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On-line version ISSN 1806-907X
Rev. Bras. Anestesiol. vol.58 no.2 Campinas Mar./Apr. 2008
Hemodynamic impact of alveolar recruitment maneuver in patients evolving with cardiogenic shock in the immediate postoperative period of myocardial revascularization
Impacto hemodinámico de maniobra de reclutamiento alveolar en pacientes evolucionando con choque cardiogénico en el postoperatorio inmediato de revascularización del miocardio
Luiz Marcelo Sá Malbouisson, TSAI; Marcelo BritoII; Maria José Carvalho Carmona, TSAIII; José Otávio Costa Auler Jr, TSAIV
em Ciências pela USP; Médico Supervisor da Divisão de Anestesiologia
do HC-FMUSP; Coordenador da UTI/RPA da Disciplina de Anestesiologia do Instituto
Central do HC-FMUSP; Especialista em Terapia Intensiva AMIB
IIMédico Estagiário do Serviço de Anestesiologia e Terapia Intensiva do Instituto do Coração (InCor) do HC-FMUSP
IIIProfessa-Associada da Disciplina de Anestesiologia da FMUSP; Diretora da Divisão de Anestesiologia do Instituto Central do HC-FMUSP
IVProfessor Titular da Disciplina de Anestesiologia da FMUSP; Diretor do Serviço de Anestesiologia Instituto do Coração (InCor) do HC-FMUSP
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.
Key Words: COMPLICATIONS: atelectasis; pulmonary collapse; SURGERY, Cardiac: myocardial revascularization; VENTILATION: alveolar recruitment maneuver, mechanical, positive end-expiratory pressure.
Y OBJETIVOS: Maniobras de reclutamiento alveolar (MRA) utilizando presiones
de 40 cmH2O en las vías aéreas son efectivas en revertir
las atelectasias después de la revascularización quirúrgica
del miocardio (RM), sin embargo, no existen estudios que evalúen el impacto
hemodinámico de esta maniobra en pacientes que evolucionaron con choque
cardiogénico. El objetivo fue probar la tolerancia hemodinámica
a la MRA en pacientes que evolucionan con choque cardiogénico después
de la RM.
MÉTODO: Después de la entrada en la UCI y de la estabilización hemodinámica, se estudiaron 10 pacientes hipoxémicos y en choque cardiogénico después de RM. Los ajustes de ventilación fueron volumen corriente de 8 mL.kg-1, PEEP 5 cmH2O, FR de 12 ipm y FiO2 de 0,6. Presión continua de 40 cmH2O se aplicó en las vías aéreas por 40 segundos en tres ciclos. Entre los ciclos, los pacientes fueron ventilados por 30 segundos y después del último ciclo, la PEEP fue ajustada en 10 cmH2O. Fueron obtenidas medidas hemodinámicas después de 1, 10, 30 y 60 minutos de la MRA y recogidas muestras de sangre arteriales y venosas para la medida de lactato y de los gases sanguíneos 10 y 60 minutos después. Datos analizados a través de ANOVA y test de Friedman. Valor de p fijado en 0,05.
RESULTADOS: La MRA aumentó la relación PaO2/FiO2 de 87 para 129,5 después de 10 minutos y 120 después de 60 minutos (p < 0,05) y redujo el shunt pulmonar de 30% para 20% (p < 0,05). No se detectaron alteraciones hemodinámicas o en el transporte de oxígeno inmediatamente o en hasta 60 minutos después de la MRA.
CONCLUSIONES: En pacientes que evolucionaron con choque cardiogénico después de RM e hipoxemia, la MRA mejoró la oxigenación y fue bien tolerada hemodinámicamente.
The development of atelectasis is commonly seen in patients undergoing cardiac surgery, representing the most important cause of hypoxemia and shunt after cardiopulmonary bypass (CPB) 1. The incidence of atelectasis in patients undergoing cardiac surgery with CPB is high, varying from 60% to 90% in the studies reported in the literature 2,3. Evaluating chest CT scans of 18 patients on the first postoperative day of mitral valve replacement or myocardial revascularization (MR) with CPB, Tenlig et al. observed the presence of bilateral dependent pulmonary densities in all but one patient. Those pulmonary densities corresponded to approximately 20% of the lung parenchyma 4.
