Design and Evaluation of Enhanced Mock Circulatory Platform Simulating Cardiovascular Physiology for Medical Palpation Training
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Disruption of Vascular Ca2+-Activated Chloride Currents Lowers Blood Pressure Christoph Heinze,1 Anika Seniuk,2 Maxim V
Research article Disruption of vascular Ca2+-activated chloride currents lowers blood pressure Christoph Heinze,1 Anika Seniuk,2 Maxim V. Sokolov,3 Antje K. Huebner,1 Agnieszka E. Klementowicz,3 István A. Szijártó,4,5 Johanna Schleifenbaum,4 Helga Vitzthum,2 Maik Gollasch,4 Heimo Ehmke,2 Björn C. Schroeder,3 and Christian A. Hübner1 1Institut für Humangenetik, Universitätsklinikum Jena, Friedrich-Schiller Universität Jena, Jena, Germany. 2Institut für Zelluläre und Integrative Physiologie, Universitätsklinikum Hamburg Eppendorf, Hamburg, Germany. 3Max-Delbrück Centrum für Molekulare Medizin (MDC) and NeuroCure, Berlin, Germany. 4Medizinische Klinik mit Schwerpunkt Nephrologie und Internistische Intensivmedizin, Charité – Universitätsmedizin Berlin, Experimental and Clinical Research Center (ECRC), Berlin, Germany. 5Interdisziplinäres Stoffwechsel-Centrum, Charité – Universitätsmedizin Berlin, Berlin, Germany. High blood pressure is the leading risk factor for death worldwide. One of the hallmarks is a rise of periph- eral vascular resistance, which largely depends on arteriole tone. Ca2+-activated chloride currents (CaCCs) in vascular smooth muscle cells (VSMCs) are candidates for increasing vascular contractility. We analyzed the vascular tree and identified substantial CaCCs in VSMCs of the aorta and carotid arteries. CaCCs were small or absent in VSMCs of medium-sized vessels such as mesenteric arteries and larger retinal arterioles. In small vessels of the retina, brain, and skeletal muscle, where contractile intermediate cells or pericytes gradually replace VSMCs, CaCCs were particularly large. Targeted disruption of the calcium-activated chloride channel TMEM16A, also known as ANO1, in VSMCs, intermediate cells, and pericytes eliminated CaCCs in all ves- sels studied. Mice lacking vascular TMEM16A had lower systemic blood pressure and a decreased hyperten- sive response following vasoconstrictor treatment. -
Blood Vessels: Part A
Chapter 19 The Cardiovascular System: Blood Vessels: Part A Blood Vessels • Delivery system of dynamic structures that begins and ends at heart – Arteries: carry blood away from heart; oxygenated except for pulmonary circulation and umbilical vessels of fetus – Capillaries: contact tissue cells; directly serve cellular needs – Veins: carry blood toward heart Structure of Blood Vessel Walls • Lumen – Central blood-containing space • Three wall layers in arteries and veins – Tunica intima, tunica media, and tunica externa • Capillaries – Endothelium with sparse basal lamina Tunics • Tunica intima – Endothelium lines lumen of all vessels • Continuous with endocardium • Slick surface reduces friction – Subendothelial layer in vessels larger than 1 mm; connective tissue basement membrane Tunics • Tunica media – Smooth muscle and sheets of elastin – Sympathetic vasomotor nerve fibers control vasoconstriction and vasodilation of vessels • Influence blood flow and blood pressure Tunics • Tunica externa (tunica adventitia) – Collagen fibers protect and reinforce; anchor to surrounding structures – Contains nerve fibers, lymphatic vessels – Vasa vasorum of larger vessels nourishes external layer Blood Vessels • Vessels vary in length, diameter, wall thickness, tissue makeup • See figure 19.2 for interaction with lymphatic vessels Arterial System: Elastic Arteries • Large thick-walled arteries with elastin in all three tunics • Aorta and its major branches • Large lumen offers low resistance • Inactive in vasoconstriction • Act as pressure reservoirs—expand -
Chapter 15 Hydrocephalus: New Theories and New Shunts?
