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Current Reviews for

Nurse Anesthetists®

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Editorial Board Chuck Biddle, CRNA, PhD Mary Jeanette Mannino, Richmond, Virginia CRNA, JD

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Coral Gables, Florida

Advisory Board Charles Barton, MSN, MEd Frank T. Maziarski, CRNA

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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, 2017. 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.

Curr Rev Nurs Anesth 38(6):69-80, 2015 71

LESSON OBJECTIVESUpon completion of this lesson, the readershould be able to:1. Identify the mechanism of action of vaso-

pressors and inotropic drugs used inanesthesia care.

2. Describe common myths associated withthe administration of vasopressors andinotropic agents.

3. Outline the management of intraopera-tive hypotension.

4. Discuss the current guidelines for themanagement of various shock states.

5. Explain the benefits of vasopressin inshock states.

6. Review the hemodynamic management ofhigh-risk surgical patients.

7. Describe tissue perfusion indicators inthe management of high-risk surgicalpatients.

8. Explain current theories for the man-agement of hypotension and the preven-tion of acute renal failure.

9. Discuss theories related to the adminis-tration of vasopressors and the preven-tion of postoperative visual loss.

10. Describe the potential adverse effects andthe prevention of hypotension in thesitting position.

Vasopressors and Inotropic Agents:Common Clinical Scenarios

Joanne Donnelly, DNP, CRNAClinical Education Director

Department of Anesthesiology/School of MedicineUniversity of Colorado Hospital

Aurora, Colorado

Current Reviews for Nurse Anesthetists designates this lesson ®

for 1 CE contact hour in Clinical pharmacology/therapeutics.

IntroductionNurse anesthetists administer vasopressors andinotropic agents for a variety of clinical scenarios.The most common scenario is hypotension. Hypo-tension during anesthesia is a common conditionthat may be related to the effects of volatile agentsand/or regional anesthesia. Hypotension and re-duced cardiac output during anesthesia may alsooccur due to shock states, patient position, type ofprocedure, or patient-specific comorbidities (such asheart failure). If hypotension is sustained and un-corrected, it may lead to adverse effects in the brain,

heart, kidneys, and fetus in a pregnant patient.More specifically, untreated hypotension may lead tostroke, myocardial infarction, or acute renal failure.

The treatment of hypotension during surgeryand anesthesia frequently includes fluids and vaso-pressors, with the addition of inotropes when nec-essary. This lesson will review a few of the commoncauses of hypotension: vasodilation from anesthesia,shock states, and procedure or surgical positionspecific causes—prone and sitting position. Decisionmaking in treatment will focus on pharmacologicchoices, receptor-specific treatment, and the preven-tion of end-organ damage.

72 Current Reviews for Nurse Anesthetists®

Anesthesia-induced Hypotension

General AnesthesiaThe induction of general anesthesia and ad-

ministration of neuraxial anesthesia may causehypotension, commonly mild and self-limiting. Thecauses of hypotension subsequent to induction ofgeneral anesthesia with propofol is due to: 1) a de-crease in sympathetic activity, 2) direct vascularsmooth muscle relaxation and 3) direct negativeinotropic effects. Studies evaluating both failing andnon-failing hearts reveal reduced contractility ineven non-failing hearts following the administrationof induction doses of propofol. Therefore, ephedrineis the vasopressor of choice for hypotension related tothe administration of propofol in lieu of the needto correct negative inotropy and smooth muscle re-laxation. Ephedrine effectively returns preoperativehemodynamics via activation of beta adrenergicreceptors, alpha adrenergic receptors, as well asstimulating the release of catecholamines fromthe adrenal medulla (Table 1). However, ephedrinepossesses unwanted effects, including an increasedheart rate and tachyphylaxis with repeated dosing.

Despite the theoretical sense of administeringephedrine to replace hemodynamic losses with in-duction, there are circumstances in which ephedrineis a poor first line choice. Such instances include allpathologies in which an increase in heart rate maybe deleterious, such as in aortic stenosis and coro-nary artery disease.

Neuraxial AnesthesiaNeuraxial anesthesia, specifically spinal anes-

thesia, causes hypotension from the sympathectomyproduced by administration of local anesthetics in

the intrathecal space. Phenylephrine, a direct-actingalpha-1 adrenergic agonist, stimulates vascularsmooth muscle resulting in vasoconstriction. In theoperating room, hypotension related to neuraxialanesthesia is commonly treated with crystalloid,ephedrine, and/or phenylephrine. The effects of bothphenylephrine and ephedrine have been studied inthe treatment of maternal hypotension secondary tospinal anesthesia for cesarean delivery, and studiesreveal no differences in fetal acidosis or Apgar scores.Therefore, the administration of both ephedrine andphenylephrine in the hypotensive maternal patientis acceptable.

