Date: September 23, 2015 From: Scott S. Schaus Andrew Teich, CRNA Valley Anesthesia, Inc. Subject: 2015 Mixed Review and Questionnaire Dear SRNA Friend and Soon-To-Be CRNA: It is our expectation that you have put a great deal of energy into your preparations for the National Certification Examination (NCE). The enclosed content updates and supplements your review materials. Some of the items are refinements of issues we have dealt with previously. You should work hard to master this material as well as the information already in your hands. Specifically, we remind you that mastering both the MemoryMaster and the Course Manual content along with the Mixed Reviews helps ensure your success on the NCE. Further study in your “go-to” anesthesia text—the text that speaks to you—is strongly recommended as well. A former Valley attendee best summarized the approach to success: “It is not enough to know the material front-to-back, up-and-down, and inside-out; you must also know it sideways!!” There are no shortcuts—work hard and stay focused! We suspect that some of the issues in the enclosed review & update packet will be new to you. You undoubtedly will be familiar with some of the items. We have worked long hours putting this information packet together and have made every attempt to document the answers to the questions accurately. If you think any of the items are incorrect, controversial, or contain grammatical errors, we would appreciate hearing from you. Please send Scott an email with your comments and suggestions. After you take the Certification Examination and have received your results, we ask a favor: please complete and return the enclosed questionnaire and send it to us. Your response, input and feedback are particularly important to us. Thank you very much for your attendance and participation in Valley Anesthesia’s Review Course and best wishes for success on the NCE. Stay focused & Never Give Up!! Sincerely yours, Scott and Andrew [email protected] | [email protected]
Transcript
!Date: September 23, 2015
From: Scott S. Schaus Andrew Teich, CRNA
Valley Anesthesia, Inc.
Subject: 2015 Mixed Review and Questionnaire
Dear SRNA Friend and Soon-To-Be CRNA:
It is our expectation that you have put a great deal of energy into your preparations for the National Certification Examination (NCE). The enclosed content updates and supplements your review materials. Some of the items are refinements of issues we have dealt with previously. You should work hard to master this material as well as the information already in your hands. Specifically, we remind you that mastering both the MemoryMaster and the Course Manual content along with the Mixed Reviews helps ensure your success on the NCE. Further study in your “go-to” anesthesia text—the text that speaks to you—is strongly recommended as well. A former Valley attendee best summarized the approach to success: “It is not enough to know the material front-to-back, up-and-down, and inside-out; you must also know it sideways!!” There are no shortcuts—work hard and stay focused!
We suspect that some of the issues in the enclosed review & update packet will be new to you. You undoubtedly will be familiar with some of the items. We have worked long hours putting this information packet together and have made every attempt to document the answers to the questions accurately. If you think any of the items are incorrect, controversial, or contain grammatical errors, we would appreciate hearing from you. Please send Scott an email with your comments and suggestions.
After you take the Certification Examination and have received your results, we ask a favor: please complete and return the enclosed questionnaire and send it to us. Your response, input and feedback are particularly important to us.
Thank you very much for your attendance and participation in Valley Anesthesia’s Review Course and best wishes for success on the NCE. Stay focused & Never Give Up!! Sincerely yours, Scott and Andrew [email protected] | [email protected]
PLEASE COMPLETE THE FOLLOWING QUESTIONNAIRE AND RETURN TO: Valley Anesthesia 424 West 33rd St, Suite 360 New York, NY 10001 Fax: (888) 803-8494
I took the Certification Exam in _____________ /__________ (month/year).
I took the Valley Review Course at ______________________ (site) in ________ (year).
