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Recognition and Management of ComplicationsDuring Moderate and Deep Sedation. Part 2:Cardiovascular Considerations

Daniel E. Becker, DDS* and Daniel A. Haas, DDS, PhD, FRCD(C)!*Associate Director of Education, General Dental Practice Residency, Miami Valley Hospital, Dayton, Ohio, and !Associate Dean, ClinicalSciences, Professor and Head of Dental Anaesthesia Faculty of Dentistry, University of Toronto, Toronto, Ontario, Canada

The risk for cardiovascular complications while providing any level of sedation orgeneral anesthesia is greatest when caring for patients already medically compro-mised. It is reassuring that significant untoward events can generally be preventedby careful preoperative assessment, along with attentive intraoperative monitor-ing and support. Nevertheless, providers must be prepared to manage untowardevents should they arise. This continuing education article will review cardiovas-cular complications and address their appropriate management.

Key Words: Medical emergencies; Sedation; Anesthesia; Complications.

Complications attributed tomoderate and deep levelsof sedation are more often associated with respira-

tory compromise and have been reviewed in a previouscontinuing education article in this journal.1 Sedation,and general anesthesia for that matter, have minimal in-fluence on overall cardiovascular function in reasonablyhealthy patients. In fact, cardiovascular complicationsmay be even more likely during dental procedures usinglocal anesthesia alone than when sedation is provided.However, respiratory compromise, excessive drug dosag-es, or inadequate anesthesia may trigger cardiovascularevents, and thewell-informedprovider should be familiarwith their recognition andmanagement.

ABNORMALITIES IN ARTERIALBLOOD PRESSURE

Neurocardiogenic (Vasovagal) Syncope

Syncope is a transient loss of consciousness due to re-duced cerebral blood flow. It may occur unexpectedlybut is often preceded by such signs and symptoms aspallor, lightheadedness, diaphoresis, and nausea. As

brain tissues are deprived of oxygen, a brief period( ie, a few seconds) of convulsive motor activity is notunusual during a syncopal episode, especially if thepatient remains in an upright posture. This event isfrequently confused as a primary seizure event.

Although syncope may be the result of a cardiac ar-rhythmia, in dental practice it is most often the resultof what is commonly referred to as a vasovagal event.Vasovagal syncope is associated with an eventual lossof sympathetic tone (vasodilatation) and increasedparasympathetic activity (bradycardia and gastrointes-tinal stimulation). The term neurocardiogenic syncopeis used to encompass both vasovagal syncope and va-sodepressor syncope in which only loss of sympathetictone occurs.2 In either event, the syncopal episode istriggered by painful or stressful events not uncommonduring dental procedures.

The pathogenesis of vasovagal syncope commenceswith increased peripheral sympathetic activity andvenous pooling. A decline in venous return leads toforceful myocardial contractions of the left ventricle.This in turn activates myocardial mechanoreceptorsand vagal afferent nerve fibers that inhibit sympatheticactivity and increase parasympathetic activity. Theseevents culminate in bradycardia, vasodilation, and thedecline in blood pressure responsible for loss of con-sciousness.2 Indeed, it is not unusual for a syncopalepisode to be preceded by a brief period of forcefulpounding of the heart and tachycardia, which contribute

Received May 17, 2011; accepted for publication June 15, 2011.Address correspondence to Dr Daniel E. Becker, Miami Valley

Hospital, Medical Education, OneWyoming St., Dayton, OH 45409;[email protected].

CONTINUING EDUCATION

Anesth Prog 58:126^138 2011

E 2011 by the American Dental Society of AnesthesiologyISSN 0003-3006/11

SSDI 0003-3006(000)

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to the subsequent neural reflexes leading to the vasova-gal event.

The depth and duration of unconsciousness duringvasovagal syncope are highly variable. In some cases,vagal influences are severe enough to induce transientperiods of asystole that persist for 30^40 seconds.3,4

Its management should be well understood by all den-tists, whether or not sedation is being administered.This consists of carrying out the primary assessmentand management of airway, breathing, and circulationwhile positioning the patient supine with legs elevat-ed. Regardless of the cause or severity, vasovagalevents will generally subside during the time primarymeasures for assessment and airway support are insti-tuted. Subsequently, attention must be directed towardabnormalities in blood pressure and heart rate thatmay or may not require pharmacologic intervention.Syncope that does not resolve spontaneously or withminor intervention is unlikely vasovagal in mecha-nism, and other causes, such as cardiac arrhythmia,stroke, and drug overdose, should be explored.

Hypotension

Episodes of hypotension in clinical practice are mostcommonly associated with vasovagal events and aregenerally transient, but they may become prolongedin the presence of central nervous system depressants.The same can be said for postural (orthostatic) hypo-tension, which normally subsides with proper reposi-tioning of the patient. The blood pressure requiredto perfuse tissues adequately varies from patient topatient and is influenced by their medical status andposture at the time of assessment.

A significant decline in blood pressure from baselineshould alert the clinician, but hypotension cannot beestablished on precise numerical values alone. Evalua-tion of tissue perfusion is the more significant compo-nent of cardiovascular assessment. Color changes inthe skin and mucosa and the rate of capillary refillsubsequent to squeezing of the nail beds can be usedas a guide for assessing perfusion of peripheral tissues.The adequacy of perfusion within the central nervoussystem can be estimated by the patient’s response toverbal and painful stimuli in the conscious patient orby pupillary reflex when they are unconscious or heavi-ly sedated. If blood pressure has declined and perfusionis considered inadequate, the clinician may elect to in-crease blood pressure.To do this appropriately, severalphysiologic principles must be considered.

Blood pressure fluctuates continuously due to thecyclic nature of the pumping action of the heart. Thehighest pressure is produced by ventricular contrac-

tion (systole) and is designated systolic blood pressure.The lowest pressure occurs during ventricular relaxa-tion (diastole) and is therefore designated as diastolicblood pressure. This is the result of arterial resistance.Mean arterial pressure is the time-weighted average ofthe blood pressure throughout the cardiac cycle and isan indication of adequacy or inadequacy of perfusion.

