The body is equipped with remarkable homeostatic mechanisms to keep the composition and volume of body fluid within narrow limits of normal. Organs involved in homeostasis include the kid-neys, lungs, heart, adrenal glands, parathyroid glands, and pitu-itary gland.
Vital to the regulation of fluid and electrolyte balance, the kid-neys normally filter 170 L of plasma every day in the adult, while excreting only 1.5 L of urine. They act both autonomously and in response to blood-borne messengers, such as aldosterone and antidiuretic hormone (ADH). Major functions of the kidneys in maintaining normal fluid balance include the following:
• Regulation of ECF volume and osmolality by selective re-tention and excretion of body fluids
• Regulation of electrolyte levels in the ECF by selective re-tention of needed substances and excretion of unneeded substances
• Regulation of pH of the ECF by retention of hydrogen ions
• Excretion of metabolic wastes and toxic substances
Given these functions, it is readily apparent that renal failure will result in multiple fluid and electrolyte problems. Renal func-tion declines with advanced age, as do muscle mass and daily ex-ogenous creatinine production. Thus, high-normal and minimally elevated serum creatinine values may indicate substantially re-duced renal function in the elderly.
The pumping action of the heart circulates blood through the kidneys under sufficient pressure to allow for urine formation. Failure of this pumping action interferes with renal perfusion and thus with water and electrolyte regulation.
The lungs are also vital in maintaining homeostasis. Through ex-halation, the lungs remove approximately 300 mL of water daily in the normal adult. Abnormal conditions, such as hyperpnea (abnormally deep respiration) or continuous coughing, increase this loss; mechanical ventilation with excessive moisture decreases it. The lungs also have a major role in maintaining acid–base bal-ance. Changes from normal aging result in decreased respiratory function, causing increased difficulty in pH regulation in older adults with major illness or trauma.
The hypothalamus manufactures ADH, which is stored in the pos-terior pituitary gland and released as needed. ADH is sometimes called the water-conserving hormone because it causes the body to retain water. Functions of ADH include maintaining the osmotic pressure of the cells by controlling the retention or excretion of water by the kidneys and by regulating blood volume (Fig. 14-2).
Aldosterone, a mineralocorticoid secreted by the zona glomerulosa (outer zone) of the adrenal cortex, has a profound effect on fluid balance. Increased secretion of aldosterone causes sodium reten-tion (and thus water retention) and potassium loss. Conversely, decreased secretion of aldosterone causes sodium and water loss and potassium retention.
Cortisol, another adrenocortical hormone, has only a fraction of the mineralocorticoid potency of aldosterone. When secreted in large quantities, however, it can also produce sodium and fluid retention and potassium deficit.
The parathyroid glands, embedded in the thyroid gland, regulate calcium and phosphate balance by means of parathyroid hormone (PTH). PTH influences bone resorption, calcium absorption from the intestines, and calcium reabsorption from the renal tubules.
Changes in the volume of the interstitial compartment within the ECF can occur without affecting body function. The vascular compartment, however, cannot tolerate change as readily and must be carefully maintained to ensure that tissues receive ade-quate nutrients.
The baroreceptors are small nerve receptors that detect changes in pressure within blood vessels and transmit this information to the central nervous system. They are responsible for monitoring the circulating volume, and they regulate sympathetic and para-sympathetic neural activity as well as endocrine activities. They are categorized as low-pressure and high-pressure baroreceptor systems. Low-pressure baroreceptors are located in the cardiac atria, particularly the left atrium. The high-pressure barorecep-tors are nerve endings in the aortic arch and in the cardiac sinus. Another high-pressure baroreceptor is located in the afferent arteriole of the juxtaglomerular apparatus of the nephron.
As arterial pressure decreases, baroreceptors transmit fewer im-pulses from the carotid sinuses and the aortic arch to the vasomotor center. A decrease in impulses stimulates the sympathetic nervous system and inhibits the parasympathetic nervous system. The out-come is an increase in cardiac rate, conduction, and contractility and in circulating blood volume. Sympathetic stimulation constricts renal arterioles; this increases the release of aldosterone, decreases glomerular filtration, and increases sodium and water reabsorption.
