Brazilian Journal of Anesthesiology
https://app.periodikos.com.br/journal/rba/article/doi/10.1590/S0034-70942008000200004
Brazilian Journal of Anesthesiology
Scientific Article

Impacto hemodinâmico de manobra de recrutamento alveolar em pacientes evoluindo com choque cardiogênico no pós-operatório imediato de revascularização do miocárdio

Hemodynamic impact of alveolar recruitment maneuver in patients evolving with cardiogenic shock in the immediate postoperative period of myocardial revascularization

Luiz Marcelo Sá Malbouisson; Marcelo Brito; Maria José Carvalho Carmona; José Otávio Costa Auler Jr

Downloads: 1
Views: 1032

Resumo

JUSTIFICATIVA E OBJETIVOS: Manobras de recrutamento alveolar (MRA) utilizando pressões de 40 cmH2O nas vias aéreas são efetivas em reverter as atelectasias após revascularização cirúrgica do miocárdio (RM), contudo não existem estudos avaliando o impacto hemodinâmico dessa manobra em pacientes que evoluíram com choque cardiogênico. O objetivo foi testar a tolerância hemodinâmica à MRA em pacientes evoluindo com choque cardiogênico após RM. MÉTODO: Após admissão na UTI e estabilização hemodinâmica, foram estudados dez pacientes hipoxêmicos e em choque cardiogênico após RM. Os ajustes ventilatórios foram volume corrente de 8 mL.kg-1, PEEP 5 cmH2O, FR de 12 ipm e FiO2 de 0,6. Pressão contínua de 40 cmH2O foi aplicada nas vias aéreas por 40 segundos em três ciclos. Entre os ciclos, os pacientes foram ventilados por 30 segundos e após o último ciclo a PEEP foi ajustada em 10 cmH2O. Foram obtidas medidas hemodinâmicas após 1, 10, 30 e 60 minutos da MRA e colhidas amostras sangüíneas arteriais e venosas para mensuração de lactato e gases sangüíneos 10 e 60 minutos após. Dados analisados por meio de ANOVA e teste de Friedman. Valor de p fixado em 0,05. RESULTADOS: A MRA aumentou a relação PaO2/FiO2 de 87 para 129,5 após 10 minutos e 120 após 60 minutos (p < 0,05) e reduziu o shunt pulmonar de 30% para 20% (p < 0,05). Não foram detectadas alterações hemodinâmicas ou no transporte de oxigênio imediatamente ou em até 60 minutos após a MRA. CONCLUSÕES: Em pacientes que evoluíram com choque cardiogênico após RM e hipoxemia, a MRA melhorou a oxigenação e foi bem tolerada sob o ponto de vista hemodinâmico.

Palavras-chave

CIRURGIA, Cardíaca, COMPLICAÇÕES, colapso pulmonar, VENTILAÇÃO, VENTILAÇÃO, VENTILAÇÃO

Abstract

BACKGROUND AND OBJECTIVES: Alveolar recruitment maneuver (ARM) with pressures of 40 cmH2 O in the airways is effective in the reversal of atelectasis after myocardial revascularization (MR); however, there is a lack of studies evaluating the hemodynamic impact of this maneuver in patients who evolve with cardiogenic shock after MR. The objective of this study was to test the hemodynamic tolerance to ARM in patients who develop cardiogenic shock after MR. METHODS: Ten hypoxemic patients in cardiogenic shock after MR were evaluated after admission to the ICU and hemodynamic stabilization. Ventilatory adjustments included tidal volume of 8 mL.kg-1, PEEP 5 cmH2O, RR 12, and FiO2 0.6. Continuous pressure of 40 cmH2O was applied to the airways for 40 seconds in three cycles. Between cycles, patients were ventilated for 30 seconds, and after the last cycle, PEEP was set at 10 cmH2O. Hemodynamic measurements were obtained 1, 10, 30, and 60 minutes after ARM, and arterial and venous blood samples were drawn 10 and 60 minutes after the maneuver to determine lactate levels and blood gases. ANOVA and the Friedman test were used to analyze the data. A p of 0.05 was considered significant. RESULTS: Alveolar recruitment maneuver increased the ratio PaO2/FiO2 from 87 to 129.5 after 10 minutes and to 120 after 60 minutes (p < 0.05) and reduced pulmonary shunting from 30% to 20% (p < 0.05). Hemodynamic changes or changes in oxygen transport immediately after or up to 60 minutes after the maneuver were not detected. CONCLUSIONS: In patients who evolved to cardiogenic shock and hypoxemia after MR, ARM improved oxygenation and was well tolerated hemodynamically.

