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and electrolytes are present in body cells, in the tissue spaces between the
cells, and in the blood that fills the vascular compartment. Body fluids transport gases, nutrients, and
wastes; help generate the electrical activity needed to power body functions;
take part in the transforming of energy; and otherwise maintain the overall
function of the body.
Environmental stresses and disease can disrupt these processes
the intracellular fluid (ICF) compartment consists of fluid contained
within all of the billions of cells in the body. It contains
approximately two thirds of the body water in healthy adults, and is
the larger of the two compartments. The remaining one third of body
water is in the extracellular fluid (ECF) compartment, which contains
all the fluids outside the cells, including that in the interstitial or
tissue spaces and blood vessels
- The composition of the ICF and ECF are strikingly different. The ECF, including the plasma and interstitial fluids, contains large amounts of
- sodium and chloride, moderate amounts of bicarbonate, but only small quantities of potassium, magnesium, calcium, and phosphate. In contrast to the ECF, the ICF contains almost no calcium; small amounts of sodium,
- chloride, bicarbonate, and phosphate; moderate amounts of magnesium;
- and large amounts of potassium (Table 8-1).
- Although blood levels usually are representative of the total body
- levels of an electrolyte, this is not always the case, particularly with
- potassium, which is approximately 28 times more concentrated inside the
- cell than outside. It is the ECF levels of electrolytes in the blood or
- blood plasma that are measured clinically
Body water, which constitutes a high percentage of body weight, is
distributed between the ICF and ECF compartments. In the adult, the
fluid in the ICF compartment constitutes approximately 40% of body
weight and that in the ECF approximately 20% of body weight
•Intracellular compartment (ICF) (66%)
The fluid in the ECF compartment is further divided into two major
the plasma compartment, which constitutes approximately 5% of body weight
the interstitial fluid compartment, which constitutes approximately 14% of body weight
A third, usually minor, subdivision of the ECF compartment is the
- transcellular compartment. It includes the cerebrospinal fluid and fluid contained in the various body spaces, such as the peritoneal, pleural, and pericardial cavities, and joint spaces. Normally, only about 1% of ECF is in the transcellular space. This amount can increase considerably in conditions such as ascites, in which large amounts of fluid are
- sequestered in the peritoneal cavity. When the transcellular fluid compartment becomes considerably enlarged, it is referred to as a third
- space, because this fluid is not readily available for exchange with the rest of the ECF.
Transport across the cell membrane
- Osmosis is the movement of water across a semipermeable membrane (i.e.,
- one that is permeable to water but impermeable to most solutes) As with solute particles, water diffuses down its concentration
- gradient, moving from the side of the membrane with greater concentration of water and lesser concentration of solute particles to
- the side with lesser concentration of water and greater concentration of solute particles. As water moves across the semipermeable membrane, it generates a pressure called the osmotic pressure.
- The magnitude of the osmotic pressure represents the hydrostatic pressure (measured in millimeters of mercury [mm Hg]) needed to oppose
- the movement of water across the membrane.
- Diffusion is the movement of charged or uncharged particles along a concentration
- gradient. All molecules and ions, including water and dissolved molecules, are in constant random motion. It is the motion of these particles, each colliding with one another, that supplies the energy for diffusion. Because there are more molecules in constant motion in a concentrated solution, particles move from an area of higher concentration to one of lower concentration.
uses transport protein to transfer molecules like glucose that can't get across the membrane
- Among the substances that are transported by primary active transport are sodium, potassium, calcium, and hydrogen ions. The active transport system studied in the greatest detail is the sodium/potassium (Na+/K+)-adenosine triphosphatase (ATPase) membrane pump. The Na+/K+-ATPase membrane pump moves sodium from inside the cell to the extracellular
- region, where its concentration is approximately 14 times greater than inside; the pump also returns potassium to the inside, where its concentration is approximately 35 times greater than it is outside the cell. If it were not for the activity of the Na+/K+-ATPase membrane pump, the osmotically active sodium particles would accumulate in the cell, causing cellular swelling because of an accompanying influx of water.
- Secondary active transport mechanisms harness the energy derived from the primary active transport of one substance, usually sodium, for the cotransport of a second substance. For example, when sodium ions are actively transported out of a cell by primary active transport,
- a large concentration gradient develops (i.e., high concentration on
- the outside and low on the inside). This concentration gradient
- represents a large storehouse of energy because sodium ions are always
- attempting to diffuse into the cell. Similar to facilitated diffusion,
- secondary transport mechanisms use membrane transport proteins. These proteins have two binding sites: one for sodium and the other for the substance undergoing secondary transport. Secondary transport systems are classified into two groups: cotransport, or symport, systems, in which sodium and the solute are transported in the same direction, and countertransport, or antiport, systems, in which sodium and the solute are transported in the opposite directions.
