SNACS MCQ Flashcards
- A 55 yr-old man has quadriplegia after undergoing suboccipital craniotomy in the sitting position for the treatment of acoustic neuroma. Which of the following is the most likely cause? A.Air embolism with the presence of probe patent foramen ovale B.Compression of the cervical cord related to neck flexion C.Jugular venous obstruction D.Postoperative pneumocephalus E.Sustained elevation of cerebral perfusion pressure
A. Air embolism with the presence of probe patent foramen ovale Venous air embolism is a known complication in the sitting position and can lead to disastrous consequences including cardiac arrest. In the presence of patent foramen ovale, it can lead to paradoxical air embolism and stroke,however isolated quadriplegia is uncommon.
B. Compression of the cervical cord related to neck flexion Cervical cord compression leading to quadriplegia is a rare complication of the sitting position. Focal pressure on the spinal cord due to extreme flexion of the head on the neck is a postulated mechanism. Regional cord perfusion may also be decreased especially when there is associated decrease in mean arterial pressure and could contribute to cord ischemia. Preventive measures could include avoidance of extreme flexion of the neck and providing a space of at least one inch between the chin and the chest, avoidance of excessive neck rotation particularly in elderly patients with cervical stenosis and maintenance of near normal mean arterial pressure. Monitoring of short latency SSEPs have been advocated to monitor the sensory pathways during the procedure. CORRECT
C. Jugular venous obstruction Jugular venous obstruction can lead to raised intracranial pressure but does not produce quadriplegia by itself.
D. Postoperative pneumocephalus Pneumocephalus is one of the differential diagnosis of delayed awakening. Collection of air under the dura can increase ICP and neurological deficit but unlikely to cause isolated quadriplegia.
E. Sustained elevation of cerebral perfusion pressure Sustained elevation in raised ICP again will not cause quadriplegia by itself.
- A 6-yr-old boy with spina bifida and a chronic indwelling urinary catheter has severe hypotension and hypoxemia during augmentation cystoplasty Which of the following is the most likely cause? A.Autonomic neuropathy B.Disseminated intravascular coagulation C.Latex allergy D.Urinary sepsis E.Venous air embolism
Autonomic neuropathy is a disorder affecting the autonomic nerves. Causes include diabetes, amyloidosis, autoimmune disorders. Patients can present with hypotension but usually not hypoxemia
Disseminated intravascular coagulation can cause abnormal bleeding and hypovolemia causing hypotension but hypoxemia is unlikely.
Latex allergy can produce anaphylaxis. It presents as severe hypotension, rash or hives, hypoxemia due to bronchoconstriction. Previous reports indicate a prevalence of latex allergy in patients with spina bifida (SB) ranging between 10% and 73%. From the initial surgical repair of the myelomeningocele, children with Spina Bifida are submitted to multiple surgeries due to the neurologic, orthopedic and urologic problems they may present. Consequently, these children are exposed to several latex-containing products during their multiple interventions and they get sensitized. Accordingly, latex allergy manifestations can be prevented. (1) Avoiding using latexcontaining products since the birth of children with SB. (2) In children already operated of myelomeningocele but without evidence of latex allergy, one should avoid the use of latex materials during their successive admissions to hospital and during further surgeries. And (3) In children known to have developed latex allergy, a latex-free operating room. Correct
Urinary sepsis would present with hypotension again hypoxemia is unlikely
Venous air embolism is again unlikely in this situation.
Which of the following statements concerning brain stem auditory evoked responses is true? A.They monitor cortical function B.They are affected by changes in paCo2 C.They are affected by mild hypothermia D.They are more resistant to anesthetic effects than somatosensory evoked responses E.They are abolished coincident with flattening of the EEG.
Cortical function is monitored by SSEPs and EEG. Auditory evoked potentials do not monitor cortical function. This answer is incorrect
Low PaCO2 and mild hypothermia affect SSEP. Auditory evoked potentials are quite resistant to changes in the above parameters. The answer is incorrect
Brainstem auditory evoked potentials are delivered by repetitive clicks using foam ear inserts attached to stimulus transducers. Cases in which they are commonly monitored include microvascular decompression of cranial nerves( V and VII), resection of acoustic neuroma,posterior fossa exploration, clipping of basilar artery aneurysm. The most common change observed during monitoring is an increase in I-V inter peak latency and loss of amplitude of wave V.The most common change is usually due to stretch of cranial nerve 8, due to cerebellar retraction. Other causes could be due to sectioning of the nerve, ischemia to the nerve, cerebellar edema or positioning of the head in retromastoid craniotomy, hypotension, hypocarbia. BAEPs are considered the easiest of the somatosensory evoked potentials to monitor and are least sensitive to changes in preoperative variables.Unlike SSEPs, BAEPs are resistant to the effects of inhalation and intravenous agents and any changes would not be confused with surgically induced changes.
