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  • Nurse Anesthesia Program Interview Prep Guide

    Attached is a prep guide created by one of our members, RebelBKM. It is extremely useful!
    CRNA Interview Preparation

    Q: Tell me about a time when you had to manage a difficult clinical situation.

    Q: Tell me about a time when you were working with someone who wasn't pulling their weight, and they had a different value system than yours. How did you deal with this person?

    Q: Tell me about a time when you failed. What happened, and how did you recover?

    Q: Tell me about a time when you had an ethical dilemma at work. What did you do?

    Q: Tell me about a time when you felt it was you against everyone else. You thought you were right and that everyone else was wrong. What did you do?

    Q: Why do you want to be a CRNA?**

    Q: What would make you a successful CRNA?**

    Q: How do you handle stress?

    Q: What kind of patients do you take care of? Your favorite and why?**

    Q: Tell us about your work experience.**

    Q: How do you describe success?

    Q: Do you foresee any barriers to your education? (finances, time commitments)

    Q: What does a CRNA do? How do you think your role as a CVICU nurse relates to the role and responsibilities of a CRNA?**

    Q: Where do you want to be in 5 years?**.

    Q: Why our program?

    Q: What questions do you have for us?**
    A: What do you look for in potential students?
    How does your program facilitate student research?
    I am very interested in teaching and education, how does your program prepare me to be an educator?
    What do you see as your school's strong points?
    On avg. how many intubations, art lines and central lines do students graduate with?
    Is there competition at clinical sites with residents for the opportunity to place those lines?
    If I am accepted what you can I do between now and the beginning of the program to adequately prepare myself?

    If you saw one of your fellow students or colleagues using drugs outside of work/classroom, what would you do? This is probably universal for most schools, which is logical since we are entrusted to an arsenal of potentially addictive drugs and have a large amount of freedom and stress.
    If you had to pick a topic for a master's thesis or doctoral dissertation, what might it be?
    Who (within the field) has influenced you the most? What do you consider the biggest issue facing the profession today? Next 5/10 years?
    How do you feel that your background will influence your research, clinical work and areas of interest?**
    How do you feel about giving up a paying job for several years?

    Me in 30 seconds:

    What is your strongest trait that will help you in your academic/professional career.**

    What is your most important weakness that you will struggle with, if any, toward this profession?

    Tell me about a typical pt in your ICU**

    What are your roles and responsibilities?**

    What do you know about XYZ School and our program?

    What if in clinical someone told you were taping your IV wrong. What would you do?

    Tell me one of your greatest accomplishments? And at your last job?

    Give an example of where you showed leadership.

    Give an example of community service.

    Give an example of when you worked on a team.

    Give me an example of your problem solving.
    What have you done to develop or change in the last few years?.

    How do others see you?

    Do you work well under pressure? Give an example.

    How do you think you will fit into the program?

    How will you be an asset to this program?

    What do you enjoy most about your job?

    What do you want written on your tombstone?

    What are your expectations of the program?

    What will you do if you don’t get into the program?

    Swan Numbers to Know!
    Cardiac Output = SV x HR and SV = preload+afterload+contractility
    Normal = 4-8 LPM

    Cardiac Index = 2.5-4 LPM

    Stroke Volume = 60-130 ml/beat
    RAP= 2-6
    CVP= 3-8
    PAP = Sys 20-30 diastolic 8-15 mean <20
    PAWP= 6-12 “normal” may need more for optimal preload. Patient specific
    SVR = 900-1400 calculated <(map-RAP) x 80> / CO
    PVR = 40-150
    Ejection fraction. Normal > 50%
    Receptor information: 1 heart 2 lungs and all those extremities
    Dopmminergic receptors are located in the vessels of renal, coronary, cerebral and mesenteric systems resulting in arterial vasodialation.

    Beta 1 effects- results in
    Inotropy- resulting in increased myocardial contractility
    Chronotropy- increased heart heart
    Dromotropy- increased conduction velocity.

    Beta 2 effects- vasodialation subclinical effects
    Alpha 1 effects- arterial vasoconstriction (increase SVR)
    Alpha 2 effects- Arterial vasodilation. (Subclinical )

    Medications to know
    Epi- dose 0.03 – 1 mcg/kg/min Endogenously released catecholamine. Intravenous (exogenous) administration results in dose dependent adrenergic receptor stimulation. Very low dose gtts may cause mild vasodilation and brochodilation via beta 2 stimulation. Intermediate and high dose gtts stimulate beta 1 receptors resulting in increased cardiac output and arterial vasoconstriction through alpha 1 stimulation. PALS calls for in ‘cold shock states’.

    Norepi dose 0.03- 2 mcg/kg/min. Pals use in warm shock. Mostly alpha stimulation for increase in SVR for increase preload and CO. maybe some mild beta 1 stim. Will have increase in HR. and increase of DBP.

