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  • 1. Aneman, A.
    et al.
    Svensson, M.
    Broome, M.
    Karolinska Institutet.
    Biber, B.
    Petterson, A.
    Fandriks, L.
    Specific angiotensin II receptor blockage improves intestinal perfusion during graded hypovolemia in pigs2000Other (Refereed)
    Abstract [en]

    OBJECTIVE: To investigate the potential of specific angiotensin II subtype 1 (AT1) receptor blockade to modify the mesenteric hemodynamic response to acute hypovolemia and retransfusion. DESIGN: Prospective, randomized, controlled experimental study. SETTING: University-affiliated animal research laboratory. SUBJECTS: Fasted, anesthetized, ventilated, juvenile domestic pigs of both sexes. INTERVENTIONS: Acute, graded hypovolemia by 20% and 40% of the total estimated blood volume followed by retransfusion in control animals (CTRL; n = 10) and animals pretreated with the AT1 receptor blocker candesartan (CAND; n = 10). MEASUREMENTS AND MAIN RESULTS: Invasive monitoring of arterial and central venous blood pressures, cardiac output, portal venous blood flow, and jejunal mucosal blood flow. Blood gases were repeatedly analyzed to calculate oxygen delivery and consumption. Thirty minutes after each level of hypovolemia at 20% and 40%, cardiac output was decreased in CTRL animals from a baseline of 2.9 +/- 0.1 to 1.8 +/- 0.2 and 1.1 +/- 0.2 L/min, with no differences compared with CAND animals. Cardiac output was restored to 3.0 +/- 0.3 L/min 30 mins after retransfusion in CTRL animals, with no significant intergroup differences. Baseline portal venous blood flow (Q(MES)) and jejunal mucosal perfusion (PU(JEJ)) were greater in CAND animals compared with CTRL animals. During graded hypovolemia, CAND animals maintained Q(MES) and PU(JEJ) at significantly higher levels compared with CTRL animals, particularly after 40% hemorrhage (+221% and + 244%, respectively, relative to the mean values in CTRL animals). The same pattern was observed after retransfusion. Moreover, the calculated mesenteric critical oxygen delivery was significantly greater in CTRL animals (74 mL/min) compared with CAND animals (34 mL/min). No animals died in the CAND group, whereas four animals died during 40% hypovolemia or retransfusion in the CTRL group. CONCLUSIONS: Specific AT1 blockade before acute hypovolemia significantly ameliorated mesenteric and, in particular, jejunal mucosal hypoperfusion. In addition, cardiovascular stability was improved, and mortality in conjunction with acute hypovolemia and retransfusion could be completely avoided. These findings support a fundamental role of the renin-angiotensin system in the mesenteric response to acute hypovolemia and indicate a substantial interventional potential for candesartan in conjunction with circulatory stress.

  • 2.
    Broome, M.
    Umeå Universitet.
    Acute effects of Angiotensin II on myocardial performance2001Other (Refereed)
    Abstract [en]

    Background: Specific angiotensin II (Ang II) receptors exist in many organs including peripheral blood vessels, cardiac myocytes and the central nervous system. This suggests multiple sites of actions for Ang II throughout the cardiovascular system. Cardiac effects of Ang II are not completely understood, though its prominent vasoconstrictor actions are well described. This study was designed to assess left ventricular function during administration of Ang II using relatively load-independent methods in a whole-animal model. Methods: Ang II was infused in incremental doses (0-200 µg/h) in anaesthetised instrumented pigs (n=10). Cardiac systolic and diastolic function was evaluated by analysis of the left ventricular pressure-volume relationship. Results: Heart rate (HR), mean arterial pressure (MAP) and systemic vascular resistance (SVR) increased dose-dependently with Ang II, while cardiac output (CO) remained unchanged. Systolic function indices end-systolic elastance (Ees) and preload recruitable stroke work (PRSW) demonstrated dose-dependent increases. The diastolic function parameter tau (t) did not change with increasing Ang II dose. Conclusion: Ang II infusion caused increases in contractility indices in anaesthetised pigs in the doses used in this study. The mechanisms for these systolic function effects may be a direct myocardial effect or modulated through changes in autonomic nervous system activity.

