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R. Reti, D. Findlay (eds.)Oral Board Review for Oral and Maxillofacial Surgeryhttps://doi.org/10.1007/978-3-030-48880-2_20
20. Electrolyte and Acid-Base Disturbances
Blood gas analysisMetabolic acidosisMetabolic alkalosisRespiratory acidosisRespiratory alkalosisHyponatremiaHyperkalemiaHypocalcemiaKussmaul’s breathingAnion gap acidosis
Definition/Pathophysiology
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Normal arterial blood pH is 7.35–7.45, and maintenance of this physiologic acid-base balance is critical to biochemical reactions in the body. In physiological solutions, an acid is a compound that contains hydrogen and reacts with water to produce hydrogen ions [H+] and a base reacts with water to form hydroxide ions [OH−] [1].
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Acidosis is defined as arterial blood pH <7.35 and is considered severe when pH <7.20. Severe acidosis produces the following [2]:
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Hypotension – direct myocardium and smooth muscle depression, reducing cardiac contractility and peripheral vascular resistance.
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Hypoxia of tissues (despite rightward shift in Hb-O2 dissociation curve).
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Ventricular fibrillation threshold is decreased.
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Hyperkalemia – K+ moves extracellularly in exchange for H+ moving intracellularly.
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CNS depression (confusion, loss of consciousness (LOC), seizures) – more pronounced in respiratory than metabolic acidosis.
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Alkalosis is defined as arterial blood pH >7.45 and is considered severe when pH >7.60. Physiologic effects of alkalosis include [2] the following:
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Hypoxia of tissues – hemoglobin has increased affinity for O2 giving up less O2 to tissues (Hb-O2 dissociation curve shifts to the left).
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Hypokalemia – H+ moves extracellularly shifting K+ intracellularly.
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Hypocalcemia – increased Ca2+ binding to plasma proteins, decreasing serum Ca2+ causing cardiovascular depression and neuromuscular irritability.
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Chemical Buffering [1–3]
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Bicarbonate (H2CO3/HCO3−) – most important for extracellular fluid (ECF) buffering.
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H2O + CO2 ←Carbonic anhydrase→ H2CO3 ↔ H+ + HCO3−
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Effective against metabolic, but not respiratory acid-base disorder.
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Hemoglobin (HbH/Hb−) – important buffer in blood.
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Intracellular proteins (PrH/Pr−) – intracellular buffering.
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Phosphates (H2PO4−/HPO42−) and ammonia (NH3/NH4+) – urinary buffers.
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Bone buffering:
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Acidic conditions will demineralize bone causing the release of alkaline compounds (CaCO3 and CaHPO4).
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Alkaline conditions will increase deposition of carbonate in bone.
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Respiratory compensation – whenever possible.
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Ventilatory changes are mediated by chemoreceptors in the brainstem.
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Minute ventilation increases with acidosis → “blowing off” CO2 to increase pH.
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Minute ventilation decreases with alkalosis → retain CO2 to decrease pH.
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Renal compensation – slower but more effective.
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Kidneys regulate bicarbonate (HCO3−) reabsorption/excretion, form new HCO3−, eliminate titratable acids and ammonium ions.
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Acid-base disorders and compensatory responses
|
Disorder |
Primary change |
Compensatory response |
|---|---|---|
|
Respiratory |
||
|
Acidosis |
Increased PaCO2 |
Increased HCO3− |
|
Alkalosis |
Decreased PaCO2 |
Decreased HCO3− |
|
Metabolic |
||
|
Acidosis |
Decreased HCO3− |
Decreased PaCO2 |
|
Alkalosis |
Increased HCO3− |
Increased PaCO2 |
Blood Gas Analysis
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Arterial or venous blood is collected in a heparin-coated syringe, air bubbles eliminated, placed on ice, and analyzed as soon as possible. Serial examinations are necessary.
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Arterial Blood Gas (ABG):
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Most commonly utilized “gold standard.”
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Invasive – risk of nerve injury or hematoma.
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Venous Blood Gas [1] :
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PO2 represents tissue extraction, not pulmonary function.
