Cardiopulmonary Monitoring in Intra-abdominal Hypertension MANU L. N. G. MALBRAIN, M.D., PH.D.,* KOEN AMELOOT, M.D.,* CARL GILLEBERT, M.D.,* MICHAEL L. CHEATHAM, M.D.†
From the *Intensive Care Unit, Ziekenhuis Netwek Antwerpen (ZNA), Antwerpen, Belgium; and the †Surgical Intensive Care Units, Orlando Medical Center, Orlando, Florida Cardiopulmonary dysfunction and failure are commonly encountered in the patient with intraabdominal hypertension (IAH) or abdominal compartment syndrome. Accurate assessment and optimization of preload, contractility, and afterload in conjunction with appropriate goal-directed resuscitation and assessment of fluid responsiveness are essential to restore end-organ perfusion. In patients with IAH, the traditional ‘‘barometric’’ preload indicators such as pulmonary artery occlusion pressure and central venous pressure are erroneously increased. Volumetric monitoring techniques have been proven to be superior in directing the appropriate resuscitation together with targeted abdominal perfusion pressure. If such limitations are not recognized, misinterpretation of the patient’s cardiac status is likely, resulting in inappropriate and potentially detrimental therapy. IAH also markedly affects the mechanical properties of the chest wall and consequently also the respiratory function. Altered mechanical properties of the chest wall may limit ventilation, influence the work of breathing, affect the interaction between the respiratory muscles, hasten the development of respiratory failure, and interfere with gas exchange. Pulmonary monitoring is important to understand the relationships between intra-abdominal pressure and chest wall mechanics and the impact of IAH on ventilator-induced lung injury, lung distention, recruitment, and lung edema.
, , , and oxygen transport are often abnormal in the critically ill P patient with intra-abdominal hypertension (IAH) and/ RELOAD
CONTRACTILITY
AFTERLOAD
or abdominal compartment syndrome (ACS) as a result of hemorrhage, ‘‘third space’’ fluid losses, and direct cellular and organ injury (sepsis, burns, trauma). The organ dysfunctions that characterize IAH/ACS may be related to either direct compressive effects such as occur with intra-abdominal pressure (IAP)-induced pulmonary or renal failure or more commonly inadequate end-organ perfusion as a result of pressure-mediated decreases in cardiac preload, contractility, and afterload.1 This review focuses on practical issues related to monitoring of cardiac and pulmonary function.
movement of the diaphragm during IAH, the intrathoracic pressure (ITP) will increase. This leads to a reduction in end-diastolic volume. Second, cardiac preload decreases resulting from decreased venous return and the systemic afterload is increased as a result of direct compression of vascular beds. This leads to decreased cardiac output (CO) as summarized in Figure 1. The cardiovascular effects of IAH are aggravated by hypovolemia and the application of positive end-expiratory pressure (PEEP). Elevated IAP negatively impacts on preload, afterload, and contractility. Accurate assessment of optimization of preload, contractility, and afterload is essential to restore end-organ perfusion and function. How Does Intra-abdominal Hypertension Affect Preload?
Pathophysiology What Are the Cardiovascular Effects Associated with Intra-abdominal Hypertension?
IAH is associated with a number of multifactorial cardiovascular effects (Table 1).1 First, as a result of cranial Address correspondence and reprint requests to Manu L. N. G. Malbrain, M.D., Ph.D., Director, Intensive Care Unit, Ziekenhuis Netwek Antwerpen (ZNA), Campus Stuivenberg/St.-Erasmus, Lange Beeldekensstraat 267, B-2060 Antwerpen 6, Antwerpen, Belgium. E-mail:
[email protected].
Cephalad deviation of the diaphragm narrows the inferior vena cava as it passes through the diaphragm, further reducing venous return, and this may occur with an IAP as low as 10 mmHg. Reduced venous return has the immediate effect of decreasing CO through decreased stroke volume.2, 3 How Does Intra-abdominal Hypertension Affect Contractility?
