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2023, Number 3

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Med Crit 2023; 37 (3)

Maximun oxygen uptake as a pronostic marker of mortality in patients with septic shock in intensive care unit

Quezada RRI, Tapia PJG, Rodríguez GVH, Moran GE

Language: Spanish
References: 58
Page: 166-177
PDF size: 318.58 Kb.


ABSTRACT

Introduction: septic shock is a state of imbalance between oxygen supply and demand in the organism, dysregulation increases progressive cellular damage that ends in multiple organ failure; knowing and using preventive maneuvers allows avoiding further damage. Oxygen transport presents both the oxygen delivery component (DO2) and the rate of oxygen consumption (VO2). Low oxygen availability is called dysoxia, and its clinical expression is the presence of multiorgan dysfunction. It may be due to inadequate oxygen supply or a defect in oxygen utilization in the mitochondria, which is called cytopathic hypoxia. VO2max (maximal oxygen uptake) is the ability to carry and consume oxygen during a stress event and can be a useful tool for early detection of patients with more severe disease. Objective: to determine the maximum oxygen consumption (VO2) in patients with septic shock criteria hospitalized in the intensive care unit (ICU) as a predictor of mortality. Material and methods: single-center, descriptive prospective cohort analysis study, patients with diagnosis of septic shock were included which were admitted to ICU during December 2021-June 2022, mortality risk variables were studied, reason for ICU discharge, sequential organ failure assessment scale (SOFA), assessment scale for severe and chronic diseases (APACHE), VO2max by Niels Uth formula VO2max = 15 × (maximum heart rate for age/basal heart rate). Sample size was calculated with expected proportion formula with a sample of n = 80. At admission, heart rate was identified to calculate VO2max based on the formula VO2max = 15 × (maximum heart rate for age/basal heart rate), then SOFA and APACHE II mortality scales were calculated, and subsequently follow-up assessment was performed 12 hours after diagnosis of septic shock, calculating VO2max, and outcome was followed up at discharge. Results: a complete analysis was performed using the SPSS 22.0.0.0 statistical package. It was divided into two groups for analysis. One group consisted of patients who survived and were discharged due to improvement and the other consisted of patients who died. The analysis of VO2max at 12 hours was divided into two risk groups using 19 mL/kg/min as the cohort point. A significant statistical difference was found with a p of 0.001. Of the patients in the low-risk group, 44 (100% of the patients in this group) were discharged due to improvement, and of the patients in the high-risk group at 12 hours, 2.3% were discharged due to improvement and 42 patients were discharged due to death (97.7% of the patients in the high-risk group). With a 47% risk difference in risk of death by maintaining a VO2max below 19 mL/kg/min at 12 hours and a VO2max above 19 mL/kg/h has a 51% risk difference for patient survival, with a sensitivity of 100% and a specificity of 76% with an RR of 0.74 with a p of 0.001. Conclusion: VO2max could be a useful tool to identify patients with adequate resuscitation. This study suggests that an increase in VO2max at 12 hours above 19 mL/kg/min represents adequate resuscitation with a decrease in mortality of the patient with septic shock.


REFERENCES

  1. Rhodes A, Evans LE, Alhazzani W, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock: 2016. Crit Care Med. 2017;45(3):486-552.

  2. De Pasquale M, Moss TJ, Cerutti S, et al. Hemorrhage prediction models in surgical intensive care: bedside monitoring data adds information to lab values. IEEE J Biomed Health Inform. 2017;21(6):1703-1710.

  3. Hall JE. Guyton and hall textbook of medical physiology, 3th ed. Elsevier: Saunders; 2011.

  4. Belletti A, Landoni G, Lomivorotov VV, et al. Adrenergic downregulation in critical care: molecular mechanisms and therapeutic evidence. J Cardiothorac Vasc Anesth. 2020;34(4):1023-1041.

  5. Vasudevan NT, Mohan ML, Goswami SK, Naga Prasad SV. Regulation of β-adrenergic receptor function: an emphasis on receptor resensitization. Cell Cycle. 2011;10(21):3684-3691.

  6. Rockman HA, Koch WJ, Lefkowitz RJ. Seven-transmembrane-spanning receptors and heart function. Nature. 2002;415(6868):206-212.

  7. Ferguson SS. Evolving concepts in G protein-coupled receptor endocytosis: the role in receptor desensitization and signaling. Pharmacol Rev. 2001;53(1):1-24.

  8. Chapleau MW, Li Z, Meyrelles SS, Ma X, Abboud FM. Mechanisms determining sensitivity of baroreceptor afferents in health and disease. Ann N Y Acad Sci. 2001;940:1-19.

  9. Rubulotta FM, Ramsay G, Parker MM, et al. An international survey: public awareness and perception of sepsis. Crit Care Med. 2009;37(1):167-170.

  10. Singer M, Deutschman CS, Seymour CW, et al. The third international consensus definitions for sepsis and septic shock (sepsis-3). JAMA. 2016;315(8):801-810. doi: 10.1001/jama.2016.0287.