In what ways did Valley Anesthesia help you prepare for the examination (attach a sheet if you need more area for comments): How might Valley Anesthesia improve the way it prepares SRNAs for the Certification Examination (attach a sheet if you need more area for comments):
1. The lungs have a dual blood supply, bronchial arteries and pulmonary arteries. Where do the bronchial arteries arise and which lung tissues are supplied by bronchial arteries? High-pressure, low-flow bronchial arteries arise from the descending thoracic aorta and sup-ply systemic arterial (oxygenated) blood to bronchi and bronchioles, terminating at the res-piratory bronchioles. The bronchial arteries also supply the supporting tissues of the lungs including nerves, pulmonary vessels and visceral pleura. [Hall JE, Guyton AC. Guyton and Hall Textbook of Medical Physiology. 12e; 2011:477; Nagelhout JJ, Plaus KL. Nurse Anes-thesia. 5e; 2013:600; Hagberg CA, Benumof J. Benumof and Hagberg’s Airway Manage-ment. 3e; 2012:18; Flood P, Rathmell JP, and Shafer S. Stoelting’s Pharmacology & Physi-ology in Anesthetic Practice. 5e; 2015:385; Butterworth JF, et al. Morgan & Mikhail’s Clinical Anesthesiology, 5e, 2013:491.]
2. The lungs have a dual blood supply, bronchial arteries and pulmonary arteries. Where do the pulmonary arteries arise and what lung tissues are supplied by pulmonary arteries? The low-pressure, high-flow pulmonary arteries supply venous blood flow to the structures distal to the terminal bronchioles, including distal nonrespiratory tissues and the alveolar capillaries where gas exchange occurs. The pulmonary artery arises from the right ventricle and branches into the right and left pulmonary arteries, which further branch to accompany the bronchi. [Hall JE, Guyton AC. Guyton and Hall Textbook of Medical Physiology. 12e; 2011:477; Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:600; Hagberg CA, Benumof J. Benumof and Hagberg’s Airway Management. 3e; 2012:18; Flood P, Rathmell JP, and Shafer S. Stoelting’s Pharmacology & Physiology in Anesthetic Practice. 5e; 2015:385; Butterworth JF, et al. Morgan & Mikhail’s Clinical Anesthesiology, 5e, 2013:491.]
3. Describe the venous drainage of the lung. The venous drainage of the bronchi occurs through the bronchial, azygous, hemiazygos, and intercostal veins, which then drain into brachiocephalic veins of the neck and ultimately the superior vena cava. The pulmonary circulation returns to the heart via the pulmonary veins, which empty into the left atrium. [Hall JE, Guyton AC. Guyton and Hall Textbook of Medi-cal Physiology. 12e; 2011:477; Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:600; Hagberg CA, Benumof J. Benumof and Hagberg’s Airway Management. 3e; 2012:18; Flood P, Rathmell JP, and Shafer S. Stoelting’s Pharmacology & Physiology in Anesthetic Practice. 5e; 2015:385; Butterworth JF, et al. Morgan & Mikhail’s Clinical Anesthesiology, 5e, 2013:491.]
4. If the immune system overreacts to an allergen, a hypersensitivity (allergic) reaction occurs. Immune-mediated hypersensitivity reactions are classified into four groups by mechanism of action: list each type of allergic reaction and give a one sentence description of the reaction. Type I reactions are anaphylactic or immediate-type hypersensitivity reactions. Type II reac-tions are cytotoxic reactions (antibody-dependent cell-mediated cytotoxicity). Type III reac-tions are immune complex reactions that produce tissue damage by deposition of the immune complexes. Type IV reactions are delayed-type hypersensitivity reactions resulting from the interaction of sensitized lymphocytes with specific antigens. [Barash PG, Cullen BF, Stoelt-ing RK, et al. Clinical Anesthesia. 7e; 2013:291–292; Nagelhout JJ, Plaus KL. Nurse Anes-thesia. 5e; 2013:1023–1024; Hines RL, Marschall KE. Stoelting's Anesthesia and Co-Existing Disease. 6e; 2012:523.]
5. Describe type I allergic (hypersensitivity) reactions: include participating cells and anti-body(ies) and list common examples of type I reactions. In type I allergic reactions (immediate-type, anaphylactic), a specific antigen—called an allergen—interacts with specific IgE antibodies on tissue mast cells or circulating basophils to trigger mediator release. The key mediator of type I reac-tions is histamine. Examples of type I reactions are allergic rhinitis, extrinsic asthma, and anaphylaxis. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:291–292; Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:1023–1024; Hines RL, Marschall KE. Stoelting's Anesthesia and Co-Existing Disease. 6e; 2012:523.]
