WATER BALANCE

NORMAL WATER CONTENT OF BODY 75% AT BIRTH 55-60% YOUNG ADULTS

MEN SLIGHTLY HIGHER THAN WOMEN (MORE FAT, LESS WATER)

45% IN ELDERLY, OBESE

WATER BALANCE
TOTAL BODY WATER ~40 LITERS SEVERAL FLUID COMPARTMENTS

65% INTRACELLULAR FLUID (ICF) 35% EXTRACELLULAR FLUID (ECF)

25% INTERSTITIAL FLUID (TISSUE FLUID) 8% BLOOD PLASMA AND LYMPH 2% TRANSCELLULAR FLUID

SYNOVIAL, PLEURAL, PERICARDIAL, ETC.

WATER BALANCE
TOTAL BODY WATER ENTERS BODY

OSMOSIS FROM DIGESTIVE TRACT

ALSO PRODUCED BY AEROBIC RESPIRATION ALSO PRODUCED BY CONDENSATION REACTIONS

EXITS BODY

URINARY, DIGESTIVE, RESPIRATORY, & INTEGUMENTARY SYSTEMS

WATER BALANCE
TOTAL BODY WATER FLUID EXCHANGED BETWEEN COMPARTMENTS

CAPILLARY WALLS, PLASMA MEMBRANES DRIVEN BY TRANSIENT OSMOTIC GRADIENTS OSMOTIC GRADIENTS DEPENDENT ON SOLUTE MOLECULES MOST ABUNDANT SOLUTES ARE ELECTROLYTES WATER BALANCE AND ELECTROLYTE BALANCE ARE CLOSELY RELATED

WATER BALANCE
WATER BALANCE FLUID GAIN = FLUID LOSS BOTH TYPICALLY ~2500 ML / DAY

WATER BALANCE
WATER GAIN TYPICALLY ~2500 ML / DAY 1600 ML FROM DRINK 700 ML FROM FOOD 200 ML FROM METABOLISM

AEROBIC RESPIRATION CONDENSATION REACTIONS

A.K.A. DEHYDRATION REACTIONS

WATER BALANCE
WATER LOSS TYPICALLY ~2500 ML / DAY 1500 ML EXCRETED AS URINE 200 ML ELIMINATED IN FECES 300 ML EXPIRED IN BREATH 100 ML SECRETED AS SWEAT 400 ML LOST AS CUTANEOUS TRANSPIRATION

DIFFUSES THROUGH EPIDERMIS, EVAPORATES

WATER BALANCE
WATER LOSS CAN VARY GREATLY

INCREASED RESPIRATORY LOSS IN COLD WEATHER INCREASED SWEAT LOSS IN WARM WEATHER INCREASED RESPIRATORY AND SWEAT LOSS, DECREASED URINE OUTPUT DURING PHYSICAL EXERTION

WATER BALANCE
WATER LOSS OBLIGATORY WATER LOSS

RELATIVELY UNAVOIDABLE EXPIRED AIR, CUTANEOUS TRANSPIRATION, SWEAT, FECAL MOISTURE, MINIMUM URINE OUTPUT (~400 ML/DAY)

WATER BALANCE
REGULATION OF WATER INTAKE GOVERNED BY THIRST

PROVOKED BY INCREASED PLASMA OSMOLARITY PROVOKED BY BLOOD LOSS RESPONDS TO SIGNS OF DEHYDRATION

THIRST CENTER IN HYPOTHALAMUS

ANGIOTENSIN II ANTIDIURETIC HORMONE (ADH) SIGNALS FROM OSMOCENTERS

INHIBITS SALIVATION

WATER BALANCE
REGULATION OF WATER INTAKE INHIBITED SALIVATION

DRY MOUTH SENSE OF THIRST INGESTION OF WATER

COOLS AND MOISTENS MOUTH DISTENDS STOMACH AND INTESTINES REHYDRATES BLOOD

THIRST INHIBITED

WATER BALANCE
REGULATION OF WATER OUTPUT CONTROLLED VIA ALTERATIONS IN URINE VOLUME URINE VOLUME AFFECTED BY

SODIUM REABSORPTION

ANTIDIURETIC HORMONE (ADH)

