10/26/2014

PowerPoint® Lecture Slides

Body Water Content
prepared by
Barbara Heard,
Human Anatomy & Physiology Atlantic Cape Community • Infants: 73% or more water (low body fat,
College Ninth Edition
low bone mass)
• Adult males: ~60% water
CHAPTER 26 • Adult females: ~50% water (higher fat
content, less skeletal muscle mass)
– Adipose tissue least hydrated of all
Fluid,
Electrolyte, • Water content declines to ~45% in old age
and Acid-Base
Balance
© Annie Leibovitz/Contact Press Images © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc.

Figure 26.1 The major fluid compartments of the body.

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

• Total body water = 40 L

Volume = 3 L, 20% of ECF

Plasma
• Two main fluid compartments
– Intracellular fluid (ICF) compartment: 2/3 in Interstitial
Intracellular fluid (ICF)
cells fluid (IF)
Volume = 25 L
Volume = 12 L
– Extracellular fluid (ECF) compartment: 1/3 40% of body weight
80% of ECF
outside cells
• 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 Extracellular
fluid (ECF)
secretions
Volume = 15 L
20% of body weight
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Electrolyte Concentration 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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Extracellular and Intracellular Fluids Extracellular and Intracellular Fluids

• Each fluid compartment has distinctive • ICF:

pattern of electrolytes – Low Na+ and Cl–
• ECF – Major cation: K+
– All similar – Major anion HPO42–
• Major cation: Na+ – More soluble proteins than in plasma
• Major anion: Cl–
– Except: higher protein, lower Cl– content of
plasma

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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 Kidneys

tract

140

120
Total solute concentration (mEq/L)

Blood plasma
Interstitial fluid 100
Blood O2 CO2 Nutrients H2O, H2O, Nitrogenous
Intracellular fluid
plasma Ions Ions wastes
Na+ Sodium
80
K+ Potassium
Ca2+ Calcium
Mg2+ O2 CO2 Nutrients H2O Ions Nitrogenous
Interstitial
Magnesium
60
wastes
HCO3– Bicarbonate fluid
Cl– Chloride
HPO42– Hydrogen 40
phosphate
SO42– Sulfate

20

Intracellular
0 fluid in tissue cells
Na+ K+ Ca2+ Mg2+ HCO3– Cl– HPO42– SO42– Protein
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anions

Figure 26.4 Major sources of water intake and output.

Water Balance and ECF Osmolality

• Water intake must = water output = ~ 2500 100 ml Feces 4%

ml/day Metabolism 10% 250 ml
200 ml
Sweat 8%

• Water intake: beverages, food, and Foods 30%

750 ml
Insensible loss
via skin and
700 ml
metabolic water lungs 28%

• Water output: urine (60%), insensible 2500 ml

water loss (lost through skin and lungs), Urine 60%

Beverages 60% 1500 ml 1500 ml
perspiration, and feces

Average intake Average output

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Figure 26.5 The thirst mechanism for regulating water intake.

Maintenance of Body fluid Osmolality ECF osmolality Plasma volume
(5 –10%)

Blood pressure

• Osmolality maintained at ~ 280 – 300 Osmoreceptors

in hypothalamus
Saliva Granular cells
in kidney

mOsm Dry mouth

Renin-angiotensin-
aldosterone
mechanism

• Rise in osmolality  Angiotensin II

– Stimulates thirst
Hypothalamic

– ADH release
thirst center

• Decrease in osmolality 
Sensation of thirst;
person takes a
drink

– Thirst inhibition Water moistens

mouth, throat;
stretches stomach,

– ADH inhibition
intestine

Water absorbed
from GI tract

Initial stimulus
Physiological response
ECF osmolality
Plasma volume Result
Increases, stimulates
© 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc. Reduces, inhibits

Figure 26.6 Mechanisms and consequences of ADH release.

