The effects of increased intra-abdominal pressure (IAP) on cardiovascular function are well recognized and include a combined negative effect on preload, afterload and contractility. The aim of this review is to summarize the current knowledge on this topic. The presence of intra-abdominal hypertension (IAH) erroneously increases barometric filling pressures like central venous (CVP) and pulmonary artery occlusion pressure (PAOP) (since these are zeroed against atmospheric pressure). Transmural filling pressures (calculated by subtracting the pleural pressure from the end-expiratory CVP value) may better reflect the true preload status but are difficult to obtain at the bedside. Alternatively, since pleural pressures are seldom measured, transmural CVP can also be estimated by subtracting half of the IAP from the end-expiratory CVP value, since abdominothoracic transmission is on average 50%. Volumetric preload indicators, such as global and right ventricular end-diastolic volumes or the left ventricular end-diastolic area, also correlate better with true preload. When using functional hemodynamic monitoring parameters like stroke volume variation (SVV) or pulse pressure variation (PPV) one must bear in mind that increased IAP will increase these values (via a concomitant increase in intrathoracic pressure). The passive leg raising test may be a false negative in IAH. Calculation of the abdominal perfusion pressure (as mean arterial pressure minus IAP) has been shown to be a better resuscitation endpoint than IAP alone. Finally, it is re-assuring that transpulmonary thermodilution techniques have been validated in the setting of IAH and abdominal compartment syndrome. In conclusion, the clinician must be aware of the different effects of IAH on cardiovascular function in order to assess the volume status accurately and to optimize hemodynamic performance.