Brazilian Journal of Anesthesiology
https://app.periodikos.com.br/journal/rba/article/doi/10.1590/S0034-70942003000500009
Brazilian Journal of Anesthesiology
Scientific Article

Comportamento hemodinâmico e metabólico do choque hemorrágico: estudo experimental no cão

Hemorrhagic shock hemodynamic and metabolic behavior: experimental study in dogs

José Fernando Amaral Meletti; Norma Sueli Pinheiro Módolo

http://dx.doi.org/10.1590/S0034-70942003000500009 Braz J Anesthesiol, vol.53, n5, p.623-632, 2003
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Resumo

JUSTIFICATIVA E OBJETIVOS: Diversos modelos experimentais têm sido utilizados para ilustrar as alterações hemodinâmicas e metabólicas que ocorrem durante o choque hemorrágico. O objetivo da pesquisa é o de observar os comportamentos hemodinâmicos e metabólicos que acontecem em um modelo seqüencial e progressivo de choque hemorrágico no cão, verificando quais índices alteram-se mais precocemente. MÉTODO: O estudo foi realizado em 13 cães sob anestesia venosa total com pentobarbital sódico, em normoventilação e previamente esplenectomizados. Os animais não foram hidratados e a velocidade do sangramento foi ditada pela pressão arterial em que o animal se encontrava. Os atributos estudados foram divididos em hemodinâmicos (freqüência cardíaca - FC, pressão arterial média - PAM, índice de resistência vascular sistêmica - IRVS, índice sistólico - IS, índice cardíaco - IC, índice de choque - I.choque, índice de trabalho sistólico do ventrículo esquerdo - ITSVE, pressão capilar pulmonar - PCP, pressão venosa central - PVC) e metabólicos (saturação venosa mista - SvO2, pressão venosa de oxigênio - PvO2, transporte de oxigênio - DO2, consumo de oxigênio - VO2, extração de oxigênio - TEO2, lactato sérico). A coleta de dados e os atributos foram estudados em 6 momentos distintos, sendo M1, o momento controle e os outros momentos correspondentes a decréscimos gradativos de 10% da volemia calculada para cada animal. RESULTADOS: A hemorragia determinou diminuição significativa da FC somente em M6; queda da PAM, IC, IS e ITSVE a cada momento estudado; discreta alteração da PVC e PCP em cada momento; diminuição da PvO2 e da SvO2 nos momentos estudados; redução do DO2, estabilização do VO2 e elevação da TEO2 nos momentos; o índice de choque apresentou elevação até M3, diminuição em M4 e nova elevação até M6; o IRVS elevou-se até M6, ficou inalterado em M5 e apresentou diminuição significativa em M6; o lactato apresentou elevações a partir de M5 e M6. CONCLUSÕES: Considerou-se que a pressão arterial média, freqüência cardíaca, pressão venosa central e pressão capilar pulmonar não refletem o real estado volêmico dos cães no nosso modelo experimental e que o transporte, consumo e a taxa de extração de oxigênio são parâmetros úteis na determinação da reversibilidade e prognóstico do choque hemorrágico.

Palavras-chave

ANIMAL, COMPLICAÇÕES

Abstract

BACKGROUND AND OBJECTIVES: Different experimental models have been used to illustrate hemodynamic and metabolic changes during hemorrhagic shock. This study aimed at observing hemodynamic and metabolic behaviors during a sequential and progressive model of hemorrhagic shock in dogs to determine which indices are earlier changed. METHODS: The study involved 13 dogs under total intravenous anesthesia with sodium pentobarbital, standard ventilation and previously splenectomized. Animals were not hydrated and bleeding velocity was dictated by animals’ blood pressure. Evaluated parameters were: hemodynamic (heart rate - HR, mean blood pressure - MBP, systemic vascular resistance index - SVRI, stroke index - SI, cardiac index - CI, shock index - i.Shock, left ventricular stroke work index - LVSWI, pulmonary capillary pressure - PCP, central venous pressure - CVP); and metabolic (mixed venous saturation - SvO2, venous oxygen pressure - PvO2, oxygen transport - O2T, oxygen consumption - VO2, oxygen extraction - TEO2, serum lactate). Results and parameters were evaluated in 6 different moments: M1 - control, and the other moments corresponding to gradual 10% decrease in calculated volume for each animal. RESULTS: Hemorrhage has determined significant heart rate decrease in M6 only; MBP, CI, i.Shock, LVSWI decrease in all studied moments; mild CVP and PCP change in all moments; PVO2 and SVO2 decrease in all moments; O2T decrease, VO2 stabilization and TEO2 increase in all moments; shock index was increased from M1 to M3, was decreased in M4 and again increased until M6; SVRI was increased from M1 to M4, remained unchanged in M5 and has significantly decreased in M6; lactate has increased as from M5 and M6. CONCLUSIONS: Mean blood pressure, heart rate, central venous pressure and pulmonary capillary pressure have not reflected real volume status of dogs in our experimental model, oxygen transport, consumption and extraction rate are useful parameters to determine hemorrhagic shock reversibility and prognosis.

