Mae URS oleNied Anesthesiologists rN es aAMERICAN SOCIETY OF ANESTHESIOLOGISTS Anesthesiology Continuing Education Program ‘Answer Key Issue 9A Ln: 35. 0. B 2G an) m. oD 3 32 mm. D aes 38 C 2 Dd heres 39. BOA CHEE 40. «6 m oD (a Mea A B.C & OB a D 7A 9 ¢ y ake) Tee i 10. 44.°«2D 78. =D prlseeeeea nF 45. B 9. B i ie 4602«< 80. D BOB OA aA 4 OB 48.0«A 8 oD isi 4. D 8. CG 1A 50. B BA m ¢ SleteD 8. D 1. D 5. A 86. ~B w C 3. sO A iG 54 OB 8&8. D aaa 55. C 8. A ane 56. a) Tata Sratea a. B 24D 58. «B 2. oD 23. oD 59.0 A atae % OC 0. 4. OB 7D a. oD %. 2B. OA A % 2 oD 6. OC OT EAl 30, -=&B oC 98. OC | ait eD. Souteec! 9. B Saeco: Sentce! 100. D 3G Siete) | 34.—O*B Can‘The self-education questions, answers, and discussions in this educational program are based on currently published medical literature and do not represent opinions or recommendations of the American Society of Anesthesiologists. Some information may be controversial, and new advances may invalidate certain statements and answers. The Editorial Board members have attempted to provide an educational experience relevant to the practice of anesthesiology. The sole purpose of the Anesthesiology Continuing Education (ACE) program is educational. Its not intended as an examination. Every effort has been made to ensure that medication selections and dosages are in accord with current recommendations and practice atthe titue of publication. However, the clinician is urged to read the package insert for each drug ptior to administration to verily indications, dosage, and added warnings and precautions ‘This self-education program is composed of 100 items each of which consists of a question, answer, discussion, and a list of references. Comments about the ACE program can be sent by email to the following: Edwin A. Bowe, MD Editorin Chief ‘eabowe@er ky.ed ASA Bxecutive Office ACEASA@asaha.org Copyright © 2012 The American Society of Anesthesiologists. All rights reserved.Tema. Intrathecal (FT) clonidine provides significant analgesia in the perioperative setting. More importantly perhaps, IT clonidine has been suggested to reduce the area of increased sensitivity to pain (hyperalgesia) that develops around the wound. This decreased area of hyperalgesia has been postulated to represent diminished “wind-up” and sensitivity of central nervous system neurons relaying pain sensation, Consistent with this interpretation, one randomized study found thae patients treated with IT clonidine experience lower rates of persistent postsurgical pain than those treated with either [T local anesthetic or IT placebo. Ziconotide, the first selective Nype voltage-sensitive caleium-channel blocker, provides potent analgesia in a novel manner independent of the opioid pathway. The US Food and Drug Administration approved ziconotide in 2004 for the management of severe chronic pain in patients for whom IT therapy is warranted and who are intolerant or refractory to other treatment, such as systemnic analgesics, adjunctive therapies, or IT morphine. Its use in the perioperative setting has not been examined. IT baclofen is used primarily for spasticity and dystonia, It may have analgesic effects when used independently or in conjunction with opioids, but IT baclofen has not been investigated as an adjuvant to perioperative pain management. Intraoperative intravenous ketamine has been suggested to reduce the proportion of patients with persistent postsurgical pains however, IT ketamine use has not been reported 0 do the same. Administration of IT ketamine has been described primarily in terminal patients but has been reported to cause neurotoxicity in the spinal cord as determined at autopsy and remains experimental. REFERENCES 1. Benzon H, Raja SN, Molloy RE, et al. Essentials of Pain Medicine and Regional Anesthesia, 2nd ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2005-471, 2. De Kock M, Lavand’homme P, Watetloos H. The shorelasting analgesia and longterm antihyperalgesic effect of intrathecal clonidine in patients unclergoing colonic surgery. Anesth Analg. 