| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
J Thorac Cardiovasc Surg 2001;122:823-824
© 2001 The American Association for Thoracic Surgery
Brief Communications |
From the Division of Thoracic and Cardiovascular Surgery, Hannover Medical School, Hannover, Germany.
Received for publication Jan 26, 2001. Accepted for publication Feb 6, 2001. Address for reprints: T. Kofidis, MD, Division of Thoracic and Cardiovascular Surgery, Hannover Medical School, Carl Neuberg Str.1, 30625 Hannover, Germany (E-mail: kofidis{at}thg.mh-hannover.de).
Low vascular resistance after cardiopulmonary bypass occurs fairly frequently.
1,3 In the early postoperative phase after heart transplantation, decrease of blood pressure might be aggravated by the effects of antigen release from the donor organ and acute inflammatory response. Decrease of systemic resistance in patients after cardiac transplantation may lead to significant organ hypoperfusion and is usually treated with vasoconstrictors. We report a case of a patient early after heart transplantation in a severe hyperdynamic state, including high cardiac output and low vascular resistance, who was successfully treated with a single dose of methylene blue.
Clinical summary
A 55-year-old man with congestive heart failure (cardiac index, 1.8 L · min–1 · m–2) with an automatic implantable cardioverter defibrillator device underwent orthotopic bicaval cardiac transplantation and explantation of the automatic implantable cardioverter defibrillator device. The underlying disease was a dilative cardiomyopathy with a history of myocarditis. Preoperative evaluation revealed impaired left ventricular systolic function (ejection fraction, 20%) and moderate pulmonary hypertension (mean pulmonary artery pressure, 28 mm Hg). The patient was on a program of furosemide, spironolactone, amiodarone, metoprolol, captopril, and digitoxin preoperatively. His clinical status reached New York Heart Association class IV. Blood pressure was 100/60 mm Hg preoperatively.
Cold ischemia time was 158 minutes, and aortic clamp time was 31 minutes. The patient was separated from cardiopulmonary bypass without problems after a reperfusion time of 60 minutes. Thereafter, his blood pressure progressively sagged. The central venous pressure was 10 mm Hg, and the hemoglobin level was 8.1 g/dL. Blood loss was negligible, and oxygen tension was 375 mm Hg on an inspired oxygen fraction of 1.0 at transfer to the intensive care unit. Online hemodynamic monitoring revealed a cardiac output of 11.2 L/min and a systemic vascular resistance of 480 dynes ·s–1 · cm–5 under norepinephrine infusion at a rate of 0.37 µg · kg–1 · min–1. Over the course of 4 hours, the requirement for norepinephrine to maintain a systolic blood pressure above 100 mm Hg escalated to 1 µg · kg–1 · min–1. Methylene blue was given intravenously (2 mg/kg body weight) over 30 minutes, resulting in an immediate rise in blood pressure. One hour after administration, norepinephrine requirements decreased to 0.22 µg · kg–1 · min–1, and 6 hours later, norepinephrine could be discontinued. Figure 1 demonstrates the norepinephrine requirements over time, together with pulmonary artery pressure, mean arterial pressure, and central venous pressure recordings. No additional methylene blue was necessary, and minimal intravenous doses of epinephrine were administered after the second postoperative day, according to our regular strategy after heart transplantation.
|
Discussion
Decrease of vascular tone after cardiac transplantation is believed to occur because of (1) general inflammatory response to cardiopulmonary bypass 1 and (2) release of antigens from graft tissue, which activate host immune mechanisms that become operative in the early reperfusion phase. 1,3 An adequate blood pressure, however, is required for sufficient organ perfusion and undisturbed graft function during the early postoperative time. Vasoplegia at this stage can be severe and refractory to conservative therapy and fluid administration. After orthotopic heart transplantation, loss of peripheral vascular resistance may become life-threatening with respect to the limitations of right-sided heart function. The underlying mechanism is believed to be increased nitric oxide synthesis, which in turn stimulates guanylate cyclase and activates the production of cyclic guanosine 3',5' monophosphate (cGMP), resulting in vascular relaxation. 4 Methylene blue inhibits guanylate cyclase, avoiding the cGMP-dependent vasorelaxant effect of nitric oxide in the smooth muscle of the vessels. Myles and colleagues 4 failed to identify an increase in nitric oxide release after CPB by means of analysis of urine nitrite-nitrate levels. Evora and colleagues 2 speculate on the existence of a distinct, nonnitric, cGMP-dependent pathway with different receptors, different G proteins, or both, or else a sensitization of vascular smooth muscle cells to the action of nitric oxide, as hypothesized by Yiu and colleagues. 3 On the basis of this theoretic background, methylene blue has also been administered to treat sepsis and anaphylactic shock. 2,5
To our knowledge, we report the first experience of vasoplegia treatment with methylene blue after heart transplantation and believe that this drug deserves our attention because of its catecholamine-saving effect, thus preventing possible malperfusion. The postoperative course of our patient after orthotopic heart transplantation did not differ from others in which methylene blue was not used, except from the impressive shortening of norepinephrine administration, volume saving, and decrease of monitoring requirements in the intensive care unit. We did not identify any adverse drug interactions with immunosuppressive drugs or significant organ malfunction. Further studies are necessary to identify possible mechanisms and side effects of the use of methylene blue after cardiac operations.
References
This article has been cited by other articles:
|
|
 |
|
  E. G. Leite, A. Ronald, A. J. Rodrigues, and P. R. B. Evora Is methylene blue of benefit in treating adult patients who develop catecholamine-resistant vasoplegic syndrome during cardiac surgery? Interactive CardioVascular and Thoracic Surgery, December 1, 2006; 5(6): 774 - 778. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Shanmugam Vasoplegic syndrome--the role of methylene blue Eur. J. Cardiothorac. Surg., November 1, 2005; 28(5): 705 - 710. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. L. Levin, M. A. Degrange, G. F. Bruno, C. D. Del Mazo, D. J. Taborda, J. J. Griotti, and F. J. Boullon Methylene blue reduces mortality and morbidity in vasoplegic patients after cardiac surgery Ann. Thorac. Surg., February 1, 2004; 77(2): 496 - 499. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. G. Leyh, T. Kofidis, M. Struber, S. Fischer, K. Knobloch, B. Wachsmann, C. Hagl, A. R. Simon, and A. Haverich Methylene blue: The drug of choice for catecholamine-refractory vasoplegia after cardiopulmonary bypass? J. Thorac. Cardiovasc. Surg., June 1, 2003; 125(6): 1426 - 1431. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. J. Gomes, M. R. Erlichman, M. L. Batista-Filho, M. Knobel, D. R. Almeida, A. C. Carvalho, R. Catani, and E. Buffolo Vasoplegic syndrome after off-pump coronary artery bypass surgery Eur. J. Cardiothorac. Surg., February 1, 2003; 23(2): 165 - 169. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
