Ebook Bedside cardiology: Part 1

(BQ) Part 1 book Bedside cardiology presents the following contents: Bedside cardiology - Is it evidence based, functional classification, syndrome and measurement, clinical instrument, first heart sound, palpation, blood pressure, arterial pulse, jugular venous pulse,...

Bedside Cardiology Bedside Cardiology Achyut Sarkar MD, D (Cardiology), DM (Cardiology) Associate Professor of Cardiology and Incharge of Congenital Heart Disease Program Institute of Post Graduate Medical Education and Research, Kolkata Senior Interventionals Cardiologist BM Birla Heart Research Center, Kolkata, West Bengal, India ® JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD New Delhi • Panama City • London • Dhaka • Kathmandu ® Jaypee Brothers Medical Publishers (P) Ltd Headquarters Jaypee Brothers Medical Publishers (P) Ltd 4838/24, Ansari Road, Daryaganj New Delhi 110 002, India Phone: +91-11-43574357 Fax: +91-11-43574314 Email: jaypee@jaypeebrothers.com Overseas Offices J.P Medical Ltd 83 Victoria Street, London SW1H 0HW (UK) Phone: +44-2031708910 Fax: +02-03-0086180 Email: info@jpmedpub.com Jaypee-Highlights Medical Publishers Inc City of Knowledge, Bld 237, Clayton Panama City, Panama Phone: +507-301-0496 Fax: +507-301-0499 Email: cservice@jphmedical.com Jaypee Brothers Medical Publishers (P) Ltd 17/1-B Babar Road, Block-B, Shaymali Mohammadpur, Dhaka-1207 Bangladesh Mobile: +08801912003485 Email: jaypeedhaka@gmail.com Jaypee Brothers Medical Publishers (P) Ltd Shorakhute, Kathmandu Nepal Phone: +00977-9841528578 Email: jaypee.nepal@gmail.com Website: www.jaypeebrothers.com Website: www.jaypeedigital.com © 2012, Jaypee Brothers Medical Publishers All rights reserved No part of this book may be reproduced in any form or by any means without the prior permission of the publisher Inquiries for bulk sales may be solicited at: jaypee@jaypeebrothers.com This book has been published in good faith that the contents provided by the author contained herein are original, and is intended for educational purposes only While every effort is made to ensure accuracy of information, the publisher and the author specifically disclaim any damage, liability, or loss incurred, directly or indirectly, from the use or application of any of the contents of this work If not specifically stated, all figures and tables are courtesy of the authors Where appropriate, the readers should consult with a specialist or contact the manufacturer of the drug or device Bedside Cardiology First Edition: 2012 ISBN 978-93-5025-985-6 Printed at Dedicated to My Teachers and Students Preface For the sake of stethoscope, please read this preface! Why another one? Why another one, when Bedside Cardiology, as a science, has been relegated in the History of Medicine and as an art, has been described an art of artifact! There is no noble intention This is only for stethoscope, for which I have a romantic nostalgia Still, I cannot accept the image that a cardiologist is giving round in the ward or seeing patient in his chamber, with the echo Doppler probe of his palmtop echocardiogram machine hanging from his neck and no stethoscope! Newer investigating tools, newer interventions are evolving almost every day and replacing the new ones We are appreciating those Even then, are we not thrilled when we detect an Austin Flint murmur or Graham Steell murmur, described two centuries back? Are we not thrilled when we detect a continuous murmur on the back of any patient? May not be that useful, we all, still enjoy Bedside Cardiology We completely agree to Dr Basil M RuDsky–“This is one of the few pleasures that can be derived from the ever-changing practice of medicine It stimulates acquisition of a good doctor-patient relationship and provides a satisfying alternative to many of the idiopathic inconsistencies and inadequacies of medical practice It is unquestionably an art and skill that must not be allowed to succumb to the way of the impossible dream of Don Quixote” Achyut Sarkar Acknowledgments I wish to thank Jaypee Brothers Medical Publishers for whom the creation of this book has become possible I wish to thank Dr Saswati Sarkar for her invaluable suggestion and inspiration I thank my father and late mother for whom I have become a doctor I thank my daughter, Parnisha and my son Arjab They themselves are my inspiration At last, to Dr Asima Sarkar, my wife, I thank with immense gratitude She has made my house a home and has shouldered all