Crash Course Cardiology 4E

Total Page:16

File Type:pdf, Size:1020Kb

Crash Course Cardiology 4E Cardiology First and second edition authors Anjana Siva Mark Noble Mohamed K Al-Obaidi Third edition authors Ajay Jain Matthew Ginks 4 th Edition CRASH COURSE SERIES EDITOR Dan Horton-Szar BSc(Hons) MBBS(Hons) MRCGP Northgate Medical Practice, Canterbury, Kent, UK FACULTY ADVISOR Michael Frenneaux MBBS(Hons) MD FRCP FRACP FACC FESC FMedSci Regius Professor of Medicine, School of Medicine and Dentistry, University of Aberdeen, Aberdeen, UK Cardiology Antonia Churchhouse BMedSci(Hons) MBChB Core Medical Trainee, London Deanery, London, UK Julian Ormerod PhD MRCP Specialist Registrar in Cardiology, Great Western Hospital, Swindon, UK Edinburgh London New York Oxford Philadelphia St Louis Sydney Toronto 2013 Senior Content Strategist: Jeremy Bowes Senior Content Development Specialist: Ailsa Laing Project Manager: Andrew Riley Designer: Christian Bilbow Icon illustrations: Geo Parkin Illustration manager: Jennifer Rose © 2013 Elsevier Limited. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein). First edition 1999 Second edition 2004 Third edition 2008 Fourth edition 2013 ISBN: 978-0-7234-3632-4 British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging in Publication Data A catalog record for this book is available from the Library of Congress Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. The Publisher's policy is to use paper manufactured from sustainable forests Printed in China Series editor foreword The Crash Course series first published in 1997 and now, 16 years on, we are still going strong. Medicine never stands still, and the work of keeping this series relevant for today’s students is an ongoing process. These fourth editions build on the success of the previous titles and incorporate new and revised material, to keep the series up-to-date with current guidelines for best practice, and recent developments in medical research and pharmacology. We always listen to feedback from our readers, through focus groups and student reviews of the Crash Course titles. For the fourth editions we have completely re-written our self-assessment material to keep up with today’s ‘single-best answer’ and ‘extended matching question’ formats. The artwork and layout of the titles has also been largely re-worked to make it easier on the eye during long sessions of revision. Despite fully revising the books with each edition, we hold fast to the principles on which we first developed the series. Crash Course will always bring you all the information you need to revise in compact, manageable volumes that integrate basic medical science and clinical practice. The books still maintain the balance between clarity and conciseness, and provide sufficient depth for those aiming at distinction. The authors are medical students and junior doctors who have recent experience of the exams you are now facing, and the accuracy of the material is checked by a team of faculty advisors from across the UK. I wish you all the best for your future careers! Dr Dan Horton-Szar v Intentionally left as blank Prefaces Authors Cardiology is an exciting and dynamic specialty that combines bedside history taking and clinical examination with a broad range of investigations and interventions. The specialty is constantly growing, and advances in diagnostics, technologies, and therapeutics are reflected in this fully revised 4th Edition. Having been through the rigours of medical school exams ourselves (some more recently than others!), we are aware that assessments are also changing. Hence we have also developed an up to date self-assessment section, the majority of which is based on the popular “Best of Five” format. We aim primarily to equip you with the knowledge needed to pass your exams, but hope that this book also gives you the opportunity to further your interest and en- joyment of cardiology. Best of luck with your studies! Antonia Churchhouse and Julian Ormerod Faculty Advisor Cardiology has seen huge advances over the past three decades and is one of the most popular and competitive specialties. Lives saved by lifestyle modification and treatment of hypertension and lipid disorders together with revascularisation and secondary prevention strategies are reflected in our national statistics which show dramatic reductions in cardiovascular mortality over the last 20 years. Impressive improvements in quality-of-life and prognosis have also resulted from contemporary treatment of systolic heart failure. Nevertheless, cardiovascular