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Management of catecholamine-induced stunned myocardium—a case report
Journal of Clinical Anesthesia (2015) xx, xxx–xxx
Case Report
Management of catecholamine-induced stunned myocardium—a case report Mohit Mittal DM (Senior Resident), M. Radhakrishnan DM (Additional Professor)⁎, G.S. UmamaheswaraRao MD (Senior Professor) Department of Neuroanaesthesia, National Institute of Mental Health and Neurosciences, Bangalore, India Received 18 August 2014; revised 3 February 2015; accepted 21 May 2015
Keywords: Catecholamines; Stunned myocardium; Subarachnoid hemorrhage; Vasospasm; Blood pressure; Cardiac output
Abstract Hypertensive, hypervolumic, and hemodilution therapy (triple-H therapy) is administered to patients with symptomatic cerebral vasospasm after intracranial aneurysm clipping. This therapy can sometimes result in cardiac dysfunction because of pharmacologically induced hyperadrenergic state. The diagnosis may be missed if blood pressure alone is monitored to guide triple-H therapy. In this report, we describe one such patient who developed cardiac failure after triple-H therapy. This was diagnosed by using a bioreactance noninvasive cardiac output monitoring. Continuous cardiac output monitoring by this technique facilitated treatment of cardiac failure with milrinone and dobutamine. At discharge, the patient had no neurologic deficits. © 2015 Elsevier Inc. All rights reserved.
1. Introduction
2. Case report
Acute stress can result in transient cardiac dysfunction caused by excess sympathetic activity [1–3]. Similar hyperadrenergic state may occur during induced hypertensive, hemodilution, and hypervolumia as a part of triple-H therapy, used to treat symptomatic cerebral vasospasm in postoperative patients after intracranial aneurysm clipping, and cause cardiac failure and pulmonary vascular congestion. Titrating triple-H therapy using only blood pressure monitoring may overlook the cardiac dysfunction associated with this therapy. Here, we report one such patient where the triple-H therapy caused cardiac dysfunction which was diagnosed and treated successfully by using a bioreactance noninvasive cardiac output monitor.
Approval from the institutional review board (National Institute of Mental Health and NeuroSciences ethics committee) was obtained for the publication of this case report. A 45year-old woman was admitted with a grade III (Fisher scale) subarachnoid hemorrhage (SAH). Cerebral angiography revealed a right posterior communicating artery aneurysm (Fig. 1). Preoperative biochemical and hematological investigations and electrocardiogram (ECG) were within normal limits. The patient underwent clipping of the aneurysm, and the postoperative course was uneventful for 5 days. On the sixth postoperative day (POD), the patient became drowsy. Cerebral angiography revealed right A1 and M1 segment vasospasm (Fig. 2). Triple-H therapy was initiated using dopamine, noradrenaline, and intravenous fluids administered through a central venous line. Doses of dopamine and noradrenaline were increased up to 23 and 0.2 μg kg− 1 min− 1, respectively, to achieve a mean arterial pressure (MAP; noninvasive) of 110 to 120 mm Hg from an MAP of 90 mm Hg. Her consciousness
⁎ Corresponding author at: Department of Neuroanaesthesia, National Institute of Mental Health and Neurosciences, Hosur Road, Bangalore, Karnataka 560029, India. Tel.: +91 80 26995415. E-mail address: [email protected] (M. Radhakrishnan). http://dx.doi.org/10.1016/j.jclinane.2015.05.025 0952-8180/© 2015 Elsevier Inc. All rights reserved.
2
M. Mittal et al.
Fig. 3 Bedside x-ray chest at ICU admission. X-ray reveals bilateral diffuse infiltrates.