Compression of the pulmonary parenchyma increases pulmonary artery pressure and pulmonary vascular
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TABLE 1. Cardiovascular Effects Related to Intra-abdominal Pressure* Diaphragm elevation and cardiac compression [ Pleural and intrathoracic pressure [ Difficult preload assessment Pulmonary artery occlusion pressure [ Central venous pressure [ Transmural filling pressure 4; Intrathoracic blood volume index 4; Global end-diastolic blood volume index 4; Right ventricular end-diastolic volume 4; Right, global, and left ventricular ejection fraction 4; Extravascular lung water 49 Stroke volume variation 9 Pulse pressure variation 9 Systolic pressure variation 9 Inferior vena caval flow Y Venous return Y Left ventricular compliance and contractility Y Downward Starling curve shift to the right Cardiac output Y Systemic vascular resistance [ Mean arterial pressure 9 4; Pulmonary artery pressure [ Pulmonary vascular resistance [ Heart rate 9 4 Lower extremity hydrostatic venous pressure [ Venous stasis, edema, ulcers [ Venous thrombosis [ Pulmonary embolismy [ Mixed venous oxygen saturation Y Central venous oxygen saturation Y False negative passive leg raising test [ Functional hemodynamic thresholds for fluid responsiveness [ * [ increased; Y decreased; 4 unchanged; 9 slightly increased; ; slightly decreased. y On decompression. Cardiovascular effects are exacerbated in case of hypovolemia, hemorrhage, ischemia, auto-PEEP, or high PEEP ventilation. PEEP, positive end-expiratory pressure.
resistance (PVR) while simultaneously reducing left ventricular preload. As right ventricular afterload increases, the right ventricle dilates with a decrease in right ventricular ejection fraction.4 Furthermore, the interventricular septum may bulge into the left ventricular chamber impeding left ventricular function with further decreases in cardiac output as a result of ‘‘ventricular interdependence.’’ This decrease in contractility results in a right- and downward shift of the Frank-Starling curve (Fig. 2). How Does Intra-abdominal Hypertension Affect Afterload?
Elevated ITP and IAP can cause increased systemic vascular resistance through direct compressive effects on the aorta and systemic vasculature and increased PVR through compression of the pulmonary parenchyma.1, 5 What Are the Pulmonary Effects Associated with Intra-abdominal Hypertension?
The interactions between the abdominal and thoracic compartments pose a specific challenge for clinicians.
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Both compartments are linked through the diaphragm and, on average, 50 per cent of the increase in IAP is transmitted to the thoracic compartment increasing ITP.6–8 As a result, both mechanical ventilation and application of PEEP (up to 15 cm H2O) will each raise IAP by 1 to 2 mmHg.9, 10 Patients with primary ACS will often develop secondary acute respiratory distress syndrome (ARDS) and require specialized ventilatory management. IAH causes an increase in alveolar pressures, dead space, and shunt fraction and a decrease in transpulmonary pressures, functional residual capacity, and dynamic and static compliance of the chest wall, resulting in hypoxemia and hypercapnia (Table 2).5 How Does Intra-abdominal Hypertension Affect Ventilator-Induced Lung Injury?
The distending force of the lung is the transpulmonary pressure (alveolar minus pleural pressure), which depends on the pressure applied to the airways and the ratio between lung and chest wall compliance. Ventilator-induced lung injury (VILI) is caused by the strain on lung structures. The transpulmonary pressure, recruitment maneuvers, and ‘‘safe’’ plateau pressures depend on chest wall compliance, pleural pressure, and IAP.5 Because IAH results in a lower transpulmonary pressure, one might expect a lower incidence of VILI. However, IAH results in poor alveolar recruitment and increased shear stress with opening and closing of alveoli, thus increasing the incidence of VILI. In primary ACS, distant organ failure and secondary ARDS are caused by circulating cytokines; increased levels of interleukin (IL)-6, IL-1b, and activated neutrophils have been demonstrated in bronchoalveolar lavage fluid during mechanical ventilation at an IAP of 20 mmHg after only 60 to 90 minutes.11 How Does Intra-abdominal Hypertension Affect Lung Distention?
