What is the capacity (L) and pressure (psig) of a full E cylinder of oxygen?
660L under a pressure of 1900 psig
What is the capacity (L) and pressure (psig) of a full H cylinder of oxygen?
6900L under a pressure of 2200psi
What is the capacity (L) and pressure (psig) of a full E cylinder of air?
625L under a pressure of 1900 psi
What is the capacity (L) and pressure (psig) of a full H cylinder of air?
6550L under a pressure of 2200 psi
What is the capacity (L) and pressure (psig) of a full E cylinder of nitrous oxide?
1590L under a pressure of 745 psi
What is the capacity (L) and pressure (psig) of a full H cylinder of nitrous oxide?
158000L under a pressure of 745 psi
Nitrous is stored as a liquid in cylinders; what does the gauge of 745 psi actually represent?
the vapor pressure of liquid nitrous oxide at room temperature
The gauge on an E cylinder of nitrous oxide reads 740 psi, explain the significance of this reading.
The nitrous gauge reads 745 psi until all the liquid is gone; at this point he cylinder is more than 3/4 empty. After all the liquid nitrous is gone, the pressure rapidly declines until the cylinder is exhausted.
Because the pressure on a nitrous oxide cylinder remains relatively constant as long as there is liquid in the cylinder, that is the only way to know the amount of liquid in the cylinder?
weight must be used to determine the amount of liquid in cylinders that store liquified gas.
What is the weight of an empty cylinder?
A patient has an arterial line in the right arm and a blood pressure cuff on the left arm; the left arm is 20 cm higher than the right arm. If the blood pressure from the arterial line is 120/80, what is the pressure from the cuff on the left arm? (Assume the a-line has been properly calibrated to the phlebostatic axis.)
The blood pressure from the cuff on the left arm is 105/65. For each 10 cm of vertical height above or below the level of the heart, 7.5 mm-Hg should be subtracted from or added to, re- spectively, the blood pressure readings (for every inch, subtract or add 1.80 mm-Hg). Since the left arm is above the arterial line in the right arm, the pressure adjustment must be sub- tracted from the readings.
What and where is the phlebostatic axis?
The phlebostatic axis approximates the position of the right atrium. In the supine position, the phlebostatic axis is the fourth intercostal space, midanteroposterior level (not midaxillary line); for the right lateral decubitus position, at fourth intercostal space midsternum; for the left lateral decubitus position, at fourth intercostal space at the left parasternal border.
Treatment of hyperkalemia can be divided into three categories, based upon mechanism of action: list these 3 categories. Give examples of agents or therapies in each category
Conceptually, treatments of hyperkalemia are divided into (1) physiologic antagonists and membrane stabilizers (calcium), (2) agents that shift or drive potassium into cells (insulin, beta adrenergic agonists, sodium bicarbonate, hyperventilation), and (3) agents or process that remove potassium from the body (sodium polystyrene sulfate (Kayexalate), diuretics, hemodialysis).
For the following treatments of hyperkalemia, state the onset (minutes) and duration of action (minutes or hours): calcium salts, sodium bicarbonate, insulin-glucose infusion, sodium poly- styrene sulfate (Kayexalate), and loop diuretics.
The onset and duration of action of various treatments of hyperkalemia, arranged from fastest to slowest: (1) calcium salts: onset in 1–3 minutes, duration of action 30–60 minutes; (2) onset of action of sodium bicarbonate is 5–10 minutes, followed by a duration of action 1–2 hours; (3) loop diuretics: onset of action 15–30 minutes with a duration of action of 2–3 hours; (4) insulin-glucose infusion, onset of action is 30 minutes, followed by a duration of action of 4–6 hours; and, (5) sodium polystyrene sulfate (Kayexalate), onset in 1–2 hours, duration of action 4–6 hours.
List 6 factors that contribute to persistent pulmonary hypertension of the newborn (PPHN).
