DOCSLIB.ORG

Diastolic-Systolic Differences in Coronary Blood Flow: Effect of Stenosis and Tachycardia in the Anaesthetized Dog

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Diastolic-Systolic Differences in Coronary Blood Flow: Effect of Stenosis and Tachycardia in the Anaesthetized Dog Physiol. Res. 43: 373-381, 1993 Diastolic-systolic Differences in Coronary Blood Flow: Effect of Stenosis and Tachycardia in the Anaesthetized Dog D. GATTULLO, M. DAMBROSIO, A. FEDERICI, R.J. LINDEN1, G. LOSANO, P. PAGLIARO Department of Anatomy and Human Physiology, University of Torino, Italy and 1 Division of Biomedical Science, King's College, London, UK Received April 13, 1993 Accepted August 2, 1993 Summary Blood flow in the left coronary artery is lower in the systole than in the diastole. This difference is attenuated in the presence of severe stenosis, which affects the flow more during the diastole than during the systole. Some explanations have been suggested: epicardial vasodilatation distal to the stenosis, a decrease in myocardial contractility and impairment of the intramyocardial pump effect. The present investigation in anaesthetized dogs showed that, in the presence of severe stenosis, the attenuation of the diastolic-systolic coronary flow differences occurs together with distal vasodilatation in the epicardial layers of the myocardium. This attenuation may be even greater if further vasodilatation is induced by increasing the heart rate. Mo evidence of reduced myocardial contractility was observed. In addition, it was found that the onset of the systolic rise of the coronary blood pressure below the stenosis occurs before that of the aortic blood pressure. This finding may serves as evidence for the role played by the intramyocardial pump mechanism in causing the systolic reduction of coronary flow. Since this mechanism is believed to propel some blood back into the aorta during the systole, the impairment of this retrograde flow caused by the stenosis could also account for the reduction of the diastolic-systolic flow differences. Key words Coronary flow - Coronary stenosis - Intramyocardial pump Introduction Arterial blood flow shows rhythmic Spaan et al. 1986, Spaan and Dankelman 1989). The fluctuations depending on cardiac activity, i.e. an extent of the systolic reduction of coronary flow has increase during the systole and a decrease during the recently been attributed to the myocardial contractility diastole. This general pattern is reversed in large (Krams et al. 1989b). It is known that the severe coronary arteries, where the flow in the systole is lower stenosis of a large coronary epicardial artery not only than in the diastole, because myocardial contraction causes a reduction in the mean flow, but also modifies compresses the intramyocardial vessels (Gregg and the pattern of the phasic flow (Furuse et al. 1975, Green 1940, Wiggers 1954, Gregg et al. 1965, Klocke Mates et al. 1978). There is a decrease in diastolic 1976). The waterfall model of Permutt and Riley coronary flow which is not accompanied by a similar (1963) has been used to describe the systolic reduction decrease in systolic coronary flow, the latter being less of coronary flow (Downey and Kirk 1975). Another reduced, unchanged or slightly increased, so that the model of the coronary circulation, "the intramyocardial differences of diastolic-systolic flow are attenuated. pump model" suggested by Spaan and his group The hypotheses proposed to explain the above provides a quantitative relationship between the changes have considered that myocardial contractility is myocardial systolic compression and diastolic reduced, that vasodilatation occurs in the epicardial relaxation and the diastolic-systolic coronary flow layers of the myocardium distal to the stenosis (Mates differences (Spaan et al. 1981, Bruinsma et al. 1985, etal. 1978) and that the effect of the intramyocardial 374 Gattullo et al. V o l. 42 pump is impaired (Spaan et al. 1981). In the present in a dose of 30 mg/kg. After the trachea had been study we tried to verify the hypothesis that intubated with a Magill tube, artificial positive pressure vasodilatation is a major factor in the attenuation of ventilation was started using a Harvard respiratory the diastolic-systolic coronary flow differences in the pump (Model 607, Harvard Apparatus Co., Dover MA, presence of severe stenosis. We examined the diastolic- U.SA.). systolic coronary flow differences before and after the The neck was opened along the ventral production of severe flow limiting stenosis; then, with midline and the right external jugular vein, the the stenosis in place, the heart rate was increased to common carotid arteries and the vagal nerves were raise oxygen consumption resulting in vasodilatation. dissected free. A catheter was inserted into the vein to Records of the left ventricular pressure were used to administer the solutions needed for the maintenance of assess possible changes in myocardial contractility. anaesthesia and of the acid-base balance. Two Preliminary results of this study have been catheters connected to Statham