Fig. 1 Four-vessel digital subtraction cerebral angiography at hospital admission. White arrow: right posterior communicating artery aneurysm.
improved. However, on the 11th POD, she developed dyspnea and productive cough. A Doppler study of the lower limbs did not show any evidence of deep venous thrombosis. Her trachea was intubated and mechanical ventilation initiated, with a
Fig. 2 Four-vessel digital subtraction cerebral angiography done on sixth POD showing proximal vessel narrowing (white arrow). A1, anterior cerebral artery; M1, middle cerebral artery.
fraction of inspired oxygen of 0. 7 (partial pressure of oxygen, arterial/fraction of inspired oxygen = 150) and 10 cm H2O positive end-expiratory pressure. Central venous pressure at this time was 20 cm H2O. The patient did not have electrocardiographic changes suggestive of myocardial ischemia, and troponin levels were not assessed. Hemodynamic parameters were continuously monitored by using an invasive femoral arterial line and bioreactance-based noninvasive cardiac output monitor (NICOM; Cheetah Medical, Tel-Aviv, Israel). The cardiac index (CI) was 1.9 L min− 1 m− 2, stroke volume (SV) was 26 mL, and systemic vascular resistance was 3751 dyne · s cm− 5 m− 2. Low SV, bilateral extensive chest infiltrates (Fig. 3), and the need for high doses of ionotropes suggested cardiac failure with a low cardiac output state which was initially treated with milrinone infusion (0.25 μg kg− 1 min− 1). This was later changed to dobutamine infusion (due to nonavailability of milrinone) at 24 hours at doses up to 20 μg kg− 1 min− 1. Transthoracic echocardiography a few hours after her hemodynamic deterioration showed left ventricular regional wall motion abnormalities in the form of apical and mid-distal anterior hypokinetic segments with an ejection fraction of 44%. As these findings were in favor of stress-induced myocardial dysfunction (precipitated by high doses of catecholamines) rather than neurogenic pulmonary complication, dopamine and noradrenaline were tapered, whereas the MAP was maintained stable at 100 to 110 mm Hg. Over a period of 7 days, dopamine and noradrenaline were tapered and stopped. The CI and SV improved to 4.4 L min− 1 m− 2 and 66 mL, respectively (Fig. 4), whereas the systemic vascular resistance decreased to 1979 dyne · s cm− 5 m− 2. Furosemide was also administered daily keeping in mind the cardiac cause of respiratory distress and a cumulative positive fluid balance of around 5 L caused by the previous triple-H therapy. A negative fluid balance of around 6 L was achieved over the next 5 days. Bacteriologic cultures of tracheobronchial secretions, urine, and blood at 48 hours of
Cardiac output monitoring and cerebral vasospasm
Fig. 4
3
Stroke volume and CI recorded during ICU stay by NICOM (noninvasive) cardiac output monitor.
intensive care unit (ICU) admission revealed no growth. Echocardiography repeated a week later revealed normal systolic function and resolution of the regional wall motion abnormalities. Once the CI stabilized with dobutamine alone, the patient was weaned off mechanical ventilation, and after a T-piece trial, the trachea was extubated on the 20th POD. The neurologic status of the patient was stable throughout her ICU stay; she was following verbal commands and did not have any focal neurologic deficits.
3. Discussion This case report highlights the successful management of myocardial dysfunction in a patient receiving triple-H therapy for symptomatic vasospasm after surgery for intracranial aneurysmal SAH. The onset of cardiac dysfunction late on the 11th POD, involvement of apical segments of myocardium, and a normal ECG result go against neurogenic stunned myocardium. Neurogenic stunned myocardium is generally seen immediately after SAH because of catecholamine surge, usually involves the basal myocardium, and is associated with elevation of cardiac enzymes and ECG changes mimicking myocardial infarction [4]. Although her respiratory distress was initially thought to be due to infection, negative bacterial cultures and the findings on cardiac output monitoring pointed toward a cardiac etiology. High doses of catecholamines, whether endogenous or exogenous, damage myocardium in the form of contraction band necrosis. This is more commonly seen in women, especially postmenopausal, as in our patient. This occurs due to lack of protective effects of estrogen that causes cardiac dysfunction even with modest elevation of circulating catecholamine levels. Our patient was receiving high doses of dopamine acting predominantly at α-adrenergic receptors.
