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ACID BASE BALANCE Lesson

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ACID BASE

BALANCE
DEFINITION OF TERMS
 Acid
 Base
 Buffer
 pH
 pK
 Equilibrium
 Law of mass action
Acid
 a substance that can yield a hydrogen ion or
hydronium ion when dissolved in water
 E.g.
HF
HCl
H2SO4
HBr
Base
 substance that can yield hydroxyl ions
 E.g.
NaOH
KOH
Sr(OH)2
Ba(OH)2
Ca(OH)2
Buffer
 combination of a weak acid or a weak base and its
salt
 a system that resists changes in pH
 effectivity depends on the pK of the buffering
system and the pH of the environment in which it is
placed
pH
 negative or inverse log of the hydrogen ion concentration
 = log (1/[H+])
 = -log[H+]
 An increase in [H+] decreases the pH
 A decrease in [H+] increases the pH

Reference value for blood plasma pH: 7.40


Hydrogen ion
 [H+] in ECF: 36 to 44 nmol/L (pH 7.34 to 7.44)
 [H+] for arterial blood: 40 nmol/L (pH 7.4)
 Acidosis: pH <7.34
 Alkalosis: pH>7.44
 -osis or -emia
pK
 negative log of the ionization constant
 also the pH in which the protonated and
unprotonated forms are present in equal
concentrations
Equilibrium
 condition wherein the number of positively-
charged electrolytes is equal to the number of
negatively-charged electrolytes
Regulation of [H+]
 Buffers
 Respiratory center and lungs
 Kidneys
BUFFERS
Bicarbonate-Carbonic acid
 Principal buffers

 H2CO3 = combines with OH- from the base to form H 2O


and HCO3-
 HCO3- = combines with H+ from the acid to form H2CO3

 pK = 6.1
Why HCO3--H2CO3 is important?
 H2CO3 dissociates into CO2 and H2O, allowing CO2
to be eliminated by the lungs and H+ as water
 Changes in CO2 modify the ventilation rate
 HCO3- concentration can be altered by the kidneys
Phosphate Buffer System
 HPO4-2 – H2PO4-
 plays a role in plasma and RBC
 involved in the exchange of sodium ion in the urine

H+ filtrate
H2PO4-(aq) H+(aq) + HPO42-(aq)
 additional H+ enter the ICF, equilibrium shifts to the

left
 additional OH- enter the ICF, shifts the equilibrium

to the right
Protein Buffer system
 depends upon the abilities of amino acids to bind or
release hydrogen ions
Hemoglobin-Oxyhemoglobin
 consists of oxygenated and nonoxygenated Hb
 plays a role in CO2 transport

HHb H+ + Hb-
HHbO2 H+ + HbO2-
Lungs
 regulate pH through retention or elimination of
CO2 by changing the rate and volume of ventilation

Problem: lungs do not remove CO2 at the rate of its production


Reason: decreased ventilation or disease
Result: CO2 accumulates in the blood, pH decreases

Problem: CO2 removal is faster than production


Reason: hyperventilation
Result: H+ concentration will be decreased, pH increases
Kidneys
 regulate pH by excreting acid, primarily in the NH 4+, &
reclaiming HCO3- from the glomerular filtrate

Problem: when HCO3- > 26-30 mmol/L


Reason: excretory capability fails (kidney failure), lactate,
acetate or HCO3- IV infusion, excessive loss of Cl- (sweating,
vomiting, prolonged nasogastric suction)
Result: HCO3- cannot be excreted

