PATHO CORNER

The Asthmatic PACU Patient ‘‘Squeaks’’ ByKim A. Noble, PhD, RN, CPAN

IN MANY WAYS, perianesthesia nursingrepresents a unique form of patient carefound in a variety of patient care settings. Pa-tients recovering from sedation or anesthesiaand surgical procedures have unique nursingcare priorities and needs compared with a va-riety of other patient care delivery settings.Some priorities of care, however, are consis-tent with any care setting, and the provisionof a patent airway is one of the first prioritiesthat is especially critical for perianesthesiapatients. Perianesthesia nurses are airwayexperts with applied experience in airwaymanagement on a daily basis. In many in-stances, airway-related complications can beprevented or treated rapidly through the pro-vision of rapid assessment and treatment. Asystematic airway assessment is completed asthe patient is being settled in the PACU bay areaand is repeated on an ongoing basis withoutawareness by the experienced PACU nurse.The patient with pre-existing respiratory dis-ease undergoing emergent surgery requirescareful handling for safe anesthetic passageand a complication-free convalescence.

Jake Jones (JJ) is a 58-year-old man who is60100and 247 lbs (112 kg.). He was admittedvia the emergency department for emergentrepair of a displaced fracture of the tibial pla-teau of the left leg. This fracture occurredwhile playing football with his adult sons andtheir friends, and JJ reports having completedseveral additional plays after the injury untilthe swelling and pain prevented his continuedparticipation. He is currently alert, reportinga 15 on a 10-point pain scale. He has received2 mg of intravenous morphine sulfate, butadditional opioids have been held pendingorthopedic and anesthesia consultation.

Journal of PeriAnesthesia Nursing, Vol 23, No 2 (April), 2008: pp 125-132

Hydromorphone hydrochloride 2 mg intra-muscularly has been ordered to be given afterthe consultation and consent completion.

JJ has a past history of moderately controlledhypertension and intermittent rapid heartrate for which he has been taking propranololhydrochloride for several months. Withoutmedical consult, JJ has recently decreased his40 mg twice daily doses to every other day be-cause he was feeling depressed while takingthe medication daily. Today was the first dayin several months he had the energy to inter-act with his family. JJ has only had one priorsurgical procedure, a tonsillectomy at age 4under general anesthesia, which was a badexperience because he had postoperativedyspnea that necessitated a longer-than-planned hospitalization. He also has a historyof multiple environmental allergies and extrin-sic asthma as a child, with his last attack occur-ring around age 14. He reports smokingapproximately a half pack per day of unfilteredcigarettes and frequent upper respiratoryinfections with dyspnea during the long win-ter season in New England. He reports havinghad a slight sore throat and cough two weeksago after babysitting his grandson. He cur-rently denies fever, shortness of breath, orchange in cough. JJ has bilateral breath soundswith slight expiratory wheezing present withdeep exhalation and occasional scattered

Dr Kim A. Noble is an Assistant Professor at Temple Univer-

sity, Philadelphia, PA.

Address correspondence to Kim A. Noble, Department of

Nursing, Temple University, 3307 N Broad St, Philadelphia,

PA 19140; e-mail address: knoble@temple.edu.

� 2008 by American Society of PeriAnesthesia Nurses.

1089-9472/08/2302-0008$34.00/0

doi:10.1016/j.jopan.2008.01.006

125

126 KIM A. NOBLE

rhonchi that clears easily with coughing. JJ hasa chest x-ray that showed changes consistentwith early, mild chronic obstructive pulmo-nary disease (COPD) and an electrocardio-gram (EKG) that shows sinus bradycardia,with an old inferior myocardial infarctionand frequent multifocal premature atrial con-tractions (PACs). JJ denies ever having hadchest pain or a heart attack. He reports fre-quent episodic heartburn that he treats withapproximately 6 to 8 antacids daily. JJ’s labwork is predominantly normal, with the onlyabnormal findings including: hemoglobin of17.2 g/dL, a room air PO2 of 78 mm Hg, a satu-ration of 91%, and a PCO2 of 57 mm Hg. Oxy-gen is applied via nasal cannula at 2 L/min.

