1. What is the appropriate dose of local anesthetic to a 10 year old, 15 kg girl with a complex scalp laceration a.

10cc 2% Lido (10ccX20mg/cc=200 mg) (15KgX5= 75 mg max) b. 30 cc 0.5% Lido with 1/200,000 epi (30ccX5mg=150 mg) (15KgX7= 105 mg max) c. 20 cc Marcaine 0.5% (20ccX5mg/cc= 100 mg) (15KgX2= 30 mg max) 2. Which of the following is a contraindication to elective surgery: a. COPD with PaCO2 of 45 mmHg b. Subendothelial myocardial infarction 1 month ago. During the 1970s, several studies reported risk of reinfarction / cardiac death: 30% MI. 15% 5% 3 to 6 months after a prior infarction. more than 6 months after the infarction. when patients were operated on within 3 months of previous

Complication rates were subsequently reduced during the 1980s.For example, Rao and colleagues[40] reported only a 6 percent reinfarction rate within 3 months after preoperative myocardial infarction and only a 2 percent re-infarction rate between 3 and 6 months after a myocardial infarction, and they then confirmed these low risks in a subsequent report. The reduction in cardiac morbidity and mortality has been attributed to the use of perioperative monitoring and careful regulation of hemodynamic status, cardiac rhythm, oxygenation, electrolytes, and hematocrit. The presence of preoperative hypoxemia identified those who required mechanical ventilation postoperatively in three studies and intraoperative blood administration was associated with those who required mechanical ventilation and who developed postoperative pneumonia. ( Murray and Nadel text book of respiratory medicine 3rd ed. ) 3. Potential complications of the sitting position during general anesthesia include: 1) Air embolism. 2) Respiratory alkalosis. 3) Hypotension. 4) Excessive scalp bleeding. (1 and 3 are correct). Hazards are associated with the sitting position. Circulatory instability, macroglossia, and quadriplegia are discussed in this section. Venous air embolism, paradoxic air embolism, and pneumocephalus are discussed later in this chapter. I could not find any reference to respiratory alkalosis or scalp bleeding (?). Miller: Anesthesia, 5th ed., 2000, p. 1906-9.

4. The anesthestist has just put the patient in reverse trendelenburg and starts to panic as the BP falls suddenly. You explain to him/her the most likely cause is: a. Bainbridge reflex. b. External compression of IVC. c. Secondary to hypotensive effects of IV induction agents. d. Decreased cardiac contractility. e. Dysfunction of baroreceptors. Baroreceptors: remember that impulses generated in baroreceptors inhibit the tonic discharge of the vasoconstrictor nerves and excite the vagal innervation of the heart, producing vasodilation, venodilation, a drop in blood pressure, bradycardia and a decrease in cardiac output. Orthostatic hypotension disruption of sympathetic nervous system sympathetic vasoconstrictor fibres compensate for the effects of gravity on circulation. Bainbridge Reflex: rapid infusion of blood or saline in anesthetized individuals sometimes produces a rise in heart rate if the initial heart rate is low. It appears to be a true reflex rather than a response to local stretch since it is abolished by bilateral vagotomy, and infusion of fluids in transplanted hearts increases the rate of the recipients atrial remnant but fails to affect the rate of the transplanted heart. The receptors may be the tachycardia-producing atrial receptors. The reflex competes with the baroreceptor-mediated decrease in heart rate produced by volumeexpansion and is diminished or absent when the initial heart rate is high. Lange Medical Books Review of Medical Physiology 17ed ch 31-33 5. Reverse Trendelenberg leads to hypotension. What is the mechanism a. Bainbridge reflex. b. Decreased CO. c. Increased intrathoracic pressure. d. Baroreceptor response. the Bainbridge reflex is an increase in HR due to direct effect of increased atrial volume to stretch the SA node in the right atrium. The stretch receptors of the atria that elicit the Bainbridge reflex transmit their afferent signals through the vagus nerves to the medulla of the brain. Then, efferent signals are transmitted back through both the vagal and the SNS nerves to increase the HR and strength of contraction - thus increasing CO

baroreceptors are stretch receptors located in the walls of the internal carotid arteries (carotid sinus) and aortic arch. Excitation of the baroreceptors by stretch causes arterial pressure to decrease because of signals to the vagus nerve to decrease peripheral resistance and decrease CO. Conversely, low pressure system (decreased stretch) causes the opposite ie. decreased vagal stimulation and increased peripheral resistance and increased CO to maintain pressure. Healthy individuals should NOT experience hypotension due to this reflex

ASIDE: - in trauma, often taught that patients in shock should be placed in Trendelenberg position, BUT this position does NOT promote venous return to the heart - Trendelenberg may interfere with respiratory exchange more than in the supine position - In Trendelenberg, see increased MAP, increased wedge pressure, increased SVR, BUT no change in CO therefore does not promote venous return to the heart Reference: Guyton, Schwartz

6. Regarding PCA : These devices allow adequate continuous pain

relief without undue somnolence. Success with this approach requires careful patient education and close nursing care. Nausea, vomiting, and respiratory depression remain potential side effects. (Schwartz p.681) (By the way, tachyphylaxix= rapid decrease of a medication effect after a few doses.) 7. All of the following are benefits of smoking cessation 6 weeks prior to surgery except a. improved ciliary function. b. decreased airway reactivity. c. decreased co2 retention. d. increased secretion clearance. e. none of the above. The importance of smoking cessation cannot be overemphasized. The annual rate of decline of FEV1 in smokers is approximately 80 ml per year, in contrast to 25 to 30 ml per year in nonsmokers. The Lung Health Study reported that patients who stopped smoking had a small improvement in FEV1 (57 ml) after 1 year. [77] Thereafter, the rate of decline in lung function is similar to age-matched nonsmokers. The short-term success rates with smoking cessation are variable (18-77 percent), but success is more likely if the patient abstains from smoking within the first 2 weeks of entry into a program. The 1994 Lung Health Study showed that patients with only a mild degree of airflow obstruction had accelerated losses of lung function if they continued to smoke. In contrast, those patients who were successful in stopping smoking, most of whom received specialized care for this purpose, had a slight improvement in airflow, followed by a minuscule decline at the end of 5 years (Fig. 96.4) .[72] The obvious conclusion from this landmark study was that smoking cessation can alter the early course and prognosis of COPD. Another interesting finding in the Lung Health Study was the cause of death, which most commonly was lung cancer followed by heart attack, stroke, and all other causes (Table 96.4) . During the course of the 5-year study, no patient died of COPD. Murray & Nadel: Textbook of Respiratory Medicine, 3rd ed., Copyright 2000

