BRS Physiology
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Chronotropic, Dromotropic and Inotropic Effects of Dilazep in the Intact Dog Heart and Isolated Atrial Preparation Shigetoshi CH
Chronotropic, Dromotropic and Inotropic Effects of Dilazep in the Intact Dog Heart and Isolated Atrial Preparation Shigetoshi CHIBA, M.D., Miyoharu KOBAYASHI, M.D., Masahiro SHIMOTORI,M.D., Yasuyuki FURUKAWA, M.D., and Kimiaki SAEGUSA, M.D. SUMMARY When dilazep was administered intravenously to the anesthe- tized donor dog, mean systemic blood pressure was dose depend- ently decreased. At a dose of 0.1mg/Kg i.v., the mean blood pressure was not changed but a slight decrease in heart rate was usually observed in the donor dog. At the same time, a slight but significant decrease in atrial rate and developed tension of the iso- lated atrium was induced. Within a dose range of 0.3 to 1mg/Kg i.v., dilazep caused a dose related decrease in mean blood pressure, bradycardia in the donor dog, and negative chronotropic, dromo- tropic and inotropic effects in the isolated atrium. At larger doses of 3 and 10mg/Kg i.v., dilazep caused marked hypotension, fre- quently with severe sinus bradycardia or sinus arrest, especially in isolated atria. When dilazep was infused intraarterially at a rate of 0.2-1 ƒÊ g/min into the cannulated sinus node artery of the isolated atrium, negative chrono- and inotropic effects were dose dependently in- duced. With respect to dromotropism, SA conduction time (SACT) was prolonged at infusion rates of 0.2 and 0.4ƒÊg/min. But at 1ƒÊg, dilazep caused an increase or decrease of SACT, indicating a shift of the SA nodal pacemaker. It is concluded that dilazep has direct negative chrono-, dromo- and inotropic properties on the heart at doses which produced no significant hypotension. -
Integration of Detailed Modules in a Core Model of Body Fluid Homeostasis and Blood Pressure Regulation
Integration of detailed modules in a core model of body fluid homeostasis and blood pressure regulation. Alfredo Hernández, Virginie Le Rolle, David Ojeda, Pierre Baconnier, Julie Fontecave-Jallon, François Guillaud, Thibault Grosse, Robert Moss, Patrick Hannaert, Randall Thomas To cite this version: Alfredo Hernández, Virginie Le Rolle, David Ojeda, Pierre Baconnier, Julie Fontecave-Jallon, et al.. Integration of detailed modules in a core model of body fluid homeostasis and blood pres- sure regulation.. Progress in Biophysics and Molecular Biology, Elsevier, 2011, 107 (1), pp.169-82. 10.1016/j.pbiomolbio.2011.06.008. inserm-00654821 HAL Id: inserm-00654821 https://www.hal.inserm.fr/inserm-00654821 Submitted on 27 Dec 2011 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Integration of detailed modules in a core model of body fluid homeostasis and blood pressure regulation Alfredo I. Hernández1,2, Virginie Le Rolle1,2, David Ojeda1,2, Pierre Baconnier3, Julie Fontecave-Jallon3, François Guillaud4, Thibault Grosse5,6, Robert G. Moss5,6, Patrick Hannaert4, S. Randall Thomas5,6 1INSERM, U642, Rennes, F-35000, France; 2Université de Rennes 1, LTSI, Rennes, F-35000, France; 3 UJF-Grenoble 1 / CNRS / TIMC-IMAG UMR 5525 (Equipe PRETA), Grenoble, F-38041, France 4INSERM U927. -
Regulation of the Systemic Circulation*
CIRCULATORY PHYSIOLOGY SECTION 6: REGULATION OF THE SYSTEMIC CIRCULATION* Summary: This set of notes integrates what we have learned about vascular and cardiac function into a whole so that we can see how the entire circulation is regulated. These are very important concepts and their mastery will move you a long way towards a real understanding of the operation of the circulatory system. I. The Systemic Vascular System -- The influence of cardiac output on the partition of blood between the venous and arterial sides of the systemic circulation. A. Earlier we have indicated that at rest most of the blood in the systemic circulation is located in the venous side. This is in part due to the relatively high capacitance of the venous system when compared to the arterial system. This gives a reserve of blood that can be used when demands for respiratory gas circulation increase as in exercise. B. When there is no circulation (death or experimental interruption of the cardiac output), there is still a blood pressure in both the arterial and venous systems. 1. As we indicated earlier, this is due to the elastic forces stored in the walls of the vessels -- since in the absence of a hemorrhage the vessels contain enough fluid to increase their volume beyond resting volume, there must be a pressure even if the blood is not moving. 2. This low pressure is referred to as the mean circulatory pressure (Guyton) and for normal blood volumes is about 7mmHg (know this value). 3. Due to the greater compliance of the venous system, the greatest relative proportion of the total blood volume will reside in the venous system when operating at the mean circulatory pressure (i.e., when the heart is stopped). -
