ACID-BASE DISORDERS
ACID/BASE BALANCE
Normal body pH is 7.35-7.45
pH greater than 7.6 is considered severe alkalemia
pH lower than 7.2 is considered severe academia
Respiratory disturbances are changes in the [CO2] levels
Metabolic disturbances are changes in the bicarbonate levels
RESPIRATORY ACIDOSIS
Definition: The pH is decreased (below 7.35), PCO2 is increased due to buildup from the lungs and HCO3 is increased due to renal compensation
This is the result of alveolar hypoventilation leading to pulmonary CO2 retention
During primary respiratory acidosis, the kidneys compensate by increase reabsorption of HCO3- and increase secretion of H+
Acute: This occurs with abrupt ventilation failure from depression of the central respiratory
center from cerebral disease or drugs; neuromuscular disease such as myasthenia gravis, ALS, Guillain-Barre, or MS; airway obstruction from asthma or COPD exacerbation.
Chronic: Occurs most commonly to COPD and neuromuscular disorders and severe restrictive
ventilator defects such as interstitial fibrosis.
RESPIRATORY ACIDOSIS
Clinical Presentation
Metabolic encephalopathy with headache and drowsiness
CNS symptoms can progress to coma
Investigations
ABG shows increased in blood PCO2 with normal to mildly changed plasma bicarb levels
Renal compensation in will increase H+ secretion and bicarb production after 3-5 days in respiratory acidosis so plasma bicarb levels will slowly rise.
Serum electrolyte levels should be normal
Treatment
Treat the underlying cause or disorder (ie: treat the COPD exacerbation)
Blood PCO2 >60mmHg likely needs assisted ventilation
RESPIRATORY ALKALOSIS
Definition: Increased blood pH above 7.45 and results from increased elimination of CO2 from the lunges.
In Respiratory alkalosis, eventually the kidneys will compensate by increasing HCO3- excretion.
Etiology is hyperventilation
An increased ventilation rate can be caused by a variety of things including anxiety, salicylate intoxication, hypoxia, primary CNS dysfunction, septicemia, liver insufficiency and pregnancy.
Clinical Presentation
Hyperventilation, obvious rapid breathing
Circumoral paresthesia of the skin, painful burning of hands and feet, light headedness
RESPIRATORY ALKALOSIS
Investigations
ABGs
Decreased PCO2
Blood pH above 7.45
Electrolytes normal
Treatment
Treat the underlying disorder (ie septicemia)
Severe alkalosis (pH>7.6) may require controlled ventilation and CO2 enriched breathing mixtures
METABOLIC ACIDOSIS
Metabolic acidosis results from an elevation in serum concentrations of H+ caused by either the loss of bicarbonate, the inability to generate bicarbonate, or the addition of hydrogen ions to the serum.
Anion gap:
The anion gap gives the level of unmeasured anions. Normal is 8-14 mEq/L, generally its accepted that anything less than 12 is fine. It helps determine the cause of metabolic acidosis and thus contributes to the treatment.
Anion gap=serum sodium-(serum bicarbonate + serum chloride)
METABOLIC ACIDOSIS
Causes resulting in increased anion gap. Think of mnemonic MUDPILES
Lactic acidosis
DKA
Starvation ketosis
Ethylene glycol, methanol or salicylate poisoning
Causes with a normal anion gap
Diarrhea
Pancreatic or biliary drainage
Ureterosigmoidostomy
Other
Renal tubular acidosis
Renal insufficiency
Adrenal insufficiency
METABOLIC ACIDOSIS
Clinical Presentation
Hyperventilation is present early as a compensatory mechanism by the lungs to blos off CO2
Ventricular arrhythmias
Neurologic changes ranges from lethargy to confusion to coma
Investigations
ABGs show a pH <7.35, decrease plasma bicarb and decreased PCO2
Note, the decreased PCO2 is a compensatory mechanism
Calculate the anion gap
METABOLIC ACIDOSIS
Treatment
Identify and treat/remove the primary cause (ie: ethylene glycol poisoning)
DKA will require insulin and IV fluids for volume repletion
Bicarbonate can be given however, this is a bit controversial as continued and ongoing avid
production will increase bicarb requirements. Blood pH should be very carefully monitored during this time. Bicarb is usually only considered when pH <7.20
Careful of K+. DKA will have lower potassium than originally appears. Many require K+ infusion as well.
METABOLIC ALKALOSIS
Definition: increase in serum bicarbonate levels with no change PCO2, causing an increase in extracellular pH >7.45
This can be caused by a loss of H+, addition of bicarbonate or a disproportionate loss of chloride
Impaired renal excretion of bicarbonate will contribute to metabolic alkalosis
Most common causes
Vomiting, NG tube suctioning, chloride diarrhea, diuretics, hypercalcemia, excessive steroids and chloride and potassium depletion
Antacids in excess can lead to alkalosis
METABOLIC ALKALOSIS
Clinical Presentation
Neurologic changes including paresthesia, light headedness, confusion, stupor and coma
Symptoms from volume depletion including weakness, muscle cramps, dizziness
If hypokalemia is present is will lead to polyuria, polydipsia and muscle weakness
Investigations
ABGs show pH> 7.45, increased serum bicarb and increase PCO2 (the lungs compensating)
Urine chloride can help differentiate between hypovolemic hypochloremic causes with chloride
<20mEq/L and volume expanded patients with mineralocorticoid excess with urine chloride > 30 mEq/L
METABOLIC ALKALOSIS
Treatment
Treat the underlying cause (ie gastric loss/volume depletion)
Increase the renal excretion of bicarbonate
Chloride responsive conditions(ie gastric loss and diuretics) are treated with sodium chloride solutions
Chloride resistant conditions (ie mineralcorticoid excess) are treated by removing an adrenal adenoma if present or with spironolactone (an aldosterone antagonist)
