MS ACID BASE IMBALANCE

WHAT IS ACID BASE BALANCE
  • Body's ability to keep pH between 7.357.35 and 7.457.45 by producing and eliminating H+.

  • Essential for cell function, oxygen delivery, and enzyme activity.

Definitions
  • Acids: Unbind H+, increasing H+ in water solution.

  • Bases: Bind with H+, lowering H+ in water solution.

  • Buffers: Can react as either an acid or a base.

ACID BASE REGULATORY ACTIONS AND MECHANISMS
  • H+ is constantly produced from normal metabolism:

    • Carbs → CO2

    • Proteins Sulfuric acids

    • Lipids → Fatty acids → Ketoacids

  • Bases (HCO3) produced mainly in pancreas, kidney, and RBCs; HCO3 can be reabsorbed by kidneys.

  • Diseased states (shock, sepsis, hypoxia, burns) can lead to excess acid production.

  • Breathing regulates CO2:

    • Excess exhalation (hyperventilation) →lose CO2 → alkalotic.

    • Insufficient exhalation (hypoventilation) → retain CO2 → acidic.

CHEMICAL ACID-BASE CONTROL ACTIONS
  • Homeostasis requires consistent H+ production and balanced CO2 loss.

  • Buffers = 1st line of defense:

    • Neutralize excess H+ to prevent dangerous pH shifts.

    • Act immediately before lungs and kidneys respond.

    • Common buffer systems:

      • Phosphate buffer system (mainly in kidneys).

      • Proteins (albumin, globulins, hemoglobin) → act like sponges, donating H+ as needed.

ACID-BASE CONTROL ACTIONS AND MECHANISMS: RESPIRATORY
  • Respiratory system = 2nd line of defense (activated when buffers are overwhelmed).

    • Lungs respond quickly (within minutes) to pH changes by regulating CO2.

  • Hyperventilation:

    • Blows off CO2 → decreased CO2 = decreased H+ → pH elevation (alkaline).

    • Causes: Anxiety, fever, pain, early sepsis, high altitude.

  • Hypoventilation:

    • Retains CO2 → increased CO2 = increased H+ →pH decrease (acidic).

    • Causes: Respiratory depression, drug overdose, COPD.

ACID-BASE CONTROL ACTIONS AND MECHANISMS: KIDNEYS
  • Renal system = 3rd line of defense (when respiratory system is insufficient).

    • Slower to respond (takes 244824-48 hours) but stronger and longer-lasting.

    • Too acidic blood: Kidneys reabsorb bicarb.

    • Too alkaline blood: Kidneys excrete bicarb.

    • Kidneys remove acids by forming phosphoric acid (phosphate + H+) and ammonium (ammonia + H+), excreted in urine.

    • Most diseased states → retain more H+.

COMPENSATION
  • Body's attempt to normalize abnormal pH.

  • Life-threatening pH: below 6.96.9 or above 7.87.8.

  • Respiratory Compensation:

    • Fast response: seconds to minutes.

    • Fixes metabolic problems by adjusting CO2 exhalation (faster/deeper breathing = more CO2 removal).

  • Kidney Compensation:

    • Slower: hours to days.

    • Fixes respiratory problems by eliminating H+ or producing more HCO3.

  • Metabolic problem → Respiratory compensation.

  • Respiratory problem → Kidney (Metabolic) compensation.

ACID-BASE IMBALANCES
  • Occur when pH is too acidic or alkalotic due to overwhelmed regulatory mechanisms.

  • Not diseases themselves, but conditions that impair organ function and can be life-threatening.

  • Treatment focuses on correcting the root cause.

ACIDOSIS - pH <7.35
  • Actual Acidosis: Too much acid production/improper acid elimination.

    • Examples: DKA, seizures, lung problems, kidney failure.

  • Relative Acidosis: Not enough base, even if acid levels are normal.

    • Examples: Diarrhea, pancreatitis, dehydration.

  • Dangers:

    • Excess H+ affects other salts (e.g., K+).

    • Small pH changes can shut down enzymes/hormones and affect nerves/muscles.

    • Cardiac dysrhythmias are common.

METABOLIC ACIDOSIS
  • H+ ions:

    • Overproduction: Excess fatty acid breakdown (DKA, starvation), anaerobic glucose metabolism (seizures), excessive toxin intake (ETOH, aspirin).

    • Under-elimination: Acid made normally, but body can't remove it (lung problems → can't exhale CO2, kidney failure → can't remove H+).

  • HCO3 ions:

    • Underproduction: Kidneys, pancreas, or liver dysfunction (kidney failure, pancreatic/liver disease).

    • Over-elimination: Lost from body (e.g., diarrhea).