An increase in IAP is the most common cause of decreased chest wall compliance in acute lung injury (ALI)/ ARDS. Compared with pulmonary ARDS, patients with extrapulmonary ARDS have decreased chest wall compliance and higher pleural pressures that both correlate with IAP.12 Measuring IAP provides an excellent method for estimating altered chest wall mechanics, because it will influence the shape of the pressure–volume (PV) curve of the total respiratory system, lung, and chest wall. The lower inflection point of the static PV curve in patients with secondary ARDS is mainly the result of the chest wall.13 Abdominal compression results in decreased static compliance and flattening and rightward shift of the inspiratory PV loop.5 The IAP level correlates with the lower inflection point of the PV curve in secondary ARDS as a result of IAH. More recently, it has
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FIG. 1. Cardiovascular effects of intraabdominal hypertension: APP, abdominal perfusion pressure; CO, cardiac output; CVP, central venous pressure; DVT, deep vein thrombosis; EDV, end-diastolic volume; IAP, intra-abdominal pressure; MAP, mean arterial pressure; PAOP, pulmonary artery occlusion pressure; PE, pulmonary embolism; Ptm transmural pressure.
injury resulted in a greater than twofold increase in pulmonary edema as measured by extravascular lung water (EVLW).13 Increased IAP also promotes lung neutrophil activation with increased pulmonary inflammatory infiltration and alveolar edema.16 How Does Intra-abdominal Hypertension Affect Lymphatic Drainage?
FIG. 2. Impact of intra-abdominal hypertension on the FrankStarling curve: intra-abdominal hypertension creates a right- and downward shift of the Frank-Starling curve so that for the same change in preload (DP), only a small change in stroke volume (DSV) can be observed.
Lymphatic fluid drainage from the lungs occurs either through the hilum, transpleurally or transabdominally. During IAH, the clearance of pulmonary edema through lymphatic pathways, pulmonary or pleural capillaries, is diminished as a result of raised ITP.17 Implications for Clinical Practice Why Are Intracardiac Filling Pressures Inaccurate during Intra-abdominal Hypertension?
been shown that the variance in transpulmonary pressure in ALI/ARDS is mainly the result of esophageal pressure (more than 54%) and thus linked to increases in IAP.14, 15 How Does Intra-abdominal Hypertension Affect Lung (de)recruitment?
Because IAP affects lung mechanics, the shape of the PV curve, and transpulmonary pressures, it will also affect alveolar recruitment and derecruitment. During IAH, higher opening pressures are needed to generate the same transpulmonary pressure for opening of the lung and higher PEEP levels are needed to prevent derecruitment. How Does Intra-abdominal Hypertension Affect Lung Edema Formation?
In a porcine model, it was found that the application of an IAP of 15 mmHg after oleic acid-induced lung
By the Frank-Starling principle, ventricular preload is defined as myocardial muscle fiber length at end-diastole (Fig. 3). Ideally, the appropriate clinical correlate would be left ventricular end-diastolic volume, but this physiological parameter cannot easily be measured. Pressurebased parameters such as left ventricular end-diastolic pressure, left atrial pressure, and pulmonary artery occlusion pressure (PAOP) have long been used clinically as surrogate estimates of intravascular volume. Although likely valid in normal healthy individuals, the multiple assumptions necessary to use PAOP and central venous pressure (CVP) as estimates of left and right ventricular preload status, respectively, are not necessarily true in the critically ill patient with IAH/ACS for a variety of reasons. First, ventricular compliance is constantly changing in the critically ill, resulting in a variable relationship between pressure and volume. As a result, changes in
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TABLE 2. Pulmonary Effects Related to Elevated Intra-abdominal Pressure Diaphragm elevation [ Intrathoracic pressure [ Pleural pressure [ Functional residual capacity Y All lung volumes Y Extrinsic compression lung parenchyma* [ Auto-PEEP [ Compression atelectasis [ Peak airway pressure [ Mean airway pressure [ Plateau airway pressure [ Pulmonary vascular resistance [ Alveolar barotrauma 4[ Alveolar volutrauma 4[ Dynamic compliance Y Static respiratory system compliance Y Static chest wall compliance YY Static lung compliance 4 Upper inflection point on pressure-volume curve Y Lower inflection point on pressure-volume curve [ Hypercarbia – PaCO2 retention [ PaO2 Y and PaO2/FiO2 Y Alveolar oxygen tension Y Oxygen transport Y Dead-space ventilation [ Intrapulmonary shunt [ Ventilation perfusion mismatch [ Ventilation diffusion mismatch [[ Oxygen consumption [ Metabolic cost and work of breathing [ Alveolar edema [ Extravascular lung water 49 Prolonged ventilation Difficult weaning Activated lung neutrophils [ Pulmonary inflammatory infiltration [ Pulmonary infection rate [ [ increased; Y decreased; 4 unchanged; 9 slightly increased; ; slightly decreased. PEEP, positive end-expiratory pressure.