Keywords

COMPLICATIONS, pulmonary collapse, SURGERY, Cardiac, VENTILATION, VENTILATION, VENTILATION

References

Magnusson L, Zemgulis V, Wicky S. Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: an experimental study. Anesthesiology. 1997;87:1153-1163.

Gale GD, Teasdale SJ, Sanders DE. Pulmonary atelectasis and other respiratory complications after cardiopulmonary bypass and investigation of aetiological factors. Can Anaesth Soc J. 1979;26:15-21.

Emhardt JD, Moorthy SS, Brown JW. Chest radiograph changes after cardiopulmonary bypass in children. J Cardiovasc Surg. 1991;32:314-317.

Tenling A, Hachenberg T, Tyden H. Atelectasis and gas exchange after cardiac surgery. Anesthesiology. 1998;89:371-378.

Magnusson L, Zemgulis V, Tenling A. Use of a vital capacity maneuver to prevent atelectasis after cardiopulmonary bypass: an experimental study. Anesthesiology. 1998;88:134-142.

Hachenberg T, Brussel T, Roos N. Gas exchange impairment and pulmonary densities after cardiac surgery. Acta Anaesthesiol Scand. 1992;36:800-805.

Brismar B, Hedenstierna G, Lundquist H. Pulmonary densities during anesthesia with muscular relaxation: a proposal of atelectasis. Anesthesiology. 1985;62:422-428.

Wasowicz M, Sobczynski P, Drwila R. Air-blood barrier injury during cardiac operations with the use of cardiopulmonary bypass (CPB): An old story? A morphological study. Scand Cardiovasc J. 2003;37:216-221.

Griese M, Wilnhammer C, Jansen S. Cardiopulmonary bypass reduces pulmonary surfactant activity in infants. J Thorac Cardiovasc Surg. 1999;118:237-244.

Pelosi P, D'andrea L, Vitale G. Vertical gradient of regional lung inflation in adult respiratory distress syndrome. Am J Respir Crit Care Med. 1994;149:8-13.

Joyce CJ, Williams AB. Kinetics of absorption atelectasis during anesthesia: a mathematical model. J Appl Physiol. 1999;86:1116-1125.

Rothen HU, Sporre B, Engberg G. Re-expansion of atelectasis during general anaesthesia: a computed tomography study. Br J Anaesth. 1993;71:788-795.

Claxton BA, Morgan P, McKeague H. Alveolar recruitment strategy improves arterial oxygenation after cardiopulmonary bypass. Anaesthesia. 2003;58:111-116.

Rothen HU, Sporre B, Engberg G. Prevention of atelectasis during general anaesthesia. Lancet. 1995;345:1387-1391.

Anyanwu E, Dittrich H, Gieseking R. Ultrastructural changes in the human lung following cardiopulmonary bypass. Basic Res Cardiol. 1982;77:309-322.

Kirshbom PM, Jacobs MT, Tsui SS. Effects of cardiopulmonary bypass and circulatory arrest on endothelium-dependent vasodilation in the lung. J Thorac Cardiovasc Surg. 1996;111:1248-1256.

Sandiford P, Province MA, Schuster DP. Distribution of regional density and vascular permeability in the adult respiratory distress syndrome. Am J Resp Crit Care Med. 1995;151:737-742.

Malbouisson LM, Busch CJ, Puybasset L. Role of the heart in the loss of aeration characterizing lower lobes in acute respiratory distress syndrome: CT Scan ARDS Study Group. Am J Respir Crit Care Med. 2000;161:2005-2012.

Froese AB, Bryan AC. Effects of anesthesia and paralysis on diaphragmatic mechanics in man. Anesthesiology. 1974;41:242-254.

Pinsky MR. Recent advances in the clinical application of heart-lung interactions. Curr Opin Crit Care. 2002;8:26-31.

Teboul JL, Pinsky MR, Mercat A. Estimating cardiac filling pressure in mechanically ventilated patients with hyperinflation. Crit Care Med. 2000;28:3631-3636.

Michard F, Boussat S, Chemla D. Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. Am J Respir Crit Care Med. 2000;162:134-138.

Jellinek H, Krafft P, Fitzgerald RD. Right atrial pressure predicts hemodynamic response to apneic positive airway pressure. Crit Care Med. 2000;28:672-678.

Auler Jr JOC, Nozawa E, Toma EK. Manobra de recrutamento alveolar na reversão da hipoxemia no pós-operatório imediato em cirurgia cardíaca. Rev Bras Anestesiol. 2007;57:476-488.

5dd6cb070e8825cf5013f286 rba Articles
Links & Downloads

Braz J Anesthesiol

Share this page
Page Sections