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Massimo Bilotta
Barbara Impiombato
Francesco Pezzo
Pasquale Mastroroberto
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Attilio Renzulli
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Ann Thorac Surg 2006;82:35-43
© 2006 The Society of Thoracic Surgeons


Original article: Cardiovascular

Intraaortic Balloon Pumping During Cardioplegic Arrest Preserves Lung Function in Patients With Chronic Obstructive Pulmonary Disease

Francesco Onorati, MD * , Lucia Cristodoro, MD, Massimo Bilotta, MD, Barbara Impiombato, MD, Francesco Pezzo, MD, Pasquale Mastroroberto, MD, Antonio di Virgilio, MD, Attilio Renzulli, MD, PhD

Cardiac Surgery Unit, Magna Graecia University, Catanzaro, Italy

Accepted for publication February 17, 2006.


Abbreviations and Acronyms AMI = acute myocardial infarction; CABG = coronary artery bypass grafting; CI = cardiac index; COPD = chronic obstructive pulmonary disease; CPB = cardiopulmonary bypass; FEV1 = forced expiratory volume in 1 second; FEV1/FVC = forced expiratory volume in 1 second/forced expiratory vital capacity; IABP = intraaortic balloon pump; ITU = intensive therapy unit; MAP = mean arterial pressure; PCWP = pulmonary capillary wedge pressure; PVRI = pulmonary vascular resistance index; RSC = respiratory system compliance; SCR = scoring of chest radiographs; SVRI = systemic vascular resistance index; TnI = troponin I


* Address correspondence to Dr Onorati, Viale dei Pini, 28 80131 Napoli, Italy (Email: frankono{at}libero.it).

Presented at the Poster Session of the Forty-second Annual Meeting of The Society of Thoracic Surgeons, Chicago, IL, Jan 30–Feb 1, 2006.


    Abstract
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 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Requirements for...
 References
 
BACKGROUND: Linear flow during cardiopulmonary bypass is considered a potential mechanism of lung damage in patients with chronic obstructive pulmonary disease (COPD). We evaluated differences in lung function of patients with COPD undergoing preoperative intraaortic balloon pumping (IABP), between linear flow during cardiopulmonary bypass (IABP-off) and maintenance of pulsatile flow (IABP-on at automatic 80 bpm) during cardioplegic arrest.

METHODS: Fifty patients with COPD undergoing preoperative IABP were randomized between January 2004 and July 2005 to receive nonpulsatile cardiopulmonary bypass with IABP discontinued during cardioplegic arrest (25 patients; group A), or IABP-induced pulsatile cardiopulmonary bypass (25 patients; group B). Hospital outcome, need for noninvasive ventilation, oxygenation (partial pressure of oxygen, arterial to fraction of inspired oxygen [PaO 2/FIO 2]), respiratory system compliance, and scoring of chest radiographs were compared.

RESULTS: There were no hospital deaths, no IABP-related complications, and no differences in postoperative noninvasive ventilation (group A: 6 of 25, 24.0% vs group B: 5 of 25, 20%; p = not significant [NS]). One patient in both groups developed pneumonia (p = NS). Intensive care and hospital stay were comparable (p = NS). Group B showed lower intubation time (8.3 ± 5.1 hours versus group A: 13.2 ± 6.0; p = 0.001), better PaO 2/FIO 2 at aortic declamping (369.5 ± 93.7 mm Hg vs 225.7 ± 99.3; p = 0.001) at admission in intensive care (321.3 ± 96.9 vs 246.2 ± 109.7; p = 0.003), and at 24 hours (349.8 ± 100.4 vs 240.8 ± 77.3; p = 0.003). The respiratory system compliance was better in group B at the end of surgery (56.4 ± 8.2 mL/cm H2O vs 49.4 ± 7.0; p = 0.004) and 8 hours postoperatively (76.4 ± 8.2 vs 59.4 ± 7.0; p = 0.0001), as well as scoring of chest radiograph at intensive care admission (0.20 ± 0.41 vs 0.38 ± 0.56; p = 0.05) and on the first day (0.26 ± 0.45 vs 0.50 ± 0.67; p = 0.025).

