Effects of endotoxic shock on right ventricular systolic function and mechanical efficiency

Lambermont, Bernard; Ghuysen, Alexandre; Kolh, Philippe; Tchana‐Sato, Vincent; Segers, Patrick; Gérard, Paul; Morimont, Philippe; Magis, David; Dogné, Jean-Michel; Masereel, Bernard; D’Orio, Vincent

doi:10.1016/s0008-6363(03)00368-7

Cited by 60 publications

(55 citation statements)

References 30 publications

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“…For the pulmonary circulation, our results evidenced significant correlation between both methods, as well as between E a ‫ء‬ (PV) and RT/T, despite dramatic changes in pulmonary vascular compliance. Our laboratory previously showed a concordant evolution between E max /E a and stroke work in pulmonary embolism or septic shock (6,13,15). This could be explained by higher basal pulmonary vascular compliance compared with the values obtained on the systemic circuit.…”

Section: Discussionmentioning

confidence: 67%

See 1 more Smart Citation

Effective arterial elastance as an index of pulmonary vascular load

Morimont¹,

Lambermont²,

Ghuysen³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Morimont P, Lambermont B, Ghuysen A, Gerard P, Kolh P, Lancellotti P, Tchana-Sato V, Desaive T, D'Orio V. Effective arterial elastance as an index of pulmonary vascular load. Am J Physiol Heart Circ Physiol 294: H2736-H2742, 2008. First published April 18, 2008 doi:10.1152/ajpheart.00796.2007.-The aim of this study was to test whether the simple ratio of right ventricular (RV) endsystolic pressure (Pes) to stroke volume (SV), known as the effective arterial elastance (E a), provides a valid assessment of pulmonary arterial load in case of pulmonary embolism-or endotoxin-induced pulmonary hypertension. Ventricular pressure-volume (PV) data (obtained with conductance catheters) and invasive pulmonary arterial pressure and flow waveforms were simultaneously recorded in two groups of six pure Pietran pigs, submitted either to pulmonary embolism (group A) or endotoxic shock (group B). Measurements were obtained at baseline and each 30 min after injection of autologous blood clots (0.3 g/kg) in the superior vena cava in group A and after endotoxin infusion in group B. Two methods of calculation of pulmonary arterial load were compared. On one hand, Ea provided by using three-element windkessel model (WK) of the pulmonary arterial system [Ea(WK)] was referred to as standard computation. On the other hand, similar to the systemic circulation, Ea was assessed as the ratio of RV Pes to SV [Ea(PV) ϭ Pes/SV]. In both groups, although the correlation between Ea(PV) and Ea(WK) was excellent over a broad range of altered conditions, Ea(PV) systematically overestimated Ea(WK). This offset disappeared when left atrial pressure (Pla) was incorporated into Ea [Ea ‫ء‬ (PV) ϭ (Pes Ϫ Pla)/SV]. Thus Ea ‫ء‬ (PV), defined as the ratio of RV Pes minus Pla to SV, provides a convenient, useful, and simple method to assess the pulmonary arterial load and its impact on the RV function.hemodynamics; pulmonary hypertension; right ventricle; ventriculoarterial coupling IN CURRENT CLINICAL practice, pulmonary arterial load [or right ventricular (RV) afterload] is usually expressed as the mean pulmonary vascular resistance, computed as the ratio of the pressure drop through the pulmonary circulation [difference between mean pulmonary arterial pressure (PAP mean ) and left atrial pressure (Pla)] to the mean pulmonary blood flow [cardiac output (CO)]. Such an evaluation ignores the pulsatile nature of both pressure and flow. Although oscillatory components of the pulmonary arterial load are low, and mean resistance may be a valuable index of the pulmonary vascular load, the pulsatile nature of the load may be prominent in numerous pathological situations. Wave reflections play an important role and should be taken into account in pulmonary hypertension resulting from several pathological conditions, like pulmonary embolism and septic shock (1,2,5,14). In this way, the pulmonary arterial impedance spectrum, which is defined in the frequency domain, provides a more precise and complete description of the pulmonary vascular load (12, 17). However, be...

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Section: Discussionmentioning

confidence: 67%

“…Our laboratory previously showed that, in heart failure due to pulmonary embolism and sepsis, the decreased value of E max /E a was related to an impaired use of energy by the failing heart (6,13,15). In combination with E max , E a (PV) appears to be a simple way to characterize ventriculo-arterial interaction (18,26,27).…”

Section: Discussionmentioning

confidence: 99%

Effective arterial elastance as an index of pulmonary vascular load

Morimont¹,

Lambermont²,

Ghuysen³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…These 9 subjects were divided into two groups with 5 pigs induced with pulmonary embolism (Desaive et al (2005); Ghuysen et al (2008)). The remaining 4 are induced with septic shock, and treated with haemofiltration starting at two hours (Lambermont et al (2003)). Both studies were under the control of the ethics committee of the medical faculty of Liege, Belgium.…”

Section: Methodsmentioning

confidence: 99%

“…Thus, it provides a good set of data to watch to progression of the disease state. For details see (Desaive et al (2005); Ghuysen et al (2008);Lambermont et al (2003)). …”