The Surviving Sepsis Campaign recom-mends maintaining a MAP of 65 mmHg orgreater; norepinephrine is the first-linevasopressor.

Vasopressor and InotropeUse in Shock States

There are several shock states that may require theadministration of vasopressors and/or inotropes. Ingeneral, the types of shock include: septic shock,hypovolemic shock, cardiogenic shock, anaphylacticshock, and neurogenic shock (Table 2). Each shockstate is described in more detail below.

First, a review of specific inotropic agents andvasopressors will allow a more receptor-specificapproach to choosing the appropriate drug. A pro-found understanding of the mechanism of action ofpositive inotropes and vasopressors aids in deter-mining which drugs will improve tissue perfusion inthe high-risk surgical patient. The most commonly

Table 1Adrenergic Receptors

Receptor Location ActivityClinical Hemodynamic

Effects if Stimulated

Alpha 1 Vascular smooth muscle Vasoconstriction Increased BP

Alpha 2 Nervous system, pre-synaptic nerve terminal

Decreased norepinephrine release

Decreased BP

Beta 1 Heart, platelets Positive inotropy, increasedchronotropy, platelet aggregation

Increased HRIncreased cardiac output

Beta 2 Bronchi, vascular smoothmuscle, uterus

Increased cAMP, bronchodilation,vasodilation

Decreased BP

Beta 3 Adipose, heart Lipolysis; possible mechanism ofnegative inotropy

Dopamine(at least 5 subtypes)

Renal, splanchnic,coronary, cerebral

Induces vasodilationSubtype causes vasoconstrictionvia norepinephrine release

Increased HRIncreased cardiac outputPotential for arrhythmias


administered positive inotropes include: dobuta-mine, norepinephrine, epinephrine, dopamine, andmilrinone. The mechanism of action and side-effectprofile for each drug is listed in Table 3.

DobutamineDobutamine is a synthetic catecholamine with

strong affinity for both beta-1 and beta-2 receptors.Vascular smooth muscle binding of dobutamineresults in alpha-1 receptor agonism (vasoconstric-tion) and beta-2 receptor agonism (vasodilation),leading to a predominant vasodilatory effect. Dosesup to 15 mcg/kg/min result in increased inotropywithout significant increased systemic vascularresistance. The end result is an increase in cardiacoutput without significant increases in afterload.Additionally, dobutamine significantly increasesmyocardial oxygen consumption, making it a usefulagent for pharmacologic “exercise” stress testing.

DopamineDopamine is an endogenous central neurotrans-

mitter and is the immediate precursor to norepineph-rine in the catecholamine synthetic pathway. Re-ceptor effects of dopamine are dose-related (althoughpreviously demonstrated “renal-dose” dopamine iscontroversial). However, at low doses, 0.5-3 mcg/kg/min, dopamine stimulates D1 postsynaptic receptorslocated in the coronary, renal, mesenteric, andcerebral beds and D2 presynaptic receptors resultingin vasodilation and increased blood flow in renaltissues. At doses of 3-10 mcg/kg/min, dopaminepossesses weak beta-1 receptor activity, promotesrelease of norepinephrine, and inhibits norepineph-rine reuptake; all of these effects lead to an increasein cardiac output, heart rate, and systemic vascularresistance. At higher doses, 10-20 mcg/kg/min, dopa-mine stimulates alpha-1 receptors leading to pro-found increases in systemic vascular resistance.

