DOCSLIB.ORG

INDE 221 Spring 2010 Syllabus Part 2

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
INDE 221 Spring 2010 Syllabus Part 2 Human Health & Disease Mondays, Tuesdays, Thursdays and Fridays 9:00 - 11:50 AM Lectures: Room M-112, Labs: Fleischmann IINNDDEE 222211 SSpprriinngg 22001100 Syllabus SSyyllllaabbuuss PPaarrtt 22 (2010) Year's Last Syllabus (2010) Year's Last Human Health & Disease Inde 221 Spring 2010 Table of Contents CARDIOVASCULAR BLOCK SYLLABUS SCHEDULE 7 SYLLABUS PREFACE 11 CARDIAC MUSCLE AND FHC 15 EXCITATION-CONTRACTION COUPLING Syllabus27 NERNST POTENTIAL AND OSMOSIS 43 EXCITABILITY AND CONDUCTION 51 CIRCULATORY VESSEL HISTOLOGY LAB 63 CARDIAC ACTION POTENTIAL 71 CONTROL OF HEART RHYTHM (2010) 85 AUTONOMIC DRUGS OVERVIEW I 97 ELECTROCARDIOGRAM (ECG) 99 LESIONS OF BLOOD VESSELS 109 THROMBOEMBOLIC DISEASE 117 CARDIAC REFLEXESYear's 123 AUTONOMIC DRUGS OVERVIEW II 141 ECG SMALL GROUPS 143 LastAUTONOMIC DRUGS: CHOLINERGICS 147 CARDIAC MUSCLE MECHANICS 149 AUTONOMIC DRUGS: ANTICHOLINERGICS 175 ARRHYTHMIAS 177 AUTONOMIC DRUGS: SYMPATHOMIMETICS I 203 VENTRICULAR PHYSIOLOGY 205 AUTONOMIC DRUGS: SYMPATHOMIMETICS II 235 STARLING CURVE AND VENOUS RETURN 237 CARDIAC OUTPUT AND CATHETERIZATION 245 AUTONOMIC DRUGS: ADRENOCEPTOR BLOCKERS 267 PHYSICS OF CIRCULATION Syllabus269 CASE DISCUSSIONS: AUTONOMIC DRUGS 289 SMOOTH MUSCLE 291 ISCHEMIC AND VALVULAR HEART DISEASE 303 RENAL CIRCULATION (2010) 323 HYPERTENSION 333 CARDIOMYOPATHY, MYOCARDITIS AND ATRIAL MYXOMA 351 ENDOTHELIUM AND CORONARY CIRCULATION 369 ANGINA PECTORIS 389 DRUGS USEDYear's IN HYPERTENSION 397 SHOCK 399 ADULT CARDIAC LAB 413 CARDIAC ANESTHESIA & BYPASS 421 LastEXERCISE PHYSIOLOGY 431 ISCHEMIC HEART DISEASE PHARMACOLOGY 441 CONGESTIVE HEART FAILURE 443 DRUGS USED IN ANGINA PECTORIS 475 AN INTRO TO CARDIAC AND TOMOGRAPHIC ANATOMY OF THE HEART 477 POSITIVE INOTROPIC AGENTS 485 CONGESTIVE HEART FAILURE PHARMACOLOGY 487 FETAL CIRCULATION AND CONGENITAL HEART DISEASE 489 CONGENITAL HEART DISEASE 527 ANTIARRHYTHMIC DRUGS Syllabus547 CARDIOVASCULAR PHARMACOLOGY CASE DISCUSSIONS 549 PEDIATRIC CARDIAC LAB 551 (2010) Year's Last Syllabus (2010) Year's Last Human Health & Disease Inde 221 Spring 2010 Syllabus Schedule Weekday Date Time Room Topic Instructor Tues 4/27 9 - 9:50 M112 Cardiac Muscle and FHC R. Tsien 10 - 10:50 M112 Excitation-Contraction Coupling R. Tsien 11 - 11:50 M112 Nernst Potential & Osmosis D. Madison Thurs 4/29 9 - 9:50 M112 Excitability & Conduction R. Tsien 10 – 11:50 FLRC Circulatory Vessel Histology Lab A. Connolly Fri 4/30 9 – 9:50 M112 Cardiac Action Potential R. Tsien 10 – 10:50 M112 Control of Heart Rhythm R. Tsien Wk 5 ends 11 – 11:50 M112 Autonomic Pharmacology Overview 1 J. Whitlock Mon 5/3 9 - 9:50 M112 ECG SyllabusR. Tsien 10 – 10:50 M112 Lesions of Blood Vessels A. Connolly 11 – 11:50 M112 Thromboembolic Disease A. Connolly Tues 5/4 9 - 10:50 M112 Cardiac Reflexes B. Kobilka 11 - 11:50 M112 Autonomic Pharmacology Overview 2 J. Whitlock Thurs 5/6 9 – 10:50 FLRC ECG Small Groups Faculty 11 - 11:50 M112 Autonomic Drugs (Cholinergics) J. Whitlock Fri 5/7 9 - 10:50 M112 Muscle Mechanics R. Turcott Wk 6 ends 11 - 11:50 M112 Autonomic Drugs (Anticholinergics) J. Whitlock Mon 5/10 9 – 10:50 M112 Arrhythmias(2010) P. Wang 11 – 11:50 