disease remains the major cause of premature death and the major challenge to clinical medicine in the 21st century, not only in western societies but increasingly in developing countries as well. There have been some notable areas in which little progress in therapy has been made, particularly in the syndrome of heart failure with normal ejection fraction. This Crash Course in Cardiology is designed to arm the reader with the knowledge base needed for a clinical introduction to this fascinating specialty. The book provides a comprehensive but we hope readable overview. We have aimed to convey the enthusiasm and excitement that the specialty inspires in us. It begins with history taking and physical examination and proceeds to describe investigations commonly used in cardiology. The next few chapters focus on the evaluation of common presenting symptoms in cardiology. Subsequent chapters focus on common presentations of patients with cardiovascular disorders and a summary of common cardiovascular disorders. vii Prefaces Like the other books in this series, the material is contemporary, the content accessible and the coverage comprehensive. We hope that students will enjoy reading this book. Michael Frenneaux viii Contents Series editor foreword . v Cardiac catheterization . 32 Prefaces . vii Cardiac computed tomography . 33 5. Chest pain . 35 1. History . 1 Differential diagnosis of chest pain . 35 Aim of history taking . 1 History to focus on the differential Presenting complaint . 1 diagnosis of chest pain . 35 Systems review . 5 Presenting complaint . 35 Past medical history . 6 Examination of patients who have chest pain . 36 Family history . 6 Investigation of patients who have Social history . 6 chest pain . 37 Drug history . 7 New onset central chest pain at rest in an Allergies . 7 ill patient . 40 Presenting history findings . 7 6. Dyspnoea . 43 2. Examination . 9 Differential diagnosis of dyspnoea . 43 How to begin the examination . 9 History to focus on the differential diagnosis of dyspnoea. 43 Observation . 9 Examination of dyspnoeic patients. 43 Examination of the hands. 10 Investigation of dyspnoeic patients . 45 Examination of the pulse . 10 Dyspnoea at rest of recent onset in an ill Taking the blood pressure . 11 patient . 47 Examination of the face . 11 7. Syncope . 49 Examination of the jugular venous pressure . 11 Differential diagnosis of syncope . 49 Examination of the praecordium . 12 History to focus on the differential diagnosis of syncope . 49 Finishing off the examination . 14 Examination of patients who present with Presenting your findings . 15 syncope . 50 3. How to write a clerking . 17 Investigation of patients who present with syncope . 51 Documentation of the history . 17 Syncope of recent onset in an ill patient . 53 Documentation of the examination findings . 18 8. Palpitations . 55 At the end of the clerking . 18 Differential diagnosis of palpitation .
Recommended publications
  • 4.17-Kronzon-M-Mode-Echo.Pdf
    M-Mode Echocardiography Is it still Alive? Itzhak Kronzon, MD,FASE Honoraria: Philips Classical M-mode Echocardiography M-Mode offers better time and image resolution. Sampling Rate M-Mode: 1800 / sec 2D: 30 / sec Disadvantages 1. Single Dimension (depth only) 2. Nonperpendicular orientation (always use 2D guidance). Normal MV MS M-Mode of RA & LA Myxomas Back cover of ECHOCARDIOGRAPHY Feigenbaum, 3rd edition MV Prolapse M-Mode in HOCM ASH / SAM Mid-systolic AV Closure Markers of LV Dysfunction A-C Shoulder (“B-Bump”) EPSS Feigenbaum, ECHOCARDIOGRAPHY What does the m-mode show? 1. MS 2. AI 3. Flail MV 4. Myxoma Answer: 3. Posterior Leaflet Motion in Flail MV Note that the posterior leaflet moves anteriorly in early diastole, before it moves posteriorly. ASD with Large L to R Shunt Note markedly dilated RV and “paradoxical” septal motion Dyssynchrony by M-Mode -LBBB 138msec Dyssynchrony of >130msec is associated with good CRT response (sensitivity 100%, specificity 63%) This M mode finding is not associated with increased risk of A. Coarctation B. Pulmonic Stenosis C. Subaortic Stenosis D. Aortic insufficiency Echo of pt with Endocarditis and Shock Best Rx is: 1. AVR 2. MVR 3. IABP 4. Can not tell Echo of pt with Endocarditis and Shock Answer: 1. AVR Note premature closure of MV & echogenic mass in LVOT (Ao veg. Vs. flail Ao cusp) Differential Dx of Premature MV Closure A. AR B. First Degree AV Block C. High Degree AV Block D. Blocked APC E. Atrial Flutter The most likely physical finding in this pt is 1. Absent left subclavian pulse 2.