the responsibilities For her only, my idea has become a book Contents Bedside Cardiology: Is It Evidence-based? Dyspnea Jugular Venous Pressure Pulse Apical Impulse Heart Sound Murmur Functional Classification NYHA Canadian Cardiovascular Society Functional Classification of Angina Pectoris Specific Activity Scale UCLA Congenital Heart Disease Functional Class WHO Classification of Functional Status in Pulmonary Arterial Hypertension The Canadian Cardiovascular Society (CCS) Severity of Atrial Fibrillation (SAF) Scale 10 Duke Activity Status Index (DASI) 10 Six-minute Walking Test 11 A Triad: Cardinal Symptoms in Cardiovascular System 14 Dyspnea 14 Physiologic Components of Dyspnea 14 Palpitation 18 Chest Pain 20 A Triad: Minor Symptoms in Cardiovascular System 25 Fatigue 25 Edema and Weight Gain 25 A Triad: Cardinal Symptoms in Congenital Left-to-right Shunt 28 Pulmonary Problems in Left to Right (L-R) Shunt 29 A Triad: Cardinal Symptoms in Congenital Cyanotic Heart Disease 31 Paroxysmal Hypoxic Spell 31 Squatting 32 Hyperviscosity Syndrome 32 xii Bedside Cardiology Syndrome and Measurement 34 Syndromes 34 Measurements 43 Clinical Instrument 46 Stethoscope 46 Electronic (digital) Stethoscope 47 Ultrasound Stethoscope (Point-of-care echocardiography) 47 Sphygmomanometer 49 A Triad: Cardinal Signs in Congenital Cyanotic Heart Disease 52 Cyanosis 52 Anemia 54 Clubbing 55 10 Jugular Venous Pulse 59 Veins 59 Jugular Venous Pressure (JVP) 60 Normal Venous Pulse 65 Abnormal Venous Pulse 67 Specific Situations 70 Other Venous Pulses 74 11 Arterial Pulse 75 Origin of Pulse 75 Rate and Rhythm 77 Rate of Rise 78 Volume 79 Character: Double-peaked/double-beating pulse 79 Condition of Arterial Wall 84 Synchrony 85 12 Blood Pressure 91 Definition 91 13 Palpation 100 Apical Impulse 100 Special Clinical Conditions 109 14 First Heart Sound 111 Mechanism 111 Splitting 111 Sound Surrounding S1 114 15 Second Heart Sound 115 Mechanism 115 Splitting 115 Contents 16 Third Heart Sound 124 Physiology 124 How to Detect it 124 17 Fourth Heart Sound 127 Physiology 127 How to Detect it 127 Pressure Over Load 128 Raised End Diastolic Pressure 128 18 Ejection Sound 130 Pulmonary Valvular Click 130 19 Non-ejection Sound 134 Midsystolic Click 134 Mitral Opening Snap (OS) 135 Pericardial Sound 138 Pericardial Rub 138 Mediastinal Crunch (Hamman Sign) 139 Prosthetic Sound 139 20 Murmur 142 Systolic Murmur 144 Ejection Systolic Murmur (Midsystolic Murmur) 144 Pansystolic Murmur 149 Early Systolic Murmur 152 Late Systolic Murmur 153 Diastolic Murmur 153 Continuous Murmur 160 21 Innocent Murmur and Sound 166 22 Dynamic Auscultation 170 Prompt Sauatting 170 Standing 171 Valsalva 172 Isometric Handgrip 174 Transient Arterial Occlusion 175 Passive Leg Raising 176 Premature Beat 176 Respiration 176 Pharmacologic Agent 176 23 Is Your Patient in Heart Failure? 179 Bedside Assessment of Heart Failure 180 Clinical Aids 181 Instrumental Aids 182 Different Criteria for Heart Failure 182 xiii xiv Bedside Cardiology 24 Clinical Assessment: Pulmonary Hypertension 186 Definition 186 Clinical Classification of PH 186 Clinical Features 186 S2 188 25 Segmental Approach in Congenital Heart Disease 191 Connection and Relation 191 Segmental Approach 191 Cardiac Position 191 Situs 193 Angiographic Identification 196 Heterotaxy 198 Atrioventricular Connection 198 Loop 203 Ventriculoarterial Connection 206 Conus 210 Great Artery Spatial Relations 211 26 Clinical Approach: Congenital Cyanotic Heart Disease 214 Pathophysiological Classification 214 Tetralogy Physiology 214 Transposition Physiology 214 Eisenmenger Physiology (EP) 214 Common Mixing Physiology 215 Mixed Physiology (Effectively Two Physiologies) 215 History-onset of Cyanosis 215 Natural History Suggestive of Increased Flow 215 History 216 General Examination 216 Pulse 216 JVP 217 Palpation 217 Heart Sound 217 Murmur 218 Thus, from Clinical Examination, Initial Impression—CCHD with 219 Next Step: To look at X-ray Chest for Vascularity 219 X-ray Chest with Increased Flow 220 X-Ray Chest with Decreased Flow 222 27 Clinical Approach: Tetralogy Physiology 224 Tetralogy Physiology 224 Tetralogy Physiology: Hemodynamics 224 Tetralogy Physiology: How to Grade Severity 225 Under Umbrella of Tetralogy Physiology 226 13 Palpation “ To remind you, your hand is more sensuous than transducer”! Apical Impulse (Fig 13-1) Normal apical impulse is defined as the thrust at the beginning of systole, small in amplitude and brief in