M112 Autonomic Drugs (Sympathomimetics 1) J. Whitlock Tues 5/11 9 – 10:50 M112 Ventricular Physiology R. Turcott 11 - 11:50 M112 Autonomic Drugs (Sympathomimetics 2) J. Whitlock Thurs 5/13 9 – 9:50 M112 Starling Curve and Venous Return J. Wong 10 – 10:50 M112 Cardiac Output and Catheterization R. Dash 11 - 11:50 M112 Autonomic Drugs (Adrenoceptor Blockers) J. Whitlock Fri 5/14 9 – 10:50 M112 Physics of Circulation M. McConnell Wk 7 ends Year's 11 - 11:50 M112 Case Discussions (Autonomic Drugs) J. Whitlock Sat 5/15 9 – 11:00 H2152 Saturday Treadmill Session #1 (Last Name A-K) – OPTIONAL Last Syllabus (2010) Year's Last Mon 5/17 9am-12pm FLRC EXAM DAY (Basic CV / Autonomics) Tues 5/18 9 – 9:50 M112 Smooth Muscle R. Tsien 10 – 10:50 M112 Ischemic Heart Disease A. Connolly 11 – 11:50 M112 Valvular Heart Disease A. Connolly Thurs 5/20 9 – 9:50 M112 Renal Circulation S. Rockson 10 - 10:50 M112 Hypertension S. Rockson 11 - 11:50 M112 Cardiomyopathy, Myocarditis and Atrial Myxoma G. Berry Fri 5/21 9 – 9:50 M112 Endothelium & Coronary Circulation J. Topper 10-10:50 M112 Angina Pectoris J. Topper Wk 8 Ends 11-11:50 M112 Drugs Used in Hypertension J. Whitlock Sat 5/22 9 – 11:00 H2152 Saturday Treadmill Session #2 (Last Name L-Z) – OPTIONAL Mon 5/24 9 – 9:50 M112 Shock M. Rosenthal 10 – 11:50 FLRC Adult Cardiac Lab SyllabusFaculty Tues 5/25 9 – 9:50 M112 Cardiac Anesthesia & Bypass M. Kanevsky 10 – 10:50 M112 Exercise Physiology R. Fishman 11 - 11:50 M112 Ischemic Heart Disease J. Whitlock Thurs 5/27 9 – 10:50 M112 Congestive Heart Failure A. Patterson 11 - 11:50 M112 Drugs Used in Angina Pectoris J. Whitlock Into to Cardiac & Tomographic Anatomy of the Fri 5/28 9 - 9:50 M112 N. Silverman Heart 10 – 10:50 M112 (2010)Positive Inotropic Agents J. Whitlock Wk 9 Ends 11 – 11:50 M112 Congestive Heart Failure Pharmacology J. Whitlock Mon 5/31 Holiday Tues 6/1 9 – 9:50 M112 Fetal Circulation & Congenital Heart Disease D. Bernstein 10 – 10:50 M112 Congenital Malformations of the Heart G. Berry 11 – 11:50 M112 Antiarrhythmic Drugs J. Whitlock Thurs 6/3 9 – 9:50 M112 Cardiovascular Pharm Case Discussions J. Whitlock 10 – 11:50 FLRC Pediatric Cardiac Lab Faculty Fri Year's6/4 9am-12pm FLRC EXAM DAY (End-CV) Mon - Tues 6/7 - 6/8 STUDY TIME Wed 6/9 9am-12pm FLRC INTEGRATED FINAL EXAM DAY Last Syllabus (2010) Year's Last Human Health & Disease Inde 221 Spring 2010 Syllabus Preface (CV) The following information has been provided to communicate any important updates in the course that have been made since the previous syllabus (Inde 221 2010 Part 1, Pulmonary and Neoplasia). TEXTBOOKS The following book is recommended for the CV Physiology sessions: Cardiovascular Physiology, by Berne and Levy, 8th edition (2000, paperback). Please note: the B&L book is available for purchase at the Stanford University Bookstore. The HHD course will not be providing copies of this book.Syllabus SATURDAY TREADMILL SESSIONS There will be two Saturday treadmill sessions that you are strongly encouraged to attend. The session dates are Saturday, May 15 and Saturday, May 22. Students whose last name begins with the letter A to K are scheduled to attend the treadmill session on May 15. Students whose last name begins with the letter L to Z are scheduled(2010) to attend the