Chapter 15 Hydrocephalus: New Theories and New Shunts? Marvin Bergsneider, M.D. Introduction The optimal and ideal management for any given clinical disorder should be fundamentally aimed at reversing or preventing the pathobiological mechanism underlying the disorder. For hydrocephalus, our current incomplete understanding of the pathophysiology is, in part, responsible for significant inadequacies of the current mainstay of treatment: the cerebrospinal fluid (CSF) shunt. The management of shunt-related problems and disorders has become a de facto subspecialty within neurosurgery. Although it is clear that the treatment of hydrocephalus was vastly improved with the introduction of the differential pressure valve by Nulsen and Spitz (25) half a century ago, it can be argued that little further improvement has occurred in the interim. A randomized, multicenter trial failed to show a benefit from “technologically advanced” valve designs compared with a standard differential pressure valve (7) similar to the one designed by John Holter. Probably one of the most refractory problems of CSF shunt diversion has been that of over-drainage. In children, excessive CSF drainage by the shunt is an important cause of shunt failure caused by ventricular catheter obstruction resulting from ventricular collapse. Over time, shunted hydrocephalic children can develop the slit-ventricle syndrome—one of the most challenging conditions to treat in neurosurgery. In older adults, shunt over-drainage can result in the devastating complication of subdural hematoma. A similar degree of ventricular reduction occurs despite the implementation of valve designs touted to prevent it, including flow-limiting valves and antisiphon devices (31). Why have efforts failed to prevent excessive CSF drainage by shunts? Although the answer is likely multifactorial, we argue that the fundamental problem lies in our incomplete and overly simplistic understanding of the hydrodynamics of hydrocephalus and in vivo shunt physiology. -
Ingeniería Cardiovascular - Del Laboratorio a La Clínica
INGENIERÍA CARDIOVASCULAR - DEL LABORATORIO A LA CLÍNICA INGENIERÍA CARDIOVASCULAR DEL LABORATORIO A LA CLÍNICA RICARDO L. ARMENTANO Departamento de Ingeniería Biológica, CENUR LITOTAL NORTE, URUGUAY Facultad de Ingeniería, UNIVERSIDAD DE LA REPÚBLICA, URUGUAY. Introducción La Ingeniería Cardiovascular integra elementos de la biología, la ingeniería eléctrica, la ingeniería mecánica, la matemática y la física con el fin de describir y comprender al sistema cardiovascular. Su objetivo es desarrollar, comprobar y validar una interpretación predictiva y cuantitativa del sistema cardiovascular en un adecuado nivel de detalle, y aplicar conceptos resultantes hacia la solución de diversas patologías. La dinámica del sistema cardiovascular caracteriza al corazón y al sistema vascular como un todo, y comprende la física del sistema circulatorio incluyendo el continente (las paredes arteriales) y el contenido (sangre), así como la interrelación entre ambos. La pared arterial y la sangre contienen la información esencial sobre el estado fisiológico del sistema circulatorio completo, en tanto que la interdependencia de estos componentes está relacionada con procesos complejos que podrían explicar la formación de lesiones en la pared vascular, tales como las placas de ateroma, o el aumento en la rigidez de la pared como está descripto en la hipertensión arterial. Los incipientes cambios morfológicos de la pared arterial inducidos por procesos patológicos pueden ser considerados marcadores precoces de futuras alteraciones circulatorias. La modelización matemática de la pared arterial, a partir de la estimación de los coeficientes de la ecuación del modelo, obtenida a través de estudios en animales conscientes, constituye una herramienta de gran valor e indispensable para una mejor comprensión de la génesis de las enfermedades cardiovasculares. -
Valve Replacement Alexander Zezulkal, John Mackinnon2 and D.G
Postgrad Med J: first published as 10.1136/pgmj.68.797.180 on 1 March 1992. Downloaded from Postgrad Med J (1992) 68, 180 - 185 i) The Fellowship of Postgraduate Medicine, 1992 Hypertension in aortic valve disease and its response to valve replacement Alexander Zezulkal, John Mackinnon2 and D.G. Beevers' 'University Department ofMedicine and 2Department ofCardiology, Dudley Road Hospital, Birmingham BT18 7QH, UK Summary: We have investigated the prevalence ofhypertension and the response ofblood pressure to operation in 87 patients with lone aortic valve disease who underwent aortic valve replacement. In patients with aortic stenosis alone 26% were hypertensive pre-operatively (age and sex adjusted blood pressure > 160 systolic and or > 95 mmHg