The most serious adverse effect of a dopamineinfusion is cardiac arrhythmias. Monitoring forarrhythmias, careful titration, and consideration ofa different positive inotropic drug may be necessary. Isoproterenol

Isoproterenol is a synthetic, nonselective betaagonist with minimal affinity for alpha adrenergicreceptors. The nonselective characteristics of iso-proterenol, specifically its actions on beta-2 recep-tors, limit its usefulness in profound hypotension. Epenephrine

Epinephrine is an endogenous catecholaminewith high affinity for beta-1, beta-2, and alpha-1receptors present in cardiac and vascular smoothmuscle. Beta adrenergic effects are more pronouncedat lower doses and alpha adrenergic effects are morepronounced at higher doses. Infusion rates rangefrom 1-10 mcg/min. Norepinephrine

Norepinephrine is a potent alpha adrenergicreceptor agonist with modest beta agonist activity.The pharmacologic profile of norepinephrine makesit a powerful vasoconstrictor with less potent directinotropic properties. Typical infusion rates rangefrom 2-4 mcg/min. Phosphodiesterase Inhibitors

Phosphodiesterase inhibitors increase the levelof cAMP by inhibiting its breakdown within the cell.Phosphodiesterase 3 is the enzyme inside the cellresponsible for the breakdown of cAMP. Preventionof this breakdown leads to increased myocardialcontractility and vasodilation. The net effect of phos-phodiesterase inhibition is increased cardiac output,decreased preload, and decreased afterload.

Table 2Shock States

Septic Shock Infectious process releasing chemicals leading to: (1) peripheral vasodilation-interstitial edema and decreased blood return to the heart, and (2) decreasedability of the cells and tissues to take up oxygen and nutrients

Anaphylactic Shock Shock due to a severe allergic antigen-antibody reaction to substances suchas drugs, contrast media, blood products, or insect or animal venom

Hypovolemic Shock 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

Cardiogenic Shock Caused by inadequate myocardial contractility from acute myocardialinfarction, coronary artery disease, or mechanical factors (valvularregurgitation, low output syndrome, arrhythmias)

Neurogenic Shock Caused by the loss of sympathetic control (tone) of resistance vessels,resulting in the massive dilatation of arterioles and venules. Caused bygeneral or spinal anesthesia, spinal cord injury, pain, and anxiety.


PhenylephrinePhenylephrine is a synthetic, potent, pure alpha-1

adrenergic agonist. Since phenylephrine has nobeta-adrenergic activity, it has no direct effect onheart rate, but may cause a reflex, transient brady-cardia. This effect is due to a baroreceptor-mediatedreflex response after rapid increases in mean arterialpressure. Infusion rates may range from 0.1-9 mcg/kg/min.

VasopressinVasopressin, also known as antidiuretic hor-

mone, is stored in the posterior pituitary gland andreleased in response to hypotension or increasedplasma osmolality. Vasopressin is also synthesizedby the heart in response to elevated cardiac wallstress and by the adrenal gland in response to in-creased catecholamine release. Vasopressin exertsdirect effects on the V1 receptors in vascular smoothmuscle and V2 receptors in the renal collecting ductcells. The stimulation of V1 receptors results invasoconstriction and the stimulation of V2 receptorsresults in an increase in water reabsorption.

Additionally, vasopressin increases the sensi-tivity of the vasculature to norepinephrine. At lowconcentrations, vasopressin mediates vasodilationin coronary, cerebral, and pulmonary arterial circu-lations. Unique to vasopressin is that its effects arepreserved in the presence of hypoxia and acidosis,making it even more useful in the presence of septicshock. Infusion rates of vasopressin range from 0.01-0.03 units/minute in the treatment of shock. In-creased doses and prolonged administration of vaso-pressin may result in decreased cardiac output,decreased hepatosplanchnic flow, and a reboundhypotension upon termination of vasopressin.

Shock States

Hypovolemic Shock Hypovolemic shock is the most common

type of shock encountered in the operatingroom. Causes of hypovolemic shock include hem-orrhage, acute volume losses from vomiting or

diarrhea, third spacing from capillary leaks, andburns. Shock ensues when the patient loses morethan 20% of the body’s blood or fluid supply. Thetreatment of hypovolemic shock requires the main-tenance of perfusion to end organs, accomplished bythe administration of fluids, blood, and potentiallyvasopressors and inotropes. It is well recognizedthat the first-line therapy in hypovolemic shockis the administration of crystalloids. While mildhypovolemic shock in surgical patients occurs fre-quently, more severe hypovolemic shock may resultin end organ damage in high-risk surgical patients.

Vasopressin 0.03 units/minute in combi-nation with norepinephrine is recom-mended in the treatment of septic shock.

