CHAPTER+THREE+NOTES

CHAPTER 3: THE CELLULAR ENVIRONMENT FLUIDS AND ELECTROLYTES, ACIDS AND BASES

YEEHAWWWW, HERE WE GO.......

(Cited references are for the information found on the linked pages, with the exception of the acid-base information at the bottom of this page)

DISTRIBUTION OF BODY FLUIDS Fluids of the body are distributed among functional compartments and provide a transport medium for cellular and tissue function. (see table 3-8 for listing of electrolytes in body fluids) ( links outside of Wiki, use your back button to return) There is a similar table on page114, but I like this one better because it shows the relationship between the values better, I think
 * Distribution
 * Intracellular fluid (ICF) makes up 2/3 of body fluid
 * extracellular fluid (ECF) is remaining 1/3
 * Two main ECF compartments are interstitial fluid (in tissues) and intravascular fluid
 * Other ECF comparments include the lymph system, joints, biliary, hepatic, pancreast, CSF, pericardial, urine
 * Sum of all fluids constitutes the total body water (table 3-1) Usally about 60% of body weight.
 * Aging and Distribution
 * Infant TBW=75%
 * First year TBW=67%
 * Childhood TBW=60-65%
 * Adolescence TBW approaches adult proportions and gender differences appear
 * With age, TBW decreases
 * Water movement between ICF and ECF is primarily a function of [|osmosis] (Brown, 1999) links out of Wikispace, use your back button to return
 * Sodium maintains balance of ECF
 * Potassium maintanins osmotic balance of ICF
 * Osmotic force of ICF protiens and non diffusable substances is maintained by active transport
 * Water movement between Plasma and Interstitial fluid
 * occur as a result of changes in hydrostatic pressur and osmotic forces at the arterial and venous ends of capillaries
 * Aquaporins are a family of water channel protiens that provide permeability to water at the capillary membrane
 * Osmotic forces in the capillaries are balanced by the hydrostatic pressure arising from cardiac contraction
 * Starling hypothesis states net filtration (across capillary membranes) = forces favoring filtration - forces opposing filtration
 * Forces favoring: hydrostatic pressure and interstitial oncotic pressure
 * forces opposing: plasma oncotic pressure and interstitial hydrostatic pressure
 * Alterations in water movement
 * Edema is the accumulation of fluid in the interstitial space.
 * problem of distribution and does not always indicate overload
 * common mechanisms are increased hydrostatic pressure, decreased plasma oncotic pressure, increased permeability of capillaries, and lymphatic obstruction
 * Increased hydrostatic pressure can result from veouns obstruction or salt and water retention
 * venous obstruction can increase the hydrostatic pressure and force fluids into the interstitial space
 * loss or decrease of plasma production decreases plasma oncotic pressure.
 * inflammation and immune response increase capillary permeability
 * lymphedema (Lymphedema therapy) occurs when lympatic channels are obstructed or surgically absent.
 * Clinical manifestations of edema
 * localized(Loyola Univeristy Medical Education Network) or generalized
 * often dependent
 * edematous fluids are trapped in the "third space" and not available for physiologic processes.
 * Sodium, Chloride, and water balance
 * water balance maintained by secretion of ADH and perception of thirst.
 * thirst is experienced when 2% of the body's fluids are lost, or when a change in osmality occurs
 * ADH secreted when plasma osmality increases, or blood pressure lowers
 * increased plasma osmality occurs with a deficit of water, or excess of sodium in relation to water
 * increased osmality results in decreased interstitial and extracellular fluid volume and stimulates osmoreceptors in the hypothalmus, and releases ADH.
 * ADH regulated by a feedback mechanism
 * with volume depletion, volume-sensitive receptors and baroreceptors stimulate release of ADH
 * baroreceptors are mainly in the heart and large arteries
 * Sodium accounts for 90% of ECF cations and regulates osmotic forces, and therefore water blance.