duration, palpable in left fifth intercostals space on midclavicular line or within ten centimeters from midsternal line Method: Patient should lie in a partial left lateral decubitus position (in 50% of adult above 50 years, apical impulse is not palpable in supine position) Sometimes elevation of the chest to about 30o may be helpful The fingertips seem best to pickup faint brief movement Fig 13-1: Normal apex cardiogram: First outward movement, due to beginning of left ventricular systolic movement, begins after S1; isovolumetric contraction ends with aortic valve opening, shortly after, outer movement ceases (at E point) Then, the retraction begins, which ends at the nadir (O) point, where the mitral valve opens From S2 to O point is the isovolumetric relaxation phase Diastolic events, including the rapid filling wave (RFW) are not palpable in normal situation Palpation Mechanism: During isovolumetric contraction, the heart rotates counterclockwise on its long axis and the lower segment of the anterior wall of the left ventricle strikes the chest wall, before or just after the ejection phase Timing: This mechanism explains the fact that normal apical impulse recedes from the chest wall and becomes impalpable after the onset of the carotid upstroke or the first heart sound, indicators of onset of ejection Medial retraction: Normal apical impulse is associated with retraction medial to interventricular sulcus This is, because of left ventricular contraction, anterior right ventricle moves away from chest wall It is a localized zone, better seen than palpable (Figs 13-2 and 13-3) Fig 13-2: Outward apical imputes is denoted by (+) and medial retraction is denoted by (–) Fig 13-3: Medial (dominant LV) and lateral retractions (dominant RV) 101 102 Bedside Cardiology (Point of maximum impulse is often used as a synonym for apical impulse This should be avoided because maximum precordial pulsation may be due to right ventricular impulse, pulmonary arterial pulsation, or aortic aneurysm.) Hyperdynamic apical impulse (forceful and ill-sustained) (Figs 13-4A to C) is defined as a thrust of large amplitude that immediately disappears from the palpating fingers So by timing, in relation to ejection phase (as measured from carotid upstroke to downstroke or from S1 to S2), hyperdynamic apical impulse extends only in early part of systole This occurs in hypermetabolic state, such as hyperthyroidism, anemia, mitral and aortic regurgitation, PDA and VSD with large left to right shunt Hypokinetic apical impulse is found in conditions with reduced stroke volume, like in acute myocardial infarction and dilated cardiomyopathy Heaving apical impulse (forceful and sustained) is defined as a thrust that is swift in upstroke, exaggerated in amplitude and is sustained throughout the ejection phase This type of powerful apical impulse is found in left ventricular outflow tract obstruction like aortic stenosis, hypertrophic cardiomyopathy, and hypertension—all conditions associated with left ventricular hypertrophy Left ventricular enlargement is defined by: a Apical impulse, in supine position, outside midclavicular line or beyond 10 centimeters from midsternal line b An enlarged area of apical impulse (in longitudinal axis)—apical impulse palpable in more than one intercostal space c An enlarged area of apical impulse—a palpable area of more than centimeter in diameter (roughly fingerbreadths) Figs 13-4A to C: Various apical impulses: A Forceful and ill-sustained apex; B Forceful and sustained apex; C Sustained, but smaller amplitude apex Palpation A displaced apical impulse to the left, in absence of left ventricular enlargement:  Pectus excavatum  Straight back  Scoliosis  Congenital absence of pericardium  Enlarged right-sided chambers pushing the left ventricle Depressed left ventricular systolic function is indicated by an sustained apical impulse, but with lesser amplitude and lower velocity of its upstroke, giving the impulse of a less powerful thrust (Evidence: How evidence-based this time old apical impulse is to predict left ventricular enlargement and left ventricular systolic dysfunction? In a comparative study, an apical impulse lateral to the midclavicular line was a sensitive (100%) but not specific (18%) indicator of left ventricular enlargement; apical impulse beyond 10 cm from mid sternal line was as TABLE 13-1 Imperceptible apical impulse * Obesity * Emphysema * Pericardial effusion * Constrictive pericarditis * Left