(BQ) Part 1 book Clinical examinations in cardiology presents the following contents: Basic anatomy and physiology, the history and symptomatology, general physical examination, general physical examination, cardiovascular system examination.
Clinical Examination in B.N Vijay Raghawa Rao ■■■ CLINICAL EXAMINATION IN CARDIOLOGY ■■■ CLINICAL EXAMINATION IN CARDIOLOGY B.N Vijay Raghawa Rao MD, DM (CARDIOLOGY), DHA, FCCP, FICC, MBA (HM) Formerly Addl Director, Professor & HOD Gandhi Medical College/Gandhi Hospital, Secunderabad, Hyderabad, India Presently Consultant Interventional Cardiologist Vijay Marie and Yashoda Superseciality Hospitals, Hyderabad, India ELSEVIER A division of Reed Elsevier India Private Limited Clinical Examination in Cardiology B.N Vijay Raghawa Rao ELSEVIER A division of Reed Elsevier India Private Limited Mosby, Saunders, Churchill Livingstone, Butterworth Heinemann and Hanley & Belfus are the Health Science imprints of Elsevier © 2007 Elsevier First Edition 2007 All rights are reserved No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission of the publisher ISBN-13: 978-81-312-0964-6 Medical knowledge is constantly changing As new information becomes available, changes in treatment, procedures, equipment and the use of drugs become necessary The authors, editors, contributors and the publisher have, as far as it is possible, taken care to ensure that the information given in this text is accurate and up-to-date However, readers are strongly advised to confirm that the information, especially with regard to drug dose/usage, complies with current legislation and standards of practice Published by Elsevier, a division of Reed Elsevier India Private Limited Sri Pratap Udyog, 274, Captain Gaur Marg, Sriniwaspuri New Delhi – 110 065, India Publishing Director: Sanjay K Singh Commissioning Editor: Sonali Dasgupta Developmental Editor: Dr Shelley Narula Manager (Editorial Projects): Dr Radhika Menon Production Executive: Ambrish Choudhary Typeset by Olympus Infotech Pvt Ltd, Chennai, India Printed and bound at Nutech Photolithographer, New Delhi Dedicated to my parents, Shri B Narsimha & Smt B Laxmamma, my wife Dr Shashikala, my daughters Dr Visha Rao & Vishala Rao and my teachers, students & patients who constantly encouraged to write & revise this clinical treatise P REFACE TO R EVISED R EPRINT First Edition of Clinical Examination in Cardiology was published in 2007 by Elsevier India Pvt Ltd which was well received and appreciated by PG students of Gen Medicine, Pediatrics and Cardiology as well as by the practicing physicians, besides being a great helpful to undergraduate students However there were some printing errors which were overlooked inadvertently These errors have been corrected and even some figures, graphs, photographs and tables have been revised and updated in this revised reprint which will be an asset to clinical decision making I am thankful to Elsevier India Pvt for their keen interest shown in revising and reprinting this clinical text book Dr B.N Vijay Raghawa Rao MD, DM (CARDIOLOGY), DHA, FCCP, FICC, MBA (HM) P REFACE TO THE E ARLIER E DITION “It is man’s mission to learn to understand” Clinical Examination in Cardiology is primarily a clinical treatise It provides a simple, lucid and comprehensive description of “Basic Anatomy and Physiology of Cardiovascular Medicine, Clinical Cardiology, and Basic Bedside Investigations (Electrocardiogram and X-ray Chest)” in a single book It is the first of its kind in the present millennium highlighting the forgotten “Clinical Cardiology, in a scenario” where cardiovascular disease is now a global problem with enormous economic consequences Besides index, this book consists of six parts with 34 chapters Part deals with “Basic Anatomy and Physiology of Cardiovascular Medicine” with ten chapters comprehensively described for better understanding of clinical cardiology Part follows the initial chapters which deal with “Cardiac Symptomatology” in two chapters Part with three chapters consists of “General Physical