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+ + HCO3

-

Types 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

+ + HPO4

2- H2PO4

-

OH- + H2PO4

- H2O + H2PO4

2-

c. 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

+ + HCO3

-

Body 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:

Oxygen deficiency at high altitudes (low

environmental O2)

Acute anxiety and emotional disturbances

Fever, anemia

Early salicylate intoxication

Cirrhosis

Gram-negative sepsis

Assisted ventilation

Hypoxemia

Pulmonary embolism

Pulmonary Edema

Cystic fibrosis

Congestive Heart Failure

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

Accumulation of tissue metabolites, including lactic

acid consequent on anaerobic metabolism

Diabetes mellitus accumulation of ketone bodies

(Aceto-acetic acid and OH butyric acid)

Non-volatile or fixed acids - not blown off

Other diseases include CHF and renal failure

Aspirin overdose with toxicity

Anion Gap

Metabolic acidosis is conveniently divided into

elevated and normal anion gap (AG) acidosis.

AG = Na+ - (Cl

- + HCO3)

Normal AG is typically 12 4 mEq/L. If AG is

calculated using K+, the normal AG is 16 4 mEq/L

Comon causes of high ion gap

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

Generation Phase

Loss of Acid (vomiting and gastric suctioning) or

gain a base (administration of NaHCO3)

Loss of fluids containing more Cl- than HCO3(use

of loop or thiazide diuretics)

Maintenance Phase

Renal excretion of HCO3 is impaired (Fluid volume

loss / contraction alkalosis)

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: 7.45

STEP 2: Assess PaCo2 to Evaluate Ventilation Normal: 35 45 mm Hg Respiratory acidosis: >45 mm Hg

Respiratory alkalosis: