The Jugular Venous Pressure Revisited
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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 -
Cardiac Symptoms and Physical Signs 11
CHAPTER 1 1 Cardiac Symptoms and Physical Signs 1.1 Common Cardiac Symptoms Angina Typical angina presents as a chest tightness or heaviness brought on by effort and relieved by rest. The sensation starts in the retrosternal region and radi- ates across the chest. Frequently it is associated with a leaden feeling in the arms. Occasionally it may present in more unusual sites, e.g. pain in the jaw or teeth on effort, without pain in the chest. It may be confused with oesopha- geal pain, or may present as epigastric or even hypochondrial pain. The most important feature is its relationship to effort. Unilateral chest pain (sub- mammary) is not usually cardiac pain, which is generally symmetrical in distribution. Angina is typically exacerbated by heavy meals, cold weather (just breath- ing in cold air is enough) and emotional disturbances. Arguments with col- leagues or family and watching exciting television are typical precipitating factors. Stable Angina This is angina induced by effort and relieved by rest. It does not increase in frequency or severity, and is predictable in nature. It is associated with ST- segment depression on ECG. Decubitus Angina This is angina induced by lying down at night or during sleep. It may be caused by an increase in LVEDV (and hence wall stress) on lying fl at, associ- ated with dreaming or getting between cold sheets. Coronary spasm may occur in REM sleep. It may respond to a diuretic, calcium antagonist or nitrate taken in the evening. Swanton’s Cardiology, sixth edition. By R. H. Swanton and S. -
Cardiology-EKG Michael Bradley
Cardiology/EKG Board Review Michael J. Bradley D.O. DME/Program Director Family Medicine Residency Objectives • Review general method for EKG interpretation • Review specific points of “data gathering” and “diagnoses” on EKG • Review treatment considerations • Review clinical cases/EKG’s • Board exam considerations EKG EKG – 12 Leads • Anterior Leads - V1, V2, V3, V4 • Inferior Leads – II, III, aVF • Left Lateral Leads – I, aVL, V5, V6 • Right Leads – aVR, V1 11 Step Method for Reading EKG’s • “Data Gathering” – steps 1-4 – 1. Standardization – make sure paper and paper speed is standardized – 2. Heart Rate – 3. Intervals – PR, QT, QRS width – 4. Axis – normal vs. deviation 11 Step Method for Reading EKG’s • “Diagnoses” – 5. Rhythm – 6. Atrioventricular (AV) Block Disturbances – 7. Bundle Branch Block or Hemiblock of – 8. Preexcitation Conduction – 9. Enlargement and Hypertrophy – 10. Coronary Artery Disease – 11. Utter Confusion • The Only EKG Book You’ll Ever Need Malcolm S. Thaler, MD Heart Rate • Regular Rhythms Heart Rate • Irregular Rhythms Intervals • Measure length of PR interval, QT interval, width of P wave, QRS complex QTc • QTc = QT interval corrected for heart rate – Uses Bazett’s Formula or Fridericia’s Formula • Long QT syndrome – inherited or acquired (>75 meds); torsades de ponites/VF; syncope, seizures, sudden death Axis Rhythm • 4 Questions – 1. Are normal P waves present? – 2. Are QRS complexes narrow or wide (≤ or ≥ 0.12)? – 3. What is relationship between P waves and QRS complexes? – 4. Is rhythm regular or irregular? -
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 -
Central Venous Pressure Venous Examination but Underestimates Ultrasound Accurately Reflects the Jugular
Ultrasound Accurately Reflects the Jugular Venous Examination but Underestimates Central Venous Pressure Gur Raj Deol, Nicole Collett, Andrew Ashby and Gregory A. Schmidt Chest 2011;139;95-100; Prepublished online August 26, 2010; DOI 10.1378/chest.10-1301 The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.chestpubs.org/content/139/1/95.full.html Chest is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright2011by the American College of Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder. (http://chestjournal.chestpubs.org/site/misc/reprints.xhtml) ISSN:0012-3692 Downloaded from chestjournal.chestpubs.org at UCSF Library & CKM on January 21, 2011 © 2011 American College of Chest Physicians CHEST Original Research CRITICAL CARE Ultrasound Accurately Refl ects the Jugular Venous Examination but Underestimates Central Venous Pressure Gur Raj Deol , MD ; Nicole Collett , MD ; Andrew Ashby , MD ; and Gregory A. Schmidt , MD , FCCP Background: Bedside ultrasound examination could be used to assess jugular venous pressure (JVP), and thus central venous pressure (CVP), more reliably than clinical examination. Methods: The study was a prospective, blinded evaluation comparing physical examination of external jugular venous pressure (JVPEXT), internal jugular venous pressure (JVPINT), and ultrasound collapse pressure (UCP) with CVP measured using an indwelling catheter. We com- pared the examination of the external and internal JVP with each other and with the UCP and CVP. -
Central Venous Pressure: Uses and Limitations