- Fluid accumulating in the
- interstitial space (between the cells) or palpable
- swelling produced by expansion of the interstitial fluid
- “Localized”-from injury
- “Generalized”-usually secondary
- to a condition: heart disease, liver disorder (anasarca)
- "Specific” to an organ: brain,
- “Dependent”-due to the effects of
- ASSESSMENT AND TREATMENT
- Daily weight, visual assment, measurement of the affected part, application of finger pressure to asses for pitting edema.
mechanisms that contribute to edema:
- •Increase in capillary filtration
- •Decrease in capillary colloidal
- osmotic pressure
- •Increase in capillary
–Burns, capillary congestion, inflammation, immune responses
•Obstruction in lymph flow
the fluid part of a solution
substance dissolved in a solution
# of particles per unit volume
concentration of solute equal to that in most cells
- concentration greater than in most
- cells-CELLS SHRINK
concentration less than in most cells-CELLS SWELL
separate into electrically charged particles called ions
Anions have a
Disorders of Electrolyte Balance
Serum Na+ <135 mEq/L
A number of age-related events make the elderly population more vulnerable to hyponatremia, including a decrease in renal function accompanied by limitations in sodium conservation. Although older people maintain body fluid homeostasis under most circumstances, the ability to withstand environmental, drug-related, and disease-associated stresses becomes progressively limited.ecause of water movement, hyponatremia produces an increase in intracellular water, which is responsible for many of the clinical manifestations of the disorder
Decreased serum osmolalityDilutional decrease in blood components, including hematocrit, blood urea nitrogen (BUN)
Signs and Symptoms of Hyponatremia
- Muscle cramps and weakness Depressed deep tendon reflexes
- Central Nervous System
- HeadacheDisorientationLethargySeizures and coma (severe)
- Gastrointestinal Tract
- Anorexia, nausea, vomitingAbdominal cramps, diarrhea
- ADH, antidiuretic hormone
- –Serum Na+>145 mEq/L
- Hypernatremia is characterized by hypertonicity of extracellular fluids and almost always causes cellular dehydration
Hypernatremia represents a deficit of water in relation to the body’s sodium stores. It can be caused by net loss of water or sodium gain. Net water loss can occur through the urine, gastrointestinal tract, lungs, or skin. A defect in thirst or inability to obtain or drink water can interfere with water replacement. Rapid ingestion or infusion of sodium with insufficient time or opportunity for water ingestion can produce a disproportionate gain in sodium.Hypernatremia occurs when there is an excess loss of body fluids that have a lower than normal concentration of sodium so that water is lost in excess of sodium. This can result from increased losses from the respiratory tract during fever or strenuous exercise, from watery diarrhea, or when osmotically active tube feedings are given with inadequate amounts of water
S/S of Hypernatremia
- Compensatory Mechanisms
- Increased thirstIncreased ADH with oliguria and high urine-specific gravity Decreased Intracellular Fluid
- Dry skin and mucous membranesDecreased tissue turgor
- Decreased salivation and lacrimation
- Hyperosmolality and Movement of Water out of Neural Tissue
- Headache Disorientation and agitation Decreased reflexes Seizures and coma (severe)Decreased Vascular VolumeWeak, rapid pulsePossible impaired temperature regulation with feverDecreased blood pressureVascular collapse (severe)
Hypokalemia represents a decrease in serum potassium levels to below 3.5 mEq/L (3.5 mmol/L). It can result from inadequate intake, excessive losses, or redistribution between the ICF and ECF compartments. The manifestations of potassium deficit include alterations in renal, skeletal muscle, gastrointestinal, and cardiovascular function, reflecting the crucial role of potassium in cell metabolism and neuromuscular function.
