Current Reviews for Nurse Anesthetists

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2 Current Reviews for Nurse Anesthetists Publisher And Editor-in-Chief FRANK MOYA, MD Coral Gables, Florida Editorial Board Advisory Board Chuck Biddle, CRNA, PhD Richmond, Virginia Linda Callahan, CRNA, PhD Klamath Falls, Oregon Nancy Gaskey-Spears CRNA, PhD Gastonbury, Connecticut Joseph A. Joyce, CRNA, BS Winston-Salem, North Carolina Mary Jeanette Mannino, CRNA, JD Laguna Niguel, California Maria Garcia-Otero, CRNA, PhD Coral Gables, Florida Sandra Ouellette, CRNA, Med, FAAN Winston-Salem, North Carolina Charles Barton, MSN, MEd Akron, Ohio Carol G. Elliott, CRNA, MPA, PhD Kansas City, Kansas Linda J. Kovitch, CRNA, MSN Bedford, Massachusetts Frank T. Maziarski, CRNA Seattle, Washington Charles Moss, CRNA, MS Larkspur, Colorado Laura Wild-McIntosh, CRNA, MSN Hillsboro, New Jersey Monte Lichtiger, MD Coral Gables, Florida Associate Publishers Joan McNulty Elizabeth Moya, JD Assistant Editor Linda G. Williams Assistant Publishers Barbara McNulty Donna Scott Circulation Assistants Carrie Scott Tiffany Lazarich Myriam Montes Kimberly Gutierrez Sponsor Frank Moya Continuing Education Programs, LLC Subscription Office - Editorial Office Current Reviews Frank Moya, M.D S.E. First Avenue 1450 Madruga Ave Ft. Lauderdale, FL Suite 207 Coral Gables, FL Phone: (954) Fax: (800) Accreditation This program has been prior approved by the American Association of Nurse Anesthetists for 26 CE credits; Code Number 33802; Expiration Date May 31, Approved by Frank Moya Continuing Education Programs, LLC. Provider approved by the California Board of Registered Nursing, Provider Number CEP 1754, for 26 contact hours and Florida Board of Nursing, Provider Number FBN 2210 for 26 contact hours. In Accordance with AANA directives, you must get 80% of the answers correct to receive one credit for each lesson and if there is a failure, there is no retaking. Disclosure Policy Frank Moya Continuing Education Programs, LLC, in accordance with the Accreditation Council for the Continuing Medical Education s (ACCME) Standards for Commercial Support, will disclose the existence of any relevant financial relationship a faculty member, the sponsor or anyone else who may be in a position to control the content of this Activity has with any commercial interest. BEFORE STARTING, PLEASE SEE LAST PAGE OF LESSON TO READ WHETHER THERE ARE ANY RELEVANT RELATIONSHIPS TO DISCLOSE AND, IF SO, THE DETAILS OF THOSE RELATIONSHIPS. Current Reviews is intended to provide it s subscribers with information that is relevant to anesthesia providers. However, the information published herein reflects the opinions of it s authors and does not represent the views of Current Reviews in Clinical Anesthesia, Current Reviews for Nurse Anesthetists, or Frank Moya Continuing Education Programs, LLC. Anesthesia practitioners must utilize their knowledge, training and experience in their clinical practice of anesthesiology. No single publication should be relied upon as the proper way to care for patients. The information presented herein does not guarantee competency or proficiency in the performance of procedures discussed. Copyright 2015 by Current Reviews. Reproduction in whole or in part prohibited except by written permission. All rights reserved. Information has been obtained from sources believed to be reliable, but it s accuracy and completeness, and that of the opinions based therein are not guaranteed. Printed in U.S.A. Current Reviews is published biweekly by Current Reviews, 1828 S.E. First Avenue, Ft. Lauderdale, FL POSTMASTER: Send address changes to Current Reviews, 1828 S.E. First Avenue, Ft. Lauderdale, FL

3 Vasopressors and Inotropic Agents: Common Clinical Scenarios Joanne Donnelly, DNP, CRNA Clinical Education Director Department of Anesthesiology/School of Medicine University of Colorado Hospital Aurora, Colorado LESSON OBJECTIVES Upon completion of this lesson, the reader should be able to: 1. Identify the mechanism of action of vasopressors and inotropic drugs used in anesthesia care. 2. Describe common myths associated with the administration of vasopressors and inotropic agents. 3. Outline the management of intraoperative hypotension. 4. Discuss the current guidelines for the management of various shock states. 5. Explain the benefits of vasopressin in shock states. 6. Review the hemodynamic management of high-risk surgical patients. 7. Describe tissue perfusion indicators in the management of high-risk surgical patients. 8. Explain current theories for the management of hypotension and the prevention of acute renal failure. 