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With CAD, Faster Is Never Better

Kim A. Noble, PhD, RN, CPAN

OU REALIZE it is another busy day in thehase I PACU as you admit 88-year-old PC fromhe OR after a total hip arthroplasty. You re-eive the following report from anesthesia: PCs female, 5=2==, weighs 112 pounds, and has aast medical history of an old anterior myocar-ial infarction on electrocardiogram (ECG), cor-nary artery disease (CAD), and osteoarthritis.C’s procedure was cancelled four weeks agoecause her hemoglobin (Hgb) was 8.7 onreadmission testing. She has been taking an

ron supplement and, although she was unableo autodonate blood, her repeat Hgb readingas 10.1 this morning. PC received a planned

egional anesthesia epidural with lidocaine andmg of duramorph, but after a late failure of thepidural block, she had general anesthesia withropofol and received the remaining 4 mg ofuramorph intravenously. During the proce-ure, PC had episodic hypotension that wasreated with a total of 25 mg of ephedrine givenn 5-mg incremental doses intravenously. Herlood loss for the procedure was 450 mL andhe was give 2200 mL of lactated Ringer’s solu-ion. A cell saver was used for the procedure,ut not enough blood was obtained to be givenack to PC.

C arrives agitated and slightly confused. Sheeports pain in her right hip area as a 6 on a0-point pain scale. Her vital signs are: bloodressure (BP) 164/104, heart rate (HR) 122,espiration rate (RR) 24, temperature 96.4° F,nd oxygen saturation 96% on 4 L of nasalxygen. She has decreased sensation from T4ilaterally, reporting a “weird” feeling to stimu-

ation application to T12 bilaterally. She hasilateral sensation on her feet with gross motor

ovement present with the right more than the

ournal of PeriAnesthesia Nursing, Vol 22, No 1 (February), 2007: pp 47-50

left. She has a urinary catheter with adequateclear yellow urine. She has a right-sided hipdressing that is dry and intact, an abductionpillow in place and compression boots bilater-ally. You notice occasional multifocal prema-ture ventricular contractions (PVCs) on herECG and she is holding her chest and reportsbeing so hungry “it hurts.” Her lungs are clear toauscultation and there is no change in the du-ration or character of chest discomfort withdeep breathing. She denies nausea and has ac-tive bowel sounds. You call the attending anes-thesiologist for additional evaluation and a 12-lead ECG is ordered. You give PC a loading doseof 4 mg of morphine and start her patient-controlled analgesia as ordered. Ten minuteslater PC reports slight improvement in her pain,now 5/10 on the pain scale, her BP is 158/98,HR 118 with continued multifocal PVCs, andher RR remains 24 per minute. The ECG iscompleted and read by anesthesia, who notesacute inferior wall changes. Intravenous nitro-glycerin and an intensive care bed are ordered.

Sympathetic Nervous SystemActivation of the CardiovascularSystem

To fully understand the interactions that resultin increases in heart rate and the myocardialoxygen requirements, one must begin with abrief review of the mechanism(s) that increase

Kim A. Noble, PhD, RN, CPAN, is an Assistant Professor atTemple University, Philadelphia, PA.

Address correspondence to Kim A. Noble, PhD, RN, CPAN,Department of Nursing, Temple University, 3307 N. Broad St,Philadelphia, PA 19140; e-mail address:knoble@temple.edu.

