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cardiovascular effects of elevated iap michael l. cheatham, md, facs, fccm director, surgical intensive care units orla

OBJECTIVES. To discuss the pathophysiologic impact of intrathoracic (ITP) and intra-abdominal (IAP) onPreloadContractilityAfterloadOxygen TransportTo consider the therapeutic interventions necessary to correct cardiac dysfunction. SETTING THE STAGE FOR IAH / ACS. Preload, contractility, afterload, and oxygen transport are commonly abnormal in the critically ill Subsequent development of sepsis, shock, or acute lung injury can further worsen cardiac functionInadequate resuscitation and fai224

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cardiovascular effects of elevated iap michael l. cheatham, md, facs, fccm director, surgical intensive care units orla

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    1. CARDIOVASCULAR EFFECTS OF ELEVATED IAP Michael L. Cheatham, MD, FACS, FCCM Director, Surgical Intensive Care Units Orlando Regional Medical Center Orlando, Florida, USA

    2. OBJECTIVES To discuss the pathophysiologic impact of intrathoracic (ITP) and intra-abdominal (IAP) on Preload Contractility Afterload Oxygen Transport To consider the therapeutic interventions necessary to correct cardiac dysfunction

    3. SETTING THE STAGE FOR IAH / ACS Preload, contractility, afterload, and oxygen transport are commonly abnormal in the critically ill Subsequent development of sepsis, shock, or acute lung injury can further worsen cardiac function Inadequate resuscitation and failure to restore cellular oxygen delivery leads to Ischemia Anaerobic metabolism Multiple organ dysfunction syndrome (MODS) Death

    4. SYSTEMIC EFFECTS OF IAH / ACS

    5. THE IMPACT OF ITP AND IAP Elevated ITP and IAP cause Cephalad deviation of the diaphragm Cardiac compression Pulmonary compression Can have marked effects on preload, contractility, afterload, and oxygen transport

    6. PRELOAD Adequate intravascular volume is essential Loss of intravascular volume may be either Absolute Hemorrhage Third-space fluid losses Relative Mechanical obstruction to blood flow Anatomic Pressure-induced Thrombosis

    7. PRELOAD Cephalad elevation of the diaphragm Induces narrowing of the inferior vena cava (IVC) Reduces blood return to the heart Elevated IAP Compresses the IVC Limits blood return from below the diaphragm Causes lower extremity and pelvic blood pooling Promotes both genital and lower extremity edema Places patient at risk for deep venous thrombosis Such changes may occur with an IAP of 10 mmHg

    8. PRELOAD Inadequate venous return decreases cardiac output (CO) through decreased stroke volume (SV) CO reduction is proportional to volume status Hypovolemic patients sustain CO reductions at lower levels of IAP than do normovolemic patients Hypervolemic patients demonstrate increased venous return in the presence of elevated IAP Volume resuscitation can to a point overcome both the anatomic and pressure-related restrictions to venous return restoring SV and CO

    9. PRELOAD ASSESSMENT IN IAH/ACS Cardiac preload is commonly assessed using central venous pressure (CVP) or pulmonary artery occlusion pressure (PAOP) Their use is based upon several assumptions: Intermittent measurements reflect a patient’s continuously changing hemodynamic state PAOP & CVP accurately reflect end-diastolic volume Ventricular compliance is unchanging

    10. THE PAOP ASSUMPTION

    11. TRANSMURAL FILLING PRESSURES Resuscitation to arbitrary, absolute PAOP or CVP values should be avoided Transmural pressures may be of greater accuracy PAOPtm = PAOPee - Ppl CVPtm = CVPee – Ppl Substituting IAP for Ppl may provide a rapid bedside estimate of transmural filling pressure

    12. IS THE PAC FLAWED OR ARE WE? Various studies have demonstrated that… 47% of physicians cannot derive basic hemodynamic information from a PAC 33% cannot identify a PAOP tracing 33% cannot describe how to increase a patient’s oxygen delivery Is it any surprise that prospective trials have failed to demonstrate a survival benefit with the use of this device?

    13. IS THE PAC REALLY FLAWED? Friese et al. Crit Care Med 2006; 34:1597-1601 Retrospective database analysis of 1,933/53,312 trauma patients managed with a PAC PAC use led to significantly decreased severity-adjusted mortality in patients with: ISS = 25 and base deficit > 11 Age > 61 years and base deficit > 6 PAC use improves survival in trauma patients with severe shock at the time of admission Suggests that early goal-directed resuscitation using a PAC has a survival benefit that may have been missed by previous smaller trials

    14. Mixed venous oximetry (SvO2) (1980’s) Assessment of oxygen transport balance Volumetric technology (1990’s) Assessment of right heart function Right ventricular ejection fraction (RVEF) Right ventricular end-diastolic volume (RVEDVI) A volumetric, as opposed to pressure-based, estimate of intravascular volume status Superior to PAOP & CVP in predicting preload recruitable increases in CO

    17. THE BENEFITS OF GOAL-DIRECTED RESUSCITATION USING A PAC

    18. ARE WE MISSING TOO MUCH? Significant physiologic changes may go undetected by conventional intermittent monitoring techniques A “snapshot” in time when a “moving picture” is what is needed

    19. CONTINUOUS THERMODILUTION Utilizes pulsed thermal energy technology Provides an updated hemodynamic assessment every 60 seconds Reduces measurement variability Automates CO measurement Averages respiratory cycle variation Standardizes injection technique Provides a constantly updated assessment of patient response to resuscitation leading to more efficient, goal-directed resuscitation

