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Cardiac Dysfunction and Lactic Acidosis During Hyperdynamic and Hypovolemic Shock

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Cardiac Dysfunction and Lactic Acidosis During Hyperdynamic and Hypovolemic Shock è - \-o(J THESIS FOR TIIE DEGREE OF DOCTOR OF MEDICINE CARDIAC DYSFUNCTION AND LACTIC ACIDOSIS DURING HYPERDYNAMIC AND HYPOVOLEMIC SHOCK DAVID JAMES COOPER DEPARTMENT OF ANAESTIIESIA AND INTENSIVE CARE FACULTY OF MEDICINE UNIVERSITY OF ADELAIDE Submitted: October,1995 Submitted in revised form: November, 1996 2 J TABLE OF CONTENTS Page 5 CH 1(1.1) Abstract (1.2) Signed statement (1.3) Authors contribution to each publication (1.4) Acknowledgments (1.5) Publications arising 9 CH2Introduction (2.1) Shock and lactic acidosis (2.2) Cardiac dysfunction and therapies during lactic acidosis (2.3) Cardiac dysfunction during hyperdynamic shock (2.4) Cardiac dysfunction during hypovolemic shock (2.5) Cardiac dysfunction during ionised hypocalcaemia l7 CH3 Methods (3. 1) Left ventricular function assessment - introduction (3.2) Left ventricular function assessment in an animal model 3.2.I Introduction 3.2.2 Anaesthesia 3.2.3 Instrumentation 3.2.4 Systolic left ventricular contractility 3.2.5 Left ventricular diastolic mechanics 3.2.6 Yentricular function curves 3.2.1 Limitations of the animal model (3.3) Left ventricular function assessment in human volunteers 3.3.7 Left ventricular end-systolic pressure measurement 3.3.2 Left ventricular dimension measurement 3.3.3 Rate corrected velocity of circumferential fibre shortening (v"¡.) 3.3.4. Left ventricular end-systolic meridional wall stress (o"r) 4 33 CH 4 Cardiac dysfunction during lactic acidosis (4.1) Introduction 4.7.1 Case report (4.2) Human studies 4.2.1 Bicarbonate in critically ill patients with lactic acidosis 4.2.2 Plasma ionised calcium and lactate in patients with lactic acidosis (4.3) Animal studies 4.3.1 Endogenous lactic acidosis in pigs 4.3.2 Infused lactic acidosis in pigs (4.4) Management strategies for patients with lactic acidosis 81 CH 5 Cardiac dysfunction during hyperdynamic shock (5.1) Introduction (5.2) Anaphylactic shock 5.2.1 Cardiac dysfunction during anaphylaxis 5.2.2 Cardiac dysfunction during histamine infusion in humans (5.3) Septic shock 5.3.1 Cardiac dysfunction during TNF - cr infusion in dogs 115 CH 6 Hypovolemic shock (6.1) Cardiac dysfunction during hypovolemic shock in pigs 131 CH7 Conclusions 133 Appendix I Published letters and abstracts based on this thesis. 135 Appendix 2 Theoretical explanation for changes in diastolic and end-systolic pressure-volume relationships in Chapter 6.1 137 Bibliography .ì1 F 'Ð Chapter L 1.1 ABSTRACT Lactic acidosis occurs during impaired tissue perfusion in both hyperdynamic and hypovolemic shock. Importantly, lactic acidosis is a key predictor of high mortality in patients' Cardiac dysfunction occurs during lactic acidosis but until recently had not been recognised to be important during hyperdynamic or hypovolemic shock. This thesis details a series of studies in patients, in human volunteers and in large animals. Haemodynamics and left ventricular systolic and diastolic mechanics are reported during lactic acidosis, during therapies for lactic acidosis, and during hyperdynamic and hypovolemic shock. These studies do not address cardiogenic or obstructive shock. The studies found in patients with shock and lactic acidosis, that infused bicarbonate does not improve cardiac function. In some patients, side effects of hypocalcemia and hypercapnia outweighed benefits. Transient haemodynamic effects of bicarbonate were due to the infusion of shock a hypertonic solution and not due to buffering. In lactic acidosis induced by hypovolemic (arterial pH 7.10), systolic left ventricular (LV) contractility was not decreased, perhaps due to endogenous catecholamines. Infusion of bicarbonate did not improve haemodynamics. In infused lactic acidosis (arterial pH 7.10), when catecholamines were blocked, systolic LV contractility was decreased and failed to increase after complete pH correction using bicarbonate. Histamine decreased LV contractility when measured using a non invasive technique in human volunteers (an H, mediated effect). Histamine may therefore be an important contributor to LV dysfunction reported during anaphylaxis. TNF - o decreased LV contractility in dogs suggesting that TNF - o may be an important contributor to LV dysfunction in the early hours of septic shock. Finally, hypovolemic shock was associated with profound LV diastolic stiffness which may account for failed resuscitation in patients with prolonged hypovolemic shock. This thesis has the unifying hypothesis that cardiac dysfunction is important in hyperdynamic and hypovolemic shock and is not caused by lactic acidosis. Accordingly, clinical patients therapies intended to improve cardiac function and rapidly normalise tissue perfusion in with shock and lactic acidosis are more likely to be successful in improving patient outcome than therapies which are intended solely to correct the acidosis' 6 I.2 STATEMENT This thesis contains no work