1
Q
- Pulmonary artery diastolic pressure increases acutely from 10 to 20 mmHg in a 28 year old man undergoing cervical laminectomy in the sitting position. The most appropriate first step in the management of this patient is to
A. administer furosemide
B. aspirate from the proximal port of the pulmonary artery catheter
C. inflate the balloon on the pulmonary artery catheter
D. place the patient in the left lateral decubitus position
E. start an infusion of nitroglycerin
A
- B The most common complications associated with the surgical sitting position includes venous air embolism (VAE), paradoxical VAE, cardiovascular instability, pneumocephalus, subdural hematoma, peripheral neuropathy, and quadriplegia (quadriplegia is possibly caused by compression ischemia of the cervical spinal cord in patients with aerrant spinal cord blood supply). Venous air embolism (VAE) occurs when air is entrained into open veins int he presence of negative intraluminal pressures (i.e., negative with respect to atmospheric pressure).Significant VAE can result in reduced cardiac output and profound hypoxia. Current devices used to detect VAE include the TEE, Doppler ultrasound, pulmonary artery catheter, mass spectrometer (to monitor changes in Peco2 and Pen2), right atrial catheter, and esophageal stethescope (to listen for a “mill wheel” cardiac murmur). The most sensitive means of diagnosing VAE include TEE or precordial Doppler monitoring. Air in the pulmonary artery can increase pulmonary vascular resistance (PVR) and cause right heart strain and dysrhythmias. The general approach to treating VAE is to: (1) stop further air entrainment; (2) aspirate entrained air; (3) prevent expansion of existing air; and (4) support cardiovascular function. Cessation of subsequent air entrainment is achieved by flooding the surgical field with irrigation fluid. Additionally, noncollapsable veins can be sealed using electrocautery, vessel ligation, or bone wax. Neck veins can be compressed as a means of increasing jugular venous pressure, which mitigates or preents further air entry and helps localize the source of air. A multiorificed right atrial catheter, placed before the event, is the most effect means of aspirating VAE. In order to prevent expansion of the VAE, nitrous oxide is immediately discontinued. Cardiovascular function is supported using ionotropes, vasopressors, and IV fluids as indicated. Approximately 20% to 30% of humans have a probe patent foramen ovale. Initiation of PEEp may increase the risk of paradoxical embolism or decrease venous effluent from the calvarium, resulting in creased CBV and ICP. (ITE 2009 Book A Q8)
2
Q
- A 75 yo man is confused, restless and disoriented two days after an aortic aneurysm repair. Serum sodium concentration is 112 mEq/L, serum osmolality is low, and urine is hypertonic. The most appropriate treatment is
A. restriction of fluid intake
B. administration of isotonic saline solution
C. administration of hypertonic (3%) saline solution
D. administration of spironolactone
C. infusion of mannitol 25 g
A
- C The triad associated with cerebral salt-wasting syndrome consists of hyponatremia, volume contraction, and urine sodium concentrations inappropriately high for the given level of serum sodium. It is mainly seen in patients with SAH. A possible etiology may be release of brain natruiretic peptide, leading to excess urinary sodium excretion. It is treated with volume replacement, utilizing normal to hypertonic IV sodium chloride solution, but avoiding overly rapid serum sodium correction as this may result in central pontine mylenolysis. Cerebral salt wasting syndrome (usually hypovolemic) is difficult to differentiate from SIADH (usually normovolemic or mildly hypervolemic) because patients with SAH can have high ADH levels secondary to trauma, pain et. A definitive diagnosis requires demonstration of a negative Na balance over several days in the setting of ongoing hypovolemia or obtaining a 24 hour urine sodium sample. Clinically, the former is often not feasible because of competing interests for prophylaxis of treatment of cerebral vasospasm with moderate hypervolemia. In the setting of cerebral salt-wasting syndrome, the 24 hour sodium value is elevated. In contrast, hyponatremia associated with SIADH is due to renal retention of free water (rather than renal loss of sodium). Accordingly, the quantity of sodium collected over the 24 hour period and CVP sould be relatively normal in SIADH patients.
3
Q
- Which of the following is the most likely to be effective in the treatment of clinically evident cerebral vasospasm occurring after subarachnoid hemorrhage?