treadmill session on May 22. If you are unable to attend your scheduled session, please find someone in the other session to switch places with you. Both sessions begin at 9:00am and last approximately two hours. Please meet in the CV Clinic, room H-2152, which is located next to the ECG Lab of the hospital (North ICU). The objective of the treadmill session is to demonstrate practical applications of ECG and Echocardiography, and show you how a treadmill diagnostic is performed.Year's Last Syllabus (2010) Year's Last HUMAN HEALTH & DISEASE Spring 2010 CCVV BBlloocckk SSyyllllaabbuuss Syllabus (2010) Year's Last Syllabus (2010) Year's Last Cardiac Muscle and FHC - Richard Tsien, Ph.D. HHD221 Spring 2010 Page 15 CARDIAC MUSCLE AND FAMILIAL HYPERTROPHIC CARDIOMYOPATHY REQUIRED READING: B&L pp. 55-61 OBJECTIVES: 1. To review the important contractile proteins for the cardiac contraction 2. To appreciate the plasticity of the heart arising from the regulation of contractile protein genes 3. To appreciate the significance of those genes in the pathophysiology of hypertrophy of the heart due to either familial hypertrophic cardiomyopathy or hypertension. I. A CLINICAL CASE: FAMILIAL HYPERTROPHIC CARDIOMYOPATHYSyllabus (FHC) A. FHC is both a sporadic and an autosomal dominant disorder characterized by unexplained myocardial hypertrophy, a wide spectrum of clinical symptoms including arrhythmias, and early death. Sudden death can occur in both symptomatic and asymptomatic individuals. Pathological change in the heart consists of focally increased cardiac mass (regional hypertrophy) and myofibrillar disarray within varied anatomic regions of the heart. The figure illustrates septal hypertrophy. In the extreme case, the mitral valve will touch the(2010) septum, causing systolic anterior motion and creating an obstruction. It turns out that FHC can arise from defects in any one of a number of heart cell contractile proteins. It is really a disease of the sarcomere. Current hypotheses suggest that FHC, while a relatively uncommon disorder, may offer clues to the basis of heart Year's failure, a very common disease that may affect half a million people a year in the U.S. alone. We will return to this theme at the end of the lecture. Last Cardiac Muscle and FHC - Richard Tsien, Ph.D. HHD221 Spring 2010 Page 16 II. THE SARCOMERE AND CONTRACTILE PROTEINS A. Here we briefly review the structure of the striated muscle cells in cardiac and skeletal muscle. Most of you will have had ample exposure to this material in earlier courses. B. The sarcomere is the basic contractile unit. The z-line marks the edges of the sarcomere. The thin filaments are attached to the z- line and these filaments contain the actin. In the center of the sarcomere is the A-band which is formed by the thick filaments containing myosin that extend to either side of the M-line. Syllabus C. The contraction of the muscle is produced by the movement of the myosin along the actin filaments. This draws the thin filaments in towards the center of the sarcomere and thereby shortens the distance from Z-line to Z-line. The overlap of actin and myosin filaments will be a short stretch at rest but in a contracted muscle, the Z-line may be pulled in almost to the edge of the thick filaments.