CONCLUSIONS: Automatic 80 bpm IABP during cardioplegic arrest preserves lung function in patients with COPD.


    Introduction
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 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Requirements for...
 References
 
The use of cardiopulmonary bypass (CPB) during cardiac operations is associated with an unspecific inflammatory reaction that correlates with the occurrence of organ dysfunction and sometimes even serious organ failure [1, 2]. Pulmonary dysfunction is a frequent complication during the postoperative course of cardiac surgery using CPB [3–6]. The severity of such dysfunction varies from mild alterations in gas exchange, to various degrees of interstitial pulmonary edema with formation of excessive bronchial secretions, to the acute respiratory distress syndrome (ARDS) [3–5, 7, 8]. In consequence, up to 20% of patients undergoing operations with the use of CPB need prolonged ventilation for more than 48 hours postoperatively [7]. Moreover, clinically manifested ARDS is one of the most common causes of in-hospital deaths and early and late complications after cardiac surgery [1–8].

Although the mechanisms behind CPB-induced lung injury are complex (involving the inflammatory reaction caused by the contact of blood with foreign surfaces [5], the type of anesthesia and ventilation [5, 9], the switch from a pulsatile to a linear flow [10], and the induction of an ischemia-reperfusion state [5–8]), the observation that maintenance of a finite pulmonary artery blood flow during CPB attenuates the degree of the lung injury suggests that lung ischemia-reperfusion plays a significant role [11]. Moreover, it has to be kept in mind that during CPB the blood flow to the lungs is almost limited to the bronchial arteries, and it has been proven in some studies that bronchial artery blood circulation is substantially reduced during CPB [11, 12]. Several experimental models have shown that the decrease in bronchial artery blood flow during and after warm CPB is the main cause of the increased pulmonary vascular permeability with formation of tissue edema and cytokine production, and severe hypoxemia secondary to intrapulmonary shunt [11, 12], which is further associated with metabolic and ultrastructural changes of the lung tissue, anticipating the worsening of CPB-related lung ischemia [7, 12]. Although the nonpulsatile blood flow obtained with standard CPB circuits is considered an acceptable, nonphysiologic compromise with few disadvantages (including the induction of the systemic inflammatory response), the theoretical benefits of pulsatile blood flow include the reduction of vasoconstrictive reflexes, the optimization of oxygen consumption, and the reduction of tissue acidosis, secondary to the improvement of organ perfusion [10, 13–16]. Furthermore, we previously demonstrated [17] that IABP-induced pulsatile flow during aortic cross-clamp time better preserves splanchnic function in patients without multiorgan comorbidities.

Finally, it is well-known that already damaged lungs, because of preoperative chronic obstructive pulmonary disease (COPD), are at high risk for CPB-induced lung dysfunction, so that COPD still represents one of the most common indications to off-pump surgery [10, 18, 19]. In fact, patients with COPD have reduced pulmonary function reserve and any injury on their lungs could have a demonstrable clinical effect after CPB [19, 20].

Therefore, it was the aim of our study to test the hypothesis that the maintenance of pulsatile perfusion during aortic cross-clamp time (ACC), with the aid of intraaortic balloon pump (IABP), may attenuate CPB-related lung damage by improving blood flow through the bronchial arteries in the subset of patients at high risk for this complication, such as those with COPD.


    Material and Methods
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 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Requirements for...
 References
 
Patients and Study Design
Between January 2004 and July 2005, we prospectively enrolled 50 patients with COPD undergoing isolated primary CABG for severe left main stem disease. All patients considered at risk for preoperative ischemic events because of severe and diffuse coronary lesions (critical left main disease greater than 90%, or severe left main lesion greater than 70% with severe right coronary stenosis greater than 75% and unstable angina despite intravenous nitrates) underwent preoperative IABP insertion. The study protocol was approved by the Institution's Ethical Committee-Institutional Review Board (September 2003). Informed consent was obtained from each patient enrolled in the study.