Anorexia, nausea, vomitingAbdominal distentionParalytic ileus (severe hypokalemia)NeuromuscularMuscle weakness, flabbiness, fatigueMuscle cramps and tendernessParesthesiasParalysis (severe hypokalemia)Central Nervous SystemConfusion, depressionCardiovascularPostural hypotensionPredisposition to digitalis toxicityElectrocardiogram changesCardiac arrhythmias
Hyperkalemia represents an increase in serum potassium to levels greater than 5.0 mEq/L (5.0 mmol/L). It seldom occurs in healthy persons because the body is extremely effective in preventing excess potassium accumulation in the ECF. The major causes of potassium excess are decreased elimination of potassium by the kidney, a transcellular shift in potassium from the ICF into the ECF compartment, and excessively rapid intravenous administration of potassium. The most serious effect of hyperkalemia is on the heart and development of serious and even fatal arrhythmias
Nausea, vomitingIntestinal crampsDiarrheaNeuromuscularWeakness, dizzinessMuscle crampsParesthesiasParalysis (severe hyperkalemia)CardiovascularElectrocardiogram changesRisk of cardiac arrest with severe hyperkalemia
Hypocalcemia represents a total serum calcium level of less than 8.5 mg/dL (2.1 mmol/L) and an ionized calcium level of less than 4.6 mg/dL (1.2 mmol/L). A pseudo-hypocalcemia is caused by hypoalbuminemia. It results in a decrease in protein-bound, rather than ionized, calcium and usually is asymptomatic.43 Thus, before a diagnosis of hypocalcemia can be made, the total calcium should be corrected for low albumin levels.
The most common causes of hypocalcemia are abnormal losses of calcium from the kidney, impaired ability to mobilize calcium from bone due to hypoparathyroidism, and increased protein binding or chelation such that greater proportions of calcium are in the nonionized form
S/S of hypocalcemia
- Paresthesias, especially numbness and tinglingSkeletal muscle crampsAbdominal muscle spasms and crampsHyperactive reflexesCarpopedal spasmTetanyLaryngeal spasm HypotensionSigns of cardiac insufficiencyDecreased response to drugs that act by calcium-mediated mechanismsProlongation of the QT interval predisposes to ventricular arrhythmias
- Osteomalacia Bone pain
Hypercalcemia represents a total serum calcium concentration greater than 10.5 mg/dL (2.6 mmol/L). Falsely elevated levels of calcium can result from prolonged drawing of blood with an excessively tight tourniquet. Increased serum albumin levels may also elevate the total serum calcium but not affect the ionized calcium.
Hypercalcemia occurs when calcium movement into the circulation overwhelms calcium regulatory hormones or the ability of the kidney to remove excess calcium ions. The two most common causes of hypercalcemia are increased bone resorption due to neoplasms and hyperparathyroidism
- PolyuriaIncreased thirstFlank painSigns of acute renal insufficiencySigns of kidney stones
- Neural and Muscle Effects (Decreased Excitability)Muscle weaknessAtaxia, loss of muscle toneLethargyPersonality and behavioral changesStupor and coma
- Cardiovascular EffectsHypertensionShortening of the QT intervalAtrioventricular block
- Gastrointestinal EffectsAnorexiaNausea, vomitingConstipation
Magnesium deficiency refers to depletion of total body stores, while severe hypomagnesemia describes a low serum magnesium concentration of less than 1.8 mg/dL (0.75 mmol/L).58 It is seen in conditions that limit intake or increase intestinal or renal losses, and it is a common finding in patients in emergency departments and critical care units
Neural and Muscle EffectsPersonality changesAthetoid or choreiform movementsNystagmusTetany TachycardiaHypertensionCardiac arrhythmias
Hypermagnesemia represents an increase in total body magnesium and a serum magnesium concentration in excess of 2.6 mg/dL (1.1 mmol/L). Because of the ability of the normal kidney to excrete magnesium, hypermagnesemia is rare
When hypermagnesemia does occur, it usually is related to renal insufficiency and the injudicious use of magnesium-containing medications such as antacids, mineral supplements, or laxatives. The elderly are particularly at risk because they have age-related reductions in kidney function and tend to consume more magnesium-containing medications, including antacids and laxatives. Magnesium sulfate is used to treat toxemia of pregnancy and premature labor; in these cases, careful monitoring for signs of hypermagnesemia is essential
S/S of hypermagnesemia
The signs and symptoms occur only when serum magnesium levels exceed 4.8 mg/dL (2.0 mmol/L).58 Because magnesium tends to suppress PTH secretion, hypocalcemia may accompany hypermagnesemia.Hypermagnesemia affects neuromuscular and cardiovascular function (see Table 8-7). Increased levels of magnesium decrease acetylcholine release at the myoneural junction, causing hyporeflexia and muscle weakness. Cardiovascular effects are related to the calcium channel–blocking effects of magnesium. Blood pressure is decreased, and the ECG shows an increase in the PR interval, a shortening of the QT interval, T-wave abnormalities, and prolongation of the QRS and PR intervals. Severe hypermagnesemia is associated with muscle and respiratory paralysis, complete heart block, and cardiac arrest
more S/S of hypermagnesemia
- Cardiovascular EffectsHypotensionCardiac arrhythmiasCardiac arrest
Sodium and Water
- suction, vomitting, diarrhea, fistulas (loss Na)
there are baroreceptors located in the low-pressure side of the circulation (walls of the cardiac atria and large pulmonary vessels) that respond primarily to fullness of the circulation. Baroreceptors are also present in the high-pressure arterial side of the circulation (aortic arch and carotid sinus) that respond primarily to changes in the arterial pressure. The activity of both types of receptors regulates renal sodium and water elimination by modulating sympathetic nervous system outflow and antidiuretic hormone (ADH) secretion
•SNS-The sympathetic nervous system
responds to changes in arterial pressure and blood volume by adjusting the glomerular filtration rate and thus the rate at which sodium is filtered from the blood. Sympathetic activity also regulates tubular reabsorption of sodium and renin release. ADH, which is secreted from the posterior pituitary glands, controls the permeability of the collecting tubules and ducts of the kidney to water, thereby regulating the amount of water that is lost in the urine.