    Vasopressin normal dose 0.3 mu/kg/min to 2 mu/kg/min
    Vasopressin AVP has two principle sites of action: the kidney and blood vessels.
    1. The primary function of AVP in the body is to regulate extracellular fluid volume by affecting renal handling of water, although it is also a vasoconstrictor and pressor agent (hence, the name "vasopressin"). AVP acts on renal collecting ducts via V2 receptors to increase water permeability (cAMP-dependent mechanism), which leads to decreased urine formation (hence, the antidiuretic action of "antidiuretic hormone"). This increases blood volume, cardiac output and arterial pressure.
    2. A secondary function of AVP is vasoconstriction. AVP binds to V1 receptors on vascular smooth muscle to cause vasoconstriction via the IP3 signal transduction pathway, which increases arterial pressure; however, the normal physiological concentrations of AVP are below its vasoactive range. Studies have shown, nevertheless, that in severe hypovolemic shock, when AVP release is very high, AVP does contribute to the compensatory increase in systemic vascular resistance
    Dopamine dose 2-20 mcg/kg/min “
    renal dosing” 2-5 mcg/kg/min results in dopaminergic stimulation.
    Intermediate dosing 5-10 mcg/kg/min predominant beta 1 stimulation.
    High dose 10-20 mcg/kg/min predominant alpha stimulation.

    Dobutamine dose 2-20 mcg/kg/min
    Synthetic catecholamine that causes beta 1 stimulation as well as vasodilation
    Vasodilation occurs because of it’s major metabolite 3-O methydobutamine, with is an inhibitor of alpha adrenoreceptors

    Milrinone dose 0.25-1 mcg/kg/min
    Positive inotrope effects are not related to stimulation of the SNS. It achieves its desired effects by inhibiting phosphodiesterase III. This in turn results in increased cAMP and subsequently, increased CA ion influx into cardiac muscle cells. Increased CA in cardiac cells results in increased force of contraction. In the vascular system, cAMP accumulation results in decreased CA ion influx resulting in vasodilation. Due to the lack of SNS stimulation dysrrhythmias are less common than with other inotropes.

    Isopril dose 0.05-0.1 mcg/kg/min used in heart transplant pt. to maintain optimum CO since the heart is now denervated.
    Niprid dose 0.5- 5 mcg/kg/min venous and arterial vasodilator with very quick onset.
    Description: Nitroprusside is an intravenous hypotensive agent effective in the acute management of hypertensive crisis and in the management of congestive heart failure. Nitroprusside is an extremely potent vasodilator with a rapid onset and a short duration of action. Nitroprusside is used primarily to manage hypertensive emergencies but can also be useful when immediate reduction of preload or afterload is needed. Other uses of the drug not currently included in the U.S. product labeling include the control of paroxysmal hypertension during surgery secondary to pheochromocytoma, treatment of peripheral vasospasm secondary to ergot alkaloid overdose, adjunctive treatment in valvular (mitral and aortic) regurgitation therapy, and reduction of afterload in patients with myocardial infarction associated with persistent chest pain. Prolonged infusions, however, have a high potential for toxicity, limiting general use of the drug. Because of its short duration, it must be administered via IV infusion. Although nitroprusside was discovered in 1850 and shown to exert hypotensive effects in humans as early as 1929, it was not approved by the FDA for clinical use until 1974.

    Mechanism of Action: The peripheral vasodilatory effects of
    nitroprusside are due to a direct action of the drug on arterial and venous smooth muscle. Other smooth muscle tissue in the body is not affected, and myocardial contractility is unaffected. Nitroprusside's hypotensive effects are enhanced by other hypotensive agents and are not inhibited by adrenergic blocking agents. Pressor agents that exert a direct stimulatory effect on the myocardial tissue (i.e., epinephrine) are the only class of drugs that can cause an increase in blood pressure during nitroprusside therapy. Almost any desired blood pressure can be maintained with various infusion rates of the drug.

    Nitroprusside-induced peripheral vasodilation results in a reduced left ventricular afterload, and this, along with a reduced venous return to the heart (due to venous pooling of the blood and decreased arteriolar resistance), results in a slight increase in heart rate and decrease in cardiac output in hypertensive patients. In patients with congestive heart failure,
    nitroprusside improves left ventricular heart performance, with increases in cardiac index, cardiac output, and stroke volume. Heart rate also slows in these patients, and arrhythmias can be reduced or abolished. Nitroprusside also can decrease myocardial oxygen demand, which is beneficial to patients with ischemia. Diuresis also occurs during nitroprusside therapy, producing increased urine volumes and increased sodium excretion.

    Nitroprusside is administered intravenously, resulting in immediate blood pressure reduction. The distribution kinetics of the drug are unknown, but it is believed to penetrate cell membranes slowly and to be distributed predominantly into the extracellular space. It is not known whether the drug crosses the placenta or the blood-brain barrier, or if it is secreted into breast milk. Nitroprusside is rapidly metabolized to cyanide radicals, which are then converted to thiocyanate in the liver via the enzyme rhodanase (see below). These metabolites are excreted almost entirely in the urine. The drug is short-acting, with hypotensive effects lasting only 1—10 minutes following infusion. The circulatory half-life of nitroprusside is 2 minutes.