Central Venous Pressure: Uses and Limitations T. Smith, R. M. Grounds, and A. Rhodes Introduction A key component of the management of the critically ill patient is the optimization of cardiovascular function, including the provision of an adequate circulating volume and the titration of cardiac preload to improve cardiac output. In spite of the appearance of several newer monitoring technologies, central venous pressure (CVP) monitoring remains in common use [1] as an index of circulatory filling and of cardiac preload. In this chapter we will discuss the uses and limitations of this monitor in the critically ill patient. Defining Central Venous Pressure What is the Central Venous Pressure? Central venous pressure is the intravascular pressure in the great thoracic veins, measured relative to atmospheric pressure. It is conventionally measured at the junction of the superior vena cava and the right atrium and provides an estimate of the right atrial pressure. The Central Venous Pressure Waveform The normal CVP exhibits a complex waveform as illustrated in Figure 1. The waveform is described in terms of its components, three ascending ‘waves’ and two descents. The a-wave corresponds to atrial contraction and the x descent to atrial relaxation. The c wave, which punctuates the x descent, is caused by the closure of the tricuspid valve at the start of ventricular systole and the bulging of its leaflets back into the atrium. The v wave is due to continued venous return in the presence of a closed tricuspid valve. The y descent occurs at the end of ventricular systole when the tricuspid valve opens and blood once again flows from the atrium into the ventricle. -
The Icefish (Chionodraco Hamatus)
The Journal of Experimental Biology 207, 3855-3864 3855 Published by The Company of Biologists 2004 doi:10.1242/jeb.01180 No hemoglobin but NO: the icefish (Chionodraco hamatus) heart as a paradigm D. Pellegrino1,2, C. A. Palmerini3 and B. Tota2,4,* Departments of 1Pharmaco-Biology and 2Cellular Biology, University of Calabria, 87030, Arcavacata di Rende, CS, Italy, 3Department of Cellular and Molecular Biology, University of Perugia, 06126, Perugia, Italy and 4Zoological Station ‘A. Dohrn’, Villa Comunale, 80121, Napoli, Italy *Author for correspondence (e-mail: [email protected]) Accepted 13 July 2004 Summary The role of nitric oxide (NO) in cardio-vascular therefore demonstrate that under basal working homeostasis is now known to include allosteric redox conditions the icefish heart is under the tonic influence modulation of cell respiration. An interesting animal for of a NO-cGMP-mediated positive inotropism. We also the study of this wide-ranging influence of NO is the cold- show that the working heart, which has intracardiac adapted Antarctic icefish Chionodraco hamatus, which is NOS (shown by NADPH-diaphorase activity and characterised by evolutionary loss of hemoglobin and immunolocalization), can produce and release NO, as multiple cardio-circulatory and subcellular compensations measured by nitrite appearance in the cardiac effluent. for efficient oxygen delivery. Using an isolated, perfused These results indicate the presence of a functional NOS working heart preparation of C. hamatus, we show that system in the icefish heart, possibly serving a both endogenous (L-arginine) and exogenous (SIN-1 in paracrine/autocrine regulatory role. presence of SOD) NO-donors as well as the guanylate cyclase (GC) donor 8Br-cGMP elicit positive inotropism, while both nitric oxide synthase (NOS) and sGC Key words: nitric oxide, heart, Antarctic teleost, icefish, Chionodraco inhibitors, i.e. -
A Review of the Stroke Volume Response to Upright Exercise in Healthy Subjects
190 Br J Sports Med: first published as 10.1136/bjsm.2004.013037 on 25 March 2005. Downloaded from REVIEW A review of the stroke volume response to upright exercise in healthy subjects C A Vella, R A Robergs ............................................................................................................................... Br J Sports Med 2005;39:190–195. doi: 10.1136/bjsm.2004.013037 Traditionally, it has been accepted that, during incremental well trained athletes (subject sex was not stated). Unfortunately, these findings were exercise, stroke volume plateaus at 40% of VO2MAX. largely ignored and it became accepted that However, recent research has documented that stroke stroke volume plateaus during exercise of increasing intensity. volume progressively increases to VO2MAX in both trained More recent investigations have reported that and untrained subjects. The stroke volume response to stroke volume progressively increases in certain 7–12 incremental exercise to VO2MAX may be influenced by people. The mechanisms for the continual training status, age, and sex. For endurance trained increase in stroke volume are not completely understood. Gledhill et al7 proposed that subjects, the proposed mechanisms for the progressive enhanced diastolic filling and subsequent increase in stroke volume to VO2MAX are enhanced diastolic enhanced contractility are responsible for the filling, enhanced contractility, larger blood volume, and increased stroke volume in trained subjects. However, an increase in stroke volume with an decreased cardiac afterload. For untrained subjects, it has increase in exercise intensity has also been been proposed that continued increases in stroke volume reported in untrained subjects.89Table 1 presents may result from a naturally occurring high blood volume. a summary of the past research that has quantified stroke volume during exercise. -
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 -
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. -
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.