Septic shock is defined as an infection withsystemic manifestations characterized by maldistri-bution of blood flow. Septic shock is the classicdistributive shock state, where there is an abnormalflow of blood to the small vessels resulting in poortissue blood flow and oxygenation. The SurvivingSepsis Campaign recommends goal-directed therapyof fluids and vasopressors to improve end-organ andcellular perfusion. The 2013 recommendations forthe treatment of septic shock include the followinggoals for the first six hours of resuscitation: main-tain a mean arterial blood pressure (MAP) of 65mmHg or greater, central venous pressure (CVP) 8-12 mmHg, urine output > 0.5 mL/kg/hr, and a cen-tral venous or superior vena cava oxygenation of >70% or a mixed venous oxygen saturation of > 65%.

Treatments recommended in septic shock tomeet hemodynamic goals are: 1) fluid resuscitationof 30 mL/kg crystalloid, 2) initiate vasopressors ifunable to maintain a MAP > 65 with crystalloidadministration, 3) norepinephrine is the first-linevasopressor, 4) epinephrine is the second-line vaso-pressor of choice when norepinephrine is insufficientto maintain a MAP of 65 mmHg, 5) vasopressin at0.03 units/minute is appropriate to use with nor-epinephrine (on a mid-range dose of norepinephrine

Table 3Inotropic Agent Receptor Activity

Agent Alpha 1 Alpha 2 Beta 1 Beta 2 Dopaminergic

Dobutamine + + +++ ++ 0

Dopamine ++/+++ ? ++++ ++ ++++

Epinephrine ++++ ++++ ++++ +++ 0

Norepinephrine +++ +++ +++ +/++ 0

Milrinone Inhibits phosphodiesterase ö increased intracellular cAMP öincreased cardiac output


5-15 mcg/min), either to improve perfusion (increaseMAP) or to reduce the required dose of norepineph-rine.

Dopamine, previously a first-line therapy in sep-tic shock, has been reported to increase cardiacarrhythmias and increase mortality. Therefore, nor-epinephrine, epinephrine, and vasopressin have be-come the recommended treatments for septic shock.

Vasopressin has been additionally supported forother clinical uses in addition to septic shock. Cur-rent data suggest its effectiveness in the treatmentof hypotension related to cardiopulmonary bypass, asa substitute to epinephrine in cardiac arrest, for thetreatment of hypotension related to the adminis-tration of ACE inhibitors, and as a potential vaso-pressor of choice in patients with pulmonary hyper-tension. Known side effects of vasopressin includea reduced splanchnic blood flow and a potential forcardiac ischemia (Table 4).

Cardiogenic ShockCardiogenic shock is defined as persistent hypo-

tension and tissue hypoperfusion due to cardiac dys-

function with adequate intravascular volume andleft ventricular filling pressure. A patient in cardio-genic shock presents clinically with tachycardia, anelevated preload and a decreased cardiac output.Causes of cardiogenic shock include myocardialinfarction, arrhythmias, pericardial tamponade, andmassive pulmonary embolism. Pharmacologic treat-ment options include dobutamine, norepinephrine,epinephrine, and milrinone. A vasopressor should beconsidered when using milrinone due to its vaso-dilatory effects.

Inotropes and vasopressors may be indi-cated to maintain tissue perfusion in high-risk surgical patients with hypovolemicshock.

Neurogenic Shock

Neurogenic shock, a form of distributive shock,most often occurs in patients with severe spinal cordinjury at the cervical or high thoracic level. A shockstate occurs due to decreased sympathetic outflow tothe cardiovascular system leading to a reduced car-diac output and systemic vascular resistance. Treat-ment with fluid therapy is followed by pharmacologicoptions to maintain mean arterial pressure > 90mmHg. Vasopressors of choice include agents withboth alpha and beta activity to improve sympathetictone and provide chronotropic cardiac support. Nor-epinephrine and dopamine are both considered suit-able treatment for neurogenic shock.

Anaphylactic ShockAnaphylactic shock, another type of distributive

shock, may result from medication, contrast dye, orblood administration as well as insect envenomation.Clinical signs include respiratory distress and cir-culatory signs of shock including tachycardia andhypotension. Treatment is aimed at eliminating theinciting agent, fluid resuscitation, and the adminis-tration of epinephrine, antihistamines, and cortico-steroids.