intracardiac pressure no longer directly reflect changes in intravascular volume. The presence of IAH will decrease left ventricular compliance by rightward shift and flattening of the Frank-Starling curve (Fig. 2). Second, the elevated ITP associated with IAH has been demonstrated to increase PAOP and CVP measurements
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by an amount that is difficult to predict, further confounding their validity. This apparent deviation from Starling’s Law of the Heart is the result of the fact that both PAOP and CVP are measured relative to atmospheric pressure but are actually the sum of both intravascular pressure and intrapleural pressure. Third, mitral valve disease can confound the use of PAOP as an estimate of intravascular volume status. Patients with IAH-induced pulmonary hypertension or ALI demonstrate increased PVR and are at significant risk for mitral valve regurgitation. Fourth, accurate PAOP measurements are dependent on proper placement of the pulmonary artery catheter (PAC). Compression of the pulmonary parenchyma as a result of elevated IAP can markedly alter the normal progression of alveolar distention and pulmonary capillary pressures defined in West’s lung Zones I, II, and III. IAH-induced cardiac and pulmonary dysfunction can further alter the normal pulmonary artery waveforms making proper placement of the PAC tip in West’s lung Zone II difficult. Inadvertent placement of the tip in apical Zone I commonly results in PAOP measurements that more appropriately reflect alveolar pressure. The Surviving Sepsis Campaign guidelines target initial and ongoing resuscitation to a CVP of 8 to 12 mmHg and a mean arterial pressure (MAP) of 65 mmHg.18 As a result of the inaccuracy of CVP measurements in IAH/ ACS, these goals should be interpreted with caution to avoid unnecessary under resuscitation. Can We Use Transmural Cardiac Filling Pressures?
Recognizing the impact of elevated IAP and ITP on the validity of intracardiac filling pressure measurements, some authors have suggested calculating the transmural PAOP (PAOPtm) or CVP (CVPtm) in an attempt to improve the accuracy of PAOP and CVP as resuscitation end points. Assuming proper placement of a PAC and the absence of other confounding factors, PAOPtm may be calculated as end-expiratory PAOP (PAOPee) minus pleural pressure (Ppl) with CVPtm calculated as CVPee – Ppl. Ppl is typically determined by
FIG. 3. The PAOP assumption: why intracardiac filling pressures do not accurately estimate preload status: LVEDV, left ventricular end-diastolic volume; LVEDP, left ventricular end-diastolic pressure; LAP, left atrial pressure; PAOP, pulmonary artery occlusion pressure.