sided pleural effusion * Dextrocardia sensitive (100%) but only marginally specific (33%); apical impulse with a diameter more than cm was the best indicator of left ventricular enlargement with the sensitivity of 92% and specificity of 75%; in this study, clinical examination was correlated with two-dimensional echocardiography In another similar study, the predictive value of sustained apical impulse for poor left ventricular ejection fraction was 56%) Right Ventricular Impulse Right ventricular impulse is normally palpable beyond neonatal age as a systolic retraction in lower left prasternal area In some children and adults with thin chest wall, a brief gentle systolic pulsation may be palpable in left lower parasternal area When palpable, this indicates either right ventricular hypertrophy or enlargement 103 104 Bedside Cardiology Right ventricular inflow is in contact with anterior chest wall in 4th and 5th parasternal space, whereas the outflow is in contact with 3rd space Thus, its area of contact with chest wall is wider than left ventricle How to look for parasternal impulse? (Figs 13-5A to C) By heel of the palm, in the third and fourth left intercostals space at sternal edge, breath-holding at end-expiration By placing three fingers in the 3rd, 4th and fifth intercostal spaces, parasternally A B C Figs 13-5A to C: How to palpate RV: (A) Ulnar side of the examining hand is placed over left parasternal area; patient asked to hold breathe at end exhalation.; (B) Alternately, three fingers are placed over left 3rd, 4th and 5th intercostal space, parasternally Patient asked to hold breath at end exhalation; (C) Hand is placed over subxiphoid area and tip of the index finger is pointed upward and left Patient is asked to hold breathe in full inspiration Palpation Ulnar border of the hand can be placed in the parasternal area Sometimes, the right ventricular impulse is better palpable from epigastric area particularly in emphysema Here the downward thrust of the right ventricle is palpable by the pad of the upward pointing fingers, at the end of deep, held inspiration Hyperkinetic impulse is found in RV volume overload like atrial septal defect, tricuspid regurgitation or pulmonary regurgitation Location is usually 4th and 5th space Forceful and sustained impulse is found in right ventricular pressure overload In infundibular stenosis, location is in 4th and 5th space, where as in valvular stenosis, it is in 3rd–5th space It may be associated with a palpable RV S4 Silent parasternal area is found in some congenital cardiac conditions affecting the right ventricle, characterized by absence of any parasternal pulsation, like Ebstein’s anomaly and Hypoplastic right heart syndrome Lateral retraction: A forceful right ventricular impulse is associated with reciprocal retraction, lateral to interventricular sulcus, further lateral to which, one can get the left ventricular impulse A grossly enlarged right ventricle can push the left ventricle backward and takes its position as apex Thus, left ventricle does not have any contact with chest wall Right ventricular apex is diffuse, extending from left parasternal area to apical area with lataral retraction at the apex (Fig 13-6) Fig 13-6: RV forming apex (+) with lateral retraction (–) 105 106 Bedside Cardiology TABLE 13-2 Grading parasternal impulse • Grade 1: Mild lift; can be perceived only by placing a pencil along the left sternal border; easily compressible by counter pressure; sustained less than one third of systole • Grade 2: Prominent lift; not easily compressible: sustained more than half of systole • Grade 3: Forceful, non-compressible by counter force; sustained throughout systole Biventricular Hypertrophy/Impulse (Fig 13-7) When both the left ventricular apical impulse and right ventricular parasternal impulses are palpable, there will be a zone of retraction in between, at the site of interventricular sulcus Fig 13-7: Bi-ventricular impulses (+) with retraction in between (–) Arterial Pulsation Pulmonary arterial pulsation is palpable as a systolic bulge in the left second intercostals space when the artery is dilated due to increased pressure or flow, poststenotic dilatation and idiopathic dilatation of pulmonary artery Similarly, aortic pulsation is palpable in upper right sternal edge or sternoclavicular junction when the aortic root is dilated, as in aortic arch aneurysm or right aortic arch Palpation (Tracheal tug: An aortic aneurysm, sometimes