Peripheral vascular response to potassium administration during cardiopulmonary bypass

J

THORAC CARDIOVASC SURG

79:237-240, 1980

Peripheral vascular response to potassium administration during cardiopulmonary bypass Potassium (K+) is often administered To patients during cardiopulmonary bypass (CPR). The effects of rapid K+ administration during CPR were studied in 30 adult patients. Each patient received one bolus dose (2,4,8,12, or 16 mEq) of potassium chloride (KCl) (2 mEq/ml) during CPR. Serum K+ was significantly increased from baseline values at KCl doses of 8 mEq and larger (p < 0.05). All increases in serum K+ returned to clinically acceptable levels within 5 minutes after the bolus. Mean arterial pressure (MAP) (torr) and total peripheral resistance (TPR) (dynes sec cm-O) changes were biphasic; after an initial transient decrease, maximal with the 16 mEq K+ bolus (MAP - 21 ± 6,t TPR - 315 ± 135t),+ these parameters increased (8 mEq K+ bolus, MAP + 15 ± 6, t TPR + 301 ± 90t; 12 mEq K+ bolus, MAP + 43 ± 9, t TPR + 998 ± 250t; 16 mEq bolus, MAP + 51 ± 9,t TPR + 1,216 ± 120tH with a peak at 3 minutes after the bolus. Hypertension, in nine of 18 patients receiving a KCl bolus of 8 mEq or larger, was of such magnitude (range 132 to 196 torr) as To require rapid therapeutic intervention to lower blood pressure. When KCl supplementation is required on CPR and slow infusion rates seem unreasonable, bolus doses of less than 8 mEq may be administered WiThoUT vascular effect,

Alan Jay Schwartz, M.D.,* Thomas J. Conahan III, M.D.,** David R. Jobes, M.D.,* Raymond W. Andrews, B.A.,*** Horace MacVaugh III, M.D.,**** and Alan Jay Ominsky, M.D.,***** Philadelphia. Pa.

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erioperative hypokalemia may precipitate ventricular arrhythmias and potentiate digitalis effect, both not From the Division of Cardiac Anesthesia, Department of Anesthesia, and Division of Cardiothoracic Surgery, Department of Surgery, University of Pennsylvania School of Medicine, Philadelphia, Pa. Presented in part at the Annual Spring Meeting of the Association of Cardiac Anesthesiologists at the Annual Meeting of the American Association for Thoracic Surgery, Toronto, Canada, April 1977. This study was supported in part by Anesthesia Training Grant USPHS-5-TOI-6M-00215-18. Received for publication May 18. 1979. Accepted for publication June 25, 1979. Address for reprints: Dr. Alan Jay Schwartz, Department of Anesthesia, University of Pennsylvania School of Medicine. 3400 Spruce St., Philadelphia. Pa. 19104. • Assistant Professor of Anesthesia. •• Assistant Professor of Anesthesia. Present address: Department of Anesthesiology, University of Arizona, Tucson, Ariz. ••• Anesthesia Research Specialist. •••• Associate Professor of Surgery. Present address: Lankenau Hospital, Philadelphia, Pa. ••••• Associate Professor of Anesthesia and Psychiatry.

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uncommon in patients undergoing cardiac operations.':" Factors cited as predisposing to hypokalemia include preoperative diuretic therapy, potassium (K+)deficient cardiopulmonary bypass (CPB) prime solutions, hemodilution with forced diuresis during CPB, and inadequate K+ replacement.l " The need for routine K+ replacement during CPB has recently been questioned.v " but if hypokalemia is present during CPB, many would agree with the need for K+ administration. Protocols for K+ supplementation during CPB vary greatly" 3, 9 but the usual end point is the resulting serum K+ level. When K+ is administered during CPB, blood pressure changes have occasionally been observed. This study was undertaken to define a bolus dose of K+ with minimum hemodynamic effects.

Patients and methods Thirty adult patients undergoing cardiac operations for coronary artery or acquired valvular disease were studied. The research protocol was approved by the University of Pennsylvania Committee on Studies Involving Human Beings. Informed consent was obtained from each participant. All patients were premedicated with morphine sul-

0022-5223/80/020237+04$00.40/0 © 1980 The C. V. Mosby Co.

237

238

The Journal of Thoracic and Cardiovascular Surgery

Schwartz et at.

