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# Fluids and electrolyte

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• The Starling Equation:\n\nJv = Kf [ (Pc-Pi) - (Pic-Pii) ] \n\nWhere:\nJv = fluid movement\nKf = Huraulic conductance\nPc = capillary Hydrostatic Pressure\nPi = interstitial hydrostatic pressure\nPi c = capillary oncotic pressure\nPi i = interstitial oncotic pressure\n
• Flow = [ (pressure of Cap - Pressure of interstitium) - (oncotic P of Cap - Oncotic P of interstitium) ]\n\n+ Pc: art dilation, venous constriction, venous pressure, Heart failure, EC volume expansion, Dependant limb edema\n- Pi c: - plasma protein, liver disease, protein starving, nephrotic syndrom, \n+ Kf: Burn, Inflammation\n
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• Perhaps because,\n- Ca outside cell makes cell relatively positive and closer to threshold.\n
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• You are basically forced to blow off all your CO2.\n
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• 1 - look at pH\n2 - look at pCO2. (see it as bicarb on chem 7) See if it is metabolic or respiratory. If outside of normal, than it is not \nthe lung&amp;#x2019;s fault.\n3 - Ex:(Acid)If pCO2 is normal, then it is acute metab. If decreased, then chronic. \n4 - Look at ion gap: Na - (CO2 + Cl) = ion gap. 10-12 = normal. \n Normal, means loss. \n Gap = DKA, LA, ingestion of antifreeze, methanol, aspirin OD, RF, \n If pCO2 elevated, its the lung. Then look at bicarb, see if acute or chronic, see if the kidneys have kicked in.\n*** do the same on the basic side. \n
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• ### Fluids and electrolyte

1. 1. Fluid and Electrolytes Acid and Base Balance Reference: Pathophysiology by Kathryn McCance Mindy Milton, MPA, PA-C July 1, 2010 1Mosby items and derived items © 2006 by Mosby, Inc.
2. 2. Distribution of Body Fluids Total body water (TBW)  Intracellular fluid Total body water aprox 42L Rest is fat, fat free solids, bones.  Extracellular fluid Mostly intracellular.  Interstitial fluid Adipose tissue has less water, so obese  Intravascular fluid have less total body water, and more risk of dehydration. age also effects, probably due to more fat. 2Mosby items and derived items © 2006 by Mosby, Inc.
3. 3. Fluid Compartment 3Mosby items and derived items © 2006 by Mosby, Inc.
4. 4. Electrolyte Distribution Major Cations:  Extracellular fluid  Plasma: Na  Interstitial Fluid: Na  Intracelluar fluid  K, Mg Major Anions  Extracellular Fluid  Plasma: Cl, HCO3, Protein  Interstitial: Cl, HCO3, HPO4, SO4  Intracellular Fluid  HPO4, Proteins, HCO3, CL,, SO4 4Mosby items and derived items © 2006 by Mosby, Inc.
5. 5. Principles of Fluid and Electrolytes Homeostatic mechanisms respond to changes in the extracellular fluid Cellular receptors respond to changes in volume and osmotic concentration Water is moved by osmotic gradients and not by active transport Water follows sodium 5Mosby items and derived items © 2006 by Mosby, Inc.
6. 6. Water Movement Betweenthe Plasma & Interstitial Fluid Osmolality represent Na consentration Osmotic forces (hydrostatic pressure) due to heart contraction Aquaporins H2O can also diffuse through memb. Starling hypothesis  Net filtration = forces favoring filtration – forces opposing filtration (oncotic) capillary bed 6Mosby items and derived items © 2006 by Mosby, Inc.
7. 7. Net Filtration  Forces favoring filtration  Capillary hydrostatic pressure (blood pressure)  Interstitial oncotic pressure (water-pulling)  Forces favoring reabsorption  Plasma oncotic pressure (water-pulling)  Interstitial hydrostatic pressure 7Mosby items and derived items © 2006 by Mosby, Inc.
8. 8. Water Movement Between Be able to do equation to ﬁgure out force. In edema, hypertension,the ICF and ECF obstruction. 8Mosby items and derived items © 2006 by Mosby, Inc.
9. 9. Edema  Factors that increase Capillary Hydrostatic Pressure  Venous obstruction THink Kinking.  Thrombophlebitis, tight clothing, prolonged sitting or standing  Salt and water retention Think osmosis drawing fluid in to make more volume.  CHF  Renal failure  Cirrhosis  Factors that decrease Capillary Oncotic Pressure  Decreased plasma proteins Less fluid in vessels  Cirrhosis  Nephrotic syndrome - centralized edema.  Malnutrition  Burns - lose proteins through skin.  Factors that increase capillary permeability  Inflammation and Immune response as a result of:  Trauma: burns, crush injury, neoplastic disease, allergic Rnx  Proteins escape from plasma  ↓ capillary oncotic pressure & ↑interstitial oncotic pressure  Factors that decrease absorption of interstitial fluids  Lymph obstruction  Infection  Tumor 9  Surgical re-sectionMosby items and derived items © 2006 by Mosby, Inc.