  • 3.
    Broome, M.
    Karolinska Institutet.
    Exogenous Angiotensin II - An experimental study of integrated circulatory effects in heart, splanchnic organs and kidney2001Other (Refereed)
    Abstract [en]

    Aim: Exogenous Angiotensin II (Ang II) is currently used for treatment of hypotensive vasodilated shock, despite limited context-specific information about regional circulatory or cardiac responses. We aimed to experimentally investigate sites of action and mechanisms for the cardiovascular acute effects of Ang II infusion with emphasis on regional circulatory control and myocardial systolic and diastolic function. Methods: In healthy anaesthetised pigs, perivascular ultrasound flowmetry, laser-doppler flowmetry and tissue micro-oximetry were employed regionally (kidney and splanchnic organs), while cardiac function was evaluated by left ventricular pressurevolume loop analysis as derived from continuous intracardiac conductance volumetry and tip-manometry. Ang II was administered either systemically (i.v.) or in the left coronary artery in a continuous, dose-variable regimen. Regional perfusion pressures were artificially controlled either by pharmacological (nitroprusside) modulation of systemic arterial pressure or by local arterial graded occlusion (perivascular clamp). Cardiac afterload was controlled by pharmacological (nitroprusside) vasodilation. Results: Ang II exerted similarly powerful vasoconstrictions in the splanchnic and renal circulations. However, the splanchnic vascular bed differed in its responsiveness to Ang II in the sense that concomitant artificial maintenance of systemic normotension fully inhibited the increase in splanchnic vascular tone. Further, splanchnic vasoconstriction by Ang II was potentiated by increases in local arterial pressure. Heart rate and systolic function indices increased dose-dependently by systemic administration of Ang II, regardless of prevailing afterload conditions. Diastolic function was impaired or unchanged. On the other hand, these cardiac effects could not be reproduced when Ang II was administered via the intracoronary route. Conclusions: In the splanchnic vascular bed, the vascular responses of Ang II are powerfully modulated by local vasomotor control. Thus, during concurrent increases in systemic arterial pressure, autoregulatory myogenic increases in vascular smooth muscle tone serves to potentiate the local vasoconstrictive actions of Ang II. This implies that blood pressure alterations have an important role for the prediction of changes in splanchnic vascular resistance during Ang II treatment. Cardiac effects of Ang II include increases in contractile function, but seem to be predominantly mediated via extracardiac structures and mechanisms. This implies that the integrity of remote mechanisms for control of myocardial function are important for the cardiac effects of Ang II treatment. Keywords: Renin-Angiotensin System, Angiotensin II, Angiotensin Amide, Nitroprusside, Swine, Conductance volumetry (non-MESH), Cardiac function, Systolic function, Diastolic function, Vasoconstriction, Splanchnic Circulation, Renal Circulation

  • 4.
    Broome, M.
    Karolinska Institutet.
    MEDIQ Anaesthesia Simulator2003Other (Other academic)
  • 5.
    Broome, M.
    Karolinska Institutet.
    MEDIQ Kinetics2003Other (Other academic)
  • 6.
    Broome, M.
    Karolinska Institutet.
    Simulation of cardiovascular physiology and pathology: The effects of mitral regurgitation on venous pulmonary flow and mitral flow.2003Other (Refereed)
    Abstract [en]

    Background: The development of simulation models and modern computers makes it possible to simulate both normal cardiovascular physiology and pathology realistically. These models can be used to aid clinicians and researchers in understanding complex phenomenon. Methods: An electrical analogue of the cardiovascular system consisting of resistances, capacitances and inductances has been constructed. The contractile function of the cardiac atria and ventricles area represented by time-varying elastances. Valvular function, pericardial volume, ventricular interaction and intrathoracic pressure are also represented by constants and functions interacting with the rest of the model. Results: A regurgitant mitral orifice of 1 cm2 during systole results in an increased volume load on the left ventricle, a decrease in cardiac output and systemic arterial blood pressures accompanied by an increase in left and right-sided cardiac filling pressures and volumes. More specifically a systolic reversal of flow in the pulmonary veins is seen. Conclusion: Simulation of cardiac normal function and pathology is a meaningful way to study the heart. Results from simulations can be used to interpret clinical invasive monitoring and echocardiography data as well as experimental research data.