    [Show full text]
  • Case Reports
    Case Reports Quadrivalvular Heart Disease An Autopsied Case with Massive Pulmonary Regurgitation Tsuguya SAKAMOTO, M.D., Zen'ichiro UOZUMI, M.D., Nobuyoshi KAWAI, M.D., Yoshiyuki SAKAMOTO, M.D., Ryoko KATO, M.D., and Hideo UEDA, M.D. SUMMARY An autopsied case of quadrivalvular heart disease was described, in which pulmonary regurgitation due to possible bicuspid valve was pre- dominant and tricuspid stenosis, mitral stenosis, and aortic stenosis with insufficiency coexisted. The patient was 47, and finally 53 years old female with long-term history of cough due to bronchial compression by the enormously dilated pulmonary artery. Clinical examination revealed massive pulmonary regurgitation, which was further substantiated by right heart catheterization and cineangiocardiography. The phono- cardiograms and the reference tracings suggested the co-existence of tricuspid stenosis, aortic stenosis with regurgitation and mitral stenosis. Cardiac catheterization, intracardiac phonocardiography and angio- cardiography also favored to the diagnosis of organic tricuspid stenosis. However, the ignorance of the presence of such an unusual combination misled to the precise antemortem diagnosis. Discussion was made on the rarity of quadrivalvular heart disease, and the pathogenesis of this unusual pulmonary regurgitation was analyzed based on the autopsy finding and the history as well as the clinical mani- festation. Finally, combination of the murmurs of organic and relative tricuspid stenosis was presented to explain the acoustical findings of the present case. Additional Indexing Words: Phonocardiography Mechanocardiography Bronchial compression Right-sided Austin Flint murmur UADRIVALVULAR heart disease was first described by Shattuck1) in 1891. However, the involvement of all four valves in a given patient is extremely rare.2) The present paper describes one of such case, in which From the Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Tokyo.
    [Show full text]
  • 1. Intermittent Chest Pain: Angina: • Stable: (Caused By
    CVS: 1. Intermittent chest pain: Angina: • Stable: (caused by chronic narrowing in one or more coronary arteries), episodes of pain are precipitated by exertion and may occur more readily when walking in cold or windy weather, after a large meal or while carrying a heavy load; the pain is promptly relieved by rest and/or sublingual glyceryl nitrate (GTN) spray, and typically lasts for less than 10 minutes. • unstable angina (caused by a sudden severe narrowing in a coronary artery), there is usually an abrupt onset or worsening of chest pain episodes that may occur on minimal exertion or at rest. • Retrosternal/ Progressive onset/ increase in intensity over 1–2 minutes/ Constricting, heavy/ Sometimes arm(s), neck, epigastrium/ Associated with breathlessness/ Intermittent, with episodes lasting 2–10 minutes/ Triggered by emotion, exertion, especially if cold, windy/ Relieved by rest, nitrates Mild to moderate. • Aggravated by thyroxine or drug-induced anemia, e.g. aspirin or NSAIDs Esophageal: • Retrosternal or epigastric/ Over 1–2 minutes; can be sudden (spasm)/ C: Gripping, tight or burning/ R: Often to back, sometimes to arms/ A: Heartburn, acid reflux/ T: Intermittent, often at night-time; variable duration/ Lying flat/some foods may trigger/ Not relieved by rest; nitrates sometimes relieve/ Usually mild but esophageal spasm can mimic myocardial infarction. 2. Acute chest pain: MI: • SOCRATES: Retrosternal/ Rapid over a few minutes/ Constricting, heavy/ Often to arm(s), neck, jaw, sometimes epigastrium/ Sweating, nausea, vomiting, breathlessness, feeling of impending death (angor animi)/ Acute presentation; prolonged duration/ ’Stress’ and exercise rare triggers, usually spontaneous/ Not relieved by rest or nitrates/ Usually severe.