© 2007 by American Society of PeriAnesthesia Nurses.1089-9472/07/2201-0007$35.00/0

doi:10.1016/j.jopan.2006.12.003

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KIM A. NOBLE48

ardiovascular (CV) functioning. Although toome extent CV control may be initiated byetabolic or humoral components, the most

apid forms of increases or decreases in CVunctioning are mediated through the activity ofhe autonomic nervous system (ANS).1 Therere two branches of the ANS, the parasympa-hetic nervous system (PSNS) and the sympa-hetic nervous system (SNS), which work inirect opposition to manipulate systemic func-ion to meet the minute-to-minute changes inystemic needs. The SNS and the PSNS are onpposite ends of the spectrum in terms ofechanism of action and physiologic re-

ponses. The PSNS exerts an effect through thenteraction of the neurotransmitter acetylcho-ine, and the muscarinic and nicotinic cholin-rgic receptors. The SNS uses the neurotrans-itters norepinephrine and epinephrine,orking through the autonomic alpha (�) andeta (�) receptors. The autonomic receptorsre further subdivided based on their location offfect, with the �-receptors residing in vascularmooth muscle, the �-1 receptors found primar-ly in cardiac muscle, and the �-2 receptorsound in the conducting airways of the lungs.

ctivation of the SNS, as would be seen in aght-or-flight response, leads to a rapid andramatic increase in CV performance. SNS fi-ers innervate multiple areas of the atria andentricles and trigger the release of norepineph-ine, which binds to �-adrenergic receptors onhe cardiac cell membranes, causing an in-reased metabolic activity,1 which can be fur-her divided into four separate events. First,-adrenergic receptors are present on the sino-trial (SA) node and conduction system of theeart, leading to an increase in heart rate andonduction velocity. Second, norepinephrinencreases the movement of calcium into theardiac cells, leading to an increase in contrac-ility of the cardiac myocytes. The third andourth events are in response to SNS stimulationf the �-adrenergic receptors, leading to con-raction and increased resistance in the vascular

mooth muscle of the blood vessels. The third

event results from the contraction of the venoussystem, causing an increased venous return tothe right atrium and increased preload orstretch of the ventricle. The fourth and finalevent is in response to the contraction of thearterial system and leads to an increase in theperipheral vascular resistance, arterial bloodpressure, and the afterload or work required bythe ventricle to eject blood. Each of theseevents independently increases myocardial ox-ygen requirements, but their summation signif-icantly increases the demand for oxygen by theheart.1 Inequalities are encountered when thesupply of oxygen via the coronary arteries isdiminished by disease such as the partial coro-nary occlusion seen with PC.

Tachycardia and CAD

Increasing the HR forces the events thattake place during depolarization (systole)and repolarization (diastole) to increase infrequency, causing a higher demand for ox-ygen. With depolarization, ion channelsopen and electrically charged ions moveacross the cell membrane, allowing the in-teraction between actin and myosin andcontraction of the myofibrils. During repo-larization, ion concentration gradients arere-established through the activity of aden-osine triphosphate-dependent, energy-burn-ing pumps, and the resting membrane po-tential for the next contraction is reset.Because of the nature of myocardial con-traction, very little blood is delivered to thecontracting myocardial cells; instead a ma-jority of blood flow to the muscle takesplace during diastole, or repolarization. In apatient with a normal HR of 70 beats perminute, depolarization or systole accountsfor one-third of the cardiac cycle, whereasdiastole or repolarization represents two-thirds of the cycle. The time of systole isrelatively fixed and increases in HR predom-inantly affect the time of diastole, or filling.Because this is the only time the myocar-dium receives its blood supply, decreasing

the time of filling reduces the supply of

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PATHO CORNER 49

xygen to the working heart. As an increasen HR simultaneously increases the demandor oxygen by myocardial cells, tachycardiareates a double-edged sword for the pa-ient with pre-existing CAD: an increase inxygen demand with a decrease of oxygenow and nutrients to the contracting myo-ytes.

mplications for the PACU Patient

AD affects approximately 13 million Ameri-ans, leading to a coronary event every 26 sec-nds and a coronary-related death everyinute.1 The chances of having a patient withAD in your PACU are good and the preventionf coronary complications is a priority. A briefummary of the implications of CAD for thewakening PACU patient follow.

