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Urine and serum potassium levels after potassium cardioplegia
J THORAC CARDIOVASC SURG 81:516-518, 1981
Urine and serum potassium levels after potassium cardioplegia Potassium cardioplegia for myocardial preservation is being used extensively in heart operations. This study was designed to determine the effect of potassium cardioplegia on serum and urine potassium levels. A control group of 11 patients was compared to a study group of 24 patients. Myocardial preservation in the control group was achieved by whole body cooling to 20° to 30° C and in the study group. by repeated injections every 30 minutes of 500 to 700 ml of cold pump blood. containing potassium chloride 30 mEq/L. into the aortic root after aortic clamping. Total potassium dose in the study group was 46 ± 21 mEq (mean ± SD). Mean serum potassium level was significantly higher during and after bypass in the study group (after bypass: control 3.65 ± O.ll mliqll., study 4.24 ± 0.10 mEq/L [mean ± SE]. p < 0.005). but was within normal limits in both groups. Urine potassium levels and excretion rates were significantly higher in the study group (potassium excretion rate after bypass: control 6.1 ± 0.7 mliqlhr, study 11.3 ± 0.9 mEq/hr [mean ± SE]. p < 0.0025). We conclude that no special measures are required to facilitate potassium excretion when total potassium cardioplegia dose in not greater than 50 mEq.
Isaac Azar, M.D.,* Tanguturi Satyanarayana, M.D.,** and Herman Turndorf, M.D.,*** New York, N. Y.
Potassium cardioplegia is an effective technique for myocardial preservation and is now being used extensively in heart operations.v " Potassium in significant amounts is repeatedly injected into the coronary circulation, and its use is a cause for concern because of potential postbypass hyperkalemia and arrhythmias.v 7 This study was done to determine the effect of potassium cardioplegia on serum and urine potassium levels during and after bypass.
Method A control group of seven men and four women, 34 to 60 years old, scheduled to undergo coronary bypass (seven), mitral valve replacement (two) and mitral annuloplasty (two), was compared to a study group of 20 From the Department of Anesthesiology. New York University Medical Center, 560 First Ave.• New York. N. Y. 10016. Presented at the annual meeting of the American Society of Anesthesiologists, San Francisco, Calif., October, 1979. Received for publication March 19, 1980. Accepted for publication Sept. 18, 1980. Address for reprints: Isaac Azar, M.D., Beth Israel Medical Center, 10 Nathan D. Perlman Place, New York, N. Y. 10003. *Assistant Professor. **Resident. ***Professor and Chairman.
516
men and four women, 40 to 73 years old, scheduled to undergo coronary bypass (14), mitral valve replacement (three), aortic valve replacement (six), and mitral commissurotomy (one). No patient in either group had history or laboratory evidence of renal failure. All were medicated preoperatively with morphine 0.1 mg/kg and scopolamine 0.4 mg. Anesthesia was induced and maintained with diazepam, fentanyl, pancuronium, and nitrous oxide in oxygen. The pump was primed with 3 L of electrolytes of (Plasma-Lyte) (sodium 140 mEq, potassium 5, magnesium 3, chlorine 98, acetate 27, and gluconate 23 mEq/L), albumin 75 gm, heparin 8,000 D, and calcium chloride 1.2 gm. Myocardial preservation in the control group was achieved by whole body cooling to 20° to 30° C and in the study group by repeated injections every 30 minutes of 500 to 750 ml of cold pump blood, containing potassium chloride 30 mEq/L, into the aortic root after aortic clamping. The study group was also cooled to 30° to 32° C. The following were measured or derived just prior to bypass, every 15 minutes during bypass, and every 15 minutes during the first postbypass hour: (1) serum and urinary potassium levels (Nova 1 Sodium/Potassium Analyzer, Curtin-Matheson Scientific, Inc., standard error ± 1%), (2) urinary output, (3) urinary excretion rate of potassium and sodium, and (4) arterial blood
0022-5223/81/040516+03$00.30/0 © 1981 The C. V. Mosby Co.
Volume 81
Potassium cardioplegia
Number 4
April, 1981
16
6
~ 12
K,mEq/hr
- Control - Study
p
5
p
o
5 17
-Control
~ -Study
P
8
2
NS
4
0
A
B
C
Fig.!. Urinary potassium excretion rate (mean ± standard error). A, Before cardiopulmonary bypass. B, During cardiopulmonary bypass. C. During first postbypass hour.