Ventricular End-Diastolic Volume (Ml)
Stroke Volume and Heart Failure Black/Blue: text. Red: very important. Green: Doctor’s notes. Pink: formulas. Yellow: numbers. Gray: notes and explanation. Physiology Team 436 – Cardiovascular Block Lecture 9 Lecture: If work is intended for initial studying. Review: If work is intended for revision. 1 Objectives Study Smart: focus on mutual topics. From the students’ guide: Explain how cardiac contractility affect stroke volume. Calculate CO using Fick’s principle equation. Explain pathophysiology of heart failure and differentiate between left and right failure. Explain how the pathophysiology associated with heart failure results in typical signs and symptoms. 2 Stroke Volume Stroke volume: is the volume of blood pumped (ejected) by each ventricle per beat (during each ventricular systole), and it is about 70-80 ml/beat. Factors Affecting It: 1- End diastolic volume (EDV) (Preload): • It is: the volume of blood present in each ventricle at the end of ventricular diastole. • Preload: load on the muscle in the relaxed state. Indices of left ventricular • Normal amount: 120-130 ml, can be increased during diastole preload: (filling of ventricles) to a volume of (120-130mL). 1- Left ventricle end diastolic • Applying preload to a muscle causes: volume Or pressure (LVEDV) 1- The muscle to stretch. 2- Right atrial pressure 2- The muscle to develop passive tension. More relaxation time, more filling, more volume. EDV Depends on: A- Filling time: the duration of ventricular diastole. B- Venous return: the rate of blood flow during ventricular diastole. 3 Stroke Volume and Factors Affecting it 1- End diastolic volume (EDV) 2- End systolic volume (ESV) (Residual): (Preload): It is: volume of blood present (that remains) in Mechanism: each ventricle at the end of ventricular systole. -
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 -
Cardio Vascular Assessment in Vasoplegia Following Cardiac Surgery Kanishka Indraratna*
Review Article ISSN 2639-846X Anesthesia & Pain Research Cardio Vascular Assessment in Vasoplegia Following Cardiac Surgery Kanishka Indraratna* *Correspondence: Kanishka Indraratna, Sri Jayewardenepura General Hospital, Sri Sri Jayewardenepura General Hospital, Sri Lanka, Postal Address- Lanka, Postal Address-7A, Claessen Place, Colombo-5, Sri Lanka, 7A, Claessen Place, Colombo, Sri Lanka. Tel: +94777578144, E-mail: [email protected]. Received: 25 July 2018; Accepted: 29 August 2018 Citation: Indraratna K. Cardiovascular Assessment in Vasoplegia Following Cardiac Surgery. Anesth Pain Res. 2018; 2(2): 1-4. ABSTRACT Severe vasodilatation during cardiac surgery has been known for many years. It is characterized by a low systemic vascular resistance, a high cardiac index, and a low blood pressure, which can be resistant to even high doses of vasoconstrictors. This condition is associated with a high mortality. After cardiac surgery, there can be cardiac dysfunction as well. However with a low systemic vascular resistance, the cardiac function curve would be shifted upwards and to the left, giving the impression of good contractility. The ejection fraction, which is the commonly used measurement of cardiac contractility, cannot therefore be relied upon for a correct assessment under these circumstances. This can affect fluid and inotrope management. Therefore a measurement which does not depend on the afterload, but measures pure myocardial contractility is required. Ventricular elastance is such a measure. A measurement of arterial elastance which reflects the flow characteristics and pulsatility of flow may be more appropriate than systemic vascular resistance to measure arterial tone. Ventricular-arterial coupling has to be maintained for optimum myocardial performance. The severe vasodilatation, the possible myocardial impairment and also its treatment with high doses of vasoconstrictors can affect the relationship between the ventricular and arterial systems. -
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. -
2.Heart As Pump
