Anesthesiology Oral Board Case #35
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“How to say it…”

A 40-year-old, 50 kg female is scheduled for open mitral commissurotomy for mitral stenosis. She had experienced an episode of atrial fibrillation during her last pregnancy 5 years prior to admission, but had otherwise been asymptomatic until the last several months, during which she has developed increasing exertional dyspnea. BP 100/60 mmHg, P 75, R20, T 37 degrees C, Hct 23. She takes no medications prior to this time. Her preoperative ECG was NSR (4 days old).

A. Preoperative Evaluation

1. Assessment of Cardiac disease. Clinical and laboratory assessment. What information from the echocardiogram is most valuable?
   
   Key points: The contractility of the right ventricle would provide an assessment of cardiac impairment sustained by the mitral stenosis. Assessment of right ventricular size and pulmonary blood flow would allow qualitative assessment of pulmonary hypertension. Assessment of the right atrium volume would allow assessment of preload status.
   
   What information from the cardiac catheterization is the most valuable? (Assessment of severity of mitral stenosis)
   
   Key points: The effective mitral valve area allows assessment of the critical nature of the stenosis, although the patient’s symptomatology would also factor into the decision as to the timing of the surgical intervention. It would also allow assessment of other cardiac manifestations of rheumatic disease (such as other valvular pathology), as well as more direct and accurate assessment of pulmonary hypertension and pathophysiology.
   
   
2. Premedication. What drug(s) would you choose to premedicate with? What dose(s):
   
   Key points: I would choose 5 mg of morphine IM and 10 mg diazepam PO approximately 2 hours prior to arrival to the OR. This would allow adequate analgesia and sedation for placement of invasive monitors.
   
   Despite premedications, the patient comes to the OR with a sinus tachycardia of 110. Why is tachycardia problematic (pathophysiology)?
   
   Key points: It would be important to maintain a calm and sedate patient and avoid tachycardia because of the patients dependency on preload and adequate ventricular filling. Tachycardia limits the time available for left-ventricular diastolic refill, and thus may lower cardiac output. Tachycardia may also precipitate ischemia.
   
   Would you delay induction? Why or why not?
   
   Key points: Yes, the priority would be to optimize the patient’s clinical condition by controlling the tachycardia. Proceeding with line placement would only exacerbate the tachycardia. Proceeding with the line placement would only exacerbate the tachycardia, and potentially lead to hypertension.
   
   How would you manage?
   
   Key points: I would supplement with more narcotic, specifically intravenous fentanyl to provide fast acting analgesia and sedation. If this failed to give prompt resolution of tachycardia, I would titrate a short acting beta blocker, such as esmolol to treat the situation.

B. Intraoperative Course

1. Selection of monitors, interpretation of data: Would you insert a pulmonary artery catheter? Why or why not?
   
   Key points: I would insert a pulmonary artery catheter. The knowledge of pulmonary artery pressures would allow a baseline for comparison for postoperative management, and following the filling pressures during the case would allow a mark of preload status for the left vertricle.
   
   What are the risks of Pa catheter placement?
   
   Key points: Patients with pulmonary hypertension have an increased risk of pulmonary artery rupture upon inflation of the balloon when the catheter is in the wedged position. There are also baseline risks with the placement of any central-vessel catheter, such as arterial placement, pneumothorax, bleeding, infection, and arrhythmias.
   
   Would pulmonary capillary wedge pressure reflect LVEDP?
   
   Key points: Because of the pressure gradient caused by the stenotic valve, the pulmonary capillary wedge pressure would not directly reflect the LVEDP, and because of pulmonary hypertension, perhaps not even the left atrial pressure. However, gross decreases in pulmonary artery pressure on serial measurement could be interpreted as a decrease in preload and thus be used to guide therapy. In this situation, the valve of the PA information comes from serial measurements over time, rather than a solitary pressure assessment.
   
   
2. Selection of anesthetic technique: What induction agent(s)? Why?
   
   Key points: I would choose a high dose of fentanyl, as this would provide hemodynamic stability and foster a lower hear rate. I would supplement this with a modest dose of etomidate as this would also tend to avoid hypotension.
   
   During induction with fentanyl, chest wall rigidity occurs. BP decreases and pulmonary arterial pressure increases rapidly. Why?
   
   Key points: Increasing intrathoracic pressures ventilation into a very low compliance chest, results in increased pulmonary artery pressure and thus a decreased cardiac output and hypotension.
   