9. Discuss theories related to the administration of vasopressors and the prevention of postoperative visual loss. 10. Describe the potential adverse effects and the prevention of hypotension in the sitting position. Current Reviews for Nurse Anesthetists designates this lesson for 1 CE contact hour in Clinical pharmacology/therapeutics. Introduction Nurse anesthetists administer vasopressors and inotropic agents for a variety of clinical scenarios. The most common scenario is hypotension. Hypotension during anesthesia is a common condition that may be related to the effects of volatile agents and/or regional anesthesia. Hypotension and reduced cardiac output during anesthesia may also occur due to shock states, patient position, type of procedure, or patient-specific comorbidities (such as heart failure). If hypotension is sustained and uncorrected, it may lead to adverse effects in the brain, heart, kidneys, and fetus in a pregnant patient. More specifically, untreated hypotension may lead to stroke, myocardial infarction, or acute renal failure. The treatment of hypotension during surgery and anesthesia frequently includes fluids and vasopressors, with the addition of inotropes when necessary. This lesson will review a few of the common causes of hypotension: vasodilation from anesthesia, shock states, and procedure or surgical position specific causes prone and sitting position. Decision making in treatment will focus on pharmacologic choices, receptor-specific treatment, and the prevention of end-organ damage. Curr Rev Nurs Anesth 38(6):69-80,

4 Anesthesia-induced Hypotension General Anesthesia The induction of general anesthesia and administration of neuraxial anesthesia may cause hypotension, commonly mild and self-limiting. The causes of hypotension subsequent to induction of general anesthesia with propofol is due to: 1) a decrease in sympathetic activity, 2) direct vascular smooth muscle relaxation and 3) direct negative inotropic effects. Studies evaluating both failing and non-failing hearts reveal reduced contractility in even non-failing hearts following the administration of induction doses of propofol. Therefore, ephedrine is the vasopressor of choice for hypotension related to the administration of propofol in lieu of the need to correct negative inotropy and smooth muscle relaxation. Ephedrine effectively returns preoperative hemodynamics via activation of beta adrenergic receptors, alpha adrenergic receptors, as well as stimulating the release of catecholamines from the adrenal medulla (Table 1). However, ephedrine possesses unwanted effects, including an increased heart rate and tachyphylaxis with repeated dosing. Despite the theoretical sense of administering ephedrine to replace hemodynamic losses with induction, there are circumstances in which ephedrine is a poor first line choice. Such instances include all pathologies in which an increase in heart rate may be deleterious, such as in aortic stenosis and coronary artery disease. Neuraxial Anesthesia Neuraxial anesthesia, specifically spinal anesthesia, causes hypotension from the sympathectomy produced by administration of local anesthetics in the intrathecal space. Phenylephrine, a direct-acting alpha-1 adrenergic agonist, stimulates vascular smooth muscle resulting in vasoconstriction. In the operating room, hypotension related to neuraxial anesthesia is commonly treated with crystalloid, ephedrine, and/or phenylephrine. The effects of both phenylephrine and ephedrine have been studied in the treatment of maternal hypotension secondary to spinal anesthesia for cesarean delivery, and studies reveal no differences in fetal acidosis or Apgar scores. Therefore, the administration of both ephedrine and phenylephrine in the hypotensive maternal patient is acceptable. The Surviving Sepsis Campaign recommends maintaining a MAP of 65 mmhg or greater; norepinephrine is the first-line vasopressor. Vasopressor and Inotrope Use in Shock States There are several shock states that may require the administration of vasopressors and/or inotropes. In general, the types of shock include: septic shock, hypovolemic shock, cardiogenic shock, anaphylactic shock, and neurogenic shock (Table 2). Each shock state is described in more detail below. First, a review of specific inotropic agents and vasopressors will allow a more receptor-specific approach to choosing the appropriate drug. A profound understanding of the mechanism of action of positive inotropes and vasopressors aids in determining which drugs will improve tissue perfusion in the high-risk surgical patient. The most commonly Table 1 Adrenergic Receptors Receptor Location Activity Clinical Hemodynamic Effects if Stimulated Alpha 1 Vascular smooth muscle Vasoconstriction Increased BP Alpha 2 Nervous system, presynaptic nerve terminal Decreased norepinephrine release Beta 1 Heart, platelets Positive inotropy, increased chronotropy, platelet aggregation Beta 2 Bronchi, vascular smooth muscle, uterus Increased camp, bronchodilation, vasodilation Beta 3 Adipose, heart Lipolysis; possible mechanism of negative inotropy Dopamine (at least 5 subtypes) Renal, splanchnic, coronary, cerebral Induces vasodilation Subtype causes vasoconstriction via norepinephrine release Decreased BP Increased HR Increased cardiac output Decreased BP Increased HR Increased cardiac output Potential for arrhythmias 72 Current Reviews for Nurse Anesthetists

