Intraabdominal hypertension and Cardiac Function
Intra abdominal hypertension adversely effects cardiac function primarily from pressure-mediated decreases in cardiac function. In addition, due to the pressure changes that develop in the abdominal and thoracic cavities, traditional measurements of fluid resuscitation status (central venous pressure - CVP and pulmonary artery occlusion pressure – PAOP or wedge pressure) can be misleading. Furthermore, dynamic indices such as stroke volume variation need to be adjusted due to the decrease in chest wall scompliance that occurs in patients with elevated IAP. Failure to recognize that these traditional measurements are misleading can lead to under or over resuscitation, persistent global ischemia and worse patient outcomes. The following paragraphs provide more detailed information into the impact of elevated intra-abdominal pressure on cardiac function.
Elevated intra-abdominal pressure - impact on cardiac
physiology:
Overview of fluid shifting:
The systemic inflammatory response of critical illness leads to massive cytokine release. These cytokines damage the capillary bed, leading to an acute capillary permeability syndrome – i.e. the capillaries leak. This capillary permeability causes intravascular fluid to leak out of the blood vessels and into the interstitial spaces – leading to hypovolemia. Clinicians response by administering IV fluid resuscitation in an effort to maintain tissue perfusion. Much of the administered IV fluid leaks out into the interstitial tissue as well. If one honestly considers where all this fluid accumulates, it is clear that after a few liters it cannot be in the compartments of the skull, thorax or muscle, leaving only the very large area of the abdomen and retroperitoneal space available to accumulate the majority of fluid administered to critically ill patients.
Preload impact:
As intravascular fluid leaks into the intersitial spaces of the bowel, mesentery and retroperitoneal spaces, the abdomen begins to swell and the abdominal wall starts to stretch. At some point the abdominal wall compliance it reached and any further sequestration of fluid leads to rapid increases in the pressure within the abdominal cavity. This has a profound impact on the vasculature – especially the venous structures of the abdomen. Once the abdominal pressure reaches levels seen in the vena cava (typically the CVP level – or less than 10-12 mm Hg) this large venous structure is compressed and blood flow is dramatically decreased through the vena cava. The result is a profound reduction in blood return to the heart (preload). In addition, the compression of the venous system within the abdominal cavity results in blood pooling in the pelvis and lower extremities further reducing venous return to the heart.[1, 2] Elevated intra-abdominal pressure also causes diaphragmatic elevation resulting in direct compression and reduction of volume within the thoracic cavity. This compression, in combination with positive pressure mechanical ventilation, leads to elevations in intra-thoracic pressure (ITP) and reduced chest wall compliance. Elevated ITP, in turn, impedes blood flow from both the inferior and superior vena cava to the thoracic cavity.[3, 4] Blood flow is further reduced by direct diaphragmatic compression of the IVC as it enters the thorax.[5] The end result is a dramatic drop in preload with a resultant drop in cardiac output.[4, 6] These effects are especially pronounced in patients who are hypovolemic. These adverse effects are initially responsive to volume loading – enough but not too much, making maintenance of adequate intravascular volume critical to maintaining cardiac output. However, the elevated pressures causing this cardiac compromise also results in misleading measurements of pressures traditionally used to determine adequacy of volume resuscitation - central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP or wedge pressure), Stroke volume variation (SVV) and pulse pressure variation (PPV). For further information of these measurements please see Hemodynamic Monitoring discussion below.