One must avoid excessive elevation of arterial resis-tance and diastolic pressure, because it can produceundo strain on the heart. For the heart to eject a strokevolume, the left ventricle must generate a pressure thatexceeds peripheral resistance. In other words, ventric-ular pressure must exceed diastolic pressure. This re-sistance to ventricular ejection is called afterload, andfor a patient with heart disease, elevated diastolic pres-sure not only stresses the heart but may also hinderejection of an adequate stroke volume. On the otherhand, coronary artery blood flow occurs during diasto-le when the heart muscle relaxes, so a reasonable dia-stolic blood pressure must be present for the heart tobe nourished before the next systolic contraction oc-curs. However, diastolic blood pressures of 30 mm Hgare generally adequate for this purpose for mostadults. In the primary care setting, systolic blood pres-sure is the target of monitoring and interventions.

Systolic blood pressure is primarily a function ofcardiac output, which is calculated as ventricular ratemultiplied by the stroke volume. Of these 2 factors,stroke volume is most significant in adults because itprovides the ‘‘surge’’ that creates the systolic pressure.Except for small children and infants, the heart rateacts merely as a ‘‘compensator’’ for changes in strokevolume. For example, slow rates are common in well-trained athletes, but rapid rates are required to sustainadequate cardiac output for patients having low strokevolumes due to heart failure. Therefore, when manag-ing a hypotensive patient, our primary goal is to im-prove stroke volume.

Stroke volume can be increased in 2 manners: (a)by improving myocardial contractility, which is aug-mented by sympathetic stimulation of beta-1 recep-tors, and (b) by increasing venous return to the heart(preload). According to the Frank-Starling law, pre-load is directly related to stroke volume, but there is alimit to this relationship. If a critical preload volumeis exceeded, congestion occurs. This volume is lowerfor patients having compromised cardiac function andshould be considered when positioning a patient. Al-though in the past the Trendelenburg position hadbeen cited as the preferred position for patients expe-riencing medical emergencies, it may allow excessivevenous return (increase preload) and compromisepatients with cardiac or respiratory disease. In fact, itappears this position offers few advantages.5,6 Thus,

Anesth Prog 58:126^138 2011 Becker and Haas 127

the more appropriate position when managing mostmedical complications in sedated patients or thosewho are unresponsive is to have the patient supinewith the legs elevated slightly. Improving venous re-turn will also increase heart rate according to theBainbridge reflex. When the right atrium is stretchedby venous return, it is sensed by receptors in the areaof the sinoatrial node, leading to an increase in heartrate to better accommodate the returning volume.Figure 1 summarizes and illustrates the influences ofvarious parameters on arterial blood pressure.

In general, a systolic blood pressure of 90 mm Hgshould sustain mean arterial pressure sufficiently toperfuse tissues in the recumbent patient. A pressurelower than this combined with evidence of inadequateperfusion requires intervention. This can be accom-plished in the following manners: (a) improve venousreturn by positioning the patient, administering intra-venous fluid, or administering drugs that provide ve-noconstriction to increase venous pressure and pre-load; (b) increase myocardial contractility ( inotropy)using drugs that activate beta-1 receptors on myocar-dial cells, providing a positive inotropic influence.

If repositioning of the patient to improve venous re-turn, such as described above, fails to improve the sit-uation, subsequent intervention should proceed in thefollowing manner. If an intravenous line is in place orcan be established readily, 250^500 mL of physiolog-ic solution, such as normal saline, should be infused

rapidly unless congestive heart failure is suspected.Generally, this will increase preload sufficiently to im-prove stroke volume and raise systolic pressure. Whenthis maneuver cannot be accomplished or provesunsuccessful, the patient’s heart rate should guide fur-ther treatment. If bradycardia is present, that is, ,60beats/min, administer intravenous atropine until therate is within normal limits. This is accomplished in0.5-mg increments. Suggested dosages for medica-tions addressed throughout this article are summa-rized in Table 2. If the rate is .60 beats/min andpressure remains low, increasing the rate further maydo little to improve systolic pressure. As heart rate in-creases, the time allocated for diastolic filling and eachsubsequent stroke volume will decline.

Although several adrenergic drugs may be accept-able to manage hypotension, ephedrine is often anideal choice for several reasons. Hypotension encoun-tered during dental practice is usually attributed toeither vasovagal episodes or the use of sedatives andanesthetics that depress sympathetic outflow to thecardiovascular system. ( In Advanced Cardiac LifeSupport courses, however, hypotension is generallycardiogenic and requires more powerful inotropics,such as dopamine and epinephrine.) In either case,ephedrine specifically counters these influences indirect-ly by stimulating norepinephrine release from sympa-thetic nerve endings. Also, ephedrine acts directly onalpha- and beta-adrenergic receptors, leading to vaso-constriction and increased rate and contractility of themyocardium. Ephedrine constricts veins to a greater ex-tent than arteries, which enables it to increase preloadmore than afterload.7 This results in less of an increase inmyocardial oxygen demand compared with other vaso-pressors. Finally, unlike epinephrine and other catechol-amines having brief durations of action, that is,5^10min-utes, the cardiovascular effects of ephedrine continue for60^90 minutes. Ephedrine can be administered intrave-nously in 5- to10-mg increments or 25 mg by sublingualor intramuscular injection. Exceeding a total dose of50mg is not recommended.

When it is secondary to hypovolemia, hypotensioncan be accompanied by tachycardia, so the cardioton-ic effects of ephedrine may be undesirable. This situa-tion occurs most often when hypotension is the resultof spinal anesthesia, hypovolemia, or dehydration andis unlikely in the dental setting, where hypotension isgenerally either vagal induced or attributed to drugsthat depress the central nervous system. However, pa-tients who have been without oral food and fluids forextended periods may present with a relative hypovo-lemia secondary to dehydration.

Phenylephrine is an alpha-adrenergic agonist thatis useful for treating hypotension when tachycardia is

Figure 1. Determinants of arterial blood pressure. The firststep for improving blood pressure is to increase venous re-turn (preload). When this proves unsuccessful, contractilitymust be improved. Arterial resistance and heart rate are rare-ly primary targets, because they produce a greater impact onmyocardial oxygen requirements.

128 Recognition and Management of Complications Anesth Prog 58:126^138 2011

present or when any increase in heart rate should beavoided, such as a patient with significant coronaryartery disease. Phenylephrine produces venoconstric-tion, improving preload and systolic pressure, andproduces arterial constriction, which increases diastolicpressure. The elevation in mean arterial pressure maytrigger a baroreceptor-mediated reduction in heartrate.7 Phenylephrine is typically administered by con-tinuous intravenous infusion or in 0.1-mg intravenousincrements. Its use should be accompanied by ade-quate fluid administration to ensure that hypovolemiais not present. The use of phenylephrine is best re-served for those with training in deep sedation and gen-eral anesthesia. An algorithm approach for managinghypotension is presented in Figure 2.