Intermittent quitters had less loss of lung function at comparable cumulative cigarette doses than continuing smokers. Interestingly, the shorter-term improvement after quitting or the decrement after relapsing was significantly related to methacholine reactivity, [145] implying that acute airway inflammation contributes to the observed FEV1 fluctuations. Sethi JM - Clin Chest Med - 01-Mar-2000; 21(1): 67-86, viii Cigarette smoking increases perioperative mortality probably because of the effects of smoking on both the cardiovascular and the respiratory systems.[100] Smokers may have increased levels of carboxyhemoglobin as a function of their brand of cigarette, how deeply they inhale, the number of puffs they take, and the level of ventilation present while they are smoking.[101] The level of carboxyhemoglobin in smokers usually ranges from 3% to 15%, and the major effects are to reduce the amount of hemoglobin available to bind with oxygen, thereby decreasing arterial oxygen content, and to shift the oxygen-hemoglobin saturation curve to the left. Smokers have a decreased oxygen delivery and an increased tissue oxygen extraction, manifested by a reduced mixed venous oxygen content.[102] Patients at greater risk for elevated carboxyhemoglobin levels are those who smoke avidly late at night and then undergo an early morning operation. Therefore, it is recommended that smokers stop smoking 12 to 18 hours preoperatively to allow sufficient time (three half-lives) for carboxyhemoglobin clearance. Nicotine has concentration-dependent effects on the cardiovascular system. It can cause systemic vasoconstriction and increases in heart rate and systemic blood pressure. Abstinence from smoking for 20 minutes is followed by decreases in heart rate, blood pressure, and systemic catecholamine levels.[103] These cardiovascular effects of nicotine may contribute to perioperative morbidity in smokers, and short-term abstinence may be beneficial. Several investigators have evaluated postoperative pulmonary complications in smokers.[104] [105] [106] [107] [108] These studies suggest that smoking may be associated with increased pulmonary complications when the patient is older, has smoked longer, is currently smoking, and perhaps already has significant underlying lung disease.[104] [105] [106] [107] [108] Although studies have not always found that a reduction in the quantity smoked or abstinence for a short interval improves perioperative outcomes,[109] patients who stop smoking before or immediately after a percutaneous cardiac revascularization have a lower risk of Q-wave infarctions and death. [110] A smoking intervention program targeted at smokers who are hospitalized for surgery produces higher long-term quit rates.[111] Recommendations suggest at least 12 to 24 hours of preoperative abstinence to achieve possible cardiovascular benefits and perhaps 4 to 6 weeks of preoperative abstinence to decrease the incidence of postoperative respiratory complications.[100] Sethi JM - Clin Chest Med - 01-Mar-2000; 21(1): 67-86, viii

8. A 4 year old boy post appendectomy weighs 15 kg , what is the best

choice of analgesia following an uncomplicated procedure ? a. Acetaminophen 160 mg PO q 4 h. b. Demerol 10 mg IM q 3h. c. Morphine 1.5 mg IV q 3h. d. Codeine 15 mg PO q 4 h prn. e. PCA.

Tylenol in Infants and children < 12 yr: 10-15 mg/kg/dose q4-6h dose in A is insufficient. Demerol : not recommended in kids Scheduled use may result in metabolite accumulation in diminished renal function, which may lead to CNS stimulation or seizures. Morphine dose is correct but IV is not preferred in children. The various physiologic responses of both neonates and fetuses to painful stimuli have been studied, and the results refute a commonly held belief that such patients do not have mature enough nervous systems to sense pain in a manner similar to adults. Despite concern that respiratory depression might result from administration of narcotic analgesics in infants, if the medications are given in the proper dose and with a proper time interval, they have an acceptable safety margin. In our hospital, virtually all-parenteral analgesics are given intravenously. For all patients with an adequate understanding of the administration system, patient-controlled analgesia (PCA) is an excellent method of pain control. There is no fixed age below which PCA is not offered; however, patients below the age of 7 years generally are poor candidates for PCA. Some attempts at parent-controlled analgesia have been made, but the emotional involvement of the parents and their desire to see the child pain- free rather than comfortable has limited the usefulness of that approach. Whenever possible, the use of anesthetic blocks, such as caudal tetracaine for hernias or thoracic epidural blocks for chest surgery, are encouraged. Two to three days of excellent pain relief can be obtained by epidural catheter administration of narcotics and/or local anesthetics, and such patients are monitored closely postoperatively. All pediatric patients having surgery, including circumcision, have pain, and should be given appropriate analgesia by the appropriate route to control that pain. 9. A patient given morphine 15mg post-op and gravol 50mg. He becomes somnolent and has a drecreased RR. The best first action would be: a. Observation. b. Administer naloxone. c. Intubate. d. Give less morphine next time. e. Use a drug other than morphine.

- Naloxone is the antidote for narcotic overdose - Adverse effects of morphine include: respiratory depression (CNS), hypotension (esp in post-op patient), profound sedation or coma - overdose symptoms include: respiratory depression, extreme somnolence, flaccidity of skeletal muscles, bradycardia, hypotension - Treatment: - ABCs first - Naloxone (0.4-2mg IV q2-3min as necessary) first unless in respiratory distress requiring immediate intubation 10.4 year old boy is comatose following a MVA. The appropriate sized endotracheal tube is? a. 2 mm b. 3 b. 4 c. 5 d. 6 Tube size= (age in years/ 4)+4 Anatomic Differences in the Pediatric AirwayImplications in Pediatric Trauma Management Differences Relatively larger tongue, which can obstruct the airway Implications Most common cause of airway obstruction in children May necessitate better head positioning or use of airway adjunct (oropharyngeal [OP] or nasopharyngeal [NP] airway) Larger mass of adenoidal tissues may make nasotracheal intubation more difficult Epiglottis is floppy and more Ushaped Larynx more cephalad and anterior NP airways may also be more difficult to pass in infants <1 year of age Necessitates use of a straight blade in young children More difficult to visualize the cords; may need to get lower than the patient and look up at 45-degree angle or greater while intubating Allows for use of uncuffed tubes in children up to size 6 mm or about 8 years of age Needle cricothyrotomy for the difficult airway versus a surgical cricothyrotomy for the same reason

Cricoid ring is the narrowest portion of the airway Narrow tracheal diameter and distance between the rings, making tracheostomy more difficult

Anatomic Differences in the Pediatric AirwayImplications in Pediatric Trauma Management Differences Implications Shorter tracheal length (4 to 5 cm in Leading to intubation of right newborn and 7 to 8 cm in 18-month- mainstem or dislodgement of the old) endotracheal tube Large airways more narrow Leads to greater airway resistance (R 1/radius4 )

