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Oral case 121

Created: 3/2/2005

 

A 70-year old 80 kg male is scheduled for right carotid endarterectoy for unilateral amaurosis fugax. Since inferior myocardial infarction eight months ago, he has had minimal angina, and sleeps on two pillows. He has a twenty-year history of hypertension, and is currently taking digoxin, furosemide, methyldopa, and nitroglycerin as needed. Blood pressure is 180/110 mmHg, heart rate is 75 bpm, respirations are 16, sodium is 145 mEq/l, and potassium is 3.5 mEq/l.

 Preoperative management

I. Hypertension

1. Should this operation be delayed in order to obtain better blood pressure control?

2. What if the blood pressure was 220/120 mmHg?

3. Would there be lower cerebral blood flow if the blood pressure is lowered? Why or why not?

II. Cardiac function

1. What is the significance of a patient's sleeping on two pillows?

2. Does an S3 gallop indicate congestive heart failure?

3. What are some causes of low stroke volume?

Hypovolemia, hypocontractility, and hypervolemia.

4. What are the uses and limitations of drugs that alter vascular tone?

Arterial vasodilators aid a failing myocardium by decreasing forward flow of cardiac output, but do not change inotropy, as do inotropic agents. Arterial vasodilators also affect venous capacitance, decreasing preload, therefore it is important to maintain volume infusion. Preload is altered by drugs that change vascular tone of the capacitance vessels.

5. What are the determinants of myocardial supply and demand?

Supply depends on the oxygen content of arterial blood, and on coronary perfusion, which depends on heart rate, diastolic pressure, and coronary blood flow. Demand is dependent on preload, afterload, inotropy, and heart rate.

3. The chest radiogram reveals a cardiac: thoracic ration of 0.7. What is your interpretation?

4. How do you differentiate left ventricular hypertrophy vs congestive heart failure?

5. Would you delay the operation?

6. If he had a myocardial infarction three months ago, would you delay the operation?

III. Digoxin

1. Would you order a blood level of digoxin?

2. The digoxin level is 3 ng/ml. What is your interpretation?

3. What are the risks of toxicity?

4. What are the risks of toxicity in light of potassium level?

5. What if the heart rate is less than 60 bpm?

6. What if there was no response to atropine?

7. Describe the pharmacology of atropine and muscarinic antagonists.

Atropine, glycopyrrolate, scopolamine, and ipratropium bromide are muscarinic antagonists, which are commonly used. They cause bronchodilation, antisialogogue actions, mydriasis, positive chronotropy, and are antispasmodic. Glycopyrrolate is a quaternary ammonium compound, lacking central nervous system effects, because it does not cross the blood-brain barrier.

 Intraoperative Course

I. Monitoring

1. Is a pulmonary artery catheter indicated?

2. What insertion site would you use?

3. What are the risks of left internal jugular insertion?

4. Is the Trendelenburg position contraindicated?

5. What electrocardiogram leads would you monitor?

6. How would you determine which leads to monitor?

7. How would you monitor the adequacy of cerebral perfusion?

8. Discuss the electroencephalogram vs stump pressure vs cerebral blood flow.

9. How would you monitor ventilation?

10. Where do you want to maintain PCO2? Explain.

11. What are the risks of a shunt?

II. Choice of anesthetic technique

1. Would a cervical plexus block be a good choice? Explain.

2. What nerves would need to be blocked.

3. Would you add sedation?

4. The patient prefers to be asleep. Would you use thiopental for induction and maintenance? Explain.

5. Would you use "brain protection" doses? Explain the evidence for or against doing so.

6. Discuss opioids vs inhaled anesthetics for maintenance.

III. Hypotension

1. The blood pressure goes from 180/110 to 120/80 mmHg after thiopental is given. Is pharmaceutical treatment indicated? Explain.

2. What if the pressure decreased to 90/70 mmHg?

3. What is your drug choice for treatment?

4. During carotid dissection, the heart rate decreases from 70 to 40 bpm, and the blood pressure decreases from 120/80 to 90/70 mmHg. What is the mechanism?

5. What is your treatment?

6. How would you prevent this from happening?

IV. ST depression

1. During emergence in the operating room, 2mm ST segment depression is noted. What is your treatment if the heart rate also rises from 70 to 110 bpm?

2. Discuss nitroglycerin vs beta-blocker vs sedation in this case.

3. What is your treatment if the blood pressure decreases to 90/70 mmHg and the pulmonary artery occlusion pressure is over 16 mmHg?

 Postoperative Care:

I. Postoperative unresponsiveness:

1. The patient is still unresponsive after one hour in the recovery room. What is your differential diagnosis?

2. Would you administer doxapram?

3. Would you administer naloxone?

4. Would you administer physostigmine?

5. Would you administer phenylephrine?

6. What are the receptor affinities for phenylephrine, ephedrine, and other adrenergic agents?

Phenylephrine is a direct-acting adrenergic agonist, acting at the receptor site. It acts on alpha-1 receptors only. Ephedrine is an indirect drug, which enters the presynaptic terminal and results in release of neurotransmitter into the synaptic junction. It acts on alpha-1, alpha-2, beta-1, and beta-2 sites. Epinephrine also works on these same sites, and norepinephrine acts on all but the beta-2 site. Isoproterenol acts on beta-1 and beta-2 sites, and clonidine acts only on alpha-1 sites. Dopamine acts on alpha-1, beta-1, and dopaminergic sites. Dobutamine is relatively beta-1 selective, and has an indirect alpha-1 agonist effect. It has some beta-2 effects as well.

7. What are side effects, which limit each beta-adrenergic agonist?

Epinephrine and isoproterenol are limited by positive chronotropy and arrhythmias. Norepinephrine, high-dose epinephrine and dopamine are limited by vasoconstriction; isoproterenol and dobutamine are limited by vasodilation.

8. How can these side effects be minimized?

Side-effects are minimized by combining with other agents, or by decreasing dosages, with phosphodiesterase inhibitors playing an important role. Common examples include the use of dopamine to maintain renal perfusion, and lidocaine to minimize arrhythmias.

6. Would you get a neurology consult?

7. Would you get an electroencephalogram?

II. Bluish-white hand and no radial pulse

1. This occurs after the nurse removes the radial artery catheter. What is the etiology?

2. Is a diagnostic workup needed?

3. What treatment would you suggest?

4. Compare drug vs surgical vs conservative treatment.

III. Enlarging hematoma at the operative site

1. What are the risks?

2. What is your management until the patient returns to the operating room?


ArticleDate:20050203
SiteSection: Article
 
   
    
                                            
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