In patients who evolved with severe ventricular dysfunction and cardiogenic shock, the presence of hypoxemia secondary to pulmonary collapse can increase pulmonary artery resistance and pressure, impairing right ventricular performance and perpetuating the state of low cardiac output. The association of tissue hypoperfusion secondary to a low cardiac output, and the reduced arterial oxygen content secondary to hypoxemia can contribute to the development of distant organic lesions. On the other hand, the possibility of noxious effects on the cardiovascular system limits the efficacy of elevated positive end-expiratory pressure (PEEP) for the length of time necessary to reverse atelectasis in this population of patients. Alveolar recruitment maneuver with 40 cmH2O pressure in the airways for brief moments has been described as effective to reverse virtually all pulmonary collapse observed after CPB 5. However, the use of elevated pressures can cause acute cardiovascular collapse. The objective of this study was to evaluate the impact of alveolar recruitment maneuver with elevated pressures on oxygenation and hemodynamic performance in patients developing severe myocardial dysfunction in the immediate postoperative period of myocardial revascularization.
After approval by the Ethics Committee of the hospital and signing of the informed consent by the family member responsible for the patient, 10 patients who developed myocardial dysfunction and required inotropic support and/or mechanical circulatory support after elective myocardial revascularization with cardiopulmonary bypass were evaluated. Inclusion criteria were as follows: a) continuous infusion of 20 µg.kg.min-1 of dobutamine and/or 0.5 µg.kg.min-1 of milrinone; b) mixed venous saturation < 75% after hemodynamic optimization; c) absence of hypovolemia, defined as pulmonary capillary wedge pressure (PCWP) < 15 mmHg; and e) severe hypoxemia, characterized by a PaO2/FiO2 below 150 in the arterial blood at the time the patient was admitted to the intensive care unit. Patients with severe pulmonary hypertension with mean pulmonary artery pressure > 40 mmHg; patients with suspected intracranial hypertension; patients with air-leaking syndrome (pneumothorax and pneumomediastinum on chest X-ray or bubbles draining out of the chest tubes); patients with pulmonary diseases requiring preoperative oxygen supplementation were excluded from the study.
According to the protocol of the institution, each patient was pre-medicated with 0.1 to 0.2 mg.kg-1 of midazolam PO 30 minutes before the surgery. After arrival to the operating room, patients were monitored with cardioscope (DII and V5 derivations) and pulse oximetry using a multiparametric Siemens monitor model SC7000 (Siemens Medical, Berlin, Germany). A 16G Teflon® catheter was used for the peripheral venipuncture. The right radial artery was punctured under local anesthesia with a 20G Teflon® catheter to monitor the mean arterial pressure. After anesthetic induction, a pulmonary artery catheter was introduced (CCO/SvO2/VIPTM TD catheter; Edwards Healthcare Co., Irvine, CA, USA) in the right jugular vein, due to the reduced ejection fraction of the patients, according to the protocol of the Anesthesiology and Intensive Care Department. Non-pulsatile flow cardiopulmonary bypass under moderate hypothermia, with an oxygenator membrane OXI Master Century (Braile, São José do Rio Preto, SP, Brazil), was applied to all patients with the circuit filled with Ringer's lactate and 50g of mannitol. Intraaortic balloon counterpulsation was used in patients difficult to wean off cardiopulmonary bypass after maximizing the pharmacological support. At the end of the procedure, patients were transferred to the intensive care unit.
After admission to the intensive care unit, hemodynamic stabilization and ventilatory support, arterial blood gases and initial hemodynamic parameters were obtained. Initial ventilatory parameters included pressure-controlled mode, respiratory rate of 12 bpm, tidal volume 8 mL.kg-1, inspiratory time 30% of the respiratory cycle, PEEP 5 cmH2O, and FiO2 0.6. Hemodynamic adjustment was done initially by optimizing the blood volume aiming at maintaining PCWP above 18 mmHg and by the administration of vasoactive drugs and use of mechanical circulatory support to keep the cardiac index above 2.5 L.min-1.m-2 and MAP above 65 mmHg. When the patient was hemodynamically stable, arterial and venous blood gases were obtained, a complete hemodynamic evaluation was undertaken and the alveolar recruitment maneuver (ARM) consisting of applying continuous 40-cmH2O pressure to the airways (CPAP) during 40 seconds for three cycles was performed. During the interval between each cycle, mechanical ventilation was resumed for 30 seconds with the same initial parameters to remove alveolar CO2. After the last cycle, PEEP was adjusted to 10 cmH2O. After ARM, a chest X-ray was obtained to evaluate the presence of pneumothorax or other air-leaking syndromes. Complete hemodynamic measurements were obtained by the thermodilution technique (3 injections of D5W at room temperature) 1, 10, 30, and 60 minutes after the ARM.