P23Db presented to the British Physiological Society (Gattullo electromanometers (Statham Laboratories, Hato Rey, et al. 1993). Puerto Rico) were inserted into the common carotid arteries: the tip of one was pushed into the aortic root Methods to transmit aortic blood pressure (ABP) near the coronary ostia; the tip of the other was pushed into the The experiments were performed on six left ventricle to transmit left ventricular pressure mongrel dogs weighing 18-27 kg. General anaesthesia (LVP). was induced by i.v. injection of sodium pentobarbitone F»g-1 Schematic drawing of the constrictor device. A= Micromanipulator. B= Joining support between the piston of the micromanipulator and the camera shutter release. C= Camera shutter release. D= Magnification of the perspex housing with the metal cylinder compressing the artery. The artery (a) is partially constricted by the metal cylinder (me). E= Positions on the heart of the constrictor, the flow probe (f), and the coronary pressure catheter (p). 1993 Coronary Stenosis in the Dog 375 After a left thoracotomy in the fourth Anaesthesia was maintained by continuous i.v. intercostal space, the pericardium was opened parallel infusion (12.5 /¿g/kg/min) of sodium pentothal, and an to the left phrenic nerve and the heart suspended in a hourly injection ( 1.0 /¿g/kg) of fentanyl (opiate-related pericardial cradle. To record coronary blood flow analgesic, Fentanest, Carlo Erba, Milano, Italy). (CBF), a flow probe connected to a 400 c.p.s. Samples of arterial blood were taken from the right electromagnetic flowmeter BL 310 (Biotronics femoral artery and analyzed for Po2, PCo2, pH, Laboratories Inc., Silver Spring, MD, U.SA.) was bicarbonate concentration and base excess using an placed around the initial part of the left circumflex IL 1302 gas analyzer (Instrument Laboratory System). coronary artery. Distal to the flow probe, a constrictor Acid-base and respiratory status were maintained device was placed around the artery (Dalla Valle and within normal limits of the dog (Altman and Dittmer Di Lavore 1988). The device surrounded the artery 1964) by regulating the respiratory pump and infusing, with curved housing of rigid Perspex and a metal a bicarbonate solution, when required. Body cylinder (Fig. 1) attached to a micromanipulator by a temperature was monitored by an Ellab DU rectal camera shutter release, about 20 cm long. The thermistor probe (Ellab Co., Copenhagen, Denmark) micromanipulator produced small movements in the and kept within normal limits using an electric pad metal cylinder which, when driven towards the housing, and/or an infrared ray lamp. constricted the artery to the required extent. Due to ECG, ABP, LVP, CBP, CBF, AF and the time the characteristics of the constrictor an eccentric rather trace were recorded using a DR -8 cathode ray recorder than a concentric stenosis could be obtained. The (Electronics for Medicine, White Plains, NY, U.SA.). extent of the constriction was read on the scale of the At the end of the experiments the animals micromanipulator. It was expressed in terms of were killed by i.v. injection of an excess of sodium percentage constriction, 100 % being the fully occluded pentobarbitone. artery and 0 % as the fully open vessel (Dalla Valle and Di Lavore 1988). The constrictor was also used to Experimental protocol occlude the artery for obtaining the level of the zero Following surgery, the experiments were flow line. started after a steady-state had been obtained with Another flow probe connected to a 1000 c.p.s. respect to the anaesthesia and the acid-base status. In 310 BL electromagnetic flowmeter was placed around each animal the heart was paced at the rate of 100 the ascending aorta, just beyond the aortic valve, to b.p.m. during the control period. Then the left record aortic flow (AF) assisting in the continuous circumflex coronary artery was constricted by about monitoring of the condition of the animal. 85 % of the range determined on the scale of the Coronary blood pressure (CBP) distal to the micromanipulator. Owing to the characteristics of the constriction was transduced by a third Statham P23Db arterial wall and the shape of the constrictor, it is electromanometer, connected to a catheter inserted possible only to indicate the degree of constriction in into the marginal artery, a branch of the left circumflex terms of a percentage change in the constrictor and not coronary artery. in terms of the actual reduction of the arterial lumen. After the vagi had been sutured, the right However, in order to quantitate the influence of the vagus distal to the occlusion was placed inside stenosis, the extent of changes in coronary resistance electrodes connected to a San’ei ES-103 stimulator has been assessed by calculating these changes in terms (San’ei Instruments Ltd.). Stimuli of 4 -7 V and 2 ms of the total coronary resistance (see below). With the in duration at 6 -8 c.p.s. were delivered to slow the artery constricted, the pacing was continued initially at heart rate and to enable pacing of the heart rate at 100 100 b.p.m. and then increased to 160 b.p.m.