  • 7.
    Broome, M.
    et al.
    Karolinska Institutet.
    Aneman, A.
    Haney, M.
    Haggmark, S.
    Johansson, G.
    Biber, B.
    Angiotensin II mesenteric and renal vasoregulation: dissimilar modulatory effects with nitroprusside2000Other (Refereed)
    Abstract [en]

    BACKGROUND: The role of systemic arterial pressure for the vascular effects of angiotensin II (Ang II) and the interactions between Ang II and perfusion pressure-dependent local vascular control mechanisms are not well understood. This study addresses these aspects of exogenous Ang II in the mesenteric and renal regional circulations. METHODS: Ang II was infused in incremental doses (0-200 microg/h) in anesthetized instrumented pigs (n=10). Renal and portal blood flows were measured by perivascular ultrasound. In the second part of the study, sodium nitroprusside (SNP) was infused at doses titrated to keep mean arterial pressure constant, in spite of concurrent Ang II administration. RESULTS: Powerful dose-dependent vasoconstrictions by Ang II were found in renal and mesenteric vascular beds (at highest Ang II doses vascular resistances increased by 109% and 88% respectively). Ang II-induced vasoconstriction was fully inhibited in the mesenteric, but not in the renal circulation, during conditions of constant mean arterial pressures achieved by SNP infusion. CONCLUSIONS: Mesenteric, but not renal, vasoconstriction by Ang II was inhibited by pharmacological maintenance of perfusion pressure. This could reflect differences between these vascular beds as regards the importance of co-acting myogenic pressure-dependent vasoconstriction. Alternatively, as the drug chosen for pressure control, sodium nitroprusside, serves as a nitric oxide donor, the relative balance between nitric oxide-mediated vasodilation and Ang II-induced vasoconstriction could have regional differences.

  • 8.
    Broome, M.
    et al.
    Umeå Universitet.
    Aneman, A.
    Lehtipalo, S.
    Arnerlov, C.
    Johansson, G.
    Winso, O.
    Biber, B.
    Splanchnic vasoconstriction by angiotensin II is arterial pressure dependent2002Other (Refereed)
    Abstract [en]

    BACKGROUND: Our hypothesis was that splanchnic vasoconstriction by exogenous angiotensin II (Ang II) is significantly potentiated by local mechanisms increasing vasomotor tone and that splanchnic tissue oxygenation during administration of Ang II is perfusion pressure dependent. The aim was to study local splanchnic circulatory effects and tissue oxygenation during intravenous infusion of Ang II at different levels of regional arterial driving pressure in a whole-body large animal model. METHODS: Ang II was infused in incremental doses (0-200 microg x h-1) in anaesthetised instrumented pigs (n=8). Mean superior mesenteric arterial pressure (PSMA) was adjusted by a local variable perivascular occluder. Perivascular ultrasound and laser-Doppler flowmetry were used for measurements of mesenteric venous blood flow and superficial intestinal blood flow, respectively. Intestinal oxygenation was evaluated by oxygen tissue tension (PtiO2) and lactate fluxes. RESULTS: Ang II produced prominent and dose-dependent increases in mesenteric vascular resistance (RSMA) when the intestine was exposed to systemic arterial pressure, but Ang II increased RSMA only minimally when PSMA was artificially kept constant at a lower level (50 mmHg) by the occluder. Although Ang II decreased PtiO2 at a PSMA of 50 mmHg, splanchnic lactate production was not observed. CONCLUSION: We demonstrate that splanchnic vasoconstriction by exogenous Ang II is dependent on arterial driving pressure, suggesting significant potentiation through autoregulatory increases in vasomotor tone. Intestinal hypoxaemia does not seem to occur during short-term infusion of Ang II in doses that significantly increases systemic arterial pressure.

