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(BQ) Part 2 book Bedside cardiology presents the following contents: Second heart sound, third heart sound, ejection sound, non-ejection sound, murmur, innocent murmur and sound, is your patient in heart failure, clinical assessment: pulmonary hypertension, segmental approach in congenital heart disea, clinical approach - eisenmenger physiology,...
15 Second Heart Sound (S2) Mechanism During the closure of the semilunar valves, clapping of the leaflets does not produce the sound Sudden deceleration of the retrograde flow of the blood column in the aorta or pulmonary artery by the closed tensed valves set the vibration of the cardiohemic system The high frequency components of this vibration produce the S2 Splitting Physiological Splitting (Fig 15-1) Left ventricular ejection begins and completes earlier than right ventricle Thus, aortic component (A2) occurs 10 to 15 ms earlier than the pulmonary component (P2) One cannot appreciate two components unless the split is more than 30–50 ms This causes the S2 single during expiration, where the split is less than 15–20 ms In inspiration, the split is appreciable because P2 is delayed and A2 occurs earlier Delayed P2 contributes 70% and early A2 30% for the inspiratory split P2 is delayed because of the effect of inspiration on the aortic and pulmonary hang out time Hang-out time is defined as the interval between the end of the ventricular ejection and closure of the semilunar valve This time is longer in pulmonary artery than the aorta Pulmonary hang out time may be up to 60 to 70 ms, whereas aortic hang-out time may be below 20 to 30 ms Semilunar valve is closed only when the pulmonary artery or aortic diastolic pressure crosses that of the respective ventricle Pulmonary vasculature is more compliant than the systemic vasculature, pulmonary vascular resistance is one tenth of that of aorta and pulmonary artery has less elastic recoil power than that of the aorta Thus, it takes a longer time for the diastolic pressure building up in the pulmonary artery than in the aorta for this cross over (Fig 15-2) 116 Bedside Cardiology Fig 15-1: Physiological splitting of S2 (A) During inspiration, P2 is delayed and A2 occurs earlier Inspiratory shifting of P2 is more than shifting of A2; (B) In lying down posture, due to increased preload, S2 may appear as persistently splitted, due to audibly wide expiratory splitting; (C) In sitting posture, expiratory splitting narrows down and becomes audibly single Thus proper assessment of S2 splitting should be done with patient in sitting posture Incisura: Point of cross over of aorta or pulmonary artery over its respective ventricle in the pressure curve is called incisura, which coincides with S2 Hang-out time can also be defined as the distance between the ventricular pressure curve and the aortic or pulmonary incisura Actual cusp apposition occurs before the incisura Due to inertia, the forward flow continues Duration of this forward flow determines the hang-out time and depends on the vascular capacitance, vascular resistance and the recoil property of the aorta vs pulmonary artery During inspiration, there is increased pulmonary vascular capacitance resulting in longer pulmonary artery hang-out time and increased venous return resulting in longer right ventricular ejection time P2 is delayed by both of these factors, more important being the hang-out time Inspiration causes decreased intrathoracic pressure, which is transmitted in the pulmonary veins with a pulling effect, without any change in the aortic capacitance Left Second Heart Sound (S2) Fig 15-2: Hang-out interval, which is defined as the interval between the end of the ventricular ejection and closure of the semilunar valve It is up to 70 ms for P2 and 30 ms for A2 ventricular stroke volume is decreased with shortening of ejection time, resulting in early A2 Pathological Splitting (Table 15-1) Pathological splitting of S2 may be related to either the wideness of the split or the effect of respiration on it TABLE 15-1 Pathological splitting of S2 A Persistent splitting Fixed Nonfixed B Reverse splitting C Persistently single Persistent