    Nitroprusside is metabolized to cyanide and thiocyanate, which, although they do not contribute to the antihypertensive action, have the potential to cause severe toxic reactions. Nitroprusside molecules begin to break down immediately after contact with sulfhydryl groups located in the cell wall. An intraerythrocytic reaction occurs, in which a molecule of nitroprusside reacts with an equivalent amount of hemoglobin, forming methemoglobin and liberating five cyanide ions. One of these cyanide ions then reacts with the methemoglobin molecule to form cyanmethemoglobin, a biologically inert compound. A patient with a normal red cell count and normal methemoglobin concentration is able to buffer approximately 175 mcg of cyanide ion per kg body weight. In other words, an otherwise healthy patient can buffer a little less than 500 mcg/kg of infused nitroprusside.

    Once the intraerythrocytic methemoglobin supply is saturated, the remaining cyanide radicals are converted to thiocyanate in the liver via the hepatic enzyme rhodanase. This reaction requires a sulfur donor, typically thiosulfate, cysteine, or cystine. Physiological concentrations of thiosulfate (11 mg/L) can convert cyanide ions to thiocyanate at about 1 mcg/kg/minute (roughly equivalent to a
    nitroprusside infusion of about 2 mcg/kg/minute). Cyanide accumulates at infusion rates that exceed this rate, and excess cyanide binds to mitochondrial cytochromes, inhibiting cellular respiration and possibly causing cell death. Thiocyanate toxicity occurs at plasma levels of 50—100 mcg/mL.
    Nicardipine dose 0.5-3 mcg/kg/min adults 5 mg/hour increased by 2.5 mg/hour every 15 minutes to a maximum of 15 mg/hour
    Inhibits calcium ion from entering the “slow channels” or select voltage-sensitive areas of vascular smooth muscle and myocardium during depolarization, producing a relaxation of coronary vascular smooth muscle and coronary vasodilation; increases myocardial oxygen delivery in patients with vasospastic angina
    Nitroglycerin, an organic nitrate available in many dosage forms, is a vasodilator proven to be the mainstay of therapy in the management of angina pectoris. Nitroglycerin is also used to control perioperative hypertension, to produce controlled hypotension during surgical procedures, to treat hypertensive emergencies, and to treat congestive heart failure associated with myocardial infarction. Nitroglycerin has also been used to treat pulmonary hypertension. Synthesized in 1846, nitroglycerin was found to cause severe headaches when placed on the tongue. The drug was later found to exhibit vasodepressor effects similar to those of the drug amyl nitrite, but with less adverse effects and better dosage control. The use of sublingual nitroglycerin for the relief of acute anginal attacks was established in 1879. Because it is inexpensive, has a rapid onset of action, and has a well-documented efficacy, sublingual nitroglycerin is still considered the drug of choice for the acute relief of angina. Although organic nitrates are still frequently prescribed for the relief of angina, they have recently come under scrutiny because of the controversy surrounding claims that nitrate tolerance and attenuation of pharmacodynamic effects have been demonstrated with all nitrate dosage forms. Nitroglycerin was granted FDA approval in 1938. In late December 2004, the FDA denied approval for Cellegesic™, a low strength 0.2% topical ointment, which was evaluated for treatment of pain associated with anal fissures and hemorrhoids.

    Mechanism of Action: Similar to other nitrites and organic nitrates,
    nitroglycerin is converted to nitric oxide (NO), a reactive free radical. Nitric oxide, the active intermediate compound common to all agents of this class, activates the enzyme guanylate cyclase, thereby stimulating the synthesis of cyclic guanosine 3',5'-monophosphate (cGMP). This second messenger then activates a series of protein kinase-dependent phosphorylations in the smooth muscle cells, eventually resulting in the dephosphorylation of the myosin light chain of the smooth muscle fiber and the subsequent release, or extrusion, of calcium ions. The contractile state of smooth muscle is normally maintained by a phosphorylated myosin light chain (stimulated by an increase in calcium ions). Thus, the nitrite- or nitrate-induced dephosphorylation of the myosin light chain signals the cell to release calcium, thereby relaxing the smooth muscle cells and producing vasodilation.

    It is believed that nitrates correct myocardial oxygen imbalances by reducing systemic and pulmonary arterial pressure (afterload) and decreasing cardiac output secondary to peripheral dilation rather than coronary artery dilation. Nitrates therefore relax peripheral venous vessels, causing a pooling of venous blood and decreased venous return to the heart, which decreases preload. Nitrates reduce both arterial impedance and venous filling pressures, resulting in a reduction of the left ventricular systolic wall tension, which decreases afterload. Thus, nitrate-induced vasodilation increases venous capacitance and decreases arteriole resistance, thereby reducing both the preload and afterload, and lowering the cardiac oxygen demand.