2005; 101:566~572, ITEM 2 Pulmonary edema occurring in patients with neurologic disorders may have a cardiovascular, neurogenic, or iatrogenic cause, oF it may be due to “negative-pressure” pulmonary edema. While the pathophysiology is complex and different for each of these states, the common presentation is a decrease in oxygen saturation and cither no change or fluffy infiltrates on a chest radiograph (Figure 1).Figure 1. Pulmonary edema. Used with kind permission, from che Loyola Univesity Health System. Neurogenic pulmonary edema (NPE), generally attributed to a massive sympathetic discharge, has been reported to occur in up to 20% of patients with severe head injury. More than half of the patients who develop NPE manifest symptoms within 4 hours of their injury. Accordingly, NPE may manifest in the intraoperative period in trauma patients. Head trauma is not the only recognized cause of NPE. Neurologic insults associated with the development of neurogenic pulmonary edema include the following: Intracranial © Trauma © Intracerebral hemorrhage © Intracranial surgery © Intracranial tumors © Other © Spinal cord trauma © Meningitis ° Multiple sclerosis © Guillain-Barré syndrome NPE is a lifehreatening condition, but scant epidemiologic data have been established on its prevalence ‘Various authors have placed morbidity at 40% to 50% anc mortality at 7%. Case reports associating NPE with isolated spinal cord injury are rare. REFERENCES 1. Cottrell JE, Young WL. Cottrell and Young's Neuroanesthesia. 5th ed. Philadelphia, PA: Elsevier Moshy; 2010:402-403, Muroi C, Keller M, Pangalt A, etal. Neurogeniec pulmonary edema in patients with subarachnoid hemorshage. J Neurosurg Anesthesiol, 2008; 20+ 188-192. 3. Sedj)J, Zicha J, Kunes J, etal. Mechanisms of neurogenic pulmonary edema development. Physiol Res. 2008; 57:499-506,4. Chen HI. Hemodynamic mechanisms of neurogenic pulmonary edema. Biol Signals. 1995; 4: 186-192. 5. Mayer SA, Fink ME, Homma S, et al. Cardiac injury associated with neurogenic pulmonary edema following subarachnoid hemorthage. Newrolog. 1994; 44:815-820. 6. Fontes RB, Aguiar PH, Zanetti MY, et al. Acute neurogenic pulmonary edema: case reports and. literature review. J Neurosurg Anesthesiol, 2003; 15:144~ 150. 7. Berlly M, Shem K. Respiratory management during the first five days after spinal cord injury. J Spinal Cord Med. 2007; 30:309-318. iTem3. Clinical scenario: A 65-year-old woman scheduled for a right upper lobectomy for adenocarcinoma is anesthetized and intubated with a leftsicled double-lumen tracheal rube. The bronchial lumen is placed in the left mainstem bronchus via fiberoptic bronchoscopy. Upon damping the tracheal lumen for one- lung ventilation, there is a significant increase in peak aitway pressure and a decrease in tidal volume, ‘Onelung ventilation is commonly achieved with a double-lumen tracheal mbe. However, cube malposition may cause impaired oxygenation or ventilation. Further, the tube malposition may manifest differently depending on operative thoracie side. In this scenario, the patient is placed in the left lateral decubitus position for het right upper lobectomy. ‘The bronchial lumen is placed in the left mainstem bronchus via fiberoptic bronchoscopy and both bronchial and tracheal cuffs are inflated. With both lungs ventilated, the tidal volume and peak airway pressures were adequate. However, after clamping the tracheal lumen with resultant onelung ventilation of the left lung, the peak airway pressure drastically increased with a decreased tidal volume, The differential diagnosis includes bronchospasm, left pneumothorax, left bronchial mucous plug, and a bronchial humen occluding the left upper lobe bronchus. The last situation results from positioning the doublelumen tube too distally in the left mainstem bronchus. The treatment is to withdraw the tube slightly with fiberoptic ‘2uidance until the rim of the bronchial cuff is visualized in the left mainstem bronchus. Heriation of the bronchial cuff into the right mainstem bronchus may occur if the double-lumen tube is not in a sufficiently distal position. In this scenario, the patient will continue to be ventilated on the left side by the dlistal endobronchial lumen and peak airway pressure would not increase. However, ifthe patient were being. ‘operated on the left side and ventilation of the lung on the right via the tracheal himen is attempted, excessive ‘peak airway pressure would result from obstruction of the right mainstem bronchus by the bronchial cuff, Likewise, a right-sided mucous plug in the given scenario would not affect onelung ventilation of the left king, ‘Tracheal cui rupture would not result in increased peak airway pressures. However, upon reinstitution of ‘tworung ventilation, a significant cuff leak may result REFERENCES 1, Miller RD. Miller's Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010+1833~ 1841, 2, Campos JH, Update on tracheobronchial anatomy and flexible fiberoptic bronchoscopy in thoracic anesthesia, Cierr Opin Anaesthesiol. 2009; 22:4~10, 3. Campos JH. Progress in lung separation. Thorac Surg Clin. 2005; 15-71-83. 