10. 10. Water Balance - two main factors  Thirst perception - stim water drinking behavior.  Osmolality receptors  Hyperosmolality and plasma volume depletion  decrease in actual H2O  ADH secretion  Increase thirst sensation  Increase permeability of Renal distal tubule to water = increased water retention. sensor in atrea, aorta, sensing 10 pressure. Used toMosby items and derived items © 2006 by Mosby, Inc. sense water.
11. 11. Other Regulatory Hormones Aldosterone  Released by the adrenal cortex  Stimulates the retention of NA and excretion of K by the distal tubule of the kidney - therefore water follows.  Aldosterone released in response to:  Increasingserum K (hyperkalemia)  Decreasing serum NA (hyponatremia)  Low renal perfusion Renin, from JGA, sensing  Renin - Angiotensin- Aldosterone System (RAAS) in the kidney. low ﬂow Start RAAS,  Increase volume (Na) and increase BP Angiotensin 2 is a vasoconstrictor. 11Mosby items and derived items © 2006 by Mosby, Inc. Normal is 136 - 145 Na per L
12. 12. Other Regulatory Hormones  Natriuretic peptides  Atrial natriuretic peptide (heart)  Brain natriuretic peptide (heart)  Urodilantin (kidney)  ANP (& BNP) is released by the cardiac muscle fibers in response to abnormal stretching of the atrial walls  Abnormal stretching can be caused by increased blood pressure or increased blood volume  Effects: reduces thirst, decreased release of ADH and Aldosterone  Will cause diuresis – water and sodium 12Mosby items and derived items © 2006 by Mosby, Inc.
13. 13. Alterations in Na+, Cl–, and Water  Total body water change with proportional electrolyte and water change  Isotonic volume depletion -- proportional exchange.  Hemorrhage  Excessive diaphoresis Cl- is the bitch, follows  Decrease fluid intake Na+.  Intestinal losses  Isotonic volume excess  Excessive NS IV - iatrogenically.  Hyperaldosteronism  cortisone - steroid 13Mosby items and derived items © 2006 by Mosby, Inc.
14. 14. Decreased water - Diabetes Insipitus. Loss of ADH: unable toHypertonic Alterations concentrate urine. Fine, as long as they can drink.  Hypernatremia Conn  Serum sodium >147 mEq/L  Related to sodium gain or water loss  Water movement from the ICF to the ECF  Intracellular dehydration (cell shrinks)  Manifestations  Intracellular dehydration, convulsions, pulmonary edema, hypotension, tachycardia 14Mosby items and derived items © 2006 by Mosby, Inc.
15. 15. Hypotonic Alterations  Decreased ECF osmolality  Caused by:  Sodium deficit (Hyponatremia) or  Fee water excess (water intoxication)  Hyponatremia will cause water movement from ECF to ICF  Intracellular overhydration (cell swells)  Cerebral edema – irritability, confusion, HA, depression, systemic edema, weakness, anorexia, nausea, diarrhea  Plasma hypovolemia  Hypotension, tachycardia, decrease urine output  Free water Excess both ICF and ECF volume increase  Intracellular overhydration (cell swells)  Plasma hypervolemia  Cellular and systemic edema as above 15Mosby items and derived items © 2006 by Mosby, Inc.
16. 16. Hyponatremia  Serum sodium level <135 mEq/L  Sodium deficits cause plasma hypoosmolality and cellular swelling  Causes: addisons disease, not  Pure sodium deficits enough cortisol or aldo.  Vomiting, diarrhea, overuse diuretics, burns Innapropriate secretion of ADH - page 104 in  Low sodium intake text.  Rare  Dilutional hyponatremia  Excessive ½ NS IV (.45) - hypotonic saline  Mannitol (shift from ICF to ECF) - not low sodium, just being diluted  Hypoosmolar hyponatremia  ARF (oliguric), severe CHF, Liver Cirrhosis  Hypertonic hyponatremia  Hyperlipidemia, hyperglycemia, hyperproteinemia 16  Displace water volume and decrease Na concentrationMosby items and derived items © 2006 by Mosby, Inc.