splitting means aortic and pulmonary components are audible in both phases of respirations Persistent nonfixed splitting means normal inspiratory widening on the backdrop of persistent splitting 117 118 Bedside Cardiology Wide Splitting (Persistent Nonfixed Splitting) (Table 15-2) S2 is said to be widely splitted: When both its components can be appreciated in expiration, particularly in standing position; there may be further widening during inspiration Inspiratory widening more than 60 msec; may be single on expiration Commonest causes are the electrical abnormalities including RBBB, WPW syndrome with left ventricular pre-excitation There is late activation of the right ventricle resulting in delayed P2 Mechanical causes include pulmonary valvular stenosis, infundibular stenosis and peripheral pulmonary artery stenosis, all of which prolong right ventricular activation time resulting in delayed P2 In pulmonary valvular stenosis, severity is directly proportional to expiratory splitting When the splitting is 70–80 ms, right ventricular systolic pressure approximates 70–80 mm Hg Severe MR and large VSD cause wide expiratory splitting due to early A2 by shortening left ventricular mechanical systole Wide inspiratoy splitting due to early A2 occurs in constrictive pericarditis Inspiration causes decreased intrathoracic pressure as well as decreased pulmonary venous pressure, which is an extracardiac structure But this thoracic pressure swinging is not reflected on cardiac chambers due to constricted pericardium Thus, left atrial pressure remains normal during inspiration This diminished pulmonary vein—left atrial pressure gradient during inspiration causes reduced left ventricular venous return and ejection time Wide split is found in Idiopathic dilatation of pulmonary artery due to prolonged hang-out time TABLE 15-2 Wide splitting of S2 Electrical causes RBBB WPW syndrome Mechanical causes Delayed P2 (RVOT stenosis) Early A2 (Severe MR, large VSD, constrictive pericarditis) Prolonged hang-out time: Idiopathic dilatation of pulmonary artery ASD (fixed) RV systolic dysfunction (fixed) Second Heart Sound (S2) Wide Fixed Splitting (Fig 15-3) The split is defined fixed when the respiratory variation is less than 20 msec This is one of the most consistent auscultatory finding and hallmark of all forms of ASD Increased pulmonary flow causes increased pulmonary Fig 15-3: ASD: In normal situation, pulmonary hang-out interval widens more in inspiration, which is responsible for insptratory split In ASD, hang-out interval is fixed in both phases of respiration, causing the fixed splitting of S2 119 120 Bedside Cardiology capacitance and prolonged hang-out time which results in persistent expiratory (wide) splitting of S2 As capacitance is already increased, inspiration does not cause any additional increase This fixed hang-out time in both phases of respiration causes the fixed splitting Another causative factor is ejection time of two ventricles Inspiration causes increased right ventricular venous return with prolonged ejection time, thus delaying P2 At the same time, increased right ventricular volume causes decreased left to right shunt, causing longer left ventricular ejection time and delayed A2 As a consequences, there is no inspiratory widening of S2 Another cause of wide fixed splitting is severe right ventricular systolic dysfunction Wide expiratory splitting is due to prolonged right ventricular ejection time During inspiration the failing right ventricle cannot increase its stroke volume or ejection time and S2 remains fixed Wide split is appreciable when RBBB is associated with right ventricular failure Pseudofixed splitting: Sometimes S2 is mistakenly diagnosed as having fixed splitting In children with rapid respiratory rate, there is little variation of right ventricular volume and S2 appears fixed A late systolic click before S2 and an opening snap after S2 may be mistaken as wide fixed S2 Narrow split in ASD: In ASD, the split may be less than 60 msec Grade of shunt, probably is not related with degree of splitting Splitting in Pulmonary Hypertension Expiratory splitting usually persists Inspiratory splitting in