6. What is anaphylaxis? Anaphylaxis is a severe, generalized, life-threatening immediate hypersensitivity reaction marked by interstitial edema—particularly laryngeal edema—bronchospasm, and cardiovas-cular collapse. The most common type of immune-mediated anaphylaxis results when previ-ous exposure to antigens in drugs or foods evokes production of antigen-specific IgE anti-bodies. Subsequent exposure to the same or a chemically similar antigen results in antigen-antibody interactions that initiate marked degranulation of mast cells and basophils. Urticaria and pruritus are common. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:291–292; Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:1023–1024; Hines RL, Marschall KE. Stoelting's Anesthesia and Co-Existing Disease. 6e; 2012:523.]
7. How does non-immune-mediated anaphylaxis (also known as anaphylactoid reaction) com-pare with anaphylaxis? Non-immune-mediated anaphylaxis (also known as anaphylactoid reaction) is nearly identi-cal to anaphylaxis; however, the triggering antigen directly stimulates mast cell and baso-phils—there is no IgE-mediated trigger. Symptoms of non-immune-mediated anaphylaxis are generally less severe than IgE-mediated anaphylaxis. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:291–292; Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:1023–1024; Hines RL, Marschall KE. Stoelting's Anesthesia and Co-Existing Dis-ease. 6e; 2012:523.]
8. Describe type II hypersensitivity (allergic) reactions: include participating cells and anti-body(ies) and list common examples of type II reactions. Type II cytotoxic reactions are mediated by IgM and IgG antibodies directed against antigens on the surface of foreign cells or extracellular tissue components. The cell damage in type II reactions is produced by (1) direct cell lysis after complete complement cascade activation, (2) increased phagocytosis by macrophages, or (3) killer T-cell lympho-cytes producing antibody-dependent cell-mediated cytotoxic effects. Examples of type II reactions include ABO-incompatible transfusion reactions, drug-induced immune hemolytic anemia, heparin-induced thrombocytopenia (HIT), myasthenia gravis, and Goodpasture’s syndrome. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:291–292; Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:1023–1024; Hines RL, Marschall KE. Stoelting's An-esthesia and Co-Existing Disease. 6e; 2012:523.]
9. Describe type III allergic (hypersensitivity) reactions: include participating cells and antibody(ies) and list more common examples of type III reactions. Type III immune complex reactions result from circulating soluble antigens and antibodies that bind to form insoluble complexes which then deposit in the microvasculature. Pro-tracted infections or autoimmune processes can lead to type III reactions. The mechanism of tissue injury is similar to that in type II reactions, involving activation of complement and recruitment of phagocytes. Systemic lupus erythemato-sus, rheumatoid arthritis, glomerulonephritis, and classic serum sickness are examples of immune complex diseases. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:291–292; Nagel-hout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:1023–1024; Hines RL, Marschall KE. Stoelt-ing's Anesthesia and Co-Existing Disease. 6e; 2012:523.]
10. Describe type IV allergic (hypersensitivity) reactions: include participating cells and anti-body(ies) and list common examples of type IV reactions. Type IV delayed-hypersensitivity reactions result from the interactions of sensitized lymphocytes with specific anti-gens. Delayed hypersensitivity reactions are mainly mono-nuclear, manifest in 18 to 24 hours, peak at 40 to 80 hours, and disappear in 72 to 96 hours. Cytotoxic T cells are pro-duced specifically to kill target cells that bear antigens identical with those that triggered the reaction. This form of immunity is important in tissue rejection, graft-versus-host reactions, contact dermatitis (e.g., poison ivy), tuberculin immunity, and Johnson-Stevens syndrome. Another form of type IV hypersensitivity is granulomatous hypersensitivity, in which chronic infection leads to the formation of granulomas in tissues. Granulomatous diseases include tuberculosis, sarcoidosis, and Crohn's disease. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:291–292; Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:1023–1024; Hines RL, Marschall KE. Stoelting's Anesthesia and Co-Existing Disease. 6e; 2012:523.]