Hypoxia, acidosis, hypothermia, hypovolemia, pneumonia, and inflammatory mediators are primary factors that contribute to persistent pulmonary hypertension of the newborn (PPHN).
Identify conditions and risks that precipitate persistent pulmonary hypertension of the new- born (PPHN).
Persistent pulmonary hypertension of the newborn (PPHN) is usually caused by precipitating conditions such as severe birth asphyxia, meconium aspiration, sepsis, congenital diaphrag- matic hernia, and maternal use of nonsteroidal anti-inflammatory drugs (NSAIDs). Risk fac- tors for PPHN include maternal diabetes or asthma, and cesarean delivery.
Describe the main physiologic function of glucagon.
The main effect of glucagon is to increase serum glucose concentration by causing hepatic gluconeogenesis and glycogenolysis (breakdown of glycogen). Glucagon plays a key role in glucose homeostasis by antagonizing the effects of insulin.
List 9 effects of glucagon, in addition to its role in glucose homeostasis.
In addition to increasing blood glucose, known effects of glucagon in human physiology include: (1) inhibited gastric motility; (2) inhibited gastric acid secretion; (3) enhanced bile secretion; (4) increased blood flow to some tissues, especially the kidneys; (5) enhanced urinary excretion of inorganic electrolytes; (6) increased insulin secretion; (7) anorexia; (8) inotropic and chronotropic cardiac effects; and, (9) relaxation of smooth muscle (e.g. biliary sphincter).
By what receptor and second messenger system does glucagon exert its positive inotropic and chronotropic effects?
Glucagon acts through its own G-protein coupled receptor (GPCR) and generation of cyclic adenosine monophosphate (cAMP). In other words, glucagon binds to glucagon receptors to promote the formation of cAMP.
The hemodynamic benefits of glucagon might be useful in what 5 situations?
The hemodynamic benefits of glucagon—positive inotropy and positive chronotropy— may be beneficial in: (1) low cardiac output syndrome following cardiopulmonary bypass; (2) low cardiac output syndrome with myocardial infarction; (3) chronic congestive heart failure; (4) anaphylactic shock with refractory hypotension; and, (5) excessive β-adrenergic blockade.
State the signs and symptoms of β receptor antagonist overdose. Which specific β receptor properties correlate with these signs and symptoms?
The manifestations of β receptor antagonist overdose depend on the characteristic of the drug, particularly its β1 selectivity, intrinsic sympathomimetic activity, and membrane- stabilizing properties. Hypotension, bradycardia, prolonged AV conduction times and wid- ened QRS complexes are common signs of beta blocker toxicity. Seizures and depression may occur, as well as hypoglycemia and bronchospasm.
Describe the treatment of β-adrenergic antagonist (beta blocker) overdose.
Overdose of β-blocking drugs may be treated with atropine, but isoproterenol, dobutamine, or glucagon infusion (or some combination) may be required along with cardiac pacing to ensure an adequate rate of contraction.
Which opioid can block voltage-dependent sodium channels, in other words, which opioid has local anesthetic properties?
Meperidine is an agonist of both μ- and κ-receptor and has been shown to block voltage- dependent sodium channels. Meperidine has well-known local anesthetic properties, particu- larly after epidural administration.
What is the metabolic syndrome? What is the prevalence of metabolic syndrome in the U. S. population?
The metabolic syndrome, also known as syndrome X and insulin resistance syndrome, is a cluster of metabolic abnormalities associated with an increased risk of diabetes and cardio- vascular events. Individuals with this syndrome have up to a fivefold greater risk of develop- ing type 2 diabetes mellitus (if not already present) and are also twice as likely to die from a myocardial infarction or stroke compared with those without the syndrome. Individuals with metabolic syndrome also have proinflammatory and prothrombotic states. There is a 35% to 40% prevalence of metabolic syndrome in the U.S. population (Miller gives a 24% age- adjusted prevalence).