JJ is evaluated by anesthesia and loudly refusesto have regional anesthesia stating ‘‘I knowpeople who are paralyzed from putting nee-dles in their back. You are NOT doing that tome!’’ He ate a large breakfast at approximately8 AM and emergent surgery with general anes-thesia for fracture repair is planned for 4 PM.

JJ is taken to the OR and anesthesia and surgerybegin as planned. He is induced with 100% ox-ygen, midazolam 3 mg, 2 mL fentanyl, 230 mgpropofol, and succinylcholine for rapid se-quence induction. Upon intubation JJ de-velops significant increased peak and plateauairway pressures and pronounced wheezing,followed by decreased breath sounds, desatu-ration, and a rise in end-tidal CO2. Sevofluraneis added and JJ receives an additional 100 mg ofpropofol and inhaled albuterol. JJ is given a sin-gle dose of methylprednisolone 125 mg intra-venously. Anesthetic maintenance wascompleted using sevoflurane and vecuroniumbromide. JJ also receives 10 mg of morphinesulfate, administered in incremental dosesover the length of the case. The surgery is com-pleted in 95 minutes, blood loss is minimal, anda total of 2,200 mL of LR is infused.

After completion of the surgery, the paralyticagent was reversed using a maximal dose ofpyridostigmine and glycopyrrolate, and JJ

was extubated without difficulty or additionalincidence of bronchospasm. Oxygen wasapplied by nasal cannula and JJ was trans-ported to the PACU.

Upon PACU admission, JJ was again noted tohave pronounced expiratory wheezing andcomplained of dyspnea. His respiratory pat-tern was very labored, saturation was 90% ona 4-L nasal cannula, and he was noted to bevery restless with frequent position changeson the stretcher. He also was reporting severeleft knee discomfort and urgency. Once allmonitoring equipment was applied, JJ wasfound to be in controlled atrial fibrillationwith a heart rate of 70 to 80 beats/minute. Anebulized respiratory treatment with ipra-tropium (Atrovent) was ordered by anesthesiaand administered. JJ’s status was changed fromoutpatient to an inpatient-monitored admis-sion for pulmonary consultation and work-up. Morphine sulfate orders were receivedand administered. Over the next hour, JJ spon-taneously converted back to sinus rhythm andhis respiratory status continued to improve.His oxygen was decreased to 2 L/min whenhis saturation reached 98%. JJ began to verbal-ize the need to smoke, stating ‘‘No one will no-tice; I just need one puff to calm me down!’’

Obstructive Pulmonary Disease

Obstructive pulmonary disease is a form ofairway obstruction that leads to the trappingof air in the distal gas exchange and conduct-ing airways, leading to a prolonged, difficultexpiration.1 This classification of disordersrepresents one of the four most frequentcauses of death2 and includes chronic bron-chitis, emphysema, and asthma. Emphysemaand chronic bronchitis frequently present asa combined disorder, leading to chronic in-flammation and airway destruction, termedchronic obstructive pulmonary disease(COPD). Asthma presents in a different fash-ion, with episodic, short-lived, triggered at-tacks leading to the release of inflammatorymediators, such as histamine, prostaglandins,

THE ASTHMATIC PACU PATIENT 127

posure to cold or smoke can lead to broncho-spasm and asthma attack, not seen in personswith ‘‘normal’’ receptor activity.4

The Autonomic Nervous System andthe Conducting Airways

The autonomic nervous system (ANS) inner-vates, coordinates, and maintains normal func-tioning of most of the organ systems of thehuman body. There are two branches of theANS with paradoxical functioning that is loca-tion dependent; in some instances SNS andPSNS work in opposition, and in some in-stances they work together to govern organsystem homeostasis. For instance, stimulationof the sympathetic branch leads to an increasein the heart rate, whereas parasympatheticnervous stimulation leads to a decrease in heartrate, but both may contribute to vasodilation.1