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measuring lower esophageal pressure using a balloon catheter. Other authors have advocated the practice of measuring PAOP during disconnection of the patient’s airway (the so-called ‘‘pop-off’’ PAOP) to minimize the effect of Ppl. Such a practice would not be valid in the patient with elevated IAP, however, because this does not reduce the contribution of IAP to the patient’s Ppl. Various studies have found that 20 to 80 per cent of IAP, or on average of 50 per cent, is transmitted to the thorax.6 As a rule of thumb, a quick estimate of transmural filling pressures can be obtained by subtracting half of the IAP from the end-expiratory filling pressure: CVPtm 4 CVPee – IAP/2 or PAOPtm 4 PAOPee – IAP/2 (Fig. 4).20 Is Volumetric Monitoring Better in Intra-abdominal Hypertension?
Using a volumetric PAC, the right ventricular ejection fraction (RVEF), reflecting the patient’s right ventricular contractility and afterload, is used to calculate the right ventricular end-diastolic volume index (RVEDVI) using the following equation: RVEDVI 4 stroke volume index (SVI)/RVEF. Independent of the effects of changing ventricular compliance and increased ITP or IAP, RVEDVI has been shown in multiple studies to be an accurate indicator of preload-recruitable increases in cardiac index (CI) in a variety of patient populations.1, 4 These studies have consistently identified a significant correlation between RVEDVI and CI and a lack of correlation between PAOP or CVP and CI during preload resuscitation. Arterial pulse contour analysis and transpulmonary thermodilution provide the calculation of several intravascular volume measurements, including global end-diastolic volume index (GEDVI) and EVLW as surrogate predictors of cardiac preload and capillary leak. It also allows the calculation of global ejection
FIG. 4. Calculation of the abdominothoracic index of transmission at the bedside: simultaneous CVP and IAP tracing before and during abdominal compression (e.g., by applying a abdominal Velcro belt). The abdominothoracic index of transmission (ATI) can be calculated as follows: the change in end-expiratory CVP (nCVPee 4 13.8 – 8.5 mmHg 4 5 mmHg) divided by the change in end-expiratory IAP (nIAPee 4 11 – 2 4 9 mmHg) and expressed as a percentage. The index of abdominothoracic transmission 4 nCVP/nIAP 4 5/9 (55.6%). CVP, central venous pressure; IAP, intra-abdominal pressure.
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fraction (GEF), an estimate of ventricular contractility using the following equation: GEF 4 (4*SVI)/GEDVI. Elevated ITP and IAP result in significant decreases in GEDVI despite paradoxical increases in measured PAOP and CVP. The value of RVEDVI and GEDVI over traditional intracardiac filling pressures is especially notable in patients with elevated ITP or IAP in which PAOP and CVP are at greatest risk for providing erroneous information regarding preload status. Because IAH significantly depletes intravascular volume and these changes in preload status are appropriately detected by volumetric preload measurements such as RVEDVI or GEDVI, these monitoring technologies are preferable to barometric preload measurements such as PAOP and CVP in patients with IAH/ACS.21 How Can We Further Improve Volumetric Indices in Intra-abdominal Hypertension?
IAH commonly results in cardiac dysfunction and decreased RVEF and GEF.22 As a result of this constantly changing ventricular compliance, there cannot be a single value of RVEDVI or GEDVI that can be considered the goal of resuscitation for all patients with IAH/ACS. Each patient must therefore be resuscitated to the end-diastolic volume that optimizes cardiac preload and systemic perfusion at that point in the patient’s critical illness (Fig. 5). Because this optimal volume will vary in response to the patient’s improving or deteriorating
FIG. 5. Ventricular function curves by GEF and RVEF: cardiac contractility in the critically ill can be described as a series of ‘‘ventricular function curves.’’ Each curve has an associated ejection fraction, describing the ventricle’s contractility, and an optimal enddiastolic volume, identifying the plateau of the ventricular function curve. Resuscitation to this plateau end-diastolic volume is widely believed to optimize a patient’s intravascular volume, cardiac function, and end-organ perfusion. As ventricular function changes, the patient ‘‘shifts’’ from one Frank-Starling curve to another with identification of both a new, optimal plateau end-diastolic volume as a resuscitation end point and a new ejection fraction. Therefore, the patient’s GEDVI and RVEDVI must be interpreted in conjunction with the patient’s GEF or RVEF. RVEDVI, right ventricular end-diastolic volume index; GEDVI, global end-diastolic volume index; RVEF, right ventricular ejection fraction; GEF, global ejection fraction.
