Does femoral venous pressure measurement correlate well with intrabladder pressure measurement? A multicenter observational trial

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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.

Section: Use Of Transpulmonary Thermodilution In Iahmentioning

confidence: 96%

Section: Effect Of Intra-abdominal Hypertension On Preload Pathophysimentioning

confidence: 99%

What every ICU clinician needs to know about the cardiovascular effects caused by abdominal hypertension

Malbrain

Waele²,

Keulenaer³

2015

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“…Pressure in the abdominal veins increases linearly with rising IAP [46][47][48]. Abdominal perfusion pressure (APP) is calculated as mean arterial pressure (MAP) -IAP [9].…”

Section: The Effect Of Iah On Splanchnic Organ Perfusionmentioning

confidence: 99%

Abdominal pressure and gastrointestinal function: an inseparable couple?

Blaser¹,

Malbrain²,

Regli³

2017

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Evaluating the degree of organ dysfunction is a cornerstone in distinguishing patients with critical illness from those without. However, evaluation of the gastrointestinal function in critically ill patients is not unified, and is still largely based on subjective clinical evaluation. Although intra-abdominal pressure has been proposed as a parameter to facilitate monitoring of abdominal compartment in critical illness, the interactions between intra-abdominal pressure and gastrointestinal function are poorly clarified. The aim of this current review is to describe interactions and associations between gastrointestinal dysfunction and intra-abdominal pressure from a pathophysiological and clinical point of view.

“…The Spiegelberg continuous intra-gastric pressure monitor using an air-filled pouch to the tip also allows one to perform continuous monitoring [11,38,39]. Inferior vena cava pressures also indirectly reflect IAP and can be measured via trans-femoral cannulation [40]. Variations exist between pressures using different techniques.…”

Section: Panel C Intravesical Pressure Monitoringmentioning

confidence: 99%

A user’s guide to intra-abdominal pressure measurement

Sugrue

Waele²,

Keulenaer³

et al. 2015

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The intra-abdominal pressure (IAP) measurement is a key to diagnosing and managing critically ill medical and surgical patients. There are an increasing number of techniques that allow us to measure the IAP at the bedside. This paper reviews these techniques. IAP should be measured at end-expiration, with the patient in the supine position and ensuring that there is no abdominal muscle activity. The intravesicular IAP measurement is convenient and considered the gold standard. The level where the mid-axillary line crosses the iliac crest is the recommended zero reference for the transvesicular IAP measurement; moreover, marking this level on the patient increases reproducibility. Protocols for IAP measurement should be developed for each ICU based on the locally available tools and equipment. IAP measurement techniques are safe, reproducible and accurate and do not increase the risk of urinary tract infection. Continuous IAP measurement may offer benefits in specific situations in the future. In conclusion, the IAP measurement is a reliable and essential adjunct to the management of patients at risk of intra-abdominal hypertension.