Load more

Recommended publications
  • Calcinosis Cutis
    Dermatology Online Journal UC Davis Calcinosis cutis: A rare feature of adult dermatomyositis Inês Machado Moreira Lobo, Susana Machado, Marta Teixeira, Manuela Selores Dermatology Online Journal 14 (1): 10 Department of Dermatology, Hospital Geral de Santo António, Porto, Portugal. [email protected] Abstract Dermatomyositis is an idiopathic inflammatory myopathy with characteristic cutaneous manifestations. We describe a case of a 55- year-old woman with dermatomyositis who presented with dystrophic calcinosis resistant to medical treatment. Dermatomyositis is an idiopathic inflammatory myopathy with characteristic cutaneous manifestations, including heliotrope rash, Gottron papules, periungual telangiectasias, photodistributed erythema, poikiloderma, and alopecia. Although heliotrope rash and Gottron papules are specific cutaneous features, calcinosis of the skin or muscles is unusual in adults with dermatomyositis. However, it may occur in up to 40 percent of children or adolescents [1]. Calcinosis cutis is the deposition of insoluble calcium salts in the skin. Calcinosis cutis may be divided into four categories according to the pathogenesis as follows: dystrophic, metastatic, idiopathic, and iatrogenic. In connective tissue diseases, calcinosis is mostly of the dystrophic type and it seems to be a localized process rather than an imbalance of calcium homeostasis. Calcium deposits may be intracutaneous, subcutaneous, fascial, or intramuscular. Clinical synopsis A 55-year-old woman was referred for evaluation because of multiple, firm nodules of the lateral hips since 1994. At that time, dermatomyositis was diagnosed based on cutaneous, muscular and pulmonary involvement. The nodules, gradually enlarging since 1999, have begun to cause incapacitation pain and many exude a yellowish material suggestive of calcium. She denied an inciting traumatic event.
    [Show full text]
  • Radionuclear Measurement of Peripheral Hemodynamics In
    RadionuclearMeasurementof Peripheral Hemodynamics in Selection of Vasodilators for Treatment of Heart Failure Yasuhiro Todo, Mitsumasa Ohyanagi, Ryu Fujisue, and Tadaaki Iwasaki Hyogo College ofMedicine, Nishinomiya, Japan Inorder to select the optimal vasodilator for the treatment of patients with congestive heart failure (CHF), the acute effects of three vasodilators (isosorbide dinitrate (ISDN) 5 mg, nifedipine 10 mg, and prazosin 1 mg) on peripheral capacitance and resistance vessels (CV and RV)were evaluated by a newly devised radionuclear technique (Study 1).Thirty-six @ patients with chronic CHF were dividedinto Group A (ejectionfraction (EF) 35%, n = 20, mean EF: 47.2 ±6.5%) and B (EF < 35%, n = 16, mean EF: 24.8 ±7.1%). ISDNproduced the strongest CVdilatation(25% in both groups). Nifedipinereduced RVtone in Groups A and B (14% and 27%, respectively),and CVtone in Group A (6%). Prazosin had the most prominent effects on both vessels in Group B. From these results, it appeared: (a) ISDN is indicated for the cases with increased CV tone, (b) nifedipine is suitable for those with @ increased RV tone, (C)in cases of increased tone in both vessels, nifedipine (when EF 35%) or prazosin (when EF < 35%) is optimal.To evaluate the validityof this assignment, 49 subjects with CHF were divided into Group 1 (n = 16, increased CV tone), Group 2 (n = 17, increased RV tone), and Group 3 (n = 16, increased CV and RV tone) in Study 2. In Group 1, the changes of all indexes were not significantly different between the subjects treated with optimal drug based on the assignment (subgroup P) and those with a non-optimaldrug (subgroup N)after 2 wk of therapy.
    [Show full text]
  • Baroreflex and Cerebral Autoregulation Are Inversely
    2460 NASR N et al. Circulation Journal ORIGINAL ARTICLE Official Journal of the Japanese Circulation Society http://www.j-circ.or.jp Hypertension and Circulatory Control Baroreflex and Cerebral Autoregulation Are Inversely Correlated Nathalie Nasr, MD, PhD; Marek Czosnyka, PhD; Anne Pavy-Le Traon, MD, PhD; Marc-Antoine Custaud, MD, PhD; Xiuyun Liu, BSc; Georgios V. Varsos, BSc; Vincent Larrue, MD Background: The relative stability of cerebral blood flow is maintained by the baroreflex and cerebral autoregulation (CA). We assessed the relationship between baroreflex sensitivity (BRS) and CA in patients with atherosclerotic carotid stenosis or occlusion. Methods and Results: Patients referred for assessment of atherosclerotic unilateral >50% carotid stenosis or oc- clusion were included. Ten healthy volunteers served as a reference group. BRS was measured using the sequence method. CA was quantified by the correlation coefficient (Mx) between slow oscillations in mean arterial blood pres- sure and mean cerebral blood flow velocities from transcranial Doppler. Forty-five patients (M/F: 36/9), with a me- dian age of 68 years (IQR:17) were included. Thirty-four patients had carotid stenosis, and 11 patients had carotid occlusion (asymptomatic: 31 patients; symptomatic: 14 patients). The median degree of carotid steno-occlusive disease was 90% (IQR:18). Both CA (P=0.02) and BRS (P<0.001) were impaired in patients as compared with healthy volunteers. CA and BRS were inversely and strongly correlated with each other in patients (rho=0.58, P<0.001) and in healthy volunteers (rho=0.939; P<0.001). Increasing BRS remained strongly associated with im- paired CA on multivariate analysis (P=0.004).
