Acid-Base Imbalances
Basics of Acid-Base Balance
Definition of Acid:
An acid is a substance that can donate hydrogen ions (H+) to a base.
Examples of acids include:
Hydrochloric acid
Nitric acid
Ammonium ion
Lactic acid
Acetic acid
Carbonic acid (H2CO3)
Definition of Base:
A base is a substance that can accept or bind H+.
Examples of bases include:
Ammonia
Lactate
Acetate
Bicarbonate (HCO3-)
Acidity and Alkalinity
Determination of Acidity or Alkalinity:
The acidity or alkalinity of a solution depends on the concentration of hydrogen ions (H+).
An increase in hydrogen ions leads to acidity, while a decrease leads to alkalinity.
Hydrogen ion concentration is expressed in negative logarithm and symbolized as pH.
Relationship between pH and H+:
Lower pH → Higher H+
Higher pH → Lower H+
Acidic and Alkaline Solutions:
Acidic solution: pH < 7
Alkaline solution: pH > 7
Normal blood pH range: 7.35 – 7.45
Acidosis: pH < 7.35
Alkalosis: pH > 7.45
Life-threatening pH range: 6.8 to 7.8
Significance of pH Range
For normal enzyme and cell function, blood pH must stay in the narrow range of 7.35 to 7.45.
If blood is acidic, the force of cardiac contractions diminishes.
If blood is alkaline, neuromuscular function becomes impaired.
Mechanisms for Maintaining Acid-Base Balance
Bicarbonate to Acid Ratio:
Ratio of bicarbonate (HCO3-) to carbonic acid (H2CO3) = 20:1.
Three Mechanisms Regulating Acid-Base Balance:
Buffer Systems:
Fastest response; acts chemically to change strong acids to weak acids or bind acids to neutralize.
Major extracellular fluid (ECF) buffer: Bicarbonate (HCO3-) – Carbonic acid (H2CO3).
Less significant buffers in ECF: Inorganic phosphates and plasma proteins.
Respiratory System:
Lungs excrete CO2 and H2O, by-products of cellular metabolism.
CO2 + H2O → H2CO3; dissociates into H+ and HCO3-.
Free H+ buffered by hemoglobin.
Renal System:
Maintains acid-base balance by absorbing or excreting acids and bases.
Normal HCO3- level: 22 to 26 mEq/L.
Acidosis: Kidneys reabsorb HCO3- and excrete H+
Alkalosis: Kidneys excrete HCO3- and retain H+.
Acid-Base Imbalances
Acid-Base Imbalance Definition:
Occurs when the ratio of acid to base (1:20) changes.
Classified as respiratory or metabolic.
Respiratory Imbalance: Affects carbonic acid concentration.
Metabolic Imbalance: Affects bicarbonate concentration.
Types of Acidosis and Alkalosis:
Acidosis Causes:
Increased carbonic acid (Respiratory acidosis).
Decreased bicarbonate (Metabolic acidosis).
Alkalosis Causes:
Decreased carbonic acid (Respiratory alkalosis).
Increased bicarbonate (Metabolic alkalosis).
Compensatory Mechanisms
To regain balance:
Lungs may compensate for metabolic disorders.
Kidneys may compensate for respiratory disorders.
Partial compensation: pH remains abnormal.
Complete compensation: pH returns to normal.
Compensatory mechanisms won’t overcompensate.
Metabolic Acidosis (Bicarbonate Deficit)
Definition:
A common clinical disturbance characterized by low pH (<7.35) and low plasma bicarbonate concentration (<22 mEq/L).
Causes: Gain of H+ (acid) or loss of bicarbonate (base).
Types of Metabolic Acidosis:
High anion gap acidosis (hyperchloremic acidosis).
Normal anion gap acidosis.
Anion Gap Calculation:
Anion gap = Na+ - (Cl- + HCO3-)
Normal value: 8 to 12 mEq/L.
High Anion Gap Indicators:
Indicates an addition of endogenously or exogenously generated acids.
Normal Anion Gap Indicators:
Indicates a loss of bicarbonate.
Causes of Metabolic Acidosis
Ingestion of acidic substances (e.g., aspirin overdose).
Excess acid production (e.g., ketosis, lactic acidosis).
Inability of kidneys to excrete adequate acid.
Loss of base (e.g., severe diarrhea, gastrointestinal fistulas, shock).
Pathophysiology and Clinical Manifestations of Metabolic Acidosis
Metabolic acidosis occurs from:
Accumulation of acids other than carbonic acid.
Loss of bicarbonate due to processes like diabetic ketoacidosis and diarrhea.
Compensatory Response:
Increased CO2 excretion by the lungs, often manifested as Kussmaul breathing (deep, rapid breathing).
Clinical Manifestations:
Headache, confusion, drowsiness, increased respiratory rate, nausea, vomiting, diarrhea, peripheral vasodilation, decreased cardiac output, decreased blood pressure, cold clammy skin, dysrhythmias, shock, bradycardia, muscular twitching.
Assessment and Management of Metabolic Acidosis
Diagnostic Findings:
ABG measurement shows low bicarbonate (<22 mEq/L) and low pH (<7.35).
May cause hyperkalemia due to potassium shifts from cells.
ECG may reveal dysrhythmias from increased potassium.
Hyperventilation to decrease CO2 as compensatory action.
Medical Management:
Correct underlying metabolic defect.
Eliminate sources of excessive chloride.
Administer bicarbonate if pH < 7.1 and bicarbonate <10 mEq/L.
Monitor closely for hypo- and hyperkalemia.