WATER FOLLOWS SODIUM REABSORPTION MORE LATER

BLOOD VOLUME , [Na+] , OSMORECEPTORS STIMULATED, PITUITARY RELEASES ADH AQUAPORINS PRODUCED IN KIDNEYS COLLECTING DUCTS FACILITATE REABSORPTION ALSO WORKS IN REVERSE

WATER BALANCE
WATER BALANCE DISORDERS FLUID DEFICIENCY

VOLUME DEPLETION (HYOVOLEMIA) DEHYDRATION VOLUME EXCESS HYPOTONIC HYDRATION

FLUID EXCESS

FLUID SEQUESTRATION

WATER BALANCE
WATER BALANCE DISORDERS FLUID DEFICIENCY: HYPOVOLEMIA CAUSED BY PROPORTIONATE LOSS OF WATER AND SODIUM WITHOUT REPLACEMENT TOTAL BODY WATER DECREASED OSMOLARITY UNCHANGED CAUSES

HEMORRHAGE SEVERE BURNS CHRONIC VOMITING OR DIARRHEA

MAJOR CAUSE OF INFANT MORTALITY

WATER BALANCE
WATER BALANCE DISORDERS FLUID DEFICIENCY: DEHYDRATION CAUSED BY LOSS OF MORE WATER THAN Na+ TOTAL BODY WATER DECREASED ECF OSMOLARITY INCREASES CAUSES

LACK OF DRINKING WATER DIABETES MELLITUS ADH HYPOSECRETION PROFUSE SWEATING OVERUSE OF DIURETICS

WATER BALANCE
WATER BALANCE DISORDERS FLUID DEFICIENCY: DEHYDRATION AFFECTS ALL FLUID COMPARTMENTS INFANTS MORE VULNERABLE THAN ADULTS

HIGHER METABOLISM MORE WASTES

MORE WASTES MORE URINE VOLUME URINE LESS CONCENTRATED GREATER WATER LOSS BY EVAPORATION

IMMATURE KIDNEYS

GREATER SURFACE AREA-TO-VOLUME RATIO

WATER BALANCE
WATER BALANCE DISORDERS EFFECTS OF FLUID DEFICIENCY CIRCULATORY SHOCK

DUE TO LOSS OF BLOOD VOLUME DUE TO DEHYDRATION OF BRAIN CELLS

NEUROLOGICAL DYSFUNCTION

WATER BALANCE
WATER BALANCE DISORDERS FLUID EXCESS LESS COMMON THAN FLUID DEFICIENCY

KIDNEYS ARE TYPICALLY ABLE TO EXCRETE MORE URINE

WATER BALANCE
WATER BALANCE DISORDERS FLUID EXCESS: VOLUME EXCESS CAUSED BY PROPORTIONATE RETENTION OF EXCESS WATER AND SODIUM TOTAL BODY WATER INCREASED OSMOLARITY UNCHANGED CAUSES

ALDOSTERONE HYPERSECRETION RENAL FAILURE

WATER BALANCE
WATER BALANCE DISORDERS FLUID EXCESS: HYPOTONIC HYDRATION WATER INTOXICATION, POS H20 BALANCE CAUSED BY RETENTION OF MORE WATER THAN SODIUM TOTAL BODY WATER INCREASED ECF OSMOLARITY DECREASES CAUSES

REPLACEMENT OF WATER AND SALT WITH WATER

ADH HYERSECRETION
LACK OF PROPORTIONATE INTAKE OF ELECTROLYTES

WATER BALANCE
WATER BALANCE DISORDERS EFFECTS OF FLUID EXCESS PULMONARY EDEMA CEREBRAL EDEMA

WATER BALANCE
WATER BALANCE DISORDERS FLUID SEQUESTRATION EXCESS FLUID ACCUMULATES IN A PARTICULAR LOCATION TOTAL BODY WATER MAY BE NORMAL CIRCULATING VOLUME MAY DROP EXAMPLES

EDEMA (IN INTERSTITIAL SPACES) HEMORRHAGE (LOST TO CIRCULATION) PLEURAL EFFUSION (IN PLEURAL CAVITY)

ELECTROLYTE BALANCE
IMPORTANCE OF ELECTROLYTES SALTS

E.G. NaCl, Ca3(PO4)2, ETC. INCLUDE IONS IN DEFINITION INVOLVED IN METABOLISM DETERMINE ELECTRICAL MEMBRANE POTENTIALS AFFECT OSMOLARITY OF BODY FLUIDS AFFECT WATER CONTENT AND DISTRIBUTION ETC.

MANY ROLES

ELECTROLYTE BALANCE
SODIUM PRINCIPAL EXTRACELLULAR CATION

90 95% OF OSMOLARITY FROM SODIUM SALTS

ROLES

DEPOLARIZATION

MUSCLES, NERVES

AFFECT TOTAL BODY WATER AFFECT WATER DISTRIBUTION COTRANSPORT

GLUCOSE, AMINO ACIDS, CALCIUM, ETC.

ETC.

ELECTROLYTE BALANCE
SODIUM HOMEOSTASIS 0.5 G / DAY DIETARY REQUIREMENT RECEIVE 3 7 G / DAY FROM OUR DIET KIDNEYS EXCRETE EXCESS (~5 G / DAY) EXCRETION REGULATED BY 3 HORMONES

ALDOSTERONE ANTIDIURETIC HORMONE (ADH) ATRIAL NATRIURETIC FACTOR (ANF)

ELECTROLYTE BALANCE
SODIUM HOMEOSTASIS REGULATION BY ALDOSTERONE SALT-RETAINING HORMONE STEROID HORMONE ALDOSTERONE SECRETION STIMULATED BY:

HYPONATREMIA HYPERKALEMIA HYPOTENSION

ELECTROLYTE BALANCE
SODIUM HOMEOSTASIS REGULATION BY ALDOSTERONE TARGET CELLS

DISTAL CONVOLUTED TUBULE COLLECTING DUCT SODIUM REABSORPTION INCREASES H+ AND K + SECRETION INCREASES URINE pH DROPS

TRANSCRIBE GENE FOR Na+-K+ PUMP

ELECTROLYTE BALANCE
SODIUM HOMEOSTASIS REGULATION BY ALDOSTERONE AVERAGE Na+ EXCRETION 5 G / DAY ALDOSTERONE REDUCES TO ~0 WATER REABSRBED PROPORTIONALLY SODIUM CONCENTRATION IN BODY UNCHANGED

ELECTROLYTE BALANCE
SODIUM HOMEOSTASIS REGULATION BY ALDOSTERONE INHIBITED BY HYPERTENSION KIDNEYS THEN REABSORB LITTLE Na+ EXCRETION INCREASED TO ~30 G / DAY

ELECTROLYTE BALANCE
SODIUM HOMEOSTASIS REGULATION BY ADH INDEPENDENTLY MODIFIES SODIUM AND WATER EXCRETION

CAN CHANGE SODIUM CONCENTRATION

INCREASES WATER REABSORPTION

HIGH BLOOD [Na+] ADH SECRETION

SODIUM CONCENTRATION DECREASED

ADH ALSO STIMULATES THIRST

ALSO HAPPENS IN REVERSE

ELECTROLYTE BALANCE
SODIUM HOMEOSTASIS REGULATION BY ANF HYPERTENSION ANF SECRETION

INHIBITS ADH AND RENIN SECRETION INHIBITS SODIUM & WATER REABSORPTION MORE SODIUM AND WATER EXCRETED BLOOD PRESSURE DECREASED

ELECTROLYTE BALANCE
SODIUM HOMEOSTASIS REGULATION BY OTHER HORMONES ESTROGENS MIMIC ALDOSTERONE

WATER RETENTION DURING PREGNANCY MENSTRUAL WATER RETENTION REDUCES SODIUM REABSORPTION DIURETIC AEFFECT PROMOTE SODIUM REABSORPTION, EDEMA

PROGESTERONE

GLUCOCORTICOIDS

ELECTROLYTE BALANCE
SODIUM HOMEOSTASIS: IMBALANCES RELATIVELY RARE HYPERNATREMIA

CAN RESULT FROM IV SALINE CAUSES WATER RETENTION, HYPERTENSION, EDEMA GENERALLY FROM WATER EXCESS HYPOTONIC HYDRATION CORRECTED BY EXCRETION OF EXCESS WATER