Hypertension

Sudden elevations in blood pressure are not that un-common in dental practice, regardless of whether se-dation is being provided. Precise blood pressures ofsignificance are not defined, but sudden elevations tosystolic blood pressure $180 mm Hg or diastolic bloodpressure $110 mm Hg are generally regarded as anacute hypertensive episode, keeping in mind that thissuggestion fails to consider the patient’s baseline read-ings.8 In patients with chronic hypertension, autoregu-lation of cerebral blood flow is reset to a higher level,and abruptly lowering pressure can lead to cerebral is-chemia. This is particularly true for geriatric patients.9

A hypertensive episode is generally regarded asurgent when the patient remains asymptomatic andrarely requires treatment other than a ‘‘time out’’ tocalm down. These episodes are most likely attributedto waning local anesthesia, a need to use the rest-room, or restlessness during lengthy procedures.

Gallagher summarized this issue vividly in an articlefor physicians in the emergency department. ‘‘Themost sensible approach to the patient in the [emergen-cy department] found to have very high blood pres-sure, without evidence of acute end organ damage, isreferral for outpatient management of serious diseasethat needs to be treated, not urgently, but for life.Focusing on the height of the column of mercuryin the sphygmomanometer confers no demonstrablebenefit on the patient and risks doing harm.’’10

Simply stated, patientswithout acute end-organ symp-toms should not receive antihypertensive agents in theoffice, and they may be safely referred to their primaryphysician for follow upwithin several days.11^13

Hypertensive emergency and crisis are terms used todescribe an acute hypertensive episode accompaniedby symptoms of end-organ damage.The event includeschest pain, headache, or visual disturbances. In thiscase, emergency medical service transport should bearranged immediately.While awaiting emergency med-ical service transport arrival, any decision to lower theblood pressure is based on the judgment and experi-ence of the provider. If treatment is elected, the goal isto lower the blood pressure by ,20% within 30^60 minutes.12^14 However, if signs or symptoms areconsistent with stroke, it is wise to avoid any interven-tion and continue to support the patient while awaitingemergency medical service transport arrival. Clinically,one cannot ascertain if injury is hemorrhagic or infarc-tion, and ischemic brain may be critically dependent oncollateral perfusion pressure. Any reduction in bloodpressure could prove catastrophic. In this scenario, onlyextremely high systolic blood pressure ($220 mm Hg)or diastolic blood pressure ($120 mm Hg) should evenbe considered for treatment.15

A variety of drugs and drug classes are suggested formanagement of hypertensive emergencies. However,nitroglycerin and labetalol are consistently mentionedand are adequate for office preparedness. Nitroglycer-in is a vasodilator that acts predominantly on the ve-nous system, decreasing venous return to the atriaand ventricles. At conventional doses, nitroglycerinhas little effect on arterial resistance and lowers bloodpressure by reducing preload and subsequent cardiacoutput. This action may be undesirable in patients withimpaired cerebral perfusion and should not be used ifstroke is suspected. However, it is ideal for those withcardiac symptoms. Nitroglycerin may be administeredeither sublingually or intravenously, but the formerroute is most appropriate in the office setting. A single0.4-mg tablet can be placed sublingually and repeatedevery 5 minutes while checking blood pressure re-sponse before each subsequent dose. Caution is ad-vised when administering more than 1 dose because

Figure 2. Hypotension algorithm. Hypotensive patients willgeneral ly respond to leg elevations or intravenous flui dadministration. When drug therapy is indicated, the choiceof drug is predicated on heart rate.


the incidence of headache may become problematic. Inany case, no more than 3 doses should be considered.

Labetalol (Trandate and Normodyne) is a selectivealpha-1blocker and nonselective beta blocker with a ra-tio of alpha/beta blockade of ,1 : 5. Labetalol lowersblood pressure by blockade of the alpha-1 receptors invascular smooth muscle and the beta-1 receptors in theheart. Because of the simultaneous beta receptor block-ade, the usual reflex tachycardia associated with othervasodilators does not occur. It can be administered in5- to 20-mg increments, depending on the response tothe initial dose, while checking blood pressure beforeeach subsequent dose. Patients under sedation or gen-eral anesthesia may be more susceptible to the lowerdose range.The expected onset of action of intravenouslabetalol is 5 minutes.The maximum dose is 0.5 mg/kgor 300 mg, but this amount will rarely be required.When administered in this manner, labetalol is safewith minimal adverse reactions.11 Like all nonselectivebeta blockers, labetalol is contraindicated in patientswith chronic obstructive pulmonary disease or asthma.Blockade of beta-2 receptors on bronchial smooth mus-cle may result in bronchoconstriction. Labetalol shouldbe used only by those with advanced training and onlywhen continuous electrocardiographic (ECG) monitor-ing and minute-by-minute blood pressure recording arein place.

Any drug that lowers blood pressure increases apatient’s risk for orthostatic (postural ) hypotension.Due to its longer duration of action, labetalol carries agreater risk than nitroglycerin and patients should beambulated with great caution. This concern is unlikely

in the office setting because any indication for usinglabetalol is likely accompanied by the need for emer-gency medical service transport. An algorithm ap-proach for managing acute hypertensive events ispresented in Figure 3.

ABNORMALITIES IN THE HEART

Cardiac Dysrhythmias

Most dentists have witnessed a patient complaining ofcardiac palpitations after administration of a local an-esthetic with epinephrine or during forceful proce-dures. Frequently this is the result of benign dysrhyth-mias, such as extrasystoles (premature contractions ),but they pass unnoticed because continuous ECGmonitoring is usually not in place. Published guide-lines for patient monitoring during sedation areconsistent in requiring continuous assessment of oxy-genation by pulse oximetry.This also provides contin-uous monitoring of pulse rate but not the specificrhythm, and guidelines for the use of ECG monitoringare less consistent. While stating that moderate andeven deep sedation have minimal impact on cardio-vascular function, theAmerican Society of Anesthesi-ologists guidelines nevertheless require ECG moni-toring for even moderate levels of sedation.16 Thishas no evidence-based scientific basis, but from thesociety’s perspective, it is understandable. All moni-toring systems used by anesthesiologists include elec-trocardiography, and any case scheduled initially forsedation may require instant conversion to a full gen-eral anesthetic. However, this requirement may beexcessive for the dentist providing only moderatesedation, and guidelines published by the AmericanDental Association are more practical for the averagemoderate sedation ^ trained dentist.17 These guide-lines do, however, require continuous ECG monitor-ing for deep sedation and general anesthesia, but itsuse for moderate sedation is suggested only for pa-tients having significant cardiovascular disease. Thiswould include patients who have known rhythm dis-turbances, including those managed with implantedpacemakers.

