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Maksuti, E., Carlsson, M., Arheden, H., Kovacs, S. J., Broome, M. & Ugander, M. (2017). Hydraulic forces contribute to left ventricular diastolic filling. Scientific Reports, 7, Article ID 43505.
Open this publication in new window or tab >>Hydraulic forces contribute to left ventricular diastolic filling
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2017 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 7, article id 43505Article in journal (Refereed) Published
Abstract [en]

Myocardial active relaxation and restoring forces are known determinants of left ventricular (LV) diastolic function. We hypothesize the existence of an additional mechanism involved in LV filling, namely, a hydraulic force contributing to the longitudinal motion of the atrioventricular (AV) plane. A prerequisite for the presence of a net hydraulic force during diastole is that the atrial short-axis area (ASA) is smaller than the ventricular short-axis area (VSA). We aimed (a) to illustrate this mechanism in an analogous physical model, (b) to measure the ASA and VSA throughout the cardiac cycle in healthy volunteers using cardiovascular magnetic resonance imaging, and (c) to calculate the magnitude of the hydraulic force. The physical model illustrated that the anatomical difference between ASA and VSA provides the basis for generating a hydraulic force during diastole. In volunteers, VSA was greater than ASA during 75-100% of diastole. The hydraulic force was estimated to be 10-60% of the peak driving force of LV filling (1-3 N vs 5-10 N). Hydraulic forces are a consequence of left heart anatomy and aid LV diastolic filling. These findings suggest that the relationship between ASA and VSA, and the associated hydraulic force, should be considered when characterizing diastolic function and dysfunction.

Place, publisher, year, edition, pages
Nature Publishing Group, 2017
National Category
Physiology
Identifiers
urn:nbn:se:kth:diva-205472 (URN)10.1038/srep43505 (DOI)000396283100001 ()28256604 (PubMedID)2-s2.0-85014668174 (Scopus ID)
Note

QC 20170511

Available from: 2017-05-11 Created: 2017-05-11 Last updated: 2018-01-13Bibliographically approved
Broomé, M. & Donker, D. W. (2016). Individualized real-time clinical decision support to monitor cardiac loading during venoarterial ECMO. Journal of Translational Medicine, 14(1)
Open this publication in new window or tab >>Individualized real-time clinical decision support to monitor cardiac loading during venoarterial ECMO
2016 (English)In: Journal of Translational Medicine, ISSN 1479-5876, E-ISSN 1479-5876, Vol. 14, no 1Article in journal (Refereed) Published
Abstract [en]

Veno-arterial extracoporeal membrane oxygenation (VA ECMO) is increasingly used for acute and refractory cardiogenic shock. Yet, in clinical practice, monitoring of cardiac loading conditions during VA ECMO can be cumbersome. To this end, we illustrate the validity and clinical applicability of a real-time cardiovascular computer simulation, which allows to integrate hemodynamics, cardiac dimensions and the corresponding degree of VA ECMO support and ventricular loading in individual patients over time.

Place, publisher, year, edition, pages
BioMed Central, 2016
National Category
Clinical Medicine
Identifiers
urn:nbn:se:kth:diva-180857 (URN)10.1186/s12967-015-0760-1 (DOI)000368057100001 ()2-s2.0-84953277113 (Scopus ID)
Note

QC 20160209

Available from: 2016-02-09 Created: 2016-01-25 Last updated: 2017-11-30Bibliographically approved
Maksuti, E., Bjällmark, A. & Broomé, M. (2015). Modelling the heart with the atrioventricular plane as a piston unit. Medical Engineering and Physics, 37(1), 87-92
Open this publication in new window or tab >>Modelling the heart with the atrioventricular plane as a piston unit
2015 (English)In: Medical Engineering and Physics, ISSN 1350-4533, E-ISSN 1873-4030, Vol. 37, no 1, p. 87-92Article in journal (Refereed) Published
Abstract [en]

Medical imaging and clinical studies have proven that the heart pumps by means of minor outer volume changes and back-and-forth longitudinal movements in the atrioventricular (AV) region. The magnitude of AV-plane displacement has also shown to be a reliable index for diagnosis of heart failure. Despite this, AV-plane displacement is usually omitted from cardiovascular modelling. We present a lumped-parameter cardiac model in which the heart is described as a displacement pump with the AV plane functioning as a piston unit (AV piston). This unit is constructed of different upper and lower areas analogous with the difference in the atrial and ventricular cross-sections. The model output reproduces normal physiology, with a left ventricular pressure in the range of 8-130 mmHg, an atrial pressure of approximatly 9 mmHg, and an arterial pressure change between 75 mmHg and 130 mmHg. In addition, the model reproduces the direction of the main systolic and diastolic movements of the AV piston with realistic velocity magnitude (similar to 10 cm/s). Moreover, changes in the simulated systolic ventricular-contraction force influence diastolic filling, emphasizing the coupling between cardiac systolic and diastolic functions. The agreement between the simulation and normal physiology highlights the importance of myocardial longitudinal movements and of atrioventricular interactions in cardiac pumping.

