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Fluid & Electrolyte Balance. Fluid Balance homeostatic value-must be maintained food & water are taken in what is not needed is excreted body is in constant.

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Presentation on theme: "Fluid & Electrolyte Balance. Fluid Balance homeostatic value-must be maintained food & water are taken in what is not needed is excreted body is in constant."— Presentation transcript:

1 Fluid & Electrolyte Balance

2 Fluid Balance homeostatic value-must be maintained food & water are taken in what is not needed is excreted body is in constant flux must be a balance between amount of water gained & amount lost Ideally-should cancel each other out digestive system-major source of water gain urinary system-primary system for fluid removal

3 Electrolyte Balance homeostatic value-must be maintained electrolytes-Cl, Na, K, etc. are ingested everyday water & sodium regulation are integrated defending body against disturbances in volume & osmolarity K imbalance –trouble with cardiac & muscle functioning Calcium imbalances –problems with exocytosis, muscle contraction, bone formation & clotting H & HCO 3 - balance –determines pH or acid-base balance

4 Maintaining Fluid & Electrolyte Balance homeostasis depends on integration of respiratory, cardiovascular, renal & behavioral systems primary route for excretion of water & ions-kidneys –essential for regulating volume & composition of fluids lungs remove H + & HCO 3 - by excreting CO 2 behavioral mechanisms –thirst & salt appetite aid in fluid & electrolyte balance

5 Osmolarity number of solute particles dissolved in 1liter of water reflected in solution’s ability to produce osmosis & alter osmotic properties of a solvent depends only on number of non penetrating solute particles in solution 10 molecules of Na + has same osmotic activity as 10 glucose or 10 amino acid molecules in same amount of fluid

6 Osmolarity important to maintain water balance since water can cross most membranes freely water balance determines osmolarity as osmolarity of ECF (extra cellular fluid) changes  water moves into or out of cells  changing intracellular volumes & cell function excess water intake  osmolarity decreases  water moves into cells  swell Na intake (osmolarity increases)  water moves out of cells  shrink changes in cell volume impairs cell function swelling –may cause ion channels to open –changing membrane permeability

7 Water major constituent of body all operations need water as diffusion medium –to distribute gas, nutrients & wastes distributed differently among various body compartments 63-65%-intracellular fluid (ICF) %-extracellular fluid (ECF) ECF-composed of three parts –interstitial or tissue fluid-25% –plasma-8% –transcellular fluid-2% miscellaneous fluids such as CSF, synovial fluid, etc.


9 Water Balance obtained when daily gains & losses are equal average intake and loss-2.5L each day Gains –metabolism (200ml/day) –preformed water-food & drink Losses –about 1.5L each day lost via urine –200ml elmininated with feces –300 ml is lost during breathing –100 ml in sweat –400ml in cutaneous transpiration water that diffuses through epidermis & evaporates output through breath & cutaneous transpiration is insensible water loss


11 Regulation of Intake Intake-governed mostly by thirst Dehydration –reduces blood volume & blood pressure –raises blood osmolarity Detected by thirst center –hypothalamus salivate less  dry mouth  sense of thirst ingest water cools & moistens mouth rehydrates blood distends stomach  inhibits thirst

12 Regulation of Output only way to control water output significantly is through urine volume kidneys cannot completely prevent water loss or replace lost water or electrolytes changes in urine volume are usually linked to adjustments in sodium reabsorption –where sodium goes water follows ADH is one way to control urine volume without sodium ADH  collecting ducts  synthesize aquaporins (water channels)  water can diffuse out of duct  water reabsorbed

13 Electrolytes participate in metabolism determine membrane potentials affect osmolarity of body fluids major cations –Na, K, Ca & H major anions –Cl, HCO 3 & P intracellular fluid contains more K + extracellular fluid has more Na + & Cl -

14 Sodium crucial role in water & electrolyte balance involved in excitability of neurons & muscle cells (resting membrane potentials) major solute in extracellular fluid determines osmolarity of extracellular fluids

15 Sodium Balance need about 0.5 grams of sodium each day typical American consumes 3-7 g/day kidneys regulate Na + levels hormonal mechanisms control Na concentrations Aldosterone –primary role ADH ANP