17. 17. orthostatic vitals:BPWater Deficit drop, pulse goes up.  Dehydration - common  Isotonic (loss of water and sodium)  Pure water deficits - rare  Hypertonic dehydration  Renal free water clearance - common  Impaired tubular function or inability to concentrate urine  Manifestations  HA, thirst, dry skin/mucous membranes, wt loss, fever, conc urine*  Tachycardia, weak pulses, and postural hypotension  Elevated hematocrit and serum sodium level * Not with diabetes insipidus 17Mosby items and derived items © 2006 by Mosby, Inc.
18. 18. Water Excess Compulsive water drinking  Psychogenic Decreased urine formation  Intrinsic renal disease or decreased renal blood flow Syndrome of inappropriate secretion of ADH (SIADH)  ADH secretion in the absence of hypovolemia or hyperosmolality  Hyponatremia with hypervolemia Manifestations  Rapid loading - cerebral edema, confusion, seizures  Slow loading - weakness, nausea, muscle twitching, headache, and weight gain 18Mosby items and derived items © 2006 by Mosby, Inc.
19. 19. Potassium Major intracellular cation Concentration maintained by the Na+/K+ ATPase pump Regulates intracellular electrical neutrality in relation to Na+ and H+ Essential for transmission and conduction of nerve impulses, normal cardiac rhythms, and skeletal and smooth muscle contraction 19Mosby items and derived items © 2006 by Mosby, Inc.
20. 20. Potassium Levels Changes in pH affect K+ balance  Hydrogen ions accumulate in the ICF during states of acidosis. K+ shifts out to maintain a balance of cations across the membrane. Aldosterone, insulin, and catecholamines influence serum potassium levels ECF acidodic, casue H to be pumped into the cell, exchanging K out. 20Mosby items and derived items © 2006 by Mosby, Inc.
21. 21. Hypokalemia Potassium level <3.5 mEq/L Etiology  Reduced intake  Shifts of potassium from the extracellular to intracellular space (alkalosis)  Loss of potassium from body stores: GI losses with vomiting, diarrhea, fistulas, laxative abuse. Renal losses from overuse of diuretics, increased aldosterone. Manifestations  Membrane hyperpolarization causes a decrease in neuromuscular excitability, skeletal muscle weakness, smooth muscle atony, and cardiac dysrhythmias 21Mosby items and derived items © 2006 by Mosby, Inc.
22. 22. Renal failure is the most common causeHyperkalemia Potassium level >5.5 mEq/L Hyperkalemia is rare due to efficient renal excretion - Caused by increased intake, shift of K+ from ICF, decreased renal excretion, insulin deficiency, or cell trauma K goes into the cells with glucose. 22Mosby items and derived items © 2006 by Mosby, Inc.
23. 23. Hyperkalemia Mild attacks  Hypopolarized membrane, causing neuromuscular irritability  Tall peaked T waves with shortened QT on ECG - rapid repolarization, poor propigation of AP.  Tingling of lips and fingers, restlessness, intestinal cramping, and diarrhea Severe attacks  The cell is not able to repolarize, resulting in muscle weakness, loss or muscle tone, and flaccid paralysis  Depressed ST segment, prolonged PR interval, widened QRS 23Mosby items and derived items © 2006 by Mosby, Inc.
24. 24. Usually inverse relationship.Calcium and Phosphate  Most calcium is stored in bone (99%)  Necessary for structure of bones and teeth, blood clotting, hormone secretion, and cell receptor function  Like calcium, most phosphate (85%) is also located in the bone  Necessary for high-energy bonds located in creatine phosphate and ATP and acts as an anion buffer  Calcium and phosphate concentrations are rigidly controlled  Increase in one will require a decrease in the other 24Mosby items and derived items © 2006 by Mosby, Inc.
25. 25. Calcium and Phosphate Regulated by three hormones - tight control.  Parathyroid hormone (PTH)  Increases plasma calcium levels  Renal activation of Vitamin D  Vitamin D  Fat-soluble steroid; increases calcium absorption from the GI tract - epidemic due to sunscreen.  Calcitonin - parafollicular cells (c cells) in pancreas.  Decreases plasma calcium levels - “tone down”. 25Mosby items and derived items © 2006 by Mosby, Inc.
26. 26. Hypocalcemia and Hypercalcemia Hypocalcemia  Hypercalcemia  < 8.5 mg/dl  > 12 mg/dl  Increased  Decreased neuromuscular neuromuscular excitability excitability (partial depolarization)  Muscle weakness  Muscle cramps  Increased bone  Think of as partial fractures!!!Wierd depolarization  Kidney stones  Constipation - hard to be able to compare/ contrast depolarize 26Mosby items and derived items © 2006 by Mosby, Inc.