11. Where is the J-point in the ECG waveform? How is the J-point used in ECG interpretation? The J-point is the point on the ECG when the QRS complex ends and the ST segment begins. ST elevation or depression is measured by comparing lead voltage at 60 or 80 milliseconds after the J-point (J+60, J+80) to the isoelectric value, usually meas-ured during the PR interval. ST elevation or depression may also be measured at the J-point. [Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:1436; Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:292; Flood P, Rathmell JP, and Shafer S. Stoelting’s Pharmacology & Physiology in Anesthetic Practice. 5e; 2015:397.]
12. What are the minimum alveolar concentration (MAC) requirements for a full-term infant, compared to the adult? The minimum alveolar concentration (MAC) value for a full-term infant is the same as for the adult. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:1196; Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:2764f.]
13. At what age (months) is the minimum alveolar concentration (MAC) highest? Which agent is the exception to this rule? By 6 months of age, the minimum alveolar concentration (MAC) is 50% greater compared to adult MAC (1.5x). For example, the MAC of desflurane for a 6-month old is 9.9% compared to 5.8% for the adult. The exception to this rule is sevoflurane: the MAC of sevoflurane is greatest in the neonate (3.3%), compared to 2% for the adult. (Updates 2015 MemoryMaster IB02g:Q9.) [Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:2764f.]
14. How are leukotrienes related to eicosanoids? Leukotrienes are metabolic derivatives of arachidonic acid, therefore leukotrienes (LT) are a category of eicosanoids. Lipoxygenase (LOX) acts on arachidonic acid to produce the leuko-triene family. Leukotrienes LTC4, LTD4, LTE4, and LTB4 increase smooth muscle contrac-tion, microvascular permeability, and airway mucus secretion.
[Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:570f; Hemmings HC, Egan TD. Pharmacology and Physiology for Anesthesia: Foundations and Clinical Application. 2013:466; Brunton LL, Chabner B, Knollman BC. Goodman & Gilman’s Pharmacological Basis of Therapeutics. 12e; 2011:938f.]
15. What action do leukotrienes (LT) have on the lungs? What cells synthesize and release LTs? Activated mast cells and basophils synthesize and release leukotrienes. Leukotrienes evoke inflammatory responses in the lungs including intense bronchoconstriction and increased pulmonary vascular permeability. Leukotrienes also promote eosinophil degranulation and attract neutrophils, both key players in the inflammatory response. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013: 292; Flood P, Rathmell JP, and Shafer S. Stoelting’s Pharmacology & Physiology in Anesthetic Practice. 5e; 2015:602; Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:411; Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:520.]
16. What is another name for the mixture of leukotrienes C4, D4, and E4? The mixture of leukotrienes C4, D4, and E4 is the classic slow-reacting substance of anaphy-laxis (SRS-A). [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:293; Hemmings HC, Egan TD. Pharmacology and Physiology for Anesthesia: Founda-tions and Clinical Application. 2013:466]
17. For what conditions are α-glucosidase inhibitors administered? The medical treatment of insulin resistance and hyperglycemia in metabolic syndrome, type 2 diabetes, and obesity is usually achieved with oral hypoglycemic drugs including α-glucosidase inhibitors, sulfonylureas, meglitinides, D-phenylalanine derivatives, diguanides, and thiazolidinediones. [Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:2205; Brunton LL, Chabner B, Knollman BC. Goodman & Gilman’s Pharmacological Basis of Therapeutics. 12e; 2011:1264–1265; Flood P, Rathmell JP, and Shafer S. Stoelting’s Pharmacology & Physiology in Anesthetic Practice. 5e; 2015:755]
18. How do α-glucosidase inhibitors work? α-Glucosidase inhibitors (acarbose, miglitol) decrease postprandial carbohydrate digestion and absorption at the intestinal brush border. By reducing absorption of starch, dextrose, and disaccharides, α-glucosidase inhibitors blunt the rise of postprandial glucose. [Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:2205; Brunton LL, Chabner B, Knollman BC. Goodman & Gilman’s Pharmacological Basis of Therapeutics. 12e; 2011:1264–1265; Flood P, Rathmell JP, and Shafer S. Stoelting’s Pharmacology & Physiology in Anesthetic Practice. 5e; 2015:755; Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:1344.]