compresses the left bronchus with each pulsation and the bronchus pulls down the trachea This downward pull of the trachea with each pulsation, can be appreciated by keeping the tip of the forefinger on the cricoid cartilage, standing behind the patient, and applying a steady upward pressure.) Heart Sound In certain conditions, first heart sound (S1) and second heart sound (S2) become palpable In mitral stenosis, S1 is loud and snapping and becomes palpable as a taping apical impulse (a misnomer because what palpable is the vibration, not the impulse) S2 is palpable when pressure is high in the great arteries These closure sounds of the semilunar valves are also called diastolic shock due to their sharp vibrant quality Aortic component of S2 is palpable in right second intercostals space in systemic hypertension and coarctation of the aorta, whereas pulmonary component is palpable in left second intercostals space in pulmonary hypertension When aorta is anterior to pulmonary artery, as in any malposition of the great arteries, a palpable S2 in left second intercostals space is actually the aortic component Third (S3), and fourth (S4) heart sound, in certain conditions, become palpable as impulses (not as vibrations as in case of S1 and S2) These are usually felt as double apical impulses—an additional outward impulse, either before or after the apical impulse These movements are best felt by the fingertips with the patient in left lateral decubitus position Using a wand as a lever at the apex beat, the impulses can be better demonstrable More common is the palpable S4, which is basically a palpable ‘a’wave or presystolic wave (hump on the apical upstroke), normally not palpable and related to an accentuated atrial filling wave This vigorous atrial contraction is found in patients with non-compliant left ventricle The clinical conditions are left ventricular outflow tract obstruction, hypertensive heart disease and ischemic heart disease Palpable S3 gallop is the early diastolic rapid filling spike, after the apical impulse The hemodynamic correlate of the palpable S3, or S4 is increased left ventricular end diastolic pressure (Triple apical impulse is sometimes found in hypertrophic obstructed cardiomyopathy Here, the forceful and sustained apical impulse is interrupted by the mid systolic obstruction and creates the impression of double apical impulse Third component is the palpable S4, produced by the vigorous atrial contraction) 107 108 Bedside Cardiology Atrial Impulse Right atrial impulse is sometimes palpable at right parasternal edge, when the aneurysm of the sinus of Valsalva ruptures in the right atrium or when the right atrium becomes ventricularized in Ebstein’s anomaly Left atrial impulse is produced by chronic severe mitral regurgitation, due to expansion of the left atrium by the regurgitant blood As left atrium is midline posterior chamber, its expansion produces the lifting of the whole heart in systole This impulse may be confused with right ventricular impulse, which is more localized A finger is placed each on apical and the parasternal impulse The left atrial impulse begins and ends later than the apical impulse, whereas the right ventricular impulse begins and ends at the same time The hemodynamic correlate of this impulse is the v wave of the left atrial pressure pulse (Fig 13-8) Fig 13-8: Precordial impulse in severe MR: Upper curve is from LV impulse Lower curve is from left atrial impulse, which begins and ends later than LV apical impulse Inward Retractions (Fig 13-9) Constrictive pericarditis is associated with systolic apical retraction followed by diastolic outward movement The usual outward impulse during systole is inhibited by the constriction and the diastolic movement coincides in timing with pericardial knock (however, as mentioned earlier, in severe Palpation constriction, precordium is quiet) Right ventricular volume overload, as in atrial septal defect, tricuspid regurgitation and pulmonary regurgitation, is also associated with systolic apical retraction along with a left parasternal outward movement producing a right ventricular rock The outward movement is due to expanding right atrium, which receives the regurgitant blood The retraction is probably due to right ventricle, which, like an overdistended balloon in diastole, empties rapidly in systole Another explanation is that the retraction in these conditions, is the palpable equivalent of the paradoxical motion of the