High-risk Surgical Patients—Vasopressors and Inotropes

Patients at high-risk for postoperative morbidityhave been identified in the literature as patientspresenting with: 1) advanced age (> 70 years old), 2)severe cardiorespiratory diseases (including COPD,asthma, pulmonary hypertension, coronary arterydisease), 3) major surgery with expected high fluidlosses (i.e., major abdominal surgery), 4) traumainvolving multiple organs, 5) severe, acute bloodloss requiring massive transfusion, and 6) vasculardisease involving major vasculature (Table 5). Pre-vention of organ failure related to hypovolemic shockin high-risk surgical patients focuses on maintenance

Table 4Vasopressin

# “Antidiuretic hormone”# Agonism of V1 receptors results in

vasoconstriction and the stimula-tion of V2 receptors results in anincrease in water reabsorption

# Effects are preserved in thepresence of hypoxia and acidosis—useful in sepsis

# Indicated in septic shock forpatients that are on a mid-rangedose of norepinephrine (5-15mcg/min)

# Dosage of 0.03 units/minute isappropriate to use with norepi-nephrine, either to improveperfusion (increase MAP) or toreduce the required dose ofnorepinephrine in the treatment of septic shock

# A substitute to epinephrine incardiac arrest

# Recommended for the treatment of hypotension related to theadministration of ACE inhibitors

# Potential vasopressor of choice inpatients with pulmonary hyper-tension

# Side effects: reduced splanchnicblood flow and a potential forcardiac ischemia


of tissue perfusion as measured by cardiac outputand cardiac index (invasive or non-invasive), deliveryof oxygen in blood (DO2I), and VO2I (oxygen con-sumption index). While these indices of tissue per-fusion require invasive monitoring, the benefits ofinformation regarding tissue perfusion may outweighthe risks associated with them.

More common measures of hypovolemic shockinclude tachycardia, hypotension, and decreasedurine output. However, the literature has shown theinsensitivity of using clinical variables such asarterial blood pressure, heart rate, consciousnesslevel, urinary volume, and perfusion of extremities todetermine the presence of tissue hypoperfusion inboth clinical and stable surgical patients. Data sug-gests that one should consider employing measuresof cardiac index and oxygen delivery in patientsknown to be at high-risk for low perfusion states.Despite the measurement employed to monitor tissueperfusion, the administration of inotropes and vaso-pressors may be indicated to maintain adequatetissue perfusion in the face of hypovolemic shock inthe high-risk surgical patient.

Vasopressor use in patients undergoingspine surgery in the prone position mayfurther impair perfusion to the opticnerve.

The risk of acute renal failure subsequent toperioperative periods of low perfusion is well under-stood. Risk factors for renal failure subsequent tointraoperative hypoperfusion are thought to include:emergent surgery, age > 59 years, and coexistingliver, pulmonary and/or vascular disease. While thedata is not conclusive regarding the administrationof specific vasopressors for the prevention of post-operative acute renal failure, data demonstrating therisk associated with mean arterial pressures less

than 40 mmHg is strong. Recommendations for theprevention of postoperative acute renal failure in-clude maintenance of mean arterial pressure withcrystalloid and vasopressors (and avoidance of heta-starch products due to their molecular weight andproven nephrotoxicity), particularly in patients withseptic shock.

Special Populationsand Use of Vasopressors

Prone Position and Spine SurgeryThe prone position has been shown to decrease

cardiac index, leading to decreased tissue perfusion.This decrease in cardiac index may be due to in-creased intrathoracic pressures causing a decrease inarterial filling, resulting in an increase in sympa-thetic activity via the baroceptor reflex. (The baro-receptor reflex in the presence of decreased bloodpressure decreases baroreflex activation and causesthe heart rate to increase in order to restore bloodpressure levels.) Additionally, decreased stroke vol-ume is accompanied by an increased sympatheticactivity (defined by increased heart rate, total per-ipheral vascular resistance, and plasma noradren-aline) in prone patients.

Hemodynamics in the prone position are furtherperturbed by the administration of total intravenousanesthesia versus general anesthesia with volatileagents. Total intravenous anesthesia is commonlyemployed in spine surgery due to the potential inter-ference of volatile anesthetics with neurophysiologicmonitoring. Propofol infusions utilized in total intra-venous anesthetics have been shown to decreasecardiac output and blood pressure, requiring theadministration of vasopressors to maintain adequatemean arterial pressures.

The prone position, coupled with reduced cardiacoutput and blood pressure, has been implicated inperioperative visual loss (POVL). However, thecause of POVL is multifactorial, caused by factorssuch as the prone position, increased crystalloidinfusion leading to hemodilution, decreased bloodpressure, and prolonged surgical time. Blood pres-sure in patients undergoing spine surgery is com-monly supported by vasopressors in an effort tomaintain blood pressure and to reduce the risk ofPOVL. However the data to support vasopressor usein this population is lacking. In fact, the adminis-tration of vasopressors may further impair per-fusion to the optic nerve. The only clear recom-mendation regarding blood pressure and POVL is toavoid intentional hypotensive technique in the proneposition for long duration spine surgeries.

