Online Letters to the Editor Pneumonia in Middle-Aged, Old, and Very Old Critically Ill Patients. Crit Care Med 2014; 42:601–609 3. Blot S: Limiting the attributable mortality of nosocomial infection and multidrug resistance in intensive care units. Clin Microbiol Infect 2008; 14:5–13 4. Vogelaers D, De Bels D, Forêt F, et al; ANTHICUS Study Investigators: Patterns of antimicrobial therapy in severe nosocomial infections: Empiric choices, proportion of appropriate therapy, and adaptation rates—A multicentre, observational survey in critically ill patients. Int J Antimicrob Agents 2010; 35:375–381 5. Blot S, Depuydt P, Vandewoude K, et al: Measuring the impact of multidrug resistance in nosocomial infection. Curr Opin Infect Dis 2007; 20:391–396 6. Norman DC: Fever in the elderly. Clin Infect Dis 2000; 31:148–151 7. Blot S, Cankurtaran M, Petrovic M, et al: Epidemiology and outcome of nosocomial bloodstream infection in elderly critically ill patients: A comparison between middle-aged, old, and very old patients. Crit Care Med 2009; 37:1634–1641 8. Blot SI, Rodriguez A, Solé-Violán J, et al; Community-Acquired Pneumonia Intensive Care Units (CAPUCI) Study Investigators: Effects of delayed oxygenation assessment on time to antibiotic delivery and mortality in patients with severe community-acquired pneumonia. Crit Care Med 2007; 35:2509–2514 DOI: 10.1097/CCM.0000000000000179
Does Therapeutic Hypothermia Improve Depressed Cardiac Functions in Postcardiac Arrest Patients? To the Editor:
W
e read with interest the article by Zobel et al (1), in which the authors stated that mild hypothermia improved variables of cardiac functions, suggesting that hypothermia could be a positive inotropic intervention in patients after the resumption of spontaneous circulation (ROSC). In the article, we found several interesting points as follows:
1. Criteria for cardiogenic shock in this study: The authors stated that criteria for determining cardiogenic shock consisted of systolic blood pressure of less than 90 mm Hg for at least 30 minutes or the need for supportive measures to maintain more than 90 mm Hg of systolic blood pressure, cool extremities, and a cardiac index of less than 2.2 L/min/m2, which were adopted in a modified version of the SHOCK trial for acute myocardial infarction (1). These criteria may be enough especially for acute coronary syndrome, but similar responses as the criteria of this study might be seen in patients in a hypovolemic state with normal cardiac contractility (2). So thorough assessments for cardiac function, for example, with echocardiography are requisite to determine cardiogenic shock after ROSC. In fact, the authors did echocardiography to show an ejection fraction of 43% ± 4% at the time of admission: this level of the ejection fraction does not seem low enough to be diagnosed as having cardiac dysfunctions. 2. Positive inotropic effects of hypothermia: We indicated that in an animal model, hypothermia induced by surface cooling produces sympathetic activation and a decrease Critical Care Medicine
in heart rate (3). Furthermore, in our previous article, we reported suppressions in heart rate responses due to blood pressure changes, that is, the “baroreceptor reflex.” These findings indicate a direct depression from hypothermia induced by surface cooling on the heart. Therefore, we need to be aware of these cardiac complications resulting from induced hypothermia especially in postcardiac arrest patients, who might be in a cardiac depressed state after ROSC (4). It has been reported that inducing therapeutic hypothermia in patients with traumatic brain injury causes a diastolic cardiac dysfunction (5), which might be due to cardiac stiffness from sympathetic activations (3). In fact, in the clinical settings, cardiotonic agents including beta-stimulating catecholamines have been applied when coping with patients with severe hypotension during therapeutic hypothermia (6). Interestingly, in this study (1), the authors stated that hypothermia at 33°C introduced by an intravascular cooling catheter elicits positive inotropic effects even in cardiogenic shock patients, who were under vasopressor support. The authors need to physiologically clarify this point. 