pulmonary hypertension depends on two opposing factors Pulmonary hypertension causes prolonged right ventricular ejection with delayed P2 At the same time it causes decreased pulmonary capacitance and hang-out time resulting in narrow S2 Inspiratory splitting is usually preserved; loud P2, however, may mask A2 in pulmonary area; then, split can better be assessed at the apex In MS with pulmonary hypertension, split is physiological In MR with pulmonary hypertension, split is wide In VSD with hyperkinetic pulmonary hypertension, split is physiological, whereas in Eisenmenger syndrome, S2 is single In ASD, both with hyperkinetic or obstructive pulmonary hypertension, split is wide and fixed In PDA with hyperkinetic pulmonary hypertension, split may be physiological or reverse, whereas in Eisenmenger syndrome, splitting is physiological In idiopathic PAH, expiratory splitting can be appreciated and inspiratory splitting is narrower Reverse Splitting (Fig 15-4) Reverse splitting is appreciable when S2 is splitted during expiration and becomes narrow or single during inspiration During expiration, A2 shifts Second Heart Sound (S2) Fig 15-4: Reverse split: S2 in AS Here, A2 is delayed In inspiration, P2 is delayed Thus, A2 merges to P2 in severe AS in inspiration In expiration, P2 occurs earlier as usual, and A2 is delayed, resulting in wider split beyond P2 Inspiration have its usual effect on S2, i.e P2 is delayed That results in either closely splitted or single S2 during inspiration Common cause of reverse splitting is delayed electrical activation of the left ventricle, like, LBBB, right ventricular pacing and pre-excitation of the right ventricle Prolonged left ventricular ejection time is another cause of reverse splitting Increased left ventricular stroke volume, like Severe AR, large PDA and left ventricular outflow obstruction, like AS, HCM cause prolonged left ventricular ejection time (Table 15-3) TABLE 15-3 Reverse splitting Electrical causes: LBBB Right ventricular pacing WPW syndrome Mechanical causes: Increased LV stroke volume (Severe AR, Large PDA) LVOT obstruction Ischemic episodes LV systolic dysfunction 121 122 Bedside Cardiology Reversed splitting can be classified as: • Type 1: S2 is usually single during inspiration, and reversely splitted in expiration • Type 2: S2 shows normal inspiratory splitting and reverse splitting in expiration • Type 3: S2 in single in inspiration, as well as in expiration, though A2P2 sequence is reverse in expiration This is because, during reverse splitting, P2-A2 separation is less than 20 ms Reverse splitting can be occasionally found in ischemic heart disease, during acute ischemic event Severe left ventricular systolic dysfunction is another cause of reverse splitting, particularly when it is associated with LBBB Persistently Single (Table 15-4) Single S2 in both phases of respiration can occur when either of the two components is absent or two components remain synchronous P2 is absent in pulmonary atresia, severe PS, dysplastic pulmonary valve, Truncus arteriosus and absent pulmonary valve Pulmonary component is present but inaudible in conditions where pulmonary artery is abnormally positioned, like DTGA or other malposed great arteries Aortic component is absent in calcific aortic stenosis or aortic atresia Both the components occur simultaneously in VSD with bidirectional shunt, having TABLE 15-4 Single S2 Absent P2 Pulmonary atresia Severe PS and dysplastic pulmonary valve Truncus arteriosus Absent pulmonary valve Occasionally in old age Inaudible P2 D-TGA MPGA Absent A2 Calcific AS Aortic atresia Inaudible A2 Loud P2 in pulmonary area Loud pansystolic murmur (VSD, MR) Prolonged ejection systolic murmur (PS) Synchronous A2 and P2 VSD with bidirectional flow Single ventricle Second Heart Sound (S2) equal pulmonary and systemic vascular resistance Sometimes, P2 is inaudible in old age with increased anteroposterior diameter of chest Intensity Loudness or intensity of S2 depends on the closing force, which is the diastolic gradient across the aortic and pulmonary valve This gradient between aorta and left ventricle is much higher than between pulmonary artery and right