This, in combination with noradrenaline, increased the afterload, maintaining the blood pressure at the target level, in spite of low cardiac output. This is clearly an unacceptable hemodynamic strategy in a patient with cerebral vasospasm. Taccone et al [5] reported 2 patients with SAH complicated by cardiogenic shock secondary to triple-H therapy for vasospasm. The authors attributed the condition to a large amount of fluids and high doses of noradrenaline to increase cerebral perfusion pressure. Their patients, in fact, required intra-aortic balloon pump counter-pulsation to maintain adequate cerebral perfusion, probably because of more severe cardiac dysfunction than in our patient as evidenced by a much lower ejection fraction. Increased cardiac output and increased arterial blood pressure may each be independently beneficial in the setting of symptomatic vasospasm. Improving CO improves the regional cerebral blood flow and O2 delivery to the brain tissue, thus reducing regional ischemia in the vasospastic territories. Joseph et al [6] demonstrated that an increase in CO without changes in MAP can elevate cerebral blood flow in the setting of vasospasm. Because CO augmentation has been shown to reverse flow deficit independent of MAP, we suggest that cardiac output be monitored in patients undergoing hemodynamic manipulation for treatment of vasospasm. This will help to avoid inadvertent aggravation of the vasospasm caused by vasopressors which are commonly used to reverse the neurologic deficit. In our patient during the initial management of vasospasm with triple-H therapy, blood pressure was monitored noninvasively. In the setting of catecholamine-induced vasoconstriction, noninvasive blood pressure reading could be falsely low prompting the clinicians to increase the doses of the vasopressors. In the ICU, it was decided to monitor the blood pressure invasively through femoral artery, as peripheral arterial measurements again could be misleading. Without cardiac output monitoring, it would have been difficult to differentiate the cardiac and respiratory causes of respiratory
4 distress. Moreover, without CO monitoring, inappropriate combination of catecholamines would have been continued with its detrimental effect on myocardial function. Although transthoracic echocardiography provided the required hemodynamic information, continuous monitoring and titration of ionotropic agents would have been impossible without continuous cardiac output monitoring. This was achieved in the current case report with NICOM. Unlike many other devices to measure cardiac output, NICOM is totally noninvasive. NICOM measures CO by bioreactance technology. It consists of a high-frequency (75 kHz) sine wave generator and 4 dual-electrode “stickers” that are used to establish electric contact with the body. Studies have shown good correlation between CO values measured by bioreactance monitor and thermodilution technique and pulse contour analysis [7,8]. Low SV measured by NICOM prompted us to choose inodilator therapy (milrinone and dobutamine) and taper vasopressors, which resulted in a dramatic improvement in CO. Reversal of myocardial dysfunction with termination of vasopressor infusion, the echocardiographic findings indicate that our patient had a catecholamine-induced cardiac dysfunction. Hypervolumic therapy had resulted in pulmonary congestion and hypoxemia. Reduced oxygen supply to the brain, in turn, resulted in cerebral dysfunction in spite of triple-H therapy. Administration of diuretics led to negative fluid balance, reduced pulmonary congestion, improved oxygenation, and successful weaning from mechanical ventilation. Intra-arterial administration of vasodilators and balloon angioplasty are other therapeutic options for the management of vasospasm when triple-H therapy becomes ineffective. Prompt recognition of the inappropriate hemodynamic management by echocardiography and continuous noninvasive cardiac output monitoring reverted the neurologic and hemodynamic deterioration in our patient.
4. Conclusion Stunned myocardium, essentially a result of massive circulating catecholamines, can occur either after SAH or after
M. Mittal et al. triple-H therapy for cerebral vasospasm. Although triple-H therapy is used for treatment of vasospasm, it may have a counterproductive effect, if the therapy targets are not properly understood. If triple-H therapy is associated with cardiac dysfunction, cerebral blood flow and oxygen supply (pulmonary congestion) may worsen, resulting in further damage to the brain. This case report stresses the need for additional hemodynamic monitoring, apart from blood pressure, especially when patients are treated with high doses of ionotropic agents. CO monitoring, in addition to BP monitoring, helps to optimize triple-H therapy and minimizes the cardiac and neurologic complications in these situations.