Sitting/Beach Chair PositionThe beach chair position was first reported in the

1980s for arthroscopic shoulder surgeries. While thisposition may provide surgical advantages, significant

Table 5Indicators of High-risk

for Postoperative Morbidity

# Advanced age (> 70 years old)# Severe cardiorespiratory disease

(COPD, asthma, pulmonary hyper-tension, coronary artery disease)

# Major surgery with expected highfluid losses (i.e., major abdominalsurgery)

# Trauma involving multiple organs# Severe, acute blood loss requiring

massive transfusion# Vascular disease involving major

vessels


alterations in hemodynamics occur. Mean arterialpressure, central venous pressure, stroke volume,and cardiac output all decrease in the sitting posi-tion. The use of volatile anesthetics further affectscerebral blood flow as the autonomic response ofincreasing systemic vascular resistance in the sittingposition is blocked. Cerebral perfusion pressure, asmeasured by the mean arterial pressure minus thecentral venous pressure, is therefore reduced in thesitting or beach chair position.

The brain MAP will be 8-24 mmHg lowerthan the measured mean brachial arterypressure in the sitting position.

Cerebral autoregulation is thought to maintaincerebral blood flow when mean arterial pressure isbetween 50 and 150 mmHg. However, the location ofthe 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 centimetergradient or a 1 mmHg decrease for each 1.25 cmdifference between the cuff and the auditory meatusor Circle of Willis. In general, the approximate dis-tance between the brain and the site of the BP cuffon the arm in the seated position will be 10-30 cmdepending on the angle of the sitting position and theheight of the patient. Hence, the brain MAP willbe 8-24 mmHg lower than the measured meanbrachial artery pressure (Table 6). The admin-istration of vasopressors to the patient in the sit-ting or beach chair position may prevent cerebralischemia related to hypotension.

Summary

Hypotension occurs frequently in conjunction withgeneral and neuraxial anesthesia. Hypotensionrelated to the induction of general anesthesia withpropofol may best be treated with ephedrine in aneffort to improve both cardiac output and systemicvascular resistance decreases due to the direct effectsof propofol. Hypotension related to neuraxial anes-thesia can be effectively treated with crystalloids,ephedrine, and/or phenylephrine. Data shows nodifference in fetal acidosis and Apgar scores whenmaternal hypotension secondary to spinal anesthesiais treated with ephedrine or phenylephrine.

Several shock states require the use of vaso-pressors and inotropic agents. The current septicshock guidelines declare norepinephrine the first-linevasopressor of choice. Vasopressin has gained morewidespread use in septic shock (to reduce the overallrequired dosage of norepinephrine), as an alternativeto epinephrine in cardiac arrest, and in the treat-ment of hypotension related to ACE inhibitors. Thechoice of inotropes for cardiogenic shock requires anunderstanding of receptor activity and desired out-comes.

Special circumstances whereby hypotensionoccurs in the operating room include the prone posi-tion in spine surgery and the sitting position. Thedata describing POVL in spine surgery proves amultifactorial cause, and indicates that vasopressorsmay be more detrimental than helpful. However, thesitting position may require the administration ofvasopressors to maintain adequate cerebral perfu-sion. ——————

Joanne Donnelly, DNP, CRNA, Clinical EducationDirector, Department of Anesthesiology/School ofMedicine, University of Colorado Hospital, Aurora,Colorado. [email protected]

Bibliography

Dellinger RP, et al: Surviving Sepsis Campaign:International guidelines for management of severesepsis and septic shock. Intensive Care Medicine 39(2):165-228, 2013. (A good reference for sepsis guidelines)

Hamilton MA, et al: A systematic review and meta-analysis on the use of preemptive hemodynamicintervention to improve postoperative outcomes inmoderate and high-risk surgical patients. Anesthesia& Analgesia 112(6):1392-1402, 2011. (A reference de-picting organ perfusion indicators)

Hoste EA, DeCorte W: Implementing the kidneydisease: Improving global outcomes/acute kidney injuryguidelines in ICU patients. Curr Opin Crit Care 19(6):544-53, 2013. (A summary of guidelines for preventionof acute kidney injury)

Kheterpal S, et al: Predictors of postoperative acuterenal failure after noncardiac surgery in patients withpreviously normal renal function. Anesthesiology 107(6):892-902, 2007. (A reference defining patients athigh risk for ARF)

Lee L: Perioperative visual loss and anesthetic man-agement. Current Opinion Anesthesiology 26:375-381,2013.