 * Chloride is the major anion in the ECF and provides electroneutrality, generally follows sodium
 * hormonal regulation of sodium is mediated by aldosterone, secreted from the adrenal cortex
 * kidneys regulate sodium balance mainly throu renal tubular reabsorption
 * when blood volume is reduced, renin is secreted by the juxtaglomerular cells of the kidney and stimulates the production of angiotensin I
 * Angiontensin I is converted to Angiotensi II, whcih acts as a hormone and stimulates the secretion of aldosterone and causes vasoconstriction
 * this cyle is known as the renin-angiotensin system
 * natriuretic peptids are hormones produced by the heart and kidneys that work to decrease blood pressure and increase sodium and water excretion when there is an increase in circulating volume
 * Alterations in sodium, chloride, and water balance
 * Isotonic alterations are accompanied by proportional changes in electrolytes and water
 * Hypertonic changes develop when the osmoloality of the ECF is elevated, usually caused by increased sodium or a loss of free water
 * hypernatremia occurs when serum sodium exceeds 147 meq/L. May be caused by acute gain of sodium such as adminstration of sodium bicarbonate, or loss of free water, or because of disease such as Cushings or primary hyperaldosteronism
 * clinical manifestations included convulsions and pulmonary edema, third spacing are most serious. Thirst, fever, dry mucous membranes, hypotension, tachycardia, low jugular venous pressure, and restlessness are associated with hypernatremia as a result of water loss
 * Treatment is D5W until the serum sodium level returns to normal
 * Water deficit may be dehydration (which includes loss of electrolytes as well) or loss of free water, usually caused by increased renal clearance due to underlying pathology such as diabetes insipidus. Comatose patients may also experience insensible water losses
 * Treatment is also D5W
 * Hyperchloremia occurs when there is an excess of sodium, or a deficit of bicarbonate
 * expected with hypernatremia or metabolic acidosis
 * treatment of underlying disorder resolves hyperchloremia
 * Hypotonic Alterations occur when the osmolality of the ECF is less than normal
 * most common cause is sodium deficit
 * serum sodium less than 135 meq/L
 * usually cause hypoosmololity with cell swelling
 * may be caused by diuretic medications
 * see table 3-7 for causes and consequences of hypotonic imbalances
 * Hypertonic hyponatremia develops with hyperlipidemia, hyperprotienemia, and hyperlycemia. Hyerpglycemia increases ECF osmolality and attracts water from ICF compartment and dilutes the ECF sodium concentration
 * symptoms are behavioral and neurologic changes such as lethargy, headache, confusion, apprehension, siezures and coma.
 * pure sodium losses result in hypovolmia with symptoms of hypotension, tachycardia, decreased urine output.
 * dilutional hyponatremia symptoms include weight gain, edema, ascites, and jugular vein distention
 * treatment related to contributing disorder
 * Water excess is almost impossible under normal circumstances. However, some compulsive water drinkers can develop water intoxication. Acute renal failure, severe CHF, and cirrhosis may also precipitate water excess. the syndrome of inappropriate secretion of ADH (SIADH) can also cause water excess.
 * symptoms are related to the rate of water intake and include convulsions, cerebral edema with confution, weakness, nausea, muscle twitching, headache and weight gain are common in chronic cases
 * ALTERATIONS IN POTASSIUM, CALCIUM, PHOSPHATE, AND MAGNESIUM BALANCE
 * Potassium is the major intracelllular electrolyte and contributes to many cellular functions
 * regulates ICF osmolality and provides the balance for intracellular electrical neutrality in relation to H+ an Na+
 * dietary intake, aldosterone, and distal tubule urine flow determine the amount of K+ excreted from the boy.
 * renal mechanism for conserving K+ is weak, even when stores are near depletion.
 * Changes in pH and thus in H+ also affect K+ balance. H+ moves from the ECF to the ICF during acidotic states, thereby diluting K+ in the urine. Body thinks you are short, so begins to retain it, and this results in serum Hyperkalemia.
 * Aldosterone is a major factor in regulating K+; increases excretion in urine and sweat
 * Insulin contributes to regulation of K+ by stimulating the sodium-Potatssiump-ATPase pump
 * Catecholoamines also influence K+ concentration in the ECF.
 * Hypokalemia
 * serum potassium less than 3.5 meq/L. changes in total body potassium are not always reflected in serum potassium.