- (vasoconstriction, water retention, corticotrophin)
- in hypothalamus
•Thirst ;polydipsia - excessive thirst. hypodipsia - decrease in ability to sense thirst
•ANP- An additional mechanism that influences sodium excretion by the kidney is the atrial natriuretic peptide (ANP). ANP, which is released from the heart in response to atrial stretch and overfilling, increases the excretion of sodium by the distal and collecting tubules of the kidney
•RAAS - Pressure-sensitive receptors in kidney, particularly in the afferent arterioles, respond directly to changes in arterial pressure through stimulation of the sympathetic nervous system and release of renin with activation of the renin-angiotensin-aldosterone system (RAAS).11 The RAAS exerts its action through angiotensin II and aldosterone (see Chapter 18). Angiotensin II acts directly on the renal tubules to increase sodium reabsorption. It also acts to constrict renal blood vessels, thereby decreasing the glomerular filtration rate and slowing renal blood flow so that less sodium is filtered and more is reabsorbed. Angiotensin II is also a powerful regulator of aldosterone, a hormone secreted by the adrenal cortex. Aldosterone acts at the level of the cortical collecting tubules of the kidneys to increase sodium reabsorption while increasing potassium elimination.
- fluid deficit or excess vs. hyponatremia or hypernatremia
Isotonic fluid volume deficit results when water and electrolytes are lost in isotonic proportions. It is almost always caused by a loss of body fluids and is often accompanied by a decrease in fluid intake The manifestations of fluid volume deficit reflect a decrease in ECF volume. They include thirst, loss of body weight, signs of water conservation by the kidney, impaired temperature regulation, and signs of reduced interstitial and vascular volumes
Hyponatremia or hypernatremia that is brought about by disproportionate losses or gains in sodium or water exerts its effects on the ICF compartment, causing water to move in or out of body cells. Many of the manifestations of changes in sodium concentration reflect changes in the intracellular volume of cells, particularly those in the nervous system.
Arterial Blood Gases:
a laboratory specimen measuring O2, CO2, pH and HCO3 in arterial blood
- PH: 7.35 – 7.45
- pCO2 : 35 – 45 mm Hg
- HCO3: 22-26 mEq/L
in acid-base balance will cause:
- by retention of CO2 from respiratory disease, O.D. (hypoventilation), trauma
- (chest / airway)
- Respiratory acidosis is associated with a serum pH below 7.35 and an arterial PCO2 above 50 mm Hg. The signs and symptoms of respiratory acidosis (Table 8-10) depend on the rapidity of onset and whether the condition is acute or chronic. Because respiratory acidosis often is accompanied by hypoxemia, the manifestations of respiratory acidosis often are intermixed with those of oxygen deficit. Carbon dioxide readily crosses the blood-brain barrier, exerting its effects by changing the pH of brain fluids. Elevated levels of CO2 produce vasodilation of cerebral blood vessels, causing headache, blurred vision, irritability, muscle twitching, and psychological disturbances. If the condition is severe and prolonged, it can cause an increase in CSF pressure and papilledema. Impaired consciousness, ranging from lethargy to coma, develops as the PCO2 rises to extreme levels. Paralysis of extremities may occur, and there may be respiratory depression. Less severe forms of acidosis often are accompanied by warm and flushed skin, weakness, and tachycardia
- is to increase oxygen intake.