The diagnosis of COPD was based on the Summit database definition: each patient required treatment for chronic pulmonary compromise or had a forced expiratory volume in 1 second (FEV1) less than 75% of predicted value or a forced expiratory volume in 1 second to forced expiratory vital capacity (FEV1/FVC) less than 0.7. Each patient underwent a spirometry test and was seen by a pneumonologist preoperatively [20].

On admission at our Institution, the patients were randomized by lottery, drawing preprepared sealed envelopes containing the group assignment. Twenty-five patients (group A) received a preoperative IABP treatment before induction of anesthesia, with IABP turned off during cardioplegic arrest, and restarted with a 1:1 IABP mode immediately after cross-clamp removal; the other 25 (group B) received standard preoperative treatment with IABP, which was switched to an automatic 80 bpm mode during cross-clamp time, and switched again to a 1:1 IABP mode after cross-clamp removal. In order to avoid misleading data, patients older than 75 years or with splanchnic organ comorbidities (renal or liver failure, abdominal aortic aneurysm, or severe autoimmune disease) were excluded from the study.

Anesthesia
All patients underwent Swan-Ganz catheter insertion through the right internal jugular vein for continuous hemodynamic monitoring before anesthetic induction. Postoperative chest roentgenogram confirmed its exact positioning.

Anesthetic technique was the same for all patients: induction of anesthesia consisted of intravenous propofol infusion at 3 mg/kg combined with fentanyl administration at 0.10 mg/kg. Neuromuscular blockade was achieved by 4 mg/hour pancuronium bromide, and lungs were ventilated to normocapnia with air and oxygen (45% to 50%). A positive end-expiratory pressure (PEEP) was set at 5 mm Hg. During CPB, ventilation was discontinued but the PEEP was maintained. Propofol infusion (150 to 200 µg/kg per minute) and isoflurane (0.5% inspired concentration) maintained anesthesia. Arterial and central venous catheters were the standard. Inotropes were started immediately after aortic cross-clamp removal to maintain adequate mean systemic pressure, always starting with enoximone at a dosage of 5 µg/kg per minute. The need for further increase in inotropes was recorded: inotropic support was defined as low-dose when enoximone was administered at a dosage lower than or equal to 5 µg/kg per minute; medium-dose when enoximone was employed at a dosage between 6 and 10 µg/kg per minute, or dobutamine was added at a dosage between 5 and 10 µg/kg per minute; or high-dose when enoximone or dobutamine infusion was greater than 10 µg/kg per minute or epinephrine was added at any dose.

Surgical Technique and Cardiopulmonary Bypass
It was institutional policy to insert IABP (8 Fr, 34 or 40 mL according to the body surface area; balloon connected to a Datascope pump [Datascope Corp, Fairfield, NJ]) percutaneously, through the best femoral artery, before induction of anesthesia, in order to better support the perioperative hemodynamic of patients undergoing surgery for severe left main stem disease. The correct placement of IABP was always assessed by postoperative chest roentgenogram or transesophageal echocardiography.

Patients received anticoagulation with enoxaparin, with a target activated partial thromboplastin time greater than 40 seconds, starting when the postoperative bleeding was controlled (usually within 6 hours). The IABP was withdrawn when hemodynamic stability was restored (ie, a cardiac index ≥ 2.0 L/m2 per minute with only minimal pharmacologic inotropic support, dobutamine, or enoximone at 5 µg/kg per minute). Cardiopulmonary bypass and surgical techniques were standardized and did not change during the study period.