HYPONATREMIA

ELECTROLYTE BALANCE
POTASSIUM PRINCIPAL INTRACELLULAR CATION AFFECTS INTRACELLULAR OSMOLARITY AFFECTS CELL VOLUME ROLES

PRODUCES RESTING & ACTION POTENTIALS COTRANSPORT THERMOGENESIS COFACTOR FOR PROTEIN SYNTHESIS

ELECTROLYTE BALANCE
POTASSIUM HOMEOSTASIS HOMEOSTASIS LINKED TO THAT OF Na+

K+ AND Na+ COREGULATED BY ALDOSTERONE

90% OF K+ REABSORBED IN PCT

REMAINDER EXCRETED IN URINE

CONTROL IMPARTED IN DCT & COLLECTING DUCT (CD)

HIGH [K+] SECRETE MORE INTO FILTRATE LOW [K+] SECRETE LESS INTO FILTRATE EXCHANGED FOR Na+

ELECTROLYTE BALANCE
POTASSIUM HOMEOSTASIS REGULATION BY ALDOSTERONE HIGH [K+] ALDOSTERONE PRODUCTION

Na+-K+ PUMP PRODUCED Na+ AND K+ COREGULATED INCREASE K+ SECRETION DECREASE Na+ SECRETION

ELECTROLYTE BALANCE
POTASSIUM HOMEOSTASIS: IMBALANCES MOST DANGEROUS ELECTROLYTE IMBALANCES HYPERKALEMIA

EFFECTS DEPEND ON SPEED OF CONC RISE QUICK RISE NERVE/MUSCLE CELLS VERY EXCITABLE CARDIAC ARREST

E.G., K+ RELEASED FROM INJURED CELLS E.G., TRANSFUSION WITH OLD BLOOD E.G., EUTHANASIA, CAPITAL PUNISHMENT LETHAL INJECTION

SLOW RISE NERVE/MUSCLE CELLS LESS EXCITABLE (Na+ CHANNELS INACTIVATED)

K+ HAS LEAKED FROM ERYTHROCYTES

E.G., ALDOSTERONE HYPOSECRETION, RENAL FAILURE, ACIDOSIS E.G., SUPPLEMENTAL K+ TO RELIEVE MUSCLE CRAMPS

ELECTROLYTE BALANCE
POTASSIUM HOMEOSTASIS: IMBALANCES HYPOKALEMIA

NERVE/MUSCLE CELLS LESS EXCITABLE MUSCLE WEAKNESS, LOSS OF MUSCLE TONE, DEPRESSED REFLEXES, IRREGULAR HEART ACTIVITY E.G., HEAVY SWEATING, CHRONIC VOMITING OR DIARRHEA, EXCESSIVE LAXATIVES, ALDOSTERONE HYPERSECRETION, ALKALOSIS E.G., DEPRESSED APPETITE, BUT RARELY FROM DIETARY INSUFFICIENCY

ELECTROLYTE BALANCE
CHLORIDE MOST ABUNDANT ANION IN ECF

MAJOR CONTRIBUTION TO OSMOLARITY FORMATION OF HCl CHLORIDE SHIFT

ROLES

CO2 LOADING/UNLOADING

REGULATION OF BODY pH

ELECTROLYTE BALANCE
CHLORIDE HOMEOSTASIS Cl- STRONGLY ATTRACTED TO SOME CATIONS (E.G., Na+, K+, Ca2+)

CANNOT KEEP THEM APART

HOMEOSTASIS ACHIEVED AS AN EFFECT OF Na+ HOMEOSTASIS

Cl- PASSIVELY FOLLOWS Na+

ELECTROLYTE BALANCE
CHLORIDE IMBALANCES HYPERCHLOREMIA

HYPOCHLOREMIA

RESULTS FROM DIETARY EXCESS RESULTS FROM INTERVENOUS SALINE ADMINISTRATION SIDE EFFECT OF HYPONATREMIA SIDE EFFECT OF HYPOKALEMIA ALTERED ACID-BASE BALANCE

