Critically ill patients who have their cardiopulmonary function optimized have reduced organ failure, reduced mortality and improved outcomes.[2-4] However, elevated intra-abdominal pressure substantially effects the cardiopulmonary system and may impact the clinicians ability to optimize function. Elevated intra-abdominal pressure causes diaphragm elevation with resulting reduction in intra-thoracic volume and increase in intrathoracic pressure. Simultaneously IAH causes vena-caval compression, pooling of blood in the pelvis and legs, restriction of flow into the chest and a dramatic drop in venous blood flow to the heart.[5-10] The end result is decreased stroke volume and cardiac output. This effect is especially pronounced in the hypovolemic patient, making hemodynamic monitoring particularly important in these patients to ensure they are not fluid under resuscitated. [7, 11]

In an attempt to optimize cardiopulmonary function, many critically ill patients undergo some form of hemodynamic monitoring. Central venous pressure (CVP) and pulmonary artery occlusion pressure (PAOP or wedge pressure) are two hemodynamic parameters commonly used to optimize care through their ability to assess fluid status, guide fluid resuscitation and to determine when to use vasopressors or diuretics. What is often not recognized is that these two hemodynamic measurements are dramatically effected by outside influences (mechanical ventilation and intra-abdominal pressure) that effect intra-thoracic pressure.[7, 9, 12-14] (See the attached figures, which graphically demonstrate the effect of elevated IAP on CVP and wedge measurements.) The result is a "false elevation" of CVP and PAOP that does not reflect actual volume status and may lead to fluid under-resuscitation. In actuality, patients with intra-abdominal hypertension will have elevated CVP and PAOP measurements despite substantial reductions in venous return to the heart and cardiac output.[13, 15-17] In many situations, patients suffering intra-abdominal hypertension will respond to fluid loading with increases in cardiac output and improvement in organ perfusion despite elevated CVP and PAOP.[13, 16]

In an attempt to improve the interpretation of CVP and PAOP data, Malbrain evaluated a number of formulas to correct for these erroneous elevations and concluded that a simple calculation will allow better estimates of transmural filling pressure.[18]

CVPcorrected = CVPmeasured - IAP/2

PAOPcorrected = PAOPmeasured - IAP/2

Optimizing cardiopulmonary function is important to improve critically ill patient outcomes. CVP and PAOP are parameters commonly used to guide therapy in critically ill patients. However, these two pressure measurements are erroneously elevated in the setting of intra-abdominal hypertension. Failure to recognize these erroneous elevations may lead to inappropriate treatment and increased morbidity and mortality. By monitoring IAP and correcting for its impact on CVP and PAOP, clinicians will be better able to optimize the cardiopulmonary status of their patients.

This figure from Citerio el al demonstrates the direct correlation between IAP and multiple other physiologic pressure measurements.[19] As demonstrated in the graph, IAP elevation leads to immediate (in seconds) and significant increases in ICP, IJP and CVP due to direct transmission of the IAP into the thorax and the central veins

For those clinicians who base fluid resuscitation and preload assessment on CVP (or on wedge pressures) this diagram graphically demonstrates that IAP causes a direct, non-fluid related increase in CVP - in effect a "false elevation" of the central venous pressure that has nothing to do with preload. Interpretation and use of CVP measurements without concomitant IAP data to correct for this false elevation may cause clinicians to misinterpret cardiac pressure data. It is not uncommon to see a very high CVP and PAOP (wedge) with poor cardiac index and suspect heart failure, when in fact these cardiac measurements are all a result of IAP elevation that has caused severe reduction in venous return to the heart with simultaneous elevations in intrathoracic pressure. In this setting, an echocardiogram of the heart will demonstrate an actively contracting left ventricle (i.e. not a failing heart) that simply cannot fill due to venous obstruction from the elevated IAP. Failure to recognize these IAP induced pathophysiologic changes may lead to treating the patient for heart failure rather than treating the cause of the problem - elevated intra-abdominal pressure.

Figure 2:

Figure: Effect of rising IAP on wedge pressure (PAOP) measurement and cardiac index As intra-abdominal pressure increases, there is a corresponding increase in intra-thoracis/pleural pressure and simultaneous increase in measured wedge pressure. However, despite an increasing wedge pressure, the cardiac index drops precipitously due to both reduced return of venous blood to the the heart and increased workload/reduced stroke volume due to the higher intra-thoracic pressure. (Diagram from Ridings, et al, Surg Forum 1994;45:74-76.)[1]

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