Keywords
Atrioventricular interaction, Cardiac function, Cardiac pumping, Longitudinal function, Cardiac model, Bond graphs
National Category
Biomedical Laboratory Science/Technology
Identifiers
urn:nbn:se:kth:diva-161634 (URN)10.1016/j.medengphy.2014.11.002 (DOI)000349585100011 ()25466260 (PubMedID)2-s2.0-84920913473 (Scopus ID)
Note

QC 20150324

Available from: 2015-03-24 Created: 2015-03-13 Last updated: 2017-12-04Bibliographically approved
Broomé, M., Frenckner, B., Broman, M. & Bjällmark, A. (2015). Recirculation during veno-venous extra-corporeal membrane oxygenation: a simulation study. International Journal of Artificial Organs, 38(1), 23-30
Open this publication in new window or tab >>Recirculation during veno-venous extra-corporeal membrane oxygenation: a simulation study
2015 (English)In: International Journal of Artificial Organs, ISSN 0391-3988, E-ISSN 1724-6040, Vol. 38, no 1, p. 23-30Article in journal (Refereed) Published
Abstract [en]

PURPOSE:

Veno-venous ECMO is indicated in reversible life-threatening respiratory failure without life-threatening circulatory failure. Recirculation of oxygenated blood in the ECMO circuit decreases efficiency of patient oxygen delivery but is difficult to measure. We seek to identify and quantify some of the factors responsible for recirculation in a simulation model and compare with clinical data.

METHODS:

A closed-loop real-time simulation model of the cardiovascular system has been developed. ECMO is simulated with a fixed flow pump 0 to 5 l/min with various cannulation sites - 1) right atrium to inferior vena cava, 2) inferior vena cava to right atrium, and 3) superior+inferior vena cava to right atrium. Simulations are compared to data from a retrospective cohort of 11 consecutive adult veno-venous ECMO patients in our department.

RESULTS:

Recirculation increases with increasing ECMO-flow, decreases with increasing cardiac output, and is highly dependent on choice of cannulation sites. A more peripheral drainage site decreases recirculation substantially.

CONCLUSIONS:

Simulations suggest that recirculation is a significant clinical problem in veno-venous ECMO in agreement with clinical data. Due to the difficulties in measuring recirculation and interpretation of the venous oxygen saturation in the ECMO drainage blood, flow settings and cannula positioning should rather be optimized with help of arterial oxygenation parameters. Simulation may be useful in quantification and understanding of recirculation in VV-ECMO.

National Category
Medical Image Processing Other Medical Engineering
Identifiers
urn:nbn:se:kth:diva-159647 (URN)10.5301/ijao.5000373 (DOI)000351285800005 ()25588762 (PubMedID)2-s2.0-84928177837 (Scopus ID)
Funder
Swedish Research Council, 2012-2800
Note

QC 20150213

Available from: 2015-02-06 Created: 2015-02-06 Last updated: 2017-12-05Bibliographically approved
Broomé, M., Maksuti, E., Bjällmark, A., Frenckner, B. & Janerot-Sjöberg, B. (2013). Closed-loop real-time simulation model of hemodynamics and oxygen transport in the cardiovascular system. Biomedical engineering online, 12(1), 69
Open this publication in new window or tab >>Closed-loop real-time simulation model of hemodynamics and oxygen transport in the cardiovascular system
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2013 (English)In: Biomedical engineering online, ISSN 1475-925X, E-ISSN 1475-925X, Vol. 12, no 1, p. 69-Article in journal (Refereed) Published
Abstract [en]

Background: Computer technology enables realistic simulation of cardiovascular physiology. The increasing number of clinical surgical and medical treatment options imposes a need for better understanding of patient-specific pathology and outcome prediction. Methods: A distributed lumped parameter real-time closed-loop model with 26 vascular segments, cardiac modelling with time-varying elastance functions and gradually opening and closing valves, the pericardium, intrathoracic pressure, the atrial and ventricular septum, various pathological states and including oxygen transport has been developed. Results: Model output is pressure, volume, flow and oxygen saturation from every cardiac and vascular compartment. The model produces relevant clinical output and validation of quantitative data in normal physiology and qualitative directions in simulation of pathological states show good agreement with published data. Conclusion: The results show that it is possible to build a clinically relevant real-time computer simulation model of the normal adult cardiovascular system. It is suggested that understanding qualitative interaction between physiological parameters in health and disease may be improved by using the model, although further model development and validation is needed for quantitative patient-specific outcome prediction.

