Acid-Base Balance, Buffering, and Urinalysis: Comprehensive Study Notes

pH basics and the bicarbonate buffer context

• pH is a logarithmic scale that measures hydrogen ion concentration; more H+ means lower pH, less H+ means higher pH. Normal blood pH is tightly regulated in a narrow range: 7.35 \le pH \le 7.45.
• Examples along the scale: extremes are caustic/toxic (battery acid, strong acids) at the low end; neutral around 7.0; basic/alkaline at the high end (less H+). Common substances with different pH ranges include:
  • Very acidic: battery acid, stomach acid, citric-rich foods like lemons.
  • Near-neutral: milk, water (distilled).
  • Mildly basic: egg whites, some antacids (Tums).
• Safety misconception: extremes on either end can be dangerous; neutral/near-neutral is safest for regular contact.
• pH relevance to physiology: small deviations in blood pH affect cellular functions; buffering systems exist to keep pH within the narrow range required for enzyme activity and metabolism.

The major buffering and compensation systems in the blood

• Buffer systems maintain pH by buffering hydrogen ions and minimizing fluctuations.
  • Carbonic acid–bicarbonate buffer system buffers the plasma:
    \mathrm{CO2} + \mathrm{H2O} \rightleftharpoons \mathrm{H2CO3} \rightleftharpoons \mathrm{H^+} + \mathrm{HCO_3^-}.
  • Respiratory compensation (lungs): adjust CO₂ elimination by changing respiratory rate to decrease or increase carbonic acid formation.
  • Renal (kidney) compensation: kidneys excrete or conserve hydrogen ions and reabsorb or generate bicarbonate (HCO₃⁻).
• Normal blood buffering range and fluctuations are shown on a teeter-totter diagram: alkalosis pushes the balance one way, acidosis the other; the system tries to keep the pH within 7.35–7.45.
• Page detail note: in guided notes there is a blank labeled CO₂ to fill; CO₂ is central to acid–base balance and buffering.

Key concepts to identify acid–base disturbances

• Alkalosis vs Acidosis:
  • Alkalosis: elevated pH, reduced hydrogen ion concentration.
  • Acidosis: reduced pH, increased hydrogen ion concentration.
• Respiratory vs Metabolic (renal) basis:
  • Respiratory disturbances involve PaCO₂ (partial pressure of carbon dioxide).
  • Metabolic disturbances involve HCO₃⁻ (bicarbonate) in plasma.
• Compensations:
  • Respiratory compensation for metabolic disorders (lungs adjust CO₂).
  • Renal compensation for respiratory disorders (kidneys adjust HCO₃⁻ and H⁺).
• Common rule summaries:
  • Respiratory opposite, metabolic equal (rough mnemonic): when the primary problem is metabolic, the compensatory change is in respiratory parameters in the opposite direction; when the problem is respiratory, the compensatory change (renal) aims to restore balance in the same direction.
• Important clinical measure: PaCO₂ and HCO₃⁻ values, along with pH, determine the disturbance and compensation stage.