ventricle For this reason, A2 is louder than P2 This loudness makes A2 audible both at the base as well as apex, whereas P2 is audible at the left second or third intercostals space That left ventricle forming the apex can be another contributing factor for the transmission of A2 at the apex A2 is louder than P2 in 95% cases, even at left 2nd intercostal space Normally, P2 is not audible down to the 2nd intercostal space and only in 5% cases, it is audible at apex Commonest cause of loud A2 is Hypertension, hyperkinetic circulation and aneurysm of the ascending aorta Hyperkinetic flow causes stretching of the aorta by increased volume during systole with vigorous recoiling during diastole contributing to loud A2 Diminished intensity of A2 is calcific AS and severe AR Cause of louder P2 is pulmonary hypertension Left to right shunt by increasing flow along with dilatation of pulmonary artery and hyperkinetic circulation by increasing flow also cause loud P2 P2 is equal to A2 in mild PAH; louder than A2 in moderate PAH; it becomes audible all through the precordium in severe PAH Apical transmission of loud P2 in PAH caused by mitral stenosis and VSD, is somehow rare A very loud P2 can mask A2 in pulmonary area P2, without PAH is usually not audible at apex When apex is formed by the right ventricle as in ASD or primary tricuspid regurgitation, P2 is audible at the apex with normal pulmonary artery pressure Depressed sternum may cause louder S2, due to the closer proximity of the chest wall with the heart Further Reading Curtis EL, Mathews RG, and Shaver JA Mechanism of normal splitting of the second heart sound Circulation 1975;51:157 Gray I: Paradoxical splitting of the second heart sound Br Heart J 1956;18:21 Harris A and Sutton G Second heart sound in normal subjects Br Heart J 1968 30:739-42 Sutton G, Harris A and Leatham A Second heart sound in pulmonary hypertension Br Heart J 1968;30:743-56 123 16 Third Heart Sound (S3) Physiology (Fig 16-1) S3 is a low frequency, low-pitched ventricular filling sound It follows A2 by 120 to 200 ms in the ventricular early rapid filling phase and coincides with y descent of the atrial pressure pulse Sudden halting of the opening AV valves in early diastole or the impact of the ventricular wall on the chest wall are some of the mechanism suggested, regarding the genesis of S3 Sudden deceleration of the blood flow after opening of the AV valve, setting the cardiohemic system in vibration and producing the S3, is the most acceptable mechanism Fig 16-1: Physiology of S3: During rapid ventricular filling phase, higher atrial-ventricular gradient, due to higher v wave causing higher atrial pressure and rapidly expanding ventricle with lower filling pressure causes S3 How to Detect it S3 is relatively a faint sound and often can be missed It can be best picked up by the bell of the stethoscope lightly pressing on the skin at the apex, the patient lying in left lateral decubitus in a quiet room Coughing a few Clinical Approach: Congential Cyanotic Heart Disease Increased flow: Truncus Arteriosus ASD, Eisenmenger Physiology Thus, X-Ray chest may identify the individual entities amongst the group Increased flow-4 common causes: TGA TAPVC Truncus arteriosus L-R shunt leading to EP 221 222 Bedside Cardiology X-Ray Chest with Decreased Flow Hilum appears less dense and smaller in size Intrapulmonary arteries appear small in size Lungs appear more translucent Then, Probabilities are Shortlisted to Entities under the umbrella of tetralogy physiology Then, to look at ECG: Left axis; vectorcardiogram: Counterclockwise depolarization in frontal plane Now, probabilities are shortlisted: Tricuspid atresia Univentricular connection, noninverted outlet chamber (From type of apex, ECG and X-Ray chest, individual entity can be established) Clinical Approach: Congential Cyanotic Heart Disease ECG: Right, occasionally left axis, counterclockwise depolarization DORV, PS Otherwise, ECG may show right axis; vectorcardiogram showing clockwise depolarization in frontal plane Then, probabilities are shortlisted to: TOF TGA, VSD, PS Univentricular connection, PS, inverted outlet chamber (Individual entities described in