Examination, Arterial Pulse and Blood Pressure” described in detail Part has two chapters describing “Jugular Venous Pulse and Jugular Venous Pressure” in detail Part follows with five chapters which describe cardiovascular examination–“Inspection, Palpation, Percussion and Precordium in Common Heart Diseases, and Auscultation” Finally, basic investigations are described in two portions, which are essential for comprehensive discussion of diagnosis and management of a cardiovascular disease This Part includes, Part 6a: “Clinical Electrocardiography” with nine chapters, which include basic concepts, normal ECG, common disease conditions, drugs effects, arrhythmias and prediction of coronary artery occlusion in a patient of acute myocardial infarction Part 6b: “Radiology of the Heart and Great Vessels” includes four chapters, describing introduction, technical facts, routine reporting of an x-ray chest, calcifications and other views Each chapter has adequate figures, tables and references, which can be used for rapid review of the material described In total, there are 749 figures, 245 tables, and 675 references This book is primarily focused for postgraduate students of “General Medicine, Cardiology and Paediatrics” However, it will also be useful for the undergraduate students for better understanding of clinical cardiology, which is a part of general medicine It may also prove useful to those who wish to broaden their knowledge of clinical cardiology and will aid in their day-to-day practice of cardiology Besides my teaching experience of undergraduate and postgraduate medical students, I have also used standard textbooks and journals of Cardiovascular Medicine as references in compiling this clinical entity I am thankful to my postgraduates, Dr Pramod, Dr Rajkiran and Dr Narender for providing beautiful photographs I am indebted to my patients at my clinic, Remedy Superspeciality Hospital and Gandhi Medical College & Hospital for their immense cooperation My special thanks to Mr Sanjay Singh and Dr Shelley Narula of Elsevier India Pvt Ltd for their constant encouragement and keen interest shown in completing this clinical treatise Dr B.N Vijay Raghawa Rao MD, DM (CARDIOLOGY), DHA, FCCP, FICC, MBA (HM) C ONTENTS Preface vii Abbreviations xi PART I BASIC ANATOMY AND PHYSIOLOGY Chapter Anatomy of the heart Chapter Lymphatic system of the heart 28 Chapter Venous drainage of the heart 31 Chapter Arterial supply of the heart 34 Chapter Nerve supply of the heart 40 Chapter The conduction system of the heart 47 Chapter Ultrastructure of the myocardium 54 Chapter Basic electrophysiological principles 66 Chapter Molecular basis of muscle contraction 73 Chapter 10 The cardiac cycle 77 PART THE HISTORY AND SYMPTOMATOLOGY 83 Chapter 11 Cardinal symptoms 85 Chapter 12 Other symptoms 144 PART GENERAL PHYSICAL EXAMINATION 159 Chapter 13 General examination 161 Chapter 14 Arterial pulse 225 Chapter 15 Measurement of the blood pressure 249 PART JUGULAR VENOUS PULSE 269 Chapter 16 Introduction and jugular venous pulse waves 271 Chapter 17 Estimation of venous pressure and JVP in diseased conditions 283 PART CARDIOVASCULAR SYSTEM EXAMINATION 297 Chapter 18 Inspection of the precordium 299 Chapter 19 Palpation of the precordium 315 x CONTENTS Chapter 20 Percussion of the precordium and precordial findings in common heart diseases 333 Chapter 21 Cardiac auscultation 354 PART 6A BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAM 457 Chapter 22 Introduction and basic concepts 459 Chapter 23 The normal electrocardiogram 474 Chapter 24 Abnormal P, T and U waves 490 Chapter 25 Ventricular hypertrophy 500 Chapter 26 Intraventricular conduction defects 516 Chapter 27 Myocardial infarction and ischemia 533 Chapter 28 Pericarditis and myocarditis 560 Chapter 29 Drug effects and electrolyte abnormalities 568 Chapter 30 Arrhythmias 580 PART 6B BASIC INVESTIGATIONS: RADIOLOGY OF THE HEART AND GREAT VESSELS 659 Chapter 31 Introduction and evaluation of heart 661 Chapter 32 The pulmonary vasculature 684 Chapter 33 Cardiac calcification 