© 2012 pearson education, inc. figure 27-1a the composition of the human body solid components...

© 2012 Pearson Education, Inc.

Figure 27-1a The Composition of the Human Body

SOLID COMPONENTS(31.5 kg; 69.3 lbs)

Proteins Lipids Minerals Carbohydrates Miscellaneous

Kg

The body composition (by weight, averaged for bothsexes) and major body fluid compartments of a 70-kgindividual.

p. 999


Figure 27-1a The Composition of the Human Body

Liters

Intracellular fluid Extracellular fluid

Interstitialfluid

Plasma

Other

WATER (38.5 kg; 84.7 lbs)

The body composition (by weight, averagedfor both sexes) and major body fluidcompartments of a 70-kg individual.

p. 999


Figure 27-1b The Composition of the Human Body

A comparison of the body compositions of adultmales and females, ages 18–40 years.

Intracellularfluid 33%

Interstitialfluid 21.5%

WATER 60%

SOLIDS 40%

Otherbodyfluids(1%)

Plasma 4.5%

Solids 40%(organic and inorganic materials)

Adult males

ECFICF

p. 999


Figure 27-1b The Composition of the Human Body

A comparison of the body compositions of adultmales and females, ages 18–40 years.

ECFICF

Adult females

SOLIDS 50%

Solids 50%(organic and inorganic materials)

Intracellularfluid 27%

Interstitialfluid 18%

Otherbodyfluids(1%)

Plasma 4.5%

WATER 50%

p. 999


Figure 27-2 Cations and Anions in Body FluidsCATIONS

ECF ICFKEY

Cations

Plasma Interstitialfluid

Intracellularfluid

Mil

lie

qu

ival

en

ts p

er l

iter

(m

Eq

/L)

Na

Ca2Mg2

KK

K

NaNa

Na

K

Ca2

Mg2

p. 1001


Figure 27-2 Cations and Anions in Body Fluids

KEY

Anions

ANIONS

ECF ICF

Plasma Interstitialfluid

Intracellularfluid

Proteins

Proteins

Org. acid

HPO42

Cl

HCO3

Organicacid

Proteins

HCO3

Cl

HPO42

SO42 HCO3

Cl

HPO42

SO42

SO42

HCO3

Cl

HPO42

p. 1001

Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc.

p. 1001

Normal Sodium Concentrations In ECF ~140 mEq/L

In ICF ~ 10 mEq/L or less

Normal Potassium Concentrations

In ICF ~ 160 mEq/L

In ECF ~ 3.5–5.5 mEq/L

Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc.

p. 1007 Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

© 2

012

Pear

son

Educ

ation

, Inc

.


Figure 27-5 The Homeostatic Regulation of Normal Sodium Ion Concentrations in Body Fluids

The secretion of ADH restricts water loss andstimulates thirst, promotingadditional waterconsumption.

Osmoreceptorsin hypothalamus

stimulated

HOMEOSTASISDISTURBED

Increased Na

levels in ECF

Because the ECFosmolarity increases,water shifts out ofthe ICF, increasingECF volume andlowering Na

concentrations.

HOMEOSTASISRESTORED

Decreased Na

levels in ECF

Recall of FluidsADH Secretion Increases

HOMEOSTASIS

Normal Na

concentrationin ECF

Start

p. 1007


Figure 27-5 The Homeostatic Regulation of Normal Sodium Ion Concentrations in Body Fluids

HOMEOSTASIS


Decreased Na

levels in ECF

Normal Na

concentrationin ECF

HOMEOSTASISRESTORED

Increased Na

levels in ECF

Water loss reducesECF volume,

concentrates ions

Osmoreceptorsin hypothalamus

inhibited

As soon as the osmoticconcentration of the ECFdrops by 2 percent or more,ADH secretion decreases, sothirst is suppressed andwater losses at the kidneysincrease.

Start

ADH Secretion Decreases

p. 1007

p. 1008

Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

© 2

012

Pear

son

Educ

ation

, Inc

.