tetralogy physiology) 223 27 Clinical Approach: Tetralogy Physiology Tetralogy Physiology Obstruction at the outlet, which is supporting pulmonary circulation, resulting in the supporting ventricular pressure at systemic level This ventricle will now decompress through large septal defect, resulting in balanced or predominontly right to left shunt Tetralogy Physiology: Hemodynamics Septal defect is a nonrestrictive, large one, resulting in equalization of two ventricular pressure Direction of the shunt will depend upon the resistance in the pulmonary and systemic circulation It may be bidirectional with dominating R-L / dominating L-R, or it may be exclusively R-L As right ventricle, though working against systemic pressure, is decompressed through large septal defect, its’ force of contraction will be not manifested in the jugular pulse pressure or precordium Clinical Approach: Tetralogy Physiology As right ventricular blood is mostly shunted through VSD in systemic circulation, pulmonary flow and pressure will be inadequate to produce an audible P2.On the other hand, enhanced flow through aorta and its malposition may produce a loud A2 and aortic click More severe will be the pulmonary stenosis, more blood will pass in the aorta, resulting in shortening and softening of the murmur across the pulmonary outflow In all the entities of tetralogy physiology, excepting TOF, great arteries may be malposed Commonly, aorta is right and anterior or left and anterior This positional abnormality may alter the clinical finding A2 may be more prominent, sometimes, palpable Best audible position may be left or right base Thus, the common hemodynamic feature in tetralogy physiology is equalization of two ventricular and aortic systolic pressure with a pressure gradient between pulmonary artery and the supporting ventricle In TOF, the aortic saturation is higher than pulmonary circulation When in mixing physiology situations, behaving as tetralogy physiology, mixing is adequate, saturation in both arteries should be same In transposition physiology behaving as tetralogy physiology, saturation in pulmonary artery may be higher than the aorta One should remember that the saturation in great arteries depend upon the mixing, streaming and location of VSD in relation of the great arteries Tetralogy Physiology: How to Grade Severity* Severity is determined by the grade of pulmonary stenosis Accordingly, it is graded as mild, moderate, severe and extremely severe Mild Usually acyanotic at rest; cyanosis is revealed on exercise Aortic click is absent A soft P2 may be audible with a wide split Pulmonary ejection murmur is loud, grade III–IV, reaches at crescendo after midsystole and extends at A2, which is not obscured by the murmur * • • Vogelpoel L, Schrire V Auscultatory and phonocardiographic assessment of fallot’s tetralogy Circulation 22: 73, 1960 Mccord M, Van Elk J and Blount S Tetralogy of Fallot: Clinical and hemodynamic spectrum of combined pulmonary stenosis and ventricular septal defect Circulation 1957;16;736-49 225 226 Bedside Cardiology Moderate Grade II cyanotic burden Aortic ejection sound is absent A2 is prominent; P2 is not audible Pulmonary ejection murmur is grade II–IV reaches peak at midsystole, and ends before A2 Severe Grade III cyanotic burden Aortic click may be found occasionally A2 is louder Pulmonary ejection murmur is grade II–III, reaches at peak before midsystole and ends well before A2 Extremely Severe Severe cyanotic burden Aortic click is consistently present A2 is louder Pulmonary ejection murmur is soft, reaches early crescendo, ends long before A2 Under Umbrella of Tetralogy Physiology Group I (Pure) Fallot’s tetralogy VSD, pulmonary atresia VSD, PS DORV, PS CC-TGA, VSD, PS Group II (Mixed physiology) A Transposition + tetralogy physiology TGA, VSD, PS B Mixing + tetralogy physiology Tricuspid atresia, VSD, PS Univentricular connection, PS Clinical Approach: Tetralogy Physiology Tetralogy Physiology: Fallot’s Tetralogy Cyanosis typically appears between weeks and months of age Hypoxic spell Squatting Single, prominent S2 (A2) Ejection systolic murmur across RVOT is best heard in left 3rd intercostal space with