Intensive Care Med (2014) 40:464–465 DOI 10.1007/s00134-013-3161-z
Antonio Maria Dell’Anna Fabio Silvio Taccone
Target mean arterial pressure after cardiac arrest
Accepted: 8 November 2013 Published online: 14 January 2014 Ó Springer-Verlag Berlin Heidelberg and ESICM 2013 A reply to this comment can be found at doi:10.1007/s00134-013-3197-0.
Dear Editor, We read with great interest the study by Beylin and coworkers [1], dealing with the principles of hemodynamic optimization after cardiac arrest (CA). In their retrospective analysis, the authors found that higher mean arterial pressure (MAP) during the first 24 h was correlated with lower mortality and improved intact neurological function. Also, the use of vasoactive agents had a negative impact on both outcomes. Although this study offers some unique findings in the management of MAP after CA, we think that some issues need to be further discussed to better understand the generability of these results. First, the authors included in the definition of ‘‘vasoactive agents’’ either vasopressors (i.e., norepinephrine, dopamine, vasopressin), inotropic agents (i.e., milrinone, dobutamine), or antihypertensive drugs (i.e., b-blockers, nitroglycerine). However, these agents have significantly different hemodynamic effects and their indications are not comparable; as an example, a patient receiving nitroglycerine for acute myocardial infarction and hypertension and another treated with dobutamine and norepinephrine for a cardiogenic shock would be analyzed
CORRESPONDENCE
in the same group, but mortality is expected to be much higher in the latter. Moreover, the investigators provided no information on the initiation, duration, and total dose of such vasoactive drugs during the study period; indeed, patients receiving high-dose norepinephrine are not similar to those treated for a few hours with low-dose dopamine and should not be considered in the same study group [2]. No data on the SOFA score or at least the cardiovascular SOFA subscore were provided; however, these findings may have better defined the severity of shock or of hemodynamic alterations in this cohort [3]. Second, the target MAP (80–100 mmHg) and central venous pressure (CVP) (8–20 mmHg) could be questionable. Deleterious effects of hypotension after CA have been reported only for systolic blood pressure below 90 mmHg [4]. Although similar MAP thresholds were used for the management of CA in randomized trials using therapeutic hypothermia (TH), patients with hypotension or shock were not specifically included in these studies [5]. These targets are also much higher than those used in patients with other forms of shock [2]. Despite autoregulation of cerebral blood flow being altered in normothermic CA patients, Bouzat et al. [6] showed that increasing MAP above 70 mmHg did not improve cerebral oxygenation in CA patients undergoing TH and raised serious concerns about the need for higher MAP targets to improve brain perfusion in this setting. Finally, the exact cause of death in this population was not reported. If optimizing hemodynamics resulted in a better cardiac function and peripheral perfusion, we would have expected a reduced number of failing organs. Unfortunately, no data on renal, hepatic, or pulmonary function were given. In contrast, if optimizing MAP resulted in a better brain perfusion, most of the deaths should have occurred because of withdrawal
of care for extended brain injury; however, a predefined strategy to assess prognosis and to limit lifesustaining therapies was not provided. In conclusion, we think that future prospective research should prospectively compare two or more different targets of MAP in comatose CA survivors to understand how these hemodynamic strategies may influence peripheral and cerebral functions. Also, the impact of different vasopressors as well as drug-related side events should be carefully monitored as they may influence patients’ outcome [2]. The combination of MAP with other surrogates of adequate tissue perfusion (i.e., mixed venous saturation, lactate concentration, urine output, cerebral oxygenation) could be a valuable option to individualize therapy in this setting. Conflicts of interest None to declare.
References 1. Beylin ME, Perman SM, Abella BS, Leary M, Shofer FS, Grossestreuer AV, Gaieski DF (2013) Higher mean arterial pressure with or without vasoactive agents is associated with increased survival and better neurological outcomes in comatose survivors of cardiac arrest. Intensive Care Med 39:1981–1988. doi:10.1007/s00134013-3075-9 2. De Backer D, Biston P, Devriendt J, Madl C, Chochrad D, Aldecoa C, Brasseur A, Defrance P, Gottignies P, Vincent JL, Investigators SI (2010) Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med 362:779–789 3. Rittenberger JC, Tisherman SA, Holm MB, Guyette FX, Callaway CW (2011) An early, novel illness severity score to predict outcome after cardiac arrest. Resuscitation 82:1399–1404 4. Kilgannon JH, Roberts BW, Reihl LR, Chansky ME, Jones AE, Dellinger RP, Parrillo JE, Trzeciak S (2008) Early arterial hypotension is common in the post-cardiac arrest syndrome and associated with increased in-hospital mortality. Resuscitation 79:410–416
465
5. Hypothermia After Cardiac Arrest Study 6. Bouzat P, Suys T, Sala N, Oddo M (2013) Effect of moderate Group (2002) Mild therapeutic hyperventilation and induced hypothermia to improve the neurologic hypertension on cerebral tissue outcome after cardiac arrest. N Engl J oxygenation after cardiac arrest and Med 346:549–556 therapeutic hypothermia. Resuscitation 84:1540–1545
A. M. Dell’Anna F. S. Taccone ()) Department of Intensive Care, Erasme University Hospital, Universite´ Libre de Bruxelles (ULB), Route de Lennik 808, 1070 Brussels, Belgium e-mail: [email protected] Tel.: ?32-2-5555587 Fax: ?32-2-5554698
Antonio Maria Dell’Anna Fabio Silvio Taccone
Target mean arterial pressure after cardiac arrest
Accepted: 8 November 2013 Published online: 14 January 2014 Ó Springer-Verlag Berlin Heidelberg and ESICM 2013 A reply to this comment can be found at doi:10.1007/s00134-013-3197-0.