References [1] Akashi YJ, Nef HM, Mollmann H, Ueyama T. Stress cardiomyopathy. Ann Rev Med 2010;61:271-86. [2] Cebelin MS, Hirsch CS. Human stress cardiomyopathy. Myocardial lesions in victims of homicidal assaults without internal injuries. Hum Pathol 1980;11:123-32. [3] Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan. J Am Coll Cardiol 2001;38:11-8. [4] Murthy SB, Shah S, Rao CP, Bershad EM, Saurez JI. Neurogenic stunned myocardium following acute subarachnoid hemorrhage: pathophysiology and practical considerations. J Intensive Care Med 2013. http://dx.doi.org/10.1177/0885066613511054. [5] Taccone FS, Lubicz B, Piagnerelli M, Van Nuffelen M, Vincent JL, Backer DD. Cardiogenic shock with stunned myocardium during tripleH therapy treated with intra-aortic balloon pump counterpulsation. Neurocrit Care 2009;10:76-82. [6] Joseph M, Ziadi S, Nates J, Malkoff M, Dannenbaum M. Increases in cardiac output can reverse flow deficits from vasospasm independent of blood pressure: a study using xenon computed tomographic measurement of cerebral blood flow. Neurosurgery 2003;53:1044-51. [7] Heerdt PM, Wagner CL, DeMais M, Savarese JJ. Noninvasive cardiac output monitoring with bioreactance as an alternative to invasive instrumentation for preclinical drug evaluation in beagles. J Pharmacol Toxicol Methods 2011;64:111-8. [8] Squara P, Rotcajg D, Denjean D, Estagnasie P, Brusset A. Comparison of monitoring performance of bioreactance vs. pulse contour during lung recruitment maneuvers. Crit Care 2009;13:R125.
Case Report
Management of catecholamine-induced stunned myocardium—a case report Mohit Mittal DM (Senior Resident), M. Radhakrishnan DM (Additional Professor)⁎, G.S. UmamaheswaraRao MD (Senior Professor) Department of Neuroanaesthesia, National Institute of Mental Health and Neurosciences, Bangalore, India Received 18 August 2014; revised 3 February 2015; accepted 21 May 2015
Keywords: Catecholamines; Stunned myocardium; Subarachnoid hemorrhage; Vasospasm; Blood pressure; Cardiac output
Abstract Hypertensive, hypervolumic, and hemodilution therapy (triple-H therapy) is administered to patients with symptomatic cerebral vasospasm after intracranial aneurysm clipping. This therapy can sometimes result in cardiac dysfunction because of pharmacologically induced hyperadrenergic state. The diagnosis may be missed if blood pressure alone is monitored to guide triple-H therapy. In this report, we describe one such patient who developed cardiac failure after triple-H therapy. This was diagnosed by using a bioreactance noninvasive cardiac output monitoring. Continuous cardiac output monitoring by this technique facilitated treatment of cardiac failure with milrinone and dobutamine. At discharge, the patient had no neurologic deficits. © 2015 Elsevier Inc. All rights reserved.
1. Introduction
2. Case report
Acute stress can result in transient cardiac dysfunction caused by excess sympathetic activity [1–3]. Similar hyperadrenergic state may occur during induced hypertensive, hemodilution, and hypervolumia as a part of triple-H therapy, used to treat symptomatic cerebral vasospasm in postoperative patients after intracranial aneurysm clipping, and cause cardiac failure and pulmonary vascular congestion. Titrating triple-H therapy using only blood pressure monitoring may overlook the cardiac dysfunction associated with this therapy. Here, we report one such patient where the triple-H therapy caused cardiac dysfunction which was diagnosed and treated successfully by using a bioreactance noninvasive cardiac output monitor.