    [Show full text]
  • Valvular Heart Disease Acute Rheumatic Fever
    Valvular heart disease Acute rheumatic fever Rheumatic fever • It typically occurs several weeks after streptococcal pharyngitis. • The most common pathogen is group A beta-hemolytic streptococci (GABHS) • Streptococcus cross-react with proteins in cardiac valves. • Time from acute streptococcal infection to onset of symptomatic rheumatic fever (RF) is usually 3–4 weeks. • RF is thought to complicate up to 3% of untreated streptococcal sore throats. • Previous episodes of RF predispose to recurrences. Diagnostic criteria for rheumatic fever (Jones criteria) • Evidence of group A streptococcal pharyngitis • Either a positive throat culture or rapid streptococcal antigen test, or an elevated or rising streptococcal antibody titer (samples taken 2 weeks apart). • Plus two major or one major and two minor Jones criteria: Major criteria Minor criteria • Polyarthritis • Fever • Carditis • Arthralgia • Chorea • Prolonged PR interval • Erythema marginatum • Elevated ESR and CRP • Subcutaneous nodules Joints • Migratory large-joint polyarthritis starting in the lower limbs in 75% of cases. Duration is <4 weeks at each site. There is severe pain and tenderness in contrast to a mild degree of joint swelling. Heart • Pancarditis occurs in 50% of cases with features of acute heart failure, mitral and aortic regurgitation, and pericarditis. • Endocarditis • affects the mitral valve (65%–70%), aortic valve (25%), and tricuspid valve (10%, never in isolation), causing acute regurgitation and heart failure but chronic stenosis. • Pericarditis • Pain • Friction rub • rarely causes hemodynamic instability/tamponade or constriction. Heart Myocarditis • Acute heart failure • Arrhythmias • Most common reason of death Skin • Erythema marginatum is an evanescent rash with serpiginous outlines and central clearings on the trunk and proximal limbs.
    [Show full text]
  • Cardiology 1
    Cardiology 1 SINGLE BEST ANSWER (SBA) a. Sick sinus syndrome b. First-degree AV block QUESTIONS c. Mobitz type 1 block d. Mobitz type 2 block 1. A 19-year-old university rower presents for the pre- e. Complete heart block Oxford–Cambridge boat race medical evaluation. He is healthy and has no significant medical history. 5. A 28-year-old man with no past medical history However, his brother died suddenly during football and not on medications presents to the emergency practice at age 15. Which one of the following is the department with palpitations for several hours and most likely cause of the brother’s death? was found to have supraventricular tachycardia. a. Aortic stenosis Carotid massage was attempted without success. b. Congenital long QT syndrome What is the treatment of choice to stop the attack? c. Congenital short QT syndrome a. Intravenous (IV) lignocaine d. Hypertrophic cardiomyopathy (HCM) b. IV digoxin e. Wolff–Parkinson–White syndrome c. IV amiodarone d. IV adenosine 2. A 65-year-old man presents to the heart failure e. IV quinidine outpatient clinic with increased shortness of breath and swollen ankles. On examination his pulse was 6. A 75-year-old cigarette smoker with known ischaemic 100 beats/min, blood pressure 100/60 mmHg heart disease and a history of cardiac failure presents and jugular venous pressure (JVP) 10 cm water. + to the emergency department with a 6-hour history of The patient currently takes furosemide 40 mg BD, increasing dyspnoea. His ECG shows a narrow complex spironolactone 12.5 mg, bisoprolol 2.5 mg OD and regular tachycardia with a rate of 160 beats/min.
    [Show full text]
  • The Austin Flint Murmur Phonocardiographic and Patho
    The Austin Flint Murmur Phonocardiographic and Patho-anatomical Study Hideo UEDA, M. D., Tsuguya SAKAMOTO, M. D., Nobuyoshi KAWAI, M. D., Hiroshi WATANABE, M. D., Zen'ichiro UozuMI, M. D., Ryozo OKADA, M. D., Tohru KOBAYASHI, M. D., Tetsuro YAMADA, M. D., Kiyoshi INOUE, M. D., and Goro KAITO, M. D. Clinical, phonocardiographic and patho-anatomical studies were made on 15 cases with the Austin Flint murmur. The phonocardio- graphic characteristics were pointed out, and the mode of production of this murmur was explained based on the patho-anatomy of the mitral valve. Several typical cases were illustrated. INCE the last century, the Austin Flint murmur, a well-known apical diastolic rumble in aortic insufficiency,1) has been extensively debated by many authors. 2)-49) However, despite the ample arguments on the incidence, acoustic and graphic characteristics, clinical background and cardiac patho- logy, a comprehensive study with the phonocardiographic as well as patho- logic confirmation has not been attempted up to the present time. The purpose of the present study is, therefore, to investigate these figures based on the clinico-pathological observations. Particular attention was paid to search for the auscultatory and phonocardiographic characteristics of the Austin Flint murmur, and to observe whether any patho-anatomical factors seem to be responsible for the production of this murmur. MATERIAL AND METHOD Out of the autopsy cases from the Second Department of Internal Medicine, Tokyo University Hospital, 14 cases of •gisolated•h aortic insufficiency had com- plete clinical examination including phonocardiography. The cases with con- comitant •gorganic•h mitral insufficiency were not included in this series.
