Acid Base Balance

Acid-base balance -- main concern two ions:

Hydrogen (H+)
Bicarbonate (HCO3-)
Acid Base Concepts
Derangement in Acid-base is common in disease processes
H+ has special significance due to the narrow range compatible with living systems
Enzymes, hormones and ion distribution are all affected by H+ concentrations
The body produces more acids than bases
Acids take in with foods
Acids produced by metabolism of lipids and proteins
Cellular metabolism produces CO2.
CO2 + H20 H2CO3 H+ + HCO3Types of Acids in the Body
1. Volatile acids:
Pco2 is most important factor in pH of body tissues.
2. Fixed Acids.
Catabolism of amino acids, nucleic acids, and phospholipids
3. Organic Acids:
By products of aerobic metabolism, anaerobic metabolism, during starvation, and diabetes.
Lactic acid, ketones
Control of Acids
1. Buffer and Buffer Systems
a. Bicarbonate buffer
Sodium Bicarbonate (NaHCO3) and carbonic acid (H2CO3)
Maintain a 20:1 ratio : HCO3- : H2CO3
HCl + NaHCO3 H2CO3 + NaCl
NaOH + H2CO3 NaHCO3 + H2O
b. Phosphate Buffer
Major intracellular buffer
H+ + HPO42- H2PO4OH- + H2PO4- H2O + H2PO42c. Protein Buffers
Includes hemoglobin, work in blood and ISF
Carboxyl group gives up H+
Amino Group accepts H+
Side chains that can buffer H+ are present on 27 amino acids.
2. Respiratory mechanisms
Exhalation of carbon dioxide
Powerful, but only works with volatile acids
Doesnt affect fixed acids like lactic acid
CO2 + H20 H2CO3 H+ + HCO3Body pH can be adjusted by changing rate and depth of breathing
3. Kidney excretion
Can eliminate large amounts of acid
Can also excrete base
Can conserve and produce bicarb ions
Most effective regulator of pH
If kidneys fail, pH balance fails
Rate of Correction
1. Chemical buffers
- react very rapidly (< 1 sec)
2. Respiratory regulation - reacts rapidly (sec to min)
3. Renal regulation
- reacts slowly (min to hr)

4 types of primary acid-base disorders

Acidosis - an excess of unwanted acid in the blood; pH may be normal
Alkalosis - an excess of unwanted alkali in the blood; pH may be normal
1. Respiratory Acidosis
Mechanism : Hypoventilation or Excess CO2 Production
Etiology
Pneumonia,Pneumothorax
Respiratory Center Depression
Inadequate mechanical ventilation
Sepsis or Burns
Neuromuscular Disease

Acute conditions:
Adult Respiratory Distress Syndrome
Pulmonary edema
Pneumothorax
Chronic Conditions
COPD
Guillain Barre syndrome (inflammatory
demyelinating polyneuropathy (AIDP)

Pathophysiology - increase in PCO2

Compensatory:
Rise in H+ is buffered by blood buffers
Renal HCO3- retention; Adjusts [HCO3- ] / [CO2] ratio to restore pH
Principal effect of acidosis is depression of the CNS through in synaptic transmission.
Generalized weakness
Deranged CNS function the greatest threat
Severe acidosis causes: Disorientation, coma, death
2. Respiratory Alkalosis
Mechanism: Hyperventilation - pulmonary ventilation; loss of CO2 exceeding production rate
Etiology
Conditions that stimulate respiratory center:
Assisted ventilation
Oxygen deficiency at high altitudes (low
Hypoxemia
environmental O2)
Pulmonary embolism
Acute anxiety and emotional disturbances
Pulmonary Edema
Fever, anemia
Cystic fibrosis
Early salicylate intoxication
Congestive Heart Failure
Cirrhosis
Gram-negative sepsis
Pathophysiology:
Compensatory
Decrease in Carbonic acid is buffered by blood buffers
Renal HCO3- excretion; Adjusts [HCO3- ] / [CO2] ratio to restore pH
Effect: Alkalosis causes over excitability of the central and peripheral nervous systems.
Numbness
Lightheadedness
Nervousness
muscle spasms or tetany
Convulsions
Loss of consciousness
Death
3. Metabolic Acidosis
Etiology:
Excessive exercise
Anion Gap
Accumulation of tissue metabolites, including lactic
Metabolic acidosis is conveniently divided into
acid consequent on anaerobic metabolism
elevated and normal anion gap (AG) acidosis.
Diabetes mellitus accumulation of ketone bodies
AG = Na+ - (Cl- + HCO3)
(Aceto-acetic acid and OH butyric acid)
Normal AG is typically 12 4 mEq/L. If AG is
Non-volatile or fixed acids - not blown off
calculated using K+, the normal AG is 16 4 mEq/L
Other diseases include CHF and renal failure
Comon causes of high ion gap
Aspirin overdose with toxicity
Lactic acidosis (anaerobic metabolism)
Diabetic ketoacidosis (accelerated lipid
metabolism)
Azotemic renal failure (end products of protein
metabolism)
Ingestion of Toxins with acid metabolites
Non-anion gap acidosis Hyperchloremic metabolic
acidosis
Compensatory:
Rise in H+ is buffered by blood buffers
Hypoventilation to increase carbonic acid level ; Adjusts [HCO3- ] / [CO2] ratio to restore pH

