Abstract
The management of patients with shock is extremely challenging because of the myriad of possible clinical presentations in cardiogenic shock, septic shock and hypovolemic shock and the limitations of contemporary therapeutic options. The treatment of shock includes the administration of endogenous catecholamines (epinephrine, norepinephrine, and dopamine) as well as various vasopressor agents that have shown efficacy in the treatment of the various types of shock. In addition to the endogenous catecholamines, dobutamine, isoproterenol, phenylephrine, and milrinone have served as the mainstays of shock therapy for several decades. Recently, experimental studies have suggested that newer agents such as vasopressin, selepressin, calcium-sensitizing agents like levosimendan, cardiac-specific myosin activators like omecamtiv mecarbil (OM), istaroxime, and natriuretic peptides like nesiritide can enhance shock therapy, especially when shock presents a more complex clinical picture than normal. However, their ability to improve clinical outcomes remains to be proven. It is the purpose of this review to describe the mechanism of action, dosage requirements, advantages and disadvantages, and specific indications and contraindications for the use of each of these catecholamines and vasopressors, as well as to elucidate the most important clinical trials that serve as the basis of contemporary shock therapy.
Keywords: Shock, cardiogenic shock, septic shock, shock therapy, endogenous catecholamines, exogenous catecholamines, inotropes, vasopressors.
Graphical Abstract
[3]
Hollenberg SM. Vasoactive drugs in circulatory shock. Am J Respir Crit Care Med 2011; 183(7): 847-55.
[4]
Sato Y, Matsuzawa H, Eguchi S. Comparative study of effects of adrenaline, dobutamine and dopamine on systemic hemodynamics and renal blood flow in patients following open heart surgery. Jpn Circ J 1982; 46(10): 1059-72.
[5]
Butterworth JFt, Prielipp RC, Royster RL. Dobutamine increases heart rate more than epinephrine in patients recovering from aortocoronary bypass surgery. J Cardiothorac Vasc Anesth 1992; 6(5): 535-41.
[6]
Prielipp RC, MacGregor DA, Royster RL, et al. Dobutamine antagonizes epinephrine’s biochemical and cardiotonic effects: Results of an in vitro model using human lymphocytes and a clinical study in patients recovering from cardiac surgery. Anesthesiology 1998; 89(1): 49-57.
[7]
Mahmoud KM, Ammar AS. Norepinephrine supplemented with dobutamine or epinephrine for the cardiovascular support of patients with septic shock. Indian J Crit Care Med 2012; 16(2): 75-80.
[8]
Kleinman ME, Goldberger ZD, Rea T, et al. 2017 American Heart Association focused update on adult basic life support and cardiopulmonary resuscitation quality: An Update to the American Heart Association Guidelines for Cardio pulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2018; 137: e7-e13.
[9]
Bassi E, Park M, Azevedo LC. Therapeutic strategies for highdose vasopressor-dependent shock. Crit Care Res Pract 2013; 2013: 654708.
[10]
Levy B, Perez P, Perny J, et al. Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study. Crit Care Med 2011; 39(3): 450-5.
[11]
Bolton JD. Clinical use of lactate testing in shock states. Seminars in Anesthesia. Perioperative Medicine and Pain 2007; 26: 35-9.
[13]
Levraut J, Ciebiera JP, Chave S, et al. Mild hyperlactatemia in stable septic patients is due to impaired lactate clearance rather than overproduction. Am J Respir Crit Care Med 1998; 157(4 Pt 1): 1021-6.
[15]
van Genderen ME, Klijn E, Lima A, et al. Microvascular perfusion as a target for fluid resuscitation in experimental circulatory shock. Crit Care Med 2014; 42(2): e96-e105.
[16]
Chertoff J, Chisum M, Garcia B. Lactate kinetics in sepsis and septic shock: A review of the literature and rationale for further research. J Intensive Care 2015; 3: 39.
[17]
Rivers EP, Elkin R, Cannon CM. Counterpoint: Should lactate clearance be substituted for central venous oxygen saturation as goals of early severe sepsis and septic shock therapy? No. Chest 2011. 140: 1408-13. Discussion 1409-13
[18]
Wutrich Y, Barraud D, Conrad M, et al. Early increase in arterial lactate concentration under epinephrine infusion is associated with a better prognosis during shock. Shock 2010; 34(1): 4-9.