Uncuffed tubes should be utilized in children under 8 years of age, as the narrowest portion of the pediatric airway in this age group is at the level of the cricoid cartilage. Rosen's Emergency Medicine: Concepts and Clinical Practice, 5th Edition, Copyright 2002 Recommended Sizes and Distance of Insertion of Endotracheal Tubes and Laryngoscope Blades for Use in Pediatric Patients RECOMMENDED INTERNAL DIAMETER OF ENDOTRACHEAL TUBE (mm) 2.5 3.0 4.0 5.0 5.5 6.5 7-8

AGE OF PATIENT Premature (<1,250 g) Full term 1y 2y 6y 10 y 18 y

a

SIZE OF LARYNGOSCOPE STRAIGHT BLADE 0 0-1 1 1-1.5 1.5-2 2-3 3

DISTANCE OF INSERTION a (cm) 6-7 8-10 11 12 15 17 19

Inserting the endotracheal tube this distance from the alveolar ridge of the mandible or maxilla places the distal end of the tube in the midtrachea. Miller: Anesthesia, 5th ed., Copyright 2000 11.Which of the following is not correct regarding anesthesia in children? a. Does not require pre-op testing in the majority of cases. b. Pre-op evaluation includes an examination of ears and throat. c. The presence of parents up until OR time increases separation anxiety. d. Is often helped by premedication. e. Requires discussion with the child.

The preoperative visit and preparation of the child for surgery are more important than the choice of premedication. [165] During this time, the anesthesiologist evaluates the medical condition of the child, the needs of the planned surgical procedure, and the psychologic makeup of the patient and family. The anesthesiologist also formulates the approach to induction of anesthesia, explains the possibilities regarding induction, and helps to soothe family concerns. Because anxiety felt by the parents may be transferred to the child, any practice that reduces anxiety in the parents may also reduce anxiety in the child. Therefore, the anesthesiologist should explain in great detail what the child and family can expect and what will be done to ensure the utmost safety. The more information the parents and child have, the more easily they will deal with the stress of surgery and hospitalization After chart review, physical examination, and the furnishing of information regarding the approximate time and length of surgery, the anesthesiologist should describe to the child what anesthesia is and what will be done to ensure good care. The purpose of all monitoring devices should be explained to the patient and family. Children need to understand that none of these devices will hurt and that they can watch during application. If an intravenous line will be started, the child needs to be told that "numbing" medicine will be used. Any special monitoring devices, such as an arterial line, a central venous line, a nasogastric tube or urine catheter, should also be described to the parents, with assurances that these devices will be inserted after induction of anesthesia. Children think in very concrete terms, so care must be taken to avoid misunderstandings. It is important to explain to children that the sleep caused by anesthetic drugs differs from normal sleep. They should know that the anesthesia medicines keep them from awakening during surgery and from remembering the operation. It should also be explained to the children that the anesthesia medicines will be removed at the end of surgery, and that they will then wake up and return to their parents. This type of explanation does not require a significant amount of time and goes a long way toward reassuring the child and family about the quality of care provided. The issue of pain must not be avoided. Children need to be reassured that everything possible will be done to minimize pain on awakening. Therefore, it should be stressed that pain medications will be administered and that local infiltration nerve blocks, patient-controlled analgesia, or continuous epidural or caudal infusions will be used. Recovery room or intensive care must also be described so that there are no surprises. Millers Anesthesia. 12.A child has seizure after injection of 1% lidocaine during an inguinal hernia repair the best initial treatement is : a. Diazepam. b. Midazolam. c. Magnesium. d. Propafol. e. Non of the above secure the airway ( ABC ). Answer A (or E if you emphasize the word initial in the question; then the answer is simply to follow ABCs.good for seizures of any etiology).

From: Wilder RT - Pediatr Clin North Am - 01-Jun-2000; 47(3): 545-58. If a patient cannot or does not warn the physician of the symptoms of impending toxicity, the first sign is seizures. If a seizure occurs, physicians should remember the ABCs of treatment.patent airway. Then, the seizure is treated with an IV dose of thiopental, 2 to 5 mg/kg, or diazepam, 50 mug/kg. For prolonged or difficult seizures, patients are paralyzed with succinylcholine, which not only decreases the systemic acidosis but also allows easier security of the airway. Treated promptly, seizures have no lasting sequelae and do not indicate any potential seizure disorder. If the physicians are not prepared to treat seizures, that is, an IV is not in place, and the seizure is prolonged, neurologic damage may ensue. Prolonged seizures can also cause systemic acidosis and hypoxia, which can worsen the potential for cardiac toxicity. Physicians should be prepared for local-anesthetic toxicity when using large doses of local anesthetics, nearing the limits of toxicity, or injecting even a small amount into a space where the potential for direct IV injection exists. The latter includes virtually all formal nerve blocks. The one situation in which IV injection is not a potential problem is SC infiltration. When making a skin wheal for an IV stick or performing another needle procedure, the amount of local anesthetic used is sufficiently small that it will not cause problems, even if deposited intravenously. When performing a field block, the needle is kept moving during the injection so that it will pass through any veins before a substantial amount of anesthetic is injected. For all other situations, physicians should be prepared to treat potential toxicity. The first part of treatment is avoidance. If a patient is able to respond, he or she is asked to report any symptoms of minor toxicity as the physician injects the material. These signs include ringing in the ears, a metallic taste in the mouth, and numbness of the lips or tongue. If any such symptoms are reported, the injection is stopped immediately. The second aspect of being prepared is to have an IV line in place. Third, the drugs and equipment to be used, including something to stop convulsions and cardiac resuscitation drugs, should be close at hand. Thiopental, a benzodiazepine, atropine, epinephrine, sodium bicarbonate, and calcium gluconate or calcium chloride should be available for resuscitation. A cardiac defibrillator and suction should also be close at hand and ready for use. If a patient cannot or does not warn the physician of the symptoms of impending toxicity, the first sign is seizures. If a seizure occurs, physicians should remember the ABCs of treatment. First and of most importance, the patient's airway is protected. Physicians should not put their fingers into the patients' mouth, however, or they may get bitten. A soft bite block, such as a roll of gauze, is placed to help the mouth stay open and provide a patent airway. Then, the seizure is treated with an IV dose of thiopental, 2 to 5 mg/kg, or diazepam, 50 mug/kg. For prolonged or difficult seizures, patients are paralyzed with succinyl choline, which not only decreases the systemic acidosis but also allows easier security of the airway. Treated promptly, seizures have no lasting sequelae and do not indicate any potential seizure disorder. If the physicians are not prepared to treat seizures, that is, an IV is not in place, and the seizure is prolonged, neurologic damage may ensue. Prolonged seizures can also cause