4. Fortier G, Coté D, Soucy], etal, Left double lumen tube malposition. Br J Anaesth, 2004; 93-475.nema ‘The American Heart Association. (AHA) 2010 neonatal resuscitation guidelines utilize an algorithmic approach to the management of the newborn after delivery (Figure 1). The AHA specifically notes that in most circumstances bradycardia in a newbom is due to hypoxemia. Accordingly, positive pressure ventilation with oxygen is the most effective treatment for bradycardia in this cireumstance. Figure 1, Neonatal flow algorithm. Used with permission, from Kattwinket J, Perlman JM, Azis Ky etal, Part I: neonatal resuscitation: 2010 American Heart Association Guidelinesfor Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science; Cirewation. 2010; 122,8909919. hheepy//cire.ahajournals.org/cgi/content/full/122/18_suppl_3/S909/FUL. Accessed February 2012, Copyright © 2004 American Heart Association, Ine Newborn Resuscitation {Ghar eee, by 1 Otgarg etston ‘gees Product, eo 708 TK70% e505In the clinical scenario where the newborn remains bradycardic despite chest compressions and adequate ventilation with supplemental oxygen, epinephrine is the recommended therapy. Tracheal intubation should also be considered. Although calcium may be useful in the management of a neonate who is experiencing weakness in. association with hypermagnesemia related to maternal administration of magnesium sulfate, itis not part of the routine AHA guidelines for the treatment of bradycardia Atropine and sodium bicarbonate are not patt of the AHA guidelines for neonatal resuscitation. REFERENCES 1. Miller RD. Mile’s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:2691-2692, 2. Rajani AK, Chitkara R, Halamek LP, Delivery room management of the newborn. Pediatr Clin North Am. 2009; 56:515-535. 3. Katewinkel J, Perlman JM, AzieK, etal. Part 15: neonatal resuscitation: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cantiovasculat Care Science. Circulation. 2010; 122:5909-919. httpx//cire-ahajournals.org/egi/content/Full/122/18_ suppl_3/S909. Accessed February 2012. ITEM 5; Postural puncture headache (PDPH) is a common complication of spinal anesthesia. The risk of PDPH may be as low as 1% (when a small gauge pencil-point needle is used) or as bigh as 80% (when the dura is punctured by a 16- or 18g Tuohy needle). The majority of these headaches resolve within 1 week. On. ‘occasion, however, these headaches may persist longer. Patients between the ages of 20 and 40 are at the greatest risk of PDPH. In contrast, pediatric, adolescent, and elderly patients are at relatively reduced risk. A patient’ sex isan important risk factor for PDPH, Worsen are significantly more likely to experience PDPH, even when risk is adjusted for age and the increased risk to parturients, Compared to cutting needles, pencil-point needles, such as the Whitacre, are associated with a reduced risk of PDPH. Previous history of migraine headache is not a described risk factor for PDPH. Patients with a history of PDPH, however, have an increased tisk of subsequent PDPH. REFERENCES 1. Benson H, Raja SN, Molloy RE, et al. Essentials of Pain Medicine and Regional Anesthesia. 2nd ed Philadelphia, PA: Elsevier Churchill Livingstone; 2005:293-297. 2. Miller RD. Miller's Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 201030753084.TEM 6 _______Caudal anesthesia can be effectively used to provide postoperative analgesia to pediatric patients undergoing lower abdominal and urological procedures. Caudal blocks in pediatric patients are commonly performed ‘while the patient is receiving general anesthesia ‘The risk for severe complications from caudal anesthesia is low. However, a possible complication from caudal anesthesia is the inadvertent injection of local anesthetic into the intrathecal space. Caudal anesthesia is typically performed at levels S4-5. The dural sac in infants has been described to terminate as low as $3. This short difference could result in inadvertent injection of local anesthetic into the intrathecal space with subsequent total spinal anesthesia. A total spinal block in an infant is typically manifested by apnea and immobility with no initial change in the heart rate or blood pressure. Apnea would develop from local anesthetic blockade to the muscles that support ventilation such as the diaphragm. Bradycardia can develop in this situation but would most likely be delayed and associated with the development of hypoxemia due to apnea. The hemodynamic stability is proposed to occur due to the relatively low sympathetic tone present in an infant compared with chat in an adult. Treatment for total spinal anesthesia in an infantis supportive; this includes supporting ventilation until the spontaneous return of respiratory function takes place. REFERENCES 1. Miller RD. Mille’s Anesthesia. 