5 Table 2 Shock States Septic Shock Anaphylactic Shock Hypovolemic Shock Cardiogenic Shock Neurogenic Shock Infectious process releasing chemicals leading to: (1) peripheral vasodilationinterstitial edema and decreased blood return to the heart, and (2) decreased ability of the cells and tissues to take up oxygen and nutrients Shock due to a severe allergic antigen-antibody reaction to substances such as drugs, contrast media, blood products, or insect or animal venom Most common type of shock that is caused by plasma loss due to burns, dehydration, traumatic shock due to blood loss and major tissue damage Caused by inadequate myocardial contractility from acute myocardial infarction, coronary artery disease, or mechanical factors (valvular regurgitation, low output syndrome, arrhythmias) Caused by the loss of sympathetic control (tone) of resistance vessels, resulting in the massive dilatation of arterioles and venules. Caused by general or spinal anesthesia, spinal cord injury, pain, and anxiety. administered positive inotropes include: dobutamine, norepinephrine, epinephrine, dopamine, and milrinone. The mechanism of action and side-effect profile for each drug is listed in Table 3. Dobutamine Dobutamine is a synthetic catecholamine with strong affinity for both beta-1 and beta-2 receptors. Vascular smooth muscle binding of dobutamine results in alpha-1 receptor agonism (vasoconstriction) and beta-2 receptor agonism (vasodilation), leading to a predominant vasodilatory effect. Doses up to 15 mcg/kg/min result in increased inotropy without significant increased systemic vascular resistance. The end result is an increase in cardiac output without significant increases in afterload. Additionally, dobutamine significantly increases myocardial oxygen consumption, making it a useful agent for pharmacologic exercise stress testing. Dopamine Dopamine is an endogenous central neurotransmitter and is the immediate precursor to norepinephrine in the catecholamine synthetic pathway. Receptor effects of dopamine are dose-related (although previously demonstrated renal-dose dopamine is controversial). However, at low doses, mcg/kg/ min, dopamine stimulates D1 postsynaptic receptors located in the coronary, renal, mesenteric, and cerebral beds and D2 presynaptic receptors resulting in vasodilation and increased blood flow in renal tissues. At doses of 3-10 mcg/kg/min, dopamine possesses weak beta-1 receptor activity, promotes release of norepinephrine, and inhibits norepinephrine reuptake; all of these effects lead to an increase in cardiac output, heart rate, and systemic vascular resistance. At higher doses, mcg/kg/min, dopamine stimulates alpha-1 receptors leading to profound increases in systemic vascular resistance. The most serious adverse effect of a dopamine infusion is cardiac arrhythmias. Monitoring for arrhythmias, careful titration, and consideration of a different positive inotropic drug may be necessary. Isoproterenol Isoproterenol is a synthetic, nonselective beta agonist with minimal affinity for alpha adrenergic receptors. The nonselective characteristics of isoproterenol, specifically its actions on beta-2 receptors, limit its usefulness in profound hypotension. Epenephrine Epinephrine is an endogenous catecholamine with high affinity for beta-1, beta-2, and alpha-1 receptors present in cardiac and vascular smooth muscle. Beta adrenergic effects are more pronounced at lower doses and alpha adrenergic effects are more pronounced at higher doses. Infusion rates range from 1-10 mcg/min. Norepinephrine Norepinephrine is a potent alpha adrenergic receptor agonist with modest beta agonist activity. The pharmacologic profile of norepinephrine makes it a powerful vasoconstrictor with less potent direct inotropic properties. Typical infusion rates range from 2-4 mcg/min. Phosphodiesterase Inhibitors Phosphodiesterase inhibitors increase the level of camp by inhibiting its breakdown within the cell. Phosphodiesterase 3 is the enzyme inside the cell responsible for the breakdown of camp. Prevention of this breakdown leads to increased myocardial contractility and vasodilation. The net effect of phosphodiesterase inhibition is increased cardiac output, decreased preload, and decreased afterload. Curr Rev Nurs Anesth 38(6):69-80,