3. A protocol of catecholamine administration for cardiogenic shock of this study is unclear. Although the authors described a method of reduction of norepinephrine administration during therapeutic hypothermia according to a target mean arterial pressure of less than or equal to 65 mm Hg, the adjustment of other catecholamines (dobutamine and epinephrine) seemed unclear. In such conditions, it seems very difficult to detect specific effects of mild hypothermia on hemodynamic variables in patients with cardiogenic shock after ROSC. In this study, cumulative doses of catecholamines at 33°C therapeutic hypothermia were found a decrease in norepinephrine but not in dobutamine, which may partly suggest vasoconstrictive effects, but not positive inotropic effects of hypothermia. Furthermore, epinephrine doses in a conventional treatment group seemed higher than those in hypothermia group even in the early phase of hospital admission. 4. The authors need to describe a protocol for normothermia including the level of the body temperature and anesthesia used. Furthermore, the authors did not report detailed hemodynamic changes in normothermia group. This may also show certain limitations of this study. The authors have disclosed that they do not have any potential conflicts of interest. Mayuki Aibiki, MD, PhD, Satoshi Kikuchi, MD, Kensuke Umakoshi, MD, Saori Ohtsubo, MD, Department of Emergency Medicine, Ehime University Graduate School of Medicine, Shitsukawa, Tohon, Ehime, Japan
REFERENCES
1. Zobel C, Adler C, Kranz A, et al: Mild Therapeutic Hypothermia in Cardiogenic Shock Syndrome. Crit Care Med 2012; 40: 1715–1723 2. Hochman JS, Sleeper LA, Webb JG: Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK www.ccmjournal.org
e315
Online Letters to the Editor Investigators. Should we emergently revascularize occluded coronaries for cardiogenic shock. N Engl J Med 1999; 341:625–634 3. Xu H, Aibiki M, Seki K, et al: Effects of induced hypothermia on renal sympathetic nerve activity and baroreceptor reflex in u rethane-anesthetized rabbits. Crit Care Med 2000; 28: 3854–3860 4. Neumar RW, Nolan JP, Adrie C, et al: Post-cardiac arrest syndrome: Epidemiology, pathophysiology, treatment, and prognostication. A consensus statement from the International Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Asia, and the Resuscitation
e316
www.ccmjournal.org
Council of Southern Africa); the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; and the Stroke Council. Circulation 2008; 118:2452–2483 5. Kuwagata Y, Oda J, Ninomiya N, et al: Changes in left ventricular performance in patients with severe head injury during and after mild hypothermia. J Trauma 1999; 47:666–672 6. Gaieski DF, Band RA, Abella BS, et al: Early goal-directed hemodynamic optimization combined with therapeutic hypothermia in comatose survivors of out-of-hospital cardiac arrest. Resuscitation 2009; 80:418–424 DOI: 10.1097/CCM.0000000000000160
April 2014 • Volume 42 • Number 4
Does Therapeutic Hypothermia Improve Depressed Cardiac Functions in Postcardiac Arrest Patients? To the Editor:
W
e read with interest the article by Zobel et al (1), in which the authors stated that mild hypothermia improved variables of cardiac functions, suggesting that hypothermia could be a positive inotropic intervention in patients after the resumption of spontaneous circulation (ROSC). In the article, we found several interesting points as follows:
1. Criteria for cardiogenic shock in this study: The authors stated that criteria for determining cardiogenic shock consisted of systolic blood pressure of less than 90 mm Hg for at least 30 minutes or the need for supportive measures to maintain more than 90 mm Hg of systolic blood pressure, cool extremities, and a cardiac index of less than 2.2 L/min/m2, which were adopted in a modified version of the SHOCK trial for acute myocardial infarction (1). These criteria may be enough especially for acute coronary syndrome, but similar responses as the criteria of this study might be seen in patients in a hypovolemic state with normal cardiac contractility (2). So thorough assessments for cardiac function, for example, with echocardiography are requisite to determine cardiogenic shock after ROSC. In fact, the authors did echocardiography to show an ejection fraction of 43% ± 4% at the time of admission: this level of the ejection fraction does not seem low enough to be diagnosed as having cardiac dysfunctions. 2. Positive inotropic effects of hypothermia: We indicated that in an animal model, hypothermia induced by surface cooling produces sympathetic activation and a decrease Critical Care Medicine