septum Fig 13-9: Apical impulse in constrictive pericarditis: Systolic retraction and diastolic outward movement, which coincides with pericardial knock Thrill It is the palpatory counterpart of a loud murmur (at least grade 4) and best palpable by the base of the fingers A thrill does not bear any other clinical information Special Clinical Conditions Ischemic heart disease: Left ventricular aneurysm causes a sustained systolic bulge in between the apex and the parasternal area, usually associated with a palpable S4 The similar impulse, in the same location is found during an ischemic episode as a result of transitory dyskinesia of the anterior segments of the ventricular wall Cyanotic heart disease: Precordium is often quiet in cyanotic heart diseases Right ventricle is the dominant ventricle (like S2) in many of the conditions As a result, a grade 1or left parasternal pulsation is the only palpatory finding Fallot’s tetralogy accompanies a right sternoclavicular pulsation, 109 110 Bedside Cardiology indicating a right aortic arch with severe pulmonary stenosis, pulmonary atresia with ventricular septal defect and Truncus arteriosus Eisenmenger syndrome is associated with a palpable pulmonary artery pulsation, palpable P2 and varying grade left parasternal pulsations TABLE 13-3 RV apex LV apex • Diffuse, palpable over wider area Localized and continuous with parasternal pulsation • Lateral retraction Medial retraction (Retraction is best appreciated in lateral decubitus position) • Found in: • Found in: – TOF – Tricuspid atresia – PS with stretched PFO – Univentricular (LV) heart – TGA, VSD, PS – Ebstein’s anomaly – DORV, PS – Pulmonary atresia, intact septum – Eisenmenger syndrome – Vena cava to left atrial communication Further Reading Benchimol A, Dimond EG and Carson JC The value of the apex cardiogram as a reference tracing in phonocardiography Am Heart J 1961;61:485 Boicourt OW, Nagle RE and Mounsey JPD The Clinical Significance of Systolic Retraction of the Apical Impulse Br Heart J 1965;27:379 Deliyannis A, Gillam PMS Mounsey JPD, et al The cardiac impulse and the motion of the heart Br Heart J 1964;26:396 Gillam PMS, Deliyannis AA and Mounsey JPD The left parasternal impulse Br Heart J 1964;26:726 14 First Heart Sound (S1) Mechanism Final halting of the closing atrioventricular valves produces the high frequency vibrations coincident with S1 Timing One must use the diaphragm to pick up this high frequency sound at the apex and the left lower sternal area Mitral valve closure occurs before the carotid upstroke because M1 precedes left ventricular ejection But this delay between M1 and upstroke is too short to be appreciated at bedside T1 coincides with the carotid upstroke Splitting Physiological Mitral component (M1) of the first sound occurs 20 to 50 ms earlier than the tricuspid component (T1) This is because of two factors Left ventricular contraction starts earlier than the right ventricle, hence mitral valve closes earlier than the tricuspid valve Besides, left atrial contraction is more effective than the right atrium in exerting the closure force, as a result of which the mitral valve is in closing position at the onset of systole and closes earlier M1 is best appreciated at the apex and T1 is at the left lower sternal area Pathological Right bundle branch block is the commonest cause of wide split of the S1 However, in many cases of RBBB, T1 is not delayed because the block is at the arborization level (peripheral) causing a delayed right ventricular upstroke, but right ventricular contraction starting at usual time In Ebstein’s anomaly, the right bundle is stunted with poor growth of the peripheral parts, 112 Bedside Cardiology causing a delayed right ventricular contraction More important here is the delayed movement of the abnormal anterior tricuspid leaflet Tricuspid stenosis and ASD are the other causes of delayed T2 Reversed splitting of S1 is very rare Severe mitral stenosis or left atrial myxoma can cause the reversed splitting LBBB should cause reversed splitting, but here also the block is at the peripheral level and onset of left ventricular contraction is not delayed Intensity (Table 14-1) The intensity of S1 is predominantly decided by the mitral component It can be compared to S2 to assess its intensity When S1 is softer than S2 at the apex, it can be described as soft When it is louder than S2 at the base, it can be described as loud S1 TABLE 14-1 Factors determining the intensity