Surgery was performed by the same senior surgeons (AR, PM, AdV) in all cases. In all patients CABG was performed through a median sternotomy. Cardiopulmonary bypass was conducted by the same perfusionist in all cases. Heparin was given at a dose of 300 IU/kg to achieve a target activated clotting time of 480 seconds or above. Blood recovery with an autotransfusion device (Autotrans Dideco, Mirandola, Modena, Italy) was performed intraoperatively in all cases. A level of hemoglobin lower than 8 g/dL suggested blood transfusion. A standard CPB circuit was used: a Dideco (Mirandola - Modena) tubing set, which included a 40 micron filter, a Stockert roller pump (Stockert Instrumente, Munich, Germany), and a hollow fiber membrane oxygenator (Monolyth, Sorin Biomedica, Saluggia, Italy). The extracorporeal circuit was primed with 1000 mL of Ringer's lactate solution and 40 mg of heparin. Systemic temperature was kept between 32°C and 34°C. Myocardial protection was always achieved with intermittent antegrade and retrograde hyperkalemic blood cardioplegia, as previously reported [21]. The CPB flow was maintained at 2.6 L · min–1 · m–2. In group A patients, IABP was turned off during cardioplegic arrest, maintaining a standard nonpulsatile CPB; group B patients underwent IABP-induced pulsatile CPB during cardioplegic arrest: pulsatile flow was maintained by an automatic 80 bpm mode until aortic declamping.

Endpoints
The primary endpoints were in-hospital mortality and morbidity, perioperative myocardial infarction, in-hospital and intensive therapy unit (ITU) stay, IABP-related complications, and investigation of lung function. In-hospital mortality was defined as any death occurring during hospital stay or in the first 30 postoperative days. Hospital morbidity was defined as any complication requiring specific therapy or causing a delay in hospital or ITU discharge. Perioperative acute myocardial infarction was defined by new Q waves of greater than 0.04 ms, and (or) a greater than 25% reduction in R waves in at least two leads on ECG, by new akinetic or dyskinetic segments at echocardiography, with a peak troponin I (TnI) greater than 3.7 µg/L or TnI concentration greater than 3.1 µg/L at 12 hours postoperatively, as previously reported [22]. The IABP-related complications were defined as any aortic dissection or perforation, limb or mesenteric ischemia, or infection or hemorrhage at the balloon entry point.

Blood samples were obtained from the peripheral systemic artery: the neutrophils were counted (Coulter counter SE-9000; Sysmex Corporation, Kobe, Japan), and the values corrected for the hematocrit values before the operation, at aortic declamping, at the end of surgery, and on the first and second postoperative days. At the same sampling time-points blood lactate concentration was measured on a commercial blood gas analyzer (GEM Premier 3000 analyzer, Lexington, MA). Determinations of blood concentration of cardiac TnI were conducted preoperatively before anesthetic induction and at 12, 24, 48, and 72 hours postoperatively. In order to evaluate the adequacy of myocardial protection techniques, TnI was measured on coronary sinus blood samples, obtained from the retrograde cardioplegic cannula, 10 minutes after completion of proximal anastomoses. The TnI assays were carried out using diagnostic kits provided by Beckman Coulter (Fullerton, California; AccuTnI Access Immunoassay System).

Lung Function
Lung function was investigated by the following (Table 1).


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Table 1. Lung Function
 
Intubation time
Defined as the time interval between orotracheal intubation and extubation of the awake patient.

Ratio of arterial oxygen tension to inspired oxygen fraction (PAO 2/FIO 2)
Arterial blood gas analysis was performed with the samples obtained from the peripheral systemic artery (GEM Premier 3000 analyzer, Lexington, MA), and the PaO 2/FIO 2 ratio was calculated preoperatively, at aortic declamping, at admission in ITU, and at 24 and 48 hours.

Respiratory system compliance (RSC)
Expressed in mL/cm H2O, the RSC was measured from the mechanical ventilator (Evita 4 Drager Medizintechnik GmbH; Lubeck, Germany) preoperatively, at the end of surgery, and at 4 and 8 hours postoperatively.

Scoring of chest radiographs (SCR)
Chest roentgenogram was performed preoperatively, at admission in ITU, and at 24 and 48 hours postoperatively. Scoring of chest radiographs was performed by a blinded radiologist according to the lung injury score, proposed by Murray and colleagues [23], ranging from 0 (no infiltrate) to 4 (extensive alveolar consolidation).

