and stimuli that increase fluid intake.
Stimuli for activating the thirst center, which occurs when fluid intake is less than fluid output, include the following: Decreased salivary secretions. Saliva production decreases, and mucous membranes are not as moist, when less fluid is available. Sensory input is relayed from sensory receptors in the mucous membranes of the mouth and throat to the thirst center. Increased blood osmolarity. This occurs most commonly from insufficient water intake and dehydration. The increase in blood osmolarity stimulates sensory receptors in the thirst center directly, and also stimulates the hypothalamus to initiate nerve signals to the posterior pituitary to release antidiuretic hormone (ADH) (see section 17.7b). ADH also stimulates the thirst center. This stimulation of the thirst center occurs with as little as a 2-3% increase in ADH. Decreased blood pressure. When fluid intake is less than fluid output, blood volume decreases with an accompanying decrease in blood pressure. Renin is released from the kidney in response to a lower blood pressure (see section 20.6b). Renin initiates the conversion of angiotensinogen to angiotensin II. An increase of 10-15% in the concentration of angiotensin II within the blood stimulates the thirst center. This mechanism is especially important when extreme volume depletion occurs; for example, when an individual is hemorrhaging. When the thirst center is activated, nerve signals are relayed to the cerebral cortex, and we then become conscious of our thirst. If we take fluid into the body by drinking or eating, water is absorbed from the GI tract into the blood, and the water then moves into the interstitial space and ultimately into the cells (figure 25.3a). Stimuli to Turn off the Thirst CenterStimuli for inhibiting the thirst center are produced when fluid intake is greater than fluid output. All of these stimuli (except distension of the stomach, described here) oppose stimuli that activate the thirst center. These include the following: Increased salivary secretions. When body fluid level is high, salivary secretions increase, and the mucous membranes of the mouth and throat become moist. Sensory input to the thirst center decreases. Distension of the stomach. Fluid entering the stomach causes it to stretch, and nerve signals are relayed to the hypothalamus to inhibit the thirst center. (Note that an empty stomach does not stimulate the thirst center; rather, only a stretched stomach wall will inhibit the thirst center.) Decreased blood osmolarity. Blood osmolarity decreases when additional fluid enters the blood. In response, the thirst center is no longer stimulated directly, and the hypothalamus decreases stimulation of ADH release from the posterior pituitary. Increased blood pressure. Blood volume and blood pressure increase with the addition of fluid. This rise in blood pressure inhibits the kidney from releasing renin, and the subsequent production of angiotensin II decreases. A decrease in angiotensin II results in a reduced stimulation of the thirst center.
Briefly describe the role of hydrogen phosphate and di-hydrogen phosphate in the phosphate buffering system.
The phosphate buffering system is found in intracellular fluid (ICF). It is especially effective in buffering metabolic acid produced by cells because phosphate (PO43-) is the most common anion within cells. The phosphate buffering system is also composed of both a weak base and a weak acid. Here hydrogen phosphate (HPO42-) is the weak base and dihydrogen phosphate (H2PO4-) is the weak acid.
Describe how fixed acids differ from volatile acids.
Fixed acid (or metabolic acid) is the wastes produced from metabolic processes (other than from carbon dioxide). Examples of fixed acids include lactic acid from glycolysis, phosphoric acid from nucleic acid metabolism, and ketoacids from metabolism of fat. Volatile (vol′ă-til; to evaporate quickly) acid is carbonic acid produced when carbon dioxide combines with water. The term "volatile acid" refers to the fact that carbonic acid is produced from a gas that is normally expired (or "evaporated"). Because CO2 is readily converted to carbonic acid in the presence of carbonic anhydrase, CO2 itself is often referred to as the volatile acid.
Describe the main sources of fluid intake.
Fluid intake is the addition of water to the body. It is divided into two categories, preformed water and metabolic water (figure 25.4): Preformed water includes the water absorbed from food and drink taken into the GI tract. On average, this is approximately 2300 milliliters (mL) of fluid intake per day. Metabolic water includes the water produced daily from aerobic cellular respiration (see section 3.4e) and dehydration synthesis (see section 2.7a). It is approximately 200 mL of fluid per day.
Name four types of acid base disturbances.
Four major types of acid-base disturbances are distinguished based on two criteria: whether the primary disturbance is respiratory or metabolic in nature; and whether the pH change is acidic or alkaline. The four categories are respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. We examine each of these in terms of the cause of the primary disturbance, and then we describe the compensation made by the physiologic buffering system that helps prevent an acid-base imbalance.
Briefly describe the role of the amine group and the carboxylic group in the protein buffer system.