of S1 Position of the valve at the onset of systole and its velocity of closure Rate of rise of ventricular pressure Valve pliability Valve cusp adequacy Increased Intensity (Table 14-2) More open the valve remains at the onset of ventricular systole, more the leaflets have to travel from the open to closed position This long travel results in the valve closure during the steeper part of the left ventricular pressure pulse, producing loud S1 Mitral stenosis and atrial myxoma (high transmitral pressure gradient), post-tricuspid left to right shunt (increased transmitral flow), short PR interval and shortened left ventricular diastole (tachycardia), by keeping the mitral valve wide open at the onset of ventricular systole, produce loud M1 Any form of increased adrenergic activity produces loud S1 by increasing the rate of rise of ventricular pressure In mitral valve prolapse, M1 is loud in spite of mitral regurgitation, probably because of increased adrenergic activity, merging of click with M1 and increase excursion of the leaflet from its prolapsed position T1 is loud in tricuspid stenosis (high transtricuspid pressure gradient), and ASD (increased transtricuspid flow) First Heart Sound (S1) TABLE 14–2 Loud S1 MS Atrial myxoma Post-tricuspid left-to-right shunt Short PR interval Tachycardia Mitral valve prolapse syndrome Tricuspid stenosis ASD Decreased Intensity (Table 14-3) Inadequate valve cusp tissue, as in severe mitral or tricuspid regurgitation may cause soft M1 or T1 Stenosed mitral or tricuspid valve with gross calcification causes loss of valve pliability with a soft S1 Semiclosure position of the mitral valve at the onset of ventricular systole, as happens in prolonged PR interval or chronic severe aortic regurgitation may cause soft S1, because the valve halting occurs at the beginning part of ventricular systole, when pressure rise is not steep Similarly, in acute severe aortic regurgitation with increased left ventricular end diastolic pressure, S1 becomes soft, sometimes inaudible In severe aortic stenosis, S1 is soft, probably because of powerful left atrial contraction causes a rapid rise of ventricular end diastolic pressure causing semiclosure position of the mitral valve at In left ventricular systolic dysfunction, poor rate of rise of pressure as well as increased end diastolic pressure causes soft S1 Pericardial effusion, obesity and COPD are other obvious causes of soft S1 TABLE 14-3 Soft S1 Severe MR or TR Grossly calcified, nonpliable valve Prolonged PR interval Chronic or acute severe AR Severe aortic stenosis Left ventricular systolic dysfunction Pericardial effusion, obesity and COPD Varying Intensity Atrial fibrillation and atrioventricular dissociation cause variable intensity of S1 Alternate loud and soft S1, auscultatory alternans, may be found in cardiac tamponade and severe left ventricular dysfunction 113 114 Bedside Cardiology Sound Surrounding S1 (Fig 14-1) M1-T1 vs S1-ejection Click S1-ejection click interval is wider than the interval between M1-T1 Aortic ejection click is widely distributed on precordium, whereas pulmonary click is best heard in left second or third intercostals space with typical decrease in intensity with inspiration M1 is usually louder than T1, whereas click is louder than S1 Fig 14-1: Events around S1 M1: Mitral component; T1: Tricuspid component; EC: Ejection click M1-T1 vs S1-non-ejection Click S1-MVP click interval is similarly wider than the M1-T1 interval Dynamic auscultation results in shifting of the click in relation to S1 The effect is less obvious for M1-T1 relation M1-T1 vs S4-S1 S4 preceding S1 is localized at the apex and best audible with the bell of the stethoscope Further Reading Kostis JB: Mcchanism of heart sound Am Heart J 1975;89:546 Leatham A: Splitting of the first and second heart sounds Lancet 1954;267:607 Warder W, Craig E: The first heart sound and ejection sounds: Echo-phonocardiographic correlation with valvular events Am J Cardiol 1975;35:346 ... 11 1 Splitting 11 1 Sound Surrounding S1 11 4 15 Second Heart Sound 11 5 Mechanism 11 5 Splitting 11 5 Contents 16 Third Heart Sound 12 4... Delhi 11 0 002, India Phone: + 91- 11- 43574357 Fax: + 91- 11- 43574 314 Email: jaypee@jaypeebrothers.com Overseas Offices J.P Medical Ltd 83 Victoria Street, London SW1H 0HW (UK) Phone: +44-20 317 08 910 ... 85 12 Blood Pressure 91 Definition 91 13 Palpation 10 0 Apical Impulse 10 0 Special Clinical Conditions 10 9 14 First Heart Sound 11 1