 * semi-trivial info again; if you have encountered the practice of giving a patient K+ because their potassium is low, then redrawing labs after infusion, your lab results are not truly reflective of the K+ status of your patient. Just because we dump a bunch of K+ into their blood stream doesn't mean its gone into the ICF where it needs to be to do its job. K+ loading is a particularly dangerous practice when it comes to surgical patients, since anesthetics already stress the heart, and serum K+ is not available to cardiac muscle to use; The K+ has to be inside the heart muscle cells before there is a demand for it. The end result may be arrythmias upon adminstration of anesthetics because the patient's //__tissues__// are still hypokalemic, even though their //__serum__// K+ reached the magic we-can-do-surgery-now number of 3.5. It is a potentially fatal practice.
 * plasma K+ may be normal or elevated when total body potassium is depleted (hey, I just said that!). In such instances, K+ shifts from the ICF to the ECF. One common cause of this is diabetic ketoacidosis. The K+ shifts results because the body is attempting to normalize pH.
 * Severe, even fatal, hypokalemia may occur if insulin is administered without also providing K+ supplements.
 * K+ losses are most commonly caused by gastrointestinal and renal disorders, with diarrhea probably being the most common.
 * Many kidney diseases result in a reduced ability to conserve sodium. The disordered sodium reabsorption creates a diuretic affect, and the increased distal tubule flow favors the secretion of potassium.
 * Several antibiotics including amphotericin B, gentamicin, and carbenicillin (aminoglycocides) are known to cause hypokalemia
 * clinical manifestations
 * metabolic dysfunction including carbohydrate metabolism, depressed insulin secretion, and glygogen synthesis
 * neuromuscular and cardiac effects produce most common symptoms including skeletal muscle weakness, smooth muscle atony, and cardiac dysrhythmias. See page 105 for discussion of membrane excitability and K+.
 * Hyperkalemia
 * Serum potassium above 5.5 meq/L constitutes hyperkalemia.
 * may be caused by increased intake, a shift of potassium to the ECF, or decreased reanal excretion
 * shift to ECF may be caused by cell trauma or chaning in permiabeility, acidosis, insulin deficiency, or cell hypoxia.
 * Burns, massive crush injuries and extensive surgery can cause a potassium shift to the ECF
 * In acidosis, H+ shifts ino the cells in exchange for K+ and Na+, hyperkalemia and acidosis therefore often occur together
 * Renal failure that results in oliguria (< 30 ml/hr) is accompanied by elevations of serum potassium
 * clinical manifestations
 * muscle weakness or paralysis
 * EKG changes and arrhythmias; Narrow tall T waves, with a shortened QT interval, depressed ST, prolonged PR interval and a widened QRS
 * neuromuscular irritability which manifests as tingling of lips and fingers
 * restlessness
 * intestinal cramping and diarrhea
 * Cell membranes become hyperpolarized so the inside of the cell becomes less negative, and the cell can repolarize more quickly (irritability)
 * Evaluation and treatment
 * related to treating underlying causes and correcting the xcess.
 * Calcium gluconate can be administered to restore normal neuromuscular irritability when K+ is dangerously high
 * Administration of Glucose (with insulin for diabetics) facilitates cellular entry of K+
 * dialysis effectively removes K+ in renal failure
 * CALCIUM AND PHOSPHATE
 * Calcium is neccessary ion for many metabolic processes
 * major cation for formation of bone and teeth
 * enzymatic cofactor for blood clottin
 * hormone secretion and cell receptors
 * regulates membrane stability and permeability
 * transmission of nerve impulses and muscle contraction
 * Phosphate is primarily in bone, with small amounts in fluid
 * High energy form ATP and creatine phosphate
 * anion buffer in the regualtion of acid-base balance
 * in the form of ATP provides energy for muscle contraction
 * Calcium and phosphate levels controlled by parathyroid hormone (PTH), vitamin D, and calcitonin
 * controls GI absorption, depostion and absorption from bone, and reabsorbtion and excretion from the kidneys
 * Hypocalcemia -serum concentration <8.5 mg/dl and ionized levels <4.0 mg/dl.