[19]
Nalos M, Leverve X, Huang S, et al. Half-molar sodium lactate infusion improves cardiac performance in acute heart failure: A pilot randomised controlled clinical trial. Crit Care 2014; 18(2): R48.
[20]
Leverve XM, Boon C, Hakim T, et al. Half-molar sodium-lactate solution has a beneficial effect in patients after coronary artery bypass grafting. Intensive Care Med 2008; 34(10): 1796-803.
[21]
Morelli A, Ertmer C, Rehberg S, et al. Phenylephrine versus norepinephrine for initial hemodynamic support of patients with septic shock: a randomized, controlled trial. Crit Care 2008; 12(6): R143.
[22]
Maas JJ, Pinsky MR, de Wilde RB, et al. Cardiac output response to norepinephrine in postoperative cardiac surgery patients: interpretation with venous return and cardiac function curves. Crit Care Med 2013; 41(1): 143-50.
[23]
Tune JD, Richmond KN, Gorman MW, et al. Control of coronary blood flow during exercise. Exp Biol Med (Maywood) 2002; 227: 238-50.
[24]
Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsiscampaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med 2013; 41(2): 580-637.
[25]
Grandy DK, Miller GM, Li JX. “TAARgeting Addiction”-The alamo bears witness to another revolution: An overview of the plenary symposium of the 2015 behavior, biology and chemistry conference. Drug Alcohol Depend 2016; 159: 9-16.
[26]
Bronwen JB, Knights KM. Pharmacology for Health Professionals. 2nd ed. Elsevier Australia 2009; p. 192.
[27]
De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med 2010; 362(9): 779-89.
[28]
Ichai C, Soubielle J, Carles M, et al. Comparison of the renal effects of low to high doses of dopamine and dobutamine in critically ill patients: A single-blind randomized study. Crit Care Med 2000; 28(4): 921-8.
[29]
Friedrich JO, Adhikari N, Herridge MS, et al. Meta-analysis: Low-dose dopamine increases urine output but does not prevent renal dysfunction or death. Ann Intern Med 2005; 142(7): 510-24.
[30]
Ungar A, Fumagalli S, Marini M, et al. Renal, but not systemic, hemodynamic effects of dopamine are influenced by the severity of congestive heart failure. Crit Care Med 2004; 32(5): 1125-9.
[31]
Juste RN, Panikkar K, Soni N. The effects of low-dose dopamine infusions on haemodynamic and renal parameters in patients with septic shock requiring treatment with noradrenaline. Intensive Care Med 1998; 24(6): 564-8.
[32]
Girbes AR, Patten MT, McCloskey BV, et al. The renal and neurohumoral effects of the addition of low-dose dopamine in septic critically ill patients. Intensive Care Med 2000; 26(11): 1685-9.
[33]
Annane D, Vignon P, Renault A, et al. Norepinephrine plus dobutamine versus epinephrine alone for management of septic shock: A randomised trial. Lancet 2007; 370(9588): 676-84.
[34]
Myburgh JA, Higgins A, Jovanovska A, et al. A comparison of epinephrine and norepinephrine in critically ill patients. Intensive Care Med 2008; 34(12): 2226-34.
[35]
Patel GP, Grahe JS, Sperry M, et al. Efficacy and safety of dopamine versus norepinephrine in the management of septic shock. Shock 2010; 33(4): 375-80.
[36]
Levy B, Perez P, Perny J, et al. Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study. Crit Care Med 2011; 39(3): 450-5.
[37]
De Backer D, Creteur J, Silva E, et al. Effects of dopamine, norepinephrine, and epinephrine on the splanchnic circulation in septic shock: Which is best? Crit Care Med 2003; 31(6): 1659-67.
[38]
Communal C, Singh K, Pimentel DR, et al. Norepinephrine stimulates apoptosis in adult rat ventricular myocytes by activation of the β-adrenergic pathway. Circulation 1998; 98: 1329-34.
[39]
Singh K, Xiao L, Remondino A, et al. Adrenergic regulation of cardiac myocyte apoptosis. J Cell Physiol 2001; 189: 257-65.
[41]
Kurita T, Kawashima S, Morita K, et al. Dobutamine, a β1 adrenoceptor agonist, increases cerebral oxygenation during acute anemia and apneic hypoxia. Neurocrit Care 2017; 27(3): 420-9.