16 ADH NaCl added to body  increased osmolarity  ADH (vaopressin) secretion & thirst increased thirst  drink  osmolarity decreases ADH  kidneys  conserves water by concentrating urine increased water reaborption increases BP returned to normal with cardiovascular reflexes


18 Aldosterone Na regulation also mediated by aldosterone –steroid hormone produced by adrenal cortex stimuli-more closely tied to blood volume & pressure & osmolarity than Na Hyponatremia & hyperkalemia  adrenal cortex  aldosterone Hypotension  renin  aldosterone secretion

19 Aldosterone tells kidneys to reabsorb Na in distal tubule & collecting ducts primary target-last 3rd of distal tubule increases activity of Na-K ATPase target cell-principal cell Apical membranes of P cells have Na & K leak channels Aldosterone enters by simple diffusion  combines with membrane receptors  Na channels increase time they remain open as intracellular Na increases  Na-K ATPase speeds up transport of Na into ECF  net result-rapid increase of Na reaborption that does not require synthesis of new channels or ATPase proteins slower phase of action  newly made channels & pumps inserted into epithelial cell membranes

20 Renin-Angiotensin-Aldosterone primary signal for aldosterone release- angiotensin II –component of renin- angiotensin system kidneys sense low blood pressure triggers specialized cells-juxtaglomerular cells (JG cells) in afferent arterioles to produce renin  angiotensinogen  angiotensin I  angiotensin II by ACE-angiotensin converting enzyme-found in lungs & on endothelium of blood vessels

21 Renin-Angiotensin-Aldosterone Path Angiotensin II  adrenal cortex  aldosterone  distal tubule  reabsorbs Na ADH secretion is also stimulated  water reabsorption increases because aldosterone is also acting to increase Na reabsorption, net effect-retention of fluid that is roughly same osmolarity as body fluids net effect on urine excretion- decrease in amount of urine excreted, with lower osmolarity Aldosterone  more NaCl reabsorbed in DCT & collecting ducts  reduces filtrate osmolarity

22 Renin-Angiotensin-Aldosterone stimuli that begin renin pathway- related directly or indirectly to blood pressure JG cells are directly sensitive to pressure & respond to low pressure by releasing renin sympathetic neurons are activated by cardiovascular control center when blood pressure drops  JG cells  renin release paracrine feedback from macula densa cells in distal tubule  stimulate renin release if fluid flow in distal tubule is high  macula densa  NO-nitric oxide  inhibits renin release GFR or BP low  fluid flow low  macula densa cells  NO lowered  JG cells  renin released

23 Sodium & Blood Pressure Na reaborption does not directly raise blood pressure retention helps stimulate fluid intake & volume expansion which increases blood volume& blood pressure

24 Angiotensin & Blood Pressure Angiotensin II has other effects on blood pressure increases it directly & indirectly through 4 pathways activates angiotensin II receptors in brain  increases vasopressin secretion  fluid retained in kidneys  constricts blood vessels Angiotensin II serves to stimulate thirst  expands blood volume & increases blood pressure Vasoconstriction-also stimulated by angiotensin II  increases blood pressure without changing blood volume angiotensin II activates receptors in cardiovascular control center  increases sympathetic output to heart & blood vessels  increases cardio output & vasoconstriction  increases blood pressure

25 ANP Na also regulated by ANP –a–atrial natriuretic peptide –p–peptide hormone made by heart atrial cells released when walls of atria are stretched ANP enhances Na excretion & urinary water loss increases GFR by making more surface area available for filtration  decreases Na & water reabsorption in collecting ducts indirectly inhibits renin, aldosterone & vasopressin release

26 K Balance most abundant cation of ICF –must be maintained within narrow range changes affect resting membrane potentials decreased K  hypokalemia  resting membrane potential becomes more negative increased K  hyperkalemia  more K inside cell  depolarization Hypokalemia  muscle weakness –more difficult for hyperpolarized neurons & muscles to fire action potentials –very dangerous –respiratory & heart muscle might fail Hyperkalemia –more dangerous of two situations depolarization of excitable tissues make them more excited initially  cells unable to repolarize fully become less excitable  action potentials smaller than normal  may lead to cardiac arrhythmias

27 Sodium & Water Balance Na & water reabsorption are separately regulated in distal nephron water does not automatically follow Na reabsorption here vasopressin (ADH) must be present proximal tubule –water reabsorption automatically follows Na reaborption