The protein buffering system is a chemical buffering system that is composed of proteins within cells and in blood plasma. It accounts for about three-quarters of the chemical buffering in body fluids. The amine group (-NH2) of amino acids acts as a weak base to buffer acid, whereas the carboxylic acid (-COOH) of amino acids acts as a weak acid to buffer base (see section 2.8 for a review of amino acid and protein structures).
Name two categories of acids in the body.
Two major categories of acid are present in the body; fixed acid and volatile acid.
Define acidosis (academia) and alkalosis (alkalemia).
Acidosis, or acidemia, is an arterial blood pH reading below 7.35, whereas alkalosis, or alkalemia, is an arterial blood pH reading above 7.45.
Briefly discuss how the kidneys regulate fixed acids to help maintain blood pH in response to DECREASED blood H+ concentration.
Although the general daily input of acid tends to decrease pH, some conditions tend to increase pH as a result of excess retention of base or loss of acid (figure 25.12b). Substances that increase blood pH also enter the blood from the GI tract. For example, this may occur if an individual regularly eats a vegetarian diet (that is rich in fruits and vegetables and low in animal protein), or regularly ingests antacids. These increase the absorption of alkaline substances into the blood, and blood H+ concentration decreases. Alkaline conditions may also be caused by the abnormal loss of HCl as a result of vomiting. When alkaline conditions are present, renal tubules respond in the following way: Do not reabsorb all of the filtered HCO3- along the length of the nephron tubule Secrete HCO3- from the blood into the filtrate, while reabsorbing H+ in exchange through type B intercalated cells Some of the filtered HCO3- (which is not reabsorbed) and secreted HCO3- is lost in the urine, while H+ is reabsorbed. Blood plasma H+ concentration increases, and blood pH decreases to normal. The kidneys therefore act as a physiologic buffering system to eliminate either excess acid or base from the body. The process is relatively slow, taking from several hours to days; however, this is the only way to eliminate fixed acid or base, and it provides the most powerful means of maintaining blood H+ concentration and preventing pH changes.
Describe the conditions that lead to the release of, and the actions of the following hormones, d. Atrial Natriuretic Peptide (ANP).
Atrial natriuretic peptide (ANP) is a peptide hormone that opposes the actions of the three hormones just discussed (figure 25.11). ANP is released into the blood from cells in the heart atria. The stimulus for its release is increased stretch of these chambers, which is an indication of both increased blood volume and blood pressure (see sections 17.10c, 20.6b, 24.5e, and 24.6d. ANP decreases both blood volume and blood pressure by binding to these target organs and causing the following responses: Blood vessels. Dilates systemic blood vessels, resulting in decreased total peripheral resistance. Systemic blood pressure decreases as a result. Kidneys. Causes vasodilation of the afferent arterioles in the kidneys and relaxation of mesangial cells; both increase the glomerular filtration rate (see section 24.5e). Page 1006 Additionally, ANP inhibits Na+ and water reabsorption by nephron tubules, resulting in additional loss of Na+ and water (see section 24.6d). These changes increase urine output. Blood volume and systemic blood pressure decreases. In addition, atrial natriuretic peptide inhibits the release of renin, the action of angiotensin II, and the release of ADH and aldosterone, thus preventing the actions of these hormones.
Describe the main sources of fluid output.
Fluid output is the loss of water from the body. Fluid output must equal fluid intake to maintain fluid balance. Fluid is lost from the body through the normal mechanisms of Breathing, Sweating, Cutaneous transpiration (evaporation of water directly through the skin), Defecation, Urination. The amount of water lost through each of these processes depends upon physical activity, environmental conditions, and internal conditions of the body. Average amounts for each type of fluid output are shown in figure 25.4. Notice that of the average fluid output, 1500 mL out of the 2500 mL (or approximately 60%) is lost in urine, and the remaining 40% of fluid is lost in expired air, through the skin by sweat and cutaneous transpiration, and in feces. Water loss can be described in two ways: either as sensible and insensible water loss or as obligatory and facultative water loss.
List the causes and explain how the fluid movement among the three fluid compartments of the body is altered under the following fluid imbalances, c. edema.
Fluid sequestration differs from the other fluid imbalances because total body fluid may be normal, but it is distributed abnormally. Fluid accumulates in a particular location, and it is not available for use elsewhere. Edema is an example of fluid sequestration in which fluid accumulates in the interstitial space around cells, and is characterized by puffiness or swelling. Anatomic or physiologic changes that can result in edema are depicted in figure 25.5. Notice as you review this figure that edema is generally a result of abnormal changes in the cardiovascular system (heart or blood vessels), blood composition, or changes to lymph vessels (the vessels that return fluid to the cardiovascular system). These changes alter the net filtration pressure (NFP) at systemic capillaries (see section 20.3c), causing additional fluid to either leave the capillaries or remain in the interstitial space.
