(A) Anaphylactic Reaction
(B) Ventricular Ischemia
(C) Pneumothorax
(D) Pulmonary Edema
(E) Septic Shock

B. 1. Ventricular ischemia is apparently leading to decreased cardiac output and congestive heart failure, as evidenced by the hypotension, elevated wedge, and elevated pulmonary artery pressures. 2. Pulmonary edema itself would result from such ischemia but would not explain (by itself) the hemodynamic changes and specifically the elevated pulmonary capillary wedge pressure.

2. K type (Remembered Question)
A 2500 gm infant, 12 hours old, undergoing repair of an omphalocele develops tachycardia to 160, decreased blood pressure to 60/15, difficulty ventilating, and decreased urine output. Appropriate therapy at this time

(1) increase depth of anesthesia
(2) additional dose of muscle relaxant
(3) give bolus D5 1/2 NS
(4) tell surgeon to forego primary closure

D.
1.  Increased abdominal pressure is apparently causing
decreased compliance, decreased venous return, and even
decreased renal perfusion.  Primary closure will not be possible
at this time.
2.  Let's review this important topic from the Big Blue Book.
3.  Omphalocele and gastroschisis (These considerations also
apply to NEC)
     a.  An omphalocele, herniation of the abdominal viscera into
     the base of the umbilical cord, has a sac.  It is caused when
     the gut fails to return to the abdominal cavity at about the
     tenth week of life.
          1)  The frequency of associated defects with omphalocele is
          twice as great as with gastroschisis.  We must always
          consider the presence of congenital heart defects with both
          groups of patients.
     b.  Gastroschisis is when the abdominal wall eviscerates
     through a defect beside (lateral to) the umbilical cord.
     There is no membrane covering of intestinal contents.  It is
     simply an evisceration through the abdominal wall.  It is
     due to intrauterine disruption of the omphalo-mesenteric
     artery.  Hypovolemia secondary to large intestinal fluid loss
     is generally more severe with gastroschisis than with
     omphalocele.
     c.  Important problems in both of these conditions are:
     HAD --hypothermia, acidosis, and dehydration, depression
     of respiration and consciousness.
     d.  What about a CVP in these patients?
          1)  It is somewhat controversial.
               a)  Adequate assessment of intravascular volume status
               can be made on the basis of intraoperative urine output
               and the character of the art line tracing and the
               development of hypotension.  In addition, the risks of
               placement of this monitor are greater in the pediatric
               population.
               b)  Dr. Berry does recommend the placement of a central
               line to monitor fluid status in these often critically ill
               patients.
     e.  Induction:  These are cases which call for awake intubation
     or for rapid sequence intubation with ketamine and sux.
     f.  Post-op extubation is hazardous because of the increased
     intraabdominal pressure after reduction of the hernia.
     g.  Treat acidosis when pH is less than 7.0.
         1)  Treat peripheral perfusion.  Warm the patient and
         make sure perfusion is adequate.
         2)  dose of bicarbonate:  base deficit    X    body weight in kg
         X    0.4 (extracellular fluid as percentage of total body weight)
Pediatrics

3. single best answer (Remembered Question) Hyperkalemia after succinylcholine in acute spinal cord injury is

(A) not clinically significant by EKG changes
(B) unlikely in the first 24 hours
(C) unlikely after 60 days
(D) reliably prevented by pretreatment with a non-depolarizer
(E) unlikely six months post-injury

B. 1. Sux is contraindicated in spinal cord injury patients for about 1 day to 1 year after injury. Sux causes the release of potassium from the motor end plate membrane and the muscle membrane in the spinal cord injury patient but not in the normal patient. Normally the muscle membrane is only electrically sensitive. In spinal cord injury patients it changes to one which is chemically sensitive (like the motor end plate) as well. If Sux causes ventricular fibrillation, treatment should be directed at ABC's, then DC shock, followed by treatment of the hyperkalemia. 2. The hyperkalemia caused by succinylcholine administration is not reliably treated by pretreatment with a nondepolarizer.

(A) adenosine
(B) verapamil
(C) digoxin
(D) lidocaine
(E) synchronized cardioversion

A. 1. Supraventricular arrhythmias a. Adenosine (6 mg initial, then 12 mg, and another 12 mg) by rapid IV push followed by a 20 cc IV fluid bolus to ensure central uptake. The drug can can cause transient standstill. b. Verapamil is a second line of defense but it can be lethal in VT. 2. Patients hemodynamically unstable with SVT should, as you know, be cardioverted.