- by excessive elimination of carbon dioxide (hyperventilation syndrome)
- and symptoms The signs and symptoms of respiratory alkalosis are associated with hyperexcitability of the nervous system and a decrease in cerebral blood flow (Table 8-10). Alkalosis increases protein binding of extracellular calcium. This reduces ionized calcium levels, causing an increase in neuromuscular excitability. A decrease in the CO2 content of the blood causes constriction of cerebral blood vessels. Because CO2 crosses the blood-brain barrier rather quickly, the manifestations of acute respiratory alkalosis are usually of sudden onset. The person often experiences light-headedness, dizziness, tingling, and numbness of the fingers and toes. These manifestations may be accompanied by sweating, palpitations, panic, air hunger, and dyspnea. Chvostek and Trousseau signs may be positive, and tetany and convulsions may occur. Because CO2 provides the stimulus for short-term regulation of respiration, short periods of apnea may occur in persons with acute episodes of hyperventilation.
- is to assist patient to retain CO2 (breathe into a paper bag, calm
- them down)
- by production of lactic acid secondary to illness, NVD, renal failure, sepsis,
- diabetic ketoacidosis
- and symptoms
- Metabolic acidosis is characterized by a decrease in serum pH (<7.35) and HCO3− levels (<24 mEq/L) due to H+ gain or HCO3− loss. Acidosis typically produces a compensatory increase in respiratory rate with a decrease in PCO2. The manifestations of metabolic acidosis fall into three categories: signs and symptoms of the disorder causing the acidosis, changes in body function related to recruitment of compensatory mechanisms, and alterations in cardiovascular, neurologic, and musculoskeletal function resulting from the decreased pH (Table 8-9). The signs and symptoms of metabolic acidosis usually begin to appear when the serum HCO3− concentration falls to 20 mEq/L or less. A fall in pH to less than 7.0 to 7.10 can reduce cardiac contractility and predispose to potentially fatal cardiac dyrhythmias.1
- ventilation (elimination of CO2 subsequently decreases hydrogen ions); fix
- underlying cause; if extreme give NaHCO3
- by excessive use of antacids and some diruetics
- and Symptoms
- Respiratory alkalosis manifests with a decrease in PCO2 and a deficit in H2CO3. In respiratory alkalosis, the pH is above 7.45, arterial PCO2 is below 35 mm Hg, and serum HCO3− levels usually are below 24 mEq/L (24 mmol/L).The signs and symptoms of respiratory alkalosis are associated with hyperexcitability of the nervous system and a decrease in cerebral blood flow (Table 8-10). Alkalosis increases protein binding of extracellular calcium. This reduces ionized calcium levels, causing an increase in neuromuscular excitability. A decrease in the CO2 content of the blood causes constriction of cerebral blood vessels. Because CO2 crosses the blood-brain barrier rather quickly, the manifestations of acute respiratory alkalosis are usually of sudden onset. The person often experiences light-headedness, dizziness, tingling, and numbness of the fingers and toes. These manifestations may be accompanied by sweating, palpitations, panic, air hunger, and dyspnea. Chvostek and Trousseau signs may be positive, and tetany and convulsions may occur. Because CO2 provides the stimulus for short-term regulation of respiration, short periods of apnea may occur in persons with acute episodes of hyperventilation.
- is to correct underlying cause.
are three mechanisms to regulate acid-base balance in the body:
–Bicarbonate buffer system
- –Transcellular hydrogen-potassium exchange
Bicarbonate buffer system
- components: bicarbonate (HCO3
- and carbonic acid (H2CO3)
- combines with hydrogen to form carbonic acid (H2CO3). It acts as a sponge, soaking it up.
- acid will then dissociate into water and carbon dioxide.
- in pCO2 causes:
- Increased respirations to eliminate CO2 which
- causes a decrease hydrogen ion and an increase in pH.
- minutes to correct problem.
- kidneys retain or secrete H+ and HCO3- as needed.
- take hours to days to correct.
- Look at pH first. Is it normal, acidotic or alkalotic?
- Look at pCO2 next. Is it normal, high (acidotic) or low
***If pCO2 is inverse with pH, it’s a respiratory problem.
- Look at HCO3 next. Is it normal, low (acidotic) or high
- ***If HCO3 is direct
- pH, it’s a metabolic problem.
what is compensation?
Compensatory mechanisms provide a means to control pH when correction is impossible or cannot be immediately achieved. Often, compensatory mechanisms are interim measures that permit survival while the body attempts to correct the primary disorder. Compensation requires the use of mechanisms that are different from those that caused the primary disorder. For example, the lungs cannot compensate for respiratory acidosis that is caused by lung disease, nor can the kidneys compensate for metabolic acidosis that occurs because of chronic kidney disease. The body can, however, use renal mechanisms to compensate for respiratory-induced changes in pH, and it can use respiratory mechanisms to compensate for metabolically induced changes in acid-base balance. Because compensatory mechanisms become more effective with time, there are often differences between the level of pH change that is present in acute and chronic acid-base disorders.