  11. Kalantari A, Mallemat H, Weingart SD. Sepsis definitions: the search for gold and what CMS got wrong. West J Emerg Med. 2017;18(5):951-956. doi: 10.5811/westjem.2017.4.32795.

  12. Lv X, Wang H. Pathophysiology of sepsis-induced myocardial dysfunction. Mil Med Res. 2016;3:30.

  13. Sevilla R, O'Horo JC, Velagapudi V, Pulido J. Correlation of left ventricular systolic dysfunction determined by low ejection fraction and 30-day mortality in patients with severe sepsis and septic shock: a systematic review and meta-analysis. J Crit Care. 2014;29:495-499.

  14. Romero M Del C, Cabrera A, Villagómez A, Méndez R, Guzmán R, Solache G. Disfunción ventricular asociada a sepsis. Rev Asoc Mex Med Crit y Ter Int. 2009;23(1):10-15.

  15. Rhodes A, Evans Le, Alhazzani W, et al. surviving sepsis campaign: international guidelines for management of sepsis and septic shock: 2016. Intensive Care Med. 2017;43:304-377. Available in: https://doi.org/10.1007/s00134-017-4683-6

  16. Vincent JL. The cardiovascular management of sepsis. year book of intensive care and emergency medicine. Germany. Spinger. 2008.

  17. Walley KR. Sepsis-induced myocardial dysfunction. Curr Opin Crit Care. 2018;24(4):292-299.

  18. Andresen M, Regueira T. Disfunción miocárdica en la sepsis. Rev Med Chile. 2010;138:888-896.

  19. Nagueh SF, Smiseth OA, Appleton CP, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2016;29(4):277-314.

  20. Suarez JC, Lopez P, Mancebo J, Zapata L. diastolic dysfunction in the critically ill patient. Med Intensiva. 2016;40(8):499-510.

  21. Peña-Juarez RA, Garrido-García LM, Zapata-Martínez SG. miocardiopatía séptica en pacientes pediátricos: fisiopatología y presentación clínica. Acta Colomb Cuid Intensivo. 2018;18(3):179-189. Disponible en: https://doi.org/10.1016/j.acci.2018.02.004

  22. Fenton KE, Parker M. cardiac function and dysfunction in sepsis. Clin Chest Med. 2016;37:289-298.

  23. Kakihana Y, Ito T, Nakahara M, Yamaguchi K, Yasuda T. Sepsis-induced myocardial dysfunction: pathophysiology and management. J Intensive Care. 2016;4:22.

  24. Hochstadt A, Meroz Y, Landesberg G. Myocardial dysfunction in severe sepsis and septic shock: ¿more question tan answers? J Cardiothorac Vasc Anesth. 2011;25:526-535.

  25. Parrillo JE, Burch C, Shelhamer Jh, Parker M, Netanson C, Schuette W. A circulating myocardial depressant substance in humans with septic shock. J Clin Invest. 1985;76:1539-1553.

  26. Balija TM, Lowry SF. Lipopolysaccharide and sepsis-associated myocardial dysfunction. Curr Opin Infect Dis. 2011;24:248-253.

  27. Li J, Carr B, Goyal M, Gaieski DF. Sepsis: the inflammatory foundation of pathophysiology and therapy. Hosp Pract (1995). 2011;39(3):99-112.

  28. Ferreira JA, Bissell Bd. Misdirected sympathy: the role of sympatholysis in sepsis and septic shock. J Intensive Care Med. 2018;33:74-86.

  29. Ostrowski SR, Gaini S, Pedersen C, Johansson PI. Sympathoadrenal activation and endothelial damage in patients with varying degrees of acute infectious disease: an observational study. J Crit Care. 2015;30:90-96.

  30. Cariou A, Pinsky MR, Monchi M, et al. Is myocardial adrenergic responsiveness depressed in human septic shock? Intensive Care Med. 2008;34:917-922.

  31. Rudiger A. Beta-block the septic heart. Crit Care Med. 2010;38:s608-612.

  32. Schmidt C, Kurt B, Holcherl K, Bucher M. Inhibition of NF-kappaB activity prevents downregulation of alpha1-adrenergic receptors and circulatory failure during CLP-induced sepsis. Shock. 2009;32:239-246.

  33. Ackland GL, Kazymov V, Marina N, Singer M, Gourine AV. Peripheral neural detection of danger-associated and pathogen-associated molecular patterns. Crit Care Med. 2013;41:e85-92.

  34. Godin PJ, Buchman Tg. Uncoupling of biological oscillators. Crit Care Med. 1996;24:1107-1116.

  35. Sharshar T, Gray F, De La Grandmaison Gl, et al. Apoptosis of neurons in cardiovascular autonomic centres triggered by inducible nitric oxide synthase after death from septic shock. Lancet. 2003;362:1799-1805.

  36. Nardocci G, Martin A, Abarzúa S, et al. Sepsis progression to multiple organ dysfunction in carotid chemo/baro-denervated rats treated with lipopolysaccharide. J Neuroimmunol. 2015;278:44-52.

