patients with coronary artery disease. Anesthesiology 1982;56:219-221 26. Quintin L, Whalley DG, Wynands JE, Morin JE: The effects of vascular catheterizations on heart rate and blood pressure before aortocoronary bypass surgery. Can Anaesth Soc J 1981;28:244-247 27. Waller JL, Zaidan JR, Kaplan JA, Bauman DI: Hemodynamic effects of vascular cannulation by residents. Anesthesiology 1982;53:S114 28. Mangano DT: Monitoring pulmonary arterial pressure in coronary artery disease. Anesthesiology 1980;53:364-370
Placement of the Pulmonary Arterial Catheter before Anesthesia for Cardiac Surgery: A Stressful, Painful, Unnecessary Crutch Ray Dzelzkalns, MD, and Theodore H. Stanley, MD Dzelzkalns R, Stanley TH: Placement of the pulmonary arterial catheter before anesthesia for cardiac surgery: A stressful, painful, unnecessary crutch. J Clin Monit 1985;1:197-200 ABSTRACT. Catheterization of the pulmonary artery (PA) in patients with cardiac or major vascular disease is a popular practice. However, controversy surrounds the question of whether the PA catheter should be inserted before or after the induction of anesthesia. Review of the literature supports insertion after induction for several reasons. First, the information provided by a PA catheter may be misleading, since it does not provide a direct measurement ofleft ventricular function, but rather, an indirect reflection that is subject to many variables. Second, pharmacologic intervention before anesthesia to correct hemodynamic abnormalities detected by a PA catheter has not been shown to improve induction of anesthesia or outcome after cardiac surgery. Induction of anesthesia with synthetic narcotics in patients with either normal or abnormal hemodynamic function is fast and uneventful, making insertion of a PA catheter before induction unnecessary. Finally, the act of inserting a PA catheter produces cardiovascular stimulation that can lead to myocardial ischemia. Thus, insertion ofa PA catheter can be more safely and rationally performed after the induction of anesthesia. KEYWORDS.Catheterization: pulmonary artery; Monitoring: hemodynamic, pulmonary artery; Anesthesia: cardiovascular, opioid
P u l m o n a r y arterial (PA) catheterization is n o w widely used in cardiac, major vascular, and noncardiac surgery for patients with c o n c o m i t a n t c o r o n a r y artery, valvular, or other serious cardiac disease. P A catheters provide h e m o d y n a m i c and metabolic information that can assist clinicians in maintaining optimal conditions intraoperatively and postoperatively. A major c o n t r o v e r s y exists concerning the timing o f insertion o f the P A catheter: Should it be done before or after the induction o f anesthesia? This discussion will examine the issues that support the a r g u m e n t for inserting the PA catheter after induction o f anesthesia for cardiac surgery. O f w h a t value is a P A catheter prior to induction? Proponents o f preanesthetic PA catheter placement feel that obtaining h e m o d y n a m i c values before induction alFrom the Department of Anesthesiology, The University of Utah School of Medicine, 50 N Medical Dr, Salt Lake City, UT 84132. Received Mar 12, 1985. Accepted for publication Mar 13, 1985. Address correspondence to Dr Stanley. 197
198 Journal of Clinical Monitoritzr Vol 1 No 3 July I985
lows for optimal patient management. However, most, if not all, of the information provided by a PA catheter is already available from the patient's cardiac cathctcrization report. This information usually includes cjcction fraction, left ventricular end-diastolic pressure, cardiac output, diseased vessels, and areas of ventricular dyskinesia. In patients with an ejection fraction greater than 0.50 and without ventricular dysyncrgy, mcasurcmcnts of central venous pressure provide a reliable estimate of left ventricular filling pressure, eliminating the need for a PA catheter [1]. In patients with an ejection fraction less than 0.40 or with vcntricular dysyncrgy, a PA catheter provides bettcr estimates of left vcntricular fdling pressure than do measurements of central venous pressure, but the information must bc critically evaluated [1]. The measurement most heavily relied upon by clinicians as an indicator of left vcntricular end-diastolic pressure (LVEDP) is the pulmonary capillary wedge pressure (PCWP). This variable also provides an estimate of left ventricular end-diastolic volume [2-5]. However, PCWP is not a reliable reflection of LVEDP. Although PCWP and LVEDP arc similar in patients with normal cardiovascular dynamics, they arc not necessarily so in patients with ischcmic myocardial disease or left ventricular hypertrophy secondary to any cause [3,4,6-8]. In patients undergoing cardiac surgcry, left ventricular compliance is frequently decreased by acute ischemia, prior myocardial infarction, and hypertrophy. The noncompliant left ventricle is morc dcpcndent on atrial contraction, or the atrial "kick," for vcntricular filling, and this results in a higher late LVEDP, which is not reflected in the PCWP [6-8]. In these situations measurements of PCWP underestimate LVEDP. Thus, a single PCWP mcasurcmcnt obtained bcforc induction in these patients frequently will bc misleading and could lead to inappropriate therapy. Furthcrmorc, construction of Frank-Starling curves with a PCWP that underestimates LVEDP will suggest better left ventricular curves than actually exist. Whether preinduction PA catheter placement provides more information concerning a patient's cardiovascular status than do cardiac catheterization data and clinical assessment (neck vein distention, gallops, rales, orthostatic hypotension, and urine output) has not been explored and is therefore unknown. Some clinicians and medical writers suggest that measurement and correction of abnormal cardiovascular variables via use ofinotropic agents or vasodilators immediately before induction of anesthesia represents superior, modern anesthetic care. Unfortunately supporters of this approach are unable to provide data to establish that correction of abnormal hemodynamic
