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