lteration in Gas Exchange

very patient emerging from general anesthesiaequires the maintenance of a patent airway anddequate respiration is priority one. The provi-ion of supplemental oxygen is imperative butn even higher priority for the patient with CADnd increased myocardial oxygen requirements.ecause the administration of more than 2 L of

ntravenous fluid and an increased workload onC’s heart may lead to a new onset of heartailure, diligent monitoring of pulse oximetrynd frequent auscultation of breath sounds isital. The reason for PC’s admission agitationust be explored and a careful evaluation ofer epidural level completed. The origination ofC’s increased respiratory rate should be deter-ined too because this also indicates an in-

rease in the work of breathing. The adminis-ration of opioids requires diligent monitoringor physiologic response and, as with any pa-ient emerging from a surgical procedure, PChould be encouraged to breathe deeply andough at intervals.

lteration in Cardiovascular Functioning

s discussed previously, the effect of height-

ned sympathetic nervous system activity in-

creases the workload and myocardial oxygenrequirements of the myocardium. This is espe-cially problematic for myocardial tissue that isnot receiving an adequate supply of oxygen andnutrients. Control of PC’s pain is importantthrough the administration of opioids and theinitiation of a nitroglycerin infusion. Nitroglyc-erin rapidly dilates the coronary and systemicvasculature, leading to an increased blood sup-ply to the myocardium and a reduction in thepreload or venous return to the heart.2 Vasodi-lation of the arterial system will also decreasethe afterload, or the amount of pressure orwork that must be completed by the left ventri-cle to eject blood through the aortic valve. Anoptimal blood pressure goal based on preoper-ative readings should be received from the at-tending anesthesiologist, and diligent monitor-ing of systemic blood pressure and the titrationof the nitroglycerin drip completed to maintainthe target blood pressure.

An ongoing nursing assessment of the epidurallevel should be conducted at intervals. Residualblockade from epidural injection may lead to aloss of sympathic tone, venous pooling, andblood pressure reduction. Caution should beused for any changes in position until the levelis below T12.3 Lab work should be ordered andobtained from the attending anesthesiologist;these include cardiac isoenzymes and troponinlevels, as well as hemoglobin and hematocrit(H&H) and serum electrolytes. Continuous car-diac monitoring is needed because PC is havingfrequent multifocal PVCs. These PVCs may beattributed to the myocardial ischemia, hypox-emia, or electrolyte imbalance, and they mayrequire the administration of an antiarrhythmicif they persist. PC’s baseline H&H was low(10.1) and it should be expected to decreasefurther with the surgical procedure, administra-tion of intravenous fluids, and blood losses. If itwas not already completed, an order for a bloodtype and screen should be obtained for a possi-ble transfusion because anemia will further

complicate PC’s ischemic myocardium.

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KIM A. NOBLE50

inally, as the cardiovascular effects of the SNSre mediated primarily through the � receptorshich innervate the myocardium, the perianes-

hesia nurse must be prepared for the adminis-ration of a �-antagonist or �-blocker if PCemains tachycardiac because these pharmaco-ogic interventions will decrease myocardial ox-gen requirements and increase the time of

iastole and blood supply to the myocardial cells.

ren

Because of the significance of CAD in Ameri-cans, the chance of recovering a patient withCAD is very good and the perianesthesia nursemust be prepared to intervene should compli-cations develop. With an understanding of thephysiologic consequences of SNS activity on thecardiovascular system, the nurse caring for thepatient with CAD emerging from anesthesia can

be anticipated, identified, and treated rapidly.

Refe1. McCance KL, Huether SE. Pathophysiology: The Biologic

asis for Disease in Adults and Children. Ed 5. St. Louis, MO:osby; 2006.

cesing. Ed 2. Philadelphia, PA: Lippincott Williams & Wilkins;2006.

3. Drain CB. PeriAnesthesia Nursing: A Critical Care Ap-

2. Aschenbrenner DS, Venable SJ. Drug Therapy in Nurs- proach. Ed 4. St. Louis, MO: Saunders; 2003.