BIOCHEMISTRY: FLUID AND ELECTROLYTES – DRA.

GABALDON

WATER BALANCE *Insensible loss – loss of water by evaporation, involuntary, either

IMPORTANCE OF WATER
 Universal biological solvent
 Property is due to:
o Polar asymmetry (H+-OH-) - hydrogen
bonding (weak bonding)
o High affinity to water molecules
 Hydrogen bonds between two
adjacent water molecules gives
liquid water a great internal
cohesion H2O has great covalent
bond
 Transport of:
o Gasses (O2 and CO2)
o Substances (nutrients and hormones)
 Dilutes toxic substances and waste products and
transports them to the kidneys and liver
o water readily dissolves compounds by
replacing solute-solute hydrogen bonds
with solute-water hydrogen bond
 Medium by which all chemical reactions occur
 Minimize temperature changes throughout the body
o Water has high specific heat
o Considerable amount of energy is needed
to break hydrogen bonds between water
molecules
o Water can absorb heat without rapidly
changing its own temperature
Total body of water = 60% of body weight (Adult)
FACTORS AFFECTING TOTAL BODY WATER
through respiratory tract or diffusion through the skin
(independent of sweat glands), cornification decreases insensible
water loss, in burn patients it is increased
*Fluid intake = fluid output
WATER COMPARTMENTS
ECF = 20%
 Blood plasma (5%) – non cellular part, important in
exchange of substances continuously w/ interstitium
(1/4 part)
 Interstitial water (15%) (3/4 part)
ICF = 40%
Total = 60%
*in ECF, blood plasma and interstitial water is separated by
capillary membrane. It has pores that solutes can pass through
except for proteins – large enough to pass through capillary pores
so it just stays in the plasma
* ICF is separated from ECF by cell membrane
Average Blood volume = 7% of body weight, (approx. 5 liters)
 60% plasma
 40% RBCs
Transcellular fluid = 1-2L
 CSF
 GIT fluids (digestive juices)
 Synovial fluid
 Eye fluids (aqueous and vitreous humors)
 Ear fluids (perilymph and endolymph)
 Pleural, pericardial and peritoneal fluids

 Age
o As person grows older, total body weight
deceases = ↑age ↑fats ↓TBW
 Degree of obesity
o Fats decreases the percentage of water in
the body
 Gender
o Men have higher % water (65%) than
women (55%) due to: Higher muscle mass
and lower amount of subcutaneous fat

SOURCES OF WATER
Osmolar substances in ECF and ICF (mOsm/LH2O)
 Preformed water = 2,100 mL/day
o water from ingested food and drink Plasma Interstitial Intracellular
+
 Metabolic water = 2000 mL/day Na 142 130 14
+
o Water produced from oxidation of K 4.2 4.0 140
++
carbohydrates Ca 1.3 1.2 0
++
Total intake = 2,300 mL Mg 0.8 0.7 20
-
Cl 108 108 4
-
DAILY INTAKE AND OUTPUT OF WATER (ml/day) HCO3 24 28.3 10
Intake Output Protein (-) 1.2 0.2 4
Fluid 2100 Insensible – 350
ingested skin
From 200 Insensible – 350 *How to remember what are the substances mostly present in the
metabolism Lungs extracellular and intracellular fluids?
Sweat 100
Feces 100 LAHAT NG MAY C EXTRACELLULAR!! NaCl, Calcium, HCO3, walang
YM,RMT
MD2021

Urine 1400 may C sa intracellular

Total input: 2300 Total output: 2300

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 BIOCHEMISTRY: FLUID AND ELECTROLYTES – DRA. GABALDON

Regulation of extracellular fluid  19mmHg is caused by dissolved proteins and 9mmHg