The American Heart Association and the National Heart, Lung, and Blood Institute define metabolic syndrome as the presence of three or more of 5 criteria. State the 5 criteria that define metabolic syndrome.
Metabolic syndrome is defined by the presence of three or more of the following 5 criteria: (1) central obesity (increased waist circumference): >102 cm (40") in males, >88 cm (35") in females; (2) dyslipidemia: triglycerides ≥150 mg/dL; (3) dyslipidemia: HDL ≤40 mg/dL in males, HDL ≤50 mg/dL in females; (4) hypertension: ≥130/85 mm-Hg or use of antihyper- tensives; and, (5) elevated fasting glucose: ≥100 mg/dL (≥5.6 mmol/L) or use of a medica- tion for hyperglycemia.
Describe a subgluteal sciatic nerve block (lithotomy approach).
A supine approach to the sciatic nerve is afforded by the subgluteal sciatic nerve block (lithotomy approach). The patient is placed supine, and the extremity to be blocked is flexed at the hip (90–120 degrees). In this position, the gluteus maximus muscle is flattened and the sciatic nerve lies relatively more superficial, making it palpable in the hollow between the semitendinosus and biceps femoris muscles. A line is drawn between the ischial tuberosity and the greater trochanter, and a wheal is raised at its midpoint. A 10- to 15-cm insulated needle is inserted perpendicular to the skin and advanced until a motor response involving the foot or ankle is elicited. Twenty to 25 mL of a local anesthetic solution is then injected.
What are the 3 muscular borders of the popliteal fossa?
The popliteal fossa is essentially a triangle, defined laterally by the tendon of the biceps femoris, medially by the common tendon of the semitendinosus and semimembranosus muscles and inferiorly by the two heads of the gastrocnemius muscle. The two heads of the gastrocnemius muscle correspond to the popliteal crease.
Describe the popliteal fossa approach to the sciatic nerve block (posterior approach).
The patient is positioned prone (or lateral, or supine with the lower extremity flexed at the hip and knee) and the borders of the popliteal fossa are identified by flexing the knee joint. A triangle is constructed—the base is the skin crease and the two sides are the semimembra- nosus (medially) and the biceps femoris (laterally). A line is drawn from the middle of the base to the apex, bisecting the triangle. The site of insertion of the needle is 1 cm lateral to the line and 7- to 10-cm above the base of the triangle. A 10-cm insulated needle connected to a nerve stimulator is introduced through a skin wheal of local anesthesia at a 45- to 60- degree anterosuperior angle. The sciatic nerve usually is located at a depth of 1 to 2 cm in an adult. After careful aspiration, 30 to 40 mL of a local anesthetic is injected.
For a fire to occur, three components of a ‘fire triangle’ must be present: list the triad of components in the fire triangle.
For a fire to occur, three components of the fire triangle must be present: a fuel source, an ignition source, and an oxidizer.
There are a number of ignition sources in the operating room, most are under the surgeon’s control. List potential ignition sources in the OR.
Potential ignition sources in the operating room are: (1) lasers; (2) electrosurgery unit (ESU); (3) argon beam coagulator; (4) fiberoptic illumina- tion; (5) defibrillator; (6) pressure regulators; (7) surgical lights; and, (8) electrical lights.
Define “fuel” and list examples of fuels in the operating room.
A fuel is anything that burns. Fuels abound in the operating room, including the patients themselves. Fuels are largely under the control of the nursing staff. Examples of fuels in the OR include: (1) tracheal tubes; (2) supraglottic airway devices; (3) drapes, towels, and dress- ings; (4) adhesives; (5) skin preparatory solutions; (6) intestinal gases; (7) oxygen cannulas; (8) petroleum-based lubricants and ointments; and, (9) body hair.
What are the 2 most common oxidizers in the operating room?