Need for noninvasive ventilation (NIV)
According to Ferrer and colleagues [24], we decided to start noninvasive positive-pressure ventilation if patients had at least one of the following parameters: respiratory acidosis (arterial pH ≤ 7.35 with partial pressure of carbon dioxide, arterial [PaCO 2] ≥ 45 mm Hg); arterial O2 saturation by pulse-oxymetry less than 90% or PaO 2 less than 60 mm Hg at inspired O2 fraction 0.5 or greater; respiratory frequency greater than 35 per minute; decreased consciousness, agitation, or diaphoresis; clinical signs suggestive of respiratory muscle fatigue, and increased work of breathing such as the use of respiratory accessory muscles, paradoxical motion of the abdomen, or retraction of the intercostal spaces.

Statistical Analysis
Statistical analysis was performed by the SPSS program for Windows, version 10.1 (SPSS Inc, Chicago, IL). Continuous variables are presented as mean ± SD, and categoric variables are presented as absolute numbers and (or) percentages. Data were checked for normality before statistical analysis.

Normally distributed continuous variables were compared using the unpaired t test, whereas the Mann-Whitney U test was used for those variables that were not normally distributed. Categoric variables were analyzed using either the {chi}2 test or the Fischer exact test. Comparison between and within groups was made using two-way analysis of variance for repeated measures. Comparisons were considered significant if p was less than 0.05.


    Results
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 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Requirements for...
 References
 
There were no differences in demographic data between the two study groups (Table 2). Similarly, intraoperative data were comparable (Table 3). Coronary sinus sampling demonstrated a similar leakage of TnI (group A: 0.70 ± 0.34 µg/L vs group B: 0.61 ± 0.48 µg/L; p = 0.095), showing a comparable myocardial protection during aortic cross-clamping. Similarly, perioperative hemodynamic data were comparable between the two groups (Table 4).


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Table 2. Patient Demographics and Characteristics
 

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Table 3. Intraoperative Data
 

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Table 4. Hemodynamic Data
 
There were no hospital deaths or perioperative myocardial infarctions in either group. Again, postoperative TnI course was similar between the two groups (Fig.1A).


Figure 1
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Fig 1. Troponin I (A), peripheral blood neutrophils (B), and peripheral blood lactate (C) measurements by group ({diamondsuit} = group A; {blacksquare} = group B) at different time points. (pa = statistical probability at each time point; pb = statistical probability within-group; pc = statistical probability between-group; ITU = intensive therapy unit.)

 
As far as inotropic support was concerned, all but 3 patients were withdrawn from low-dose enoximone on the third postoperative day: 2 patients in group A required medium doses of enoximone (7.5 µg/kg per minute), starting intraoperatively until the third and the fourth postoperative days, respectively; one patient in group B required medium doses of inotropes because of intraoperative association with low-dose intravenous (IV) dobutamine due to a cumbersome weaning from CPB.

Mean in-ITU stay (group A: 2.3 ± 0.5 days versus group B: 2.1 ± 0.9; p = 0.880) and mean postoperative hospital stay (group A: 7.5 ± 1.1 days versus group B: 6.9 ± 1.6; p = 0.176) were similar between the two groups. There were no major or minor IABP-related complications in either group.

There were six postoperative complications among the entire study period. One patient in group A (4%; p = 0.500) developed perioperative ileus requiring rehydration and IV fenoldopam; 1 patient in each group (4%; p = 0.755) experienced lung pneumonia requiring NIV and oral antibiotics; 2 patients (8%) in group A and 1 patient (4%; p = 0.500) in group B developed postoperative atrial fibrillation requiring IV amiodarone. However, all patients recovered during hospital stay and were discharged home in sinus rhythm and in healthy condition.

As far as lung function was considered we found the following.

Intubation time
Group B showed lower intubation time (8.3 ± 5 .1 hours versus group A: 13.2 ± 6.0; p = 0.001).

PAO 2/fIO 2 ratio
The PaO 2/FIO 2 ratio proved to be better in group B at aortic declamping, at admission in ITU, and at 24 hours (Table 1). It is noteworthy, the different behavior of the PaO 2/FIO 2 ratio in the two groups: patients undergoing standard CPB with linear flow during ACC demonstrated a gradual decrease of oxygenation during the entire surgical period, showing a gradual increase in the late postoperative time and reaching the pre-CPB values only on the second postoperative day. On the other side, the ratio demonstrated an early amelioration at aortic declamping in patients undergoing automatic IABP during ACC, and maintaining a better, or at least the same, value than that of the preoperative time during the entire postoperative course.