Figure 27-6 The Integration of Fluid Volume Regulation and Sodium Ion Concentrations in Body Fluids

Natriuretic peptidesreleased by cardiacmuscle cells

Rising bloodpressure and

volume

Increased bloodvolume andatrial distension


Rising ECF volume by fluid

gain or fluid and Na gain

HOMEOSTASISRESTORED

Falling ECFvolume

StartHOMEOSTASIS

Normal ECFvolume

Reducedbloodvolume

CombinedEffects

Reducedbloodpressure

Increased Na loss in urine

Responses to Natriuretic Peptides

Increased water loss in urine

Reduced thirst

Inhibition of ADH, aldosterone,epinephrine, and norepinephrinerelease

p. 1008


Figure 27-6 The Integration of Fluid Volume Regulation and Sodium Ion Concentrations in Body Fluids


Falling ECF volume by fluidloss or fluid and Na loss

Decreased bloodvolume andblood pressure Increased renin secretion

and angiotensin IIactivation

Increased aldosteronerelease

Increased ADH release

Increased urinary Na

retention

Endocrine Responses Combined Effects

Decreased urinary waterloss

Increased thirst

Increased water intake

Rising ECFvolume

HOMEOSTASISRESTORED

StartHOMEOSTASIS

Normal ECFvolume

Falling bloodpressure and

volume

p. 1008


Figure 27-9 The Basic Relationship between PCO2 and Plasma pH

PCO2

40–45mm Hg HOMEOSTASIS

If PCO2 rises

When carbon dioxide levels rise, more carbonic acidforms, additional hydrogen ions and bicarbonate ionsare released, and the pH goes down.

PCO2

pH

H2O CO2 H2CO3 HCO3H

p. 1013


Figure 27-9 The Basic Relationship between PCO2 and Plasma pH

pH

PCO2

When the PCO2 falls, the reaction runs in reverse, and

carbonic acid dissociates into carbon dioxide and water.This removes H ions from solution and increases thepH.

pH

7.35–7.45HOMEOSTASIS

If PCO2 falls

H HCO3 H2CO3 H2O CO2

p. 1013


Figure 27-10 Buffer Systems in Body Fluids

Buffer Systems

Intracellular fluid (ICF)

Phosphate BufferSystem

Protein Buffer Systems

The phosphatebuffer systemhas an importantrole in bufferingthe pH of the ICFand of urine.

Protein buffer systems contribute to the regulationof pH in the ECF and ICF. These buffer systems interactextensively with the other two buffer systems.

Hemoglobin buffersystem (RBCs only)

Amino acid buffers(All proteins)

Plasma proteinbuffers

The carbonic acid–bicarbonate buffersystem is mostimportant in the ECF.

Carbonic Acid–Bicarbonate BufferSystem

Extracellular fluid (ECF)

occur in

p. 1014


Figure 27-11 The Role of Amino Acids in Protein Buffer Systems

Neutral pH

If pH fallsIf pH rises

Amino acidIn alkaline medium, aminoacid acts as an acid

and releases H

In acidic medium, aminoacid acts as a base

and absorbs H

p. 1014


Figure 23-24 A Summary of the Primary Gas Transport Mechanisms

Systemiccapillary

Cells inperipheral

tissues

Chlorideshift

CO2 pickup


Figure 23-24 A Summary of the Primary Gas Transport Mechanisms

Alveolarair space

Pulmonarycapillary

CO2 delivery


Figure 27-12a The Carbonic Acid–Bicarbonate Buffer System

CARBONIC ACID–BICARBONATE BUFFER SYSTEM

H2CO3

(carbonic acid)CO2 H2OCO2

Lungs

Basic components of the carbonic acid–bicarbonatebuffer system, and their relationships to carbon dioxideand the bicarbonate reserve

HCO3

(bicarbonate ion)

H

BICARBONATE RESERVE

Na

HCO3

NaHCO3

(sodiumbicarbonate)

p. 1015


Figure 27-12b The Carbonic Acid–Bicarbonate Buffer System

Fixed acids ororganic acids:

add H

The response of the carbonic acid–bicarbonatebuffer system to hydrogen ions generated by fixed ororganic acids in body fluids

CO2

Lungs

CO2 H2OIncreased

H2CO3HCO3

–H Na

HCO3 NaHCO3

p. 1015


Figure 27-13a Kidney Tubules and pH Regulation

The three major buffering systems in tubular fluid,which are essential to the secretion of hydrogen ions