(A) pulmonary edema
(B) neonatal hypotonia
(C) hypokalemia
(D) sensitivity to nondepolarizers
(E) maternal hypotension

C. 1. Hyperkalemia is a known side effect. Hypokalemia is not. 2. Let's review the side effects of magnesium in the context of the treatment of severe pre-eclampsia. As you know, major therapy revolves around bedrest and magnesium. If the patient is seizing, the initial goal is support of oxygenation, ventilation, and circulation. Control the seizure with thiopental or diazepam. a. Bedrest b. MgSO4 (therapeutic range is 4-6 meq/l) 1) Use 20% solution with recommended 4 gram loading dose over 15 minutes and 1 gm/hr IV thereafter.) 2) Effects: They are VAST! a) V: vasodilator (probably on the basis of smooth m. relax.) b) A: anticonvulsant c) S: sedative, skeletal muscle relaxant: it decreases the release of acetylcholine and decreases the sensitivity of the motor end plate to acetylcholine. d) T: tocolytic (decreases uterine activity) which increases uterine blood flow. 3) Side effects a) prolonged PR interval and wide QRS, muscle weakness and loss of DTR's, respiratory insufficiency, and cardiac failure are the classic signs and symptoms. Therapeutic level is 5 meq/l. First sign is a prolonged PR interval and widened QRS (5-10 meq/l), muscle weakness and loss of DTR's (10 meq/l), respiratory paralysis (15 meq/l), and cardiac \arrest (20 meq/l). The neonate can have decreased muscle tone after birth and this is manifested by respiratory depression and apnea. Treatment is CaCl2 by IV route. b) Increased sensitivity to depolarizing and nondepolarizing muscle relaxants certainly occurs. No fasciculation after sux. If mag has been used do not use a defasiculating dose of nondepolarizer and decrease the dose of sux by about one-half. c) Side effects in the newborn include flaccidity, respiratory depression, and apnea. The treatment is calcium. d) Other side effects include the following: (U of I Drug Info) Vasodilatation-Hypotension Hyperthermia Hyperkalemia Hypocalcemia-Hypophosphatemia Diarrhea CNS depression Pulmonary edema: rare; 2 cases reported c. Hydralazine: Does not decrease uterine blood flow as SNP does. In fact, it increases both uterine and renal blood flow. There is an effect in 15-20 minutes which lasts for 2 hours. This should be given if MgSO4 does not work in controlling the blood pressure. SNP has two potential serious effects: it decreases uterine blood flow and it crosses the placenta and increases the risk of fetal toxicity from cyanide. 1) Captopril has been associated with fetal death

(A) pain in lateral aspect of thigh
(B) inability to abduct thigh
(C) weakness below the knee
(D) inability to dorsiflex the foot
(E) burning pain in the hip

A. Lower extremity nerve block 1. The nerve supply to the lower extremity consists of the lumbar and sacral plexus. a. The Lumbar Plexus: T12, L1,L2, L3,L4---Femoral, Obturator, and Lateral Femoral Cutaneous Nerves b. The Sacral Plexus: L4, L5, S1, S2---Sciatic Nerve 2. Sciatic nerve block a. This is really a block of the sacral plexus b. The sciatic nerve leaves the pelvis through the greater sciatic notch and descends into the popliteal region. In the popliteal fossa it divides into the tibial and the common peroneal nerves. c. The sciatic nerve innervates the hamstrings and all muscles of the leg and foot. d. It is sensory to the front (superficial and deep peroneal nerves), back (posterior tibial nerve) and lateral (sural nerve) aspect of the ankle. Sensation to the medial aspect of the ankle is by the saphenous nerve, a branch of the femoral nerve. 3. Femoral nerve block a. It enters the pelvis and passes under the inguinal ligament. b. It divides under the inguinal ligament into anterior and posterior divisions. c. It is sensory to the anterior and medial thigh and leg. d. It is sensory to the medial aspect of the ankle as the saphenous nerve. 4. Lateral Femoral Cutaneous Nerve a. It is sensory to the anteriolateral aspect of the thigh down to the knee. b. Meralgia Paresthetica: Compression of the lateral femoral cutaneous nerve by the inguinal ligament to produce pain, numbness, and paresthesias over the anteriolateral aspect of the thigh. 5. Obturator Nerve a. It supplies the adductors of the thigh.