    [Show full text]
  • Soft Tissue Calcification and Ossification
    Soft Tissue Calcification and Ossification Soft-tissue Calcification Metastatic Calcification =deposit of calcium salts in previously normal tissue (1) as a result of elevation of Ca x P product above 60-70 (2) with normal Ca x P product after renal transplant Location:lung (alveolar septa, bronchial wall, vessel wall), kidney, gastric mucosa, heart, peripheral vessels Cause: (a)Skeletal deossification 1.1° HPT 2.Ectopic HPT production (lung / kidney tumor) 3.Renal osteodystrophy + 2° HPT 4.Hypoparathyroidism (b)Massive bone destruction 1.Widespread bone metastases 2.Plasma cell myeloma 3.Leukemia Dystrophic Calcification (c)Increased intestinal absorption =in presence of normal serum Ca + P levels secondary to local electrolyte / enzyme alterations in areas of tissue injury 1.Hypervitaminosis D Cause: 2.Milk-alkali syndrome (a)Metabolic disorder without hypercalcemia 3.Excess ingestion / IV administration of calcium salts 1.Renal osteodystrophy with 2° HPT 4.Prolonged immobilization 2.Hypoparathyroidism 5.Sarcoidosis 3.Pseudohypoparathyroidism (d)Idiopathic hypercalcemia 4.Pseudopseudohypoparathyroidism 5.Gout 6.Pseudogout = chondrocalcinosis 7.Ochronosis = alkaptonuria 8.Diabetes mellitus (b) Connective tissue disorder 1.Scleroderma 2.Dermatomyositis 3.Systemic lupus erythematosus (c)Trauma 1.Neuropathic calcifications 2.Frostbite 3.Myositis ossificans progressiva 4.Calcific tendinitis / bursitis (d)Infestation 1.Cysticercosis Generalized Calcinosis 2.Dracunculosis (guinea worm) (a)Collagen vascular disorders 3.Loiasis 1.Scleroderma
    [Show full text]
  • Angiotensin II Protocol
    Angiotensin II (Giapreza ™) Protocol Background Sepsis and septic shock are medical emergencies that affect millions of people each year and killing as many as 1 in 4.1 The cornerstones of therapy are fluid resuscitation, early appropriate antibiotics, source control if needed and vasopressors. A small portion of patients fail to respond to these therapies and develop refractory shock. The definition of refractory septic shock varies in the literature but is generally considered to be hypotension, with end-organ dysfunction, requiring high-dose vasopressor support.2 The associated mortality of refractory septic shock is up to 60% and as high as 80-90% in patients requiring more than 1 mcg/kg/min of norepinephrine.2,3 Patients who develop refractory septic shock comprise a very small portion of the population in large randomized controlled trials therefore limited data is available regarding outcomes and management. Indications: Angiotensin II (Ang II) is a vasoconstrictor used to increase blood pressure in adults with septic or other distributive shock. Administration: Starting dose of 5 (nanograms) ng/kg/min intravenously via central line only. Titration: Every 5 minutes by increments of 5 ng/kg/min as needed. Maximum dose should not exceed 80 ng/kg/min (During the first 3 hours of administration); after the first 3 hours the maintenance (maximum) dose is 40 ng/kg/min. Monitoring: Critical care setting only with telemetry, arterial blood pressure, and continuous SpO2 monitoring. DVT Prophylaxis should be started (unless contraindicated)
    [Show full text]
  • Pathophysiology of the Cardiovascular System and Neonatal Hypotension
    Pathophysiology of the Cardiovascular System and Neonatal Hypotension Sandra L. Shead, RNC-NIC, MSN, CNS, NNP-BC Continuing Nursing Education BSTRACT (CNE) Credit A A total of 2.5 contact Hypotension is common in low birth weight neonates and less common in term newborns and is hours may be earned as CNE credit associated with significant morbidity and mortality. Determining an adequate blood pressure in for reading the articles in this issue neonates remains challenging for the neonatal nurse because of the lack of agreed-upon norms. Values identified as CNE and for completing an online posttest and evaluation. for determining norms for blood pressure at varying gestational and postnatal ages are based on To be successful the learner must empirical data. Understanding cardiovascular pathophysiology, potential causes of hypotension, and obtain a grade of at least 80% on assessment of adequate perfusion in the neonatal population is important and can assist the neonatal the test. Test expires three (3) years from publication date. Disclosure: nurse in the evaluation of effective blood