Each branch of the ANS has two forms of recep-tors, different locations and terminal neuro-transmitters (NT) (Figure 1). The conductingairways are innervated by both branches ofthe ANS: the sympathetic nervous system(SNS) and the parasympathetic nervous system(PSNS). The activation of the beta-1 receptorsby circulating epinephrine (catecholamine)leads to the relaxation of the smooth muscle lin-ing of the conducting airways and bronchodila-tion. Activation of the PSNS works in anopposite fashion with the neurotransmitteracetylcholamine binding to muscarinic recep-tors causing bronchoconstriction. Just as the re-sistance to airflow and airway size can beinfluenced by stimulation of the SNS/PSNS,pharmacologic manipulation and receptorblockade can lead to changes in the size and re-activity of the airway. For example, JJ was takingpropranolol hydrochloride, a nonselectivebeta-adrenergic antagonist for the treatmentof long-standing hypertension and sporadictachycardia. Nonselective beta-adrenergic an-tagonists successfully block the beta-1 recep-tors, leading to a decrease in heart rate,contractility, and, therefore, blood pressure.As a nonspecific agent, there is also

and leukotrienes, and activation of immunecells, including mast cell degranulation and ac-tivation of lymphocytes, neutrophils, and mac-rophages.1 This cascade leads to increasedresistance and swelling in the smooth musclelining of the airways and heightened activityof the autonomic nervous system and cate-cholamine release, leading to increased bron-chial responsiveness.3

Asthma is one of the most common obstruc-tive respiratory diseases in the United States,affecting approximately 11 million individ-uals,1 with an increasing incidence also beingreported. Bronchial hyperreactivity, found inapproximately 10% of the population of theUnited States, is a characteristic trait ofasthma. Ninety percent of anesthesia-inducedbronchospasm is associated with endotra-cheal intubation, most often thought to bethe result of mechanical irritation of the largeairways and the associated dramatic inflamma-tory and smooth muscle response.4

The Physiology of Asthma andReactive Airway Disease

The respiratory center of the brain stemreceives and processes information from a vari-ety of sources to determine the depth, rate,and rhythm of the ventilatory cycle. In addi-tion to the chemoreceptors, which provide in-formation to the respiratory center about theCO2 and PO2 levels, receptors are located inlung tissue that govern and protect ventila-tion. One set of receptors, termed irritant re-ceptors, are found in the large airways andare triggered by the mechanical manipulationof intubation. Insertion of a laryngoscopeand endotracheal tube causes nervous infor-mation to travel via parasympathetic afferent,or ascending, tracts to the respiratory centerin the central nervous system (CNS). Nervousinformation rapidly returns to the smoothmuscle that lines the conducting airways, lead-ing to cough and bronchospasm. In patientswho have a heightened response to stimuliapplied to the parasympathetic receptors, ex-

KIM A. NOBLE

history, including the frequency, trigger, andsymptoms associated with dyspnea attacks,and the timing of those attacks focusing onwheezing or dyspnea that occurs at night orin the early morning. This pattern of symp-toms would indicate a poorly controlled disor-der that would require medical interventionbefore surgery. Also important to discover isthe type of treatment that is required for thepatient’s symptom management and a currentmedication schedule. Also important is thepresence of any symptoms today, includingan upper respiratory infection in the prior 4to 6 weeks, because this will increase therisk for the development of bronchospasmon intubation. The health care practitionerneeds to elicit the presence of asthma orwheezing triggers that include cold or smoke,because this would indicate a heightened re-sponse by irritant receptors and again indicatean increased risk of instability during anesthe-sia. The final point to ask is about prior anes-thetic experience(s) and any wheezingdevelopment or dyspnea because this couldagain indicate an increased risk. The comple-tion of this type of detailed respiratory anddyspnea assessment in a planned surgical pro-cedure allows for the luxury of time to preparethe patient. JJ presented with a past history ofbronchospasm under anesthesia and an upperrespiratory infection 2 weeks before his injury,both placing him at increased risk for a bron-chospastic response.

Several forms of diagnostic testing are recom-mended for patients reporting dyspnea, in-cluding pulmonary function testing, chestradiograph, and arterial blood gas (ABG) sam-pling. Patients with decreased forced expira-tory values (, 80% of predicted values)should receive inhaled administration ofa beta-2 adrenergic agonist and the test shouldbe repeated 15 to 20 minutes later. An improve-ment (.15%) indicates the need of treatmentand stabilization with inhalation agents. Pa-tients exhibiting elevated resting PCO2 values(PCO2 .45 mm Hg) are at increased risk andhave a potential need for intensive care

a pharmacologic blockade of the beta-2 recep-tors, decreasing the bronchodilatory effect ofthe SNS and placing patients with pulmonarydisease at significant risk for the developmentof bronchospastic disorders. The use of cardio-selective beta-1 antagonism with the desired ef-fects of decreasing heart rate and contractilitycan be obtained without the beta-2 antagonism.