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cardiac status, the true value of continuous hemodynamic monitoring becomes clear. Why Is Abdominal Perfusion Pressure Important?
A single threshold value of IAP cannot be globally applied to the decision-making of all critically ill patients. Assessment of abdominal perfusion as a resuscitation end point can overcome this problem.22 Analogous to the widely accepted and used concept of cerebral perfusion pressure, calculated as mean arterial pressure (MAP) minus ICP, abdominal perfusion pressure (APP), calculated as MAP minus IAP, has been proposed as a more accurate marker of critical illness and end point for resuscitation in patients with IAH. Target APP values may be achieved through a balance of judicious fluid resuscitation and application of vasoactive medications such as dopamine and norepinephrine. Maintaining an APP above 60 mmHg has been demonstrated to significantly improve patient survival from IAH/ACS.23 How Does Intra-abdominal Pressure Affect Fluid Responsiveness?
An increase in IAP will result in a concomitant increase in ITP and thus in stroke volume variation and pulse pressure variation (PPV). This means that we cannot use the same thresholds for different conditions.24 Where we normally use a cutoff of 10 to 12 per cent to define fluid responsiveness, we must use 20 to 25 per cent in patients with ACS. This threshold value depends on the patient’s tidal volume, PEEP level, increased ITP and consequent changes in pleural pressure
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and chest wall elastance, the presence of obesity, heart failure with changes in right and left ventricular preload and afterload, pulmonary hypertension, and degree of increased IAP. The resuscitative goals also differ in children or neonates. Can I Use the Passive Leg Raising Test in Intra-abdominal Hypertension to Assess Fluid Responsiveness?
Recent data show that approximately 25 per cent of critically ill patients with a PPV above 12 per cent are not fluid-responsive, suggesting different thresholds exist for different clinical conditions.25 Similar falsepositive PPV values have been related to right ventricular dysfunction, which is common during critical illness. The passive leg raising (PLR) test can similarly be false-negative related to increased IAP and diminished venous return from the legs and mesenteric veins. Care should be taken when a PLR test is performed and IAP measurement is needed to interpret the results of a PLR test. During IAH, one can expect an increase in baseline PPV, especially if the patient’s head of bed (HOB) is elevated (Fig. 6).9 Performing a PLR maneuver with the HOB elevated (the position of least risk for ventilator-associated pneumonia) will further increase IAP and will only result in a marginal venous return from the legs, but not from the mesenteric veins. Performing a PLR maneuver from the supine position will have a neutral effect on IAP and result in a better venous return from the legs, but not from the mesenteric veins. A PLR maneuver in the Trendelenburg position will have a beneficial effect on IAP and, depending on body anthropomorphism, may
FIG. 6. Schematic overview comparing the possible effects and (dis)advantages of different PLR tests during increased IAP: the passive leg raising (PLR) test can be performed from HOB (A) or supine (B) position or putting the patient in the Trendelenburg position (C). Endogenous fluid resuscitation comes from venous return from the legs (oblique arrow) and the mesenteric veins (horizontal arrow). The amount endogenous fluid resuscitation is indicated by the thickness of the arrow (dotted line is the smallest, whereas 3-mm line is the largest amount), a dotted line marked with an ‘‘X’’ indicates the absence of endogenous transfusion. HOB, head of bed; IAH, intra-abdominal hypertension; IAP, intra-abdominal pressure; ICP, intracranial pressure; PLR, passive leg raising; PPV, pulse pressure variation; VAP, ventilator-associated pneumonia: [ increase, [[ large increase, 9 small increase, ; small decrease, Y decrease, YY large decrease.
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result in a more pronounced venous return from the legs as well as from the mesenteric veins. How Can I Perform Alveolar Recruitment in My Patient with Intra-abdominal Hypertension?