693 Chapter 34 Evaluation of extracardiac structures and chest X-ray in other views 701 Index 708 A BBREVIATIONS PART ADP: adenosine diphosphate AHA: american heart association AJR: abdominal jugular reflux AML: anterior mitral leaflet ANP: atrial natriuretic peptide ATP: adenosine triphosphate AV node: atrio ventricular node AV: atrioventricular AVT: anterior interventricular trunk CICR: calcium induced calcium release CLN: cardiac lymph node CT: chordae tendinae CVA: cerebrovascular accident CVC: cardiac vagal center IVC: inferior vena cava JSR: junctional sarcoplasmic reticulum LA: left atrium LAD: left anterior descending LBB: left bundle branch LCx: left circumflex LCC: left coronary channel LMCA: left main coronary artery LV: left ventricle MHC: myosin heavy chain MLC: myosin light chain MSC: main supracardiac channel OM: obtuse marginal OMT: obtuse marginal trunk PDA: patent ductus arteriosus PFO: patent foreman ovale PML: posterior mitral leaflet PM: papillary muscle pCO2: partial pressure of carbon dioxide pO2: partial pressure of oxygen PVT: posterior interventricular trunk RA: right atrium RBB: right bundle branch RCA: right coronary artery RCC: right coronary channel RFW: rapid filling wave RLD: right lymphatic duct RV: right ventricle SA node: Sinoatrial node SERCA: sarco endoplasmic reticulum calcium ATPase SFW: slow filling wave SL: semilunar SVC: superior vena cava VMC: vasomotor center PART Af: atrial fibrillation ALCAPA: anomalous left coronary artery from pulmonary artery AMI: acute myocardial infarction AP: angina pectoris AR: aortic regurgitation ARVD: arrhythmogenic right ventricular dysplasia AS: aortic stenosis ASD: atrial septal defect AVRT: atrioventicular reciprocating tachycardia BBB: bundle branch block CAD: coronary artery disease CCS: Canadian cardiovascular society CHF: congestive heart failure CHD: congenital heart disease CHB: complete heart block CM: cardiomyoapthy COA: coarctation of aorta COPD: chronic obstructive pulmonary disease CRF: chronic renal failure CT: cardiac tamponade CVA: cerebrovascular accident DCM: dilated cardiomyoapthy DORV: doublet outlet right ventricle HCM: hypertrophic cardiomyopathy HOCM: hypertrophic obstructive cardiomyopathy LAD: left anterior descending LAHB: left anterior hemi block LBBB: left bundle branch block 442 CARDIOVASCULAR SYSTEM EXAMINATION Table 21.29 Etiology of diastolic murmurs Early diastolic murmur Mid diastolic murmur Pre systolic murmur Pan diastolic murmur AR Functional PR (Graham Steell murmur) LV inflow obstruction: MS RV inflow obstruction: TS MS TS Severe AR Severe PR Mitral diastolic flow murmurs: severe MR, left-to-right shunts (VSD, PDA) Tricuspid diastolic flow murmurs: severe TR, left-to-right shunts (ASD, RSOV into RA, PAPVC) Severe AR (Austin Flint murmur) Acute rheumatic carditis (Carey Coombs murmur) Organic PR AR (Austin Flint murmur) Complete heart block RSOV: rupture of sinus of Valsalva, PAPVC: partial anomalous pulmonary venous connection between systole and diastole They have to be differentiated from to and fro murmurs of VSD ϩ AR, AS ϩ AR, MS ϩ MR (see Fig 21.64) Causes of Continuous Murmurs: Due to high to low pressure shunts (i) From systemic artery to pulmonary artery ● Aortic run off into pulmonary artery: PDA, AP window, truncus arteriosus with pulmonary artery stenosis, surgically created aortopulmonary anastomosis (Blalock, Waterston or Pott’s shunts) ● Bronchial collaterals (bronchial to precapillary pulmonary arterial anastomosis and resultant aortic pulmonary fistula): Pulmonary atresia, TOF.134 ● Anomalous left coronary artery from pulmonary artery (ALCAPA) (ii) From systemic artery to right heart: ● Aortic run off into right heart: RSOV into RA or RV ● Coronary cameral fistula: Coronary artery fistula into RA or RV (LA) (iii) Other shunts: ● Left to right atrial shunts with mitral valve obstruction: Lutembacher’s syndrome (MS with ASD), mitral atresia with ASD, Post PTMC ● Arteriovenous fistula ● Venovenous shunts: Anomalous pulmonary venous drainage, porto-systemic shunt in