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Chapter 27: Fluid, Electrolyte and Acid-base Balance

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1 Chapter 27: Fluid, Electrolyte and Acid-base Balance
BIO 211 Lecture Instructor: Dr. Gollwitzer

2 Today in class we will discuss:
The importance of water and its significance to fluid balance in the body Definitions and the importance of: Fluid Balance Electrolyte balance Acid-base balance Extracellular fluid (ECF) and intracellular fluid (ICF) and compare their composition Fluid and electrolyte balance Hormones that regulate them Importance of key electrolytes

3 Introduction Water critical to survival
50-60% total body weight 99% of extracellular fluid (ECF) Essential component of cytosol (intracellular fluid, ICF) All cellular operations rely on water Diffusion medium for gases, nutrients, waste products

4 Body Fluid Compartments
Body must maintain normal volume and composition of: ICF ECF = all other body fluids Major - IF, plasma Minor - lymph, CSF, serous and synovial fluids ICF > total body water than ECF Acts as water reserve

5 Body Fluid Compartments
Figure 27–1a-2

6 Body Fluid Balance Must maintain body fluid:
Volume (fluid balance) Ionic concentration (electrolyte balance) pH (acid-base balance) Gains (input) must equal loss (output) Balancing efforts involve/affect almost all body systems

7 Fluid (Water) Balance = amount of H20 gained each day equal to amount of H2O lost Regulates content and exchange of body water between ECF and ICF Gains GI (from food, liquid)* Catabolism Losses Urine* Evaporation (from skin, lungs) Feces * Primary route

8 Fluid Gains and Losses Figure 27–3

9 Electrolyte (Ion) Balance
Balances gains and losses of all electrolytes (ions that can conduct electrical current in solution) Gains GI (from food, liquid) Losses Urine Sweat Feces

10 Acid-base (pH) Balance
Balances production and loss of H+ Gains GI (from food and liquid) Metabolism Losses Kidneys (secrete H+) Lungs (eliminate CO2)

11 Fluid Components ECF components (plasma and IF) very similar
Major differences between ECF and ICF ICF very different because of cell membrane Selectively permeable Specific channels for ions Active transport into/out of cell Water exchange between ECF and ICF occurs across cell membranes by: Diffusion Osmosis Carrier-mediated transport

12 Cations in Body Fluids Figure 27–2 (1 of 2)

13 Anions in Body Fluids Figure 27–2 (2 of 2)

14 Cations and Anions in Body Fluids
In ECF Na+ Cl- HCO3- In ICF K+ (98% of body content) Mg2+ HPO42- Negatively charge proteins

15 Principles of Fluid and Electrolyte Regulation
All homeostatic mechanisms that monitor and adjust body fluid composition respond to changes in ECF, not ICF Because: A change in ECF spreads throughout body and affects many or all cells A change in ICF in one cell does not affect distant cells

16 Principles of Fluid and Electrolyte Regulation
No receptors directly monitor fluid or electrolyte balance Electrolyte balance = electrolytes gained equals the electrolytes lost Monitor secondary indicators Baroreceptors – for plasma volume/pressure Osmoreceptors – for osmotic (solute) concentration Solutes = ions, nutrients, hormones, all other materials dissolved in body fluids

17 Principles of Fluid and Electrolyte Regulation
Cells cannot move water by active transport Passive in response to osmotic gradients Fluid balance and electrolyte balance are interrelated Body’s content of water and electrolytes: Increases if gains exceed losses Decreases if losses exceed gains

18 Primary Hormones for Fluid and Electrolyte Balance
ADH Aldosterone Natriuretic peptides (e.g., ANP)

19 ADH Produced by osmoreceptor neurons in supraoptic nuclei in hypothalamus (and released by posterior pituitary) Osmoreceptors monitor osmotic concentrations in ECF Osmotic concentration increases/decreases when: Na+ increases/decreases or H2O decreases/increases Increased osmotic concentration  increased ADH

20 ADH  Water conservation
Increases water absorption  decreased osmotic concentration (by diluting Na+) Stimulates thirst center in hypothalamus  increased fluid intake

21 Figure 27–4

22 Aldosterone Mineralocorticoid secreted by adrenal cortex
Produced in response to: Decreased Na+ or increased K+ In blood arriving at: Adrenal cortex Kidney (renin-angiotensin system

23 Renin-Angiotensin System
Renin released in response to: Decreased Na+ or increased K+ in renal circulation Decreased plasma volume or BP at JGA Decreased osmotic concentration at DCT Renin   angiotensin II activation in lung capillaries Angiotensin II  Adrenal cortex  increased aldosterone Posterior pituitary  ADH Increased BP (hence it’s name)

24 Aldosterone In DCT and collecting system of kidneys 
Increased Na+ absorption (and associated Cl- and H2O absorption) Increased K+ loss  Increased sensitivity of salt receptors on tongue  crave salty foods

