Fluid Intake and Output

Fluid Intake and Output

The human body loses about 2,500 mL of water every day through urine, feces, and insensible perspiration, which involves gradual movement across the epithelia of the skin and respiratory tract. Other losses occur via sensible respiration, which is secre-tion through the sweat glands. Maximum perspi-ration rates can reach 4 liters per hour in extreme circumstances. Fever can also increase water loss, so a patient with fever should drink plenty of fluids to offset this condition.

The human body takes in about 2,500 mL of water every day. Via liquids, 1,500 mL are gained; via foods, 750 mL are gained; and via metabolic generation, 250 mL are gained. Metabolic generation of water is defined as the production of water within cells. For example, when 1 g of a lipid is broken down, 1.7 mL of water is generated. This is higher than the amount generated by the breakdown of proteins or carbo-hydrates. TABLE 23-1 lists sources of water input and methods of water output.

Water Intake Regulation

Thirst is primarily responsible for the regulation of water intake. Intense thirst comes from osmotic pres-sure affecting extracellular fluids on the thirst center in the hypothalamus. Loss of body water increases osmotic pressure to stimulate osmoreceptors in the thirst center. Whenever total body water decreases by as small an amount as 1%, thirst is triggered. Drink-ing fluids triggers nerve impulses that inhibit the thirst mechanism, stopping drinking before the swallowed fluids are absorbed. This keeps a person from consum-ing too many liquids.

Water intake is regulated by several major types of stimuli: the effects of osmoreceptors, dryness of the mouth, and a decrease in blood volume or blood pressure. In the hypothalamus, the osmo-receptors monitor osmolality of the extracellular fluid by identifying changes in the stretching of plasma membranes, which are caused by the intake or output of water. Only a 1–2% change will acti-vate them. Dry mouth develops when the osmotic pressure of the blood increases, causing the salivary glands to produce less saliva. They do this because the osmotic gradient that pulls water from the blood into the salivary glands is reduced. A large decrease in blood volume or blood pressure, of between 5% and 10%, also triggers thirst. Changes are based on signaling from baroreceptors, directly activating the thirst center, and from the effects of angiotensin II. Altogether, thirst increases because of these events. Thirst is influenced by consuming sodium, such as in a snack food, because sodium influences the events. When the amount of sodium ions in the extracel-lular fluid is increased, the osmoreceptors are stim-ulated. Therefore, there is a temporary increase in blood volume.

Water Output Regulation 

Water output occurs on a regular basis, and we cannot survive for long without consuming water. The kidneys­ are powerful but cannot compensate for a lack of water intake. Obligatory water loss  food residue  in  the feces, and the minimum daily sensible water loss. The kidneys must flush 600 mmol of urine solutes, which are the end products of metabolism and other activities, out of the body via the urine every day. Because the maximum concentration of urine is approximately 1,200 mOsm, at least 500 mL of water need to be excreted.

In addition to obligatory loss of water, urine volume and solute concentration are based on intake of fluids, the diet, and other forms of water loss. Excessive sweating causes the kidneys to excrete much lower quantities of urine to maintain water balance. In normal individuals, the kidneys start to eliminate excess water about 30 minutes after drinking. This is the amount of time required to inhibit the release of ADH. About one hour after drinking water, diuresis has reached its peak. This declines to the lowest level after about three hours.

Role of Antidiuretic Hormone (ADH)

The release of ADH is proportional to the amount of water reabsorbed in the collecting ducts of the kidneys. Low ADH levels mean that most water that reaches the collecting ducts will not be reabsorbed. This is because a lack of aquaporins in principal cells’ apical membranes prevents water movement. 

The water flows by without being reabsorbed. The urine is dilute, and there is reduced body fluid volume. High ADH levels cause aquaporins to be inserted in principal­ cell apical membranes. Almost all water that is filtered is reabsorbed. Only a small volume of urine, highly concentrated, is excreted. ADH secretion is regulated by two receptors, one in the brain and one in the heart (FIGURE 23-5).

In the hypothalamus, osmoreceptors sense the solute­ concentration of the extracellular fluid, ­triggering or inhibiting release of ADH from the posterior­ pituitary. Increased osmolality of the ­extracellular fluid causes the hypothalamic osmore-ceptors to be ­stimulated, and ADH is released. Oppo-sitely, decreased extracellular fluid osmolality slows ADH release. More water is excreted in the urine, and the blood osmolality is restored to normal. Sig-nificant blood volume or blood pressure changes also affect ADH secretion. If blood pressure is decreased, ADH release increases. This may be direct, because of baroreceptors in the atria and certain blood ves-sels, or indirect, because of the renin-angiotensin-­ aldosterone mechanism.

The changes that cause this must be significant because extracellular fluid osmolality changes are greatly important as daily stimulatory or inhibi-tory factors. Release of ADH may occur because of excessive sweating, diarrhea, or vomiting as well as ­hemorrhaging, severe burns, or a prolonged fever. When any of these occur, high ADH levels cause arteriole constriction, which directly increases blood pressure. This is where the alternate name for ADH, vasopressin, is derived.

1. What is the effect of ADH when you drink water?

2. What is water of metabolism?

3. Differentiate between sensible and insensible perspiration.

4. List the primary factors that regulate water intake and output.

Role of Aldosterone

Aldosterone helps in the regulation of water bal-ance. Produced by the cortex of each adrenal gland, aldosterone is a mineralocorticoid hormone. Its levels in the blood are controlled by blood pressure and by the volume of the fluid in the nephrons of the kidneys. FIGURE­ 23-6 illustrates the mechanisms involved in aldosterone secretion. Specific cells in the kidneys produce the enzyme known as renin when they are stimulated by a decline in blood pressure and in the volume of nephron filtrate.

When renin contacts the large plasma protein known as angiotensinogen in the bloodstream, it removes a segment of this protein. This process pro-duces angiotensin I, a small peptide molecule. Because angiotensin I is inactive, it must be converted into its active form, angiotensin II. This requires enzymes found in the blood inside the lungs. Angiotensinogen is produced in the liver.

The secretion of aldosterone from the adrenal glands is stimulated by angiotensin II. When aldoste-rone moves through the blood to reach the kidneys, it stimulates nephron cells to increase how much sodium they reabsorb, increasing the tubular reab-sorption of sodium. Water then follows the sodium ions, moving out of the nephron into the peritubular capillaries, increasing blood volume and blood pres-sure. These processes then shut the feedback loop off. Water balance is additionally affected by chemicals found in the diet, of which the most influential are caffeine and alcohol.

The Role of Atrial Natriuretic Peptide

Atrial natruiretic peptide (ANP) is a hormone pro-duced by specialized myocardial cells. ANP is secreted by neurons originating in the hypothalamus. It acts as both hormone and neurotransmitter. Atrial natri-uretic peptide increases the glomerular filtration rate and inhibits the release of renin. This hormone also reduces thirst, blocks the release of ADH and inhib-its the release of aldosterone, resulting in decreased blood pressure.