 Plasma and interstitium is separated from one another by Donnan effect – extra osmotic pressure caused by
by capillary membrane which possesses intercellular sodium, potassium and other cations held by plasma
clefts or capillary pores through which water soluble proteins
substances will pass through
 Intercellular clefts are not uniform in size in all the Interstitial Fluid Osmotic Pressure (IFOP)
capillaries, in some areas – liver have larger clefts  Osmosis of fluid outward
because all metabolic processes happens there and in  Drawing force of interstitium because of leaked out
kidneys for the excretion of substances. Due to the proteins
presence of larger clefts, some of the proteins will be  About 8mmHg
able to leak out (accounts for the amount of proteins
in the interstitial CHP = capillary → interstitium
IFHP = interstitium → capillary
What happens with your lipid soluble substances? COP = interstitiun (H2O) → capillary
 It doesn’t need the cleft, it can readily pass through IFOP = capillary (H2O) → interstitium
the endothelial cells because of the presence of lipid
bilayer Net Fluid Filtration Pressure (NFP)
 difference between pushing force and pulling force
*Exchange of water and substances through the capillary
membrane is through DIFFUSION If sum of these forces:
*Exchange of water and substances between ECF and ICF is  NFP Positive: there will be net fluid filtration across
through OSMOSIS capillaries (outward)
 NFP negative: there will be net fluid absorption from
Forces affecting Fluid movement through the capillary interstitial spaces into the capillaries (inward)
membrane
NFP = (CHP+IFOP) – (COP-IFHP)
Hydrostatic Pressure (OUTWARD FORCE) = pushing force – pulling force
 Due to the weight of water pushing against a surface
o Capillary Hydrostatic Pressure (CHP)  The COP and IFOP are the same at both ends of the
o Pressure of blood in the capillaries – capillary; however, the CHP differs at the arterial and
FILTRATION FORCE venous ends of the capillary (about 30mmHg at
arterial end and 10mmHg at the venous end
Osmotic Pressure (PULLING FORCE)  Average capillary pressure at arterial ends = 15 to
 Due to the attraction of water to large molecules into 25mmHg, greater than that of venous ends.
the capillaries such as protein (albumin – most Forces causing FILTRATION at the ARTERIAL END of the capillary
abundant) INWARD OUTWARD
 Also called plasma oncotic pressure CHP (arterial end) 30 COP 28
 Proteins are more abundant in the blood vessels than Negative interstitial 3
outside, it tends to attract water in from the interstitial free fluid pressure
space IFOP 8
Total: 41 Total: 28
When each compartment of the body contains the appropriate Summation of
concentration of water and electrolytes, the body is said to be in forces:
fluid balance. Electrolyte concentration can be controlled by the Outward 41
action of kidneys Inward 28
Net outward force 13
Starling forces (4 primary forces) (arterial end)
 Determines whether the fluid will move out of the
blood into the interstitial fluid or in the opposite  The summation of forces at the arterial end of the
direction capillary shows a NF of 13mmHg, tending to move
fluid outward through the capillary pores
Capillary Hydrostatic Pressure (CHP)  It is at the aterial end where we perfuse our organs
 Forces fluid outward through the capillary membrane
 30-40mmHg in the arterial ends of capillary Forces causing REABSORPTION at the VENOUS END of the
 10-15mmHg in the venous ends capillary
 Plasma → interstitium
INWARD OUTWARD
COP 28 CHP (venous end) 10
Interstitial Fluid Hydrostatic Pressure (IFHP)
Negative interstitial 3
 Moves fluid inward through the capillary membrane
free fluid pressure
 Average interstitial fluid pressure in loose connective
IFOP 8
tissue is about 3mmHg
Total: 28 Total: 21
 Interstitium → capillary
Summation:
Inward 28
Capillary Colloid Osmotic Pressure (COP)
Outward 21
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MD2021

 Pull water into capillary membrane

Net inward force 7
 Osmosis of fluid inward
(venous end)
 Average COP in normal human plasma = 28mmHg

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 BIOCHEMISTRY: FLUID AND ELECTROLYTES – DRA. GABALDON

 The force that causes fluid to move into the capillary is
greater than the opposing outward force, the
difference, 7mmHg is the net reabsorption pressure
Starling’s Law of the Capillaries
 The amount of fluid filtered in the arterial end of the
capillaries is almost equal to the fluid returned to the
circulation by reabsorption
 Slight disequilibrium accounts for the fluid that will be
eventually returned to the circulation by the way of
lymphatics
Baroreceptors
 Located in the atria of the heart, pulmonary artery and
vein
 Send messages to the hypothalamus via the vagus
nerve
 ADH secretion is stimulated by changes in the
circulating volume of body fluid that results in an
increase or decrease of internal pressure
 Reduction of around 8-10% from the normal body
volume of water due to hemorrhage or excess
perspiration will result in ADH secretion