Oxygen and nitrous oxide are the most common oxidizers in the operating room and are un- der control of the anesthetist. Nitrous oxide supports combustion and in the process releases the energy of its formation, providing increased heat.
A desiccated CO2 absorbent can serve as one of the 3 components of the fire triangle—which one? Explain the process.
Desiccated CO2 absorbent is a possible source of ignition in the breathing circuit. When a desiccated strong base CO2 absorbent is exposed to sevoflurane, absorber temperature of several hundred degrees may result from their interaction. The buildup of very high tempera- tures, the formation of combustible degradation byproducts (formaldehyde, methanol, and formic acid), plus the oxygen- or nitrous oxide-enriched environment provide all the sub- strates necessary for a fire to occur.
List the sequence of steps to take to manage an intraoperative airway fire.
The specific sequence of steps to take in managing an intraoperative airway fire depends to a certain extent upon the reference: Barash combines many steps into a short, 4-point list, whereas Nagelhout and Plaus have 2 different descriptions, a short version and lengthy list of discrete steps. The 4-step Barash version: (1) simultaneously remove the endotracheal tube and stop gases/disconnect circuit; (2) pour saline into airway; (3) remove burning materials; (4) mask ventilate patient, assess injury, consider bronchoscopy, reintubate. The short Nagel- hout and Plaus version: (1) stop oxygen flow; (2) stop ventilation; (3) extubate patient; (4) extinguish fire; (5) mask ventilate; (6) reintubate. The patient will require airway assess- ment and medical treatment including bronchoscopy, lavage, and steroids.
In the previous question, shorter versions of airway fire management were given; Nagelhout and Plaus provide a more expansive 15-step version—list these 15 steps.
Nagelhout and Plaus’ more extensive 15-step version: (1) discontinue use of laser; (2) in rapid succession, remove ETT, turn off all gases, remove sponges and any flammable mate- rial, and pour saline into airway; (3) extinguish burning ETT/LMA in basin of water (always available during laser surgery); (4) resume ventilation with air, ventilate with 100% O2 only when the fire is extinguished; (5) examine airway and remove residual debris with rigid bronchoscope, consider lavage with normal saline, examine small and distal airways with flexible fiberoptic bronchoscope; (6) administer humidified O2 by mask if airway damage is minimal and risk of laryngeal edema is low; (7) if indicated, reintubate with a smaller ETT; (8) assess extent of thermal trauma with ABG, carboxyhemoglobin levels, and CXR; (9) keep patient intubated and administer 40% to 60% humidified O2 if airway burn is pre- sent or suspected; (10) consider tracheostomy and mechanical ventilation for postoperative management; (11) consider administration of steroids; (12) admit patient to ICU for a mini- mum 24-hour observation; (13) retain all equipment and materials involved in the fire for further inspection; (15) reassemble surgical team to identify the sequence of events that led to the surgical fire; (16) report fire as a sentinel event to The Joint Commission, ECRI, and the FDA. (NB: Miller takes an intermediate approach, closer to the discrete listing of Nagel- hout and Plaus).
Match the major classes of diuretics with their tubular (nephron) site of action.
Inhibitors of carbonic anhydrase (acetazolamide) act at the proximal tubules. Osmotic diuret- ics (mannitol, glycerin, isosorbide) work at the proximal tubule and/or loop of Henle. (NB: the ‘classic’ teaching has been osmotic diuretics act at the proximal tubules; the latest evidence—presented in Goodman & Gilman’s The Pharmacologic Basis of Therapeutics, one of the NBCRNA reference texts—is osmotic diuretics work on the loop of Henle.) Loop diuretics (furosemide, bumetanide, torsemide, ethacrynic acid) are inhibitors of Na+-K+-2Cl– symport acting at the thick ascending limb (TAL) of the loop of Henle. Thiazides and thia- zide-like diuretics (bendroflumethiazide, chlorothiazide, hydrochlorothiazide, hydroflumethi- azide, methylclothizide, polythiazide, trichlorthiazide, chlorthalidone, indapamide, metola- zone, quinethazone) inhibit Na+-Cl– symport at distal tubules. Potassium-sparing diuretics (triamterene and amiloride) inhibit renal sodium channels in the late distal tubule and collect- ing ducts. Antagonists of mineralocorticoid receptors (spironolactone and eplerenone) work in the late distal tubule and collecting ducts as well. Nesiritide (human recombinant BNP) acts at the inner medullary collecting duct (not shown on figure).