that has been accepted for the award of any other degree or diploma in any university or other tertiary institution, and to the best of my knowledge and belief, contains no material previously published or written by another person except where due reference has been made in the text. I give consent to this copy of my thesis, when deposited in the University Library, being available for loan and photocopying. ,qr',ltqîk SIGNED DATE 1.3 CONTRIBUTION OF THE AUTHOR TO EACH STUDY Each of the seven studies detailed in this thesis Chs (4.2.2 - 6.1) was conceived, designed and performed by myself, in each case with advice and assistance from my Critical Care Fellowship supervisors Dr Keith Walley and Dr Jim Russell. Data analysis was done with the assistance of Mr Barry Wiggs and Keith V/alley. Manuscript writing and revision in Ch (4.2.7, 4.2.2, 4'3.2, and 5.2.2) was done by myself with the advice and assistance of co-authors. Manuscript writing for publication in Ch (4.3.1, 5.3.7, and 6.1) was done in collaboration with the co-authors, principally Keith \Malley. The published review papers (4.4, and,2.Z.l) which provide background and amplification for the original studies, and the two book chapters, (see Ch 1.5) were written by myself. 1 I.4 ACKNOWLEDGMENTS This body of research would never have been completed, nor would this thesis have been written, without the support, assistance, guidance and encouragement of a large number of people. The work was done while an external postgraduate student of the University of Adelaide, predominantly during the tenure of a Critical Care Research Fellowship (1988 to 1990) at St. paul's Hospital, University of British Colombia, Canada, in the Department of Critical Care Medicine and the Pulmonary Research Laboratory. Dr Jim Russell structured the Fellowship years and facilitated everything that I accomplished including the coordination of grant support. Dr Keith Walley was my model of scientific excellence and rigour, my teacher, and friend. Drs Jim Hogg and Dr Peter Pare nurtured the Pulmonary Research Laboratory to its present world class standing and endlessly provided grass roots support to me and the other Fellows. Dianne Minshall and Lisa Baile taught me laboratory skills and assisted with technical expertise for each of the animal studies. Prof WB Runciman supported the project with enthusiasm, provided encouragement, and kept at me with persistence until the thesis reached completion. Dr LIG V/orthley, my earliest mentor, instilled both a love of Intensive Care and a need to always do better and provided constant encouragement. Finally, Cate Cooper gave unflagging support through nearly three years of the overseas Fellowship, three children, and a dislocated home life. My sincere thanks are due to all. 8 1.5 PUBLICATIONS ARISING FROM THIS THESIS PAPERS l. Cooper DJ, Worthley LIG. Adverse haemodynamic effects of sodium bicarbonate in metabolic acidosis. Intensive Care Med. 1987 ;13:425 -427 . 2' Cooper DJ. Walley KR, Russell JA. Bicarbonate does not improve haemodynamics in human lactic acidosis: a prospective, controlled study. Ann Intern Med 1990; I 12:492-498. 3. Cooper DJ. and Vy'orthley LIG. Buffer therapies for patients who have lactic acidosis? Intensive and Crit Care Digest 1990; 9:30-31. (Editorial). 4. Walley KR, Cooper DJ. Diastolic stiffness impairs left ventricular function during hypovolemic shock, in pigs. Am J Physiol 199 | ;260:Hi O2-H1 12. 5. Cooper DJ. Management of Lactic Acidosis in Critically Ill Patients. Appl Cardiopul pathophys 1992;4:245- 252. rWalley 6. KR, Cooper DJ. Neither hypertonic saline nor bica¡bonate improve left ventricula¡ contractility during hypovolemic shock, in pigs. J Crir Care 1992;7:14-2L rWalley 7. Cooper DJ, KR, Dodek P, Rosenberg F, Russell JA. Plasma ionised calcium and blood lactate concentrations a¡e inversely related in human lactic acidosis. Intensive Care Med 1992; 18:296-289. 8. Cooper DJ. Thompson C, Walley KR, et al. Histamine decreases human left ventricular contractility. J Appl Physiol 1992; 73: 2530 - 2531. 9. Cooper DJ. Cardiac Dysfunction during Anaphylaxis. Appl Cardiopul. Pathophys 1993; 5:9-18. 10. Cooper DJ, Walley KR. Bica¡bonate does not improve decreased left ventricular contractility during lactic acid infusion, in pigs. Am Rev Resp Dis 1993;148:3lj-322. 11. Walley KR, Hebert PC, Wakai Y, Wilcox PG, Road JD, Cooper DJ. Decrease in left ventricular contractility after tumour necrosis factor alpha infusion in dogs. J Appl physiol 1994;j6:1060- 1067 12' V/ilcox P, Wakai Y, Walley KR, Cooper DJ. Road J. Tumor Necrosis Factor-ü, decreases in vivo diaphragm contractility in dogs. Wilcox PG, V/akai Y, Walley KR, Cooper DJ, Road J. Am J Resp Crit Care Med 1994;150:1368-73. 13. Cooper D, Schellenberg R, \Valley K. Different effects of histamine H, and H, stimulation on left ventricula¡ contractility in pigs. Am J Physiol 1995;269:H959-H964 BOOK CIIAPTERS l. Cooper DJ shock. in Dziukas L (ed): TextBookof EmergencyMedicine. lsted. McGrawHill. (in press 1996). 2. Cooper DJ: Acidosis and sodium bicarbonate therapy, in Keneally J.
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