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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 -
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 -
Bio 104 Cardiovascular System
29 Bio 104 Cardiovascular System Lecture Outline: Cardiovascular System Hole’s HAP [Chapters 14, 15, 16] Blood: Introduction (Chapter 14) - - - - A. Characteristics of Blood 1. Blood Volume - - - 2. Blood Composition a. Blood Cells Red blood cells White blood cells Platelets b. Plasma 3. Origin of Blood Cells - - 30 Bio 104 Cardiovascular System B. Red Blood Cells 1. Characteristics - - - oxyhemoglobin - deoxyhemoglobin - 2. Red Blood Cell Counts 4.6 – 6.2 4.2. – 5.4 reflects blood’s ___________________________ 3. Red Blood Cell Production low blood oxygen ________________________ RBC production vitamin B12, folic acid, Fe are necessary Dietary Factors Affecting RBC Production 31 Bio 104 Cardiovascular System 4. Life Cycle of RBC lifespan worn out RBCs destroyed by Hb heme and globin 5. Anemia Def. = C. White Blood Cells 1. Functions & Types diapedesis positive chemotaxis granulocytes - - - agranulocytes - - 32 Bio 104 Cardiovascular System 2. White Blood Cell Counts 5, 000 - 10,000 leukopenia leukocytosis differential WBC count Granulocytes Agranulocytes Neutrophils (segs, PMNs, bands) Monocytes Eosinophils Lymphocytes Basophils D. Platelets - cell fragments -130,000 - 360,000 - helps control _______________ Plasma A. Characteristics 33 Bio 104 Cardiovascular System B. Plasma Proteins C. Gases and Nutrients Gases Nutrients - - - - - - D. Nonprotein Nitrogenous Substances Urea - Uric acid - Amino acids – Creatine – Creatinine – BUN – E. Plasma Electrolytes Absorbed from the _____________ or released as by-products -
Effects of Vasodilation and Arterial Resistance on Cardiac Output Aliya Siddiqui Department of Biotechnology, Chaitanya P.G
& Experim l e ca n i t in a l l C Aliya, J Clinic Experiment Cardiol 2011, 2:11 C f a Journal of Clinical & Experimental o r d l DOI: 10.4172/2155-9880.1000170 i a o n l o r g u y o J Cardiology ISSN: 2155-9880 Review Article Open Access Effects of Vasodilation and Arterial Resistance on Cardiac Output Aliya Siddiqui Department of Biotechnology, Chaitanya P.G. College, Kakatiya University, Warangal, India Abstract Heart is one of the most important organs present in human body which pumps blood throughout the body using blood vessels. With each heartbeat, blood is sent throughout the body, carrying oxygen and nutrients to all the cells in body. The cardiac cycle is the sequence of events that occurs when the heart beats. Blood pressure is maximum during systole, when the heart is pushing and minimum during diastole, when the heart is relaxed. Vasodilation caused by relaxation of smooth muscle cells in arteries causes an increase in blood flow. When blood vessels dilate, the blood flow is increased due to a decrease in vascular resistance. Therefore, dilation of arteries and arterioles leads to an immediate decrease in arterial blood pressure and heart rate. Cardiac output is the amount of blood ejected by the left ventricle in one minute. Cardiac output (CO) is the volume of blood being pumped by the heart, by left ventricle in the time interval of one minute. The effects of vasodilation, how the blood quantity increases and decreases along with the blood flow and the arterial blood flow and resistance on cardiac output is discussed in this reviewArticle. -
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. -
CARDIAC CYCLE & CONTROL (All Cd References Refer to Interactiv
Biology 251 Fall 2015 TOPIC 15: CARDIOVASCULAR SYSTEM: CARDIAC CYCLE & CONTROL (All cd references refer to Interactive Physiology cd, Cardiovascular menu) I. Mechanical Events in the Cardiac Cycle (Figs 13.18 to 13.21; cd cardiac cycle 5 to 17) A. Introduction 1. Systole: Contraction and emptying of the chambers 2. Diastole: Relaxation and filling of the chambers 3. Atria and Ventricles go through separate cycles of systole and diastole 4. The contraction status (being in systole or diastole) determines heart chamber pressure which determines whether valves are open or closed. B. TP interval: Ventricular diastole 1. Atria and ventricles are in diastole (i.e., relaxed). 2. Blood flows from veins into atria 3. Ventricuclar Pressure < Aortic Pressure = Aortic Valve closed 4. Atrial pressure > Ventricular Pressure = AV valve open so 5. Blood flows from atria directly into ventricles. C. P wave and PQ interval: Late ventricular diastole 1. Ventricuclar Pressure < Aortic Pressure = aortic valve closed 2. SA node reaches threshold and fires. 3. Atrial depolarization occurs. 4. Atria contract = atrial systole 5. Atrial Pressure > Ventricular Pressure = AV valves open. 6. Blood squeezed by atrial contraction from atria into ventricles. D. QR Interval: End of ventricular diastole 1. Ventricuclar pressure < Aortic Pressure = Aortic Valve closed 2. Atrial Pressure > Ventricular Pressure = AV valves open. 3. Blood squeezed from atria into ventricles. 4. Electrical impulse enters ventricles from the AV node. 5. Ventricles begin to depolarize. 6. R peak is end of ventricular diastole and start of ventricular systole. E. RS interval: Early ventricluar systole 1. Ventricles begin to contract. 2. Atrial Pressure < Ventricle Pressure = AV valves close 3. -