    [Show full text]
  • The Recognition and Management of Valvular Heart Disease
    VALVULAR HEART DISEASE THE RECOGNITION AND MANAGEMENT OF VALVULAR HEART DISEASE Discussion of heart murmurs tends to be associated with specialist ward rounds in teaching hospitals, but a good understanding of this clinical sign provides valuable information. AUSCULTATING A HEART MURMUR When does it occur? •Time the murmur in systole or diastole to the first heart sound and by palpating the upstroke of the carotid artery as systole. • Is the murmur early, mild, late, holosystolic, or diastolic? How loud is it? •Grade I — very soft, only heard with special effort • Grade II — soft, faint, but heard immediately • Grade III — moderately loud • Grade IV — so loud that a thrill can be felt •Grade V — very loud, heard with only part of the stethoscope on the chest wall J A KER • Grade VI — heard with the stethoscope removed from the chest wall. MB ChB, MMed (Int), MD Professor Where is it maximal? Department of Internal Medicine • Apex, left parasternal area, aortic area, pulmonary area. School of Medicine Where does it radiate to? University of Pretoria • Neck, axilla, back. Categories of heart murmurs There are three broad categories of heart murmurs: • systolic (murmur begins with S1 or after S1, ends at S2) • diastolic (murmur begins after S2, ends before S1) • continuous (murmur continues without interruption from systole through S2 into diastole. Typical in patent ductus arteriosus). Systolic heart murmurs Systolic murmurs are illustrated in Fig. 1 and are classified as: • early systolic • midsystolic •late systolic • holosystolic (pansystolic) Early systolic murmurs occur in acute severe mitral regurgitation, tricuspid regurgitation (with normal right ventricular (RV) pressures) and ventricular septal defect (VSD).
    [Show full text]
  • 12 ACE (Angiotensin-Converting Enzyme)
    Index Ablation, radiofrequency, 58–59 Antihypertensive and Lipid Ablative therapy, 65–66 Lowering Treatment to Accupril (quinapril), 12 Prevent Heart Attack Trial ACE (angiotensin-converting (ALLHAT), 18 enzyme) inhibitors, 7 Antihypertensive drug classes, Acebutolol (Sectral), 13, 61 7–18 Aceon (perindopril), 13 Antihypertensive drug selection, Adalat Procardia (nifedipine), 14 19–20 Adenocard (adenosine), 64 Antihypertensive drugs, 12–16 Adenosine (Adenocard), 64 Antiplatelet therapy, 40 Adolescents Aortic insufficiency, 98–99 sudden cardiac death in, 218–219 Aortic stenosis, 105–107 syncope in, 213 Aspirin Alcohol, 158 angina pectoris and, 36 Aldactone (spironolactone), 16 low-dose, 188 Aldomet (methyldopa), 15 Atenolol (Tenormin), 13, 61 ab-blockers, 15 Atherosclerosis, 186–187 a1-blockers, 14, 17 premature, 148–149 Altace (ramipril), 13 Athletes Amiloride (Midamor), 15 murmurs in, 111–112 Amiodarone (Cordarone), 63 sudden cardiac death in, 219–220 Amlodipine (Norvasc), 14 Atorvastatin (Lipitor), 163 Aneurysm, 196–197 Atrial fibrillation, 191–192, 76–80 Angina pectoris, 27–28, 32–41 Atrial flutter, 80–81 aspirin and, 36 Atrial premature beats, 70 unstable, 36–41 Atrial tachycardia, 73 Angiotensin-converting enzyme Atrioventricular (AV) nodal (ACE) inhibitors, 7 reentrant tachycardias, 74–75 Angiotensin receptor antagonists, Atrioventricular node, 53 9 Atrioventricular reciprocating Ankle-brachial index, 282 tachycardias, 75–76 Antiadrenergic agents, 11–18 Austin Flint murmur, 104 Antiarrhythmic drugs, 59–65 AV, see Atrioventricular
    [Show full text]
  • Ministry of Health of Ukraine Kharkiv National Medical University