(1) angle of the mandble
(2) cricothyroid membrane
(3) sternal notch
(4) greater cornu of the hyoid bone

D. One could answer E. but then we get into the business of the whole body being a landmark. I believe they want you to be more restrictive. Anatomy of the airway 1. Pharynx (glossopharyngeal (9th) nerve) a. Hypopharynx: glossopharyngeal (9) and hypoglossal (12) nerves 2. Larynx (vagus (10th) nerve) a. Major cartilages of the larynx: There are five. 1) Hyoid 2) Thyroid 3) Cricoid 4) Arytenoid: attached to the cricoid and have attached to them the VC's. 5) Epiglottic b. Sensory and motor supply of the larynx and trachea are branches of the vagus, namely the superior laryngeal nerve and the recurrent laryngeal nerve. c. Superior laryngeal nerve: blocked as it passes below the greater cornu of the hyoid bone. Two main branches: 1) Internal laryngeal branch: It pierces the thyrohyoid membrane and provides sensation to the area above the vocal cords (epiglottis to the vocal cords). 2) External laryngeal branch: It provides innervation to the cricothyroid muscle, a major tensor of the vocal cords. d. Recurrent laryngeal nerve: It enters the larynx just posterior to the cricothyroid articulation. 1) It is blocked by a transtracheal approach through the cricothyroid membrane. 2) It runs in a groove between the trachea and the esophagus. It can be easily blocked while performing a stellate ganglion block. 3) The recurrent laryngeal nerve provides sensation to the area below the vocal cords as well as control over all of the laryngeal muscles except the cricothyroid. 4) Bilateral bruising is the only injury which can cause rapid, severe respiratory obstruction. 3. Trachea (vagus (10th) nerve)

(1) narrowed subglottic space
(2) postoperative diabetes insipidus
(3) TMJ involvement
(4) large tongue

E. A. Hypophysectomy 1. Performed for acromegaly, Cushing's disease, or metastatic cancer. 2. Most common problem postoperatively is DI, which is a lack of ADH. a. Hallmark of DI is a low urine osmolality and a low urine specific gravity. The osmolality is usually less than 150 mOsm/kg and the S.G. is usually less than 1.005. b. The urine osmolality is never greater than the serum osmolality. 3. Treatment is D51/4NS and ADH infusion.   B. Acromegaly: 1. The anterior pituitary secretes several hormones: luteinizing hormone, follicle stimulating hormone, growth hormone, thyroid stimulating hormone, ACTH, prolactin, and melanocyte stimulating hormone. 2. Growth hormone is especially important. Excess growth hormone before the epiphyses are closed leads to gigantism and to acromegaly after they have closed. In both, there is overgrowth of skeletal, soft, and connective tissues. 3. Effects upon the airway are important: the mandible increases in thickness and length and this can lead to sketal problems, especially involving the TMJ. The tongue and epiglottis enlarge, pharyngeal tissue overgrowth leads to soft tissue upper airway obstruction, and tracheal subglottic diameter is reduced. 4. There are several other considerations of anesthetic mportance: a. hypertension b. increased risk of coronary artery disease c. increased V/Q mismatching 5. Acromegaly has no effect upon our selection of drugs for the maintenance of anesthesia but it does influence our approach to the induction. While there can be ample distance between the submentum and the hyoid, good mouth opening, good neck range of motion (an apparently manageable airway). Often our hands aren't big enough and our grip not strong enough to overcome the forces leading to airway obstruction. The huge mandible, large tongue, floppy epiglottis, small glottic opening place acromegalics at high risk to obstruct with apnea and awake fiberoptic intubation is most frequently the best approach.

(A) tachycardia
(B) hypertension
(C) tachypnea
(D) metabolic alkalosis (severe)
(E) increased ETCO2

E. 1. The classic initial signs of malignant hyperthermia are tachycardia and tachypnea. These are secondary to sympathetic stimulation from hypermetabolism and underlying hypercarbia. 2. These signs are, however, rather nonspecific. The differentials covering each is long. Light anesthesia and pain are difficult to rule out. 3. The ABG, on the other hand, is more reliable. It consistently reveals hypercarbia, hypoxia, and both a respiratory and metabolic acidosis. Hypercarbia is therefore more specific and reliable. 4. The differential for hypercarbia includes reduced minute ventilation, increased dead space, and increased production of carbon dioxide--as in MH.

(A) reassure the patient and re-evaluate the next morning
(B) pull the catheter
(C) add local anesthetic
(D) obtain magnetic resonance imaging
(E) add fentanyl

D. 1. Neurologic problems of this type must be taken seriously. For example, the epidural catheter could have migrated and now be wrapped around a nerve root. Pulling it could worsen the situation. The best approach would be to obtain an MRI and diagnose the problem. A neurologist and/or a neurosurgeon would then guide treatment.