EEG is sensitive to high doses of volatile anesthetics however auditory evoked potentials are quite resistant.
A patient who is paraplegic secondary to spinal cord transection at T3 develops bradycardia and facial flushing during a nephrectomy under general anesthesia with nitrous oxide, fentanyl and isoflurane The most likely cause of this response is
A.Release of histamine B.Stimulation of carotid sinus
C.Release of prostaglandins
D.Vagal response to peritoneal traction E.Release of epinephrine
Release of histamine can cause facial flushing but unlikely to cause bradycardia and could cause tachycardia and hypotension.
Autonomic hyperreflexia is a syndrome of vascular instability commonly brady cardia, hypertension, facial flushing occurring after spinal cord injury usually above T7. The trigger to this response is usually a cutaneous, proprioceptive or visceral stimulus(full bladder, surgical stimulation as in the above case). The sensation enters the spinal cord and causes a spinal reflex, which in normal persons is inhibited from above. Sudden increases in blood pressure are sensed in the pressure receptors of the aorta and carotid sinus. The resultant vagal hyperactivity produces bradycardia,ventricular ectopy and heart block. Reflex vasodilation occurring above the level of the lesion may lead to flushing of the head and neck. Treatment of autonomic reflexia is with ganglion blocking drugs like trimethaphan, alpha adrenergic blocking drugs like phentolamine, vasodilators like nitroprusside or nitroglycerin, deep general or regional anesthesia. Patients with autonomic hyperreflexia should not be treated with beta blockers alone leaving the alpha receptors unopposed. Correct
Release of prostaglandins can cause hypotension and facial flushing but does not cause tachycardia
Vagal response to peritoneal traction can cause bradycardia or even systole, unlikely to be the cause in this situation.
Release of epinephrine is unlikely in this situation. It is unlikely to cause bradycardia
1.A 4 month old child is undergoing a craniectomy for craniosynostosis under general anesthesia. Suddenly the systolic BP drops from 75 mmHg to 30 mmHg and the EtCO2 decreases from 35 to 6 mmHg. Which of the following maneuvers is LEAST likely to have a beneficial effect??
A.Administration of a fluid bolus B.Administration of a vasopressor C.Application of PEEP D.Aspiration of the central line E.Flooding of the wound with saline
Children undergoing craniosynostosis repair are subject to significant hemodynamic changes, including venous air embolism and significant blood loss. Administration of fluid bolus would be very helpful in correcting a low blood pressure in this situation. The goal of hydration is reducing the gradient between the right atrium and the entraining vessel.
Hemodynamic support often includes vasopressor support. Due to the obstruction being mainly to the right side of the heart by the entrained air, the increase in right ventricular afterload subsequently causes left ventricular failure. Hence, right ventricular support should be kept in mind. Therefore, dopamine, dobutamine and epinephrine, are effective in supporting blood pressure and restoring cerebral blood flow, even in very low birth weight infants.
C. APPLICATION OF PEEP- The application of positive end-expiratory pressure increases central venous pressure but also decreases cardiac filling pressure, cardiac output, and blood pressure-unlikely to be beneficial. It may increase the chance of paradoxical air embolism and further cardiovascular compromise. The following are the likely steps to be taken in suspected venous air embolism Inform surgeon immediately. Discontinue N2O if being administered, increase O2 flows. Have the surgeon flood the surgical field with fluids. Change the patient’s position to lower the head to the heart level Aspirate the right atrial catheter. Provide cardiovascular support. Jugular venous compression although a recommendation could dislodge atherosclerotic plaques, cause venous engorgement and brain edema and so should be used with caution.
Attempts should immediately be made to identify and occlude the site of air entry, either by flooding the operative field with saline when appropriate (such as during a posterior fossa craniotomy) or by applying bone wax to bone edges
- Which of the interventions to be carried out in the emergency department is most likely to reduce intracranial pressure rapidly in traumatic brain injury? A. Intubate and hyperventilate B.Intravenous administration of opioid C.Intravenous administration of corticosteroid D.IV administration of nitroprusside E.IV administration of furosemide Please click on answer choices
Administration of opioids would not help with intracranial pressure reduction. Although opioids are used to treat pain in trauma patients, negative side effects like drop in mean arterial pressure and decrease in cerebral perfusion pressure should be watched for.