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Fig. 1. Change from control serum potassium and mean arterial pressure after bolus KCI administration (2,4, 8, 12, or 16 mEq) during CPB (mean zr S.E.M.). fate (0.1 mg/kg) and scopolamine (0.04 to 0.06 mg/ kg), anesthetized with nitrous oxide and halothane in oxygen, and paralyzed with succinylcholine infusion for endotracheal intubation and pancuronium bromide (0.02 to 0.04 mg/kg) for maintenance. Monitoring included a radial artery catheter for continuously recording mean arterial pressure (MAP) and for intermittent blood sampling. CPB was instituted with a Sams Model 1800 or 2000 pump (Sams Inc., Ann Arbor, Mich.) with a Travenol Model 5M0317 bubble oxygenator (Artifical Organs Division, Travenol Laboratories, Deerfield, Ill.) and a prime consisting of 2,000 ml of Normosol R (Abbott Laboratories, North Chicago, Ill.) and 1,000 ml of 5% plasma protein (Buminate 5% Hyland Division, Travenol Laboratories, Costa Mesa, Califor.). A pump index of 2.2 Llm 2/min was maintained throughout the study period. Only patients meeting the following criteria at the time of potassium chloride (KCl) (KCI injection (2 mEq/ml), USP, Elkins-Sinn, Inc., Cherry Hill, N. J.) administration were included in the study: (I) MAP on CPB not in excess of 100 torr, (2) serum K+ level not in

excess of 5.0 mEq/L, and (3) urine output at least 0.5 ml/kg/hr. Each patient was randomly assigned to one of five treatment groups determining the single bolus dose of KCI (2, 4, 8, 12, or 16 mEq) they were to receive after the establishment of stable CPB. KCI was administered directly into the oxygenator reservoir. After the bolus had been administered no further KCI was given during the 10 minute study period. In addition to the measured MAP, total peripheral resistance (TPR) was calculated from the equation: TPR (dynes' sec . crrr s) = [MAP (torr) - central venous pressure (torr)] x 80 cardiac output (L'min) Hypertension during CPB was defined as a MAP greater than 120 torr, a pressure often exceeding cerebrovascular autoregulation. 10. 11 Blood was sampled 1 minute prior to and 45 seconds, 1112,3,5, and 10 minutes after the administration of KCI. Each sample was analyzed for arterial blood gases and pH (lL213 meter with 127 micro electrode system, Instrumentation

Volume 79

Potassium administration during CPR

Number 2 February, 1980

Laboratories , Lexington , Mass .), hematocrit (capillary tube method), sodium and K+ (Orion Space-Stat 30 Sodium/Potassium Analyzer, Orion Biomedical, Cambridge, Mass.), calcium (Orion Model 99-20 Ionized Calcium System), magnesium (Atomic Absorption Spectrophotometer, Varian Techtron Type AA-5, Florham, N. J.), osmolarity (Model 3L osmometer, Advanced Instruments, Needham Heights , Mass.), and total protein (TS Meter to read refractive index, Bausch and Lomb, Rochester, N. Y.) . Administration of vasoconstrictors, aortic cross-clamping, and nasopharyngeal temperature were recorded during the 10 minute study period. Data were analyzed with Student's t test for independent samples where appropriate, with p < 0 .05 considered to be significant. Results Patient ages, weights, and body surface areas and serum K+, MAP, and TPR on CPB prior to bolus KCl administration were similar among the five treatment groups. Statistical analysis revealed that at no time during the study period were there differences among the five groups with regard to vasoconstrictor administration, aortic cross-clamping, nasopharyngeal temperature , arterial blood gases, pH, hematocrit, sodium, calcium, magnesium, osmolarity, or total protein (p < 0.05) . Serum K+ was significantly increased from baseline values at KCI doses 8 mEq and larger (p < 0.05). Even after the largest (16 mEq) dose , the acute serum Ktrise returned to clinically acceptable levels within 5 minutes after the KCI bolus. MAP and TPR changes were biphasic in nature (Fig. I). Following an initial transient decrease in both MAP and TPR, maximal with the 16 mEq K+ bolus, (MAP -21 ± S.E.M . 6, TPR -315 ± S .E .M. 135, P < 0.05), these parameters increased (8 mEq K+ bolus, MAP + 15 ± S.E.M . 6, TPR +301 ± S.E.M. 90; 12 mEq K+ bolus , MAP +43 ± S.E.M . 9, TPR +998 ± S.E .M . 250; 16 mEq bolus, MAP +51 ± S.E.M . 9, TPR + 1,216 ± S.E .M . 120, P < 0.05) with a peak at 3 minutes after the bolus KCl administration (Fig . I). The peak of the hypertension invariably occurred later than the peak in the serum K+ (Fig. I). Hypertension during CPB , associated with administration of bolus KCI doses of 12 mEq or larger, was of such clinical magnitude (range 132 to 196 torr) in eight of 12 patients as to require temporary reduction in the pump output and intravenous therapy with a vasodilator such as Arfonad (Roche Laboratories, Division of

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Fig. 2. Typical mean arterial pressure trace in a patient receiving a 16 mEg bolus of KCI during CPB. Arrow J: KCl bolus injected. Arrow 2: Halothane-inspired concentration 1.5%. CPB flow reduced 10% below calculated. Arrow 3: Monad I mg bolus injected. Note: Blood sampling artifacts are seen in the pressure trace at 1.5, 3, and 5 minutes.

