Lecture 6: Acid Base Homeostasis Imbalance

ACID–BASE HOMEOSTASIS:

• Refers to the body’s ability to maintain a stable pH in bodily fluids, especially blood

• pH scale:
  ○ Range: 0–14
  ○ 7 = neutral
  ○ <7 = acidic
  ○ >7 = alkaline

• Metabolic processes continuously produce acids

• Balance between acids and bases is required to maintain homeostasis

BODY ACIDS: VOLATILE AND NON-VOLATILE:

Volatile acids

• Eliminated by lungs

• Carbonic acid (H₂CO₃)
  ○ Weak acid
  ○ Breaks down into H₂O and CO₂
  ○ CO₂ eliminated through ventilation

Non-volatile acids

• Not eliminated by lungs

• Examples:
  ○ Hydrochloric acid (HCl)
  ○ Sulfuric acid
  ○ Phosphoric acid

• Secreted into urine and eliminated by kidneys

MEASUREMENT OF ACID–BASE BALANCE: BLOOD pH:

• Reflects hydrogen ion (H⁺) concentration

• More H⁺ → lower pH → acidic

• Less H⁺ → higher pH → alkaline

• Body balances:
  ○ CO₂ = acid → lowers pH
  ○ HCO₃⁻ = base → raises pH

REGULATION OF pH (COMPENSATION):

Chemical buffers

• Immediate response

• Act within seconds

Respiratory system

• Eliminates CO₂ (acid)

• CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻

• Exhaling CO₂ raises pH

• Hypoventilation → CO₂ retention → ↓ pH

Renal system

• Slower response (hours to days)

• Ultimate regulator

• Eliminates:
  ○ H⁺ (acid) in urine
  ○ Reabsorbs or excretes HCO₃⁻

BUFFERS:

• Stabilize pH by absorbing or releasing H⁺

• Present in both ICF and ECF

Chemical buffers

• Immediate but temporary

• Include:
  ○ Carbonic acid–bicarbonate system
  ○ Hemoglobin/oxyhemoglobin
  ○ Phosphate buffer
  ○ Protein buffer
  ○ K⁺/H⁺ exchange

Physiological buffers

• Lungs and kidneys

• Required for long-term balance

RESPIRATORY SYSTEM AND ACID–BASE BALANCE:

• Controls CO₂ levels in blood

• Respiratory center in medulla regulates breathing

• Responds within minutes to hours

• Increased ventilation:
  ○ Removes CO₂
  ○ Raises pH

• Decreased ventilation:
  ○ Retains CO₂
  ○ Lowers pH

RENAL SYSTEM AND ACID–BASE BALANCE:

• Regulates acids and bases

• Functions:
  ○ Excrete H⁺
  ○ Reabsorb or excrete HCO₃⁻

• Reabsorption of HCO₃⁻:
  ○ Neutralizes acid
  ○ Raises pH

• Excretion of HCO₃⁻:
  ○ Lowers pH

• Responds in hours to days

CLASSIFICATION OF ACID–BASE IMBALANCES:

• Metabolic:
  ○ HCO₃⁻ problem
  ○ Kidney or metabolic origin

• Respiratory:
  ○ CO₂ problem
  ○ Lung origin

• Acidosis:
  ○ Low pH
  ○ Excess acid

• Alkalosis:
  ○ High pH
  ○ Excess base

ARTERIAL BLOOD GASES (ABGs):

• Assess:
  ○ Acid–base status
  ○ Cause of imbalance
  ○ Compensatory response
  ○ Oxygenation

Normal values

• pH: 7.35–7.45

• PaCO₂: 35–45 mmHg

• HCO₃⁻: 22–28 mEq/L

• PaO₂: >80 mmHg

ABG INTERPRETATION (STEP-BY-STEP):

1. Evaluate pH
   ○ <7.35 = acidosis
   ○ >7.45 = alkalosis

2. Evaluate PaCO₂

3. Evaluate HCO₃⁻

4. Identify primary disorder

5. Determine compensation:
   ○ Uncompensated: one value abnormal
   ○ Partially compensated: all three abnormal
   ○ Fully compensated: pH normal