(1) pancuronium
(2) sufentanyl
(3) isoflurane
(4) halothane

B. Aortic Insufficiency: Volume overload of the LV leading to Angina, CHF, and Ischemia because of decreased aortic diastolic pressure. 1. The murmur is a decrescendo diastolic murmur. 2. The goals are to achieve small increases in heart rate and decreases in SVR. a. A slow heart rate leads to an increased diastolic time and therefore worsened regurgitation (leading to decreased diastolic blood pressure and lower coronary perfusion pressure.) b. An increased SVR also increases the regurgitant fraction. c. Maintain contractility and volume. 3. The problem here is volume overload of the left ventricle. 4. Sufentanyl and halothane could lead to bradycardia. Pancuronium would be beneficial from the standpoint of the moderate tachycardia it causes. Isoflurane would lead to a small reduction in SVR and increase in HR--both desirable in aortic regurgitation.

(A) 10 milli amps
(B) 100 milli amps
(C) 1 amp
(D) 10 amp
(E) 10 micro amps

E. 1. MACROSHOCK MICROSHOCK 1 mA perception 10 uA rec. max leakage current 10 mA "let go"; >10 sustained contractions   100 mA V Fib 100 uA V fib ( milliamps ) ( microamps ) 2. Recall definitions: a. Macroshock: The amount of current applied to the outside of the body. b. Microshock: The amount of current applied to the inside of the body. 3. They want you to know some basic numbers. Memorize them!

(1) small increase in heart rate, minimal change in SVR
(2) minimal change in heart rate, slight increase in SVR
(3) heart rate unchanged, slight decrease in SVR
(4) minimal change in either heart rate or SVR

D. 1. Second generation long-acting nondepolarizers: Doxacurium and Pipecuronium (These were asked about first on the written exam in 1993) a. Doxacurium 1) long-acting bisquaternary ammonium compound 2) does not release histamine, no cardiovascular side-effects 3) similar to pancuronium in elim. half-life and dep. upon renal clearance 4) may not trigger MH b. Pipecuronium 1) long-acting steroidal non-depolarizing agent 2) does not release histamine, no cardiovascular side-effects 3) similar to pancuronium in elim. half-life and dep. upon renal clearance 4) compared to children and adults, potency is increased and duration is shortened in infants.

(A) 10 mg of ketorolac has the analgesic equivalent of 50 mg meperidine
(B) 10 mg of ketorolac has the analgesic equivalent of 6 mg of morphine
(C) Ketorolac is a cyclooxygenase inhibitor which has a half-life of about 3 hours
(D) Bronchospasm is a contraindication to the use of ketorolac
(E) Ketorolac may inhibit platelet aggregation and prolong bleeding time

C. We know that ketorolac was on the written in 1993. Here is the information you need to know. I. Ketorolac Tromethamine (Toradol) [Information from the package insert] 1. Ketorolac is a NSAID which has very effective analgesic, anti-inflammatory, and antipyretic actions. 2. It inhibits the synthesis of prostaglandins (cyclo-oxygenase inhibition) and is a peripherally acting analgesic. The IM doses available are 15, 30, and 60 mg. Ten milligrams of Ketorolac is comparable to 50 mg of meperidine or 6 mg of morphine. a. Ketorolac causes less drowsiness, nausea, and vomiting than morphine. b. The half-life of Ketorolac is about 6 hours. 3. Ketorolac is not recommended as a preoperative medication because it inhibits platelet aggregation and may prolong bleeding time. Its role in obstetrical anesthesia has not been adequately studied. 4. Contraindications: a. Bronchospasm b. Angioedema c. Nasal polyps 5. Complications: a. Gastrointestinal: ulceration, bleeding, perforation b. Renal: acute renal failure, nephritis c. Hemorrhage: d. Hypersensitivity: anaphylaxis, bronchospasm, angioedema

(1) Posterior superior iliac spine
(2) Iliac crest
(3) Greater trochanter
(4) Ischial tuberosity

B. (Review anatomy chapter of Big Blue) Sciatic nerve block a. The sciatic nerve arises from the sacral plexus b. The sciatic nerve leaves the pelvis through the greater sciatic notch and descends into the popliteal region. In the popliteal fossa it divides into the tibial and the common peroneal nerves. c. The sciatic nerve innervates the hamstrings and all muscles of the leg and foot. d. It is sensory to the front (superficial and deep peroneal nerves), back (posterior tibial nerve) and lateral (sural nerve) aspect of the ankle. Sensation to the medial aspect of the ankle is by the saphenous nerve, a branch of the femoral nerve. e. The classic approach is with the patient lying in a lateral position with the hip and knee flexed. A line should be drawn between the posterior superior iliac spine and the greater trochanter. At the midpoint of this line a perpendicular (bisecting line) line should be drawn 3 cm downward. This is the target for the block. f. No significant complications resulting from this block have been documented. g. The only surgical procedure which may possibly be done using the sciatic nerve block as the sole anesthetic would involve the sole of the foot. If surgery involves the lower extremity blocking the sciatic nerve is usually combined with femoral, obturator, or lateral femoral cutaneous nerve blocks.

