From the notes

Question 1

Increased anion gap metabolic acidosis causes:

Answer 1

Increased production of endogenous nonvolatile acids

(Renal failure, Ketoacidosis, Lactic acidosis, Mixed-
hyperosmolar or alcoholic coma, Inborn errors of
metabolism); Ingestion of toxin (salicylate, methanol,
ethylene glycol, paraldehyde, toluene, sulfur);
Rhabdomyolysis

Question 2

Normal anion gap metabolic acidosis:

Answer 2

Increased gastrointestinal losses of [HC03-]: diarrhea, anion exchange resins, ingestion of CcCl or MgCI2,
fistulae - pancreatic, biliary or small bowel; Increased
renal losses of [HC03-] (renal tubular acidosis, carbonic
anhydrase inhibitors, hypoaldosteronism); Dilutional;

Total parenteral nutrition; Increased intake of chloride-
containing acids (lysine, arginine)

Question 3

Anesthetic considerations in patients with acidosis:

Answer 3

• Can potentate the depressant effects of most sedatives.
• Can increase the fraction of the drug in the nonionized form and facilitate
  penetration of the opioid into the brain.
• Increase depression of airway reflexes-may predispose to pulmonary
  aspiration.
• Increase depression (respiratory and cardiac) effects of both volatile and
  intravenous anesthetics.
• The most important complication of acidosis is a greatly increased propensity for arrhythmia.

Question 4

Causes of respiratory alkalosis:

Answer 4

Central Pain; Ischemia; Stroke; Tumor; Infection; Fever; Drugs
stimulation
Peripheral
stimulation

(Salicylates, progesterone, analeptics)
Hypoxemia; High altitude; pulmonary disease (cardiogenic and
noncardiogenic pulmonary edema, asthma, pulmonary emboli);
Severe anemia

Unknown Sepsis; Metabolic encephalopathies
mechanism
Iatrogenic Ventilator-induced

Question 5

Chloride sensitive causes of metabolic alkalosis:

Answer 5

Gastrointestinal vomiting, gastric drainage,
diarrhea); Renal (diuretics, low chloride intake;
Sweating; cystic fibrosis)

Question 6

Chloride resistant causes of metabolic alkalosis:

Answer 6

Increased mineralocorticoid activity (primary and secondary
hyperaldosteronism, Cushing’s syndrome); Severe hypokalemia.

Question 7

Explain the difference between chloride resistant and chloride sensitive causes of metabolic acidosis:

Answer 7

In the first case we have losses of Cl as in vomiting because of loss of acid HCl.
HCO3-is relatively increased. NaCl 0,9 % brings Cl and is an adequate therapy. In the second case Na is avidly reabsorbed by the kidneys and H+ are exchanged and excreted. That is why it is not chloride sensitive.

Question 8

Anesthetic considerations in a patient with alkalemia:

Answer 8

• Respiratory alkalosis appears to prolong opioid-induced depression
• Cerebral ischemia from reduction in cerebral blood flow during
  respiratory alkalosis (cerebral hypotension)
• Severe ventricular dysrhythmia from combination of alkalemia and hypokalemia
• Potentiation of nondepolarizing neuromuscular blockade

Question 9

Defibrillation maximum:

Answer 9

360J monophasic
150J biphasic

Question 10

Dosages in CPR:

Answer 10

• Epinephrine 1 mg every 4 min
• Atropine 1mg up to 2 mg
  Amiodarone in case of ventricular tachycardia/fibrillation 2x150 mg
• Lidocain 100 mg bolus iv up to 300 mg
• Sodium Bicarbonate only if severe acidosis pH<7,20 other ways might produce intracellular acidosis

Question 11

Spinal anesthetic used in labor:

Answer 11

10 mcg sufentanyl / fentanyl 25mcg w/ bupivicaine 1.25-2.5mg

Question 12

Emergency C-section:

Answer 12

Ranitidine 50 mg slow IV (45 min minimum to produce effect)
Metocloprarnide 10 mg IV (improves lower esophageal barrier pressure)

Metocloprarnide 10 mg IV (improves lower esophageal barrier pressure)

0,3 M Sodium citrate 30 ml PO during the 30 min preinduction