25 Natriuretic Peptides Released by cardiac muscle cells stretched by:
Increased BP or blood volume Oppose angiotensin II and cause diuresis  Decreased ADH  increased H2O loss at kidneys  Decreased aldosterone  increased Na+ and H2O loss at kidneys Decreases thirst  decreased H2O intake Net result = decreased stretching of cells

26 Figure 27–5, 7th edition

27 Fluid and Electrolyte Balance
When body loses water: Plasma volume decreases Electrolyte concentrations increase When body loses electrolytes: Electrolyte concentrations decrease Water also lost

28 Disorders of Fluid and Electrolyte Balance
Dehydration = water depletion Due to: Inadequate water intake Fluid loss, e.g., vomiting, diarrhea Inadequate ADH (hypothalamic/pituitary malfunction) Leads to: Too high Na+ = hypernatremia Thirst, wrinkled skin Decreased blood volume and BP Fatal circulatory shock

29 Disorders of Fluid and Electrolyte Balance
Overhydration = water excess Due to: Excess water intake (>6-8 L/24 hours) Seen in hazing rituals (water torture) Marathon runners/paddlers Ravers on ecstasy who overcompensate for thirst Chronic renal failure Excess ADH Leads to Too low Na+ = hyponatremia Increased blood volume and BP CNS symptoms (water intoxication); can proceed to convulsions, coma, death

30 Disorders of Fluid and Electrolyte Balance
Hypokalemia Too low K+ Caused by diuretics, diet, chronic alkalosis (plasma pH >7.45) Results in muscle weakness and paralysis Hyperkalemia Too high K+ Caused by diuretics (that block Na+ reabsorption) Renal failure, chronic acidosis (plasma pH<7.35) Results in severe cardiac arrhythmias

31 Summary: Disorders of Electrolyte Balance
Most common problems with electrolyte balance Caused by imbalance between gains/losses of Na+ Uptake across digestive epithelium Excretion in urine and perspiration Problems with potassium balance Less common, but more dangerous

32 Today in class we will discuss:
Acid-base balance and Three major buffer systems that balance pH of ECF and ICF Compensatory mechanisms involved in maintaining acid-base balance Respiratory compensation Renal compensation Causes, effects, and the body’s response to acid-base disturbances that occur when pH varies Respiratory acid-base disorders Respiratory acidosis Respiratory alkalosis Metabolic acid-base disorders Metabolic acidosis Metabolic alkalosis

33 Acid-Base Balance Control of pH
Acid-base balance = = production of H+ is precisely offset by H+ loss Body generates acids (H+) during metabolic processes Decrease pH Normal pH of ECF = 7.35 – 7.45 <7.35 = acidosis (more common than alkalosis) >7.45 = alkalosis <6.8 or >7.7 = lethal

34 Acid-Base Balance Deviations outside normal range extremely dangerous
Disrupt cell membranes Alter protein structure (remember hemoglobin?) Change activities of enzymes Affects all body systems Especially CNS and CVS

35 Acid-Base Balance CNS and CVS especially sensitive to pH fluctuations
Acidosis more lethal than alkalosis CNS deteriorates  coma  death Cardiac contractions grow weak and irregular  heart failure Peripheral vasodilation  decreased BP and circulatory collapse

36 Acid-Base Balance Carbonic acid (H2CO3)
Most important factor affecting pH of ECF CO2 + H2O  H2CO3  H+ + HCO3-

37 Relationship between PCO2 and pH
PCO2 inversely related to pH Figure 27–9

38 Acid-Base Balance H+ Gained Eliminated
At digestive tract Through cellular metabolic activities Eliminated At kidneys by secretion of H+ into urine At lungs by forming H2O and CO2 from H+ and HCO3- Sites of elimination far from sites of production As H+ travels through body, must be neutralized to avoid tissue damage Accomplished through buffer systems

39 Buffers Compounds dissolved in body fluids Stabilize pH
Can provide or remove H+

40 Buffer Systems in Body Fluids
Phosphate buffer system (H2PO4-) In ICF and urine Protein buffer systems In ICF and ECF Includes: Hb buffer system (RBCs only) Amino acid buffers (in proteins) Plasma protein buffers (albumins, globulins…) Carbonic acid-bicarbonate buffer system Most important in ECF

41 Figure 27–7

42 Carbonic Acid–Bicarbonate Buffer System
Figure 27–9

43 Maintenance of Acid-Base Balance
For homeostasis to be preserved: H+ gains and losses must be balanced Excess H+ must be: Tied up by buffers Temporary; H+ not eliminated, just not harmful Permanently tied up in H2O molecules Associated with CO2 removal at lungs Removed from body fluids Through secretion at kidneys Accomplished by: Respiratory mechanisms Renal mechanisms