    Total coronary blood flow can be increased by nitrites and nitrates in patients with normal hearts, but in patients with ischemia,
    nitroglycerin does not increase total coronary blood flow but simply redistributes blood to ischemic areas. This effect is believed to be due to the drug's preferential dilation of the larger conductive vessels of the coronary circulation, which, in the presence of coronary atherosclerosis, redirects the distribution of the coronary blood supply to ischemic areas.

    Nitrates cause a transient compensatory increase in heart rate and myocardial contractility that normally would increase myocardial oxygen consumption, yet the nitrate-induced decrease in ventricular wall tension results in a net decrease in myocardial oxygen demand and amelioration of the pain of angina pectoris. In addition,
    nitroglycerin relaxes all other types of smooth muscle including bronchial, biliary, GI, ureteral, and uterine. Nitrites and nitrates are functional antagonists of acetylcholine, norepinephrine, and histamine.

    In individuals who have minimal reflex tachycardia, syncope can result from the decrease in blood pressure that occurs following higher doses of nitrates and nitrites. Although this is not likely to occur with doses of nitrates that do not cause blood pressure reduction, patients should be sitting or lying down during and immediately after administration of nitroglycerine.

    The antihypertensive actions of
    nitroglycerin are secondary to pharmacologic properties that make it an effective antianginal agent but are primarily a result of its peripheral vasodilatory effects. With the exception of greater vascular (venous) specificity and the greater variety of pharmaceutical preparations available, nitroglycerin (NTG) is similar to nitroprusside in many respects. Both agents are capable of producing venous (more so with NTG) and arterial dilation, with beneficial effects on redistribution of myocardial blood flow.

    Nitroglycerin can be administered by the oral, lingual (spray), sublingual, intrabuccal, topical, or intravenous routes. Nitroglycerin is well absorbed across the oral mucosa, transdermally, and following systemic oral administration. Irrespective of the route of administration, organic nitrates are virtually completely metabolized by the enzyme glutathione-organic nitrate reductase, so the systemic or presystemic hepatic biotransformation is the key determinant of the bioavailability and duration of action of the various preparations.

    The onset of action for each
    nitroglycerin preparation is as follows: IV, immediate; translingual, 2—4 minutes; extended-release capsules and tablets, 20—45 minutes; sublingual, 1—3 minutes; transmucosal (buccal) extended-release tablets, 2—3 minutes; ointment, 20—60 minutes; and transdermal, 40—60 minutes. Duration of action is as follows: IV, several minutes (dose-dependent); translingual, 30—60 minutes; extended-release capsules and tablets, 8—12 hours; sublingual, 30 minutes; transmucosal (buccal) extended-release, 5 hours; ointment, 4—8 hours; and transdermal, 18—24 hours.

    Nitroglycerin distributes widely throughout the body tissues and is approximately 60% plasma protein-bound. The metabolites of nitroglycerin, 1,3- and 1,2-glyceryl dinitrate, are much less potent than the parent compound and have a half-life of approximately 40 minutes, compared to a parent half-life of 1—3 minutes. The metabolites are excreted by the kidneys.

    Esmolol 25-250 mcg/kg/minEsmolol
    Esmolol is a rapid-onset and short-acting selective beta-1 receptor antagonist. These characteristics may make esmolol a useful drug for preventing or treating adverse blood pressure and heart rate increases that occur intraoperatively in response to noxious stimulation, as during intubation of the trachea Menkhaus et al, 1985. Administered as a continuous infusion (200 mg kg -1 min -1 IV) beginning 5 minutes before induction of anesthesia, esmolol prevents increases in heart rate associated with noxious stimulation in patients undergoing coronary artery-bypass graft operations Girard et al. 1986. Alternatively, a bolus of esmolol, 80 mg IV, followed by a continuous infusion (12 mg min -1 IV) lowers heart rate and blood pressure in adult patients undergoing noncardiac surgery Gold et al, 1989. Other reports describe prevention of perioperative tachycardia and hypertension with esmolol, 100 to 200 mg IV, administered over 15 seconds before the induction of anesthesia 1990,Sheppard et al, 1990. Prior administration of esmolol, 500 mg kg -1 min -1 IV, to patients undergoing electroconvulsive therapy with anesthesia induced by methohexital and succinyl-choline results in attenuation of the heart rate increase and a decrease in the length of the electrically induced Seizures Howie et al, 1990. Esmolol has been used during resection of pheochromocytoma and may be useful in the perioperative management of thyrotoxicosis, pregnancy-induced hypertension (toxemia of pregnancy), and epinephrine- or cocaine-induced cardiovascular toxicity Nicholas et al, 1988,Ostman et al, 1988,Pollan and Tadjziechy, 1989,Thorne and Bedford, 1989,Zakowski et al, 1989. The beta-1 selectivity of esmolol may unmask beta-2-stimulated vasodilation by epinephrine-secreting tumors. Administration of esmolol to patients chronically treated with beta-antagonists has not been observed to produce additional negative inotropic effects deBruijn et al, 1987. The presumed reason for this observation is that esmolol, in the dose employed, does not occupy sufficient additional beta-receptors to produce detectable increases in beta-blockade.