Legal controversies aside, there is an intangiblereassurance provided by an ECG monitor that adds tothat provided by periodic measurement of blood pres-sure and continuous pulse oximetry. This of coursepresumes the operator understands and can interpretelectrocardiograms and is comfortable witnessing oc-casional benign dysrhythmias and the subtle mechan-ical nuances all monitors present during routine use.The precise interpretation of a particular dysrhythmia

Figure 3. Hypertension algorithm. Episodes of hyperten-sion rarely require treatment. Asymptomatic episodes willgenerally correct after addressing possible causes. If pressureremains elevated, referral to the primary care physicianshould be considered. When accompanied by symptoms,emergency medical service transport should be arrangedand nitroglycerin or labetalol may be considered.


is not as important as recognizing that a disturbanceis occurring and deciding whether it is compromisingthe patient’s hemodynamic status. This will be ourapproach when addressing selected dysrhythmias andtheir management. A review of basic electrocardio-gram interpretation has been published in a previouscontinuing education article in this journal.18

Supraventricular Bradydysrhythmias

Bradycardia is defined as a heart rate of ,60 beats/min, but symptoms normally do not arise unless therate falls to ,50 beats/min. Supraventricular brady-dysrhythmias may be sinus or junctional in origin, orthey may be caused by various degrees of atrioventricu-lar block. In most cases, these events are vagally in-duced, but central nervous system depressants are po-tential culprits and may potentiate vagal activity whenpresent. Hypoxemia can also be a common cause, andefforts should be made to investigate and correct thispossibility.19 The precise diagnosis of the arrhythmia isnot so important as evidence of hemodynamic compro-mise (hypotension) or ventricular ectopy (prematureventricular contraction [PVC]) due to ventricular es-cape.When either of these events is present, the brady-cardia should be treated with atropine, as previouslyexplained in the discussion of hypotension in thisarticle.

If a bradyarrhythmia does not respond after 2 dosesof atropine, a second or third degree atrioventricularblock should be investigated. Second-degree type IIand third-degree blocks are located below the atrio-ventricular node, where there is no parasympatheticinnervation. Atropine is seldom effective for infrano-dal block, and these cases require EMS transport foreventual pacemaker insertion. If hypotension remainssignificant while awaiting EMS transport, the recom-mended treatment is epinephrine by continuous infu-sion titrated from 2^10 mg/min.19 This can be accom-plished by adding 1 mL of 1 : 1000 epinephrine to a500-mL bag of normal saline or 5% dextrose, whichprovides a concentration of 2 mg/mL. Titration withan infusion pump should commence at 1 mL/minwith incremental increases guided by blood pressureand heart rate. An epinephrine infusion should beused only by those with advanced training and whencontinuous ECG monitoring and minute-by-minuteblood pressure recording are in place.

Sinus and Supraventricular Tachydysrhythmias

Tachycardia is defined as a heart rate .100 beats/min,but usually it is not until rates exceed 150 that patients

become symptomatic. Transient episodes of tachycar-dia are triggered most often by pain, stress, and vaso-pressors included in local anesthetic solutions. It maybe an indication that the sedation being administeredis not sufficient to manage the patient’s fear. It is impor-tant to establish whether the tachycardia is secondaryto pain, stress, or vasopressors or whether the tachycar-dia is truly cardiogenic, which may lead to hypotensionor myocardial ischemia. This tachycardia is almost al-ways controlled by the sinoatrial node and is called si-nus tachycardia; a P wave precedes each QRS complex.Sinus tachycardia can also be an initial reflex responseto hypoxia or hypotension, and these should be consid-ered before further treatment. Once these possibilitieshave been attended, persistent tachycardia may causethe patient to complain of palpitations. In this case,intravenous fluids should be administered to supportblood pressure in the event the rapid heart rate is at-tempting to sustain the blood pressure in a hypovole-mic patient. If the episode continues, a selective beta-1receptor antagonist, such as esmolol (Brevibloc), can beadministered. Due to its relatively brief duration of ac-tion (T1/2 ,9 minutes), esmolol is generally adminis-tered as a bolus of 0.5 mg/kg over 2 minutes followedby a continuous intravenous infusion. For office use, wesuggest it be titrated intravenously in 20-mg incrementsevery 2^3 minutes until the heart rate declines to an ap-propriate level. There is no maximum dose publishedfor esmolol, but 80^100 mg is a reasonable limit beforedetermining it is ineffective. If the tachycardia does notrespond to this dosage or recurs after the effects of es-molol have waned, EMS transport should be consid-ered. Compared with nonselective beta blockers, suchas labetalol, esmolol is less likely to produce broncho-spasm, but it must nevertheless be used with caution inpatients with chronic obstructive pulmonary diseaseor asthma. Esmolol should be used only by thosewith advanced training and only when continuousECG monitoring and minute-by-minute blood pressurerecording are in place.

Sinus and supraventricular tachydysrhythmias aredistinguished from ventricular dysrhythmias by narrowQRS complexes. If P waves are not evident precedingthe QRS, the rhythm is not sinus in origin and isdescribed as supraventricular. These dysrhythmias in-clude atrial flutter, atrial fibrillation, and supraventricu-lar tachycardia. It must be emphasized that atrial flutterand fibrillation are fairly common chronic conditionsthat are usually well tolerated due to medications thatcontrol ventricular rate. They introduce concern onlywhen ventricular rate accelerates or they present as anew onset.

In contrast to atrial flutter and fibrillation, sup-raventricular tachycardia is not a chronic condition,


although a patient may have a history of paroxysmalepisodes. An onset of supraventricular tachycardia isalways a concern. It is generally more rapid, produc-ing heart rates .150 beats/min, and can be distin-guished from the others by its regular ventricularrhythm (ie, regular R to R intervals). A precise diagno-sis can be challenging, but the important feature deter-mining a need for treatment is hemodynamic instabi-lity, that is, hypotension. Although adenosine isregarded as the drug of choice for confirmed supra-ventricular tachycardia, a beta blocker, such as esmo-lol, is also an option.19 Furthermore, esmolol is also anoption in treating symptomatic atrial flutter and fibril-lation. For this reason, esmolol is an acceptable choicefor managing any of the atrial tachyarrhythmias. Com-pared with sinus tachycardias, any of the supraventric-ular dysrhythmias that become symptomatic are a fargreater concern, and EMS transport should be ar-ranged as treatment is rendered.

