How the Heart Works Topic Overview
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Chapter 20 *Lecture Powerpoint the Circulatory System: Blood Vessels and Circulation
Chapter 20 *Lecture PowerPoint The Circulatory System: Blood Vessels and Circulation *See separate FlexArt PowerPoint slides for all figures and tables preinserted into PowerPoint without notes. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Introduction • The route taken by the blood after it leaves the heart was a point of much confusion for many centuries – Chinese emperor Huang Ti (2697–2597 BC) believed that blood flowed in a complete circuit around the body and back to the heart – Roman physician Galen (129–c. 199) thought blood flowed back and forth like air; the liver created blood out of nutrients and organs consumed it – English physician William Harvey (1578–1657) did experimentation on circulation in snakes; birth of experimental physiology – After microscope was invented, blood and capillaries were discovered by van Leeuwenhoek and Malpighi 20-2 General Anatomy of the Blood Vessels • Expected Learning Outcomes – Describe the structure of a blood vessel. – Describe the different types of arteries, capillaries, and veins. – Trace the general route usually taken by the blood from the heart and back again. – Describe some variations on this route. 20-3 General Anatomy of the Blood Vessels Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Capillaries Artery: Tunica interna Tunica media Tunica externa Nerve Vein Figure 20.1a (a) 1 mm © The McGraw-Hill Companies, Inc./Dennis Strete, photographer • Arteries carry blood away from heart • Veins -
4B. the Heart (Cor) 1
Henry Gray (1821–1865). Anatomy of the Human Body. 1918. 4b. The Heart (Cor) 1 The heart is a hollow muscular organ of a somewhat conical form; it lies between the lungs in the middle mediastinum and is enclosed in the pericardium (Fig. 490). It is placed obliquely in the chest behind the body of the sternum and adjoining parts of the rib cartilages, and projects farther into the left than into the right half of the thoracic cavity, so that about one-third of it is situated on the right and two-thirds on the left of the median plane. Size.—The heart, in the adult, measures about 12 cm. in length, 8 to 9 cm. in breadth at the 2 broadest part, and 6 cm. in thickness. Its weight, in the male, varies from 280 to 340 grams; in the female, from 230 to 280 grams. The heart continues to increase in weight and size up to an advanced period of life; this increase is more marked in men than in women. Component Parts.—As has already been stated (page 497), the heart is subdivided by 3 septa into right and left halves, and a constriction subdivides each half of the organ into two cavities, the upper cavity being called the atrium, the lower the ventricle. The heart therefore consists of four chambers, viz., right and left atria, and right and left ventricles. The division of the heart into four cavities is indicated on its surface by grooves. The atria 4 are separated from the ventricles by the coronary sulcus (auriculoventricular groove); this contains the trunks of the nutrient vessels of the heart, and is deficient in front, where it is crossed by the root of the pulmonary artery. -
Young Adults. Look for ST Elevation, Tall QRS Voltage, "Fishhook" Deformity at the J Point, and Prominent T Waves
EKG Abnormalities I. Early repolarization abnormality: A. A normal variant. Early repolarization is most often seen in healthy young adults. Look for ST elevation, tall QRS voltage, "fishhook" deformity at the J point, and prominent T waves. ST segment elevation is maximal in leads with tallest R waves. Note high take off of the ST segment in leads V4-6; the ST elevation in V2-3 is generally seen in most normal ECG's; the ST elevation in V2- 6 is concave upwards, another characteristic of this normal variant. Characteristics’ of early repolarization • notching or slurring of the terminal portion of the QRS wave • symmetric concordant T waves of large amplitude • relative temporal stability • most commonly presents in the precordial leads but often associated with it is less pronounced ST segment elevation in the limb leads To differentiate from anterior MI • the initial part of the ST segment is usually flat or convex upward in AMI • reciprocal ST depression may be present in AMI but not in early repolarization • ST segments in early repolarization are usually <2 mm (but have been reported up to 4 mm) To differentiate from pericarditis • the ST changes are more widespread in pericarditis • the T wave is normal in pericarditis • the ratio of the degree of ST elevation (measured using the PR segment as the baseline) to the height of the T wave is greater than 0.25 in V6 in pericarditis. 1 II. Acute Pericarditis: Stage 1 Pericarditis Changes A. Timing 1. Onset: Day 2-3 2. Duration: Up to 2 weeks B. Findings 1. -
Basic Rhythm Recognition