systemic acidosis and hypoxia, which can worsen the potential for cardiac toxicity. Finally, if a large dose of local anesthetic is given rapidly and intravenously, cardiac toxicity may occur. This is worst with bupivacaine or etidocaine but may occur with any local anesthetic in sufficiently high doses. Cardiac toxicity is usually in the form of dysrhythmias, primarily ventricular contractions, or fibrillation. Again, physicians should remember their ABCs: secure the airway, provide respiration with 100% oxygen, and start artificial circulation. Epinephrine is used to treat hypotension, and defibrillation is begun as soon as possible. If this is ineffective, bretylium, 5 mg/kg IV per dose to a maximum of 30 mg/kg, is given Bretylium is more effective than lidocaine for the treatment of bupivacaine-induced cardiac toxicity Pediatric Clinics of North America Volume 47 Number 3 June 2000 13.A 60 y.o. female, with severe emphysema, is seen in the ER for suspected sepsis. After the initial assessment, she becomes agitated and is given 10mg of diazepam IV. 30 min. later, she is found stuporous and her ABGs show : pCO2 80, pO2 60. What is the next step in treatment? a. O2 by mask. b. Dexamethasone. c. Intubate. I dont know if there is an option to reverse her with flumazinil. But I think intubation is the safest thing to do. 14.Several weeks following a major multiple trauma, succinylcholine is C/I because : a. Hyperkalemia will result because the motor end plate is more sensitive to depolarizing agents. b. Hyperkalemia will result because of calcium release from the sarcoplasmic reticulum. 15.Why does succinylcholine cause hyperkalemia in patients with burns and trauma? a. Due to increased sensitivity to depolarizing muscle relaxant. b. Due to increased calcium release from the ER. c. Etc Hyperkalemia The administration of succinylcholine to an otherwise well individual for an elective surgical procedure increases plasma potassium levels by approximately 0.5 mEq/L. This increase in potassium is due to the depolarizing action of the relaxant. With activation of the acetylcholine channels, movement of sodium into the cells is accompanied by movement of potassium out of the cells. This slight increase in plasma potassium levels is well tolerated by individuals and generally does not cause dysrhythmias. Several early reports suggested that patients in renal failure may be susceptible to a hyperkalemic response to succinylcholine.[105] [106] [107] Nevertheless, more controlled studies have shown that renal failure patients are no more susceptible to an exaggerated

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response to succinylcholine than are those with normal renal function. [108] [109] [110] [111] [112] One might postulate that patients who have uremic neuropathy may be susceptible to succinylcholine-induced hyperkalemia, although evidence supporting this view is scarce.[107] [112] Severe hyperkalemia may follow the administration of succinylcholine to patients with severe metabolic acidosis and hypovolemia.[113] In rabbits, the combination of metabolic acidosis and hypovolemia results in a high resting potassium level and an exaggerated hyperkalemic response to succinylcholine. [114] In this situation, the potassium originates from the gastrointestinal tract and not from muscle, as in the classic hyperkalemic response.[115] In patients with metabolic acidosis and hypovolemia, correction of the acidosis by hyperventilation and sodium bicarbonate administration should be attempted before administration of succinylcholine. Should severe hyperkalemia occur, it can be treated with immediate hyperventilation, 1.0 to 2.0 mg calcium chloride intravenously, 1 mEq/kg sodium bicarbonate, and 10 U regular insulin in 50 mL 50% glucose for adults or, for children, 0.15 U/kg regular insulin in 1.0 mL/kg 50% glucose. Kohlschtter and colleagues[116] found that four of nine patients with severe abdominal infections had an increase in serum potassium concentrations of as much as 3.1 mEq/L above baseline values after succinylcholine administration. These investigators found that in the case of intra-abdominal infections that persist for longer than 1 week, the possibility of a hyperkalemic response to succinylcholine should be considered. Stevenson and Birch[117] described a single, well-documented case of a marked hyperkalemic response to succinylcholine in a patient with a closed head injury without peripheral paralysis. In studying soldiers who had undergone trauma during the Vietnam War, Birch and associates[118] found that a significant increase in serum potassium did not occur in 59 patients until about 1 week after the injury, at which time a progressive increase in serum potassium occurred after the infusion of succinylcholine. Three weeks after injury, three of these patients with especially severe injuries showed marked hyperkalemia with an increase in serum potassium of greater than 3.6 mEq/L, sufficient to cause cardiac arrest. Birch and coworkers[118] found that prior administration of 6 mg dTc prevented the hyperkalemic response to succinylcholine. In the absence of infection or persistent degeneration of tissue, a patient is susceptible to the hyperkalemic response probably for at least 60 days after massive trauma or until adequate healing of damaged muscle has occurred.

In addition, patients with any number of conditions that have resulted in the proliferation of extrajunctional acetylcholine receptors, such as those with neuromuscular disease, are likely to have an exaggerated hyperkalemic response after the administration of succinylcholine. The response of these patients to neuromuscular blocking agents is reviewed in detail later in this chapter. Some of these disease states include cerebrovascular accident with resultant hemiplegia or paraplegia, muscular dystrophies, and Guillain-Barr

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syndrome. The hyperkalemia after administration of succinylcholine may be to such an extent that cardiac arrest ensues. For an in-depth discussion of the clinical and

pathophysiologic aspects of succinylcholine-induced hyperkalemia, the reader is referred to a review by Gronert and Theye.[119] Miller's Anesthesia, 6th ed **The mechanism is by translocation of potassium from the cells into the ECF and burns and trauma are well documented contraindications to using succinylcholine. This is from an anesthesia text available online through the CMA Clinical reports and experimental studies have clearly shown that, in patients with certain diseases or conditions, an exaggerated release of potassium in response to succinylcholine may occur, occasionally of such magnitude that cardiac arrest ensues. [66D] [66G] Conditions that render the patient especially susceptible to the hyperkalemic response from succinylcholine are burns, trauma, nerve damage, neuromuscular disease, closed head injury, intra-abdominal infections, and renal failure. Then in an anesthesia journal I found that the increase is due to upregulation of acetylcholine receptors in the area of the burn due to immature tissue beneath the eschar so I think the answer is A. GREAT CAUTION should be observed if succinylcholine is administered to patients during the acute phase of injury following major burns, multiple trauma, extensive denervation of skeletal muscle, or upper motor neuron injury . The risk of hyperkalemia in these patients increases over time and usually peaks at 7-10 days after the injury. Mosby's Drug Consult Copyright 2002. The prolonged depolarization produced by succinylcholine is accompanied by a large efflux of potassium out of muscle cells, and this results in a transient rise in serum potassium of 0.5 to 1.0meq/L. Life-threatening increases in serum K have been recorded in patients with acute neurologic injury and burns. (ICU book).