    Autonomic Agents

    Cardiovascular Agents

    Cardiovascular Agents
    Class II antiarrhythmics

    Cardiovascular Agents
    Antihypertensive Agents

    Esmolol is an extremely short-acting beta1-selective beta-blocker. However, unlike other beta1-selective beta-blockers (e.g., metoprolol, atenolol), esmolol is administered via continuous IV infusion. Because of the extremely short duration of action of esmolol, it is useful for acute control of hypertension or certain supraventricular arrhythmias. Esmolol was approved by the FDA in 1986 for the acute, temporary control of ventricular rate in certain supraventricular arrhythmias such as sinus tachycardia and atrial flutter and/or fibrillation in the perioperative, postoperative, or emergency setting. Nonapproved indications include short-term control of perioperative hypertension, management of tachyarrhythmias complicating acute MI, and minimization of acute myocardial ischemia secondary to acute MI or unstable angina.

    Mechanism of Action: Beta-adrenergic antagonists counter the effect of sympathomimetic neurotransmitters (e.g., catecholamines) by competing for receptor sites. Similar to metoprolol and atenolol,
    esmolol, in low doses, selectively blocks sympathetic stimulation mediated by beta1-adrenergic receptors in the heart and vascular smooth muscle. Esmolol possesses roughly 100 times more activity on beta1-receptors than on beta2-receptors. Consequently, the pharmacologic effects of esmolol are primarily limited to the myocardium. As with all 'selective' adrenergic agonists, higher doses of esmolol (>300 mcg/kg/min) result in attenuated or lost selectivity for the beta1-receptors. At doses typically used clinically, esmolol does not demonstrate appreciable intrinsic sympathomimetic or membrane-stabilizing activity; however, these effects may be seen at higher doses.

    The antiarrhythmic properties of
    esmolol occur at the nodal level of pacemaker control, increasing sinus cycle length and sinus node recovery time and slowing conduction through the AV node. The pharmacodynamic consequence of this activity is a negative chronotropic effect and, occasionally, conversion to sinus rhythm in the case of atrial fibrillation and/or flutter.

    Actions that make
    esmolol useful in treating hypertension include its negative chronotropic and inotropic activity (which also decreases cardiac output), a reduction in sympathetic outflow from the CNS, and suppression of renin release from the kidneys. The pharmacodynamic consequence of this activity is reduction of both systolic and diastolic blood pressure. Thus, like other beta-blockers, esmolol affects blood pressure via multiple mechanisms. Esmolol is effective in treating angina and post-MI ischemia because the drug decreases the oxygen demand of the heart through its negative chronotropic and inotropic effects as well as its antihypertensive activity.

    Esmolol is administered via IV infusion. Onset of action after IV injection is extremely rapid, with steady-state concentrations achieved within 5 minutes after a loading dose is given. Steady-state esmolol concentrations are proportional to the infusion rate. Following discontinuation, esmolol effects begin to decline in 1—2 minutes, with beta-antagonist activity completely reversed within approximately 20 minutes.

    Esmolol is rapidly and widely distributed (apparent volume of distribution is 3.4 L/kg), although the specific body tissues and fluids into which esmolol distributes have not been determined. Esmolol is 55% protein-bound, primarily to albumin and alpha-1-acid glycoprotein.

    Esmolol is rapidly hydrolyzed in the blood by plasma esterases to the free acid of the methyl ester of esmolol and methanol. The terminal half-life of esmolol averages 9 minutes, so esmolol-induced beta-blockade is virtually eliminated within 20 minutes after drug discontinuation. This property offers a distinct clinical advantage over IV propranolol, which persists for up to 60 minutes after discontinuation. Within 24—48 hours, the majority of an esmolol dose is excreted renally, primarily as inactive metabolites, with less than 2% as unchanged drug. The remainder of a dose may be excreted via the fecal route.

    PGE dose 0.01-0.1 mcg/kg/min
    Genitourinary Agents
    Impotence Agents

    Hormones and Hormone Modifiers

    Description: Alprostadil is naturally occurring prostaglandin E1. Alprostadil and other prostaglandins in the E series are naturally present in the seminal vesicles and cavernous tissues of males and in the placenta and ductus arteriosus of the fetus. Alprostadil is used to treat impotence in adult males and to maintain the patency of the ductus arteriosus in neonates up until the time of corrective or palliative surgery. The efficacy of alprostadil in treating impotence varies with the cause. The response rate is generally lower in patients with impotence due to mixed etiologies compared to those with impotence due to neurogenic, psychogenic, or vasculogenic causes. Two dosage forms are marketed for treating impotence: a transurethral product (Muse®) which uses a medicated pellet administered into the urethra and an injection (Caverject® or Edex®) that is directly injected into the corpus cavernosa. Other dosage forms such as a topical gel and a non-invasive liposomal delivery system are under investigation. Topiglan™ is one such investigational topical formulation of alprostadil under development by MacroChem (www.macrochem.com). The company expects the licensee of the product to conduct phase III trials in order to pursue marketing. Prostin VR Pediatric® is the commercial intravenous preparation of alprostadil used in neonates for maintaining the patency of the ductus arteriosus. The drug is generally more effective in those neonates with low pretreatment blood PO2 and who are 4 days old or less. Intravenous alprostadil requires respiratory monitoring during administration because apnea develops in 10—12% of neonates. Prostin VR Pediatric® was approved by the FDA in 1981, Caverject® in July 1995, MUSE® in October 1996, and Edex® in June 1997.