Distribution of Fluids between ECF and ICF

Osmosis
 Moves water from one compartment to another
 Water transfers from dilute to concentrated
compartment
 Chiefly influences by dissolved solutes
 Most of these solutes are electrolytes

Osmolaity vs Osmolarity
 Both are measure of solute concentration of a solution
but in different units
Osmolality –osmoles per kg of H2O (Osm/kg H2O)
Osmolarity –osmoles per liter of solution (Osm/L)
+
Primary ECF cation = Na , accounts for the 80% of ECF osmolarity
+
Primary ICF cation = K , accounts for the ICF osmolarity
Total osmolarity of both ECF and ICF = 300 mOsm/L Thirst response
*plasma osmolarity is slightly higher due to the presence of  Connected to response of osmoreceptors
proteins o ↑plasma osmolarity stimulates
osmoreceptors which in turn stimulates
Regulation of Body Fluid Volume and ECF osmolarity sensation of thirst
 The mechanism for the regulation of the body fluid are  Thirst center is also located in the hypothalamus
centered in the hypothalamus  Other factors involved:
 The regulation if BF and ECF osmolarity is under o Degree of dryness of mucosal linings of
control of ADH and Aldosterone mouth and pharynx
Primary factors that trigger release of ADH: o Stretch receptors in the GIT
 Osmoreceptors
 Baroreceotors (pressure receptors)

Secondary factors:
 Stress
 Pain
 Hypoxia
 Potassium alteration

Osmoreceptors
 Found in hypothalamus
 Trigger ADH production in response to:
o Dehydration due to water loss or lack of
fluid intake
o Relative dehydration: no overall loss of
water content but there is gain of sodium
loss Effects of different concentration on cell volume
 Common determinant : ↑plasma osmolarity ECF osmol = 280 mOsm/L, same concentration inside the cell

*Water deficit – there is increase ECF osmolarity, it will stimutale ISOTONIC

osmoreceptors in hypothalamus, osmoreceptors will shrink, it  same concentration in both compartments, no net
fires nerve signals to pituitary to secrete ADH, increasing now the movement
plasma ADH resulting to increase water permeability of DT and CD HYPOTONIC
for more water reabsorption and decreasing water excretion  ECF is <280 mOsm/L, more concentration inside the
thereby correcting water deficit cell than in ECF, water will go inside the cell = swell
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MD2021

HYPERTONIC
 more concentration in ECF than inside cell, water will
go out from the cell = shrink