16.The BEST way to administer analgesia post-operatively in a morbidly obese female post-thoracotomy is: a. continuous IV narcotic. b. Nurse gives IV bolus narcotic PRN. c. Nurse gives IM narcotic PRN. d. Epidural analgesia. e. Background PO narcotic with nurse gives IM narcotic for breakthrough pain. 17.Contraindication to nasotracheal intubation : a. Basal skull fracture. b. NG tube in place.

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18.What system is most commonly effected by lidocaine toxicity? a. Cardiovascular b. Neurological c. Respiratory d. Musculoskeletal e. Renal 19.Which of the following is true about the side effects of local anaesthetics: a. cardiac side effects prior to neurologic side effects b. increased by use of epinephrine Complications of LA : Neuro : (general inhibition follows excitation), tinnitus, metal taste, dizziness, seizures, coma. Neuro side effects arise prior to cardiac side effects. CNS manifestations are excitatory and/or depressant. The excitatory manifestations may be very brief or may not occur at all, in which case the first manifestation of toxicity may be drowsiness merging into unconsciousness and respiratory arrest. Drowsiness following the administration of lidocaine is usually an early sign of a high blood level of the drug and may occur as a consequence of rapid absorption. Mosby's Drug Consult Copyright 2002 Cardiac : more resistant than CNS, bupivicaine 70X more cardiotoxic than xylocaine xylo : ST, SVT, myocardial depression bupi : SVT, AV block, PVCs, VT, Widened QRS, myocardial depression toxicity increases with : high PCO2, low pH, high serum K Epinephrine decreases the side effects. 20.Best therapy for treatment administration? a. Diazepam IV. of seizures following lidocaine

All local anesthetics have a similar toxicity profile. CNS effects include lightheadedness, tongue numbness, and restlessness at low levels, progressing to perioral paresthesias, slurred speech, and excitability or drowsiness at higher levels, to seizures and coma with respiratory arrest and cardiovascular depression in severe toxicity. Cardiovascular effects include palpitations, cardiac dysrhythmias (particularly bupivacaine), hyper- or hypotension, and cardiovascular collapse. Treatment for seizures is symptomatic, with IV benzodiazepines as the treatment of choice. Cardiac dysrhythmias are more difficult to treat, and fatalities have been reported, particularly with bupivacaine. Anesthesiology Clinics of North America Volume 18 Number 2 June 2000 Copyright 2000 W. B. Saunders Company

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21.Halothane anesthesia has been shown to be unrelated to massive postop hepatic necrosis and is safe to use in hepatobiliary surgery. Repeated exposures to halothane over short periods, however, may cause mild hepatitis, though the incidence is extremely low. Hepatitis may be caused by an allergic reaction. It is associated with eosinophilia, and more severe liver dysfunction follows repeated exposure to halothane or one of its metabolites. The incidence of spontaneous abortion in female operating room personnel is 1 1/2-2 times the normal rate, but whether this is due to inhalation of trace concentrations or to other aspects of their work is not known. Thousands of OR personnel are chronically exposed to trace concentrations of inhaled anesthetics; this is a concern because of potential mutagenicity, teratogenicity, and carcinogenicity. However, there has been no demonstrated cause-and-effect relationship. Current p.184-185

22. 25 mls of a 2% lidocaine solution contains how much lidocaine :

a. b. c. d. e. 5 mg 10 mg 50 mg 100 mg 500 mg

23.

Of the following anesthetic agents, which of the following is not an ester : a. Procaine b. Lidocaine c. Tetracaine d. Cocaine e. All of above

Local Anesthetic Molecule : The typical local anesthetic molecule, exemplified by lidocaine and procaine , is a tertiary amine attached to a substituted aromatic ring by an intermediate chain. The tertiary amine is a base (proton acceptor). The chain always contains either an ester or amide linkage; local anesthetics may therefore be classified as amino-ester or amino-amide compounds. The aromatic ring system gives a lipophilic character to its portion of the molecule, whereas the tertiary amine end is relatively hydrophilic, particularly because it is partially protonated and thus bears some positive charge in the physiologic pH range. Lidocaine, for example, is 65 percent protonated at pH 7.4.

Ester-type agents include procaine, chloroprocaine, cocaine, and tetracaine. The amide-type agents include lidocaine, mepivacaine, prilocaine, bupivacaine (Marcaine), and etidocaine. The main difference between esters and amides is their metabolic pathways. Esters are hydrolyzed by plasma pseudocholinesterase, whereas amides are metabolized in the liver through enzymatic degradation. Within the ester or amide group, alterations in chemical structure to either the aromatic or the hydrophilic portion may affect the rate of metabolism and create a different activity profile for each agent within a given group. Chemically, local anesthetics are poorly soluble weak bases. To be commercially available in solution, an agent is combined with hydrogen chloride to produce the salt of a weak acid. In the resulting acidic solution, salts exist both as uncharged molecules (nonionized) and as positively

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charged cations (ionized). The uncharged form is lipid soluble, enabling it to diffuse through tissues and across nerve membranes, which the charged form cannot do. The ratio of uncharged to charged forms depends on the pH of the medium (vial solution or tissue milieu) and on the pKa of the specific agent. The pKa is the pH at which 50% of the solution is in the uncharged form, and 50% is in the charged form. Because the pKa is constant for a specific agent, the relative proportion of these forms is dependent on the pH of the solution in accordance with the HendersonHasselbalch equation: pH = pKa + log [uncharged]/[charged] When the pH of the solution or tissue decreases, a given agent exists more in its ionized, charged form; conversely, when a pH increases, the agent exists more in its nonionized, uncharged form. Because the nonionized portion is the form of drug that can diffuse through tissues and nerves, manipulation of the pH of the solution is a useful tool for the physician.