7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:2532-2534. 2. Afshan G, Khan FA. Total spinal anaesthesia following caudal block with bupivacaine and buprenorphine. Paediatr Anaesth. 1996; 6239-242. EM 7 Clinical scenario: A 115-kg, 68.yearold man presents 40 your preoperative clinic to be evahiated prior to his elective lumbar diskectomy scheduled for tomorrow. He has 2 history of type 2 diabetes, tobacco abuse, and hypercholesterolemia. His blood pressure is 175/90 mm Hg, pulse 75 beats/min, and oxygen saturation 92% on room air. Hlis exercise is severely limited by his back pain. He denies chest pain. His preoperative electrocadiogtam is shown below.Certain findings on an electrocardiogram (ECG) are indicative of acute STeelevation myocardial infarction (STEMI), While ECG findings may vary according to the infarct area, commonalities do exist Depolarization (QRS) and repolarization (ST) abnormalities should be sought, particularly in patients with risk factors for coronary artery disease. A patient, particularly one with diabetes, with a STEML ‘may initially present without significant symptoms. The ECG in this patient demonstrates an evolving inferoposterolateral STEMI, with prominent Q waves, ST elevation, and T wave inversion in the inferior leads along with reciprocal changes as seen in Figure 1. Figure 1. Evolving inferoposterolateral infarction. Note the prominent Q waves in If, Ill ancl VE, along with ST elevation and T wave inversion in these leads, as well as V3 through V6. ST depression in L, VL, VI, and V2 is consistent with a reciprocal change. Relatively cll R waves are also present in V1 and V2. Used with permission, from Libby P, Bonow RO, Mann DL, etal, Braunwald’s Heart Disease: A Textbook of Caxdiovsculay Medicine, 8th ed. Philadelphia, PA: Elsevier Saumders; 2008:Figure 1239, Copyright © Elsevier Inc.All rights reserved. t ave -_t_l,—,—_4 Me Le : ‘When a STEM is suspected, emergency cardiology consultation with notification of cardiac catheterization laboratory personne! should be initiated immediately for definitive diagnosis and possible coronary intervention (Figure 2). Further diagnostic testing, particularly stress testing (ex, dobutamine stress echocardiography), is not recommended in patients with ECG evidence of STEMI due to the resultant delay in tevascularization as well as the associated increase in myocardial oxygen demand, i | iFigure 2. Bvidencebased approach 1 need or catheterization (cath) and revasculaiation after STEML ‘This algorithm shows treatment paths for patents who intially undergo a primary invasive strate, receive “bale the inden ‘apy for STEMI Patients who have not undergo 2 primary iewasive serategy and have no highsrsk features should undergo fonetional evaluation with one ‘of the noninvasive tots shown. When clinically sgnficant ischemia is detected, patients should under catheeerization and revasculariztion as indicated if no clinically significant ischemia is detects, medical therapy is prescribed ater STEML STEMI indicates STelevation myocardial infarction; EF, eection rations OG, clectrocardography. Used with permission, fforn Angman EM, Anbe DT, Armstrong PW, etal American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing ‘Committee t Revise the 1999 Guidelines fr the Management of Paints With Acute Myocardial Infaretion) ACC/AHA guidelines forthe management of patents with STlevation myocardial infartion-excautive summary-areportof the American Collegeof Cardiology/American Heart Associaton Tisk Force on Practice Guidelines (Writing Committe to Revise the 1999 Guidelines for dhe Management of Patients With Acute Myocardial Infarction), Credation, 2004; 11:588-636. Copyright © 2004 American Heart Assocation, Inc » 7 Taye [Lites = ‘ave == wo) fata meer] [ae fees eecee| Tecoma x + Ripe Tae mace #—!of_Aiewcacie | ¥ ate See Oe senet ll oencarise ace | | soit! |PHEO| | Sse |] Barc aaa =] ==}—[ Coronary bypass is not recommended in the setting of an acute STEMI and may even be harmful. The ‘treatment of choice for STEMI is percutaneous intervention, including angioplasty or stenting, in the cardiac catheterization laboratory. In cases where a catheterization laboratory is not immediately available, thrombolytic therapy may be appropriate until intervention can commence. However, in the STEMI population, coronary.teperfusion via percutaneous coronary intervention improves survival and decreases major cardiovascular events compared to thrombolytic therapy. Proceeding with elective surgery during an evolving myocardial infarction is inappropriate.REFERENCES 1. Libby P, Bonow RO, Mann DL, et al. Braunwwald’s Heate Disease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, PA: Elsevier Saunders; 2008:172. 