19. List the most common side effects of α-glucosidase inhibitors. Flatulence, abdominal cramping, and diarrhea are side effects that frequently result from undigested carbohydrates that reach bacteria in the lower colon. With the exception of occa-sional increases in liver transaminases, α-glucosidase inhibitors are considered nontoxic. [Flood P, Rathmell JP, and Shafer S. Stoelting’s Pharmacology & Physiology in Anesthetic Practice. 5e; 2015:755.]
20. Antiemetic agents typically block one (or more) of six receptors—list these six receptors. Antiemetic agents are usually antagonists at: (1) dopamine receptors (D2); (2) histamine receptors (H1); (3) muscarinic ACh receptors; (4) serotonin receptors (5-HT3); (5) GABAA receptors; and, (6) NK1 (neurokinin-1) receptors. [Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:2963t; Flood P, Rathmell JP, and Shafer S. Stoelting’s Pharmacology & Physiology in Anesthetic Practice. 5e; 2015:693t; Brunton LL, Chabner B, Knollman BC. Goodman & Gilman’s Pharmacological Basis of Therapeutics. 12e; 2011:1341–1346]
21. Correlate (match) the clinically used antiemetics with their primary mechanism (receptor). Dopamine receptors (D2 predominantly): metoclopramide, droperidol, haloperidol, aliza-pride, perphenazine, and prochlorperazine. Histamine receptors (H1): dimenhydrinate, diphenhydramine, cyclizine, and promethazine. Muscarinic ACh receptors: hyoscine. Serotonin receptors (5-HT3): ondansetron, dolasetron, granisetron, tropisetron, ramosetron, and palonosetron. GABAA receptors: midazolam, diazepam, and lorazepam. Neurokinin-1 receptors (NK1): aprepitant. NB: the antiemetic mechanism of action of dexamethasone is unknown. [Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:2963t; Flood P, Rathmell JP, and Shaf-er S. Stoelting’s Pharmacology & Physiology in Anesthetic Practice. 5e; 2015:693t; Brunton LL, Chabner B, Knollman BC. Goodman & Gilman’s Pharmacological Basis of Therapeu-tics. 12e; 2011:1341–1346]
22. Research has validated that use of a single ECG lead for ischemic monitoring in patients with documented CAD is inadequate; monitoring with multiple leads enhances patient safety. A 5-cable (5-lead) ECG monitoring system is currently the standard for monitoring patients with suspected myocardial ischemia. Describe the placement of the 5 electrodes in the 5-cable system. In the five-electrode (5-cable) monitoring system, the four limb electrodes, LA, RA, LL, and RL placed at their corresponding monitoring locations allow any of the six bipolar limb leads ( I, II, III, aVR, aVL, and aVF) to be obtained, and a fifth chest electrode can be placed in any of the standard precordial V1 to V6 locations. [Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:1436; Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:295; Flood P, Rathmell JP, and Shafer S. Stoelting’s Pharmacology & Physiology in Anesthetic Practice. 5e; 2015:397.]
23. Describe the proper placement of RA, LA, LL, and RL electrodes according to the Mason-Likar lead position scheme. Proper placement of the RA electrode is over the outer right clavi-cle and of the LA electrode is over the outer left clavicle. The LL electrode is placed near the left iliac crest or midway between the costal margin and left iliac crest along the anterior axillary line. The RL electrode may be placed at any convenient location on the body. [Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:296t.]
24. Which unipolar lead in the 5-lead monitoring system is preferred when arrhythmias are anticipated? Which unipolar leads are pre-ferred for monitoring ischemia? In the 5-lead system, V1 is preferred for special arrhythmia monitoring, whereas V3 to V5 are the preferred leads for monitoring ischemia. [Miller RD, Cohen NH, Eriksson LI, et al. Mil-ler’s Anesthesia. 8e; 2015:1436; Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:295; Flood P, Rathmell JP, and Shafer S. Stoelting’s Pharmacology & Physiology in Anesthetic Practice. 5e; 2015:397.]