Cells of PCT,DCT, andcollectingsystem

Peritubularfluid

Peritubularcapillary

Carbonic acid–bicarbonatebuffer system

Phosphate buffer system

Ammonia buffer system

KEY

Countertransport

Active transport

Exchange pump

Cotransport

Reabsorption

Secretion

Diffusion

p. 1018


Figure 27-13b Kidney Tubules and pH Regulation

KEY Countertransport

Active transport

Exchange pump

Cotransport

Reabsorption

Secretion

Diffusion

Production ofammonium ions andammonia by thebreakdown of glutamine

Tubular fluidin lumen

Glutaminase

Carbonchain

Glutamine

p. 1018


Figure 27-13c Kidney Tubules and pH Regulation

KEY Countertransport

Active transport

Exchange pump

Cotransport

Reabsorption

Secretion

Diffusion

The response ofthe kidney tubuleto alkalosis

Tubular fluidin lumen

Carbonicanhydrase

p. 1018


Figure 27-14 Interactions among the Carbonic Acid–Bicarbonate Buffer System and Compensatory Mechanisms in the Regulation of Plasma pH

The response to acidosis caused by the addition of H

Addition

of HStart

(carbonic acid) (bicarbonate ion)H

Otherbuffer

systems

absorb H

KIDNEYS

Increased respiratory

rate lowers PCO2,

effectively convertingcarbonic acidmolecules to water.

Lungs

CO2 CO2 H2O

Respiratory Responseto Acidosis

Secretion

of H

H2CO3 HCO3 HCO3

Na

BICARBONATE RESERVE

NaHCO3

Generation

of HCO3

Renal Response to Acidosis

(sodium bicarbonate)

Kidney tubules respond by (1) secreting H

ions, (2) removing CO2, and (3) reabsorbing

HCO3 to help replenish the bicarbonate

reserve.

CARBONIC ACID-BICARBONATE BUFFER SYSTEM

p. 1019


Figure 27-14b Interactions among the Carbonic Acid–Bicarbonate Buffer System and Compensatory Mechanisms in the Regulation of Plasma pH

BICARBONATE RESERVE

Removal

of H

H

(carbonic acid) (bicarbonate ion)H2CO3 HCO3

Otherbuffer

systems

release H

Generation

of H

Secretion

of HCO3

KIDNEYS

H2OCO2Lungs

Respiratory Responseto Alkalosis

Decreased respiratory

rate elevates PCO2,

effectively converting

CO2 molecules to

carbonic acid.

Renal Response to Alkalosis

HCO3 NaHCO3Na

(sodium bicarbonate)

Kidney tubules respond by

conserving H ions and

secreting HCO3.

The response to alkalosis caused by the removal of H

Start

CARBONIC ACID-BICARBONATE BUFFER SYSTEM

p. 1019


Figure 27-15a Respiratory Acid–Base Regulation

Responses to Acidosis

Respiratory compensation:Stimulation of arterial and CSF chemo-receptors results in increasedrespiratory rate.

Renal compensation:

H ions are secreted and HCO3

ions are generated.

Buffer systems other than the carbonicacid–bicarbonate system accept H ions.

Respiratory Acidosis

Elevated PCO2 results

in a fall in plasma pH


Hypoventilation

causing increased PCO2

HOMEOSTASIS

Normalacid–base

balance

HOMEOSTASISRESTORED

Plasma pHreturns to normal

Decreased PCO2

Decreased H and

increased HCO3

Combined Effects

IncreasedPCO2

Respiratory acidosis

p. 1021


Figure 27-15b Respiratory Acid–Base Regulation


Hyperventilation

causing decreased PCO2

Respiratory Alkalosis

Lower PCO2 results

in a rise in plasma pH

Responses to Alkalosis

Respiratory compensation:Inhibition of arterial and CSFchemoreceptors results in a decreasedrespiratory rate.

Renal compensation:H ions are generated and HCO3

ions

are secreted.