Table 6Sitting Position

# Cerebral autoregulation occurs

when mean arterial pressures isbetween 50 and 150 mmHg

# There is a 0.77 mmHg decrease inblood pressure for every centimetergradient between the BP cufflocation and the auditory meatus (1 mmHg for each 1.25 cm)

# The brain MAP will be 8-24 mmHglower than the measured meanbrachial artery pressure


Pestana D, et al. Perioperative goal-directed hemo-dynamic optimization using nonivasive cardiac out-put monitoring in major abdominal surgery: A pro-spective, randomized, multicenter trial: POEMASstudy (Peri-Operative goal-directed thErapy in majorAbdominal Surgery). Anesthesia & Analgesia 119(3):579-587, 2014. (A good reference for goal-directedtherapy)

Russel JA, et al: Vasopressin versus norepinephrineinfusion in patient with septic shock. The New EnglandJournal of Medicine 358(9):877-887, 2008.

Sanderland T, et al: Maintaining tissue perfusion inhigh-risk surgical patients: A systematic review ofrandomized clinical trials. Anesthesia & Analgesia 112(6):1384-1391, 2011.

Tips for your Clinical Practice: Key Points

# Maternal hypotension due to neuraxial blockade may result in adverse outcomes; both ephedrineand 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 involvesfluid administration and vasopressors including norepinephrine and dopamine.

# Hypotension occurring in high risk patients such as the elderly, those with severe comorbidity, andtrauma-induced hypovolemia, should be managed in a goal-directed manner with carefully titratedvasoactive agents and fluid therapy.

Chuck Biddle, CRNA, PhDRichmond, Virginia

FRANK MOYA CONTINUING EDUCATION PROGRAMS, INC. & FACULTY DISCLOSURE

THIS AUTHOR’S AND FM CEP’S SPECIFIC DISCLOSURES:

C The author / faculty has indicated that there is no relevant financial interest or relationship with any com m ercial interest.

C 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.

C As a m atter of policy, FM CEP does not have any relevant financial interest or relationship with any com m ercial interest. In addition, all m em bers

of the staff, Governing Board, Editorial Board and CM E Com m ittee who m ay have a role in planning this activity have indicated that there is no

relevant financial interest or relationship with any com m ercial interest.

C Current Reviews is intended to provide its subscribers with inform ation that is relevant to anesthesia providers. However, the information published

herein reflects the opinions of its authors. Anesthesia practitioners m ust 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 m eet the standards and criteria of the Am erican Association of Nurse Anesthetists

(AANA) for the prior-approved continuing m edical education activity, Provider-Directed Independent Study, also known as hom e study. CRNA is an

approved program provider.

CRNA has designated the lessons which m eet specific content areas such as pharm acology, H IV/AIDS, etc. However, only the Board of Nursing

of an individual State is the final authority in the determ ination of whether or not these lessons meet the State’s licensure requirem ents.

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.

6MARK ONLY THE ONE BEST ANSWER PER QUESTION ON YOUR

ANSWER CARD. MARK THIS PAGE AND KEEP FOR YOUR RECORDS.

In accordance with AANA directives, you must get 80% of the answers correctto 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 septicshock 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 tissueperfusion 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 per-

fusion.G C. Cardiac index is a reliable indicator of tissue per-

fusion.G D. Use of pulmonary artery catheters is required in

all of these patients.

4. Treatment of neurogenic shock requires adminis-tration 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 significantvasodilation: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. As a first-line therapy for septic shock.G C. In the treatment of anaphylactic shock.G D. For the prevention of perioprative visual loss

(POVL).

7. A patient in the sitting position whose BP cuff andpressure 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 myocardialcontractility 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 thematernal patient following spinal anesthesia in-cludes: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’tmiss any issues of your subscription. The post office will not forward your subscriptionto Current Reviews for Nurse Anesthetists .®

Phone: (954) 763-8003Fax: (954) 762-9111 or (800) 425-1995

Documents

Current - School of Nurse Anesthesia · This program has been prior approved by the American Association of Nurse Anesthetists ... you must get 80% of the answers correct to receive