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 BIOCHEMISTRY: FLUID AND ELECTROLYTES – DRA. GABALDON

o Diabetic insepedus
CLINICAL PROBLEMS WITH FLUID BALANCE o Iatrogenic : prolonged NPO, tube feedings
 Hypotonic dehydration with inadequate amounts of water
 Isotonic dehydration  Manifestations:
 Hypertonic dehydration o Thirst
 Hypotonic overhy o Decreased skin turgor
 Isotonic overhydratio o Dry mucous membrane
 Hypertonic overhydration o ↑serum sodium and serum osmolarity
o ↑urine SG
Dehydration – water is the problem o Sins of shock are usually not present
Overhydration – depending on solute concentration
Hypotonic Overhydration
Hypotonic Dehydration  Hypotonic expansion of the ECF
 Hypotonic contraction of ECF  Decreased serum osmolarity leads to fluid shifting
 Fluid has fewer solutes than normal plasma from the blood stream into the cells
 Relatively uncommon – loss of more solutes (usually  Causes: interstitial edema, cellular swelling and
Na) than water electrolyte dilution
 Seen in: heat stroke and exhaustion  Causes:
 Causes fluid to shift from the blood stream into the o Too much IV D5W: the body metabolizes
cells, leading to decreased vascular volume and the glucose rapidly, leaving plain hypotonic
eventual shock fluid in the blood stream
 Increased cellular swelling o Keeping patient NPO with ice chips over
 Cerebral edema causes increase intracranial pressure, long period of time
headache, confusion o Tap water enema
 Manifestations: o Psychogenic cause: excessive drinking of
o Hypotension plain water
o Tachycardia  Manifestations:
o Changes in level of consciousness o Overall headache and photophobia
o Low serum osmolarity o Confusion and disorientation
o Low urine SG o Muscle twitching
o Increased urine volume o Hyperirritability
o Nausea and vomiting
Isotonic Dehydration o Polyuria in persons with normal kidneys
 Loss of equal amounts of fluids and electrolytes o Convulsions and coma
 Most common form of dehydration
 No intracellular shifts Isotonic Overhydration
 Causes:  Isotonic expansion of the ECF
o Diuretic therapy  Hypervolemia
o Excessive vomiting  Fluid equilibrate between blood and interstitial
o Excessive urine loss compartments
o Hemorrhage  Edema
o Decreased fluid intake  Rarely happens in persons with normal HR and kidneys
 Manifestations:  Causes:
o Weight loss o Over administration of IV isotonic fluids
o Hypotension and orthostatic hypotension o Excessive saline enemas
o Rapid, weak pulse o ↑sodium intake resulting to compensatory
o Oliguria (dark, concentrated, scanty urine) water retention
o Decreased skin turgor  Manifestations:
o Dry mucous membranes  Weight gain, distended neck veins
o Elevated urine SG  Polyuria if kidneys are normal
o Altered level of consciousness  Hypertension
o Inc. hematocrit, serum protein, BUN  Full bounding pulses
o When severe can lead to shock  Crackles in lungs (pulmonary edema)
 Elevated respirations
Hypertonic Dehydration
 Hypertonic contraction of ECF Hypertonic Overhydration
 Fluid has more solutes than normal plasma  Hypertonic expansion of the ECF
 Second most common type of dehydration  ↑ serum osmolarity leads to shifting of fluids from
 Occurs when water loss from ECF > solute loss cells into the blood stream
 Cause fluid to be pulled from the cells into the blood  Causes cell shrinkage and fluid volume overload
stream leading to cellular shrinkage or dehydration increased cardiac workload
 Causes:  Eventually lead to ↓Cardiac Output and CHF
o Excessive insensible fluid loss:  Causes:
hyperventilation and pure water loss with o Over administration of hypertonic IV fluids
YM,RMT
MD2021

high fever o over use of hypertonic enemas

o Water diarrhea o hypertonic tube feedings
o Diabetic ketoacidosis o ingestion of sea water

