MS ACID BASE IMBALANCE
WHAT IS ACID BASE BALANCE
Body's ability to keep pH between and 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 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 or above .
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.