  • 9.
    Broome, M.
    et al.
    Umeå Universitet.
    Haney, M.
    Haggmark, S.
    Johansson, G.
    Aneman, A.
    Biber, B.
    Acute effects of angiotensin II on myocardial performance2001Other (Refereed)
    Abstract [en]

    BACKGROUND: Specific angiotensin II (Ang II) receptors exist in many organs including peripheral blood vessels, cardiac myocytes and the central nervous system. This suggests multiple sites of actions for Ang II throughout the cardiovascular system. Cardiac effects of Ang II are not completely understood, though its prominent vasoconstrictor actions are well described. This study was designed to assess left ventricular function during administration of Ang II using relatively load-independent methods in a whole-animal model. METHODS: Ang II was infused in incremental doses (0-200 microg x h(-1)) in anaesthetised instrumented pigs (n=10). Cardiac systolic and diastolic function were evaluated by analysis of the left ventricular pressure-volume relationship. RESULTS: Heart rate (HR), mean arterial pressure (MAP) and systemic vascular resistance (SVR) increased dose-dependently with Ang II, while cardiac output (CO) remained unchanged. Systolic function indices, end-systolic elastance (Ees) and preload recruitable stroke work (PRSW), demonstrated dose-dependent increases. The diastolic function parameter tau (tau) did not change with increasing Ang II dose. CONCLUSION: Ang II infusion caused increases in contractility indices in anaesthetised pigs in the doses used in this study. The mechanisms for these systolic function effects may be a direct myocardial effect or modulated through changes in autonomic nervous system activity.

  • 10.
    Broome, M.
    et al.
    Umeå Universitet.
    Haney, M.
    Osterlund, B.
    Haggmark, S.
    Johansson, G.
    Biber, B.
    The cardiac effects of intracoronary angiotensin II infusion2002Other (Refereed)
    Abstract [en]

    Angiotensin II (Ang II) is a potent vasoconstrictor, which recently has been shown to also have significant inotropic effects. Previous results regarding the mechanisms of the acute inotropic effects of Ang II are not conclusive. We designed this study to investigate the local cardiac effects of intracoronary Ang II infusion in doses not affecting systemic circulation. Ang II (2.5-40 microg/h) was infused in the left coronary artery of Yorkshire pigs (n = 9) reaching calculated intracoronary Ang II concentrations of 842 +/- 310, 3342 +/- 1238, and 12448 +/- 4393 pg/mL, respectively. Cardiac systolic and diastolic function was evaluated by analysis of the left ventricular pressure-volume relationship. Coronary flow was measured by using a coronary sinus catheter and the retrograde thermodilution technique. No significant changes were seen in the systolic and diastolic function variables of heart rate, end-systolic elastance, preload recruitable stroke work, the time constant for isovolumetric relaxation, or in coronary vascular resistance and flow. The positive inotropic and chronotropic effects of Ang II seen in previous studies seem thus to be mediated via extracardiac actions of Ang II. Coronary vascular tone is not affected by local Ang II infusion in anesthetized pigs. IMPLICATIONS: The positive inotropic and chronotropic effects of angiotension II (Ang II) seen in previous studies seem to be mediated via extracardiac actions of Ang II. Coronary vascular tone is not affected by local Ang II infusion in anesthetized pigs.