24. A 4 year old boy, 25kg, scalp laceration how much lidocaine : a. 10 ml of 1% xylo b. 10 ml of 2% xylo
c. 30 ml of 1% xylo with epi d. 15 cc of 0.5% marcaine e. 25cc of 0.5% marcaine 1 ml xylocaine 1% 1ml xylocaine 2% 1ml of 0.5% marcaine = = = 10 mg of xylocaine 20 mg of xylocaine 5 mg of marcaine

xylocaine max. dose is 4 mg/kg for plain and 7 mg/kg with epi bupivacaine max dose is 2 mg/kg and 2 - 3 mg/kg with epi 25X 4= 100mg is the maximum xylocaine that can be used 25X7= 175mg is the max. xylo with epi. If using bupivacaine, the maximums will be respectively 25X2=50mg and 25X2 3=50mg to 75mg Note : marcaine is not recommended in children <2 years of age ( CPS under Xylocaine and marcaine )

25. What is the maximum lidocaine dose you can use in a 20kg boy
using a. b. c. d. e. 1% lidocaine with 1:100 000 epi: 6cc 8cc 10cc 12cc 14cc

26. A patient receives spinal anesthesia the surgeon requests the patient to be placed in trendelenburg position and the patient the patient become hypotensive the most likely cause is a. Anaphylactic shock. b. Sympathetic block.

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c. Injection of the anesthetic into a spinal artery. d. Aorta/inferior Vena Cava injury. e. Non of the above. Answer B. From: Sabiston, 16th ed., p. 277. Complications of subarachnoid block include hypotension (sometimes refractory), postdural puncture headache, transient radicular neuropathy, backache, urinary retention, infection, epidural hematoma, and excessive cephalad spread resulting in cardiorespiratory compromise. Frank neurologic injury, although recently described with continuous techniques using small-bore catheters, is rare. Hypotension, occurring as a consequence of sympathectomy, usually responds readily to fluids and small doses of pressors, such as ephedrine. Spinal anesthesia, or subarachnoid block, has many applications for urologic, lower abdominal, perineal, and lower extremity surgery. Spinal anesthesia is induced by injection of local anesthetic, opiates, or both into the subarachnoid space. A well-performed subarachnoid block provides excellent sensory and motor blockade below the level of the block. The block generally has a relatively rapid and predictable onset. Several factors determine the level, speed of onset, and duration of spinal blocks.

1. Local anesthetic agent. Local anesthetics have varying potencies,

durations of action, and speeds of onset after subarachnoid administration (Table 16-8) . These properties are determined by the lipid solubility, protein binding, and pK a , respectively, of each agent. Volume and dose of local anesthetic. Increasing the dose generally increases the extent of cephalad spread and duration of subarachnoid block. In one study, 18 volunteers received one of three doses (4, 8, or 12 mg) of bupivacaine and one of three doses of ropivacaine for subarachnoid analgesia. Ropivacaine is half as potent and in equipotent doses has a similar profile with a higher incidence of side effects (such as a 28% incidence of pain on injection). [88] Rapidly injecting local anesthetic solutions leads to turbulent flow and unpredictable spread. Patient position and local anesthetic baricity. Local anesthetic solutions can be prepared as hypobaric, isobaric, and hyperbaric solutions. Cerebrospinal fluid (CSF) has a low specific gravity (i.e., similar to that of water). Local anesthetic solutions prepared in water have a slightly lower specific gravity than CSF and ascend within the CSF. Plain local anesthetic solutions are isobaric, and local anesthetics mixed in 5% dextrose are hyperbaric relative to CSF. The baricity of the local anesthetic solution and the position of the patient at the time of injection and until the local anesthetic firmly binds to nervous tissue determine the level of block. For example, administration of hyperbaric bupivacaine at the low lumbar level to a patient in the sitting position results in an intense lumbosacral block. The cephalad spread of the block is determined by how long the patient remains in the sitting position. Vasoconstrictors. The addition of epinephrine, particularly to shortacting local anesthetics, increases the duration of action. Addition of opioids. In eight volunteers undergoing subarachnoid anesthesia in a cross-over design, the addition of 20 mug of

2.

3.

4. 5.

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fentanyl to plain 5% lidocaine in dextrose prolonged the duration of analgesia and increased the duration of tolerance for tourniquet pain by 48%. [83] 6. Anatomic and physiologic factors. Anatomic factors that decrease the relative volume of the subarachnoid space, such as obesity, pregnancy, increased intra-abdominal pressure, prior spine surgery, and abnormal spinal curvature, can result in a higher than expected level of spinal anesthesia. Elderly patients tend to be more sensitive to intrathecally injected local anesthetics. Spinal anesthesia provides the advantage of avoiding manipulation of the airway and the potential complications of tracheal intubation as well as the potential side effects of general anesthetics, including nausea, vomiting, and prolonged emergence or drowsiness. Spinal anesthesia also provides advantages for several types of surgery, including endoscopic urologic procedures, particularly transurethral resection of the prostate, in which an awake patient provides a valuable monitor for assessment of hyponatremia or bladder perforation. Less confusion and postoperative delirium have been reported in elderly patients after repair of hip fractures under spinal anesthesia. Intrathecal opiate administration can provide high-quality postoperative analgesia for patients undergoing abdominal, lower extremity, urologic, and gynecologic procedures. In most cases, spinal anesthesia is administered as a single bolus injection. Therefore, the block is of limited duration and is not suitable for prolonged procedures. The practice of continuous spinal anesthesia using small-bore catheters has been largely abandoned because of neurologic complications associated with local anesthetic toxicity. Four cases of cauda equina syndrome were reported, three with 28-gauge catheters and 5% lidocaine and one with tetracaine through an epidural catheter that had inadvertently been placed subdurally. [103] However, continuous spinal anesthesia with relatively large-bore epidural catheters can provide the advantages of incremental titration and the ability to administer additional doses in selected elderly patients. Unfortunately, this technique has a high likelihood of inducing a postdural puncture headache in young patients. Complications of subarachnoid block include hypotension (sometimes refractory), postdural puncture headache, transient radicular neuropathy, backache, urinary retention, infection, epidural hematoma, and excessive cephalad spread resulting in cardiorespiratory compromise. Frank neurologic injury, although recently described with continuous techniques using small-bore catheters, is rare. Hypotension, occurring as a consequence of sympathectomy, usually responds readily to fluids and small doses of pressors, such as ephedrine. Sabiston , 16th edition. Pharmacologic sympathectomy with local anesthetics is a very effective way of inducing hypotension. Epidural or spinal anesthesia produces arteriolar and venous dilation and hypotension. These effects are enhanced by a pooling of blood in the venous system that decreases venous return and cardiac output. If the block is extended to the midthoracic region, sympathetic innervation of the heart (T1-T4) is also affected, thereby preventing compensatory tachycardia. [37] The unpredictable degree of hypotension and the necessity for large infusions of fluids are the principal drawbacks of this technique. It was recently