~
- Control -StUdy
p
140
80 Na~mEq/hr
Na~mEq/L
60
-Control - Study NS
138 136
40
134
20
132
0
c
Fig. 3. Serum potassium level (mean ± standard error). A, Before cardiopulmonary bypass. B, During cardiopulmonary bypass. C. During first postbypass hour.
~ 100
B
A
A
B
C
130
A
B
C
Fig. 2. Urinary sodium excretion rate (mean ± standard error). A. Before cardiopulmonary bypass. B. During cardiopulmonary bypass. C, During first postbypass hour.
Fig. 4. Serum sodium level (mean ± standard error). A, Before cardiopulmonary bypass. B, During cardiopulmonary bypass. C. During first postbypass hour.
gases and pH. The unpaired Student's t test was used to analyze the results. Any p values smaller than 0.05 were considered significant.
in the study group. Serum sodium was often abnormally low in the control group but was always normal in the study group. No significant differences were observed in urinary output, arterial pH, or arterial Pco.,
Results (Tables I and II and Figs. 1 to 4) Total potassium dose in the study group was 46 ± 21 mEq (mean ± SD). Mean serum potassium levels during and after cardiopulmonary bypass were higher in the study group. However, they were within normal limits at all times in both groups. Some individuals in the study group had serum potassium levels as high as 5.9 mEq/L and others as low as 3.3 mEq/L, but no case of persistently high serum potassium occurred. The rate of urinary potassium excretion was significantly higher and that of sodium significantly lower
Discussion Serum potassium abnormalities are common after bypass and are of great concern during that period of time." Low serum potassium concentrations resulting from dilutional bypass and excessive diuresis occur often. The recent popularity of potassium cardioplegia has introduced a new risk factor of high serum potassium and refractory arrhythmia to the postoperative period. 6.1 Some surgeons resort to a prophylactic administration of
The Journal of
5 18
Azar, Satyanarayana, Turndorf
Thoracic and Cardiovascular Surgery
Table I. Serum potassium and sodium after potassium cardioplegia (mean ± standard error)
I
Before CPB During CPB After CPB Before CPB During CPB After CPB
Control (n
= 11)
I
Study (n
= 24)
Potassium (mEq/L) 3.98 ± 0.16 3.91 ± 0.10 4.15 ± 0.14 4.77 ± 0.15 3.65 ± 0.11 4.24 ± 0.10 Sodium (mEq/L) 138.8 ± 1.0 137.4 ± 0.5 133.4 ± 0.7 137.0 ± 0.3 133.7 ± 0.7 137.7 ± 0.3
I
p Value
NS <0.01 <0.005
NS <0.0005 <0.0005
Legend: CPB, Cardiopulmonary bypass. NS, Not significant.
Table II. Urine potassium and sodium after potassium cardioplegia (mean ± standard error) _ _ _ _ _1
Control (n = 11)
I Study (n
Low serum sodium level after bypass has been reported before." Our observation that potassium cardioplegia reduces renal sodium excretion is in agreement with the concept of sodium-potassium excretion interdependency": The increased availability of potassium ions to renal tubuli decreased sodium excretion and protected the study group from excessive loss of sodium. Although serum level in our control group was never below 130 mEq/L, there was a potential danger of postbypass hyponatremia. Therefore, we recommend liberal supplementation of potassium during and after bypass to protect the patient from low levels of both serum potassium and sodium, provided renal function is adequate. REFERENCES
= 24) I-p-v:-a-lu-e-
Before CPB During CPB After CPB
Potassium (mEq/L) 70.0 ± 7.8 67.6 ± 4.3 11.3 ± 1.6 20.3 ± 1.7 32.6 ± 1.6 37.5 ± 1.6
<0.0025 <0.05
Before CPB During CPB After CPB
Potassium (mEq/hr) 3.6 ± 0.3 3.0 ± 0.2 7.1 ± 0.3 12.4 ± 0.7 6.1 ± 0.7 11.3±0.9
<0.0025 <0.0025
Before CPB During CPB After CPB
Sodium (mEq/L) 56.0 ± 11.0 52.8 ± 8.5 133.6 ± 2.2 II 1.3 ± 2.4 109.6 ± 3.7 86.0 ± 4.9
<0.0005 <0.0025
Before CPB During CPB After CPB
Sodium (mEq/hr) 5.0 ± 0.8 4.7 ± 0.5 88.2 ± 8.8 64.8 ± 5.7 65.8 ± 10.8 31.9 ± 3.9
<0.05 <0.005
NS
NS
NS
NS
2
3
4
5 6
Legend: CPB, Cardiopulmonary bypass. NS, Not significant.
diuretics and insulin to facilitate potassium excretion and potassium transport into cells. It has been our impression that this was superfluous and that patients with normal renal function could easily handle 50 mEq or less of potassium given in intermittent doses. That this is indeed the case is confirmed by this study. Persistently high concentrations of serum potassium did not occur in either group. A few cases of low serum potassium occurred in both groups, and this was easily corrected by intravenous potassium administration.
