ACS OVERVIEW
» Overview
» Impact on Outcome
» Does monitoring and
   intervention improve
   outcome in IAH?
» IAH and Cardiac
» ACS and Pulmonary
» IAH and Renal
» IAH and Gut
» IAH and Brain
» IAH and Hemodynamic
   Monitoring Errors
» IAH and Pancreatitis
» IAH and Sepsis
» IAH and Burns
» IAH and Pediatrics
» IAH Interventions
» ACS and IAH Prevalence
» ACS and Multiple Organ
   Failure
» Volume of Infusion
» Abdominal Perfusion Pressure
» No such thing as an open abdomen
» Catheter Associated UTI
ACS Overview >>
Overview: 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.[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]

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 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


Dynamic variables of fluid responsiveness: Pulse pressure variation (PPV), Stroke volume variation (SVV) (See figure 3)

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.[19] The conclusions from what data is available is that SVV is not reliable for predicting fluid responsiveness in the face of significant IAH, while PPV is still predictive but the threshold for determining fluid responsiveness increases from about 10% to 20%. 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.[19] 

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 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.[20] 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.[21-23] 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.[19, 21]

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.  Again, understanding their flaws and knowledge of the patients IAP will assist in proper interpretation of 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.  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.

Figure 1: 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.[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]


IAP_SVV_ROC

Figure 3: Impact of elevated IAP (via pneumoperitoneum) on SVV, PPV, and GEDV - from Renner 2009 - Receiver operating curves showing the usefulness of PPV, SVV and GEDV for predicting fluid responsiveness in the face of norma IAP versus high IAP.  (The greater the area under the curve, the more meaningful and predictive the data). As can be seen on these ROC curves - as the IAP is elevated, SVV loses its ability to predict fluid responsiveness while PPV and GEDV retain their predictiveness - though PPV thresholds go up.

 

References
  1. Ridings, P.C., C. Blocher, and H. Sugerman, Cardiopulmonary effects of raised intra-abdominal pressure. Surg Forum, 1994. 45: p. 74-76.
  2. Boyd, O., R.M. Grounds, and E.D. Bennett, A randomized clinical trial of the effect of deliberate perioperative increase of oxygen delivery on mortality in high-risk surgical patients. Jama, 1993. 270(22): p. 2699-707.
  3. Wilson, J., et al., Reducing the risk of major elective surgery: randomised controlled trial of preoperative optimisation of oxygen delivery. Bmj, 1999. 318(7191): p. 1099-103.
  4. Rivers, E., et al., Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med, 2001. 345(19): p. 1368-77.
  5. Goodale, R.L., et al., Hemodynamic, respiratory, and metabolic effects of laparoscopic cholecystectomy. Am J Surg, 1993. 166(5): p. 533-7.
  6. Caldwell, C.B. and J.J. Ricotta, Changes in visceral blood flow with elevated intraabdominal pressure. J Surg Res, 1987. 43(1): p. 14-20.
  7. Kashtan, J., et al., Hemodynamic effect of increased abdominal pressure. J Surg Res, 1981. 30(3): p. 249-55.
  8. Richardson, J.D. and J.K. Trinkle, Hemodynamic and respiratory alterations with increased intra-abdominal pressure. J Surg Res, 1976. 20(5): p. 401-4.
  9. Diamant, M., J.L. Benumof, and L.J. Saidman, Hemodynamics of increased intra-abdominal pressure: Interaction with hypovolemia and halothane anesthesia. Anesthesiology, 1978. 48(1): p. 23-7.
  10. Barnes, G.E., et al., Cardiovascular responses to elevation of intra-abdominal hydrostatic pressure. Am J Physiol, 1985. 248(2 Pt 2): p. R208-13.
  11. Diebel, L.N., et al., Effect of increased intra-abdominal pressure on hepatic arterial, portal venous, and hepatic microcirculatory blood flow. J Trauma, 1992. 33(2): p. 279-82.
  12. Cheatham, M.L., et al., Right ventricular end-diastolic volume index as a predictor of preload status in patients on positive end-expiratory pressure. Crit Care Med, 1998. 26(11): p. 1801-6.
  13. Cheatham, M.L., et al., Preload assessment in patients with an open abdomen. J Trauma, 1999. 46(1): p. 16-22.
  14. Chang, M.C., et al., Effects of abdominal decompression on cardiopulmonary function and visceral perfusion in patients with intra-abdominal hypertension. J Trauma, 1998. 44(3): p. 440-5.
  15. Cullen, D.J., et al., Cardiovascular, pulmonary, and renal effects of massively increased intra-abdominal pressure in critically ill patients. Crit Care Med, 1989. 17(2): p. 118-21.
  16. Ridings, P.C., et al., Cardiopulmonary effects of raised intra-abdominal pressure before and after intravascular volume expansion. J Trauma, 1995. 39(6): p. 1071-5.
  17. Diebel, L.N., et al., End-diastolic volume. A better indicator of preload in the critically ill. Arch Surg, 1992. 127(7): p. 817-21; discussion 821-2.
  18. Malbrain, M., et al., Effect of intra-abdominal pressure on pleural and filling pressures. Intensive Care Med, 2003. 29: p. S73.

  19. Renner, J., et al., Influence of increased intra-abdominal pressure on fluid responsiveness predicted by pulse pressure variation and stroke volume variation in a porcine model*. Crit Care Med, 2009.

  20. Malbrain, M. and I. De laet, Functional hemodynamics and increased intra-abdominal pressure:same threholds for different conditions? Crit Care Med, 2009. 37: p. 781.

  21. Cheatham, M.L. and M.L. Malbrain, Cardiovascular implications of abdominal compartment syndrome. Acta Clin Belg Suppl, 2007(1): p. 98-112.

  22.  Malbrain, M.L. and I.E. De Iaet, Intra-abdominal hypertension: evolving concepts. Clin Chest Med, 2009. 30(1): p. 45-70, viii.

  23. Michard, F., S. Alaya, and V. Zarka, Global end-diastolic volume as an indicator of cardiac preload in patients with septic shock. Chest, 2003. 124: p. 1900-1908.

  24. Citerio, G., et al., Induced abdominal compartment syndrome increases intracranial pressure in neurotrauma patients: a prospective study. Crit Care Med, 2001. 29(7): p. 1466-71.