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demonstrated, however, that if hemodynamic stability is maintained by intravenous infusion of low-dose epinephrine (1-5 mug/min), this technique can be used safely. [25] [35] An epidural anesthetic technique is most commonly used to minimize blood loss during lower abdominal or pelvic surgery. Miller anesthesia. 27.Which drug is necessary in the treatment of malignant hyperthermia? a. Halothane. b. Dantrolane. c. Succinaylcholine. d. Pancuronium. e. Lidocaine. Discontinuation of the trigger may be adequate treatment for acute MH if the onset is slow or if there was a brief administration of the trigger. However, if MH is fulminant (i.e., Pa CO2 greater than 60 mm Hg and increasing, mixed venous P CO2 greater than 90 mm Hg and increasing, base deficit greater than 5 mEq/L and falling, and temperature increasing 1C/15 min), then adequate therapy is urgently needed for survival. In some patients, cardiac output falls rapidly, and there are minor metabolic and acid-base changes because of minimal tissue perfusion. This can result in rapid demise. Dantrolene is the specific therapeutic drug, but it must be given while adequate muscle perfusion is present. [13] [31] It is also important to use symptomatic therapy to control body temperature, acid-base balance, and renal function. Adjunctive drugs are seldom necessary if proper treatment is begun soon enough. Dantrolene rapidly halts the increases in metabolism and secondarily results in a return to normal levels of catecholamines and potassium. [12] [13] The homeostatic mechanisms of the body then rapidly restore arterial blood pressure, heart rate, and sympathetic hyperactivity back toward normal. Malignant hyperthermia is a myopathy, usually subclinical, that features an acute loss of control of intracellular calcium (Ca 2+ ). Dantrolene is therapeutic because it reduces Ca2+ release from the SR without altering Ca2+ re-uptake. ( Miller anesthesia ) 28.A patient has a brother who had a reaction to a general anesthetic that sounds like malignant hyperthermia. The best agent to use for this operation would be? a. An amide (this is safe, but not sufficient for general anaesthesia). b. Succinyl choline. c. Halothane. d. Isofluorane. e. Thiopental (a barbiturate). 29.Which of the following anesthetics do not cause malignant hyperthermia:

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a. b. c. d. e.

Amide local anesthetics. (can cause) Enflurane. Ester local anesthetics. Pancuronium. Succinaylcholine.

Anesthesia should consist of nitrous oxide, barbiturates, etomidate, propofol, opiates, tranquilizers, and/or nondepolarizing muscle relaxants. Potent volatile agents, such as halothane, enflurane, sevoflurane, desflurane, and isoflurane, and the depolarizing muscle relaxants, such as SCh, must be avoided, even in the presence of dantrolene. Some human patients have experienced a hypermetabolic state despite these precautions; however, these patients have always responded favorably to intravenous dantrolene. [16] The consensus is that in most instances, preoperative dantrolene is not needed in susceptible patients because the use of non-triggering agents is almost always associated with uneventful anesthesia. If used, the dose is 1 to 2 mg/kg given intravenously just before induction. This approach avoids the side effects of lengthy pretreatment. Miller: Anesthesia, 5th ed., Copyright 2000 TABLE 27-2 -- Drugs in Patients Susceptible to Malignant Hyperthermia UNSAFE Volatile anesthetics Desflurane Enflurane Halothane Isoflurane Sevoflurane
[110] [31]

SAFE Amide anesthetics Barbiturates Calcium

[42] [12] [13] [42] [15] [31]

Dantrolene

Digitalis drugs Epinephrine Etomidate Ketamine

[10] [82] [83] [31] [64]

Ester anesthetics Cyclopropane Ether

[3] [91]

Relaxants Succinylcholine Cautious use: Dantrolene in combination with calcium antagonist [37] [38] [39] [40] [41]

Nitrous oxide

[31] [89]

Nondepolarizing relaxants [87] (except curare, a weak depolarizer [90] ) Norepinephrine

[62] [63] [64]

Opiates [31] Propofol [94] [95] Tranquilizers in general (except chlorpromazine)

The incidence of malignant hyperthermia is estimated to be approximately 1 in 100,000 general anesthetic procedures. The syndrome consists of a rapid rise in body temperature, usually during the initiation of a general anesthetic after administration of succinylcholine or potent inhalation

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agents, particularly halothane. Metabolic acidosis and electrolyte imbalances quickly develop, with associated hypercalcemia. In most patients there is hypotonicity of skeletal muscle resulting in the acidosis. The final stages of the event are marked by temperatures approaching 42C, oxygen desaturation, hypercapnia, and cardiac dysrhythmia. Prevention is the safest method of limiting the risk to susceptible patients. A family history of complications associated with anesthetics is a warning of this possibly lethal complication. Once the syndrome unfolds, dantrolene is administered intravenously in a dose of 1 mg/kg and repeated as necessary to a total dose of 10 mg/kg. Support measures are initiated promptly, including positive pressure ventilation on 100 percent oxygen, correction of the acidosis and electrolyte imbalance, cooling blankets, monitoring of urine output, and treatment of possible myoglobinuria. After the acute episode, oral administration of dantrolene up to 1 to 2 mg/kg four times a day may be necessary for 1 to 3 days to prevent recurrences.

30.Which of the following local anaesthetics has vasoconstrictor properties? a. Bupivicane. b. Cocaine. c. Lidocaine. Cocaine is pyrogenic, augmenting heat production in stimulating muscular activity and causing vasoconstriction which decreases heat loss. Cocaine is known to interfere with the uptake of norepinephrine by adrenergic nerve terminals, producing sensitization to catecholamines, causing vasoconstriction and mydriasis. Mosby's Drug Consult Copyright 2002.

31. A young healthy patient is brought into the operating room and
becomes drowsy and hypoxic with a decreased respiratory rate. The most likely cause is? a. Pulmonary embolism. b. Pneumothorax. c. Pre-operative sedation. d. Cardiac insufficiency. e. Upper airway obstruction. 32.A person who is ASA III is likely : a. Expected to die imminently. b. Suffering severe major medical illness. c. Healthy. d. Asymptomatic systematic disease. e. Suffering symptomatic systemic disease. ASA is related to the anesthetic risk class : I Perfectly healthy patient II Mild systemic disease, no functional limitations III Severe systemic disease, definite functional limitation but not incapacitating

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IV Severe systemic disease that is a constant threat to life V Deathly ill, not expected to survive greater than 24hours