6 Phenylephrine Phenylephrine is a synthetic, potent, pure alpha-1 adrenergic agonist. Since phenylephrine has no beta-adrenergic activity, it has no direct effect on heart rate, but may cause a reflex, transient bradycardia. This effect is due to a baroreceptor-mediated reflex response after rapid increases in mean arterial pressure. Infusion rates may range from mcg/ kg/min. Vasopressin Vasopressin, also known as antidiuretic hormone, is stored in the posterior pituitary gland and released in response to hypotension or increased plasma osmolality. Vasopressin is also synthesized by the heart in response to elevated cardiac wall stress and by the adrenal gland in response to increased catecholamine release. Vasopressin exerts direct effects on the V1 receptors in vascular smooth muscle and V2 receptors in the renal collecting duct cells. The stimulation of V1 receptors results in vasoconstriction and the stimulation of V2 receptors results in an increase in water reabsorption. Additionally, vasopressin increases the sensitivity of the vasculature to norepinephrine. At low concentrations, vasopressin mediates vasodilation in coronary, cerebral, and pulmonary arterial circulations. Unique to vasopressin is that its effects are preserved in the presence of hypoxia and acidosis, making it even more useful in the presence of septic shock. Infusion rates of vasopressin range from units/minute in the treatment of shock. Increased doses and prolonged administration of vasopressin may result in decreased cardiac output, decreased hepatosplanchnic flow, and a rebound hypotension upon termination of vasopressin. Shock States Hypovolemic Shock Hypovolemic shock is the most common type of shock encountered in the operating room. Causes of hypovolemic shock include hemorrhage, acute volume losses from vomiting or diarrhea, third spacing from capillary leaks, and burns. Shock ensues when the patient loses more than 20% of the body s blood or fluid supply. The treatment of hypovolemic shock requires the maintenance of perfusion to end organs, accomplished by the administration of fluids, blood, and potentially vasopressors and inotropes. It is well recognized that the first-line therapy in hypovolemic shock is the administration of crystalloids. While mild hypovolemic shock in surgical patients occurs frequently, more severe hypovolemic shock may result in end organ damage in high-risk surgical patients. Vasopressin 0.03 units/minute in combination with norepinephrine is recommended in the treatment of septic shock. Septic shock is defined as an infection with systemic manifestations characterized by maldistribution of blood flow. Septic shock is the classic distributive shock state, where there is an abnormal flow of blood to the small vessels resulting in poor tissue blood flow and oxygenation. The Surviving Sepsis Campaign recommends goal-directed therapy of fluids and vasopressors to improve end-organ and cellular perfusion. The 2013 recommendations for the treatment of septic shock include the following goals for the first six hours of resuscitation: maintain a mean arterial blood pressure (MAP) of 65 mmhg or greater, central venous pressure (CVP) 8-12 mmhg, urine output > 0.5 ml/kg/hr, and a central venous or superior vena cava oxygenation of > 70% or a mixed venous oxygen saturation of > 65%. Treatments recommended in septic shock to meet hemodynamic goals are: 1) fluid resuscitation of 30 ml/kg crystalloid, 2) initiate vasopressors if unable to maintain a MAP > 65 with crystalloid administration, 3) norepinephrine is the first-line vasopressor, 4) epinephrine is the second-line vasopressor of choice when norepinephrine is insufficient to maintain a MAP of 65 mmhg, 5) vasopressin at 0.03 units/minute is appropriate to use with norepinephrine (on a mid-range dose of norepinephrine Table 3 Inotropic Agent Receptor Activity Agent Alpha 1 Alpha 2 Beta 1 Beta 2 Dopaminergic Dobutamine Dopamine ++/+++? Epinephrine Norepinephrine /++ 0 Milrinone Inhibits phosphodiesterase increased intracellular camp increased cardiac output 74 Current Reviews for Nurse Anesthetists

7 Table 4 Vasopressin # Antidiuretic hormone # Agonism of V1 receptors results in vasoconstriction and the stimulation of V2 receptors results in an increase in water reabsorption # Effects are preserved in the presence of hypoxia and acidosis useful in sepsis # Indicated in septic shock for patients that are on a mid-range dose of norepinephrine (5-15 mcg/min) # Dosage of 0.03 units/minute is appropriate to use with norepinephrine, either to improve perfusion (increase MAP) or to reduce the required dose of norepinephrine in the treatment of septic shock # A substitute to epinephrine in cardiac arrest # Recommended for the treatment of hypotension related to the administration of ACE inhibitors # Potential vasopressor of choice in patients with pulmonary hypertension # Side effects: reduced splanchnic blood flow and a potential for cardiac ischemia 5-15 mcg/min), either to improve perfusion (increase MAP) or to reduce the required dose of norepinephrine. Dopamine, previously a first-line therapy in septic shock, has been reported to increase cardiac arrhythmias and increase mortality. Therefore, norepinephrine, epinephrine, and vasopressin have become the recommended treatments for septic shock. Vasopressin has been additionally supported for other clinical uses in addition to septic shock. Current data suggest its effectiveness in the treatment of hypotension related to cardiopulmonary bypass, as a substitute to epinephrine in cardiac arrest, for the treatment of hypotension related to the administration