  37. Ramchandra R, Wan L, Hood Sg, Frithiof R, Bellomo R, May CN. Septic shock induces distinct changes in sympathetic nerve activity to the heart and kidney in conscious sheep. Am J Physiol Integr Comp Physiol. 2009;297:r1247-1253.

  38. Vayssettes-Courchay C, Bouysset F, Verbeuren Tj. Sympathetic activation and tachycardia in lipopolysaccharide treated rats are temporally correlated and unrelated to the baroreflex. Auton Neurosci. 2005;120:35-45.

  39. Pavlov VA, Tracey KJ. The cholinergic anti-infammatory pathway. Brain Behav Immun. 2005;19:493-499.

  40. Tracey KJ. The inflammatory reflex. Nature. 2002;420:853-859.

  41. Bravi A, Longtin A, Seely AJE. Review and classification of variability analysis techniques with clinical applications. Biomed Eng Online. 2011;10:90.

  42. Jarkovska D, Valesova L, Chvojka J, et al. Heart rate variability in porcine progressive peritonitis-induced sepsis. Front Physiol. 2016;6:412.

  43. Fairchild KD, Saucerman JJ, Raynor LL, et al. Endotoxin depresses heart rate variability in mice: cytokine and steroid effects. Am J Physiol Integr Comp Physiol. 2009;297:r1019-1027.

  44. Venditti P, Di Stefano L, Di Meo S. Mitochondrial metabolism of reactive oxygen species. Mitochondrion. 2013;13(2):71-82.

  45. Gifford JR, Garten RS, Nelson AD, et al. Symmorphosis and skeletal muscle VO2 max: in vivo and in vitro measures reveal differing constraints in the exercise? trained and untrained human. J Physiol. 2016;594(6):1741-1751.

  46. Lundby C, Montero D. Crosstalk opposing view: diffusion limitation of O2 from microvessels into muscle does not contribute to the limitation of VO2max. J Physiol. 2015;593(17):3759-3761.

  47. Fink MP. Cytopathic hypoxia. mitochondrial dysfunction as a mechanism contributing to organ dysfunction in sepsis. Crit Care Clin. 2001;17:219-237.

  48. Koutlianos N, Dimitros E, Metaxas T, Cansiz M, Deligiannis A, Kouidi E. Indirect estimation of VO2max in athletes by ACSM's equation: valid or not? Hippokratia. 2013;17(2):136-140.

  49. Elliott AD, Skowno J, Prabhu M, Noakes TD, Ansley L. Evidence of cardiac functional reserve upon exhaustion during incremental exercise to determine VO2max. Br J Sports Med. 2015;49(2):128-132.

  50. Bazerbashi H, Merriman KW, Toale KM, et al. Low tissue oxygen saturation at emergency center triage is predictive of intensive care unit admission. J Crit Care. 2014;29(5):775-779.

  51. Malekmohammad M, Ahmadi-Nejad M, Adimi P, Jamaati HR, Marashian SM. Evaluation of maximum O2 consumption: using ergo-spirometry in severe heart failure. Acta Med Iran. 2012;50(9):619-623.

  52. Annane D, Bellissant E, Cavaillon J. Septic shock. Lancet. 2005;365(9453):63-78.

  53. Makey I, Berger RL, Cabral HJ, Celli B, Folch E, Whyte RI. Maximal oxygen uptake--risk predictor of NSCLC resection in patients with comorbid emphysema: lessons from NETT. Semin Thorac Cardiovasc Surg. 2015;27(2):225-231.

  54. Bolliger CT, Jordan P, Soler M, et al. Exercise capacity as a predictor of postoperative complications in lung resection candidates. Am J Respir Crit Care Med. 1995;151(5):1472-1480. doi: 10.1164/ajrccm.151.5.7735602.

  55. Licker M, Schnyder JM, Frey JG, et al. Impact of aerobic exercise capacity and procedure-related factors in lung cancer surgery. Eur Respir J. 2011;37(5):1189-1198. doi: 10.1183/09031936.00069910.

  56. Cabezas GA, Meleán LM, Torrealba HE. Consumo máximo de oxígeno (vo2max) para predecir riesgos postoperatorios en cirugía abdominal electiva. Revista de la Facultad de Medicina. 2001;24(2):163-171.

  57. Astorino T, DeRevere J, Anderson T. Blood lactate concentration is not related to the increase in cardiorespiratory fitness induced by high intensity interval training. Int J Environ Res Public Health. 2019;16(16):2845.

  58. Vincent JL, de Mendonça A, Cantraine F, Moreno R, Takala J, Suter PM, et al. Use of the SOFA score to assess the incidence of organ dysfunction/failure in intensive care units: results of a multicenter, prospective study. Working group on "sepsis-related problems" of the European Society of Intensive Care Medicine. Crit Care Med. 1998;26(11):1793-800. doi: 10.1097/00003246-199811000-00016.




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