SCIT 1408 Applied Human Anatomy and Physiology II - Fluids Chapter 26

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Body Water Content Infants 73% or >, water Females ~ 50%, water Males ~ 60%, water Old age ~ 45%, water

Total water content declines with age


Fluid Compartments ICF – intracellular fluid; (2/3 total fluid volume) ECF – extracellular fluid; (1/3 total fluid volume)

Plasma – the fluid portion of the blood Interstitial fluid (IF) – fluid in spaces between cells

Other minor ECFs Lymph, CSF, eye humors, synovial fluid, serous

fluid, and GI secretions


Fluid Compartments

PLAY InterActive Physiology ®: Introduction to Body Fluids, page 10

Figure 26.1


Composition of Body Fluids Water = universal solvent Solutes are:

Electrolytes inorganic salts, all acids and bases, & some proteins

Dissociate in H20, > particles, > osmosis factor

Nonelectrolytes glucose, lipids, creatinine, & urea Do not dissociate, 1 particle, < osmosis factor

Water moves according to osmotic gradientsPLAY InterActive Physiology ®:

Introduction to Body Fluids, page 11


Electrolyte Concentration mEq/L - # electrical charges/ L soln mEq/L = (concentration of ion in [mg/L]/the

atomic weight of ion) number of electrical charges on one ion

For single charged ions, 1 mEq = 1 mOsm For bivalent ions, 1 mEq = 1/2 mOsm 1 mOsm = # solute particles in 1 g or 1 ml H20


Electrolyte Composition of Body Fluids

Figure 26.2

Body Fluid Compartments

ECF

ICF


Fluid Movement Among Compartments Compartmental exchange is regulated by osmotic

and hydrostatic pressures IF in capillary beds returned to blood via lymph Exchanges between IF & ICF via semi-permeable

cell membranes Two-way water flow is substantial Nutrients flow into ICF, wastes flow out (1-way

flow)


Extracellular and Intracellular Fluids Osmolalities of all body fluids are equal

changes in solute concentrations are quickly followed by osmotic changes

ICF volume due to ECF [solute]

Plasma – only fluid that circulates throughout the body links external and internal environments

PLAY InterActive Physiology ®: Introduction to Body Fluids, pages 19–22


Continuous Mixing of Body Fluids

Figure 26.3


Water Intake and Output for Proper Hydration

Figure 26.4

> plasma osmolality triggers release of ADH & stimulates thirst


Regulation of Water Intake The hypothalamic thirst center is stimulated:

By a decline in plasma volume of 10%–15% By increases in plasma osmolality of 1–2% Via baroreceptor input, angiotensin II, other stimuli Not always stimulated when fluid vol is < as in

exercise

Thirst turned off by mouth moisture, stomach stretch receptors

PLAY InterActive Physiology ®: Water Homeostasis, page 18


Regulation of Water Intake: Thirst Mechanism

Figure 26.5


Regulation of Water Output Obligatory H20 losses include:

Insensible water losses from lungs and skin

H20 in undigested food residues in feces

Kidneys excrete 900-1200 mOsm of solutes to maintain blood homeostasis

Urine solutes must be flushed out of the body in H20 ---- H20 follows Na+

PLAY InterActive Physiology ®: Water Homeostasis, pages 3–10


Influence and Regulation of ADH Water reabsorption in collecting ducts directly

proportional to ADH release < ADH = dilute urine, < volume of body fluids > ADH = concentrated urine, > body fluids via > of

aquaporins in collecting duct membranes

Regulation of ADH release = hypothalmus > ADH release: > fever; > sweating, vomiting,

diarrhea; severe blood loss, burns



Mechanisms and Consequences of ADH Release

Figure 26.6


Disorders of Water Balance: Dehydration H20 loss > H20 intake; negative fluid balance From: hemorrhage, burns, vomiting, diarrhea,

sweating, water deprivation, > diuretics Signs/symptoms: cottonmouth, thirst, dry flushed

skin, oliguria Prolonged dehydration: < H20 in ECF

wt loss Fever mental confusion hypovolemic shock, < electrolytes


Disorders of Water Balance: Dehydration

Figure 26.7a


Disorders of Water Balance: Hypotonic Hydration

Figure 26.7b


Disorders of Water Balance: Hypotonic Hydration From: Renal insufficiency or >>> ingestion of H20

Hyponatremia ECF diluted – sodium level normal but > water

H20 moves into cells

Nausea, vomiting, cramping, cerebral edema Immediate threat to neurons


Disorders of Water Balance: Edema > fluid in the interstitial space, tissue swelling Caused by: > flow of fluids out of the blood or

< return of fluids to blood > flow of fluids out of the blood :