diastolic) and 24% were hypertensive post-operatively. In those with aortic regurgitation alone, hypertension was present in 65% before and 57% after valve replacement using the same criterion. For combined stenosis and regurgitation, the prevalence was 54% and 62%, respectively. The post-operative increase in systolic pressure in patients with aortic stenosis occurred mainly in those with a history of left ventricular failure. In those with aortic regurgitation or combined stenosis with regurgitation, diastolic pressure rose after valve replacement resulting in a prevalence of diastolic hypertension of 44% and 35%, respectively. Blood pressure changes were not predicted by the type of valve inserted nor its size. Our data show that despite severe symptomatic aortic valve disease, systolic hypertension was common in aortic stenosis and diastolic hypertension was found in aortic regurgitation. This underlines the by copyright. importance of blood pressure monitoring in patients following aortic valve replacement. -
Simple Models of the Cardiovascular System for Educational and Research Purposes
56 ORIGINAL ARTICLE SIMPLE MODELS OF THE CARDIOVASCULAR SYSTEM FOR EDUCATIONAL AND RESEARCH PURPOSES Tomáš Kulhánek*, Martin Tribula, Jiří Kofránek, Marek Mateják Institute of Pathological Physiology, 1st Faculty of Medicine, Charles University in Prague, Prague, Czech Republic * Corresponding author: [email protected] Article history AbstrAct — Modeling the cardiovascular system as an analogy of an electri- Received 14 September 2014 cal circuit composed of resistors, capacitors and inductors is introduced in many Revised 30 October 2014 research papers. This contribution uses an object oriented and acausal approach, Accepted 4 November 2014 which was recently introduced by several other authors, for educational and re- Available online 24 November 2014 search purpose. Examples of several hydraulic systems and whole system model- ing hemodynamics of a pulsatile cardiovascular system are presented in Modelica Keywords language using Physiolibrary. Modelica modeling physiology cardiovascular system Physiolibrary INTRODUCTION grown technology from the scientific community, such as SBML [10], JSIM [11] or CellML [1,12] or industrial The mathematical formalization of the cardiovas- standard technology implemented by several vendors, cular system (CVS), i.e. the models, can be divided such as the Modelica language [8,9]. into two main approaches. The first approach builds This article introduces a modeling method which 3D models with geometrical, mechanical properties follows the second approach for modeling CVS as and the time-dependence -
Time-Varying Elastance and Left Ventricular Aortic Coupling Keith R
Walley Critical Care (2016) 20:270 DOI 10.1186/s13054-016-1439-6 REVIEW Open Access Left ventricular function: time-varying elastance and left ventricular aortic coupling Keith R. Walley Abstract heart must have special characteristics that allow it to respond appropriately and deliver necessary blood flow Many aspects of left ventricular function are explained and oxygen, even though flow is regulated from outside by considering ventricular pressure–volume characteristics. the heart. Contractility is best measured by the slope, Emax, of the To understand these special cardiac characteristics we end-systolic pressure–volume relationship. Ventricular start with ventricular function curves and show how systole is usefully characterized by a time-varying these curves are generated by underlying ventricular elastance (ΔP/ΔV). An extended area, the pressure– pressure–volume characteristics. Understanding ventricu- volume area, subtended by the ventricular pressure– lar function from a pressure–volume perspective leads to volume loop (useful mechanical work) and the ESPVR consideration of concepts such as time-varying ventricular (energy expended without mechanical work), is linearly elastance and the connection between the work of the related to myocardial oxygen consumption per beat. heart during a cardiac cycle and myocardial oxygen con- For energetically efficient systolic ejection ventricular sumption. Connection of the heart to the arterial circula- elastance should be, and is, matched to aortic elastance. tion is then considered. Diastole and the connection of Without matching, the fraction of energy expended the heart to the venous circulation is considered in an ab- without mechanical work increases and energy is lost breviated form as these relationships, which define how during ejection across the aortic valve. -
04. the Cardiac Cycle/Wiggers Diagram