For the different acid-base imbalances RESPIRATORY ALKALOSIS do the following, a. define them. b. identify several causes. c. describe the change in pH, pCO2, and bicarbonate before compensation. d. briefly explain renal and/or respiratory compensation. e. describe the change in pH, pCO2, and bicarbonate after compensation.
Respiratory alkalosis occurs when the Pco2 decreases to levels below 35 mm Hg due to an increase in respiration. Faster breathing (hyperventilation) may occur in response to the following: Severe anxiety Any condition in which an individual is not receiving sufficient oxygen (e.g., as might occur when climbing to a high altitude where there is a decrease in the partial pressure of oxygen [Po2]; during congestive heart failure; as a result of severe anemia; or due to low blood pressure) Aspirin overdose (a condition that stimulates the respiratory center) Continued elimination of CO2 results in decreased levels of blood CO2 that in turn cause a decrease in blood H2CO3 and lowered H+ concentration as the chemical reaction shifts to the left:
Compare and contrast the electrolytes, SODIUM and potassium ions, with regards to their, a. main location, b. functions, and c. regulation.
SODIUM Approximately 99% of Na+ is in the ECF and only 1% in the ICF, a gradient that is maintained by Na+/K+ pumps. Sodium functions in a number of physiologic processes, many of which have been presented in previous chapters (e.g., neuromuscular functions and cotransport in kidney tubules). We now describe how Na+ concentration is regulated to maintain its balance, and how it functions in determining plasma osmolarity and regulating fluid balance. As the most common cation in the ECF—composing approximately 90% of the solute concentration in the ECF—Na+ is therefore the most important electrolyte in determining blood plasma osmolarity and in regulating fluid balance. The ECF becomes temporarily hypertonic if Na+ concentration increases from either elevated Na+ intake or decreased water content. Consequently, water moves from the other compartments into the blood plasma in an attempt to reestablish the normal Na+ concentration (figure 25.6b). Sodium is the principal cation in the extracellular fluid (ECF). (a) Normal blood plasma Na+ concentration is between 135 mEq/L and 145 mEq/L and is important in maintaining fluid balance. Sodium level increases through the diet and decreases through urine, feces, and sweating. Sodium content and concentration are regulated by aldosterone, antidiuretic hormone (ADH), and atrial natriuretic peptide (ANP). (b) Changes in Na+ concentration cause movement of water between fluid compartments.
Extracellular Fluid (ECF)
The fluid outside of cells is referred to collectively as extracellular fluid (ECF).
Briefly describe the two factors that influence the percentage of body fluid.
The fluid percentage depends upon two variables: the age of an individual, and the relative amounts of adipose connective tissue and skeletal muscle tissue: Age. Infants have the highest percentage of fluid, at approximately 75% fluid by weight. In contrast, elderly individuals have the lowest percentage of fluid at 45%. Children and young and middle-aged adults are usually somewhere in between these two extremes, with a general trend of decreasing percentage of body fluid seen with increasing age. Relative amounts of adipose connective tissue to skeletal muscle tissue. The percentage of fluid in the body at each age depends upon the ratio of adipose connective tissue and skeletal muscle tissue because of the difference in water content of these tissues. Adipose connective tissue is approximately 20% water, whereas skeletal muscle tissue is approximately 75% water. This accounts for the general differences in the percentage of body fluid that are noted between females and males of the same age after puberty.
For the different acid-base imbalances RESPIRATORY ACIDOSIS do the following, a. define them. b. identify several causes. c. describe the change in pH, pCO2, and bicarbonate before compensation. d. briefly explain renal and/or respiratory compensation. e. describe the change in pH, pCO2, and bicarbonate after compensation.
The most common acid-base disturbance occurs because of impaired elimination of CO2 by the respiratory system (caused by either a decrease in breathing rate or impaired gas exchange at the respiratory membrane). Respiratory acidosis is defined as occurring when the Pco2 in the arterial blood becomes elevated above 45 mm Hg. Causes include the following: Injury to the respiratory center, perhaps caused by trauma or by poliovirus infection Disorders of the nerves or muscles involved with breathing, such as the loss of muscle strength associated with muscular dystrophy Airway obstruction (e.g., chronic obstructive pulmonary disease) Decreased gas exchange due to reduced respiratory surface area or thickened width of the respiratory membrane (these two conditions are associated with emphysema or pulmonary edema, respectively) Continued impairment results in the accumulation of CO2 in the blood that ultimately causes an increase in blood H2CO3 and a subsequent increase in H+ concentration as the chemical reaction shifts to the right: Infants are more susceptible to respiratory acidosis because their smaller lungs and lower residual volume (see section 23.5f) do not eliminate CO2 as effectively. CO2 accumulates in the blood, with a subsequent increase in carbonic acid (H2CO3).