The use of steroids is not recommended for improving outcome or reducing the intracranial pressure in traumatic brain injury. According to the brain trauma foundation guidelines, there is strong evidence that steroids are deleterious: thus their use is not recommended. The CRASH(Corticosteroid Randomization After Severe Head Injury) trial in 2004 reported the results of an international randomized control trial in which 10,008 patients were randomized to receive methylprednisolone or placebo. The study was halted after about 5 years when interim analysis showed a deleterious effect of methylprednisolone. Specifically, the two week mortality in the steroid group was 21% versus 18% in the controls, with a 1.18 relative risk of death in the steroid group(95% CI 1.09-1.27, p=0.0001)
Sodium nitroprusside should not be used in patients with raised intracranial pressure due to its ability to dilate cerebral blood vessels resulting in a rise in intracranial pressure and a decrease in cerebral perfusion pressure consequent to lowering of the mean arterial pressure. Incorrect Try again!! Cottrell J.E: J Neurosurg. 1978 Mar;48(3); 329-31
Although furosemide reduces CSF production and consequently can lower the intracranial pressure, this is not the standard of care in the above situation. However, mannitol may be used for osmotic diuresis and decreasing the raised ICP
- WHICH OF THE FOLLOWING STATEMENTS CONCERNING AUTONOMIC HYPERREFLEXIA IS TRUE?? A.It occurs within 24 hours after injury B.It occurs with lesions below T 10 C.It occurs with reflex increase in parasympathetic outflow D.It is characterized by paroxysmal hypotension and tachycardia E.It is prevented by blocking afferent visceral pathways
Autonomic hyperreflexia is a potentially life threatening condition characterized by a sudden uncontrolled sympathetic response secondary to noxious stimuli. It occurs usually in the first six months after injury. It does not occur within 24 hours after injury.
This choice is incorrect.The incidence is reported to be between 48% and 98% in patients with quadriplegia and high paraplegia (lesion above T6)
Autonomic hyperreflexia is triggered by a noxious stimulus below the level of the lesion, which then activates unopposed sympathetic activity.
The noxious stimulus carried by the sensory nerves below the level of the lesion of the spinal cord, activates sympathetic nerves causing massive vasoconstriction, increased blood pressure and bradycardia. Hypotension and tachycardia are not the manifestations of autonomic hyperreflexia.
Autonomic hyperreflexia occurs following spinal shock and in association with return of reflexes. Stimulation (bladder and bowel usually) below the spinal cord transection initiates afferent impulses that enter the spinal cord. These impulses initiate a sympathetic nervous system activity which is uninhibited by inhibitory impulses from above the level of the transection, leading to systemic hypertension and reflex bradycardia which are the hallmarks of this condition. Blocking the afferent visceral pathways by spinal anesthesia could be effective in prevention. Epidural anesthesia, deep general anesthesia and local anesthesia may or may not prevent the occurence. Regardless of the technique used, vasodilator drugs with a short half life should be readily available.
During carotid endarterectomy, blood pressure suddenly decreases from 140/90 mm Hg to 80/50 mm Hg.The EKG shows a HR of 42/min with normal sinus rhythm and occasional premature ventricular contractions. The most appropriate therapy is IV administration is A. Atropine B. Epinephrine C. Isoproterenol D. Lidocaine E. Phenylnephrine Please click on answer choices
Surgical manipulation of the carotid sinus with activation of the baroreceptor reflexes can cause abrupt bradycardia and hypotension. Although cessation of surgical manipulation could promptly restore the hemodynamics, administration of IV atropine would help this situation. Infiltration of the carotid bifurcation with 1% lidocaine usually prevents further episodes. A recent, large retrospective study reported asystole in 4.9% of patients after carotid stenting. Asystole was more likely to occur in patients undergoing a rightsided procedure, in those with significant contralateral stenosis, and in those with a reduced left ventricular ejection fraction. The administration of prophylactic atropine before balloon inflation decreases the incidence of intraoperative bradycardia and cardiac morbidity in primary carotid stenting patients. Correct
Epinephrine would not be the first choice in this situation. Using epinephrine could also contribute to increase myocardial demand in these patients with pre-existing predisposition to myocardial ischemia.