Buffer systems other than the carbonic

acid–bicarbonate system release H

ions.Respiratory alkalosis

Decreased

PCO2

Combined Effects

Increased PCO2

Increased H and

decreased HCO3

HOMEOSTASISRESTORED


Normalacid–base

balance

HOMEOSTASIS

p. 1021


Figure 27-16a Responses to Metabolic Acidosis

Responses to Metabolic Acidosis


Renal compensation:

H ions are secreted and HCO3 ions

are generated.

Buffer systems accept H ions.

Metabolic Acidosis

Elevated H resultsin a fall in plasma pH


Increased H production

or decreased H excretion

HOMEOSTASIS

Normalacid–base

balance

HOMEOSTASISRESTORED


Decreased H andincreased HCO3

Decreased PCO2

Combined Effects

Increased

H ions

Metabolic acidosis can result from increasedacid production or decreased acid excretion,leading to a buildup of H in body fluids.

p. 1023


Figure 27-16b Responses to Metabolic Acidosis


Bicarbonate loss;depletion of bicarbonate

reserve

Metabolic Acidosis

Plasma pH falls becausebicarbonate ions are

unavailable to accept H

Responses to Metabolic Acidosis


Renal compensation:H ions are secreted and HCO3

ions

are generated.

Buffer systems other than the carbonic

acid–bicarbonate system accept H

ions.

Metabolic acidosis can resultfrom a loss of bicarbonateions that makes the carbonicacid–bicarbonate buffersystem incapable ofpreventing a fall in pH.

Decreased

HCO3 ions

Combined Effects

Decreased PCO2

Decreased H and

increased HCO3

HOMEOSTASISRESTORED


Normalacid–base

balance

HOMEOSTASIS

p. 1023


Figure 27-17 Metabolic Alkalosis


Loss of H;

gain of HCO3

Metabolic Acidosis

Elevated HCO3 results

in a rise In plasma pH Responses to Metabolic Alkalosis

Respiratory compensation:Stimulation of arterial and CSFchemoreceptors results in decreasedrespiratory rate.

Renal compensation:H ions are generated and HCO3

Ions are secreted.

Buffer systems other than thecarbonic acid–bicarbonate system

donate H ions.

Decreased

H ions, gain

of HCO3 ions

Combined Effects

Increased H and

decreased HCO3

Increased PCO2

HOMEOSTASISRESTORED


Normalacid–base

balance

HOMEOSTASIS

p. 1024


Figure 27-18 A Diagnostic Chart for Suspected Acid–Base Disorders

Respiratory AcidosisPCO2

increased (50 mm Hg)

Primary cause is hypoventilation

Check PCO2

Acidosis pH 7.35 (acidemia)

Metabolic AcidosisPCO2

normal or decreased

Check HCO3

AcuteRespiratory

Acidosis

Chronic(compensated)

Respiratory Acidosis


Metabolic Acidosis

AcuteMetabolicAcidosisPCO2

normal PCO2 decreased

(35 mm Hg)Examples:• respiratory failure• CNS damage• pneumothorax

Examples:• emphysema• asthma

HCO3 normalHCO3

increased

(28 mEq/L)

Reduction due torespiratorycompensation

Examples:• diarrhea

Examples:• lactic acidosis• ketoacidosis• chronic renal failure

Due to generation orretention of organicor fixed acids

Due to loss of HCO3

or to generation oringestion of HCl

Normal Increased

Check anion gap

Check pH

Suspected Acid–Base Disorder

p. 1025


Figure 27-18 A Diagnostic Chart for Suspected Acid–Base Disorders

Check pH

MetabolicAlkalosis

RespiratoryAlkalosis

PCO2 increased

(45 mm Hg)

PCO2 decreased

(35 mm Hg)

Alkalosis pH 7.45 (alkalemia)

Check PCO2

Primary cause ishyperventilation

Check HCO3

(HCO3 will

be elevated)Examples:• vomiting• loss of gastric acid

AcuteRespiratory

Alkalosis


RespiratoryAlkalosisNormal or slight

decrease

in HCO3

Decreased HCO3

(24 mEq/L)

Examples:• fever• panic attacks

Examples:• anemia• CNS damage

Suspected Acid–Base Disorder

p. 1025

© 2012 pearson education, inc. figure 27-1a the composition of the human body solid components...

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