Renin is an enzyme that converts angiotensinogen, an inactive substance formed by the liver, into angiotensin I. Renin is released by the juxtaglomerular cells of the kidneys in response to decreased renal perfusion. Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II. Angiotensin II, with its vasocon-strictor properties, increases arterial perfusion pressure and stim-ulates thirst. As the sympathetic nervous system is stimulated, aldosterone is released in response to an increased release of renin. Aldosterone is a volume regulator and is also released as serum potassium increases, serum sodium decreases, or adrenocortico-tropic hormone increases.
ADH and the thirst mechanism have important roles in main-taining sodium concentration and oral intake of fluids. Oral intake is controlled by the thirst center located in the hypothalamus. As serum concentration or osmolality increases or blood volume de-creases, neurons in the hypothalamus are stimulated by intra-cellular dehydration; thirst then occurs, and the person increases oral intake of fluids. Water excretion is controlled by ADH, aldosterone, and baroreceptors, as mentioned previously. The presence or absence of ADH is the most significant factor in deter-mining whether the urine that is excreted is concentrated or dilute.
Located on the surface of the hypothalamus, osmoreceptors sense changes in sodium concentration. As osmotic pressure increases, the neurons become dehydrated and quickly release impulses to the pos-terior pituitary, which increases the release of ADH. ADH travels in the blood to the kidneys, where it alters permeability to water, causing increased reabsorption of water and decreased urine output. The retained water dilutes the ECF and returns its concentration to normal. Restoration of normal osmotic pressure provides feedback to the osmoreceptors to inhibit further ADH release (see Fig. 14-2).
Atrial natriuretic peptide (ANP) is released by cardiac cells in the atria of the heart in response to increased atrial pressure.
Any disorder that results in volume expansion or increased cardiac filling pressures (eg, high sodium intake, heart failure, chronic renal fail-ure, atrial tachycardia, or use of vasoconstrictor agents) will increase the release of ANP. The action of ANP is the direct opposite of the renin–angiotensin–aldosterone system and decreases blood pressure and volume (Fig. 14-3). The ANP measured in plasma is normally 20 to 77 pg/mL (20—77 ng/L). This level increases in acute heart failure, paroxysmal atrial tachycardia, hyperthy-roidism, subarachnoid hemorrhage, and small cell lung cancer.The level decreases in chronic heart failure and with the use of medications such as urea (Ureaphil) and prazosin (Minipress).
Normal physiologic changes of aging, including reduced renal and respiratory function and reserve and alterations in the ratio of body fluids to muscle mass, may alter the responses of an elderly person to fluid and electrolyte changes and acid–base disturbances.
In addition, the frequent use of medications in older adults can affect renal and cardiac function and fluid balance, thereby increasing the likelihood of fluid and electrolyte disturbances. Routine pro-cedures, such as the vigorous administration of laxatives before colon x-ray studies, may produce a serious fluid volume deficit, necessitating the use of intravenous (IV) fluids to prevent hy-potension and other effects of hypovolemia.
Alterations in fluid and electrolyte balance that may produce minor changes in young and middle-aged adults have the poten-tial to produce profound changes in older adults, accompanied by a rapid onset of signs and symptoms. In other elderly patients, the clinical manifestations of fluid and electrolyte disturbances may be subtle or atypical. For example, fluid deficit or reduced sodium levels (hyponatremia) may cause confusion in the elderly person, whereas in young and middle-aged people the first sign commonly is increased thirst. Rapid infusion of an excessive vol-ume of IV fluids may produce fluid overload and cardiac failure in the elderly patient. These reactions are likely to occur more quickly and with the administration of smaller volumes of fluid than in healthy young and middle-aged adults because of the de-creased cardiac reserve and reduced renal function that accom-pany aging.
Increased sensitivity to fluid and electrolyte changes in the elderly patient requires careful assessment, with attention to in-take and output of fluids from all sources and to changes in daily weight; careful monitoring of side effects and interactions of med-ications; and prompt reporting and management of disturbances.
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