  • 11.
    Broome, M.
    et al.
    Karolinska Institutet.
    Hokfelt, T.
    Terenius, L.
    Peptide YY (PYY)-immunoreactive neurons in the lower brain stem and spinal cord of rat1985Other (Refereed)
  • 12.
    Broome, Michael
    KTH, School of Technology and Health (STH), Medical Engineering.
    Aplysia CorVascSim2012Other (Other academic)
  • 13.
    Broome, Michael
    Karolinska Institutet.
    MEDIQ CorVascSim2011Other (Other academic)
  • 14.
    Broome, Michael
    Karolinska Institutet.
    Simulation of Cardiovascular Physiology and Pathology: The Effects of Mitral Regurgitation on Mitral and Pulmonary Venous Flow2004Other (Other academic)
    Abstract [en]

    Background: The development of simulation models and modern computers makes it possible to simulate both normal cardiovascular physiology and pathology realistically. These models can be used to aid clinicians and researchers in understanding complex phenomenon. Methods: An electrical analogue of the cardiovascular system consisting of resistances, capacitances and inductances has been constructed. The contractile function of the cardiac atria and ventricles area represented by time-varying elastances. Valvular function, pericardial volume, ventricular interaction and intrathoracic pressure are also represented by constants and functions interacting with the rest of the model. Results: A regurgitant mitral orifice of 1 cm2 during systole results in an increased volume load on the left ventricle, a decrease in cardiac output and systemic arterial blood pressures accompanied by an increase in left and right-sided cardiac filling pressures and volumes. A systolic reversal of flow in the pulmonary veins is seen. The magnitude of systolic flow reversal in the pulmonary veins is dependent on left atrial compliance. Conclusion: Simulation of cardiac normal function and pathology is a meaningful way to study the heart. Results from simulations can be used to interpret clinical invasive monitoring and echocardiography data as well as experimental research data. Left atrial compliance may be of importance for interpretation of pulmonary venous flow profiles in mitral regurgitation.

  • 15.
    Broome, Michael
    Karolinska Institutet.
    Simulation of cardiovascular physiology and pathology with CorVascSim: A PC software for advanced education and research2004Other (Other academic)
    Abstract [en]

    Background and Goal: The rapid development of computer technology makes simulation of cardiovascular physiology and pathology possible. The current work presents a scientifically based cardiovascular model, with a self-explanatory interface. Material and Methods: An electrical analogue of the cardiovascular system including resistances, capacitances and inductances was constructed. The contractile function of the cardiac atria and ventricles are represented by time-varying elastances. Valvular function, pericardial volume, ventricular interaction and intrathoracic pressure are represented by constants and functions, which can interact. Pressures, flows and volumes are recalculated every millisecond and presented on-line as numerical and high-resolution graphics. Results and Discussion: The validity of the simulation models is based on the references (1-4). The software makes it possible to illustrate a great diversity of circulatory pathological findings including systolic and diastolic heart failure, valve diseases, pericardial effusion, arteriosclerosis and effects of changes in intrathoracic pressure. The model is being used to educate doctors and nurses in cardiac surgery, cardiac anaesthesia, and cardiology, but its pedagogical value remains to be validated. Conclusion: Simulation of cardiac physiology and pathology provides a new way to study the heart. Results from simulations can be used in education as well as in interpretation of clinical invasive monitoring, echocardiography and experimental research.

  • 16.
    Broome, Michael
    Karolinska Institutet.
    The Effects of Mitral Regurgitation on Venous Pulmonary Flow and Mitral Flow2004Other (Other academic)
  • 17.
    Broome, Michael
    et al.
    Karolinska Institutet.
    Palmer, K.
    Schersten, H.
    Frenckner, B.
    Nilsson, F.
    Prolonged extracorporeal membrane oxygenation and circulatory support as bridge to lung transplant2008In: Annals of Thoracic Surgery, ISSN 0003-4975, E-ISSN 1552-6259, Vol. 86, no 4, p. 1357-1360Article in journal (Refereed)
    Abstract [en]

    A 38-year-old man with progressive alveolitis secondary to polymyositis was treated for 52 days with venovenous and venoarterial extracorporeal membrane oxygenation as a bridge to bilateral lung transplantation. The patient survived, despite multiple complications, and is now back home with good pulmonary function. He is working part-time nearly 3 years post-transplant. This case shows that long-term extracorporeal lung assist is a viable but demanding alternative for bridging patients to pulmonary transplantation. This case also shows that right ventricular failure necessating conversion to veno-arterial assist does not necessarily predict right ventricular failure post-transplant.