of ACE inhibitors, and as a potential vasopressor of choice in patients with pulmonary hypertension. Known side effects of vasopressin include a reduced splanchnic blood flow and a potential for cardiac ischemia (Table 4). Cardiogenic Shock Cardiogenic shock is defined as persistent hypotension and tissue hypoperfusion due to cardiac dysfunction with adequate intravascular volume and left ventricular filling pressure. A patient in cardiogenic shock presents clinically with tachycardia, an elevated preload and a decreased cardiac output. Causes of cardiogenic shock include myocardial infarction, arrhythmias, pericardial tamponade, and massive pulmonary embolism. Pharmacologic treatment options include dobutamine, norepinephrine, epinephrine, and milrinone. A vasopressor should be considered when using milrinone due to its vasodilatory effects. Inotropes and vasopressors may be indicated to maintain tissue perfusion in highrisk surgical patients with hypovolemic shock. Neurogenic Shock Neurogenic shock, a form of distributive shock, most often occurs in patients with severe spinal cord injury at the cervical or high thoracic level. A shock state occurs due to decreased sympathetic outflow to the cardiovascular system leading to a reduced cardiac output and systemic vascular resistance. Treatment with fluid therapy is followed by pharmacologic options to maintain mean arterial pressure > 90 mmhg. Vasopressors of choice include agents with both alpha and beta activity to improve sympathetic tone and provide chronotropic cardiac support. Norepinephrine and dopamine are both considered suitable treatment for neurogenic shock. Anaphylactic Shock Anaphylactic shock, another type of distributive shock, may result from medication, contrast dye, or blood administration as well as insect envenomation. Clinical signs include respiratory distress and circulatory signs of shock including tachycardia and hypotension. Treatment is aimed at eliminating the inciting agent, fluid resuscitation, and the administration of epinephrine, antihistamines, and corticosteroids. High-risk Surgical Patients Vasopressors and Inotropes Patients at high-risk for postoperative morbidity have been identified in the literature as patients presenting with: 1) advanced age (> 70 years old), 2) severe cardiorespiratory diseases (including COPD, asthma, pulmonary hypertension, coronary artery disease), 3) major surgery with expected high fluid losses (i.e., major abdominal surgery), 4) trauma involving multiple organs, 5) severe, acute blood loss requiring massive transfusion, and 6) vascular disease involving major vasculature (Table 5). Prevention of organ failure related to hypovolemic shock in high-risk surgical patients focuses on maintenance Curr Rev Nurs Anesth 38(6):69-80,

8 of tissue perfusion as measured by cardiac output and cardiac index (invasive or non-invasive), delivery of oxygen in blood (DO2I), and VO2I (oxygen consumption index). While these indices of tissue perfusion require invasive monitoring, the benefits of information regarding tissue perfusion may outweigh the risks associated with them. More common measures of hypovolemic shock include tachycardia, hypotension, and decreased urine output. However, the literature has shown the insensitivity of using clinical variables such as arterial blood pressure, heart rate, consciousness level, urinary volume, and perfusion of extremities to determine the presence of tissue hypoperfusion in both clinical and stable surgical patients. Data suggests that one should consider employing measures of cardiac index and oxygen delivery in patients known to be at high-risk for low perfusion states. Despite the measurement employed to monitor tissue perfusion, the administration of inotropes and vasopressors may be indicated to maintain adequate tissue perfusion in the face of hypovolemic shock in the high-risk surgical patient. Vasopressor use in patients undergoing spine surgery in the prone position may further impair perfusion to the optic nerve. The risk of acute renal failure subsequent to perioperative periods of low perfusion is well understood. Risk factors for renal failure subsequent to intraoperative hypoperfusion are thought to include: emergent surgery, age > 59 years, and coexisting liver, pulmonary and/or vascular disease. While the data is not conclusive regarding the administration of specific vasopressors for the prevention of postoperative acute renal failure, data demonstrating the risk associated with mean arterial pressures less Table 5 Indicators of High-risk for Postoperative Morbidity # Advanced age (> 70 years old) # Severe cardiorespiratory disease (COPD, asthma, pulmonary hypertension, coronary artery disease) # Major surgery with expected high fluid losses (i.e., major abdominal surgery) # Trauma involving multiple organs # Severe, acute blood loss requiring massive transfusion # Vascular disease involving major vessels than 40 mmhg is strong. Recommendations for the prevention