7
8 9
Mundth ED, Goel IP, Morgan RJ, et al: Effect of potassium cardioplegia and hypothermia on left ventricular function in hypertrophied and non-hypertrophied hearts. Surg Forum 26:257-258, 1975 Goldstein SM, Nelson RL, McConnell DH, et al: Cardiac arrest after aortic cross-clamping. Effects of conventional vs pharmacologic arrest on myocardial supply/demand balance. Surg Forum 26:271-273, 1975 Tyers GFO, Manley NJ, Williams EH, Shaffer CW, Williams DR, Kurusz M: Preliminary clinical experience with isotonic hypothermic potassium-induced arrest. J THORAC CARDIOVASC SURG 74:674-680, 1977 Adams PX, Cunningham IN Jr, Brazier J, Pappis M, Trehan N, Spencer FC: Technique and experience using potassium cardioplegia during myocardial revascularization for preinfarction angina. Surgery 83:12-19, 1978 Levitsky S, Feinberg H: Intraoperative protection of the myocardium. Surg Annu 10:305-320, 1978 Tucker WY, Ellis RJ, Mangano DT, Ryan CJM, Ebert PA: Questionable importance of high potassium concentrations in cardioplegic solutions. J THORAC CARDIOVASC SURG 77:183-190, 1979 Kopman EA, Ramirez-lnawat RC: Persistent electromechanical cardiac arrest following administration of cardioplegic and glucose-insulin-potassium solutions. Anesth Analg 59:69-71, 1980 Nuutinen L, Hollmen A: Cardiopulmonary bypass time and renal function. Ann Chir Gynaecol 65:191-199, 1976 Swales JD: Sodium Metabolism in Disease, London, 1975, Lloyd-Luke Ltd., pp 272-298
Urine and serum potassium levels after potassium cardioplegia Potassium cardioplegia for myocardial preservation is being used extensively in heart operations. This study was designed to determine the effect of potassium cardioplegia on serum and urine potassium levels. A control group of 11 patients was compared to a study group of 24 patients. Myocardial preservation in the control group was achieved by whole body cooling to 20° to 30° C and in the study group. by repeated injections every 30 minutes of 500 to 700 ml of cold pump blood. containing potassium chloride 30 mEq/L. into the aortic root after aortic clamping. Total potassium dose in the study group was 46 ± 21 mEq (mean ± SD). Mean serum potassium level was significantly higher during and after bypass in the study group (after bypass: control 3.65 ± O.ll mliqll., study 4.24 ± 0.10 mEq/L [mean ± SE]. p < 0.005). but was within normal limits in both groups. Urine potassium levels and excretion rates were significantly higher in the study group (potassium excretion rate after bypass: control 6.1 ± 0.7 mliqlhr, study 11.3 ± 0.9 mEq/hr [mean ± SE]. p < 0.0025). We conclude that no special measures are required to facilitate potassium excretion when total potassium cardioplegia dose in not greater than 50 mEq.
Isaac Azar, M.D.,* Tanguturi Satyanarayana, M.D.,** and Herman Turndorf, M.D.,*** New York, N. Y.
Potassium cardioplegia is an effective technique for myocardial preservation and is now being used extensively in heart operations.v " Potassium in significant amounts is repeatedly injected into the coronary circulation, and its use is a cause for concern because of potential postbypass hyperkalemia and arrhythmias.v 7 This study was done to determine the effect of potassium cardioplegia on serum and urine potassium levels during and after bypass.
Method A control group of seven men and four women, 34 to 60 years old, scheduled to undergo coronary bypass (seven), mitral valve replacement (two) and mitral annuloplasty (two), was compared to a study group of 20 From the Department of Anesthesiology. New York University Medical Center, 560 First Ave.• New York. N. Y. 10016. Presented at the annual meeting of the American Society of Anesthesiologists, San Francisco, Calif., October, 1979. Received for publication March 19, 1980. Accepted for publication Sept. 18, 1980. Address for reprints: Isaac Azar, M.D., Beth Israel Medical Center, 10 Nathan D. Perlman Place, New York, N. Y. 10003. *Assistant Professor. **Resident. ***Professor and Chairman.