(A) administer sodium nitroprusside IV
(B) papaverine intra-arterial
(C) administer nitroglycerine IV
(D) perform a stellate ganglion block
(E) reassure the patient and take no action at present

B. 1. Steps in the management of intra-arterial injection of thiopental: (1993 exam) (Information from package insert from Abbott) a. Leave needle in place if possible b. Inject the artery with dilute papaverine (40-80 mg) or 10 cc of 1% procaine. These steps inhibit smooth muscle spasm. According to the AMA Drug Evaluation, lidocaine is also acceptable in place of procaine. (p. 172, 1993) c. If necessary perform sympathetic block of the brachial plexus and/or stellate ganglion. d. Heparinize to prevent thrombus formation. e. Consider a-adrenergic blockade (phentolamine). 2. At present, with the hand pink, a stellate ganglion block does not seem indicated.

(A) rise in both end tidal carbon dioxide and end tidal nitrogen
(B) fall in end tidal nitrogen and rise in end tidal carbon dioxide
(C) fall in end tidal carbon dioxide with a rise in end tidal nitrogen
(D) no change in end tidal nitrogen but a fall in end tidal carbon dioxide
(E) no change in either end tidal nitrogen or end tidal carbon dioxide

C. A significant venous air embolus is detected by the the mass spectrometer. End tidal nitrogen rises and end tidal carbon dioxide falls.

1. The celiac plexus is formed by the greater and lesser splanchnic nerves at L3
2. The celiac plexus is located at L1
3. One of the side effects is hypertension
4. When performed with alcohol is one of the most definitive pain treatments for pancreatic cancer pain

C. Celiac Plexus Block: 1. The plexus is formed from the greater and lesser splanchnic nerves at L1 vertebral level. 2. Used when malignant tumors are present in the pancreas, liver, gall bladder, and/or stomach leading to intractable pain. 3. The plexus lies clustered around the celiac artery, lateral to the aorta. 4. Problems and complications: a. Hypotension b. Diarrhea (relative vagal over-activity leads to increased peristalsis and gut constriction) 5. An alcohol celiac plexus block is the most effective of all therapeutic endeavors in the treatment of pancreatic cancer pain.

(1) Is actually a neuralgia in the distribution of the occipital nerve
(2) Is characterized by a dull, aching pain
(3) Injection of steroids is most effective
(4) Treatment is a block of the gasserian ganglion, located in the middle cranial fossa

D. Trigeminal Neuralgia (tic douloureux) , 1. Characterized by a sharp pain in the face--roughly in the distribution of the maxillary branch of trigeminal nerve. 2. The treatment is a Gasserian ganglion block if all branches of the nerve are involved. 3. The definitive treatment is a neurolytic nerve block, usually with glycerol. 4. The gasserian ganglion is located in the middle cranial fossa. It is adjacent to Meckel's Cave, which contains CSF.

(1) cryoprecipitate
(2) DDAVP
(3) FFP
(4) factor VIII concentrate-Humate-P (virus deactivated)

E. 1. Type 1 von Willebrand's is the mildest of the three forms of the disease. von Willebrand's disease is characterized by lack of von Willebrand's factor which leads to a relative lack of factor VIII as well as a platelet abnormality in that von Willebrand's factor is necessary to activate platelets. von Willebrand's factor is a "big brother", protecting factor VIII. In von Willebrand's disease there is less factor VIII in the plasma. Factor VIII does not circulate as a free molecule. It is accompanied by von Willebrand's factor.   2. I spoke to a hematologist about this confusing question. Basically, the answer is that all "could" be used--depending upon the circumstances. Cryoprecipitate, DDAVP, and FFP could all be used in this situation but currently the most favored product would likely be a purified factor VIII concentrate which is virus deactivated, e.g. Humate P. The problem is that many hospitals do not have it. If that is the case, since most type 1 von Willebrand's patients are DDAVP responsive one would administer DDAVP. Cryo and FFP take time to thaw anyway. If the patient has a history of poor responsiveness to DDAVP, however, and virus deactivated, purified concentrate is not available, cryoprecipitate or FFP (in this order) should be administered. 3. See Big Blue (Blood and Coag)