Respiratory acidosis

• Definition: elevated PaCO₂ with a decrease in pH due to impaired ventilation.
  • Mechanism: ↑ CO₂ leads to more carbonic acid, increasing H⁺ and lowering pH.
  • Primary equation impact: \mathrm{CO2} + \mathrm{H2O} \rightleftharpoons \mathrm{H2CO3} \rightleftharpoons \mathrm{H^+} + \mathrm{HCO_3^-}.
• Common causes:
  • Hypoventilation or respiratory depression (e.g., postoperative respiratory depression from opioids/anesthetics).
  • Airway obstruction; COPD, bronchitis, pneumonia; pneumothorax/atelectasis; sleep apnea.
  • CNS depression (head trauma, central nervous system depressants like sedatives, benzodiazepines, opioids; alcohol).
  • Excessive depressants on respiration (opioids, benzodiazepines) and ARDS with impaired gas exchange.
• Typical clinical presentation and changes:
  • Neurologic: lethargy, confusion, dizziness, headache; can progress to coma.
  • Cardiovascular: hypotension; dysrhythmias related to hyperkalemia (H⁺ shifts into cells, K⁺ shifts out).
  • Respiratory: primary problem is hypoventilation; compensation involves the respiratory system attempting to exhale more CO₂ if possible, but underlying lung disease may blunt this.
  • Skin: warm, flushed appearance due to peripheral vasodilation.
  • Muscular: seizures possible due to severe acidemia; weakness from hyperkalemia.
• ABG pattern:
  • pH decreased (acidic);
  • PaCO₂ increased;
  • HCO₃⁻ may be normal or increased if renal compensation has begun (chronic cases).
• Medical management:
  • Treat the underlying cause (e.g., reverse drug overdose, manage COPD/exacerbation, improve oxygenation, relieve obstruction).
  • Airway protection and supportive ventilation as needed.
  • Oxygen administration if hypoxemic.
  • Encourage airway clearance: turn, cough, deep breathe; hydration to thin secretions; bronchodilators if airway obstruction present.
  • Avoid sedation and opioids that depress respiration further.
  • Noninvasive ventilation (BiPAP/CPAP) can be used to improve ventilation; suction the airway as needed.
  • Endotracheal intubation and mechanical ventilation if CO₂ rises above about 50 mmHg with signs of acute respiratory distress or if the patient tires out and cannot maintain ventilation.
  • In COPD patients, avoid aggressive lowering of CO₂ that could remove their baseline compensatory mechanism; tailor to underlying comorbidities.
• Practical notes:
  • CO₂ management is time-sensitive; collaboration with respiratory therapists is crucial.
  • The rate of correction matters; overcorrecting CO₂ in chronic CO₂ retainers can cause harm.

Respiratory alkalosis

• Definition: decreased PaCO₂ with an increased pH due to excessive ventilation.
  • Mechanism: hyperventilation reduces carbonic acid formation, leading to fewer H⁺ and higher pH.
• Common causes:
  • Hyperventilation from anxiety, pain, fever, agitation, severe dehydration, pregnancy, sepsis; mechanical ventilation with too-rapid settings.
  • Hypoxemia stimulating respiratory drive can also cause hyperventilation.
• Typical clinical presentation and changes:
  • Neurologic: dizziness, lightheadedness, confusion, headaches; possible syncope.
  • Cardiovascular: hypotension; tachycardia; dysrhythmias; chest discomfort.
  • GI: nausea, vomiting.
  • Neuromuscular: tetany, numbness/tingling (paresthesias), hyporeflexia, seizures in severe cases.
  • Respiratory: compensation by hypoventilation to retain CO₂; the lungs reduce ventilation to raise CO₂ levels.
• ABG pattern:
  • pH increased (alkalotic);
  • PaCO₂ decreased;
  • HCO₃⁻ may decrease slightly if metabolic compensation occurs; overall, compensation is typically limited and slow.
• Medical management:
  • Identify and fix underlying cause (reduce anxiety, manage fever/pain, treat hypoxemia).
  • Calming interventions and breathing retraining; consider anxiolytics only if appropriate.
  • Paper bag technique has been used to re-inhale CO₂ (controversial and must be prescribed; risks include delay of treating hypoxemia).
  • If on mechanical ventilation, adjust settings to avoid excessive CO₂ removal.
  • In persistent metabolic compensation or if necessary, adjust ventilator to avoid overventilation.