cirrhosis of liver i.e Cruveilheir Baumgarten syndrome Due to rapid blood flow ● ● Cervical venous hum Mammary souffle CARDIAC AUSCULTATION AR Functional PR (GSM) AR (AFM) CHB Early DM PreSM Diastolic murmur (DM) Organic PR Mid DM LV inflow obstruction: MS LAM Cor at MS TS Fig 21.63 Severe AR Severe PR Holo DM MD flow murmur: Severe MR Shunts: VSD, PDA, AP window, RSOV into RV Hyperkinetic states: anemia, pregnancy, thyrotoxicosis Complete heart block RV inflow obstruction: TS RAM Carcinoid syndrome Ebstein’s anomaly MV opening interference: Severe AR (AFM) Acute Rh carditis (CCM) 443 TV opening interference: Severe PR with normal PA pressure (right-sided AFM) TD flow murmur: ASD RSOV into RA Gerbode’s shunt PAPVC, TAPVC CA to RA SA and causes of diastolic murmurs-VSD: ventricular septal defect, | Classification PDA: patent ductus arteriosus, ASD: atrial septal defect, PH: pulmonary hypertension, AR: aortic regurgitation, PR: pulmonary regurgitation, MR: mitral regurgitation, MS: mitral stenosis, TS: tricuspid stenosis, AP: aortopulmonary, RSOV: rupture of sinus of Valsalva, RV: right ventricle, RA: right atrium, PAPVC: partial anomalous pulmonary venous connection, TAPVC: total anomalous pulmonary venous connection, CA: coronary artery to right atrial communication, SA: single atrium, LAM: left atrial myxoma, RAM: right atrial myxoma, Cor at: Cor triatriatum, Rh: rheumatic, AFM: Austin Flint murmur, CCM: Carey Coomb’s murmur, GSM: Graham Steell murmur, PA: pulmonary artery, Pre SM: presystolic or late diastolic murmur, MD: mitral diastolic, TD: tricuspid diastolic ● ● ● Hyperthyroidism Hemiangioma Hyperemia of neoplasm: Hepatoma, renal cell carcinoma, Paget’s disease Secondary to localized arterial obstruction ● ● ● ● ● ● Coarctation of aorta Branch pulmonary artery stenosis Carotid occlusion Femoral artery occlusion Celiac mesenteric artery occlusion Renal artery occlusion 444 CARDIOVASCULAR SYSTEM EXAMINATION S1 S2 S1 Continuous murmur (PDA) S1 MSM S2 EDM S1 To-Fro murmur (AS and AR) Fig 21.64 murmur in patent ductus | Continuous arteriosus (PDA) vs to and fro murmur i.e mid systolic murmur (MSM) of aortic stenosis (AS) and early diastolic murmur (EDM) of aortic regurgitation (AR) Fig 21.65 murmur is best heard in infra| PDA clavicular and pulmonary areas during expiration Table 21.30 Continuous murmur of PDA Features Findings Proper name Frequency Character Gibson’s murmur Combination of high and low Rough machinery, crescendo-decrescendo murmur peaking at S2 In left infraclavicular and pulmonary areas during expiration Augments the murmur Murmur decreases/disappears >Diastolic component Best heard Isometric hand grip Valsalva maneuver Amylnitrate inhalation Continuous Murmurs Due to High-to-Low Pressure Shunts 1) Continuous murmur in patent ductus arteriosus (PDA): The classic description of the PDA murmur was given by George Gibson in 1900 and hence also known as Gibson’s murmur.135 ● ● ● ● ● It is classically described as a rough machinery murmur due to the combination of high and low frequency vibrations and associated thrill is common It peaks at S2, after which it gradually wanes until it terminates before S1 (crescendodecrescendo murmur) The murmur is best heard in the left infraclavicular and pulmonary areas during expiration (see Fig 21.65) The systolic component is widely audible, while the diastolic component is restricted to pulmonary and infraclavicular areas Isometric hand grip increases the intensity and duration of the murmur and may bring out the diastolic component when it is not heard The murmur decreases or disappears with Valsalva maneuver (see Table 21.30) CARDIAC AUSCULTATION 445 Table 21.31 PDA with no continuous murmur Young infants Very small ductus Very large ductus With pulmonary hypertension With Eisenmenger’ syndrome When associated with: (i) Preductal coarctation of aorta (ii) Aortic stenosis (iii) Large ventricular septal defect The murmur is not continuous in the following conditions ● ● ● ● In young infants (due to high pulmonary vascular resistance), when ductus