Although isoproterenol has been used for heart block, it is not indicated and could be detrimental in this patient with sinus bradycardia due to carotid manipulation.
IV lidocaine is not indicated at this point. Infiltration of the carotid bifurcation with 1% lidocaine usually helps to prevent further episodes. Infiltration may, however, increase the incidence of both intraoperative and postoperative hypertension.
Since the cause of this bradycardia is surgical manipulation of the carotid sinus, administration of the above medication would not be the first choice. However, arterial blood pressure should be maintained in the highnormal range throughout the procedure which may need utilization of a medication like phenylephrine with its vasopressor effect particularly during the period of carotid clamping in an attempt to increase collateral flow and prevent cerebral ischemia. This may be of use particularly in patients with contralateral internal carotid artery occlusion or severe stenosis. I
1.A 55-year-old man who is scheduled to undergo carotid endarterectomy (CEA) has a persistent myocardial filling defect at three hours on a dipyridamole-thallium scan. Which of the following statements is correct? (A) Coronary autoregulation is effective in this segment (B) Coronary revascularization should precede CEA (C) Isoflurane is contraindicated (D) Myocardial infarction is impending (E) There is a segment of nonviable myocardium
In the setting of severe coronary disease, perfusion reserve may be reduced from flow-limiting stenosis, endothelial dysfunction, and adrenergic stimulation. •When coronary arteries are narrowed by atherosclerotic disease, coronary auto regulation attempts to normalize myocardial blood flow by reducing the resistance of distal perfusion beds. •Fixed perfusion defects are usually due to myocardial scarring. Due to exhausted perfusion reserve in those areas of severe stenosis and blocked arteries, coronary auto regulation is unlikely to be effective
Results from the randomized, prospective CARP( Coronary Artery Revascularization Prophylaxis)trial demonstrated that an aggressive strategy of prophylactic coronary artery revascularization before vascular surgery in patients with stable cardiac symptoms does not improve short-term outcome or long-term survival. At 2.7 years after randomization, mortality was 22% and 23% in patients with and without revascularization, respectively. Postoperative MI, defined by increased troponin levels, occurred in 12% and 14% of patients with and without revascularization, respectively. the best approach to managing coexisting severe carotid and coronary disease remains uncertain.
Early studies indicated that isoflurane caused coronary steal and should therefore be avoided in patients with coronary heart disease. Subsequently, more detailed trials have disputed this and have shown that as long as coronary perfusion pressure is maintained, isoflurane does not cause coronary steal or myocardial ischemia Studies using EEG and regional cerebral blood flow (rCBF) measurements suggest that the critical rCBF (the rCBF below which EEG changes of cerebral ischemia occur) is lower for isoflurane than for halothane or enflurane. Sevoflurane is a good alternative because its critical rCBF in patients undergoing endarterectomy is similar to that determined with isoflurane and it may facilitate more rapid emergence.
Impending myocardial infarction has 3 common presentations: Onset of ischemic cardiac pain in a patient previously free of symptoms. Intensification of angina of effort in a patient with previous angina of several months’ or years’ duration. Recurrence of pain, at rest or on slight provocation, in a patient who has been pain free after a previous myocardial infarction.