Regulation of Water Output: Influence of ECF osmolality
Na+ concentration

ADH
in plasma

Plasma volume

• Other factors may trigger ADH release

Stimulates
(5–10%), BP

– Large changes in blood volume or pressure Osmoreceptors

in hypothalamus
Inhibits

• E.g.,  BP   ADH release due to blood vessel

Negative
feedback
inhibits
Baroreceptors
in atria and
Stimulates
baroreceptors and renin-angiotensin-aldosterone large vessels

mechanism Posterior pituitary

Stimulates

• Factors lowering blood volume: intense sweating, Releases ADH

vomiting, or diarrhea; severe blood loss; traumatic Antidiuretic

hormone (ADH)

burns; and prolonged fever Targets

Collecting ducts
of kidneys

Effects

Water reabsorption

Results in

ECF osmolality Scant urine

Plasma volume

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Disorders of Water Balance Disorders of Water Balance: Hypotonic

Hydration
• Principal abnormalities of water balance • Cellular overhydration, or water
– Dehydration intoxication
– Hypotonic hydration • Occurs with renal insufficiency or rapid
– Edema
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

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Figure 26.7b Disturbances in water balance. Slide 1

Disorders of Water Balance: Edema

• Atypical accumulation of IF  tissue swelling

1 Excessive 2 ECF osmotic 3 H2O moves (not cell swelling)
H2O enters pressure falls into cells by
the ECF osmosis; cells swell • Result of  fluid out of blood or  fluid into blood
•  fluid out of blood caused by
– Increased capillary hydrostatic pressure or
permeability
• Capillary hydrostatic pressure increased by incompetent
venous valves, localized blood vessel blockage, congestive
heart failure,  blood volume
Consequences of hypotonic hydration (water gain). • Capillary permeability increased by ongoing inflammatory
If more water than solutes is gained, cells swell. response

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Edema Electrolyte Balance

•  fluid returning to blood result of • Electrolytes are salts, acids, bases, some
– Imbalance in colloid osmotic pressures, e.g., proteins
hypoproteinemia ( plasma protein levels  • Electrolyte balance usually refers only to
low colloid osmotic pressure)
salt balance
• Fluids fail to return at venous ends of capillary
beds • Salts control fluid movements; provide
• Results from protein malnutrition, liver disease, or minerals for excitability, secretory activity,
glomerulonephritis membrane permeability
• Salts enter body by ingestion and
metabolism; lost via perspiration, feces,
urine, vomit
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Table 26.2 Sodium Concentration and Sodium Content

Central Role of Sodium

• 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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Regulation of Sodium Balance: Aldosterone Aldosterone

• Regardless of aldosterone presence • Aldosterone  decreased urinary output;

– 65% Na+ reabsorbed in proximal tubules; 25% increased blood volume
reclaimed in nephron loops – By active reabsorption of remaining Na+ in
– Na + never secreted into filtrate distal convoluted tubule and collecting duct
• Water in filtrate follows Na+ if ADH is • Also causes increased K+ secretion
present
–  Na+ in urine   water loss

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Regulation of Sodium Balance: Aldosterone Regulation of Sodium Balance: Aldosterone

• Renin-angiotensin-aldosterone • Renin catalyzes production of

mechanism main trigger for aldosterone angiotensin II
release – Prompts aldosterone release from adrenal
– Granular cells of JGC secrete renin in cortex
response to –  Na+ reabsorption by kidney tubules
• Sympathetic nervous system stimulation • Aldosterone release also triggered by
•  filtrate NaCl concentration
elevated K+ levels in ECF
•  stretch (due to  blood pressure) of granular
cells • Aldosterone brings about its effects slowly
(hours to days)

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Figure 26.8 Mechanisms and consequences of aldosterone release. Figure 26.9 Mechanisms and consequences of ANP release.

K+ concentration Body Na+ content Stretch of atria

in the ECF triggers renin release, of heart due to BP
increasing angiotensin II Releases
Negative Atrial natriuretic peptide
feedback (ANP)
Stimulates
Targets

Adrenal cortex

Releases JG complex Hypothalamus and Adrenal cortex

of the kidney posterior pituitary

Aldosterone Effects
Effects

Targets Renin release*

ADH release Aldosterone

release
Kidney tubules
Angiotensin II Inhibits
Inhibits

Collecting ducts
Effects of kidneys
Vasodilation
Effects

Na+ reabsorption K+ secretion Na+ and H2O reabsorption

Results in

Restores Blood volume

Results in
Homeostatic plasma
levels of Na+ and K+
Blood pressure

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

Filtrate NaCl
Stretch in afferent concentration in ascending Inhibits baroreceptors

• Female sex hormones

arterioles limb of nephron loop in blood vessels

(+) (+) (+)