RESPIRATORY ACIDOSIS
  • Cause: CO2 retention due to ineffective breathing → increased free H+ → acidic blood.

  • Causes of CO2 retention:

    • Slow/shallow breathing (head injury, opioids).

    • Inadequate chest expansion (rib fractures).

    • Airway obstruction (asthma, mucous plug).

    • Reduced alveolar capillary diffusion (pneumonia).

ACIDOSIS ASSESSMENT
  • Neurological Signs: Cognitive changes (awareness, time, place, person) due to retained H+.

  • Cardiovascular Signs: Hypotension, tachycardia, dysrhythmias (reduced O2 carrying capacity due to vasodilation).

  • Respiratory Signs: Kussmaul respirations (deep, rapid breathing in metabolic acidosis), shallow/slow breathing (respiratory acidosis), cyanosis (severe hypotension).

  • Integumentary: Warm, flushed skin (respiratory acidosis); cool, clammy skin (metabolic acidosis from shock).

ACIDOSIS - DIAGNOSTIC ABG’S
  • ABGs measure lung/kidney efficacy in acid-base and O2 balance.

  • Metabolic Acidosis:

    • pH <7.35

    • PaO2 normal

    • PaCO2 normal or slightly decreased

    • HCO3 low (<22 mEq/L)

    • Serum potassium high (H+ kicks K+ out of cells)

  • Respiratory Acidosis:

    • pH <7.35

    • PaO2 low

    • PaCO2 high

    • HCO3 variable

    • Serum potassium may be high

ACIDOSIS - CARE
  • Metabolic Acidosis:

    • Goal: Treat underlying problem.

    • DKA → insulin.

    • Diarrhea → rehydration, antidiarrheals.

    • Restore fluid balance and monitor electrolytes.

  • Respiratory Acidosis:

    • Goal: Improve gas exchange.

    • Drug therapy (bronchodilators, steroids, reversal agents).

    • O2 therapy.

    • Ventilatory support if needed.

    • Prevent worsening respiratory failure (caution with COPD pts).

ALKALOSIS - pH >7.45
  • Actual Alkalosis: Body makes too much base (bicarb) or can't get rid of it.

    • Example: Antacid overuse.

  • Relative Alkalosis: Amount of acids decreases, even if bases don't increase.

    • Examples: Prolonged vomiting, diuretic overuse.

  • Dangers:

    • K+ shifts into cells → hypokalemia.

    • Can lead to hypoventilation and hypoxia.

  • Acidosis is generally more life-threatening, but alkalosis is also dangerous.

METABOLIC ALKALOSIS (less common than metabolic acidosis)
  • Caused by either increase of bases (base excess) or decrease of acids (acid deficit).

  • Base excess: Excessive intake alkaline substances.

    • Bicarbs, acetates, citrates (e.g., from preserved blood).

  • Acid deficit: Loss of acids from disease or treatments.

    • NG suctioning, loop/thiazide diuretics (loss of H+ ions), excess vomiting, Cushings/Hyperaldosteronism (bicarb retention, H+ loss).

RESPIRATORY ALKALOSIS
  • Cause: Excessive loss of CO2 through hyperventilation.

  • Causes of hyperventilation:

    • Anxiety/panic attacks, fever, pain, sepsis, high altitude.

    • Brain injury affecting respiratory control.

  • Hallmark sign: ABG result with elevated pH and low CO2.

ALKALOSIS ASSESSMENT
  • Neurological Signs: Confusion, dizziness, lightheadedness, possible seizure.

  • Cardiovascular Signs: Possible hypotension, dysrhythmias (due to low K+).

  • Respiratory Signs: Shallow breathing, hypoventilation.

  • Neuromuscular Signs: Muscle twitching/cramping, numbness, tingling (especially around mouth and fingers), Trousseau's/Chvostek's signs (due to hypocalcemia).

ALKALOSIS - DIAGNOSTIC ABG’S
  • Metabolic Alkalosis:

    • pH >7.45

    • PaO2 normal

    • PaCO2 increased or normal

    • HCO3 high (>28)

  • Respiratory Alkalosis:

    • pH >7.45

    • PaO2 low or normal

    • PaCO2 low (<35)

    • HCO3 low or normal

  • Hypocalcemia and hypokalemia often occur with alkalosis.

  • O2 is low when cause is respiratory in nature.

ALKALOSIS - CARE
  • Prevent further losses of H+, K+, Ca2+, Cl-.

  • Stop or adjust causative treatment.

  • Drug therapy:

    • Antiemetics for vomiting.

    • Electrolyte replacement.

    • Fluids.

  • Examples: Stop bicarb antacids, change diuretics.