For the different acid-base imbalances METABOLIC ACIDOSIS do the following, a. define them. b. identify several causes. c. describe the change in pH, pCO2, and bicarbonate before compensation. d. briefly explain renal and/or respiratory compensation.
The most common metabolic acid-base disturbance occurs as a result of a decrease in HCO3-. This decrease may result from an excessive loss of HCO3-, but more generally it occurs when there is an accumulation of fixed acid. The excess H+ binds with HCO3- to form H2CO3; thus, HCO3- levels in the blood decrease. Metabolic acidosis occurs when arterial blood levels of HCO3- fall below 22 mEq/L. This condition is usually caused by unhealthy changes in physiologic processes that were described earlier in the chapter (see figure 25.12a). These include the following: Increased production of metabolic acids, such as ketoacidosis from diabetes mellitus, increased lactic acid from glycolysis, or excessive production of acetic acid from excessive intake of alcohol Decreased elimination of acid due to renal dysfunction Increased elimination of HCO3- as a result of severe diarrhea Infants are especially vulnerable to this condition because they produce larger amounts of acidic metabolic wastes due to a higher metabolic rate.
State the role of chemical buffers.
The physiologic buffering systems previously described are extremely effective in helping to maintain body fluid pH. The physiologic processes within the kidneys occur over several hours to several days, whereas those of the respiratory system require only a few minutes to respond. In contrast, chemical buffering systems act quickly and temporarily to help prevent pH changes that would occur in response to the addition of acid or base, such as happens shortly after a meal, or as a result of abnormal loss of acid or base. Chemical buffering systems are composed of one or two types of molecules that can bind and release H+ within a fraction of a second to prevent large pH changes. The molecule, or molecules, of chemical buffering systems are composed of both a weak base that can bind excess H+ and a weak acid that can release H+. Remember that chemical buffers cause both temporary and limited adjustments until the body can eliminate the excess acid or base through physiologic buffering systems (namely, the kidneys or the respiratory system).
Describe the conditions that lead to the release of, and the actions of the following hormones, b. Antidiuretic hormone (ADH).
The release and action of ADH can be summarized as follows: ADH is released under conditions of low blood pressure (action of angiotensin II), low blood volume (detected by stretch receptors in the heart and blood vessels), and high blood osmolarity (dehydration) to stimulate both fluid intake and water reabsorption in the kidneys. If fluid intake occurs, then blood pressure increases, blood osmolarity is further decreased, and blood volume increases. As the stimuli return to within normal homeostatic levels, ADH release is decreased through negative feedback.
Name and identify the location(s) of the three most important chemical buffering systems.
The three most important chemical buffering systems include the following: The protein buffering system within both cells and the blood The phosphate (PO43-) buffering system within cells The bicarbonate (HCO3-) buffering system within the ECF, particularly the blood Although similar in the mechanism to buffer both acid and base, the three chemical buffering systems differ in their locations and in the molecules that compose them.
Describe the conditions that lead to the release of, and the actions of the following hormones, a. Angiotensin II.
We previously described angiotensin II as a potent vasoconstrictor that helps regulate blood pressure (see sections 17.10c, 20.6b, and 24.5e). Recall that angiotensinogen is an inactive hormone synthesized and released continuously from the liver. Its activation, which occurs within the blood, is initiated by the enzyme renin. Renin is released from the juxtaglomerular (JG) apparatus of the kidneys in response to either (1) low blood pressure (as detected by decreased stretch of baroreceptors within granular cells, or by decreased NaCl detected by chemoreceptors within macula densa cells; see section 24.3c); or (2) stimulation by the sympathetic division. The sequential action of renin and angiotensin converting enzyme (ACE) (which is bound to the endothelial lining of blood vessels) cause the formation of angiotensin II (the active form of the hormone). The formation and action of angiotensin II can be summarized as follows: It is synthesized either when blood pressure is low or the sympathetic division is activated. It causes an increase in resistance, decrease in fluid output (which helps to maintain blood volume and blood pressure), and an increase in blood volume (if fluid intake occurs). Consequently, blood pressure increases. Increasing blood pressure is aided by the release of both ADH and aldosterone. As blood pressure returns to within normal homeostatic levels, both renin release and angiotensin II synthesis are decreased by negative feedback.