In asthma, bronchoconstriction is the founda-tional pathophysiological mechanism andrequires further description. There are threetypes of PSNS muscarinic receptors that havedifferent roles in the bronchoconstrictiveresponse: M1, M2, and M3. M1 receptors func-tion in the control of neurotransmitter releasefrom the vagus nerve; M3 receptors are foundin the bronchial smooth muscle and, whenbound to the neurotransmitter acetylcholine,lead to bronchoconstriction. The final typeof muscarinic receptor is the M2, which are lo-cated close to the M3 receptors and functionto prevent the overstimulation of the M3 re-ceptor, therefore preventing excessive bron-choconstriction.2 Pharmacologic treatment mayaffect one form of receptor in a preferentialfashion and, in the case of blocking theaction of the M2 receptor, cause an in-creased, bronchospasm by the loss of the reg-ulatory action of the receptor. This responseis seen with the administration of low doseatropine, an anticholinergic that blocks theaction of the PSNS, but because of its selec-tive action on the M2 receptor, is not a firstline choice for the treatment of broncho-spasm.

Anesthesia and Asthma

The best way to manage an asthmatic patientwho requires surgery is to gather a respiratory

Autonomic Nervous System

Sympathetic Nervous System Parasympathetic Nervous System

Alpha Beta Muscarinic Nicotinic

Fig 1. Autonomic Nervous System

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can increase secretions and cause coughing,laryngospasm, and bronchospasm.2 Lightanesthesia may trigger bronchospasm in a sen-sitive patient, and one of the first treatmentsfor the development of intraoperative wheez-ing is to increase the concentration of theinhalational anesthetic agent.2

Intravenous Anesthetics

The use of propofol for induction is currentlythe main agent used for induction that doesnot lead to wheezing in asthmatic patients.Thiopental was found to stimulate wheezingduring the induction of healthy asthmatics(46%) and methohexital (26%); however theuse of etomidate and ketamine were not. Ifpropofol cannot be used, ketamine is a viableoption because it stimulates the SNS, leadingto direct bronchodilation from smooth musclerelaxation. Different derivatives of ketamineare now available that have less associatednegative CNS effects.2 As noted previously, ifa patient has bronchospasm from a light planeof anesthesia and bronchospasm from endo-tracheal tube (ETT) irritation, additional pro-pofol can be given to deepen the anesthesia.It is also recommended that patients areextubated while still under deep anesthesiato prevent ETT-mediated bronchospasm onemergence from anesthesia.3

Opioids

Opioids are a frequently used and effectiveadjunct to the administration of general anes-thetic agents. Despite the histamine releaseassociated with the administration of relativelyhigh-dose morphine sulfate, opioids can beused effectively to decrease the cough reflexand deepen the anesthetic plane as needed.2 Fi-nally, patient comfort is very important in asth-matic patients because the anxiety associatedwith acute pain may trigger bronchospasm.

Muscle Relaxants

The mechanism of action in muscle relaxantsis to interfere with acetylcholine binding atthe neuromuscular junction, leading to theelimination of neurotransmission and

monitoring postoperatively.2 Finally chest ra-diograph analysis is used to rule out an acute in-fection or as a global assessment of currentpulmonary status. However, chest radiographsare frequently normal in patients with asthma.2

JJ again had several identified abnormalities.His emergent need of surgery eliminated thepossibility of completing pulmonary functiontesting and his elevated PCO2 and arterial hy-poxemia and abnormal chest radiograph placehim at an increased risk for pulmonary compli-cations during general anesthesia.

Conflicting reports have been presented forthe incidence of the development of wheezingfrom bronchoconstriction during the induc-tion of general anesthesia from 0.17%4 to14%.5 The best approach to patients with a his-tory of asthma is to use regional anesthesia,if possible; however, bronchospasm is pre-vented relatively easily and managed withthe administration of anesthetic agents, andthe contribution of individual agents usedwill be discussed.