29 Acid-Base Balance water must be strictly monitored to keep it at a certain pH –not too acidic or too alkaline metabolism depends on functioning enzymes –very sensitive to changes in pH pH changes also disrupt stability of cell membranes –alter protein structure normal pH range neutral side

30 pH measurement of hydrogen ion concentration –lower pH indicates higher hydrogen concentration-higher acidity –higher pH indicates lower hydrogen concentration-higher alkalinity pH-below 7.35-acidosis pH-above 7.45-alkalosis Strong acids dissociate readily in water giving up H which lowers pH Weak acids ionized slightly –keep most of hydrogen bound bases accept hydrogen ions –strong base has strong tendency to bind hydrogen ions –raises pH weak base binds less hydrogen ions –less effect on pH HNO2 H+ + NO2

31 Disruptions of Acid-Base Balance pH imbalances produce problems that can be life threatening intracellular proteins comprising enzymes, membrane channels, etc very sensitive to pH functions of proteins depend on 3-d shape can become altered by pH changes must balance gain & loss of H ions

32 Compensations for Acid-Base Imbalances Buffers –f–first line of defense –a–always present –a–attempt to suppress changes in H + Kidneys –c–change in rate of hydrogen ion secretion by renal tubules – greatest effect –r–requires days to take effect Lungs –c–can have rapid effect –c–cannot change pH as much as urinary system –c–change pulmonary ventilation- expel or retaining carbon dioxide

33 Chemical Buffers any substance that can bind or release H ions such that they dampen swings in pH three major chemical buffer systems of body Bicarbonate System Phosphate System Protein System

34 Carbonic Acid-Bicarbonate Buffer System most important extracellular buffer system CO 2 + H 2 O  H 2 CO 3 H + + HCO 3 - __ add H  equation shifts to left  more HCO 3 made  increases CO 2 & H 2 O

35 Phosphate Buffer System important in buffering ICF & urine H 2 PO 4  H + HPO 4 H + HPO 4  H 2 PO4

36 Protein Buffer System involves amino acids accepting or releasing H +  pH: COOH  COO - + H +  pH: NH 2 + H +  NH 3 + amino group accepts H

37 Respiratory Compensation change in respiratory rate directly affects carbonic acid- HCO 3 buffer system any change in PCO 2 affects H ion & HCO 3 concentrations increasing or decreasing rate of respiration alters pH by lowering or raising PCO 2 PCO 2 increases  pH decreases PCO 2 decreases  pH increases excess CO 2 ventilation increases to expel more low CO 2 ventilation is reduced

38 Renal Compensation slower than buffers or lung compensation changes rate of H & HCO 3 secretion or reabsorption in response to changes in pH directly-excretes or reabsorbs H ions indirectly-changes reabsorption or excretion of HCO 3 during times of acidosis renal tubule secretes H + into filtrate HCO 3 - & K + blood pH increases pH levels-secretion of H ions decreased & bicarbonates not reclaimed

39 Disorders of Acid-Base Balance Acidosis –low pH  neurons less excitable  CNS depression  confusion & disorientation  coma  death Alkalosis –high pH  neurons hyperexcitable  numbness & tingling  muscle twitches  tetanus Acid-base imbalances fall into two categories Respiratory Metabolic

40 Respiratory Acidosis respiratory system cannot eliminate all CO 2 made by peripheral tissues accumulates in ECF  lowers its pH primary symptom of hypercapnia-respiratory acidosis typical cause Hypoventilation-low respiratory rate

41 Respiratory Alkalosis uncommon usually due to hyperventilation (plasma PCO 2 decreases) can be modulated by breathing into paper bag & rebreathing exhaled CO 2

42 Metabolic Acidosis due to drop in blood bicarbonate levels drop –l–lost due to renal dysfunction –l–lost through severe diarrhea due to accumulation of non- volatile acids-organic acid Lactic acidosis Ketoacidosis –g–generation of large amount of ketone bodies occurs during starvation & diabetes may also be caused by impaired ability to excrete H ions at kidneys or by severe HCO 3 loss as occurs during diarrhea or overuse of laxatives

43 Metabolic Alkalosis HCO 3 ions become elevated Rare can be due to non respiratory loss of acid excessive intake of alkaline drugs excessive vomiting causes a loss of HCl.


45 Compensations for Decreased pH

46 Compensations for Increased pH


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