– Estrogens:  NaCl reabsorption (like

Granular cells (+) Sympathetic
of kidneys nervous system
Release (+)

aldosterone) Renin

Catalyzes conversion
Systemic arterioles
Causes

•  H2O retention during menstrual cycles and Angiotensinogen

(from liver)
Angiotensin I Vasoconstriction
Results in

pregnancy Converting enzyme (in lungs)

Angiotensin II
Peripheral resistance (+)
Posterior pituitary
(+)

– Progesterone:  Na+ reabsorption (blocks (+)

Systemic arterioles
(+)
Adrenal cortex
Releases

ADH (antidiuretic
hormone)
Secretes
aldosterone) Causes

Vasoconstriction Aldosterone
(+)

Collecting ducts
of kidneys

• Promotes Na+ and H2O loss

Results in Targets
Causes
Peripheral resistance Distal kidney tubules
H2O reabsorption

• Glucocorticoids:  Na+ reabsorption and

Causes

Na+ (and H2O)

reabsorption
Results in

promote edema Blood volume

(+) stimulates
Renin-angiotensin-aldosterone
Blood pressure Mechanism
Neural regulation (sympathetic
nervous system effects)
ADH release and effects
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Regulation of Potassium Balance Regulation of Potassium Balance

• Importance of potassium • Hyperkalemia - too much K+

– Affects RMP in neurons and muscle cells • Hypokalemia - too little K+
(especially cardiac muscle)
• Both disrupt electrical conduction in heart
•  ECF [K+]  RMP  depolarization  reduced
excitability 
•  ECF [K+]  hyperpolarization and – Sudden death
nonresponsiveness

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Regulation of Potassium Balance Influence of Plasma Potassium

Concentration
• K+ part of body's buffer system • Most important factor affecting K+
• H+ shifts in and out of cells in opposite secretion is its concentration in ECF
direction of K+ to maintain cation balance, • High K+ diet   K+ content of ECF  K+
so entry into principal cells  K+ secretion
– ECF K+ levels rise with acidosis • Low K+ diet or accelerated K+ loss reduces
– ECF K+ levels fall with alkalosis its secretion
• Interferes with activity of excitable cells

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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+ – Calcium phosphate salts
reabsorption) by principal cells • Ca2+ in ECF important for
– Adrenal cortical cells directly sensitive to K+ – Blood clotting
content of ECF
– Cell membrane permeability
• Increased K+ in adrenal cortex causes
– Release of aldosterone  K+ secretion – Secretory activities
• Abnormal aldosterone levels severely – Neuromuscular excitability - most important
influence K+ levels

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Regulation of Calcium Influence of PTH

• Hypocalcemia   excitability and • PTH promotes increase in calcium levels

muscle tetany by targeting
• Hypercalcemia  inhibits neurons and – Bones – osteoclasts break down matrix,
muscle cells, may cause heart arrhythmias releasing calcium and phosphate to blood
– Kidneys – increases calcium reabsorption;
• Calcium balance controlled by parathyroid
decreases phosphate ion reabsorption
hormone (PTH) from parathyroid gland
– Small intestine – increases calcium
– Rarely deviates from normal limits 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.
Influence of PTH Hypocalcemia
(low blood Ca2+)

• 98% filtered calcium reabsorbed due to

PTH release from
parathyroid gland

PTH
• If ECF calcium levels normal PTH
secretion inhibited Osteoclast activity Ca2+ reabsorption Activation of
in bone causes Ca2+

• 75% of filtered phosphates reabsorbed in

in kidney tubule vitamin D by kidney
and PO43- release
into blood

PCT
– PTH inhibits this by decreasing the T m
• Phosphate reabsorption also affected by
Ca2+ absorption
from food in small
intestine

insulin (increases it) and glucagon

(decreases it) Ca2+ in blood

Initial stimulus
Physiological response

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Regulation of Anions Acid-base Balance

• Cl– is major anion in ECF • pH affects all functional proteins and

– Helps maintain osmotic pressure of blood biochemical reactions, so closely
– 99% of Cl– is reabsorbed under normal pH regulated
conditions • Normal pH of body fluids
• When acidosis occurs, fewer chloride ions – Arterial blood: pH 7.4
are reabsorbed – Venous blood and IF fluid: pH 7.35
• Other anions have transport maximums – ICF: pH 7.0
and excesses are excreted in urine • Alkalosis or alkalemia: arterial pH >7.45
• Acidosis or acidemia: arterial pH <7.35