Dear Editor, We read with great interest the study by Beylin and coworkers [1], dealing with the principles of hemodynamic optimization after cardiac arrest (CA). In their retrospective analysis, the authors found that higher mean arterial pressure (MAP) during the first 24 h was correlated with lower mortality and improved intact neurological function. Also, the use of vasoactive agents had a negative impact on both outcomes. Although this study offers some unique findings in the management of MAP after CA, we think that some issues need to be further discussed to better understand the generability of these results. First, the authors included in the definition of ‘‘vasoactive agents’’ either vasopressors (i.e., norepinephrine, dopamine, vasopressin), inotropic agents (i.e., milrinone, dobutamine), or antihypertensive drugs (i.e., b-blockers, nitroglycerine). However, these agents have significantly different hemodynamic effects and their indications are not comparable; as an example, a patient receiving nitroglycerine for acute myocardial infarction and hypertension and another treated with dobutamine and norepinephrine for a cardiogenic shock would be analyzed
CORRESPONDENCE
in the same group, but mortality is expected to be much higher in the latter. Moreover, the investigators provided no information on the initiation, duration, and total dose of such vasoactive drugs during the study period; indeed, patients receiving high-dose norepinephrine are not similar to those treated for a few hours with low-dose dopamine and should not be considered in the same study group [2]. No data on the SOFA score or at least the cardiovascular SOFA subscore were provided; however, these findings may have better defined the severity of shock or of hemodynamic alterations in this cohort [3]. Second, the target MAP (80–100 mmHg) and central venous pressure (CVP) (8–20 mmHg) could be questionable. Deleterious effects of hypotension after CA have been reported only for systolic blood pressure below 90 mmHg [4]. Although similar MAP thresholds were used for the management of CA in randomized trials using therapeutic hypothermia (TH), patients with hypotension or shock were not specifically included in these studies [5]. These targets are also much higher than those used in patients with other forms of shock [2]. Despite autoregulation of cerebral blood flow being altered in normothermic CA patients, Bouzat et al. [6] showed that increasing MAP above 70 mmHg did not improve cerebral oxygenation in CA patients undergoing TH and raised serious concerns about the need for higher MAP targets to improve brain perfusion in this setting. Finally, the exact cause of death in this population was not reported. If optimizing hemodynamics resulted in a better cardiac function and peripheral perfusion, we would have expected a reduced number of failing organs. Unfortunately, no data on renal, hepatic, or pulmonary function were given. In contrast, if optimizing MAP resulted in a better brain perfusion, most of the deaths should have occurred because of withdrawal
of care for extended brain injury; however, a predefined strategy to assess prognosis and to limit lifesustaining therapies was not provided. In conclusion, we think that future prospective research should prospectively compare two or more different targets of MAP in comatose CA survivors to understand how these hemodynamic strategies may influence peripheral and cerebral functions. Also, the impact of different vasopressors as well as drug-related side events should be carefully monitored as they may influence patients’ outcome [2]. The combination of MAP with other surrogates of adequate tissue perfusion (i.e., mixed venous saturation, lactate concentration, urine output, cerebral oxygenation) could be a valuable option to individualize therapy in this setting. Conflicts of interest None to declare.
References 1. Beylin ME, Perman SM, Abella BS, Leary M, Shofer FS, Grossestreuer AV, Gaieski DF (2013) Higher mean arterial pressure with or without vasoactive agents is associated with increased survival and better neurological outcomes in comatose survivors of cardiac arrest. Intensive Care Med 39:1981–1988. doi:10.1007/s00134013-3075-9 2. De Backer D, Biston P, Devriendt J, Madl C, Chochrad D, Aldecoa C, Brasseur A, Defrance P, Gottignies P, Vincent JL, Investigators SI (2010) Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med 362:779–789 3. Rittenberger JC, Tisherman SA, Holm MB, Guyette FX, Callaway CW (2011) An early, novel illness severity score to predict outcome after cardiac arrest. Resuscitation 82:1399–1404 4. Kilgannon JH, Roberts BW, Reihl LR, Chansky ME, Jones AE, Dellinger RP, Parrillo JE, Trzeciak S (2008) Early arterial hypotension is common in the post-cardiac arrest syndrome and associated with increased in-hospital mortality. Resuscitation 79:410–416
465
5. Hypothermia After Cardiac Arrest Study 6. Bouzat P, Suys T, Sala N, Oddo M (2013) Effect of moderate Group (2002) Mild therapeutic hyperventilation and induced hypothermia to improve the neurologic hypertension on cerebral tissue outcome after cardiac arrest. N Engl J oxygenation after cardiac arrest and Med 346:549–556 therapeutic hypothermia. Resuscitation 84:1540–1545
A. M. Dell’Anna F. S. Taccone ()) Department of Intensive Care, Erasme University Hospital, Universite´ Libre de Bruxelles (ULB), Route de Lennik 808, 1070 Brussels, Belgium e-mail: [email protected] Tel.: ?32-2-5555587 Fax: ?32-2-5554698