Load more

Recommended publications
  • 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
    [Show full text]
  • 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
    [Show full text]
  • 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
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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
    [Show full text]
  • 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.
    [Show full text]
  • JUGULAR VENOUS PRESSURE Maddury Jyotsna
    INDIAN JOURNAL OF CARDIOVASCULAR DISEASES JOURNAL in women (IJCD) 2017 VOL 2 ISSUE 2 CLINICAL ROUNDS 1 WINCARS JVP- JUGULAR VENOUS PRESSURE Maddury Jyotsna DEFINITION OF JUGULAR VENOUS PULSE AND The external jugular vein descends from the angle of the PRESSURE mandible to the middle of the clavicle at the posterior Jugular venous pulse is defined as the oscillating top of border of the sternocleidomastoid muscle. The external vertical column of blood in the right Internal Jugular jugular vein possesses valves that are occasionally Vein (IJV) that reflects the pressure changes in the right visible. Blood flow within the external jugular vein is atrium in cardiac cycle. In other words, Jugular venous nonpulsatile and thus cannot be used to assess the pressure (JVP) is the vertical height of oscillating column contour of the jugular venous pulse. of blood (Fig 1). Reasons for Internal Jugular Vein (IJV) preferred over Fig 1: Schematic diagram of JVP other neck veins are IJV is anatomically closer to and has a direct course to right atrium while EJV does not directly drain into Superior vena cava. It is valve less and pulsations can be seen. Due to presence of valves in External Jugular vein, pulsations cannot be seen. Vasoconstriction secondary to hypotension (as in congestive heart failure) can make EJV small and barely visible. EJV is superficial and prone to kinking. Partial compression of the left in nominate vein is usually relieved during modest inspiration as the diaphragm and the aorta descend and the pressure in the two internal
    [Show full text]
  • The Heart and Cardiovascular Function
    18 The Heart and Cardiovascular Function Lecture Presentation by Lori Garrett © 2018 Pearson Education, Inc. Section 1: Structure of the Heart Learning Outcomes 18.1 Describe the heart’s location, shape, its four chambers, and the pulmonary and systemic circuits. 18.2 Describe the location and general features of the heart. 18.3 Describe the structure of the pericardium and explain its functions, identify the layers of the heart wall, and describe the structures and functions of cardiac muscle. 18.4 Describe the cardiac chambers and the heart’s external anatomy. © 2018 Pearson Education, Inc. Section 1: Structure of the Heart Learning Outcomes (continued) 18.5 Describe the major vessels supplying the heart, and cite their locations. 18.6 Trace blood flow through the heart, identifying the major blood vessels, chambers, and heart valves. 18.7 Describe the relationship between the AV and semilunar valves during a heartbeat. 18.8 Define arteriosclerosis, and explain its significance to health. © 2018 Pearson Education, Inc. Module 18.1: The heart has four chambers that pump and circulate blood through the pulmonary and systemic circuits Cardiovascular system = heart and blood vessels transporting blood Heart—directly behind sternum . Base—superior • where major vessels are • ~1.2 cm (0.5 in.) to left • 3rd costal cartilage . Apex—inferior, pointed tip • ~12.5 cm (5 in.) from base • ~7.5 cm (3 in.) to left • 5th intercostal space © 2018 Pearson Education, Inc. Borders of the heart © 2018 Pearson Education, Inc. Module 18.1: Heart location and chambers Heart = 2-sided pump with 4 chambers . Right atrium receives blood from systemic circuit .
    [Show full text]