Chapter 27: Fluid, Electrolyte and Acid-base Balance

BIO 211 LectureInstructor: Dr. Gollwitzer

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• 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

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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

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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

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Figure 27–1a-2

Body Fluid Compartments

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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

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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

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Fluid Gains and Losses

Figure 27–3 8

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

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Acid-base (pH) Balance

• Balances production and loss of H+

• Gains– GI (from food and liquid)– Metabolism

• Losses– Kidneys (secrete H+)– Lungs (eliminate CO2)

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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

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Cations in Body Fluids

Figure 27–2 (1 of 2) 12

Anions in Body Fluids

Figure 27–2 (2 of 2) 13

Cations and Anions in Body Fluids

• In ECF– Na+ – Cl-

– HCO3-

• In ICF– K+ (98% of body content)– Mg2+

– HPO42-

– Negatively charge proteins

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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

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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

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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

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Primary Hormones for Fluid and Electrolyte Balance

• ADH• Aldosterone• Natriuretic peptides (e.g., ANP)

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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

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ADH

• Water conservation– Increases water absorption decreased osmotic

concentration (by diluting Na+)– Stimulates thirst center in hypothalamus

increased fluid intake

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Figure 27–4 21

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

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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)

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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

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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

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Figure 27–5, 7th edition 26

Fluid and Electrolyte Balance

• When body loses water:– Plasma volume decreases– Electrolyte concentrations increase

• When body loses electrolytes:– Electrolyte concentrations decrease– Water also lost

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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

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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, death29

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

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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

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• 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

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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 = lethal33

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

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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

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Acid-Base Balance

• Carbonic acid (H2CO3)– Most important factor affecting pH of ECF

• CO2 + H2O H2CO3 H+ + HCO3-

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Figure 27–9

Relationship between PCO2 and pH• PCO2 inversely related to pH

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Acid-Base Balance• H+

– Gained• 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

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Buffers

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

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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

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Figure 27–7 41

Carbonic Acid–Bicarbonate Buffer System

Figure 27–942

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

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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

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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

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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

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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 levels47

Carbonic Acid–Bicarbonate Buffer System

Figure 27–9 48

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

- reabsorbed49

The Carbonic Acid–Bicarbonate Buffer System and

Regulation of Plasma pH

Figure 27–11a 50

The Carbonic Acid–Bicarbonate Buffer System and

Regulation of Plasma pH

Figure 27–11b 51

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

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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

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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

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Respiratory Acidosis

Figure 27–12a, 7th edition 55

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

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Respiratory Alkalosis

Figure 27–12b, 7th edition 57

Metabolic Acid-Base Disorders• Result from:– Production of acids during metabolic processes– Conditions that affect concentration of HCO3

- in ECF

• Metabolic– Acidosis– Alkalosis

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Metabolic Acidosis• Results from:– Production of large numbers of acids• H+ overloads buffer systems

– Inability to excrete H+ at kidneys– Severe HCO3

- loss

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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

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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+

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Figure 27–13

Responses to Metabolic Acidosis

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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

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Metabolic Alkalosis

Figure 27–1464

Detection ofAcidosis and Alkalosis

• Includes blood tests for:– pH– PCO2

– HCO3-

• Recognition of acidosis or alkalosis• Classification as respiratory or metabolic

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Diagnostic Chart for Acid-Base Disorders

Figure 27–18 66

Blood Chemistry and Acid–Base Disorders

Table 27–4 67