RSC
Respiratory system compliance worsened in both groups after CPB, with a slow but progressive improvement in the first few hours after surgery. Again, patients undergoing pulsatile CPB during ACC showed better values of RSC at the end of surgery, and a greater improvement either at 4 and 8 hours postoperatively (Table 1).

SCR
We registered a slight worsening of chest radiographs in both groups during the postoperative course; however, patients belonging to group B demonstrated better SCR compared with groupA, either at ITU admission or on the first postoperative day (Table 1).

Need for NIV
No differences were found in postoperative NIV (group A: 6 of 25, 24.0% vs group B: 5 of 25, 20%; p = NS).

As far as perioperative hemochrome was considered, neutrophils proved to be lower in group B at aortic declamping, at the end of surgery, and on the first postoperative day, as shown in Figure 1B. Finally, peripheral blood lactate proved to be lower in group B at the same time-points (Fig 1C).


    Comment
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 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Requirements for...
 References
 
Since the early days of cardiac surgery, it has been recognized that CPB is associated with systemic inflammation, and that occasionally this leads to major organ dysfunction [6]. In particular, pulmonary dysfunction after CPB was first described 40 years ago [25]. Many studies have focused on the pathophysiologic mechanisms of CPB-induced lung injury, involving the systemic inflammatory response through the contact of blood with the artificial surfaces of the bypass circuit [5], the type of anesthesia and artificial ventilation [5, 9], the switch from a physiologic pulsatile flow to an artificial linear flow [10], and the induction of an ischemia-reperfusion state of the lung [5–8]. In particular, during CPB both the heart and the lungs are excluded from the circulation: while the myocardium is generally protected by cardioplegia, no measures are taken to protect the lung [26]. Moreover, of the two circulatory systems of the lungs, the blood is limited to flowing to the lungs during CPB almost always through the bronchial arteries [7, 10, 26]. Finally, if under normal conditions the predominant function of the bronchial circulation is to nourish the nonalveolar lung tissues [27], when the pulmonary blood flow seizes bronchial blood flow may be expected to increase as a compensatory measure [28]. However, Schlensak and colleagues [26] demonstrated that although CPB reduced pulmonary artery blood flow, it did not increase the bronchial flow to the lungs, adding another mechanism of ischemic injury to the lungs. On the other side, Kuratani and colleagues [29] demonstrated that during partial CPB the lungs are perfused mainly by the bronchial arteries, and that the regional blood flow to the lungs decreased to 40% of the pre-bypass values. Moreover, there are some data showing that the maintenance of a finite pulmonary artery blood flow during CPB attenuates the degree of the lung injury, suggesting the critical role of an ischemia-reperfusion mechanism on the pathophysiology of postoperative pulmonary dysfunction [11].

Patients with COPD have an increased risk of organ-failure morbidity after cardiac surgery [30]. Bevelaqua and colleagues [31] demonstrated that although nonpulsatile CPB is used more extensively than pulsatile CPB, it causes a more pronounced pulmonary dysfunction in patients with preoperative COPD. Therefore, although the nonpulsatile blood flow obtained with standard CPB circuits is considered an acceptable nonphysiologic compromise with few disadvantages, first of all the induction of the inflammatory response, the theoretical benefits of pulsatile blood flow include the reduction of vasocontrictive reflexes, the optimization of oxygen consumption, and the reduction of acidosis, secondary to the improvement of organ perfusion [10, 13–16]. According to these findings, because of the avoidance of blood contact with foreign surfaces and the maintenance of a physiologic pulsatile perfusion, a recent study by Staton and colleagues [19] has shown off-pump surgery to achieve better gas exchange and earlier extubation than on-pump surgery in patients with COPD.