27. 27. pH Inverse logarithm of the H+ concentration If the H+ are high in number, the pH is low (acidic). If the H+ are low in number, the pH is high (alkaline). The pH scale ranges from 0 to 14: 0 is very acidic, 14 is very alkaline. Each number represents a factor of 10. If a solution moves from a pH of 6 to a pH of 5, the H+ have increased 10 times. 27Mosby items and derived items © 2006 by Mosby, Inc.
28. 28. pH Acids are formed as end products of protein, carbohydrate, and fat metabolism To maintain the body’s normal pH (7.35-7.45) the H+ must be neutralized or excreted The bones, lungs, and kidneys are the major organs involved in the regulation of acid and base balance 28Mosby items and derived items © 2006 by Mosby, Inc.
29. 29. pH Body acids exist in two forms  Volatile - can blow off.  H2CO3 (can be eliminated as CO2 gas)  Nonvolatile  Sulfuric, phosphoric, and other organic acids  Eliminated by the renal tubules with the regulation of HCO3– 29Mosby items and derived items © 2006 by Mosby, Inc.
30. 30. Buffering Systems A buffer is a chemical that can bind excessive H+ or OH– without a significant change in pH A buffering pair consists of a weak acid and its conjugate base  Ex: H2CO3 ; HCO3- see the kidney work with both of these.  HHb ; Hb- - in plasma. (Hemoglobin system) The most important plasma buffering systems are the carbonic acid–bicarbonate system and hemoglobin The most important intracellular buffering systems are phosphate and protein 30Mosby items and derived items © 2006 by Mosby, Inc.
31. 31. Carbonic Acid–Bicarbonate Pair If the amount of bicarbonate decreases, the pH decreases, causing a state of acidosis The pH can be returned to normal if the amount of carbonic acid also decreases  This type of pH adjustment is referred to as compensation The respiratory system compensates by increasing or decreasing ventilation The renal system compensates by producing acidic or alkaline urine Renal compensatio H2O + CO2 <-->H2CO3 <--> HCO3- + H+ take days. Lungs in minutes to hours. 31Mosby items and derived items © 2006 by Mosby, Inc.
32. 32. Other Buffering Systems Protein buffering  Proteins have negative charges, so they can serve as buffers for H+ Renal buffering  Secretion of H+ in the urine and reabsorption of HCO3– Cellular ion exchange  Exchange of K+ for H+ in acidosis and alkalosis 32Mosby items and derived items © 2006 by Mosby, Inc.
33. 33. Acid-Base Imbalances Normal arterial blood pH  7.35 to 7.45  Obtained by arterial blood gas (ABG) sampling Acidosis  Systemic increase in H+ concentration  < 7.35 Alkalosis  Systemic decrease in H+ concentration  > 7.45 33Mosby items and derived items © 2006 by Mosby, Inc.
34. 34. Acidosis and Alkalosis Four categories of acid-base imbalances:  Respiratory acidosis—elevation of pCO2 due to ventilation depression  Respiratory alkalosis—depression of pCO2 due to alveolar hyperventilation  Metabolic acidosis—depression of HCO3– or an increase in non-carbonic acids  Metabolic alkalosis—elevation of HCO3– usually due to an excessive loss of metabolic acids lactic acidosis - shock, DKA, 34Mosby items and derived items © 2006 by Mosby, Inc. Met Alk - diarrhea/ vomiting.
35. 35. Metabolic Acidosis SLower. 35Mosby items and derived items © 2006 by Mosby, Inc.
36. 36. Metabolic Alkalosis Have alk urine.Depression of breathing. 36 Mosby items and derived items © 2006 by Mosby, Inc.
37. 37. Respiratory Acidosis etiology: depression of respiration. Can be acute and chronic. pCO2 will triggar compensation.head trauma and drug OD,compensation will nothappen.Chronic - will causerespiration to adapt,changing set pint.Kidneys are the one. 37 Mosby items and derived items © 2006 by Mosby, Inc.
38. 38. Respiratory Alkalosis Cause: ICU ventilated patients, anxiety, anemia (less Hb), pulm/cv disorders. Happens rapidly. Kidneys compensate for chronic. 38Mosby items and derived items © 2006 by Mosby, Inc.
39. 39. Acid Base Response Issue is either a production or excretion problem. Buffering systems in the plasma (RBC). bicarb/carbonic acid system and Hb. 39Mosby items and derived items © 2006 by Mosby, Inc.
40. 40. Approach to Acid Base Disturbances 40Mosby items and derived items © 2006 by Mosby, Inc.
41. 41. Questions? 41Mosby items and derived items © 2006 by Mosby, Inc.