radiation to 2nd and 1st spaces Axis is downward and right with clockwise depolarization RVH: Tall R eave in V1 with a transition to rS pattern from V2 onwards T wave in right precordial leads may be upward or downward in equal number of cases Persistent rS pattern up to V6 indicates minimal pulmonary flow with under filled LV A prominent R wave and initial q in V5–6 indicate reasonable pulmonary flow with balanced shunt Tetralogy Physiology: VSD, Pulmonary Atresia Cyanosis appears earlier than TOF (when pulmonary circulation is supported by large PDA or several MAPCAs, cyanosis may be delayed or inconspicuous) History of spell or squatting is uncommon S2 is always single Aortic click, best heard at right upper sternal border and may be audible at left sternal edge and apex, i.e it has wider range of audibility The click does not vary with respiration Its later onset in systole gives the impression of “wide splitting” of the first sound Pulmonary ejection murmur is absent A soft systolic murmur, due to flow into the aorta may be present Continuous murmur is the hallmark It is present in 80% cases, best heard beneath the clavicle, back of the chest, right or left or both Systolic portion may be prominent and one may miss the diastolic part X-ray Chest: VSD, Pulmonary Atresia Vessels pattern is prominent but disorganized with a stringy or reticulated appearance 227 228 Bedside Cardiology Most importantly, the hila are not large and are disorganized or even inappearent in the lateral view The arteries seem most prominent over the area of the main stem bronchi Tetralogy Physiology: DORV, PS Clinically, it is indistinguishable from Fallot’s tetralogy When great arteries are malpositioned and aorta is more anterior, A2 is more prominent When VSD is restrictive, an obligatory flow from left ventricle to right ventricle can produce a long systolic murmur Left ventricle may be hypertrophied and may impart a palpable impulse Other than RVH and right axis, the distinguishable features in ECG from Fallot’s tetralogy are: Counterclockwise depolarization, with q waves in lead I and aVL.(*) Deep and prolonged terminal forces like, broad and slurred S in lead I, aVL, V5–6, and wide R in aVR When PS is mild and occasionally when it is severe, axis may be left.(*) Prominent left ventricular forces.(**) Right bundle branch block (**) AV delay with prolonged PR interval (**) * Krongard E, Ritter DG, Weidman WH and Dushane JW Hemodynamic and anatomic correlation of electrocardiogram in double outlet right ventricle Circulation 46: 995, 1972 ** Mirowski M, Mehrlizi A and Taussig HB The Electrocardiogram in patients with both great vessels arising from the right ventricle combined with pulmonary stenosis Circulation 28: 1116, 1963.) Clinical Approach: Tetralogy Physiology Right axis deviation, counterclockwise depolarization, RVH, preserved LV force in V6 in DORV, VSO, PS Tetralogy Physiology: CC–TGA, VSD, PS Left-anterior ascending aorta Aorta anterior to pulmonary artery As ascending aorta forms a leftward sweep, aortic click and A2 are more prominent Aortic pulsation and A2 may be palpable All these are, rather in pulmonary area, away from left sternal edge Pulmonary ejection murmur radiates more rightward (as) Tetralogy Physiology: Univentricular Connection, PS Most commonly, apical impulse is left ventricular type A2 and aortic clicks are more prominent A prominent long systolic murmur, pansystolic in nature, may be audible at mid left sternal edge, due to obligatory flow from ventricle through bulboventricular foramina into outlet chamber When the bulboventricular communication is restrictive, murmur becomes midsystolic in nature It radiates towards right base with noninverted outlet chamber and left base with inverted outlet chamber Tetralogy Physiology: Univentricular Connection, PS Noninverted Outlet Chamber Left axis/indeterminate axis 229 230 Bedside Cardiology Counterclockwise depolarization Classical stereotyped rS complex from V1 to V6 Inverted Outlet Chamber Rightward axis Prominent R in V1 rS from V2 to V5 If there is R in V6, initial q wave will be absent Tetralogy Physiology: TGA, VSD, PS • As with other malposition, A2 is loud