Cardiovascular Responses to Hypoxemia in Sinoaortic-Denervated Fetal Sheep
003 1-399819 1 /3004-038 1$03.0010 PEDIATRIC RESEARCH Vol. 30. No. 4, I991 Copyright ID1991 International Pediatric Research Foundation. Inc. I1riiirc~c/it1 U.S. ,.I Cardiovascular Responses to Hypoxemia in Sinoaortic-Denervated Fetal Sheep JOSEPH ITSKOVITZ (ELDOR), EDMOND F. LAGAMMA. JAMES BRISTOW, AND ABRAHAM M. RUDOLPH Ccirdiovascz~karResearch Instillrle. Unlver:c.i/yqf Califi~rniu,Sari Francisco. Sun Francisco. Cu11fi)rilia94/43 ABSTRACT. Fetal cardiovascular response to acute hy- hypoxemia in postnatal life (1 3). The vascular effects of periph- poxemia is characterized by bradycardia, hypertension, and eral chemoreceptor stimulation, with ventilation held constant, redistribution of cardiac output. The role of aortic and include coronary vasodilation and vasoconstriction in the carotid chemoreceptors in mediating these responses was splanchnic organs and the skeletal muscles. Stimulation of the examined in eight sinoaortic-denervated and nine sham- carotid body chemoreceptors results in reflex bradycardia and operated fetal lambs. Blood gases, pH, heart rate, arterial negative inotropic responses. The bradycardia and peripheral pressure, and blood flow distribution were determined be- vasoconstriction during carotid chemoreceptor stimulation can fore and during hypoxemia. In intact fetuses, heart rate be reversed by effects arising from concurrent hypernea (13). fell from 184 -+ 12 to 165 + 23 beatslmin (p< 0.01) but The arterial chemoreceptors (aortic and carotid bodies) are increased from 184 + 22 to 200 + 16 beatslmin (p< 0.05) active in the fetal lamb and are responsive to hypoxemia (14- in the sinoaortic-denervated fetuses. Intact fetuses showed 21). Stimulation of the fetal arterial chemoreceptors result in an early hypertensive response to hypoxemia, whereas the bradycardia, which is abolished by SAD (19, 20, 22). -
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. -
The Duration of Left Ventricular Systole in Mitral Incompetence
Br Heart J: first published as 10.1136/hrt.24.4.464 on 1 July 1962. Downloaded from THE DURATION OF LEFT VENTRICULAR SYSTOLE IN MITRAL INCOMPETENCE BY P. G. F. NIXON AND G. R. WAGNER From the Department of Medicine and Thoracic Surgery, in the General Infirmary at Leeds Received December 11, 1961 In mitral incompetence the left ventricle has two exits and it has been suggested that diminished resistance to emptying causes left ventricular systole to be shorter than normal (Brigden and Leatham, 1953). Theoretically the elevation of left ventricular end-diastolic pressure that is found in severe mitral incompetence (Ross et al., 1958; Nixon, 1961a) should result in prolongation of systole. The purpose of this communication is to report measurements of left ventricular systole in patients with mitral incompetence, and to consider their significance. MATERIAL AND METHODS Patients with chronic rheumatic mitral valvular disease submitted to diagnostic left heart catheteri- zation were selected for this study provided they were free from evidence of congestive heart failure, aortic valvular, hypertensive, or ischaemic heart disease: six had atrial fibrillation and were severely http://heart.bmj.com/ disabled by their mitral disease. During cardiac catheterization mean arterial blood pressure lay between 80 and 100 mm. Hg in five cases; in one it was 110 mm. Hg. Pulmonary hyper- tension was present, average pulmonary arterial systolic pressures lying between 40 and 60 mm. Hg. The diagnosis of pure or predominant incompetence was made from the presence of all ofthe follow- ing findings: clinical and radiological evidence of left ventricular enlargement; left ventricular apical impulse displacement curves (Schneider and Klunhaar, 1961) showing a prominent "third heart sound wave ", and evidence ofventricular stasis in diastole (Fig. -
Blood Vessels and Circulation