Electrocardiographic Interpretation Basic Rhythm Recognition William Brady, MD Department of Emergency Medicine Cardiac Rhythms Anatomy of a Rhythm Strip A Review of the Electrical System Intrinsic Pacemakers Cells These cells have property known as “Automaticity”— means they can spontaneously depolarize. Sinus Node Primary pacemaker Fires at a rate of 60-100 bpm AV Junction Fires at a rate of 40-60 bpm Ventricular (Purkinje Fibers) Less than 40 bpm What’s Normal P Wave Atrial Depolarization PR Interval (Normal 0.12-0.20) Beginning of the P to onset of QRS QRS Ventricular Depolarization QRS Interval (Normal <0.10) Period (or length of time) it takes for the ventricles to depolarize The Key to Success… …A systematic approach! Rate Rhythm P Waves PR Interval P and QRS Correlation QRS Rate Pacemaker A rather ill patient……… Very apparent inferolateral STEMI……with less apparent complete heart block RATE . Fast vs Slow . QRS Width Narrow QRS Wide QRS Narrow QRS Wide QRS Tachycardia Tachycardia Bradycardia Bradycardia Regular Irregular Regular Irregular Sinus Brady Idioventricular A-Fib / Flutter Bradycardia w/ BBB Sinus Tach A-Fib VT PVT Junctional 2 AVB / II PSVT A-Flutter SVT aberrant A-Fib 1 AVB 3 AVB A-Flutter MAT 2 AVB / I or II PAT PAT 3 AVB ST PAC / PVC Stability Hypotension / hypoperfusion Altered mental status Chest pain – Coronary ischemic Dyspnea – Pulmonary edema Sinus Rhythm Sinus Rhythm P Wave PR Interval QRS Rate Rhythm Pacemaker Comment . Before . Constant, . Rate 60-100 . Regular . SA Node Upright in each QRS regular . Interval =/< leads I, II, . Look . Interval .12- .10 & III alike .20 Conduction Image reference: Cardionetics/ http://www.cardionetics.com/docs/healthcr/ecg/arrhy/0100_bd.htm Sinus Pause A delay of activation within the atria for a period between 1.7 and 3 seconds A palpitation is likely to be felt by the patient as the sinus beat following the pause may be a heavy beat. -
Abnormally Enlarged Singular Thebesian Vein in Right Atrium
Open Access Case Report DOI: 10.7759/cureus.16300 Abnormally Enlarged Singular Thebesian Vein in Right Atrium Dilip Kumar 1 , Amit Malviya 2 , Bishwajeet Saikia 3 , Bhupen Barman 4 , Anunay Gupta 5 1. Cardiology, Medica Institute of Cardiac Sciences, Kolkata, IND 2. Cardiology, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong, IND 3. Anatomy, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong, IND 4. Internal Medicine, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong, IND 5. Cardiology, Vardhman Mahavir Medical College (VMMC) and Safdarjung Hospital, New Delhi, IND Corresponding author: Amit Malviya, [email protected] Abstract Thebesian veins in the heart are subendocardial venoluminal channels and are usually less than 0.5 mm in diameter. The system of TV either opens a venous (venoluminal) or an arterial (arterioluminal) channel directly into the lumen of the cardiac chambers or via some intervening spaces (venosinusoidal/ arteriosinusoidal) termed as sinusoids. Enlarged thebesian veins are reported in patients with congenital heart disease and usually, multiple veins are enlarged. Very few reports of such abnormal enlargement are there in the absence of congenital heart disease, but in all such cases, they are multiple and in association with coronary artery microfistule. We report a very rare case of a singular thebesian vein in the right atrium, which was abnormally enlarged. It is important to recognize because it can be confused with other cardiac structures like coronary sinus during diagnostic or therapeutic catheterization and can lead to cardiac injury and complications if it is attempted to cannulate it or pass the guidewires. -
Basic ECG Interpretation
12/2/2016 Basic Cardiac Anatomy Blood Flow Through the Heart 1. Blood enters right atrium via inferior & superior vena cava 2. Right atrium contracts, sending blood through the tricuspid valve and into the right ventricle 3. Right ventricle contracts, sending blood through the pulmonic valve and to the lungs via the pulmonary artery 4. Re-oxygenated blood is returned to the left atrium via the right and left pulmonary veins 5. Left atrium contracts, sending blood through the mitral valve and into the left ventricle 6. Left ventricle contracts, sending blood through the aortic Septum valve and to the body via the aorta 1 http://commons.wikimedia.org/wiki/File:Diagram_of_the_human_heart 2 _(cropped).svg Fun Fact….. Layers of the Heart Pulmonary Artery – The ONLY artery in the body that carries de-oxygenated blood Pulmonary Vein – The ONLY vein in the body that carries oxygenated blood 3 4 Layers of the Heart Endocardium Lines inner cavities of the heart & covers heart valves (Supplies left ventricle) Continuous with the inner lining of blood vessels Purkinje fibers located here; (electrical conduction system) Myocardium Muscular layer – the pump or workhorse of the heart “Time is Muscle” Epicardium Protective outer layer of heart (Supplies SA node Pericardium in most people) Fluid filled sac surrounding heart 5 6 http://stanfordhospital.org/images/greystone/heartCenter/images/ei_0028.gif 1 12/2/2016 What Makes the Heart Pump? Electrical impulses originating in the right atrium stimulate cardiac muscle contraction Your heart's -
What Is Single Ventricle?