    Ministry of Health of Ukraine Kharkiv National Medical University AUSCULTATION OF THE HEART. NORMAL HEART SOUNDS, REDUPLICATION OF THE SOUNDS, ADDITIONAL SOUNDS (TRIPLE RHYTHM, GALLOP RHYTHM), ORGANIC AND FUNCTIONAL HEART MURMURS Methodical instructions for students Рекомендовано Ученым советом ХНМУ Протокол №__от_______2017 г. Kharkiv KhNMU 2017 Auscultation of the heart. normal heart sounds, reduplication of the sounds, additional sounds (triple rhythm, gallop rhythm), organic and functional heart murmurs / Authors: Т.V. Ashcheulova, O.M. Kovalyova, O.V. Honchar. – Kharkiv: KhNMU, 2017. – 20 с. Authors: Т.V. Ashcheulova O.M. Kovalyova O.V. Honchar AUSCULTATION OF THE HEART To understand the underlying mechanisms contributing to the cardiac tones formation, it is necessary to remember the sequence of myocardial and valvular action during the cardiac cycle. During ventricular systole: 1. Asynchronous contraction, when separate areas of myocardial wall start to contract and intraventricular pressure rises. 2. Isometric contraction, when the main part of the ventricular myocardium contracts, atrioventricular valves close, and intraventricular pressure significantly increases. 3. The ejection phase, when the intraventricular pressure reaches the pressure in the main vessels, and the semilunar valves open. During diastole (ventricular relaxation): 1. Closure of semilunar valves. 2. Isometric relaxation – initial relaxation of ventricular myocardium, with atrioventricular and semilunar valves closed, until the pressure in the ventricles becomes lower than in the atria. 3. Phases of fast and slow ventricular filling - atrioventricular valves open and blood flows from the atria to the ventricles. 4. Atrial systole, after which cardiac cycle repeats again. The noise produced By a working heart is called heart sounds. In auscultation two sounds can be well heard in healthy subjects: the first sound (S1), which is produced during systole, and the second sound (S2), which occurs during diastole.
    [Show full text]
  • Dynamic Auscultation
    TOP 10 TAKEAWAYS… Jane A. Linderbaum MS, APRN, CNP, AACC Assistant Professor of Medicine Department of cardiovascular disease No Disclosures No off-label discussions 73% of survey respondents identified a need for improved knowledge of CV pathophysiology #10 CARDIAC CIRCULATION, KNOW IT AND LOVE IT The Cardiac Cycle The heart sounds • S1 Mitral (and tricuspid) valve closure Soft if poor EF, loud if good EF • S2 Aortic and pulmonary valve closure Loud if aortic (pulm) pressure • S3 – means “restrictive” filling • S4 – means “abnormal” filling Listening Posts for Auscultation AV – 2nd RICS PV – 2nd LICS MV – 5-6th LICS @ the apex TV – 5-6th LICS parasternal 83% of survey respondents identified themselves as early career in clinic/hospital consult practices # 9 COMMON SYSTOLIC MURMURS YOU WILL DIAGNOSE AND MANAGE MITRAL REGURGITATION MR Treatment • Treat underlying conditions • Consider MV repair when possible at experienced center • Consider MV replacement before ventricle dilates and/or function decreases MITRAL VALVE PROLAPSE Mitral Valve Prolapse Pearls • CHANGE in Murmur (from click-murmur or isolated late sys murmur to holosystolic without audible click) • Skeletal deformities in up to 50% • Upright posture enhances auscultation of the mid-late systolic murmur • May develop severe MR, refer for additional testing as patient may be candidate for mitral valve repair • Murmur may INCREASE with Valsalva • Typically do not require SBE prophylaxis Hypertrophic Cardiomyopathy Hypertrophic Cardiomyopathy • Vigorous LV apical impulse – sustained
    [Show full text]
  • Valvular Heart Disease Systolic Murmurs (ASMR) Diastolic Murmurs (MSAR) Aortic Stenosis (AS) Mitral Regurg