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PCO2 usually 4–6 mm Hg higher than PaCO2, except in case of severe shock, or PaCO2 >45 mm Hg.
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pH is usually 0.03–0.04 lower than arterial pH.
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Bicarbonates, lactates, and base excess are similar to ABG.
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Blood Gas Interpretation
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Correlate changes in pH with changes in CO2 or HCO3 (Tables 20.1 and 20.2)
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Respiratory disorder → pH and CO2 change in the opposite direction.
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Each 10 mm Hg change in CO2 should change arterial pH by about 0.08 in the opposite direction.
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Metabolic disorder → pH and CO2 change in the same direction.
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Each 6 mEq change in HCO3 also changes arterial pH by 0.1 in the same direction.
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If the pH change is greater or less than predicted, a mixed acid-base disorder is present.
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In metabolic acidosis, calculate the plasma anion gap. In metabolic alkalosis, measure urinary chloride.
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Acid-base disorders’ diagnosis
|
pH |
→ Increased |
PaCO2 |
→ Increased |
Metabolic alkalosis |
|
→ Decreased |
Respiratory alkalosis |
|||
|
→ Decreased |
PaCO2 |
→ Increased |
Respiratory acidosis |
|
|
→ Decreased |
Metabolic acidosis |
Metabolic Acidosis
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Defined as a primary decrease in bicarbonate [HCO3−]. It is further categorized as anion gap or non-ion gap acidosis.
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Anion gap in plasma is defined as the difference between the 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.
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Increased anion gap is the result of:
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Either increased unmeasured cations such as K+, Ca2+, Mg2+
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Or decreased unmeasured anions such as plasma proteins (albumin), lactic acids, keto acids, phosphates, sulfates.
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Causes:
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Anion gap “MUDPILERS” mnemonic – caused by either the ingestion of toxins or increased production of endogenous nonvolatile acids.
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Methanol ingestion
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Uremia – renal failure causes the inability to excrete non-volatile acids
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Diabetic ketoacidosis, starvation keto-acidosis
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Paraldehyde, paracetamol/acetaminophen ingestion
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Iron, isoniazid ingestion
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Lactic acidosis
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Ethanol, ethylene glycol ingestion
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Rhabdomyolysis
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Salicylate/aspirin ingestion
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Non-ion gap (hyperchloremic) – primarily either GI or renal wasting of bicarbonate.
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GI losses of HCO3− – diarrhea, intestinal/pancreatic fistulas, and ileal obstruction.
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Renal losses of HCO3− – renal tubular acidosis, hypoaldosteronism.
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Dilutional – rapid and large volume bicarbonate-free fluid (0.9% NaCl).
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Respiratory compensation – Kussmaul’s breathing : hyperventilation in response to acidemia.
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Decreased blood pH stimulates respiratory centers to increase minute ventilation, which in turn lowers PaCO2 by “blowing off” CO2, shifting pH toward normal.
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Treatment – correction of underlying cause:
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ESRD – hemodialysis.
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Lactic acidosis – supplemental O2, fluid resuscitation, circulatory support.
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DKA – IV fluids, insulin.
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Hemorrhage – RBC transfusion: Hb buffers both CO2 (carbonic acid) and nonvolatile acids.
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Sodium bicarbonate (NaHCO3) – effective in non-gap metabolic acidosis because problem is bicarbonate loss. It is not effective in anion gap acidosis.
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Metabolic Alkalosis
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Defined as a primary increase in bicarbonate [HCO3−]. Metabolic alkalosis can be subdivided into chloride-sensitive and chloride-resistant metabolic alkalosis.
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Chloride -sensitive alkalosis is associated with extracellular fluid depletion and NaCl deficiency. Sodium (Na+) and volume depletion cause bicarbonate (HCO3−) to be reabsorbed in the kidney because physiologic maintenance of ECF volume is given priority over acid-base balance. Diuretics are the most common cause of chloride-sensitive metabolic alkalosis.
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Chloride-resistant alkalosis is associated with extracellular fluid expansion secondary to mineralocorticoid excess, causing increased aldosterone-mediated Na+ and ECF reabsorption in exchange for H+ secretion.
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