LifeLife withwith aa SingleSingle VentricleVentricle StephenStephen Crumb,Crumb, APNAPN CoordinatorCoordinator CColumbusolumbus OOhiohio AAdultdult CCongenitalongenital HHearteart DiseaseDisease ProgramProgram Biology 101 Q. Your heart has ______ chambers? A. ___3____ Wrong! You need to study!! But you asked how many chambers MY heart has! My heart has only 3 chambers because I have a single ventricle !! ObjectivesObjectives DescribeDescribe thethe congenitalcongenital heartheart defectsdefects thatthat leadlead toto singlesingle ventricleventricle DiscussDiscuss longlong--termterm issuesissues thatthat maymay arisearise inin peoplepeople withwith singlesingle ventricleventricle andand howhow toto treattreat themthem DiscussDiscuss waysways toto staystay healthyhealthy LearnLearn fromfrom eacheach otherother TheThe NormalNormal HeartHeart WhatWhat isis SingleSingle Ventricle?Ventricle? AbnormalAbnormal heartheart structurestructure presentpresent atat birthbirth OnlyOnly oneone functionalfunctional pumpingpumping chamberchamber (ventricle)(ventricle) SeveralSeveral congenitalcongenital heartheart defectsdefects leadlead toto singlesingle ventricle,ventricle, aa featurefeature ofof allall isis cyanosiscyanosis CyanosisCyanosis BlueBlue colorcolor duedue toto lowlow bloodblood oxygenoxygen CausedCaused byby mixingmixing ofof oxygenoxygen--poorpoor (blue)(blue) bloodblood andand oxygenoxygen--richrich (red)(red) bloodblood MixingMixing isis necessarynecessary forfor initialinitial survivalsurvival HypoplasticHypoplastic LeftLeft -
Visualizing Real Tim E Vasomotion in Vivo Using Optical Coherence
A Visualizing real time vasomotion in vivo using Optical Coherence Tom ography Suhir Abuhajar 2012 Lancaster University-Physics Department-Nonlinear Biomedical Physics Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy in Physics ProQuest Number: 11003436 All rights reserved INFORMATION TO ALL USERS The quality of this reproduction is dependent upon the quality of the copy submitted. In the unlikely event that the author did not send a com plete manuscript and there are missing pages, these will be noted. Also, if material had to be removed, a note will indicate the deletion. uest ProQuest 11003436 Published by ProQuest LLC(2018). Copyright of the Dissertation is held by the Author. All rights reserved. This work is protected against unauthorized copying under Title 17, United States C ode Microform Edition © ProQuest LLC. ProQuest LLC. 789 East Eisenhower Parkway P.O. Box 1346 Ann Arbor, Ml 4 8 1 0 6 - 1346 C ontents Declaration v Abstract vi Acknowledgment vii 1 Introduction 1 1.1 Motivation .................................................................................................... 1 1.2 Structure of the th esis ............................................................................. 2 1.3 Physiology of the skin ............................................................................. 5 1.3.1 Functions of the s k i n ................................................................... 7 1.3.2 Structure of human s k i n ............................................................ 9 1.3.3 -
The American Society of Echocardiography
1 THE AMERICAN SOCIETY OF ECHOCARDIOGRAPHY RECOMMENDATIONS FOR CARDIAC CHAMBER QUANTIFICATION IN ADULTS: A QUICK REFERENCE GUIDE FROM THE ASE WORKFLOW AND LAB MANAGEMENT TASK FORCE Accurate and reproducible assessment of cardiac chamber size and function is essential for clinical care. A standardized methodology creates a common approach to the assessment of cardiac structure and function both within and between echocardiography labs. This facilitates better communication and improves the ability to compare results between studies as well as differentiate normal from abnormal findings in an individual patient. This document summarizes key points from the 2015 ASE Chamber Quantification Guideline and is meant to serve as quick reference for sonographers and interpreting physicians. It is designed to provide guidance on chamber quantification for adult patients; a separate ASE Guidelines document that details recommended quantification methods in the pediatric age group has also been published and should be used for patients <18 years of age (3). (1) For details of the methodology and the rationale for current recommendations, the interested reader is referred to the complete Guideline statement. Figures and tables are reproduced from ASE Guidelines. (1,2) Table of Contents: 1. Left Ventricle (LV) Size and Function p. 2 a. LV Size p. 2 i. Linear Measurements p. 2 ii. Volume Measurements p. 2 iii. LV Mass Calculations p. 3 b. Left Ventricular Function Assessment p. 4 i. Global Systolic Function Parameters p. 4 ii. Regional Function p. 5 2. Right Ventricle (RV) Size and Function p. 6 a. RV Size p. 6 b. RV Function p. 8 3. Atria p. -