    Valvular heart disease Systolic murmurs (ASMR) Diastolic murmurs (MSAR) Aortic stenosis (AS) Mitral regurg. (MR) Mitral stenosis (MS) Aortic regurg. (AR) Causes 1-Calcification and degeneration of 1-Rheumatic heart disease 1- Rheumatic Fever; 1-Rheumatic heart disease a normal valve (elderly) 2- MVP (prolapse) 2- Other less common 2-Aortic aneurysm \ Dissection. 2-Calcification and fibrosis of a 3- Endocarditis causes: 3-Inflammation congenitally bicuspid aortic valve 4- Ischemic heart disease Congenital Mitral Stenosis, SLE, 4-Degeneration 3-Rheumatic valvular disease 5- Myocarditis Rheumatoid Arthritis, Atrial 5- Severe Hypertension 6- Cardiomyopathies Myxoma (tumor), Malignant 6-Bicuspid aortic valve 7- Myxomatus degenration Carcinoid, Bacterial Endocarditis 7-Endocarditis 8- Marfan's syndrome Pathophysiology 1.Obstructed LV emptying 1. increased LA pressure and 1.LA hypertension: - Stroke volume increased (high (pressure overload) decreased forward CO and - Pulmonary interstitial edema. Systolic BP) 2. Left ventricular hypertrophy Afterload. - Pulmonary hypertension - Regurgitant volume increased 3. ↑LV diastolic pressure: 2. Volume overload occurs, - Leads to right heart failure / CHF (Low Diastolic BP) → Pulmonary - ↑ LA pressure → pulmonary increasing preload. - LA stretch & atrial fibrillation venous congestion venous congestion 2. Limited LV filling & cardiac - ↓ perfusion pressure. output. symptoms - Angina (imbalance - Fatigue & weakness - Malar flush - Dyspnea on exertion (most between supply & demand) - Dyspnea - Dyspnea on exertion common complaint) - Syncope with exertion - Orthopnea, PND - Fatigue - Fatigue. - Dyspnea - Right sided HF (in the late - Orthopnea, PND, - Diminished exercise - Congestive heart failure stages of the disease) & - Palpitation, Chest pain, tolerance. (CHF) eventually may lead to Peripheral edema. - Angina (Imbalance CHF. - Hoarseness between myocardial supply - Systemic embolism & demand) - Hemoptysis (10%) Signs - Pulsus Parvus et Tardus - Systolic thrill.
    [Show full text]
  • Cardiovascular Semiotics: the Personalities Behind the Eponyms
    International Journal of Cardiovascular Sciences. 2016;29(5):396-406 396 REVIEW ARTICLE Cardiovascular Semiotics: The Personalities Behind the Eponyms Renata Gudergues Pereira de Almeida1, Juliana dos Santos Macaciel1, Érico Araújo Reis Santos1, Thiago Calvet Cavalcanti Garcia1, Anastacia Midori Hashimoto1, Cláudio Tinoco Mesquita1,2 Departamento de Medicina Clínica – Faculdade de Medicina – Universidade Federal Fluminense1, Programa de Pós-Graduação em Ciências Cardiovasculares da UFF2, Niterói, RJ – Brazil Abstract observed in life today is also present in medicine and its teaching. Currently, many teachers and students Since its inception, medicine has been based tend to neglect cardiac auscultation in favor of on observation of signs and specific findings in ill imaging examinations to evaluate the heart, such as patients. Semiotics is, therefore, an ancient study. echocardiography and magnetic resonance imaging. Cardiac semiology, although more recent, is more However, it is worth noting that, in many cases, the complex in its learning due to difficulties in the reality of medicine distances patients from access interpretation of auscultatory findings. Austin Flint, to cardiovascular imaging examinations, even in Rivero Carvallo, Antonio Valsalva, and Adolf Kussmaul large centers. are some of the many physicians who have dedicated The lack of competence for cardiac auscultation themselves to the academic study of cardiac semiology can be seen in several countries around the world. and became eternalized in the medical field through
    [Show full text]