   How would you treat?
   
   Key points: I would relax the chest wall musculature with a dose of muscle relaxant. I would choose vecuronium because of it’s lack of significant hemodynamic side effects.
   
   What maintenance agent(s) would you choose?
   
   Key points: I would continue to maintain the high plasma level of fentanyl with supplemental doses given by a continuous infusion. Likewise, I would maintain muscle relaxation with vecuronium. I would titrate in small doses of midazolam to provide amnesia and supplement this with isoflurane to treat autonomic responses such as increases in heart rate or blood pressure.
   
   What hemodynamics are you trying to achieve during maintenance?
   
   Key points: Management goals would be to: maintain a low heart rate to allow adequate diastolic filling, maintain sinus rhythm to further augment diastolic filling, maintain adequate preload to favor the pressure gradient and foster adequate left ventricular filling, maintain a decreased afterload to augment left ventricular ejection fraction and increase cardiac output, and limit any decrease in inotropy and systolic ejection of blood.
   
   Would you avoid N2O?
   
   Key points: Yes. Due to the potential for the nitrous-induced expansion of microbubbles introduced during establishment of cardiopulmonary bypass and the possibility of cerebral embolic sequelae, I would avoid N2O for this procedure.
   
   
3. Management of cardiac arrhythmias. After sternotomy, the surgeon touches the right atrium and atrial fibrillation with a rapid ventricular response suddenly occurs. Treatment options?
   
   Key points: Adenosine would slow the ventricular response, and may convert if the fibrillation is due to re-entrant phenomenon. Esmolol, or a calcium channel blocker like verapamil would be effective but may exacerbate hypotension. Digoxin would most likely take too long for a clinical effect. Diltiazem bolus and infusion may be effective. Since the heart is exposed, direct electric cardioversion in also a reasonable first – line option.
   
   
4. Weaning from cardiopulmonary bypass. At the end of bypass, there is considerable difficulty in wearing due to low cardiac output; CVP and pulmonary arterial pressures are elevated, left atrial pressure is low.
   
   What is your diagnosis?
   
   Key points: I would be concerned about pulmonary vasoconstriction and hypertension. This may be secondary to an idiosyncratic reaction to protamine administration, or exacerbation of an underlying insult to the pulmonary vascular endothelium by air or thrombosis embolization.
   
   How would you treat?
   
   Key points: I would provide supportive care by augmenting right ventricular cardiac contractility with inotropes, such as epinephrine, and continue to monitor for decreased pulmonary arterial pressures and CVP.
   
   If the hypotension failed to resolve in the face of a decreased CVP, I would administer more volume to treat the decreased preload. If the hypotension continued to persist I would recommend to the surgeon that we out the patient back on bypass. I would attempt to convert the inotropes to an agent such as dobutamine, which would offer the advantage of pulmonary vasodilatation along with increased inotropy.

C. Postoperative Course

1. Postoperative ventilatory care. Would you plan controlled ventilation overnight? Why or why not?
   
   Key points: Yes. Given the volatile intraoperative hemodynamics, I would expect the patient to be at high risk for further episodes of hypotension, or perioperative hemorrhage. I would wan to insure adequate sedation, analgesia, oxygenation and ventilation for the immediate postoperative period. This would prevent untoward sympathetic responses which might complicate postoperative management.
   
   What agents would you use for sedation and/or analgesia overnight?
   
   Key points: I would choose fentanyl for paid and profound analgesia, and propofol infusion for rapidly titratable and easily reversible sedation.
   
   
2. Management of postoperative bleeding: In the intensive care unit, the patient has “excessive bleeding” from chest tubes. What is “excessive” in this setting?
   
   Key point: This is a subjective assessment, but I would be concerned with a hemorrhage rate greater than 200 cc/hr in this 50 kg patient.
   
   What is the differential diagnosis of bleeding?
   
   Key points: There maybe inadequate reversal of the heparin, return of coagulation interference resulting from protamine before the levels of heparin subside, surgical hemorrhage from leaking suture lines and oozing from the surgical sites. Finally, disseminated intravascular coagulation resulting fom complement activation within a large hematoma could cause excessive bleeding.
   
   What are your treatment options?
   