Therefore, it seems that a pulsatile perfusion and an augmentation of lung perfusion through the collateral bronchial arteries can ameliorate functional results in patients with COPD undergoing on-pump surgery. We hypothesized that this goal could be achieved with the aid of IABP, switching it to an automatic 80 bpm mode during aortic cross-clamping. In fact, it is common practice to discontinue IABP during cardioplegic arrest because of the loss of ECG signal, although switching it to an automatic mode a pulsatile flow could be achieved. We have evaluated this aspect of perioperative support with IABP.

When pulmonary outcome is considered, we found better functional results in patients belonging to group B, either in terms of intubation time, PaO 2/FIO 2 ratio, RSC, or SCR. It is noteworthy that differences were found to be significant at very early time-points, such as aortic declamping (PaO 2/FIO 2 ratio), at the end of surgery (RSC), at admission in ITU (PaO 2/FIO 2 ratio, SCR), during the first few postoperative hours (RSC), and on the first postoperative day (PaO 2/FIO 2 ratio, SCR). Our data correlated with those of Tarcan and colleagues [10], who found in patients with COPD undergoing pulsatile CPB (with the aid of a second roller pump integrated in the CPB circuit) shorter intubation time, lower pulmonary vascular resistance, and lower neutrophil count. Similarly, an increase in alveolar septal thickening, a decreased alveolar surface area, and a reduced capacity to oxygenate blood associated with a CPB-induced reduction of bronchial blood flow [26] have been demonstrated. Kuratani and colleagues [29] demonstrated that pulmonary dysfunction and the derangement of the ultrastructural lung tissue after CPB were less severe among the patients whose bronchial blood flow exceeded 25% of the systemic blood flow. Another experimental work by Serraf and colleagues [32] showed that a pulmonary blood flow of 35 mL/kg per minute obviated the lung injury. Although these studies failed to clarify the optimal flow rate of the bronchial arterial system during CPB, it is likely that more than normal bronchial blood flow is the prerequisite for protection of the lung during CPB [33]. According to this, it is well-known that one of the main goals achieved by IABP is the amelioration of organ perfusion by an augmentation of the blood flow [34]. Therefore, we can hypothesize that automatic IABP mode during ACC improves bronchial blood flow, furthermore maintaining somewhat pulsatile perfusion, reducing the ischemic-reperfusion mechanism of CPB-induced lung injury. According to a limited ischemic injury, we found lower lactate levels from aortic declamping to the first postoperative day in patients undergoing pulsatile perfusion during ACC. These data may correlate with the recent evidence of higher lung-tissue lactate production parallel to the reduction of bronchial blood flow during CPB [26]. Moreover, it has been demonstrated that the augmentation of bronchial flow improves the lung lymph flow, which clears excess of lung fluid, especially in cases of lung inflammatory response [35]. In this way we can interpret our findings of better RSC in patients belonging to group B.

Except for a shorter intubation time, we did not find significant differences in hospital outcome or in terms of major lung complications such as pneumonia and need for NIV. Similarly, we found comparable hospital stay and ITU stay between the two groups. It is possible that the short difference in the time course of linear versus pulsatile flow (ie, the duration of the aortic cross-clamp time, at present ranging from about 20 to 60 minutes) did not account for a significantly impaired organ perfusion in patients in whom IABP was turned off during cardioplegic arrest. It can be hypothesized that partial CPB (as in CABG) did not account for a severe impairment of bronchial perfusion, as in total CPB, in which it has been shown that bronchial blood flow decreased to 11% of the pre-bypass value [29]: this would indicate that partial CPB attenuates the degree of the ischemic-reperfusion lung injury, limiting therefore the incidence of major complications.

Finally, we found a significant lower neutrophil count in the peripheral blood of patients belonging to group B. Cardiopulmonary bypass-induced lung damage is mediated by neutrophil activation, which infiltrated the alveoli during the ischemia-reperfusion period [36], and can be easily detected in the bronchial lavage fluid after CPB [12]. Suzuki and colleagues [34] demonstrated that the neutrophil sequestration in the lung was less severe in patients undergoing pulmonary perfusion during CPB; similarly, Schlensak and colleagues [12] found a significant accumulation of neutrophils in bronchoalveolar lavage of piglets undergoing CPB, parallel to the reduction of the bronchial perfusion. Our data also confirm those of Tarcan and colleagues [10], who demonstrated a lower white cell count together with a higher percentage of neutrophils in the peripheral blood of COPD patients undergoing nonpulsatile CPB. It may be argued that an IABP-induced pulsatile perfusion during ACC, together with an improvement of blood flow through the bronchial arteries, may attenuate the neutrophil-related CPB-induced lung injury.

