10/26/2014

PowerPoint® Lecture Slides prepared by Barbara Heard, Atlantic Cape Community Ninth Edition College

Human Anatomy & Physiology

CHAPTER

26

Fluid, Electrolyte, and Acid-Base Balance © Annie Leibovitz/Contact Press Images

© 2013 Pearson Education, Inc.

Fluid Compartments

Body Water Content

• Infants: 73% or more water (low body fat, low bone mass) • Adult males: ~60% water • Adult females: ~50% water (higher fat content, less skeletal muscle mass) – Adipose tissue least hydrated of all

• Water content declines to ~45% in old age

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Figure 26.1 The major fluid compartments of the body.

Total body water Volume = 40 L 60% of body weight

– Intracellular fluid (ICF) compartment: 2/3 in cells – Extracellular fluid (ECF) compartment: 1/3 outside cells

Intracellular fluid (ICF) Volume = 25 L 40% of body weight

Interstitial fluid (IF) Volume = 12 L 80% of ECF

• Plasma: 3 L • Interstitial fluid (IF): 12 L in spaces between cells – Usually considered part of IF: lymph, CSF, humors of the eye, synovial fluid, serous fluid, and gastrointestinal secretions © 2013 Pearson Education, Inc.

Electrolyte Concentration

Plasma Volume = 3 L, 20% of ECF

• Total body water = 40 L • Two main fluid compartments

Extracellular fluid (ECF) Volume = 15 L 20% of body weight © 2013 Pearson Education, Inc.

Electrolyte Concentration • For single charged ions (e.g. Na+), 1 mEq = 1 mOsm • For bivalent ions (e.g. Ca2+), 1 mEq = 1/2 mOsm • 1 mEq of either provides same amount of charge

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© 2013 Pearson Education, Inc.

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Extracellular and Intracellular Fluids

Extracellular and Intracellular Fluids

• Each fluid compartment has distinctive pattern of electrolytes • ECF

• ICF: – Low Na+ and Cl– – Major cation: K+ – Major anion HPO42– – More soluble proteins than in plasma

– All similar • Major cation: Na+ • Major anion: Cl–

– Except: higher protein, lower Cl– content of plasma

© 2013 Pearson Education, Inc.

© 2013 Pearson Education, Inc.

Figure 26.2 Electrolyte composition of blood plasma, interstitial fluid, and intracellular fluid.

Figure 26.3 Exchange of gases, nutrients, water, and wastes between the three fluid compartments of the body.

160

Lungs

Gastrointestinal tract

Kidneys

Blood plasma Interstitial fluid Intracellular fluid Na+

Sodium

K+

Potassium

Ca2+

Calcium

Mg2+

Magnesium

HCO3– Bicarbonate Cl–

Chloride

HPO42– Hydrogen phosphate SO42–

Total solute concentration (mEq/L)

140

120

100

Blood plasma

O2

CO2

Nutrients H2O, Ions

H2O, Nitrogenous Ions wastes

Interstitial fluid

O2

CO2

Nutrients H2O

Ions Nitrogenous wastes

80

60

40

Sulfate

20

0 © 2013 Pearson Education, Inc.

Na+

K+

Ca2+

Mg2+ HCO3–

Cl–

HPO42– SO42–

Protein anions

Water Balance and ECF Osmolality • Water intake must = water output = ~ 2500 ml/day • Water intake: beverages, food, and metabolic water • Water output: urine (60%), insensible water loss (lost through skin and lungs), perspiration, and feces

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Intracellular fluid in tissue cells © 2013 Pearson Education, Inc.

Figure 26.4 Major sources of water intake and output.

100 ml Metabolism 10%

250 ml 200 ml

Foods 30%

750 ml

700 ml

Feces 4% Sweat 8% Insensible loss via skin and lungs 28%

2500 ml

Beverages 60%

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1500 ml

1500 ml

Average intake per day

Average output per day

Urine 60%

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Maintenance of Body fluid Osmolality

Figure 26.5 The thirst mechanism for regulating water intake. Plasma volume (5 –10%)

ECF osmolality

Blood pressure

• Osmolality maintained at ~ 280 – 300 mOsm • Rise in osmolality 

Osmoreceptors in hypothalamus

Saliva

Granular cells in kidney

Renin-angiotensinaldosterone mechanism

Dry mouth

Angiotensin II

– Stimulates thirst – ADH release

Hypothalamic thirst center

• Decrease in osmolality 

Sensation of thirst; person takes a drink

– Thirst inhibition – ADH inhibition

Water moistens mouth, throat; stretches stomach, intestine

Water absorbed from GI tract Initial stimulus Physiological response

ECF osmolality Plasma volume

Result Increases, stimulates

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Regulation of Water Output: Influence of ADH

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Reduces, inhibits

Figure 26.6 Mechanisms and consequences of ADH release. ECF osmolality Na+ concentration in plasma