and may be palpable • Pulmonary ejection murmur is usually inaudible due to posterior location of pulmonary artery When audible, it is usually transmitted rightward direction, due to the disposition of pulmonary artery Classical TGA X-ray chest Classical picture of simple TGA is lost Egg-on-side is not seen, as left heart chambers are small, occupied by right–sided chambers There is decreased vascularity Narrow pedicle is widened because of dilated ascending aorta ECG Peaked p for enlarged RA; right axis; RVH; T waves are seldom inverted in right precordial leads TGA, VSD, PS Clinical Approach: Tetralogy Physiology Tetralogy Physiology: Tricuspid Atresia, VSD, PS • A prominent a wave in the jugular pulse • Left ventricular type apical impulse • Absent right ventricular impulse • Always single S1 ECG • Left axis deviation and counterclockwise depolarization • Prominent p wave • Adult progression in precordial lead • X-Ray chest • Prominent right atrium, convex LV, absent RV (best seen in LAO view) 231 Index Page numbers followed by f refer to figure and t refer to table A Abdominal aortic disease 85 Abnormal venous pulse 67 Anacrotic pulse 79 Anderson classification 207 Anemia 54 Angina 235 Angiographic identification 196 Aortic arch syndrome 85 click 218 dissection 85 pressure 132f valve 132f valvular click 132f Apical impulse 2, 100 in constrictive pericarditis 109f Atrial septal defect 237 Atrioventricular connection 191, 198 Augmentation index 98 Axillary artery aneurysm 57 B Becker’s sign 85 Bedside assessment of heart failure 180 Bisferiens pulse 79 Biventricular impulses 106f Bladder length 51f Brachial arteriovenous malformation 57 Bronchial asthma 84 C Canadian Cardiovascular Society 7, 10 Carcinoid disease 159 Cardiac causes of hemoptysis 27 defects 40, 41 malposition 191 myxoma 57 Carotid aortic bodies 14 arteries 88 pulse 66f Cause of death 239 Center of right atrium and sternal angle 62f Central point of bladder 51f Changes of pulse waves during peripheral transmission 76f Chest pain 20 Chronic severe MR 152f Classification of angina pectoris Clinical classification of pulmonary hypertension 186 Coarctation of aorta 85, 87f Common atrium 234 Commonest diseases 18 Condition of arterial wall 84 Congenital absence of pericardium 103 cyanotic heart disease 219 heart disease Congenitally corrected transposition of great arteries 229 Congestive heart failure 28 Conotruncal facies 42f Constrictive pericarditis 159 Continuous murmur 160 of PDA 161f Corrigan’s sign 85 Cyanosis 52 Cyanotic heart disease 109 D De Musset’s sign 85 Definition of pulmonary hypertension 186 Dennison’s sign 86 Depressed left ventricular systolic function 103 Diastolic murmur 153 Dicrotic pulse 79 Different diastolic murmur 154f prosthetic valves 140f shapes of murmur 143f systolic murmur 145f Dilated aortic knuckle 238 242 Bedside Cardiology Dissection of aorta 85 Double beating pulse 79 inlet right ventricle 199 ventricle 198, 199 outlet right ventricle 228 peaked pulse 80 Down’s syndrome 37f, 232 Duke activity status index 10 Duroziez’s murmur 86, 155 Dyspnea 1, 14, 235 Hypercalcemia 40 Hyperdynamic apical impulse 102 Hyperkinetic impulse 105 Hypertensive PR 157f Hypertrophic cardiomyopathy 147 Hyperviscosity syndrome 32, 235 Hypokinetic apical impulse 102 Hypoxia 14 Hypoxic spell 227 I Early systolic murmur 152 Ebstein’s anomaly 217, 218 Eisenmenger complex 238 physiology 214, 217 syndrome 26, 233, 234, 237-239 Ejection systolic murmur 144 Electronic stethoscope 47 Infective endocarditis 57 Inner intercanthal distance 41 interorbital distance 43 Innocent murmur and sound 166 Interpupillary distance 41 Irregular cannon waves 71 Ischemic heart disease 109 Isolated tricuspid stenosis 159 Isometric handgrip 174 Isovolumeric contraction 132f F J Fallot’s tetralogy 227 Fatigue 25 Femoral pulse 87 First heart sound 111 Forceful and sustained impulse 105 Forearm pressure 94f Functional capacity Jugular venous pressure 1, 60 pulse 59, 217 E K Kartagener syndrome 197 L G Gerhardt’s sign 86 Graham Steell murmur 218, 236 Great artery spatial relations 191, 211 H Hamman sign 139 Hand-held echocardiogram 48f Heart failure 182 symptoms 235 sound 2, 66f, 217 