Limitations
The main limitation of the study is related to the small sample size of patients enrolled in the study.

This is a result of the single-center design of the study itself, which, on the other hand, guarantees uniformity of the perioperative management of the patient population throughout the experimentation. Moreover, on an intention-to-treat basis, we enrolled patients with the most similar risk profile, as patients with severe coronary lesions, without severe organ comorbidities other than COPD or extensive extracardiac atherosclerosis, which may mislead the results. Finally, patients were operated on by the same senior surgeons and underwent the same CPB, led by the same perfusionist, thus reducing the risk of human bias. However, the small sample size of the population remains, as well as the small incidence of some major complications (mortality, IABP-related complications, etc), which failed to demonstrate differences other than lung function in some of the established primary endpoints.

Conclusions
We conclude that although automatic 80 bpm IABP during cardioplegic arrest does not influence major clinical outcomes, it significantly preserves lung function in COPD patients undergoing CABG. These differences are already evident even for cross-clamp time lower than 60 minutes. Consequently, there is no reason, in COPD patients undergoing preoperative IABP support, to turn off the pump during cardioplegic arrest, but our data suggest that a switch to the automatic mode is ideal.


    Requirements for Recertification/Maintenance of Certification in 2006
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 Abstract
 Introduction
 Material and Methods
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 Comment
 Requirements for...
 References
 
Diplomates of the American Board of Thoracic Surgery who plan to participate in the Recertification/Maintenance of Certification process in 2006 must hold an active medical license and must hold clinical privileges in thoracic surgery. In addition, a valid certificate is an absolute requirement for entrance into the recertification/maintenance of certification process. if your certificate has expired, the only pathway for renewal of a certificate is to take and pass the Part I (written) and the Part II (oral) certifying examinations.

The American Board of Thoracic Surgery will no longer publish the names of individuals who have not recertified in the American Board of Medical Specialties directories. The Diplomate's name will be published upon successful completion of the recertification/maintenance of certification process.

The CME requirements are 70 Category I credits in either cardiothoracic surgery or general surgery earned during the 2 years prior to application. SESATS and SESAPS are the only self-instructional materials allowed for credit. Category II credits are not allowed. The Physicians Recognition Award for recertifying in general surgery is not allowed in fulfillment of the CME requirements. Interested individuals should refer to the Booklet of Information for a complete description of acceptable CME credits.

Diplomates should maintain a documented list of their major cases performed during the year prior to application for recertification. This practice review should consist of 1 year's consecutive major operative experiences. If more than 100 cases occur in 1 year, only 100 should be listed.

Candidates for recertification/maintenance of certification will be required to complete all sections of the SESATS self-assessment examination. It is not necessary for candidates to purchase SESATS individually because it will be sent to candidates after their application has been approved.

Diplomates may recertify the year their certificate expires, or if they wish to do so, they may recertify up to two years before it expires. However, the new certificate will be dated 10 years from the date of expiration of their original certificate or most recent recertification certificate. In other words, recertifying early does not alter the 10-year validation.

Recertification/maintenance of certification is also open to Diplomates with an unlimited certificate and will in no way affect the validity of their original certificate.

The deadline for submission of applications for the recertification/maintenance of certification process is May 10 each year. A brochure outlining the rules and requirements for recertification/maintenance of certification in thoracic surgery is available upon request from the American Board of Thoracic Surgery, 633 N St. Clair St, Suite 2320, Chicago, IL 60611; telephone: (312) 202-5900; fax: (312) 202-5960; e-mail: mailto:info{at}abts.org. This booklet is also published on the website: www.abts.org.


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