During alveolar recruitment maneuvers in patients with IAH/ACS, higher opening pressures are needed as a result of the compression of the pulmonary parenchyma and decrease in transpulmonary pressures. An appropriate recruitment maneuver would consist of serially increasing recruitment pressures, up to a maximum of 40 + IAP/2 cm H2O, for 40 seconds guided by the patient’s response and improvement in oxygenation. What Is the Impact of Intra-abdominal Pressure on Acute Respiratory Distress Syndrome Definitions and Management?
The ARDS consensus definitions should take into account PEEP and IAP values. The PAOP criterion in the ARDS consensus definitions is inappropriate in the case of IAH as a result of the inaccuracy of PAOP measurements and must be adjusted upward because most patients with IAH and secondary ARDS will have a PAOP above 18 mmHg as a result of transmission of IAP to the intrathoracic compartment and intracardiac filling pressure measurements. During lung protective ventilation, the plateau pressure should be limited to transmural plateau pressures (Pplattm 4 Pplat – IAP/2) below 30 to 35 cmH2O What Is the Role of Neuromuscular Blockade in Intra-abdominal Hypertension/Abdominal Compartment Syndrome?
Neuromuscular blockade (NMB) can be very beneficial in reducing IAP and improving both cardiac and pulmonary function in the setting of IAH/ACS. The risks of NMB must be weighed against the potential benefits of improving abdominal wall compliance, improving atelectasis, decreasing ventilator pressures, improving patient-ventilator dyssynchrony, decreasing IAP, increasing APP, and improving end-organ perfusion and function.19 When used, NMB is typically necessary for only 24 to 48 hours, allowing time for the patient’s cardiopulmonary dysfunction to improve and IAP to decrease. Conclusions
Increased IAP has a tremendous impact on cardiopulmonary function. The presence of IAH reduces preload and contractility and increases afterload while it facilitates lung edema formation, alveolar derecruitment, and VILI. Close cardiopulmonary monitoring is
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needed and adequate treatment should be performed to restore cardiopulmonary function in critically ill patients with IAH/ACS. REFERENCES
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17. De Laet I, Malbrain ML. ICU management of the patient with intra-abdominal hypertension: what to do, when and to whom? Acta Clin Belg Suppl 2007;62:190–9. 18. Malbrain ML, Wilmer A. The polycompartment syndrome: towards an understanding of the interactions between different compartments! Intensive Care Med 2007;33:1869–72. 19. Malbrain ML, De Potter TJ, Dits H, Reuter DA. Global and right ventricular end-diastolic volumes correlate better with preload after correction for ejection fraction. Acta Anaesthesiol Scand 2010;54:622–31. 20. Cheatham ML, White MW, Sagraves SG, et al. Abdominal perfusion pressure: a superior parameter in the assessment of intraabdominal hypertension. J Trauma 2000;49:621–6. 21. Malbrain ML, de Laet I. Functional hemodynamics and increased intra-abdominal pressure: same thresholds for different conditions. . . ? Crit Care Med 2009;37:781–3.
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22. Mahjoub Y, Touzeau J, Airapetian N, et al. The passive legraising maneuver cannot accurately predict fluid responsiveness in patients with intra-abdominal hypertension. Crit Care Med 2010; 38:1824–9. 23. Malbrain ML, Reuter DA. Assessing fluid responsiveness with the passive leg raising maneuver in patients with increased intra-abdominal pressure: be aware that not all blood returns! Crit Care Med 2010;38:1912–5. 24. De Keulenaer BL, De Waele JJ, Powell B, Malbrain ML. What is normal intra-abdominal pressure and how is it affected by positioning, body mass and positive end-expiratory pressure? Intensive Care Med 2009;35:969–76. 25. Verzilli D, Constantin JM, Sebbane M, et al. Positive endexpiratory pressure affects the value of intra-abdominal pressure in acute lung injury/acute respiratory distress syndrome patients: a pilot study. Crit Care 2010;14:R137.
