New Approaches to Monitoring of Cardiac Function Emil Söderqvist Doctoral Thesis, Royal Institute of Technology, 2006
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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 -
Chronotropic Incompetence: a Proposal for Br Heart J: First Published As 10.1136/Hrt.70.5.400 on 1 November 1993
400 Br Heart3' 1993;70:400-402 FOR DEBATE Chronotropic incompetence: a proposal for Br Heart J: first published as 10.1136/hrt.70.5.400 on 1 November 1993. Downloaded from definition and diagnosis Demosthenes Katritsis, A John Camm Between 1958 and 1960 Astrand docu- exercise testing that is <75%16 or <80%"7 of mented the normal heart rate response to the predicted MPHR. Other arbitrary defini- exercise in healthy individuals and noted that tions such as a maximum exercise heart rate the maximum heart rate decreased with age.' 2 <100 beats/min" or <120 beats/min'8 have A reduced cardiac chronotropic response to also been used. However, the achievement of isoprenaline has been reported in elderly sub- maximum exercise is not always possible. jects and alterations in catecholamine- Elderly cardiac patients, especially those adrenergic receptor interactions may be disabled by chronotropic incompetence, are responsible for this change of cardiovascular unable to perform sufficient exercise on the regulation in the elderly.35 In addition the treadmill. Furthermore, everyday life activi- parasympathetic innervation of the sinus ties of these patients usually correspond to node is currently under investigation.6 Over low work loads up to 6 metabolic equivalents the years it has also been recognised that corresponding to the first stage of the stan- an inadequate chronotropic response dard Bruce protocol. In addition, not much is (chronotropic incompetence) at maximal known about the patterns of heart rate accel- exercise is common in patients with cardiac eration and deceleration in the presence of disease78 and much interest has centred chronotropic incompetence. -
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: 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. -
Electrocardiography in Horses – Part 2: How to Read the Equine ECG
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Ghent University Academic Bibliography Vlaams Diergeneeskundig Tijdschrift, 2010, 79 Thema: electrocardiography in horses 337 Electrocardiography in horses – part 2: how to read the equine ECG Elektrocardiografie bij paarden – deel 2: interpretatie van het EKG T. Verheyen, A. Decloedt, D. De Clercq, P. Deprez, S. U. Sys, G. van Loon Department of Large Animal Internal Medicine Faculty of Veterinary Medicine, Ghent University Salisburylaan 133, 9820 Merelbeke, Belgium [email protected] ABSTRACT The equine practitioner is faced with a wide variety of dysrhythmias, of which some are physiological. The recording of an exercise electrocardiogram (ECG) can help distinguish between physiological and patholog- ical dysrhythmias, underlining the importance of exercise recordings. The evaluation of an ECG recording should be performed in a highly methodical manner in order to avoid errors. Each P wave should be followed by a QRS complex, and each QRS complex should be preceded by a P wave. The classification of dysrhythmias according to their origin helps to understand the associated changes on the ECG. In this respect, sinoatrial nodal (SA nodal), atrial myocardial, atrioventricular nodal (AV nodal) and ventricular myocardial dysrhythmias can be distinguished. Artefacts on the ECG can lead to misinterpretations. Recording an ECG of good quality is a prerequisite to prevent misinterpretations, but artefacts are almost impossible to avoid when recording during exercise. Changes in P or T waves during exercise also often lead to misinterpretations, however they have no clinical significance. SAMENVATTING De paardendierenarts wordt geconfronteerd met een waaier van dysritmieën, waarvan sommige fysiologisch zijn. -
Presentation Title
Meet the experts: Cardiogenic Shock Inotropes: effects on the heart, the microcirculation and other organs ACCA Masterclass 2017 Alessandro Sionis Director Acute & Intensive Cardiac Care Unit Hospital de la Santa Creu I Sant Pau Universitat de Barcelona Spain Disclosures (last 5 years) ► Speaker: Abiomed, Maquet, Novartis, Orion-Pharma ► Clinical trials: Cardiorentis, Novartis, Orion-Pharma ► Research grants: Novartis, Orion-Pharma ► Royalties: No PATIENT WITH AHF Bedside assessment to identify haemodynamic profile CONGESTION? YES (95% of AHF patients) NO (5% of AHF patients) “Wet” “Dry” POOR PERFUSION? NO YES NO YES “Wet” & “Warm” “Wet” & “Cold” “Dry” & “Warm” “Dry” & “Cold” Adapted from 2016 ESC HF Guildeines PATIENT WITH AHF Bedside assessment to identify haemodynamic profile CONGESTION? YES (95% of AHF patients) NO (5% of AHF patients) “Wet” “Dry” POOR PERFUSION? NO YES NO YES “Wet” & “Warm” “Wet” & “Cold” “Dry” & “Warm” “Dry” & “Cold” Adapted from 2016 ESC HF Guildeines Definitions of Terms Used in Cardiogenic Shock Diagnosis Term Definition Symptoms/signs of congestion (left-sided) Orthopnoea, paroxysmal nocturnal dyspnoea, pulmonary rales (bilateral), peripheral oedema (bilateral). Symptoms/signs of congestion (right-sided) Jugular venous dilatation, peripheral oedema, congested hepatpmegaly, hepatojugular reflux, ascites, symptoms of gut congestionsymptoms of gut congestion. Symptoms/signs of hypoperfusion Clinical: cold sweated extremities, oliguria, mental confusion, dizziness, narrow pulse pressure. Laboratory measures: metabolic -
