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. Failure to recognize that these traditional measurements are misleading can lead to under 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:

Preload and Cardiac output:
Elevated intra-abdominal pressure 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). Elevated ITP, in turn, impedes blood flow from the inferior vena cava to the thoracic cavity.[1, 2] Blood flow is further reduced by direct diaphragmatic compression of the IVC as it enters the thorax, and by venous compression and blood flow restriction within the abdominal cavity.[3] 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.[4, 5] The end result is a dramatic drop in preload with a resultant drop in cardiac output.[2, 6] These effects are especially pronounced in patients who are hypovolemic. Fortunately, these adverse effects are responsive to volume loading, 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) and pulmonary artery occlusion pressure (PAOP or wedge pressure). For further information of these measurements please see IAH and Hemodynamic Monitoring Errors.

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. 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 (See separate section on this topic for more details):
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.[2, 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.

Pulse pressure variation (PPV) and stroke volume variation (SVV) are also impacted by IAP.[16, 17] 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.  .  Again, understanding their flaws and knowledge of the patients IAP will assist in proper interpretation of these measurements. 

Summary:
Intra-abdominal hypertension and the resulting elevations in intra-thoracic pressure lead to substantial cardiovascular dysfunction. Most of these adverse effects will respond to fluid resuscitation, but these fluids will also lead to increased edema and may exacerbate intra-abdominal hypertension. Eventually, the only solution to the vicious cycle may be the need for decompressive laparotomy. In patients with limited cardiopulmonary reserve, early decompression should be considered. Traditional pressure based measurements of vascular volume status such as CVP and PCWP are erroneously elevated and do not reflect the patients volume status. Volumetric measurements such as RVEDVI and GEDVI should be used instead to determine the point when fluid resuscitation endpoints are met.

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