Keywords
Cardiovascular simulation, Time-varying elastance functions, Lumped parameter model, Valve model, Oxygen transport model, Computer simulation
National Category
Medical Image Processing
Identifiers
urn:nbn:se:kth:diva-128495 (URN)10.1186/1475-925X-12-69 (DOI)000323346300001 ()2-s2.0-84882957482 (Scopus ID)
Funder
Swedish Research Council, 2012-2800
Note

QC 20130916

Available from: 2013-09-16 Created: 2013-09-12 Last updated: 2017-12-06Bibliographically approved
Broomé, M., Maksuti, E., Waldenström, A. & Bjällmark, A. (2013). Simulation of arterial hypertension and progressive arteriosclerosis with a 0-D multipurpose cardiovascular model. In: CMBE13: 3rd International Conference on Computational & Mathematical Biomedical Engineering. Paper presented at CMBE13 3rd International Conference on Computational & Mathematical Biomedical Engineering; City University of Hong Kong, HK SAR, China, 16–18 December, 2013 (pp. 433-436).
Open this publication in new window or tab >>Simulation of arterial hypertension and progressive arteriosclerosis with a 0-D multipurpose cardiovascular model
2013 (English)In: CMBE13: 3rd International Conference on Computational & Mathematical Biomedical Engineering, 2013, p. 433-436Conference paper, Published paper (Refereed)
Abstract [en]

The effects of systemic vascular resistance and progressive stiffening/arteriosclerosis inthe vascular tree on arterial blood pressure is explored in a 0D cardiovascular simulationmodel. Pulse pressure is both sensitive and specific for increases in stiffness and meanarterial pressure both sensitive and specific for changes in vascular resistance.

Series
CMBE Proceedings, ISSN 2227-3085
Keywords
0D vascular model, arterial hypertension, arteriosclerosis
National Category
Engineering and Technology
Identifiers
urn:nbn:se:kth:diva-138317 (URN)978-0-9562914-2-4 (ISBN)
Conference
CMBE13 3rd International Conference on Computational & Mathematical Biomedical Engineering; City University of Hong Kong, HK SAR, China, 16–18 December, 2013
Note

QC 20140328

Available from: 2013-12-18 Created: 2013-12-18 Last updated: 2014-03-28Bibliographically approved
Broome, M. (2012). Aplysia CorVascSim. Stockholm: Aplysia Medical AB
Open this publication in new window or tab >>Aplysia CorVascSim
2012 (English)Other (Other academic)
Place, publisher, year, pages
Stockholm: Aplysia Medical AB, 2012
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:kth:diva-58837 (URN)
Note

QC 20150218

Available from: 2012-01-10 Created: 2012-01-09 Last updated: 2015-02-18Bibliographically approved
Broome, M. (2011). MEDIQ CorVascSim. Stockholm: MEDIQ Abraxas AB
Open this publication in new window or tab >>MEDIQ CorVascSim
2011 (English)Other (Other academic)
Place, publisher, year, pages
Stockholm: MEDIQ Abraxas AB, 2011
National Category
Anesthesiology and Intensive Care Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:kth:diva-58838 (URN)
Note

QC 20150218

Available from: 2012-01-10 Created: 2012-01-09 Last updated: 2015-02-18Bibliographically approved
Larsson, M., Talving, P., Palmér, K., Frenckner, B., Riddez, L. & Broomé, M. (2010). Experimental extracorporeal membrane oxygenation reduces central venous pressure: an adjunct to control of venous hemorrhage?. Perfusion, 25(4), 217-223
Open this publication in new window or tab >>Experimental extracorporeal membrane oxygenation reduces central venous pressure: an adjunct to control of venous hemorrhage?
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2010 (English)In: Perfusion, ISSN 0267-6591, E-ISSN 1477-111X, Vol. 25, no 4, p. 217-223Article in journal (Refereed) Published
Abstract [en]