of postoperative acute renal failure include maintenance of mean arterial pressure with crystalloid and vasopressors (and avoidance of hetastarch products due to their molecular weight and proven nephrotoxicity), particularly in patients with septic shock. Special Populations and Use of Vasopressors Prone Position and Spine Surgery The prone position has been shown to decrease cardiac index, leading to decreased tissue perfusion. This decrease in cardiac index may be due to increased intrathoracic pressures causing a decrease in arterial filling, resulting in an increase in sympathetic activity via the baroceptor reflex. (The baroreceptor reflex in the presence of decreased blood pressure decreases baroreflex activation and causes the heart rate to increase in order to restore blood pressure levels.) Additionally, decreased stroke volume is accompanied by an increased sympathetic activity (defined by increased heart rate, total peripheral vascular resistance, and plasma noradrenaline) in prone patients. Hemodynamics in the prone position are further perturbed by the administration of total intravenous anesthesia versus general anesthesia with volatile agents. Total intravenous anesthesia is commonly employed in spine surgery due to the potential interference of volatile anesthetics with neurophysiologic monitoring. Propofol infusions utilized in total intravenous anesthetics have been shown to decrease cardiac output and blood pressure, requiring the administration of vasopressors to maintain adequate mean arterial pressures. The prone position, coupled with reduced cardiac output and blood pressure, has been implicated in perioperative visual loss (POVL). However, the cause of POVL is multifactorial, caused by factors such as the prone position, increased crystalloid infusion leading to hemodilution, decreased blood pressure, and prolonged surgical time. Blood pressure in patients undergoing spine surgery is commonly supported by vasopressors in an effort to maintain blood pressure and to reduce the risk of POVL. However the data to support vasopressor use in this population is lacking. In fact, the administration of vasopressors may further impair perfusion to the optic nerve. The only clear recommendation regarding blood pressure and POVL is to avoid intentional hypotensive technique in the prone position for long duration spine surgeries. Sitting/Beach Chair Position The beach chair position was first reported in the 1980s for arthroscopic shoulder surgeries. While this position may provide surgical advantages, significant 76 Current Reviews for Nurse Anesthetists

9 alterations in hemodynamics occur. Mean arterial pressure, central venous pressure, stroke volume, and cardiac output all decrease in the sitting position. The use of volatile anesthetics further affects cerebral blood flow as the autonomic response of increasing systemic vascular resistance in the sitting position is blocked. Cerebral perfusion pressure, as measured by the mean arterial pressure minus the central venous pressure, is therefore reduced in the sitting or beach chair position. The brain MAP will be 8-24 mmhg lower than the measured mean brachial artery pressure in the sitting position. Table 6 Sitting Position # Cerebral autoregulation occurs when mean arterial pressures is between 50 and 150 mmhg # There is a 0.77 mmhg decrease in blood pressure for every centimeter gradient between the BP cuff location and the auditory meatus (1 mmhg for each 1.25 cm) # The brain MAP will be 8-24 mmhg lower than the measured mean brachial artery pressure Cerebral autoregulation is thought to maintain cerebral blood flow when mean arterial pressure is between 50 and 150 mmhg. However, the location of the blood pressure cuff, frequently the upper arm, and the distance to the head must be considered. There is a 0.77 mmhg decrease for every centimeter gradient or a 1 mmhg decrease for each 1.25 cm difference between the cuff and the auditory meatus or Circle of Willis. In general, the approximate distance between the brain and the site of the BP cuff on the arm in the seated position will be cm depending on the angle of the sitting position and the height of the patient. Hence, the brain MAP will be 8-24 mmhg lower than the measured mean brachial artery pressure (Table 6). The administration of vasopressors to the patient in the sitting or beach chair position may prevent cerebral ischemia related to hypotension. Summary Hypotension occurs frequently in conjunction with general and neuraxial anesthesia. Hypotension related to the induction of general anesthesia with propofol may best be treated with ephedrine in an effort to improve both cardiac output and systemic vascular resistance decreases due to the direct effects of propofol. Hypotension related to neuraxial anesthesia can be effectively treated with crystalloids, ephedrine, and/or phenylephrine. Data shows no difference in fetal acidosis and Apgar scores when maternal hypotension secondary to spinal