Cardiac contractility:
Compression of the lungs by the diaphragms combined with elevation of intra-thoracic pressure causes increases in pulmonary vascular resistance and reduction in vascular return to the left heart. The resulting pulmonary hypertension causes right ventricular dilation, leftward ventricular septal bulging, higher right ventricular wall tension and increased right ventricular work. The result is both higher right ventricular oxygen demand and lower left ventricular cardiac output leading to reduced coronary blood flow and possibly subendocardial ischemia – further reducing cardiac function in a vicious cycle.[7, 8]
Afterload:
Reduced cardiac output leads to increased systemic vascular resistance as the body attempts to maintain a stable blood pressure and cerebral perfusion. This leads to an increase in cardiac work while simultaneously leading to reduction of blood flow to the gut – which in turn causes further ischemia and capillary leakage, further increases in intra-abdominal pressure and further exacerbation of cardiac dysfunction.[9-11]
Hemodynamic Monitoring
(Click here to see more detailed section on this topic):
Traditional intra-cardiac filling pressures such as central venous pressure (CVP) and pulmonary artery wedge pressure (PCWP or PAOP) are directly impacted by the pressure within the thoracic cavity.[4, 12-15] Because intra-thoracic pressure is elevated in patients who are suffering from intra-abdominal hypertension and in patients on mechanical ventilation with positive end-expiratory pressure, these traditional pressure-based measurements tend to be erroneously elevated and are not reflective of intravascular volume status. In many situations, patients with elevated CVP and PCWP are still fluid under resuscitated and will response to fluid loading with increases in cardiac output and improvement in organ perfusion. At some point, however, a cycle of futile crystalloid preloading is entered and further fluid resuscitation is actually harmful.[16, 17]
Pulse pressure variation (PPV), stroke volume variation (SVV) and fluid responsiveness predicted by passive leg raising are also impacted by IAP.[18-20] Because elevations in IAP result in reduced thoracic wall compliance, there is increased variation in these parameters during ventilation resulting in less predictiveness of fluid responsiveness. Furthermore, the obstruction of the vena cave by high abdominal pressure makes passive leg raising less effective as a fluid bolus. Understanding these issues and interpreting SVV, PPV and PLR results with knowledge of simultaneous IAP levels will assist in proper interpretation of these measurements.
In contrast, right ventricular end-diastolic volume index (RVEDVI) and/or global end-diastolic volume index (GEDVI) – volumetric measurements rather than a pressure-based measurements – more accurately predict preload status and are a useful indicators of volume status. A number of studies have noted direct correlations with RVEDVI and patient outcome, noting that patients with higher RVEDVI (>110 to 133 mL/m2) had reduced incidence of MODS and lower mortality than those who had lower volumetric indices.[13, 21]
Summary:
Intra-abdominal hypertension and the resulting elevations in intra-thoracic pressure lead to substantial cardiovascular dysfunction. Most of these adverse effects will initially respond to fluid resuscitation, but these fluids will also lead to increased edema and may exacerbate intra-abdominal hypertension. Once IAH is present, further fluids may lead to worsening of the patients condition. Traditional pressure based measurements of vascular volume status such as CVP and PCWP are erroneously elevated and do not reflect the patients volume status. Newer cardiovascular indices such as SVV, PPV and PLR are also impacted by IAP. Utilizing intraabdominal pressure as another piece of the cardiovascular puzzle will assist clinicians in interpreting fluid status in these complex patients.
References:
1. 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.
2. MacDonnell, S.P., O.A. Lalude, and A.C. Davidson, The abdominal compartment syndrome: the physiological and clinical consequences of elevated intra-abdominal pressure. J Am Coll Surg, 1996. 183(4): p. 419-20.
3. 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.
4. Kashtan, J., et al., Hemodynamic effect of increased abdominal pressure. J Surg Res, 1981. 30(3): p. 249-55.
5. Schein, M., et al., The abdominal compartment syndrome: the physiological and clinical consequences of elevated intra-abdominal pressure. J Am Coll Surg, 1995. 180(6): p. 745-53.
6. Baxter, J.N. and P.J. O'Dwyer, Pathophysiology of laparoscopy. Br J Surg, 1995. 82(1): p. 1-2.
7. Eddy, A.C., C.L. Rice, and D.M. Anardi, Right ventricular dysfunction in multiple trauma victims. Am J Surg, 1988. 155(5): p. 712-5.
8. 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.
9. Luca, A., et al., Hemodynamic effects of acute changes in intra-abdominal pressure in patients with cirrhosis. Gastroenterology, 1993. 104(1): p. 222-7.
10. Bloomfield, G.L., et al., Elevated intra-abdominal pressure increases plasma renin activity and aldosterone levels. J Trauma, 1997. 42(6): p. 997-1004; discussion 1004-5.
11. 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.
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. 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.
15. 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.
16. Balogh, Z., et al., Patients with impending abdominal compartment syndrome do not respond to early volume loading. Am J Surg, 2003. 186(6): p. 602-7; discussion 607-8.
17. Balogh, Z., et al., Supranormal trauma resuscitation causes more cases of abdominal compartment syndrome. Arch Surg, 2003. 138(6): p. 637-43.
18. 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.
19. 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.
20. Mahjoub, Y., et al., The passive leg-raising maneuver cannot accurately predict fluid responsiveness in patients with intra-abdominal hypertension. Crit Care Med, 2010.
21. Chang, M.C. and J.W. Meredith, Cardiac preload, splanchnic perfusion, and their relationship during resuscitation in trauma patients. J Trauma, 1997. 42(4): p. 577-82; discussion 582-4.