Approval from the institutional review board (National Institute of Mental Health and NeuroSciences ethics committee) was obtained for the publication of this case report. A 45year-old woman was admitted with a grade III (Fisher scale) subarachnoid hemorrhage (SAH). Cerebral angiography revealed a right posterior communicating artery aneurysm (Fig. 1). Preoperative biochemical and hematological investigations and electrocardiogram (ECG) were within normal limits. The patient underwent clipping of the aneurysm, and the postoperative course was uneventful for 5 days. On the sixth postoperative day (POD), the patient became drowsy. Cerebral angiography revealed right A1 and M1 segment vasospasm (Fig. 2). Triple-H therapy was initiated using dopamine, noradrenaline, and intravenous fluids administered through a central venous line. Doses of dopamine and noradrenaline were increased up to 23 and 0.2 μg kg− 1 min− 1, respectively, to achieve a mean arterial pressure (MAP; noninvasive) of 110 to 120 mm Hg from an MAP of 90 mm Hg. Her consciousness
⁎ Corresponding author at: Department of Neuroanaesthesia, National Institute of Mental Health and Neurosciences, Hosur Road, Bangalore, Karnataka 560029, India. Tel.: +91 80 26995415. E-mail address: [email protected] (M. Radhakrishnan). http://dx.doi.org/10.1016/j.jclinane.2015.05.025 0952-8180/© 2015 Elsevier Inc. All rights reserved.
2
M. Mittal et al.
Fig. 3 Bedside x-ray chest at ICU admission. X-ray reveals bilateral diffuse infiltrates.
Fig. 1 Four-vessel digital subtraction cerebral angiography at hospital admission. White arrow: right posterior communicating artery aneurysm.
improved. However, on the 11th POD, she developed dyspnea and productive cough. A Doppler study of the lower limbs did not show any evidence of deep venous thrombosis. Her trachea was intubated and mechanical ventilation initiated, with a
Fig. 2 Four-vessel digital subtraction cerebral angiography done on sixth POD showing proximal vessel narrowing (white arrow). A1, anterior cerebral artery; M1, middle cerebral artery.
fraction of inspired oxygen of 0. 7 (partial pressure of oxygen, arterial/fraction of inspired oxygen = 150) and 10 cm H2O positive end-expiratory pressure. Central venous pressure at this time was 20 cm H2O. The patient did not have electrocardiographic changes suggestive of myocardial ischemia, and troponin levels were not assessed. Hemodynamic parameters were continuously monitored by using an invasive femoral arterial line and bioreactance-based noninvasive cardiac output monitor (NICOM; Cheetah Medical, Tel-Aviv, Israel). The cardiac index (CI) was 1.9 L min− 1 m− 2, stroke volume (SV) was 26 mL, and systemic vascular resistance was 3751 dyne · s cm− 5 m− 2. Low SV, bilateral extensive chest infiltrates (Fig. 3), and the need for high doses of ionotropes suggested cardiac failure with a low cardiac output state which was initially treated with milrinone infusion (0.25 μg kg− 1 min− 1). This was later changed to dobutamine infusion (due to nonavailability of milrinone) at 24 hours at doses up to 20 μg kg− 1 min− 1. Transthoracic echocardiography a few hours after her hemodynamic deterioration showed left ventricular regional wall motion abnormalities in the form of apical and mid-distal anterior hypokinetic segments with an ejection fraction of 44%. As these findings were in favor of stress-induced myocardial dysfunction (precipitated by high doses of catecholamines) rather than neurogenic pulmonary complication, dopamine and noradrenaline were tapered, whereas the MAP was maintained stable at 100 to 110 mm Hg. Over a period of 7 days, dopamine and noradrenaline were tapered and stopped. The CI and SV improved to 4.4 L min− 1 m− 2 and 66 mL, respectively (Fig. 4), whereas the systemic vascular resistance decreased to 1979 dyne · s cm− 5 m− 2. Furosemide was also administered daily keeping in mind the cardiac cause of respiratory distress and a cumulative positive fluid balance of around 5 L caused by the previous triple-H therapy. A negative fluid balance of around 6 L was achieved over the next 5 days. Bacteriologic cultures of tracheobronchial secretions, urine, and blood at 48 hours of
Cardiac output monitoring and cerebral vasospasm
Fig. 4
3
Stroke volume and CI recorded during ICU stay by NICOM (noninvasive) cardiac output monitor.