Part I Anaesthesia Refresher Course – 2018 4 University of Cape Town The Cardiac Cycle The “Wiggers diagram” Prof. Justiaan Swanevelder Dept of Anaesthesia & Perioperative Medicine University of Cape Town Each cardiac cycle consists of a period of relaxation (diastole) followed by ventricular contraction (systole). During diastole the ventricles are relaxed to allow filling. In systole the right and left ventricles contract, ejecting blood into the pulmonary and systemic circulations respectively. Ventricles The left ventricle pumps blood into the systemic circulation via the aorta. The systemic vascular resistance (SVR) is 5–7 times greater than the pulmonary vascular resistance (PVR). This makes it a high-pressure system (compared with the pulmonary vascular system), which requires a greater mechanical power output from the left ventricle (LV). The free wall of the LV and the interventricular septum form the bulk of the muscle mass in the heart. A normal LV can develop intraventricular pressures up to 300 mmHg. Coronary perfusion to the LV occurs mainly in diastole, when the myocardium is relaxed. The right ventricle receives blood from the venae cavae and coronary circulation, and pumps it via the pulmonary vasculature into the LV. Since PVR is a fraction of SVR, pulmonary arterial pressures are relatively low and the wall thickness of the right ventricle (RV) is much less than that of the LV. The RV thus resembles a passive conduit rather than a pump. Coronary perfusion to the RV occurs continuously during systole and diastole because of the low intraventricular and intramural pressures. In spite of the anatomical differences, the mechanical behaviour of the RV and LV is very similar. -
Chapter 9 Monitoring of the Heart and Vascular System
Chapter 9 Monitoring of the Heart and Vascular System David L. Reich, MD • Alexander J. Mittnacht, MD • Martin J. London, MD • Joel A. Kaplan, MD Hemodynamic Monitoring Cardiac Output Monitoring Arterial Pressure Monitoring Indicator Dilution Arterial Cannulation Sites Analysis and Interpretation Indications of Hemodynamic Data Insertion Techniques Systemic and Pulmonary Vascular Resistances Central Venous Pressure Monitoring Frank-Starling Relationships Indications Monitoring Coronary Perfusion Complications Electrocardiography Pulmonary Arterial Pressure Monitoring Lead Systems Placement of the Pulmonary Artery Catheter Detection of Myocardial Ischemia Indications Intraoperative Lead Systems Complications Arrhythmia and Pacemaker Detection Pacing Catheters Mixed Venous Oxygen Saturation Catheters Summary References HEMODYNAMIC MONITORING For patients with severe cardiovascular disease and those undergoing surgery associ- ated with rapid hemodynamic changes, adequate hemodynamic monitoring should be available at all times. With the ability to measure and record almost all vital physi- ologic parameters, the development of acute hemodynamic changes may be observed and corrective action may be taken in an attempt to correct adverse hemodynamics and improve outcome. Although outcome changes are difficult to prove, it is a rea- sonable assumption that appropriate hemodynamic monitoring should reduce the incidence of major cardiovascular complications. This is based on the presumption that the data obtained from these monitors are interpreted correctly and that thera- peutic decisions are implemented in a timely fashion. Many devices are available to monitor the cardiovascular system. These devices range from those that are completely noninvasive, such as the blood pressure (BP) cuff and ECG, to those that are extremely invasive, such as the pulmonary artery (PA) catheter. To make the best use of invasive monitors, the potential benefits to be gained from the information must outweigh the potential complications. -
Estimation of Central Systolic Blood Pressure Using an Oscillometric Blood Pressure Monitor
Hypertension Research (2010) 33, 592–599 & 2010 The Japanese Society of Hypertension All rights reserved 0916-9636/10 $32.00 www.nature.com/hr ORIGINAL ARTICLE Estimation of central systolic blood pressure using an oscillometric blood pressure monitor Hao-Min Cheng1,2, Kang-Ling Wang2,3, Ying-Hwa Chen2,3, Shing-Jong Lin1,4, Lung-Ching Chen2,3, Shih-Hsien Sung2,3, Philip Yu-An Ding2,3, Wen-Chung Yu2,3, Jaw-Wen Chen1,4 and Chen-Huan Chen1,2,4 Current noninvasive techniques for assessing central aortic pressure require the recording of an arterial pressure wave using a high-fidelity applanation tonometer. We therefore developed and validated a novel method to estimate the central aortic systolic pressure using an oscillometric blood pressure monitor alone. Invasive high-fidelity right brachial and central aortic pressure waves, and left-brachial pulse volume plethysmography from an oscillometric blood pressure monitor, were obtained at baseline and 3 min after administration of sublingual