Metabolic Alkalosis (Base Bicarbonate Excess)
Definition:
Clinical disturbance characterized by high pH (decreased H+ concentration) and high plasma bicarbonate concentration.
Causes: Gain of bicarbonate (base) or loss of H+ (acid).
Common Causes:
Vomiting or gastric suction (loss of H+ and Cl-).
Pyloric stenosis.
Diuretic therapy promoting potassium loss (e.g., thiazides, furosemide).
Pathophysiology:
Metabolic alkalosis occurs with loss of acid (such as prolonged vomiting or gastric suction) or gain of bicarbonate (e.g., ingestion of baking powder).
Compensatory mechanisms: Decreased respiratory rate to increase CO2, renal excretion of bicarbonate.
Clinical Manifestations:
Tingling fingers and toes, dizziness, decreased respiration (compensatory action), atrial tachycardia, decreased motility, paralytic ileus, headache, lethargy, tetany, seizures.
Assessment and Diagnostic Findings:
ABGs show pH > 7.45 and serum bicarbonate concentration > 26 mEq/L.
PaCO2 increases as lungs compensate by retaining CO2.
Hypokalemia may accompany metabolic alkalosis.
Management:
Supply sufficient chloride for kidneys to absorb sodium with chloride (facilitating bicarbonate excretion).
Administer sodium chloride fluids to restore normal volume.
Administer potassium as KCl to replace K+ and Cl- losses.
Respiratory Acidosis (Carbonic Acid Excess)
Definition:
Clinical condition with pH < 7.35 and PaCO2 > 45 mm Hg; can be acute or chronic.
Acute Respiratory Acidosis Causes:
Emergency situations such as acute pulmonary edema, foreign object aspiration, atelectasis, sedative overdose.
Pathophysiology:
Due to inadequate CO2 excretion resulting in elevated plasma CO2 levels and increased carbonic acid levels.
The kidneys conserve bicarbonate and increase urinary excretion of H+; compensation begins within 24 hours.
Clinical Manifestations:
Increased pulse and respiratory rate, increase in blood pressure, mental cloudiness, fullness in the head, cyanosis, tachypnea, ventricular fibrillation.
Assessment and Diagnostic Findings:
ABG shows pH < 7.35, PaCO2 > 45 mm Hg.
Variations in bicarbonate level depend on the duration of acidosis.
Chest X-ray and ECG may be indicated to identify pulmonary disease and cardiac involvement.
Management:
Improve ventilation; measures vary with the cause.
Bronchodilators for bronchial spasm, antibiotics for respiratory infections.
Thrombolytics or anticoagulants for pulmonary emboli.
Semi-Fowler’s position for improved chest wall expansion.
Adequate hydration (2-3 L/day) to keep mucous membranes moist for secretion removal.
Respiratory Alkalosis (Carbonic Acid Deficit)
Definition:
Clinical condition where arterial pH > 7.45 and PaCO2 < 35 mm Hg.
Common Causes:
Extreme anxiety, hypoxemia, salicylate intoxication, inappropriate ventilator settings.
Pathophysiology:
Due to hyperventilation, which causes excessive CO2 expulsion and decreases plasma carbonic acid concentration.
Compensatory mechanism: Renal excretion of bicarbonate.
Clinical Manifestations:
Lightheadedness, inability to concentrate, numbness, tingling, tinnitus, loss of consciousness, tachycardia, dysrhythmias, confusion, hyperventilation.
Assessment and Diagnostic Findings:
ABG confirms respiratory alkalosis with elevated pH, low PaCO2, and normal bicarbonate.
Management:
Correct the underlying cause, such as anxiety; instruct the patient to breathe more slowly.
In cases of severe anxiety, sedatives may be necessary.
ABG Analysis
Overview:
ABG analysis assesses ventilation effectiveness and acid-base balance.
Critical tests: pH, PaCO2, and HCO3-.
Normal Values for Adults:
pH: 7.35 to 7.45
PaCO2: 35 to 45 mm Hg
HCO3-: 22 to 26 mEq/L
Steps in ABG Analysis:
Step 1: List essential values: pH, PaCO2, HCO3-.
Step 2: Check against normal values:
Indicate abnormal results with:
"A" for excessive acid,
"B" for excessive base,
"N" for normal balance.
Step 3:
Circle results:
If pH and PaCO2 are circled, indicates respiratory disorder.
If pH and HCO3- are circled, indicates metabolic disorder.
If all three are circled, indicates combined disturbance.
Step 4: Check for compensation:
If uncircled value is abnormal in the opposite direction, compensation is occurring.
If it remains normal, no compensation.
Notes:
In respiratory disorders, pH and PaCO2 move in opposite directions; HCO3- remains normal.
In metabolic disorders, pH and HCO3- move in the same direction; PaCO2 remains normal.
Remember ROME: Respiratory Opposite, Metabolic Equal.
Case Studies
Case Study 1:
Patient: Mary Marfo, 34, presents with acute shortness of breath and pain.
ABG Results:
pH: 7.50
PaCO2: 29 mm Hg
PaO2: 64 mm Hg
HCO3-: 24 mEq/L
Interpretation:
Respiratory alkalosis without compensation.
Administer O2 therapy, encourage slow breathing; consider pulmonary embolism as probable cause.
Case Study 2:
ABG Results:
pH: 7.20
PaCO2: 35 mm Hg
HCO3-: 14 mEq/L
Interpretation:
Patient in metabolic acidosis due to low pH and low HCO3-.
Conclusion
Understanding and managing acid-base imbalances is essential in clinical practice to maintain homeostasis and ensure patient safety and health.