EFFECTS

KIDNEYS RETAIN K+ BY SECRETING Na+, Cl- FOLLOWS

ELECTROLYTE BALANCE
CALCIUM ROLES

STRENGTHENS BONE MUSCLE CONTRACTION SECOND MESSENGER FOR HORMONES ACTIVATES EXOCYTOSIS BLOOD CLOTTING

ELECTROLYTE BALANCE
CALCIUM BINDS TO PHOSPHATE ION

CAN FORM Ca3(PO4)2 HIGH CONCENTRATIONS OF BOTH IONS WILL FORM PRECIPITATE CRYSTALS INTRACELLULAR [Ca2+] MUST BE KEPT LOW Ca2+ PUMPED OUT & INTO E.R.

ELECTROLYTE BALANCE
CALCIUM HOMEOSTASIS REGULATED BY PTH & CALCITROL

ALSO BY CALCITONIN IN CHILDREN BONE DEPOSITION & REABSORPTION INTESTINAL ABSORPTION URINARY EXCRETION

BLOOD [Ca2+] REGULATED VIA

ELECTROLYTE BALANCE
CALCIUM IMBALANCES HYPERCALCEMIA

REDUCES EMBRANE PERMEABILITY TO Na+ INHIBITS DEPOLARIZATION OF NERVES/MUSCLES MUSCULAR WEAKNESS, CARDIAC ARRHYTHMI, ETC. RESULTS FROM

ALKALOSIS HYPERPARATHYROIDISM HYPOTHYROIDISM

ELECTROLYTE BALANCE
CALCIUM IMBALANCES HYPOCALCEMIA

INCREASES EMBRANE PERMEABILITY TO Na+ NERVES/MUSCLES OVERLY EXCITABLE TETANUS IF CONCENTRATION DROPS TO LOW RESULTS FROM

ACIDOSIS VITAMIN D DEFICIECY DIARRHEA PREGNANCY OR LACTATION HYPOPARATHYROIDISM HYPERTHYROIDISM

ELECTROLYTE BALANCE
PHOSPHATES RELATIVELY CONCENTRATED IN ICF ROLES

COMPONENTS OF BONES COMPONENTS OF DNA & RNA COMPONENTS OF PHOSPHOLIPIDS ACTIVATE / DEACTIVATE ENZYMES BUFFER pH OF BODY FLUIDS

ELECTROLYTE BALANCE
PHOSPHATES COMPONENTS OF

NUCLEIC ACIDS (DNA, RNA) NTPs AND dNTPs (ATP, dATP, GTP, dGTP, etc) cAMP PHOSPHOLIPIDS VARIOUS OTHER PHOSPHORYLATED MOLECULES

GENERATED VIA ATP HYDROLYSIS, ETC. EXIST AS MIXTURE OF THREE FORMS

PO43HPO42H2PO4-

(PHOSPHATE ION) (MONOHYDROGEN PHOSPHATE ION) (DIHYDROGEN PHOSPHATE ION)

ELECTROLYTE BALANCE
PHOSPHATE HOMEOSTASIS DIET PROVIDES AMPLE PHOSPHATE READILY ABSORBED BY SMALL INTESTINE REGULATION

RENAL TUBULES SITE OF REGULATION PTH INCREASES PHOSPHATE EXCRETION EXCRETION RATE AFFECTED BY URINE pH

ELECTROLYTE BALANCE
PHOSPHATE IMBALANCES PHOSPHATE HOMEOSTASIS NOT VERY CRITICAL BODY CAN TOLERATE WIDE VARIATIONS OF PHOSPHATEE CONCENTRATION WITH LITTLE EFFECT

ACID-BASE BALANCE
ACIDS, BASES, AND pH ACID

BASE

ANY SUBSTANCE RELEASING H+ [H+] INCREASES (pH DECREASES)

pH

ANY SUBSTANCE ACCEPTING H+ [H+] DECREASES (pH INCREASES)