Extrasystoles (Premature Contractions)

Extrasystoles are ectopic impulses that occur in addi-tion to the underlying rhythm and occur in most indi-viduals. By convention, the term contraction is appliedto these extra impulses, although a true mechanicalcontraction may not always occur. The source of theseectopic impulses can be anywhere throughout theatria and ventricles: premature atrial contractions, pre-mature junctional contractions, or PVCs. In general,they are all relatively benign rhythms, and any newonset may reflect some sort of stress response thatshould be addressed.

PVCs are distinguished from other extrasystoles bytheir bizarre and widened QRS complex.They are gener-ally benign, but when they occur with considerable fre-quency, they dohave agreater potential for complicationsthan other extrasystoles. They may produce hemody-namic instability or lead to lethal dysrhythmias, such asventricular tachycardia and fibrillation.The Lown criteria

are used to classify PVCs according to their frequenciesand patterns (Table 1).20 After myocardial infarction,Lown classes 3^5 have been found to be associated witha greater risk for conversion to lethal dysrhythmias, butthis correlation has not been established for otherpatients.20 Nevertheless, a reasonable caveat is thattreatment is unlikely necessary forPVCshavingauniformappearance, regardless of frequency, unless the patientbecomes hypotensive. For classes 3^5, treatment andEMS transport are reasonable decisions.

There are many antidysrhythmic drugs advocatedfor treating patients with PVCs, but lidocaine is thesafest and least sophisticated to administer. It can beadministered as a single 0.5- to 1-mg/kg dose and re-peated every 5 minutes up to 3 mg/kg. Its influencewill generally last 15^20 minutes, after which a con-tinuous infusion of 1^2 mg/min is required if thecondition persists. However, when a patient remainssymptomatic after 1 or 2 incremental doses or the con-dition recurs after its effects have waned, EMS trans-port should be arranged.

Before electing to use lidocaine for PVCs, it isimportant to confirm that the underlying rhythm isnot a bradycardia, in which the PVCs represent effortsat ventricular escape. In this case, atropine should beadministered to increase the underlying heart rate. Theventricular escape beats will then hopefully subside.

Ventricular Tachycardia

Unlike ventricular fibrillation, ventricular tachycardiamay not be accompanied by cardiac arrest. It can bedistinguished from atrial tachydysrhythmias by wideQRS complexes and the absence of atrial waveforms.It is not uncommon for patients to remain relativelystable while experiencing this dysrhythmia, but it candeteriorate rapidly to cardiac arrest. EMS transportshould be summoned immediately. Current advancedcardiovascular life support guidelines suggest procain-amide, amiodarone, and sotalol as preferred agents,but lidocaine is still regarded as an acceptable alterna-tive and can be administered in the identical regimenaddressed for management of PVCs. If the patient de-velops chest pain or becomes hypotensive, synchro-nized cardioversion is recommended if available. Theoffice team should prepare for cardiac arrest, shouldit occur. Figure 4 provides an algorithm approach formanaging atrial and ventricular tachydysrhythmias.

Chest Pain: Angina/Myocardial Infarction

When any of the previously discussed complicationsbecome extremely severe, they can either strain the

Table 1. Lown Classif ication of Premature Ventricu larContractions*

Class Description

0 None1 ,30/hr2 $30/hr3 Multiform (or multifocal )4A 2 consecutive (couplet )4B $3 consecutive (run of

ventricular tachycardia)5 R-on-Tphenomenon

*Adapted fromYeally and Delbridge.20


heart or compromise coronary perfusion to the pointthat the patient may experience an episode of anginapectoris. However, this form of chest pain is most like-ly to occur if the patient has preexisting coronary ar-tery disease. The event may represent an episode ofstable angina or a more serious event labeled acutecoronary syndrome. To understand this difference, abasic understanding of the pathogenesis of coronaryartery disease must be appreciated.

The fundamental defect in coronary artery disease isstenosis, or narrowing of the lumen of coronary arter-ies due to atherosclerosis. The condition is not acutelylife threatening so long as the lesion remains stable

and does not rupture. The patient may experiencechest pain if cardiac stress suddenly increases becausecoronary ‘‘supply’’ is outweighed by myocardial oxygendemand. These episodes of chest pain are regarded as‘‘stable angina’’ and can be precipitated by the stressof dental treatment. The angina will dissipate whencardiac stress is reduced by calming the patient andperhaps administering a dose of nitroglycerin.

A more serious consequence occurs when athero-sclerotic lesions become unstable and rupture, produc-ing the so-called ‘‘acute coronary syndrome.’’ In thiscase, coronary perfusion becomes even further com-promised. Added to the preexisting stenosis, debris

Table 2. Relevant Data for Emergency Drugs*

Indication/Drugs Action Administration

Bradycardia/hypotensionAtropine (1.0 mg/mL) Cholinergic (muscarinic) receptor

antagonistIV: 0.5 mg q 2^3 min (3 mg total )IM/SLI: 0.5 mg q 5^10 min (3 mg total )

Ephedrine (50 mg/mL) Releases norepinephrine; alpha/betareceptor agonist

IV: dilute1mL in 5 mL510 mg/mL; then10 mg q 2^3 min (50 mg total )

IM/SLI: (undiluted) 25 mg q 5^10 min(50 mg total )

Phenylephrine (10 mg/mL)! Selective alpha agonist IV: double dilute1mL in10 mL51mg/mL;then discard 9 mL and dilute remaining1mL in10 mL5 0.1mg/mL; administer0.1-mg increments q 2^3 min (0.5 mgtotal ) or by infusion

HypertensionNitroglycerin (0.3- or 0.4-mg

tablet or 0.4-mg spray)Venodilator Sublingual:1 tablet q 5 min3 3

Labetalol (5 mg/mL)! Alpha/beta receptor antagonist IV: 5^20 mg q 5 min (300 mg total)AV blocksAtropine (1.0 mg/mL) Cholinergic (muscarinic) receptor

antagonistSee bradycardia/hypotension above.

