Abstract
Sepsis is a very important medical problem occuring in approximately 1% of all hospitalized patients [1] with an incidence of approximately 1500 cases per million per year [2]. The key clinical features of sepsis are largely the result of release of inflammatory mediators so that the accompanying disturbances in organ system physiology are frequently termed the systemic inflammatory response syndrome (SIRS). These clinical signs include fever or hypothermia, tachycardia, and tachypnea as well as evidence of dysfunction of multiple organ systems [1]. Dysfunction of the cardiovascular system occurs in 40% of patients with sepsis [3, 4]. Mortality rate increases from 20 to 30% in sepsis without cardiovascular dysfunction [3, 5] to approximately 40-70% in septic shock [3, 6]. Cardiovascular dysfunction in sepsis occurs as part of the systemic inflammatory response. The cause of the systemic inflammatory response is complex and involves early exogenous chemical signals (typically bacterial cell wall products) which trigger expression of multiple endogenous signalling cytokines and mediators which, in turn, activate cells involved in the inflammatory response including leukocytes, endothelial cells and even parenchymal cells, which in turn release more signalling cytokines or effector molecules (e.g. lytic enzymes and oxygen free radicals).
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Balk RA, Bone RC (1989) The septic syndrome. Crit Care Clinics 5: 1–8
Ziegler EJ, Fisher CJ, Sprung CL, et al (1991) Treatment of Gram-negative bacteremia and septic shock with HA-1A human monoclonal antibody against endotoxin. A randomized, double-blind, placebo-controlled trial. N Engl J Med 324: 429–436
Bone RC, Fisher CJ Jr, Clemmer TP, et al (1987) A controlled clinical trial of high-dose methylprednisolone in the treatment of severe sepsis and septic shock. N Engl J Med 317: 653–658
Hess ML, Hastillo A, Greenfield LJ (1981) Spectrum of cardiovascular function during Gram-negative sepsis. Prog Cardiovasc Dis 23: 279–298
Hinshaw L, Peduzzi P, Young E, Sprung C, Shatney C, Sheagren (1987) Effect of high-dose glucocorticoid therapy on mortality in patients with clinical signs of systemic sepsis. N Engl J Med 317: 659–665
Sprung CL, Panagiota VC, Marcial EH, Pierce M, Gelbard MA, Long WM (1984) The effects of high dose corticosteroids in patients with septic shock: A prospective, controlled study. N Engl J Med 311: 1137–1143
Walley KR (1995) Ventricular dysfunction during sepsis. In: Vincent JL (ed) Yearbook of Intensive Care and Emergency Medicine 1995. Springer-Verlag, Berlin, pp 505–517
Siegel JH, Greenspan M, Del Guerico LRM (1967) Abnormal vascular tone, defective oxygen transport and myocardial failure in human septic shock. Annals Surg 165: 504–517
Tuchschmidt J, Fried J, Astiz M, Rackow E (1992) Elevation of cardiac output and oxygen delivery improves outcome in septic shock. Chest 102: 216–220
Parker MM, Shelhamer JH, Bacharach SL, Green MV, Natanson C, Frederick TM (1984) Profound but reversible myocardial depression in patients with septic shock. Ann Intern Med 100: 483–490
Parrillo JE, Burch C, Shelhamer JH, Parker MM, Natanson C, Schuette W (1985) A circulating myocardial depressant substance in humans with septic shock. J Clin Invest 76: 1539–1553
Parker MM, Suffredini AF, Natanson C, Ognibene FP, Shelhamer JH, Parriello JE (1989) Responses of left ventricular function in survivors and non-survivors of septic shock. J Crit Care 4: 19–25
Suffredini AF, Fromm RE, Parker MM, Brenner M, Kovacs JA, Wesley RA (1989) The cardiovascular response of normal humans to the administration of endotoxin. N Engl J Med 321: 280–287
Natanson C, Fink MP, Ballantyne HK, MacVittie TJ, Conklin JJ, Parrillo JE (1986) Gram-negative bacteremia produces both severe systolic and diastolic cardiac dysfunction in a canine model that simulates human septic shock. J Clin Invest 78: 259–270
Walley KR, Hebert PC, Wakai Y, Wilcox P, Road J, Cooper 1 (1994) Decrease in left ventricular contractility after tumor necrosis factor-a infusion in dogs. J Appl Physiol 76: 1060–1067
Russell JA, Ronco JJ, Lockhat D, Belzberg A, Kiess M, Dodek PM (1990) Oxygen delivery and consumption and ventricular preload are greater in survivors than in non-survivors of the adult respiratory distress syndrome. Am Rev Respir Dis 141: 659–665
Sibbald WJ (1985) Myocardial function in the critically ill: Factors influencing left and right ventricular performance in patients with sepsis and trauma. Surg Clinics N Am 65: 867–893
Kass DA, Maughan WL, Guo ZM, Kono A, Sunagawa K, Sagawa K (1987) Comparative influence of load versus inotropic state on indexes of ventricular contractility: Experimental and theoretical analysis based on pressure-volume relationships. Circulation 76: 1422–1436
Herbertson MJ, Werner HA, Goddard CM, et al (1995) Anti-tumor necrosis factor-a prevents decreased ventricular contractility in endotoxemic pigs. Am J Respir Crit Care Med 152: 480–488
Walley KR, Cooper DJ (1991) Diastolic stiffness impairs left ventricular function during hypovolemic shock in pigs. Am J Physiol 260: H702 - H712
Thomas F, Smith J, Orme J Jr, Clemmer T, Hagan A, Elliott G (1986) Reversible segmental myocardial dysfunction in septic shock. Crit Care Med 14: 587–588
Herbertson MJ, Werner HA, Walley KR (1996) Nitric oxide synthase inhibition partially prevents decreased LV contractility during endotoxemia. Am J Physiol 270 (Heart Circ Physiol 39): H1979 - H1984
Gilbert JC, Glantz SA (1988) Determinants of left ventricular filling and of the diastolic pressure-volume relation. Circulation 64: 827–832
Stahl TJ, Alden PB, Ring WS, Madoff RC, Cerra FB (1990) Sepsis-induced diastolic dysfunction in chronic canine peritonitis. Am J Physiol 258: H625 - H633
Werner HA, Herbertson MJ, Walley KR (1995) Amrinone increases ventricular contractility and diastolic compliance in endotoxemia. Am J Respir Crit Care Med 152: 496–503
Strieter RM, Kunkel SL, Bone RC (1993) Role of tumor necrosis factor-a in disease states and inflammation. Crit Care Med 21: 5447 - S463
Tracey KJ, Lowry SF (1990) The role of cytokine mediators in septic shock. Adv Surg 23: 21–56
Finkel MS, Oddis CV, Jacob TD, Watkins SC, Hattler BG, Simmons RL (1992) Negative inotropic effects of cytokines on the heart mediated by nitric oxide. Science 257: 387–389
Brady AJ, Poole-Wilson PA, Harding SE, Warren JB (1992) Nitric oxide production within cardiac myocytes reduces their contractility in endotoxemia. Am J Physiol 263 (Heart Circ Physiol 32): H1963 - H1966
Massey KD, Strieter RM, Kunkel SL, Danforth JM, Standiford TJ (1995) Cardiac myocytes release leukocyte-stimulating factors. Am J Physiol 269 (Heart Circ Physiol 38): H980 - H987
Goddard CM, Allard MF, Hogg JC, Herbertson MJ, Walley KR (1995) Prolonged leukocyte transit time in coronary microcirculation of endotoxemic pigs. Am J Physiol 269 (Heart Circ Physiol 38): H1389 - H1397
Goddard CM, Allard MF, Hogg JC, Walley KR (1996) Myocardial morphometric changes related to decreased contractility after endotoxin. Am J Physiol 270 (Heart Circ Physiol 39): H1446 - H1452
Herbertson MJ, Werner HA, Russell JA, Iversen K, Walley KR (1995) Myocardial oxygen extraction ratio is decreased during endotoxemia in pigs. J Appl Physiol 79: 479–486
Gomez A, Wang R, Unruh H, Light RB, Bose D, Chau T (1990) Hemofiltration reverses left ventricular dysfunction during sepsis in dogs. Anesthesiology 73: 671–685
Lefer A, Inge T (1973) Differentiation of a myocardial depressant factor present in shock plasma from known plasma peptides and salts. Proc Soc Exp Biol 142: 422–433
Hallstrom S, Vogl C, Redl H, Schlag G (1990) Net inotropic plasma activity in canine hypovolemic traumatic shock: Low molecular weight plasma fraction after prolonged hypotension depresses cardiac muscle function in vitro. Circ Shock30: 129–144
Carli A, Auclair MC, Benassayag C, Nunez E (1981) Evidence for an early lipid soluble cardiodepressant factor in rat serum after a sublethal dose of endotoxin. Circ Shock 8: 301–312
Echtenacher B, Falk W, Mannel DN, Krammer PH (1990) Requirement of endogenous tumor necros factor/cachectin for recovery from experimental peritonitis. J Immunol 145: 3762–3766
Bagby GJ, Plessala KJ, Wilson LA, Thompson JJ, Nelson S (1991) Divergent efficacy of antibody to tumor necrosis factor-a in intravascular and peritonitis models of sepsis. J Infect Dis 163: 83–88
Tracey KJ, Fong Y, Hesse DG, et al (1987) Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia. Nature 330: 662–664
Schulz R, Pauas DL, Catena R, Moncada S, 011ey PM, Lopaschuk GD (1995) The role of nitric oxide in cardiac depression induced by interleukin-1f3 and turner necrosis factor-a. Br J Pharmacol 114: 27–34
Decking UKM, Flesche CW, Godecke A, Schrader J (1995) Endotoxin-induced contractile dysfunction in guinea pig hearts is not mediated by nitric oxide. Am J Physiol 268 (Heart Circ Physiol 37): H2460 - H2465
Natanson C (1990) Studies using a canine model to investigate the cardiovascular abnormality of and potential therapies for septic shock. Clin Res 38: 206–214
Herbertson MJ, Werner HA, Studer W, Russell JA, Walley KR (1996) Decreased left ventricular contractility during porcine endotoxemia is not prevented by ibuprofen. Crit Care Med 24: 815–819
Strieter RM, Koch AE, Antony VB, Fick RB Jr, Standiford TJ, Kunkel SL (1994) The immunopathology of chemotactic cytokines: The role of interleukin-8 and monocyte chemoattractant protein-1. J Lab Clin Med 123: 183–197
Granton IT, Goddard CM, Allard MA, Hogg JC, Walley KR (1995) Removal of circulating leukocytes attenuates myocardial dysfunction in an isolated-supported rabbit heart during endotoxemia.Am J Respir Crit Care Med 151: A316 (Abst)
Poon BY, Goddard CM, Leaf CD, Russell JA, Walley KR (1996) Gluthathione repletion prevents endotoxin-induced decrease in left ventricular contractility in isolated rabbit hearts. Am J Respir Crit Care Med 153: A251 (Abst)
Song H, Tyml K (1993) Evidence for sensing and integration of biological signals by the capillary network. Am J Physiol 265: H1235 - H1242
Lam C, Tyml K, Martin C, Sibbald W (1994) Microvascular perfusion is impaired in a rat model of normotensive sepsis. J Clin Invest 94: 2077–2083
Walley KR (1996) Heterogeneity of oxygen delivery impairs oxygen extraction by peripheral tissues: Theory. J Appl Physiol 81: 885–894
Humer MF, Phang PT, Friesen BP, Allard MF, Goddard CM, Walley KR (1996) Heterogeneity of gut capillary transit times and impaired gut oxygen extraction in endotoxemic pigs. J Appl Physiol 81: 895–904
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1997 Springer-Verlag Berlin Heidelberg
About this paper
Cite this paper
Walley, K.R. (1997). Mechanisms of Decreased Cardiac Function in Sepsis. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 1997. Yearbook of Intensive Care and Emergency Medicine, vol 1997. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-13450-4_23
Download citation
DOI: https://doi.org/10.1007/978-3-662-13450-4_23
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-662-13452-8
Online ISBN: 978-3-662-13450-4
eBook Packages: Springer Book Archive