if the diuretic site of action was a hotspot question, what would you do for the agents that have multiple sites of action, such as the potassium-sparing agents (late distal tubule and collecting ducts)? Multiple hotspots are permissible, thus place the marker in either location. If the question was a matching style drag-and-drop format, you should be able to eliminate a choice that only matches with another agent in the question.
Where is positive end- expiratory pressure (PEEP) applied in the anesthesia cir- cuit?
A positive end-expiratory pressure (PEEP) valve must be placed in the expiratory side of the breathing system. Possible locations for the PEEP valve are shown in the accompanying figure (A, B, C).
What does the ASTM standard require of disposable PEEP valves?
The ASTM standard requires that a PEEP valve be marked with an arrow indicating proper direction of gas flow or the words inlet and outlet or both.
The trigeminal nerve has three divisions—the ophthalmic, maxillary, and mandibular—as you know. Describe the anatomy and functions of the mandibular division (V3).
The anterior branch of the mandibular nerve (V3) gives rise to the masseter nerve, which provides motor innervation to the muscles of mastication (chewing, “moves the mandible”). The posterior branch of the mandibular nerve provides sensory innervation to the lower teeth and gums (“feels the mouth inside and out”). The lingual nerve is a terminal branch of the mandibular nerve: the lingual nerve supplies general sensory innervation to the lingual mucous membranes, the anterior two-thirds of the tongue, and floor of the mouth.
What is the relationship between the chorda tympani nerve (a branch of the facial nerve, CN VII) and the lingual nerve (a terminal branch of CN V3)?
The chorda tympani nerve, a branch of the seventh cranial nerve (facial nerve, CN VII) joins the lingual nerve, shortly after the origin of the lingual nerve, and courses with the lingual nerve to the anterior two-thirds of the tongue. The chorda tympani supplies special sensory fibers to the taste buds on the anterior two-thirds of the tongue. (Tip: Hagberg’s text has a wonderful one paragraph summary of the innervation of the tongue, p51.)
Which three cranial nerves supply sensory innervation to the oropharynx?
The oropharynx is supplied by a plexus derived from the vagus (CN X), facial (CN VII), and glossopharyngeal (CN IX) nerves.
Describe the anatomy and functions of the glossopharyngeal nerve (CN IX).
The glossopharyngeal nerve (GPN) supplies general and special (taste) sensory innervation to the posterior third of the tongue via the lingual branch (caution: not the lingual nerve, which is a terminal branch of the mandibular division of CN V), the vallecula, the anterior surface of the epiglottis, the posterior and lateral walls of the pharynx, and the tonsillar pil- lars. Motor innervation from the glossopharyngeal nerve is to one of the muscles of degluti- tion (swallowing).
Block of which nerve abolishes the gag reflex and decreases the hemodynamic response to laryngoscopy?
The glossopharyngeal (GPN) block is highly effective in abolishing the gag reflex and decreasing the hemodynamic response to laryngoscopy, including awake laryngoscopy.
Explain the anterior approach to the glossopharyngeal nerve block.