> BP, > capillary permeability (inflammation) Damaged venous valves, blocked blood vessels CHF, hypertension, high blood volume


Edema < return of fluids to blood (imbalance in colloid

osmotic pressures) Hypoproteinemia – < plasma proteins In capillary beds, fluid leaves at the arterial ends, < plasma

proteins fail to pull fluid back in at venous end From: protein malnutrition, liver disease,

glomerulonephritis Blocked lymphatic vessels

Leaked proteins collect in IF, > fluid from blood; leads to < BP, < circulation

InterActive Physiology ®: Electrolyte Homeostasis, pages 12–16


Electrolyte Balance Electrolyte balance refers mainly to salt balance Salts ingested, lost in urine, feces, sweat Na+, K+, Ca++ regulation very important:

Neuromuscular excitability Secretory activity Membrane permeability Controlling fluid movements


Sodium in Fluid and Electrolyte Balance Sodium > cation in the ECF; > osmotic pressure Sodium salts: NaHCO3, NaCl

Account for 90-95% of all solutes in the ECF Contribute 280 mOsm of the total 300 mOsm ECF

solute concentration Plasma membranes fairly impermeable to Na+ but

some does leak into cells & is pumped out by Na+-K+ pumps

When [Na+] changes, H20 volume changes- ECF [Na+] remains pretty constant


Sodium in Fluid and Electrolyte Balance Changes in plasma sodium levels affect:

Plasma volume & BP ICF & IF volumes

Na+ levels chiefly controlled by kidneys & coupled to acid-base balance

PLAY InterActive Physiology ®: Electrolyte Homeostasis, pages 4–6, 18–22


Regulation of Sodium Balance: Aldosterone Sodium reabsorption

65% of Na+in filtrate reabsorbed in PCT 25% reclaimed in the loops of Henle

IF, > aldosterone levels

1. all remaining Na+ is reabsorbed

2. > aquaporins inserted into DCT & collecting ducts, increasing membrane permeability to H20

3. H20 follows Na+ & both are reabsorbed


Regulation of Sodium Balance: Aldosterone JGA stimulates renin-angiotensin mechanism to

release aldosterone when:

1. Sympathetic nervous system stimulation

2. Decreased filtrate osmolality

3. Decreased stretch (due to decreased blood pressure)


Regulation of Sodium Balance: Aldosterone Adrenal cortex releases aldosterone if :

1. > K+ in plasma (ECF)

2. < Na+ in plasma (not nearly as sensitive)

> Aldosterone- effects mediated very slowly

1. < urine output

2. > BP



Regulation of Sodium Balance: Aldosterone

Figure 26.8


Addison’s Disease Hypoaldosteronism Hypovolemia a high risk


Maintenance of Blood Pressure Homeostasis

Figure 26.9

Correcting < BP

Baroreceptors in aorta, carotids, heart


Mechanisms and Consequences of ANP Release

Figure 26.10

Correcting > BP


Influence of Other Hormones on Na+ Balance Estrogens:

> NaCl reabsorption by renal tubules May cause water retention during menstrual cycles > edema during pregnancy

Progesterone: < Na+ reabsorption, > Na+ & H20 loss

Glucocorticoids > Na+ reabsorption, > edema


Regulation of Potassium Balance K+ > intracellular cation; Maintains RMP

> ECF K+ (hyperkalemia), < membrane potential < ECF K+ (hypokalemia) = hyperpolarization &

nonresponsiveness Imbalance effects excitable cells especially

Neurons Muscles Heart- sudden death


Regulation of Potassium Balance

ICF: ECF- H+ exchange with K+ for cation balance Acidosis, ECF K+ rises Alkalosis, ECF K+ falls


Regulatory Site: Cortical Collecting Ducts 10- 15% of filtrate K+ lost in urine regardless of need

Must ingest K+ foods over time to keep proper K+ levels

> ECF K+, principal cells in collecting ducts > K+ secreted into filtrate; from diet high in K+

< ECF K+, < secretion/excretion; from diet low in K+ Type A intercalated cells can reabsorb some K+ left in

the filtrate


Influence of Aldosterone on K+ secretion > Aldosterone, > K+ secretion, > Na+ reabsorption

by principal cells > ECF K+ around the adrenal cortex causes:

Release of aldosterone Potassium secretion

Potassium controls its own ECF concentration via feedback regulation of aldosterone release


Homeostatic Imbalance Dietary Salt substitutes contain > K+ Must have adequate aldosterone levels to prevent

hyperkalemia Too much aldosterone, (adrenocortical tumor),

hypokalemia, hyperpolarization of neurons & paralysis


Regulation of Calcium Ca++ in ECF is important for:

Blood clotting, membrane permeability, secretory behavior, neuromuscular cells

Hypocalcemia: > excitability, causes muscle tetany

Hypercalcemia: < excitability, May cause heart arrhythmias

Calcium balance is controlled by parathyroid hormone (PTH) and calcitonin (minor)


Regulation of Calcium and Phosphate PTH > ECF Ca++ from:

Bones – mostly from here Small intestine – > intestinal absorption Kidneys – > Ca++ reabsorption, which goes with

< phosphate reabsorption Normal Ca++ inhibits PTH release


Acid-Base Balance Normal pH of body fluids:

Arterial blood = 7.4 Venous blood & IF = 7.35 ICF = 7.0

Alkalosis or alkalemia = arterial blood pH > 7.45 Acidosis or acidemia = arterial pH < 7.35

(physiological acidosis b/c it is below normal even though it is above neutral pH & not “acidic”)


Hydrogen Ions Most from cellular metabolism [H+] Regulation:

Chemical buffer systems – act within seconds Respiratory center – acts within 1-3 minutes Renal – require hrs- days

Acids- H+ donors Bases- H+ acceptors


Strong and Weak Acids

Figure 26.11

Completely dissociates

Partially dissociates

Strong: Weak:


Chemical Buffer Systems 3 major chemical buffer systems

Bicarbonate buffer system- important ECF buffer Phosphate buffer system Protein buffer system

Any drifts in pH are resisted by the entire chemical buffering system


Bicarbonate Buffer System A mixture of carbonic acid (H2CO3) – weak acid

& sodium bicarbonate (NaHCO3) – weak base

If HCl added: Bicarbonate ties up H+, > H2CO3

HCl + NaHCO3 H2CO3 + NaClInterActive Physiology ®: Acid/Base Homeostasis, pages 16–17


Phosphate Buffer System Nearly identical to the bicarbonate system

Sodium salts of dihydrogen phosphate (H2PO4¯), a

weak acid

Monohydrogen phosphate (HPO42¯), a weak base

This system is an effective buffer in urine and intracellular fluid

PLAY InterActive Physiology ®: Acid/Base Homeostasis, page 18


Protein Buffer System Plasma & intracellular proteins - most plentiful and

powerful buffers; eg. hgb Some amino acids of proteins have:

Carboxyl groups- (weak acids) Amino groups- (weak bases)

Amphoteric molecules are protein molecules that can function as a weak acid or a weak base



Physiological Buffer Systems The respiratory system regulation:

CO2 + H2O H2CO3 H+ + HCO3¯

reversible rxn

PLAY InterActive Physiology ®: Acid/Base Homeostasis, page 20–26


Physiological Buffer Systems During carbon dioxide unloading, H+ incorporated

into H2O

When hypercapnia or rising plasma H+ occurs:

Deeper, more rapid breathing expels > CO2

< H+ Alkalosis causes slower, shallow breathing, > H+

Lung dysfunction causes acid-base imbalance (respiratory acidosis or respiratory alkalosis)



Renal Mechanisms of Acid-Base Balance Chemical buffers can tie up excess acids or bases,

but they cannot eliminate them from the body The lungs can eliminate carbonic acid by

eliminating carbon dioxide Only the kidneys can rid the body of metabolic

acids (phosphoric, uric, & lactic acids, & ketones) and prevent metabolic acidosis

The ultimate acid-base regulatory organs are the kidneys


Renal Mechanisms of Acid-Base Balance

1. Conserving (reabsorbing) or generating new HCO3¯

2. Excreting HCO3¯

Losing a HCO3¯ is the same as gaining a H+

Reabsorbing a HCO3¯ is the same as losing a H+


Renal Mechanisms of Acid-Base Balance Hydrogen ion secretion occurs in the PCT and in

type A intercalated cells Hydrogen ions from the dissociation of carbonic

acid

H2CO3 H+ + HCO3¯

Tubules impermeable to HCO3¯; cannot reabsorb but can conserve via an indirect way



Reabsorption of Bicarbonate

1. In tubule cells : CO2 + H2O H2CO3

2. H2CO3 H+ + HCO3¯

3. For each H+ secreted, a Na+ & HCO3¯ are reabsorbed by the PCT cells

4. Secreted H+ form H2CO3 in filtrate - in tubule lumen

5. H2CO3 then dissociates to CO2 + H2O

6. CO2 diffuses into tubule cell, > H+ secretion

thus, HCO3¯ disappears from filtrate at the same rate that it enters the peritubular capillary blood



Reabsorption of Bicarbonate Carbonic acid formed

in filtrate dissociates to release carbon dioxide and water

Carbon dioxide then diffuses into tubule cells, where it acts to trigger further hydrogen ion secretion