Metabolic acidosis

• Definition: a decrease in bicarbonate (HCO₃⁻) or accumulation of acids with a concomitant drop in pH; base deficit with a high hydrogen ion concentration.
  • Key phrase: metabolic disturbances are characterized by a decrease in HCO₃⁻ and a low pH; the pH and bicarbonate move in the same direction (metabolic disturbances align vs respiratory disturbances that oppose).
• Common causes:
  • Diabetic ketoacidosis (DKA): insulin deficiency -> increased fat metabolism -> ketone production -> accumulation of acids and loss of bicarbonate.
  • Renal failure: inability to excrete acids and retain bicarbonate; increased waste products.
  • Severe diarrhea: loss of bicarbonate-rich fluids from gut.
  • Lactic acidosis: inadequate oxygen delivery/metabolism leading to lactate accumulation.
  • Ingestion/toxins: aspirin overdose, toxins, antifreeze (ethylene glycol).
  • Ketosis from high-fat diets or alcohol (alcoholic ketoacidosis).
• Special concept: anion gap metabolic acidosis
  • Anion gap (AG) helps classify acidosis and points to underlying causes:
    \text{Anion Gap} = (\mathrm{Na^+} + \mathrm{K^+}) - (\mathrm{Cl^-} + \mathrm{HCO_3^-})
  • A high AG suggests accumulation of unmeasured anions (e.g., ketones, lactate, toxins).
• Typical clinical presentation and changes:
  • Neurologic: lethargy, confusion, dizziness, headache, potential coma with severe acidosis.
  • Cardiovascular: hypotension; dysrhythmias related to hyperkalemia from H⁺/K⁺ shifts (as H⁺ enters cells, K⁺ exits).
  • Respiratory: compensatory hyperventilation (Kussmaul respirations) in metabolic acidosis to blow off CO₂ and raise acidity balance;
  • GI: nausea, vomiting, abdominal pain; may have decreased appetite.
  • Muscular: weakness due to electrolyte shifts and hyperkalemia.
• ABG pattern:
  • pH decreased; HCO₃⁻ decreased; PaCO₂ may be low due to respiratory compensation (ventilation increases) or near normal depending on the stage.
  • Anion gap may be elevated (when unmeasured anions accumulate).
• Medical management:
  • Treat underlying cause (insulin for DKA; antibiotics for sepsis; fluids for dehydration; dialysis for renal failure).
  • Diabetes/DKA: aggressive IV fluids, insulin therapy to suppress ketogenesis, monitor potassium (shifts with insulin and corrected acidosis).
  • Renal failure: dialysis to remove acids and waste products; dietary adjustments (lower protein waste products).
  • Severe acidosis may warrant bicarbonate therapy in select cases, but use is cautious and tailored to the cause and stability.
• Additional notes:
  • Volume status and polyuria in DKA can lead to osmotic diuresis and extracellular volume deficits; monitor hydration closely.
  • In lactic acidosis and sepsis, address tissue perfusion and oxygen delivery to reduce lactate production.

Metabolic alkalosis

• Definition: increased bicarbonate (HCO₃⁻) or loss of acid with a relative gain of base, leading to high pH.
• Common causes:
  • Loss of hydrogen ions and chloride via diuresis (e.g., loop or thiazide diuretics).
  • Excessive vomiting or nasogastric suctioning that removes gastric acid (HCl).
  • Hyperaldosteronism increasing renal hydrogen ion loss and sodium reabsorption.
  • Excessive ingestion of sodium bicarbonate or antacids (i.e., iatrogenic bicarbonate load).
  • Massive blood transfusions (citrate metabolized to bicarbonate).
  • Hypokalemia: cause and consequence in alkalosis; potassium shifts can contribute to alkalosis by facilitating hydrogen ion loss from cells.
• Signs and symptoms:
  • Neurologic: lethargy, irritability, confusion, headaches; seizures in severe cases.
  • Cardiovascular: hypotension; dysrhythmias associated with hypokalemia (e.g., U waves, other dysrhythmias); tachycardia.
  • GI: nausea, vomiting, anorexia; persistent GI symptoms due to electrolyte disturbances.
  • Neuromuscular: tetany, tremors, tingling (paresthesias); muscle cramps; seizures possible.
  • Respiratory: compensatory hypoventilation to retain CO₂ and acidify the blood.
• ABG pattern:
  • pH increased; HCO₃⁻ increased; PaCO₂ increased as a respiratory compensation attempt.
• Medical management:
  • Correct the underlying cause (stop diuretics causing volume depletion or adjust dosing; treat vomiting; correct electrolyte disturbances).
  • IV fluids with chloride (e.g., normal saline) to replete chloride and aid in correcting alkalosis.
  • Correct potassium: provide potassium supplementation if hypokalemic.
  • Avoid excessive bicarbonate administration; treat the root cause rather than simply pushing bicarbonate.
  • In some cases, address hyperaldosteronism or other endocrine contributors.