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. -
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. -
Electrical Activity of the Heart: Action Potential, Automaticity, and Conduction 1 & 2 Clive M
Electrical Activity of the Heart: Action Potential, Automaticity, and Conduction 1 & 2 Clive M. Baumgarten, Ph.D. OBJECTIVES: 1. Describe the basic characteristics of cardiac electrical activity and the spread of the action potential through the heart 2. Compare the characteristics of action potentials in different parts of the heart 3. Describe how serum K modulates resting potential 4. Describe the ionic basis for the cardiac action potential and changes in ion currents during each phase of the action potential 5. Identify differences in electrical activity across the tissues of the heart 6. Describe the basis for normal automaticity 7. Describe the basis for excitability 8. Describe the basis for conduction of the cardiac action potential 9. Describe how the responsiveness relationship and the Na+ channel cycle modulate cardiac electrical activity I. BASIC ELECTROPHYSIOLOGIC CHARACTERISTICS OF CARDIAC MUSCLE A. Electrical activity is myogenic, i.e., it originates in the heart. The heart is an electrical syncitium (i.e., behaves as if one cell). The action potential spreads from cell-to-cell initiating contraction. Cardiac electrical activity is modulated by the autonomic nervous system. B. Cardiac cells are electrically coupled by low resistance conducting pathways gap junctions located at the intercalated disc, at the ends of cells, and at nexus, points of side-to-side contact. The low resistance pathways (wide channels) are formed by connexins. Connexins permit the flow of current and the spread of the action potential from cell-to-cell. C. Action potentials are much longer in duration in cardiac muscle (up to 400 msec) than in nerve or skeletal muscle (~5 msec). -
60 Arterial Pressure–Based Cardiac Output Monitoring 525
PROCEDURE Arterial Pressure–Based Cardiac 60 Output Monitoring Susan Scott PURPOSE: Arterial pressure–based cardiac output monitoring is a minimally invasive technology that can be used to obtain hemodynamic data on a continuous basis. PREREQUISITE NURSING • The difference between the systolic and diastolic pressures KNOWLEDGE is called the pulse pressure, with a normal value of 40 mm Hg. • Arterial pressure is determined by the relationship between • Knowledge of the anatomy and physiology of the cardio- blood fl ow through the vessels (cardiac output), the com- vascular system is necessary. pliance of the aorta and larger vessels, and the resistance • Knowledge of the anatomy and physiology of the vascu- of the more peripheral vessel walls (systemic vascular lature and adjacent structures is needed. resistance). The arterial pressure is therefore affected by • Understanding of the pathophysiologic changes that occur any factors that change either cardiac output, compliance, in heart disease and affect fl ow dynamics is necessary. or systemic vascular resistance. • Understanding of aseptic technique is needed. • The average arterial pressure during a cardiac cycle is • Understanding of the hemodynamic effects of vasoactive called the mean arterial pressure (MAP). It is not the medications and fl uid resuscitation is needed. average of the systolic plus the diastolic pressures, because 1 • Understanding of the principles involved in hemodynamic at normal heart rates systole accounts for 3 of the cardiac 2 monitoring is necessary. cycle and diastole accounts for 3 of the cardiac cycle. • Knowledge of invasive cardiac output monitoring is needed. The MAP is calculated automatically by most patient • Knowledge of arterial waveform interpretation is needed. -
Cardiovascular System: Heart
Cardiovascular System: Heart Cardiovascular System – Heart Conducting cells: Cardiac Electrophysiology Cardiac cells specialized to quickly spread action potentials across myocardium • Weak force generators System allows for orderly, sequential depolarization and Intrinsic Conduction System: contraction of heart Normal sinus rhythm: 1) AP originates at SA node 2) SA node fires at 60 – 100 beats / min Atrial internodal tracts Sinoatrial node: (SA node) 3) Correct myocardial activation sequence • Located in right atrial wall • Initiates action potentials (APs) • Pacemaker (~ 80 beats / min) Bundle branches Atrioventricular node: (AV Node) • Connects atria to ventricles • Slowed conduction velocity • Ventricular filling Purkinje Bundle of His fibers Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.14 1 Cardiovascular System – Heart Cardiac Electrophysiology The autonomic nervous system can directly affect the heart rate; these effects are called chronotropic effects Recall: spontaneous depolarization = VG Na+ channels Positive chronotrophic effects: (increase heart rate) • Under sympathetic control Leads to g ; cells SA Na NE node reach threshold more rapidly Sinoatrial node Pharmacology: β1 receptors β-blockers (e.g., propanolol) Negative chronotrophic effects: (decrease heart rate) • Under parasympathetic control Leads to gNa; cells reach threshold SA less rapidly ACh node Leads to gK; cells hyperpolarized during Muscarinic receptors repolarization stage (further from threshold) Costanzo (Physiology, 4th ed.) – Figure