25. Which blood components are found in packed red blood cells (PRBC)? Packed red blood cells (PRBC) contains red blood cells in anticoagulated plasma. Most plasma is removed (by centrifugation) and is replaced by preservative, most commonly cit-rate phosphate dextrose adenine-1 (CPDA-1). [Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:888t; Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:416.]
26. The addition of adenine to CPD extends the storage time of packed red blood cells (PRBC) from 21 days to ___ days. The addition of adenine to citrate phosphate dextrose (CPD) solution allows RBCs to resyn-thesize adenosine triphosphate (ATP), which extends the storage time from 21 to 35 days. As a result, RBCs or whole blood can be stored for 35 days when stored in CPDA-1. [Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:1835.]
27. Name three preservatives that extend the storage time of packed red blood cells (PRBC) from 35 days to 42 days. The shelf life of packed red blood cells (PRBC) can be extended to 42 days when AS-1 (Adsol), AS-3 (Nutricel), or AS-5 (Optisol) is used. [Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:1835.]
28. Extending blood storage to 42 days is a mixed blessing. Describe the biochemical alterations of stored blood. (Hint: what substances are increased? Decreased?) During storage, RBCs metabolize glucose to lactate, hydrogen ions accumulate, and plasma pH decreases. The storage temperatures of 1° to 6 °C depress the sodium-potassium pump, thus RBCs lose K+ and gain Na+. Some RBCs undergo lysis, resulting in increased plasma Hb levels. Progressive decreases in ATP and 2,3-diphosphoglycerate (2,3-DPG) occur during storage and factors V and VII (most labile factors) are decreased as well. Summary of plasma changes in stored blood: fewer RBCs in an acidic, hyponatremic, hyperkalemic, hypoglyce-mic plasma, with increased free hemoglobin and decreased 2,3-DPG. [Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:1835; Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:418; Butterworth JF, et al. Morgan & Mikhail’s Clinical Anesthesiology, 5e, 2013:1171–1172.]
29. Which blood components are present in fresh-frozen plasma (FFP)? Fresh-frozen plasma contains ALL clotting factors, naturally occurring inhibitors of coagula-tion, and antithrombin (formerly antithrombin III). FFP is devoid of red blood cells and plate-lets. [Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:888t.]
30. Which blood components are present in cryoprecipitate? Cryoprecipitate is a protein fraction collected from the top of thawing FFP and therefore contains concentrated factors I, VIII, vWF, XIII, and fibronectin. [Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:888t.]
31. Which blood product contains the greatest concentration of fibrinogen (factor I)? Cryoprecipitate contains more fibrinogen per volume than fresh-frozen plasma, specifically 15 g/L in cryo compared to 2.5 g/L in FFP (6x more fibrinogen in cryo). [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:422.]
32. State the threshold for fibrinogen replacement. The traditional threshold for fibrinogen replacement is fibrinogen levels less than 80 to 100 mg/dL. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:422.]
33. How many bags of cryoprecipitate constitute a single dose? What is the expected fibrinogen increase following one dose of cryoprecipitate? A single dose—five pooled bags of cryoprecipitate—typically raises the fibrinogen concen-tration by 50 mg/dL. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:422.]
34. According the the ASA’s 2006 updated practice guidelines, at what hemoglobin level is RBC transfusion rarely indicated? At what hemoglobin level is always indicated? According to the ASA’s 2006 updated practice guidelines, transfusion is rarely indicated when the Hb concentration is more than 10 g/dL. and is almost always indicated when it is less than 6 g/dL, especially when the anemia is acute. (Note: the ASA practice guideline will be updated in 2015.) [Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:1836–1837.]
35. According to the ASA 2006 updated practice guidelines, what factor justifies RBC transfu-sion when hemoglobin levels are intermediate (6–10 mg/dL)? The determination of whether intermediate Hb concentrations (6 to 10 g/dL) justify or re-quire RBC transfusion should be based on the patient’s risk for complications of inadequate oxygenation. [Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:1836–1837.]