By Adam Hollingworth 2.Heart as a Pump Table of Contents Cardiac Cycle ......................................................................................................................................................... 2 CVS Pressures .................................................................................................................................................................... 3 Heart Failure ..................................................................................................................................................................... 3 Pericardium ....................................................................................................................................................................... 3 Timing .................................................................................................................................................................................. 4 Length of Systole & Diastole ......................................................................................................................................... 4 Arterial Pulse ........................................................................................................................................................ 4 JVP ............................................................................................................................................................................. 4 Cardiac Graph ...................................................................................................................................................... -
Control of Cardiac Output in Thyrotoxic Calves. Evaluation of Changes in the Systemic Circulation
Control of cardiac output in thyrotoxic calves. Evaluation of changes in the systemic circulation. S Goldman, … , M Olajos, E Morkin J Clin Invest. 1984;73(2):358-365. https://doi.org/10.1172/JCI111220. Research Article The contribution of peripheral vascular factors to the high output state in thyrotoxicosis was examined in 11 calves treated with daily intramuscular injections of L-thyroxine (200 micrograms/kg) for 12-14 d. Thyroxine treatment increased cardiac output from 14.1 +/- 1.4 to 24.7 +/- 1.4 liters/min (P less than 0.001) and decreased systemic vascular resistance from 562 +/- 65 to 386 +/- 30 dyn-s/cm5 (P less than 0.01). Blood volume was increased from 65 +/- 4 ml/kg in the euthyroid state to 81 +/- 6 ml/kg when the animals were thyrotoxic (P less than 0.05). The role of low peripheral vascular resistance in maintenance of the high output state was evaluated by infusion of phenylephrine at two dosages (2.5 and 4.0 micrograms/kg per min). In the euthyroid state, no significant decrease in cardiac output was observed at either level of pressor infusion. In the thyrotoxic state, the higher dosage of phenylephrine increased peripheral resistance to the euthyroid control level and caused a small (6%) decrease in cardiac output (P less than 0.05). This small decrease in cardiac output probably could be attributed to the marked increase in left ventricular afterload caused by the pressor infusion as assessed from measurements of intraventricular pressure and dimensions. Changes in the venous circulation were evaluated by measurement of mean circulatory filling pressure and the pressure gradient […] Find the latest version: https://jci.me/111220/pdf Control of Cardiac Output in Thyrotoxic Calves Evaluation of Changes in the Systemic Circulation Steven Goldman, Marcey Olajos, and Eugene Morkin Department of Internal Medicine, Veterans Administration Medical Center, Tucson, Arizona 85723; Departments of Internal Medicine and Pharmacology, University ofArizona College of Medicine, Tucson, Arizona 85724 Abstract. -
Chronic Chagasic Cardiomyopathy (CCC) with Severe Biventricular Involvement and Intraventricular Dromotropic Disturbances