516
men and four women, 40 to 73 years old, scheduled to undergo coronary bypass (14), mitral valve replacement (three), aortic valve replacement (six), and mitral commissurotomy (one). No patient in either group had history or laboratory evidence of renal failure. All were medicated preoperatively with morphine 0.1 mg/kg and scopolamine 0.4 mg. Anesthesia was induced and maintained with diazepam, fentanyl, pancuronium, and nitrous oxide in oxygen. The pump was primed with 3 L of electrolytes of (Plasma-Lyte) (sodium 140 mEq, potassium 5, magnesium 3, chlorine 98, acetate 27, and gluconate 23 mEq/L), albumin 75 gm, heparin 8,000 D, and calcium chloride 1.2 gm. Myocardial preservation in the control group was achieved by whole body cooling to 20° to 30° C and in the study group by repeated injections every 30 minutes of 500 to 750 ml of cold pump blood, containing potassium chloride 30 mEq/L, into the aortic root after aortic clamping. The study group was also cooled to 30° to 32° C. The following were measured or derived just prior to bypass, every 15 minutes during bypass, and every 15 minutes during the first postbypass hour: (1) serum and urinary potassium levels (Nova 1 Sodium/Potassium Analyzer, Curtin-Matheson Scientific, Inc., standard error ± 1%), (2) urinary output, (3) urinary excretion rate of potassium and sodium, and (4) arterial blood
0022-5223/81/040516+03$00.30/0 © 1981 The C. V. Mosby Co.
Volume 81
Potassium cardioplegia
Number 4
April, 1981
16
6
~ 12
K,mEq/hr
- Control - Study
p
5
p
o
5 17
-Control
~ -Study
P
8
2
NS
4
0
A
B
C
Fig.!. Urinary potassium excretion rate (mean ± standard error). A, Before cardiopulmonary bypass. B, During cardiopulmonary bypass. C. During first postbypass hour.
~
- Control -StUdy
p
140
80 Na~mEq/hr
Na~mEq/L
60
-Control - Study NS
138 136
40
134
20
132
0
c
Fig. 3. Serum potassium level (mean ± standard error). A, Before cardiopulmonary bypass. B, During cardiopulmonary bypass. C. During first postbypass hour.
~ 100
B
A
A
B
C
130
A
B
C
Fig. 2. Urinary sodium excretion rate (mean ± standard error). A. Before cardiopulmonary bypass. B. During cardiopulmonary bypass. C, During first postbypass hour.
Fig. 4. Serum sodium level (mean ± standard error). A, Before cardiopulmonary bypass. B, During cardiopulmonary bypass. C. During first postbypass hour.
gases and pH. The unpaired Student's t test was used to analyze the results. Any p values smaller than 0.05 were considered significant.
in the study group. Serum sodium was often abnormally low in the control group but was always normal in the study group. No significant differences were observed in urinary output, arterial pH, or arterial Pco.,
Results (Tables I and II and Figs. 1 to 4) Total potassium dose in the study group was 46 ± 21 mEq (mean ± SD). Mean serum potassium levels during and after cardiopulmonary bypass were higher in the study group. However, they were within normal limits at all times in both groups. Some individuals in the study group had serum potassium levels as high as 5.9 mEq/L and others as low as 3.3 mEq/L, but no case of persistently high serum potassium occurred. The rate of urinary potassium excretion was significantly higher and that of sodium significantly lower
Discussion Serum potassium abnormalities are common after bypass and are of great concern during that period of time." Low serum potassium concentrations resulting from dilutional bypass and excessive diuresis occur often. The recent popularity of potassium cardioplegia has introduced a new risk factor of high serum potassium and refractory arrhythmia to the postoperative period. 6.1 Some surgeons resort to a prophylactic administration of
The Journal of
5 18
Azar, Satyanarayana, Turndorf
Thoracic and Cardiovascular Surgery
Table I. Serum potassium and sodium after potassium cardioplegia (mean ± standard error)
I
Before CPB During CPB After CPB Before CPB During CPB After CPB
Control (n
= 11)
I
Study (n
= 24)
Potassium (mEq/L) 3.98 ± 0.16 3.91 ± 0.10 4.15 ± 0.14 4.77 ± 0.15 3.65 ± 0.11 4.24 ± 0.10 Sodium (mEq/L) 138.8 ± 1.0 137.4 ± 0.5 133.4 ± 0.7 137.0 ± 0.3 133.7 ± 0.7 137.7 ± 0.3
I
p Value
NS <0.01 <0.005
NS <0.0005 <0.0005
Legend: CPB, Cardiopulmonary bypass. NS, Not significant.