intensive care unit (ICU) admission revealed no growth. Echocardiography repeated a week later revealed normal systolic function and resolution of the regional wall motion abnormalities. Once the CI stabilized with dobutamine alone, the patient was weaned off mechanical ventilation, and after a T-piece trial, the trachea was extubated on the 20th POD. The neurologic status of the patient was stable throughout her ICU stay; she was following verbal commands and did not have any focal neurologic deficits.
3. Discussion This case report highlights the successful management of myocardial dysfunction in a patient receiving triple-H therapy for symptomatic vasospasm after surgery for intracranial aneurysmal SAH. The onset of cardiac dysfunction late on the 11th POD, involvement of apical segments of myocardium, and a normal ECG result go against neurogenic stunned myocardium. Neurogenic stunned myocardium is generally seen immediately after SAH because of catecholamine surge, usually involves the basal myocardium, and is associated with elevation of cardiac enzymes and ECG changes mimicking myocardial infarction [4]. Although her respiratory distress was initially thought to be due to infection, negative bacterial cultures and the findings on cardiac output monitoring pointed toward a cardiac etiology. High doses of catecholamines, whether endogenous or exogenous, damage myocardium in the form of contraction band necrosis. This is more commonly seen in women, especially postmenopausal, as in our patient. This occurs due to lack of protective effects of estrogen that causes cardiac dysfunction even with modest elevation of circulating catecholamine levels. Our patient was receiving high doses of dopamine acting predominantly at α-adrenergic receptors.
This, in combination with noradrenaline, increased the afterload, maintaining the blood pressure at the target level, in spite of low cardiac output. This is clearly an unacceptable hemodynamic strategy in a patient with cerebral vasospasm. Taccone et al [5] reported 2 patients with SAH complicated by cardiogenic shock secondary to triple-H therapy for vasospasm. The authors attributed the condition to a large amount of fluids and high doses of noradrenaline to increase cerebral perfusion pressure. Their patients, in fact, required intra-aortic balloon pump counter-pulsation to maintain adequate cerebral perfusion, probably because of more severe cardiac dysfunction than in our patient as evidenced by a much lower ejection fraction. Increased cardiac output and increased arterial blood pressure may each be independently beneficial in the setting of symptomatic vasospasm. Improving CO improves the regional cerebral blood flow and O2 delivery to the brain tissue, thus reducing regional ischemia in the vasospastic territories. Joseph et al [6] demonstrated that an increase in CO without changes in MAP can elevate cerebral blood flow in the setting of vasospasm. Because CO augmentation has been shown to reverse flow deficit independent of MAP, we suggest that cardiac output be monitored in patients undergoing hemodynamic manipulation for treatment of vasospasm. This will help to avoid inadvertent aggravation of the vasospasm caused by vasopressors which are commonly used to reverse the neurologic deficit. In our patient during the initial management of vasospasm with triple-H therapy, blood pressure was monitored noninvasively. In the setting of catecholamine-induced vasoconstriction, noninvasive blood pressure reading could be falsely low prompting the clinicians to increase the doses of the vasopressors. In the ICU, it was decided to monitor the blood pressure invasively through femoral artery, as peripheral arterial measurements again could be misleading. Without cardiac output monitoring, it would have been difficult to differentiate the cardiac and respiratory causes of respiratory
