REVIEW
WHY DO WE CARE SO MUCH ABOUT ACID -BASE DISTURBANCES?
(hint-why is pH so important?)
Biological processes require a very narrow pH to function correctly
RESPIRATORY ACIDOSIS
WHAT IS THE PRIMARY PROBLEM?
Increased PaCO
2(typically >45mmHg)
Increased CO
2is caused by decreased alveolar ventilation or
increased CO
2production:
CAUSES OF RESPIRATORY ACIDOSIS
ALVEOLAR
HYPOVENTILATION
CNS Depression
Neuromuscular Disorders
Pleural Effusion or Pneumothorax
Airway Obstruction
Asthma, foreign body,
laryngospasm, COPD, Tumor, OSA
Pneumonia
Aspiration
Pulmonary Edema
Ventilator Malfunction
INCREASED CO
2
PRODUCTION
Shivering
Malignant Hyperthermia
Prolonged Seizure
Thyroid storm
Extensive burns
Respiratory Acidosis Compensation
Compensation varies depending on whether it is ACUTE versus CHRONIC
Resp. Acidosis
ACUTE: Limited compensation available
Hgb can act as a buffer
Exchange of potassium and H
+
ions
Minimal increased renal retention of Bicarb
CHRONIC
Significant renal compensation with Bicarb retention in about 24h, with peak effect in 3-
5 days
***Special consideration for the anesthetist: patients with chronically elevated CO
2
should be ventilated to their “Normal” pCO
2
Respiratory Acidosis Compensation
METABOLIC ACIDOSIS
WHAT IS THE PRIMARY PROCESS CAUSING METABOLIC ACIDOSIS?
Decreased Bicarb (HCO
3
-
) –usually <21mEq/L
Occurs via 3 primary processes
Consumption of bicarb
Excess Wasting
Rapid dilution of plasma via non-barb containing fluid (Like Normal Saline)
CALCULATE THE ANION GAP FIRST!
Anion Gap= Major cations –major anions= 12mEq/L (range 7-14)
Equation:
Electrical Neutrality must exist!
Erroneously low AG can occur in the setting of low albumin (as in
chronic liver disease).
For every 1g/dL decrease in albumin AG decreases by 2.5mEq/L
Causes of Metabolic Acidosis
Increased Anion Gap
Increased Production of Acid
Ketoacidosis, renal failure (GFR
<20mL/min), lactic acidosis
(hypoxemia, hypoperfusion or
cyanide poisoning)
Toxins
Salicylate, methanol, ethylene
glycol, etc
Rhabdomyolosis
Normal Anion Gap
GI loss of bicarb:
Diarrhea, biliary/bowel/pancreatic
fistulas, etc
Renal loss of bicarb
Renal tubular acidosis (defect in
secretion of H+), carbonic
anhydrase inhibitor,
hypoaldosteronism
Dilutional
**large volume NaCl administration
TPN
Trick to remember High AG
Metabolic Acidosis
Metabolic Acidosis Compensation
Winter’s Formula:
Anesthesia and Acidosis
Increase the availability of opioids
Increased depressant effects of most sedatives
Increased risk of aspiration if airway reflexes are not intact
Difficult to control hypotension
Increased risk of arrhythmia with Halothane if acidemia is present
Acidosis is often accompanied by hyperkalemia AVOID
succinylcholine
RESPIRATORY
ALKALOSIS
PRIMARY PROCESS THAT CAUSES RESPIRATORY
ALKALOSIS:
Decreased pCO
2–typically via increased
hyperventilation
Causes
Pain, anxiety, ischemia, stroke, infection, fever,
progesterone (pregnancy), asthma, anemia,
ventilator induced
RESPIRATORY ALKALOSIS
COMPENSATION
METABOLIC ALKALOSIS
Primary process is an increase in plasma bicarb
Chloride Sensitive
GI
Vomiting, NGT
Renal
**Diuretics (furosemide, thiazides,
etc)
Post hypercapnic
Cystic Fibrosis
Chloride Resistant
Severe Hypokalemia
Licorice Ingestion
Hyperaldosteronism
Other
Massive Transfusion
Anesthesia and Alkalosis
Prolonged opioid induced respiratory depression
Severe respiratory alkalosis can lead to decreased cerebral blood
flow
Alkalemia often is accompanied by hypokalemia increased risk
of arrhythmias
Possible potentiation of nondepolarizing NMBs