[42]
Romson JL, Leung JM, Bellows WH, et al. Effects of dobutamineon hemodynamics and left ventricular performance after cardiopulmonary bypass in cardiac surgical patients. Anesthesiology 1999; 91(5): 1318-28.
[43]
Richard C, Ricome JL, Rimailho A, et al. Combined hemodynamic effects of dopamine and dobutamine in cardiogenic shock. Circulation 1983; 67(3): 620-6.
[44]
Butterworth JFt, Prielipp RC, Royster RL. Dobutamine increases heart rate more than epinephrine in patients recovering from aortocoronary bypass surgery. J Cardiothorac Vasc Anesth 1992; 6(5): 535-41.
[45]
Jentzer J, Coons J, Pharm D, et al. Pharmacotherapy update on the use of vasopressors and inotropes in the intensive care unit. J Cardiovasc Pharmacol Ther 2015; 20(3): 249-60.
[46]
Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: A report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction). Circulation 2004; 110(9): e82-e292.
[47]
Werdan K, Russ M, Buerke M, et al. Cardiogenic shock due to myocardial infarction: Diagnosis, monitoring and treatment: A German-Austrian S3 Guideline. Dtsch Arztebl Int 2012; 109(19): 343-51.
[48]
Volkow ND, Wang GJ, Kollins SH, et al. Evaluating dopamine reward pathway in ADHD: Clinical implications. JAMA 2009; 302(10): 1084-91.
[49]
Mozayani A, Raymon L. Handbook of Drug Interactions: A Clinical and Forensic Guide. Springer Science & Business Media 2003; pp. 541-2.
[50]
Rhodes A, Evans LE, Alhazzani W, et al. Surviving sepsis campaign: International guidelines for the management of sepsis and septic shock. Intensive Care Med 2017; 43(3): 304-77.
[51]
Leone M, Boyadjiev I, Boulos E, et al. A reappraisal of isoproterenol in goal-directed therapy of septic shock. Shock 2006; 26(4): 353-7.
[52]
Morelli A, Lange M, Ertmer C, et al. Short-term effects of phenylephrine on systemic and regional hemodynamics in patients with septic shock: A crossover pilot study. Shock 2008; 29(4): 446-51.
[53]
Jain G, Singh DK. Comparison of phenylephrine and norepinephrine in the management of dopamine-resistant septic shock. Indian J Crit Care Med 2010; 14(1): 29-34.
[54]
Bangash MN, Kong ML, Pearse RM. Use of inotropes and vasopressor agents in critically ill patients. Br J Pharmacol 2012; 165(7): 2015-33.
[55]
Baruch L, Patacsil P, Hameed A, et al. Pharmacodynamic effects of milrinone with and without a bolus loading infusion. Am Heart J 2001; 141(2): 266-73.
[56]
Carceles MD, Fuentes T, Aroca V, et al. Effects of milrinone on contractility and cyclic adenosine monophosphate production induced by beta1- and beta2-adrenergic receptor activation in human myocardium. Clin Ther 2007; 29: 1718-24.
[57]
Rossinen J, Harjola VP, Siirila-Waris K, et al. The use of more than one inotrope in acute heart failure is associated with increased mortality: A multi-centre observational study. Acute Card Care 2008; 10(4): 209-13.
[58]
Royster RL, Butterworth JFt, Prielipp RC. Combined inotropic effects of amrinone and epinephrine after cardiopulmonary bypass in humans. Anesth Analg 1993; 77(4): 662-72.
[59]
Anderson DA (2012). Dorland’s Illustrated Medical Dictionary. 32nd ed. New York. Elsevier.ISBN 978-1-4160-6257-8.
[60]
Caldwell HK, Young WS III. Oxytocin and Vasopressin: Genetics and Behavioral Implications (PDF).In: Lajtha A, Lim R Handbook of Neurochemistry and Molecular Neurobiology: Neuroactive Proteins and Peptides. 3rd ed. Berlin: Springer 2006; pp. 573-607.
[62]
Morelli A, Ertmer C, Rehberg S, et al. Continuous terlipressin versus vasopressin infusion in septic shock (TERLIVAP): A randomized, controlled pilot study. Crit Care 2009; 13(4): R130.
[63]
Luckner G, Mayr VD, Jochberger S, et al. Comparison of two dose regimens of arginine vasopressin in advanced vasodilatory shock. Crit Care Med 2007; 35(10): 2280-5.