36. List four (4) variations of head-elevated surgical positions. Four variations of head-elevated positions are: (1) sitting, including lounge chair and beach chair variation; (2) supine—tilted head up; (3) lateral—tilted head up, also called the “park bench” position; and, (4) prone—tilted head up. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:818–820.]
37. Venous air embolism is the most feared complication of head up surgical positions, as you know. Edema of the face, neck, and tongue in head up positions may compromise the airway. What is the cause of edema in these areas in a head up position? Edema of the face, neck, and tongue in head up positions, including severe postoperative macroglossia, is purportedly due to venous and lymphatic obstruction caused by prolonged, marked neck flexion. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:820]
38. What precautions should be taken to minimize the occurrence of face, neck, and tongue ede-ma in the head up positions? In order to minimize the risk of edema in the face, neck, and tongue during surgical proce-dures in a head up position, avoid placing the patient’s chin against the chest—do not force the chin into the suprasternal notch—and use an oral airway to protect the endotracheal tube. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:820]
39. What nerve injury may occur from a sternal retractor? Spreading of the sternal retractor during cardiac surgery causes the clavicle to move posteri-orly and the first rib to move upward thus pinching the brachial plexus between the two bones. Dissection of the internal mammary artery requires wide, asymmetric chest retraction and may lead to brachial plexus neuropathy, most often manifest as sensory deficit in the dis-tribution of the ulnar nerve. [Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:409; Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:1260; Cousins MJ, Briden-baugh PO. Cousins and Bridenbaugh’s Neural Blockade in Clinical Anesthesia and Pain Medicine. 4e; 2009:493]
40. What is the purpose of the second lumen on an LMA ProSeal? The LMA ProSeal was the first double-lumen supraglottic airway. The second lumen is used for: (1) diagnosis of malposition, (2) passive emptying of the stomach, and (3) active empty-ing of the stomach (OGT insertion). The LMA Supreme is a single-use version of the ProSeal. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:773; Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:450–451; Miller RD, Cohen NH, Eriks-son LI, et al. Miller’s Anesthesia. 8e; 2015:1664.]
41. When choosing an LMA ProSeal, should you use the same size, size up, or size down from the appropriate LMA classic size? When selecting an LMA ProSeal, you should size down from the appropriate LMA classic size. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:773t.]
42. Many fiberoptic bronchoscopes (FOB) have a notch in the eyepiece at the 12-o’clock posi-tion; what is the purpose of this notch? Many fiberoptic bronchoscopes have a notch in the eyepiece at the 12-o’clock position to aid with orientation. [Hagberg CA, Benumof J. Benumof and Hagberg’s Airway Manage-ment. 3e; 2012:367.]
43. One of the most important goals of premedication for awake intubation (AI) is drying of the airways, because secretions can obscure the view of the glottis and may prevent the local an-esthetic from reaching target areas. What is the drug of choice for drying airways prior to AI? The antisialagogue of choice for awake intubation is glycopyrrolate, 0.2–0.3 mg IV or IM, unless contraindicated. The antisialagogue effects of glycopyrrolate last longer than 4 hours and the drug does not cross the blood-brain barrier (no sedative effect). Note: anticholiner-gics only prevent formation of new secretions, therefore administer at least 30 minutes before topicalization. [Hagberg CA, Benumof J. Benumof and Hagberg’s Airway Management. 3e; 2012:247; Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:606; Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:1672.]
44. What are four (4) goals of adding hyaluronidase to peribulbar local anesthetic blocks? The addition of hyaluronidase to a local anesthetic as a spreading factor facilitates diffusion of drugs into the tissues. Hyaluronidase added to an ophthalmic block may: (1) improve the quality of the block; (2) increase speed of onset; (3) limit the acute increase in intraocular pressure; and, (4) decrease the incidence of postoperative strabismus. [Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:133; Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:1387; Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:2516.]