Hoffmann-La Roche Inc., Nutley, N. J.). These bloodpressure- reducing interventions were necessary despite inspired halothane concentrations often exceeding 1.0% (Fig. 2). With smaller K+ doses less hypertension was seen. In only one patient given an 8 mEq KCI bolus was a reduced pump flow or vasodilator judged clinically necessary. Discussion KCl administration during CPB is primarily intended to raise serum K+ acutely and hence to stabilize the post-CPB cardiac rhythm . 12-14 Repletion of total body K+ deficits, if they truly exist, will not occur with this therapy. Rather, the acute increase in the extracellular relative to intracellular K+ concentrations results in a diminished arrhythmia potential necessary for successful termination of CPBY' 15 If the serum K+ level is sufficiently decreased that a heightened arrhythmia potential exists , guidelines for K+ administration are needed so that serum K+ can be increased safely. While problems may be avoided with slow infusions of dilute solutions of KCl, rapid administration may be needed. Occasionally, situations exist near the termination of a long CPB where K+ is low and the prolongation of CPB required to infuse KCI slowly seems unjustified. The data presented in this study show that in patients on stable CPB, bolus administration of KCl in doses of 8 mEq and larger does increase serum K+. However, at bolus doses of 8 mEq and larger acute hypertension

The Journal of Thoracic and Cardiovascular

240 Schwartz et al.

results. The magnitude of the hypertension in nine out of 18 patients was sufficient to require rapid therapeutic intervention. Recognition of this vascular response in the first few patients prompted us to intervene much more rapidly and vigorously in subsequent patients. Hypertensive responses occurred in no patient receiving a dose less than 8 mEq KCI. Vascular effects of hyperkalemia are well known from animal studies'" but are not always recognized in man because the cardiac effects occur much more rapidly and, in the absence of CPB, have devastating results. The CPB situation is unique, however, because the vasculature is isolated from the heart, unmasking vascular effects. We have shown that rapid administration of K+ in doses of 8 mEq or greater during CPB frequently results in a significant increase in MAP. It is recommended therefore that bolus doses of less than 8 mEq be administered during CPB in those situations where even slower infusion rates seem contraindicated. We thank Drs. Bryan E. Marshall and Theodore C. Smith for their guidance in the completion of this study, Mr. C. Medsker for performing the laboratory analyses, The Hospital of the University of Pennsylvania Heart Lung Team for their technical assistance during cardiopulmonary bypass, Ms. B. Ewing, B. A., for the illustration, and Ms. T. Kearns for the preparation of the manuscript. REFERENCES Teasdale SJ: Editorial. J THoRAc CARDIOVASC SURG 76:678-679, 1978 2 Lockey E, Longmore DB, Ross DN, et al: Potassium and open-heart surgery. Lancet 1:671-675, 1966 3 Dieter RA, Neville WE, Pifarre R: Hypokalemia following hemodilution cardiopulmonary bypass. Ann Surg 171:17-23, 1970 4 Dieter RA, Neville WE, Pifarre R: Serum electrolyte changes after cardiopulmonary bypass with Ringer's lac-

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tate solution used for hemodilution. J THoRAc CARDIOVASC SURG 59:168-177, 1970 Marcial MB, Vedoya RC, Zerbini EJ, et al: Potassium in cardiac surgery with extracorporeal perfusion. Am J Cardiol 23:400-408, 1969 Morgan DB, Mearns AJ, Burkinshaw L: The potassium status of patients prior to open-heart surgery. J THoRAc CARDIOVASC SURG 76:673-677, 1978 Todd EP, McAllister RG, Campbell HC, et al: Effect of propranolol on hypokalemia induced by cardiopulmonary bypass. Circulation 56:222, 1977 (abst) Tyers GIO, Manley NJ, Williams EH, et al: Preliminary clinical experience with isotonic hypothermic potassiuminduced arrest. J THORAC CARDIOVASC SURG 74:674-681, 1977 Babka R, Pifarre R: Potassium replacement during cardiopulmonary bypass. J THoRAc CARDIOVASC SURG 73:212-215, 1977 Strandgaard S, MacKenzie ET, Sengupta D, et al: Upper limit of autoregulation of cerebral blood flow in the baboon. Circ Res 34:435-440, 1974 Shapiro HM: Intracranial hypertension. Anesthesiology 43:445-471, 1975 Cohen 11: Disorders of potassium balance. Hosp Pract 14:119-128,1979 Stockigt JR: Potassium metabolism. Anaesth Intens Care 5:317-325, 1977 Black DAK: Potassium metabolism, Maxwell MH, Kleeman CR, eds: Clinical Disorders of Fluid and Electrolyte Metabolism, New York, 1972, McGraw-Hill Book Co., Inc., pp /28-132 Weiner MW, Epstein FH: Signs and symptoms of electrolyte disorders. Maxwell MH, Kleeman CR, eds: Clinical Disorders of Fluid and Electrolyte Metabolism, New York, 1972, McGraw-Hill Book Co., Inc., pp 635-641 Friedman SM, Friedman CL: Effects of ions on vascular smooth muscle, Hamilton WF, ed: Handbook ofPhysiology, Sect 2, Circulation, Vol 2, Baltimore, 1963, The Williams & Wilkins Co., pp 1145-1149