Table II. Urine potassium and sodium after potassium cardioplegia (mean ± standard error) _ _ _ _ _1
Control (n = 11)
I Study (n
Low serum sodium level after bypass has been reported before." Our observation that potassium cardioplegia reduces renal sodium excretion is in agreement with the concept of sodium-potassium excretion interdependency": The increased availability of potassium ions to renal tubuli decreased sodium excretion and protected the study group from excessive loss of sodium. Although serum level in our control group was never below 130 mEq/L, there was a potential danger of postbypass hyponatremia. Therefore, we recommend liberal supplementation of potassium during and after bypass to protect the patient from low levels of both serum potassium and sodium, provided renal function is adequate. REFERENCES
= 24) I-p-v:-a-lu-e-
Before CPB During CPB After CPB
Potassium (mEq/L) 70.0 ± 7.8 67.6 ± 4.3 11.3 ± 1.6 20.3 ± 1.7 32.6 ± 1.6 37.5 ± 1.6
<0.0025 <0.05
Before CPB During CPB After CPB
Potassium (mEq/hr) 3.6 ± 0.3 3.0 ± 0.2 7.1 ± 0.3 12.4 ± 0.7 6.1 ± 0.7 11.3±0.9
<0.0025 <0.0025
Before CPB During CPB After CPB
Sodium (mEq/L) 56.0 ± 11.0 52.8 ± 8.5 133.6 ± 2.2 II 1.3 ± 2.4 109.6 ± 3.7 86.0 ± 4.9
<0.0005 <0.0025
Before CPB During CPB After CPB
Sodium (mEq/hr) 5.0 ± 0.8 4.7 ± 0.5 88.2 ± 8.8 64.8 ± 5.7 65.8 ± 10.8 31.9 ± 3.9
<0.05 <0.005
NS
NS
NS
NS
2
3
4
5 6
Legend: CPB, Cardiopulmonary bypass. NS, Not significant.
diuretics and insulin to facilitate potassium excretion and potassium transport into cells. It has been our impression that this was superfluous and that patients with normal renal function could easily handle 50 mEq or less of potassium given in intermittent doses. That this is indeed the case is confirmed by this study. Persistently high concentrations of serum potassium did not occur in either group. A few cases of low serum potassium occurred in both groups, and this was easily corrected by intravenous potassium administration.
7
8 9
Mundth ED, Goel IP, Morgan RJ, et al: Effect of potassium cardioplegia and hypothermia on left ventricular function in hypertrophied and non-hypertrophied hearts. Surg Forum 26:257-258, 1975 Goldstein SM, Nelson RL, McConnell DH, et al: Cardiac arrest after aortic cross-clamping. Effects of conventional vs pharmacologic arrest on myocardial supply/demand balance. Surg Forum 26:271-273, 1975 Tyers GFO, Manley NJ, Williams EH, Shaffer CW, Williams DR, Kurusz M: Preliminary clinical experience with isotonic hypothermic potassium-induced arrest. J THORAC CARDIOVASC SURG 74:674-680, 1977 Adams PX, Cunningham IN Jr, Brazier J, Pappis M, Trehan N, Spencer FC: Technique and experience using potassium cardioplegia during myocardial revascularization for preinfarction angina. Surgery 83:12-19, 1978 Levitsky S, Feinberg H: Intraoperative protection of the myocardium. Surg Annu 10:305-320, 1978 Tucker WY, Ellis RJ, Mangano DT, Ryan CJM, Ebert PA: Questionable importance of high potassium concentrations in cardioplegic solutions. J THORAC CARDIOVASC SURG 77:183-190, 1979 Kopman EA, Ramirez-lnawat RC: Persistent electromechanical cardiac arrest following administration of cardioplegic and glucose-insulin-potassium solutions. Anesth Analg 59:69-71, 1980 Nuutinen L, Hollmen A: Cardiopulmonary bypass time and renal function. Ann Chir Gynaecol 65:191-199, 1976 Swales JD: Sodium Metabolism in Disease, London, 1975, Lloyd-Luke Ltd., pp 272-298