An overview of ABG interpretation and practical management tips

• Disturbance recognition sequence:
  • Step 1: Look at pH to determine if acidemia or alkalemia is present.
  • Step 2: Check PaCO₂ and HCO₃⁻ to identify whether the primary disturbance is respiratory or metabolic.
  • Step 3: Determine if there is compensation by the other system (partial vs full compensation).
• Common clinical anchors mentioned in the notes:
  • Respiratory acidosis: increased PaCO₂; pH down; underlying causes include hypoventilation, airway obstruction, COPD, ARDS, CNS depression. Management focuses on improving ventilation and addressing the cause.
  • Respiratory alkalosis: decreased PaCO₂; pH up; causes include hyperventilation due to anxiety, fever, pain, hypoxemia. Management focuses on calming the patient and addressing the trigger; ventilation settings may need adjustment if on a ventilator.
  • Metabolic acidosis: decreased HCO₃⁻; pH down; common with DKA, renal failure, diarrhea, lactic acidosis; management includes treating the underlying cause and sometimes bicarbonate.
  • Metabolic alkalosis: increased HCO₃⁻; pH up; causes include vomiting, diuretics, antacids, citrate from transfusions; management includes correcting electrolyte disturbances and the underlying cause.
• Clinical notes and tips:
  • “Base stored in the intestines” mnemonic helps remember bicarbonate handling; losses (diarrhea, vomiting) affect acid–base state.
  • Potassium balance is tightly linked to acid–base status; hydrogen ion movement can drive potassium in or out of cells, altering serum K⁺ and relevant dysrhythmias.
  • In metabolic acidosis with an elevated anion gap, evaluate for lactate, ketones, toxins; in non-gap acidosis, consider bicarbonate loss (diarrhea, renal tubular acidosis).
  • For respiratory disturbances, consult a respiratory therapist for ventilator adjustments; CO₂ targets must be individualized, especially in COPD.

Urinalysis: essential clues to renal and systemic conditions

• Urine composition and normal ranges:
  • Color: pale yellow to deep amber; hydration status affects color.
  • Odor: usually odorless or mild.
  • Volume: ~715 to 2000 mL/24 h.
  • pH: range typically 4.5 to 8.0 (wide normal range).
  • Specific gravity: 1.003 \le SG \le 1.032. Osmolarity: 40 \le \text{osmolarity} \le 1350 \text{ mOsm/kg} (varies by method).
  • Urobilinogen: 0.2 \text{ to } 1.0 \text{ mg/100 mL}.
  • Leukocytes: 0–2 HPF (on microscopic exam); Leukocyte esterase on dipstick test indicates presence of leukocytes.
  • Nitrites: positive suggests bacterial infection.
  • Glucose: should be negative; presence indicates elevated plasma glucose (diabetes).
  • Protein: normally trace or negative; significant protein indicates glomerular injury.
  • Ketones: should be negative (suggests altered metabolism or dehydration).
  • Bilirubin: typically negative; positive can indicate liver or biliary disease.
  • Blood: normally negative; positive may indicate infection, stones, trauma, or menstruation contamination.
• Dipstick vs microscopy:
  • Leukocyte esterase: enzyme produced by leukocytes; rapid dipstick indicator of leukocytes.
  • Microscopy assesses actual cells (RBCs, WBCs), casts, crystals, bacteria.
• Stepwise urinalysis approach:
  • Gross appearance: volume, color, clarity; odor.
  • Biochemistry: pH, osmolarity, glucose, protein, ketones, bilirubin, nitrites, leukocyte esterase.
  • Microscopy: spin down sample; evaluate for cells, bacteria, crystals, casts.
• Practical interpretation cues:
  • Color can reflect hydration or vitamin intake (e.g., bright yellow from B vitamins; orange from rifampin or phenazopyridine).
  • Abnormal pH and specific gravity can reflect metabolic state and hydration; persistent abnormalities require clinical correlation.
• Urinalysis case snippet (educational example):
  • 19-year-old male with increased appetite and thirst for six months and polyuria; this presentation raises suspicion for diabetes or metabolic imbalance and will be explored via urinalysis in the lab activity.