Thallium201 is a monovalent cation with biologic properties similar to those of potassium. 201 Tl is a well-suited radionuclide for differentiation of normal and ischemic myocardium from scarred myocardium. After initial uptake into the myocyte, an equilibrium is created between the intracellular and extracellular concentrations of thallium. After blood levels diminish during the redistribution phase, the equilibrium favors egress of thallium out of the myocyte. On the basis of that equilibrium, thallium concentration diminishes over time in zones of normal uptake while diminishing more slowly in zones with less initial thallium uptake(zone of ischemia). Fixed perfusion defect is due to decreased blood flow to an area of heart muscle, due to permanently damaged muscle (essentially a scar in the heart muscle). When scarred myocardium is present, the initial rest or stress thallium defect persists over time; such deficits are termed irreversible or fixed defects . Correct
- A 75-yr-old woman with significant carotid artery stenosis is scheduled for general anesthesia for repair of a fractured hip. Which of the following is the greatest disadvantage of using propofol as an induction agent in this patient?? A) Decreased arterial blood pressure (B) Pain during IV injection (C)Prolonged apnea after induction (D) Prolonged awakening (E) Prolonged elimination half life
The most prominent effect of propofol is a decrease in arterial blood pressure during induction of anesthesia. Independent of the presence of cardiovascular disease, an induction dose of 2 to 2.5 mg/kg produces a 25% to 40% reduction of systolic blood pressure. Similar changes are seen in mean and diastolic blood pressure. The decrease in arterial blood pressure is associated with a decrease in cardiac output and cardiac index (± 15%), stroke volume index (± 20%), and systemic vascular resistance (15% to 25%). Left ventricular stroke work index also is decreased (± 30%). Anesthetic management goals for carotid endarterectomy include protection of the heart and brain from ischemic injury. Propofol appears safe and superior in terms of hemodynamic stability in carotid endarterectomy and prevention of myocardial ischemia in two studies listed below. Both the studies studied hemodynamic stability and incidence of myocardial ischemia during carotid endarterectomy and compared propofol with isoflurane. Correct
Induction of anesthesia with propofol is often associated with pain on injection. Pain on injection is reduced by using a large vein(antecubital vein), avoiding veins in the dorsum of the hand, and adding lidocaine to the propofol solution or changing the propofol formulation. Pretreatment with opiates, nonsteroidal anti-inflammatory drugs, ketamine, esmolol or metoprolol, magnesium, , a clonidine-ephedrine combination, dexamethasone,dexmedetomidine and metoclopramide all have been tested with variable efficacy. However pain on injection is not a reason to avoid propofol at induction of anesthesia during a carotid endarterectomy.
Apnea occurs after administration of an induction dose of propofol; the incidence and duration of apnea depend on dose, speed of injection, and concomitant premedication. An induction dose of propofol results in a 25% to 30% incidence of apnea from the respiratory depressant effects of propofol. The duration of apnea occurring with propofol may be prolonged to more than 30 seconds. The incidence of prolonged apnea (>30 seconds) is increased further by addition of an opiate, either as premedication or just before induction of anesthesia. However, since we are going to manually control the patient’s respiration after induction, apnea will not be a problem during induction of anesthesia.
After a single bolus dose, whole blood propofol levels decrease rapidly as a result of redistribution and elimination. The initial distribution half-life of propofol is 2 to 8 minutes. The context-sensitive half-time for propofol for infusions of up to 8 hours is less than 40 minutes. Because the required decrease in concentration for awakening after anesthesia or sedation with propofol is generally less than 50%, recovery from propofol remains rapid even after prolonged infusion
The rapidity with which the drug level decreases is directly related to the time of infusion (i.e., the longer the drug is infused, the longer the half-time). Propofol, has a significantly short half-time(4-7 hrs) and this makes them more suitable for prolonged infusion.
EEG changes of cerebral ischemia during carotid endarterectomy occurs when regional cerebral blood flow is
45-50 ml/min/100g B. 35-40 ml/min/100g C. 25-30 ml/min/100g D. 15-20 ml/min/100g E. 5-10 ml/min/100g
Carotid endarterectomy requires temporary clamping leading to cerebral ischemia. The ipsilateral cerebral hemisphere will be dependent on collateral blood flow from the vertebral artery and contralateral carotid artery through the circle of Willis. Ischemic EEG changes may be seen with shunt malfunction, hypotension or cerebral emboli. Typical regional cerebral blood flow is 5055ml/min/100g of brain tissue. EEG deterioration would not occur. Incorrect Try again
This is not the correct answer. EEG changes have not been observed at 35-40ml/min/100g.
The above value is incorrect.EEG changes have not been observed at 25-30 ml/min/100g.
Changes in EEG are usually seen with flows between 1520ml/min/100g. However analysis of xenon decay curves for regional cerebral blood flow along with EEG monitoring have provided some important insights. The critical rCBF values depend upon the volatile agent used along with nitrous oxide and is approximately 20, 15, 10 and 10ml/100g of brain tissue for halothane, enflurane, sevoflurane and isoflurane respectively. The changes usually consist of replacement of the faster background activity with higher amplitude theta and lower amplitude irregular delta components. The changes usually reverse with placement of a shunt.
In patients anesthetized with isoflurane critical regional cerebral blood flow for EEG changes measured was approximately 10-11ml/100g/min. Isoflurane and sevoflurane lower the critical regional cerebral blood flow at which EEG changes occur. In areas of focal cerebral ischemia such as carotid or middle cerebral artery occlusion, cerebral auto regulation of blood flow is lost and flow is dependent on perfusion pressure and blood volume.
