20. Electrolyte and Acid-Base Disturbances Flashcards
Normal arterial blood pH
7.35-7.45
Acidosis
pH
sequelae
Arterial blood pH <7.35 (severe when pH >7.20)
-Hypotension - direct myocardium and smooth muscle depression, reducing contractility and PVR
- Hypoxia of tissues
- Ventricular fibrillation threshold decreased
- Hyperkalemia (K+ moves extracellularly in exchange for H+ moving intracellularly)
- CNS depression (more pronounced in respiratory vs. metabolic acidosis).
Alkalosis
pH
sequelae
Arterial blood pH >7.45 (severe pH>7.60)
- Hypoxia of tissues
- Hypokalemia (H+ moves extracellularly, shifting K+ intracellularlY)
- Hypocalcemia (increased Ca2+ binding to plasma proteins, decreasing serum Ca2+ causing cardiovascular depression and neuromuscular irritability
Respiratory acidosis: primary change and compensatory response
Respiratory acidosis
Primary change: increased PaCO2
Compensatory response: increased HCO3-
Respiratory alkalosis: primary change and compensatory response
Respiratory alkalosis
Primary change: decreased PaCO2
Compensatory response: decreased HCO3-
Metabolic acidosis: primary change and compensatory response
Metabolic acidosis
Primary change: decreased HCO3-
Compensatory response: decreased PaCO2
Metabolic alkalosis: primary change and compensatory response
Metabolic alkalosis
Primary change: increased HCO3-
Compensatory response: increased PaCO2
Compensatory mechanisms for acid/base disorders (3)
- Chemical buffering (bicarbonate for ECF buffering, hemoglobin for blood, intracellular proteins for intracellular buffering, phosphates and ammonia for urine, alkaline compounds released by bone in acidic conditions).
- Respiratory compensation (minute ventilation increases with acidosis to “blow off” CO2 to increase pH and vice versa in alkalosis).
- Renal compensation (slower, but more effective - kidneys regulate bicarbonate reabsorption/excretion, form new HCO3-, eliminate titratable acids and ammonia ions.)
Blood gas analysis (ABG vs. VBG)
Arterial or venous blood collected in heparin-coated syringe, air bubbles eliminated, placed on ice, and analyzed as soon as possible.
- ABG: “gold standard” but more invasive, risk of nerve injury or hematoma
- VBG: PO2 represents tissue extraction, not pulmonary function. PCO2 is usually 4-6mm Hg higher than PaCO2, except in case of severe shock. pH usually 0.03-0.04 lower than arterial pH. Bicarbonates, lactates, and base excess are similar to ABG.
How are blood gases interpreted (respiratory disorder vs. metabolic disorder)
Correlate changes in pH with changes in CO2 or HCO3
- RESPIRATORY DISORDER: pH and CO2 change in opposite direction. Each 10mm Hg change in CO2 should change arterial pH by about 0.08 in the opposite direction.
- METABOLIC DISORDER: pH and CO2 change in the same direction. Each 6mEq change in HCO3 also changes arterial pH by 0.1 in the same direction
pH increased
PaCO2 increased
metabolic alkalosis
pH increased
PaCO2 decreased
respiratory alkalosis
pH decreased
PaCO2 increased
respiratory acidosis
pH decreased
PaCO2 decreased
metabolic acidosis
In metabolic acidosis, calculate ___
Plasma anion gap
What is metabolic acidosis?
A primary decrease in bicarbonate (further classified as anion gap or non-ion gap acidosis)
What is anion gap? What causes it?
Anion gap in plasma is the difference between measured cations (Na+) and measured anions (Cl- and HCO3-).
In actuality, it represents the difference in unmeasured anions and cations. Because electroneutrality must be maintained, a true anion gap cannot exist.
Increased anion gap is the result of: increased unmeasured cations such as K+, Ca2+, Mg2+ or decreased unmeasured anions such as plasma proteins (albumin), lactic acids, keto acids, phosphates, sulfates.
Causes of anion gap metabolic acidosis
Anion gap metabolic acidosis: MUDPILERS
- Methanol ingestion
- Uremia (renal failure)
- Diabetic ketoacidosis
- Paraldehyde, paracetamol/acetaminophen ingestion
- Iron, isoniazid ingestion
- Lactic acidosis
- Ethanol, ethylene glycol ingestion
- Rhabdomyolysis
- Salicylate/aspirin ingestion
Causes of non-ion gap (hyperchloremic) metabolic acidosis
Non-ion gap metabolic acidosis
Primarily either GI or renal wasting of bicarbonate
- GI losses of HCO3- (diarrhea, intestinal/pancreatic fistulas, ileal obstruction)
- Renal losses of HCO3- (renal tubular acidosis, hypoaldosteronism)
- Dilutional (rapid and large volume bicarbonate-free fluid like 0.9% NaCl)
What is Kussmaul’s breathing
Respiratory compensation - hyperventilation in response to acidemia
Treatment of metabolic acidosis
- ESRD (hemodialysis)
- Lactic acidosis (supplemental O2, fluid resuscitation, circulatory support)
- DKA (IV fluids, insulin)
- Hemorrhage (RBC transfusion, Hb buffers both CO2 [carbonic acid] and non-volatile acids)
- Sodium bicarbonate (NaHCO3) effective in non-gap metabolic acidosis because the problem is bicarbonate loss. Not effective in anion-gap acidosis.
This treatment is effective in non-gap metabolic acidosis but not in anion gap acidosis
Sodium bicarbonate (NaHCO3)
What is metabolic alkalosis?
How can it be subdivided?
A primary increase in bicarbonate (can be subdivided into chloride sensitive and chloride resistant metabolic acidosis)
What is chloride-sensitive metabolic alkalosis?
Associated with extracellular fluid depletion and NaCl deficiency.
- Sodium and volume depletion cause bicarbonate to be reabsorbed in the kidney because physiologic maintenance of ECF volume is given priority over acid-base balance.
- Diuretics most common cause of chloride-sensitive metabolic acidosis.
What is chloride-resistant metabolic alkalosis?
Associated with extracellular fluid expansion secondary to mineralocorticoid excess, causing increased aldosterone-mediated Na+ and ECF reabsorption in exchange for H+ secretion.
Causes of chloride-sensitive alkalosis
ECF depletion and NaCl deficiency
- GI: vomiting, gastric drainage (continuous NG suction)
- Renal: diuretics, post-hypercapnic, low chloride intake
- Sweat: cystic fibrosis
Causes of chloride-resistant alkalosis
ECF expansion and enhanced mineralocorticoid activity
- Hyperaldosteronism, refeeding syndrome
What is respiratory acidosis?
A primary increase in PaCO2 due to increased production or reduced ventilation.
- Hypoventilation
- Increased CO2 production (MH, thyroid storm, sepsis, prolonged seizure activity, burn injury)
What is respiratory alkalosis?
A primary decrease in PaCO2 due to hyperventilation
- Central stimulation such as pain, anxiety, ischemia, stroke, tumor, infection, fever, drug induced
- Peripheral stimulation such as hypoxemia, altitude, asthma, pulmonary edema, CHF, PE, severe anemia
Normal blood sodium range
135-145 mEq/L
Normal blood potassium range
3.5-5.5 mEq/L