4 distress. Moreover, without CO monitoring, inappropriate combination of catecholamines would have been continued with its detrimental effect on myocardial function. Although transthoracic echocardiography provided the required hemodynamic information, continuous monitoring and titration of ionotropic agents would have been impossible without continuous cardiac output monitoring. This was achieved in the current case report with NICOM. Unlike many other devices to measure cardiac output, NICOM is totally noninvasive. NICOM measures CO by bioreactance technology. It consists of a high-frequency (75 kHz) sine wave generator and 4 dual-electrode “stickers” that are used to establish electric contact with the body. Studies have shown good correlation between CO values measured by bioreactance monitor and thermodilution technique and pulse contour analysis [7,8]. Low SV measured by NICOM prompted us to choose inodilator therapy (milrinone and dobutamine) and taper vasopressors, which resulted in a dramatic improvement in CO. Reversal of myocardial dysfunction with termination of vasopressor infusion, the echocardiographic findings indicate that our patient had a catecholamine-induced cardiac dysfunction. Hypervolumic therapy had resulted in pulmonary congestion and hypoxemia. Reduced oxygen supply to the brain, in turn, resulted in cerebral dysfunction in spite of triple-H therapy. Administration of diuretics led to negative fluid balance, reduced pulmonary congestion, improved oxygenation, and successful weaning from mechanical ventilation. Intra-arterial administration of vasodilators and balloon angioplasty are other therapeutic options for the management of vasospasm when triple-H therapy becomes ineffective. Prompt recognition of the inappropriate hemodynamic management by echocardiography and continuous noninvasive cardiac output monitoring reverted the neurologic and hemodynamic deterioration in our patient.
4. Conclusion Stunned myocardium, essentially a result of massive circulating catecholamines, can occur either after SAH or after
M. Mittal et al. triple-H therapy for cerebral vasospasm. Although triple-H therapy is used for treatment of vasospasm, it may have a counterproductive effect, if the therapy targets are not properly understood. If triple-H therapy is associated with cardiac dysfunction, cerebral blood flow and oxygen supply (pulmonary congestion) may worsen, resulting in further damage to the brain. This case report stresses the need for additional hemodynamic monitoring, apart from blood pressure, especially when patients are treated with high doses of ionotropic agents. CO monitoring, in addition to BP monitoring, helps to optimize triple-H therapy and minimizes the cardiac and neurologic complications in these situations.
References [1] Akashi YJ, Nef HM, Mollmann H, Ueyama T. Stress cardiomyopathy. Ann Rev Med 2010;61:271-86. [2] Cebelin MS, Hirsch CS. Human stress cardiomyopathy. Myocardial lesions in victims of homicidal assaults without internal injuries. Hum Pathol 1980;11:123-32. [3] Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan. J Am Coll Cardiol 2001;38:11-8. [4] Murthy SB, Shah S, Rao CP, Bershad EM, Saurez JI. Neurogenic stunned myocardium following acute subarachnoid hemorrhage: pathophysiology and practical considerations. J Intensive Care Med 2013. http://dx.doi.org/10.1177/0885066613511054. [5] Taccone FS, Lubicz B, Piagnerelli M, Van Nuffelen M, Vincent JL, Backer DD. Cardiogenic shock with stunned myocardium during tripleH therapy treated with intra-aortic balloon pump counterpulsation. Neurocrit Care 2009;10:76-82. [6] Joseph M, Ziadi S, Nates J, Malkoff M, Dannenbaum M. Increases in cardiac output can reverse flow deficits from vasospasm independent of blood pressure: a study using xenon computed tomographic measurement of cerebral blood flow. Neurosurgery 2003;53:1044-51. [7] Heerdt PM, Wagner CL, DeMais M, Savarese JJ. Noninvasive cardiac output monitoring with bioreactance as an alternative to invasive instrumentation for preclinical drug evaluation in beagles. J Pharmacol Toxicol Methods 2011;64:111-8. [8] Squara P, Rotcajg D, Denjean D, Estagnasie P, Brusset A. Comparison of monitoring performance of bioreactance vs. pulse contour during lung recruitment maneuvers. Crit Care 2009;13:R125.