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 BIOCHEMISTRY: FLUID AND ELECTROLYTES – DRA. GABALDON

 manifestations:  Manifestations:
o ↑BP and central venous pressure (CVP) o Confusion, headache
o Distended neck veins o Nausea and vomiting
o Full, bounding pulses o Generalized muscle weakness
o Thirst from cellular shrinkage Hypernatremia
o ↑serum Na and serum osmolarity  ↑Na levels
o ↓urine output, body retains water to dilute  Causes:
sodium o Renal failure (inability to excrete Na)
o ↑urine Na levels in persons with normal o Excessive salt ingestion
kidneys o Over administration of hypertonic IV fluids
o Disorientation, lethargy and coma o Salt water drowning
o ↓fluid intake
ELECTROLYTE BALANCE o Diabetes insipidus (def. of ADH)
Major Electrolytes  Aldosterone
 Sodium  Consequence: water transfer from cell into the ECF
 Potassium causing cellular dehydration
 Calcium  Manifestations: hyper reflexes, hypertension, seizure
 Magnesium
 Chloride POTASSIUM
 Phosphate  NV: 3.5 – 5.5 mEq/L
 Bicarbonate  Critical for electrical conduction of nerve impulses –
particularly cardiac electrical conduction
NORMAL VALUES!!  Major cation in the ICF
Sodium = 135 – 145 mEq/L  K imbalance at the cellular level is maintained by the
Potassium = 3.5 – 5.5 mEq/L Na-K pump
Calcium = 4.0 – 5.5 mEq/L or 8.5 – 10 mg/dL  Kidney can excrete K and in exchange for Na-
Magnesium = 1.5 – 2.5 mEq/L controlled by aldosterone
 Body is much more sensitive to small changes b serum
SODIUM K levels than to small changes in other serum
 NV: 135 – 145 mEq/L electrolytes
 Predominant CATION in the ECF
 Plays crucial role in excitability of muscles and neurons Hypokalemia
 Important in regulating fluid balance  ↓K levels
 Na regulation at cellular level is controlled by the Na-K  Common cause:
pump o Loss of K: excessive vomiting, suctioning,
 Body levels of Na retention/ excretion are controlled diarrhea
by aldosterone o Hemodilution from overhydration
 Aldosterone is controlled by renin-angiotensin o Alkalosis
system (RAAS) o Acute alcoholism
 Medications:
o Diuretics, laxative, insulin
 Manifestations:
o Hypotension and elevated pulse due to
increased cardiac output
o Weakness, constipation, motility ileus
Hyperkalemia
 ↑ K levels
 Common cause:
o Use of K supplements
o Receiving old or improperly administered
blood (hemolyzed)
o Inadequate K excretion – from ↓
aldosterone related to Addison disease
o Cell destruction: crushing injuries, burns
 Manifestations:
Hyponatremia o Diarrhea, apathy, confusion
 ↓ sodium levels o numbness in hands and feet
 Causes: o acidosis
o Loss of Na in fluid ECG changes in Hypo-Hyperkalemia
o Excessive sweating, vomiting, diuretics HYPOKALEMIA HYOERKALEMIA
o Renal failure (inability to conc. and save Na) P wave ↑amplitude and width Flat
o Dilution of Na from fluid overload PR interval Prolonged Prolonged
o Over administration of hypotonic fluids QRS interval Prolonged
o Fresh water drowning T wave Flattening or inversion Peak ( ↑amplitude
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MD2021

 Consequence – water moves into cell (such as brain and width

cells) causing brain expansion within the limited space U wave ↑ prominence
inside the cranium

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 BIOCHEMISTRY: FLUID AND ELECTROLYTES – DRA. GABALDON

Normal ECG, changes in Hyperkalemia and Hypokalemia Hypercalcemia

 ↑Ca++ levels
 Causes:
o Disturbances in regulation
o ↓ renal excretion
o Diuretic use that enhances Ca++
reabsorption
o Excess PTH
o Hormone
o Hyperthyroidism
o Cancer
o Excess intake of calcium
 Manifestations:
o Muscle weakness, nausea, vomiting,
constipation
o Hypoactive vowel sounds
CALCIUM o Extreme thirst
 NV: 4.0 – 5.5 mEq/L o Polyuria (if kidney function is normal)
 Required for normal skeletal, cardiac and smooth o Kidney stones, blood clots
muscle contraction o Homan’s sign
 Needed for blood clotting o Arrythmias, ECG changes
 Intestinal absorption of dietary calcium requires
vitamin D
 Calcium metabolism is regulated by PTH and Vit D

Hypocalcemia
 ↓ Ca++ levels
 Causes:
o Due to failure of normal regulatory
mechanisms, such as acute or chronic renal
failure
 Pathophysiology:
o Calcium functions as membrane stabilizer,
so ↓ levels increases excitability of nerves
and muscles
o Although calcium is needed for blood
clotting, prolonged deficiency or very low
levels are needed before blood clotting MAGNESIUM
mechanisms are altered  NV: 1.5 – 2.5 mEq/L
o Bones store calcium, if serum levels are  Needed to prevent over excitability of muscles
low, bones release calcium and becomes  Has a sedative effect on neuromuscular junction,
osteoporotic inhibits acetylcholine release and admonishes muscle
 Manifestations: cell excitability
o Tetany, muscle spasms, cramps  Acts as cofactor in enzyme reactions
o Tremors, hyperactive reflexes  Participates in bone and teeth production
o Diarrhea
o Tingling of fingers, toes, lips and face Magnesium Balance
o (+) Trousseau’s sign: carpopdeal spasm  Mostly found in ICF and bone
(hans spasm when blood pressure cuff  Within cells, it functions in the Na-K pump
inflated 3-4 mins)  Aldosterone controls Mg concentration in the ECF
o (+) Chvostek’s sign: tap facial nerve; facial o ↓ Mg levels results in an ↑ aldosterone
muscles go into spasms secretion
o Seizures, arrhythmia, and ECG changes  Aldosterone increases Mg reabsorption by the kidneys