    Mechanism of Action: For the treatment of impotence, alprostadil relaxes the smooth muscles of the corpus cavernosum; however, the exact mechanism of action is unknown. It appears that the effects are due to increasing the intracellular concentrations of cyclic AMP. Alprostadil interacts with specific membrane-bound receptors that stimulate adenylate cyclase and elevate intracellular cyclic AMP, leading to activation of protein kinase and resultant smooth muscle relaxation. This action is in contrast to papaverine which inhibits oxidative phosphorylation mediated inactivation of cyclic AMP and interferes with calcium mobilization during muscle contraction. Alprostadil may also antagonize the vasoconstrictive actions of norepinephrine by preventing the neuronal release of norepinephrine and may enhance the actions of nonadrenergic, noncholinergic vasodilatory neurotransmitters. In treating impotence, alprostadil induces erection by relaxing trabecular smooth muscle and dilating cavernosal arteries and their branches. Dilation of the cavernosal arteries is accompanied by increased arterial inflow velocity and increased venous outflow resistance. As a result, the lacunar spaces expand and blood becomes entrapped secondary to compression of venules against the tunica albuginea. To achieve adequate tumescence and rigidity, the tunica albuginea must be sufficiently stiff to compress the venules penetrating it and thus block venous outflow. This process is also referred to as the corporal veno-occlusive mechanism. Alprostadil does not directly affect ejaculation or orgasm.

    In the treatment of ductus arteriosus-dependent congenital heart defects, alprostadil maintains ductal patency by relaxing the smooth muscles of the ductus arteriosus. Alprostadil is only effective if given prior to complete anatomic closure of the ductus arteriosus. Administration of alprostadil to neonates with cyanotic congenital heart defects (restricted pulmonary blood flow) results in an increase in pulmonary blood flow and/or increase in mixing between the systemic and pulmonary circulation which leads to a temporary increase in arterial oxygen partial pressure (PaO2) and oxygen saturation. The response of the cyanotic neonate to alprostadil therapy is also inversely related to pretreatment PO2. The greatest response appears to be in those neonates with low pretreatment PaO2 (< 20 torr), narrowing ductus arteriosus, and who are 4 days old or younger. Neonates with PaO2 values of 40 torr or more usually have little response to alprostadil.

    In neonates with restricted systemic blood flow, administration of alprostadil can result in prevention or correction of acidemia, increased cardiac output with increased systemic blood pressure, increased femoral pulse volume, increased renal blood flow and function, decreased gradient of descending to ascending aortic blood pressures (in neonates with coarctation of the aorta), and/or decreased ratio of pulmonary artery pressure to descending aortic pressure (in neonates with interruption of the aortic arch). Unlike in cyanotic neonates, the efficacy of alprostadil in acyanotic neonates does not depend on age or pretreatment PaO2.

    Pharmacokinetics: Alprostadil is administered by intravenous infusion, intracavernosal injection, or via an urethral suppository. Intravenous administration of alprostadil requires a continuous infusion of the drug because approximately 80% of the dose is metabolized in one pass through the lungs, mostly by beta- and omega-oxidation. After intracavernosal or intraurethral administration, minimal systemic absorption occurs. Any alprostadil absorbed by these routes is rapidly metabolized. Alprostadil given via the urethra is delivered directly to the urethral lining for transfer via the corpus spongiosum to the corpora cavernosa. The onset of effect is within 5—10 minutes after urethral administration and the duration of effect is approximately 30—60 minutes and will vary from patient to patient. Following intracavernosal administration, erection usually occurs within 2—25 minutes and may last for about 1 to several hours. Tolerance to the beneficial vascular effects does not appear to occur.

    Once in the systemic circulation, alprostadil is bound primarily to albumin (81%). No significant binding to erythrocytes or white blood cells occurs. Alprostadil is completely metabolized to several metabolites which are primarily excreted in the urine. There is no evidence of tissue retention of alprostadil or its metabolites following IV administration.