  • 18.
    Broomé, Michael
    et al.
    KTH, School of Technology and Health (STH), Medical Engineering, Medical Imaging. Karolinska University Hospital and Karolinska Institutet, Sweden.
    Donker, D. W.
    Individualized real-time clinical decision support to monitor cardiac loading during venoarterial ECMO2016In: Journal of Translational Medicine, ISSN 1479-5876, E-ISSN 1479-5876, Vol. 14, no 1Article in journal (Refereed)
    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.

  • 19.
    Broomé, Michael
    et al.
    KTH, School of Technology and Health (STH), Medical Engineering, Medical Imaging.
    Frenckner, Björn
    Broman, Mikaeö
    Bjällmark, Anna
    KTH, School of Technology and Health (STH), Medical Engineering, Medical Imaging.
    Recirculation during veno-venous extra-corporeal membrane oxygenation: a simulation study2015In: International Journal of Artificial Organs, ISSN 0391-3988, E-ISSN 1724-6040, Vol. 38, no 1, p. 23-30Article in journal (Refereed)
    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.

  • 20.
    Broomé, Michael
    et al.
    Umeå Universitet.
    Haney, M.
    Häggmark, S.
    Johansson, G.
    Åneman, A.
    Biber, B.
    Pressure-independent cardiac effects of angiotensin II in pigs2004In: Acta Physiologica Scandinavica, ISSN 0001-6772, E-ISSN 1365-201X, Vol. 182, no 2, p. 111-119Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Angiotensin II (Ang II) is a potent vasoconstrictor with an important role in the development of cardiovascular disease. Earlier results have shown a positive acute inotropic effect of Ang II in anaesthetized pigs together with significant vasoconstriction. This investigation was designed to study cardiac effects of Ang II, when blood pressure was maintained constant by experimental means. METHODS: Ang II (200 microg h(-1)) was infused in anaesthetized pigs (n = 10) at two different arterial blood pressures, the first determined by the effects of Ang II alone, and the second maintained at baseline blood pressure with nitroprusside. Cardiac systolic and diastolic function was evaluated by analysis of left ventricular pressure-volume relationships. RESULTS: Heart rate, end-systolic elastance (Ees) and pre-load adjusted maximal power (PWRmax EDV(-2)) increased at both blood pressure levels, although less when blood pressure was kept constant with nitroprusside. The time constant for isovolumetric relaxation (tau(1/2)) was prolonged with Ang II alone and shortened with Ang II infused together with nitroprusside. CONCLUSION: Ang II infusion in the pig has inotropic and chronotropic properties independent of arterial blood pressure levels, although the effects seem to be blunted by pharmacological actions of the nitric oxide donor nitroprusside.

  • 21.
    Broomé, Michael
    et al.
    KTH, School of Technology and Health (STH), Medical Engineering, Medical Imaging.
    Maksuti, Elira
    KTH, School of Technology and Health (STH), Medical Engineering, Medical Imaging.
    Bjällmark, Anna
    KTH, School of Technology and Health (STH), Medical Engineering, Medical Imaging.
    Frenckner, Björn
    Janerot-Sjöberg, Birgitta
    KTH, School of Technology and Health (STH), Medical Engineering, Medical Imaging.
    Closed-loop real-time simulation model of hemodynamics and oxygen transport in the cardiovascular system2013In: Biomedical engineering online, ISSN 1475-925X, E-ISSN 1475-925X, Vol. 12, no 1, p. 69-Article in journal (Refereed)
    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.