pressure. This article reviews cardiovascular pathophysiology The author/planning committee as it relates to blood pressure and discusses potential causes of hypotension in the term and preterm has no relevant financial interest or affiliations with any commercial neonate. Variation in management of hypotension across centers is discussed. Underlying causes and interests related to the subjects pathophysiology of hypotension in the neonate are described. discussed within this article. No commercial support or sponsorship was provided for this educational Keywords: neonatal hypotension; definition; physiology; cardiovascular system; preterm; management; activity. ANN/ANCC does not assessment; cerebral; autoregulation; blood pressure endorse any commercial products discussed/displayed in conjunction with this educational activity.
    [Show full text]
  • Cardiovascular Physiology
    CARDIOVASCULAR PHYSIOLOGY Ida Sletteng Karlsen • Trym Reiberg Second Edition 15 March 2020 Copyright StudyAid 2020 Authors Trym Reiberg Ida Sletteng Karlsen Illustrators Nora Charlotte Sønstebø Ida Marie Lisle Amalie Misund Ida Sletteng Karlsen Trym Reiberg Booklet Disclaimer All rights reserved. No part oF this book may be reproduced in any Form on by an electronic or mechanical means, without permission From StudyAid. Although the authors have made every efFort to ensure the inFormation in the booklet was correct at date of publishing, the authors do not assume and hereby disclaim any liability to any part For any inFormation that is omitted or possible errors. The material is taken From a variety of academic sources as well as physiology lecturers, but are Further incorporated and summarized in an original manner. It is important to note, the material has not been approved by professors of physiology. All illustrations in the booklet are original. This booklet is made especially For students at the Jagiellonian University in Krakow by tutors in the StudyAid group (students at JU). It is available as a PDF and is available for printing. If you have any questions concerning copyrights oF the booklet please contact [email protected]. About StudyAid StudyAid is a student organization at the Jagiellonian University in Krakow. Throughout the academic year we host seminars in the major theoretical subjects: anatomy, physiology, biochemistry, immunology, pathophysiology, supplementing the lectures provided by the university. We are a group of 25 tutors, who are students at JU, each with their own Field oF specialty. To make our seminars as useful and relevant as possible, we teach in an interactive manner often using drawings and diagrams to help students remember the concepts.
    [Show full text]
  • Arterial System Lecture Block 10 Vascular Structure/Function
    Arterial System Lecture Block 10 Arterial System Bioengineering 6000 CV Physiology Vascular Structure/Function Arterial System Bioengineering 6000 CV Physiology Functional Overview Arterial System Bioengineering 6000 CV Physiology Vessel Structure Aorta Artery Vein Vena Cava Arteriole Capillary Venule Diameter 25 mm 4 mm 5 mm 30 mm 30 µm 8 µm 20 µm Wall 2 mm 1 mm 0.5 mm 1.5 mm 6 µm 0.5 µm 1 µm thickness Endothelium Elastic tissue Smooth Muscle Fibrous Tissue Arterial System Bioengineering 6000 CV Physiology Aortic Compliance • Factors: – age 20--24 yrs – athersclerosis 300 • Effects – more pulsatile flow 200 dV 30--40 yrs C = – more cardiac work dP 50-60 yrs – not hypertension Laplace’s Law 100 70--75 yrs (thin-walled cylinder): [%] Volume Blood T = wall tension P = pressure T = Pr r = radius For thick wall cylinder 100 150 200 P = pressure Pr Pressure [mm Hg] σ = wall stress r = radius σ = Tension Wall Stress w = wall thickness w [dyne/cm] [dyne/cm2] Aorta 2 x 105 10 x 105 Capillary 15-70 1.5 x 105 Arterial System Bioengineering 6000 CV Physiology Arterial Hydraulic Filter Arterial System Bioengineering 6000 CV Physiology Arterial System as Hydraulic Filter Arterial Cardiac Pressure • Pulsatile --> Output t Physiological smooth flow t Ideal • Cardiac energy conversion Cardiac • Reduces total Output Arterial cardiac work Pressure t Pulsatile t Challenge Cardiac Output Arterial Pressure t Filtered t Reality Arterial System Bioengineering 6000 CV Physiology Elastic Recoil in Arteries Arterial System Bioengineering 6000 CV Physiology Effects of Vascular Resistance and Compliance Arterial System Bioengineering 6000 CV Physiology Cardiac Output vs.