    Nitric Oxide 10-40 Nitric Oxide/Oxygen blends are used in critical care to promote capillary and pulmonary dialation to treat Primary Pulmonary Hypertenson in neonatal patients post meconium aspiration and related to birth defect. These are often a last-resort gas mixture before the use of ECMO

    Fentanyl 1-2 mcg/kg
    Versed dosing 0.05-1 mg/kg
    Ketamine 1mg/kg
    Ketamine is a racemic mixture of an R (-) and S (+) optical isomers. The S (+) isomer has been shown to be more potent than the R (-) isomer. It has also been shown to have fewer side effects than either the R (-) isomer or the racemic mixture (Kohrs & Dureux, 1998). Ketamine has a rapid onset (30 seconds), relative short duration (5-15 minutes), high lipid solubility and a low degree of plasma protein binding (12 %) (White, 1997). These properties are reflected in the following parameters from Goodman and Gillman (1996). Ketamine has a molecular weight of 238. It has a pKa of 7.5, elimination half-life of 2.3 +/- 0.5 hours, volume of distribution of 1.8+/- 0.7 L.kg-1, clearance of 15+/- 5 ml.min.kg-1. The drug is extensively metabolized in the liver via the cytochrome P-450 enzymes. Ketamine undergoes N-demethylation to form norketamine, an active metabolite that is one fifth to one third as potent as the parent drug (Stoelting, 1991). Norketamine is then hydroxylated on the cyclohexanone ring in two places. This forms hydroxynorketamine metabolites III and IV. These metabolites can be further metabolized by heat to metabolites II or conjugated to inactive glucuronide metabolites (White, 1997). The metabolites and a small amount of the drug are excreted in the urine.
    Ketamine affects the CNS, producing a state of dissociative anesthesia. Ketamine appears to work at the thalamoneocortical projection system and in the medial medullary reticular formation. These actions play a pivotal role in emotional components of nociception from the spinal cord to the brain (Miller, 2000). Ketamine produces profound analgesia but the patient’s cough, corneal and swallowing reflex often remain intact. Lacrimation and horizontal nystagmus are present and airway secretions increase. Purposeful movements, not related to painful stimuli, occur and skeletal muscle tone increases. Ketamine increases cerebral blood flow (CBF) 60% to 80% but blood flow returns to normal within approximately half an hour after administration. This increase in CBF causes both the metabolic oxygen consumption and intracranial pressure to increase. Electroencephalogram can determine ketamine’s effects. Alpha waves give way to
    theta-waves while the drug is active and return to alpha-waves upon emergence.
    Ketamine, at high doses, may cause emergence delirium, night terrors, sympathetic stimulation and hallucinations.
    Ketamine stimulates the cardiovascular system. This drug has direct myocardial depressant effects but is offset by the centrally produced sympathetic outflow. There is a subsequent increase in heart rate, blood pressure, and cardiac output. These affects on the cardiovascular system can be attenuated with the use of α and β-adrenergic antagonists (Miller, 2000). Inhalational agents will also blunt the cardiovascular response of ketamine (Miller, 2000). Catecholamine-depleted patients may exhibit a decline in blood pressure and cardiac output (White, 1996).
    Ketamine has minimal effects on the respiratory system, airway reflexes are relatively preserved and the carbon dioxide response is not blunted. There is an increase in tracheal, bronchial and salivary gland secretions. The use of an antisialogogue may be necessary to attenuate increased secretions. The increase of circulating catecholamines is thought to give ketamine its bronchodilating properties.
    Kohrs and Durieux (1998) reported that ketamine’s antagonistic action at the NMDA receptor accounts for most of the anesthetic properties of the drug. It is at the phencyclidine site, on the NMDA receptor, that
    ketamine non-competitively inhibits the action of glutamate. Ketamine also acts at opioid, nicotinic, muscarinic, monoaminergic and non-NMDA glutamate receptors.

    Etomdate 0.3 -0.6mg/kg
    Propofol 1-2 mg/kg
    General Anesthetics

    Propofol (2,6-diisopropylphenol) is an intravenous, nonbarbiturate anesthetic that is chemically unrelated to other intravenous anesthetics. Propofol is used to induce anesthesia that can be maintained by continuous infusion or with inhalation anesthetics. Propofol induces anesthesia as quickly as thiopental, but emergence from anesthesia is 10-times more rapid than with thiopental and is associated with minimal postoperative confusion. Only desflurane has a more rapid recovery time than propofol, but desflurane is associated with nausea/vomiting. Propofol has no analgesic activity and causes sedation at a lower dosage than that needed for anesthesia. Unlike many other general anesthetics, propofol possesses antiemetic activity. Propofol (Diprivan®) received FDA approval in October 1989. In March 1997, the FDA granted exclusivity until 2015 to Zeneca for a modified formulation that contains disodium edetate (EDTA) to retard microorganism growth. A generic formulation of propofol is available, but it contains sodium metabisulfite and not EDTA as the preservative.

    Mechanism of Action:
    Propofol appears to inhibit the NMDA subtype of glutamate receptors by channel gating modulation and has agonistic activity at the GABAA receptor. Propofol enhances the amplitude of currents evoked by subthreshold concentrations of gamma-aminobutyric acid (GABA) and directly activates the GABAA receptor in the absence of GABA. Propofol activates chloride channels in the β1 subunit of GABAA, but it is unknown if propofol binds directly to the receptor, binding sites, or if the effects are a result of mediation of distinct mechanisms, such as second messengers. Propofol and benzodiazepines have similar effects on GABAA receptor deactivation but different effects on desensitization. Receptor desensitization causes a fall from a peak (activation) due to agonist application to an apparent steady state. Deactivation is the rate of decay to baseline following the termination of drug application. Both drugs slow the rate of deactivation, but only propofol decreases the rate and extent of receptor desensitization in the presence of saturating concentrations of GABA. In the presence of sub-maximal concentrations of GABA, both drugs slow the rate and extent of receptor desensitization. The anesthetic and amnesic properties of propofol may be or partly a result of NMDA-mediated excitatory neurotransmission depression. The utility of propofol for refractory migraine, status epilepticus, and delirium tremens may be due to enhanced inhibitory synaptic transmission from GABAA receptor agonism or glutamate receptor inhibition.