  • 22. Broomé, Michael
    et al.
    Maksuti, Elira
    KTH, School of Technology and Health (STH), Medical Engineering, Medical Imaging.
    Waldenström, Anders
    Bjällmark, Anna
    KTH, School of Technology and Health (STH), Medical Engineering, Medical Imaging.
    Simulation of arterial hypertension and progressive arteriosclerosis with a 0-D multipurpose cardiovascular model2013In: CMBE13: 3rd International Conference on Computational & Mathematical Biomedical Engineering, 2013, p. 433-436Conference 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.

  • 23. Frenckner, B.
    et al.
    Broomé, Michael
    Karolinska Institutet.
    Lindström, M.
    Radell, P.
    Platelet-derived growth factor inhibition: a new treatment of pulmonary hypertension in congenital diaphragmatic hernia?2008In: Journal of Pediatric Surgery, ISSN 0022-3468, E-ISSN 1531-5037, Vol. 43, no 10, p. 1928-1931Article in journal (Refereed)
    Abstract [en]

    Increased pulmonary vascular resistance causing pulmonary artery hypertension is a major problem in the treatment of congenital diaphragmatic hernia with a strong association to mortality. We here report a patient with intractable pulmonary hypertension at 4 weeks of age unresponsive to conventional treatment. After administration of the platelet-derived growth factor (PDGF) receptor antagonist imatinib, pulmonary artery pressure gradually decreased to acceptable levels and the patient's clinical condition gradually improved.

  • 24. Holzgraefe, B.
    et al.
    Broome, Michael
    Karolinska Institutet.
    Kalzen, H.
    Konrad, D.
    Palmer, K.
    Frenckner, B.
    Extracorporeal membrane oxygenation for pandemic H1N1 2009 respiratory failure2010In: Minerva Anestesiologica, ISSN 0375-9393, E-ISSN 1827-1596Article in journal (Refereed)
    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.

  • 25. Larsson, M.
    et al.
    Talving, P.
    Palmér, K.
    Frenckner, B.
    Riddez, L.
    Broomé, Michael
    Karolinska Institutet.
    Experimental extracorporeal membrane oxygenation reduces central venous pressure: an adjunct to control of venous hemorrhage?2010In: Perfusion, ISSN 0267-6591, E-ISSN 1477-111X, Vol. 25, no 4, p. 217-223Article in journal (Refereed)
    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.

  • 26.
    Maksuti, Elira
    et al.
    KTH, School of Technology and Health (STH), Medical Engineering, Medical Imaging.
    Bjällmark, Anna
    KTH, School of Technology and Health (STH), Medical Engineering, Medical Imaging. Karolinska Institute, Sweden .
    Broomé, Michael
    KTH, School of Technology and Health (STH), Medical Engineering, Medical Imaging. Karolinska Institute, Sweden .
    Modelling the heart with the atrioventricular plane as a piston unit2015In: Medical Engineering and Physics, ISSN 1350-4533, E-ISSN 1873-4030, Vol. 37, no 1, p. 87-92Article in journal (Refereed)
    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.

  • 27.
    Maksuti, Elira
    et al.
    KTH, School of Technology and Health (STH), Medical Engineering.
    Carlsson, Marcus
    Arheden, Hakan
    Kovacs, Sandor J.
    Broome, M.
    KTH, School of Technology and Health (STH), Medical Engineering.
    Ugander, Martin
    Hydraulic forces contribute to left ventricular diastolic filling2017In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 7, article id 43505Article in journal (Refereed)
    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.

  • 28. Osterlund, B.
    et al.
    Jern, C.
    Seeman-Lodding, H.
    Johansson, G.
    Haggmark, S.
    Broome, M.
    Umeå Universitet.
    Biber, B.
    Intracoronary beta2 receptor activation induces dynamic local t-PA release in the pig2003Other (Refereed)
    Abstract [en]

    To investigate beta2 -adrenergic agonist-mediated effects on coronary fluxes of local fibrinolytic factors, healthy anaesthetised and instrumented pigs (n=10) were studied during infusion of isoprenaline (IPR) into the left main coronary artery. Coronary net fluxes of total t-PA antigen, active t-PA and total PAI-1 antigen were determined at baseline and at 3, 5, 7 and 10 minutes of IPR infusion. During IPR, net release of total t-PA increased in a biphasic pattern with transiently high levels at 3 (+440 %) and 7 minutes (+620%) and returned towards baseline at 10 minutes. Net coronary release of active t-PA increased with maximum levels at 3 minutes (+50%). Baseline coronary net flux of total PAI -1 showed a decrease which was most pronounced at 10 minutes. To conclude, a fast beta2 agonist-mediated local release of t-PA into the coronary vasculature was demonstrated. For total t-PA, this response was characterised by a biphasic release profile.