    [Show full text]
  • Non-Coding Rnas in the Cardiac Action Potential and Their Impact on Arrhythmogenic Cardiac Diseases
    Review Non-Coding RNAs in the Cardiac Action Potential and Their Impact on Arrhythmogenic Cardiac Diseases Estefania Lozano-Velasco 1,2 , Amelia Aranega 1,2 and Diego Franco 1,2,* 1 Cardiovascular Development Group, Department of Experimental Biology, University of Jaén, 23071 Jaén, Spain; [email protected] (E.L.-V.); [email protected] (A.A.) 2 Fundación Medina, 18016 Granada, Spain * Correspondence: [email protected] Abstract: Cardiac arrhythmias are prevalent among humans across all age ranges, affecting millions of people worldwide. While cardiac arrhythmias vary widely in their clinical presentation, they possess shared complex electrophysiologic properties at cellular level that have not been fully studied. Over the last decade, our current understanding of the functional roles of non-coding RNAs have progressively increased. microRNAs represent the most studied type of small ncRNAs and it has been demonstrated that miRNAs play essential roles in multiple biological contexts, including normal development and diseases. In this review, we provide a comprehensive analysis of the functional contribution of non-coding RNAs, primarily microRNAs, to the normal configuration of the cardiac action potential, as well as their association to distinct types of arrhythmogenic cardiac diseases. Keywords: cardiac arrhythmia; microRNAs; lncRNAs; cardiac action potential Citation: Lozano-Velasco, E.; Aranega, A.; Franco, D. Non-Coding RNAs in the Cardiac Action Potential 1. The Electrical Components of the Adult Heart and Their Impact on Arrhythmogenic The adult heart is a four-chambered organ that propels oxygenated blood to the entire Cardiac Diseases. Hearts 2021, 2, body. It is composed of atrial and ventricular chambers, each of them with distinct left and 307–330.
    [Show full text]
  • Overview of Partial Left Ventriculectomy
    Prepared by ASERNIP-S NATIONAL INSTITUTE FOR CLINICAL EXCELLENCE INTERVENTIONAL PROCEDURES PROGRAMME Interventional procedure overview of Partial Left Ventriculectomy Introduction This overview has been prepared to assist members of IPAC advise on the safety and efficacy of an interventional procedure previously reviewed by SERNIP. It is based on a rapid survey of published literature, review of the procedure by specialist advisors and review of the content of the SERNIP file. It should not be regarded as a definitive assessment of the procedure. Procedure name Partial Left Ventriculectomy The Batista Procedure Specialty society Society of Cardiothoracic Surgeons of Great Britain and Ireland Executive Summary Left partial ventriculectomy (PLV) seeks to treat dilated cardiomyopathy by reducing cardiac volume and hence heart wall pressure through the resection of a portion of the left ventricle. Patients receiving it are generally suitable for cardiac transplant but unable to receive it, often for social or economic reasons. PLV is an emerging procedure and the vast majority of evidence is case series, although there has been one retrospective comparative study of PLV and transplantation. Hospital mortality was reported for up to 30% of patients and overall mortality was around 40% of patients. Thirty day survival ranged from 50% to 99%, and no significant difference was found between PLV and transplant. One-year survival ranged from 46% to 80% and three- year survival was reported in one study as 60%. Event-free survival was reported as 80% at 30 days, 49% at 1 year and 26% at three years. Use of a left ventricular assist device or relisting for cardiac surgery was reported in one study at between 5% and 15% of patients at 30 days and in 43% at 1 year and 58% at 3 years.