6. Assess oxygenation (PaO₂)

ROME METHOD (ABGs):

• Respiratory = Opposite

• Metabolic = Equal

Examples

• pH ↓ + PaCO₂ ↑ → Respiratory acidosis

• pH ↓ + HCO₃⁻ ↓ → Metabolic acidosis

• pH ↑ + PaCO₂ ↓ → Respiratory alkalosis

• pH ↑ + HCO₃⁻ ↑ → Metabolic alkalosis

RESPIRATORY ACIDOSIS:

Cause

• Carbonic acid excess (↑ CO₂)

Etiology

• Hypoventilation

• Respiratory depression (opioids, stroke)

• Chest trauma

• Airway obstruction

• COPD, pulmonary edema

• Respiratory failure

Compensation

• Kidneys retain HCO₃⁻

• Kidneys excrete H⁺

Clinical manifestations

• Headache

• Confusion

• Lethargy

• Dysrhythmias

• Hyperkalemia

Interventions

• Assess airway and breathing

• High Fowler’s position

• Pulmonary hygiene

• Monitor ABGs, ECG, electrolytes

• Pursed-lip breathing

Treatment

• Bronchodilators

• Antibiotics

• Steroids

• Narcan if opioid-related

RESPIRATORY ALKALOSIS:

Cause

• Carbonic acid deficit (↓ CO₂)

Etiology

• Hyperventilation

• Anxiety

• Pain

• Fever

• Pulmonary embolism

• Hypoxemia

Compensation

• Renal excretion of HCO₃⁻ (limited)

Clinical manifestations

• Lightheadedness

• Confusion

• Tachycardia

• Hypokalemia

• Hypocalcemia

• Paresthesias

• Seizures

Interventions

• Calm environment

• Slow breathing

• Rebreathing CO₂ (paper bag)

• Monitor ABGs, ECG, electrolytes

Treatment

• Sedatives

• Anti-anxiety medications

METABOLIC ACIDOSIS:

Cause

• Increased acid or decreased bicarbonate

Etiology

• Diabetic ketoacidosis

• Lactic acidosis (shock, sepsis)

• Severe diarrhea

• Kidney disease

• Malnutrition

• Aspirin toxicity

Clinical manifestations

• Kussmaul respirations

• Hypotension

• Hyperkalemia

• Cold, clammy skin

• Abdominal pain

• Diarrhea

Interventions

• Monitor I&O

• Assess LOC

• Monitor ABGs, ECG, electrolytes

• Teach diarrhea and DKA warning signs

Treatment

• Treat underlying cause

• Sodium bicarbonate

• Fluid and electrolyte replacement

METABOLIC ALKALOSIS:

Cause

• Loss of acid or gain of bicarbonate

Etiology (LAVA-UP)

• Loop diuretics

• Antacid use

• Vomiting

• Aldosterone excess

Compensation

• Hypoventilation

• Renal excretion of HCO₃⁻

Clinical manifestations

• Dizziness

• Confusion

• Hypokalemia

• Hypocalcemia

• Muscle cramps

• Seizures

Interventions

• Monitor respiratory status

• Monitor LOC and I&O

• Monitor ABGs, ECG, electrolytes

• Teach proper antacid use

Treatment

• Treat cause

• IV fluids (NS or 0.45 NS)

KEY EXAM POINTS:

• CO₂ = acid; HCO₃⁻ = base

• Lungs regulate CO₂ only

• Kidneys regulate H⁺ and HCO₃⁻

• Respiratory imbalances = PaCO₂ problem

• Metabolic imbalances = HCO₃⁻ problem

• Respiratory compensation is fast

• Renal compensation is slow but permanent

• Kussmaul respirations = metabolic acidosis

• Hypoventilation → respiratory acidosis

• Hyperventilation → respiratory alkalosis

• Always identify the underlying cause first

• ABGs determine type and compensation status