The Kolmogorov-Smirnov test was used to evaluate the normal distribution of the hemodynamic parameters and blood gases. The one-way Analysis of Variance for repeated measurements or the Friedman test, followed by the multiple comparison test (Student-Neumann-Keuls or Wilcoxon test) was used to analyze the data according to their distribution. It was considered a level of significance of 0.05. Data are presented as mean ± standard error or discriminated if presented in a different form.
After admission to the intensive care unit and initial hemodynamic stabilization for a mean period of two hours, 10 patients who remained severely hypoxemic were enrolled in the study. Table I shows hemodynamic and oxygenation parameters and the need of pharmacological and mechanical circulatory support of patients immediately before the alveolar recruitment maneuver. Patients had a mean cardiac index of 2.6 L.min-1.m2, SvO2 64% (normal: 75%), oxygen extraction 34% (normal: 25%), and arterial lactate 31.6 md.dL-1 (normal: up to 14 mg.dL-1), characterizing cardiogenic shock. All patients received infusion of 20 µg.kg-1.min-1 of dobutamine, seven received infusion of up to 0.7 µg.kg-1.min-1 of milrinone, and eight received infusion of noradrenaline (0.1 ± 0.03 µg.kg-1.min-1). Five patients required mechanical circulatory support with intraaortic balloon counterpulsation due to failure of inotropic and vasopressor pharmacologic support. After the initial optimization, mean mixed venous saturation was 64%, oxygen extraction 34%, and arterial lactate 31.6mg.dL-1. In patients selected for this study, mean PaO2/FiO2 immediately after hemodynamic stabilization was 87 and static complacency 36 ± 2 mL.cm-1H2O-1.
Pneumothorax or other signs of air leakage were not detected on the chest X-ray done after the maneuver. As can be seen in the upper panel of Figure 1, there was a significant increase in the mean values of PaO2/FiO2 to 129.5 10 minutes after ARM, which was maintained at 120 one hour after the maneuver; and reduction in pulmonary shunting from 30% to 20% ten minutes after ARM, which was maintained at 23% sixty minutes after the maneuver. Significant hemodynamic changes immediately after and 60 minutes after ARM were not observed. Cardiac index and MAP remained stable at all study moments (Figure 1 lower panel). Significant changes in pulmonary artery pressure, pulmonary capillary wedge pressure, central venous pressure, heart rate, and left and right ventricular work load indexes (Figure 2) were not observed, and the same is true for systemic and pulmonary vascular resistance (Figure 3 lower panel). There were no statistically significant changes on oxygen transportation (Figure 3 upper panel).
In this study, we observed that in patients who develop cardiogenic shock in the immediate postoperative period of myocardial revascularization, alveolar recruitment maneuver with airways pressures of 40 cmH2O improved oxygenation without significant changes in hemodynamic performance, immediately or up to 60 minutes after the maneuver.
Alveolar collapse followed by hypoxemia is a common complication in patients undergoing cardiac surgeries 6. Atelectasis develop especially in dependent and caudal pulmonary regions during the first moments of anesthetic infusion and muscular relaxation, affecting up to 20% of the pulmonary parenchyma, up to 5 minutes after anesthetic induction 4,7. In patients undergoing cardiac surgery with cardiopulmonary bypass, the increase in pulmonary extravascular water and changes in the normal activity of the surfactant system, secondary to the activation of inflammatory and coagulation cascades by the contact between the blood and non-endothelial surfaces, contribute to the increased weight of the pulmonary parenchyma and additional alveolar collapse, further decreasing the efficacy of gas exchange 8-10. In hypoxemic patients with hemodynamic instability, the use of increased inspired fraction of oxygen to compensate the hemodynamic intolerance to PEEP, can also contribute to the development of atelectasis 11. In the present study, it was observed a mean pulmonary shunt of 30% after hemodynamic stabilization in the intensive care unit, and mean PaO2/FiO2 of 87, which configure severe acute pulmonary lesion.
Alveolar recruitment maneuver resulted in a significant increase of mean PaO2/FiO2 values of 48%, which were maintained for at least 60 minutes, and a significant and lasting reduction in pulmonary shunting by 10% reflecting the partial opening of collapsed lung areas. Experimental animal studies and studies in humans with normal pulmonary and cardiovascular functions undergoing cardiopulmonary bypass under general anesthesia demonstrated that pressures of 40 cmH2O are effective in re-opening virtually all areas of lung collapse 5,12,13, as well as the efficacy of a PEEP of 10 cmH2O in preventing new areas of pulmonary collapse 14. Despite the evidence of improved gas exchange after ARM and implementation of PEEP of 10 cmH2O, it is most likely that some areas of the pulmonary parenchyma remained collapsed and were unable to provide adequate gas exchange, since PaO2/FiO2 remained below 200 and pulmonary shunting remained around 20%, suggesting the presence of residual ventilation/perfusion imbalance. In this group of patients who evolved with cardiogenic shock, alveolar edema 15, changes in pulmonary vascular regulation induced by the CPB 16, or the use of elevated pressures in the airways below those necessary to open and/or maintain opened previously collapsed pulmonary areas can explain the presence of residual hypoxemia. It is possible that repeating the alveolar recruiting maneuver followed by higher PEEP would have lead to supplementary improvement in oxygenation.