45. Which congenital anomaly is characterized by a short neck, irregular dentition, a high, arched palate, macroglossia, micrognathia, and subglottic stenosis? Patients with trisomy 21 (Down’s syndrome) have a short neck, irregular dentition, a high, arched palate, macroglossia, micrognathia, and subglottic stenosis. Airway obstruction and hypoxemia upon induction should be expected. Oral airways should always be available to help reestablish airway patency. [Hines RL, Marschall KE. Stoelting's Anesthesia and Co-Existing Disease. 6e; 2012:634–635, 634t; Butterworth JF, et al. Morgan & Mikhail’s Clini-cal Anesthesiology, 5e, 2013:903; Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anes-thesia. 7e; 2013:887]
46. During neonatal and pediatric surgery, every effort must be made to maintain the infant’s temperature to minimize thermal stress. What operating room temperature is recommended for procedures on a full-term infant? For a premature infant? To minimize the stress of hypothermia during pediatric procedures, the surgical environment should be warmed to ensure that the entire room constitutes a giant incubator. Operating room temperatures of 27 °C and 29 °C are recommended for full-term and premature new-borns, respectively. [Davis PJ, Cladis FP, Motoyama EK. Smith’s Anesthesia for Infants and Children. 8e; 2011:176–178; Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:2789.]
47. List four (4) potential risks to the fetus during nonobstetric surgery during pregnancy. Of the 4 risks, which is the leading cause of perinatal morbidity and mortality? Possible risks to the fetus of antenatal surgery include: (1) the effects of the disease process itself, or related therapy; (2) the teratogenicity of anesthetic agents or other drugs adminis-tered during the perioperative period; (3) intraoperative perturbations of uteroplacental perfu-sion and/or fetal oxygenation; and (4) the risk for abortion or preterm delivery. Premature delivery is the leading cause of perinatal morbidity and mortality. Premature delivery is im-plicated in more than 50% of all perinatal deaths. [Chestnut DH, Wong CA, Tsen, LC et al. Obstetric Anesthesia, 5e; 2014:358; Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:1150.]
48. Define premature labor. Premature labor is defined as regular uterine contractions that occur before 37 weeks of ges-tation or before 259 days from the last menstrual cycle and that result in dilation or efface-ment of the cervix. Late preterm births, defined as those of 34 to 36 weeks’ gestation, com-pose approximately 70% of all preterm births. [Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5e; 2013:1150; Chestnut DH, Wong CA, Tsen, LC et al. Obstetric Anesthesia, 5e; 2014:787.]
49. What three (3) maternal catastrophes pose the greatest acute risks to the fetus during nonob-stetric surgery during pregnancy? Maternal catastrophes involving severe hypoxia, hypotension, and acidosis pose the greatest acute risk to the fetus during nonobstetric surgery during pregnancy. [Chestnut DH, Wong CA, Tsen, LC et al. Obstetric Anesthesia, 5e; 2014:358.]
50. Which two general procedures are associated with the greatest risk of preterm labor in non-obstetric surgery during pregnancy? Abdominal and pelvic procedures are associated with the greatest incidence of preterm labor. Intra-abdominal procedures during the third trimester are most likely to be associated with preterm labor. [Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. 7e; 2013:1173; Fleisher LA. Anesthesia and Uncommon Diseases. 6e; 2012:540.]
Note: Page numbers followed by an “f” indicate a figure in the listed reference (e.g., [Miller RD, Cohen NH, Eriks-son LI, et al. Miller’s Anesthesia. 8e; 2015:2764f.]). Page numbers followed by a “t” indicate a table in the listed reference (e.g., [Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 8e; 2015:2963t.]).
• Keep in mind that mastery of the entire content of Valley Anesthesia’s study resources—Review Course Manual (“Sweat Book”), MemoryMaster, and Mixed Reviews—is highly recommended.
• The NBCRNA has an NCE Bibliography, a list of the texts used by the
NBCRNA as the basis for questions on the certification examination. To obtain the PDF and further information, visit: http://www.nbcrna.com/certification/Pages/NCE-Bibliography.aspx.
The MemoryMaster App is available for iPhone, iPad, and iPod Touch!
Please visit the iTunes Store or App Store on your Apple device to get your copy.
(Search for Certified Registered Nurse Anesthetist app.)