Fluid compartments and movement of water and solutes

• Body fluid compartments:
  • Intracellular fluid (ICF): inside cells (cytosol).
  • Extracellular fluid (ECF): outside cells, including plasma (blood) and interstitial fluid (IF).
• Definitions:
  • Cytosol vs cytoplasm: cytosol is the fluid inside cells; cytoplasm includes cytosol plus organelles.
  • Plasma: liquid component of blood (part of the ECF).
  • Interstitial fluid (IF): fluid between cells/tissues (part of the ECF).
• Movement rules (concentration gradients):
  • Solutes move from high concentration to low concentration (down their gradient).
  • Water moves from high water concentration to low water concentration (i.e., toward higher solute concentration).
• Practical implication: movement of solutes and water between ICF and ECF depends on solute gradients, membrane permeability, and osmotic pressures; this underpins fluid balance and edema/volume status.

Quick note on practical lab interpretation and study cues

• Respiratory rate as a mnemonic:
  • Respiratory rate is slow in respiratory acidosis; respiratory rate is fast in respiratory alkalosis.
• The “buffers, compensation, and monitoring” workflow:
  • Identify primary disturbance (respiratory vs metabolic).
  • Check compensatory responses (partial vs complete) and assess the urgency of intervention.
• Practical management priorities in acute settings:
  • Protect airway and ensure adequate oxygenation for respiratory disturbances.
  • Treat underlying cause first (DKA, COPD flare, pneumonia, dehydration, toxins).
  • Monitor ABGs and electrolytes closely; coordinate with respiratory therapy, nephrology, or critical care teams as needed.

Summary of clinical relevance and real-world connections

• Buffer systems and compensation are central to maintaining cellular function; disruptions can rapidly affect neurological, cardiovascular, respiratory, and muscular systems.
• Anion gap metabolic acidosis is a key diagnostic concept, especially in diabetic ketoacidosis and lactic acidosis scenarios encountered in hospital settings.
• Diuretics, vomiting, and excessive bicarbonate or citrate can push patients toward metabolic alkalosis, highlighting the importance of electrolyte balance and careful management.
• Urinalysis provides essential clues to renal and systemic health, including hydration status, glycemic control, kidney function, infection, and liver-related issues.
• Real-world care requires teamwork (nurses, physicians, respiratory therapists, nephrologists) to interpret ABGs, adjust ventilator settings, and treat underlying causes with attention to patient-specific comorbidities (e.g., COPD, ARDS, renal failure).

Quick reference formulas and numeric checkpoints

• Buffer reaction (carbonic buffer):
  \mathrm{CO2} + \mathrm{H2O} \rightleftharpoons \mathrm{H2CO3} \rightleftharpoons \mathrm{H^+} + \mathrm{HCO_3^-}
• Anion gap:
  \text{Anion Gap} = (\mathrm{Na^+} + \mathrm{K^+}) - (\mathrm{Cl^-} + \mathrm{HCO_3^-})
• Normal blood pH range: 7.35 \le pH \le 7.45
• Normal urine pH range: 4.5 \le pH \le 8.0
• Normal urine specific gravity: 1.003 \le SG \le 1.032
• Typical CO₂ management threshold in acute respiratory distress with acidosis: consider escalation when PaCO₂ remains elevated and pH remains acidic; intubation/ventilation considered if CO₂ rises above roughly 50\ \text{mmHg} with signs of respiratory distress (case-by-case depending on COPD baseline and overall status).