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Acid-base Balance Acid-base Balance

• Most H+ produced by metabolism • Concentration of hydrogen ions regulated

– Phosphorus-containing protein breakdown
releases phosphoric acid into ECF
– Lactic acid from anaerobic respiration of
glucose
– Fatty acids and ketone bodies from fat
metabolism
– H+ liberated when CO2 converted to HCO3– in
blood
sequentially by
– Chemical buffer systems: rapid; first line of
defense
– Brain stem respiratory centers: act within 1–3
min
– Renal mechanisms: most potent, but require
hours to days to effect pH changes

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Figure 26.11 Dissociation of strong and weak acids in water.

Acid-base Balance: Chemical Buffer
Systems
• Strong acids dissociate completely in
water; can dramatically affect pH
• Weak acids dissociate partially in water;
are efficient at preventing pH changes
• Strong bases dissociate easily in water;
quickly tie up H+
• Weak bases accept H+ more slowly

A strong acid such as A weak acid such as

HCI dissociates H2CO3 does not
completely into its ions. dissociate completely.
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Chemical Buffer Systems Phosphate Buffer System

• Chemical buffer: system of one or more • Action nearly identical to bicarbonate

compounds that act to resist pH changes buffer
when strong acid or base is added • Components are sodium salts of:
– Bind H+ if pH drops; release H+ if pH rises – Dihydrogen phosphate (H2PO4–), a weak acid
1. Bicarbonate buffer system – Monohydrogen phosphate (HPO42–), a weak
2. Phosphate buffer system base
3. Protein buffer system • Unimportant in buffering plasma
• Effective buffer in urine and ICF, where
phosphate concentrations are high

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Respiratory Regulation of H+ Respiratory Regulation of H+

• Hypercapnia activates medullary • Alkalosis depresses respiratory center

chemoreceptors
–  Increased respiratory rate and depth
• Rising plasma H+ activates peripheral
chemoreceptors
–  Increased respiratory rate and depth
– More CO2 is removed from the blood
– H+ concentration is reduced
– Respiratory rate and depth decrease
– H+ concentration increases
• Respiratory system impairment causes
acid-base imbalances
– Hypoventilation  respiratory acidosis
– Hyperventilation  respiratory alkalosis

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Renal Mechanisms of Acid-Base Balance Renal Mechanisms of Acid-base Balance

• Most important renal mechanisms • Renal regulation of acid-base balance

– Conserving (reabsorbing) or generating new depends on kidney's ability to secrete H+
HCO3– • H+ secretion occurs in PCT and collecting
– Excreting HCO3– duct type A intercalated cells:
• Generating or reabsorbing one HCO3– – The H+ comes from H2CO3 produced in
same as losing one H+ reactions catalyzed by carbonic anhydrase
• Excreting one HCO3– same as gaining one inside cells
H+ – As H+ secreted, Na+ reabsorbed
– See Steps 1 and 2 of following figure

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Figure 26.12 Reabsorption of filtered HCO3– is coupled to H+ secretion. Slide 1

Renal Mechanisms of Acid-base Balance
1 CO2 combines with water 2 H2CO3 is quickly split, forming
within the tubule cell, forming H+ and bicarbonate ion (HCO3−).
H2CO3.

Filtrate in
tubule
Nucleus
3a H+ is secreted
into the filtrate. • Rate of H+ secretion changes with ECF
Peri-
lumen PCT cell tubular
capillary
3b For each H+ secreted, CO2 levels
a HCO3− enters the
ATPase peritubular capillary
blood either via symport –  CO2 in peritubular capillary blood   rate
with Na+ or via antiport
with CI−. of H+ secretion
3a 3b
4 ATPase
2 4 Secreted H+
combines with HCO3− in
– System responds to both rising and falling H+
5 CA *
1 CA
the filtrate, forming
carbonic acid (H2CO3).
concentrations
6 HCO3− disappears from
the filtrate at the same
rate that HCO3− (formed
Tight within the tubule cell)
junction enters the peritubular
capillary blood.
Primary active transport Transport protein 6 CO diffuses into the tubule 5 The H CO formed in
Secondary active transport 2 2 3
CA Carbonic anhydrase
Simple diffusion cell, where it triggers further H+ the filtrate dissociates to
secretion. release CO2 and H2O.