anesthesia is treated with ephedrine or phenylephrine. Several shock states require the use of vasopressors and inotropic agents. The current septic shock guidelines declare norepinephrine the first-line vasopressor of choice. Vasopressin has gained more widespread use in septic shock (to reduce the overall required dosage of norepinephrine), as an alternative to epinephrine in cardiac arrest, and in the treatment of hypotension related to ACE inhibitors. The choice of inotropes for cardiogenic shock requires an understanding of receptor activity and desired outcomes. Special circumstances whereby hypotension occurs in the operating room include the prone position in spine surgery and the sitting position. The data describing POVL in spine surgery proves a multifactorial cause, and indicates that vasopressors may be more detrimental than helpful. However, the sitting position may require the administration of vasopressors to maintain adequate cerebral perfusion. Joanne Donnelly, DNP, CRNA, Clinical Education Director, Department of Anesthesiology/School of Medicine, University of Colorado Hospital, Aurora, Colorado. joannedonnelly@comcast.net Bibliography Dellinger RP, et al: Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock. Intensive Care Medicine 39(2): , (A good reference for sepsis guidelines) Hamilton MA, et al: A systematic review and metaanalysis on the use of preemptive hemodynamic intervention to improve postoperative outcomes in moderate and high-risk surgical patients. Anesthesia & Analgesia 112(6): , (A reference depicting organ perfusion indicators) Hoste EA, DeCorte W: Implementing the kidney disease: Improving global outcomes/acute kidney injury guidelines in ICU patients. Curr Opin Crit Care 19(6): , (A summary of guidelines for prevention of acute kidney injury) Kheterpal S, et al: Predictors of postoperative acute renal failure after noncardiac surgery in patients with previously normal renal function. Anesthesiology 107 (6): , (A reference defining patients at high risk for ARF) Lee L: Perioperative visual loss and anesthetic management. Current Opinion Anesthesiology 26: , Curr Rev Nurs Anesth 38(6):69-80,

10 Pestana D, et al. Perioperative goal-directed hemodynamic optimization using nonivasive cardiac output monitoring in major abdominal surgery: A prospective, randomized, multicenter trial: POEMAS study (Peri-Operative goal-directed therapy in major Abdominal Surgery). Anesthesia & Analgesia 119(3): , (A good reference for goal-directed therapy) Russel JA, et al: Vasopressin versus norepinephrine infusion in patient with septic shock. The New England Journal of Medicine 358(9): , Sanderland T, et al: Maintaining tissue perfusion in high-risk surgical patients: A systematic review of randomized clinical trials. Anesthesia & Analgesia 112 (6): , Tips for your Clinical Practice: Key Points # Maternal hypotension due to neuraxial blockade may result in adverse outcomes; both ephedrine and phenylephrine are safe and effective for use in this setting. # Vasopressin has experienced a large increase in clinical use due to its pronounced efficacy at V1 (vascular smooth muscle) and V2 (renal distal tubule and collecting duct) receptors. # Recent clinical research reveals that a combination of norepinephrine and vasopressin is effective in the management of distributive (septic) shock states. # A classic form of neurogenic shock can occur in the wake of spinal cord injury; treatment involves fluid administration and vasopressors including norepinephrine and dopamine. # Hypotension occurring in high risk patients such as the elderly, those with severe comorbidity, and trauma-induced hypovolemia, should be managed in a goal-directed manner with carefully titrated vasoactive agents and fluid therapy. Chuck Biddle, CRNA, PhD Richmond, Virginia FRANK MOYA CONTINUING EDUCATION PROGRAMS, INC. & FACULTY DISCLOSURE THIS AUTHOR S AND FMCEP S SPECIFIC DISCLOSURES: The author / faculty has indicated that there is no relevant financial interest or relationship with any commercial interest. The author / faculty has indicated that, as appropriate, he/she has disclosed that a product is not labeled for the use under discussion, or is still under investigation. As a matter of policy, FMCEP does not have any relevant financial interest or relationship with any commercial interest. In addition, all members of the staff, Governing Board, Editorial Board and CME Committee who may have a role in planning this activity have indicated that there is no relevant financial interest or relationship with any commercial interest. Current Reviews is intended to provide its subscribers with information that is relevant to anesthesia providers. However, the information published herein reflects the opinions of its authors. Anesthesia practitioners must utilize their knowledge, training and experience in their clinical practice of anesthesiology. No single publication should be relied upon as the proper way to care for patients. DESIGNATON OF SPECIFIC CONTENT AREAS: Current Reviews for Nurse Anesthetists (CRNA) is designed to meet the standards and criteria of the American Association of Nurse Anesthetists (AANA) for the prior-approved continuing medical education activity, Provider-Directed Independent Study, also known as home study. CRNA is an approved program provider. CRNA has designated the lessons which meet specific content areas such as pharmacology, HIV/AIDS, etc. However, only the Board of Nursing of an individual State is the final authority in the determination of whether or not these lessons meet the State s licensure requirements. 78 Current Reviews for Nurse Anesthetists