19 Blood Vessels and Circulation Lecture Presentation by Lori Garrett © 2018 Pearson Education, Inc. Section 1: Functional Anatomy of Blood Vessels Learning Outcomes 19.1 Distinguish between the pulmonary and systemic circuits, and identify afferent and efferent blood vessels. 19.2 Distinguish among the types of blood vessels on the basis of their structure and function. 19.3 Describe the structures of capillaries and their functions in the exchange of dissolved materials between blood and interstitial fluid. 19.4 Describe the venous system, and indicate the distribution of blood within the cardiovascular system. © 2018 Pearson Education, Inc. Module 19.1: The heart pumps blood, in sequence, through the arteries, capillaries, and veins of the pulmonary and systemic circuits Blood vessels . Blood vessels conduct blood between the heart and peripheral tissues . Arteries (carry blood away from the heart) • Also called efferent vessels . Veins (carry blood to the heart) • Also called afferent vessels . Capillaries (exchange substances between blood and tissues) • Interconnect smallest arteries and smallest veins © 2018 Pearson Education, Inc. Module 19.1: Blood vessels and circuits Two circuits 1. Pulmonary circuit • To and from gas exchange surfaces in the lungs 2. Systemic circuit • To and from rest of body © 2018 Pearson Education, Inc. Module 19.1: Blood vessels and circuits Circulation pathway through circuits 1. Right atrium (entry chamber) • Collects blood from systemic circuit • To right ventricle to pulmonary circuit 2. Pulmonary circuit • Pulmonary arteries to pulmonary capillaries to pulmonary veins © 2018 Pearson Education, Inc. Module 19.1: Blood vessels and circuits Circulation pathway through circuits (continued) 3. Left atrium • Receives blood from pulmonary circuit • To left ventricle to systemic circuit 4. -
Basic Cardiac Rhythms – Identification and Response Module 1 ANATOMY, PHYSIOLOGY, & ELECTRICAL CONDUCTION Objectives
Basic Cardiac Rhythms – Identification and Response Module 1 ANATOMY, PHYSIOLOGY, & ELECTRICAL CONDUCTION Objectives ▪ Describe the normal cardiac anatomy and physiology and normal electrical conduction through the heart. ▪ Identify and relate waveforms to the cardiac cycle. Cardiac Anatomy ▪ 2 upper chambers ▪ Right and left atria ▪ 2 lower chambers ▪ Right and left ventricle ▪ 2 Atrioventricular valves (Mitral & Tricuspid) ▪ Open with ventricular diastole ▪ Close with ventricular systole ▪ 2 Semilunar Valves (Aortic & Pulmonic) ▪ Open with ventricular systole ▪ Open with ventricular diastole The Cardiovascular System ▪ Pulmonary Circulation ▪ Unoxygenated – right side of the heart ▪ Systemic Circulation ▪ Oxygenated – left side of the heart Anatomy Coronary Arteries How The Heart Works Anatomy Coronary Arteries ▪ 2 major vessels of the coronary circulation ▪ Left main coronary artery ▪ Left anterior descending and circumflex branches ▪ Right main coronary artery ▪ The left and right coronary arteries originate at the base of the aorta from openings called the coronary ostia behind the aortic valve leaflets. Physiology Blood Flow Unoxygenated blood flows from inferior and superior vena cava Right Atrium Tricuspid Valve Right Ventricle Pulmonic Valve Lungs Through Pulmonary system Physiology Blood Flow Oxygenated blood flows from the pulmonary veins Left Atrium Mitral Valve Left Ventricle Aortic Valve Systemic Circulation ▪ Blood Flow Through The Heart ▪ Cardiology Rap Physiology ▪ Cardiac cycle ▪ Represents the actual time sequence between -
The Jugular Venous Pressure Revisited
REVIEW CME EDUCATIONAL OBJECTIVE: Readers will measure and interpret the jugular venous pressure in their patients CREDIT with heart failure JOHN MICHAEL S. CHUA CHIACO, MD NISHA I. PARIKH, MD, MPH DAVID J. FERGUSSON, MD Cardiovascular Disease, John A. Burns School Assistant Professor, John A. Burns School Clinical Professor of Medicine, Department of Medicine, University of Hawaii, Honolulu of Medicine, University of Hawaii; of Cardiology, John A. Burns School The Queen’s Medical Center, Honolulu of Medicine, University of Hawaii; The Queen’s Medical Center, Honolulu The jugular venous pressure revisited ■■ ABSTRACT n this age of technological marvels, I it is easy to become so reliant on them as Assessment of the jugular venous pressure is often inad- to neglect the value of bedside physical signs. equately performed and undervalued. Here, we review Yet these signs provide information that adds the physiologic and anatomic basis for the jugular venous no cost, is immediately available, and can be pressure, including the discrepancy between right atrial repeated at will. and central venous pressures. We also describe the cor- Few physical findings are as useful but as rect method of evaluating this clinical finding and review undervalued as is the estimation of the jugular the clinical relevance of the jugular venous pressure, venous pressure. Unfortunately, many practi- especially its value in assessing the severity and response tioners at many levels of seniority and experi- to treatment of congestive heart failure. Waveforms ence do not measure it correctly, leading to a vicious circle of unreliable information, lack reflective of specific conditions are also discussed.