  • 29. Sundeman, H.
    et al.
    Aneman, A.
    Broome, M.
    Umeå Universitet.
    Haney, M.
    Johansson, G.
    Haggmark, S.
    Biber, B.
    Winso, O.
    Effects of desflurane on the pig intestinal circulation during hypotension1999Other (Refereed)
    Abstract [en]

    BACKGROUND: The aim of the present study was to analyze the perfusion pressure dependency for the splanchnic vascular effects of desflurane (DES). METHODS: We measured portal blood flow (QPORT, perivascular ultrasound) and jejunal mucosal perfusion (JMP; laser Doppler) in pentobarbital-anesthetized pigs (n=10). Experimentally, decreases in mean arterial pressure (MAP) were produced by pericardial infusions of dextran. The protocol included sets of measurements at incremental doses of DES (1, 2, 4 and 6%) prior to and during pericardial infusions. RESULTS: Although QPORT and JMP decreased significantly during pericardial infusions, DES, irrespective of dose, did not reduce QPORT until MAP had decreased below 65-70 mm Hg. In higher MAP ranges, vasodilation in pre-portal tissues was powerful enough to maintain QPORT in spite of concurrent decreases in driving arterial pressure, as produced by either DES or pericardial infusion, or by a combination of both. We found no effects of DES on JMP even at very low MAP (about 40 mm Hg during pericardial infusion), indicating that the normal physiological response of the small intestine to redistribute blood flow from deeper to more superficial layers during hypotension was unimpaired by DES. CONCLUSIONS: Our data suggest a wide dose-tolerability of DES as regards the splanchnic circulation during hypotensive states.

  • 30. Sundeman, H.
    et al.
    Haney, M.
    Broome, M.
    Umeå Universitet.
    Haggmark, S.
    Johansson, G.
    Winso, O.
    Biber, B.
    The effects of desflurane on cardiac function as measured by conductance volumetry in swine1998Other (Refereed)
    Abstract [en]

    The purpose of the investigation was to assess the effects of desflurane (DES) on left ventricular heart function during basal barbiturate anesthesia in a closed-pericardium, closed-chest acute swine model. The study was performed in 11 normoventilated adult pigs. Hemodynamic measurements were obtained using arterial, central venous, and pulmonary artery catheters, as well as a conductance volumetry and tip manometry catheter placed in the left ventricle. Hemodynamic measurements were recorded during basal pentobarbital anesthesia and with the addition of 1%, 2%, 4%, and 6% DES. DES dose-dependently decreased mean arterial pressure, systemic vascular resistance, left ventricular end-systolic pressure, dP/dtMAX and dP/dtMIN. At doses >1%, decreases in CO, stroke volume, ejection fraction, end-systolic elastance, preload recruitable stroke work, preload adjusted maximal power, and peak filling rate were observed. Heart rate decreased at 4% and 6% DES. Isovolumetric relaxation time increased only at 6% DES. We conclude that smaller doses of DES have a significant cardiodepressive effect in the setting of barbiturate infusion, as measured by conductance volumetry. IMPLICATIONS: Desflurane, in very small doses, depressed cardiac function during pentobarbital anesthesia with ketamine and benzodiazepine premedication in swine, as assessed by conductance volumetry and left ventricular pressure and volume relationship analysis. These results suggest that desflurane, in combination with certain anesthetics, can be cardiodepressive even in very small doses.

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