Figure 26.12


Generating New Bicarbonate Ions Type A intercalated cells of Collecting ducts

generate new HCO3¯ by 2 mechanisms:

1. Renal excretion of acid via secretion and excretion of H+

2. Renal excretion of acid via secretion and excretion of NH4

+ ( ammonium ions)



Hydrogen Ion Excretion Dietary H+ must be counteracted by generating

new HCO3¯ The excreted H+ must bind to buffers in the urine

(phosphate buffer system) Intercalated cells actively secrete H+ into urine,

which is buffered and excreted HCO3¯ generated is:

Moved into the interstitial space via a cotransport system

Passively moved into the peritubular capillary blood


Hydrogen Ion Excretion In response to

acidosis: Kidneys generate

bicarbonate ions and add them to the blood

An equal amount of hydrogen ions are added to the urine

Figure 26.13


Ammonium Ion Excretion This method uses NH4+ produced by the

metabolism of glutamine in PCT cells Each glutamine metabolized produces two

ammonium ions and two bicarbonate ions Bicarbonate moves to the blood and ammonium

ions are excreted in urine


Ammonium Ion Excretion

Figure 26.14


Bicarbonate Ion Secretion When the body is in alkalosis, type B intercalated

cells:

Secrete HCO3¯

Reabsorb H+ , acidify the blood

The mechanism is the opposite of type A intercalated cells and the HCO3¯ reabsorption process

Even during alkalosis, the nephrons and collecting ducts excrete fewer HCO3¯ than they conserve



Respiratory Acidosis and Alkalosis Respiratory system fails to balance pH

Abnormal PCO2 indicates < respiratory function

Normal PCO2 : 35 - 45 mm Hg

Respiratory acidosis: PCO2 > 45mm Hg

Respiratory alkalosis: PCO2 < 35 mm Hg


Respiratory Acidosis and Alkalosis Respiratory acidosis:

> common cause of acid-base imbalance > CO2, < pH From shallow breathing or < gas exchange

pneumonia, cystic fibrosis, emphysema

Respiratory alkalosis: < CO2, > pH Hyperventilation

Stress, pain


Metabolic Acidosis Second most common cause of acid-base

imbalance < pH, < HCO3¯ From:

> alcohol, > loss HCO3¯ > lactic acid from exercise or shock, ketosis,

kidney failure


Metabolic Alkalosis

> pH, > HCO3¯

From: Vomiting of the acid contents of the stomach Intake of excess base (e.g., from antacids) Constipation, in which excessive bicarbonate is

reabsorbed


Effects of Acidosis & Alkalosis pH < 7.0

CNS depressed Coma Death

pH > 7.8 CNS overstimulated

Muscle tetany > agitation, nervousness convulsions


Respiratory and Renal Compensations Respiratory System attempts to correct metabolic

acid-base imbalances Renal System attempts to correct imbalances

caused by respiratory disease


Respiratory Compensation of Metabolic Acidosis

> rate & depth of breathing b/c > H+ & < HCO3¯ stimulate respiratory centers

As CO2 is “blown off” during respiratory compensation to get rid of H+, PCO2 levels <

In respiratory acidosis, the respiratory rate is often depressed and is the immediate cause of the acidosis


Respiratory Compensation of Metabolic Alkalosis

Compensation exhibits slow, shallow breathing, allowing CO2 to accumulate in the blood

Compensation is revealed by: > pH (over 7.45)

> HCO3¯

Rising PCO2



Renal Compensation of Respiratory Acidosis To correct respiratory acid-base imbalance, renal

mechanisms are stepped up

Acidosis has > PCO2 and > HCO3¯

> PCO2 is the cause of acidosis

> HCO3¯ indicate the kidneys are retaining HCO3¯ to offset the acidosis


Renal Compensation of Respiratory Alkalosis < PCO2

> pH

The kidneys eliminate HCO3¯ by:

failing to reclaim it actively secreting it


Developmental Aspects Water content of the body is > at birth (70-80%);

declines with age; 58% at adulthood > muscle mass, > water (adult males) Homeostatic mechanisms slow down with age Elders > risk of dehydration- < responsive to thirst The very young and the very old are the most

frequent victims of fluid, acid-base, and electrolyte imbalances


Problems with Fluid, Electrolyte, and Acid-Base Balance Occur in the young, reflecting:

Low residual lung volume High rate of fluid intake and output High metabolic rate yielding more metabolic

wastes High rate of insensible water loss Inefficiency of kidneys in infants

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SCIT 1408 Applied Human Anatomy and Physiology II - Fluids Chapter 26

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