Hemodynamic congestion 179 Hemoptysis 234, 235 Hepatic pulsation 86 Hill’s sign 86 Holt-Oram syndrome 40f Landolfi’s sign 85 Late systolic murmur 153 Law of conservation of energy 92 Left anterior ascending aorta 213 carotid artery 88f ventricular end-diastolic pressure 28 enlargement 102 systolic movement 100f Leg pressure 95f Leriche syndrome 85 Lower pulmonary artery 130f M Marfan syndrome 36f Mayne sign 86 Index Mean corpuscular volume 55 pressure 91 Mediastinal crunch 139 Medullary center 14 Metacarpal index 34 Mid-diastolic murmur 236 Midsystolic click 134 murmur 144 pulmonary flow murmur 236 Minervini’s sign 85 Minor symptoms in cardiovascular system 25 Mitral component 111, 114f opening snap 135 regurgitation 150 stenosis 26 Muller’s sign 85 Multiple heart sound 218 Murmur 3, 218 of AR 155f of PR 157 N New York Heart Association Noncardiac surgery 239 Nonejection click 134f Noonan syndrome 39f Normal apex cardiogram 100f ear 44f venous pulse 65 ventriculoarterial connection 208 O Ocular hypertelorism 43 Orbital hypertelorism 43 Origin of pulse 75 Osler’s sign 98 Outer intercanthal distance 41 interorbital distance 43 P Palfrey’s sign 86 Pansystolic murmur 149 Paroxysmal hypoxic spell 31 Patent ductus arteriosus 237 Pectus carinatum 36f excavatum 36f, 103 Pericardial rub 138 sound 138 Persistent splitting 117 Physiologic components of dyspnea 14 Plateau murmur of VSD 161f Polysplenia 197 Popliteal artery pulse 89 Position of aorta relative to midline 198 atria 198 cardiac apex 198 liver and gallbladder 198 Premature beat 176 Pressure curves 67f overload 128 Proportional pulse pressure 91 Prosthetic sound 139 Proximal aortic pulse 76f Pulmonary arterial hypertension 233 artery 213 atresia 227 click 218 ejection click 236 murmur 230 stenosis 147, 218 valvular click 130 Pulmonic stenosis 228-231 Pulsatile cervix 86 Pulse in hypertension 85 pressure 91 widens 82f Q Quincke’s sign 85 R Raised end diastolic pressure 128 Range of acceptable arm circumference 51f Regular cannon waves in junctional rhythm 72f Respiratory muscles 14 Retinal artery pulsation 85 243 244 Bedside Cardiology Reverse differential cyanosis 53 Right atrial myxoma 159 carotid artery 88 ventricular end-diastolic pressure 130f Rightward axis 230 Rosenbach’s sign 86 S Scamroth’s sign 57f Scoliosis 103 Second heart sound 115 Severity of AS 147 atrial fibrillation scale 10 MS 158f PS 148 Silent valvular disease Simultaneous palpation of both brachial arteries 88f radial and femoral arteries 89f Situs ambiguous 192 inversus 192 solitus 192 Six-minute walking test 11 Sphygmomanometer 49 Splenic pulsation 86 Stethoscope 46 Subclavian artery obstructive disease 85 Substernal chest pain 21 Subvalvular stenosis 146 Supraclavicular fossa 168 murmur 168f Supravalvular stenosis 85, 146 Systolic murmur 144 T Telecanthus 43 Timing of murmur with carotid artery 143f Tracheal tug 107 Transient arterial occlusion 175 Transposition of great arteries 230 Traub’s sign 86 Trepopnea 18 Tricuspid atresia 217, 222, 226, 231 regurgitation 151 Triple apical impulse 107 Truncal regurgitation 218 Truncus arteriosus 216, 219, 221, 232, 234 Turner syndrome 37f U Ultrasound stethoscope 47 Univentricular heart 216, 217 Uvular pulsation 85 V Valsalva maneuver 174f Venous pulsation in atrial fibrillation 72f constrictive pericarditis 73f pulses 74 Ventricular loope 191 septal defect 151, 227, 229-231, 237 Ventriculoarterial connection 191, 206, 208 Visual analog scale 17, 17f W WHO classification of functional status in pulmonary arterial hypertension Wide pulse pressure 98 William syndrome 41f ... 19 -2 and Fig 19-4) TABLE 19 -2 MS vs ASD Similarities S2-OS/A2-P2 Diastolic murmur Differences Inspiration Standing MS ASD S2-OS MS A2-P2 Flow murmur A2-P2-OS S2-OS narrows OS intensity downs S2-OS... downs S2-OS widens A2-P2 A2-P2 widens P2 intensity ups A2-P2 narrows Fig 19-4: MS vs ASD: In ASD, in both phases of respiration, there will be two components around S2 (A2 and P2) In MS, whereas... mentioned Fig 20 -2: Timing of the murmur with carotid artery 143 144 Bedside Cardiology Dynamic Auscultation Described separately Systolic Murmur (Table 20 -2) (Fig 20 -3) TABLE 20 -2 Types of systolic