Epinephrine (1mg/mL)! Alpha/beta agonists IV infusion: add1mg (1mL) to 500 mLnormal saline or 5% dextrose in water52 mg/mL; start titration at1mL/min

TachycardiasEsmolol (10 mg/mL)! Beta-1 receptor antagonist IV: 20 mg q 2^3 min (0.5 mg/kg bolus if

severe); repeat as neededLidocaine (2%) 20 mg/mL, 5-mL

prefilled syringe!Sodium channel blocker IV:1.0^1.5mg/kg q 3^5min (3mg/kg total)

Angina/myocardial infarctionNitroglycerin (0.3- or 0.4-mg

tablet or 0.4-mg spray)Venodilator Sublingual:1 tablet q 5 min3 3 if needed

Morphine Opioid receptor agonist IV: 2.5mg q 3^5min to10mg; ifmorphine isunavailable, may consider either 25 mgfentanyl or 2.5 mg nalbuphine, which52.5 mgmorphine

Aspirin Antiplatelet agent Chew and swallow:1 full-strength (325 mg)tablet or 4 baby-strength (81mg) tablets

* This table summarizes emergency drugs addressed in this article.! Indicates medications the authors suggest be used only by those with advanced formal training in deep sedation and general

anesthesia and that require minute-by-minute blood pressure and electrocardiographic monitoring. Advanced providers may alsoconsider additional agents suggested in advanced cardiovascular life support guidelines.

` IV indicates intravenous; IM, intramuscular; SLI, sublingual injection; and AV, atrioventricular.


from fractured atherosclerotic plaques obstructs coro-nary flow more severely and subsequent chest pain isdescribed as unstable angina. This form of angina canoccur at rest or with stress andmay evolve to thrombosiswith total occlusion of a coronary vessel. If this occurs,myocardial cells will undergo necrosis, defined as myo-cardial infarction. Therefore, the acute coronary syn-drome is produced by unstable atherosclerotic lesionsand manifests as either unstable angina or myocardialinfarction, described collectively as acute coronarysyndrome.

The dentist can do little to improve coronary bloodflow. Patient management must be devoted to reduc-ing cardiac stress and subsequent myocardial oxygenrequirement, which hopefully will render the compro-mised coronary perfusion adequate. When a patientexperiences chest pain, a complete primary assess-ment that includes not only blood pressure and heartrate but also hemoglobin saturation via pulse oximetryshould be performed. This will assure that adequateoxygenation is present. Regardless of these results,supplemental oxygen should be provided via nasalcannula (4 L/min) or nasal hood (6 L/min). Any

benefit of supplemental oxygenation has not been es-tablished for patients who sustain normal hemoglobinsaturation on room air, but short-term administrationhas no adverse effects. Comforting the patient may re-duce stress-induced increases in heart rate and bloodpressure. If pain persists, nitroglycerin (either a 0.3- or0.4-mg tablet or a 0.4-mg spray) should be adminis-tered sublingually, provided that the systolic bloodpressure is .90 mm Hg. Nitroglycerin dilates systemicveins and reduces venous return, that is, preload. Thisreduction in diastolic wall tension or stress may alsoallow improved coronary perfusion, especially in thesubendocardial regions. Nitroglycerin can be repeatedevery 5 minutes until symptoms improve or sideeffects (eg, hypotension, reflex tachycardia) occur. Hy-potension is particularly troublesome because it couldcompromise coronary perfusion further and reflextachycardia increases myocardial oxygen demand. Al-though reclined patients are not likely to experiencethese problems, blood pressure and pulse should beassessed before administering each subsequent doseof nitroglycerin.

Nitroglycerin is contraindicated if the patient hastaken an erectile dysfunction agent, such as sildenafil(Viagra) and vardenafil (Levitra), within 24 hours orwithin 48 hours if tadalafil (Cialis ) is used.21 Further-more, we must reemphasize the importance of assess-ing blood pressure before administering nitroglycerinto any patient. In some cases of myocardial infarction,nitroglycerin can produce a more significant drop inblood pressure. This is particularly true if the infarctioninvolves the inferior wall and right ventricle.22,23 Al-though this diagnosis requires 12-lead ECG analysis,successful management of these particular infarctionsis dependent on improving preload, which is reducedby nitroglycerin. Systolic blood pressure .90 mm Hgshould be confirmed before administering each dose.

The actual criteria for need and timing for activationof EMS transport are not well established.The packageinserts for nitroglycerin formulations instruct patientswith angina pectoris to access EMS transport when 3doses of nitroglycerin over15^20 minutes fail to relievesymptoms. Pollack and Braunwald24 have suggestedthat EMS transport is indicated after administration of3 doses of nitroglycerin over a15- to 20^minute periodfor stable angina but only1dose if angina is deemed un-stable. Current American Heart Association guide-lines25 address only suspected acute coronary syn-drome (unstable angina or myocardial infarction) andencourage immediate EMS transport. They do not ad-dress stable angina. However, it may be impossible forthe dentist to ascertain if the condition represents a sta-ble or unstable event, and personal judgment must beused regarding subsequent action. For a patient with

Figure 4. Sudden-onset tachycardia algorithm. Current ad-vanced cardiovascular life support guidelines provide severalsuggestions for managing tachycardias. Although lidocaine isnot listed as the preferred agent for ventricular tachycardia, itis nevertheless mentioned as an acceptable alternative. Clini-cians will determine the most suitable drugs based on theirexperience and training. A sinus tachycardia that respondsto a beta blocker, such as esmolol, does not necessarily re-quire emergency medical service transport. However, emer-gency medical service transport should be considered for asudden onset of all remaining atrial tachydysrhythmias (sup-raventricular tachycardia, atrial flutter, atrial fibrillation) orventricular tachycardia, whether or not treatment is per-formed.While awaiting emergency medical service transport,unstable patients may be managed using antidysrhythmicdrugs if cardioversion is not available. Adapted and abridgedfrom the 2010 American Heart Association advanced cardio-vascular life support guidelines.19


preexisting coronary disease, chest pain provoked by aparticularly stressful intervention may well represent atypical episode of stable angina. In this case, the patientwill respond nicely after a primary assessment or a sin-gle dose of nitroglycerin and could very well be senthome after the dental treatment is completed. In con-trast, patients having no prior history of angina or whorequire more than their usual dose to relieve symptomsshould be transported to an emergency department forfurther evaluation. In all cases, it is professionally cour-teous to inform the patient’s primary physician whenpossible.