Problem: when HCO3- < 26-30 mmol/L


Reason: diuretics favoring excretion of HCO3-, excessive loss
of cations, kidney dysfunction (chronic nephritis or infections)
Result: HCO3- reabsorption is impaired
Lungs and Kidneys
 Lungs (respiratory): hyperventilate or
hypoventilate (CO2)
 Kidneys (metabolic): reabsorb or excrete
bicarbonate
Acid Base disorders
 Acidemia: blood pH < 7.35, excess acid
 Alkalemia: blood pH > 7.45, excess base
 Primary respiratory acidosis/alkalosis: disorder due
to ventilatory dysfunction (PCO2 change)
 Nonrespiratory or metabolic disorder: disorder
resulting in the change in HCO3-
 Mixed respiratory and nonrespiratory disorders
Compensation
 the body tries to restore acid base homeostasis
during an imbalance
 how? By altering a factor not affected by the
pathologic process
 E.g. Imbalance of metabolic origin, the body
compensates by ventilation
 Lungs: respond immediately but short term
 Kidneys: respond slower but long term
 Fully compensated or partially compensated
Primary Metabolic Acidosis
 <24 mmol/L HCO3-, resulting in decreased pH
 Causes: acid producing substance (NH4Cl, CaCl2)
or by excessive formation of organic acids (diabetic
ketoacidosis and starvation), reduced excretion of
acids (renal tubular acidosis), excessive loss of
HCO3- (diarrhea or drainage from a biliary,
pancreatic, or intestinal fistula)
 Compensation: hyperventilation
Primary Respiratory Acidosis
 due to decreased in alveolar ventilation
(hypoventilation), causing a decreased elimination
of CO2 by the lungs
 hypercarbia
 Causes: chronic obstructive pulmonary disease
(COPD), hypoventilation caused by drugs like
barbiturates, morphine, or alcohol, mechanical
obstruction, asphyxiation, CHF
 Compensation: kidneys increase the excretion of
H+ and increase the reclamation of HCO3-
Primary Metabolic Alkalosis
 gain of HCO3-, causing an increase in pH
 Causes: excess administration of sodium
bicarbonate, ingestion of bicarbonate producing
salts (sodium lactate, citrate or acetate), excessive
loss of acid through vomiting, nasogastric
suctioning, or prolonged use of diuretics
 Compensation: respiratory depression
(hypoventilation)
Primary Respiratory Alkalosis
 increased rate of alveolar ventilation lowering CO2
 Causes: hypoxemia, chemical stimulation by drugs
like salicylates, increased in environmental
temperature, fever, hysteria (hyperventilation),
pulmonary emboli, pulmonary fibrosis
 Compensation: kidneys excrete HCO3- in the urine
and reclaim H+ to the blood
Normal values

pH 7.35-7.45
PCO2 (mmHg) 35-45
HCO3- (mmol/L) or (mEq/L) 22-26
H2CO3 (mEq/L) 1.14-1.26
Total CO2 content (mmol/L) 23-27
PO2 (mmol/L) 80-110
SO2 (%) >95
O2Hb (%) >95
Formula
 Henderson Hasselbach equation
pH = pKa + log [A-]/[HA]
 Total CO = H CO + HCO -
2 2 3 3

 H2CO3 = PCO2 X 0.0307


Problems:
1. pH = 7.51
PCO2 = 40 mmHg
HCO3- = 36 mmol/L
2. pH = 7.31
PCO2 = 50 mm Hg
PO2 = 62 mm Hg
HCO3- = 24 mmol/L
SO2 = 78%
3. pH = 7.11
PCO2 = 60 mmHg
HCO3- = 24 mmol/L
4. pH = 7.5
PCO2 = 15 mmHg
HCO3- = 25 mmol/L
5.
Total CO2 = 28.7 mmol/L
H2CO3= 1.84 mmol/L
6. Total CO2 = 37.3
H2CO3 = 1.25
7. pOH = 6.42
PCO2 = 39 mmHg
HCO3- = 35 mmol/L
SPECIMEN CONSIDERATIONS
 arterial blood samples
 venous sx may be used if pulmonary function or O2 transport is not
measured
 sources of error:
 collection device
 form & concentration of heparin
 speed of syringe filling
 maintenance of anaerobic environment
 mixing of sx to ensure dissolution & distribution of the heparin
anticoagulant
 transport & storage time before analysis
OTHER CONSIDERATIONS
 conditions of the px at the time the sx is drawn
should be documented
 ventilation (room air or supplemented)
 temperature
 posture
 blood collection device: preheparinized plastic
syringe (dry form)
 adequate mixing
OTHER CONSIDERATIONS
 slow filling of syringe: small needle may produce
bubbles and may cause hemolysis
 Sx is kept at RT and analyzed in < 30 min
 anaerobic environment be kept
METHODS FOR BLOOD GAS
DETERMINATION
 PO2
 pH
 PCO2
PO2 Measurement
1. Clarke electrodes
 measure the amount of current flow in a circuit that is related to
the amount of O2 being reduced at the cathode
 microammeter: measures the movement of electrons
  CHON build up, bacterial contamination
2. Transcutaneous electrodes: O2 depends on O2
diffusing from the capillary bed through the tissue to
the electrode
 Neonates and infants
  skin thickness & tissue perfusion w/ arterial blood
pH Measurement
 Potentiometric measurement
 Glass membrane sensitive to H+ is

placed around the Ag-AgCl electrode to


form a measuring electrode
 Reference elec: (calomel: Hg-HgCl or

Ag-AgCl half cell)


PCO2 Measurement
 uses Severinghaus electrode
 semipermeable membrane, bicarbonate buffer
 CO2 diffuse into the membrane reacts w/ the buffer
and form H2CO3, then dissociates to form HCO3-
and H+
 H+ is measured by pH electrode and related to
PCO2
  protein build up on the membrane
Arterial puncture

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