variables before anesthetic induction improves outcome after cardiac procedures. In patients with poor left ventricular function who were undergoing coronary artery bypass grafting (CABG) procedures, Wynands et al [9] observed that the mean LVEDP was 29 torr and the mean PCWP was 22 torr. These investigators found that even without pharmacological intervention, anesthesia could be induced with high doses of a potent narcotic with no occurrence of hemodynamic alterations throughout the entire operation. Proponents of preanesthetic PA catheterization feel that obtaining preinduction hemodynamic values allows a more rational selection of the "best anesthetic approach" for induction and maintenance of anesthesia. These proponents feel that it is worth the effort and time to obtain additional hcmodynamic information, such as PCWP, cardiac outputs in triplicate, and systemic vascular resistance, to help guide the anesthetic induction. However, anesthetic induction for the large majority of cardiac and major vascular surgical procedures usually involves the use of one of the new synthetic narcotics, fentanyl or sufcntanil. Results from many studies using these agents for induction of anesthesia have shown the process to bc characteristically fast and hcnaodynaniically uneventful. Wc have assessed cumulative data from eleven recently published studies (239 subjects) in patients who had rcasonably good left vcntricular function and wcrc undergoing CABG procedures. After induction with fcntanyl, sufcntanil, or alfcntanil there occurred minimal or no changes in heart rate, blood pressure, cardiac output, the ECG tracing, or PCWP [10-20]. Indeed almost all measured cardiovascular values wcrc unchanged in all these studies. There arc fcwcr data available in patients with little or no ventricular reserve, but the results are similar. Wynan& and colleagues [9] studied patients with poor left ventricular function (ejection fraction less than 0.3, left ventricular end-diastolic pressure greater than 20 tort, and significant dyskinesia) who wcrc given 30 p.g/kg of fentanyl for induction of anesthcsia. They observed no change in any hcmodynamic variablc either during induction or after tracheal intubation. In another study these same investigators evaluated patients with moderate to severe left vcntricular impairment (NYHA classification of III and IV) [21]. In these patients anesthetic induction with 50 I-tg/kg of fcntanyl produced only a small decrease (17%) in systolic blood pressure, and the systolic pressure returned to baseline values following endotracheal intubation. In patients undergoing mitral valve replacement, Stanley and Webster [22] observed no significant changes in heart rate, stroke volume, cardiac output, peripneral vascular resistance, and mean arterial and
Clinical Controversy: Dzelzkahls and Stanley: Preoperative PA Catheterization
central venous pressures during induction of anesthesia with 11 + 3 p,g/kg of fentanyl and after endotracheal intubation. In a similar investigation, Bovill et al [23] compared fentanyl, sufentanil, and alfentanil for induction of anesthesia in 60 patients with various forms of valvular heart disease. They found no changes in hemodynamic functioning and no ECG evidence of myocardial ischemia during or after the induction-intubation sequence. Preinduction hemodynamic abnormalities can result from insertion of a PA catheter. Placement of a PA catheter in unanesthetized patients can produce considerable stimulation of the cardiovascular system [24-25]. Lunn et al [24] evaluated PA catheter insertion in awake and anesthetized patients undergoing CABG or valve replacement operations. All patients were premedicated with 10 mg ofdiazepam orally and 0.1 mg/kg of morphine and 0.5 mg of scopolaminc intramuscularly, and all were judged adequately premedicated upon arrival to the opcrating room. In spitc of continued verbal assurance, as well as the use of local ancsthetics and appropriate mechanical maneuvers, thcse authors found that systolic blood prcssure and hcart rate increased significantly above baseline values in awake patients during implantation of the catheters. In contrast, in anesthetized patients thcre were no changes in any cardiovascular variable. Four of 40 patients in the unanesthetized patient groups complained of angina and three of those had ST wavc depression greater than 1 mm requiring treatment with oral nitroglycerin, de Lange and co-workers [25] studied paticnts who were about to undergo CABG or valve replacement surgery, who were heavily premedicated with lorazepam (0.08 rag/ kg) and atropine (0.1 mg/15 kg), and who had a PA catheter inserted via the basilic or cephalic vein before induction of anesthesia. They found that insertion of the PA catheter resulted in an increase in systolic arterial blood pressure in all groups, as well as an increase in heart rate in patients who werc not receiving betaadrenergic blockers. T w o of 84 patients had angina and demonstrated significant ST wave depression on the ECG. A recent study by Slogoff and Keats [26] looked for perioperative myocardial ischemia in patients scheduled for CABG operations. The patients were given their usual beta-adrenergic blockers and nitrates preoperatively, along with moderate or heavy preanesthetic medication. These investigators observed that 18% of patients (182 of 1,023) arrived in the operating room with new ischemic ECG changes. These results suggest that the anxiety and stress associated with transportation to the operating room and/or insertion of a venous catheter can in themselves result in serious problems.
