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Oral case 46

Created: 5/10/2004

Weaning from cardiopulmonary bypass

A 65-year old male had a mitral valve replacement for mitral regurgitation. He is having difficulty separating from bypass due to hypotension.

1. How do you evaluate causes?

2. How do you manage now?

3. Would you give calcium after bypass?

Yes. It has been traditional to give calcium routinely after bypass, to increase myocardial contractility. Since this has been challenged, studies have shown that myocardial performance is not improved after calcium boluses, even though cardiac output and blood pressure may improve. Calcium given in this setting may blunt effects of beta agonists, and cause intracellular myocardial calcium overload, and resultant tissue injury, necrosis, and pancreatic injury as well. Using one gram is given to counteract hyperkalemia from potassium cardioplegia after reperfusion has been established, and before bypass termination, continues to be common practice.

CO2 monitoring

A high expired PCO2 is read on the mass spectrometer.

1. What are the possible causes?

The amount of CO2 in the blood is inversely related to alveolar ventilation. Causes of hypercarbia include hypoventilation, increased CO2 production, and iatragenic causes.

Common causes of hypoventilation include muscle paralysis, inadequate ventilation, volatile anesthetics, and narcotics. CO2 production is increased with malignant hyperthermia, hyperthyroidism and thyroid storm, fever, and hypermetabolic states. Iatragenic causes include the administration of bicarbonate or CO2, and depletion of the CO2 absorbent granules.

2. How would you evaluate this?

3. If the end-tidal PCO2 reads 35 mmHg, can the patient be hypercapneic?

4. What effects can hypoxia and hypercarbia cause?

Hypoxia and hypercarbia can lead to hypertension, tachycardia, myocardial depression, cyanosis, bradycardia, and cardiac arrest.

Management of chronic pain

A patient has had chronic pain in the right arm for six months, after receiving a gunshot wound there.

1. What is your differential diagnosis?

2. How would you evaluate this patient?

3. What treatment would you give?

4. What is the prognosis?

A 65-year old patient on codeine for leg pain secondary to a fall presents with epigastric pain. She has a significant cardiac history, with a myocardial infarction occurring three months ago.

1. Name several drugs that relieve opioid-induced spasm of the sphincter of Oddi.

Naloxone, nitroglycerine, atropine, and glucagon.

2. What drug can you give her that would relieve opioid-induced epigastric pain, but would not relieve angina pectoris?


3. Which drug relieves both types of discomfort, and are therefore not useful in diagnosis?


4. What is the mechanism by which naloxone works?

It competitively antagonizes opioids at the mu receptors.

5. Name the side effects of naloxone.

Reversal of ventilatory depression and analgesia, leading to a surge of catecholamines and resultant tachycardia, hypertension, pulmonary edema, and dysrhythmias. It may also cause nausea and vomiting, and has been used in hypovolemic shock to increase myocardial contractility and survival.

6. What is an agonist-antagonist?

Agonist-antagonists were thought to act as agonists at the kappa receptor, and as antagonists at the mu receptor. They are better understood now to act as partial agonists at multiple receptors, either increasing overall opioid effect when added to a small concentration of pure agonist, or decreasing opioid effect when added to a large concentration of pure agonist.

7. Why use an agonist-antagonist?

To reverse respiratory depression without reversing analgesia markedly, and to avoid cardiac and pulmonary complications.

8. What are the advantages of using an opioid partial agonist?

They are fewer side effects, they have a lower potential for abuse, and there is a ceiling effect for respiratory depression.

9. Do opioids have peripheral effects?

This is an area of controversy, but peripheral opioid analgesia occurs when inflamed tissue is infiltrated with opioids. The inflammation may disrupt the usual barrier around peripheral nerves, allowing access to opioid receptor sites.

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