Keywords

ANIMAL, COMPLICATIONS

References

Velasco IT, Rocha e Silva M. Choque hipovolêmico: ressuscitação hipertônica. Rev Bras Terap Intens. 1990;2:16-21.

Rocha e Silva M, Braga GA, Prist R. Physical and physiological characteristics of pressure drisen hemorrhage. Am J Physiol. 1992;263:H1402-H1410.

Giesecke AN, Laurence DE. Anestesia para Cirurgia dos Traumatismos. Tratado de Anestesiologia. 1992:1877-1893.

Alexander RH, Proctor HJ. Advanced Trauma Life Support Instruction Manual. 1996:77.

Velasco IT. Clinical and therapeutic aspects of states of shock. Rev Paul Med. 1997;115:1329.

Horton JW, Longhurst JC, Coln D. Cardiovascular effects of haemorrhagic shock in spleen intact an in splenectomized dogs. Clin Physiol. 1984;4:533-548.

Kim SI, Desai JM, Shoemaker WC. Sequence of cardiorespiratory alterations after gradual prolonged hemorrhage in conscious dogs. Am J Physiol. 1969;216:1044-1050.

Schwartz S, Frantz RA, Shoemaker WC. Sequential hemodynamic and oxygen transport responses in hypovolemic, anemia and hypoxia. Am J Phisiol. 1981;241:864-871.

Erstad BL. Oxygen transport goals in the resuscitation of critically ill patients. Ann Pharmacother. 1994;28:1273-1284.

Shoemaker WC. Relation of oxygen transport patterns to the pathophysiology and therapy of shock states. Intensive Care Med. 1987;13:230-243.

Shoemaker WC. Circulatory mechanisms of shock and their medicators. Crit Care Med. 1987;15:787-794.

Morrison DF. Multivariate Statistical Methods. 1990:495.

Curi PR. Metodologia e Análise da Pesquisa em Ciências Biológicas. 1998:265.

Dillon AR, Hankes CH, Machreiner RF. Experimental hemorrhage in splenectomized an nonsplenectomized dogs. Am J Vet Res. 1980;41:707-711.

Massone F. Anestesiologia Veterinária: Farmacologia e Técnicas. 1988:23.

Priano LL, Traber DL, Wilson RD. Barbiture anesthesia an abnormal physiologic situation. J Pharmacol Exp Ther. 1969;165:126-135.

Manders WT, Watner SF. Effects of pentobarbital anesthesia on left ventricular function and distribution of cardiac output in dogs with particular reference the mechanism for tachycardia. Circ Res. 1976;39:512-517.

Nelson AW, Swan H. Hemorrhage: response determining survival. Arc Shock. 1974;4:273-285.

Greene NM. Reports of scientific meetings. Anesthesiology. 1971;34:104-105.

Olmsted F, Page IH. Hemodynamic changes in dogs caused by sodium pentobarbital anesthesia. Am J Physiol. 1966;210:817-820.

Gilmore JP. Pentobarbital sodium anesthesia in the dog. Am J Physiol. 1965;209:404-408.

Barlow G, Knott DH. Hemodynamic alterations after 30 min of pentobarbital sodium anesthesia in dogs. Am J Physiol. 1964;207:764-766.

Schwartz S, Frantz RA, Shoemaker WC. Sequential hemodynamic and oxygen transport responses in hypovolemic, anemia and hypoxia. Am J Physiol. 1981;241:864-871.

Ilkim JE, Haskins SC, Patz JO. Cardiovascular and respiratory effects of thiopental administration in hipovolemics dogs. Am J Vet Res. 1991;52:576-580.

Orkin FK, Cooperman LH. Complication in Anesthesiology. 1983:220-240.

Guyton AC. Tratado de Fisiologia Médica. 1992:230-238.

Allgower M, Burn C. Shock index. Ger Med Mon. 1968:14-19.

Rody MY, Sittle RR, Kirkiman E. Resuscitation fluids and oxygen transport in haemorrhagic shock. Adv Exp Med Biol. 1992;316:409-418.

Pianim NA, Liu SY, Klein SR. Tissue oxygenation in hypovolemic shock. J Surg Res. 1993;55:338-343.

Vaughin S, Puri VK. Cardiac output changes and continuous mixed venous oxygen saturation measurement in the critically ill. Crit Care Med. 1988;16:495-498.

Abyt JW, Scottlile FO, Durbin CG. Continuous SVO2 or Predictor of Changes in Output: Clinical Observation. Continuous Measurement of Blood Oxygen Saturation in the High Risk Patient. 1982;1:45-58.

Kazavan KK, Del Guelcio LR. The risk of mixed venous blood gas determination traumatic shock. Ann Emerg Med. 1980;9:174-182.

Shoemaker WC. Circulatory mechanisms of shock and their medicators. Crit Care Med. 1987;15:787-794.

Shoemaker WC, Kran HB, Appel PL. Therapy of shock losed on athophysiology, monitoring and outcome prediction. Crit Care Med. 1990;18:19-25.

Revelly JP, Gardaz JP, Nussler J. Effect of epinephrine on oxygen consumption and delivery during progressive hemorrhage. Crit Care Med. 1995;23:1272-1278.

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