 * Deficits related to inadequate absorption, deposition of calcium to bone or other tissues, blood administration, or decreases in PTH or vitamin D
 * nutritional deficits may occur in the avoidance of dairy products, or consumption of large amounts of phosphorus (its found in sodas, BTW), The citrate solution used to store whole blood in binds with calcium
 * Vitamin D deficiency, can result from inadequate intake or avoidance of sunlight and causes decreased intestinal absorption of calcium
 * Clinical Manifestations
 * increase in neuromuscular excitability. Calcium deficits cause partial depolarization of nerves and muscles
 * Chvostek signs is elicited by tapping on the facial nerve just below the temple and a positive sign in a twitch on the nose or lip
 * Trousseau's sign is positive with contraction of the hand and fingers when the arterial blood flow is occluded for five minutes
 * Severe symptoms include convulsions and tetany
 * characteristic EKG change is a prolonged QT interval
 * Evaluation and Treatment
 * severe condition requires IV adminstration of 10% calcium gluconate.
 * oral calcium replacements initiated and intake of phosphates decreased
 * Hypercalcemia -serum concentration >12 mg.dl
 * can be caused by chronic diseases including hyperparthyroidism, bone mets, sarcoidosis, and excess vitamin D. Many tumors produce PTH and elevate serum calcium. Sarcoid appears to increase vitamin D levels
 * clinical manifestations
 * many symptoms are nonspecific. fatigue, weakness, lethargy, anorexia, nausea, and constipation ore common.
 * kidney stones may form from precipitates of calcium salts
 * A shortened QT segment and depressed T waves may be observed with varying degrees of heart block
 * Evaluation and treatment
 * treatment of underlying disorder
 * when renal function is normal, oral phosphate is effective
 * IV administration of large amounts of normal saline to enhance renal secretion
 * corticosteriods and the cytotoxic drug mirhramycin may also be used as treatment
 * Hypophosphatemia - serum level < 2.0 mg/dl
 * most common cause are malabsorption and renal excretion
 * associated with vitamin D deficiency, use of magnesium and aluminum containing antacids, and long term alcohol abuse
 * clinical manifestations
 * consequences related to reducted capacity of red blood cells to transport oxygen
 * leukocyte and platelet dysfunction may also occur limiting blood clottin ability and increasing risk of infection
 * Nerve and muscle function can be affected because of derangement in energy metabolism.
 * irritability, confusion, numbness, coma, and convulsions may develop
 * muscle weakness severe enough to cause respiratory failure and cardiomyopathies may also develop
 * evaluation and treatment
 * again related to underlying causes. administration of phosphate salts in dangerous, and low levels are not usually life threatening
 * Hyperphosphatemia
 * serum > than 4.5 mg/dl develops with exogenous or endogenous addition of phosphorus to the ECF, or with significant loss of glomerular filtration
 * Cell destruction associated with treatment of metastatic tumors can release large amounts of phophorus into the serum
 * Long term use of phosphate enemas can also contribute to elevated levels
 * clinical manifestations
 * similar to symptoms of hypocalcemia. With prolonged hyperphosphortemia, calicfication of the soft tissues occurs in the lungs, kidneys, and joints.
 * Evaluation and treatment
 * underlying pathologic condition must be treated. Aluminum hydroxide may be administered because it binds with phosphate in the gut and prevents uptake.
 * MAGNESIUM
 * Major intracellular cation, about 40-60 % stored in muscle and bone, with 30% in cells. small amount in serum
 * Hypomagnesemia- serum level < 1.5 meq/l
 * increases in neuromuscular excitability and tetany are present
 * caused by malnutrition, alcholism, renal tubular dysfunction, metabolic acidosis and loop and thiazide diruetics
 * symptoms are muscle weakness, increased reflexes, ataxia, nystagmus, tetany, and convulsions
 * treatment is IV adminstration of Mag sulfate
 * Hypermagnesemia- serum level > 2.5 meq/L i
 * rare and usually caused by renal failure
 * depresses skeletal muscle contraction and nerve function,
 * symptoms include nausea and vomiting, weakness, hypotension, bradycardia, and respiratory depression
 * treatment is removal of mag by dialysis and avoidance of magnesium containing substances
 * ACID BASE BALANCE (OH, LORD, I JUST HATE THIS PART...)
 * Hydrogen Ion and pH
 * H+ concentration is commonly expressed as the pH, the negative logarithm of hydrogen ions in a solution (SEE! Its just no fun at all....)
