and Acid-Base Disturbances

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© Springer Nature Switzerland AG 2021

R. Reti, D. Findlay (eds.)Oral Board Review for Oral and Maxillofacial Surgerydoi.org/10.1007/978-3-030-48880-2_20

20. Electrolyte and Acid-Base Disturbances

Simon Bangiyev1  , Dustin R. Altmann2, Tarek Korban3 and Damian Findlay4
(1)

Yale New Haven Hospital, Oral and Maxillofacial Surgery, New Haven, CT, USA
(2)

Providence Regional Medical Center, Division of Oral and Maxillofacial Surgery, OM3 Oral and Maxillofacial Surgery, Everett, WA, USA
(3)

The Mount Sinai Hospital, Department of Otolaryngology – Head and Neck Surgery, New York, NY, USA
(4)

Oral Facial Surgery Institute, St. Louis, MO, USA
 
Keywords

Blood gas analysisMetabolic acidosisMetabolic alkalosisRespiratory acidosisRespiratory alkalosisHyponatremiaHyperkalemiaHypocalcemiaKussmaul’s breathingAnion gap acidosis

Definition/Pathophysiology

  • 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].

  • Acidosis is defined as arterial blood pH <7.35 and is considered severe when pH <7.20. Severe acidosis produces the following [2]:

    • Hypotension – direct myocardium and smooth muscle depression, reducing cardiac contractility and peripheral vascular resistance.

    • Hypoxia of tissues (despite rightward shift in Hb-O2 dissociation curve).

    • Ventricular fibrillation threshold is decreased.

    • Hyperkalemia – K+ moves extracellularly in exchange for H+ moving intracellularly.

    • CNS depression (confusion, loss of consciousness (LOC), seizures) – more pronounced in respiratory than metabolic acidosis.

  • 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:

    • Hypoxia of tissues – hemoglobin has increased affinity for O2 giving up less O2 to tissues (Hb-O2 dissociation curve shifts to the left).

    • Hypokalemia  – H+ moves extracellularly shifting K+ intracellularly.

    • Hypocalcemia – increased Ca2+ binding to plasma proteins, decreasing serum Ca2+ causing cardiovascular depression and neuromuscular irritability.

Compensatory mechanisms – protection of physiologic pH, which occurs in three phases (Table 20.1):

  • Chemical Buffering [13]

    • Bicarbonate (H2CO3/HCO3) – most important for extracellular fluid (ECF) buffering.

      • H2O + CO2 ←Carbonic anhydrase→ H2CO3 ↔ H+ + HCO3

      • Effective against metabolic, but not respiratory acid-base disorder.

    • Hemoglobin (HbH/Hb) – important buffer in blood.

    • Intracellular proteins (PrH/Pr) – intracellular buffering.

    • Phosphates (H2PO4/HPO42−) and ammonia (NH3/NH4+) – urinary buffers.

    • Bone buffering:

      • Acidic conditions will demineralize bone causing the release of alkaline compounds (CaCO3 and CaHPO4).

      • Alkaline conditions will increase deposition of carbonate in bone.

  • Respiratory compensation – whenever possible.

    • Ventilatory changes are mediated by chemoreceptors in the brainstem.

      • Minute ventilation increases with acidosis → “blowing off” CO2 to increase pH.

      • Minute ventilation decreases with alkalosis → retain CO2 to decrease pH.

  • Renal compensation – slower but more effective.

    • Kidneys regulate bicarbonate (HCO3) reabsorption/excretion, form new HCO3, eliminate titratable acids and ammonium ions.

Table 20.1

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

  • 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.

  • Arterial Blood Gas (ABG):

    • Most commonly utilized “gold standard.”

    • Invasive – risk of nerve injury or hematoma.

  • Venous Blood Gas [1] :

    • PO2 represents tissue extraction, not pulmonary function.

    • PCO2 usually 4–6 mm Hg higher than PaCO2, except in case of severe shock, or PaCO2 >45 mm Hg.

    • pH is usually 0.03–0.04 lower than arterial pH.

    • Bicarbonates, lactates, and base excess are similar to ABG.

Blood Gas Interpretation

  • Correlate changes in pH with changes in CO2 or HCO3 (Tables 20.1 and 20.2)

    • Respiratory disorder → pH and CO2 change in the opposite direction.

      • Each 10 mm 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 6 mEq change in HCO3 also changes arterial pH by 0.1 in the same direction.

    • If the pH change is greater or less than predicted, a mixed acid-base disorder is present.

    • In metabolic acidosis, calculate the plasma anion gap. In metabolic alkalosis, measure urinary chloride.

Table 20.2

Acid-base disorders’ diagnosis

pH

→ Increased

PaCO2

→ Increased

Metabolic alkalosis

→ Decreased

Respiratory alkalosis

→ Decreased

PaCO2

→ Increased

Respiratory acidosis

→ Decreased

Metabolic acidosis

Metabolic Acidosis

  • Defined as a primary decrease in bicarbonate [HCO3]. It is further categorized as anion gap or non-ion gap acidosis.

  • 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.

    • Increased anion gap is the result of:

      • Either increased unmeasured cations such as K+, Ca2+, Mg2+

      • Or decreased unmeasured anions such as plasma proteins (albumin), lactic acids, keto acids, phosphates, sulfates.

  • Causes:

    • Anion gap “MUDPILERS” mnemonic – caused by either the ingestion of toxins or increased production of endogenous nonvolatile acids.

      • Methanol ingestion

      • Uremia – renal failure causes the inability to excrete non-volatile acids

      • Diabetic ketoacidosis, starvation keto-acidosis

      • Paraldehyde, paracetamol/acetaminophen ingestion

      • Iron, isoniazid ingestion

      • Lactic acidosis

      • Ethanol, ethylene glycol ingestion

      • Rhabdomyolysis

      • Salicylate/aspirin ingestion

    • Non-ion gap (hyperchloremic) – primarily either GI or renal wasting of bicarbonate.

      • GI losses of HCO3 – diarrhea, intestinal/pancreatic fistulas, and ileal obstruction.

      • Renal losses of HCO3 – renal tubular acidosis, hypoaldosteronism.

      • Dilutional – rapid and large volume bicarbonate-free fluid (0.9% NaCl).

  • Respiratory compensation – Kussmaul’s breathing : hyperventilation in response to acidemia.

    • Decreased blood pH stimulates respiratory centers to increase minute ventilation, which in turn lowers PaCO2 by “blowing off” CO2, shifting pH toward normal.

  • Treatment – correction of underlying cause:

    • ESRD – hemodialysis.

    • Lactic acidosis – supplemental O2, fluid resuscitation, circulatory support.

    • DKA  – IV fluids, insulin.

    • Hemorrhage – RBC transfusion: Hb buffers both CO2 (carbonic acid) and nonvolatile acids.

    • Sodium bicarbonate (NaHCO3) – effective in non-gap metabolic acidosis because problem is bicarbonate loss. It is not effective in anion gap acidosis.

Metabolic Alkalosis

Jul 23, 2021 | Posted by in Oral and Maxillofacial Surgery | Comments Off on and Acid-Base Disturbances
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