• Other factors may trigger ADH release

Plasma volume (5–10%), BP

Stimulates

– Large changes in blood volume or pressure

Osmoreceptors in hypothalamus

• E.g.,  BP   ADH release due to blood vessel baroreceptors and renin-angiotensin-aldosterone mechanism • Factors lowering blood volume: intense sweating, vomiting, or diarrhea; severe blood loss; traumatic burns; and prolonged fever

Inhibits

Negative feedback inhibits Baroreceptors in atria and large vessels

Stimulates

Stimulates Posterior pituitary Releases

ADH

Antidiuretic hormone (ADH) Targets

Collecting ducts of kidneys Effects

Water reabsorption Results in

ECF osmolality Plasma volume

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Disorders of Water Balance • Principal abnormalities of water balance – Dehydration – Hypotonic hydration – Edema

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Scant urine

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Disorders of Water Balance: Hypotonic Hydration • Cellular overhydration, or water intoxication • Occurs with renal insufficiency or rapid excess water ingestion • ECF osmolality   hyponatremia  net osmosis into tissue cells  swelling of cells  severe metabolic disturbances (nausea, vomiting, muscular cramping, cerebral edema)  possible death • Treated with hypertonic saline © 2013 Pearson Education, Inc.

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Figure 26.7b Disturbances in water balance.

1 Excessive H2O enters the ECF

2 ECF osmotic pressure falls

Slide 1

3 H2O moves into cells by osmosis; cells swell

Disorders of Water Balance: Edema • Atypical accumulation of IF  tissue swelling (not cell swelling) • Result of  fluid out of blood or  fluid into blood •  fluid out of blood caused by – Increased capillary hydrostatic pressure or permeability

Consequences of hypotonic hydration (water gain). If more water than solutes is gained, cells swell.

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• Capillary hydrostatic pressure increased by incompetent venous valves, localized blood vessel blockage, congestive heart failure,  blood volume • Capillary permeability increased by ongoing inflammatory response

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Edema

Electrolyte Balance

•  fluid returning to blood result of

• Electrolytes are salts, acids, bases, some proteins • Electrolyte balance usually refers only to salt balance • Salts control fluid movements; provide minerals for excitability, secretory activity, membrane permeability • Salts enter body by ingestion and metabolism; lost via perspiration, feces, urine, vomit

– Imbalance in colloid osmotic pressures, e.g., hypoproteinemia ( plasma protein levels  low colloid osmotic pressure) • Fluids fail to return at venous ends of capillary beds • Results from protein malnutrition, liver disease, or glomerulonephritis

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Central Role of Sodium

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Table 26.2 Sodium Concentration and Sodium Content

• Most abundant cation in ECF – Sodium salts in ECF contribute 280 mOsm of total 300 mOsm ECF solute concentration

• Only cation exerting significant osmotic pressure – Controls ECF volume and water distribution – Changes in Na+ levels affects plasma volume, blood pressure, and ECF and IF volumes

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© 2013 Pearson Education, Inc.

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Regulation of Sodium Balance: Aldosterone

Aldosterone

• Regardless of aldosterone presence

• Aldosterone  decreased urinary output; increased blood volume

– 65% Na+ reabsorbed in proximal tubules; 25% reclaimed in nephron loops – Na + never secreted into filtrate

• Water in filtrate follows Na+ if ADH is present

– By active reabsorption of remaining Na+ in distal convoluted tubule and collecting duct

• Also causes increased K+ secretion

–  Na+ in urine   water loss

© 2013 Pearson Education, Inc.

© 2013 Pearson Education, Inc.

Regulation of Sodium Balance: Aldosterone

Regulation of Sodium Balance: Aldosterone

• Renin-angiotensin-aldosterone mechanism main trigger for aldosterone release

• Renin catalyzes production of angiotensin II

– Granular cells of JGC secrete renin in response to • Sympathetic nervous system stimulation •  filtrate NaCl concentration •  stretch (due to  blood pressure) of granular cells

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– Prompts aldosterone release from adrenal cortex –  Na+ reabsorption by kidney tubules

• Aldosterone release also triggered by elevated K+ levels in ECF • Aldosterone brings about its effects slowly (hours to days) © 2013 Pearson Education, Inc.

Figure 26.8 Mechanisms and consequences of aldosterone release.

K+ concentration in the ECF

Figure 26.9 Mechanisms and consequences of ANP release.

Body Na+ content triggers renin release, increasing angiotensin II

Stretch of atria of heart due to BP Releases Negative feedback

Stimulates

Atrial natriuretic peptide (ANP) Targets

Adrenal cortex Releases

Hypothalamus and posterior pituitary

JG complex of the kidney

Aldosterone

Adrenal cortex

Effects Effects Renin release*

Targets

ADH release

Kidney tubules

Aldosterone release

Inhibits

Angiotensin II

Inhibits Collecting ducts of kidneys

Effects Vasodilation

Effects

Na+ reabsorption

K+ secretion

Na+ and H2O reabsorption Results in

Restores

Blood volume Results in

Homeostatic plasma levels of Na+ and K+

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Blood pressure

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Influence of other Hormones

Figure 26.10 Mechanisms regulating sodium and water balance help maintain blood pressure homeostasis. Systemic blood pressure/volume