The pressure applied on the airways to reverse the pulmonary collapse should be higher than the pressures that caused the atelectasis. In other words, the alveolar pressure has to be higher than the sum of the components responsible for the increase in pleural pressure, namely the pressure imposed by the weight of the edematous lung parenchyma 10,17, compression of the lower lobes by the weight of the heart 18, and compression of caudal regions by the weight of the abdominal viscera 19. However, the use of 40 cmH2O-pressures on the airways, necessary to reverse atelectasis, can cause hemodynamic collapse especially in patients who develop severe myocardial dysfunction after cardiopulmonary bypass and, therefore, it is avoided. In this study, although patients were evolving with shock and had signs of tissue hypoperfusion, characterized by a mean cardiac index of 2.6 L.min-1.m2 in the presence of maximal pharmacological and mechanical circulatory support, SvO2 64% (normal: 75%), oxygen extraction 34% (normal: 25%), and arterial lactate 31.6 mg.dL-1 (normal: up to 14 mg.dL-1), ARM was performed without deterioration of contractility indexes, increase in pulmonary vascular resistance or worsening tissue oxygenation.
Important elevations in intra-thoracic pressure cause a reduction in venous return and the volume of intra-thoracic blood, and increase impedance to right ventricular ejection, independent of the direct compression of the heart in the cardiac groove caused by the increased pulmonary expansion 20. Immediate consequences of the alveolar recruitment maneuver include sudden reduction in right and left ventricular blood volume, increase in pulmonary vascular resistance, and reduction in cardiac output secondary to the reduced venous return and blood volume in the cardiac chambers. The hemodynamic tolerance to ARM observed in patients in circulatory shock can be partly explained by a reduction in the transmission of the airways pressure to the cardiovascular system due to the low pulmonary complacency. Teboul et al. 21 demonstrated a proportional relationship between the impact caused by an elevation of airways pressure on cardiac filling pressures and static complacency of the respiratory system. The mean static complacency of the respiratory system was 36 mL.cmH2O-1, much lower than expected for patients with normal lungs whose pressures are above 100 mL.H2O-1. Another mechanism that explains the hemodynamic tolerance to ARM is the optimization of blood volume, which reduces the interference of the maneuver on venous return and, consequently, on cardiac output. Michard et al. 22 observed, in patients with septic shock and respiratory failure that the ventilatory interference on hemodynamic performance was greater in hypovolemic patients causing cyclic reductions in cardiac output. Jellineck et al. 23 observed that a CVP below than 12 mmHg was associated with a reduction in cardiac output with pulmonary hyperinsuflation with pressures of 30 cmH2O in the airways, while this interference was less accentuated in patients with CVP higher than 12 mmHg. In the present study, ventricular filling pressures were optimized in all patients before ARM, with a mean PCWP of 19.6 mmHg in face of a PEEP of 5 cmH2O. Besides, in patients whose cardiac index did not reach 2.5 L.min-1.m-2 just with volume replacement, the infusion of vasoactive drugs was increased and the hemodynamic goals were achieved in all patients before ARM. It is possible that the association of optimized hemodynamic parameters and the reduction in the static complacency of the respiratory system allowed for ARM without hemodynamic consequences 24.
According to the results of the present study, alveolar recruitment maneuver in patients with circulatory shock after myocardial revascularization with CPB promoted a significant improvement in oxygenation without jeopardizing the hemodynamic performance. The benefits of the ARM go beyond reversion of atelectasis. By promoting better distribution of the ventilation to previously collapsed areas, it reduces the possibility of volumetric trauma, reduces pulmonary vascular resistance associated with hypoxia, improves right ventricular performance and reduces the need for postoperative mechanical ventilation. However, further studies are necessary to compare the benefits of ARM to the risks of adverse events, such as pneumothorax and inflammatory lung damage associated with sustained pulmonary hyperinflation.