[64]
Russell JA, Fjell C, Hsu JL, et al. Vasopressin compared with norepinephrine augments the decline of plasma cytokine levels in septic shock. Am J Respir Crit Care Med 2013; 188(3): 356-64.
[65]
Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med 2013; 41(2): 580-637.
[66]
Polito A, Parisini E, Ricci Z, et al. Vasopressin for treatment of vasodilatory shock: An ESICM systematic review and meta-analysis. Intensive Care Med 2012; 38(1): 9-19.
[67]
Argenziano M, Chen JM, Choudri AF, et al. Management of vasodilatory shock after cardiac surgery: Identification of predisposing factors and use of a novel pressor agent. J Thorac Cardiovasc Surg 1998; 116: 973-80.
[68]
Argenziano M, Chen JM, Cullinane S, et al. Cardiac transplantation for end-stage heart disease. Cardiol Rev 1999; 7(6): 349-55.
[69]
Torgersen C, Dunser MW, Wenzel V, et al. Comparing two different arginine vasopressin doses in advanced vasodilatory shock: A randomized, controlled, open-label trial. Intensive Care Med 2010; 36(1): 57-65.
[70]
Luckner G, Mayr VD, Jochberger S, et al. Comparison of two dose regimens of arginine vasopressin in advanced vasodilatory shock. Crit Care Med 2007; 35(10): 2280-5.
[71]
Tayama E, Ueda T, Shojima T, et al. Arginine vasopressin is an ideal drug after cardiac surgery for the management of low systemic vascular resistant hypotension concomitant with pulmonary hypertension. Interact Cardiovasc Thorac Surg 2007; 6(6): 715-9.
[72]
He X, Su F, Taccone FS, et al. A selective V1A receptor agonist, selepressin, is superior to arginine vasopressin and to norepinephrine in ovine septic shock. Crit Care Med 2016; 44(1): 23-31.
[73]
Maybauer MO, Maybauer DM, Enkhbaatar P, et al. The selective vasopressin type 1a receptor agonist selepressin (FE 202158) blocks vascular leak in ovine severe sepsis. Crit Care Med 2014; 42(7): e525-33.
[74]
Rehberg S, Ertmer C, Vincent JL, et al. Role of selective V1a receptor agonism in ovine septic shock. Crit Care Med 2011; 39(1): 119-25.
[75]
Rehberg S, Yamamoto Y, Sousse L, et al. Selective V1a agonism attenuates vascular dysfunction and fluid accumulation in ovine severe sepsis. Am J Physiol Heart Circ Physiol 2012; 303(10): H1245-54.
[76]
Russell J, Vincent J, Kjølbye A, et al. Selepressin, a novel selective vasopressin V1A agonist, is an effective substitute for norepinephrine in a phase IIa randomized, placebo-controlled trial in septic shock patients. Crit Care 2017; 21: 213.
[77]
Lehtonen L, Põder P. The utility of levosimendan in the treatment of heart failure. Ann Med 2007; 39(1): 2-17.
[78]
Gordon AC, Perkins GD, Singer M, et al. Levosimendan for the prevention of acute organ dysfunction in sepsis. N Engl J Med 2016; 375(17): 1638-48.
[79]
Ukkonen H, Saraste M, Akkila J, et al. Myocardial efficiency during calcium sensitization with levosimendan: A noninvasive study with positron emission tomography and echocardiography in healthy volunteers. Clin Pharmacol Ther 1997; 61: 596-607.
[80]
Wang Q, Yokoo H, Takashina M, et al. Anti-inflammatory profile of levosimendan in cecal ligation-induced septic mice and in lipopolysaccharide-stimulated macrophages. Crit Care Med 2015; 43: e508-20.
[81]
Hasslacher J, Bijuklic K, Bertocchi C, et al. Levosimendan inhibits release of reactive oxygen species in polymorphonuclear leukocytes in vitro and in patients with acute heart failure and septic shock: A prospective observational study. Crit Care 2011; 15: R166.
[82]
Paraskevaidis IA, Parissis JTTh, Kremastinos D. Anti-inflammatory and anti-apoptotic effects of levosimendan in decompensated heart failure: A novel mechanism of drug-induced improvement in contractile performance of the failing heart. Curr Med Chem Cardiovasc Hematol Agents 2005; 3(3): 243-7.
[83]
du Toit EF, Genis A, Opie LH, Pollesello P. A role for the RISK pathway and K(ATP) channels in pre- and post-conditioning induced by levosimendan in the isolated guinea pig heart. Br J Pharmacol 2008; 154(1): 41-50.
[84]
Morelli A, Donati A, Ertmer C, et al. Levosimendan for resuscitating the microcirculation in patients with septic shock: A randomized controlled study. Crit Care 2010; 14: R232.
[85]
Memiş D, Inal MT, Sut N. The effects of levosimendan vs dobutamine added to dopamine on liver functions assessed with noninvasive liver function monitoring in patients with septic shock. J Crit Care 2012; 27: 318.e1-e6.
[86]
Buerke M, Lemm H, Krohe K, et al. Levosimendan in the treatment of cardiogenic shock. Minerva Cardioangiol 2010; 58(4): 519-30.
[87]
Shang G, Yang X, Song D. Effects of levosimendan on patients with heart failure complicating acute coronary syndrome: A meta-analysis of randomized controlled trials. Am J Cardiovasc Drugs 2017; 17: 453.
[88]
Russ MA, Prondzinsky R, Christoph A, et al. Hemodynamic improvement following levosimendan treatment in patients with acute myocardial infarction and cardiogenic shock. Crit Care Med 2007; 35(12): 2732-9.
[89]
Mebazaa A, Nieminen MS, Packer M, et al. Levosimendan vs dobutamine for patients with acute decompensated heart failure: The SURVIVE Randomized Trial. JAMA 2007; 297(17): 1883-91.
[90]
Mehta RH, Leimberger JD, van Diepen S, et al. Levosimendan in patients with left ventricular dysfunction undergoing cardiac surgery. LEVO-CTS Investigators. N Engl J Med 2017; 376(21): 2032-42.
[91]
Levin R, Degrange M, Del Mazo C, et al. Preoperative levosimendan decreases mortality and the development of low cardiac output in high-risk patients with severe left ventricular dysfunction undergoing coronary artery bypass grafting with cardiopulmonary bypass. Exp Clin Cardiol 2012; 17(3): 125-30.
[92]
Toller W, Heringlake M, Guarracino F, Algotsson L. Preoperative and perioperative use of levosimendan in cardiac surgery: European expert opinion. Int J Cardiol 2015; 184: 323-36.
[93]
Levin RL, Degrange MA, Porcile R, et al. The calcium sensitizer levosimendan gives superior results to dobutamine in postoperative low cardiac output syndrome. Rev Esp Cardiol 2008; 61(5): 471-9.
[94]
De Hert SG, Lorsomradee S, Cromheecke S, et al. The effects of levosimendan in cardiac surgery patients with poor left ventricular function. Anesth Analg 2007; 104(4): 766-73. [Erratum in: Anesth Analg 2007; 104]. (6): 1544.
[95]
Aronson D, Krum H. Novel therapies in acute and chronic heart failure. Pharmacol Ther 2012; 135(1): 1-17.
[96]
Liu LC, Dorhout B, van der Meer P, et al. Omecamtiv mecarbil: A new cardiac myosin activator for the treatment of heart failure. Expert Opin Investig Drugs 2016; 25(1): 117-27.
[97]
Shen YT, Malik FI, Zhao X, et al. Improvement of cardiac function by a cardiac Myosin activator in conscious dogs with systolic heart failure. Circ Heart Fail 2010; 3(4): 522-7.
[98]
Teerlink JR, Metra M, Zacà V, et al. Agents with inotropic properties for the management of acute heart failure syndromes. Traditional agents and beyond. Heart Fail Rev 2009; 14(4): 243-53.
[99]
Malik FI, Hartman JJ, Elias KA, et al. Cardiac myosin activation: a potential therapeutic approach for systolic heart failure. Science 2011; 331(6023): 1439-43.
[100]
Teerlink JR, Felker GM, McMurray JJ, et al. Acute treatment with omecamtiv mecarbil to increase contractility in acute heart failure: The ATOMIC-AHF study. J Am Coll Cardiol 2016; 67(12): 1444-55.
[101]
Teerlink JR, Felker GM, McMurray JJ, et al. Chronic oral study of myosin activation to increase contractility in heart failure (COSMIC-HF): A phase 2, pharmacokinetic, randomised, placebo-controlled trial. Lancet 2016; 388(10062): 2895-903.
[102]
Utter MS, Ryba DM, Li BH, et al. Omecamtiv mecarbil, a cardiac myosin activator, increases Ca2+ sensitivity in myofilaments with a dilated cardiomyopathy mutant tropomyosin E54K. J Cardiovasc Pharmacol 2015; 66(4): 347-53.
[103]
Mamidi R, Gresham KS, Li A. Molecular effects of the myosin activator omecamtiv mecarbil on contractile properties of skinned myocardium lacking cardiac myosin binding protein-C. J Mol Cell Cardiol 2015; 85: 262-72.
[104]
Bakkehaug JP, Kildal AB, Engstad ET, et al. Myosin activator omecamtiv mecarbil increases myocardial oxygen consumption and impairs cardiac efficiency mediated by resting myosin ATPase activity. Circ Heart Fail 2015; 8: 766-75.
[105]
Cleland JGF, Teerlink JR, Senior R, et al. The effects of the cardiac myosin activator, omecamtiv mecarbil, on cardiac function in systolic heart failure: A double-blind, placebo-controlled, crossover, dose-ranging phase 2 trial. Lancet 2011; 378: 676-83.
[106]
Nánási P Jr, Gaburjakova M, Gaburjakova J, et al. Omecamtiv mecarbil activates ryanodine receptors from canine cardiac but not skeletal muscle. Eur J Pharmacol 2017; 809: 73-9.
[107]
Planelles-Herrero VJ, Hartman JJ, Robert-Paganin J, et al. Mechanistic and structural basis for activation of cardiac myosin force production by omecamtiv mecarbil. Nat Commun 2017; 8(1): 190.
[108]
Horváth B, Szentandrássy N, Veress R, et al. Frequency-dependent effects of omecamtiv mecarbil on cell shortening of isolated canine ventricular cardiomyocytes. Naunyn Schmiedebergs Arch Pharmacol 2017; 390(12): 1239-46.
[109]
PharmaPoint: Heart Failure—Global Drug Forecast and Market Analysis to 2026 New York, New York: Global Data. July 2017.
[110]
Gheorghiade M, Ambrosy AP, Ferrandi M, et al. Combining SERCA2a activation and Na-K ATPase inhibition: A promising new approach to managing acute heart failure syndromes with low cardiac output. Discov Med 2011; 12(63): 141-51.
[111]
Colucci WS, Elkayam U, Horton DP, et al. Intravenous nesiritide, a natriuretic peptide, in the treatment of decompensated congestive heart failure. Nesiritide Study Group. N Engl J Med 2000; 343(4): 246-53.
[112]
O’Connor CM, Starling RC, Hernandez AF, et al. Effect of nesiritide in patients with acute decompensated heart failure. N Engl J Med 2011; 365(1): 32-43.
[113]
Holmes DR Jr, Bates ER, Kleiman NS, Sadowski Z. Contemporary reperfusion therapy for cardiogenic shock: The GUSTO-I trial experience. The GUSTO-I Investigators. Global utilization of streptokinase and tissue plasminogen activator for occluded coronary arteries. J Am Coll Cardiol 1995; 26(3): 668-74.
[114]
Babaev A, Frederick PD, Pasta DJ, et al. Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock. JAMA 2005; 294(4): 448-54.
[115]
Anderson ML, Peterson ED, Peng SA, et al. Differences in the profile, treatment, and prognosis of patients with cardiogenic shock by myocardial infarction classification: A report from NCDR. Circ Cardiovasc Qual Outcomes 2013; 6(6): 708-15.
[116]
Martin C, Papazian L, Perrin G, et al. Norepinephrine or dopamine for the treatment of hyperdynamic septic shock? Chest 1993; 103(6): 1826-31.
[117]
Levy B, Dusang B, Annane D, et al. Cardiovascular response to dopamine and early prediction of outcome in septic shock: A prospective multiple-center study. Crit Care Med 2005; 33(10): 2172-7.
[118]
Mager G, Klocke RK, Kux A, et al. Phosphodiesterase III inhibition or adrenoreceptor stimulation: milrinone as an alternative to dobutamine in the treatment of severe heart failure. Am Heart J 1991; 121(6 pt 2): 1974-83.
[119]
Metra M, Nodari S, D’Aloia A, et al. Beta-blocker therapy influences the hemodynamic response to inotropic agents in patients with heart failure: A randomized comparison of dobutamine and enoximone before and after chronic treatment with metoprolol or carvedilol. J Am Coll Cardiol 2002; 40(7): 1248-58.
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