Stretch in afferent arterioles

• Female sex hormones

Granular cells of kidneys

(+) Sympathetic nervous system

(+)

Release

(+)

Renin

Systemic arterioles Causes

Catalyzes conversion

•  H2O retention during menstrual cycles and pregnancy

– Progesterone:  aldosterone)

Inhibits baroreceptors in blood vessels

(+)

– Estrogens:  NaCl reabsorption (like aldosterone)

Na+

Filtrate NaCl concentration in ascending limb of nephron loop

(+)

Vasoconstriction

Angiotensin I

Angiotensinogen (from liver)

Results in Converting enzyme (in lungs)

(+)

Peripheral resistance

Angiotensin II

Posterior pituitary

(+)

reabsorption (blocks

Systemic arterioles

Secretes

(+)

Vasoconstriction

Aldosterone

Results in Peripheral resistance

ADH (antidiuretic hormone)

Adrenal cortex

Causes

• Promotes Na+ and H2O loss

Releases

(+)

(+)

Collecting ducts of kidneys

Targets

Causes

Distal kidney tubules

• Glucocorticoids:  Na+ reabsorption and promote edema

H2O reabsorption

Causes Na+ (and H2O) reabsorption Results in Blood volume

(+) stimulates

Blood pressure

Renin-angiotensin-aldosterone Mechanism Neural regulation (sympathetic nervous system effects) ADH release and effects

© 2013 Pearson Education, Inc.

© 2013 Pearson Education, Inc.

Regulation of Potassium Balance

Regulation of Potassium Balance

• Importance of potassium

• Hyperkalemia - too much K+ • Hypokalemia - too little K+ • Both disrupt electrical conduction in heart 

– Affects RMP in neurons and muscle cells (especially cardiac muscle) •  ECF [K+]  RMP  depolarization  reduced excitability •  ECF [K+]  hyperpolarization and nonresponsiveness

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– Sudden death

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Regulation of Potassium Balance

Influence of Plasma Potassium Concentration

• K+ part of body's buffer system • H+ shifts in and out of cells in opposite direction of K+ to maintain cation balance, so

• Most important factor affecting K+ secretion is its concentration in ECF • High K+ diet   K+ content of ECF  K+ entry into principal cells  K+ secretion • Low K+ diet or accelerated K+ loss reduces its secretion

– ECF K+ levels rise with acidosis – ECF K+ levels fall with alkalosis • Interferes with activity of excitable cells

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© 2013 Pearson Education, Inc.

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Regulation of Potassium Balance

Regulation of Calcium

• Influence of aldosterone

• 99% of body's calcium in bones

– Stimulates K+ secretion (and Na+ reabsorption) by principal cells – Adrenal cortical cells directly sensitive to K+ content of ECF • Increased K+ in adrenal cortex causes – Release of aldosterone  K+ secretion

• Abnormal aldosterone levels severely influence K+ levels

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– Calcium phosphate salts

• Ca2+ in ECF important for – Blood clotting – Cell membrane permeability – Secretory activities – Neuromuscular excitability - most important

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Regulation of Calcium

Influence of PTH

• Hypocalcemia   excitability and muscle tetany • Hypercalcemia  inhibits neurons and muscle cells, may cause heart arrhythmias • Calcium balance controlled by parathyroid hormone (PTH) from parathyroid gland

• PTH promotes increase in calcium levels by targeting

– Rarely deviates from normal limits

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Influence of PTH

– Bones – osteoclasts break down matrix, releasing calcium and phosphate to blood – Kidneys – increases calcium reabsorption; decreases phosphate ion reabsorption – Small intestine – increases calcium absorption (indirectly through stimulation of kidney to activate vitamin D precursor)

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Figure 16.13 Effects of parathyroid hormone on bone, the kidneys, and the intestine. Hypocalcemia (low blood Ca2+)

• 98% filtered calcium reabsorbed due to PTH • If ECF calcium levels normal PTH secretion inhibited • 75% of filtered phosphates reabsorbed in PCT

PTH release from parathyroid gland

Osteoclast activity in bone causes Ca2+ and PO43- release into blood

Ca2+ reabsorption in kidney tubule

Activation of vitamin D by kidney

– PTH inhibits this by decreasing the T m

• Phosphate reabsorption also affected by insulin (increases it) and glucagon (decreases it)

Ca2+ absorption from food in small intestine

Ca2+ in blood Initial stimulus Physiological response

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© 2013 Pearson Education, Inc.

Result

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Regulation of Anions

Acid-base Balance

• Cl– is major anion in ECF

• pH affects all functional proteins and biochemical reactions, so closely regulated • Normal pH of body fluids

– Helps maintain osmotic pressure of blood – 99% of Cl– is reabsorbed under normal pH conditions

• When acidosis occurs, fewer chloride ions are reabsorbed • Other anions have transport maximums and excesses are excreted in urine

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– Arterial blood: pH 7.4 – Venous blood and IF fluid: pH 7.35 – ICF: pH 7.0

• Alkalosis or alkalemia: arterial pH >7.45 • Acidosis or acidemia: arterial pH