Acid-Base Disorders

Acid-Base Disorders

Happen when bicarb buffer (1st mechanism) is overwhelmed

Acid-Base Balance

Two independent variables:

1. Respiratory mechanism (regulates pCO2)

2. Renal mechanism (regulates HCO3-)

Acidosis - pH

Acidosis vs. Alkalosis

1. metabolic or respiratory

2. can be primary or compensatory

-determined by pH

metabolic is usually primary (then resp compensates)

Buffer Systems

1. Bicarbonate

2. Respiratory

3. Renal

Low pH (acidity) vs High pH (alkalinity)

exhale CO2 when you have low pH

resp system kicks in and retains pCO2 to buffer when you have high pH

Renal

alkaline pH - excrete bicarb, retain H+

acidic pH - excrete H+, retain bicarb

Metabolic Acidosis

LOW pH, LOW HCO3-

Elevated anion gap acidosis (increased acid production leads to HCO3- consumed)

-diabetic ketoacidosis

-lactic acidosis (intense exercise, renal failure, sepsis)

-poisoning (methanol or ethylene glycol)

Normal anion gap acidosis:

-HCO3- loss from kidneys or GI tract --> H+ elevation

-diarrhea

-renal tubular acidosis (bicarb lost in urine)

-diuretics

Anion Gap - Metabolic Acidosis

Is bicarbonate low from high acids or from bicarb loss?

- high anion gap = high acids (normal to high Cl-)

-HCO3- consumed by buffering excess H+ ions

-Normal anion gap = HCO3- loss and high Cl-

Metabolic Acidosis Compensatory Mechanisms

1. Respiratory (primary):

- Kausmaul breathing (hyperventilation) - lowers pCO2

2. Renal (secondary):

- Excrete H+ ions

- Increase ammonia formation

- Absorb HCO3- (if possible)

Lab Findings:

1. pH < 7.35

2. LOW pCO2 (if compensating)

3. LOW HCO3- (consumed trying to buffer excess acid or excreted)

4. Increased or normal anion gap

Metabolic Alkalosis

HIGH pH, HIGH HCO3-

1. Increased ingestion of bases

-antacids

-IV fluids high in bicarbonate

-blood transfusions (citrate is basic)

2. Decreased excretion of bases (diuretics)

3. Increased excretion of H+ (Cushing and high aldosterone)

4. Loss of acidic fluid (vomiting)

5. Cystic Fibrosis (impaired H+ production)

Metabolic Alkalosis Compensatory Mechanisms

Respiration (primary):

1. Hypoventilation leads to increased pCO2

Renal (secondary):

1. H+ retention

2. Less ammonia formation

3. Increase HCO3- excretion

Lab Findings:

1. pH> 7.45 (>7.55--> tetany)

2. HIGH HCO3-

3. Normal pCO2

Respiratory Acidosis

LOW pH, HIGH pCO2

Cause: decreased CO2 expelled from lungs

Chronic hypoventilation

1. COPD

2. Brain damage

Acute hypoventilation

1. Drugs

2. Asthma, pneumothorax, pleural effusion

3. Wrong ventilator settings

Respiratory Acidosis Compensatory Mechanisms

Immediate compensation by Hb and protein buffer systems

Renal compensation (takes 2-3 days):

1. Excrete H+ ions

2. Form more ammonia

3. Absorb bicarbonate

4. Increased Na+ reabsorption in exchange for H+

Lung compensation: depends on lung's ability to function

Lab Findings:

1. pH

Respiratory Alkalosis

HIGH pH, LOW pCO2

Hyperventilation (CO2 removal)

1. increases [HCO3-] : [pCO2] ratio -> pH elevation

2. acute or chronic

Excessive Elimination

1. anxiety

2. fever

3. drugs

4. Gram neg septicemia

5. cerebrovascular incidents (stroke)

6. mechanical ventilators

Respiratory Alkalosis Compensatory Mechanisms

Immediate compensation by Hb and protein buffer systems

Renal compensation:

1. Retain H+ ions

2. Excrete bicarbonate

Lab Findings:

1. pH > 7.45

2. LOW pCO2

3. normal HCO3-

Interpreting Blood Gas Analyses

Systematic Approach

1. Review pH result - acidotic or alkalotic

2. Review HCO3- changes

- abnormal - metabolic

- normal - respiratory

3. Review pCO2 changes

- indicate respiratory issue

4. Look for compensation

- none

- partial

- full

Blood Gas Levels

pH: 7.35 - 7.45

HCO3-: 22 - 29 mmol/L

pCO2: 35 - 45 mmHg