Abstract
Shock is defined by an impaired tissue perfusion which causes malfunction of vital organs. An inadequate cardiac output and/or maldistribution of blood flow can induce shock providing that vital organs are underperfused. An inappropriate cardiac output may result from an inadequate filling of the heart and/or an impairment of pump function. Restrictive changes of the heart walls or obstruction within the cardiac chambers may jeopardize cardiac filling, but the most common cause of heart failure in shock is a reduction of venous return due to absolute or relative hypovolemia. Changes in autonomic function which occur with hypovolemia limit many of the detrimental effects of reduced cardiac output. If the hypovolemia is severe or persists over a long period of time, the compensatory changes of cardiac function may deteriorate to progressive cardiac failure. Cardiac output is determined by four physiologic parameters: preload (end-diastolic fiber length), afterload (ventricular wall tension during ejection), contractility, and heart rate (Weems and Downey 1992; Guyton 1991). The changes in the cardiac factors induced by lack of intravascular volume and the associated systemic response of the organism are primarily dependent on the amount of volume loss (Table 1).
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References
Alyono D, Ring WS, Chao RYN, Alyono MM, Crumbley AJ, Larson VE, Anderson RW (1983) Characteristic of ventricular function in severe hemorrhagic shock. Surgery 94:250–258.
Barriot P, Riou B (1987) Hemorrhagic shock with paradoxical bradycardia. Intensive Care Med 13:203–207.
Brown JM, Grosso MA, Moore EE (1990) Hypertonic saline and dextran: impact on cardiac function in the isolated rat heart. J Trauma 30:646–650.
Dhainaut JF, Devaux JY, Monsallier JF, Brunet F, Villemant D, Huyghebaert MF (1986) Mechanisms of decreased left ventricular preload during continuous positive pressure ventilation in ARDS. Chest 90:74–80.
Goodyer AVN (1967) Left ventricular function and tissue hypoxia in irreversible hemorrhagic and endotoxin shock. Am J Physiol 212(2):444–450.
Granger DN (1988) Role of xanthine oxidase and granulocytes in ischemia-reperfusion injury. Am J Physiol 255:H1269–H1275.
Guyton AC (1991) Textbook of medical physiology. Saunders, Philadelphia.
Hallström S, Vogl C, Krosl P, Redl H, Schlag G (1987) Studies on low molecular weight inotropic plasma substances in prolonged hypovolemic traumatic shock. Prog Clin Biol Res 236A:591–597.
Johnson G, Tsao P, Lefer AM (1990) Synergism between superoxide dismutase and sodium nitrite in cardioprotection following ischemia and reperfusion. Am Heart J 119:530–537.
Klausner JM, Paterson IS, Kobzik L, Valeri CR, Shepro D, Hechtman HB (1989) Leukotrienes but not complement mediate limb ischemia-induced lung injury. Ann Surg 209:462–470.
Kramer GC, Walsh JC, Perron PR, Günther RA, Holcroft JW (1989) Comparison of hypertonic saline/dextran versus hypertonic saline/hetastarch for resuscitation of hypovolemia. Braz J Med Biol Res 22:279–282.
Lefer AM (1987) Interaction between myocardial depressant factor and vasoactive mediators with ischemia and shock. Am J Physiol 252:R193–R205.
Lehr HA, Guhlmann A, Nolte D, Keppler D, Messmer K (1991) Leukotrienes as mediators in ischemia-reperfusion injury in a microcirculation model in the hamster. J Clin Invest 87:2036–2041.
Mazzoni MC, Borgstrom P, Arfors KE, Intaglietta M (1988) Dynamic fluid redistribution in hyperosmotic resuscitation of hypovolemic hemorrhage. Am J Physiol 255:H629–H637.
Mazzoni MC, Lundgren E, Arfors KE, Intaglietta M (1989) Volume changes of an endothelial cell monolayer on exposure to anisotonic media. J Cell Physiol 140:272–280.
Mazzoni MC, Borgstrom P, Intaglietta M, Arfors KE (1990) Capillary narrowing in hemorrhagic shock is rectified by hyperosmotic saline-dextran reinfusion. Circ Shock 31:407–418.
Moss GS, Gould SA (1988) Plasma expanders. An update. Am J Surg 155:425–434.
Neidhart PP, Suter PM (1988) Changes of right ventricular function with positive end-expiratory pressure (PEEP) in man. Intensive Care Med 14[Suppl 2]:471–473.
Pearson PJ, Schaff HV, Vanhoutte PM (1990a) Acute impairment of endothelium-dependent relaxations to aggregating platelets following reperfusion injury in canine coronary arteries. Circ Res 67:385–393.
Pearson PJ, Schaff HV, Vanhoutte PM (1990b) Longterm impairment of endothelium-dependent relaxations to aggregating platelets after reperfusion injury in canine coronary arteries. Circulation 81: 1921–1927.
Prasad K, Kalra J, Buchko G (1988) Acute hemorrhage and oxygen free radicals. Angiology 39:1005–1013.
Reilly JM, Cunnion RE, Burch Whitman C, Parker MM, Shelhamer JH, Parrillo JE (1989) A circulating myocardial depressant substance is associated with cardiac dysfunction and peripheral hypoperfusion (lactic acidemia) in patients with septic shock. Chest 95:1072–1080.
Schreuder JJ, Jansen JR, Versprille A (1985) Hemodynamic effects of PEEP applied as a ramp in normo-, hyper-, and hypovolemia. J Appl Physiol 59: 1178–1184.
Secher NH, Bie P (1985) Bradycardia during reversible haemorrhagic shock — a forgotten observation? Clin Physiol 5:315–323.
Thompson D, Adams SL, Barrett J (1990) Relative bradycardia in patients with isolated penetrating abdominal trauma and isolated extremity trauma. Ann Emerg Med 19:268–275.
Velasco JT, Baena RC, Rocha D, Loureiro MI (1990) Central angiotensinergic system and hypertonic resuscitation from severe hemorrhage. Am J Physiol 259: H1752–H1758.
Walley KR, Cooper DJ (1991) Diastolic stiffness impairs left ventricular function during hypovolemic shock in pigs. Am J Physiol 260:H702–H712.
Weems WA, Downey JM (1992) Regulation of venous return and cardiac output. In: Johnson LR (ed) Essential medical physiology. Raven, New York, pp 189–194.
Wildenthal K, Mierzwiak DS, Mitchell JH (1969) Acute effects of increased serum osmolality on left ventricular performance. Am J Physiol 216:898–904.
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© 1993 Springer-Verlag Berlin Heidelberg
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Traber, D.L., Meyer, J., Traber, L.D. (1993). Cardiac Function During Hypovolemia. In: Schlag, G., Redl, H. (eds) Pathophysiology of Shock, Sepsis, and Organ Failure. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76736-4_14
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DOI: https://doi.org/10.1007/978-3-642-76736-4_14
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