01. Magnusson L, Zemgulis V, Wicky S et al. Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: an experimental study. Anesthesiology, 1997;87:1153-1163. [ Links ]
02. Gale GD, Teasdale SJ, Sanders DE et al. Pulmonary atelectasis and other respiratory complications after cardiopulmonary bypass and investigation of aetiological factors. Can Anaesth Soc J, 1979;26:15-21. [ Links ]
03. Emhardt JD, Moorthy SS, Brown JW et al. Chest radiograph changes after cardiopulmonary bypass in children. J Cardiovasc Surg (Torino), 1991;32:314-317. [ Links ]
04. Tenling A, Hachenberg T, Tyden H et al. Atelectasis and gas exchange after cardiac surgery. Anesthesiology, 1998;89:371-378. [ Links ]
05. Magnusson L, Zemgulis V, Tenling A et al. Use of a vital capacity maneuver to prevent atelectasis after cardiopulmonary bypass:an experimental study. Anesthesiology, 1998;88:134-142. [ Links ]
06. Hachenberg T, Brussel T, Roos N et al. Gas exchange impairment and pulmonary densities after cardiac surgery. Acta Anaesthesiol Scand, 1992;36:800-805. [ Links ]
07. Brismar B, Hedenstierna G, Lundquist H et al. Pulmonary densities during anesthesia with muscular relaxation: a proposal of atelectasis. Anesthesiology, 1985;62:422-428. [ Links ]
08. Wasowicz M, Sobczynski P, Drwila R et al. 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. [ Links ]
09. Griese M, Wilnhammer C, Jansen S et al. Cardiopulmonary bypass reduces pulmonary surfactant activity in infants. J Thorac Cardiovasc Surg, 1999;118:237-244. [ Links ]
10. Pelosi P, D'andrea L, Vitale G et al. Vertical gradient of regional lung inflation in adult respiratory distress syndrome. Am J Respir Crit Care Med, 1994;149:8-13. [ Links ]
11. Joyce CJ, Williams AB Kinetics of absorption atelectasis during anesthesia:a mathematical model. J Appl Physiol, 1999;86: 1116-1125. [ Links ]
12. Rothen HU, Sporre B, Engberg G et al. Re-expansion of atelectasis during general anaesthesia:a computed tomography study. Br J Anaesth, 1993;71:788-795. [ Links ]
13. Claxton BA, Morgan P, McKeague H et al. Alveolar recruitment strategy improves arterial oxygenation after cardiopulmonary bypass. Anaesthesia, 2003;58:111-116. [ Links ]
14. Rothen HU, Sporre B, Engberg G et al. Prevention of atelectasis during general anaesthesia. Lancet, 1995;345:1387-1391. [ Links ]
15. Anyanwu E, Dittrich H, Gieseking R et al. Ultrastructural changes in the human lung following cardiopulmonary bypass. Basic Res Cardiol, 1982;77:309-322. [ Links ]
16. Kirshbom PM, Jacobs MT, Tsui SS et al. Effects of cardiopulmonary bypass and circulatory arrest on endothelium-dependent vasodilation in the lung. J Thorac Cardiovasc Surg, 1996;111: 1248-1256. [ Links ]
17. 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. [ Links ]
18. Malbouisson LM, Busch CJ, Puybasset L et al. 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. [ Links ]
19. Froese AB, Bryan AC Effects of anesthesia and paralysis on diaphragmatic mechanics in man. Anesthesiology, 1974;41: 242-254. [ Links ]
20. Pinsky MR Recent advances in the clinical application of heart-lung interactions. Curr Opin Crit Care, 2002;8:26-31. [ Links ]
21. Teboul JL, Pinsky MR, Mercat A et al. Estimating cardiac filling pressure in mechanically ventilated patients with hyperinflation. Crit Care Med, 2000;28:3631-3636. [ Links ]
22. Michard F, Boussat S, Chemla D et al. 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. [ Links ]
23. Jellinek H, Krafft P, Fitzgerald RD et al. Right atrial pressure predicts hemodynamic response to apneic positive airway pressure. Crit Care Med, 2000;28:672-678. [ Links ]
24. Auler Jr JOC, Nozawa E, Toma EK et al. Manobra de recrutamento alveolar na reversão da hipoxemia no pós-operatório imediato em cirurgia cardíaca. Rev Bras Anestesiol, 2007;57: 476-488. [ Links ]
Dr. Luiz Marcelo Sá Malbouisson
Av. Dr. Enéas de Carvalho Aguiar, I Cerqueira César
05403-900 São Paulo, SP
Submitted em 9
de fevereiro de 2007
Accepted para publicação em 5 de dezembro de 2007
* Received from Instituto do Coração do Hospital da Clínicas da Faculdade de Medicina da Universidade de São Paulo (HC-FMUSP), São Paulo, SP