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Figure 26.13 New HCO3– is generated via buffering of secreted H+ by HPO42– (monohydrogen phosphate). Slide 1
1 CO2 combines with water 2 H2CO3 is quickly 3a H+ is Ammonium Ion Excretion
within the type A intercalated split, forming H+ and secreted into
cell, forming H2CO3. bicarbonate ion the filtrate by a
(HCO3−). H+ ATPase
pump.
Filtrate in
tubule
Nucleus
Peri-
• More important mechanism for excreting
lumen Tight junction 3b For
tubular
capillary each H+ acid
secreted, a
HCO3− enters
the peritubular • Involves metabolism of glutamine in PCT
1 capillary blood
via an antiport
carrier in a
cells
2 HCO3− -CI−
3a 3b exchange
process.
• Each glutamine produces 2 NH4+ and 2
"new" HCO3–
ATPase (new)
4 4 Secreted
Type A H+ combines
intercalated
cell of collecting duct
with HPO42−
in the tubular • HCO3– moves to blood and NH4+ is
5 filtrate,
out in urine Forming
H2PO4−.
excreted in urine
Primary active transport
Secondary active transport
Transport protein
Ion channel
5 The H PO −
2 4
• Replenishes alkaline reserve of blood
Simple diffusion Carbonic anhydrase is excreted
Facilitated diffusion in the urine.
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Figure 26.14 New HCO3– is generated via glutamine metabolism and NH4+ secretion. Slide 1
1 PCT cells 2a This weak acid NH4+ 2b For each NH4+ secreted, Bicarbonate Ion Secretion
metabolize (ammonium) is secreted into a bicarbonate ion (HCO3−)
glutamine to the filtrate, taking the place of enters the peritubular capillary
NH4+and HCO3−. H+ on a Na+ -H+ antiport carrier. blood via a symport carrier.

• When body in alkalosis, type B

Filtrate in Nucleus
tubule lumen
Peri-
PCT tubule cells
tubular
capillary intercalated cells
Glutamine Glutamine
Deamination,
Glutamine
– Secrete HCO3–
1 oxidation, and
acidification
(+H+)
– Reclaim H+ to acidify blood
2a 2b
(new)
3

out in urine
ATPase

Tight junction

Primary active transport Simple diffusion 3 The NH4+ is

Secondary active transport Transport protein excreted in the urine.
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Bicarbonate Ion Secretion
• Mechanism is opposite of bicarbonate ion
reabsorption process by type A
intercalated cells
• Even during alkalosis, nephrons and
collecting ducts conserve more HCO3–
than they excrete
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Respiratory Acidosis and Alkalosis
• PCO2 below 35 mm Hg  respiratory
alkalosis
– Common result of hyperventilation often due
to stress or pain
• CO2 eliminated faster than produced
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Metabolic Acidosis and Alkalosis
• Metabolic alkalosis much less common
than metabolic acidosis
– Indicated by rising blood pH and HCO3–
– Causes include vomiting of acid contents of
stomach or by intake of excess base (e.g.,
antacids)
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10/26/2014
Respiratory Acidosis and Alkalosis
• Most important indicator of adequacy of
respiratory function is PCO2 level (normally
35–45 mm Hg)
– PCO2 above 45 mm Hg  respiratory acidosis
• Common cause of acid-base imbalances
• Due to decrease in ventilation or gas exchange
• CO2 accumulates in blood
• Characterized by falling blood pH and rising P CO2
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Metabolic Acidosis and Alkalosis
• Metabolic acidosis – low blood pH and
HCO3–
– Causes
• Ingestion of too much alcohol ( acetic acid)
• Excessive loss of HCO3– (e.g., persistent diarrhea)
• Accumulation of lactic acid (exercise or shock),
ketosis in diabetic crisis, starvation, and kidney
failure
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Respiratory Compensation
• Changes in respiratory rate and depth
• In metabolic acidosis
– High H+ levels stimulate respiratory centers
– Rate and depth of breathing elevated
– Blood pH is below 7.35 and HCO3– level is
low
– As CO2 eliminated by respiratory system,
PCO2 falls below normal
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