 * The logarithmic value means that as the pH changes one unit (from 6.0 to 7.0), the H+ changes tenfold.
 * The more H+, the lower the pH, the less H+, the higher the pH. __**Inverse proportion-**__remember that, its important!
 * Different body fluids have different pH values, some are listed on page 110
 * Body acids are formed as end products of metabolism and there are two kinds
 * Volatile acids can be eliminated as carbon dioxide
 * Non volatile acids must be eliminated through the kidneys
 * Thus, the lungs and kidneys, along with the buffer systems, are the primary regulators of acid-base balance
 * Buffer systems
 * Buffering occurs both int he ICG and ECG compartments, and the buffers systems function at different rates
 * Buffers can absorb excessive acid (H+) or excessive base (OH-) without a significant change in pH
 * See table 3-9 for a list of buffer systems
 * Carbonic acid-Bicarbonate buffering
 * operates in both the lungs and the kidneys
 * the greater the Pco2, the more carbonic acid is formed
 * the relationship that exists between carbonic acid (H2CO3) and Carbon dioxide (Pco2) can be expressed as follows
 * H2CO3=0.03 X Pco2(mmHg) where 0.03 is the solubility coefficient of carbon dioxide in water
 * The relationship between bicarbonate and carbonic acid is usually expressed as a ratio. When pH is 7.4, this ratio is 20:1 (bicarb:Carbonic acid)
 * protien buffering- most protien are inside cells, so primarily an intracellular buffer system
 * Hemoglobin is an excellent intracellular buffer because of its ability to bind with H+ and CO2
 * Unsaturated Hemoglobin is a better buffer because it has a better binding capacity
 * See figure 3-9
 * renal buffering - the distal tubule of the kidney regulates acid-base balance by secreting H+ into the urine and reabsorbing bicarbonate
 * Dibasic phosphate and ammonia are two important renal buffers
 * ACID-BASE IMBALANCES
 * H[|ERE IS A GAME YOU CAN PLAY TO LEARN ABOUT ACID-BASE IMBALANCES] (Study Stack)
 * This is acid-base imbalances in a nutshell; sometimes simplification is a beautiful thing.
 * Metabolic disorders will show altered pH and altered Bicarb
 * Respiratory disorders will show altered pH and altered PaCO2
 * If the patient is compensated:
 * Metabolic states: the pH and the buffers will be abnormal in the same direction, that is pH, HCO3, and PaCO2 will all be high, or they will all be low
 * Respiratory states: the pH and the buffers will still be abnormal, but in opposite directions, that is pH will be low and HCO3 and PaCO2 will be high, or vice versa
 * **Acid­base disorder** || **Primary event** || **Compensatory response** ||
 * Metabolic acidosis || **[[image:http://www.lakesidepress.com/pulmonary/books/physiology/eqn/eqn7_c.gif]]** || **[[image:http://www.lakesidepress.com/pulmonary/books/physiology/eqn/eqn7_d.gif]]** ||
 * Metabolic alkalosis || **[[image:http://www.lakesidepress.com/pulmonary/books/physiology/eqn/eqn7_g.gif]]** || **[[image:http://www.lakesidepress.com/pulmonary/books/physiology/eqn/eqn7_h.gif]]** ||
 * Respiratory acidosis || **[[image:http://www.lakesidepress.com/pulmonary/books/physiology/eqn/eqn7_i.gif]]** || **[[image:http://www.lakesidepress.com/pulmonary/books/physiology/eqn/eqn7_j.gif]]** ||
 * Respiratory alkalosis || **[[image:http://www.lakesidepress.com/pulmonary/books/physiology/eqn/eqn7_k.gif]]** || **[[image:http://www.lakesidepress.com/pulmonary/books/physiology/eqn/eqn7_l.gif]]** ||

In all cases, the underlying causes must be treated to completely resolve the acid-base imbalance. It should be noted that some people are perpetually imbalanced (referring to acid-base) because of chronic illness. Chronic lungers come to mind rather easily. Ventilated patients often develop these issues as well. (Lakeside Press)

I think that's it!! Hope my Wiki was helpful!

References