Intra-abdominal pressure and associated hemodynamic monitoring errors
Critically ill patients who have their
cardiopulmonary function optimized have reduced organ failure,
reduced mortality and improved outcomes.[1-3]
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.[4-9]
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 not fluid under resuscitated. [6, 10]
Click here for an overview of the pathophysiologic changes seen with IAH / ACS
Static barometric variables of preload: CVP and Pulmonary Wedge (occlusion) pressures
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 presumed 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.[6, 8, 11-13] (See the figures below, 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.[12, 14-16] 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.[12, 15] However, once a critical threshold is passed – further fluid loading is detrimental in these patients – a phenomenon termed “futile crystalloid preloading.”[17, 18]
In attempt to improve the interpretation of CVP and PAOP data, Malbrain assessed many patients and found that approximately 50% of the IAP is transmitted across the diaphragm and onto the hemodynamic catheter. Using this data he evaluated a number of formulas to correct for these erroneous elevations and concluded that a simple calculation will allow the easiest estimates of transmural filling pressure.[19]
CVPcorrected = CVPmeasured – IAP/2
PAOPcorrected = PAOPmeasured – IAP/2
Basically, he recommends that you subtract half of
the IAP from your measured CVP or wedge pressure and use this
corrected number as your filling pressure. If it is low – then the
patient is probably fluid responsive. On the other hand, over
utilization of fluid will exacerbate the situation and make the
patients worse.[17, 18] Ennis utilized this concept in burn patients
to simplify their protocol for military field hospitals – once both
IAP and CVP were elevated – patients were no longer given IV fluids
regardless of urine output. Implementing this very simple approach
they have accomplished a substantial drop in onset of abdominal
compartment syndrome and in mortality (reduced from 36% to 18%) for
a slight increase in transient renal insufficiency.[20]
Dynamic variables of fluid responsiveness: Pulse pressure
variation (PPV), Stroke volume variation (SVV)
Pulse pressure variation (PPV), Stroke volume
variation (SVV) and systolic pressure variation (SPV) have not been
well studied in the setting of intraabdominal hypertension. The
existing data – all from animal studies, demonstrates that intraabdominal
hypertension limits the ability of these dynamic variables to
predict fluid responsiveness by altering chest wall compliance and
consequently pleural pressure swings for a given tidal volume.[21,
29]
The conclusions from what data is available is that SVV may not be
very
reliable for predicting fluid responsiveness in the face of
significant IAH, while PPV is still somewhat predictive but the
threshold for determining fluid responsiveness increases in both
instances from about
12% to 20% or more. The reason for this increase in threshold is felt to be
due to a decrease in chest wall compliance that occurs during IAH,
which then results in increased transmission of airway pressure to
the pleura and an increase in these dynamic variables of fluid
responsiveness for a given tidal volume.[21, 29, 30]
Passive leg raising has also come under question in terms of
its accuracy during IAH – because the vena cava is fairly compressed
from the pressure in the abdomen it is more difficult to get a fluid
infusion into the chest with simple leg raising.[22] Some suggest
full reverse Trendelenburg to achieve an effect but this is not well
investigated and risks VAP and ICP problems.
When
experts in the field are questioned about their utilization of SVV
and PPV parameters during care of the patient with IAH – rather than
relying on SVV for estimating fluid responsiveness, they recommend
using more aggressive passive leg raising or small incremental fluid
boluses followed by observation of individual beat to beat stroke
volumes. If stroke volumes rise in the face of these small fluid
challenges, then the patient is still fluid responsive and should be
further resuscitated.[23] As human data becomes available these
recommendations may or may not change.
Volumetric preload indices: Global end diastolic volume index
(GEDVI), right
ventricular end diastolic volume index (RVEDVI)
Volumetric estimates of preload status, such as right ventricular
end diastolic volume index (RVEDVI) or global end diastolic volume
index (GEDVI), are especially useful because of the changing
ventricular compliance and elevated ITP.[24-26] These parameters
have been noted to be very predictive of fluid responsiveness and
the preferred measurement if available in patients with significant
elevations in intra-abdominal pressure.[21, 24]
Summary:
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 and their use in these patients must be undertaken with knowledge of their flaws and adjustments in decision making. Functional dynamic monitoring parameters such and SVV and PPV also are impacted by elevated intra-abdominal pressure and can be non-predictive of fluid responsiveness. This does not mean they are useless, rather it means that the clinician must understanding their flaws in the face of elevated IAP (and must know the IAP) to properly interpret these measurements. Volume index catheters appear to provide the most reliable data regarding hemodynamics and fluid responsiveness and may be appropriate in the complex patient with elevated IAP. Echocardiography may also be very useful but data are lacking. 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.
Figures:
Figure 1: Impact of intraabdominal pressure increase on pressure transmitted across diaphragm, into chest and onto CVP catheter
This slide shows a cartoon and a real time pressure tracing that demonstrates the transmission of IAP across the diaphragm with resulting "false" elevation of measured vascular pressure on a hollow catheter placed within a thoracic vessel.
(Click here to enlarge diagram)
Figure 2: Effect of IAP elevation on CVP & ICP
This figure from Citerio el al demonstrates the direct correlation between IAP and multiple other physiologic pressure measurements.[27] 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.
(Click here to enlarge diagram)
Figure 3 : 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.)[28]
(Click here to enlarge diagram)
Figure 4: Effect of IAH on the predictive value of PPV, SVV and GEDV for fluid responsiveness
Receiver operating curves (ROC curves) demonstrating the influence of elevated IAP on the sensitivity and specificity of SVV, PPV and GEDV for predicting fluid responsiveness. Ideally a test will be 100% sensitive and specific which would place the curve peak in the upper left side of the graph. As can be noted on these graphs, the ROC curves are fairly good in the face of no elevated IAP, but once a pneumoperitoneum is introduced – leading to IAH – the predictability of fluid responsiveness with these tests is more limited.(Diagram from Renner, Crit Care Medicine 2009)
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