Premedication

Anxiety from surgical anticipation may lead tothe release of catecholamines and exacerbatebronchoconstriction. Careful patient evaluationmust be completed and effective use of anxio-lytic agents may be helpful in patients who donot demonstrate an elevation in resting CO2

or have a reduction in their respiratory drive.Benzodiazepines are effective in the reductionof anxiety and do not affect bronchial tone.2

Volatile Inhalation Agents

Volatile anesthetic gases lead to a reduction inbronchospasm by a direct blockade of the irri-tant pathways of the PSNS, leading to a relaxa-tion of the smooth muscle of the airways.3

Halothane is a potent bronchodilator at lowconcentrations that was used frequently inchildren; however, it carries a risk of hepatitis.Newer agents, such as enflurane, isoflurane,and sevoflurane offer similar bronchodilatoryeffects, with the best effect seen with sevoflur-ane.3 Desflurane should be avoided because it

THE ASTHMATIC PACU PATIENT

130 KIM A. NOBLE

results can also be obtained with the topicaladministration during intubation.2

Implications for the PACU Patient

As with many disorders, the best approach toreactive airway disease and asthma is to usea proactive approach with thorough data col-lection related to respiratory symptoms andpulmonary assessment. In this fashion, thehealth care provider can potentially anticipateand prevent the occurrence of acute dyspnea.As mentioned previously, patients withasthma are at risk for bronchospasm with air-way instrumentation and this should be antic-ipated and prevented if possible. The Phase IPACU care of the asthmatic patient centerson the completion of ongoing respiratoryassessments, with rapid intervention and treat-ment if air exchange difficulty reoccurs.

Alteration in Gas Exchange

The patient who experiences bronchospasmin the OR is no different than any emergingpatient; the provision of an adequate airwayfor gas exchange is the PACU nurse’s first pri-ority. For this patient, diligence in pulmonaryassessment and monitoring is essential. Theprovision of adequate hydration through theadministration of IV fluids and humidificationof inhaled gases will assist the patient withthe mobilization of secretions and the preven-tion of airway drying from inhalation of drygases.3 The provision of continuous pulseoximetry and cardiac monitoring is needed,as is frequent pulmonary auscultation forbreath sounds and the presence of adventi-tious sounds. The presence of wheezingwould indicate the development of broncho-spasm and may necessitate the administrationof additional beta-2 agonist administration innebulized inhalation route. JJ may also requirethe administration of additional corticoste-roids to reduce the spasm and inflammatoryresponse. Arterial blood gas (ABG) should becompleted as ordered and results obtainedand reported in a timely fashion.6

paralysis. The effect of the paralytic agent is de-pendent on the muscarinic receptor (M1, M2,or M3) that is affected, leading to great variabil-ity in the associated changes in bronchial tone.Agents that have a greater effect on M2 recep-tors (gallamine, pipecuronium) can eitherdirectly cause an increase in bronchospasm,whereas agents that have a greater effect onthe M3 muscarinic receptor (vecuronium, ro-curonium, mivacurium, and pancuronium)do not cause bronchospasm. Atracurium andmivacurium should be eliminated as potentialchoices as they cause a histamine release thatmay exacerbate bronchospasm in a sensitivepatient. Also imperative in the selection ofthe paralytic agent is the consideration forthe reversal as the mechanism of action is toprevent the breakdown of acetylcholine inthe neuromuscular junction, allowing the re-establishment of normal passage of impulseswith the resultant muscle contraction. The ad-ministration of a pharmacologic agent thatmimics the PSNS can lead to systemic effects,including bradycardia, nausea and vomiting,and bronchospasm. The PSNS effect is antago-nized by the administration of atropine or gly-copyrrolate. There are no clear establishedguidelines for the use of paralytic and reversalagents in asthmatic patients and these medica-tions need to be individually titrated based onpatient response and the need of a paralyticagent.2

Local Anesthetics

The administration of an amide local anes-thetic decreases the transmission of nervousimpulses to the CNS and can be very effectiveto decrease the cough reflex and broncho-spasm related to the release of histamine inasthmatic patients.2 Intravenous dosing oflidocaine of 1.0 to 2.0 mg/kg body weightcan be used to decrease the endotrachealirritation associated with the mechanicalmanipulation of intubation. Intravenous ad-ministration was not found to be an effectivetreatment modality to treat established bron-chospasm once wheezing is present. If sys-temic lidocaine is not desired, effective