2. O'Connor RE, Brady W, Brooks SC, etal. Part 10: acute coronary syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular (Care. Circulation, 2010; 122:8787-S817. 3. Antman EM, Anbe DT, Armstrong PW, et al; American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarctionexecutive summary: a report of the American College of Cardiology/ American Heart Association Task Force on Practice ‘Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). Circulation, 2004; 110:588-636. iTem 8 Local anesthetics decrease the rate of depolarisation in the fastconduction tissues, including ventricular ‘muscle and Purkinje fibers. Bupivacaine in particular decreases this rate of depolarization more than other local anesthetis, prolonging the recovery phase. The dysthythmogenic nature of bupivacaine occurs as a resul€ of incomplete restoration of sodinm channel activation between beats. Accidental intravascular administration of bupivacaine has resulted in fatal cardiac dysthythmias. A relatively new addition to the treatment of local anesthetic-induced dysrhythmias is the administration of 20% lipid emulsion (ie, Intralipid [Baxter, Deerfield, llinois)). While the exact mechanism is not known, lipid emulsion may extract the lipid soluble bupivacaine from the aqueous plasma, rendering bupivacaine unavailable to tissue. Treatment of cardiac arrest secondary to local anesthetic roxicity includes a 1 mL/kg bolus of Intralipid followed by an infusion of 0.25 mL + kg! * min for 10 minutes, while continuing advanced life support ‘There is no role for propofol, insulin, or caleium administration in efforts to resuscitate from. bupivacaine toxicity. REFERENCES 1. Miller RD. Miller's Anesthesia. 7ch ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010.933-934. 2. Weinberg G, Ripper R, Feinstein DL, et al. Lipid emulsion infusion rescues dogs from bupivacaine- induced cardiac toxicity. Reg Anesth Pain Med. 2003; 28:198-202. 3, Weinberg G, Hertz P, Newman J. Lipid, not propofol, treats bupivacaine overdose. Anesth Analg. 2004; 99:1875- 1876, 4, Resuscitation for cardiac toxicity. LipidRescue Web site: hetps//lipidrescue.squarespace.comy. { |ITEM 9, __Although not originally included in the American Society of Anesthesiologists (ASA) physical status __ classification, since 1993 patients who have been declared brain dead and who are coming to the operating room for organ retrieval for donation are assigned ASA. physical status VI. The current system consists of 6 categories as follows: ‘+ ASA physical status I-A normal healthy patient ‘© ASA physical status IIA patient with mild systemic disease ‘* ASA physical starus III-A patient with severe systemic disease ASA physical starus IVA patient with severe systemic disease that is a constant threat to life ASA physical status VA moribund patient who is not expected to survive without the operation © ASA physical status VI-A declared braindead patient whose organs are being removed for donor purposes REFERENCES 1. Miller RD. Mille’s Anesthesia. Tth ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010:1002~1003, 2, ASA Physical Status Classification System. American Society of Anesthesiologists Web site. https//www.asahq.org/ For Members/Clinicallnformation/ASA-Physical StatusClassification- System.aspx. Accessed February 2012, ITEM 10 Patients with severe mitral stenosis have a propensity for decreased cariac output secondary to diminished ventricular filling during diastole. Specifically, patients with mitral stenosis are dependent on preload and a telatively low heart rate. Adequate preload is necessary for left ventricular filling. However, as many patients with mitral stenosis have elevated pulmonary vascular pressure, careful titration of preload is essential to avoid pulmonary congestion. Invasive monitoring is useful, although the pulmonary artery occlusion pressure will overestimate the actual left ventricular end-diastolic pressure in patients with mitral stenosis. ‘While milrinone may be useful in reducing pulmonary artery pressures, the decrease in afterload in the presence of diminished left ventricular stroke volume may exacerbate hypotension. Maintaining a relatively low heart rate increases diastolic time and improves ventricular filling. Therefore, agents that increase heart rate, including epinephrine and dobutamine, may reduce stroke volume and ultimately cardiac output in patients with mitral stenosis. Similarly, these patients have a fixed obstruction, and may be quite dependent on atrial contraction during diastole; atrial fibrillation and atrial flutter are often poorly tolerated. Increasing afterload with phenylephrine will decrease the abnormal transvalvular pressure gradient between the left atrium and the left venticle, In addition, perfusion pressure will be restored, REFERENCES 1. Kaplan JA. Essentials of Cardiac, Anesthesia. Philadelphia, PA: Elsevier Saunders; 2008.347-352. 