    [Show full text]
  • Nitric Oxide, the Biological Mediator of the Decade: Fact Or Fiction?
    Eur Respir J 1997; 10: 699–707 Copyright ERS Journals Ltd 1997 DOI: 10.1183/09031936.97.10030699 European Respiratory Journal Printed in UK - all rights reserved ISSN 0903 - 1936 SERIES 'CLINICAL PHYSIOLOGY IN RESPIRATORY INTENSIVE CARE' Edited by A. Rossi and C. Roussos Number 14 in this Series Nitric oxide, the biological mediator of the decade: fact or fiction? S. Singh, T.W. Evans Nitric oxide, the biological mediator of the decade: fact or fiction? S. Singh, T.W. Evans. Unit of Critical Care, National Heart & ERS Journals Ltd 1997. Lung Institute, Royal Brompton Hospital, ABSTRACT: Nitric oxide (NO), an atmospheric gas and free radical, is also an London, UK. important biological mediator in animals and humans. Its enzymatic synthesis by constitutive (c) and inducible (i) isoforms of NO synthase (NOS) and its reactions Correspondence: T.W. Evans with other biological molecules such as reactive oxygen species are well charac- Royal Brompton Hospital Sydney Street terized. NO modulates pulmonary and systemic vascular tone through its vasodila- London SW3 6NP tor property. It has antithrombotic functions and mediates some consequences of UK the innate and acute inflammatory responses; cytokines and bacterial toxins induce widespread expression of iNOS associated with microvascular and haemodynam- Keywords: Acute respiratory distress syn- ic changes in sepsis. drome Within the lungs, a diminution of NO production is implicated in pathological hypoxic pulmonary vasoconstriction states associated with pulmonary hypertension, such as acute respiratory distress nitric oxide syndrome: inhaled NO is a selective pulmonary vasodilator and can improve ven- nitric oxide synthase tilation-perfusion mismatch. However, it may have deleterious effects through mod- pulmonary hypertension ulating hypoxic pulmonary vasoconstriction.
    [Show full text]
  • Thursday Poster Assignment
    Corresponding Author Paper Title Board Assignment Number ‐ Thursday Classification of Typical Developing and Autism Spectrum Disorder Using Connectivity A.R., Jac Fredo Matrix and Support Vector Machine 111 Abbaszadeh, Behrooz Probabilistic Prediction of Epileptic Seizures Using SVM 220 Abe, Takuto Surrogate Modeling for Neuroprotective Focal Brain Cooling Device 110 Comprehensive Comparison of 2D vs. 3D Resource Usage in Large Volumetric Medical Agris, Jacob Image Segmentation 109 On Smartphone Sensability of Bi‐Phasic User Intoxication Levels from Diverse Walk Agu, Emmanuel Types in Standardized Field Sobriety Tests 327 The Effect of Perceived Sound Quality of Speech in Noisy Speech Perception by Akbarzadeh, Sara Normal Hearing and Hearing Impaired Listeners 370 Towards the Development of an Optrode Biopotential Sensor: Characterization Using Al Abed, Amr in Vitro Cardiac Tissue Recordings 108 Spatially Filtered Low‐Density EMG and Time‐Domain Descriptors Improves Hand Al‐Jumaily, Adel Movement Recognition 419 Optimizing Stimulation Strategies for Retinal Electrical Stimulation: A Modelling Study Alqahtani, Abdulrahman 287 An Automatic Navigation and Pressure Monitoring for Guided Insertion Procedure Alsunaydih, Fahad Nasser 326 A Statistical Determination of the Energy Delivered to Muscular Tissue in Amador, Alejandro Electrostimulation Protocols 149 Analysis of Muscle Fatigue During Exercise and Exercise Combined with Electrostimulation 151 Signal‐To‐Noise Ratio Determination in a Hybrid System of Electrostimulation and Electromiography 150 Continuous Prediction of Cognitive State Using a Marked‐Point Process Modeling Amidi, Yalda Framework 286 Antônio Freire Teixeira, Marcos Automatic Counting of Erythrocytes Using Image Processing 153 Feature Extraction from Radiographic Images for Bone Age Identification 152 Arantes, Ana Paula Bittar Britto Towards the Improvement of Algorithms Used in Robot‐Assisted Therapies 107 Arce‐Diego, José L.
    [Show full text]