A. administration of nimodipine
B. administration of thiopental
C. decreasing cerebral perfusion pressure
D. hypercarbia
E. hypocarbia
A
- A Intracranial aneurysms are the most common cause of intracranial hemorrhage. Occur in 2-4% of population with 1-2% rupturing per year. They are most frequently manifested as hemorrhage together with a sudden, severe headache, nausea, vomiting, focal neurologic signs and depressed consciousness. Major complications of aneurysmal rupture include death, rebleeding, and vasospasm and they may be treated with either endovascular coiling or surgery. Short term outcomes are similar in patients treated surgically versus endovascular insertion. Some pts are unsuitable candidates for insertion of platinum coils because of the anatomy and location of aneurysms and they require surgery. Early treatment is advocated for prevention of rebleeding but surgery may be associated with technical difficulty because of a swollen inflamed brain, whereas delayed treatment increases the risk of rebleeding. Vasopasm is generally manifested clinically 3-5 days after SAH and is the foremost cause of morbidity and death. Transcranial Doppler and cerebral arteriography can detect cerebral vasospasm before clinical symptoms. Treatment of vasospasm includes “triple H” therapy (hypervolemia, hypertension, hemodilution), which consists of the IV administration of fluids or ionotropic drugs, or both. The IV administration of a calcium channel blocker, nimodipine, decreases the risk of morbidity and death from vasospasm. Other treatment modalities include selective intra-arterial injection of vasodilators and balloon dilation (angioplasty) of the affected cerebral vessels using interventional radiology. (ITE 2009 Book A Q 20)
4
Q
- A 50 year old male with amyotrophic lateral sclerosis (ALS) is to undergo surgical repair of a fractured wrist. He currently has a gastrostomy tube due to bulbar dysfunction. Which statement about the anesthetic management of this patient is MOST likely true?
A. He is at increased risk for developing malignant hyperthermia
B. General anesthesia with a laryngeal mask airway is recommended
C. Succinylcholine should not be administered
D. The procedure can safely be performed in an outpatient setting.
A
- C Amyotrophic lateral sclerosis (ALS) is a progressive neuromuscular disease characterized by skeletal muscle weakness, atrophy, and spasticity resulting from upper and lower motor neuron degeneration. It typically presents in middle age (40-50 yo) and occurs predominantly in men. Early in the disease, isolated muscle weakness in the extremities may be the only deficit. However, over time the disease progresses such that muscle weakness becomes generalized. Weakness of the muscles of respiration results in progressive deterioration of pulmonary status culminating in the need for ventilator support. Swallowing and feeding difficulties also develop due to bulbar muscle weakness, increasing the risk for pulmonary aspiration. Patients with ALS have successfully undergone general and regional anesthesia. In order to minimize the respiratory depressant effects of opioids and general anesthetic agents, regional anesthesia - especially peripheral nerve blocks- may be preferred when appropriate for the surgical procedure. Regional anesthesia has not been associated with disease progression. Neuroaxial anesthesia has been performed successfully in patients with ALS. However, due to the respiratory muscle weakness associated with the disease, care should be taken to avoid level of block that could interfere with ventilatory function. When performing general anesthesia in the patients with ALS, succinylcholine must be avoided to prevent hyperkalemia resulting from the response of extrajunctional acetylcholine receptors on the membranes of denervated muscles. Nondepolarizing neuromuscular blocking agents should be used judiciously and with careful neuromuscular monitoring in these patients. There is evidence that increased sensitivity to these drugs may occur. In addition, residual muscle weakness postoperatively would not be well tolerated and could lead to the need for mechanical ventilation. ALS patients whoare experiencing bulbar muscle weakness, such as the patient in the scenario who requires a gastrostomy tube due to feeding difficulties, are at increased risk for aspiration of gastric contents. Aspiration prophylaxis measures should be taken and use of a laryngeal mask airway would not be recommended. ALs is not a risk factor for malignant hyperthermia. Due to the compromised pulmonary function that occurs in ALS patients, these patients are at risk for postoperative pulmonary complications and may require postoperative ventilator support. Therefore, these patients should not undergo surgery as an outpatient. (ACE 2008 5B)
5
Q
5. Massive venous air embolism occurs in a patient who is undergoing craniotomy in the sitting position with nitrous oxide, oxygen, fentanyl anesthesia. Which of the following changes in end-tidal (ET) concentrations of carbon dioxide, nitrogen, and nitrous oxide are most likely in this patient? ETCO2 ETN2 ETN2O A. increased increased decreased B. decreased decreased increased C. decreased decreased decreased D. decreased increased decreased E. increased decreased decreased
A
- D A sudden decrease in end-tidal concentration of carbon dioxide reflects increased dead space secondary to continued ventilation of alveoli no longer being perfused because of obstruction of their vascular supply by air bubbles. An increased end-tidal nitrogen concentration may reflect nitrogen from venous air embolism but is rarely available. And decreased end-tidal concentration of nitrous gas could be because of the same reason CO2 is decreased? (any ideas). (ITE 2009 Book A Q95)
Anesthesiology
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