   Key points: I would reassess the ACT and if elevated, provide a supplemental dose of protamine. I would also expect the patient to have ongoing volume loss and hypovolemia. I would replace this with packed red blood cells and fresh frozen plasma. This would replace ongoing hemoglobin and clotting factor losses.
   
   Finally, if the coagulopathy does not appear to respond to these measures, the patient should be considered for surgical exploration. Many times, even if no direct bleeding source is found, the removal of the hematoma also removes the inciting factor of the ongoing coagulopathy.

D. Additional Topics

1. Cervical spine fracture: An 18 year old male is brought to the emergency room after a diving accident; he is unable to move his arms or legs and has swallow ventilation. How would you manage this?
   
   Key points: This patient has probably sustained a cervical spine fracture with cord injury. His ability to sustain adequate ventilation efforts is also probably compromised. In addition we must assume he has a full stomach. I would immediately make sure that the cervical spine is immobilized in a collar or secured between two sand bags. And then place the patient on 100% oxygen, preferably with a sealed face mask and Jackson-Reese circuit. Because of the known neurologic compromise, I would elect to not place the cervical spine at any further risk and proceed to a cricothyroidotomy under local anesthesia.
   
   Appropriate equipment cannot be located. What would you do? What precautions would you employ for intubation?
   
   Key points: The patient requires endotracheal intubation for positive- pressure ventilation. I would attempt a blind nasal intubation after brief topical application of Neo-Synephrine to the nares and 4% lidocaine spray to the oropharynx. With this approach I would take care to avoid manipulation of the neck.
   
   The nasal approach is unsuccessful, the respirations are qualitatively weaker, how would you proceed?
   
   Key points: I would proceed with an oral intubation with a rapid- sequence induction with the patient’s cricoid cartilage under a modest amount of pressure.
   
   I would remove the collar or sandbags and have an assistant hold the mastoid process with gentle traction in-line with the cervical spine. I would administer the drugs and proceed with gentle laryngoscopy.
   
   One of your colleagues suggests the use of a laryngeal mask aiway. How would you respond?
   
   Key points: I would not agree, because while I could then avoid manipulation of the neck, the patient would still be susceptible to the risks of aspiration of gastric contents, and the ability to provide positive- pressure ventilation would be very limited.
   
   
2. A previously healthy patient develops wheezing after induction and intubation: What is your differential diagnosis?
   
   Key points: Wheezing after intubation may be caused by bronchospasm brought on by the irritation of the tracheal by the endotracheal tube. The sympathetic response of inadequate anesthesia may also account for the reactivity of the airways. Induction drugs or relaxants may also cause the release of histamine or other provocative mediators. In addition, a malpositioned endotracheal tube at the level of the carina, or an overinflated cuff may produce the sound of wheezing. Finally, the patient may have a history of asthma and now is having an acute attack.
   
   What would be your initial treatment?
   
   Key points: I would deepen the anesthetic by increasing the inhaled agent. I would then confirm the position of the endotracheal tube by laryngoscopy and deflate and re inflate the cuff.
   
   Would you use halothane as you anesthetic due to its bronchodilating properties?
   
   Key points: Since all the anesthetics produce bronchodilation, I would prefer to use desflurane due to it’s faster onset.
   
   The clinical situation deteriorates after initial treatment (blood pressure and O2 saturation decreases). Discuss some additional management options.
   
   Key points: I would continue to asses the situation by switching to hand ventilation and monitoring intrathoracic compliance. I would also assess breath sounds for continued wheezing and symmetry. Hypotension and oxygen desaturation may be seen in the face of marked hypovolemia and decreased venous return exacerbated by increased intrathoracic pressure.
   
   Hypotension may limit the use of potent agents if the patient has continued wheezing and bronchospasm, but additional bronchodilators such as beta agonists should be administered via the endotracheal tube. If the breath sounds are asymmetric, consideration should be given to a pneumothorax (especially in patients with COPD), and if the degree of hypotension and desaturation are not life threatening, I would order a chest x-ray for confirmation.
   
   Key points: I would recommend placement of a thoracostomy tube and proceed with the case.
   
   Could you decompress the pneumothorax with an angiocatheter and place the thoracostomy after the procedure?
   
   Key points: Yes. But, at some point during the case, if the angiocatheter fails to maintain the decompression while the patient is being ventilated, the pneumothorax will recur, and this time, suction may be required to resolve the situation. Ultimately, this might require violation of the sterile field for urgent placement of a thoracostomy tube.

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