in heart rate (3). Furthermore, in our previous article, we reported suppressions in heart rate responses due to blood pressure changes, that is, the “baroreceptor reflex.” These findings indicate a direct depression from hypothermia induced by surface cooling on the heart. Therefore, we need to be aware of these cardiac complications resulting from induced hypothermia especially in postcardiac arrest patients, who might be in a cardiac depressed state after ROSC (4). It has been reported that inducing therapeutic hypothermia in patients with traumatic brain injury causes a diastolic cardiac dysfunction (5), which might be due to cardiac stiffness from sympathetic activations (3). In fact, in the clinical settings, cardiotonic agents including beta-stimulating catecholamines have been applied when coping with patients with severe hypotension during therapeutic hypothermia (6). Interestingly, in this study (1), the authors stated that hypothermia at 33°C introduced by an intravascular cooling catheter elicits positive inotropic effects even in cardiogenic shock patients, who were under vasopressor support. The authors need to physiologically clarify this point. 3. A protocol of catecholamine administration for cardiogenic shock of this study is unclear. Although the authors described a method of reduction of norepinephrine administration during therapeutic hypothermia according to a target mean arterial pressure of less than or equal to 65 mm Hg, the adjustment of other catecholamines (dobutamine and epinephrine) seemed unclear. In such conditions, it seems very difficult to detect specific effects of mild hypothermia on hemodynamic variables in patients with cardiogenic shock after ROSC. In this study, cumulative doses of catecholamines at 33°C therapeutic hypothermia were found a decrease in norepinephrine but not in dobutamine, which may partly suggest vasoconstrictive effects, but not positive inotropic effects of hypothermia. Furthermore, epinephrine doses in a conventional treatment group seemed higher than those in hypothermia group even in the early phase of hospital admission. 4. The authors need to describe a protocol for normothermia including the level of the body temperature and anesthesia used. Furthermore, the authors did not report detailed hemodynamic changes in normothermia group. This may also show certain limitations of this study. The authors have disclosed that they do not have any potential conflicts of interest. Mayuki Aibiki, MD, PhD, Satoshi Kikuchi, MD, Kensuke Umakoshi, MD, Saori Ohtsubo, MD, Department of Emergency Medicine, Ehime University Graduate School of Medicine, Shitsukawa, Tohon, Ehime, Japan
REFERENCES
1. Zobel C, Adler C, Kranz A, et al: Mild Therapeutic Hypothermia in Cardiogenic Shock Syndrome. Crit Care Med 2012; 40: 1715–1723 2. Hochman JS, Sleeper LA, Webb JG: Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK www.ccmjournal.org
e315
Online Letters to the Editor Investigators. Should we emergently revascularize occluded coronaries for cardiogenic shock. N Engl J Med 1999; 341:625–634 3. Xu H, Aibiki M, Seki K, et al: Effects of induced hypothermia on renal sympathetic nerve activity and baroreceptor reflex in u rethane-anesthetized rabbits. Crit Care Med 2000; 28: 3854–3860 4. Neumar RW, Nolan JP, Adrie C, et al: Post-cardiac arrest syndrome: Epidemiology, pathophysiology, treatment, and prognostication. A consensus statement from the International Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Asia, and the Resuscitation
e316
www.ccmjournal.org
Council of Southern Africa); the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; and the Stroke Council. Circulation 2008; 118:2452–2483 5. Kuwagata Y, Oda J, Ninomiya N, et al: Changes in left ventricular performance in patients with severe head injury during and after mild hypothermia. J Trauma 1999; 47:666–672 6. Gaieski DF, Band RA, Abella BS, et al: Early goal-directed hemodynamic optimization combined with therapeutic hypothermia in comatose survivors of out-of-hospital cardiac arrest. Resuscitation 2009; 80:418–424 DOI: 10.1097/CCM.0000000000000160
April 2014 • Volume 42 • Number 4