With activation of EMS transport, the decision hasbeen made that the condition is possibly an acute coro-nary syndrome, and aspirin (300 mg) should be admin-istered. This is accomplished ideally by chewing andswallowing either 3 or 4 chewable, flavored baby aspi-rins (81 mg each) or a regular 325-mg tablet. Plateletaggregation is a key factor during coronary thrombosis,and the maximum antiplatelet influence of aspirin isachieved within 1 hour of administration. Nitroglycerincan be continued every 5 minutes, provided systolicpressure is at least 90 mm Hg and the heart rate is with-in normal limits.

If pain is severe and persistent, an opioid (narcotic )can be administered. Opioids not only relieve painand anxiety but also reduce peripheral resistance (af-terload ) and venous capacitance (preload). This re-duces myocardial oxygen demand, that is, a nitroglyc-erin- like effect. Although morphine is ideal and thusthe conventional agent recommended, fentanyl andnalbuphine are acceptable alternatives. Opioids aremore likely to produce hypotension if nitroglycerin

has been administered, and the clinician should mon-itor blood pressure carefully and often. An opioidshould be considered only if an intravenous infusionis in place and the clinician is familiar with its use. Asuggested algorithm for management of chest pain isprovided in Figure 5.

Cardiac Arrest

Cardiac arrest is the absence of a pulse. In the officesetting, the ECG status will most likely commencewith ventricular tachycardia, which deteriorates toventricular fibrillation. This can subsequently deterio-rate further to asystole or pulseless electrical activity.Cardiac arrest is most often attributed to myocardialinfarction but may also be triggered by other factors,such as sustained hypoxemia due to severe respiratorydepression or airway obstruction.

Once primary assessment confirms cardiac arrest,EMS transport must be obtained immediately and theoffice team should commence cardiopulmonary resus-citation following the 2010 American Heart Associa-tion guidelines as instructed in all health care providercourses in basic life support.26 An exemplary officeprotocol is presented in Figure 6. Ventilations shouldbe performed using a bag-valve-mask device (eg,Ambu-Bag) attached to a 100% oxygen source. Chestcompressions must be rapid (100/min) with pauses af-ter 30 compressions to allow for 2 adequate ventila-tions. There is little excuse for the entire office staffnot being certified in basic life support at the health

Figure 5. Chest pain algorithm. It may be difficult to deter-mine whether sudden onset of chest pain is an episode of stableanginaor acute coronary syndrome. If the episodewasprovokedin a patient with a known history of ischemic heart disease andspontaneously subsides or responds to his or her usual dose ofnitroglycerin, treatment may be continued and emergencymedical support transport is not necessary.

Figure 6. Office protocol for basic life support.26 This algo-rithm summarizes the actions that should be followed when apatient unexpectedly loses consciousness and primary assess-ment reveals no evidence of breathing. Unlike the AmericanHeart Association guidelines for lay rescuers, health care pro-viders should check for a pulse and provide ventilations alongwith chest compressions. AED indicates automated externaldefibri l lator; CPR, cardiopu lmonary resuscitation; BVM,bag-valve-mask device; EMS, emergencymedical service.


care provider level on a regular basis ( ideally on an an-nual basis). Definitive treatment requires electrical de-fibrillation as soon as it is available. The beneficial roleof cardiopulmonary resuscitation likely rests in itsmodest influence on coronary perfusion and minimiz-ing hypoxemia, which may sustain electrical activityuntil defibrillation is available. Supporting this con-cept are data illustrating greatest success when cardio-pulmonary resuscitation is initiated immediately and isfollowed by defibrillation within 5^8 minutes of cardi-ac arrest. For offices equipped with automated exter-nal defibrillators, the device should be turned on andits instructions followed. If an automated externaldefibrillator is not available, the office team shouldconcentrate on proper delivery of cardiopulmonaryresuscitation until EMS transport arrives.

Although many sedation and all general anesthesiaproviders train in advanced cardiac life support, it isessential to appreciate that the bulk of this curriculumbenefits patient management during the prearrest andpostarrest period. The actual success of resuscitationfrom cardiac arrest is predicated on an effective basiclife support protocol, including early defibrillation.However, once basic life support measures are inplace, providers may proceed according to the Ameri-can Heart Association cardiac arrest algorithm.19

An abridged version of this protocol is provided inFigure 7. Once an advanced airway is in place, chestcompressions should no longer be interrupted. A

single ventilation can be provided every 6^8 secondswhile compressions continue.

SUMMARY

Appropriate preoperative assessment and optimiza-tion of patients undergoing moderate or deep sedationare essential to minimize complications that may ariseintraoperatively. Furthermore, continual monitoringof cardiovascular status provides timely informationto also minimize potential occurrence of adverseevents. Understanding the relevant cardiovascularphysiology provides the basis for the clinician to deter-mine the most proper means of management. In turn,this allows for optimal care for patients receiving mod-erate or deep sedation for their dentistry. A summaryof medications addressed in this article is foundin Table 2.

REFERENCES

1. Becker DE, Haas DA. Management of complicationsduring moderate and deep sedation. Part 1: respiratoryconsiderations. Anesth Prog. 2011;58.

2. Carlson MD. Syncope. In: Fauci AS, Braunwald E, &Kasper DL, et al., eds. Harrison’s Principles of Internal Medi-cine. 17th ed. NewYork, Ny: McGraw Hill; 2008.

3. Deihl RR, Linden D. Images in clinical medicine:neurocardiogenic syncope. N Engl J Med. 1998;339:312.

4. Thrush DN, Downs JB. Vagotonia and cardiac arrestduring spinal anesthesia.Anesthesiology.1999;91:1171^1173.

5. Sibbald WJ, Paterson NA, Holliday RL, Baskerville J.The trendelenburg position:hemodynamic effects in hypo-tensive and normotensive patients. Crit Care Med. 1979;7:218^224.

6. Coonan TJ, Hope CE. Cardio-respiratory effects ofchange of body position.CanAnaesth Soc J.1983;30:424^437.

7. Lawson NW, Johnson JO. Autonomic nervous system:physiology and pharmacology. In: Barash PG, Cullen BF, &Stoelting RK, eds. Clinical Anesthesia. 5th ed. Philadelphia,Pa: Lippincott-Raven Publishers; 2006.

8. Chobanian AV, Bakris GL, Black HR, et al. Seventhreport of the Joint National Committee on Prevention, Detec-tion, Evaluation, and Treatment of High Blood Pressure. Hy-pertension. 2003;42:1206^1252.