11 Letters to the Editor... Thank you for providing Current Reviews for Nurse Anesthetists. This service has enabled me to stay current with the practice of anesthesia for many years. My subscription has ensured that I continued to practice safe effective anesthesia for the past 35 years. Now I am retiring from anesthesia and looking forward to enjoying the Golden Years with my wife and family. Thank you again for your service to the nurse anesthesia community. Glen Hardesty, CRNA Winter Haven, FL Response... Glenn, Many thanks for your 35 year loyalty to Current Reviews for Nurse Anesthetists. Enjoy your Golden Years Frank Moya, MD Publisher The views and opinions expressed in the Letters to the Editor are those of the authors and do not necessarily reflect the views of Current Reviews or the Editorial Board. Letters submitted for consideration should not exceed 100 words in length. The Editor has the authority to accept, reject, or edit any letter submitted for publication. Personal correspondence to the Editor must be clearly indicated as Not for Publication if so requested by the sender. Letters must be signed (although name may be withheld on request) and are subject to editing and abridgement.

12 MARK ONLY THE ONE BEST ANSWER PER QUESTION ON YOUR ANSWER CARD. MARK THIS PAGE AND KEEP FOR YOUR RECORDS. 6 In accordance with AANA directives, you must get 80% of the answers correct to receive one credit for each lesson, and if there is a failure, there is no retaking. POST-STUDY QUESTIONS 1. Current guidelines for the management of septic shock advise the administration of vasopressin: G A. As a first line therapy for septic shock. G B. In patients with septic shock on norepinephrine at doses of 5-15 mcg/min. G C. Added to a phenylephrine infusion. G D. Only when epinephrine is not effective. 2. Dopamine for the treatment of septic shock: G A. Is superior to norepinephrine. G B. Has a lower mortality than norepinephrine. G C. Has a higher incidence of cardiac arrhythmias. G D. Has equivalent mortality to norepinephrine. 3. The TRUE statement regarding monitors of tissue perfusion in high-risk surgical patients is: G A. Heart rate and blood pressure are sensitive indicators of tissue perfusion. G B. Urine output is a reliable indicator of tissue perfusion. G C. Cardiac index is a reliable indicator of tissue perfusion. G D. Use of pulmonary artery catheters is required in all of these patients. 4. Treatment of neurogenic shock requires administration of: G A. Alpha adrenergic agonists only. G B. Beta receptor antagonists. G C. Fluids only. G D. Alpha and beta adrenergic agonists. 5. The following inotropic agent may cause significant vasodilation: G A. Dopamine. G B. Milrinone. G C. Norepinephrine. G D. Vasopressin. 6. Vasopressin should be considered: G A. In hypotensive patients on ACE inhibitors. G B. G C. G D. As a first-line therapy for septic shock. In the treatment of anaphylactic shock. For the prevention of perioprative visual loss (POVL). 7. A patient in the sitting position whose BP cuff and pressure gauge are on the arm: G A. Will have a higher cerebral BP than the reading from their cuff. G B. Will have equivalent BP in their brain to the arm cuff reading. G C. Will have a lower cerebral BP than their arm cuff reading. G D. The BP in the brain cannot be approximated from the arm cuff reading. 8. Norepinephrine is: G A. A potent alpha adrenergic receptor agonist with modest beta agonist. G B. A pure beta agonist. G C. A pure alpha agonist. G D. A potent alpha adrenergic receptor agonist with modest dopaminergic activity. 9. Phosphodiesterase inhibitors increase myocardial contractility by: G A. Stimulating beta-1 adrenergic receptors. G B. Stimulating alpha-1 adrenergic receptors. G C. Increasing the concentration of camp inside the cell. G D. Increasing the concentration of AMP inside the cell. 10. The recommended treatment of hypotension in the maternal patient following spinal anesthesia includes: G A. Ephedrine only. G B. Epinephrine. G C. Phenylephrine only. G D. Both ephedrine and phenylephrine are safe. Moving? Please notify us at least six weeks before you move to your new address, so you won t miss any issues of your subscription. The post office will not forward your subscription to Current Reviews for Nurse Anesthetists. Phone: (954) Fax: (954) or (800)