Hypomagnesemia
 Causes:
o ↓GI absorption, malnutrition
o Total Prenatal Nutrition (TPN) without Mg
o Vomiting, prolonged nasogastric suctioning
o Laxative abuse, diarrhea, malabsorption
o Alcoholism, cancer chemotherapy
o Excessive intake of Ca++, Vit D
o ↑ dose steroids
o Hypoaldosteronism
YM,RMT
MD2021

 Manifestations:
 Tachycardia, cardiac arrhythmias, hypotension
 Painful paresthesia and muscle spasms

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 BIOCHEMISTRY: FLUID AND ELECTROLYTES – DRA. GABALDON

 Tetany, hyoeractive reflexes Bases

+
 (+) Chvostek’s and Trousseau’s sign  an ion or a molecule that can accept H
 Confusion, agitation, seizure  referred to as proton acceptors
- -
Hypermagnesemia  ex: HCO3 : It can combine with H to form H2CO3
 Causes:  Strong base: NaOH
o Relatively rare
o Usually caused by a combination of ↑intake Buffers
and ↓renal function  a compound that limits the change in hydrogen ion
o Antacid and laxatives concentration (and pH) when hydrogen ions are added
 Manifestations: or removed from the solution
o Lethargy and drowsiness  all buffers are weak acids or bases
o Depressed respirations
o ↓BP, bradycardia progressing to cardiac Mechanism on regulating changes in H+ concentration and Acid-
arrest Base balance
o Hypoactive reflexes
o Coma 3 primary systems that regulate H+ conc. in body fluids
 Chemical Buffers
ACID-BASE BALANCE o Immediately combine with acid or base to
Regulation of Hydrogen Ion prevent changes in H+ concentration
+
 Precise H regulation is essential because activities of  Respiratory Center
almost all enzyme system in the body are influenced by o Regulates the removal of CO2 from the ECF
H+ concentration  Renal Mechanism
 A hydrogen ion is a single free proton released from a o Eliminates excess acid or base from the
hydrogen atom body
Hydrogen ion and pH o Slow to respond, but the most powerful
 The process of metabolism generates H ion
+ acid base regulatory mechanism
 Small amounts are formed from metabolism of amino
acids and anaerobic metabolism of glucose to lactic or Chemical Acid Base Buffer System
pyruvic acid  Reacts within seconds
 More acid is produced as a result of CO2 released from  Do not eliminate H+ from or add them to the body but
anaerobic metabolism only keep them tied up until balance can be re-
 pH is inversely proportional to H+ concentration established
+
 ↑pH = ↓H
 the pH is calculated by taking the negative logarithm of Buffer System
hydrogen ion concentration:  Rapidly acting
 Composed of weak acid and its salt
+
pH = -log10(H )  Buffers in the plasma:
o Bicarbonate buffer = NaHCO3 / H2CO2
o Phosphate buffer = Na2HPO4 / NaH2PO4
ACID, BASES AND BUFFERS o Protein buffer
Acids
 defined as any compound which can release hydrogen Buffers in the RBC
ions in solution  Bicarbonate Buffer
 examples: HCl, H2HCO3  Phosphate buffer
 referred to as proton donors  Hgb buffer
Strong Acids
 a compound that ionizes completely in a solution to Bicarbonate Buffer System
form hydrogen ions and a base. (ex. HCl)  Chief buffer for fixed, non-volatile acids
Weak Acids  Most important buffer in ECF
 compounds that are only partially ionized in a solution Sodium Bicarbonate
 Alkali reserve of the body
 Deficiency = metabolic acidosis
Ionization of an acid in solution:  Excess = metabolic alkalosis
 2 components: weak acid and salt
HA ↔ H + A
+ -  NaHCO3 (sodium bicarbonate)
(acid) ↔ (H+) + (conjugate base)
Hemoglobin Buffer
+
Strong Acid:  Chief buffer for H generated by CO2
+
HA → H + A
-  Responsible for 60% of the buffering capacity of the
*reaction moved to the right resulting in complete ionization of blood
the acid  pH in cells slightly lower than ECF