9. Varon J, Marik PE. The diagnosis and management ofhypertensive crisis. Chest. 2000;118:214^227.

10. Gallagher EJ. Hypertensive urgencies: treating themercury? Ann Emerg Med. 2003;41:530^531.

11. Gray RO. Hypertension. In: MarxJA, Hockberger RS, &Walls RM, et al., eds. Rosen’s EmergencyMedicine:Concepts andClinicalPractice.7th ed.Philadelphia, Pa:MosbyElsevier,2010.

12. Papadopoulos DP, Mourouzis I, Thomopoulos C,MakrisT, Papademetriou V. Hypertension crisis. Blood Press.2010;19:328^336.

Figure 7. Abridged version of the advanced cardiovascularlife support cardiac arrest algorithm. When cardiac arrest isdetermined, the emergency medical service (911) should bealerted and cardiopulmonary resuscitation commenced im-mediately as presented in Figure 6.The office team may thenfollow this abridged version of the 2010 American HeartAssociation cardiac arrest algorithm.19 Analysis of the timerequired for each step in this sequence will reveal that anydecision regarding choice of antidysrhythmic drug will likelybe unnecessary because the emergency medical service willhave arrived.


13. Rodriguez MA, Kumar SK, De Caro M. Hypertensivecrisis. Cardiol Rev. 2010;18:102^107.14. Marik PE, Varon J. Hypertensive crises: challenges

and management. Chest. 2007;131:1949^1962.15. Jauch EC, Cucchiara B, Adeoye O, et al. Part 11: adult

stroke. 2010 American Heart Association Guidelines forCardiopulmonary Resuscitation and Emergency Cardiovas-cular Care. Circulation. 2010;122:S818^S828.16. American Society of Anesthesiologists Task Force on

Sedation and Analgesia by Non-Anesthesiologists. Practiceguidelines for sedation and analgesia by non-anesthesiologists.Anesthesiology. 2002;96:1004^1017.17. AmericanDentalAssociation,ADAGuidelines for theUse

of Sedation and General Anesthesia by Dentists. Available at:http://www.ada.org/prof/resources/positions/statements/anesthesia_guidelines.pdf. Accessed July1, 2011.18. Becker DE. Fundamentals of ECG interpretation.

Anesth Prog. 2006;53:53^64.19. NeumarTW, Otto CW, Link MS, et al. Part 8: adult ad-

vanced cardiovascular life support.2010AmericanHeartAssoci-ation Guidelines for Cardiopulmonary Resuscitation and Emer-gencyCardiovascularCare.Circulation. 2010;122:S729^S767.20. Yealy DM, Delbridge TR. Dysrhythmias. In: Marx JA,

Hockberger RS, & Walls RM, et al., eds. Rosen’s Emergency

Medicine: Concepts and Clinical Practice. 7th ed. Philadel-phia, Pa: Mosby Elsevier, 2010.21. Kloner RA. Cardiovascular effects of the 3 phospho-

diesterase-5 inhibitors approved for the treatment of erectiledysfunction. Circulation. 2004;110:3149^3155.22. Ferguson JJ, Diver DJ, Boldt M, Pasternak RC. Signifi-

cance of nitroglycerin-induced hypotension with inferior wallacute myocardial infarction. Am J Cardiol.1989;64:311^314.23. Moye S, Carney MF, Hostege C, Mattu A, Brady WJ.

The electrocardiogram in right ventricular myocardial infarc-tion. AmJ Emerg Med. 2005;23:793^799.24. Pollack CV Jr, Braunwald E. 2007 update to theACC/

AHA guidelines for the management of patients with unsta-ble angina and non-ST-segment elevation myocardial infarc-tion: implications for emergency department practice. AnnEmerg Med. 2008;51:591^606.25. O’Connor RE, BradyW, Brooks SC, et al. Part 10: acute

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CONTINUING EDUCATIONQUESTIONS

1. You have sedated a 62-year-old man with a historyof hypertension managed with losartan (Cozaar )and hydrochlorothiazide. His preoperative bloodpressure was 138/88 and 126/81 after sedation.Approximately 30minutes into the procedure, yourmonitor records a pressure of 182/102, which yousubsequently reconfirm. The patient is calm andasymptomatic.Which of the following is the mostappropriate action?

A. If signs of stroke develop, 20 mg of intrave-nous labetalol should be administered.

B. 0.4 mg of nitroglycerin should be adminis-tered.

C. The patient should be transported by emer-gency medical service for further evaluation.

D. Treatment should be paused and possiblecauses ( eg, inadequate local anesthesia )ruled out.

2. Which of the following is correct regarding tachy-cardias and ectopy?

A. Supraventricular tachycardias always havea P wave before every QRS.

B. Emergency medical service should be calledfor a patient experiencing any form of tachy-cardia.

C. Drug administration is NOTrequired for a pa-tient having uniform-appearing prematureventricular contractions at a rateof1or 2/min.

D. Tachycardias with narrow QRS complexesare ventricular in origin and should be man-aged with1mg/kg lidocaine.

3. Your patient is a 57-year-old man with a history ofcoronary artery disease. His medications includemetoprolol and nitroglycerin. He has not used thenitroglycerin in the previous 6 months.While an ex-traction is being attempted, he complains that thearea is not numb and that he is experiencing chestpain.Which of the following is the most appropriatemanagement for this patient?

A. Nitroglycerin should be administered sublin-gually in a dose of 0.3 or 0.4 mg.

B. Emergency medical service transport shouldbe called.

C. An automated external defibri llator shouldbe applied to the patient.

D. A 1-mg dose of epinephrine should be ad-ministered intravenously.

4. Your patient is a 24-year-old woman scheduledfor a third molar extraction under sedation. Shehas a negative medical history other than Zoloftfor panic disorder. After administration of localanesthetic, she loses consciousness.Your primaryassessment reveals that she is breathing and has apulse. Her oxygen saturation is 98%, blood pres-sure is 70/50, and pulse rate is 74. All of the fol-lowing are appropriate for managing this situationEXCEPT:

A. Administer or increase supplemental oxygen.B. Administer 0.5 mg of atropine intravenously,

intramuscularly, or injected sublingually.C. Administer 10 mg of ephedrine intravenous-

ly or 25 mg intramuscularly or injected sub-lingually.

D. Administer 250^500 mL intravenous fluid.


continuing education recognition and management of ...tion of tissue perfusion is the more...

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