Management:
Treatment of underlying disorder
Respiratory support assisted mechanical ventilation
Administration of Exogenous alkali (NaHCO3)
4. Metabolic Alkalosis
Etiology
Excessive intake of alkali or renal defects
Maintenance Phase
Generation Phase
Renal excretion of HCO3 is impaired (Fluid volume
Loss of Acid (vomiting and gastric suctioning) or
loss / contraction alkalosis)
gain a base (administration of NaHCO3)
Loss of fluids containing more Cl- than HCO3(use
of loop or thiazide diuretics)
Management:
Treatment of the underlying cause
Administration of Acetazolamide (Diamox)
Administration of Exogenous acid HCl or HCl precursors (ammonium chloride, arginine
monohydrochloride)
Analysis of Arterial Blood Gases
STEP 1: Classify the pH
Normal: 7.35 7.45
Acidemia: <7.35
Alkalemia: >7.45
STEP 2: Assess PaCo2 to Evaluate Ventilation
Normal: 35 45 mm Hg
Respiratory acidosis: >45 mm Hg
Respiratory alkalosis: <35 mm Hg
STEP 3: Assess HCO3 // Evaluate Metabolic Process Normal: 22 - 26mEq/L
Metabolic acidosis: <22 mEq/L
Metabolic alkalosis: >26 mEq/L
Level of Base Excess-5 -4 -3 -2 +2 +3 +4 +5
STEP 4: Determine Presence of Compensation
No Compensation present:
Abnormal pH
Abnormal pH
Abnormal PaCO2
Normal PaCO2
Normal HCO3
Abnormal HCO3
Partial Compensation: with opposite directions
Abnormal pH
Abnormal PaCO2
Abnormal HCO3
Complete or full Compensation
pH Normal
Abnormal PaCO2 and HCO3
* Only a state of acidosis can cause the pH to become acidotic.
Example 1
Example 2
pH
7.25 acid
pH
7.25 acid
paCO2 = 55 acid
paCO2 = 55 acid
HCO3 = 25 normal
HCO3 = 35 alkaline
BE
= +2 normal
BE
= +8 alkaline
Non Compensatory Respiratory Acidosis
Respiratory acidosis with partial compensation
Example 3
pH 7.35 acid normal
paCO2 = 50 acid
HCO3 = 30 alkaline
BE
= +5 alkaline
Respiratory acidosis with complete compensation
STEP 5:
Evaluate Oxygenation
SaO2 = 94 100%
SaO2 below 93 = Hypoxemia (pulse oximeter)
pAO2 = 80 100 mm/Hg Adequate Oxygenation
paO2 = 60 79 mm/Hg Mild hypoxemia
paO2 = below 39 = Severe hypoxemia
STEP 6: Interpret
Maria was brought to ER department semi-coma, breathing deeply with a respiratory rate of 32 cycles per minute.
ABG was done at room air after which shes given Oxygen at 2L/minute
ABG results as follows
pH
7.28
paCO2 = 28.9
HCO3 = 11 BE
= -13
PO2
= 96% O2 Sat =90%
Partially compensated metabolic acidosis with adequate oxygenation