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One can only wonder what the incidence of myocardial ischemia would have been if a PA catheter had been inserted before induction of anesthesia. With adequate preanesthetic medication, and perhaps additional intravenous sedation administered in the operating room, it is possible to insert a PA catheter without evidence ofischemia [27-29]. However, the degree of central nervous system depression required can produce respiratory depression. Quintin [27] compared arterial blood gases obtained the day before CABG surgery with those sampled after preinduction placement of the PA catheter. They showed an increase in arterial carbon dioxide tension from 39 to 45 torr and a decrease in arterial oxygen tension from 76 to 69 torr. Thus, the generous preoperative medication given to blunt stress responses from preinduction catheterization may pose a risk to the patient with marginal respiratory and cardiac reserve. Furthermore, sedated patients often experience hypoxemia and hypercapnia secondary to rebreathing associated with placement of drapes over the face [30-31]. Despite lack of data, many clinicians continue to place PA catheters before induction of anesthesia. What motivates them to use this unnecessary and potentially dangerous crutch is unclear, since the placement ofa PA catheter in unanesthetized patients needlessly provides ideal conditions for increased cardiovascular stimulation and myocardial ischemia. Evidence from many studies using modern anesthetic induction agents indicates that anesthesia can be initiated rapidly and maintained uneventfully without need of a PA catheter. Changes in hemodynamic functioning are generally minimal, usually restricted to heart rate and blood pressure, and easily managed with the usual ECG and blood pressure monitoring. Placement of a PA catheter after induction of anesthesia eliminates the risk of stress-induced myocardial ischemia and allows for catheterization under more ideal and controlled conditions.
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22. Stanley TH, Webster LR: Auesthetic requirements and cardiovascular effects of fentanyl-oxygen and fcntanyldiazepam-oxygcn anesthesia in man. Anesth Analg 1978;57:411-416 23. Bovill JG, Warren PJ, Schuller JL, ct al: Comparison of fcntanyl, st, fentanil, and alfcnta,lil anesthesia in patients undergoing valvular heart surgery. Anesth Analg 1984;63: I{181- 1086 24. Lunn JK, Stanley TH, Webster LR, Bidwai AV: Arterial blood-pressure and pulse-rate responses to pulmonary and radial arterial catheterization prior to cardiac and major vascular operations. Anesthesiology 1979;51:256-269 25. de Langc SS, Boscoe MJ, Stanley TH: Pcrcutancous pulmonary artery catheterization via tile arm before anaesthesia: Success rate, freque,~cy of complications and arterial pressure and heart rate responses. Br J Anacsth 1981;53:1167-1171 26. SlogoffS, Keats AS: Does perioperativc myoca,-dial ischcmia lead to postoperative myocardial infarction? Anesthesiology 1985;62:1117-114 27. Quintin L, Whalley I)G, Wynauds JE, Morin JE: Tile effects of vascular catheterizations upon heart rate and blood prcssu,c before aortocoronary bypass surgery. Can Anaesth Soc J 1981;28:244-247 28. Waller JL, Zaidan JR, Kaplan JA, Bauman 1)1: Hcmody,namic responses to preoperative vascular cannulation m patients with coronary artery disease. Anesthesiology 1982;56:219-221 29. WallcrJL, ZaidanJR, Kaplan JA, Bauman 1)1: Hcmody,namic effects of vascular cannulation by residents. Anesthesiology 1980;53:S114 30. Weisman H, Christensen RE, l)illon jB: An airconditioned, adjustable table frame for cyc surgery. Arch Ophthal 1970;83:448-449 31. Ramanathan S, Capan L, Chalon J, ct al: Minienvironmental control under the drapes during operations on the eyes of conscious patients. Anesthesiology 1974;48:286-288