THE ASTHMATIC PACU PATIENT 131

dioselective beta-blocker would be a betterchoice for JJ because of his potential for pul-monary disease. JJ also needs to receive educa-tion relating to his accelerated heart ratebecause he has a reduction in the coronaryblood flow and an increased heart rate de-creases the supply of oxygen to the myocardialcells and at the same time increases the de-mand for oxygen by the myocardium. Perhapsthe addition of another antiarrhythmic or anti-coagulation would be needed if fibrillation isseen frequently. Compression boots need tobe applied throughout JJ’s hospitalization toprevent venous stasis and the developmentof a deep vein thrombosis.

Potential for Anxiety and Incisional Pain

The development of anxiety can lead towheezing in the patient prone to broncho-spasm, so careful education needs to be pro-vided, with the goal of anxiety reduction. JJshould not expect to be pain–free, but heshould have adequate pain medication admin-istration to control his pain and enable pulmo-nary functioning and early mobilization.

Alteration in Mobility

As mentioned previously, JJ is at risk for the de-velopment of deep vein thrombosis related tohis immobility and potential for irregular heartrate. Compression boots should be appliedwhenever JJ is in bed and education as to theirimportance and rationale for use provided. JJshould receive ordered anticoagulation and,if he is to continue the anticoagulation afterdischarge, he will need education relating todosage and administration. JJ needs also to un-derstand the importance of early and frequentmobilization as he recovers from this injuryand surgery. From an orthopedic perspective,early mobility will facilitate healing and frac-ture repair and enable JJ to return to his previ-ous level of activity. JJ also needs educationrelating to crutch-walking, cast care, or thecare of an immobilized joint. He will need tohave dressing changes as ordered by the sur-geon and will need to learn to care for his

As soon as the patient is hemodynamicallystable, the head of the bed may be raised to a45-degree angle to ease the work of breath-ing. JJ should be encouraged to cough anddeep breathe, and suction should be readilyavailable if needed. The potential for reintu-bation and mechanical ventilation should beanticipated and personnel, equipment, andmedications that would be needed immedi-ately available. Planning for discharge fromthe Phase I PACU should include theavailability of intensive care observation ifordered by the attending physician oranesthesiologist.

JJ needs to be taught to cough and deepbreathe postoperatively to prevent the devel-opment of an upper respiratory infection.This can be facilitated with the use of incen-tive spirometry, with instruction and rein-forcement offered as needed. JJ also needs tobe encouraged to stop smoking and this maybe facilitated in the acute care setting withthe use of transdermal nicotine patches.

Alteration in Cardiovascular Functioning

In the PACU, JJ needs careful monitoring for thedevelopment of additional dysrhythmias orchest pain. His arrival in new-onset atrial fibril-lation with an accelerated rate and his historyof silent myocardial infarction indicate theneed for careful monitoring. JJ needs to be ques-tioned for the development of indigestion anda coronary mechanism as the trigger for the dis-comfort explored. The presence of further EKGchanges or chest discomfort may indicate theneed of monitoring serum cardiac enzymesand treatment with nitrates as needed.

Because JJ has a history of an abnormal accel-erated heart rate for which he is receivingpharmacologic beta blockade, he needs edu-cation relating to the use and dosage schedulefor this drug because it is not a medication hemay titrate to meet his liking. Changes in thedosage of beta-blockers require weaning andcareful planning to prevent the developmentof cardiovascular side effects. Perhaps a car-

132 KIM A. NOBLE

surgical incision to prevent the developmentof an infection.

In conclusion, JJ has experienced a rare andfrightening complication of general anesthesia

and the manipulation of his airway. With carefulassessment and rapid communication with theattending anesthesiologist and medical inter-ventions as required, the perianesthesia nursemay minimize the consequences of COPD.

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3. Huford WE. The bronchospastic patient. Int Anesthesiol

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4. Warner DO, Warner MA, Barnes RD, et al. (1996). Perioper-

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5. Rooke GA, Choi HJ, Bishop J. (1997). The effect of isoflur-

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