Chronic Chagasic Cardiomyopathy (CCC) with severe biventricular involvement and intraventricular dromotropic disturbances Andrés Ricardo Pérez-Riera, M.D. Ph.D. Raimundo Barbosa-Barros, MD Design of Studies and Scientific Writing Chief of the Coronary Center of the Hospital de Messejana Dr. Carlos Laboratory in the ABC School of Medicine, Alberto Studart Gomes. Fortaleza – CE- Brazil Santo André, São Paulo, Brazil https://ekgvcg.wordpress.com Portuguese Relato de caso Paciente de 29 anos, branca, procedente de área rural endêmica, casa de pau a pique, vários membros da família infectados, portadora de miocardiopatia chagásica crônica com quadro clínico de severa cardiopatia dilatada em classe funcional IV, mesmo com medicação plena. ECO: severo comprometimento da função sistólica biventricular por hipocinesia difusa e fração de ejeção do VE = 22%. Insuficiência mitral e tricúspide ostial severas; diâmetro diastólico do VE = 4.7 Altura / cm / m, pressão sistólica da artéria pulmonar = 44 mmHg. Em uso regular de carvedilol 25 mg 2xdia, furosemida 40 mg 2xdia, espironolactona 25 mgxdia, maleato de enalapril 20 mg 2xdia, amiodarona 100 mg x dia, ácido acetilsalicílico 100 mg x dia. Perguntas: 1. Qual o diagnóstico ECG/VCG? 2. Qual a conduta adequada? English Case report 29-year-old, female, Caucasian, from an endemic rural área for Chagas disease, a stick-up house, several family members infected, carrier of chronic chagasic cardiomyopathy with clinical signs of severe dilated cardiomyopathy functional class IV, even with full medication. ECO: severe impairment of biventricular systolic function due to diffuse hypokinesia and LV ejection fraction = 22%. Severe ostial mitral regurgitation and tricuspid insufficiency; LV diastolic diameter = 4.7 LV/ height/cm/m, pulmonary artery systolic pressure = 44 mmHg. -
Calcium Channel Blockers (Ccbs)
DRUG CLASSES CALCIUM CHANNEL BLOCKERS Calcium channel blockers (CCBs) or calcium antagonists, are among the most widely used drugs in cardiovascular medicine with roles not only in hypertension but also in angina and (for some CCBs) tachyarrhythmias. Examples Amlodipine Diltiazem Felodipine Isradipine Lacidipine Lercanidipine Nicardipine Nifedipine Nisoldipine Verapamil Mechanism of action CCBs promote vasodilator activity (and reduce blood pressure) by reducing calcium influx into vascular smooth muscle cells by interfering with voltage-operated calcium channels (and to a lesser extent receptor-operated channels) in the cell membrane. Interference with intracellular calcium influx is also important in cardiac muscle, cardiac conduction tissue and gastrointestinal smooth muscle. In cardiac tissues, CCBs have potential for negative inotropic, chronotropic and dromotropic activity while the gastrointestinal effects predispose to constipation. These effects vary with different agents according to ability to penetrate cardiac and other tissues, relative affinity for calcium channels in different tissues and the influence of reflux cardiac stimulation secondary to peripheral vasodilation. 1 Although often considered as a single class, CCBs can be subdivided according to structural and functional distinctions. Dihydropyridine derivates : amlodipine, felodipine, isradipine, lacidipine, lercanidipine, nicardipine, nifedipine, nisoldipine Phenylalkylamine : verapamil Benzothiazepine derivative : diltiazem Dihydropyridine derivatives have pronounced -
Cardiac Output Venous Return
Circulatory Physiology As a Country Doc Episode 3 Cardiac Output and Venous Return Patrick Eggena, M.D. Novateur Medmedia, LLC. Circulatory Physiology As a Country Doc Episode 3 Cardiac Output and Venous Return Patrick Eggena, M.D. Novateur Medmedia, LLC. i Copyright This Episode is derived from: Course in Cardiovascular Physiology by Patrick Eggena, M.D. © Copyright Novateur Medmedia, LLC. April 13, 2012 The United States Copyright Registration Number: PAu3-662-048 Ordering Information via iBooks: ISBN 978-0-9663441-2-7 Circulatory Physiology as a Country Doc, Episode 3: Cardiac Output and Venous Return Contact Information: Novateur Medmedia, LLC 39 Terry Hill Road, Carmel, NY 10512 email: [email protected] Credits: Oil Paintings by Bonnie Eggena, PsD. Music by Alan Goodman from his CD Under the Bed, Cancoll Music, copyright 2005 (with permission). Illustrations, movies, text, and lectures by Patrick Eggena, M.D. Note: Knowledge in the basic and clinical sciences is constantly changing. The reader is advised to carefully consult the instruc- tions and informational material included in the package inserts of each drug or therapeutic agent before administration. The Country Doctor Series illustrates Physiological Principles and is not intended as a guide to Medical Therapeutics. Care has been taken to present correct information in this book, however, the author and publisher are not responsible for errors or omissions or for any consequence from application of the information in this work and make no warranty, expressed or implied, with re- spect to the contents of this publication or that its operation will be uninterrupted and error free on any particular recording de- vice.