Background: Venoarterial ECMO has been utilized in trauma patients to improve oxygenation, particularly in the setting of pulmonary contusions and ARDS. We hypothesized that venoarterial ECMO could reduce the central venous pressure in the trauma scenario, thus, alleviating major venous hemorrhage. Methods: Ten swine were cannulated for venoarterial ECMO. Central venous pressure, mean arterial pressure, portal vein pressure and portal vein flow were recorded at three different flow rates in both a hemodynamic normal state and a setting of increased central venous pressure and right ventricular load, mimicking acute lung injury. Results: Venoarterial ECMO reduced the central venous pressure (CVP(sup)) from 9.4 +/- 0.8 to 7.3 +/- 0.7 mmHg (p < 0.01) and increased the mean arterial pressure from 103 +/- 8 to 119 +/- 10 mmHg (p < 0.01) in the normal hemodynamic state. In the state of increased right ventricular load, the CVP(sup) declined from 14.3 +/- 0.4 to 11.0 +/- 0.7mmHg (p < 0.01) and the mean arterial pressure (MAP) increased from 66 +/- 6 to 113 +/- 5 mmHg (p < 0.01). Conclusion: Venoarterial ECMO reduces systemic venous pressure while maintaining or improving systemic perfusion in both a normal circulatory state and in the setting of increased right ventricular load associated with acute lung injury. ECMO may be a useful tool in reducing blood loss during major venous hemorrhage in both trauma and selected elective surgery.

Keywords
ECMO, trauma; injury, hemorrhage, central venous pressure
National Category
Anesthesiology and Intensive Care
Identifiers
urn:nbn:se:kth:diva-58862 (URN)10.1177/0267659110375864 (DOI)000280750500006 ()20573652 (PubMedID)1477-111X (Electronic) 0267-6591 (Linking) (ISBN)
Note
QC 20120111Available from: 2012-01-10 Created: 2012-01-09 Last updated: 2017-12-08Bibliographically approved
Holzgraefe, B., Broome, M., Kalzen, H., Konrad, D., Palmer, K. & Frenckner, B. (2010). Extracorporeal membrane oxygenation for pandemic H1N1 2009 respiratory failure. Minerva Anestesiologica
Open this publication in new window or tab >>Extracorporeal membrane oxygenation for pandemic H1N1 2009 respiratory failure
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2010 (English)In: Minerva Anestesiologica, ISSN 0375-9393, E-ISSN 1827-1596Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Severe respiratory failure related to infection with the pandemic influenza A/H1N1 2009 virus is uncommon but possibly life-threatening. If, in spite of maximal conventional critical care, the patient's condition deteriorates, extracorporeal membrane oxygenation (ECMO) may be a life-saving procedure. METHODS: An observational study approved by the local ethics committee was carried out. Data from all patients treated with ECMO at the ECMO Center Karolinska for influenza A/H1N1 2009-related severe respiratory failure were analyzed. The main outcome measure was survival three months after discharge from our department. RESULTS: Between July 2009 and January 2010, 13 patients with H1N1 2009 respiratory failure were treated with ECMO. Twelve patients were cannulated for veno-venous ECMO at the referring hospital and transported to Stockholm. One patient was cannulated in our hospital for veno-arterial support. The median ratio of the arterial partial oxygen pressure to the fraction of inspired oxygen (P/F ratio: PaO2 /FiO2) before cannulation was 52.5 (interquartile range 38-60). Four patients were converted from veno-venous to veno-arterial ECMO because of right heart failure (three) or life-threatening cardiac arrhythmias (one). The median maximum oxygen consumption via ECMO was 251 ml/min (187-281 ml/min). Twelve patients were still alive three months after discharge; one patient died four days after discharge due to intracranial hemorrhage. CONCLUSION: Patients treated with veno-venous or veno-arterial ECMO for H1N1 2009-related respiratory failure may have a favorable outcome. Contributing factors may include the possibility of transport on ECMO, conversion from veno-venous (v-v) or veno-arterial (v-a) ECMO if necessary, high-flow ECMO to meet oxygen requirements and active surgery when needed.

Keywords
Adult, Analgesics/therapeutic use, Anoxia/therapy, Cohort Studies, Cross Infection/therapy, *Extracorporeal Membrane Oxygenation/adverse effects/instrumentation, Female, Humans, Hypnotics and Sedatives/therapeutic use, *Influenza A Virus, H1N1 Subtype, Influenza, Human/complications/*therapy/virology, Male, Middle Aged, Pandemics, Pregnancy, Respiration, Artificial, Respiratory Function Tests, Respiratory Insufficiency/etiology/*therapy/virology, Treatment Outcome
National Category
Anesthesiology and Intensive Care
Identifiers
urn:nbn:se:kth:diva-58863 (URN)21178913 (PubMedID)1827-1596 (Electronic) 0375-9393 (Linking) (ISBN)
Note
QC 20120116Available from: 2012-01-10 Created: 2012-01-09 Last updated: 2017-12-08Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-8987-9909

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