nitroglycerin in 100 patients during cardiac catheterization. In the initial 50 patients (Generation Group), Central systolic blood pressure was predicted by a multi-variate prediction model generated from the comprehensive analysis of the invasive brachial pressure wave, including brachial late-systolic shoulder pressure value and parameters related to wave reflection and arterial compliance. Another prediction model was similarly constructed from the noninvasively calibrated pulse volume plethysmography. Both models were validated in the subsequent 50 patients (Validation Group) with results: r¼0.98 (Po0.001) and mean difference¼0.5±4.5 (95% confidence interval À8.3 to 9.3) mm Hg for the invasive model, and r¼0.93 (Po0.001) and mean difference¼À0.1±7.6 (95% confidence interval À15.0 to 14.8) mm Hg for the noninvasive model. -
Monitoring of the Central Blood Pressure Waveform Via a Conformal Ultrasonic Device
HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Nat Biomed Manuscript Author Eng. Author Manuscript Author manuscript; available in PMC 2019 March 21. Published in final edited form as: Nat Biomed Eng. 2018 September ; 2(9): 687–695. doi:10.1038/s41551-018-0287-x. Monitoring of the central blood pressure waveform via a conformal ultrasonic device Chonghe Wang#1, Xiaoshi Li#2, Hongjie Hu#2, Lin Zhang1, Zhenlong Huang1, Muyang Lin7, Zhuorui Zhang1, Zhenan Yin3, Brady Huang5, Hua Gong1, Shubha Bhaskaran3, Yue Gu2, Mitsutoshi Makihata6, Yuxuan Guo1, Yusheng Lei1, Yimu Chen1, Chunfeng Wang8, Yang Li1, Tianjiao Zhang1, Zeyu Chen4, Albert Pisano6, Liangfang Zhang1, Qifa Zhou4, and Sheng Xu1,2,3,9,* 1Department of Nanoengineering, University of California San Diego, La Jolla, CA, 92093-0448, USA. 2Materials Science and Engineering Program, University of California San Diego, La Jolla, CA, 92093-0418, USA. 3Department of Electrical and Computer Engineering, University of California San Diego, La Jolla, CA, 92093-0407, USA. 4Department of Ophthalmology and Biomedical Engineering, Viterbi School of Engineering, University of Southern California, Los Angeles, CA 90089-1111, USA. 5Department of Radiology, School of Medicine, University of California San Diego, La Jolla, CA, 92103, USA. 6Department of Mechanical and Aerospace Engineering, University of California San Diego, La Jolla, CA, 92093-0411, USA. 7School of Precision Instrument and Optoelectronic Engineering, Tianjin University, Tianjin, 300072, China. 8The Key Laboratory of Materials Processing and Mold of Ministry of Education, School of Materials Science and Engineering, School of Physics & Engineering, Zhengzhou University, Zhengzhou, 450001, Henan, China. 9Department of Bioengineering, University of California San Diego, La Jolla, CA, 92093-0412, USA. -
Effects of Inhibition of Nitric Oxide Formation on Basal Vasomotion and Endothelium-Dependent Responses of the Coronary Arteries in Awake Dogs
Effects of inhibition of nitric oxide formation on basal vasomotion and endothelium-dependent responses of the coronary arteries in awake dogs. A Chu, … , S Moncada, F R Cobb J Clin Invest. 1991;87(6):1964-1968. https://doi.org/10.1172/JCI115223. Research Article The role of nitric oxide in basal vasomotor tone and stimulated endothelium-dependent dilations in the coronary arteries in chronically instrumented awake dogs was studied by examining the consequences of inhibiting endogenous nitric oxide formation with the specific inhibitor of nitric oxide formation, NG-monomethyl-L-arginine (L-NMMA). In four awake dogs, coronary dimension crystals were chronically implanted on the circumflex artery for the measurement of epicardial coronary diameter, and Doppler flow probes were implanted for quantitation of phasic coronary blood flow (vasomotion of distal regulatory resistance vessels). Basal epicardial coronary diameter, acetylcholine-stimulated endothelium-dependent dilation, and flow-induced endothelium-dependent dilation of the epicardial arteries and phasic blood flow were recorded before, and after 5, 15, 50, and 120 mg/kg of L-NMMA. L-NMMA induced a dose-related increase in basal epicardial coronary vasomotor tone. There was an accompanying increase in aortic pressure and a decrease in heart rate. At doses greater than or equal to 50 mg/kg, rest phasic coronary blood flow was also decreased. Left ventricular end-diastolic pressure and contractility were not significantly changed. In contrast, the flow-induced or acetylcholine-stimulated endothelium-dependent responses were attenuated only after infusion of the highest does of L-NMMA (120 mg/kg). The changes in the basal vasomotor tone and acetylcholine-stimulated endothelium-dependent responses returned towards the control states in the presence of L-arginine (660 mg/kg).