The anterior approach to the glossopharyngeal block, which isolates the lingual branch of the glossopharyngeal nerve and is better tolerated by the patient, involves injecting local anes- thetic at the base of the anterior tonsillar pillar (palatoglossal arch). The practitioner first anesthetizes the tongue with topical anesthesia and then has the patient open his or her mouth and protrude the tongue forward. The anesthetist then displaces the tongue to the opposite side with a tongue blade, resulting in the formation of a gutter. Where the gutter meets the base of the palatoglossal arch, a 23- or 25-gauge spinal needle is inserted approximately 0.25 to 0.5 cm and aspirated for air. If air is obtained on aspiration, the needle has been placed too deeply and should be withdrawn until no air is aspirated. If blood is obtained, the needle must be withdrawn and repositioned more medially. After correct positioning, 1 to 2 mL of 2% lidocaine is injected, and the block is then repeated on the opposite side.
List 8 treatments for hypercalcemia.
hypercalcemia is treated with (1) volume expansion with normal saline (4–6 L in first 24 hours), (2) loop diuretics (enhances renal excretion of calcium), (3) bisphosphonates (zoledronic acid, pamidronate, etidronate) to inhibit bone resorption of calcium (4) mithra- mycin, (5) calcitonin, (6) glucocorticoids, (7) phosphates, and (8) rarely, plicamycin.
Flexible fiberoptic bronchoscopy is essential to verify placement of a double-lumen tube (DLT), as you know. What feature of the endobronchial cuff facilitates visualization of this cuff during flexible fiberoptic bronchoscopy?
Bright blue, low-volume, low-pressure endobronchial cuffs are incorporated on the double- lumen tube for easier visibility during fiberoptic bronchoscopy.
What is the location of the blue endobronchial cuff when a left-sided double-lumen tube is properly placed?
When a left-sided double-lumen tube (DLT) is properly positioned, the top surface of the blue endobronchial cuff should be seen in the left bronchus, approximately 5 mm below the tracheal carina (Nagelhout and Plaus state 1–2 mm below the carina). The blue endobron- chial cuff should not be too proximal or overinflated such that it herniates across the carina and obstructs the contralateral bronchus or pushes the carina to the right
What is the normal serum magnesium concentration (mg/dL)? In mEq/L? In mmol/L?
Normal serum magnesium is 1.8–2.5 mg/dL (1.5–2.1 mEq/L, 0.75–1.5 mmol/L).
What are the manifestations of hypomagnesemia when serum [Mg2+] <1.0– 1.5 mEq/L, 0.5–0.75 mmol/L)?
When serum [Mg2+] <1.0–1.5 mEq/L, 0.5–0.75 mmol/L), neuromuscular irritability, hypokalemia, and hypocalcemia ensue.
Tetany, seizures, and arrhythmias occur when serum magnesium falls below what level?
Tetany, seizures, and arrhythmias occur when serum magnesium concentrations are <0.5 mmol/L).
What manifestations occur when serum magnesium levels reach 5–7 mg/dL (4.2–5.8 mEq/L, 2.1–2.9 mmol/L)?
Hypermagnesemia with serum [Mg2+] = 5–7 mg/dL (4.2–5.8 mEq/L, 2.1–2.9 mmol/L) leads to lethargy, drowsiness, flushing, nausea and vomiting, and diminished patellar tendon reflexes.
What signs occur when serum magnesium levels reach 7–12 mg/dL (4.2–5.8 mEq/L, 2.1–2.9 mmol/L)?
Serum magnesium concentration in the range of 7–12 mg/dL (5.8–10 mEq/L, 2.9–5 mmol/L) leads to somnolence, hypotension, ECG changes, and loss of patellar tendon reflexes.
Complete heart block, cardiac arrest, respiratory arrest, paralysis, and coma occur with what degree of hypermagnesemia?
When serum magnesium levels are >12 mg/dL (>10 mEq/L, >5 mmol/L), complete heart block, cardiac arrest, respiratory arrest, paralysis, and coma occur. NB: According to Chest- nut, respiratory arrest occurs more specifically at magnesium levels of 15 to 20 mg/dL, and asystole occurs when the serum magnesium concentration exceeds 25 mg/dL.