2. Frogel J, Galusca D. Anesthetic considerations for patients with advanced valvular heart disease undergoing noncardiac surgery. Anesthesiol Clin. 2010; 28:67-85. 10ITEM 14, The ED, is an important pharmacodynamic principle used to develop dosing strategies to target specific ‘effects and to compare the potency and efficacy of drugs for the specific effect: The ED,, is commonly defined as either the dose to achieve a drug's effect in 50% of the exposed patients or che dose required to achieve 50% of the drug's desited effect. ‘The BD, is not defined as the dose to reach 50% of the steady state serum concentration, nor as the duration of a drug’ effect in 50% of the exposed patients, nor as the time required to achieve 50% elimination of the drug. REFERENCES 1. Batash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 6th ed. Philadelphia, PA: Wolters Kluwer/Lippincote Williams & Wilkins; 2009:151, 2. AlSallami HS, Pavan Kumar WV, Landersdorfer CB, et al. The time course of drug effects. Pharm Stat, 2009; 8:176~185, 3, Kern SE, Stanski DR. Pharmacokinetics and pharmacodynamics of intravenously administered anesthetic drugs: concepss and lessons for drug development. Clin Pharmacol Ther. 2008; 84:153-157. ITEM 12 ‘When performing regional anesthesia, nerve stimulation commonly has been used to identify nerves prior to injection of local anesthetic. Electrical stimulation can result in depolarization of the nerve, which produces muscular contraction (if motor fibers are stimulated) or paresthesias (if sensory fibers are stimulated), Factors that influence whether or not a nerve will respond to an electrical stimulus include total electrical charge (the product of inensity and duration) as depicted in the following equation: QeIxT Where Q> total charge |= stimulus intensity ‘Te stimulus duration ‘The result determines if a nerve will be depolarized (Figure 1), Factors thar determine the minimum stimulation threshold include the theabase (che minimum current intensity necessary to depolarize a nerve) and the chronaxie (the minimum duration of the stimulus when the intensity is twice the theobase). iFigure 1. Stength-duration curve. The curve illustrates the relationship between the ehteshold current aiensity and pulse uration. Used with permission, from Hadi A. Tetbuok of Regional Aneshera and Acute SEE ~ Ra agement New Yorks NY McGrase Hill 2007 Figure 1 igure haw adapted With from Pither CE, Raj PP, Ford D}. The use of peripheral nerve stamulators for regional anaesthesia a review of experimental characteristics, technique, and clinical applications, Reg Anesth Pain Med. 1985, 1049-58, ‘Strength Duration Curve Cat ‘Scale Newe 0 ‘Stimulus Strenght (mA) i ooo 500 ‘Chronaxle Pulse Duration (sec) Different nerves have different minimum stimulation thresholds (Figure 2). The ability to elicit a motor response without inducing pain or paresthesia is due to the fact that the chronaxy in motor nerves (A-alpha fibers) is lower than that of sensory nerves (A-delta and C fibers). Use of a longduration pulse of high intensity will result in depolarization of the nerve even ifthe stimulus is applied at a substantial distance from the nerve (Figure 3). The objective of ensuring that the needle is positioned close to the nerve is defeated by use of a stimulus of high intensity or long duration since a response may be elicited even if the needle is not in the correct position, In addition, stimull of longer duration are more likely o be perceived as painful | Figure 2. Intensity of the stimulating current required to obtain specific visible motor response during interscalene (biceps contractions) and femoral block (quadriceps contractions). Current of longer lueation elicits motor response aca significantly lower current intensity, Used with permission, from Hadsic A. Textbook of Regional Anesthesia and Acute Pain Management. New York, NY: McGraw-Hill, 2007:Figuee 5-2, a igure that was adapted with petmission, from Pither CE, Raj PP, Ford DJ. The use of peripheral nerve stimulators for regional anaesthesia: a review of experimental characteristics, ‘technique, and clinical applications. Reg Anesth Pain Med, 1985; 10:49-58. 2 interscalene 1m Femoral “He ia 12