is too small (valve-like) or too large (when equalization of pulmonary and systemic pressures occurs) the diastolic component may be very short or absent So also in severe PH as the pulmonary vascular resistance increases, PADP approaches and reaches systemic levels, diminishing and finally abolishing the diastolic flow and diastolic component of the murmur When associated with preductal coarctation of aorta (due to lower aortic pressure), AS (due to lower aortic pressure and elevated LVEDP), large VSD (due to equalization of pulmonary and systemic pressures), severe PH secondary to MS, peripheral pulmonary artery stenosis When the equalization of pulmonary and systemic pressures occurs in Eisenmenger’s syndrome, the systemic flow across the shunt diminishes and finally ceases leaving the ductus silent (see Table 21.31) 2) Continuous murmur associated with bronchial collaterals: It is heard in the same location as that of PDA, but radiates widely especially over the posterior thorax 3) Continuous murmur in anomalous origin of left coronary artery from pulmonary artery (ALCAPA): The murmur is continuous when the left-to-right shunt is large and is usually best heard at left sternal border The child may have chest pain with ECG evidence of myocardial infarction 4) Continuous murmur in RSOV (rupture of sinus of valsalva) ● ● ● ● The murmur is usually continuous when RSOV occurs into RA or RV It may be continuous when RSOV occurs into LA But it is early diastolic when sinus of Valsalva aneurysm ruptures into LV It also becomes early diastolic when PH supervenes with high RVSP which shortens or abolishes systolic flow and systolic component of the murmur It is more of a superficial murmur with very prominent diastolic thrill, which is described as ‘purring of a cat’ It is maximally heard at the lower left sternal border or over the xiphoid corresponding to the fistulous tract.136 It is often well audible to the right of the sternum with no significant changes with respiration 446 CARDIOVASCULAR SYSTEM EXAMINATION 5) Continuous murmur in coronary cameral fistula ● ● ● ● ● In general, the murmur is soft, superficial and high pitched In 90%, coronary artery (CA) fistula drains into right heart and resultant murmur is continuous But in case of CA fistula draining into RV, the murmur softens during systole (when the systolic flow decreases due to compression of the fistula during RV contraction) The murmur is louder in systole as the pressure gradient is more in systole in case of CA fistula draining into RA or LA The murmur is not continuous if it empties into LV It may be purely diastolic or systolic and diastolic Continuous murmur is also absent and may be silent if multiple coronary artery fistulas empty into pulmonary artery Site ● ● ● The murmur is best heard either left or right of the lower sternal area when CA drains into RA It is maximally heard at left mid to lower sternal border or in subxiphoid region in CA draining into RV In CA draining into LA, it is best heard in upper to mid left sternal border and may radiate leftward as far as the anterior axillary line 6) Continuous murmur in left-to-right atrial shunts with MV obstruction ● ● ● As in Lutembacher’s Syndrome, mitral atresia with ASD Continuous murmur is also heard when a small ASD is produced following transseptal catheterization or percutenous transmitral commisurotomy (PTMC), due to high velocity flow across the septal defect especially if the mitral obstruction is not adequately relieved by the balloon valvuloplasty The murmur increases during inspiration and decreases with Valsalva maneuver 7) Continuous murmur in venovenous shunts ● ● Total anomalous pulmonary venous drainage into a systemic vein (usually superior vena cava or innominate veins) may produce a continuous murmur (venous hum) usually heard in pulmonary or left infraclavicular areas.137 Portosystemic shunts: In portal hypertension usually secondary to cirrhosis of liver, tortuous collateral veins are seen radiating from the umbilicus (Caput medusae) A continuous murmur (venous hum) may be heard over these collaterals (CruveilheirBaumgarten syndrome) (see Fig 21.66) 8) Continuous murmur in arteriovenous fistula ● Arteriovenous fistulas could be congenital or acquired which give rise to continuous murmurs – Congenital AV fistulas include coronary arterial fistula, RSOV, ALCAPA – Acquired AV fistulas include surgically created fistula for hemodialysis, posttraumatic or after catherization CARDIAC AUSCULTATION Fig 21.66 ● 447 murmur is heard over the Caput medusae which is described | Aascontinuous Cruveilheir Baumgarten syndrome Systolic accentuation of the continuous murmur occurs in peripheral arteriovenous fistulas and is best heard over the site of the fistula – Local compression may: (i) Decrease the intensity of the murmur by raising venous pressure and thereby reducing the AV pressure gradient (ii) A baroreceptor-mediated reflex bradycardia may occur (Branham’s sign) and reflex tachycardia occurs on release (see Table 21.32) Continuous Murmurs Due to Rapid Blood Flow High velocity blood flow through veins and arteries may cause a continuous murmur 1) The Venous Hum was first recognized by Potain in 1867 ● ● ● ● The normal flow of blood across the normal veins in the neck is noiseless But increased velocity of blood flow gives rise to a continuous bruit over the neck veins which is known as cervical venous hum It may be rough and noisy and typically louder in diastole.34 The venous hum is best heard in sitting posture with head rotated to the opposite side and chin upwards, placing the bell of the stethoscope at the base of the neck in between the two heads of the sternomastoid muscle and may be more prominent on the right side Sometimes it may radiate below the clavicles and may be confused with the continuous murmur of PDA if not evaluated carefully (see Fig 21.67) The murmur is abolished by the digital compression of the internal jugular vein with head in neutral position (see Fig 21.68) – It is poorly heard in supine position, while – Anemia and thryotoxicosis initiate or reinforce the venous hum (see Table 21.33) 448 CARDIOVASCULAR SYSTEM EXAMINATION Table 21.32 Continuous murmurs Due to high-to-low pressure shunts Due to rapid blood flow Due to localized arterial obstruction PDA AP window Truncus arterosus with PA stenosis Pulmonary atresia Blalock, Waterston and Pott’s shunts ALCAPA RSOV into RA, RV Coronay artery fistula into RA, RV Lutembacher’s syndrome 10 Mitral atresia with ASD 11 Post PTMC with ASD 12 AV fistula 13 TAPVC into systemic veins 14 Portosytemic shunt Coarctation of aorta Branch pulmonary artery stenosis Carotid occlusion Femoral artery occlusion Renal artery occlusion Celiac mesenteric artery occlusion Cervical venous hum Mammary soufflé Hemangioma Hyperthyroidism Hyperemia of neoplasm (hepatoma, renal cell carcinoma, Paget’s disease) RSOV: rupture of sinus of Valsalva, TAPVC: total anomalous pulmonary venous connection, PTMC: percutaneous transmitral commisurotomy, ALCAPA: anomalous left coronary artery from pulmonary artery Fig 21.67 to elicit the venous hum| Maneuver patient’s chin is pulled to the left and Fig 21.68 upward stretching the neck to abolish the venous hum by | Maneuver digital compression of right internal jugular vein with head in neutral position Causes of cervical venous hum include: i) Physiological causes: Healthy children and young adults, later stages of pregnancy ii) Pathological causes: ● ● ● Hyperkinetic circulatory states (due to = velocity and > viscosity of blood): Anemia, thyrotoxicosis, beriberi Intracranial AV fistula with bruit over the skull Compression of the jugular vein by the fascia or bony structures in the neck CARDIAC AUSCULTATION 449 Table 21.33 The venous hum Features Findings Due to = flow into Character Initiated or = by Abolished by Best heard with bell of the stethoscope Fig 21.69 Internal jugular veins Rough, noisy, louder in diastole Anemia, thyrotoxicosis Digital compression of internal jugular vein In sitting posture with head rotated to opposite side with chin upward at the base of the