Section: Methodsmentioning

confidence: 99%

Estimating afterload, systemic vascular resistance and pulmonary vascular resistance in an intensive care setting

Stevenson

Revie

Chase

et al. 2012

IFAC Proceedings Volumes

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Poor management and delayed diagnosis for both pulmonary embolism and septic shock are common and lead to increased cost, length of stay and mortality. Despite a wealth of information coming from commonly placed catheters much of this information remains unknown to an intensive care clinician. Data was gather from two porcine trials, 5 subjects induced with pulmonary embolism, and 5 with septic shock (treated with haemofiltration). Methods for real-time estimating afterload, systemic vascular resistance and pulmonary vascular resistance are presented. Knowledge of these parameters would greatly increase management of patients with pulmonary embolism and septic shock, and help the accuracy and speed of diagnosis. All estimations tracked trends very well. The estimating for afterload has a percentage error of 21.6% in pulmonary embolism and 11.8% in septic shock, systemic vascular resistance has a percentage error of 12.51% and 13.5% for pulmonary embolism and septic shock respectively while pulmonary vascular resistance showed percentage errors of 12.2% and 44.5%. From these estimations, the drop in systemic vascular resistance and afterload can be clearly identified in the septic shock cohort, as well as the recovery after haemofiltration was started, while the pulmonary embolism cohort showed the expected increase in pulmonary vascular resistance.

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“…19 Endotoxic shock-induced increase in PVR was associated with early preservation of RV-arterial coupling but deterioration as soon as 1 hour after the initial insult because of an unsustained adaptive increase in contractility. 21 Chronic aortopulmonary shunting as a model of persistent ductus arteriosus in growing piglets was associated with preserved RV-arterial coupling after 3 months, 24,37 but with uncoupling after 6 Note: E max : maximum right ventricular elastance; E a : pulmonary arterial elastance; PA: pulmonary artery; AP; aortopulmonary; RVF: right ventricular failure. months because of RV systolic function failure.…”

Section: Coupling Of Systolic Function To Afterloadmentioning

confidence: 99%

Biomechanics of the Right Ventricle in Health and Disease (2013 Grover Conference Series)

Naeije¹,

Brimioulle²,

Dewachter³

2014

Pulm. circ.

107

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Right ventricular (RV) function is a major determinant of the symptomatology and outcome in pulmonary hypertension. The normal RV is a thin-walled flow generator able to accommodate large changes in venous return but unable to maintain flow output in the presence of a brisk increase in pulmonary artery pressure. The RV chronically exposed to pulmonary hypertension undergoes hypertrophic changes and an increase in contractility, allowing for preserved flow output in response to peripheral demand. Failure of systolic function adaptation (homeometric adaptation, described by Anrep's law of the heart) results in increased dimensions (heterometric adaptation; Starling's law of the heart), with a negative effect on diastolic ventricular interactions, limitation of exercise capacity, and vascular congestion. Ventricular function is described by pressure-volume relationships. The gold standard of systolic function is maximum elastance (E max ), or the maximal value of the ratio of pressure to volume. This value is not immediately sensitive to changes in loading conditions. The gold standard of afterload is arterial elastance (E a ), defined by the ratio of pressure at E max to stroke volume. The optimal coupling of ventricular function to the arterial circulation occurs at an E max /E a ratio between 1.5 and 2. Patients with severe pulmonary hypertension present with an increased E max , a trend toward decreased E max /E a , and increased RV dimensions, along with progression of the pulmonary vascular disease, systemic factors, and left ventricular function. The molecular mechanisms of RV systolic failure are currently being investigated. It is important to refer biological findings to sound measurements of function. Surrogates for E max and E a are being developed through bedside imaging techniques.Keywords: right ventricle, pulmonary hypertension, preload, afterload, maximum elastance, end-systolic elastance, arterial elastance. One must inquire how increasing pulmonary vascular resistance results in impaired right ventricular function.-J. T. Reeves, 1989 1 In 1988, Jack Reeves and his colleagues noted that pulmonary hypertension is a common complication of cardiac and pulmonary diseases, that associated alterations in right ventricular (RV) function cause symptoms and limit survival, and that, paradoxically, research in this area had been relatively scarce. 1 Accordingly, they called for more studies to improve the understanding of RV failure in health and disease. Twenty-five years later, there has been significant progress, but our present knowledge remains incomplete, and calls for more research have been repeated. 2,3 The right ventricle (RV) in mammals and birds is a thin-walled flow generator, designed to accommodate the entire systemic venous return undergoing gas exchange in the pulmonary circulation, which is a separate high-flow, low-pressure system. 4 The pulmonary vascular pressures at rest and at mild levels of exercise are so low that a mean systemic filling pressure in the range of 10-15 m...

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Effects of endotoxic shock on right ventricular systolic function and mechanical efficiency

Cited by 60 publications

References 30 publications

Effective arterial elastance as an index of pulmonary vascular load

Effective arterial elastance as an index of pulmonary vascular load

Estimating afterload, systemic vascular resistance and pulmonary vascular resistance in an intensive care setting

Biomechanics of the Right Ventricle in Health and Disease (2013 Grover Conference Series)

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