44 Conditions Affecting Acid-Base Balance
Disorders affecting buffers, respiratory or renal function Emphysema, renal failure Cardiovascular conditions Heart failure or hypotension Can affect pH, change glomerular filtration rates, respiratory efficiency Conditions affecting CNS Neural damage/disease that affects respiratory and cardiovascular reflexes that regulate pH

45 Disturbances of Acid-Base Balance
Serious abnormalities have an: Acute (initial) phase pH moves rapidly out of normal range Compensated phase If condition persists Physiological adjustments move pH back into normal range Cannot be completed unless underlying problem corrected Types of compensation Respiratory Renal

46 Respiratory Compensation
Changes respiratory rate Increasing/decreasing respiratory rate changes pH by lowering/raising PCO2 Helps stabilize pH of ECF Occurs whenever pH moves outside normal limits Has a direct effect on carbonic acid-bicarbonate buffer system

47 Respiratory Compensation
Increased PCO2  Increased H2CO3  increased H+  decreased pH (acidosis) Increased respiratory rate  more CO2 lost at lungs  CO2 decreases to normal levels Decreased PCO2  Decreased H2CO3  decreased H+  increased pH (alkalosis) Decreased respiratory rate  less CO2 lost at lungs  CO2 increases to normal levels

48 Carbonic Acid–Bicarbonate Buffer System
Figure 27–9

49 Renal Compensation Changes renal rates of H+ and HCO3-
Secretion Reabsorption In response to changes in plasma pH Increased H+ or decreased HCO3-  Decreased pH (acidosis)  more H+ secreted and/or less HCO3- reabsorbed Decreased H+ or increased HCO3-  Increased pH (alkalosis)  less H+ secreted and/or more HCO3- reabsorbed

50 The Carbonic Acid–Bicarbonate Buffer System and Regulation of Plasma pH
Figure 27–11a

51 The Carbonic Acid–Bicarbonate Buffer System and Regulation of Plasma pH
Figure 27–11b

52 Disturbances of Acid-Base Balance
Conditions named for: Uncompensated or Compensated Primary source of problem Respiratory or metabolic Mixed (both) Primary effect Acidosis or alkalosis e.g., Compensated or uncompensated Respiratory acidosis or alkalosis Metabolis acidosis or alkalosis

53 Respiratory Acid-Base Disorders
Result from imbalance between: CO2 generated in peripheral tissues (ECF) CO2 excreted at lungs Cause abnormal CO2 levels in ECF  Respiratory Acidosis Alkalosis

54 Respiratory Acidosis Most common challenge to acid-base equilibrium
Primary sign is hypercapnia (increased PCO2) Develops when respiratory system cannot eliminate all CO2 generated by peripheral tissues Usual cause is hypoventilation Acute situation may be immediate, life-threatening condition Requires bronchodilation or mechanical breathing assistance (ventilator) pH can get as low as 7.0

55 Respiratory Acidosis Figure 27–12a, 7th edition

56 Respiratory Alkalosis
Relatively uncommon Primary sign is high pH Develops when increased respiratory activity (hyperventilation) lowers plasma PCO2 to below normal levels (hypocapnia) Seldom of clinical significance pH can get as high as 7.8 – 8.0

57 Respiratory Alkalosis
Figure 27–12b, 7th edition

58 Metabolic Acid-Base Disorders
Result from: Production of acids during metabolic processes Conditions that affect concentration of HCO3- in ECF  Metabolic Acidosis Alkalosis

59 Metabolic Acidosis Results from: Production of large numbers of acids
H+ overloads buffer systems Inability to excrete H+ at kidneys Severe HCO3- loss

60 Metabolic Acidosis Production of large number of acids
Lactic acidosis from anaerobic respiration After strenuous exercise From prolonged tissue hypoxia (O2 starvation) Ketoacidosis from generation of ketone bodies during metabolism When peripheral tissues cannot obtain adequate glucose from bloodstream and begin metabolizing lipids and ketone bodies), e.g., Starvation Complication of poorly controlled diabetes mellitus

61 Metabolic Acidosis Inability to excrete H+ at kidneys
With severe kidney damage (glomerulonephritis) Caused by diuretics that interfere with H+ secretion into urine Severe HCO3- loss From chronic diarrhea Loss interferes with buffer system ability to remove H+

62 Responses to Metabolic Acidosis
Figure 27–13

63 Metabolic Alkalosis Relatively rare Occurs after repeated vomiting
Stomach continues to generate HCl to replace lost acids Is associated with increased HCO3- in ECF HC03- + H+  H2CO3 Reduces H+  alkalosis

64 Metabolic Alkalosis Figure 27–14

65 Detection of Acidosis and Alkalosis
Includes blood tests for: pH PCO2 HCO3- Recognition of acidosis or alkalosis Classification as respiratory or metabolic

66 Diagnostic Chart for Acid-Base Disorders
Figure 27–18

67 Blood Chemistry and Acid–Base Disorders
Table 27–4


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