neck | Auscultation for mammary soufflé Probable mechanism of the venous hum: The laminar flow in internal jugular vein may be disturbed by the deformation of the vein at the level of the transverse process of the atlas during head rotation designed to elicit the hum.138 2) The mammary soufflé: (soufflé ϭ puff in French) This innocent continuous arterial murmur occurs in 10–15% of pregnant women during 2nd and 3rd trimesters and in early postpartum period in lactating mothers.139 ● ● ● ● It is due to increased blood flow to the breast tissue This medium to high pitched murmur is best heard over the breast on either side between 2nd and 6th anterior intercostal spaces with no significant change with respiration and may be confused with the continuous murmur of PDA or AV fistula.140 The mammary soufflé usually begins after S1 with a distinct gap and systolic component is the loudest Light pressure with the stethoscope augments the murmur, whereas the firm pressure with the stethoscope or digital compression abolishes the murmur (see Fig 21.69) Valsalva maneuver has no significant effect on the murmur It disappears after the termination of lactation (see Table 21.34) Continuous Murmurs Secondary to Localized Arterial Obstruction ● Localized stenosis of systemic or pulmonary arteries produce a continuous murmur or bruit if the obstruction is critical (Ն80%) with no adequate collaterals so that a 450 CARDIOVASCULAR SYSTEM EXAMINATION Table 21.34 Mammary soufflé Features Findings Type Cause Occurs in Continuous arterial murmur = Blood flow to breast tissue 10–15% of pregnant women in 2nd–3rd trimester and early post partum period Medium to high pitched Begins after S1 with a definite gap, with loudest systolic component Augments the murmur Abolishes the murmur No effect on the murmur Murmur disappears Frequency of the murmur Description Light pressure over the breast Firm pressure over the breast Valsalva maneuver Termination of lactation Cervical venous hum Mammary soufflé Hyperthyroidism Hemiangioma Hepatoma, renal cell carcinoma Continuous murmur (CM) Rapid blood flow Localized arterial obstruction High to low pressure shunts Aortic runoff into PA: PDA AP window Truncus arteriosus with PA stenosis After shunt surgery Bronchial collaterals: P At TOF Fig 21.70 COA Branch PA stenosis CA occlusion FA occlusion RA occlusion CMA occlusion SA to PA: ALCAPA Other shunts: Lutembachers syndrome M At with ASD Post PTMC AV fistula Anomalous PVD CM syndrome SA to right heart: RSOV into RA or RV Coronary cameral fistula and causes of continuous murmurs—PDA: patent ductus arte| Classification riosus, ASD: atrial septal defect, PA: pulmonary artery, M At: mitral atresia, P At: pulmonary atresia, TOF: tetralogy of Fallot, AP: aorto-pulmonary, PTMC: percutaneous transmitral commisurotomy, AV: arteriovenous, PVD: pulmonary venous drainage, CM syndrome: Cruveilheir-Baumgarten syndrome, RSOV: rupture of sinus of Valsalva, RA: right atrium, RV: right ventricle, COA: coarctation of aorta, CA: carotid artery, FA: femoral artery, RA: renal artery, CMA: celiac mesenteric artery, SA: systemic artery, ALCAPA: anomalous left coronary artery from pulmonary artery, after shunt surgery e.g Blalock, Waterston and Pott’s shunts CARDIAC AUSCULTATION ● ● ● ● 451 continuous pressure gradient is produced throughout the cardiac cycle and often with systolic accentuation.141 With adequate collateral arteries, only systolic gradient persists with no diastolic gradient across the obstructed artery as the collaterals around the obstructed artery deliver adequate flow and hence only systolic murmur may 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PART GENERAL PHYSICAL EXAMINATION 15 9 Chapter 13 General examination 16 1 Chapter 14 Arterial pulse 225 Chapter 15 Measurement of the blood pressure 249 PART JUGULAR VENOUS PULSE 269 Chapter 16 ... Semilunar (SL) Valves REFERENCES 16 16 17 17 17 17 18 22 24 27 GROSS ANATOMY OF THE HEART The heart is a conical, hollow muscular organ situated in the middle mediastinum behind the sternum and costal