    Propofol with hypocarbia increases cerebrovascular resistance and decreases cerebral blood flow, cerebral metabolic oxygen consumption, and intracranial pressure. The decrease in cerebral blood flow and intraocular pressure is likely a result of a decrease in systemic vascular resistance. Propofol does not affect cerebrovascular reactivity to changes in arterial carbon dioxide tension.

    Propofol has been shown to possess antiemetic properties. Propofol reduces the concentration of serotonin and 5-hydroxyindoleacetic acid in the area postrema. The reduction may be mediated by the GABAA receptor. Propofol also reduces the synaptic transmission in the olfactory cortex, which suggests a decrease in the release of excitatory amino acids like glutamate and aspartate. Propofol does not affect gastric emptying time or dopamine D2 receptors.

    Propofol is administered intravenously and, due to its high lipophilicity, is rapidly distributed to all tissues in the body. There is fast equilibration between the plasma and the brain. Loss of consciousness usually occurs within 40 seconds, although the onset of action varies with the dose, rate of administration, and extent of premedication. Propofol crosses the placenta and is distributed into breast milk. Propofol is 95—99% protein-bound. The time to tissue saturation depends on the rate and duration of the infusion. Propofol is metabolized in the liver where it rapidly undergoes glucuronide conjugation to inactive metabolites. Initially, the fall in plasma concentration is roughly 50% due to tissue distribution and 50% due to metabolic clearance. The duration of action of a 2—2.5 mg/kg bolus injection is 3—5 minutes despite a delayed release of drug from deep compartments. The steady state concentration is generally proportional to the infusion rate. The clearance of propofol exceeds estimated hepatic blood flow, which suggests extrahepatic routes of metabolism. The elimination half-life of 3—12 hours is the result of slow release of propofol from fat stores. About 70% of a single dose is excreted renally in 24 hours (90% in 5 days). The terminal half-life is 1—3 days after a 10-day infusion.

    Recovery from anesthesia is rapid (8—19 minutes for 2 hours of anesthesia) and is associated with minimal psychomotor impairment. The time to awakening is affected by the tissue drug concentration. The longer the infusion, the greater time to awakening, which usually occurs at a
    propofol concentration of 0.5 µg/mL or less. Emergence from light sedation (Ramsey score from 3 to 2) is usually less than 35 minutes if the infusion has lasted 3 days or less. The emergence time could be up to 3.5 hours or longer for patients that receive more than 3 days of propofol even if the sedation score is kept at 3. The more heavily sedated the patient, the longer the emergence time will likely be, especially for long infusion times. Longer emergence times may occur in obese patients. Significant propofol accumulation may occur with long-term propofol use. Due to peripheral tissue saturation, the rate at which the propofol concentration will fall becomes more dependent on metabolic clearance than tissue redistribution.

    Special populations: Total body clearance and volume of distribution of
    propofol are decreased in the elderly whereas these values in children between 3 and 12 years of age are similar to those of adults. The pharmacokinetics of propofol do not appear to be affected by chronic hepatic or renal disease.

    Precedex load with 1mcg/kg (optional)and then following with infusion of 0.2-0.7 mcg/kg/hr Dexmedetomidine is an alpha-2 agonist, a novel sedative with analgesic properties that controls stress, anxiety and pain. When facilitating a patient's adaptation to mechanical ventilation, the current standard of care is the use of a combination of agents including propofol, opioids, and benzodiazepines. These agents can be associated with a number of side effects, including respiratory depression, especially when agents are used concurrently.
    Dexmedetomidine, as a single agent, will produce sedation, pain relief, anxiety reduction, stable respiratory rates, and predictable cardiovascular responses. Dexmedetomidine facilitates patient comfort, compliance and comprehension by offering sedation with the ability to rouse patients. This "rousability" allows patients to remain sedated yet communicate with health care workers.
    This article was originally published in forum thread: Nurse Anesthesia Program Interview Prep Guide started by ADMIN View original post
    Comments 3 Comments
    1. mwilliams7425's Avatar
      mwilliams7425 -
      Great article on how to ace the anesthesia school interview on www.simplyanesthesia.com. Highlights types of questions asked, clinical scenarios and possible 'test' questions. Very helpful
    1. Christine0717's Avatar
      Christine0717 -
      thank you for this!
    1. TEVA_BELIEVA's Avatar
      this was very helpful, thank you for posting it.