A 40-year old 100 kg woman is to undergo clipping of an anterior communicating artery aneurysm. She sustained a subarachnoid hemorrhage two days ago, with no altered consciousness, and no cerebral vasospasm. A gastric stapling procedure done two years ago resulted in a 50 kg weight reduction. Blood pressure is 160/100 mmHg, pulse is 100 bpm, respirations are 18, oral temperature is 37.5 degrees centigrade, and hemoglobin is 11 gm/dl.
I. Evaluation of cerebral status
1. What evidence of increased intracranial pressure would you seek?
2. What is the significance of increased intracranial pressure to anesthetic management?
3. What is the importance of vasospasm?
4. What is the significance of her hypertension?
5. Should hypertension be treated in this setting? Why or why not?
II. Problems associated with obesity
1. What is the significance of obesity to anesthetic care?
2. What are potential circulatory effects?
3. What are the effects of obesity on anesthetic requirements?
III. Selection of premedication
1. Should she receive sedatives? Why or why not?
2. Should she receive analgesics? Why or why not?
No. Although this patient may have a headache, she should not be in extreme pain. Opioid therapy could result in respiratory depression, hypercapnia and increased cerebral blood flow, muscular rigidity and inability to ventilate, histamine release and hypotension requiring pressor support, pruritus and agitation, nausea/vomiting and increased intracranial pressure, oversedation with decreased gag reflex, orthostatic depression, delayed gastric emptying, and sphincter of Oddi spasm.
I. Selection and interpretation of date from monitors
1. Deliberate hypotension is planned. Does this influence monitor selection? Explain.
2. Would you use central venous line vs a pulmonary artery catheter? Explain.
3. What is the level at which one should measure systemic artery pressure? Explain.
4. Are air emboli monitors indicated? Why or why not?
II. Choice and management of anesthesia
1. A colleague believes that rapid intravenous induction is mandatory. Do you agree? Explain your rationale.
2. What methods would you use to accomplish this?
3. Compare and contrast ketamine vs thiopental in this circumstance.
Sodium thiopental has an induction dose of about 4 mg/kg, with loss of consciousness within fifteen seconds intravenously. It is 99% metabolized by the liver, with an elimination half-life of 6-12 hours
Ketamine is a phencyclidine derivative, and is actually a racemic mixture of two isomers. It is ten times more lipid-soluble than thiopental, and produces unconsciousness within thirty seconds after 1-2 mg/kg, and lasts 20-30 minutes. It produces sedation, amnesia, and analgesia. It is metabolized by the liver to a weakly active metabolite, norketamine. The elimination half-life is 3 hours, and it depends on hepatic blood flow. It increases heart rate, blood pressure, and cardiac output, relaxes bronchial smooth muscle, increases secretions, can cause hypertension and cardiac dysrhythmias when used with tricyclic antidepressants, and increases intracranial pressure, cerebral metabolism, and in contraindicated in patients with intracranial mass lesions or increased intracranial pressure.
4. Discuss the properties and effects of propofol.
Propofol is a 2,6 diisopropylphenol, and is highly lipophilic, therefore easily crosses the blood-brain barrier. Loss of consciousness occurs within less than one minute, after an induction dose of about 2 mg/kg. It is rapidly cleared by the liver, and patients have less residual cloudiness, and less nausea and emesis. Induction decreases blood pressure by 20-30%.
4. Compare and contrast succinylcholine vs metocurine in this circumstance.
5. Discuss intravenous vs topical lidocaine in this setting.
6. Is enflurane a reasonable choice for maintenance? Explain.
7. What would you use for maintenance? Give your reasons.
III. Management of deliberate hypotension
1. The plan is for profound hypotension at the time of aneurysm clipping, and moderate hypotension at other times. What methods would you use to produce each?
2. How will you determine the safe lower limit for blood pressure?
3. Which organs are at risk?
4. What methods of management would you use to prevent organ damage?
5. How would you manage paCO2 and hemoglobin?
IV. Management of ventilation
1. An airway pressure of 55 cm H2O is required to deliver the calculated tidal volume. What are possible causes?
2. Is this hazardous? Why or why not?
3. Despite the usual tidal volume, blood gas shows a paCO2 of 46 mmHg and a paO2 of 70 mmHg on 50% FIO2. What explains this?
4. What is your management?
5. Should positive end-expiratory pressure be applied? Why or why not?
I. Management of hypertension
1. The patient is intubated and breathing spontaneously on arrival to the recovery room. Blood pressure is 200/100 mmHg. What are likely causes?
2. What are the risks?
3. A colleague suggests chlorpromazine. Do you agree?
4. What is your management?
5. Would you extubate this patient now?
II. Evaluation of postoperative jaundice
1. Six days postoperatively, scleral icterus is noted, and urine contains bile. Could this be due to anesthetic drugs?
2. How do you determine the etiology?