Weak acid: Phosphate Buffer System

HA ↔ H + A
+ -  important in buffering acids in the distal tubules of the
YM,RMT
MD2021

+
*partial ionization resulting in an equilibrium with HA, H and A
+ kidney
all present in the solution  becomes greatly concentrated in the tubules
 composed of 2 parts:

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 BIOCHEMISTRY: FLUID AND ELECTROLYTES – DRA. GABALDON

 Na or KH2PO4 – acid part Acid-Base Plasma Primary Compensation

 Na or K2HPO4 – basic part Imbalance pH disturbanc
e
Respiratory Mechanism Respiratory Low ↑pCO2 ↑renal NAE with
 Quick acting Acidosis ↑H+ resulting in ↑ HCO3-
 Emergency mechanism Respiratory High ↓pCO2 ↓ renal NAE w/
 Cannot completely restore acid-base equilibrium by Alkalosis ↓H+ resulting in ↓HCO3-
itself Metabolic Low ↓HCO3- Hyperventilation w/
 Regulates primarily CO2 level in the blood (intracellular Acidosis reslting ↓pCO2
metabolism), removal of CO2 from ECF Metabolic high ↑HCO3- Hypoventilation w/
 Factors: Alkalosis resulting ↑pCO2
o Rate of metabolic formation of CO2
o Change in pulmonary ACID-BASE IMBALANCE
o ↑alveolar ventilation = ↓pCO2 RESPIRATORY TYPE
Respiratory Acidosis
Renal Mechanism  Due to hypoventilation and consequential ↑pCO2
 Slow acting  Ex: status asthmaticus, morphine poisoning,
 Can completely restore acid-base balance pulmonary edema
 Regulates primarily the sodium-bicarbonate  Destruction of respiratory center
o Respiratory tract obstruction
The renal role in maintaining acid-base balance is two fold o Pneumonia
 Reclaim filtered bicarbonate and therefore, avoid o ↓ respiratory exchange gases
bicarbonate loss
 Regenerate bicarbonate in an amount equal to that Respiratory Alkalosis
used as buffer  Due to hyperventilation and consequential ↓pCO2
 Examples:
Proximal Tubule o Occurs in high altitude, psychoneurosis
 Main site for bicarbonate reabsorption accounting for o Hystei, early stage salicylate poisoning
75-90% of the filtered load o Injudicious use of respiration
 Bicarbonate is reabsorbed with sodium, it is filtered
and reabsorbed METABOLIC TYPE
 H+ enters the tubules via secretion; not filtered at Metabolic Acidosis
Bowman’s capsule because there is little free H+ in the  Due to ↓bicarbonate content of the blood
plasma  Causes:
 DM with ketosis
Distal Tubule  Renal insufficiency
 Loss of intestinal content as in diarrhea, vomiting
 Remaining 10-25% of bicarbonate is reabsorbed  Treatment: Sodium Bicarbonate
 Generation of new bicarbonate at a rate of 1.0-1.5
mmol/kg/day Metabolic Alkalosis
 Phosphate anion is filtered and not reabsorbed  ↑bicarbonate fraction
 Ammonia is formed in cells lining tubule from amino  Causes:
acids through deamination (takes place after 1-2 days)  Treatment of peptic ulcer with alkali (NaHCO 3 tablets)
of increased H+  Hypokalemic alkalosis (prolonged vomiting, high
intestinal obstruction)
Phosphate buffer system -
 Loss of Cl due to vomiting – pyloric stenosis
+
 Any excess H can combine with HPO4 and other
tubular buffers
+
 After the H combine with HPO4 to form H2PO4 it can
be excreted as sodium salt (NaH 2PO4), carrying with
the excess hydrogen

Abnormal Acid-Base Balance

 Acid base imbalances can be defined as acidosis or
alkalosis
o Acidosis - excess H+
o Acidemia - blood pH <7.35
o Alkalosis – excess HCO3-
o Alkalemia – blood pH >7.45
 When acid-base disturbance results from a primary
change in HCO3-, it is a metabolic disorder
 When primary disturbance alters blood pCO2, it is a
respiratory disorder
YM,RMT
MD2021