    20. CONTINUOUS THERMODILUTION Most invasive and labor-intensive of the monitoring technologies demanding a thorough understanding of PAC monitoring principles Provides a continuous assessment of Preload (RVEDVI) Contractility (CO, RVEF) Afterload (SVR, RVEF) Oxygen transport balance (SvO2) Improves patient resuscitation and outcome Appropriate for the most critically ill patients

    21. ARTERIAL PULSE CONTOUR ANALYSIS Estimation of SV from the arterial pressure waveform was first described almost 100 years ago CO is proportional to the area under the arterial pressure waveform Proposed as a less invasive alternative to the PAC Requires only an arterial pressure catheter and a central venous catheter (CVC)

    22. Accuracy is dependent upon arterial resistance, compliance, and impedance Initial calibration via iced saline thermodilution Recalibration every 8 hours Provides continuous assessment of Left ventricular SV and CO Global ejection fraction (GEF) Global end-diastolic volume (GEDV) Intrathoracic blood volume (ITBV) Extravascular lung water (EVLW) Stroke volume variation (SVV) ARTERIAL PULSE CONTOUR ANALYSIS

    23. A less invasive alternative to a PAC Provides continuous assessment of Preload (GEDVI, ITBVI, EVLW, SVV) Contractility (CO) Afterload (SVR) Multiple studies have demonstrated that CO correlates better with GEDVI and ITBVI than with PAOP in the presence of elevated ITP and IAP A minimally invasive option for continuous hemodynamic monitoring in IAH/ACS ARTERIAL PULSE CONTOUR ANALYSIS

    24. OPTIMAL RVEDVI / GEDVI Initial studies suggested an RVEDVI of 130-140 mL/m2 or GEDVI of 640-800 mL/m2 were optimal This oversimplifies what is actually a complex and dynamic relationship Ventricular function and compliance are constantly changing in the critically ill RVEF / GEF must be considered when determining the optimal volume for resuscitation End-diastolic volume ? 1 / Ejection Fraction

    25. FAMILIES OF STARLING CURVES

    26. CORRECTED TARGET VOLUMES

    27. CONTRACTILITY Diaphragmatic elevation and direct cardiac / pulmonary compression… Reduces biventricular preload Elevates pulmonary artery pressures Elevates pulmonary vascular resistance In response, the thin-walled right ventricle dilates The interventricular septum may bulge into the left ventricular chamber, impeding left ventricular function and decreasing cardiac output May result in systemic hypotension and worsening right coronary artery blood flow

    28. CONTRACTILITY At a time when right ventricular function is essential to maintaining CO Right ventricular ejection fraction decreases Right ventricular wall tension increases Myocardial oxygen demand increases Subendocardial ischemia may occur Right ventricular dysfunction can become severe resulting in left ventricular failure due to "ventricular interdependence"

    29. CONTRACTILITY Volume resuscitation and inotropic support will improve biventricular contractility at mild to moderate levels of IAH Restores preload Improves ventricular function Increases coronary perfusion pressure The cardiac dysfunction of severe IAH and ACS can only be reversed by decompressive laparotomy Delayed intervention may prove to be futile

    30. AFTERLOAD Generally increases to compensate for reduced venous return and falling SV Elevated ITP and IAP pathologically… Increases systemic vascular resistance through direct compressive effects on the aorta and systemic vasculature Increases pulmonary vascular resistance through compression of the pulmonary parenchyma

    31. AFTERLOAD Increased afterload is poorly tolerated by patients with… Inadequate intravascular volume Marginal cardiac contractility / prior dysfunction Acute lung injury requiring PEEP Preload augmentation appears to initially ameliorate the increased afterload Decompressive laparotomy is most effective for reducing vascular resistance to appropriate levels

    32. OXYGEN TRANSPORT Cellular delivery of oxygen is essential to avoiding multiple organ dysfunction Efficient oxygen delivery requires appropriate Preload Contractility Afterload Alveolar oxygenation Interventions aimed at reducing ITP and IAP are essential to improving oxygen delivery and transport balance

    33. WSACS RECOMMENDATIONS Avoid overresuscitation Fluid resuscitation volume should be carefully monitored to avoid over-resuscitation in patients at risk for IAH/ACS (Grade 1B) Hypertonic crystalloid and colloid-based resuscitation should be considered in patients with IAH to decrease the progression to secondary ACS (Grade 1C) Fluid resuscitation is a cornerstone of management Consider goal-directed hemodynamic monitoring

    34. RESUSCITATION ALGORITHM Each patient should be resuscitated to restore end-organ function and normalize markers of perfusion adequacy APP > 60 mmHg predicts survival from IAH / ACS Unnecessary over-resuscitation should be avoided May lead to secondary ACS, lung dysfunction PAOP and CVP may be used to guide resuscitation with the explicit understanding that transmural estimates of PAOP and CVP must be utilized

    35. CONCLUSIONS Cardiovascular dysfunction plays a major role in the organ dysfunction and failure that characterizes IAH/ACS Optimal cardiac function is essential to avoiding multiple organ dysfunction and improving outcome Preload, contractility, afterload, and oxygen transport balance are all interrelated Correction of one component frequently mandates treatment of all

    36. CONCLUSIONS Hemodynamic monitoring and goal-directed resuscitation are essential to improving patient outcome from IAH / ACS PAOP and CVP are commonly erroneous in IAH Reliance on such parameters may lead to under-resuscitation and inappropriate therapeutic interventions Volumetric preload estimates such as RVEDVI and GEDVI are superior to PAOP and CVP as predictors of preload-recruitable increases in cardiac output

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