A MEASURE OF [H+] -LOG [H+] SCALE 0 14, 7 IS NEUTRAL

ACID-BASE BALANCE
WHY IS ACID-BASE BALANCE IMPORTANT? METABOLISM REQUIRES NUMEROUS ENZYMES ENZYMES ARE PROTEINS pH AFFECTS PROTEIN STRUCTURE PROTEIN STRUCTURE AFFECTS FUNCTION DEVIATIONS FROM NORMAL pH CAN INACTIVATE ENZYMES AND SHUT DOWN METABOLIC PATHWAYS

ACID-BASE BALANCE
BLOOD pH BLOOD AND TISSUE pH 7.35 7.45

ENZYMES FUNCTION WELL WITHIN THIS RANGE ENZYMES FUNCTION POORLY (OR NOT AT ALL) WHEN SIGNIFICANTLY OUTSIDE OF THIS RANGE THIS RANGE MUST BE MAINTAINED

ACID-BASE BALANCE

ACID-BASE BALANCE
BUFFERS ANY MECHANISM OF RESISTING SIGNIFICANT CHANGES IN pH ACCOMPLISHED BY CONVERTING:

STRONG ACID WEAK ACID STRONG BASE WEAK BASE

ACID-BASE BALANCE
BUFFERS PHYSIOLOGICAL BUFFER

SYSTEM STABILIZING pH BY CONTROLLING BODYS OUTPUT OF ACIDS, BASES, OR CO2

URINARY SYSTEM

BUFFERS GREATEST QUANTITY REQUIRES HOURS OR DAYS TO EXERT EFFECT SMALLER EFFECT EXERTS EFFECT WITHIN MINUTES

RESPIRATORY SYSTEM

ACID-BASE BALANCE
BUFFERS CHEMICAL BUFFER SYSTEM

COMBINATION OF WEAK ACID AND WEAK BASE BINDS TO H+ AS [H+] RISES, AND RELEASES H+ AS [H+] FALLS CAN RESTORE NORMAL pH ALMOST IMMEDIATELY THREE MAJOR CHEMICAL BUFFER SYSTEMS

BICARBONATE SYSTEM PHOSPHATE SYSTEM PROTEIN SYSTEM

ACID-BASE BALANCE
BICARBONATE BUFFER SYSTEM CARBONIC ACID (H2CO3)

WEAK ACID

BICARBONATE ION (HCO3-)

WEAK BASE

CO2 + H20 H2CO3 H+ + HCO3WORKS IN CONCERT WITH RESPIRATORY AND URINARY SYSTEM

THESE SYSTEMS REMOVE CO2 OR HCO3-

ACID-BASE BALANCE
PHOSPHATE BUFFER SYSTEM DIHYDROGEN PHOSPHATE ION(H2PO4-)

WEAK ACID

MONOHYDROGEN PHOSPHATE ION (HPO42-)

WEAK BASE

H2PO4- H+ + HPO42STRONGER THAN BICARBONATE BUFFERING SYSTEM MORE IMPARTANT IN BUFFERING ICF AND RENAL TUBULES THAN IN ECF

ACID-BASE BALANCE
PROTEIN BUFFER SYSTEM PROTEINS ARE MORE CONCENTRATED THAN BICARBONATE AND PHOSPHATE BUFFERS ACCOUNTS FOR ~75% OF ALL CHEMICAL BUFFERING OF BODY FLUIDS BUFFERING ABILITY DUE TO CERTAIN FUNCTIONAL GROUPS OF AMINO ACID RESIDUES

CARBOXYL GROUPS

--COOH -COO- + H+
--NH3+ -NH2 + H+

AMINO GROUPS

ACID-BASE BALANCE
RESPIRATORY CONTROL OF pH CO2 + H20 H2CO3 H+ + HCO3 ADDITION OF CO2 INCREASES [H+] REMOVAL OF CO2 DECREASES [H+] CAN NEUTRALIZE 2-3 X MORE ACID AS CHEMICAL BUFFERS

ACID-BASE BALANCE
RENAL CONTROL OF pH CAN NEUTRALIZE MORE ACID OR BASE THAN BOTH RESPIRATORY SYSTEM AND CHEMICAL BUFFERS RENAL TUBULES SECRETE H+

H+ EXCRETED IN URINE EXCHANGED FOR SODIUM ION (Na+) ONLY POSSIBLE WHEN [H+] INSIDE TUBULE CELLS IS > [H+] IN TUBULAR FLUID

ACID-BASE BALANCE
ACID-BASE BALANCE DISORDERS AT pH 7.4, 20:1 HCO3-:H2CO3 RATIO IF [H2CO3] INCREASES, pH DROPS

pH BELOW 7.35 = ACIDOSIS pH ABOVE 7.45 = ALKALOSIS

IF [HCO3-] INCREASES, pH INCREASES

ACID-BASE BALANCE
ACID-BASE BALANCE DISORDERS RESPIRATORY ACIDOSIS

CO2 PRODUCTION EXCEEDS RESPIRATORY CO2 ELIMINATION CO2 ACCUMULATES IN ECF pH DROPS RESPIRATORY CO2 ELIMINATION EXCEEDS CO2 PRODUCTION EXCESSIVE VENTILATION (HYPERVENTILATION) pH RISES

RESPIRATORY ALKALOSIS

ACID-BASE BALANCE
ACID-BASE BALANCE DISORDERS METABOLIC ACIDOSIS

INCREASED PRODUCTION OF ORGANIC ACIDS INGESTION OF ACIDIC DRUGS

E.G., FERMENTATION LACTIC ACID E.G., ALCOHOLISM, DIABETES MELLITUS KETONE BODIES

LOSS OF BASE

E.G., ASPIRIN

METABOLIC ALKALOSIS

E.G., CHRONIC DIARRHEA, OVERUSE OF LAXITIVES

RARE OVERUSE OF BICARBONATES

LOSS OF STOMACH ACID FROM CHRONIC VOMITING

E.G., ANTACIDS

ACID-BASE BALANCE
ACID-BASE BALANCE DISORDERS ACIDOSIS H+ PASSIVELY DIFFUSES INTO CELLS K+ DIFFUSES OUT

ELECTRICAL BALANCE MAINTAINED

H+ BUFFERED BY INTRACELLULAR PROTEINS NET LOSS OF CATIONS FROM CELL MEMBRANE IS NOW HYPERPOLARIZED NERVE & MUSCLE CELLS DIFFICULT TO STIMULATE

CENTRAL NERVOUS SYSTEM DEPRESSED

CONFUSION, DISORIENTATION, COMA

ACID-BASE BALANCE
ACID-BASE BALANCE DISORDERS ALKALOSIS H+ PASSIVELY DIFFUSES OUT OF CELLS K+ DIFFUSES INTO CELLS

MEMBRANE POTENTIAL SHIFTED NERVOUS SYSTEM HYPEREXCITABLE

GAIN IN POSITIVE INTRACELLULAR CHARGE

NEURONS FIRE SPONTANEOUSLY SKELETAL MUSCLES OVERSTIMULATED

MUSCLE SPASMS, TETANY, CONVULSIONS, RESPIRATORY PARALYSIS

ACID-BASE BALANCE
ACID-BASE IMBALANCE COMPENSATION RESPIRATORY SYSTEM COMPENSATION ADJUSTS PCO2 IN ECF

EFFECTIVE VS RESPIRATORY ACIDOSIS AND ALKALOSIS NOT VERY EFFECTIVE VS METABOLIC ACIDOSIS AND ALKALOSIS

CO2 EXCESS INCREASED VENTILATION CO2 DEFICIENCY DECREASED VENTILATION

I.E., CANNOT RID BODY OF KETONE BODIES

NOT ALL THE WAY TO 7.4

CAN CORRECT pH 7.0 TO 7.2 OR 7.3

ACID-BASE BALANCE
ACID-BASE IMBALANCE COMPENSATION RENAL SYSTEM COMPENSATION SLOWER TO RESPOND CAN FULLY RESTORE NORMAL pH URINE pH NORMALLY 5 6

MAY DROP TO 4.5 WITH EXCESS H+

MAY RISE TO 8.2 WITH EXCESS HCO3

RESPONSE TO ACIDOSIS RENAL TUBULES INCREASE H+ SECRETION H+ IN URINE IS BUFFERED RESPONSE TO ALKALOSIS HCO3- CONCENTRATION IN URINE ELEVATED