ECG P Wave Abnormalities
E lectrocardiography S eries Singapore Med J 2013; 54(1) : 4 CMEARTICLE ECG P wave abnormalities Li Ling Tan1, MBBS, MRCP, Swee Guan Teo1,2, MBBS, MRCP, Kian Keong Poh1,2, FRCP, FACC Fig. 1 ECG shows bifid P waves in leads II, III and aVF. CASE 1 tomography (CT) of his brain showed an infarct involving the CLINICAL PRESENTATION right putamen and internal capsule. He was otherwise A 58-year-old man presented to the emergency department asymptomatic. What does the electrocardiogram (ECG) in Fig. 1 with a one-week history of left-sided weakness. Computed show? 1Cardiac Department, National University Heart Centre, National University Health System, 2Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore Correspondence: A/Prof Poh Kian Keong, Senior Consultant and Associate Professor, Cardiac Department, National University Heart Centre, 1E Kent Ridge Road, NUHS Tower Block, Level 9, Singapore 119228. [email protected] E lectrocardiography S eries 2a 2b Fig. 2 (a) Echocardiogram in the parasternal long axis view shows a calcified mitral valve. There is restricted opening and closing of the posterior mitral valve leaflet (thick arrow), as well as doming of the anterior mitral valve leaflet (thin arrow); (b) At diastole, the mitral valve opening is markedly reduced (outlined and labeled with an asterisk). RV: right ventricle; LV: left ventricle; LA: left atrium ECG INTERPRETATION CLINICAL COURSE ECG shows the presence of ‘P mitrale’ in multiple leads – inferior Transthoracic echocardiogram showed moderately severe mitral leads II, III and aVF, and also leads V2, V3 and V4. The duration stenosis (Fig. -
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. -
Effect of Mental Stress on Myocardial Blood Flow and Vasomotion in Patients with Coronary Artery Disease
Effect of Mental Stress on Myocardial Blood Flow and Vasomotion in Patients with Coronary Artery Disease Heiko Schoder, Daniel H. Silverman, Roxana Campisi, Harold Karpman, Michael E. Phelps, Heinrich R. Schelbert, and Johannes Czernin Department ofMolecular and Medical Pharmacology, Division ofNuclear Medicine, School ofMedicine, University of California, Los Angeles; and Laboratory ofStructural Biology and Molecular Medicine, University ofCalifornia, Los Angeles, California dial oxygen demand is physiologically accommodated by an In patients with coronary artery disease (CAD), mental stress increase in myocardial blood flow (MBF). Therefore, in may provoke ischemic electrocardiographchanges and abnor healthy individuals mental stress induces coronary artery malities in regionaland global left ventricularfunction. However, vasodilatation (3,4). In patients with coronary artery disease little is known about the underlyingmyocardialblood flow (CAD), however, mental stress modeled in a laboratory or response(MBF)inthesepatients.Methods: We investigatedthe experienced in daily life can induce myocardial ischemia as hemodynamic, neurohumoral, and myocardial blood flow re sponses to mental stress in 17 patients with CAD and 17 healthy evidenced by ischemic changes on electrocardiography volunteers of similar age. Mental stress was induced by asking (ECG) (5), left ventricular wall motion abnormalities, and a individualsto solve mathematicsubtractionsin a progressively decline in left ventricular ejection fraction (6, 7). Such challenging sequence; MBF was quantified at rest and during abnormal responses to mental stress may also predict mentalstressusing13NammoniaPET.Results:Mentalstress ischemic events, such as unstable angina pectoris or myocar induced significant (P < 0.01) and comparable increases in dial infarction, in daily life (8,9). rate—pressureproduct, measured in beats per minute x mm Hg, The mechanisms underlying these mental stress—induced in bothpatients(from7826 ±2006to 10586±2800)and healthy volunteers (from 8227 ±1272 to 10618 ±2468).