33. With respect to regional and general anaesthetics: a. GA is preferred for long cases. b. GA is preferred for a patient with known ischemic heart
disease. patient. Choice of anaesthetic depends on: 1- patient factors: - medical status, preferences 2- surgical factors: - dermatomes to be covered, length of procedure, position, complexity, cost of patient movement is regional or local anaesthetic safer than GA no evidence in the healthy population, no evidence in cardiac population relative contraindication to local or regional anaesthesia is uncooperative patient (confused or agitated) Reference: Dr. Raymer POS anaesthesia session 34.Which anaesthetic has the shortest duration of action, making it the preferred drug for use in outpatient surgery: a. Thiopental. b. Versed. c. Propofol. d. Isoflurane. Thiopental acts within 20s, duration 5-15 minutes Versed acts within 3-6 minutes, duration 30min-2h Propofol acts within 40s, duration 5-8 minutes Isoflurane induction agent 35. A patient has been on prednisone 20mg od for two weeks for an asthma exacerbation. For his perioperative care, he should recieve: a. Fludrocortisone b. Hydrocortisone 100mg IV tapering over 3 days c. This dose of prednisone is not enough to suppress pituitary function d. Hydrocortisone 50 mg IV od for 7 days The Patient Taking Corticosteroids Primary adrenal insufficiency (Addison's disease) is quite uncommon, as is secondary adrenal insufficiency on the basis of an intrinsic deficit of corticotropin. Adrenal suppression by exogenous corticosteroid administration is, on the other hand, quite prevalent. Patients who receive potentially suppressive doses of exogenous corticosteroids are most often those with severe dermatoses, inflammatory rheumatologic conditions, hematologic or lymphoproliferative disorders, or asthma or other forms of COPD. Individuals who have received more than 40-mg prednisone per day, or its equivalent, for more than 1 week in the preceding year are at risk of adrenal suppression. Smaller doses of oral corticosteroids administered for longer periods, and even the inhaled corticosteroids

c. Regional anaesthesia is preferred for the confused, agitated

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employed now as mainline therapy in the management of reactive airways disease, may also result in adrenal suppression. Of note in this regard is the recent report of a small randomized trial of preoperative patients maintained on oral prednisone with evidence of adrenal suppression on cosyntropin stimulation test. Patients all received their usual prednisone dose and were randomized to either supplemental stress doses of hydrocortisone in saline, or saline alone. No differences were noted in perioperative hypotension or tachycardia.[6] Due to small sample size, the power of this study is limited. Alternate-day administration of relatively low doses of oral corticosteroids (less than 20-mg prednisone equivalent) reduces the risk of suppression. Long-term treatment with very low doses of corticosteroids (less than 5 mg per day prednisone equivalent) is also associated with a low likelihood of adrenal suppression.Until more data are available, the goal of perioperative management for patients with known or suspected adrenal suppression remains the provision of sufficient exogenous corticosteroid to match the maximal physiologic output caused by the stress of surgery and anesthesia. This has been established at 300to 400-mg cortisol equivalent in the first 24 hours after general anesthesia and major surgery. Hydrocortisone sodium succinate or hydrocortisone sodium phosphate should be employed preferentially to achieve combined glucocorticoid and mineralocorticoid effects. Protocols using the intramuscular route of administration have demonstrated variable effectiveness. Repeated intravenous boluses or combined bolus and infusion protocols are the most reliable means of supporting patients through surgery. Up to 40% of bolus-administered hydrocortisone may be lost in the urine. See Box 13-10 for management points on the patient taking corticosteroids Box 13-10. Management Points: Patient Taking Corticosteroids Suspected adrenal suppression may be excluded by a normal response to a cosyntropin stimulation test performed preoperatively . If adrenal suppression is confirmed or is suspected in a patient who requires surgery urgently or in whom a cosyntropin stimulation test has not been performed, the following apply: When possible, a priming dose of hydrocortisone (100 mg) may be administered orally, intramuscularly, or intravenously at midnight before the patient's surgery. Administer hydrocortisone sodium succinate or hydrocortisone sodium phosphate, 100 mg, intravenously on call to the operating room and every 6 to 8 hours thereafter for 24 hours. After initial bolus, an infusion of hydrocortisone at 10 mg per hour may be substituted for repeated boluses. After complicated or prolonged surgery, consider extending stress-dose steroid coverage with hydrocortisone, 50 mg, every 6 to 8 hours on postoperative day 1 and hydrocortisone, 25 mg, every 6 to 8 hours on postoperative day 2. For intraoperative or postoperative hypotension include intravenous bolus administration of hydrocortisone, 50 to 100 mg, in the treatment regimen.

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TABLE 25-7 -- Relative Potency and Equivalent Doses for Commonly Used Glucocorticoids RELATIVE GLUCOCORTICOID POTENCY 1.0 0.8 4.0 4.0 5.0 5.0 EQUIVALENT GLUCOCORTICOID DOSE (mg) 20.0 25.0 5.0 5.0 4.0 4.0

STEROIDS Short-acting Cortisol (hydrocortisone) Cortisone Prednisone Prednisolone Methylprednisolone Intermediate-acting Triamcinolone Long-acting Betamethasone Dexamethasone

25.0 30.0

0.60 0.75

36.An adjustment of lidocaine dose is necessary in a patient with which one of the following: a. Hepatic insufficiency. b. Renal insufficiency. c. Patient with congestive heart failure. d. Respiratory insufficiency. e. Patient on propranolol. Im actually not sure what the answer is. In the Physicians Drug Handbook pg 566-567: Metabolism: lidocaine is metabolized in the liver to 2 active metabolites. Less than 10% of a parental dose escapes metabolism and reaches the kidney unchanged. Metabolism is affected by hepatic blood flow, which may decrease after MI and CHF. Liver disease also may limit metabolism. Use cautiously in the elderly; patients with renal or hepatic disease, complete or 2nd degree heartblock, sinus brady or CHF. Concomitant use of lidocaine with betablockers may cause lidocaine toxicity from reduced hepatic clearance. Comcomitant use with other antiarrhythmic agents, including phenytoin, procainamide, propranolol and quinidine, may cause additive or antagonist effects as well as additive toxicity. However, no guidelines are given for adjusting the dose. Any thoughts? 37.In pediatric surgery, which is true for infants? a. Having parents come to the OR increases separation anxiety. b. Infants require IV fluids during the 6 hours they are NPO. c. No preoperative testing is required.

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while infant is NPO, require maintenance fluids for sensible and insensible losses for 24 hours: 100ml/kg for upto 10kg for ml/hr: 4ml/kg/hr for upto 10kg 50ml/kg from 11 to 20kg 2ml/kg/hr for 11-20kg 25ml/kg for each additional kg 1ml/kg/hr for each add kg use 5% dextrose in or 1/3 normal saline I have no idea about option a) but if this question requires only one answer, then answer b) makes the most sense

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